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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
Western University ojHealth Sciences
Department oJOsteopathic Manipulative Medicine
Pomona, California
College oJOsteopathic Medicine oJthe Pacific
ROBERT E. KAPPLER, D.O., F.A.A.O.
Western University ojHealth Sciences
Professor and Chair
Pomona. California
Department oJOsteopathic Manipulative Medicine
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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© 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
THIS PAGE INTENTIONALLY LEFT BLANK
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.
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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
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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
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OSTEOPATHIC PHILOSOPHY AND HISTORY
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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
1. Osteopathic 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
1. Osteopathic Philosophy and History
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
1. Osteopathic Philosophy
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
1. Osteopathic Philosophy and History
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.
1. Osteopathic Philosophy
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
f Osteopathic Philosophy and History
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,
1. Osteopathic Philosophy
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
1. Osteopathic Philosophy
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
I. Osteopathic Philosophy and History
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.
1. Osteopathic Philosophy and History
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
I. Osteopathic Philosophy and History
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
1. Osteopathic Philosophy and History
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;
2. Major Events in Osteopathic History
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
2. Major Events in Osteopathic History
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
I. Osteopathic Philosophy and History
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
2. Major Events in Osteopathic History
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
f Osteopathic Philosophy and History
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
Today, t h e practice of med i c i ne needs as never before t h e guiding and i n teraction o f a l l body systems. I t should apply known truths
of osteopathic
tion. Available at: http://www.aoa-net.org/AOAGeneral/tenets.htm. Ac
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.
2. Major Events in Osteopathic History
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.
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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.
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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.
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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.
Osteopathic Considerations in the Basic Sciences
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.
Osteopathic Considerations in the Basic Sciences
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.
Osteopathic Considerations in the Basic Sciences
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.
Osteopathic Considerations in the Basic Sciences
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.
Osteopathic Considerations in the Basic Sciences
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<1r fa.�ial. �q;ptuTT\
FIGURE 4.19. Diagrammatic representation of a transverse section through the arm, illustrating the organization of superficial and deep fascia. Deep fascia divides the arm into compartments by way of inter muscular septa.
perficial fascia (Figs. 4.5 and 4 . 1 9) . It contains collagen fibers as well as variab le amou nt s of fat . Superficial fascia serves ro i ncrease skin mob i l it y, acts as a t hermal insu laror, and srores energy for met abolic use. The dense connect ive t issue enve lope, wh ich invests and separates individual muscles of the l i mb s and t ru nk, is deep fascia. It is also composed primarily of collagen fibers. Between individual muscles there is a fas cial plane, which represents t he separat ion of t he connect ive
Medial antebrachial
Median n.
Basilic v.
Musculocutaneous n.
Med. brach. cutaneous n.
Fascia and Neurovascular Bund le
Fascia is a derivat ive of mesoderm. Throughout the b ody t here is a sub cut aneous layer of loose connect ive t issue called the su -
Neurovascular
l&�rfj�@����-- Cephalic v.
bundle Medial inter-
---ttffl�;:;;:::
muscular septum
���I!f!ijR\1rN�- Brachialis m. ���TtFI'1t-- Humerus
Lateral inter
'ii!.5.�it9-+l--_ muscular septum
Penetrating fibers
Ulnar n.
Neurovascular bundle: Radial
Muscle flber
Sup. ulnar
collateral a.
collateral
Radial n.
a. and v.
Int. perimysium-
Triceps m.:
{
lateral head
Ext. perimysiumMu,de fa,d
collateral Subcutaneous fat and connective tissue
I
Tendon FIGURE 4.18. Diagrammatic representation of how muscle attaches to bone. (Source unknown.)
Long head FIGURE 4.20. Transverse section through the arm. Neurovascular bun dles are found between skeletal muscles in anterior and posterior compartments.
4. Anatomy
53
\1; ....-- Psoas fascia Anterior layer of thoracolumbar fascia (quadratus lumborum fascia) Transversus aponeurosis Transversus aponeurosis
A
Internal oblique External oblique
J
Middle
Latissimus dorsi Intertransversarius
Interspinalis
Tip of transverse process
L-____ Posterior
Layers of thoracolumbar fascia
Erector spinae, aponeurosis of origin
Rotatores Transversospinalis
Erector spinae
Trapezius
Serratus posterior Latissimus dorsi
FIGURE 4.21. Transverse section through the back, illustrating the organization of deep fascia. The deep fascia serves to divide the back into compartments for muscles of similar function.
tissue invest ment (wrapper) of the indiv idual muscles. In the li mbs, back, an d neck, deep fascia passes over and between mus cle groups an d connects t o bone periosteum. The deep fasci a passing between muscle groups in the l i mbs is called intermus cular septa. These intermuscular septa, toget her wit h the deep fascia in the limbs an d deep fascia in the back an d neck, pass over an d between muscle groups serving to compartmentaliz e muscle groups of similar fun ctions an d innerv at ions (Figs. 4.204.22). Deep fasci a between individual muscles, which move ex-
ten sively, i s loose conn ect ive tissue and faci litates movement . As a connect ive t issue, fascia provides for mobility an d stab il ity of the musculoskeletal system. Myofascial contin uity can be found t h roughout t he body. This will be d iscussed in detail later in t he chapter. Furt her det ails regarding t he st ructure and fun c t i on of fascia can be foun d in Chapter 3, "R ules of Anatomy" (11). Peripheral n erves an d blood an d lymph vessels lie in fascia, loose connective t i ss ue, between muscles. This fascia serves to
54
Jf
Osteopathic Considerations in the Basic Sciences Nuchal ligament Vertebral arch of
POSTERIOR
cervical vertebra
Supertical cervical fascia (subcutaneous tissue)
Middle scalene Retropharyngeal space Lymph node
������I§�����!;� ���t=�
Anterior scalene Longus colli --Alar fascia
-Tr--r'Ti'� === ---iT-rinM mr
Omohyoid
--�-w
Sternocleido· mastoid
---'���
Skin
Carotid sheath
Vagus nerve
Internal jugular vein Common carotid artery Esophagus
Pretracheal fascia
A
Investing fascia
Prevertebral fascia Retropharyngeal space
Mandible Investing fascia ---;-:;JI�\
Pre tracheal fascia ---hm-'-;�
B
Manubrium --H-' E
FIGURE 4.22. Transverse section through the neck, illustrating the organization of the deep fascia. The deep fascia divides the neck into muscular, visceral , and neurovascular compartments.
bind together these n erves and vessels, an d collect ively t h e com ponents form the neurovascular bun dle (Fig. 4.20). Muscle Action
A muscle contracts because it is st i m ulated by a motor nerve. A single motor n erve fi ber innervates more than one skeletal muscle fi ber. The nerve fiber an d all the m uscl e fibers it innervates are
called the motor unit (Fig. 4.23). In general, small muscles that react quickly (e.g., extraocular muscles) have ten or fewer muscle fi bers innervated by a single nerve fiber. In contrast , large muscles which do n ot require fine cent ral nervous system cont rol (e.g., deep back muscles) may have up t o 1,000 muscle fibers in a motor un it. When a muscle is rest ing, some motor un its are always discharging. It may n ot be the same motor un its at each instance in t ime. This type of motor act ivity (muscle tone) is the
4. Anatomy
55
Most movements require the combined action of several mus cles. The term " prime mover" is used for those muscles that act directly to bring about the desired movement. Every muscle. which acts on a joint, is paired with another m uscle that has the opposite action on the same joint. These muscles are antagonists of each other (e.g., biceps brachi i , A ex o r; triceps, ex tensor) . An antagonist does not signi ficantly block the action of the prime mover. Its pri mary effect only occurs at the i n i tiation of the move ment after which it relaxes until the movement is fi n ished. There are times when prime movers and antagonists con t ract tOgether and are called fixatO rs. T h i s occurs to stabil ize a joint or hold a part of the body in an appropriate position. Muscles that con tract at the same time as pri me movers are called synergists. These can be either muscles that aid the p rime movers in the perfo r mance of the desired action or a ntago n ist muscles that contract at the same time as a prime mover and thereby p revent unwant ed movement, which would be counterproductive to the desi red action. I n d ividual muscles should not always be co nsidered as units with a si ngle function. Different parts of the same mus cle may have different, even an tagonistic, actions (e.g delroid muscle). .•
FIGURE 4.23. A motor unit.
background for muscular contraction in the performance of a purposeful movement. When most muscles contract, their fibers act through tendons on moveable bones to get the desi red action ( Fig. 4 . 1 8 ) . Move ments result in the activation of motO r u n i ts in some muscles and the simultaneous relax ation of motO r units in other muscles. Movement that comes about from muscle contraction causes the muscles to change in length. When this occurs, tension created within the muscle re mains constant and the contracti o n is called isotOnic. I f movement does not occur as a result of muscle con traction and muscle length stays constant with el evated tension generated within the muscles, the contraction is called isometric (e.g., posterior compartment muscles of the leg in standing) . Iso tO nic contractions may be concen tric (shorten ing of the muscle) or eccentric (lengthen ing of the muscle).
Post. ne rve
AnL nt2rve
SEGMENTAL ORGANIZATION OF THE NEUROMUSCULOSKELE TAL AND VASCULAR SYSTEMS
A typical transverse section th rough the thoracic region demon strates the basic organization of the ax ial skeleton ( Figs. 4.3 and 4 .2 4) . Throughout the thoracic region, each verteb ral level is organized symmetrically about a central ax is composed of the vertebra, spinal cord, and aorta. The d istribution of a typical spinal nerve and posterior i ntercostal artery are repeated at each segmental level of the thoracic spine (Tl through TI 2). The typical spinal nerve is formed by the union of the ante rior and posterior roOtS j ust lateral to rhe in tervertebral foramen. Within a short distance, the spinal nerve divides to form a pos terior primary ramus and an anterior primary ramus (F ig. 4 . 24) .
,.amus---==��_/
ramus or i nteTcosio\ n
l�fJrco5101
���nCi!OU5 br.
Ext.
'-int.rcoslal 4;.u mczmbron"'--,,<�=...� �""'-'.r-'''-'''' '''
Ani. culoneou� br. -----"
---
(Jnl. mornma,,{
0.1.1
lnt. thora.cic a.rt.
'----perforating (cutoneou�) br.
FIGURE 4.24. Transverse section illustrating contents of a seg mental level through the thorax.
56
If.
Osteopathic Considerations in the Basic Sciences
S2----'.:.;;;-h S3
C6
1+---- L3
�T---L4 S2
S2
S1 \IT"--L4 FIGURE 4.25. Dermatomal maps o f body.
T he pos terior primary ramus is dis tributed to the deep (" true" ) bac k m usc les , t h e s kin over these m uscles , an d t h e j oin ts, whic h the musc les func tionally move. Posterior primary rami dis tribute segmen tally from the base of the skull to the coccyx. The an terior primary ram us in the thorac ic region ( in tercos tal nerve) passes between the muscle layers of the interc os tal s pace an d d is tributes laterally and an teriorly t o s upply t h e m usc les and s kin o f t h e thorax and abdomen. T h e pattern o f thorac ic an d abdominal dis tribution is cI in ically demonstrated as dermatomal bands ft om the bas e of the neck to the pubis (Fig. 4 . 25 ) . The an terior pri mary rami are dis tributed in a more complex manner above an d below the thoracic region (Fig. 4 . 26 ) . The an terior primary ram i of C 1-3 an d C4 form t h e cervical plexus . T he anterior primary rami of C5-8 an d T I form the brac h ial plexus, whic h s uppl ies the upper limb. L umbar an d s ac ral an terior primary rami (Ll-4 an d L5 , S 1-3) form the lumbos ac ral plexus , whic h is dis tributed to the pelvis , perineum, and lower limb.
In the thorac ic region the abdominal aorta gives rise to right and left pos terior in terc os tal arteries , whic h segmentally supply the thorac ic and abdominal walls (Fig. 4 .24). This area of s up p ly incl udes the s kin , s u perfic ial and deep fasc ia, interc os tal and abdominal m usc ulature, ribs , vertebrae, and paravertebral mus c u lature. The costal groove on the in ternal inferior s ur face of eac h rib contains a s egmen tal neurovasc ular bundle, whic h inc ludes the interc os tal nerve and artery, ven ae commitans of the intercos tal artery (in tercos tal veins ) , an d segmental interc os tal lymphatics ( Fig. 4 . 24). T hese s tructures s upply and drain the musc le, con n ec t ive tissue, an d s kin within and over the thorax an d abdomen . The segmental pattern o f neurovasc ular d is tribu tion in the thorax an d abdomen is an example of developmental segmenta tion that the body main tains in the adult. H owever, this segmen tal pattern is modified in the limbs by di fferent ial growth an d development.
4. Anatomy
Terminal Cords Divs. Trks. Roots , , , , branches, ,
, , 'Suprascapular n. , ,
Lat. pect. n. Musculocutaneous
'
Circumflex -----:�"....,.�-�� Radial ---+.,.c--(CJA Median
Med. pect. n.
Ulnar-----f-
To subscapularis teres major lat. dorsi
c
Med. cutaneous nerves of arm and forearm
Iliohypogastric n.
A
'�".....� :...,..,.
Lateral
_ _
femoral
Lumbosacral trunk
Femoral n.---!
Great auricular
Obturator n. ------'--h.
D
'-;:l�_,--t.'C3
Ant. cutaneous
C4
To brachial plexus
B
Phrenic
'\.J.¥-"-t--I--
E FIGURE 4.26. Sp inal cord and plexuses. A: Sagittal view of spinal cord and plexuses. C: Brachial plexus. 0: Lumbar plexus. E: Sacral plexus.
B: Cervical plexus.
Sciatic nerve
57
58
!1.
Osteopathic Considerations in the Basic Sciences
LIMB ANATOMY Upper and Low er Limb s
The anatomy of the upper and lower l imbs is comparable. I f one is to understand this basic anatomy, as well as how the l imbs func tion, then one must understand limb development. The l i m bs are divided i n to four majo r parts. The upper limb is divided i nto the shoulder (shoulder girdle) , arm, forearm, and hand while the lower limb consists of the pelvic girdle, th igh, leg, and foot. The bones of the upper and lower limbs form the appendicular skeleto n . These bones form in situ in the developing limb buds. They begin as mesenchyme, which condenses and differentiates into hyal ine cart i l age bone models. These cartilaginous models eventually ossifY th rough endochondral ossification . Limb mus culature is also derived from mesenchyme but, unlike that which form the bones, muscle mesenchyme is derived from somites ad jacent to the developing neural tube and migrates i n to the limb bud from the hypomere, where it condenses adjacent to the devel oping bones ( Fig. 4.4). As the l i m b elongates, the muscular tissue splits i nto Aexor (anterior) and extensor (posterior) components. I n itially the muscles of the li mbs are segmental i n character, but in ti me, they fuse and are com posed of m uscle tissue from sev eral segments. Upper limb buds are opposite neural tube (spinal cord) segments C5 -8 and T I , while lower l i m b buds lie opposite segments L2-5 and S I and S2. As the l imbs grow, posterior and anterior branches derived from a n terior primary ram i of spinal nerves penetrate i n to the developing muscles ( Fig. 4.4). Poste rior branches enter extensor m usculature while anterior branches enter Aexor m usculatu re. Wirh development, the segmental posterior and a n terior branches from each anterior primary ramus unite to form large posterior and a n terior nerves. This union of the original segmental posterior and anterior branches from each anterior primary ramus is the basis for the formation of the brachial and lumbosacral plexuses (Fig. 4 . 26 ) , and comes about with the fusion of segmental muscles. The large posterior and anterior nerves are represented i n the adult upper l i m b as the radial nerve supplying extensor musculature and the median and ulnar nerves innervati ng Aexor musculature, respectively (Fig. 4 . 26 ) . I n the adult lower limb, the large posterior and anterior nerves are represented as the femoral and common fibular nerves supplying extensor musculature and the tibial nerve supplying flexor mus culature, respectively (Fig. 4 . 26 ) . Contact between nerves and differentiating muscle cells is a prerequisite for complete func;onal muscle differentiation. The segmental spi nal nerves also provide sensory i n nervation of the l i m b dermatomes. The origi nal segmental dermatomal patrern is modified with growth of the li mbs, but an orderly sequence is presem i n the adult (Fig. 4.27). As d iscussed earlier, the development of the upper and lower limbs is similar. H owever, there are two differences. First, the lower l i m b develops later than the upper limb. Second, the l i mbs rotate in opposite directions. The upper limb rotates 90 degrees laterally so that the elbow poi n ts posteriorly; the extensor mus culature l ies on lateral and posterior surfaces while the Aexor musculature lies on anterior and medial surfaces; and the thumb lies laterally on the amerior facing palm. The lower limb rotates 90 degrees med ially so that the knee points anteriorly, the exten sor muscles are on the amerior surface while the Aexor muscles
Preaxial
5th week
border
(
----
'-.
D
A
)
..2
-......,
L
3J
Postaxial border Later in 5th week
Ventral axial lines Adult
84
C8
T1
T1
F
c Anterior Aspect
Posterior Aspect
FIGURE 4.27. Developing dermatomal patterns in upper (A-C) and lower (D-F) limbs. A-C: A nterior view, upper limb. 0 and F: Posterior view, lower limb. A, B, 0 and E: Limb buds in embryo. C and F: Adult limbs.
are on the posterior surface, and the big toe is medial. These rotations are necessary based on the functions that the limbs per form. Deep fascia and i ntermuscular septa connecting with bone in the l imbs separate or compartmental ize groups of muscles. The muscles in each compartment share similar fu nctions, develop men tal histories, nerve and arterial supply, as well as venous and lymphatic drainage. Functional Ad aptation
Through their development, the upper and lower li mbs have anatomically adapted to perform different fu nctions. The up per limb is involved in manual activity. It moves freely, espe cially the hand, which is adapted for manipulating and grasp i ng. The stab i l i ty of the upper limb has been sacrificed for mobi l i ty. The digits are the most mobile parts of the upper li mb. The lower l i m b is involved in locomotion, weight bearing, and main taining equilibrium. Because of its weight-bearing funcrion, some movement has been sacrificed in order to ach ieve stabili ty.
MYOFASCIAL CONTINUITY
The concept of myofascial conti nuity is best understood by ex a m i n i ng the attachment of a tendon to a bone. The dense fibrous
4. Anatomy
���������;::---
,"-��--
����il�I���IT= '11b���""�:T>�-
Trapez ius m . Deltoid m. I nfraspinatus m . Teres minor m. Teres major m. Rhomboideus major m. Triangle of auscultation
_Y.�':7f:7H---+--/t-��\�---+--it---
//.���rrr-----il--
59
Through the attachment of the dense regular fi b rous tissue of tendon and l igament to bone a m icroscopic fiber continui ty is found, with the periosteum covering the substance of each bone. The tendon attachment provides d i rect cont i n u i ty of a m uscle at i ts origin and i nsertion to bone. The con nection of tendon to bone provides functional i n tegrity of each part of the body across each synovial j o i n t by way of the muscle-tendon complex, which can best be described as myofascial conti n u i ty (Fig. 4.18). The latissimus dorsi muscle exemplifies the myofascial con tinuity concept. Through attachment to the l umbar spine and i liac crest by way of the lumbodorsal (thoracolumbar) fascia the latissim us dorsi tendon/aponeurosis has continuity with the Aat sheet of skeletal m uscle, which covers the posterior and lateral trunk. The latissimus dorsi muscle then converges to a nar row Aat tendon , which crosses the posterior axilla and i nserts i nto the Aoor of the i n tertubercular groove on the anterior as pect of the h umerus (Figs 4.28 and 4.29). The latissi mus dorsi
Latissimus dorsi m. Ext. abdominal oblique m. Lumbar triangle
Ilium FIGURE 4.28. Superficial muscles of the upper limb located on the back. Notice extensive broad attachment of latissimus dorsi muscle as it covers the posterior and lateral trunk.
connective tissue is anchored to the compact cortical substance of bone by microscopic connective tissue penetrating fibers (Sharpey fi bers). The connective tissue, which then forms the mass of the tendon, becomes feathered to i n terdigitate with the skeletal mus cle fibers, which will form the substance of a given muscle. The same arch itecture is duplicated at the proximal and distal m uscle attachments to bone (Fig. 4.18).
Ax.illary
n.
(Circumflex
n.l � Po!ot. humeraL c:i.rcumn�1(. a.
Triangular 'pa.ce q,.. c:i.Tcumfl.. ,ca�\.Ilar
a.
FIGURE 4.29. Posterior wall of axilla showing attachment of latissimus dorsi muscle into the intertubercular groove of humerus.
FIGURE 4.30. Deep muscles of back provide myofascial continuity from the cranium through the vertebral column to the pelvis.
60
[J.
Osteopathic Considerations in the Basic Sciences TraplZziuc;, S�rn\.�pinali� Capi tis
�-I--.:'��_-
o� -�__������:�� St�rn� i��W: mastoid.
Sup. Obtiqu�
Longis�. Capiti�
���f1"- lrans. prOC(l5S, C 1
Inf. Oblique --Tf.fii1
fI--'=:- Ve rtebrc.l art�ry
GrlZa.tlZr
Trans. p rocess, C Z
occipital n.
5 pleniu""
Interspinali':>
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
Jf
Osteopathic Considerations in the Basic Sciences
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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
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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!.
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Osteopathic Considerations in the Basic Sciences
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.)
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Osteopathic Considerations in the Basic Sciences
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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Osteopathic Considerations in the Basic Sciences
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
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Osteopathic Considerations in the Basic Sciences
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
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Osteopathic Considerations in the Basic Sciences
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
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Osteopathic Considerations in the Basic Sciences
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
77
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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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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Osteopathic Considerations in the Basic Sciences
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
82
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Osteopathic Considerations in the Basic Sciences
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
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Osteopathic Considerations in the Basic Sciences
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.
85
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.
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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.
•
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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5. Biomechanics
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73. Bigliani LU, Kelkar R, Flarow EL, et al. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop. 1 996;330: 1 3-30. 74. Zuckcrman JD, Matsen FA. Biomechanics of the shoulder. In: Nordin M, Frankel V[-I , eds. Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, PA: Lea & Febiger; 1 989:225-247. 75. Poppcn N K, Walker PS. Forces at the glenohumeral joint in abduction. Clin Orthop. 1 978; 1 35: 1 65- 1 70. 76. King AI, Prasad P, Ewing CL. Mechanism of spinal injury due ro cau docephalad accelcration. Orthop Clin North Am. 1 975;6: 1 9-3 1 . 77. EI-Bohy AA, King A I . I n tervertebral disc and facet contact pressure in axial rorsion. In: Lantz SA, King AJ, eds. Advances in Bioengineering. New York, NY: American Society of Mechanical Engineers; \ 986:26-27. 78. Gower WE, Pedrini, V. Age related variations in protein-polysaccharides from human nuclcus pulposus, annulus Iibrosus and costal cartilage. J Bone Joint Surg. 1 969;5 I A: 1 1 54-1 1 62. 79. Urban J PG, McMullin JE Swelling pressure of the i nrervertebtal disc: inAuence of proreoglycan and collagen conrenrs. Biorheology. 1 985;22: 1 45- 1 57. 80. Nachcmson A. Lumbar inrradiscal pressure. Acta Orthop Scand Suppl. 1 960;43: 1 - 1 40. 8 1 . White AA, Panjabi MM. ClinicaL Biomechanics ofthe Spine. Philadelphia, PA: J B Lippincott Co; 1 978. 82. Lindh M. Biomcchanicsofthe lumbar spine. In: Nordin M, Frankel V H , eds. Basic Biomechanics of the MusculoskeletaL System. 2nd ed. Philadel phia. PA: Lea & Febiger; 1 989; 1 83-207.
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AUTONOMIC NERVOUS SYSTEM FRANK H. WILLARD
KEY CONCEPTS • •
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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.
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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
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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
/
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Collateral ganglia and Prevertebral Plexuses
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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 +-<::
P rega n glioni c fi be rsCentral Origin
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parasympathet ic divisions of autonomic system. From Harati
Y. Anatomy
of the spinal and peripheral autonomic nervous system. In: Low P, ed.
Clinical Autonomic Disorders. Boston, MA: L i ttle, Brown and Company; 1 993, with permission.
Pelvic nerve
( n ervus eri ge n s)
Sex organs FIGURE 6.5.
Parasympathetic division of peripheral autonomic system.
JG.
Correlative Neuroanatomy and Functional Neurology. Los Altos, CA: Lange Medical Publishers; 1 985, with permission.
From Chusid
sympathetic system arises from cholinergic preganglionic neu rons located in the lateral horn of the thoracic and lumbar spi nal cord; it is also called the thoracolumbar system. I n general, the postganglionic neurons of the sympathetic system are adrener gic and secrete norepinephrine. H owever, there are i mportant exceptions. For example, some cholinergic ganglionic neurons contribute to the in nervation of the hair follicles and sweat glands as well as possibly innervating the vasculature in skeletal muscle (7). The parasympathetic system arises from chol inergic pregan glionic neurons located in either cranial nerve nuclei of the brain stem or the lateral horn of the sacral spinal cord, and it is therefore called the craniosacral system. The postganglionic neurons of the
parasym pathetic system secrete acetylcholine and a wide variety of other neuron modulators such as the neuropeptides. G iven that these two divisions of the autonomic nervous system can be differ entiated on the basis of their anatomy and chemistry, it is not sur prisi ng that they have differing in Auences on their target organs. Sympathetic Auto nomic Nervous System
The sympathetic autonomic nervous system has two major components: vascular and visceral. The vascular component is associated with the spinal nerves and innervates: Fascia Smooth muscle of vasculature Smooth m uscle of hair follicles Secretory cells in the sweat glands of the skin The visceral component innervates: Smooth muscle Cardiac muscle Nodal tissue Glandular organs of the thoracic, abdomi nal, pelvic, and perineal viscera
6. A utonomic Nervous System
Paravertebral ganglionic trunk
Greater splanchnic nerve
Celiac
Superior mesenteric plexus splanchnic nerve
Inferior mesenteric plexus
Superior hypogastric plexus
Sacral splanchnic nerve
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FIGURE 6.7.
Inferior hypogastric plexus
Paravertebral ganglia (sympathetic trunk) lying along me·
dian axis of body. From Rohen JW, Yokochi C. Color Atlas of Anatomy. New York, NY: Igaku-Shoin Medical Publishers; 1 983, with permission.
Also, portions of the sympathetic visceral system provide an innervation ro the neurons of the parasympathetic ganglia i n the walls of the visceral organs. The ganglionic neurons of the sympathetic nervous system are located in two types of ganglia: paravertebral and preverte bral (Fig. 6.4). The paravertebral ganglia form two long chains called the sympathetic trunks, which are located on either side of the vertebral col umn ( Fig. 6.7). Each sympathetic trunk ex tends from the upper cervical vertebrae along the heads of the ribs in the thorax, on the sides of the lumbar vertebral bodies in the abdomen, and along the ventromedial aspect of the sacroiliac joint in the pelvis. Inferiorly, the two trunks terminate by unit i ng to form the gangl ion impar, a small neural structure on the ventral aspect of the coccygeal vertebrae. The three major prever tebral gangl ia are found in clusters, embedded i n the abdominal plexuses that surround the anterior branches of the aorta. Addi-
95
tional small clusters of prevertebral ganglia are found scattered i n t h e autonomic plexus of t h e pelvic basin. The detailed organization of the sympathetic system is illus trated in Fig. 6.4. The following features are critical: 1.
AJI pregangl ionic cell bodies are located in the lateral horn of spinal cord segments primarily between Tl and l2; however, they can extend as high as C7 and as low as l3. Their axons leave the spi nal cord through ventral roots Tl-l2 and course along the corresponding spi nal nerves to reach white commu nicating rami ( Fig. 6.8). The wh i te ram i carry the myelinated, pregangl ionic fibers from the spi nal nerve d i rectly i n to the par avertebral gangl ia. They also carry sensory processes from the vasculature and viscera back to the spinal nerve.
2. The paravertebral ganglia are present on both sides of the spinal cord i n the following distribution (8): • Three cervical segments (superior, middle, and stellate) • Ten to 12 thoracic segments • Four lumbar segments • At least four or five sacral segments Often the upper thoracic and lower cervical gangl ia are fused to form the stellate ganglion. Only the ganglia between T1 and L2 receive whi te ram i , because preganglionic fibers arise from only these segments. 3 . Neurons in paravertebral ganglia located either above Tl or below L2 receive their innervation from p regangl ionic fibers arising in spinal segments TI-L2. These pregangl ionic axons enter the sympathetic trunk at their segmental level of origin and ascend or descend through the trunk to reach ganglia positioned above or below T I -L2. 4 . Ganglionic neurons destined to i n nervate blood vessels, smooth muscles, and glands of the skin are found in all the par avertebral gangl ia. Their postganglionic axons gai n access to spinal nerves by passing over gray ram� (Fig. 6.8). AJI paraver tebral ganglia give rise to gray rami; each spinal nerve receives at least one gray ramus. The postganglionic axons follow the spi nal nerves distally before shifting to assume a posi tion in the fascia along the wall of a blood vessel. 5. Ganglionic neurons with axons i nnervating thoracic, abdom inal, and pelvic viscera are found in the three cervical gangl ia, the upper five thoracic paravertebral ganglia, and the p reverre bral ganglia. These are the celiac and the superior and i nferior mesenteric ganglia, as well as small scattered ganglia in the pelvic plexus. These prevertebral ganglia receive their pregan gl ionic axons through thoracic, lumbar, and sacral splanchnic nerves. The term splanch nic refers to the viscera; splanch nic nerves are si mply v isceral nerves. Thoracic, lumbar, and sacral splanchnic nerves carry sympathetic fibers and pelvic splanch nic nerves carry parasympathetic fibers. The sympathetic ganglia receive information from the central nervous system through the axons of the pregangl ionic neurons. A preganglionic axon of the sympathetic system has a n umber of options after passing through a white ramus between Tl and L2 to enter a paravertebral ganglion: 1 . I t can i nnervate a gangl ionic neuron in the paravertebral gan glion at i ts spi nal cord level of entry.
96
If. Osteopathic Considerations in the Basic Sciences
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Postganglionic unmyelinated fibers FIGURE 6.8.
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Neuronal circuitry present in typical periph
eral thoracic spinal segment. From Harati Y. Anatomy
To prevertebral ganglia or adrenal medulla
of the spinal and peripheral autonomic nervous system. In: Low P, ed. Clinical Autonomic Disorders. Boston, MA: Little, Brown and Company; 1 993, with permission.
2. It can pass e ither up or down in the sympathetic trunk to innervate ganglionic neurons located at levels not serviced by white rami .
3. I t can proceed through t h e paravertebral ganglia without
forming synaptic contacts, j oin a thoracic, lumbar, or sacral splanchnic nerve, and subsequently innervate neurons in one of the retroperitoneal prevertebral ganglia. These options are diagrammed in Fig. 6.8, which i llustrates a rypical thoracic spinal segment and i ts accompanying spinal nerve and paravertebral ganglia. The significance of these innervation patterns is fur ther considered as the innervation of specific organs is examined. Parasympathetic Autonomic Nervous System
Nucleus Edinger Westphal nucleus
Nerve
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End
Ciliar y
Organs
Eye
Superior salivatory nucleu s Inferior salivatory nucleus Dorsal motor
The parasympathetic autonomic nervous system, unlike its sym pathetic counterpart, innervates only visceral organs and blood vessels in the: Head and neck Thorax Abdomen Pelvis
./
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The parasympathetic nervous system lacks a division inner vating the peripheral vasculature of the extremi ties and trunk. I t i s divided into two portions: cranial and sacral. These are based on the location of its p reganglionic neurons (Figs. 6.5 and 6.9). The cranial portion consists of several brainstem nuclei and their preganglionic nerves. Cranial nerves [ll, V11, and IX give rise to parasympathetic p reganglionic fibers that innervate ganglia located in the: Orbit (ciliary ganglion) Sphenopalatine fossa (sphenopalatine ganglion) Inferior temporal fossa (otic ganglion) Floor o f the mouth (submandibular and sublingual ganglia)
Respiratory tract and lungs Gastrointestinal tract, liver and
and rectum Genitourinary tract FIGURE 6.9.
Summary of parasympathetic nervous system emphasiz
ing distribution of cranial nerves III, VII, IX, and X. From Barron KD, Chokroverty S. Anatomy of the autonomic nervous system: brain and brainstem. In: Low P, ed. Clinical Autonomic Disorders. Boston, MA: Lit tle, Brown and Company; 1 993, with permission.
6. A utonom ic Nervous System
Cranial nerve X, the vagus nerve, i n nervates ganglia i n the organs of the cervical, thoracic, and superior portions of the ab dominal viscera. The vagus nerve is a significant source of parasympathetic i n nervation to the thoracic and upper abdominal viscera. I t enrers the thoracic cavity along the upper portion of the mediastinal wall and passes posterior to the root of the lung to gain a po sition on the walls of the esophagus. Vagal branches are given off to the cardiac and pulmonary plexuses and to the esophageal plexus. Through the upper portion of the vagus, the n ucleus ambiguous of the medulla conrributes i nnervation to the phar ynx, larynx, and skeletal m uscle portion of the upper esophagus. Preganglionic vagal fibers from the dorsal motor n ucleus of the . medulla terminate i n ganglia on the walls ofeach organ begll1nll1g in the upper esophagus and extending to the splenic flexure of the colon. From these ganglia, postganglionic fibers arise and course in and around the smooth muscle layers and glands of the organ. The left and right trunks of the vagus rotate around the esoph agus (due to the fetal rotation of the gut), formi ng the anrerior and posterior trunks of the vagus, respectively. At the distal end of the esophagus, these [wo trunks slip through the esophageal hiatus of the diaphragm riding in the fatty advenri tial fasci a of the esophageal walls. Although the idenrity of the vagus nerve is lost as i ts axons join the celiac plexus, its pregangli o n ic fibers continue in the celiac and superior mesenreric plexus evenrually reaching the full extent of these [wo corresponding neurovascu lar territories. The vagal p reganglionic axons reach only as far inferiorly as the splenic flexure of the colon. The lower portion of the gastroinrestinal tract located distal to the splenic flexure, as well as the pelvic viscera, receives their parasympathetic in nervation from the pelvic splanchnic nerves. These latter nerves form the sacral componenr of the parasym pathetic nervous system. The preganglionic neurons are locate i n the lateral horn of spi nal cord segmenrs S2-4. Their axons eXit the spinal cord by traveling in the sacral nerve roots. As these roots pass through the endopelvic fascia, small pelvic splanch nic nerves branch off. These branches quickly join the i n ferior hypogastric plexus (pelvic plexus), which is also located in the endopelvic fascia. Through this plexus, the pregangli o n ic axons can reach the visceral organs of the pelvic bas i n such as the uri nary bladder, the i nrernal reproductive organs, and the rectum. By ascending along the hypogastric plexus, these axons al� o enrer the inferior mesenteric plexus of the abdomen. From the II1fenor mesenteric plexus, these preganglionic axons follow the vascular branches of the inferior mesenreric artery to service structures such as the descending and sigmoid colon. The preganglionic axons of the vagus and of the pelvic splanchnic nerves terminate in ganglia located in the walls of the abdom inopelvic viscera. Shorr, postganglionic axons invade the organ to terminate in lay ers of smooth muscle and in surrounding glands. The pattern of parasympathetic innervation of the visceral organs conrinues in an uninterrupted manner through the abdominopelvic cavity even though the source of this i n nervation shifts fro m cranial origins to sacral origins at the splenic flexure of the large bowel. The auronomic nervous system provides input to the:
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Vasculature and fascias throughout the body The visceral organs of the head and neck The visceral organs of the thoracoabdominopelvic cavity
97
Spleen Thymus Bone marrow Lymph modes The remainder of the chapter focuses on the i nnervation of the vasculature, fascia, and major organs. Primary Afferent Fibers
The autono m ic nervous system is not strictly an efferent system (9). All nerves conrain i ng autonomic efferenr axons also carry primary afferenr fibers. The principal targets of these primary afferenr fibers are the: Dorsal horn of the spinal cord fro m approximately T I -L2 and S2-4 Solitary n ucleus of the vagal complex in the medulla Although the majority of primary afferent fibers i n autonomic nerves are of the small-caliber variety ( B-afferenr system), a few larger, myelinated fibers are also presenr (A-afferent system). I n general, the input over visceral afferent fibers t o the medullary brainstem i nvolves the n onnoxious regulation of organ function. Conversely, many of the primary afferenr fibers targeting the spinal cord have the characteristics of nociceptive fibers. They produce neuropeptides such as substance-P and calcitonin gene related polypeptide and respond to nociceptive sti m ul i . In ad dition, some are capable of elicit i ng a neurogenic i n flammatory response in the surrounding tissue ( 1 0, 1 1 ) . Nociceptive input from these fibers to the spinal cord can facilitate spinal segmenrs. This i n i tiates vasomotor changes and alters the output to somatic musculature (viscerosomatic reflexes) and refers pain to the so matic structures ( 1 2, 1 3). (The relationship of the visceral affer enr fibers to viscerosomatic reflexes is reviewed elsewhere in this text.)
REGIONAL DISTRIBUTION OF THE AUTONOMIC NERVOUS SYSTEM Trunk and Limbs Peripheral Vasculature
The vascular tree is divided i n to fou r different types of vessels based on their distinctive functions (14): 1. Conduit vessels comprise the arterial system prior to arterioles. 2. Resistance vessels represenr arterioles. 3 . Exchange vessels are capillaries. 4 . Capacitance vessels consist of veins. Most aspects of the vascular tree receive an i nnervation that controls the resistance of these vessels to blood flow (7, 1 4, 1 5) . Different types ofaxons i n these vascular nerves can b e idenrified by their neurochemistry. Sensory fibers, coursing in the vascu lar nerves, typically conrain neuropeptides such as substance-P and calcitonin gene-related polypeptide. Efferenr axons in the peripheral autonomic nerves can be ( 1 4): Adrenergic Choli n ergic
98
II. Osteopathic Considerations in the Basic Sciences
H istaminergic Purinergic I n general, the adrenergic fibers function as conscrictors, con tracting smooth muscle i n the tunica media and increasing the resistance in the peripheral vasculature. These norepinephrine contai ning fibers arise fro m the paraverrebral ganglia of the sym pathetic nervous system and i n nervate all vasculature of the body. Chol inergic fibers are much fewer in number in most tissue, and are vasod ilating i n nature. These nerves are of mixed origin, and most often arise from the parasympathetic ganglia i nnervating the vasculature i n the head and neck and the visceral organs of the thorax, abdomen, and pelvis. Cholinergic vasodilator fibers, in nervating blood vessels i n the extremities, arise i n the sympathetic trunk of some mammals; however, the i m portance of this system is in humans is not known ( 1 6) . Purinergic and histami nergic axons also mediate relaxation of vascular wall smooth m uscle, but their origin and role i n vasodilation are not clear ( 1 4). The sympathetic i nnervation of blood vessels i n muscle and skin is accomplished by preganglionic neurons located i n the lateral horn of spinal segments T2 through L2-3. Their axons leave the spinal cord in the ventral roots and pass through whi te rami to in nervate neurons located in the paravertebral ganglia (Fig. 6. 8). Vasomotor neurons present i n the paravertebral ganglia give rise to axons rhat leave the ganglia over the gray ram i to rejoin the spi nal nerves. I n this way, they reach the somatic peripheral tissue where they i nnervate blood vessels, swear glands, and hair follicles. A topographic map of the vasculature i n the body is contained within paravertebral ganglia such that ( J 7, 1 8): 1 . The vasomotor fibers to the head and neck come from spinal segments T I -4. Their axons travel superiorly in the sympa thetic crunk to reach the cervical ganglia. Postganglionic axons follow the carotid vascular tree to reach the head and neck. Seg ments T I -2 provide i n nervation for the brain and meninges; T2-4 provides i nnervation to the vasculature of the face and neck. 2. The vasomotor fibers to the upper extremity come from spinal segments T5-7. Their axons course superiorly in the sym pathetic tru nk to reach the upper thoracic and lower cer vical ganglia. Postganglionic axons join the spinal nerves of the brachial plexus to reach the vasculature of the upper extremity. 3. The vasomotor fibers to the lower excremity come from spinal segments Tl 0 through L2-3 . Their axons descend in the sym pathetic crunk to reach the lower l umbar and sacral ganglia. Postgangl ionic axons j o i n the spinal nerves of the lumbosacral plexus to reach the vasculature of the lower extremity. Sympathetic fibers course along the outer border of the tun ica med ia of the artery and secrete their neuroregulators into the extracellular A uids surroun d i ng the vascular smooth mus cle. Most sympathetic fibers release norepinephr i ne from small swelli ngs along the termi nal distribution of the axon. This neu romodulator i nteracts with its specific receptors o n the vascular smooth muscle cell membranes. Both Ci- and ,B-adrenergic recep tors are present on these plasma membranes ( 1 9). Activation of Ci-adrenoceptors leads to contraction of the smooth muscle cells and vasoconstriction, while activation of the ,B-adrenoceptors mediates relaxation of the muscle cell, resulting in vasodilatation.
I n general, the Ci-adrenoceptors predominate on the smooth mus cle of resistance vessels; therefore adrenergic stimulation yields vasoconscriction in skeletal muscle. Addi tional control of skeletal muscle resistance arteries is ac complished through numerous endothel iu m-derived substances such as the vasodilator n i tric oxide or the vasoconstrictors prosta cycli n , endothelin, and angiotensin (20). The tone in the vessel wall is the product of a complex i nteraction of these vasoactive substances ( 2 1 ). Neurally mediated, active vasodilation of cu taneous capi llary bed is well established in the literature ( 1 6). Sympathetic cholinergic fibers do not appear to innervate the cu taneous vascular cree; i nstead, a nonadrenergic, noncholinergic vasodilatory mechanism exists for these vessels (22). Neurally me diated, active vasodilation of skeletal muscle vascular beds appears to be doubtful and has recendy been questioned ( 1 6). Along with the efferent innervation of the vascular cree, affer ent or sensory fibers also course in the walls of the blood vessels. Little is known of the sensory feedback to the spi nal cord pro vided by these fibers. The nomenclature of rhese afferent fibers is confusing because it is not clear whether they are somatic or vis ceral afferent fibers. Jinkins and colleagues (23) have termed the vascular afferent fibers found in somatic tissue "somatosympa thetic fibers" because they course through somatic tissue but are related to the autonomic nervous system. However, because these afferent fibers are generally small caliber and contain an array of neuropeptides such as substance-p, m uch of the information they carry is most l i kely related to nociceptive stimul i . The normal, basel i ne release of neuropeptides such as substance-P from these fibers may play an important role in maint aining vascular tone (24). Thus, the small-cal iber, primary afferent fibers appear to have additional homeostatic fu nctions in the peripheral tissue beyond that of nociception. When irritated, some of these small-caliber, sensory axons can secrete quantities of substance-P (a proinAammatory, vasodila tory neuropeptide) into the surrounding tissue. This release of an i nAammatory agent from a peripheral nerve term i nal is in volved i n i ni t iating the processes of neurogenic in Aammation and edema (25). Neurogenic i n Aammation is a critical component in inAam matory joint d isease, which suggests an imporrant role for the small-caliber, primary afferent fibers in these diseases (26). An interaction between sensory axons and sympathetic neu rons appears to occur i n the peripheral tissues. Sympathetic adren ergic terminals often end in close association with the peripheral processes of sensory neurons. Secretion of norepinephrine can i ncrease the levels of prostaglandins E2 and 12 in the tissue (27). Prostaglandins are i rritating to many small-cal iber, primary affer ent fibers. Sufficient sympathetic discharge therefore can resul t i n a nociceptive input t o the spinal cord. [ n addition, evidence strongly suggests that small-cal iber, primary afferent fibers can become sensitized to sympathetic nervous system acti�ity (27). This interaction between sympathetic efferent axons and primary afferent neurons is a possible mechanism for sympathetically de pendent hyperalgesia such as that present in reAex sympathetic dystrophy (28). Sweat Glands and Connective Tissue
Along with i nnervating the vasculature, the peripheral autonomic fibers also provide an i n nervation to sweat glands and fascia.
6. A utonomic Nervous System
Sweat glands receive an exclusively cholinergic i n nervation from the sympathetic rrunk ganglia; these fibers are termed the sym pathetic chol inergic system ( 1 5). The cholinergic fibers stimulate secrerory activity in the gland. Small-cali ber, neuropeptide-con raining, primary afferent fibers in nervate all forms of connective tissue. These fibers of ten course in close association with adrenergic sympathetic axons and blood vessels. A close relationship between these fibers and the connective tissue componenrs of the fascia is seen in such tissue as the: Cranial dura (29 ,30) Gastrointestinal tract (3 1 ) Synovium of diarthrodial joints (32) I n several locations, such as joints, these fibers have been demonstrated ro play a role in modulating the cellular compo nents (mast cells) of the connective tissue and ro contribute ro the maintenance of tissue i ntegrity (32,33). Finally, the i nrerac tion of these two fiber types appears ro play an i mportant role in the maintenance of normal vascular rone in connective tissue (24) . Head and Neck
The auronomic innervation of the head and neck arises from two general sources: sympathetic and parasympathetic. The sympa thetic in nervation originates in the intermediolateral nucleus of the upper thoracic segments (T l -4) of the spinal cord, and their gangl ionic neurons are located in the cervical sympathetic gan glia of the neck. Postganglionic fibers from the superior cervical ganglion enter the head following the course of the carotid and vertebral arteries and the j ugular vein. The parasympathetic in nervation originates from several nuclei in the brai nstem, and the gangl ionic neurons are located in these ganglia (Fig. 6.9): Ciliary sphenopalatine Otic Geniculate Recently, additional parasympathetic ganglia located on the walls of the internal carotid artery have been described (34-36). The auronomic in nervation of the cranial viscera, the function of these nerves, and the neurology of their dysfunction are amply described elsewhere ( I 7,37-40). The third cranial nerve conrains parasympathetic axons that arise in the Ed inger-Westphal nucleus of the midbrain and in nervate the ciliary ganglion of the eye ( Fig. 6.9). These axons are responsible for consrricting the pupil through the pupillary sphincter muscles and contracting the cil iary body ro thicken the lens in the accommodation reflex. The facial (VI I) cranial nerve carries parasympathetic pregangl ionic axons from the superior salivarory and lacrimal nuclei in the ponrine region of the brain stem. These secreromoror and vasomotor axons course along the superficial petrosal nerve to reach the sphenopalatine ganglion. Postganglionic axons fol low branches of the rrigeminal nerve to reach the lacrimal gland and mucosal glands of the nasal and oral cavities. Preganglionic axons from the superior salivatory nucleus also follow the chorda tympani, a branch of the facial nerve, to reach the submandibular and sublingual ganglia. Postganglionic axons from these ganglia supply the salivatory glands o n the floor
99
of the mouth. The glossopharyngeal nerve carries secretomotor and vasomotor axons from the inferior salivatory nucleus located at the ponromedullary border to the otic ganglion. These laner axons pass over the lesser perrosal nerve. Postganglionic axons from the otic ganglion extend to the parotid gland over branches of the third division of the rrigem inal nerve. Cranial nerve X, the vagus, is the largest of the parasympa thetic nerves. It supplies preganglionic parasympathetic i n ner vation of the viscera in the thorax and abdomen to the level of the splenic flexure in the transverse colon. Efferenr vagal ax ons arise in the dorsal motor nucleus and nucleus ambiguous of the medulla. The vagus is largely a sensory nerve; afferent fibers outnumber efferent fibers in the mammalian vagus by more than 1 0: 1 (4 1 ). These sensory fibers include the afferent in nervation of the thoracoabdominal viscera and the general sensory i nnervation of the: Pharynx Larynx Ski n of the ear External auditory meatus External surface of the tympanic membrane The cell bodies for these afferenr fibers are located in the two nuclei of the vagus: the superior (j ugular) ganglion and the infe rior ganglion. Their central brainstem targets i nclude the nucleus soli tarius, n ucleus ambiguous, and spinal trigeminal nucleus. An area of much recent i nrerest is the autonomic in nervation of the vascular and dural systems in the head. Preganglionic sym pathetic input to the cranial vasculature and dura arises in the upper thoracic spinal segments. Those con troll ing the vascula ture of the brain and meni nges are located in segments T I -2, and those involved with the vasculature of the face and neck are located in T2-4 ( I 7). Ganglionic neurons are located in the supe rior cervical sympathetic ganglion and in small ganglia embedded in the fibers of the i n ternal carotid nerve ( I 8). Their axons course along the carotid arteries; those going to the cerebral vessels and dura form the well-developed inrernal carotid nerve. Within the dura, the adrenergic fibers diverge away from the vasculature to form a dense plexus within the connective tissue substrate of the dura itself (30). The extensive autonomic innervation may play a role in regulating the metabolic activity of the dural tissue. The sympathetic i nnervation of the dura and associated vasculature is of i n terest due to i ts proposed role in the cause of migraine headache (42). Parasympathetic axons innervating the cerebral vasculature arise in these ganglia: sphenopalatine, otic, and inrernal carotid (36,43-45). Axons fro m the ganglia contain acetylcholine and neuropeptides such as vasoactive intestinal polypeptide and neuropeptide-Y, among others (35 ,46). The axons form a delicate plexus wrapped around cerebral arteries as they travel through the subarach noid space. Primary afferenr fibers conraining neuropep tides such as substance-P and calcironin gene-related polypep tide are also present in the plexus surrounding the cerebral ves sels. These fibers arise in the ophthalmic and maxi llary divisions of the trigeminal ganglion (47) and consti tu te the "trigemino vascular system" (48). Similar primary afferenr fibers contai ning substance-P and calcitonin gene-related polypeptide have been described in the dura mater (30). Some of these fibers form free
1 00
If Osteopathic Considerations in the Basic Sciences
endings and are postulated to have trophic relationships with the connective tissue cells i n the dura such as the fibroblast and mast cells. Release of these proinflammatory peptides has been i ndi cated in the pathogenesis of certain in flammatory headaches such as the migraine and cluster varieties (49, 5 0).
Sympathetic
-+
Thorax
A large autonomic plexus of fibers extends fro m the superior mediastinum inferiorly through the posterior mediastinum and con ti nues into the abdominopelvic cavity, using the esophageal hiatus of the diaphragm as a conduit (Fig. G . 1 0) . In total, this complex arrangement of fibers is best termed the thoracic plexus, although it has several regionally named components. The tho racic plexus is derived from the vagus nerve and its branches and from splanch n ic branches from the paravertebral ganglia. The thoracic plexus i s located near the m idline and divided ap proximately i n to two pans: superior and i n ferior. Superiorly, this complex arrangement of fibers contains the i n terwoven cardiac and pulmonary plexuses that are distributed around the great ves sels of the heart and the large airways. I nferiorly, it contains the esophageal plexus wrapped around the esophagus as it courses through the posterior mediastinum. Fig. G. 1 1 is a schematic
Grey rami to C1 -----''"<-c!'f7 Superior cervical ganglion
Right vagus ------jttr1:�h.___r_...-:.�-- nerve Cardiac branches
M iddle cervical ganglion
���.--_-- Deep cardiac plexus
����;W--:���I,-_ Esophageal
Anterior ramus, T1
plexus
Inferior cervical ganglion
Anterior vagal trunk
\������M.--- Celiac
plexus (cut) Superior mesenteric plexus
Right inferior hypogastric plexus
*:Si���
Pelvic-oe:== splanchnic nerves
;;!!!I:;�:=:-./
Coccygeal nerve
FIGURE
Inferior mesenteric plexus Superior hypogastric plexus Vesical and prostate plexus
6 . 1 0. G reat autonomic plexus extending from the lower cervi
cal region through the thorax and abdomen to reach the pelvis. From Bann i ster LH, Berry MM, Collins P, et ai, eds. Gray 's Anatomy. New York, NY: Churchill Livingstone; 1 995, with permiss i o n .
Cardiac Pulmonary And Esophageal Nerves
-+
Parasympathetic
Thoracic Plexus
/~ Nerve
Cardiac Plexus Pulmonary
-+
Plexus
-+
Esophageal Plexus
FIGURE
6.1 1 . A schematic d i agram illustrating the thoracic plexus and
its associated systems. The thoracic, cardiac, pulmonary, and esophageal nerves are a source of sympathetic postganglionic fibers into the plexus . The vagus nerve is a source of parasympathetic preganglionic fibers to the plexus. Organ ganglia for the parasympathetic system will be found within the parts of the thoracic plexus.
diagram illustrating the thoracic plexus. Branches from this au tonomic plexus in the thorax supply the following with afferent and efferent nerves: Heart Trachea Bronchi Lungs Esophagus Thoracic duct Sympathetic i nnervation of the thoracic viscera arises in spinal cord segments T 1 through T5 or TG. Axons from these pregan glionic neurons synapse with ganglionic neurons in the superior, m iddle, and inferior cervical ganglia as well as i n the sympathetic trunk ganglia Tl to T5-G. Sympathetic postgangl ionic axons fro m these paravertebral ganglia join the thoracic plexus via a se ries of smal l , delicate cardiac, pulmonary, and esophageal nerves. With i n the thoracic plexus, sympathetic cardiac and pulmonary nerves descend through the superior mediasti num join ing with s i m ilarly named parasympathetic branches from the vagus and recurrent laryngeal nerves. They form the complex cardiopul monary plexus of fibers surrounding the great vessels of the heart (Fig. G. 1 2) and the vasculature and airway structures of the lungs (Fig. G. 1 3). The individual superior, middle, and inferior cardiac nerves of the sympathetic trunk and vagus are extremely i ncon sistent in actual form (5 1 ). The esophageal sympathetic nerves arise fro m the thoracic paravertebral ganglia and course d iago nally downward across the thoracic vertebral bodies to reach the adventitial fascia surrounding the esophagus in the posterior me diastinum. Here, they join with the main trunks of the vagus nerve (parasympathetic) to form the esophageal plexus. The m ixing of parasympathetic and sympathetic axons begins in the most superior aspect of the thoracic autonomic plexus as it extends upward i nto the cervical region. Scattered communi cating branches unite the vagus and recurrent laryngeal nerves
6. A u tonomic Nervous System
Vagus nerve -
Cervical
_------
Sympathetic trunk,
_
cardiac branches
Conjoined cervical
/" sympathetic cardiac
nerve
Cervico thoracic cardiac branches
Thoracic
-- Aortic
cardiac
arch
branches
and plexus
Right pulmonary artery and plexus
FIGURE
6.12. Nerve supply of heart. From Bonica JJ. General consid
erations of pain in the chest. In: Bonica JJ. The Management of Pain. Philadelphia, PA: Lea
&
Febiger; 1 990, with permission.
with the sympathetic rrunk. Therefore, even at the most superior aspect of the plexus, there are no pure sympathetic or parasym pathetic nerves. Also, all fibers in the plexus contain a mixture of afferent and efferent axons, so the plexus cannot be considered a purely efferent structure either.
Cardiovascular Plexus
The cardiac plexus represents a region of the thoracic plexus closely related to the i nnervation of the heart. The cardiac plexus consists of a mixture of sympathetic and parasympathetic fibers (as well as afferent fibers) woven atound the great vessels of the heart (Fig. 6. 1 2). Sympathetic input to the cardiac plexus arises from preganglionic neurons located in the nucleus intermedi olateral is of the lateral horn of the spinal cord extending from segments T l to T 5 . This column of spinal cord neurons contains a topographic map of the heart. The ventricular i nnervation is represented i n the h igher thoracic segments, b ut the atrial rep resentation is found in the lower segments ( 52). This inverted cardiac map results from the embryologic origin of the heart; the ventricular system forms superior to the atrial system (53). The preganglionic axons of the spinal cord neurons enter the sympathetic rrunk by passing over white rami in the upper tho racic segments. Once i n the rrunk, most of these fibers ascend to reach their ganglionic neurons located primarily in the two to three cervical gangl ia. Variable numbers of cervical and thoracic
101
sympathetic cardiac nerves leave t h e cervical a n d upper thoracic ganglia, course through the fascia of the mediastinum, and join the cardiac branches of the vagus to form the cardiac plexus. This plexus i s primarily located o n the walls of the pulmonary arterial tree ( 54). The parasympathetic input to the cardiac plexus arises from preganglionic neurons i n the dorsal motor n ucleus of the vagus and the nucleus ambiguous of the medulla ( 5 5 , 56). These pregan glionic axons leave the vagus nerve over its variable (one to three) cardiac branches begi n n i ng i n the neck and extending i n to the superior mediastinum. The axons target a parasympathetic gan glion embedded in the cardiac plexuses, termed Wristberg's gan glion. Short cholinergic axons fro m these ganglia reach the si noa trial and atrioventricular nodes and course in the myocardium of the ventricles. The parasympathetic i nnervation of the ventric ular wall is m uch less dense than that of the sympathetic fibers ( 57). From the cardiac plexus, sympathetic adrenergic and parasym pathetic cholinergic, postganglionic axons form a rich network of fibers distributed along the coronary vasculature, coursing throughout the myocardium of the atria and ventricles, and reaching the s inoatrial and atrioventricular nodes ( 57). The in nervation of the intrinsic nodal system of the heart is bilaterally asymmetric; the right side of the plexus favors the s inoatrial (SA) node but the left side of the plexus tends to target the atrioven tricular (AV) node. Thus, stim u lation of the sympathetic fibers on the left side accelerates cardiac output but is arrhythmogen ic because it is directed to the AV node ( 58). A similar reaction is obtained by cooling the right sympathetic fibers, indicati ng that cardiac activity is i n fluenced by the balance of activity between the two sympathetic i n pu ts ( 58). Stimulation of the parasym pathetic vagal fibers tends to stabilize heart rate. It appears that the balance of tonic neural activity occurring in the vagus and sympathetic systems i n fluences, in part, heart rate and vol u me o u tput. Cardiac afferent nerves are an i m portant consideration in un derstanding reflex control of the heart, patterns of referred cardiac pain, and patterns of cardiac-facil itated segments. Small-cali ber, primary afferent fibers are distributed throughout the ( 59-6 1 ): Myocardium Coronary vasculature Roots of its great vessel Parietal pericard i u m There are at least two different pathways for these cardiac sen sory fibers. Those coursing with the sympathetic nerves have their cell bodies located in dorsal root ganglia extending from C6 to T7, and their central processes terminate i n the dorsal horn of the spinal cord (62,63). Sensory axons coursing with the parasympa thetic nerves have cell bodies located in the nodose ganglion of the vagus nerve and central processes that terminate in the soli tary nucleus of the medulla. I n addition to the autonomic nerves supplying an afferent i nnervation of the pericardium, afferent fibers reach this srructure over the phren ic nerve as well . These phrenic afferent fibers enter the spinal cord over segments C3- 5 . Along with t h e dual origin of sensory nerves, there is a differential distribution of these two sensory pathways in the
1 02
fl. Osteopathic Consideration�in the Basic Sciences
_ R i g ht vagus nerve
Left vagu s nerve - Vagus nerve
Posterior
Aortic _ _
_
arch _
surface of trachea
Trachea
1 R ight
Thoracic sympathetic
:_ posterior
cardiac nerves
J R ight
pulmonary
plexus
_
posterior
Esophagus and plexus
p u l m onary plexus
Left vagus
Sympathetic
nerve
thoracic cardiac n.
_Aortic arch
Right
Cardiac
- lu ng
R ig h t
rent laryn
I
_:
anterior
p u l monary plexus " D i a phragm
Left recur
plexus
(reflected)
R ight coronary-
geal nerve
I Left I . r anterior I p u lmonary .J plexus
I
I
- .,...,.,·-#,.1
Left - coronary
plexus
plexus
B
A FIGURE 6.13.
Innervation of l u ng. From Bonica JJ. General considerations of pain
Bonica JJ, ed. The Management o f Pain. P h i la d e l p h i a, PA: Lea
cardiovascular system . The afferent fibers of the vagus nerve rer m i nate in the (6 1 ): Ascend i ng aorta Aortic arch Pulmonary trunk Arterial walls Atrial walls Atrioventricular valve Ventricular walls The afferent fi bers from the sympathetic nerves reach the (60): Atrial walls Pulmonary arteries Arrioventricular and aortic valves Parietal peritoneum Afferent fibers fro m both systems reach the coronary arteries. Those from the vagus extend to a more distal level of the vas culatu re closer to the apex of the heart than do afferent fibers associated with the sympathetic nervous system. Both A8- and
&
in
the chest.
Febiger; 1 990:98 1 , w i t h permission.
In:
C-afferent fibers are present in the heart (64). Many of rhese fibers contain neuropeptides such as substance-P or calcitonin gene related polypeptide that are typical of small-caliber, primary af ferent fibers. At least one population of these cardiac C-fibers has the physiologic properries of nociceprive axons. In general, rhe afferent fibers coursing wirh the sympathetic nerves are involved with cardiac nociception, and those following the parasympathetic nerves are mainly involved in reflexogenic regulation of heart functions through their brainstem connec tion (62). Section of the sympathetic nerves to the heart can relieve cardiac pain in the chest, arms, and neck (65). These car diac afferent fibers enter the spinal cord over a range of segmenrs fro m C6 to T7, but the i n fluence of these nerves can extend ar least two segments below T7 (66). The signs of segmental facil iration due to cardiac d isease can present i n the vicinity of the cervicothoracic j uncrion and extend downward through at least T9 (67). Importantly, rhe nociceprive afferent fibers reaching the dorsal horn of the spi nal cord i nfluence neurons with concomi tant somatic receprive fields. This viscerosomaric convergence of nociceprive i n formarion provides an explanarion for rhe referral of pain from cardiac strucrures to the body wall and exrremity (68).
6. A utonomic Nervous System
Respiratory Plexus
The ai rways of the respiratory system receive their i nnervation th rough the large pulmonary plexus that surrounds rhe pul monary artery and extends onto the posterior surface of the tra chea and bronchi ( Fig. 6. 1 3) . Sympathetic preganglionic neurons that contribute to this plexus are located in the lateral horn of spinal segments T2-7, and their gangl ionic neurons are located in the cervical and first four thoracic ganglia. Postganglionic ax ons from these gangl ia course through cardiac and esophageal nerves from the sympathetic trunk to reach the pulmonary plexus. These adrenergic axons primarily target the glandular tis sue surrounding the bronchi and bronchioles; l ittle direct adren ergic innervation of the bronchial muscularure has been noted. /3-adrenergic receptors are present on the glandular cells and on bronchial smooth muscle cells. Stimulation of the /3-adrenergic, sympathetic nervous system leads to bronchial dilation and the release of a more viscous secrerion (69) . The vagus nerve is the source of parasympathetic i n nervation for the respiratory ai rways. After entering the thorax, the vagus shifts posteriorly in the mediastinum to pass behind the root of rhe lung. Anterior and posterior pulmonary branches are given off that contribute to the pulmonary plexus. Parasympathetic gan glia located in the walls of the ai rways receive preganglionic fibers from these vagal branches. Postganglionic parasympathetic fibers course in the arteriobronchial tree to terminate around bronchial smooth muscularure, mucosal glands, and blood vessels. Stimu lation of these cholinergic fibers causes (69 ) : Bronchoconstriction Hypersecretion of a serous secrerion Vasod ilation The pulmonary plexus and ganglia contain intrinsic neurons, i.e., cells whose processes remain in the peripheral tissue and do not innervate the central nervous system. Such cells are called interneurons. Some of these cells produce a variety of neuropep tides, among which is vasoactive i ntestinal polypeptide, a potent bronchodilator (70). I n addition, several neuropeptides corelease with norepinephrine From sympathetic terminals and with acetyl choline from parasympathetic terminals. These ubiquitous neu ropeprides have recently gained considerable interest due to their role i n controlling the diameter of the bronchial l u men and the initiation of bronchial wall inAammation (7 1 ) . Small-caliber, primary afferent fibers are also present in the pulmonary plexus. These fibers provide sensory inFormation to the brainstem via the vagus and to the spinal cord via the sympa thetic trunk. This information is involved in reAex arcs related to: Sneezing Coughing Bronchospasms Pulmonary congestion Many of these fibers, and particularly the smallest of them , contain neuropeptides such as substance-P and calcitonin gene related polypeptide, among others. I rritation of these sensory fibers results in the release of proinflammatory substances, leading to neurogenic edema and inflammation in the l ung. Substance- P, released From these sensory axons i nto the pul-
1 03
monary parenchyma, is a potent bronchoconstrictor, vasodilator, and secretagogue (72). Activation of these primary afferent nociceptors can also fa cili tate segments in the spinal cord extending fro m the cervical region i n to the low thoracic cord (67). The extended range of activation most l i kely relates to the wide distribution of the cen tral processes of these primary afFerent fibers. Changes in spi nal cord activity are seen i n response to pulmonary aFferent stim ula tion. Electrical stimulation of inflamed tracheobronchial mucosa produces a decrease in electrical skin resistance in the T2-5 der matomes Followed by cutaneous hyperalgesia hours later (65). Unlike the heart, pain From the l ungs and bronchial tree is car ried in the vagal fibers as well as in the spinal aFferent fibers. Lung rumors can refer pain to the skin around the ear (73) , which is a region of the head i nnervated by small cutaneous branches of the vagus nerve. Electrical stimulation of the laryngeal and tra cheal m Llcosa refers pain to the neck, and similar irritation of the bronchial tree refers pain to the anterior chest wal l . Section of the vagus nerve below the recurrent laryngeal branch ameliorates the pain (74) , suggesting that the nerve is the conduit for this reFerred pain. The costal parietal pleura receive an aFFerent in nervation de rived from the intercostal nerves of the thorax. The mediastinal pleura are i nnervated by sensory fibers From the phrenic nerve, and diaphragmatic pleura is i nnervated by twigs From the inter costal nerves (65). The parietal p lural membrane is sensitive to noxious stimuli. The visceral pleura i n the l ungs receive sympa thetic and sensory fibers from the autonomic plexuses surround ing the bronchi, but is i nsensitive to pain (65). Esophageal Plexus
The esophagus extends fro m an upper sphincter region located at the i n Ferior border of the pharynx to a lower sph incter region located at the border of the stomach. Along i ts route, the body of the esophagus is lodged in the loose connective tissues of the superior and posterior mediastinum. The upper esophageal sphincter is mainly derived Fro m the cricopharyngeus and thyropharyngeus m uscles (together they compose the i n ferior pharyngeal constrictor), which receive their innervation fro m the pharyngeal plexus composed of the superior laryngeal and pharyngeal branches of the vagus nerve (75). The body of the esophagus is surrounded by a plexus of autonomic nerves derived from the inFerior laryngeal branch of the vagus and esophageal branches of the sympathetic trunk (76) . The superior portion of the esophagus is a mixture of skeletal and smooth muscle, although the lower portion is composed of smooth mus cle only. The preganglionic parasympathetic i n nervation to the superior portion of the esophagus (skeletal m uscle portion) is de rived from rhe n ucleus ambiguous. The smooth muscle of the esophagus is derived primarily from the dorsal motor nucleus of the vagus nerve (77) . The left and right vagal trunks approach the esophagus at the root of the l u ng and form an elaborate plexus, which follows this structure through the esophageal hiarus i n the diaphragm. The postganglionic parasympathetic neurons are contained in two i ntrinsic ganglia in the walls of the esophagus: Auerbach's, or the myenteric plexus, and Meissner's, or the sub mucosal plexus. Sympathetic preganglionic neurons are located
1 04
II. Osteopathic Considerations in the Basic Sciences
in the inrermediolateral n ucleus of spinal cord segmenrs ranging from T2-8 (78): Cervical esophageal porrion T2-4 Thoracic esophageal porrion T3-6 Abdominal porrion T5-8 The pregangl ionic axons synapse i n the cervical and upper thoracic sympathetic ganglia. Small esophageal branches, derived from the cervical to fourrh and fi fth thoracic ganglia and carrying postgangl ionic sympathetic fibers, j o i n the vagal plexus along the walls of the esophagus (78). At rest, the cricopharyngeus and thyropharyngeus muscles maintain a tonic conrraction driven by the vagal fibers from the nucleus ambiguous (75). During swallowing, the tonic vagal drive is i n hibited and the upper esophageal sphincter relaxes. Peristalsis i n the upper portion (skeletal m uscle portion) of the esophagus is driven by the n ucleus ambiguous of the vagus nerve (75), al though that in the body and lower portion of the esophagus is driven by the dorsal motor n ucleus of the vagus. The relaxation of the lower esophageal sphincter is accomplished by the n itrergic neurons in Aurbach's plexus driven by the dorsal motor n ucleus of the vagus nerve (79). Afferent fibers from the esophageal walls follow the vagus nerve back to the solitary n ucleus of the medulla. They also fol low the sympathetic fibers back to the dorsal horn of the upper segment of the spinal cord (80). Vagal afferent fibers ending i n the sol i tary n ucleus o f the medulla contribute to a viscerovisceral reAex arc by synapsing on premotor neurons of the n ucleus am biguous and preganglionic neurons of the dorsal motor n ucleus of the vagus nerve (75). The premotor neurons subsequently innervate the motor neurons of the n ucleus ambiguous. The pre motor neurons form the central pattern generator for organized movements of the esophagus such as swallowing (79). The spinal afferent fibers from the esophagus contribute to the referral of pain. These afferent fibers i nnervate spinal segments that also receive afferent information fro m the: Heart Pulmonary tree Chest Upper back and torso Esophageal pain can refer substernally (heartburn) or posteri orly through the back into the area of the scapula ( 8 1 ). Referred pain from the esophagus has n umerous patterns, the more com mon of which are gripping, p ressing, bori ng, or stabbing (82). Aortic Plexus
The thoracic aorta has an inrimate relationsh i p with both divi sions of the autonomic nervous system. Sympathetic input and sensory fibers reach the superior thoracic aorta through cardiac and pulmonary nerves as well as by following d i rect branches from the sympathetic trunk. The i n ferior thoracic aorta receives branches of the thoracic splanchnic nerves. The preganglionic sympathetic axons arise i n the upper five thoracic spinal segments and the postganglionic fibers arise fro m the upper five thoracic paravertebral ganglia. Once o n the wall of the aorta, these fibers form an adrenergic plexus i n the advenritial tissue. Afferent fibers
from this large, elastic arrery follow the sympathetic nerves back to the upper five thoracic spinal segments (65). This observation accounts for the referral of pain from the thoracic aorra to the thoracic spinal segments, resulting in thei r subsequent facilita tion. Vagal cardiac nerves traverse the walls of the aorta as they descend toward their targets. Small twigs from these branches provide afferenr as well as parasympathetic efferent in nervation (Fig. 6. 1 4). Thoracic Duct Innervation
The thoracic duct, located i n the posterior mediastinum near the esophagus, receives an i nnervation similar to the vascular i n nervation elsewhere in the trunk. Its m uscular walls receive cholinergic innervation from the vagus nerve and sympathetic adrenergic i nnervation fro m branches of the i ntercostal nerves in a segmental pattern. The eleventh thoracic ganglion and the left splanchn ic nerve innervate the cisterna chyli, which is the origi n of the thoracic duct (83). Norepinephrine and epinephrine act to increase the flow of lymph through the thoracic duct (84). The effect of these adrenergic compounds on lymph vessels appears to be mediated through a-receptors on the smooth m uscle cells of the lymph vessel wall (85). Abdominopelvic Regio n
The thoracic plexus passes through the diaphragm to con tinue inferiorly in the abdomi nopelvic cavity as the abdominopelvic plexus. This plexus is a massive network of fibers lying along the m i dline astride the aorra and extending from the abdominal diaphragm to the pelvic diaphragm. At the level of the abdominal diaphragm, the plexus has two major components: parasympathetic and sympathetic. The two vagal trunks and their associated branches, representing the para sym pathetic com ponen t, en ter the abdomen ridi ng on the walls of the esophagus. The sympathetic component (or thoracic splanch nic nerves) passes directly through the crura of the diaphragm or under the medial arcuate l igament to enter the abdomen. Once in the abdomi n al cavity, the vagal trunks and thoracic splanchnic nerves u n i te around the aortic prevertebral ganglia. The resultanr abdomi nopelvic plexus of fibers follows the abdominal aorta to the pelvic brim and bifurcates slightly above the sacral promon tory, and the resulting two divisions of the plexus descend into the pelvic basin (Fig. 6. 1 5). Throughout the abdomen, the plexus contains both sympathetic and parasympathetic axons and also has numerous afferent fibers. Toward the inferior end of the ab dominopelvic plexus, addi tional sympathetic conrributions arise in the l u mbar and sacral splanchnic nerves, although addi tional parasympathetic contributions come from the pelvic splanchnic nerves i n the pelvic basin. Like the thoracic plexus, the abdominopelvic plexus can be divided into several geographical regions. Along the abdom inal aorra, the major prevertebral ganglia mark out d i ffering territo nes: Celiac Superior mesenteric I n ferior mesenreric
6 A utonomic Nervous System
Aort ic arch and plexus I
Vagus nerve - - From stellate ganglion
Ascending thoracic " aorta
From thoracic sympathetic ganglia
"-
From cardiac plexus
-
-
/'
I
I
I
/
,/
-
Celiac trunk
___ ---
Celiac ganglion
Su perior ....... mesenteric ganglion
_ _
=.
Inferior thoracic splanc hnic nerve
---
/'
Renal ---..r- � arteries
Superior thoracic splanchnic nerve
Aorticorenal ganglion
.��4JWb "'�;' From lumbar ganglia
Inferior - mesenteric artery
FIGURE
6 . 1 4. Innervation of thoracic and abdominal aorta . From
JJ, & Febiger; 1 990:979,
Bonica JJ. General considerations of pain in the chest. In: Bonica
ed. The Management of Pain. Philadelphia, PA: Lea with permission.
105
The superior hypogastric plexus l ies between the inferior mesenteric plexus and the sacral promontory. Below the sacral promonto ry, the plexus splits to pass laterally around the pelvic organs. This region is called the inferior hypogastric plexus or, simply, the pelvic plexus. Frequently, rhe fibers of the superior hy pogastric plexus unite i nto a few large cords in the region d i rectly over the sacral promontory and j us t prior to bifurcation i nto the two inferior hypogastric plexuses. These cords are often referred to in the surgical l iterature as the presacral nerve (86). Although the abdom inal autonomic nervous system has regional names, in reality the components blend together to form one great ab dominopelvic plexus. The abdomi nal portion of this great plexus supplies efferent and afferent nerves to the organs of the ab dominal cavity i nduding the gastrointestinal organs, spleen, and kidneys. The pelvic portion of this plexus suppl ies the rectu m, urinary organs, and reproductive organs. I n add ition to the or gans, the abdom i nopelvic plexus also i nnervates the vasculatu re of the abdominopelvic cavity.
Gastrointestinal Tract
The gastrointestinal system receives a complex pattern of extrinsic i nnervation i nvolving splanch n ic nerves derived from the thora columbar and sacral portions of the spi nal cord and the term inal portion of the vagus and pelvic splanchnic nerves ( Figs. 6.4 and 6 . 5 ) . These nerves form a complex network of fibers lying along the abdomi nal aorta and extending from the thoracoabdomi nal diaphragm to the pelvic diaphragm ( Fig. 6. 1 5) . This elaborate plexus, l i ke its visceral blood supply, can be divided into three zones based on embryologic partitions of the gastrointestinal system: Celiac (foregut) Superior mesenteric (midgut) I n ferior mesenteric (hi ndgut) A complex network of i n trinsic fibers and neurons called the enteric nervous system is found within the walls of the gut. The enteric or i nt r i nsic neural system controls rhe activity of gut smooth muscle and glands. I n turn, it is modulated by the extrin sic fibers from the central nervous system via the sympathetic and parasympathetic nerves. N umerous sensory feedback loops exist i n the gastroi ntestinal system. Afferen t fibers withi n the luminal surface and gut wall form short feedback loops within the enteric nervous system. Longer feedback loops connect the gut to the prevertebral ganglia, and still longer loops connect the gut with the spinal cord and brainstem (6, 1 3 ,87-90) . Figure 6. 1 6 is a schematic diagram of the abdomi nopelvic plexus demonstrating i ts input from sympathetic and parasympathetic sources. The gastrointestinal tract has a special pattern of sympathetic i nnervation that differs significantly from that of the thoracic viscera. Preganglionic fibers arise i n the lateral horn of spinal segments T9- L2, but they do not terminate i n the paravertebral ganglia. Instead they pass through a series of thoracic, lumbar, and sacral splanchnic nerves (branches off of the sympathetic truck) to reach the prevertebral sympathetic ganglia on the anterior wall of the abdomi nal aorta ( Fig. 6 . 1 5 ) .
1 06
J!. Osteopathic Considerations in the Basic Sciences
Gastric- hepatic branch, Ant. vagal truk
R. phrenic plexus
"
R. phrenic nerve --
-- .......
"
/ ,
/
"
Post. vagal trunk,
R. sup. thoracic splanchnic n.
"-
Celiac ganglia
L phrenic n.
_ -
"
"-
"
celiac division
...- -
and plexus
L. sup. thoracic splanchnic n . __
Adrenal nerves _
_
_
_
R. middle splanchnic n. R. aorticorenal
_
Adrenal nerves
L. middle splanchnic n. _ and L. aorticorenal
_
ganglion
_
_
ganglion
Sup. mesenteric - gang. and artery
R . renal artery and plexus
R . kidney - -
- - L. kidney - _ L. renal artery
- -
and plexus -
- Intermesenteric
R. spermatic (or
plexus
ovarian) artery - -
and plexus
-
_
_ _
L. spermatic (or ovarian) a . and plexus
-- - L. lumbar sympathetic chain
Renal branch from superior hypogastric plexus
Abdom inal aorta -
--
- -
- - -
-
- _
_
Inf. mesenteric gang., artery and plexus
_
R. lumbar sympathetic - - -
_
- Sup. hypogastric plexus
chain
- - L. ureter R. common iliac artery -
-
- -- - - -L. common iliac artery
R. hypogastric nerve - -
FIGURE 6.15.
- - - L. hypogastric nerve Position of major prevertebral sympathetic ganglia in great autonomic plexus of ab
domen. From Bonica J J . General considerations of pain in the chest. In: Bonica JJ, ed. The Management
of Pain. Philadelphia, PA: Lea
&
Febiger; 1 990: 1 1 57, with permission.
The major prevertebral ganglia are disuibuted around the three abdom i nal arteries: Cel iac Superior mesenteric I n ferior mesenteric Anatomical authorities subdivide the cel iac ganglia i nto nu merous parts based o n its location about the celiac artery and aorta; however, from a practical perspective, i t is si m pier to con sider it as one anatom ical unit. Also, the celiac and superior mesenteric ganglia are often fused together i n to an inseparable mass surrounding the trunks of their cwo arteries. An older term for this arrangement is the solar plexus. Additional clusters of sympathetic ganglia neurons are found scattered i n the hypogas tric plexus as it enters the pelvic basin. Neurons i n each prevertebral ganglion give rise to postgan gl ionic fibers that in nervate abdo m i nal and pelvic viscera. These axons travel to their target organs by hitchhiking on abdomi-
nal and pelvic arteries. Each prevertebral ganglion in nervates a d i fferent region of the viscera. Celiac Ganglia
The celiac ganglionic mass surrounds the celiac trunk. It is of ten fused to the superior mesenteric ganglia to form one large, complex mass. When carefully dissected, the precise shape of the ganglion complex is very irregular and defies meani ngful classi fication (5 1 ) . The celiac ganglia receive afferenr fibers from the thoracic splanchnic nerves (T5-9) . In rurn, it supplies postgan glionic sympathetic axons to the vascular territory of the celiac artery including the (Figs.6. 1 7 and 6 . 1 8) : D istal esophagus Stomach Proxi mal duoden u m Liver Gall bladder Spleen Portions of the pancreas
1 07
6. A utonomic Nervous System
Superior Mesenteric Ganglia Sympathetic
Parasympathetic
Abdominopelvic Thoracic
-
Splanchnic
CO SMO
N. Lumbar
-
Splanchnic
IMG
N.
Sacral Splanchnic N.
1-
HG
Plexus
I I
� Abdomen
E
N T E
R
/1
[;J Nerve
I
I C
� G
A
N
I
Pelvis
G \ L
� I A
\
Pelvic N.
lustrating its g a n g l i a and sources of i n put. Thoracic, l u mbar, and sacral splanchnic nerves for the sympathetic trunk carry sympathetic pregan gl ionic fi bers to the paravertebral g a n g l i a located i n the plexus. Post ganglionic axons from the paravertebral g a n g l i a target the i ntrinsic enteric g a n g l i a of the organ wa l ls. Parasympathetic fibers a rise i n the vagus nerve superiorly and the pelvic splanchnic nerves i nferiorly. These fibers also target the intrinsic enteric g a n g l i a located on the organ walls.
_
Distal duodenum Portions of the pancreas Jej unum Ileum Ascending colon Proximal two-thirds of the transverse colon
Splanchnic
FIGURE 6.16. A schematic diagra m of the abdominopelvic plexus i l
Esophagus
This ganglion is found wrapped around rhe superior mesemeric artery. As memioned above, ir is ofren fused wirh rhe celiac gan gl ia. The superior mesemeric ganglia also receive pregangl ionic axons fro m rhe rhoracic splanch nic nerves. Irs distribution of postganglionic axons reaches the territory supplied by the supe rior mesemeric artery (Fig. 6. 1 9) :
Inferior Mesenteric Ganglia
The most ventral of the rhree preverrebral ganglia, the i n ferior mesemeric ganglia, surrounds the abdom inal artery of the same name. It receives axons from the three lumbar splanch nic nerves and supplies postganglionic axons to the vascular rerritory of the i n ferior mesemeric vessels, namely the (Fig. 6. 1 8): Distal third of the transverse colon Descending colon Sigmoid colon Rectum
Vag u s nerves
_
L
6
Liver l i fted u p a n d t o side \
Posterior hepatic \ \ plexus
Gai ibladder l
7
\
\
\
T(5)
8 9
\���S;��i!����
10 (1 1 )
Celiac
/
/
Anterior hepatic plexus
/
Duodenum
\
G a's trod uodenal plexus
FIGURE 6.17. Connections of celiac g a n g l ion a n d i n nervation of stomach. From Kim mey MB, Silverstein FE. D i seases of the gastroi ntest i n a l tract. I n : Bon ica JJ, ed. The Management of Pain. P h i l a d e l p h i a , PA: Lea & Febiger; 1 990: 1 1 89, with permission.
1 08
II. Osteopathic Considerations in the Basic Sciences
Vagus nerves
Esophagus
-
_
Liver lifted u p a n d t o side
6 Anterior vagal trunk
\
Posterior hepatic \ \ plexus
\ \
Gai ibladder l
\
T(5)
L
\
\
7 8 9
\��:=��i��� \ \ ��
10 (1 1 )
G a l l bladder
\ \ \
:
.
:
Celiac
::: ganglia : : // A
: : I
/:.. :. .:/ "
/
/
Anterior hepatic plexus
/ ----�
Duodenum
\
G astroduodenal plexus
/
/
/
Pancreas
Posterior hepatic plexus
FIGURE 6.18. Connections of celiac g a n g l i a and the i n nervation of the l iver and b i l ia ry tree. From M u l h o l l a n d MW, Debas HT. Diseases of the l i ver, b i l iary system, and pancreas. In: Bon ica JJ, ed. The Management of Pain. P h i la d e l p h ia, PA: Lea & Febiger; 1 990: 1 2 1 5, with permission.
Postganglionic fibers From the preverrebral ganglia Follow their specific blood supplies through the mesenreric ligamenrs ro reach the specific organs. The termination of these noradrenergic fibers is primarily on the neurons in the enreric ganglia (9 1 ). Sympa thetic fibers also terminate in the m uscular coat of blood vessels, and an abundance of these fibers reaches the sphincter m uscu lature of the enteric wall . Only scattered sympathetic fibers are present in the m uscularis externa and submucosa of the gastroin testinal tract (92) . There are almost no adrenergic cell bodies i n t h e enreric plexus; therefore, most enteric adrenergic fibers are of external origin. [ n general, stimulation o f the sympathetic fibers inhibits the activiry oFcholi nergic neurons of the parasym patheti c system a n d slows peristalsis a n d motiliry. The parasym pathetic i n nervation o f the organs located below the thoracoabdomi nal d iaphragm has a dual origin, which also segregates along vascular and embryologic divisions. The organs of the Foregut and m i dgut, serviced by the celiac and superior mesenreric arteries, receive parasympathetic p reganglionic fibers From the vagus nerve (Figs. 6. 1 7 through 6 . 1 9) . The vagus nerve follows the esophagus through the diaphragm ro enrer the abdom inal caviry on the walls of the sromach. The esophageal hiatus of the diaphragm is the last place the vagus can be identified as a dis tinct nerve. Vagal axons, however, continue into the abdominal cavi ry, joining those o f the sympathetic system i n the celiac and superior mesenteric ganglia and Forming m ixed nerves, which
pass along celiac and superior mesenteric blood vessels eventually ro reach the abdomi nal viscera. Vagal fibers are plenti ful in the walls of the sromach and small bowel, and a Few reach as Far dis tally in the enteric plexus as the splenic flexure of the large colon. The pregangl ionic vagal axons term inate on neurons in enreric gangl ia. Short postganglionic fibers From these neurons in ner vate the glands and course with i n the layers of smooth m uscle of the alimentary canal. Choli nergic sti mulation increases glandular secretions and peristaltic activiry. The organs of hindgut origin (transverse colon ro anus) re ceive parasympathetic preganglionic in nervation from the pelvic splanchni c nerves (Fig. 6.20). These nerves arise in the lateral horn of the S2-3 spinal cord segments and exit the spinal canal with the sacral nerve roots. As the roots pass along the pelvic wall on their way ro the greater sciatic foramen, the delicate pelvic splanchnic nerves are given oFf. These thin nerves course through the endopelvic fascia ro reach the i n ferior hypogastric plexus sur rounding the walls of the rectum. Once in the hypogastric plexus, these parasympatheti c preganglionic fibers can ascend ro the ori gin of the i n ferior mesenteric artery. By hitchhiking along the branches of this artery, they reach upward ro the splenic flexure of the large colon. Not all parasympathetic axons From the pelvis follow this route ro reach the inferior abdominal organs. Some preganglionic fibers in the inFerior hypogastric plexus gain ac cess ro the enteric plexus in the wall of the rectum and ascend
1 09
6. A utonomic Nervous System
Vagus nerves
T7
Left
8
T8
9
9
10
10
1 1
11
nerve
- Right - a n d left celiac ganglia
R i g ht
12 R. I I
L . celiac g .
,,
,
- - --
\
, I
\
, '.
Jej u n u m
I
II
I
,
I
I I I
I I
,
I
"
\
"
B
I
, -I
/
,
\
\
I
,
\
I
A
I
I
S u perior mesenteric plexus
/
I
I
Ileum
FIGURE 6.19. Connections o f superior mesenteric g a n g l ion and t h e i n nervation o f t h e s m a l l bowel. From
Kimmey MB, Si lverste i n FE. Diseases of the gastrointest i n a l tract. I n : Bon ica JJ, ed. The Management of & Febiger; 1 990: 1 1 98, with permission.
Pain. P h i l ad e l p h ia, PA: Lea
along the colon ro reach more proximal levels of the hindgut. The pregangl ionic axons of the pelvic splanchnic nerves even tually terminate on the neurons of the enteric nervous system. Stimulation of the parasympathetic fibers i ncreases gut peristalsis and mobility. The enteric ganglia and plexus within the walls of the gut form a highly complex and elaborate network, often referred ro as the third division of the auronomic nervous system. It exerts a major influence over all activities in the gut (6,93). The enteric nervous system is estimated ro possess as many neurons as are found in the entire spinal cord (94). The enteric system is divided i n to two layers: The external layer is the myenteric plexus (Auerbach's) controll ing the muscularis externa, and the i n ternal layer is the submucosal ( Meissner's) control ling the glandular and immune components of the subm ucosal layers. A full understanding of these structures requires a knowledge of the gastroi ntestinal his rology and is beyond the scope of this review (95 ,96) . Numerous neurotransmi tters and neuromodularors are found within enteric neurons, for example: Acerylcholine Seroronin Purines Gamma-ami no buryric acid H istamine
There are also many peptides such as: Substance-P Somarostatin Vasoactive i n testinal polypeptide Enkephalins Recently, ni tric oxide has been described as a significant non cholinergic, nonadrenergic mechanism of neurotransmission i n t h e enteric nervous system a s well a s elsewhere (97,98). Nitric oxide is synthesized from the amino acid argi nine by neurons i n the myenteric plexus and is a potent smooth muscle relaxing facroL For this reason, it is postulated ro be important i n d i lation of the alimentary canal. Three levels of sensory i nformation processing are necessary for the proper regulation of gastroi n testinal tract function (6,87). The fi rst level features afferent neurons that form a shorr loop i n terconnecting the gut mucosa, submucosa, or m uscle ro the enteric gangl ia only. These neurons are responsible for local re flexes along the gut wall. The second level of sensory informa tion processi ng i nvolved is arranged i n a longer loop involving afferent neurons from the mucosa that project ro the preverre bral ganglia along the aorta. These sensory neurons partici pate in i ntraabdominal reflex arcs coord i nating various regions of the gastrointestinal system. Neither of these two sensory levels can
1 10
11. Osteopathic Considerations in the Basic Sciences
&�� v
Transverse colon
Celiac g a n g l i a
Superior mesenteric ganglion and Plex us
.. /
�
/
\.-'(� � ._
x/X
- ....-r-
Vagus nerves
-
/ ) � ;--
-..,.
- I_�
� ,
Aorta
1,;
'/ 1
0('
Lu mbar trunk
\
c
.2 o u
I n ferior mesenteric ganglion a n d plexus
Ol c 1J c ., u
'"
«
S u perior hypogastric plexus
Sacral sympathetic trunk
,/
Sacral plexus
/
/
I n ! . hypogastric
A
( pelvIc) plexus
-----
Sigmoid colon
FIGURE 6.20. Connections of inferior mesenteric ganglion and the i n n e rvation of the large bowel and rectum. SSSN, sacra l sympathetic splanchnic nerve. From Kim mey MB, S i lverstein F E . Diseases of the gas troi ntest i n a l tract. In: Bonica JJ, ed . The Management of Pain. P h i l a d e l p h i a , PA: Lea & Febiger; 1 990: 1 1 99, with permission.
reach consciousness, thus we are generally unaware of the reAex control activity occurring in the gut wal l . Final ly, the third level of sensory feedback loops i nvolves afferent neurons that project from the gut wall to the brainstem via the vagus nerve or [0 the spinal cord via the thoracic, lumbar, and pelvic splanchnic nerves. These visceral afferent neurons assist the central nervous system i n i n tegrating the activity of the alimentary canal with that of external environmen tal conditions. I n formation in this third sensory level can, on occasion, reach consciousness. There are significant differences in distribution , morphology, and neurochem istry between the visceral afferent fibers associated with sympathetic nerves and those coursing with the parasympa thetic nerves. There are very few large, encapsulated nerve end i ngs in the gut wal l , most of which are related to axons fro m the parasympathetic vagus nerve. However, the majority of afferent terminals in the gut are smal l-caliber, naked nerve endings (87). In the vagus nerve, mechanoreceptive, chemoreceptive, and poly modal fibers have been described w i th their receptive fields in the mucosa and subm ucosa of the gut wal l . At least in the stom ach, very few of these vagal fibers contain calcitonin gene-related polypeptide, a neuropeptide typically related in nociceptive af ferent fibers of the somatic tissue. However, some nociceptive information is carried in the vagus nerve because pain fro m a
hiatal hernia can be referred to the face (99) via the vagus nerve. Little is known of nociceptive function in vagal fibers below the level of the diaphragm. The visceral afferent fibers that follow the sympathetic nerves to the spinal cord are mechanoreceptive and chemoreceptive, and they tend to be distributed to the mesen teries and peritoneal l igaments of the gut and along its vascu lar system. I n contrast to the vagal fibers, those projecting to the spinal cord are mostly of small caliber and are rich in calci toni n gene-related polypeptide, suggesting that they have a role i n nociception. Their endings are com monly distributed within the mesentery and supporting l igaments of the abdominal or gans (88). These nerve endi ngs are frequently present near the branch points for the vasculature in the peri [Oneal lining. Few small-caliber nerve endings are present within the visceral organs themselves. (See additional com ments concern ing vagal activity in Chapter 8 . ) Physiologic (68) a n d clinical studies support the general sepa ration of regulatory information in to the vagal system and noci ceptive i n formation i n to the spi nal cord. Stimulating the greater thoracic splanchn i c nerve at surgery elicits severe pai n; however, blockade of rhe splanchnic nerve relieves pain ( I OO). I n addi tion, applying local anesthetic to rhe greater thoracic splanchnic nerve after abdo m inal surgery prevents the endocrine metabolic
6. A utonomic Nervo us System TA BLE 6 . 1 . V I SCERAL ORGANS A N D T H E I R APPROXI MATE SPINAL CORD LEVEL FOR T H E O R I G I N OF T H E I R PREGAN G L I O N I C N EURONSa Heart
T l ·T5
Stomach
T5-T9
liver and g a l l bladder
T6-T9
Pancreas
T5-T 1 l
Sma l l intestine
T9-T 1 l
Colon and rectum
TS-l2
Kidney and ureters
T l 0-ll
U r i nary bladder
T l 0-ll
Ovary and fallopian tube
T9-T 1 0
Testicle a n d epid idymus
T9-T l 0, L 1 - L2
Uterus
T l 0- L l
Prostate
l l -l2
Cerv ix
52·54
111
Those afferent axons rraveling with the vagus nerve respond ro such stimuli as plasma glucose concentration, POrtal venous blood osmotic pressure, and temperarure changes. The visceral afferem fibers associated with the splanch nic n erves are h igh-threshold mechanoreceprors and chemoreceprors located i n the walls of the bil iary system, among other places, and are responsive ro stretch and bradykinin concentration. The evidence available ro date suggests that all pain sensation from the liver and biliary tree is transmitted via the splanch n i c nerves and not the vagus nerve.
52-54 52-54 52-54
These levels create a viscerotopic map i n the lateral horns of the spinal cord.
•
responses such as increased plasma cortisol and urinary adrenaline levels that are usually presem in rhe early srages of recovery ( 1 0 I ) . The projecrion of the viscera afferem fibers through the sympa theric system creares a nociceptive map of rhe abdominopelvic organs on the dorsal horn of the spinal cord. This map has been demonstrared in h umans by sectioning the whire ram i commicans during rhe surgical rrearmem of visceral pain [Whire and Sweer, as cited in Janig and Morrison ( 88 ) ) . A sum mary of rhe organ oropic map of rhe human viscera is p resemed in Table 6 . 1 . The posirion of a specific organ in rhe visceral afferem organoropic map of the spinal cord coincides approxi marely with rhe origin of the sympathetic efferem system ro that specific organ. The nociceptive input ro the spinal cord over these visceral afferem fibers is not precisely mapped; i nstead, i nput from any one organ overlaps considerably w i th rhat from surrounding organs (88). Hepatobiliary Tree a n d Pancreas
The vascularure and parenchyma of rhe l iver and pancreas, as well as their associared ducts, receive i n nervarion fro m both di visions of rhe auronomic nervous system ( Fig. 6. 1 8) . I n addi tion, rhese organs have an abundam supply of visceral afferem fibers thar course in rhe vagus and rhoracic splanch nic nerves. Pregangl ionic sympathetic i n nervation ro these organs arises i n thoracic segments at approximately T 6 r o T9- l l a n d approaches the abdomen through the rhoracic splanchnic nerves. Sympa thetic gangl ionic neurons are located in the celiac ganglia. Their postganglionic axons reach rhe l iver and pancreas by h itchhiki ng on the heparic and pancrearic branches of the celiac trunk. Pre gangl ionic parasym pathetic axons, derived from the vagus nerve, pass through the fascia of the celiac region and follow the vascu larure ro the rarger organs. Little is known concerni ng rhe effects of auronomic nerve sti mulation on liver function. However, i n general, sympatheric activation drives t h e liver roward i ncreasing the ourpur of glucose ( 1 02 ) . A significant percemage o f t h e axons in t h e vagus and rhoracic splanchnic nerves traveling ro the liver and pancreas are sensory in narure. Approxi mately 90 of the vagal axons and 50 of the splanchnic axons ro the l iver are visceral afferem fibers ( 1 03 ) . These fW O afferem systems perform differem functions ( 1 3) .
Kidney and Urinary Tract Kidney
Although the kidney is primarily con trolled by endocrine mech anisms, ir does receive significant i n nervation from the sympa thetic adrenergic system that regulates, i n part , the retention of sodium (Table 6 . 1 ) ( 1 04- 1 07) . Alterations in the neural activity i n sympathetic fibers are involved i n the generation of certain forms of hypertension ( 1 08 ) . Very li ttle vagal parasympathetic (cholinergic) input ro the kidney has been reported. This organ does, however, receive neuropeptide-con tai ning, primary afferent fibers that course along with the adrenergic fibers ( Fig. 6.2 1 ) . The kidney receives most of i ts i n nervation from the thora columbar spinal cord. Preganglionic sympathetic neurons regu lati ng the kidney are located in the lateral horn of rhe spi nal cord extending approxi mately from segments T i l ro L1 . Their axons enter the abdominopelvic plexus over the lower thoracic and fi rst lumbar splanchnic nerves (Table 6. 1 ) . The postganglionic sym parhetic adrenergic fibers are derived from laterally positioned ganglia (someti mes called aorticorenal ganglia) in the celiac and superior mesenteric plexuses and course i nro the hilus of the kid ney along the renal vascularure. The adrenergic axons of the mammalian kid ney terminate on the ( 1 09 ) : Afferent a n d efferent glomerular arterioles Proxi mal and d istal renal rubules Ascending limb of Hen le's loop J uxraglomerular appararus All portions of the corrical tubular nephron are under neu ral inAuence. The relative density of adrenergic fibers is grearest around rhe ascending limb of the loop of H enle, followed in decreasing relative density by rhe d isral convoluted rubule and rhe proximal convolured rubule ( J 1 0, I l l ) . a -adrenoceprors have been located on the proximal convoluted rubule ( 1 1 2) as well as on the smooth m uscle of rhe vasculature. Sympathetic i n nerva tion of the kidney is i n volved in the normal regulation of sodium retemion, both by i ncreasing the transport of sodium across the tubule walls and by direcrly increasing the release of ren i n from the j uxtaglomerular apparatus ( 1 1 3, 1 1 4) . Srudies have shown that there is increased activity in the renal sympathetic nervous system in essential hypertension in h u mans ( 1 08 ) . A dual sensory i nnervation of t h e kidney ex ists: afferent fibers follow the thoracic splanchnic nerves back ro rhe spinal cord and the vagus nerve back ro the brainstem. Wirhin the kidney, pe ripheral endi ngs of both mechanoreceprors and chemoreceprors are found in close association with ureteric blood vessels (arter ies and veins) and in the walls of the pelvis of rhe ureter ( 1 1 5) .
112
/1. Osteopathic Considerations in the Basic Sciences
Left vagus n . Anterior -- vaga l tru n k Celiac
Posterior
/' vagal ./" /'
/' ,-/
t r u nk
./" S u perior
thoracic
splanchnic n
.-/
M i ddle thoraCIC spla n c h n i C n renal Celiac ganglion
ganglion
I n ferior thoracIc splanchnic n Aort lcorenal ganglion ---- R e n al ple x u s
gastric plexus
--
'�.
- Sympathetic trunk
H y pogast r i c n .
- I n ! . hypogastric ( pe l v i c ) p l e x u s
Inf
\"
1·... /. \'"
hypogastric -
( pelv I c ) p l e x u s Middle ureteric
A
nerve
FIGURE 6.21.
/ S2
,.
Aort i c plexus
/�/3 (:
// / 4 I: /I I (: II I '\ . .'\., --: I
�' :..:-�� - ::?
B
Innervation of the kidney. From Ansell J5, Gee WF. Diseases of the kidney. In: Bonica
ed. The Management of Pain. Philadelphia, PA: Lea
Their cell bodies are in rhe dorsal root ganglia located mainly in segmenrs at the thoracolumbar j unction (T I O-L3), and rheir cenrral processes rerm i nare i n rhe dorsal horn o f the spinal cord. These afferenr axons are classified as A and C-fibers. Vagal afferenr fibers, borh mechanoreceptors and chemoreceptors, play a role in renorenal reAexes. The mechanoreceptors are also i nvolved in modulating cardiovascular reAexes, thus regulating blood pres sure ( I 1 5) . Pain is the only detectable sensory perception that can be elicited from the kidney ( 1 3) . This modal i ry is carried in the visceral afferent fibers of the thoracic splanchnic nerves to reach the spi nal cord and the spinothalam ic tracts. In a study of the sym pathetic renal afferen t fibers i n the pri mate, all spinotha lamic tract cells excited by renal afferenr fibers were also excited by somatic afferenr fibers, indicating a powerful somatovisceral convergence on these cells ( 1 1 6) . This convergence has been sug gested as a mechanism to explain the referral of pain from the kidney ou( to somatic structures such as the Aank of the body. I n addition, this relationship may explain the changes i n the tone of muscle in nervated by the segmenrs T 1 0- L 1 that accompany renal infection or i nAammation. Ureter
Primary fu nction of the u reter is the unidirectional Row of urine from the kid ney to the urinary bladder. Although i t is richly i nvested with nerves ( J 1 7) , peristalsis i n rhe ureter is pri marily myogenic in nature, d riven by specialized pacemaker cells ( I 1 8) .
&
Febiger; 1 99 0 : 1 233, with permission.
Ureter
Bladder
JJ,
The course of the ureter is retroperitoneal, lying along the pos terior abdomi nal body wall and embedded in the transversalis fascia. The walls of the ureter consist of i n terlacing bundles of smooth m uscle fibers woven into a theca muscularis. Individual smooth m uscle cells inrerconnect via numerous gap j unctions, making the m uscularis a functional syncytium ( 1 1 9) . Modified smooth m uscle cells within the muscular layer serve as pacemak ers, initiating peristal tic contractions ( 1 20). A plexus of efferenr and afferenr nerve fibers that are capable of regulating the pace maker cells is wrapped around the m uscularis ( 1 1 9) . The ureter receives its in nervation in a segmental fashion. The upper portion is i nnervated by the lower thoracic and upper lumbar segmenrs (Tl 0-L1 ) and by the vagus nerve. The lower portion of the ureter is i n nervated by the upper lumbar segmenrs ( L 1 -2) and the pelvic splanch nic nerves (Table 6. 1 ) . The sym pathetic i n nervation reaches the upper ureter through the lesser thoracic and l umbar splanchnic nerves. Gangl ionic neurons are located in the celiac and associated renal and gonadal ( testicu lar or ovarian) ganglia. The lower ureter receives its sympathetic innervation from lumbar and sacral splanch nic nerves that con tribute to ganglia located in the superior and inferior hypogastric plexus ( 1 2 1 ) . F i bers containing ryrosine hydroxylase and neuropeptide-Y, markers for sympathetic axons, are in the outer muscle layers and the surrounding adventi tia of the human ureter ( 1 22- 1 24). Ac tivation of a-adrenergic receptors increases ureter peristalsis and
6. A 71to nomic Nervous System
elevates lumi nal pressures; whereas activation of tJ -adrenergic re ceptors decreases ureter peristaltic frequency and lowers intrau reter pressures ( 1 25). The actual role of the noradrenergic system in human ureter peristalsis has been questioned, and it appears that control over the surrounding vascular system is the dom i nant theme for the ureteric nerves (I 1 8). Parasympathetic in nervation for the upper portion of the ureter arises in the vagus nerve and reaches the ureter through the celiac and superior mesenteric plexus. The lower portion receives its cholinergic i nnervation from spi nal segments S2-4. These pelvic splanch nic nerves communicate with the ureter via the inferior hypogastric plexus. Acetylcholine-con taining neu rons are present in the mural gangl ia of the u reter, and fibers containing acetylcholine are present i n the mammalian ureter. These fibers are of greatest densi ry as the ureter enters the vesi cal wall. Stimulation of the u reter wall with acetylcholine results in an increased contractile activity and an increased basal tone of the mural smooth muscle ( 1 25 , 1 26). Acetylchol ine also re laxes the ureter resistance arteries using a mechanism involving endothelium-derived ni tric oxide ( 1 25). Afferent fibers to the ureter are derived from dorsal root gangl ia ranging from L2-3 to S 1 -2 (in guinea pigs) ( 1 27). Two classes of mechanoreceptors have been described i n the ureter walls ( 1 2 8). One class has low thresholds and is responsive to peristaltic-type contractions of the ureteric smooth muscle. The other class of mechanoreceptor has higher thresholds of activation and is most likely related to nociception. M any ofthese primary afferent fibers contain neuropeptides such as substance-P and calcitonin gene related polypeptide, thereby suggesting that they are i nvolved in nociceptive activities. Pain, presumably from �hese nociceptors, is the only sensory perception obtainable from the human ureter ( 1 3). I n the tho racolumbar dorsal horn of the spinal cord, inpu t from the ureter converges with somatic input from thoracol umbar spinal seg ments. Pain from distention of the ureter is often referred to the somatic body wall over a range of body segments. From the upper ureter, pain refers to the area from the anterior superior spine of the ileum anteriorly to the border of the rectus abdominis muscle (TI I - 1 2). From the middle ureter, pain refers to the area from the inguinal l igament anteriorly to the rectus abdomi n is muscle (T 1 2-L 1 ). From the lower ureter, pain refers to the suprapubic area ( L l ) and below i nto the scrotum or labia ( L2) ( 1 2 1 ). This descending segmental pattern of primary afferent fibers from the ureter is responsible for the descending movement of faci l itated segments as any obstructing material moves through the ureteric lumen. Urinary Bladder
The muscular components of the urinary bladder can be divided into two anatomical and functional parts: the body (or detrusor urinae muscle) and the base (or the trigone m uscle). The detrusor urinae muscle is the larger of the two parts and is active dur i ng ex pulsion of urine from the bladder. The trigone m uscle surrounds the openi ngs of the ureter in the base and the opening of the urethra i n the neck of the bladder. It acts as an i n ternal sphincter and, when contracted, helps to prevent the Aow of urine fro m the bladder. The detrusor and the trigone tend to oppose each other in activity. Both detrusor and trigone muscles comprise multiple
113
layers of smooth muscle fibers and receive an efferent innervation from the large autonom ic pelvic plexus. A th i rd muscle related to bladder fu nction is located inferior ro the trigone in the layers of the perineum. It is the deep transverse perineal muscle; the portion of this muscle that surrounds the urethra is called the sphi ncter urethra. Unlike the detrusor and trigone, this compo nent of the peri neal diaphragm is com posed of skeletal muscle and innervated by branches of the pudendal nerve, a somatic nerve (S2-4). The autonom ic i n nervation of the urinary bladder is ac complished through the hypogastric plexus that is embedded in endopelvic fascia (Fig. 6.22). Parasympathetic pregangl ionic (cholinergic) fibers from the i n termediolateral nucleus of spinal segments S2-4 enter the hypogastric plexus via the pelvic splanch nic nerves. These axons continue anteriorly i n to the vesicle plexus to termi nate on gangl ionic neurons located in the walls of the bladder. Their postgangl ionic (chol inergic and purinergic) ax ons supply motor i n nervation to all portions of the bladder wall. Sti mulation of the parasympathetic system, which occurs during voiding, is excitatory to the detrusor m uscle and inhibitory to the trigone muscle ( 1 29). Sympathetic pregangl ionic fibers arise i n the i ntermediolat eral n ucleus of spinal segments T I 1 -L2 ( Fig. 6. 22). They leave the sympathetic trunk cours i ng on lumbar and sacral splanch nic nerves to enter the inferior hypogastric plexus, eventually targeting prevertebral ganglia ( 1 30 ) . Sympathetic postganglionic (adrenergic) axons pass anteriorly through the inferior hypogas tric plexus and ultimately contribute to the vesicle plexus in the bladder adventitia. Their major target is the smooth muscle cells of the trigone m uscle with a m uch smaller contribution to the smooth muscle of the detrusor urinae. Sympathetic tone facil i tates contraction of the trigone muscles and relaxation of the detrusor urinae muscle, which is necessary to allow expansion of the bladder while i t i s filling ( 1 30 ) . The vesicle plexus con tains many gangl ionic neurons tradi tionally associated w i th the parasympathetic system. H owever, it is now clear that these neurons also receive input from adren ergic axons i n the sympathetic system. Thus, the sympathetic system can i n A uence the activity of the parasympathetic system by modulating the activity of the gangl ion cells. The ganglion cells i n nervating the trigone m uscle have a -adrenoceptors on their membranes and respond ro sympathetic sti mulation wirh contraction . Conversely, gangl ion cells in nervating the detrusor m uscle have tJ-adrenoceptors on thei r membranes and respond to sympathetic stim ulation with relaxation. It is through this differential distribution of adrenoceptors thar the sympathetic nervous system is capable of increasing the tone i n the trigone while simultaneously relaxing the detrusor uri nae ( 1 30). The sphi ncter urethrae muscle, or external ureth ral sph incter, at the base of the bladder, is skeletal m uscle; it receives i ts innerva tion from the perineal branches of the pudendal nerve ( Fig. 6 . 2 2). This is a somatic nerve containing axons from motoneurons lo cated i n the ventral horn of the spinal cord (S2-4). The release of urine from the bladder requi res an integrated viscerosomatic reAex i nvolving: l . Exc i tation of the parasympathetic system to activate the de trusor uri nae m uscle.
1 14
11. Osteopathic Considerations in the Basic Sciences
T1 1
't--f"""'--'-
Paravertebal ganglia
T1 2 1---P'-'-'-t-'-'+'c.:.:
Lumbar splanchric nerves
L1 L2 Superior
��� - hypogastric
Sacral para sympa thetic
Inferior masenteric ganglion
plexus Right hypogastric
Trigone muscle
1?m77JJ#m>-- External sphincter muscle
nerve
A
Right inferior hypogastric (pelvic) plexus
B
Pelvic splanchric nerves
Pudendal nerve
FIGURE
6.22. A: Inferior hypogastric plexus as it i n nervates the viscera of the pelvic bas i n . B: Somatic i n nervation of the u r i n a ry bladder and its external s p h i n cter. From Gee WF, Ansell JS. Pelvic and perineal pa i n of urologic orig i n . In: Bon ica JJ, ed. The Management of Pain. Ph i l adelphia, PA: Lea & Febiger; 1 990: 1 369, with permission.
2. I n hibition of the sympathetic system to relax the trigone and internal sphincteral muscles. 3 . Subsequent inhibition of the pudendal nerve to relax the ex ternal sphincteral muscles. Vesicle afferent fibers arise from mechanoreceptor endi ngs in the connective tissue and epithelium of the vesicle mucosa and travel over the lumbar and pelvic splanchnic nerves as well as pudendal nerves to reach the cord at the U -2 and 52-4 levels. Cell bodies for these nerves are ptesent in the associated dorsal root ganglia. Many of these fibers contain neuropeptides such as those represented in the small-caliber, primary afferent fibers system ( 1 30 ) . The afferent fibers reach only to the dorsal horn of the spi nal cord near their segmental level of entry; however, a small number of these fibers enter the spinal cord and follow the ascending tracts rostrally to terminate in the lower regions of the medulla. Sensory information from d istension of the bladder initiates the reA exes i nvolved in voidi ng. I ni tial filling of the bladder trig gers low-level afferent volleys that increase the tone in the trigone muscle and external sphi ncter muscles and inhibit the tone i n the detrusor urinae muscle, allowing the bladder to serve as a reser voi r for urine. After a certain level of filling is reached, a higher intensity of afferent volleys from the bladder wall reverse these reA exes such that the detrusor urinae muscle tone is enhanced and the tone of the trigone and external sphincter is inhibited.
This reversal of reAexes prepares the bladder for voidi ng. The last step, relaxation of the external sphi ncter, requires cooperation of the suprasegmental control of the bladder musculature, allowing volitional control of voiding ( 1 30). Reproductive Tract
The pelvic and peri neal organs of the male and female re productive systems receive both sympathetic and parasympa thetic innervation through the complex abdominopelvic plexus ( Fig. 6.23). This in nervation targets the glandular cells and smooth muscle of the vasculature as well as the mural smooth muscle present in the tubular portions of these organs. The ori gin of this i nnervation varies accord i ng to the embryonic origin o f the specific organs. The testis and ovary, which arise i n the gonadal ridge of the posterior abdominal wall, receive thei r af ferent and efferent supply from the abdominal portions of the abdominopelvic plexus. The remain ing pelvic organs of repro duction are innervated from the pelvic portion of the plexus. Afferent fi bers are present i n each of these organs, and their input to the spinal cord is a key feature in the presentation of pelvic palll . Testis an d Ovary
Gonadal tissue receives sympathetic innervation from pregan glionic neurons located in spinal segments T I 0 and T I l . These
6 A utonomic Nervous System
T ( 1 1 ) _-F"-�-:.I
1 2 '1---P....,�:.:..: L1 '1'--r-"':":':k
Tl l
,+--p'"'-'-f.-.:J..
115
Sympathetic trunk
T1 2 't--P....,�:.:..:
L2 l---'-¥'--'4
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L2
Aortic plexus
Inferior Mesenteric ganglion Sacral splanchnic nerves
Superior hypogastric plexus
Uterus
Pudendal nerve
A
R ight inferior hypogastric ( pelvic) plexus
B
FIGURE 6.23. A: I n nervation of the m a l e reproductive organs. B: I n nervation of the female reproduc tive organs. From Gee WF, Ansel l JS. Pelvic and perineal pa i n of urolog i c o r i g i n . In: Bon ica JJ, ed. The Management of Pain. Phi ladelphia, PA: Lea & Febiger; 1 99 0 : 1 369, with permission.
pregangl ionic axons target neurons i n the celiac and superior mesenteric ganglia. The gonadal (spermatic or ovarian) plexus of fibers arises from these ganglia and follows the course of the gonadal aneries. Additional sympathetic postganglionic axons join the gonadal plexus from the superior hypogastric plexus in the lower abdomen. In females, the gonadal (ovarian) plexus in nervates the ovary and extends on to reach the uterine tubes. In males, the gonadal (spermatic) plexus j o i ns the spermatic cord with the vas deferens and proceeds through the i nguinal canal to reach the scrotum. Adrenergic fibers in the testis are present around blood vessels and i nterstitial cells of the seminiferous tubules and in the tubules of the epididymis ( 1 2 5 ) . Stimula tion of the sympathetic nervous system initiates strong peristaltic waves i n the vas deferens, which is responsible for the propulsion of sperm. Parasympathetic i n nervation of the gonadal tissue is less dense than that of the sympathetic fibers. Choli nergic fibers arise from the vesical plexus and join the gonadal plexus as i t passes though the pelvis. These fibers primarily target the vas deferens and the seminal vesicles. Afferent fibers from the testis, epididymis, and vas deferens extend through the gonadal plexus to reach the thoracolumbar spinal cord. Fibers arising i n the testis target segment T I O, those from the epididym is enter the spi nal cord at T I l and T I 2, al though those from the vas deferens enter at Tl 0-L 1 ( 1 3 1 ) . Af ferent fibers from the ovary also ascend in the gonadal plexus to enter the spinal cord at the T l 0 level. The return of afferent axons from the gonadal tissue to the lower thoracic level of the spi nal
cord is responsible for the referral of pain to the thoracolum bar j unction and the facili tation of segments in this area consequent to irritation of the gonadal tissue. Uterus, Uterine Tube, Cervix, and Vagina
The distal portion of the abdominopelvic plexus bifurcates as it descends over the sacral promontory to enter the pelvic bas i n . T h e pelvic portion of t h i s complex neural structure is called the inferior hypogastric or pelvic plexus. This network of gangl ia and fibers sweeps laterally along the pelvic walls to surround the midline organs of the female pelvis. As this plexus crosses over the transverse cervical l igamen t, its fibrous network thickens to form the elaborate plexus of Frankenhuser (a regional subset of the inferior hypogastric plexus ) . From here, autonomic axons ac company the uterine vessels medially along the transverse cervical ligament to gai n access to the uterus, cervix, and vagi na. The re mainder of the i n ferior hypogastric plexus extends anteriorly to surround the bladder (this collection of fibers is often referred to as the vesical plexus). Sympathetic pregangl ionic neurons capable ofin Auencing the uterus and cervix are located i n the T 1 0-L2 spi nal segments ( Fig. 6.23). Their axons target neurons in the celiac ganglia and other prevenebral ganglia. Postgangl ionic fibers from these gan glia descend i nto the pelvic basin coursing i n the superior and inferior hypogastric plexus to eventually reach the uterus. For the most pan, these adrenergic fibers end on the vasculature of the uterus. Some axons term i nate in the s11100th muscle of the
116
ff. Osteopathic Considerations in the Basic Sciences
myometrium, particularly i n the longitudinal layer ( 1 32) and among the glands of the endometrium. The parasympathetic i nput to the uterus and cervix arises i n the i n termediolateral nu cleus of spinal segments 52-4. These axons target ganglia located in the plexus of Frankenhuser; whereas postgangl ionic (cholin ergic) axons extend from this plexus i nto the uterus following the uterine artery. Most of the choli nergic i nput to the uterus is confi ned to the vascular supply with a small amount reaching the glands of the endometrium and a few fibers i n the circular muscle layer of the myometrium ( 1 32). Beyond regulation of the vasculature, the function of this elaborate autonomic inner vation of the uterus is not well known. Evidence suggests that stimulation of the adrenergic and chol i nergic i nputs can enhance the contraction of mammalian uterine myometrium ( 1 33 ) . The number and size of adrenergic nerves appears to i ncrease in the uterus dur i ng pregnancy ( 1 34), further suggesting a role for these fibers in the uteri ne contractions o f l abor and delivery. The uterus, cervix, and vagina receive a complex afferent in nervation that inAuences the referral of pain during parturition ( 1 35 ) . Experimental studies i n cats demonstrate that afferent fibers from the uterus and cervix enter the spinal cord over a range of levels (T I 2-53) ( 1 36) . The majority of fibers from the fallopian tubes have cell bodies in the dorsal root ganglia of the lu mbar segments; whereas the majority of fi bers from the cervix have cell bodies in the dorsal root ganglia of the sacral segments. Clinical studies suggest that the afferent fibers from the human uterus project to even higher levels of the spinal cord (T 1 0) ( 1 35) and that the majority of pain fibers from the uterus enter the thoracolumbar spinal cord 0 37, 1 38). Nocicep tive fibers from the uterus pass upward through the superior hypogastric plexus and lumbar splanch nic nerves to enter the spinal cord over the wh i te rami of the lower thoracic and lum bar segments. For this reason, the white ramus at Ll can be particularly large. The pathways handling sensory i n formation from the female reproductive tract are split. I nput from above the cervix ascends through the superior hypogastric plexus to the thoracolumbar junction although afferent fibers from the cervix and below descend into the sacral spinal cord (68) . This arrange ment of primary afferent fibers is responsible, in part, for the presentation oflow-back pain late i n pregnancy as well as accom panying facil itation of spinal segments around the thoracolumbar j unction. Erectile Tissue of the Penis and Clitoris
The sympathetic in nervation of the vasculature and erectile tis sue in the pen is and clitoris has i ts origin in the in termediolateral cell column of spinal cord segments T I I -L2 ( Fig. 6.23). At least two routes exist through which these fibers reach the penis. One route involves preganglionic axons that arise in the thoracolumbar spinal cord and synapse i n the associated paravertebral ganglia. From these ganglia, adrenergic postganglionic fibers join the hy pogastric plexus to pass i n to the pelvic basin, eventually entering the pen is at its root on the perineal d iaphragm. The second route comprises sympathetic preganglionic axons from thoracolumbar segments that pass by the paravertebral ganglia to terminate in pelvic ganglia located deep in the pelvic plexus. Postgangl ionic adrenergic axons from these ganglia reach the root of the penis or cl i toris by following the associated perineal vasculature.
Parasympathetic in nervation of the vasculature and erectile tissue arises in the sacral (52-4) spi nal cord. Postgangl ionic ax ons from neurons in the scattered ganglia of the pelvic plexus join the sympathetic axons entering the pen is or clitoris over its root. Nonadrenergic, noncholi nergic axons, presumably from cells located i n the pelvic ganglia, also i nnervate the erectile tis sue. Somatic motor i nnervation of the clito ris and penis arises in Onuf's nucleus of the ventral horn of spinal cord segments 52-4 . Their axons travel the course of the pudendal to the perineum where they innervate the followi ng structures, all of which are composed of skeletal m uscle: Bulbocavernosus muscles Ischiocavernosus muscles Superficial and deep perineal muscles External urethral sphincters Anal sphincters The sex act requi res coordinated viscerosomatic reAexes in volving the organs and musculature of the pelvic and perineal region ( 1 30). I n itially, somatic and/or emotional stimuli activate parasympathetic outAow from the sacral cord to the vasculature of the erectile tissue. The cholinergic fibers activate the release of nitric oxide from endothelial cells, which relaxes the vessel walls and results in increased perfusion of the tissue. Once the erectile tissue is engorged, additional stimuli initiate a sympathetic bar rage fro m the thoracolumbar ju nction of the cord. Th is output results in contraction of smooth muscle in the vas deferens in the male and in the walls of the vagina in the female. Coordinated reAex activation of the perineal nerve subsequently results in con traction of the bulbospongiosus, ischiocavernosus, and transverse perineal muscles. The rhythmic contraction of these muscles as sists in forcing the ejaculate along the urethra in the male and constricts the vestibule of the vagina in the female. Integration of these three efferent pathways (parasympathetic, sympathetic, and somatic) occurs i n the circuitry of the sacral spinal cord segments and is necessary for successful completion of the sex act.
CONCLUSION
The autonomic nervous system is a major factor orchestrating the diverse functions of i nternal structures. Through an exten sive network of connections, the autonomic nervous system helps maintain the normal rhythm of activity in the visceral organs as well as adjust their output to accommodate any external chal lenge. This conglomerate of interlocking systems, with its per vasive i n Auence on our physiology and psychology, is called the neuroendocri ne-immune network. This network is described in more detail in Chapter 8 and in Chapter 9 of the previous edi tion of this book ( 1 39).
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NEUROPHYSIOLOGIC MECHANISMS OF INTEGRATION AND DISINTEGRATION MICHAEL M. PATTERSON ROBERT D. WURSTER
KEY CONCEPTS • • • • • • •
• • • • •
The background of neurophysiologic research i n osteopathic medicine The reflex and the interactions affecting reflex activity Types of reflex interactions and the importance of reflexes in body function Neural basis of reflex interaction and integration and how reflex integration is exhibited in cardiac control How spinal and higher nervous areas interact in reflex control Concept of the facilitated area or segment of the spinal cord and how it affects function Effects of nociception on peripheral tissues and how nerve fibers transmit materials to and from peripheral structures Central excitation changes and four stages of alteration of spinal neuron excitability What causes the changes of spinal neuron excitability and the time course of each I m portance of trophic factors for normal function The implications of alterations in neural integrative function for health I mportance of manipulative treatment in maintaining optimal function and health
The human body is a machine run by the unseenforce called lifo, and that it may be run harmoniously it is necessary that there be liberty ofblood, nerves, and arteries .from the generating point to destination (1). The foundations of the osteopathic profession, laid by its founder, Andrew Taylor Still, M D , DO, recognize that the state of health is a continuum from complete b reakdown to perfect function. One of Still's basic beliefs about function was that the body was a totally integrated unit, its structures working together harmo niously to produce a state of health. Lacking that harmonious function, the body produced conditions promoting loss of heal th,
or disease. I mplicit i n these assumptions is the idea that the var ious parts of the body are functionally i nterconnected, allowing for necessary adaptations when demands on the body change. This view necessitates that the supply and maintenance organs, mainly the visceral structures, are functionally connected with the primary energy consumer of the body, the m usculoskeletal system. This i nterrelationshi p has long been neglected in medical practice. The communicating systems of the body, including the i mmune, endocrine, and neural systems, provide this intercon nectedness. When a problem develops in the integrating systems of the body, function cannot help but be compromised, and the stage is set for a lowered state of health, and eventually disease, to occur. The field of neurophysiology is important to the physician. A thorough knowledge of anatomy and the structural relationships within the body are vital. The physician must also know how these structures function and relate to each other. He or she needs a basis for providing the patient with a rational course of treat ment, especially manipulative treatment. The physician must be aware of what palpatory diagnosis is telling him or her about the underlying state of the body, and therefore of the person. Many excellent neurophysiology texts are available that outline the basics of the field. This chapter does not attempt to give an overview of the entire field or all the areas of special interest to the osteopathic physi cian. It focuses on the integration of somatic and visceral function through the reflex pathways and relates these interactions to their specific neural basis. Functional alterations in reflex pathways that can disrupt integration are reviewed, along with the noni mpulse based or trophic function of the nervous system, and how this provides a means of rwo-way communication within the body not dependent on the better understood neural impulse-based communication. These aspects of the integrative activity of the nervous system are i mportant in the osteopathic clinical experi ence and the role of manipulative treatment in health care. As Still recognized before the turn of the century, proper function necessitates the free interaction and integration of all body sys tems. Rational treatment of functional problems likewise requires an understanding of how these interactions occur and what can alter their function.
7.
NeurophysioLogic Mechanisms ofIntegration and Disintegration
NEUROPHYSIOLOGY IN THE OSTEOPATHIC PROFESSION
The search for mechanisms underlying the efficacy of osteopathic methods began with the founding of the osteopathic p rofession. Although Still did not pursue what we would call organized re search, he certainly was a fi ne researcher. He constantly ques tioned his observations and searched for better ways to find health and ameliorate disease. His early students at the American School of Osteopathy soon began to actively investigate the basis for the treatments they were developing. Their observations resulted i n the formulation o f the concept of the osteopathic lesion (now known as the somatic dysfunction) . The osteopathic lesion was a set of palpatory cues and signs that indicated a functional distur bance in the body that predisposed i t to disease. The early pioneers of the profession believed that somatic dysfunctions were primary causes of clinical breakdowns that resulted in the many manifes tations of disease, either by themselves or by allowing, through reduced function, microorganisms to overwhelm the body de fenses. When viewed in this perspective, the statement by Still that "all diseases are mere effects, the cause being a partial or complete failure of the nerves to properly conduct the fl uids of life" (1) is more meaningful. Still believed that various types of diseases were not entities unto themselves but were the result of the body's efforts to regain optimal function in the face of adverse influences, which is a view that is becoming more strongly supported by the current idea of the "illness response" (2,3). Thus, the events that led to the disrup tion of the body's normal function became the primary events to treat in the osteopathic physician's efforts to remove the influences resulting in clinical illness. The osteopathic lesion was viewed as one of the primary factors i nfluencing body function. In addition, the osteopathic lesion was amenable to physical manipulations. In addition, Still and his students realized that the body was of necessity an integrated unit; the visceral systems were tightly connected to the somatic systems. They felt strongly that visceral disturbances would cause manifestations in the somatic structures and that somatic disturbances would cause visceral dysfunctions. This reciprocal relationship became very important in the pro fession's thinking, clinical practice, and research endeavors. Early research efforts in the profession largely aimed at pro viding evidence for the somatic problems identified as the os teopathic lesion and the effects of these dysfunctions on various aspects of function (4) . I n their efforts to find objective measmes of the osteopathic lesion, researchers at the American School of Osteopathy used skiography, an early form of x-ray, to look at bony placement and circulatory function as early as 1898. An other early research thrust was the effects of somatic disturbances on visceral function. Louisa Burns began research in this area early in the 1900s with studies on dogs that showed that stim ulation of the lower dorsal region increased muscle contraction in the stomach and i ntestines bur that steady pressure for a time tended to inhibit such contractions (4) . Burns eventually be came head of the A. T. Still Research I nstitute in Chicago and produced a body of research suggesting that strains produced in the vertebral column would, over time, have definite and re producible effects on visceral function and morphology. Aided later by Wilber Cole, effects of somatic strains on neural endplate
121
function controlling visceral o rgans were found and documented by neural stains. In addition, Cole was able to well delineate the pathways for the effects of somatic influences on visceral func tion (5) . The early research efforts of the osteopathic profession by Burns, Cole, and others were attempts to describe the effects of somatic disturbances on visceral function and the effects of ma nipulative treatment on immune and general function, among other things. They established a firm interest in the profession on the interrelationships between somatic and visceral function. Beginning i n the late 1930s, a new era of research in osteo pathic medicine began. In an effort to enhance the profession's repuration, ]. S. Denslow began a program of research at the Kirksville College of Osteopathy and Surgery that was to span 40 years and add m uch to the understandi ng of the methods of manipulative treatment. With his colleagues, Denslow used the then cutting edge technology of electro myographic (EMG) recordi ng to obtain objective evidence of specific alterations in somatic function that correlated almost exactly to palpatory find i ngs (G). Joined by Irvin M . Korr i n 1945, Denslow used the EMG technology to show that one of the u nderlying causes of palpa tory findings was, i n deed, altered muscle excitability. Korr then i n terpreted these findings in terms of neural function and the concept of the facilitated segment was developed as an underpin ning of the osteopathic lesion (7) . The research of the Kirksville group (see discussion later in this chapter) fi rmly placed the inter actions between somatic and visceral structures in the forefront of the underpinnings of osteopathic clinical practice and philos ophy. It became obvious that the i nteractions between visceral and somatic structures were important in health maintenance and disease processes. These interactions also provided an ex planatory framework for the i mpact of manipulative treatment as not only influencing somatic function but also having a real and often vital effect on visceral function. Thus, this chapter will focus on the interactions between visceral and somatic structures and how they are o rganized. In addition, the alterations in spinal cord function that can occur with somatic input and its i nflu ence on visceral function will be discussed. Understanding these i n teractions and alterations, beginning with the organization of the basic reflex arc, is important in understanding the value of osteopathic treatment techniques and the neural basis of health.
THE REFLEX
In 1 905, Charles Sherrington (8) published The Integrative Ac tion of the Nervous System. This classic text represented current knowledge about the fundamental aspects of how the nervous system handled and i n tegrated information. Over the ensuing years, considerably more has been learned about the function of the nervous system and how it integrates the many functions of the body. A great deal is known about how the basic structural unit of the nervous system, the neuron, i nteracts with other cells through synaptic structures and the release of neurotransmitters and neuromodulators. The billions of neurons and glial cells that make up the nervous system are organized i n to functional groups, often with widely differing structural and functional characteris tics. Many of the neurons are involved in networks that respond to stimuli impinging on or even originating in the body, which
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11. Osteopathic Considerations in the Basic Sciences
results in commands to muscles and glands that produce activ ity or secretions. These networks, the reflexes, have been more fully analyzed in recen t years. What were previously considered to be almost autonomous units of function are actually complex and i n teractive aspects of an organizational whole. The reflex has been found to be anything but a static unit of i nput/output re lationships, but rather it is an active and ever-changing mosaic. The characteristics of reflex function are modulated by messages from other areas of the nervous system and by activity of the en docrine and immune systems. In fact, reflexes must not be viewed as separate entities but as parts of various programs that con trol motor and secretory actions. Thus, an i ndividual reflex may serve differing functions depending on which control program is operating (9) . However, for purposes of analysis, reflexes have usually been isolated for study, a practice that has erroneously led many students to view reflexes as simple and unchanging entities.
Afferent limb
Sense organ (e.g., skin) Central limb
Structure
The common concept of the reflex is basically one of a relation shi p between an input stimulus to the body and an output action to either a m uscle or a secretory organ. Sherrington viewed the reflex as an input/output relationship between i n formation com ing into the body and a response to that i n formation. He viewed a reflex as always inherited and innately given (8) . The concept of a reflex i ncludes an afferent or i ncoming limb from a sen sory receptor, which is a central component in the spin al cord or brain. It also includes an output (efferent) limb that is usually a motor component to either somatic (musculoskeletal) or visceral structures terminating in synaptic connections that may either activate o r i nhibit activity i n these structures (Fig. 7.1). The usual concept of the reflex suggests that the reflex limbs are fai rly well defined and limited primarily to one i nput and one output channel, with little i n teraction with other reflex networks (Figs. 7.2 and 7.3) . Almost all reflex networks can be i nfluenced by a wide variety ofother excitatory and inhibitory signals, including those coming fro m higher or lower levels of the central nervous system. The picture of a reflex as a simple message pathway from the patellar tendon that causes the quadriceps femoris muscle to contract, resulting i n a knee jerk, is a vast oversimplification of the interactions that occur when a stimulus causes a response. The tendon tap reflex, exemplified by the patellar tap/knee jerk reflex activation, is, however, a prime example of the simplest reflex structure. The tendon tap, or myotatic reflex, is a monosynaptic reflex. It is the only monosynaptic reflex present in the human. The stimulus of a tap to a tendon stretches the m uscle attached to the tendon, which in turn stretches the muscle spindle organs i n the muscle. Neural signals, or action potentials, are sent from the spindle organs to the spinal cord on the i ncoming, or afferent, limb of the reflex. I n this case, the signals travel through the spinal cord on the axons from the spindles directly to the motoneurons that innervate the muscle that was stretched. They make synaptic contact with the motoneurons causing them to generate action potentials that travel over the efferent, or outgoing, limb of the reflex network back to the m uscle, which causes i t to contract. It would be a simple picture if this was all that happened.
Effector organ (e.g., muscle)
Efferent
limb
FIGURE 7.1. Schematic of reflex as it is usually envisioned, with affer ent, central, and efferent limbs.
However, the i ncoming axons send off branches that go to other neurons in the spinal cord that, in turn, send axons to the mo toneurons of the antagonist of the stretched muscle. These axons provide signals that inhibit the motoneurons innervating the an tago nist muscle. When the stretched muscle contracts, the antag on ist muscle is i nhibited to allow a smooth movement to occur.
Dorsal
Ventral FIGURE 7.2. A common, mistaken concept of how a reflex is con stru cted. Afferent limb simply connects with central limb, which acti vates efferent limb. Left. monosynaptic reflex; right, pol ysynaptic reflex. Actual complexity is better represented in Fig. 7.3.
7.
Neurophysiologic Mechanisms 0/Integration and Disintegration
Dorsal
123
Many somato-somatic reflexes have been documented and studied. The simple somato-somatic reflexes are exemplified by defensive withdrawal actions such as when accidentally touching a hot object and the arm jerks back. Very complex activities, such as the righting reflexes that occur, for example, when a cat is dropped upside down and lands on its feet are also found, but even these reflexes do not occur in isolation; as with the myotatic reflexes, they are accompanied by a spread of activity throughout the nervous system.
VISCERa-VISCERAL
Ventral
FIGURE 7.3. Schematic of neural interactions at the spinal level, indi cating the complexity of even s imple reflexes. Input to the spinal cord sends collaterals up and down the cord and is acted on by ascending and descending influences, as well as input from the opposite side of the cord. Input courses through several synapses and interneurons before acting (in thoracolumbar cord) on both somatic and sympathetic mo toneurons. In cervical and sacral cord areas, parasympathetic pathways are involved.
A second type of reflex is the viscero-visceral reflex, in which sen sory input from a visceral structure causes activity in a visceral organ. These reflexes are involved, for example, in distention of the gut that results in increased contraction of the gut mus cle. Viscero-visceral reflexes involve afferent activity flowing from the receptors into the spinal cord through interneurons to pro duce efferent or outflow activity within the sympathetic and/or parasympathetic motoneurons.
REFLEX INTERACTIONS
In addition, other branches from the incoming axons go up the spinal cord to other spinal areas (for example, to the arms if the patellar reflex was stimulated) , to the brainstem, as well as down the spinal cord to lower spinal centers. What appeared to be a simple reflex network has become a complex set of pathways within the spinal cord and brainstem. In addition, pathways from both above and below the level of the input axons can directly influence the basic excitability of the motoneurons involved and, hence, alter the reflex activity observed when the tendon is tapped. I ndeed, when elicited clinically, the tendon tap reflex is used as a porthole into the nervous system to see how i t is functioning, and the clinician is not usually interested in that reflex per se. I n fact, the main purpose o f using the tendon tap reflex clinically i s t o test the excitability o f the motoneurons, a s a function o f both local and distant infl uences.
SOMATa-SOMATIC
Although the tendon tap reflex is used a great deal clinically, the most familiar of the spinal reflexes are the defensive reflexes, such as the withdrawal movements of a limb to a noxious stim ulus. These somato-somatic reflexes occur when some stimulus is applied to a somatic structure. This initiates a volley of neural activity (often nociceptive) through the afferent limb of the re flex to the spinal cord. The afferent input activity flows through synapses into the interneurons of the spinal cord central gray, and finally into the ventral horn motoneurons. These motoneurons then cause somatic muscle contraction. The reflexes have at least one interneuron between the sensory input in the dorsal horn of the cord and the motoneu rons of the ventral horn (Fig. 7.3) . They are named from the origin of the information and the locus of action, both somatic.
We might expect to find that afferent input from somatic struc tures has some influence on visceral organs and that input from visceral structures has some effect on somatic o rgans. Somato visceral and viscero-somatic reflexes have been known for many years but, until recently, have received little attention from the research and medical community. H owever, these types of reflex i nteractions are very i mportant for the practice and understand ing of osteopathic palpatory diagnosis and treatment and for the integration of body function. A fami liar example of a viscero-somatic reflex is pain and muscle tightness in the left shoulder with onset of a myocar dial infarction (MI). The nociceptive input from the compro mised myocardium (a visceral structure) is exciting not only the pathways that are interpreted as shoulder pain (a somatic structure) but is also causing the motoneurons supplying the shoulder muscles to become active. In a classic study, Eble (J 0) showed several such reflexes by stimulating visceral structures and recording somatic m uscle activity. He demonstrated that stim ulation of various visceral structures produced somatic muscle activity. Conversely, activity in a somatic structure can alter visceral function. In a number of studies over the last several years, Sato (11) clearly demonstrated the effect of somatic stimulation on var ious visceral functions, ranging from heart rate to adrenal output. These studies have also shown that some of these reflex interac tions occur directly in the spinal cord. With others, the afferent activity from the somatic stimulation travels up the spinal cord to the brainstem, resulting in a cascade of activity from the brain stem back down to the spinal autonomic motoneurons. In both viscero-somatic and somato-visceral reflex networks, activity resulting from the stimulation of a structure can have either an excitatory or inhibitory influence on the motoneurons involved. For example, stimulation of the belly skin usually results
124
fI. Osteopathic Considerations in the Basic Sciences
in inhibition of gut activity (a somato-visceral reflex) bur increases heart rate. In daily life, the body's somatic system is active. The skeletal muscles are the machines that carry out activities. The visceral organs are the means by which the energy demands and mainre nance of the muscles are met and by which waste is disposed of. Without a continuous and highly inregrated comm unication be tween these two systems, the body could not conrinue to achieve a balance among: Its energy needs and supply The amounr of blood necessary to carry nutrienrs and waste and fulfill the demands of the muscles and bones Supply and demand in general
, ,
Neural Basis for Reflex Interactions
Evidence is accumulating about the neural basis of viscero somatic and somato-visceral inreractions. When a stimulus is applied, afferenr input from either visceral or somatic structures flows into the spinal cord along the dorsal roots and enrers the upper areas of the spinal gray maner. The spinal gray maner is com monly divided inro ten layers, fi rst documented on cytoarchi tectural evidence by Rexed (12) (Fig. 7.4). Large-diameter, cuta neous afferent input that signals nonnociceptive stimuli enters the spinal gray of the dorsal horn and terminates primarily in layers 1l I and IV. Nociceptive afferenrs from both somatic and visceral structures enrer the cord and send branches rostrally and caudally in Lissauer's tract that runs along the apex of the dorsal horn. Branches of this nociceptive input then terminates in layers I , n, Y, V1I, and X. Layers I and V display an especially tremendous overlap of the input fro m somatic and visceral nociceptors (13) . It now appears that in most areas of the spinal cord, practically every inrerneuron that receives inpur from a visceral nociceptor also receives inpur from a somatic source. It also appears that al most 80% of interneurons that receive input from somatic struc tures also receive visceral input. Presently, there is no evidence for any ascending pathway that transmits only visceral sensory signals from the spinal cord to the brain. This raises the question of how an individual can distinguish visceral fro m somatic pain or sensa tion at all. In many cases, visceral pain is fel t as a diffuse and poorly localized sensation and is referred to somatic structures. The over lap of somatic and visceral input explains the referral of visceral pain to somatic structures, which is designated as referred pain.
.
, , .
The neural connections represenred by these reflex systems are one of the primary ways this inregration is carried out. For the osteopathic physician, the viscero-somatic and somato-visceral reflexes are of extreme importance. When us ing palpatory diagnosis to detect subtle problems in function, whether it be tissue texture changes, motion characteristics, or temperature variations of the body, the physician is sensing clues from the musculoskeletal system, skin, muscles, and fascias. These clues reflect not only aspects of these tissues but also func tional characteristics of the underlying visceral organs and tissues through the viscero-somatic reflex networks. When the physician uses manipulative treatmenr to correct somatic dysfunctions, un derlying visceral function is affected through the somato-visceral reflex networks. Thus, for both palpation and treatment, an un derstanding of reflex function is necessary.
.
X
.
0
,
VII "
"
"
"
,
..
,
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FIGURE 7.4. Rexed layers. Laminae at the L-7 segment of a cat spinal cord. From Rexed B. The cytoarchitectonic organi zation of the spinal cord in the cat. J Comp Neural. 1952;96:415 -495 , with permission.
I mpulses arriving from visceral structures and converging onto inrerneurons also receiving somatic afferenrs activate ascending pathways to the brain that result in the perception of pain in the somatic structure. In addition, more somatic than visceral input occurs because the viscera are much more sparsely inner vated with sensory receptors. This suggests that visceral input has much more diffuse functional effects than the corresponding somatic afferents do. For example, it appears that many of the somatic C fibers terminate primarily in focal areas of layer If of the cord. Visceral C fibers extend for several segments and give off collaterals at regular intervals. Only about 10% of the inflow into the thoracolumbar spinal cord comes from visceral structures (14) . This sparse innervation but wide distribution of visceral af ferenrs may be the basis for the diffuse nature of most visceral pain. The evidence indicates that the widespread effects ofvisceral input is due more to functional (spread of activity through net works) than anatomic (many collateral branches) divergence (15). Figure 7.5 shows the afferent terminations of somatic and visceral afferent fibers in the various levels of the spinal cord. The overlap of input onto common inrerneurons within the gray maner of the spinal cord is also the basis for the activation of somatic muscle activity seen with visceral disturbances. The excitatory drive provided onto common interneurons by visceral input activates not only sympathetic outflow back to visceral structures but also motoneurons (both alpha and gamma) that innervate skeletal musculature. The result is a tonic activation of skeletal muscles in the referral area of visceral input. This is the viscero-somatic reflex manifestation, or splinring, that is seen, for example, in appendicitis.
7.
125
Neurophysiologic Mechanisms ofIntegration and Disintegration
Lissauer's tract
C-pol ymodal nocicept or
resulting in decreased vasoconstriction and better fl uid flow in the thoracic area (16). Although much of Out information on the activation of sym pathetic afferents by skeletal input has come from nociceptive input, there is evidence that sympathetic output can also be strongly driven independent of nociception by m uscle propri oceptors. For example, Kaufman (I7) has shown large effects on sympathetic outflow driven by alteration of proprioceptive input from m uscles. Thus, the evidence for activation and con trol of sympathetic activity by somatic input strongly suggests a basis for musculoskeletal activity in the regulation of body func tion through somato-visceral reflexes. Likewise, recen t research by Jou and Foreman (18) has shown that cardiac efferenrs can have dramatic influences on m uscle activity, supporting the role of viscero-somatic reflex connections as u nderlying the effective ness of palpatory diagnosis in visceral disease states.
CARDIAC CONTROL
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We will now consider a model of viscero-somatic and somato visceral interactions shown in cardiac control. Neural input from somatic structures may affect neural activity to both somatic and visceral structures. A good example of the interaction between so matic afferents and autonomic outflow is the control of the heart. As with most visceral structures, the heart receives its autonomic innervation from both sympathetic and parasympathetic nerves .
FIGURE 7.5. Terminal patterns of pri mary afferent collaterals i n the transverse plane of spi nal cord. Left, pri mary afferent termi nations of axons not associated with nociception. A, (-low threshold mechanore ceptor; B, i nnocuous cooling receptor; C, A hair afferent; D, G-1 and G-2 hair receptors; E, slowly adapting type I and II afferents; F, primary and secondary muscle spi ndle afferents; G, Golgi tendon organ. The ar row indicates that the parent axon bifu rcates and ascends and descends the spinal cord for 17 segments giving off collaterals along this course. Right, nociceptor afferents from both somatic and visceral structures. Both visceral and somatic A and ( fiber nociceptor afferents termi nate in Rexed lamina I, II, V, and to some extent in VII and X. Lamina are i ndicated on the right and ou tlined by dotted lines. From Light AR. The Initial Processing of Pain and Its Descending Control: Spinal and Trigem inal Systems. Basel, Switzerland: Karger; 1992:88, with permission.
These relationships also underlie the reverse phenomenon, that of the somato-visceral reflex, in which somatic input alters sympathetic and parasympathetic outflow. The data on the con vergence of somatic and visceral input are beginning to explain the interrelations between visceral and somatic structures, espe cially when nociceptive input is activated. There are descending infl uences on the activity of both so matic and visceral reflex pathways. In many of the reflex loops driven by both visceral and somatic input, there is a strong ef fect of descending pathways on the long-lasting excitability of the reflex outflow. These descending influences can maintain the excitability of the reflex for extended periods. They may account for some of the long-term increases in sensitivity, muscle con tractions, and hyperexcitable sympathetic output seen especially with visceral disturbances. Likewise, the long-lasting descend ing influences can be inhibitory, resulting in lowered somatic or autonomic outflow. For example, the effects of rib-raising tech niques (a somatic stimulation) on sympathetic outflow seems to be primarily inhibitory through the descending brain influences,
SYMPATHETIC INNERVATION OF THE HEART
Excitation of the cardiac sympathetic nerves (Fig. 7.6) causes th ese effects: I ncreased heart rate I ncreased atrial and ventricular contractility Decreased conduction time fro m the atrium to the ventricle
e
+ Heart rate + Atrial and ventricular contractility
ventricular conductivity FIGURE 7.6. Sympathetic i nnervation of heart. A, ventral root; B, stel late ganglion; C, spinal nerve; D, vagosympathetic trunk; E, vagus nerve; F, cardiac nerves; G, middle cervical ganglion.
If Osteopathic Considerations in the Basic Sciences
126
Brainstem and upper spinal cord
Ascending pathways
Descending pathways
T1
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T2
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T3
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T4
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T5
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heart
Ascending pathways
Lower spinal co rd FIGURE 7.7. Spinal sympathetic innervation of the heart and related ascending and descending pathways. The heart receives spinal cord con trol vi a T1 to T5 spinal cord levels with T2 making the largest fu nctional contribution. Lesions above T1 and below T5 block brai n control of cardiac sympathetic activity and reflex responses to ascending afferent activation, respecti vely.
The heart's spinal in nervation is associated with spinal cord levels from Tl to about T5, with T2 probably contributing the most (Fig. 7.7). The preganglionic fibers leave the spinal cord via the ventral roots and course a short distance in the spinal nerves (Fig. 7.6). The preganglionic fibers then exit the spinal nerves to enter the adjoining sympathetic chain ganglia. Most preganglionic sym pathetic fibers con troll i ng the heart course though the stellate ganglion to the middle cervical ganglion. There, they excite gan gl ion cells that send their axons, the postganglionic fibers, via the cardiac nerves to in nervate: Pacemaker cells Myocardium Conductile system Coronary arteries
The first paravertebral ganglion associated with the heart is the stellate ganglion, where some preganglionic axons excite ganglion cells whose axons also run directly to the heart (19). Segmental-li ke innervation to different portions of the heart does not seem to occur (20). In other words, a particular spinal level (e.g., T4), sends its sympathetic influences to most areas of the heart, not to one area. One should be cautious in relating problems in one portion of the heart to problems associated with one spinal level. However, different spinal segmental levels in nervate different organs, for example, heart versus lungs. Some degree of segmental-like innervation does occur. Understanding the spinal cord levels that control the heart is helpful in understanding responses of spi nal cord-inj ured pa tients (Fig. 7.7) (21,22). With spinal cord lesions above Tl, the brain has no control of the heart via the spinal cord and sympathetic nerves, but it can still activate the parasympathetic pathways. However, m arked cardiac alterations may occur via reflexes mediated by sensory input that en ters the spinal cord below the CS level. For example, i nput from the urinary bladder may cause markedly i n creased sympathetic activity to the heart. Patients with spinal lesions below Tl have some brain control of the heart via descending spinal pathways. Patients with le sions below T5 rarely show any spinal reflexes influencing the heart from the spinal afferents entering the cord below the lesion level. Specifi c levels of the spinal cord i nnervate specific visceral organs. Sympathetic motoneurons located in both sides of the spinal cord and their corresponding sympathetic nerves i nnervate the heart. There are some quantitative differences in the regions of the heart that are innervated (20). For example, stimulation of sympathetic preganglionic nerves from both sides of the spinal cord causes increases in heart rate. The right side has a greater i n fluence on hean rate and the sinoatrial node function. Both sides i nnervate the atrioventricular node, both ventricles, and atria. However, sympathetic output from the left spi nal cord has a greater effect on cardiac output and myocardial contractility (20,22). Visceral organs receive asymmetrical autonomic control from the left and right sides of the spinal cord. Several different descending spinal pathways can affect auto nomic outflow from the spinal cord. Many of these pathways are located in the lateral funiculus of the spinal cord. Both anatomic (23) and physiologic (24) evidence suggests that the descend i ng spinal pathways are organized according to a viscerotropic pattern. Localized lesions of the spinal cord, or portions of the descending spinal pathways, may result in loss of brain control of one particular visceral organ, which also suggests that the brai n has the potential to separately control different visceral organs (Fig. 7.S).
PARASYMPATHETIC INNERVATION OF THE HEART
Parasympathetic i nnervation of the heart is via the vagus nerve that causes the following (Fig. 7.9): Decreased heart rate Slowed atrioventricular conduction
7.
Descending pathways
Decreased atrial contraction Limited decrease of ventricular contractility
1 �::: ---�.
127
Neurophysiologic Mechanisms oflntegration and Disintegration
Kidney
'-----+ Leg
FIGURE 7.8. Viscerotropic organization of the descending spinal path· ways controlling autonomic outflow.
The cardiac vagal fibers travel in the cervical vagus nerve (vagosympathetic trunk) i n to the thorax where they separate from the vagus nerve to form the cardiac n erves. These cardiac vagal nerves have their cell bodies in the medulla, that is, the nucleus ambiguous and the dorsomotor nucleus (25-29). These rwo medullary regions may subserve different cardiac functions. For example, the nucleus ambiguous may mediate heart rate while the dorsomotor nucleus regulates ventricular contractility (27). Not only are there regions of the brainstem controlling cardiac function that seem to be distinct from those controlling gastroi ntestinal function and other visceral organs but different brainstem regions may control separate cardiac functions.
VISCERAL FUNCTION CONTROL
Vagosympathetic trunk
Cardiovascular function can be reflexively controlled by somatic afferents via the somatosympathetic reflexes. These reflexes may be mediated at the spinal cord level o r via suprasegmental con nections. The spinal somatosympathetic reflexes demonstrate de pendency on segmental organization. These sympathetic reflex responses at one segmental level are larger if the somatic afferent activity enters at the same spinal level than if i t en ters at adjoin ing levels (30,31). These reflexes also demonstrate laterality, because they are larger for ipsilateral reflexes than for contralateral reflexes (Fig. 7.10). Visceral afferents can also influence somatic reflexes, and mus cle tone may be altered by visceral i n put. Many of these reflex possibili ties are very i m portant for osteopathic palpatory diagno sis and treatment because they provide mechanisms for the use of muscle tone as an indicator of visceral disturbances. The work by Eble (32) showed activation of skeletal m uscles with stim ulation of visceral structures, and Schoen and Finn (33) reported EMC activity in shoulder muscles of the cat following experimental myocardial infarction. The cardiac viscero-somatic reflex has an influence on somatic musculature (18). Rostral
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128
II. Osteopathic Considerations in the Basic Sciences
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Central Afferents nervous system � Ganglion -------. Effector FIGURE 7. 1 1 . Afferent reflex control of autonomic effectors may be mediated v i a reflexes within peripheral autono m i c gangl i a as well as v i a central nervou s system connections.
Not only can there be activity from somatic or visceral struc tures that influences the opposite structures, but another type of activity, independent of the brain or spinal cord, may also occur. Recently, neural activity has been recorded from in vitro sympa thetic ganglion cells and i nt racardiac ganglion cells, demonstrat ing considerable action potential activity even when the neuronal connections to the central nervous system are severed (25,27-29). These observations suggest that the autonomic ganglia may func tion as little brains with in peripheral ganglia and the heart. These ganglia may have the neural circuitry to act almost independently and have the ability to integrate i ntrinsic cardio-cardiac reflexes as well as information ftom the central nervous system. However, the functional roles of these peripheral nervous system int e rac tions are presently unknown (Fig. 7. 1 1) . The possibility o f little brains with i n the autonomic ganglia presents many more possibilities. If visceral afferents have re flexes within the autonomic ganglia, somatic afferents could also have reflex connections within them. Some somatic afferent fibers pass through the autonomic gangl ia. It is possible that somatic afferents influence sympathetic activity not only to the somatic structure bLlt also to visceral structures such as the heart. Acti vation of somatic afferents might cause reflex alteration of car diac function via di rect ganglionic reflexes as well as via the cen tral nervous system-mediated reflexes. Likewise, visceral afferents might activate sympathetic gangl ion cells with axons supplying somatic structures (34-37). The therapeutic impl ications of re flexes with in autonomic ganglia may be important.
INTERACTIONS OF SOMATIC AFFERENTS AND BARORECEPTOR CONTROL OF AUTONOMIC ACTIVITY
Blood pressure and cardiac function are reflexively controlled through alteration of autonomic activity mediated by arterial blood pressure afferent receptors called baroreceptors. I ncreased arterial blood pressure excites baroreceptor activity, which is car ried to the brainstem via the glossopharyngeal and vagus nerves. In the brainstem, the baroreceptor afferent activity eventually
leads to excitation of the medullary cardiac vagal cell bodies. It also leads to inhibition of the sympathetic activity to the cardio vascular system via descending brainstemlspinal pathways (38). Baroreceptor reflexes i nvolving the cardiac vagus nerves have par allel inhibitory effects on the sinoatrial node (slowing heart rate) and atrioventricular node (slowing atrioventricular conduction) (39). Although these baroreceptor reflexes have powerful influences on cardiovascular function, they also interact with other spinal reflexes, especially from small, high-threshold, afferent fibers. With activation of these spinal afferents, reflex changes in sym pathetic activity (somatosympathetic reflexes) occur at the spinal cord level and through suptasegmental reflexes involving ascend ing and then descending pathways to and from the brainstem (40,41). Baroreceptor reflexes inhibit both spinal and supraspinally me diated somatosympathetic reflexes (42). Presumably, other vis ceral afferents that also mediate sympathetic reflexes are also in hibited by these powerful baroreceptor reflexes. Somatic afferent activity can modulate baroreceptor reflex va gal control of the heart. Baroreceptor activation excites the car diac vagus nerve activity. However, somatic afferent stimulation attenuates or blocks the baroreceptor influence of vagal cardiac nerves. Somatic afferents and baroreceptors compete for control of autonomic activity. The ascending and descending pathways for these reflexes have been localized in the dorsal portion of the lateral funiculus of the spi nal cord (43-45). Sum mation Characteristics of Somato-Visceral Reflexes
Somato-visceral reflexes demonstrate temporal and spatial sum mation as indicated by the wind-up phenomenon and the ef fect of inpur from different parts of the body. These somato visceral reflexes do not reach their maximal activity immediately (46). Rather, when stim ulated at a slow repetition rate, these re flexes exhibit wind-up. With each repetition of the stimulation up to about 20 times, the autonomic response increases in size (Fig. 7.12). The wind-up, or as i t has also been termed, sensitization phe nomenon suggests that maximal effectiveness of therapeutic pro cedures involving somatic afferent influences on autonomic con trol may require frequent repetitions of the procedure to allow the response to build to its maximum. Furthermore, afferent in put from different portions of the body can summate to activate autonomic responses (47). Accordingly, one would expect that a sublim inal or noneffective sti mulus to one part of the body might
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FIGURE 7 . 1 2. Wind-up or sensiti zation. When a sti m u lus is repeated at a rate of once every second or two, response to stim ulus may continue to grow for 20 seconds or more. Finally. a stable response level is reached that can continue at an increased level as long as the stimulus is continued.
7.
Afferent i nput
Neurophysiologic Mechanisms ofIntegration and Disintegration
Autonomic response
Location
Location Stimulation FIGURE 7.13. Su mmati on of autonomic responses. Input from two dif ferent locations add together to produce a larger autonomic response than e i ther input produces when it occurs alone.
acrually have an eFFecr iF combined wirh srimularion ro anorher area (Fig. 7.13). The reflex sysrem is rruly a complex i nregrating network. Per haps most important For rhe osreoparh is the Fact that somatic inpur can and does influence visceral Funcrion, j ust as input from the viscera causes changes in output ro rhe somatic strucrures. This can often be felt as altered tissue rensions or changes in mo rion characrerisrics of joints. Maps have been published lisring somaric areas that become abnormal ro palpation with various visceral disrurbances (48). A corollary of rhis is rhar manipularion of the somaric srruc tures can alrer the funcrion of visceral strucrures rhrough rhe same parhways. The reflexes are nor simple sysrems wirh only local influences, but interconnecred networks rhar receive inpur From many sources and process rhat inFormarion For distriburion ro both local and disranr areas of the body.
ALTERATION OF INTEGRATIVE FUNCTION
I npur from each area of the body and from descending brain areas interacrs on a h ighly overlapping and integrated neural net work in rhe spinal interneurons. Afferent input from any source influences both visceral and somaric structures. For normal func rioning of organs, muscles, fluid morion, and other body activi ries, these complex and interacring networks within the nervous sysrem musr acr in concert. Should one area of rhe neural net work respond either more or less rhan normal, rhe finely runed balance necessary for normal and oprimal physiologic funcrion will be disturbed. Not only must the control mechanisms from rhe brain be normal for proper reflex funcrion, but rhe networks of neurons that make up the reflexes must also be acting nor mally. Unfortunarely, rhese networks rhemselves can be altered, resulring in a loss of proper function. Although Sherringron postulated thar reflexes are innately given, evidence is accumularing that the function of reflex net works can be infl uenced by many facrors. They are subjecr ro both short-term and long-rerm changes thar can have consequences for rhe healrh of rhe individual. [n rhe early and mid-1940s, Denslow and colleagues (4951) were among the firsr ro show rhe resulrs of changes in rhe inregrative function of reflex networks in humans. They per formed a series of studies on normal, young adul r volunteers ro derermine wherher the reflex excitabiliries at various spinal levels of rhe body were stable and comparable. They measured how much srimulation ir rook ro evoke muscle activity ( EMG) in rhe
129
paraspinal muscles of rhe back ar several levels of rhe rhoracic spll1e. They found rhar, on the average, reflex excitability ro pressure on the spinous processes was highest in the upper thoracic area and lowest in the midlumbar area. Although decreased excitability fro m rhe upper rhoracic ro rhe lower lumbar areas was seen overall in rhe subjects studied, pracrically all individuals studied had areas rhat were very highly excitable, responding ro small amounts of pressure on the spinous process at that spi nal level. In normal areas, in contrasr, even a fairly heavy pressure in the spinous processes did not produce any muscle activity in the associared muscles. The highly excitable areas were characterized by not only the i ncreased muscle acrivity ro pressure on rhe spi nous p rocess but also often by pain and tenderness in the area. The areas of increased sensirivity to sti m ulation were not uniform fro m individual to i ndividual and were long-lasting (some cases remaining almost the same for years). In most cases, the individual did not realize that any change was present. These long-lasting, low-threshold areas to afferent inpur could be acrivared not only by srimularing tissues at rhe same level of the spinal cord bur also by srim ulating orher areas of rhe back or even by providing a psychological suess to the individual. With remore i npur, such as pressure o n a spinous process four verrebrae away from rhe level of rhe low-rhreshold area, the muscles ar rhe level of rhe inpur remained silent while rhose at the level of rhe low rhreshold became acrive. The same pattern occurred wirh psychological srressors. The normal areas remained silent, but rhe low-rhreshold areas showed muscle activity. I n larer srudies, Denslow and co-workers (52,53) found rhar nor only was muscle activity affecred bur so were rhe activiries of visceral organs rhrough altered symparheric output. Here, again, rhe i n terrelaredness of rhe somaric and visceral portions of the body was shown. Alrhough many orherwise normal subjects had low-threshold or high-excirability areas, ir became evident fro m subject-to subjecr variability, and from further dara showing thar the ex cirability i ncreases often accompanied inj ury and disease, thar rhe excirability changes were nor a normal state. They represented ar eas of neural funcrion rhar were operaring out of synchrony wirh orher areas of the neural sysrem, causing the organs served by rhose neural supplies also to be our of synchrony wirh rhe toral body function. Korr (7) suggested thar rhese low-rhreshold spinal reflexes rep resenred pathways rhar were being held in a hyperexcired srare, perhaps by continued bombardment of i nput. He rermed these areas facil irared. He pointed our rhar rhey acted to magnify inpur to rhe area fro m any source and to cause a magnified ourflow to rhe organs i nnervared by rhar level of rhe spinal cord. Thermo graphic srudies were also conducted (52,53) . Not only did rhe skeleral muscles respond in an exaggerared fashion in rhe low threshold areas bur the symparheric ourflow also i ncreased. Such areas of abnormally increased excirability or decreased rhreshold wirhin rhe orherwise normal areas of the spinal cord m usr acr to decrease the overall inregration of body funcrion. No m atter rhe source of input to a facilirared spinal area, rhe neural outflow would be exaggerated relarive to rhe same response ar orher spinal levels. Such a situarion lasring over rime can have o n ly undesirable consequences for toral body function.
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Beg i nning and Mai ntenance of Reflex Fac i l i tation
The finding that facilitated or low-threshold areas could comi nue for long periods of time and the faG that these areas were not the same berween individuals suggested that some process could occur that would establish these chronically hyperactive areas. Initial speculation suggested that the hyperexcirabiliry was main tained by ronic afferem inpuL Most input from either somatic or visceral srrucrures, however, decreases dramatically with activities such as sleep or other forms of relaxation. Why should the hyper excitabiliry cominue even with the loss of afferem activiry? What is the nature of the neural processing within the reflex pathways ro afferem stimuli that might explain the appearance of regions of hyperexcitabiliry? More recem srudies have provided some an swers that have a bearing on how changes i n reflex excitabiliry can at ti mes be an adaptive process and at ti mes a derrimemal one.
ALTERATION OF REFLEX EXCITABILITY
The concepr of the reflex as a simple, unchanging, static in put/output relationship is oversimpl ified. Although he character ized reflex function as i nnately given, even Sherri ngron recognized that reflex excitabiliry could be momemarily alrered by infl uences such as signals from higher brain structures or by rapid and re peated use, wh ich, he noted, caused reflex fatigue. The norion that reflexes are fundamemally unchanging, Hatic i npur/ourpur relarionsh ips is sril1 widespread despite the faG that i r is now clear that rhe excirabiliry of spinal reflex parhways can be al tered by many influences. These changes can range from shorr lasting, fleering changes ro very long-lasting ones that may even become permanenr. These long-lasting alrerations may well be the basis for the changes shown by Denslow in his srudies of human moroneuron excirabiliry and for the faci l i rared srare hy porhesized by KorL These rhrears ro functional i megrarion of rhe body may be related ro the effects of nociceptive stimuli at the periphery.
ALTERATION OF NOCICEPTIVE STIMULI
Inflammation from strong stimulation of rhe skin or ocher pe ri pheral somatic or visceral srructures produces a ser of changes in rhe sensory receprors of the organ that dramatically alters the amoum of neural activiry sem ro the spinal cord (54). Most tissues are innervated by various sensory receprors, such as: Touch Tem perarure Stretch Nociceprors The nociceprors are composed primarily of naked (unmyeli nared) nerve endi ngs that respond ro potemially tissue-damaging stimuli. In the hollow visceral organs, rhey respond ro strerch or dilarion of the organ, for example. These receprors send i m pulses rhrough rhin myelinared (group I I I or A) or unmyel inared (group
IV or C) fibers i nro rhe spinal gray maner, where they synapse primarily in Rexed layers I and V. When acriviry occurs in rhese pathways, the resulting sensarion is usually d iscomforr or pain, alrhough the i nput may be blocked (by orher neural activiry) fro m reaching rhe areas of rhe brainsrem where rhey are appre ciated as pain. However, even though a nociceptive input ro the spinal cord does not reach the conscious level, it may affect the dynamics of rhe spinal parhways (55). Once a stimulus sufficienrly srrong ro acrivare nociceptive in pur begi ns, i mpulses crave I i mo the spinal cord via rhe dorsal roots. At the branches of the peripheral neurons, the afferem im pulses i nvade the afferem branches and are conveyed back our ro rhe nerve term inals where they cause release of various peptides inro the surrounding tissues. The sites of peptide release may be some distance from the original stim ulus. The resulr of th is release is the starr of a cascade of evems that leads ro involvemem of the sympathetic posrganglionic nerve termi nals and ro the release of serum from the surrounding capillaries. Prostaglandins released from the sympathetic nerve terminals cominue the serum release that leads ro local inflammation. This p rocess begins the healing process, although i t may be sufficienrly severe that the healing process is retarded (56). The in flammarion also produces dramatic changes in the characteristics of the local nociceprors in the area. Schmidt (54) demonstrated in the cat knee joim that the nu mber of nociceprors responding ro a stretch stimulation may be berween 3,000 and 4,000 arrer inflammation. In con trast, even severe scretch of the normal joint may cause only 400 nociceprors ro fire. Also, the receprive fields of the active nociceprors enlarge dramatically i n the inflamed area, and the threshold ro acrivation significanrly decreases. The result of an inflammarory process (or a srrong stimulus that pro duces rissue damage) will be ro lower nocicepror thresholds and dramatically i ncrease i nput ro the spinal cord. Peri pheral evems can lead ro dramatic changes in the amoum of stimuli caused by changes in the peripheral receprors. What happens ro spinal reflex nerworks when stimulus input changes? I n the normal reflex pathway, repeated activation of the pathway by a weak afferem input results in a temporary decrease in the output of the nerwork. Sherringron described this shorr term decrease in reflex pathway excitabi l i ry as reflex fatigue. This process, now termed habiruation, has been srudied extensively and is a characteristic of polysynaptic reflex pathways in the spi nal cord and brainstem. Habi tuation is characterized by a decrease in output from a neural pathway that has repeated stimulus input ofa mild ro mod erate i mensiry. A stimulus may initially produce a response of a certain magnitude, but if the stimulus is repeated several times, the response decreases. If the stimulus is then terminared, the re sponse returns ro i ts initial level in a matter of seconds ro mi nutes (57). The process of habi tuation is a ubiquirous phenomenon, occurring in almost all animals and in all mammalian reflex path ways except the monosynaptic myotatic reflex. It is a necessary parr of the neural i megration, because it allows nonessential stim uli ro be muted i n rheir effecrs on rhe nervous sysrem. The opposire of habiruarion is an increase in reflex excirabil i ry. Earlier we described rhe phenomenon of wind-up, i n which a srimulus repeared several rimes causes an increased number of neural fi ri ngs. Wind-up has also been called sensitizarion in earlier
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NeurophysioLogic Mechanisms ofIntegration and Disintegration
studies (Fig. 7. 1 2) . In this process, a repetitive stim ulus can cause an increase in output rather than a decrease. A stimulus causing habiwation can cause sensitization simply by increasing i ts in tensity. This causes more nociceptors to become active, or the same nociceptors to produce more impulses. Like habiwation, sensitization can occur within a matter of seconds, and it can also dissipate in a matter of seconds when the stimulus is terminated (57). Both habituation and sensitization have been extensively swd ied at the cellular level. In the mammal, both occur within the spinal central gray matter in the interneuron pathways. They are probably subserved by two different sets of interneurons, which then synapse on the motoneurons of both the sympathetic and somatic systems. Both sensitization and habituation are appar ently presynaptic processes that either inhibit (habituation) or enhance (sensitization) the release of neurotransmitter with each activation of the presynaptic terminal (58) . They are i ndepen dent of descending influences from higher nervous centers. Both processes can be demonstrated in humans with spinal cord tran sections. Habiwation and sensitization are different p tocesses but occur at the synaptic level and can occur over a few seconds of sensory input. AJthough the process of sensitization may not be a unitary one (because there may be more than one form of sensitization), when the initiating stimulus is terminated, both processes do appear to dissipate in a fairly short time. Habiwation allows the organism to damp the response to nonthreatening stimuli while sensitization allows the individual to respond more forcefully to a stimulus that is stronger and thus threatens tissue damage. These two processes are valuable i n maintaining the organism in its everyday existence. Under normal conditions, the opposing processes of habituation and sensitiza tion function to maintain a balance between overreaction and underreaction to normal stimuli. When the i n flammation pro cess occurs, whether it is a minimal or maximal inflammation, the balances of habiwation and sensitization are disrupted. The normal damping effects ofhabituation are shifted toward the sen sitization process. This is caused by the larger and more extreme responses of the peripheral receptors to what would usually be a nonthreatening stimulus. The result is a larger than normal motor output to both the visceral and somatic structures innervated by the affected reflex pathways and, thus, to an overresponse to stim uli. The process disrupts the normal integration of physiologic function. Once the process of sensitization has begun, often over a few seconds of strong input, a secondary process begins to occur. Sen sitization dissipates a few seconds or minutes after the stimulus is gone. A longer lasting process, termed long-term sensitization, begins to develop in the reflex pathways once sensitization has been in place for several minutes. This process precludes the ex citability of the neural pathways from rewrning to normal for some time, often hours. The effects of this process can often be seen in laboratory experiments when bursts of stimulation are given followed by an occasional stimulus pulse to test the responsiveness of the reflex system. After initial sensitization and the rapid decrease of reflex excitability after stimulus termination, the response being tracked does not return to its prestim ulation baseline but remains a small
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but significant amount above the base level. This hyperexcitabi lity does not decay for varying amounts of time depending on the time and strength of the stimulus. Unlike sensitization, long term sensitization is thought to be a postsynaptic event, possibly involving the elaboration of proteins in the postsynaptic neuron that remain active for some time after the initiating event. Recently, Mantyh and colleagues (59) have shown dramatic changes in the substance P receptors and even structural reorga nization of the dendrites of spinal i n terneurons after nociceptive input. These changes could be the basis for long-term sensiti zation. Long-term sensitization involves a different mechanism than the short-term process does and can have effects that far outlast the originating stimulus. Once a stimulus has acted o n a reflex network for a longer t ime, the results can be even more dramatic. For many years, a process known as spinal fixation has been known but not fully recognized. First shown i n anesthetized animals, spinal fixation was manifest as remaining active leg flexion after 3 to 4 hours of limb flexion secondary to a cerebella lesion. The lesion produced disrupted outflow fro m the postural centers in the cerebellum, resulting in sustained flexion of a leg. When the spinal cord was sectioned im mediately after the lesion, the limb dropped to the usual flaccid paralysis of the animal. However, if the spinal cord was allowed to remain i ntact for 3 to 4 hours after the lesion and then transected, the limb remained flexed to some extent. The ex planation was that the strong outflow from the injured cerebellum caused a hyperexcitability to develop i n the target i n terneurons of the cord that remained active after spinal transection and resulted in continued motor activity. In the m id- l 960s, research showed that the m i n i mal time nec essary for the fixation of this excitability was approximately 45 minutes. A n i mals receiving the spinal transection within 35 min utes showed no remaining flexion, but those having 45 minutes between lesion and transection showed remai ning flexion (60). This effect has now been shown to occur not only as a result of a cerebella lesion but also with stimulation of the skin of the hind limb, and it has also been shown to occur in either i ntact or animals with spinal transection (61-63) . The change in the spinal reflexes produced by the cerebella lesion was caused not by pain or nociceptive input but by changes in outflow fro m the postural centers. This, along with more recent research, shows that changes in the reflex functions can occur with both nociceptive and nonno ciceptive i nput, although nociceptive input produces the changes more quickly than nonnociceptive input does. Reflex excitability changes can be influenced by many factors, includi ng: Stress ptior to stimulation Length and severity of stimulation Whether the spinal cord is i ntact o r sectioned The changes have been traced for 3 to 7 days after only 45 minutes of fairly i n tense nociceptive stimulation and may last even longer. With intense stimulus i nput, the effect is seen after as little as 20 minutes of stimulation (64). Obviously, strong input, especially nociceptive in nature, can have rapid and long lasting effects on the excitability of reflex circuits. Although the locus of the changes seen in fixation is not yet known, i t seems
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likely that the alterations observed are processes akin ro long term sensitizarion but which last a much longer rime. Ir appears rhar the fixation process is also dependent on rhe e1aborarion of proteins in the postsynaptic cells and that it would affecr rhe re sponsiveness of those cells nor only ro rhe original inpur bur also ro all inpur to the cell. Another l i ne of evidence of long-lasting i ncreases in reflex excitability comes from studies of peripheral inflammation thar show that there are peripheral effects of i nflammarion on afferent input and receptive fields. Contin ued afferent input from pe ripheral inflammation produces dramatic changes in the respon siveness of spinal interneurons. I n terneurons on which afferent fibers from affected nociceptors synapse begin to respond much more easily to i nput fro m a variety of sources, such as touch, pres sure, and even the movement of distant muscles. These dramatic changes in excitability also last for long periods (days and weeks) and develop duri ng the initial i nflammarory episode (65,66) . Knowing something abour rhe mechanisms of rhe changes may allow us to restore more normal funcrion. Dubner, Ruda, and Gold (67,68) summarized a series of i ntracellular changes thar are linked to the excitabil i ty alterations seen wirh the i n flammation p rocess. The cells activated by nociceptive input fro m i nflamed peripheral structures begin to show enhanced activation of spe cific parts of the postsynaptic cell membrane called N-methyl 0aspartate (NMDA) receptors. When these receptors become more active, the excitability of the cell is increased. If cellular activation continues even longer, changes in the acrivity of genes within the neuron are seen. A class of genes called intermediare-early genes, c-fos, and c-j un, become more acrive, causing increased dynor phin release wirhin the cell. Dynorphin is a subsrance rhar causes increased cell excir�rion. With more o f i r being produced, the cell is rhen held in a hyperexcirable srate. Wol paw provided strong evidence thar excitability increases and decreases can be produced nor only by nociceptive inpur to rhe spinal circuits, bur also by nonnociceprive input (69) . In Wolpaw's studies, both increased and decreased spinal reflex excirability were produced by long rerm i n pur rhar was nonnociceprive. Thus, ir is beginning to appear rhar spinal circuirs can be altered rapidly by nociceprive inpur, and more slowly by nonnociceprive i nput. Other studies have begun ro show thar a fourth type of spinal circuir excitability alterarion can occur. Wirh heighrened ex citability over several days, a p rocess begins to occur in rhe in rerneuron cell body rhar fi nally desrroys rhe cell. Although borh inhibitory and exciratory interneurons should rheorerically borh be affecred by rhis process, i r appears rhar inhibitory interneurons are affecred primarily (70). Thus, after rhe long-rerm excirability increases of rhe fixarion type are esrablished, contin ued acrivarion of rhe parhways may result in the loss of inhibirory interneurons. This is certainly an almosr permanent event. However, it is ap parenrly nor rhe end of rhe story. I n some cases where i nhibitory interneurons have been lost, rhere may be new exciratory synapses acrually formed to replace rhe losr inhibitory synapses (71) . These cwo addirional processes would further shift rhe balance of ex citarion in rhe spinal cord roward enhanced excirability, perhaps permanen dy. We have oudined four steps rhar have been shown to occur in rhe spi nal cord reflex circuitry to alrer the excitability of rhose pathways:
Sensirizarion Long-rerm Sensirizarion Fixarion Loss of i nhibitory interneurons/new exciratory synapse for manon These four overlapping and progressive srages in spinal ex cirability alrerations are underlain by differenr neural processes, ranging from simple synapric transmission alrerations ro com plex changes in the generic function of rhe cell. Wirh increased undersranding of the underlying processes involved, it may be possible to find ways to stop or even reverse them and, hence, reestablish normal excitability in an affected region. In addition, rhe restorarion of normal input to an affecred spinal area would have an ameliorative effect on the function. However, at present, l irrle is known abour how to reverse the effects of these excitability al rerations. These four sreps are a progression from short-term ro long rerm and even permanent alrerations of spinal excirability. I r seems almost certain rhat these sreps underlie the changes recorded by Denslow (49) and i nterpreted by Korr (7) as the facil irated segment. They saw these alrerations as having widespread and often grave consequences for rhe patient. Alrhough they had no way to undersrand rhe basis of rhe facilitated segment at that time, rhey righdy viewed these alrerarions in funcrion as a real rhreat to rhe health and function of the parient. An area of spinal reflex pathways that are either temporarily or permanenrly in a srare of increased excirability would respond to all input in an exaggerated way, with the resulr thar the organs or rissues inner vared by rhose areas of rhe spinal cord would receive exaggerated neural drive. Thus, rhe affecred rissues, somatic or visceral, would be driven ro respond in a fashion rhat was not in harmony with rhe resr of rhe body. Over rime, rhis increased drive on the tissues would be expecred to rake a toll on rhe funcrional ability of the rissues and could resulr in premarure breakdown or loss of normal function. Ir is also evidenr rhat areas of increased spinal excirability would respond to central commands in an inappropriate way. This could be rhe reason why some people respond ro stress with heart palpitations while others respond with gastric distress. The abnormally excirable area of the cord would be the one to re spond wirh abnormal drive onro the innervated rissues, resulring in clinical manifesrations not seen in other tissues. Thus, a clini cal problem may be the result of a long-standing facilitated area of rhe spinal cord. In addirion ro spinal circuir changes, it is now becoming ap parenr rhat nociceptive i npur may cause changes in the brai n stem and even in rhe corrical areas rhat could account for many of the usual symproms seen wirh chronic pain. I ndeed, rhere is evidence rhat in the prefrontal COiTex, cortical neurons anal ogous ro rhe spinal inhibirory interneurons may be destroyed with some types of pain input (72). The probable result of these changes in rhe brainstem and even cortex rhat may be analo gous ro those seen in the spi nal cord will be ro alter the abil i ty of rhe system ro respond ro environmenral stress, and may predispose ro disease, alrered imm une function, and depressive srares (see Chaprer 8 by Willard in this section for furrher discussion) .
7.
NeurophysioLogic Mechanisms of Integration and Disintegration
Thus, the spinal excitability alterations first seen by Denslow and Korr seem to be underlain by a series of progressively longer lasting spinal circuit alterations that result in altered outflow to central brain areas and to both somatic and visceral tissues i n nervated b y that area. A s noted above, the restoration of normal input to the area from somatic and visceral tissues would almost surely help normalize the function of the affected areas in all but extreme cases. The restoration of normal tissue function by manipulative procedures would be expected to help restore nor mal function in the spinal circuits. Thus, given an altered reRex network, that area can no longer respond in concert with other networks, producing diminished functional i ntegration, and be gin ning the loss of health associated with disease.
NONIMPULSE-BASED INTEGRATION
Neurons not only convey impulses throughout the body to i nte grate function but also a steady stream of material Rowing from the neural cell body out the axon and dendrites. This flow is called axoplasmic flow. It transports materials from where they are man ufactured in the cell body down a complex microtubular structure within the axon. Materials to supply rebuilding of the axon walls, to resupply the transmitter substances, and so forth are carried on this system. The most common clinical effects of the loss of this transport system can be seen when neural contact is wi thdrawn from an end organ, such as when a muscle is denervated by cutting its motor nerve (a relatively common occurrence). Not only does the muscle cease to contract but unless the nerve regrows again to contact the muscle, the muscle fibers eventually lose their abili ty to contract. They change their structure to that of noncontractile connective tissue. Likewise, if an end organ is damaged, i ts nerve supply often retracts and the synapses are lost. The end organ sup plies something to the nerve that allows the synapses to remain viable. A great deal of study has been done on the uptake of sub stances supplied by the end organ by nerve terminals. A family of substances known as nerve gtowth factor (NGF) is essential to continued nerve contact with an end organ and for contin ued viability of con tacts between nerves higher up the chain. If the end organ does not supply N G F, the synaptic contact is lost. This factor is also essential in development, allowing appro priate nerves to reach and establish contact with the appropri ate end organs. Loss of appropriate N G F causes deterioration of the nerve and its contacts. NGF is elaborated in the end or gan and taken up by the presynaptic membranes, where it is transported up the axon to the cell body, a process called ret rograde transport. There, it regulates the function of the nerve and the nerve's ability to mai n tain synaptic contacts. Many other substances can be taken up and transported to the cell body, but not all of them are helpful to nerve function. The tetanus toxi n , tetanospasmin, is made in peripheral structures after in fection by the Clostridium tetani bacterium. The toxin is taken up by nerve terminals and transported to the central nervous sys tem, where it affects neural function, causing the clin ical signs of tetanus.
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Many common nerve-tracing techniques rely on the ability of the neuron to take up substances and transport them from the periphery of the nerve to the cell body. For example, horseradish peroxidase is used as a nerve tracer by i njecting it i n to the area of nerve terminals, where it is taken into the cell and transported up the axon , eventually filling the cell body and even dendri tes. A fixative can then be used to turn the horseradish petoxidase a dark brown-black, providing an easily visualized portrait of the cell. Many other dyes and materials are commonly used in this way to visualize nerve cells. Although much is known about the N G F family and some other substances and about the actual transport mechanisms within the axon , less is known about the delivery of substances to end organs through transport from cell body to axon (anterograde flow) , such as what is delivered to keep a muscle functional. I n 1967, Korr e t al (73) published the results o f a study that showed that amino acids placed on the cell bodies of the hypoglossal nu cleus o n the floor of the fourth ventricle were i ncorporated i n to the cell body and transported down the axon to the tongue mus cle, where they were delivered into the muscle fibers. Later work showed that not only was the material transported bur it was also transported at several different rates of Row. That study and others since have shown that Row rates with i n an axon vary from as slow as 0.5 mm/day to as fast as 400 m m/day. The observed rates are (74): Slow (0.52 mm/day) Medium (25 mm/day) Fast (up to 400 mm/day) Very fast (up to 2,000 mm/day) Although much of the anterogradely transported materials are related to support of the neuron and synaptic functions (such as supply of neurotransmitter components) , materials del ivered by the nerve to its end organ are necessary for either its function or con tinued existence (75). The nervous system is not only the network for rapid com mun ications within the body, but it serves as a vast network for a far slower two-way communication between the central nervous structures and every part of the body. Disruption of this slow transport of materials has consequences for con ri n ued function that may not be immediately evident but that range from subtle to disastrous. Complete withdrawal of NGF or of the materi als delivered by the nerve to i ts end organ may result in loss of function. Disturbance of the Row of materials in either direction results in less than optimal function of the organs i nvolved. Many questions remain about the two-way commun ication of axoplasmic Row. What substances are being del ivered? How necessary are they? What do the materials transported from the periphery to the nerve cell bodies do to the function of the cell or of the entire CNS? Al·e there crucial times for delivery of nerve factors to end organs for proper development? H owever these questions are answered, it is important to recognize the vast i ntegrating nature of the non impulse-based transport systems of the nervous system and the importance of proper function of this system. Many things have been shown to affect the material Row within the nerve cells. Even small pressure on axons can impede
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proper axoplasmic flow. A sustained i ncreased n umber of im pulses carried by the neuron (as i n those originating i n facilitated areas of the cord) may decrease flow rates. I mproper supplies of nutrients and oxygen to the cell body or axon alter the flow. The occurrence of the tissue tensions and fluid flow disturbances of ten associated with somatic dysfunctions can be factors in altering axoplasm ic flows. The somatic dysfunctions treated with the use of manipulation would be expected to have a positive effect on the flow of materials in axons of the area and, hence, to improve body function and integration.
CONCLUSION
In the normal, in tegrative function of the nervous system, a great number of influences obviously act on any neural pathway. Af ferent input activates reflex outflow. Descending activities from higher nervous centers modulate excitability ofinterneurons. As cending influences from lower spinal areas i ncrease or decrease activity. Psychological effects are played out on all levels of the neuraxis. The nerves deliver the materials necessary for normal function to thei r end organs while the end organs send the sub stances necessary for continued synaptic viability to the nerves. These influences come together to determine the moment-to moment excitability of any area of the central nervous system and to determine overall outflow to both somatic and visceral struc tures. If all of these influe nces are working in harmony, optimally integrated function can be expected from the various organs. I f, however, o n e area i s in a hyperexcitable state, the output from that area of the system will not be in harmony with the output of the other areas. In that case, the optimal function is disrupted and the i ndividual becomes i ncreasingly prone to loss offunction and disease. The long-term alterations in spinal reflex excitability (now well-demonstrated by various studies) seem almost certain to underlie the alterations demonstrated by Denslow and his col leagues. These b reaks in the normal i n tegration of the nervous system were shown to affect both visceral and somatic structures. The i n teraction between visceral and somatic input in the spinal cord provides the basis for that common effect. The changes shown in response to nociceptive input can easily account for the long-lasting nature of the facilitation identified in those stud ies. The facilitation was hypothesized by Korr to be the basis for the somatic dysfunctions long recognized by the osteopathic profession. Because the neurons involved i n the altered excitability are i n terneurons (the neurons on which a variety of different pathways synapse), the data also support the effects of excitability changes on both somatic and autonomic outflow. The i nput from both visceral and somatic structures ends o n common i nterneurons. When the excitability of those interneurons is altered, the out flow to all structures innervated by motoneurons to which those i n terneurons connect is affected. The reflex networks of the nervous system are not at all static, genetically determined entities. They are a vast network of highly interconnected pathways that are continually changing to meet local needs and to main tain i ntegration of function. These pro cesses allow the delicate moment-to-moment i ntegration that
characterizes optimal functional capacity. The integration, how ever, can be turned against the very system it serves. When abnor mal or very strong input occurs, the result can be a long-term dis ruption of the normal excitatory/inhibitory balances and a shift to excessive excitability (or in some cases, to excessive inhibition) . The result, in either case, is the loss o f functional integration and a decrease i n functional capacity of the individual. There are many factors that i n fl uence the total function of the individual, i ncluding their: Accumulated effects of life Habits Living environment Food Psychological and spiritual makeup and state The role of the state of the nervous system is but one of the factors i n fl uencing the total health of the person. Because i t affects a l l organs a n d structures with which it communicates, an area of central excitation or facilitation delivers the effects of all other stressors on the individual to the end organs. In essence, it is the final common factor in communicating with the end organ. Most of the other stressors in life are difficult to change, and the osteopathic physician has little impact on or control over them. H owever, the physician can directly affect the course of the facilitation and its effects by recognizing that it occurs and by using modalities, especially manipulative treatment, that alter it. Rational therapy dictates the normalization ofafferent input as quickly as possible. I n chronic situations, use methods to reduce the abnormal i nput to allow the body to restore normal balances of excitation and inhibition as fully as possible. In this way, the goal of total osteopathic treatment, to optim ize each individual's function and to restore the individual's dynamic functional bal ance of optimal health, can be brought closer to reality.
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7.
NeurophysioLogic Mechanisms ofIntegration and Disintegration
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Neurol. 1 980; 1 93:467-508. 29. Hopkins D, Armour J. Medullary cclls of origin of physiologically iden tified cardiac nerves in the dog. Brain Res Bull., 1 982;8:359-365. 30. Beacham W, Perl E. Background and reAex discharge of sympathetic preganglionic neurons in the spinal car. } Physiol. 1 964; 1 72:400-4 1 6. 3 1 . Beacham W, Perl E. Characterisrics of a spinal sympathetic reAex. } Physiol. 1 964 ; 1 73:43 1 -448. 32. Eble IN. Parrerns of response of the paraverrebral muscularure ro visceral stimuli. Am} Physiol. 1 960; 1 98(2):429-433. 33. Schoen RE, Finn WE. A model for studying a viscerosomatic reAex induced by myocardial infarction in the car. } Am Osteopath Assoc. 1 978;78( 1 ) : 1 22- 1 23. 34. Amour J. Activiry of in siru stellate ganglion neurons of dogs recorded extracellularly. Crln } Physiol Pharmacol. 1 986;64: 1 0 1 - 1 1 1 . 35. Amour J . ACtiviry of i n situ middle cervical gangl ion neurons in dogs, using extracellular record ing techniques. Can } Physiol Pharma col. 1 985 ;63:704-7 1 6. 36. Boznjak Z, Kampine J . I nrracellular recordings from the stellate ganglion of the car. } Physiol. 1 982;324:273-283.
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37. Gagliardi M, Randall W, B iegel' D , et a!' Activity ofin vivo canine cardiac plexus neurons. A m } Physiol. 1 98 8 ; 2 5 5 : 789-800. 38. Terui N, Koizumi K. Responses of cardiac vagus and sympathctic nerve ro excitation of somatic and visceral nerves. } A uton Nero Syst. 1 9 84; 1 0:73-9 1 . 39. O'Toole M , Wurster R, Phill ips J , et al. Parallel barorecepror con trol of si noatrial rate and atrioventricular conduction. Am } Physiol. 1 984;246: H 1 49-H 1 53 . 40. Koizumi K, B rooks e. T h e inregration of auronomic system reactions: Discussion of auronomic teAexes, their conrrol and their association with somatic reactions. Ergeb PhysiolBiol Chern Exp Pharrnakol. 1 972;67: 1 68.
4 1 . Saro A, Sch midr R. Somarosymparhetic reAexes: Afferent fibers, ccntral pathways, d ischarge characteristics. Physiol Reo. 1 973;53:9 1 6-947. 42. Barman S, Wurster R. I nreraction of descending sympathetic path ways and afferenr nerves. A m } Physiol. 1 978;234:H 223-H229. 43. Geis G , Wurster R. Local ization ofascending inotropic and chronotropic pathways i n the car. eirc Res. 1 98 1 ;49: 7 1 1 -7 1 7. 44. Kozelka J , Chrisry G, Wurster R. Somaro-auronomic reA exes in anes thetized and unanesthetized dogs. } A uton Nero Syst. 1 982;5 :63-70. 45. Kozelka j, Chung j, Wurster R. Ascending spinal pathways mcdiating somaro-cardiovascular reAexes. } A uton Nero Syst. 1 98 1 ;3: 1 7 1 - 1 7 5 . 46. Chung J , Webber C , Wurster R. Ascending spinal pathways fo r the so marosympathetic A and C reAex. Am} Physiol. 1 979;237:H 342-H347. 47. Chung J , Wurster R. Neurophysiological evidence for spatial summation i n the C N S from unmyeli natcd afferenr fibers. Brain Res. 1 978; 1 53: 59660 1 . 48. Te Poorren BA. Spinal palparory diagnosis of visceral disease. Osteopathic Annals. 1 979:52-53. 49. Denslow JS, Korr 1M, Krems AD . Quanritative studies of chronic facil itation i n h u ma n moroneuron pools. A m } Physiol. 1 947; 1 0 5 (2):229238. 50. Denslow JS. The cenrral excitarory state associated with postural abnor malities. } Neurophysiol. 1 942 ; 5 ( 5 ) : 393-402. 5 1 . Denslow JS. An analysis of the variabi l ity of spinal reAex thrcsholds. } Neurophysiol. 1 944;7(July): 207-2 1 5 . 52. Korr 1 M , Thomas PE, Wright H M . Parrerns of electrical skin resistance in man . } Neural Transm. 1 95 8 ; 1 7:77-96. 53. Wright H M . Local and regional variations i n cutaneous vasomoror rone of the h u man trunk. } NeltraI 7l'flnsm. 1 960;22:34-52. 54. Schmidt RF. Neurophysiological mechanisms of arrhriric pai n. I n : Parrerson M M , Howell I N , eds. The Central Connection: Somato1Jis cerallViscerosomatic Interaction. I ndianapolis, I N : American Academy of Osteopathy; 1 992: 1 30- 1 5 1 . 5 5 . Schmidt RF. Nociception and pai n . I n : Sch midt RF, Thews G , eds. Human Physiology. Heidelberg, Germany: Springer-Vcrlag; 1 987. 56. Payan D G . Peripheral neuropeptides, i n Aammation, and nociception. I n : Willard F H , Parrerson M M , eds. Noriception and the Neuroendocrine Immune Connection. I ndianapolis, I N : American Academy of Osteopa thy; 1 994: 34-42. 57. Groves P, Thompson R. Habiruation: A dual-process theory. Psychol Rev. 1 970;77( 5):4 1 9-450. 58. Kandel ER, B r u n el l i M, B yrne J , et al . A common presynaptic locus for the synaptic changes underlying shorr-term habituation and sen sitization of the gill-withdrawal reAex i n aplysia. Cold Spring Harbor
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NOCICEPTION, THE NEUROENDOCRINE IMMUNE SYSTEM, AND OSTEOPATHIC MEDICINE FRANK H. WILLARD
INTRODUCTION Somatic Dysfunction Represents a Critical Concept in Osteopathic Medicine
Paramount ro the osteopathic concept of patient care is the no tion that the health of the body-soma and viscera-has a direct influence of the abiliry of rhe patient ro fend off disease states. Thus, a critical aspect of osteopathic evaluation involves a struc rural examination of the patient ro locate and characterize somatic and visceral dysfunction. These dysfu nctions, usually detected by palpation, have been described as manifesting with
I. changes i n tissue texture, 2. i ncreased sensitivity ro rouch, termed hyperalgesia, 3. altered ease or range of motion, and
moral facrors and rhe enhanced neural activiry summate ar rhe level of rhe brainsrem ro in itiate general arousal and associated, protective endocrine and neural reflexes. Many aspects of this process relate ro the general adaptive response of described by Selye (2). Although such neuroendocrine reflexes can be bene ficial and protective in the acute si tuation, chronic exposure ro this compensated state, termed allostasis (3) is pathologic. A sig nificant portion of this chapter will focus on rhe drives ini tiating allostatic processes and the consequent i n flammarory and de generative inj ury chronic allostasis infl icts on body and m i nd. A major conclusion of the chapter will be that the osteopathic ap proach ro patient care is aimed at helping the patient ro resrore a more natural homeostatic condition. This is accomplished by de faci litating allostaric drives, thereby creating a condition in which the person will be berter capable of fending off diseases states.
4 . anaromic asymmetry of the effected region ( 1 ) . As one can determ ine simply from the clinical man i festations, somatic dysfunction involves sign ificant alteration in the under lying tissue; Denslow ( 1 ) was able ro relate these changes ro ede matous and inflammarory processes using h istopathologic inves tigation. Somatic Dysfunction Results in Facilitation of the Spinal Cord
The physical process of somatic dysfunction releases signals lead ing ro alteration of activiry in the nervous system, endocrine sys tem, and immune system. This chapter and several orhers in this text will review the changes occurring i n the spinal cord segments consequent ro somatic dysfunction. In the spinal cord, altered or enhanced neuronal activiry is termed facilitation. The result of spinal facilitation is significant change in outflow over both so matic and auronomic routes from the spinal cord. Numerous manifestations of altered spinal outflow can be seen clinically i n the target peripheral tissue. Somatic Dysfunction, Spinal Facilitation, and General Health
Along wirh activating related spinal cord circuits, somatic dys function also releases humoral facrors. Both the circulating hu-
NOCICEPTION AND SOMATIC DYSFUNCTION Pathophysiology of Somatic Dysfunction Biopsies of Palpable Lesions Reveal Signs of Inflammation and Edema
The term somatic dysfunction or osteoparhic lesion has been used throughout osteopathic literature. I ts effecr on the activity of skeletal m uscle was demonstrated by Korr and Parterson 0 in the 1 950s and 1 960s; but, until the 1 970s, these terms still lacked a solid pathophysiologic basis. Using the four cardinal manifesta tions of somatic dysfunction as criteria ro identify these lesions i n volunteers, Denslow (I) biopsied t h e lesions and reported overt signs of i nflammation and edema as underlying causes.
Inflammatory Events Signal the Spinal Cord Through Peripheral Nerves
Given rhat somatic dysfunction has an underlying inflammatory basis, we can now examine the events i n the body i n itiated by the i nflam marory process. Chemical mediators released from numer ous rypes of cells in fascia act ro stimulate wound repai r and tissue growth. At the same time, these mediarors also stimulate noci ceptive nerve endi ngs in the local tissue resulting in a signal being sent ro the spi nal cord ( Fig. 8 . 1 ) . The nature of th is i nteraction
1 38
tt. Osteopathic Considerations in the Basic Sciences
Spinal nerve Penpheral proc ess (of B-atferent fibres)
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in the peripheral nervous system is critical ro the formation of spi nal facilitation and its subsequent i mpact on body function. The Peripheral Nervous System and Primary Afferent Nociceptors The Peripheral Sensory Nervous System Can Be Divided Into Two Components
The neuronal processes (fibers) contained i n peripheral sensory nerves (termed pri mary afferent fibers) , whether they supply so matic or visceral tissue, can be divided structurally and function ally inro twO major categories: primary afferent fibers from large sensory neurons involved i n detecting discriminative and propri oceptive events, and small, sensory neurons that are more rypically involved i n detecting general warn i ngs of potential danger (4). Al though numerous studies poi nt ro the small fiber system as being critical ro the establishment of demonstrable spinal facilitation (5-7), once established, both large and small fiber systems can become major components i n the relationship between somatic dysfunction and spinal facilitation (8). Large Fiber System Provides Discriminative Touch and Proprioception Characteristics of the Large Fiber System
The large-cal iber primary afferent fibers rypically are well myeli nated and rapidly conducting. They term inate in peripheral tissue with specialized, encapsulated endings such as Pacinian or Meissner corpuscles, Merkel discs, or Ruffini endings. Within the central nervous system , the large-caliber fibers ascend the spi nal cord ro terminate in the dorsal column nuclei of the cau dal medulla. From the dorsal col u m n nuclei, projections ascend ro the thalamus and then ro the somatic sensory cortex where they are precisely mapped with respect ro body structure (9). The large fiber system rypically responds ro low-level energy stimuli such as light rouch , vibration, or tissue movements. Thus,
FIGURE 8.1. Interac tion between neuropeptides and im munoc ytes : produc tion of a f eed-f orward inf lammatory c ascade. The peripheral terminal of the primary aff er ent noc ic eptor (PAN) is illus trated and ends in c onnec tive tissue near a c apil lary. A nox ious s timulus has trig gered the releas e of neuropeptide (s ubs tanc e- P) from the PAN terminals . The s ubs tanc e P (SP) has triggered the releas e of his tamine f rom the s urrounding mas t c ells , pros taglandins from the c apillary endothelial c ells , and the f ormation of brady k inin from the plasma protein preprobrady k inin. White blood c ells migrate to the tis s ue and releas e proinf lammatory c y tok ines . Many of thes e s ubs tanc es are c apable of triggering inc reas ed ac tivity of the PAN and f urther s ec retion of neuropeptides . Thus , a f eed-f orward s ituation is es tablis hed, leading to edema in the loc al tissue with sens itization of the PAN. From Willard FH . Neuroendoc rine-immune network , noc ic ep tive s tress, and the general adaptive res pons e. In: Everett T, Dennis M, Ric k etts E, eds . Physiotherapy in Mental Health: A Practical Approach. Ox f ord, UK: Butterworth H einemann; 1995: 102-126, with permiss ion.
this system is i nvolved in discri mi narive rouch and propriocep tion. Under normal conditions, stimulating components of the large fiber system produce a perception that is very specific ro the rype of ending on the p rocess and nor sensitive ro the source of stimulation. For example, sti m ulating a Pacin ian corpuscle will produce the sensation of vibration regardless of how it is stimulated-either mechanically or electrically, or of how in tensely it is stimulated (l0). Another major characteristic of the I::.rge fiber system is its adaptabi l iry. Under repeated stimulation, many of these fibers will adapt such that the number of action potentials generated diminishes (1 1 ) . Thus, the large fiber system is best stimulated by novel activiry and will tend ro adapt ro repetitive sti muli, thereby reduci ng its detection of this information.
Small Fiber System Provides Nociception and General Adaptation Characteristics of the Small Fiber System
The small-caliber primary afferent fibers are rypically unmyeli nated or very l ightly myel inated, They terminate in peripheral tissue with naked nerve endi ngs, devoid of any encapsulation. Within the brain, i n formation from the small-caliber system is d istributed ro numerous brainstem and thalamic areas before be ing sent ro the cerebral cortex (9) . The small fiber system is capable of detecting high-energy stimuli such as that wh ich is either damaging or potentially dam aging ro the surroundi ng tissue. Thus, major functions of this sys tem involve protection and defense. Mapping of this information on the cerebral cortex is not as precise as that seen in rhe large caliber fiber system. Not only does this system activate somatic sensory cortex, it also has projections reaching m uch of the lim bic forebrain 02- 1 4), Furthermore, the sensation obtained from intensely stim ulating a small-caliber fiber often differs from that derived from low-level stimulation. Low-level stimulation can produce the sensation of crude rouch or contact while intense
8. Nociception, the Neuroendocrine Immune System, and Osteopathic Medicine
aCtlvlry in the fiber produces the sensation of pain . More im portantly, i ntense activation of the small-caliber system i n i tiates brainstem responses involving arousal and general adaptation. Thus the small fiber system is an i mportant avenue i n to the arousal system of the brainstem. Activation of the arousal system serves to alter endocrine and i mmune functions thtoughout the body and represents the major focus of this chapter. Finally, another major characteristic of the small fiber system is i ts ability to sensitize to repetitive stimuli (11 ) . Under such stimulation, many of the neurons in the small fiber system will lower their thresholds of activation, thereby becoming sensitized to the stim ulus. Location of the Small Fiber System
Small-caliber, primary afferent fibers are distributed throughout the tissues of the body. They extend throughout the connective tissue of the dermis and enter the deep layer of the epidermis. Small fibers can be found coursing i n the fascial wrappings of blood vessels and nerves and i n the connective tissue support network throughout muscle, tendon, and ligament as well as in the capsules and synovial linings of joints. This includes the outer third of the i ntervertebral discs that are also i nnervated by components of the small-caliber fiber system. I n addition, similar processes can also be found i n the support l igaments and organ walls of the viscera. The meningeal layers of the central nervous system also contain small-caliber fibers that course along, and fan out from the meningeal blood vessels. The only tissues i n the body that d o not receive a n i nnervation fro m the small fiber system are the articular and hyaline cartilages, nucleus polposus, and the parenchyma of the central nervous system . Activation of the Small Fiber System
Because the small fiber system represents an i mportant compo nent of the arousal system, it is necessary to consider i ts activiry. Three forms of energy are capable of activating components of the small fiber system: mechanical, thermal, and chemical. In under standing somatic dysfunction, mechanical and chemical forms of activation are of major concern. Mechanical energy appears to activate primary afferent fibers by distorting their membranes and opening associated ion channels, allowing depolarization of the fiber. Chemical energy works through a myriad of receptors located on the surface of the primary afferent fiber. Receptors are present for such chemicals as bradykinin, serotonin, histamine, norepi nephrine, and a variety of neuropeptides ( 1 5) . Importantly, the receptor composition of the primary afferent fiber is not static and can shift consequent to the condition of the tissue. Thus re ceptors for norepi nephrine are not normally active on these fibers but sensitiviry to sympathetic catecholamines can develop after tissue inj ury (16) . Nociception is the physical action of exciting small-caliber, primary afferent endings (whether by mechanical, thermal, or chemical means) . Therefore, the small-caliber fibers that are sen sitive to tissue damaging stimuli are often termed primary afferent nociceptors or PANs (15) . Human Perception o f Small Fiber Activity
Primary afferent fiber activiry can be studied using the technique of m icroneurography ( 1 7) . From such studies, i t has become clear
1 39
that nociception can occur in the peripheral tissue and primary af ferent nociceptors can be active without our knowledge of these event s . Thus, low-level firing of PANs can occur without our perception, or at best, perhaps giving us the sensation o f poorly localized touch. Conversely, we can perceive high-level or rapid firing of PANs as pain. Most cri tical , however, is the fact that high-level activiry of the PANs can alter the ptoperties and be havior of components of the surrounding large fiber system and, under these pathologic conditions, we then also perceive large fiber activiry as pain ( 1 8) . Peripheral Sensitization o f Primary Afferent Nociceptors Primary Afferent Nociceptors Are Involved in the Process of Somatic Dysfunction and Spinal Facilitation
The observation that palpable somatic dysfunction i nvolves the histologic signs of i n flammation and edema opens the door for understanding the role of PANs in this rype of lesion. PANs can be extremely sensitive to the chemical mediators of i nflam mation ( 1 5) and, in many situations, release proinflammatory neuropeptide mediators that will worsen the si tuation (Fig. 8.2). This condition is termed neurogenic i nflammation (19). Chemoreceptor Primary Afferent Nociceptors Respond to Proinflammatory Compounds
D ur i ng an i nflammatory event, vascular endothelial cells release prostaglandins and local mast cells release h istamine. White blood cells are attracted i n to the tissue and release various cytokines such as i n terleukin-1, i n terleukin-6, and tumor necrosis factor. Within the area of i nflammation, the pH drops i ndicating an increase in the concentration of protons, a condition known to
Neurogenic Inflammatory Cycle
Tissue
Inflammation
Neuropeptides
Sensitized
Spinal
Primary Afferent Fibers
Cord
FIGURE 8.2. Summary diagram illustrating the tissue inf lammatory cycle and the sensitization of primary af f erent f ibers.
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fl. Osteopathic Considerations in the Basic Sciences
activate PANs in human skin (20) . I n addi tion, the plasma protein preprobradyki n i n is unblocked to yield bradykinin. Receptors for most of these compounds are present on the PANs and these com pounds have been demonstrated to i ncrease the firing rate of the PANs. Furrhermore, when the smallest of the PAN s (the C fibers) become active, they not only carry an action potential toward the spinal cord but also release neuropeptides from their peripheral term i nals (19) . Typical neuropeptides released are substance-p, calcitonin gene-related polypeptide, and somatostatin among others. Not only are some of these peptides vasodilatory (cre ating neurogenic extravasation) but they also can sti mulate mast cells to degranulate thereby releasing more h istamine i n ro the tissue. Fi nally, a t least one of the secreted peptides, substance-p, is also capable of direct i rritation of the PANs.
Peripheral Sensitization Contributes to the Increased Sensitivity to Touch or Hyperalgesia
The lowered thresholds of the PANs con tribute to the increased sensitivity to touch or hyperalgesia, representing the second of the four criteria for the diagnosis of somatic dysfunction. Thus, knowledge of the i nflammatory process and the PAN response allows an understanding o f the first two criteria used in diagnosing somatic dysfunction. [n the next section, the response of the spinal cord to PAN activity will be examined in an effort to gain understanding of the last two cri teria used in osteopathic palpatory diagnosis.
NOCICEPTION AND SPINAL FACILITATION Alteration of Primary Afferent Nociceptor
Termination and Activity of Primary Afferent
Phenotype by Inflammatory Chemicals
Nociceptors in the Dorsal Horn
Normally, members of the large fiber system-such as the AfJ fibers-do not secrete peptide when activated. During the i n flammatory process, however, the AfJ fibers have been observed to undergo a phenotypic change developing behaviors similar to the C fibers of the small fiber system including the secretion of neuropeptide (18 ) . Not only does this finding demonstrate that the large fiber system can cont ribute to the i nflammatory pro cess, but it also demonstrates how plastic the peripheral nervous system can be in response to challenge.
Based on the model of an inflammatory process, somatic dysfunc tion in the peripheral tissue produces inflammatory chemicals that irritate PANs; these fibers then relay action potentials i n to the dorsal horn of the spinal cord. Activity in the dorsal horn plays a crucial role i n determining the outcome of the dysfunction. I n one sense, the dorsal horn neurons can convert the nociceptive activity of primary afferen t fibers i nt o a signal that the brain can i nterpret as pain. Woolf and colleagues (23) divided the activity o f the dorsal horn neurons i n to four functional states.
Increased Responsiveness of Primary Afferent
The Four Modes of Activity in the Dorsal Horn
Nociceptors Results in Peripheral Sensitization
As PANs become active in an i nflammatory situation, an impor tant change man i fests i n their behavior. Under repetitive stimuli, there is a shift in their response properties such that they become much more sensitive to low thresholds of energy ( Fig. 8.2). I n this condition, a previously noxious stimulus now elicits a greater pain sensation. This condition is termed pri mary hyperalgesia (21). I f the t issue is so sensitive that typically nonnoxious stim uli can elicit the sensation of pain , then the condition is termed allodyn ia-a special subset o f the hyperalgesic cond i tion. When PANs alter their thresholds to produce an area of primary hyper algesia, they are said to have undergone a process of peripheral sensi tization (22). Hyperalgesia that develops around the imme diate area of noxious stimulation is termed pri mary hyperalgesia; whereas that which develops outside o f the area o f stimulation is termed secondary hyperalgesia. I n some situations, the area of secondary hyperalgesia is not in conti nu i ty with the area of primary hyperalgesia ( 1 7) . Application to Understanding Somatic Dysfunction
I n the first mode, which represents normal function, the input to the dorsal horn is balanced with the output; in essence, the output is in normal proporrion to the i nput received by the dor sal horn neurons. This allows a given nociceptive input to be converred i n to an acute pai n signal sen t to the brainstem and forebrai n . Tn the second state, the output of the dorsal horn is partially inhibi ted; therefore, the response to a given input is suppressed. This is also a normal mode and allows the brain to reduce the amount of pain that is experienced consequent to a given nociceptive stimulus. The third mode is the converse of the second and is also normal in function; here, the dorsal horn output to a given nociceptive signal is increased or facilitated. In this mode, the dorsal horn neurons have become sensitized to the nociceptive i nput and are generating an enhanced pain signal to the brain. This latter mode is considered to be a pro tective defense against fur ther injur y by usage. Final ly, the fourth mode o f dorsal horn activity is pathologic i n nature. Here, the output from dorsal horn neurons is way out of proportion from the i nput; thus a stimulus, nociceptive or otherwise, produces an enlarged and prolonged output from the dorsal horn. Each of these modes will be considered briefly.
Edematous Response Underlies the Tissue Texture Changes
Mode One: Normal Input-Normal Output
The extravasation of fluid i n to the extracellular space during in flammation al ters the tissue compos i tion and changes i ts pal patory presentation. These observations account for the tissue texture changes that represent the first cri terion for the diagnosis of somatic dysfunction.
Distribution of Central Terminals in the Dorsal Horn
The central processes of the PANs enter the dorsal horn from i ts dorsal surface and termi nate primarily in the upper layers of the structure-laminae I and I I . Some of these fibers also extend in
8. Nociception, the Neuroendocrine Im m une System, and Osteopathic Medicine
Mode 1
-
141
Normal Transmission
Innocuous or noxious stimulation
Afferent input
IIII
SP glutamate
o AMPA
� O�-----40r--NK1
�
__
Postsynaptic output
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Normal Sensibility
eo the deep porrion of the dorsal horn, lamina V. I n con([ast, the cenrral terminals of the large fiber system, such as the Af3 fibers, pass medially over the dorsal horn eo enrer the spinal cord along me margin of the dorsal columns. From here, the large-caliber fibers climb up the dorsal columns ro reach the dorsal column nuclei at rhe base of the brainstem, from which i nformation is passed oneo thalamus and, evenrually, the cerebral cortex. How ever, before ascending the spinal cord, many of these axons give off a collateral fiber thar enrers the dorsal horn synapsing in layers I I I and IV.
Chemistry of Primary Afferent Nociceptor Central Processes in the Dorsal Horn
Within the dorsal horn, all fibers appear ro release amino acids, such as asparrate and glutamate, as neurotransmi((ers. Typically, these amino acids are released inro the clefts of synapses on dorsal
FIGURE 8.3. Mode 1 demons trating balanced in put/output relations between the pre- and pos t s y naptic element. From Doubell TP, Mannion RJ, Woolf CJ. The dors al horn: s tate- dependent s ens ory processing, plas ticity and generation of pain. In: Wall PD, Melzack R, eds . Textbook of Pain. Edinburgh, Scotland: Churchill Livingstone; 1999:165-181, with permiss ion.
horn neurons. The PANs, however, also release a neuropeptide rransmi((er, substance-p, not necessarily i nro the synaptic cleft, but inro the extracell ular spaces o f the dorsal horn. The neu ropeptide then diffuses o n ro receprors on the membranes of surrounding dorsal horn neurons.
Normal Activity of the Dorsal Horn
The depolarization of PANs by a nociceptive stimulus activates the rapid release of excitarory amino acids i nro the clefts of synapses on dorsal horn neurons. The resultanr firing (action potential) pa((ern of the dorsal horn neurons is directly related eo the amounr o f ([ansmitter released ( Fig. 8.3). This is experienced i n a healthy individual when, for example, their skin is pinched and they feel a q u ic k sensation of pain that term inates shorrly af ter the stimulus is ceased. The stimulus is noxious and can trigger rapid, protective reflexes, but has not damaged the tissue.
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11. Osteopathic Considerations in the Basic Sciences
Mode 2
-
Suppressed Transmission
Activation of segmental and descending inhibitory systems
Afferent input
IIII
SP glutamate
Reduced transmitter release
o
o
�IP,-.A _- � �
Postsynaptic
FIGURE 8.4. Mode 2 demonstrating the pre- and postsy naptic inhibition of ac tiv ity resulting in the suppression of firing in the dorsal horn neuron. From Doubell TP, Mannion RJ, Woolf Cl The dorsal horn: state-dependent sensory proc essing, plas tic ity and generation of pain. In: Wall PD, Melzac k R, eds. Textbook of Pain Ed inburgh, Sc otland: Churc hill Livingstone; 1999:165-181, with permission.
Postsy naptic output
I
Reduced Sensibility
Mode Two: Normal Input-Suppressed Output Two Systems Combine to Suppress Dorsal Horn Activity
In the second mode, a normal nociceptive i nput generates a re duced output from the dorsal horn. I n this condition, the dorsal horn neurons are being inhibited by two mechanisms (Fig. 8.4). From the periph ery, through a complex mechanism, the large caliber (Af3) fibers whose collateral branches terminate in the m iddle layers of the dorsal horn trigger a n i nhibition of neurons i n the upper layers of the structure. This represents the classic gate-control theory of Melzack and Wal l (24) . Additional sup pression of dorsal horn neuronal activity comes from descending supraspinal pathways. These descending pathways allow the cere-
bral cortex and brainstem, especially its l imbic or emotional com ponents, to exercise control over the conversion of nociceptive input into pain signals by the dorsal horn . Using these endoge nous pain control systems, the body can reduce the amount of pain it is experiencing. This can be useful i n critical situations such as escape behavior where pain needs to be m i n imized. Mode Three: Normal Input-Enhanced Output
I n this mode, neural activity in the primary afferent fiber results i n an enhanced response ftom the neurons in the dorsal horn (Fig. 8.5) . This enhancement of activity represents a mode of spinal facilitation and is underwritten by a complex series of i n teractions.
8. Nociception, the Neuroendocrine Immune System, and Osteopathic Medicine
Mode 3
-
1 43
Facilitated Transmission
Increased excitation/reduced inhibition
Afferent input
II II Adenostne 5HT
Presynaptic
Reduced presynaptic
augmentation
inhibition
mGluR
vL.-.
----- --___-'"
,,
__
Retrograde signals e.g
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...,
,
NO
\ \ \ I I
Postsynaptic
"
facilitation I
Reduced postsynaptic inhibition
I
-----
". ./
/
t Postsynaptic activity
111111111111111111 I III FIGURE 8.5. Mode 3 demonstrating the enhanced activity in the dorsal horn neuron indicating a state of sensitization. From Doubell TP, Mannion RJ, Woolf CJ. The dorsal horn: state-dependent sensory processing, plasticity and generation of pain. In: Wall PD, Melzack R, eds. Textbook of Pain. Edinburgh, Scotland: Churchill Livingstone; 1999:165-181, with permission.
Release of Peptide and Activation of Voltage-Gated Channels
Prolonged PAN stimulation results i n the release of neuropeptide, such as substance-P, in the exrracell ular spaces of the dorsal horn. Responding ro the neuropeptide signal , neurons rrigger i n rernal phosphorylation evenrs that resulr in the opening of voltage gated membrane channels for glutamate. These channels allow calcium in Aux to the cell. Evenrs that are triggered by a change in the cell's vol tage due to repeated firing are referred to as "activity dependent."
Activity-Dependent Changes Lead to Altered Gene Expression and Protein Synthesis
The calcium inAux from the vol tage-gated channels is involved in gene i nduction. An example of an activity-dependenr, i n duced gene expression is the gene encoding for dynorphin. A barrage of activity on the PANs can result i n the induction of
m RNA for dynorp h i n and, ulrimately, its synrhesis in nu mer ous dorsal horn neurons. Dynorphin is known to i ncrease the facilitation of neurons; therefore, i t can i ncrease the sensitivity of dorsal horn neurons. This is particularly i nreresting because it means that excessive activity in the PANs can resu lt i n a molecu lar change ( involving altered gene expression) in the dorsal horn neurons.
Mode Four: Subnormal Input-Grossly Enhanced Output
I n this mode, dorsal horn neurons have altered their membrane properties such that they overrespond to very minimal i nput, and i n some cases, to no input at all. This hypersensitivity state is a pathologic condition that is most l i kely related to at least three conditions: the sprouting of processes from damaged nerves, the activation of dorsal horn glial cells, and cell death of overexci ted inhibitOry i n rerneurons in the dorsal horn ( Fig. 8.6).
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ll. Osteopathic Considerations in the Basic Sciences
Mode 4 Structural reorganization
Aberrant connections with facilitated transmission
C-fibre
______-r-_����---L---l
r-
I I I
II
0
0 0
o
o
II
0
i
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o
IlIIlV/V
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-------'---., C-fibre terminal atrophy
'D1'-r5111 T,O-ri'l
1
Nerve injury
A-fibre sprouting
Normallerminalion pattern
Interneuron degeneration
Pain hypersensibility - persistent
FIGURE 8_6_ Mode 4 demonstrating pathologic changes in the loss of C f ibers secondary to nerve injury
and the sprouting larger f ibers f rom the deeper levels of the dorsal horn. From Doubell TP, Mannion RJ, Woolf CJ. The dorsal horn: state-dependent sensory processing, plasticity and generation of pain. In: Wall PD, Melzack R, eds. Textbook of Pain. Edinburgh, Scotland: Churchill Livingstone; 1999: 165-181, with permission.
The Central Terminals of Af3 Fibers in an Injured Nerve Sprout Within the Dorsal Horn
Damage to a peripheral nerve can lead to enhanced sprouring o f peripheral a n d central fibers of dorsal roor ganglion neurons. I n addirion , rhe damage o f rhe small PAN fibers secondary t o nerve inj ury will result in rhe withdrawal of rheir axons fro m lamina I I o f the dorsal horn. Sprouting from rhe central rermi nals o f Af3 fibers i n rhe deeper laminae can then i nvade rhe upper layers and replace rhese rerm inals by formi ng abnormal synaptic contacts with neurons in lamina II (25) . [n rhis condirion, light touch, which is usually a non noxious stimulus, can result i n Af3 fiber acriviry and the subsequent activarion o f upper level dorsal horn neurons whose acriviry rypically encodes rhe signals for pai n .
Excessive Primary Afferent Nociceptor Activity Can Activate Dorsal Horn Glial Cells
Recenr srudies have proposed an i nteresri ng role for glial cells i n rhe development a n d maintenance of spinal faci lirarion (26,27). In rhis model, excessive release of neurorransm irrers from rhe cenrral rerm inals of PAN fibers resulrs i n the acrivarion of dor sal horn astrocytes and microglial cells. This appears to be a receptor-mediared process. The activared glial cells respond by releasi ng proinflam marory cyrokines, reacrive oxygen species, ni rric oxide, prosraglandins, excirarory amino acids, and adenosine rriphosphare; all of which are compounds rhat can contribute ro rhe excirarion of dorsal horn neurons. Interesringly, bloclcing the merabolic acriviry of spinal glial cells or antagonizing rhe produc-
rion or release of p roinflammatory cytolcines i n rhe spinal cord prevents rhe development of hyperalgesic srares consequent to viral antigens (28). Thus, glial acrivarion appears exacerbare rhe ongoing activiry of rhe PAN-dorsal horn neuron couple leading to rhe excessive acriviry stares characrerisric of spi nal facilirarion. Excessive Neuronal Activity in the Dorsal Horn Can Result in Cell Death.
I n siruarions i nvolving rissue i njury and subsequenr PAN acriviry, such as chronic consrriction injury to a nerve (29) or a surgical i ncision (30), damage occurs in the population oflaminae [ ro I I I dorsal horn neurons. This damage i s seen as darkened, pynoric neurons. It is proposed rhar rhey represent neurons dying rhrough a process of excitatory toxiciry due ro excessive exposure ro excira rory amino acids released from excessively acrive PANs. The facrs rhar rhese dying neurons are rypically rhe smaller neurons in rhe dorsal horn and rhar rhe dorsal horn loses inhibitory rransmir rer after nerve inj uries suggest that rhe dying cells are inhibirory interneurons involved in modularing acriviry in rhe dorsal horn circuits (31). The loss of inhibirory neurons from a dorsal horn circuir would allow grearer facilirarion of pain parhways. Central Sensitization of Spinal Cord Neurons
In modes rhree and four of dorsal horn operarion, rhe primary i nput encounters a hypersensirive neuronal circuirry. The hyper activiry represents a form of central sensirizarion rhar is to be disti nguished from sensirization of rhe peripheral terminals of
8. Nociception, the Neuroendocrine Im mune System, and Osteopathic Medicine
the primary afferent fibers (23). I n mode three, the central sensi tization is related to phosphorylation events, altered membrane properties, and subsequent gene i nductions. These activities have a reversible nature, unl ike the situation in mode four. I n this later mode, pathologic changes in the tissue such as terminal sprouting or neuronal cell death have indelibly altered the activity of the dor sal horn. Development of mode four in a patient underlies some of the changes experienced i n shift from acute to chronic pai n . Spinal Facilitation and Altered Spinal
145
have afferent terminals fro m visceral PANs (35). Thus, nocicep tive activity converges on neurons i n the spi nal cord that are capable of responding to excessive i nput with facilitation. Us ing this model , it can be seen that either somatic or visceral (or both) dysfunction (s) can serve to facilitate the spinal cord. Once facilitated, i nput of somatic or visceral origin can function to activate spi nal cord neurons, generating the subsequent somatic or visceral peripheral changes com monly associated with somatic dysfunction . These somatovisceral and viscerosomatic reA exes are further d iscussed in Chapter 7.
Cord Output
Central sensitization in the spinal gray matter creates a condition of spinal faci litation. In this condition, circuits i n the spinal cord have lowered thresholds of activation and can therefore be more easily engaged by the synaptic drive of the primary afferent fibers.
SUMMARY: THE NOCICEPTIVE MODEL
Spinal Facilitation Is the Product of Multiple Factors
in the Establishment of Spinal Facilitation
Multiple events are involved in facilitation of the spinal cord. As previously outl ined, primary afferent fibers release amino acid and peptide neurotransmitter, dorsal horn neurons undergo mem brane property changes due to phosphorylation events, and gene induction occurs in the nucleus of these neurons, producing fa cilitatory compounds such as dynorphi n .
Spinal facilitation involves changes in cellular membrane prop erties, gene expression, and in the distribution of synaptic ter m inals i n the spinal gray matter, as previously described. These structural and functional alterations in neurons depend on the excessive synaptic drive from the PANs. In fact, i n experimen tal paradigms, outward manifestations of spinal faci l i tation are difficult or i mpossible to obtain without elevating the stimulus parameters to the level of activating the PANs (8).
OF SOMATIC DYSFUNCTION The Role of the PANS Primary Afferent Nociceptors Are Important
Spinal Facilitation Suggests a Form of Spinal Memory
The facilitation of dorsal horn circuits secondary to intense PAN activity and the long-term to permanent nature of these changes suggest the existence of a spi nal memory. This memory would allow the ingraining of old pain patterns and their reactivation by mi lder stimuli at a later date (5,32). Spinal Facilitation Leads t o Altered Output On the Ventral Root
Facilitation of the spinal cord by PANs results in altered activity i n the ventral roots (33). Because the ventral roots contain somatic efferent axons in nervating skeletal muscle, the outward manifes tation of this activity involves altered muscle tone in the associated spinal segments. These changes in muscle tone suggest a neuro physiologic basis for the altered ease or range of motion present in patients with somatic dysfunction. Furthermore, the altered somatic muscle tone would be expected to create an anatomic asymmetry in the effected region of the body, thus explaining the third and fourth criteria for the diagnosis of somatic dysfunction. The ventral root also carries visceral efferent fibers i nnervating glands and vascular and organ wall smooth muscle as well as associated fascia and immunocytes. Evidence suggests that spinal facilitation also alters the output of the visceral afferent fibers (34), thereby accounting for the vasomotor, sudomotor, and organ specific changes often associated with somatic dysfunction. Convergent Input to the Spinal Circuit and Spinal Facilitation
Finally, it is significant to point out that many of the dorsal horn neurons that receive afferent terminals from somatic PANs also
Primary Afferent Nociceptors Are Not Necessary to Maintain Spinal Facilitation
Once spinal facil itation has been established, elim i nating periph eral spinal input by section o f the dorsal roots does not elimi nate the outward signs o f faci litation (8); instead, the increased muscle tone abates slowly with time. Thus although PANs are necessary to establish facilitation, they appear not to be necessary to maintain the facili tation. Alterations in Spinal lnterneurons Results in Long-term Memory of Circuit Facilitation
Spi nal facil itation survives transection of the spinal cord, which suggests that i t arises i n the spinal gray matter itself and not from descending brai nstem i nfluences (8). These observations are in line with the above-cited l i terature that implicates the neu rons and possibly the glial cells of the spinal gray matter as the main culprits in facilitation of the spi nal cord (27). The emphasis placed o n the PANs has given rise to the "nociceptive model of spinal facil i tation" (36) .
SPINAL FACILITATION AND THE BRAINSTEM AROUSAL SYSTEM Ascending Spinal Pathways
Somatic dysfunction that occurs in peripheral tissue generates a signal carried by the PANs into the dorsal horn of the spinal cord. This nociceptive i n formation is processed by spinal neurons and relayed upstream to the brainstem and thalamus en route to the cerebral cortex. Most of the ascending i n formation is carried in the classically defined anterolateral system, which contains
1 46
II. Osteopathic Considerations in the Basic Sciences
spinothalamic fibers, spinohypothalamic fibers, and spi noreticu lar tract. Anterolateral System The Spinothalamic Tract carries Information on Pain Localization to the Parietal Cortex
The spi nothalamic tract eX[ends from the segmental levels of the cord ro the posterior and ventral portions of the thalamus. As it ascends, most of its fibers lie in the both the lateral and ventral regions of the anterolateral tract. The tract arises from neurons located i n three cl usters i n the spinal gray: lamina 1, lami nae I V and V, and lami nae V I I and V I I I ( J 3 ) . The target of this pathway is the contralateral thalamus, especially its lateral and posterior portions. Although the activities of the spinothalamic tract are complex and multifacrorial, a major fu nction o f the structure ap pears ro be the conduction of information on stimulus localiza tion from the spi nal cord th rough the lateral positions of thai am us ro the somatic sensory areas of cerebral cortex (1 1 ) (Chapter 9 ) . The Spinohypothalamic Tract carries Nociceptive Information to the Limbic Forebrain
Projections from the spi nal cord ro the contralateral hypothala mus have been described in nu merous studies (37) . All o f the neurons involved with this tract appear ro be responsive only ro noxious stimuli, strongly suggesting that the tract is involved i n l i mbic response r o nociceptive stimuli ( 3 8 ) . Recent studies have also demonstrated trigemi nohypothalamic tracts carrying nox ious i n formation from the oro facial region ro the hypothalamus (39). Although functional studies o f the trigemino- and spi nohy pothalamic tracts have yet ro be done, they both appear ro carry noxious i n formation and they both are in a position ro activate or inAuence neuroendocrine and emotional response. The Spinoreticular Tracts carry Warning Information to the Brainstem and Prefrontal Cortex
Projections from spi nal cord neurons ro the brainstem form a complex system involved in auronomic regulation and protec tion of homeostasis. These pathways arise from spinal laminae I , V, and VI I , and project ro the reticular formation as well as ro other regions of the brainstem such as the parabrachial nucleus, periaqueductal gray, hypothalamus, and amygdala (40). Addi tionally, projections from the spinal trigemi nal nucleus i nro the brai nstem reticular formation also exist (41) . These pathways are predomi nantly contralateral i n distribution; however, some of these fibers, especially those going ro the lower brainstem , are bi lateral. Ascending pathways from the reticular formation lead ro the medial nuclei of the thalamus, from which fibers project ro the prefrontal and anterior cingulate cortex. Thus, the spinoreticular tracts target the limbic forebrain, the major emotional compo nent of the brai n. Information in the Spinoreticular and Spinal Hypothalamic Tracts Is of Both Somatic and Visceral Origin
Activity in the spinoreticular tracts is both somatic and visceral i n origin a n d is typically o f a nociceptive nature. T h e spinoreticular
pathways i n itiate protective, suprasegmental reAexes related ro cardiovascular, respirarory, and endocrine control system as well as provide the affective and emotional components of pain ( 1 2) . Taken rogether, this older and slower ascending system activates a brainstem arousal system that is protective in nature but that has a huge inAuence on the homeostatic mechanisms of the body. Brainstem Reticular Formation Anatomy
The reticular formation represents a broad col umn of cells and fibers extending through the center of the brainstem and arising from the spi nal gray matter at the cervicomedullary j unction and blending i n ro the hypothalamus at the rostral end of the midbrai n . The cranial nerve nuclei are embedded in the reticular formation (42). The reticular formation of the brainstem is a major target of ascending fibers carrying nociceptive information from either somatic or visceral dysfunctions. The Reticular Formation Is the Integral Core of the Brainstem, Extending from the Medulla to the Thalamus
The reticular formation contains many of the phylogenetically oldest cell clusters of the brain and plays a major role in con tro l l i ng the defense mechanisms for protecting homeostasis. The formation is divided functionally inro caudal and rostral portions. The Caudal Reticular Formation Contains Areas Controlling the Autonomic Nervous System
The caudal portion of the reticular formation is contained In the medulla and pons. It has cell clusters associated with car diovascular and respirarory control located ventrally and laterally (41) and surrounding a central portion that inAuences posture by modulating skeletal m uscle rone. Other regions of the caudal reticular formation are i nvolved with modulating spinal facil ita tion. These regions receive sign ificant input from the anterolateral fibers systems ( nociceptive i n formation) and, in turn, control sev eral descending pathways that reach the dorsal and ventral horns. These descending brainstem-spinal projections can either inhibit or excite neurons i n the spinal gray. The Rostral Reticular Formation Contains Areas Controlling Attention and Arousal
The rostral portion of the reticular formation begins in the pons and extends through the midbrain inro the caudal regions of the hypothalamus. A major component of the rostral brainstem is the arousal system (43) . This system consists of two in terconnected components. A medially positioned cluster of nuclei forms the reticular activating system that is capable of modulating cerebral cortical activity between states of sleep and wakefulness. More dorsal and laterally, monoamine-producing nuclei (such as the lo cus coeruleus) function ro integrate the hormonal and auronomic nervous system components of the arousal response. Both aspects of the arousal system respond ro nociception from somatic or vis ceral dysfunction. It is critical ro consider how the arousal system works and its overall or long-term im pact on body function.
8. Nociception, the Neuroendocrine Imm u ne System, and Osteopathic Medicine
Arousal System of the Brainstem The Rostral Portion of the Brainstem Plays a Key Role in the Arousal System
Protection of the body from external or i nternal threat requires that the individual be awake and capable offocusing attention on the surrounding environment. The midbrain plays an essential role in this process. Projections extend i nto the generalized nuclei of the thalamus from the neurons i n the reticular formation of the midbrain, which, in turn, form a diffuse projection to the neocortex. Long known as the reticular activating system, this circuitry is deeply i nvolved in controlling the activity of cerebral cortex, determining such states as sleep and wakefulness (44) . I n addition to the reticular activating system, several monoamine pathways arise i n the brainstem and i n nervate both thalamus and neocortex. Like the reticular activating system, the monoamine pathways modulate the activity of neocortical neurons i n various ways. One system that arises from the locus coeruleus in the mid brain plays an important role i n arousal (45 ) . Flucruations i n the activity of coeruleus neuron are directly reflected i n the activity of the cortical electroencephalogram. Together, the reticular ac tivating system and the associated monoamine pathways control the attention and arousal states of the individual; this circuitry forms the basis for the arousal system. The Arousal System Is Most Responsive to Novel, Unexpected, or Unwanted Stimuli
Any unexpected or unanticipated stimulus can activate the arousal system of the brainstem. This includes visual, acoustic, and somatic sensory stimuli. Nociceptive stimuli represent a par ticularly strong drive on the arousal system. Stimulation of the sciatic nerve at a level that activates its PANs results in i ncreased neuronal activity in the locus coeruleus (46) . Although the path way from the spinal cord ro the locus coeruleus is multisynaptic (47), the effect on the coeruleus is still very powerful. Somatic Dysfunction and the Arousal System
I ncreased activity of PANs secondary to somatic dysfunction will be detected by the arousal system . Thus, somatic dysfunction can alter the state of arousal in the brain. This is most clearly seen in acute injuries. The peripheral nervous system becomes active either through mechanical irritation or through the re lease of proinflammatory cyrokines. Spinal cord neurons respond with increased activity, and the individual becomes aware of the injury. Rapid adaptive changes, detailed below, also occur i n the endocrine and autonomic nervous systems after activation of the midbrai n arousal circuitry. In the short-term siruation, these reflex responses are beneficial to survival of the i ndividual. However, long-term exposure to these adaptive changes, such as chronic somatic or visceral dysfunction, can have pathologic consequences. Visceral Dysfunction and the Arousal System
Visceral afferent fibers i n the vagus nerve carry signals concern ing visceral dysfunction to the solitary nucleus of the brainstem. Mechanical irritation, i n fection, or inflammation of visceral
1 47
tissue results in the release of proinAammatory cytokines by macrophages, dendritic cells, and other i mmune cells, some of which occurs i n the vicinity of the vagal nerve endings. Re cent srudies demonsrrated that the proinflammatory cytokine, i n terleuki n- l ,B i n teracts in various ways with the vagus nerve to activate its primary afferent fibers (48) . These relationships have given rise to the concept of an "immunosensory system" (49). I n this concept, dendritic cells and other antigen-presenting cells interact with foreign substances through immune-type receptors; the activated antigen-presenting cell releases proin Aammatory cy tokine that i n teracts with receptors on the vagal primary afferent fibers. Thus, the antigen-presenting cell is behaving as a highly variable receptor, capable o f detecting the enormous range of stimuli typical of the i m m une system but then generating a com mon signal that peripheral nerves can understand. The activated vagal fibers transmit signals to the soli tary nucleus of the brain stem from which i m munosensory i n formation ascends th rough the brainstem to the thalamus and l imbic forebrain. The response to such i nformation has been termed sickness behavior or the acute-phase response (50). S ickness behavior is characterized by physiologic changes: fever, increased sleep, alterations in blood chemistry; behavioral changes: decreased locomotion, decreased l ibido, decreased exploration and aggression, and decreased food and water i n take; and by hormonal changes: activation of the sympathetic nervous system (SNS) and o f the hypothalamic piruitary-adrenal axis (50). Thus, the i m m une system and the nervous system combine their activity such that the i m mune sys tem's amazing abilities to detect an infi nite n umber of substances is coupled ro the nervous system's abilities to generate a rapid adaptive and protective response.
Emotional Stimuli and the Arousal System
Not only does the arousal system respond to unexpected or un wanted sensory stimuli but i t also is sensitive to emotional activity. Strong connections exist between the forebrain limbic system (the center o femotional activity in the brain) and the arousal system of the midbrain. For example, the amygdala n uclear complex in the medial aspect o f the temporal lobe-a major component of fear o r negative memory system-has a prominent descending pro jection to the area i mmediately s urrounding the locus coeruleus i n the brainstem ( 5 1 ) . Viewed in this light, the arousal system of the brainstem is performing as a convergence point. It re ceives sensory stimuli (somatic, visceral, visual, and acoustic) and emotional stimuli and channels this warning i n formation into a wide-ranging output circuitry that significantly alters activity i n t h e nervous, endocrine, and i m m u n e systems.
AROUSAL AND THE NEUROENDOCRINE IMMUNE NETWORK Output of the Arousal System Alters Hemostasis
Activation of the arousal system consequent to physical (somatic or visceral) or emotional stimuli has a profound i m pact on home ostatic mechanisms in the body. I n i tiating a strong systemic sympathetic response and triggering the release of the adrenal cortical steroid hormones to accomplish this effect. These two
1 48
11. Osteopathic Considerations in the Basic Sciences
systems, neural and endocri ne, i nteract with a third, the immune system, to inAuence the release ofcytokines. The neuroendocrine im mune network Functions to prepare the body for defense by faci l i tating healing, suppressing the pain pathways, and modu lating the im mune system for optimal response.
The Autonomic Nervous System and Catecholamine Release
The locus coeruleus and portions of the rostral ventral medulla are closely l i n ked functionally. Much of the noxious somatic and visceral sensory i n formation that ulti mately activates the locus coeruleus does so by targeting the rostral ventral medulla, specifically a structure termed the n ucleus paragigatocell ularis. This later nucleus has direct projections to the locus coeruleus. Thi� circui try-the locus coeruleus and associated medullary structures-has been described as the SNS o f the brain (52,53). Activated by unexpected or noxious stimuli, this system releases the catecholami ne norepinephrine i n to many forebrai n regions, such as the hypothalamus and amygdala. The locus coeruleus, although containing only a moderate number of neurons (approximately 50,000 to 65,000; see reF. 54) , has extremely wide-ranging Forebrai n axonal projections that reach m uch of the neocortex, h ippocampal Formation, amygdala, thalamus, and hypothalamus. In addition to the Forebrain structures, the locus coeruleus has projections to the spinal cord and some brainstem nuclei. Finally, the rostral ventral medulla has projections i nto the cardiovascular and respi ratory control centers of the caudal brainstem.
Activation of Cardiovascular and Respiratory Centers in the Brain Stem
The inAuence of the locus coeruleus-rostral ventral medulla over the caudal brainstem cardiovascular and respiratory control cen ters helps to explain the changes in circulatory and respiratory parameters that can accompany unexpected or noxious stimuli ( 5 5 , 56) . Acute nociceptive stimuli can result i n an i mmediate rise in blood pressure and heart rate. A drop in blood pressure Fol lowed by a slow gradual climb in cardiac parameter occurs after th is i n itial event. Long-term exposure to excess activity in these central as well as peripheral sympathetic systems has been l i n ked to essential hypertension and to progressive fai lure of the heart (57). These studies emphasize the important l i n k between the somatic and visceral nervous system, the SNS, and the cardiovas cular system.
Descending Systems Influence the Lateral Horn of the Spinal Cord
When activated by the arousal system, descending noradrenergic fibers From the locus coeruleus and other brainstem nuclei can exert a modulatory inAuence o f the activity o f presynaptic fibers and neurons in the dorsal horn (58). After nociceptive stimuli are received, the noradrenergic system functions to inhibit trans mission in the spinal dorsal horn, which reduces the sensation of palll.
The Hypothalamic-Pituitary-Adrenal Axis and Glucocorticoids Release
Along with activating the brainstem SNS, nociceptive drive From somatic or visceral dysfunction also triggers a complex of pro tective responses from the hypothalamus and pituitary. The pathways used to evoke these responses i nvolve both direct, nociceptive-carrying spi nohypothalamic fibers and spinoreticular fibers that result i n activation of ascending noradrenergic projec tions in the locus coeruleus that reach the hypothalamus. Little is known concerning the action of the spinohypothalamic fibers (38); however, norepi nephrine from the coeruleus projections triggers neurons in the paraventricular nucleus of the hypothala mus to release the peptide corticotropin-releasing hormone (59). In addition, a h umoral pathway to the brain also exists. Proin flammatory cytokines released in areas of trauma, inflammation, or i n Fection can become systemic, crossing the blood-brain bar rier in the vicinity of the circumven tricular organs (60,6 1 ) . These latter organs contain neurons that project to ·the hypothalamus and are known to orchestrate the fever response as well as the neuroendocrine response typical of arousal (62) .
The Locus Coeruleus-Norepinephrine System Stimulates the Release of Corticotropin-releasing Hormone
The coupling between the locus coeruleus and the paraven tricu lar n ucleus of the hypothalamus serves to coordinate the release of corticotropin-releasing hormone (CRH) and norepinephrine. Norepinephrine released into the paraventricular nucleus stimu lates the release of CRH; in turn, CRH can stim ulate the pro duction and release of norepinephrine Form the locus coeruleus (63,64). The observation that they exist in a Feed-Forward inter active circuit means that systemic levels of these two substances can rise quickly in response to external or internal threats.
Corticotropin-releasing Hormone and the Activation of the Anterior Pituitary and Adrenal Glands to Produce Cortisol
Neurons producing CRH in the paraventricular nucleus have axons that release this peptide i nto the neural-hemal zone of the median emi nence. The peptide enters the bloodstream and is passed to the capillary network in the anterior pituitary. In response to CRH, corticotropes in the anterior pituitary pro duce and secrete adrenocorticotropin (ACTH). This later pep tide is released i n to systemic circulation and stimulates cells in the adrenal cortex to produce and release gl ucocorticoids such as cortisol ( Fig. 8.7). This mechanism, which leads to cortisol production, has been termed the hypothalamic-pituitary-adrenal ( H PA) axis. Each of the substances involved in regulating the H PA axis (CRH , ACT H , and cortisol) participates in a feedback loop that is capable of suppressing the axis iF plasma levels of adrenal cortical steroids rise too high. Major drives on the H PA axis i nclude a retinohypothalamic connection involved in ci rca dian release of cortisol, unexpected or noxious somatic or visceral stimuli, and a strong emotional drive from such limbic structures as the prefrontal cortex and the amygdala (65 ) .
8. Nociception, the Neuroendocrine Im mune System, and Osteopathic Medicine
Limbic Forebrain
The Cytokine Network
1(- )
(( \
f-J/7_) � b�
.o!oo k--
CR H
l �\
8
H
nt
I
(
-
)
1 49
)
Retina
:�::::�
Dy'f,"",o"
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FIGURE 8.7. Diagram illustrating the hypothalamic-pitu itary- adrenal axis. H , humoral pathway s; N, neural pathways.
The Arousal-Stress Response System
The H PA axis and its compatriot, the locus coeruleus norepinephrine ( LC-N E) axis, represent the major stress system of the body. Driven by unexpected or noxious stimuli such as physical or emotional dysfunction that activates the arousal sys tem of the brainstem, and coupled through the coeruleohypotha lamic l i nk, these two axes provide for the quick release of nore pinephrine and cortisol in the face of an external or i n ternal stressor. Cortisol Functions to Prepare the Body for Repair and Survival
Cortisol has extensive and very complex functions throughout the body (66). When considering an i m mediate stress, these func tions have been summarized i nto three categories: permissive, suppressive, and stimulating. A fourth category, termed prepara tory, is used to describe anticipatory changes when the individual has a warn ing of an impending stress. Permissive functions are typified by the necessity of cortisol presence for many calorigen ic metabolic reactions to occur (67) . I n particular, the prolonged glucose-generating, metabolic actions of glucagons and the cat echolamines, such as norepinephrine, require cortisol. Most no tably, cortisol is known for its suppressive effects on the produc tion of cytoki nes and the cytotoxic arm of the immune system. However, it also appears to have a stimulatory effect on the hu moral side of the immune system in some circumstances (68). From this brief consideration, it is evident that cortisol is mo bilizing resources needed in threateni ng situations to establish a wi ndow of optimal performance for the immune system, thereby preventing a runaway response from ful m inating (69 ) .
Wh ite blood cells establish a communication network between themselves using small polypeptides termed cytoki n es. These pleiotropic molecules are released from both the monocytic (monokines) and lymphocytic (Iymphoki nes) cell li nes in re sponse to i n fection or trauma. At a local level, cytokines fu nction to coordinate the immune response; as such , they perform in an autocrine and paracrine fashion. H owever, it has also become apparent that some of these molecules can survive in circulation long enough to influence immune cells at a distance as well as i nteract with nonimmune tissue such as the central nervous sys tem (70) and the endocrine system as well as in some organs such as the lung and the liver. In this sense, cytokines are acting as hormones. A critical function of cytokines is their role in inflamma tion. Here, two fundamental types of cytokines have been de fined: proinflammatory cytokines such as interleuki n- l and tu mor necrosis factor, and antiinflammatory cytokines such as i n terleuki n-4 and - 1 O. Some cytoki nes, such as i nrerleukin-6, can demonstrate both pro- and anti inflammatory tendencies depend ing on the circumstances. The extent of inflam mation present in tissue depends, in part, on the ratio o r balance between the pro and antiinflammatory cytokines. G iven that palpable, somatic dysfunction demonstrated the presence of an ongoing, underlying i nflam matory response, it be comes of much i n terest to consider the rami fications of cytokine release i nto system ic circulation. Massive release of cytokines is known to occur in some bacterial infections; i n this case, organs such as the lung may respond by progressing toward respiratory distress (7 1 ) . At extreme levels of systemic cytokines, such as in system ic i nflammatory disease (72), multiple organ system failur e can occur (73 ) . Little is known concern ing cytokine release from locally inflamed tissue o utside of the observation that it does hap pen in disease states (74). Once systemic, cytokines can i nteract with the vasculature in the lung i ncreasing its permeabil ity and resulting in the extravasation of fluid. Also, systemic cytokines can i n teract with the hypothalamus to trigger thermeogenesis and stimulate the H PA axis to i ncrease output o f C R H , ACTH , and cortisol (69.75). Thus, cytokines that are system ically released from a local inflammatory event can i n fl uence activity in the other organ systems of the body. A number of conditions foster the release of cytokines i nto the bloodstream i ncluding i njury, infection, the i nflammatory and autoimmune p rocesses, as well as some psychiatric and demented d isorders (69 ) . Systemic proi nflam matory cytokines c a n result i n the release of cytoki nes from glial cells in the spi nal cord and brain. The output of the glial cytokine response is enhanced pain percep tion (hyperalgesia) and activation of the arousal system. This response has been termed sickness behavior (50). The triggers for this type of cytokine release i nclude peripheral tissue i n fection, i nflammation , and traumatic i n j ury. This observation is impor tant because it demonstrates that a somatic dysfunction, with its h istologically demonstrated inflammatory response, would be expected to release cytokines as well as generate increased activity in PANs. The cytoki nes can in teract at the spinal cord level to alter pain thresholds and i n the bra i n to alter the function of the neuroendocrine-immune network.
1 50
If Osteopathic Considerations in the Basic Sciences
Output of the Neuroendocrine-Immune Network Is Protective
Humoral Route
The major output chemicals of the neuroendocrine-immune axis are norepinephrine, cortisol, and a mixture of cytokines. The nu merous i nteractions between these substances fostered the con cept that communications in the neuroendocrine-immune net work are "bidirectional" (77) . Cells i n each component of the network-neural, endocrine, and immune-contain receptors for the other's regulatory products. Thus, neural cells in the hy pothalamus and other locations, as well as immunocytes through out the body, can respond to hormones such as CRH, ACTH, and cortisol. Conversely, cells i n the anterior pituitary and adrenal gland can respond to some cytokines and neurotransmitters. This concept has given rise to the term "bidirectional communica tion" between these systems (78 ) . Clearly, the boundaries be tWeen these systems have been transcended and the network is functioni ng i n a unitary manner. The neural and immune com ponents serve as the sensory i nputs to the network (79) (detecting external and i nternal signals) and the complex output of chem icals serves to regulate the homeostatic mechanisms of the body (3). The regulatory effect of the neuroendocrine-immune sys tem on homeostasis is protective i n nature, and has been termed allostasis, which means the "maintenance of stability through change" (80). Allostasis Homeostasis is Critical to Survival
FIGURE 8.8. Diagr am ill ust r at ing t he neur al and humor al r out e us ed i n act iv at in g the arousal s ystem of t he brainstem. AS, arousal s ystem:
The Neuroendocrine-Immune Network Integration of a Neural-Endocrine-Immune Reaction
Two significant observations arise from the preceding sections. First, acting through the nervous system, somatic dysfunction relays an excitatory drive on the LC-N E and H PA axes of the midbrain and hypothalamus. Second, acting through humoral routes and the release of cytokines from i n flammatory tissue, that same dysfunction also stimulates the HPA axis (Fig. 8 . 8) . Studies i nducing small, local i n flammatory reactions similar to those seen in somatic dysfunction and examining the response of the H PA axis have verified these observations (76) . The H PA axis has a biphasic response to an acute, local i n flammatory event; the first phase is acute (less than an hour) and is fol lowed by a second phase that develops more slowly (after 3 hours) and parallels the rise in the inflammatory event (69,76). The first phase is mediated via the peripheral nervous system whereas the second p hase is mediated h umorally through the release of cytokines. These, and similar studies, demonstrate a neuroendocrine-immune network that responds both acutely and in a more prolonged manner to threat or injury.
Homeostasis includes the carefully controlled rhythms of param eters such as heart rate, blood pressure, fluid ionic balance, tem perature, and plasma glucose levels. All of these values are in a state of constant flux; however, not only must the values for these items be maintained within narrow limits to be compatible with life, but many o f these items must also be closely regulated with respect to each other. Any situation, of either external or i nternal origin , that threatens homeostasis is considered stressful (8 1 ) . I n a potentially threatening situation , the neuroendocrine-immune system is capable of rapidly modulating homeostatic rhythms i n a coordinated manner, effecting the appropriate changes necessary for promoting the survival of the i ndividual. The Impact of Norepinephrine and Cortisol on the Body rearranges Its Homeostatic Rhythms Into a State Termed "Allostasis "
When threatened, the neuroendocrine-immune network is capa ble of responding with rapid release of an i mpressive list of chem icals that alter the normal homeostatic rhythms: norepinephrine, adrenal cortical steroids, and cytokines. This altered state of body function has been termed allostasis to distinguish it from the nor mal mechanism of homeostasis. Its feedback control is critical to proper function of the allostatic system. As the threat diminishes, the feedback control systems should suppress the levels of allo static compounds, returning the body to its normal function. Disease p rocesses all represent threats to the body and, as such, wil l activate the allostatic response. This has been demonstrated in studies of very ill patients; their body markedly shifts i nto
8. Nociception, the Neuroendocrine Im mune System, and Osteopathic Medicine
excessive production of cortisol in a last eFFort chance at survival (82). [ F the individual survives the d isease, the feedback control systems attempt to return the body to normal homeostasis.
1 51
TABLE 8 . 1 . MARKERS ASSAYED TO DETE R M I N E ALLOSTATIC LOAD Sys tolic b lood pressure Dias tolic b lood pressure Wais t to hip r atio
The AI/ostatic State and Defense: Short-Term Gains,
Total cholesteral-HDL ratio
Long-Term Losses
Total glycos y lated hemoglob in level
Enhanced production of norepi nephri ne, cortisol, and cytokines can create a protective environment for rapid deFense of the body against threat. The short-term gains of this system can be enor mous because they can determ ine the very su rvival of the i ndivid ual. However, recent studies have demonstrated that long-term exposure to this al tered chemical mi lieu is cumulative and ap pears to' be pathologic (3), giving rise to the term "allostatic load" to describe the accumulation of damage i n the system due to prolonged activation of the allostatic mechanism.
U rinary cortis ol level U rinary norepineph rine level U rinary epineph rine level HDL ch oles terol level Dih ydroepiand ros terone
such as adult survivors of child sexual abuse, may also suffer from dysregulation of the arousal-allostatic response system (86,87) . Degenerative and Inflammatory Diseases May Have
Allostati c Load Somatic, Visceral, and Inescapable Emotional Stimuli Are Strong Drives on the AI/ostatic Mechanism
Through the arousal system, most stressors can activate the SNS H PA couple, which results in an allostatic response. Examples i nclude emotional events acting through l i mbic forebrain con nections as well as physical stressors acting via the spinoreticular and spinohypothalamic pathways. Physical stressors can be di vided i nto somatic and visceral origins. Somatic stressors include any Form of trauma or injury including somatic dysFunctions. Visceral stressors range From traumatic injury, i n fection, o r in Aammation of visceral organs to more subtle, diet-related events. Long-Term Activation of the AI/ostatic Mechanism Results in Extensive Wear and Tear on the Organ Systems of the Body
Continual or repeated activation of the SNS- H PA couple creates an abnormal state that is stressFul to the body. In this condition of repeated allostasis, organ systems are literally damaging one another with their activity (3). Evidence suggests that the expo sure to allostatic substances (such as catecholamines and cortisol) is cumulative; that is, the effects of stressors add up progressively. This concept of the summating effects of stress exposure has been termed allostatic load (8 1 ) . Thus, allostatic load represents the price paid for chronic (either contin ual or repeated) exposure to the stress-mediated neuroendocrine adaptations. Another effect of increased exposure to allostatic chemicals is the gradual loss of the effectiveness of Feedback pathways meant to reestablish normal homeostasis (83). Specifically, long-term exposure to al lostatic chemistry has been demonstrated to destroy h ippocampal Formation neurons that contain cortisol receptors and that Func tion in a long-loop feedback pathway to the hypothalamus, which controls the secretion ofcorticotropin-releasing factor (84). Thus, the more the arousal system stimulates release of allostatic sub stances, the worse the body becomes at reestablishing homeosta sis. Animal models are available to demonstrate this phenomena (83,85), but more recent evidence suggests that human situations,
Their Roots in the AI/ostatic Mechanism
McEwen and co-workers devised a method For indexing allo static load (88). In this study, they developed a l ist of markers that could be measured in an aging population. Their markers are l isted in Table 8. 1 . Whether the person was in the h igh-risk category was determined For each parameter. A1lostatic load was the sum of the number of categories in which the person exceeded high-risk level. Thus, each participant in the study received an in dex number indicating his or her allostatic load. The participants were then assessed For cognitive and physical functions and, based on this i n Formation, divided i nto three groups: high-, med ium-, and low-Functioning groups. When functional status was com pared with allostatic load scores, the results were remarkable. The h igher allostatic load score correlated with lower cognitive and physical Functioning scores in a cross-sectional view o f the popula tion. Furthermore, h igher allostatic load baseline scores predicted greater decline in cognitive and physical functions over a seven year period of follow-up (89). These results strongly support the concept that long-term exposure to the allostatic chemical envi ron ment (catecholamines, cortisol, and cytoki nes) is damaging to organ systems. The Consequences of Increasing AI/ostatic Load
Allostasis is the adaptive condition that results From activation of the arousal system of the brainstem . Evidence suggests that long-term exposure to the allostatic response is cumulative and results i n the gradual destruction of organ systems. This section examines specific examples of systems breakdown that can be correlated to i ncreased drive on the allostatic mechanism. AI/ostasis Has Been Correlated to Increased Occurrence of Cardiovascular Disease
Evidence that prolonged activation of the allostatic system is detrimental to the cardiovascular system is extensive. N u mer ous studies demonstrate the effect of psychosocial and men tal stress on i ncreased blood pressure, obesity, enhanced activ ity of the fibrinogenic system , and i ncreased atherosclerosis (3). A recent review (90) h ighlights the devastating eFfects of i ncreased
1 52
II. Osteopathic Considerations in the Basic Sciences
sympathetic tone on the cardiovascular system i ncluding con gestive heart fai l ure, left ventricular hypertrophy, hypertension, and atherosclerosis. I t is i nstructive to look at some possible mechanisms by which these pathologies occur. I ncreased SNS activiry has been correlated with essential hypertension (57). Fac tors contributing to i ncreased SNS activiry i nclude psychosocial stress as well as somatic and visceral nociceptive activiry. Acute and chronic pain from either somatic or visceral origins will in crease the SNS output and i n A uence cardiovascular function. Both acute and chronic somatic sti m u l i can elevate blood pres sure ( 5 5 , 9 J ,92). I ncreased cortisol levels promote insulin resis tance at the tissue level (93). This results in i ncreased production of insu l i n to cou nteract the resistance. Elevated levels of i nsuli n secretion stimulate more S N S activiry (94) and lead to enhance atherosclerosis. I n addi tion, the i nsulin resistance serves to raise the level of plasma glucose, which i ncreases the risk of i n fection and kidney damage (95). AI/ostasis Has Been Related t o Demise o f the Central Nervous System
Memory loss and depression are [wo cardinal manifestations of the effect of allostasis on the nervous system (3). Cortisol uses portions of the b ra i n , such as the h ippocampus, as a feedback mechanism to control the production of corticotropin-releasing hormone from the hypothalamus (96). Long-term exposure to elevated levels ofcortisol has been associated with sign ificant dam age to the h ippocampal formation, ranging from reversible den dritic regression to the excitotoxic death of hi ppocampal neurons (the latter being a permanen t event) (97,98). The h ippocampal formation plays a central role i n the memory process; cell loss from this structure underlies, in part, the notable memory loss reported clinically. AI/ostasis Has Multiple, Complex Effects on the Immune System
The classic response of the immune system to long-term exposure to elevated cortisol and catecholami ne levels is immunosuppres sion (99, J 00). Thus, in patients with chronic hypercorticism, one manifestation is i m m u nosuppression (63 ,64 ) . However, acute ex posure to elevated cortisol levels can enhance certain i m m une system fu nction (3) . One mechanism for i m m unoenhancement following stress would be for a1lostatic chemicals to shift the balance of activiry i n the i m mune system from Th 1 toward Th2 immunocytes by suppressing the Th 1 cells ( 1 0 1 ) . Corticosteroids and sympathetic stim ulation are known to be i n h ibitory to T h l cel l activities and often are stimulatory to Th2 cytokines ( 1 02). Th 1 lym phocytes are known to enhance cell-mediated forms of immuniry, and Th2 lymphocytes are i nvolved i n enhancing an tibody production from plasma cells ( 1 02). If the Th2 pathways are enhanced, more antibody-mediated auto i mm une and allergic rypes of diseases would be expressed ( 1 02 ) .
flow resulted in increased water retention, retention of sodium, hypervolemia, and hypertension ( J 04). Long-term pathologic consequences occur in the kidney secondary to exposure to el evated sympathetic activiry ( l 0 5 ) . In the gastrointestinal sys tem and skin, elevated cortisol and catecholami nes increase the responsiveness of delayed-rype hypersensitivi ry (95, 1 06, 1 07).
SUMMARY: AROUSAL, ALLOSTASIS, AND ALLOSTATIC LOAD Allostasis, the General Compensatory Response and Disease The Healthy Body Has the Capability to Defend Against Disease
[n health, the human body and mind have remarkable abili ties to resist d isease. These capabi l ities can be inAuenced by genetic background as well as environmental history.
The Concept of AI/ostasis Represents an Aspect of the General Compensatory Response
Allostasis is the body's attempt to compensate for a stressful sit uation in a protective way, whether the stress is physical or psy chosocial in nature. Both forms of stressors activate the arousal system of the brainstem, leading to SNS and H PA responses, and the elevation of plasma catecholamines and cortisol ( F ig. 8.9). I n this manner, the SNS a n d H PA couple acts a s the last common pathway through whi ch multiple forms of a stressor may i ni ti ate the appropriate compensatory responses. The convergence of multiple, different pathways on a common mechanism also fa cilitate summation of differing drives to obtain a more i n tense response. Thus, somatic or visceral dysfunction can exacerbate the response of the arousal system in a person with an emotional dysfunction.
Physical Stress Somatic
---
Visceral
The Arousal System
NeuroEndocrineI mmune Axis Psychosocial Stress Emotional
•
Norepinephrine Cortisol Cytokines
AI/astatic Shifts Have a n Impact o n Numerous Other Systems
SNS activiry plays a major role i n the regulation of the kid ney ( 1 03). Stressful si tuations that activated the sympathetic out-
A l J ostasis FIGURE 8.9. A diag r am illustrating the al los tas is- ar ous al s ys tem and its impact on the homeos tatic mechanis m of the body.
8. Nociception, the Neuroendocrine Im m une System, and Osteopathic Medicine
In the Compensated State, There Is Less Room for Further Adaptation
In this compensated state, the body is less capable offurther adap tation to an i ncreased stress or a new stressor. This is true whether the compensation is in the form ofstructural or metabolic change, or more typically, both.
1 53
one drive on the arousal system . Others i nclude visceral dysfunc tions (stressors) signali ng through ascending spinal cord tracts and both somatic and visceral dysfunctions using cytokines traveling through h u moral routes to reach the hypothalamus and arousal system . Finally, descending connections from l i m bic forebrai n structures such as the p refron tal cortex and amygdala provide a strong drive for emotional dysfunction (stress) on the arousal system .
Long-term Existence in the Compensated State Can Be Destructive
Long-term exposure to elevated levels of SNS-H PA output forces organ systems in the body to function abnormally and, l i terally, grind each other down (3) . Neurons and endocrine cells operated in an excited state are susceptible to excitotoxic cell death; im mune cells maintai ned in an excited state can be more responsive, attacking the wrong tissues, stimulating surrounding cells to pro liferate creating plaques in i nappropriate locations, or becoming repressed and improperly defending the body. Many inflammatory, neoplastic, and degenerative processes that we accept as common occurrences of aging may, in fact, be the result of a compensated individual, unable to adequately stave off disease.
REEXAMINATION OF THE OSTEOPATHIC
The Arousal System o f the Brain Stem i s Coupled to the AI/ostatic Response
The arousal system is coupled to two major efferent pathways: the SNS and the hypothalamic-pituitary-adrenal axis ( H PA) . In creased drive on the arousal system leads to the release of cat echolamines from the SNS and adrenal cortical steroids from the H PA. Norepinephrine and cortisol modifY the production of n umerous cytokines from the i m mune system. All three sys tems (neural, endocrine, and immune) function together in a network to alter homeostatic p rocesses i n to a protective state termed allostasis. The defensive compensation created by the allostatic response can be very beneficial to escape behavior and wound repair as well as the prevention or containment of i nfection .
Feedback Pathways Restore Homeostasis via
PHILOSOPHY OF MEDICINE
Adequate Function of the Neural and
Events in Peripheral Tissue and at the Spinal
Circulatory Systems of the Body
Cord Level Suggest an Understanding
The allostatic response occurs in the face of a stressor. As the stressor abates, feedback pathways-both neural and h u moral function to restore natural homeostatic balance. Failure of the neural or h u moral routes or excessive exposure to the allostatic chemistry can result in i nappropriate feedback and failure to re turn to baseline homeostatic values; thus, the body exists in a chronic compensatory state.
of Somatic Dysfunction
This chapter began by exami n i ng the pathophysiology of a so matic dysfunction (edema and i nflammation) and demonstrated that there are two routes by which this event can signal the spinal cord. The neural route is by far the best known; however, recent studies suggest that the mediators of in flammation can also reach the central nervous system through humoral routes. In the spinal cord, neural and humoral signals combine to produce short-term changes in dorsal horn neuronal activity. In situations of exces sive or repeated inj ury, long-term (and in some cases, permanent) changes in spinal cord neural circuitry can occur, thus underlying various pai n states. Altered segmental activity in the spinal cord leads to somatic responses that manifest as altered ease or range of motion in skeletal muscles and anatomical asymmetries in joint position. I n addition, spinal cord sympathetic outflow can also change, thus accounting for cl inically well-known somatovisceral reflexes.
Failure to Restore Homeostasis Exposes the Body to Increased Risk of Disease
Long-term exposure to the allostatic response forces organ sys tems to work with each other i n u n natural or compensated states. I n this condition, the organ systems literally grind each other down (3) . Epidemiologic research has related this compensated situation to the chronic and i nsidiously progressive development of numerous degenerative and i nflammatory d iseases.
The Osteopathic Approach to the Patient Is Focused Somatic Dysfunction Triggers the Arousal System of the Brainstem
The arousal system is composed of a complex neural circuitry ex pending from the medulla, pons, and midbrain. Its connections descend i n to the spinal cord to modulate spinal circuitry and as cend into the forebrain to trigger behavioral states. It is responsive to any kind of unexpected or unwanted stressor. Somatic dysfunc tion (stress) that works through ascending spinal cord tracts is but
on Relieving the Drives on the AI/ostatic Mechanism
The osteopathic approach to the patient helps that person find his way back to baseline homeostatic condition. In this chapter, two major drives on the arousal-allostatic response have emerged: physical and psychosocial. Both are very capable of signi ficantly altering baseline homeostasis. In the physical category, we find somatic dysfunction and visceral dysfunction; i n the psychosocial category, we find emotional and cognitive sources. The i m portant
1 54
ll. Osteopathic Considerations in the Basic Sciences
concept is that these drives, working through the common path way of the arousal-a1lostatic system, appear to summate with each other to augment the a1lostatic impact on normal home ostasis. Thus, regaining health for the i ndividual is dependent on reestabl ish i ng baseline homeostatic values by m itigating the drives on the arousal-allostatic system. In one sense, these drives represent the handles available for modulating the activity of the arousal-allostatic system. To best address the status of these han dles, the osteopathic physician needs to consider the i ndividual, not only i n terms of their specific com plaints but also i n terms of the general status of thei r body (soma) and visceral functions, as well as their i n tegration with their surroundi ng fam ily, social, and work environments. The treatment plan is then based on a rational approach to normalizing these processes. The ability of the osteopathic physician (by virtue of h is or her train ing) to assess the patient's somatic and visceral status as well as the spe cific complai nt underscores the unique osteopathic approach to medicine.
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TISSUE RESPIRATION AND CIRCULATION HARVEY V. SPARKS, JR.
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Cells need a relatively constant and favorable environment to produce the energy needed for normal function. The circulatory system provides cells with a lifeline to the outside world, bringing the required nutrients and taking away the waste products of metabolism. ATP is the direct source of energy for most chemical reactions in cells. Creatine phosphate is a quick source oflimited amounts of ATP. Glycolysis is a source of limited amounts of ATP and does not require oxygen. Most ATP is formed as the result of oxidative phosphorylation, involving the conversion of oxygen, substrate, ADP and inorganic phosphate (Pi) to produce CO2, H20, and ATP. ADP and Pi stimulate oxidative phosphorylation, but under many conditions the main stimuli are probably NADH and calcium ion. Cellular oxygen demand is the net stimulus for oxidative phosphorylation. As we understand it p resently, this is a function of cytosolic concentrations of ADp, Pi, and calcium ion as well as NADH delivery to the mitochondrial respiratory chain. Supply of blood containing oxygen and substrates is locally regulated by three mechanisms: metabolic, myogenic, and paracrUle. Metabolic regulation i nvolves the cellular release of metabolites tllat cause vasodilatation. This release is stimulated when oxygen supply falls below oxygen demand. Myogenic regulation i nvolves a change in the stretch of microvessels by a change in blood pressure. Increased blood p ressure causes constriction and decreased blood p ressure causes dilatation. Paracrine regulation involves the release of a number of chemical mediators fro m nearby cells. These mediators cause vasodilatation or vasoconstriction. There are four elements of local control of blood flow: active hyperemia, reactive hyperemia, autoregulation, and the response to injury.
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Active hyperemia is the increase in blood flow associated with i ncreased metabolic activity and is caused by metabolic and paracrine regulation. Reactive hyperemia is the i ncrease in blood flow that follows a period of restricted blood flow and is caused by metabolic, myogenic, and paracrine regulation. Autoregulation ofblood flow refers to the tendency ofblood flow to rema i n constant despite variation in arterial p ressure and is caused by metabolic and myogenic regulation. The vascular response to injury is the changes in resistance to blood flow as well as capillary permeability to plasma protein that follows a variety of i nsults, including mechanical, thermal, and allergic injuries. It is caused by paracrine regulation. Coronary blood flow is determined by the interactions of five factors: diastolic arterial p ressure, myocardial compression, active hyperemia, endothelial function, and sympathetic nerve tone. Because intramural vessels are compressed during cardiac contraction, perfusion of the myocardium is u niquely dependent on diastolic arterial p ressure. Active hyperemia is the main determinant of coronary blood flow. Coronary reserve refers to the ability of coronary arterioles to dilate in response to a m ismatch between oxygen supply and demand. As atherosclerosis i mpedes flow through major distributi ng coronary arteries, coronary reserve is used to maintain normal resti n g coronary blood flow, reducing the remaining reserve that may be required under conditions of increased demand. Myocardial stu n ning is a reversible reduction in myocardial contractility that fol lows one or more periods of reduced oxygen supply relative to demand. Myocardial h ibernation is a chronic depression in myocardial contractility following repeated bouts of myocardial stunning, or after a sustai ned period of suboptimal blood Row. When coronary blood Row increases, larger coronary a rteries participate because of Row-induced vasodilatation.
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This is caused by shear forces on endothelial cells that release n i tric oxide. Although the direct effect of stimulation of sympathetic nerves to the heart is coronary constriction, this is overwhelmed by the active hyperemia resulting fro m the increased metabolism of cardiac muscle. Skin blood flow is influenced both by local and core body temperature. The cutaneous response to injury includes a red line, a flare, and a wheal. The red .line is caused by release of paracrines. The flare is caused by a local axon reflex, involving the release of substance P and calcitonin gene-related peptide. The wheal is local edema resulting a combination of increased transport of plasma proteins into the interst itial space and is caused by substance P, histamine and bradykinin, and increased capillary hydrostatic pressure accompanying arteriolar vasodilatation.
A major role of the physician is to encourage the normal physi ologic processes responsible for maintenance of a favorable envi ronment for each cell of the body, and when necessary, to fight pathologic events that disrupt this environment ( 1 ) . Each cell m ust meet i ts needs for energy by producing adenosine triphos phate (ATP) in sufficient quanti ties. In most cells, this is primarily done by oxidative phosphorylation. Oxidative phosphorylation requires a cellular environment that provides a steady supply of oxygen and substrate and a route for the d isposal of the byprod ucts of cellular respiration, CO2 and H20. Circulation of the blood plays a key role in maintaining the internal environment of cells. The circulation is the cell's connection to the outside world, bringing oxygen and substrates and removing the waste products of metabolism. This chapter d iscusses the regulation of cellular respiration and the local mechanisms that regulate circu lation to maintain the internal environ ment.
REGULATION OF TISSUE RESPIRATION ATP is the common intermediate that provides chem ical energy for cellular function. Motility, pumping of ions, and metabolic pathways all use ATP as a source of energy ( 1 ). The cell makes use of ATP by enzymatically transforming ATP to adenosine 5'-di phosphate (ADP) and in the process capturing the chemical energy released. A cell needs a supply of ATP calibrated to meet its needs at a given time. In some cells, such as muscle fibers, energy requirements may vary greatly in just a few seconds, as the cells go from resting to high activity (2). When ATP is rapidly broken down, it must be resynthesized from ADP in a timely fashion . I n many cells, including skeletal and cardiac muscle, phos phocreatine provides a quick source of ATP by the following reaction (3): ADP + PCr
+---+
ATP + Cr
The equilibrium constant for this reaction favors the forma tion ofATp, so that PCr falls to approximately 10% of i ts maximal value before a physiologically significant decrease in ATP occurs. Although phosphocreatine is a rapid means for replenishing ATp, the amount of ATP available via this pathway is limited. Cells m ust turn to other pathways for a more sustained supply of ATP. Glycolysis, the breakdown of glucose to pyruvate is a rapid source of ATp, although nor as quick as the phosphocreatine reaction. Glycolysis captures only a small fraction of the energy available in the glucose molecule for the formation of ATP, but it does this quickly and without requiring oxygen. In a few cell types, including red blood cells, glycolysis is the source of ATP. However, in most cells, glycolysis serves to provide ATP for a few seconds before oxidative phosphorylation begins to meet the steady-state requirements for ATP. When short bursts of energy are needed, or when the supply of oxygen is limited, glycolys is is a significant source of ATP (4). Under most circumstances, in most cells, oxidative phospho rylation is the mainstay for the synthesis of ATP from ADP. Ox idative phosphorylation is capable of supplying ATP for a wide range of cellular energy requirements. As the rate of oxidative phosphorylation increases, the circulation must deliver an in creasing supply of oxygen and substrates. Later, we will consider how this delivery is regulated. For the moment, let us assume that oxygen and substrate are available. If that is the case, ATP supply from oxidative metabolism exactly matches ATP use. The regulation of oxidative metabolism is our next topic. The cellular controls that match ATP supply to ATP use are not fully understood, but recent studies involving the use of in vivonuclear magnetic i maging have provided i mportant cl ues. We will use the muscle cells of the heart as our example in dis cussing regulation of oxidative metabolism. This is a good choice because cardiac muscle cells exhibit a wide range ofrates of oxida tive phosphorylation. In addition, energy supply to cardiac cells is vital to survival and is the main issue in coronary artery disease, a major cause of morbidity and mortality in Western societies (2). Later we will return to a discussion of coronary blood flow to complete our consideration of energy supply of the myocardium. The m itochondrion is the intracellular site of the events that make use of oxygen, substrate, ADp, and inorganic phosphate (Pi) to produce CO2, H20, and ATP. Isolated mitochondria are stimulated to produce ATP by increased concentrations of ADP and Pi. One view is that this pertains directly to the regulation of m itochondria inside cells ( 5 ) . According to this view, as ATP is used, cytosolic ADP and Pi concentrations rise. The mito chondria, bathed in the cytosol, respond to the increased ADP and Pi by producing more ATP. However, recent observations of m i tochondrial function in intact heart and brain as well as other tissues demonstrate that there can be large changes in ATP synthesis by mirochondria without significant changes in the cy tosolic concentrations of ADP and Pi. This raises the question of what regulates oxidative phosphorylation in the absence of changes in ADP and Pi. At least two factors stimulate ATP synthesis independent of a change in ADP or Pi. First, nicotinamide adenine dinucleotide (NADH) is formed at a nu mber of steps in the metabolism of substrates, most i mportantly in the citric acid cycle, and it is a thermodynamic driving force increasing the rate of oxidative phosphorylation (6). Second, an increase in cytosolic calcium
9. Tissue Respiration and CircuLation
ion concemration stimulates mitochondrial ATP synthesis (7). It appears that increased cytosolic calcium ion concentration raises the effectiveness ofNADH in driving oxidative phosphorylation. This observation raises the possibility that in the presence of increased calcium concentration, minimal changes in ADp, Pi, and NADH may be adequate to drive oxidative phosphorylation. This view is compatible with the available information fro m the study of oxidative phosphorylation in intact hearrs. The view that calcium ions are i ntegral to the normal regula tion of oxidative phosphorylation putS this ion in a central role in both the synthesis and the use of ATP. For example, in cardiac muscle, increased cytosolic calcium ion concentration unleashes actomyosin cross bridge cycl i ng and contraction. This event dra matically increases the hydrolysis of ATP. At the same time, the increase in cytosolic calcium ion concentration stimulates oxida tive phosphorylation. In this scenario, a rise in ADP and Pi is not requ ired for an increased rate of ATP synthesis. Instead, the same stimulus, cytosolic calcium ion concentration, is responsible for increasing ATP hydrolysis and also increasi ng ATP symhesis (7). This discussion of the regulation of m i tochondrial ATP syn thesis brings us to the defi nition of oxygen demand. Oxygen demand is the net stimulus for oxidative phosphorylation. As we presently understand, it is dependent on the cytosolic concentra tions of ADp, Pi, and calcium ion as well as NADH del ivery to the m itochondrial respi ratory chain. The next section discusses the factors that inRuence the supply of oxygen by circulation. Mainrenance of the balance of supply and demand for oxygen is necessary if cells are to cont inuously carry our their functions.
REGULATION OF TISSUE CIRCULATION Blood Row in tissue is determi ned by the pressure difference be tween the arterial and venous sides of its circulation and the resis tance to Row offered by its own vasculature. The heart generates the pressure difference across a tissue. Elaborate control mecha nisms adjust cardiac output and systemic vascular resistance to mainrain adequate arterial pressure. G iven an adequate p ressure head, tissue blood Row is regulated by local mechanisms that allow precise regional adjustment of blood Row. The systemic control of arterial pressure and the regulation of the arterial par tial pressure of O2 and CO2 by the lungs is beyond the scope of this chapter. In the fol lowing discussion, we will assume that arterial pressure and arterial blood gas composition is normal, unless otherwise speci fied. We will focus our attention on the local regulation of blood Row. Blood vessels in systemic circulation can be categorized ac cording to thei r function. The aorta and large arteries distribute blood to organs and tissues with a very small drop in pressure. Smaller arteries and arterioles are the main site of resistance to blood Row. Capil laries and small venules are the locus of exchange of substances between tissues and blood. Larger venules and veins hold the largest share of blood volume and therefore are said to have a capaci tance fu nction. These terms will be used below. After discussion of the general mechan isms governing the lo cal regulation of blood Row, two contrasting vascular beds will be considered in some detail. Regulation of coronary blood Row is dom inated by the requiremem to balance oxygen supply and demand. We will use this vascular bed as our example of local
159
regulation of Row in a tissue that undergoes large changes in respi ration. Regulation of skin blood Row provides us with a contrast to coronary blood Row. Under most ci rcumstances, skin receives sufficient blood Row to meet its metabolic needs. However, skin is the site of heat loss to the external environment. Blood Row to skin plays a major role i n the extent of this loss, and its control reRects this fact. In addition, skin is juxtaposed to the external environment and is frequently injured. We will also d iscuss the changes in skin blood Row in response to injury.
GENERAL MECHANISMS GOVERNING LOCAL REGULATION OF BLOOD FLOW Local regulation of blood Row occurs by means of three basic regulatory mechanisms: metabolic, myogenic, and paracrine. The control of blood Row in any one tissue can be understood as a particular application of these three mechanisms. A discussion of these mechanisms will serve as a background for the description of blood Row in particular tissues. Metabolic regulation refers to changes in blood Row that oc cur in response to alterations in the ratio of blood Row to the metabolic requirements of tissues (8). It is med iated by vasodila tor metabolites, i ncluding adenosine, potassium ions, CO2, and hydrogen ions released from parenchymal cells. These vasodila tors relax the smooth muscle of nearby arterioles. The resulting vasodi latation results in reduced resistance to Row and, in the presence of a constant arterial pressure, increased blood Row. In creased blood Row suppl ies more O2 and other nutrients. The sti mulus for release of vasodi l ator metabol ites can be either in creased metabolic activity of parenchymal cells or decreased P02 resul ting from reduced O2 supply relative to the use of oxygen. Tissue P02 decreases with increased use of O2 relative to supply and under conditions when arteriolar wall P02 decreases, which contributes to vasod ilatation. In general, if arterial P02 is normal, P02 of the arteriolar wall is normal . This is because O2 diffuses readily from blood i n to the arteriolar wall. The relative impor tance of the various metabolic vasodilator mechanisms depends on the parenchymal cel l in question, the m ix of tissue activi ty, and blood supply. A feedback loop describing metabol i c regulation is shown in F igure 9.1. In this feedback loop, a decrease in arterial pres sure reduces blood Row and the delivery of oxygen. The mis match between O2 supply and use lowers tissue P02. Lowered tissue P02 l i m i ts the formation of ATP and results in the release of vasodilator metabolites: adenosine, for example. Vasodi l ator metabol i tes raise Row toward normal. Al ternatively, increased tissue metabolism leads to increased O2 use and lowers tissue P02. Lowered P02 l i m its formation of ATP from ADP and in creases the same vasodilator metabolites. Increased blood Row re stores tissue P02. In Figure 9. 1, tissue P02 is used as the error sig nal in the negative feed back loop. However, some metabolites are not ordinarily released in response to lowered tissue P02. A good example is K+, which is released with each action potential of the tissue. It acts as a feed-forward mechanism, initiating vasodilata tion before the action potentials that release it have time to trigger the cellular events that will ultimately result in i ncreased O2 use. Myogenic regulation refers to changes in the tone of resistance vessels in response to alterations in their transmural pressure. It
11. Osteopathic Considerations in the Basic Sciences
160
I
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I j I Blood Flow
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I
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. . Flow
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FIGURE 9.1. Metabolic regulation of blood flow. Either reduced arte rial pressure or increased tissue metabolism reduces tissue P02. This leads to release of vasodilator metabolites, relaxation of arteriolar smooth muscle, and decreased vascular resistance. In the case of de creased arterial pressure, blood flow returns toward the original value (autoregulation). In the case of increased metabolism, blood flow in creases (active hyperemia). Metabolic regulation of blood flow also plays a role in reactive hyperemia.
occurs when a change i n transmural pressure results i n i ncreased or decreased stretch of the vascular smooth m uscle of resistance vessels ( Fig. 9.2). Increased stretch results i n contraction of vas cular smooth muscle. The myogenic response counteracts the influence of increased or decreased transmural pressure o n resis tance vessel diameter. For example, when we stand up, transmura l pressure increases dramatically in t h e resistance vessels of the legs and feet. These resistance vessels are stretched and their response is to constrict. This response has at least two beneficial effects. First, it prevents the dilatation that would otherwise occur as a re sult of the i ncreased transmural pressure. Second, constriction of the resistance vessels lessens the hydrostatic pressure transmined to the capillaries of the legs and feet as a result of standing. The error signal for myogenic regulation is stretch of vas cular smooth muscle cells within the wall of resistance vessels (9). Stretch of vascular smooth m uscle causes opening of stretch-
i[
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i Arteriolar
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i
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FIGURE 9.3. Paracrine regulation of blood flow results from media tors released from blood elements and endothelial cells. Platelets re lease thromboxane A2, thrombin, and serotonin that, in the absence of intact endothelium, cause contraction of the underlying vascular smooth muscle. Thrombin, serotonin, and ADP cause release of nitric ox ide and/or prostacyclin from endothelial cells, which results in vascular smooth muscle relaxation. Thus, activated platelets cause vasoconstric tion only in the presence of locally disrupted endothelium. Histamine released from mast cells also causes vasodilatation via endothelial cells. Two elements of local control that are not paracrine are flow-induced vasodilatation and vasodilators released from collaterals of axons me diating nociception.
activated cation channels that carry Ca++ and initiate contraction ( 1 0) . Stretch also activates signaling pathways involving phospho lipase C and protein kinase C ( 1 1 ) . Paracrine regulation refers r o the local release o f chemical me diators that cause vasodilatation or vasoconstriction. Only a small fraction of these m ediators will be mentioned. Many paracrines have effects on smooth muscle growth andlor apoptosis (in addi tion to their effects on tone), but only effects on tone will be con sidered here. E ndothelial cells and platelets release mediators that i nfluence vascular smooth muscle tone ( 1 2) . [n a n umber of cases, endothelial cells modifY the effects of substances released from platelets. Seroronin , ADP, and thrombin released from platelets cause vascular smooth muscle relaxation in the presence of en dothelium. Bur these agents act directly on vascular smooth mus cle to cause contraction. Perhaps the most significant interaction is between thromboxane A2 (TxA2) and prostacyclin ( PGI2)· Platelets release TxA2 , a vasoconstrictor, and this effect predom i nates when the endothelial layer of the blood vessel is damaged. However, normal endothelium releases PGI2, a vasodilator, and it has the dominant effect in normal blood vessels ( 1 3) . Figure 9.3 shows two other phenomena that are not strictly paracrine, but are of significance. Flow-induced dilation (14) plays an important role in producing high flows in the heart dur ing metabolic hyperemia. The axon reflex is also shown in this fig ure and will be described in the discussion of skin blood flow ( 1 5) .
arteriolar smooth muscle
FIGURE 9.2. Myogenic regulation of blood flow results from a change in arteriolar tone in response to a change in stretch of arteriolar smooth muscle. Increased transmural pressure, (ordinarily the effect of increased arterial pressure) stretches the vascular wall, which causes contraction of arteriolar smooth muscle, arteriolar constriction, and a decrease in blood flow. Myogenic regulation plays a role in autoregu lation of blood flow and reactive hyperemia.
ELEMEN TS OF LOCAL CON TROL OF BLOOD FLOW The three mechanisms described above underlie in varying de grees fou r elements of local control of blood flow: active hyper emia (metabolic and paracrine regulation), reactive hyperemia ( metabolic, myogenic, and paracrine regulation), auroregulation
9. Tissue Respiration and Circulation
(metabolic and myogenic regulation) , and the vascular response to injury (paracrine regulation) . Active hyperemia occurs when tissue metabolism is increased. This leads to release of vasodilator metabolites in proporrion to the level of activity of the tissue. Paracrines such as prostaglandins are also released during increased metabolic activity, and as metabolic activity increases, so does tissue blood flow. In many tissues, including cardiac muscle, skeletal muscle, brain, and gut , there is a linear relationship berween oxygen consumption and blood flow. In this way, oxygen supply, oxygen demand, and oxygen consumption are matched. The precise mix of metabo lites and paracrines depends on the conditions of the increased metabolism, how well oxygen supply meets oxygen demand, and the tissue type. Reactive hyperemia occurs when blood flow is stopped due to occlusion of the artery supplying the region. The occlusion can be caused by compression of the artery by external pressure or by thrombus formation in the lumen. In the case of reactive hyperemia, the time period of the occlusion is short enough so that, although there may be metabolic adjustments in the tissue in response to a lack of oxygen, there is no sustained cell inj ury or death. When the occlusion is removed, flow increases well above the level observed before the occlusion. It then returns to baseline with a time course dependent on the duration of the occlusion : the longer the occlusion, the longer the duration o f the reactive hyperemia. The local vasodilatation responsible for reactive hy peremia is caused by three mechanisms: metabolic, paracrine, and myogenic regulation. When flow to the affected region i s stopped and tissue P02 drops, vasodilator metabolites and paracrines are released. They accumulate in the tissue because there is no blood flow to wash them out. In time, they completely dilate the resis tance vessels. The occlusion of the arrery supplying a region of tissue lowers transmural pressure in the resistance vessels beyond the occlusion. This reduces stretch of the vascular smooth muscle and results in its relaxation. In general, the myogenic response dominates in occlusions of shorr duration when there is little time for the build-up of metabolites and paracrines. In longer occlu sions, the paracrine and metabolic responses gain in importance. Autoregulation of blood flow refers to the ability of tissues to maintain flow within a narrow range despite changes in ar terial pressure. Most tissues including brain, heart, kidney, skin, and gut display autoregulation. Autoregulation depends on rwo mechanisms: metabolic and myogenic regulation. The reduction in flow. accompanying a decrease in perfusion pressure allows the build-up of locally released metabolic vasodilators. These vasodilators decrease vascular resistance and restore flow. The converse happens when perfusion pressure is elevated. A fall in perfusion pressure also reduces transmural pressure i n resistance vessels. The myogenic response leads to a reduction in vascular smooth muscle tone and a decrease in resistance to blood Row. Thus, both mechanisms tend to restore flow to its original level despite the reduction in perfusion pressure. The vascular response to inj ury refers to the constellation of vascular changes after local tissue inj ury. In general, paracrines such as histamine, bradykinin, and prostanoids are released and cause dilatation of resistance and capacitance vessels as well as increased leakiness of exchange vessels to plasma proteins. The cutaneous circulation provides the prototypical vascular response to injury and this subject will be expanded in that context.
161
REGULATION OF BLOOD FLOW IN THE MYOCARDIUM Coronary blood flow ( 1 6) is determined by the interactions of five factors: diastolic arterial pressure, myocardial compression, active hyperemia, endothelial function, and sympathetic nerve tone. Because intramural vessels are compressed during cardiac con traction, perfusion of the myocardium is uniquely dependent on diastolic arterial pressure (17). The larger distributing coronary arteries run over the epicardial surface of the heart. Transmu ral branches penetrate the myocardium and deliver blood flow throughout the thickness of the wall. It is the transmural ves sels and their branches within the myocardium that are subject to the compressive forces of each cardiac contraction. During systole, blood flow ceases in the myocardium near the suben docardium because myocardial compression completely closes the vessels supplying this region. Vessels supplying myocardium near the subepicardiu m are not occluded by cardiac contraction; therefore, this region has steady blood flow across the entire car diac cycle. However, on the average, over the complete cardiac cycle, myocardial blood flow is as high or higher in the subendo cardium. This is because very high flow during diastole balances the lack of flow during systole. The high flow during diastole can be viewed as reactive hyperemia in response to the cessation of flow with each systole. With stenosis of the distributing arteries on the surface of the heart (as occurs in coronary atherosclero sis), subendocardial flow is more threatened than subepicardial flow because more coronary reserve is used to provide adequate perfusion under normal conditions (see below) . Coronary flow stops at a diastolic arterial pressure well above zero. This is primarily because of the "waterfall" phenomenon (17). Coronary veins of the left ventricle are usually compressed by the relatively high tissue pressure that results from the ven tricular cavity pressure present, even during diastole. Pressure upstream from the point of compression builds up until the vessels are forced open and flow proceeds to the coronary si nus. This is of consequence because the pressure head for an organ is the upstream (ordinarily mean arterial) pressure minus the downstream (ordinarily venous) pressure. We have al ready seen that in the case of the coronary bed, the upstream pressure is diastolic arterial pressure. The down stream pressure is j ust above tissue pressure, the pressure required to keep tissue pressure from collapsing coronary veins. Tissue pressure is close to diastolic ventricular cavity pressure. This n umber is ordinarily low com pared with diastolic arterial pressure, and its effect can be ignored. However, in the p resence of elevated diastolic pressure (as occurs with decreased diastolic ventricular compliance), the downstream pressure can become a significant factor in l i miting coronary flow. This occurs, for example, with myocardial hypertrophy. Active hyperemia (8, 1 6) is the main determinant of coronary blood flow. Because three-fourths of arterial O2 is extracted by the myocardiu m under resting conditions, significant i ncreases in the requirement for O2 must be served by higher blood flow. Physio logic increases in myocardial metabolism are almost always the re sult of increased sympathetic nerve activity to the heart. Depend ing on the circumstances, part of the i ncrease in coronary blood flow may be provided by i ncreased arterial (primarily diastolic) pressure. However, coronary arteriolar vasodilatation resulting
11. Osteopathic Considerations in the Basic Sciences
162
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FIGURE 9.4. Coronary reserve refers to the ability of vessels down stream from a stenosis to dilate. It is manifested in the autoregulatory range by reactive hyperemia andlor increased flow in response to a va sodilator. Below the autoregulatory range, vessels downstream from a stenosis are completely dilated and so a vasodilator stimulus such as reactive hyperemia or a drug does not increase flow. Within the au toregulatory range, the magnitude of coronary reserve depends on how much downstream dilatation is necessary to compensate for an upstream stenosis; that is, more coronary reserve is found when the pressure distal to the stenosis is 100 mm Hg than when it is 75 mm Hg.
from release of vasoactive metabolites is usually required to pro vide adequate supply of O2. In general, there is a linear relation ship between coronary blood Row and myocardial metabolism. Flow-induced dilatation (see below) of epicardial-distributing ar teries is necessary to maintain the full pressure gradient across the wall of the heart. The concept of coronary reserve in the face of coronary artery stenosis is closely tied to active hyperemia and autoregulation ( 18). Stenosis of coronary arteries occurs in individuals with coronary atherosclerosis. Until a stenosis becomes quite severe, it has little or no effect on resting coronary blood Row. This is due to autoregulation of blood Row. Figure 9.4 shows coronary Row as a fu nction of coronary perfusion pressure downstream from stenosis of a major epicardial coronary artery. The region of the curve where changes in pressure are accom panied by small changes in Row is the result of autoregulation. If the coronary cir culation is within the autoregulatory range, reactive hyperemia can be elicited by brieRy stopping Row. Furthermore, i n fusion of a vasodilator such as adenosine causes increased Row. Both of these responses require that the resistance vessels downstream from the stenosis are capable of dilating. The resistance vessels can respond to an added vasodilator stimulus to the extent that they are not maximally dilated to maintain resting Row in the face of an upstream stenosis. The remaining ability for resistance vessels to dilate in the face of an upstream stenosis is called coro nary reserve. The magnitude of the increase in Row observed with reactive hyperemia or drug infusion gives an estimate of the coro nary reserve. If pressure distal to a stenosis falls below the autoregulatory range ( Fig. 9.4), Row decreases in proportion to the drop i n pressure. This i s because the abiliry o f the resistance vessels to
dilate (coronary reserve) has been com pletely exhausted. At this point, reactive hyperemia and increased Row in response to a vasodilator do not occur. There is a third method for estimating coronary reserve. It can be observed by measuri ng the pressure drop across the stenosis during infusion of a vasodilator ( 18). This method relies on the assumption that the resistance across the stenosis does not change. In this situation, if increased Row occur s because of downstream resistance vessel dilatation, the pressure drop across the stenosis increases. If no change in the pressure drop across the stenosis is observed, the conclusion is that no increase in Row was possible and that coronary reserve is exhausted. The issue of reduced Row caused by coronary stenosis is made more complex by the fact that if coronary Row is reduced, the my ocardium quickly adjusts to this new situation . During a period of reduced Row that results in a reduced oxygen supply relative to myocardial demand, a rapid decrease in myocardial contractiliry is found in the region served by the reduced Row. After one or more periods of reduced oxygen supply relative to demand, myocar dial con tractiliry may be reduced for minutes to hours, despite a return to normal resting coronary blood Row. This is called my ocardial stu n ning ( 19). The reduction (s) in the supply/demand ratio that causes myocardial stu n ning may be the result of either periods of reduced coronary blood Row or increased myocardial oxygen consumption . The cause of myocardial st unning appears to involve the liberation of oxygen free radicals and a decrease in the sensitiviry of the contractile machinery to calcium ions (20). After repeated bouts of myocardial stun ning or after a sus tained period of suboptimal blood Row, a chronic depression in myocardial contractility may ensue. This is called hibernation ( 19,2 1,22), and it is not the result of infarction of myocardium. At first, duringfonctionaL hibernation, the causes may be similar to those of stu n ning. Hibernation of a more severe and/or longer nature is referred to as structuraL hibernation and involves rarefac tion of contractile proteins, reduced mitochondria, and other later changes, i ncluding apoptosis. If notmal Row is restored by coronary artery bypass or angioplasry, hibernating myocardium can retur n to normal function (23). The myocardium is protected from stunning, hibernation, and infarction by previous short bouts of ischemia. This is called ischemic preconditioning (24 ) . Ischemic preconditioning occurs in many organs, including brai n , lung, liver, and skeletal muscle. Although there appear to be multiple mechanisms responsible for preconditioning, adenosine seems to play a central role. Coronary endothelial cells are im portant in the regulation of coronary blood Row. The full development of active hyperemia is dependent on normal endothelial cell function . The primary event causing increased coronary blood Row during active hyper emia is dilatation of arterioles by local metabolites and patacrines. However, if the epicardial-distributing arteries do not participate in this dilatation, there is an increased pressure drop along their length. This means that the pressure available to drive blood Row across the wall through transmural coronary arteries is de creased and happens when endothelial communication with vas cular smooth muscle is curtailed by atherosclerosis, hypertension, and other conditions. If the coronary endothelium is normal, in creased Row velociry in distributing arteries causes release of ni tric oxide from endothelial cells. Nitric oxide diffuses to vascular
9. Tissue Respiration and Circulation
smooth muscle where it causes relaxation by elevating smooth muscle cyclic guanylic acid ( G MP). The resulting increase in di ameter of distributing arteries is sufficient to minimize the drop in pressure that would otherwise accompany the i ncreased flow associated with active hyperemia (25). Coronary endothelium also plays an i mportant role in protect i ng vascular smooth muscle fro m the constrictor effects of a num ber of agonists in the blood. These i nclude platelet-derived sero tonin and thrombin ( 1 2,26). Coronary artery spasm is thought to occur in the absence of the normal vasodilator influences of nitric oxide, prostacyclin, and perhaps other substances that are released from normal endothelium. Stimulation of the sympathetic nerves to the heart has two competing effects. Norepinephrine released from sympa thetic nerves acts on a I -adrenergic receptors to cause i ncreased heart rate and contractility; these effects i ncrease myocardial metabolism and result in active hyperemia. Norepinephrine also acts on f3 I -adrenergic receptors to cause contraction of coronary smooth muscle. The net effect of these opposing effects of sympa thetic nerve stimulation is to raise coronary blood flow in propor tion to the increase in myocardial oxygen consumption. Coronary blood flow increases almost as m uch as it does in the absence of the a I -adrenergic-mediated coronary constrictive effect ( 1 6).
REGULATION OF SKIN BLOOD FLOW Skin has a low metabolic rate; therefore, its nutrient require ments are ordinarily met unless severe pathologic reductions i n blood flow occur. For the most part, changes in skin blood flow are unrelated to changes in local metabol ism. Skin blood vessels demonstrate impressive reactive hyperemia. This is evidenced by the erythema and i ncrease in surface temperature that is com monly seen after a period of external compression.
163
Skin temperature both influences and is influenced by blood flow. Skin is crucial in the elimi nation of heat fro m the body by radiation, convection, and evaporation. As core body temperature increases, cutaneous blood flow rises (27,28). This is a result of at least two events (29) ; the first i s withdrawal of sympathetic vasoconstrictor tone, and the second is release of a vasodilator from the sympathetic cholinergic nerve endings that stimulate sweat glands. The vasodilator has not been identified. A third possibility is that the bradykin i n released from active sweat glands causes i ncreased skin blood flow during sweati ng. The evidence currently available i ndicates that bradykin i n may play a role, but i t is not necessary to achieve maximum skin blood flow during body heating. Local skin temperature also influences skin blood flow (30). At a given core temperature, placing skin in a warmer local tempera ture raises blood flow. This is because increased local temperature reduces sensitivity of cutaneous vessels to norepinephrine. At ex tremely high or low temperatures, other mechanisms come i nto play. At local temperatures over 45°C, the vascular response to inj ury occurs (see below). At local temperatures below 1 Do C, the phenomenon of cold vasodilatation is observed. At this tempera ture, vascular smooth m uscle contraction fai ls and cutaneous ves sels dilate; however, the increased blood flow warms the smooth m uscle and it then contracts. Once it contracts, blood flow de creases and the temperature of the vascular smooth m uscle drops again. The smooth m uscle fai ls to contract and blood flow in creases. This establishes periodic oscillations in skin blood flow. The cutaneous response to i nj ury ( F ig. 9 . 5 ) is observed in re sponse to many stimuli ranging from mechanical and thermal damage, to insect b i tes, to allergic reactions (3 1 ) . With mechan ical injury, a red line appears at the site of the insult. This i s the resulr of local release of a number of vasodilators, i ncluding his tami ne, b radykini n , prostaglandins, and n itric oxide, all of which increase the filling of the subcutaneous venous plexus causing a
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FIGURE 9.5. The cutaneous response to injury consists of three el ements. local di latation at the site of the injury (red reac tion) results from local release of a num ber of vasodilators, including histamine, bradykinin, prostaglandins, and nitric ox ide. Edema results from a combination of increased transport of proteins across the capillary wall stimulated by histamine and bradykinin, and increased capillary hydrostatic pressure resulting from arte riolar dilatation. Col laterals of nocicep tive C fibers that release calcitonin gene related peptide and other vasodilators cause the flare around an injury.
164
II. Osteopathic Considerations in the Basic Sciences
red line. A nociceprive srim ulus also acrivares pain fi bers rhar give offcollarerals char i nnervare rhe region near rhe sensory nerve end i ngs (32) . These collaterals arise directly from the sensory nerve axon without passing through a synapse. When the nerves are ac tivated, they release a number of peptides, including substance-P and calcitonin gene-related peptide (CGRP) fro m the collaterals. This is called an axon reflex. CG RP causes dilatation around the inj ury: aflare. Finally, the combination of i ncreased m icrovascular transport of plasma protein and increased capillary hydrostatic pressure causes local edema formation: a wheal. The increased transport of plasma proteins i nt o the i n terstitial space is caused by substance-p, hisrami ne, and bradykinin. The i ncrease capil lary hydrostatic pressure is caused by the vasodilators menrioned above.
6. Moreno-Sanchez R, Hogue BA, Hansford RC. I n R uence of NAD l i n ked dehydrogenase activity on Rux through oxidative phosphoryla tion. Biochern ). 1 990;268:42 1 --428. 7. Terriro PR, Mootha VK, French SA, et al. Ca2+ activation of heart mirochondrial oxidarive phosphorylarion: role of the FOIF I -ATPase.
A m } Physiol Cell Physiol. 2000;278:C423-C4 3 5 . 8. Laughli n M H , Korrhuis RJ , Duncker D J , et a l . Control of blood Row to cardiac and skeletal muscle during exercise. In: Rowell LB, Shepherd JT.
Handbook ofPhysiology Section 12: Exercise: Regulation and Integration of Multiple Systems. New York, NY: Oxford University Press; 1 996. 9 . Davis MJ , H i ll MA. Signaling mechanisms underlying rhe vascular myo genic response. Physiol Rev. 1 999;79:387--423. 1 0 . Jackson
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Hypertension.
2000;35: 1 73- 1 78. I I . Bakker E N , KerkhofCJ, Sipkema
P Signal transducrion in sponraneous
myogenic tone in isolated arterioles from rat skeletal muscle. Cardiovasc
Res. 1 999; 4 1 ( 1 ) :229-236. 1 2. Vanhoutte PM. Endothelial dysfunction and inhibition of converting enzyme. Eur Heart). 1 998; Suppl J :J7-J 1 5 .
SUMMARY Tissue respiration is marched to the cellular requirements for ATP. In cardiac muscle, the regulation of the synthesis of ATP appears to be linked to the maj o r cytosolic signal responsible the level of contractile activity, calcium ions. This links the use of ATP by contractile machinery to the supply of ATP by the mi tochondria. The ability of rhe m i rochondrion to supply ATP is dependenr on rhe circulatory supply of O2 and substrares. This is largely a matrer of adjusrment of blood flow to rhe active rissue by local mechanisms. Local mechanisms responsible for regulation of blood flow can be divided i n to rhree caregories: merabolic, myogenic, and paracrine regularion. These basic mechanisms ac count for acrive hyperemia, reacrive hyperemia, autoregularion of blood flow, and rhe vascular response to inj ury. Coronary blood flow provides an excellent example of a tis sue in which local regularion of blood flow is primarily concerned with marching oxygen supply to the demand created by oxidarive phosphorylation. The hean also provides an iliuSC/'arion of rhe interacrion between blood supply and Funcrion rhrough consider arion of myocardial srunning, hibernarion, and preconditioning. Skin blood flow is a counter example in which matching of merabolism and blood flow is nor usually of grear significance. I nsread, regularion of skin blood flow i s primarily concerned with rem perature regularion and rhe local response ro injury.
1 3 . Ware JA, Heistad DO. Platelet-endothelium interactions. N Engl} Med. 1 993;328:628-635. 14. Bevan JA. Shear stress, (he endothelium and the balance between Row i nduced contraction and dilation in animals and man. Int } Microcirc
Clin Exp. 1 997; 1 7:248-256. 1 5 . Owman C. Peptidergic vasodilator nerves i n the peripheral circula tion and in the vascular beds o f the heart and brain. Blood Vessels. 1 990;27:73-93. 1 6. Feigl EO. Coronary physiology. Physiol Rev. 1 983;63: 1 -205. 17. Downey J M. Extravascular coronary resistance. In: Sperelakis N, ed.
Physiology and Pathophysiology ofthe Heart, 2nd ed. Boston, MA: K1uwer Academic Publishers; 1 989. 1 8 . Pijls NH, De Bruyne B . Coronary pressure measurement and fractional Row reserve. Heart. 1 99 8; 80 : 539-542. 1 9 . Camici PG, Dutka DP Repetitive stunning, hibernation, and heart fail ure: contribution of PET to establishing a link. Am} Physiol Heart Circ
Physiol. 200 1 ;280(3) : H 929-H936. 20. Bolli R, Marban E . Molecular and cellular mechanisms of myocardial stunning. Physiol Rev. 1 999;79(2) :609-634. 2 1 . Canty J r. JM , Fallavollita JA. Chronic hi bernation and chronic stunning: a continuum. } Nue! Cardiol. 2000;7( 5 ) : 5 09-527. 22. Heusch G , Schulz R. The biology of myocardial hi bernation. Trends
Cardiovasc Med. 2000; 1 0( 3 ) : 1 08- 1 1 4 . 2 3 . Rahimtoola S H . Concept and evaluation of hibernating myocardium.
Annu Rev Med. 1 999;50:75-86. 24. Ferrari R, Ceconi C, Curello S, et al. Ischemic preco nditioning, myocardial stunning, and hibernation: basic aspects. Am Heart ). 1 999; 1 3 8 : S 6 1 -S68. 25. Spatks H V, Wangler RD, Corman M W. COl1(rol of the coronary circu lation. In: Sperelakis N, ed. Physiology and Pathophysiology ofthe Heart, 2nd ed. Boston, MA: Kluwer Academic Publishers; 1 989. 26. Fleming I , Busse R. N O: the primary ED RF. } Mol Cell Cardiol. 1 999;3 1 : 5- 1 4.
REFERENCES
27. Rowell LB. Human Circulation Regulation during Physical Stress. New York, NY: Oxford University Press; 1 986: 1 77- 1 78. 28. Rowell LB. Human Cardiovascular Control. New York, NY: Oxford Uni
I . Boyer P D . The ATP synrhase-a splendid molecular machine. Annu
Rev Biochern. 1 997;66:7 1 7-749. 2 . Korzeniewski B . Regulation of ATP supply in mammalian skeletal mus cle during resting state ro i l1(ensive work transition. Biophys Chem. 2000;83: 1 9-34. 3. Sal,lin K, Tonkonogi M, Soderlund K. Energy supply and muscle fatigue in humans. Acta Physiol Scand. 1 998; 1 62(3):26 1 -266. 4 . Hardie DC. Metabolic control: a new solution ro an old problem. Curr
Bioi. 2000; I 0 : R757-R7 59. 5 . Chance B, Williams G . Respirarory enzymes in oxidative phosphoryla tion: I . Kinetics of oxygen utilization. } Bioi Chem. 1 9 5 5 ; 2 1 7:383-393.
versity Press; 1 993. 29. Joyner M J , Halliwill J R. Sympathetic vasod ilatation in human limbs.
} Physiol. 2000;526(Pt 3) :47 1 --480. 30. Minson CT, Berry LT, Joyner MJ . N i tric oxide and neurally medi ated regulation of skin blood Row during local heating. } Appl Physiol. 200 1 ; 9 1 (4 ): 1 6 1 9- 1 626. 3 1 . Botici-Mazi R, Kouridakis S, KOl1(ou-Fili K. Cutaneous responses to substance P and calcitonin gene-related peptide in chronic urticaria: the effect of cetirizine and dimethindene. Allergy. 1 999;54:46-56. 32. Sann H, Pierau FK. Efferent functions ofC-fiber nociceptors Z Rheuma
tol. 1 998; 57(Suppl 2) : 8- 1 3 .
MICROBIOLOGIC CONSIDERATIONS AND INFECTIOUS DISEASES LAURITZ A. JENSEN JAMES B. JENSEN
KEY CONCEPTS • • • • • • • •
Global and national significance of microbial d iseases in terms of morbidity and mortality Germ theory of disease and its credence in osteopathic medicine Limitations of the germ theory of disease Microbial virulence and pathogenicity Structural and physiologic barriers and defenses; nonspecific and specific immunologic mechanisms Positive nutritional status and its role in tempering the Immune response Therapeutic and antimicrobial considerations Vaccinations and other preventive measures to control infectious diseases
Life expectancy in the United States has increased significantly during the past century, from 47 years in 1 900 to nearly 77 years (both sexes) in 2000. This tremendous improvement is due in part to a marked drop in the impact of infectious diseases. Four princi pal factors responsible for this dramatic betterment of the quality of human life are improved nutrition, improved personal and community hygiene, the development of antibiotics, and the de velopment ofvaccines. This chapter will discuss the role infectious diseases play on human morbidity and mortality and the impact of these four factors on the improvement ofthe human condition.
HAS THE WAR AGAINST INFECTIOUS DISEASE INDEED BEEN WON?
During the early days of the 20th century, Americans were ter rified of infectious diseases, mainly because they did not un derstand how to prevent "catching" them and understood even less about how to "cure" them. The influenza A outbreak that emerged at the close of World War I is perhaps the supreme ex ample of just how devastating and feared a disease could be. The
Spanish flu-so named because it was fi rst reported in the Spanish newspapers-engulfed Europe within a few months, overwhelm ing public health services and killing millions of people who were otherwise healthy and in the prime of their lives. When General Pershing's troops returned home to America, they brought this influenza virus with them. Although Americans may have fared better than much of the affected world, the death toll was still staggering. Approximately 675,000 died 0), and more than 25% of the country suffered intense illness. Because this strain of virus was so lethal, many people died within 48 hours of onset of symptoms. At its height, thousands perished each week, prompt ing health officials to close public schools and forbid people ftom attending chur<;h services or theaters. Worldwide, between 20 and 40 million lost their lives (2). The history of infectious diseases contains many grim tales, but medicine has come a long way since those early years of the 20th century. Just 5 1 years following the devastating pandemic of influenza, the United States Surgeon General, William H. Stewart, enthusiastically proclaimed that the war against microbes had been won and that it was time to "close the book on infectious diseases." In 1 969, this point of view seemed reasonable. Antibiotics could knock out almost any bacterial infection, smallpox had been eradicated in most regions of the world, the risk of tuber culosis (TB) was presumed to be in decline, and poliomyelitis and other scourges of children were being effectively controlled by hard-hitting immunization programs. In retrospect, however, Stewart was a bit optimistic. The rise of antibiotic resistance and the overflow of Third World disease problems into the United States-not to mention the emergence of new diseases and the reemergence of previously controlled diseases-were looming on the horizon. Physicians were about to be faced with many new and somewhat ominous challenges. Worldwide Importance
Globally, microbial or infectious diseases are more destructive than malignancies or cardiovascular disease. One-third of the world is infected with the tubercle bacillus, and TB lcills at least 2 million annually (3). In 200 1 , the Centers for Disease Control
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FIGURE 10.1. Ascarid worm passed by a Guatemalan child. (Photo l.D. Goldsmith.)
FIGURE 10.2. Positive Gram stain from a male patient with gonorrhea. (Photo by l.A. Jensen.)
and Prevention (CDC) reported that an estimated 36 million peo ple are afflicted with the human immunodeficiency virus (HIV) (4). We are losing more people to malaria each year than we were 30 years ago; five children die of malaria in the world every minute. In Africa, this computes to the death of 1 million chil dren each year (5). Surely these figures are conservative estimates. One of us OBJ) has spent 1 8 years working on malaria in remote African villages and has personally witnessed hundreds of malaria deaths in children who were buried within an hour of passing. None of these deaths were ever reported. Worldwide, 2 billion people are infected with Ascaris (Fig. 1 0. 1 ), another 1.3 billion with whipworm and hookworms, 1 20 million with lymphatic filariasis, and 200 million with schistosomes (6). What these data do not reflect is the toll these infections extract in human well being, creative energy, and vitality (7).
Other microbial diseases of significance included in the year ro-date or cumulative reports are hepatitis A, legionellosis, Lyme disease (Fig. 1 0.3), hemorrhagic Escherichia coLi infections, in vasive HaemophiLus influenzae, meningococcal disease, and per tussis. Outbreaks of Norwalk-like virus account for 23 million cases of gastroenteritis each year ( 1 3). Furthermore, foodborne bacterial pathogens, including CampyLobacter and gram-negative enterobacterial organisms, produce an estimated 1 3.8 million cases of gasrrointestinal (GI) disease annually ( 1 4). Giardia, the most commonly detected intestinal prorozoan parasite in the United States, is responsible for up ro 2.5 million cases of diarrhea each year-a prevalence equal to that of SaLmoneLLa and ShigeLLa combined ( 1 5). Not only do treatable infectious dis eases present substantial health challenges by themselves, but the emergence of antibiotic-resistant organisms, such as methicillin resistant StaphyLococcus au reus (16), vancomycin-resistant entero cocci ( 1 7), multidrug-resistant strains of Streptococcuspneumoniae ( 1 8), and Mycobacterium tubercuLosis ( 1 9), threaten ro overturn years of progress in antimicrobial therapy. Moreover, genetically engineered antibiotic-resistant bacteria, if intentionally released as biological warfare agents-similar to the anthrax-laced letters that resulted in the contamination of U.S. government buildings,
courtesy of
National Importance
In the United States, infectious diseases pose a real threat to people of all age groups. Each year, 2 to 3 million cases of community acquired pneumonia- Streptococcus pneumoniae being the usual agent-are identified. Approximately 1 1 0,000 Americans are hospitalized annually because of influenza or influenza-related complications. Sadly, about 20,000 of these people will die (8). Older Americans are particularly vulnerable, as microbes account for one-third of all deaths (9). Strep throat, although ordinarily not as debilitating as pneumonia and mostly involving children or young adults, ranks third on the list of common complaints to the office-based physician ( 1 0). Probably 6 million Americans have periodontal disease-not usually thought of as an infectious disease-but because of its polymicrobial etiology, it is rightfully placed in this category. Recent studies have even shown a posi tive connection between unhealthy dentition and cardiovascular disease ( 1 1 ). The number of cases of sexually transmitted dis ease (STD) reported nationally is not only striking; bur seems to be increasing. Surveillance data in recent years indicate that at least 15 million STD infections occur annually, with genital warts, genital herpes, gonorrhea (Fig. 1 0.2), chlamydia, and tri chomoniasis being commonly reported in young, sexually active Americans (12).
FIGURE 10.3. Lyme disease from a patient in the Midwestern United States. (Photo by l.A. Jensen.)
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media offices, and postal facilities i n the fall of2001, could have catastrophic consequences. In addition to these old and famil iar infectious scourges, we face fresh enemies in that more than 22 newly recognized diseases that have emerged since 1973, in cluding acquired immunodeficiency syndrome (AlDS), rotavirus infections, Ebola virus, Lyme disease, Hantaan virus infections, and others (20). And so it goes. A century ago, Americans were terrified of infectious disease. Today bacteria, viruses, and par asites are still making us sick-even killing us-and infectious disease specialists are not sanguine about the future. Indeed, as one scientist remarked: "The war has been won . . . by the other side" (21). GERM THEORY OF DISEASE: KOCH'S POSTULATES AND THEIR LIMITATIONS The Origin and Early History
The German physician Robert Koch changed forever the way we look at communicable diseases by his elegant demonstra tion in 1876 that the endospore-forming bacterium Bacillus anthracis was the etiologic agent of splenic fever, otherwise known as anthrax. His 1882 paper to the Berlin Physiological Society is universally considered by microbiologists as a signature moment in medical science and the cornerstone of the germ theory of disease, although many scientists laid the foundation for Koch's seminal studies. The thought process likely began with the Ger man anatomist Jacob Henle, Koch's mentor. It was Henle who put forth the idea of a "parasite" or contagium as the inducer of cerrain diseases (i.e., disease communicability). But Henle did not know how to prove this. It was Koch's genius to develop methods of pure culture so that only one species of bacterium at a time could be examined for its ability to induce disease. In 1884, Koch outlined his methods as a series of rules-later to be called Koch's postulates-that he developed during his studies on the etiology of tuberculosis. Tn fact, within 20 years of the pub lication of Koch's classic papers, the agents of most of the major bacrerial diseases were discovered by carefully following his postu lates (22,23). Along with the French bacteriologist Louis Pasteur, Koch is recognized as the co-founder of medical mictobiology (24). Although some of Koch's postulates cannot be applied ex perimentally (these exceptions will be discussed subsequently), they represent the keystone in the history of infectious diseases. These postulates are succinctly stated in the 1890 paper given at another scientific forum-the Tenth International Congress of Medicine. The translation that follows is by T.M. Rivers (25): However, if it can be proved: first that the parasite occurs in every case of the disease in question, and under circumstances which can account for the pathological changes and clinical course of the dis ease; secondly, that it occurs in no other disease as a forruirous and nonpathogenic parasite; and thirdly, that if, after being fully isolated from the body and repeatedly grown in pure culture, can induce the disease anew; then the occurrence of the parasite in the disease can no longer be accidental, bur in this case no other relation between it and the disease except that the parasite is the cause of the disease can be considered.
A fourrh condition dealing with reisolating the parasite (mi croorganism) from the experimental infection was eventually
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added, which only strengthened belief in Koch's blueprint of causality. Undoubtedly, Koch's research on anthrax, published in 1876, kindled his interest in defining a standard for disease causation. It is possible that anthrax transmission as the paragon for the germ theory may have been one of the reasons why the medical com munity in the U.S. initially fought against the premise. Even in the 1800s, anthrax was a disease primarily of domestic animals. It seemed to have little relevance to the U . S. physician. Koch's work on the tubercle bacillus was somewhat more compelling but only because of its diagnostic value. No useful therapy to effectively combat tuberculosis existed in those days, and furthermore, the newly developed isolation and culture techniques in clinical bac teriology had no practical application in the art of healing for the average practitioner. In his historical vignette on medicine in the United States, King gives a clear account of the circumstances and prevailing medical beliefs (e.g., miasmatic-contagious origin of disease, attitudes of physicians) of the era (26). Osteopathy and the Germ Theory of Disease
In the first decade of the 20th century, osteopathic physi cians gradually recognized microorganisms as potential causative agents for various diseases. In 1906, McConnell and Teall es poused sttong views on good hygiene and sanitary practices (27). To their credit, they confessed that the germ theory was a correct principle, plainly acknowledging that a bacillus was the "exciting cause" of typhoid fever. Other diseases like scarlet fever, diphthe ria, and malaria also were believed to have direct mictobial links, bur usually microorganisms were considered to be of secondary importance only. Viral diseases were obviously ill-defined, being impossible to identifY in that era. Hulett, in 1903, had a similar view (28): These [Pasreur, Klebs, and Koch], wirh others, placed the theory upon fairly sure ground in showing by methods ro which no objections could be raised that in certain cases there is such a definite relationship between the pathologic condition and the presence of the micro organism. The question is not yet entirely settled as to the nature of that relation. 1s the disease as it exists responsible for the presence of the micro-organism or do the bacteria produce the pathologic condition? [The italics are the author's.]
He further suggested that because the healthy person often har bors "so-called" pathogenic bacteria, their presence in the sick patient may not be sufficient proof of a causal relationship but merely an incidental finding (28). The limitations with regards to causality were quite apparent in Hulett's day. Health care professionals still have many of the same ques tions a century later. Is merely bringing the host and the microbe together sufficient to cause disease or are there other issues that should be factored into the equation to answer the question? Perhaps certain strains of microbes are less virulent and require a larger infective dose to produce infection and illness. Host parasite relationships and innate abilities to resist active disease likely produce the carrier state or result in subclinical infections. And what about adaptive immune responses? It is clear that dis ease results from complex interactions berween pathogens and their hosts, and many such interactions, remain ill-defined even today.
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Constraints of the Germ Theory of Disease When Attempting to Show Causality
In many respects, the basic premise of "cause and effect" is v iewed as a working theory; hence, it is constantly being refined. With this in mind, Fredricks and ReIman (29) point out some ob vious encumbrances with Koch's postulates. Sometimes all the postulates cannot possibly be fulfilled. For example, chlamy diae, rickettsiae, viruses, and many eukaryotic parasites do not grow in pure culture, but require elaborate cell culture and sim ilar techniques for successful in vitro propagation. Furthermore, pathogenic strains of the syphilis spirochete cannot be indefinitely transferred in conventional media or in tissue culture. Polymicro bial causation is even more perplexing. Hepatitis D virus cannot complete its life cycle and produce disease unless it coexists with hepatitis B. Often, bacteria will secrete exotoxins, whose site of cellular or tissue damage is located far from the site of bacterial colonization. The historical example of this is diphtheria, where the bacteria colonize only the nasopharynx, but the d isease results in notable damage to the heart, kidney, and tissues of the central nervous system. Moreover, staphylococcal food poisoning and Aspergillus aHatoxicosis are not infections at all, but are diseases due to the ingestion of toxins produced in foods. As such, they are classified as intoxications, and one would not find the causative organism in the body of the host during the clinical presentation. Finally, using genotype-based microbial identification, such as hybridization and amplification (PCR or polymerase chain reac tion) technology, a high degree of sensitivity and specificity and can provide persuasive evidence of a cause-and-effect association sufficient for a laboratory diagnosis without the specific ident i fication of the actual organism. Thus, it can be seen that Koch's postulates are not totally satisfied when identifYing microorgan Isms that may be the cause of disease. In summary, Fredricks and ReIman state it this way: "A microbe that fulfills Koch's postulates is most likely the cause of the disease in question. A microbe that fails to fulfill Koch's postulates may still represent the etiologic agent of disease or may be a simple commensal" (29). So, what makes one microorganism a fierce pathogen while a closely related strain of the same species is nothing more than a harmless commensal? The short answer, at least from the perspec tive of the microbe, is the acquisition and phenotypic expression of one or more virulence factors.
contributes to pathogenicity (30). Recently, however, Casadevall and Pirofski refined the overall concept of pathogenicity, along With subordll1ate terms. Accordingly, a pathogen is a microorgan Ism that damages a host directly or as a result of an immunologic response, and pathogenicity refers to the organism's ability to cause damage to host cells. Virulence pertains to the relative ca pacity of a microorganism to damage the host, and a virulence factor is a bacterial component that damages the host (31). These new definitions are not microbe centered as such, but reAect a combined effort of both the pathogen and host to produce a dis ease state. In other words, disease is a multifactorial process. To ignore the complexity of the human host by focusing solely on the pathogen produces an incomplete picture of the disease. For tunately, these definitions also take into account the variant na ture of host-pathogen interactions (e.g., opportunistic pathogens producing disease in the immunodeficient host, degree of host specificity by the pathogen, specificity of tissue involved). Host Peculiarities and Disease
Sometimes, a classic pathogen like Salmonella produces oven dis ease in one person but is asymptomatic in another. Subclinical infections are always a concern since they serve as reservoirs for the spread of pathogens to others, whose infections are likely to be symptomatic. Typhoid Mary (Fig. 10.4), a somewhat pejorative nickname given to an immigrant Irish cook in New York City, represents the classic example of the carrier state. Although Mary Mallon, her real name, never presented with symptoms (at least denied ever being ill), she repeatedly tested positive for Salmonella (32). Over the course of her career as a cook, she infected 47 peo ple with typhoid fever, three of whom died (33). But the point is this: harboring the microbe does not necessarily mean that the person will present with overt disease. The complexities of the host-pathogen interaction including genetic makeup, variations in physiology, and innate and adaptive immunity, all must be considered-and not all of these factors are well understood. Some persons are genetically predisposed to resist specific in fections. In the case of falciparum malaria, sickle cell heterozy gotes typically have low parasite counts in the bloodstream. A single amino acid substitution (valine in place of glutamic acid)
VIRULENCE AND PATHOGENICITY: MICROBIAL WEAPONRY AND WARFARE AT THE CELLULAR LEVEL Attributes of the Microbe That Contribute to Disease
What constitutes a pathogen has been an issue that microbiolo gists have wrestled with for more than a century. Before this ques tion can be answered, basic definitions for terms like pathogenic ity, virulence, and virulence factors must be explained. Classically defined, these terms focus only on the microbe. Furthermore, pathogen refers to a microbe that is capable of producing dis ease, pathogenicity as the microbe's capacity to cause infection or disease, and a virulence factor as a microbial component that
FIGURE 10.4. Grave ofTyphoid Mary, Bronx, N. Y. (Photo by l.A. Jensen.)
10.
FIGURE 10.5. Eat at Duffy's cartoon. (Illustration by K.L. Rhodes. DO.)
in the .B-polypeptide chain of hemoglobin accounrs for the dif ference. People with the homozygous condition usually die early in adulthood, but a heterozygous genome provides protection for individuals living in areas where malaria is prevalenr. The patho logic mechanism is still unclear; it has been suggested that sick ling encourages increased desrruction of parasitized erythrocytes by the reticuloendothelial system or it may be that the reduced oxygen blood levels are deleterious to the Plasmodium parasite. Regardless of the exact mechanism, people of African heritage are more likely to carry this abnormal gene, and as such, have a selective advanrage against the lethal form of malaria (34). Another form of inherited resistance to malaria, specifically to Plasmodium vivax, is cenrered around a cyrokine receptor on the erythrocyte. The site is referred to as the Duffy antigen or glycoprotein (named after a patient who received transfusion for hemolysis in 1950), which normally serves as the receptor for proinflammatory cytokines (e.g., inrerleukin-8). Bur, it also func tions as the merozoite receptor in P. vivax infections (Fig. 10.5), so erythrocytic cells that are Duffy negative are less likely to carry the parasite. Since West Africans lack this anrigen, they ordinarily are resistanr to vivax malaria (35). Specific Examples of How Microorganisms Make Us Sick
[n order for microorganisms to cause disease they must pene rrate the host's natural barriers (skin, mucous membranes, etc.), then colonize the tissues-generally by specific attachmenrs and evenrually begin to reproduce (36). To accomplish this they must also avoid the host's immune response. Pathogenic organ isms have developed an astonishing array of molecules to as sist them with cellular penetration, colonization, and immune avoidance. If, as is often the case, such molecules are injurious to the host or augmenr colonization, they are called virulence
Microbiologic Considerations and Infectious Diseases
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factors (sometimes referred to as virulence determinanrs, traits, or mechanisms). An ordinary characteristic involved with some housekeeping chores, like the fermenration of glucose, is not generally classified as a virulence facror (30). Again, virulence factors are linked ro the microbe's capacity to produce disease. Examples include structural e1emenrs (e.g., pili, pneumococcal or cryptococcal polysaccharide capsule, influenza virus hemag glutinins) that conrribute to cellular adherence and colonization, and secreted products, such as those that directly injure cells and tissues-perhaps to provide nurrienrs for the bacteria or allow the microbes to penetrate to other areas of the body. Sometimes these determinants work in concert to elicit dis ease. Case in poinr, in order to be pathogenic, Bacillus anthracis must possess genes capable of expressing a potent tripartite toxin as well as genes for a polygluramyl capsule. A toxigenic strain of B. anthracis that fails to assemble a capsule and thus avoids the immune response, is incapable of inducing disease (37). Con versely, a strain of B. anthracis that produces a polygluramyl cap sule but not the toxin is nonvirulent as well. Hence, in order to be pathogenic, both virulence factors must be expressed (38). Many population and evolutionary biologists have questioned the notion that pathogenesis is simply an artifact of a recent as sociation between the microparasite and the host (39). Virulence mechanisms likely afford the causative agent a competitive ad vantage in terms of perpetuation, dispersal, and survival in a parasitic niche. Malignant pests they are, bur only because they are "sophisticated opponenrs" or "artful contenders" snuggling to make a living at our expense (40). Many successful parasites have evolved clever means of avoiding the immune response. For example, Trypanosoma brucei, the causative agent of African sleep ing sickness, is the "artful dodger" of the microbial world, hiding from the host by perpetually switching its surface glycoproteins (i.e., anrigenic switching). The bait-and-switch scheme renders the host powerless to mount an effective immunologic defense. Schistosomes (blood flukes) employ a slightly differenr strategy to conceal themselves from the host. By disguising themselves with a coating of blood anrigens, the body defenses are easily warded off (35). Staphylococcus aureus avoids antibody responses because of the surface component, protein A, which binds immunoglobulin G (IgG) in reverse. Neisseria spp. (agents of gonorrhea and spinal meningitis) actually destroy immunoglobulin A (IgA) found on mucosal surfaces with 19A proteases (41). Molecular mimicry, undermining and nullifying the killing effects of neutrophils and macrophages, and manipulation of host physiology during an infection (e.g., bloody diarrhea, excessive sneezing) are compre hensible and sensible strategies only when viewed through the lens of natural selection. These responses are not merely acci dental accompaniments or incidenrals of disease. To clarify this concept further, other examples follow. The bacterium Legionella pneumophila naturally infects the free-living soil amoeba Acanthamoeba. When it is phagocytosed, the bacterium will prevent phagolysosome development (42). In fact, the bacillus is also capable of multiplying within the phagosome of alveolar macrophages if a bountiful supply of iron (also cysteine) is available. The cytoplasm of the macrophage, however, is normally an iron-poor environment. Legiobactin, a siderophore or iron-chelating compound, provides the means to overcome this obstacle. The result is inrracellular replication and
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FIGURE 10.6. Yersinia injecting virulence proteins into the host cell ASM News, 2000.)
cytoplasm. (Courtesy of
increased virulence (43). Another advamage of the imracellular niche is rhat the microbe, LegioneLIa in this case, is able to hide from specific immune mechanisms. Yops (Yersinia outer membrane proteins) are a series of plasmid-mediared virulence proteins that prevem phagocytic destruction of these organisms. Essemially rhe phagocyte (Fig. 10.6) is hijacked, paralyzed, and disarmed because Yops prevcm phagocyric oxidarive bursts and inhibit the release of proinAammatory cytokines. The Yersinia organism will then be disseminated deeper imo rhe body (e.g., lymph nodes, liver, spleen) and evemually elicir a phagocyric apoptosis (44). Sometimes a bacterial or viral component elicits exagger ared immunologic responses. Virulence factors thar induce rhese altered immune responses are called superantigens, such as rhe sraphylococcal enrerotoxin, the most common cause of food poisoning, and toxic shock syndrome toxin-I, which induces the often fatal toxic shock syndrome. Such superamigens non specifically acrivate T lymphocytes, producing a nondirected cy tokine cascade, leading to multiple organ and rissue dysfunc rions expressed as fever, nausea, vomiring, and desquamarion (45). The mechanisms and straregies rhar microbes employ are seemingly endless and beyond rhe scope of this presemarion. Suffice it to say thar a berrer undersranding of rhe nature of a pathogen is crucial when comemplaring anribioric, amiinAam matory, and orher rherapeuric oprions to conrrol rhe parhogenesis caused by microorganisms.
IMMUNITY-BORDER INCURSIONS AND THE BODY'S "TOP GUNS" The Historical Perspective and General Principles
The word immunity comes from rhe Larin, immunis, which means exempt. The rerm was coined in recognirion of rhe ob servation rhar many people who experienced a disease were ofren
"exempr" from suffering the same malady in rhe furure. In 1890, von Behring and Kitasato imroduced the concept of humoral im munity by showing that serum from laboratory animals immu nized against the toxigenic diseases of tetanus or diphtheria would neutralize the effects of the respective disease (46,47). This inno vative work actually followed the studies by Elie Metschnikoff, who in 1884, noted that certain white blood cells regularly "ear" or phagocytose disease-producing microorganisms (48). This principle became known as cellular immunity. For decades the field of immunology was sharply divided into what appeared to be irreconcilable factions-cellular versus humoral immunity. These seemingly opposing views were finally reconciled in the 1950s when it became clear that both humoral and cellular im munity were collective effects of the multiple functions of the lymphocytes. The capability to resist invasion and pathogenic insulrs by microbes is divided into two categories of immunity-innate or nonspecific and adaptive or specific immuniry. There is some overlap berween the two. By definirion, innare immunity in cludes rhose mechanisms of resistance that basically remain the same regardless of previous experience with microbes. In other words, such mechanisms have no immunologic memory and, thus, are not "boosted" by subsequent exposures. On the other hand, adaptive or specific immunity improves with experience and often results in a profound resistance to an otherwise highly virulenr disease agent. Innare immunity can be divided into four domains: anatomic, physiologic, endocytic, and inAammatory. ln essence, these four domains are barriers to invasion by pathogenic microorganisms. Barriers That Limit the Success of Microbes
Anatomic barriers include the skin, which has several unique pro tective properties. Skin is made up of two major componems. The inner componenr, the dermis, is richly vascularized and conrains sebaceous glands, which secrete sebum (an oily secretion or coat ing), and accommodates immense numbers of macrophages and other phagocytic cells. The outer portion, the epidermis, is non vascular and layered. The outermost layer is dead at maturation, contains the waxy protein keratin, and is constanrly being shed. This shedding or desquamation prevents the excessive accumu lation of bacteria. Furthermore, the epidermis is salty and acidic, due in part to the sebum. (Similarly, the antibacterial properries of cerumen prorect the auditory canal.) Lysozyme is another an tibacterial substance that is found on the skin (it is also found in tears and other body secretions). Lysozyme attacks the peptido glycan layer of the prokaryotic cell wall, which results in lysis of many rypes of bacterial cells. Truly, rhis is an inhospirable place for rhe survival and multiplicarion of mosr pathogens; however, many types of bacteria, which are benign in that they normally do not produce disease, have become adapted to rhe skin and other body surfaces. These so-called friendly bacteria are known as normal Aora, and their mere presence affords the host protec rion since they out compete or crowd out pathogenic organisms. The low pH of the skin is due in part to metabolic by-products of normal bacterial Aora. In spite of these defenses, a few pathogens are able to colo nize the skin. The anaerobic bacterium Propionibacterium acnes
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FIGURE 10.7. Tinea corporis, or ringworm of the body, o n the leg of a college student. (Photo by l.A. Jensen.)
readily multiplies in hair follicles and crevices, producing acnes vulgaris-an inAammatory condition that is the nemesis of many adolescents. Cutaneous mycoses, like those that cause ringworm in prepubescent children (Fig. 10.7) or athlete's foot in young adults (Fig. 10.8), are ordinarily confined to keratinized surfaces and tissues such as skin, nails, and hair. What is more, pathogens are only rarely capable of penetrating intact skin. The spirochete Treponema palLidum and infective stages of some helminths (e.g., schistosome cercariae, filariform hookworm larvae) are notable exceptions and easily pass through the epidermal barrier, even if it is undamaged. Like the epidermis, the mucosal layer of the GI tract is a nonspecific defensive barrier. The stomach's' acidic environment destroys sizable numbers of microbes, but a few pathogens are acid-tolerant, such as ShigelLa dysenteriae and Heficobacter pylori, and other organisms are spared because they are evidently insu lated in chunks of food. Progressing down the alimentary canal, the number of bacteria increases until the intestinal content con tains 25% to 30% bacterial load by dry weight. The intestinal mucosa is prime real estate, so to speak, and certain types of
FIGURE 10.8. A severe case of tinea pedis, or athlete's foot, in a home less man. (Photo courtesy of A.H. Dekker.)
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microorganisms compete vigorously for space. Like the skin Aora, these organisms are generally not pathogenic. They are highly adapted to specialized GI niches and, as such, control pathogenic organisms. In short, the indigenous microbiota out compete would-be pathogens for space and nutrients. Mucous membranes, such as those that line the respiratory and urogenital tracts, possess numerous innate defenses (e.g., mucus, ciliated epithelial cells, lysozyme). In the case of the res piratory tract, mucous secretions effectively bog down would-be invaders, and the resident ciliated epithelial cells, located deep in the system, constantly sweep the mucous-trapped microbes, dust, and pollen into the pharynx where they are swallowed into the stomach. The outer third of the urinary tract contains some resident bacteria, but the ourward Aow of acidic urine helps keep the upper system sterile. The female genital tract has its own microAora, composed in part of acidophilic streptococci and lac tobacilli. During their initial anempt to get a foothold in the vagi nal canal, many invading pathogens are overwhelmed by these microorganisms, possibly as a result of the low p H and again, simply by being crowded out. When microorganisms do pervade these physical and chemical barriers, they encounter billions of phagocytes, such as macrophages and neutrophils, which attempt to destroy the invaders. Inflammation and Other Nonspecific Defenses
From time to time, regardless of the physical barricades and patrols of white blood cells, violations do occur and microbial pathogens are successful in colonizing a site in the body. This incursion will generally lead to the initiation of inAammatory responses. InAammation consists of a highly complex series of events that sometimes acts as a rwo-edged sword, killing or re straining microbes on the one hand and exacerbating disease conditions on the other. InAammation means "setting on fire" and represents a series of events that have been recognized since ancient times. The Roman physician Celus aptly described in Aammarion as "rubor et tumor cum calore et dolore" which means redness and swellingwith heat and pain. The events behind this de scription are complex and difficult to thoroughly describe within the context of rhis chapter, and thus will only be brieAy described. When microbial invasion occurs (also, sprain and contusion), released inAammatory mediators like histamines, prostaglandins, and cytokines induce vasodilation and increased blood Aow to the compromised or injured tissue site. This inAux of blood not only results in erythema (rubor) but also raises the local tem perature (calore). These mediators also increase the permeability of the dilated blood vessels, allowing for the escape of plasma components and circulating leukocyres. Localized edema (tumor) follows, and an accumulation of fibrin prevents the spread of the invaders. Finally, to help protect the already damaged tissues from further insults, these mediators of inAammation upregu late pain receptors (dolore). The clotting componenrs of the es caped plasma form a fibrin barrier to restrict further invasion, and other intrinsic antimicrobial blood components (e.g., com plement) begin to destroy the pathogens. Finally, the neutrophils and macrophages clear our the microbial invaders. Hence, in nate immunity represents a collection of preventive measures,
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blocking the incursion and colonization of pathogenic organ isms. Such nonspecific mechanisms are generally not influenced by repeated experience with pathogens. Under certain conditions, inAammation may have systemic impacts such as fever (the cardinal symptom) and shock. Fever occurs when certain exogenous pyrogens, such as the bacterial cell wall components, peptidoglycan and lipopolysaccharide (LPS), arouse macrophages and other immunologic cells that release proinAammatory cytokines, such as tumor necrosis factor (TNF), interleukin- l ( I L- l ), and I L-6. These cytokines, described as en dogenous pyrogens, provoke the hypothalamus to increase the body temperature above the normal 37°C set-point (49). Fever is a defensive measure of the host-not simply an incidental con sequence of disease. In theory, a febrile temperature will dam age the pathogen. Fever evidenrly subdues certain temperature sensitive pathogens, such as T pafiidum. This was the driving principle that inspired Julius Wagner-Jauregg, an Austrian physi cian in the early 1900s, to employ malariotherapy as a means to ameliorate the devastating sequelae of neurosyphilis (50). Thus, fever-suppressing therapy like aspirin and ibuprofen might ag gravate the infection; however, a fever that is excessively high must obviously be dealr with aggressively. Furthermore, febrile temperatures are believed to enhance phagocytic capacities and activation of the alternative complement pathway. Also, a slighrly higher than normal temperature has a positive inAuence on spe cific T-Iymphocyte-mediated cytotoxicity (51). Hence, the pro duction offever, although nonspecific, is an effective way to retard pathogenic growth. Another nonspecific defensive strategy that checks the growth of many pathogens-organisms like streptococci, legionellae, shigellae, yeasts, intestinal amoebae, and malaria sporozoans involves the tying up of free iron in the human body. Many pathogenic species require iron to reproduce. Iron-binding pro teins, such as lactoferrin and transferrin, which are found in breast milk, tears, respiratory mucus, and GI and reproduc tive tract secretions, inhibit these pathogens (30). High lev els of free iron-perhaps from supplements-will exacerbate TB and amoebic dysentery, and children afflicted with cerebral malaria will probably get better faster when therapeutic mea sures include iron-binding drugs. Good evidence suggests that the practice of providing iron therapy to a patient with an in fection who is also experiencing an apparent transitory iron deficiency anemia might actually be counterproductive (21). On the other hand, a true iron-deficient anemia could de press the immune system by decreasing lymphoid cell develop ment and I L- l production (52). Undoubtedly, it is a matter of degree. Other nonspecific protective mechanisms include coughing, sneezing, pain, and diarrhea. People who are unable to remove bacterial-laden mucus from their respiratOry tract have a good chance of dying of pneumonia (21). Diarrhea and vomiting are importaJ1( as clearing mechanisms for diarrheagenic bacterial or viral tOxins. A bout of diarrhea will aid healing by decreasing the contact time berween the invasive bacterial pathogen (e.g., Shigella) and the intestinal mucosal surface. Antimotility ther apy, therefore, is generally not recommended for shigellosis and salmonellosis (53). Ofcourse, some ofthese mechanisms induced
by microbes have undesired consequences-at least from the hu man perspective-like the enhanced spread of disease through aerosolization or contamination of food and water. Specific Immunologic Mechanisms
Unlike the innate or nonspecific immune mechanisms, adaptive or specific immunity becomes more focused, more profound, and more efficient at dealing with microbial pathogens (espe cially repeat microbial experiences). Specific immunity has four characteristics: specificity, diversity, memory, and the ability to differentiate self from nonself. Specificity is determined by the molecular configuration of the pathogens-structural compo nents known as aJ1(igens which are loosely defined as molecular sequences that evoke immune responses. Amazingly, the immune system can differentiate berween rwo proteins that vary only by a single amino acid. Moreover, it can recognize billions of separate antigens. These characteristics are due to the fact that leukocytes, known as lymphocytes, recognize and respond only to the specific aJ1(igen to which they are committed. Thus, in each person there exists billions of unique lymphocytes, each dedicated to a given antigen providing the immune response its incredible diversity. The seminal event of immunity is called immunologic memory. This means that once the lymphocytes respond to a given anti gen, any subsequent appearance of the same aJ1 (igen will elicit a rapid, profound, and highly focused reprisal. Finally, the immune system has the ability to differentiate most proteins, as well as all cells that belong to an individual, from molecules and cells de rived from other living things, including viruses, bacteria, fungi, and parasites. The immune system is second to the central nervous system in complexity and, as such, simple explanations as to how it works are challenging, to say the least. Nonetheless, the key partici pants in specific immunity are the lymphocytes and a group of cells known as antigen-presenting cells (APCs) and their prod ucts. Lymphocytes are derived from pluripotent stem cells in the bone marrow. Some lymphocytes develop in the bone mar row before being released intO the bloodstream-these are the B lymphocytes or B cells. Other lymphocytes are derived in the bone marrow but are further altered in the thymus gland, becoming thymus-derived lymphocytes or T cells. Both B and T lymphocytes have specific aJ1(igen recognition molecules on their surfaces, called antibodies on B cells and T-cell receptors (TCR) on T cells. Thus, for each antigen that a person can re act to, there are specific lymphocytes already committed to that aJ1(igen. The activation ofthe lymphocyte triggers the specific im mune response and requires an intimate interaction berween the ' antigen and its corresponding lymphocyte. As a means ofdifferen tiating self from nonself, each individual has a unique molecular code that annotates every nucleated cell in the body. This unique code comes from a gene complex called the major histOcompat ibility complex (MHC). Thus, each individual has a particular MHC molecular complex; only identical rwins have the same set of M H C markers. These MHC markers or proteins are classi fied intO M H C class I and MHC class II. M HC class II markers are found only on certain cells of the immune system (APCs), whereas all nucleated cells express MHC class I markers on their
10.
plasma membranes. Several immune system cells act as APCs, but generally these are the macrophages, B lymphocytes, and dendritic cells. Before lymphocytes interact with their antigens they are known as naive lymphocytes. Naive lymphocytes do not undergo the cell cycle, but after leaving the bone marrow or thymus as B cells they circulate for a period of time and, unless activated by their respective antigens, undergo apoptosis and are replaced by other identical cells from the bone marrow stem cells. The B cells can react directly with their antigens by means of their antibody surface receptors. The binding of antigen to the surface antibody, along with receipt by the B cell of other signals delivered from T-helper cells, stimulates the B cell to undergo a reproductive process called clonal expansion, which results in numerous iden tical cells. Plasma cells and memory B cells are the products. The plasma cells are generally short-lived, but they produce copious quantities of antibody-up to 2,000 antibody molecules per sec ond. These antibody molecules circulate throughout the body in blood and tissue Auids and react only with the antigen that initiated its production. The memory B cells constitute a major component of recall of the immune system. Following the ini tial antigenic stimulation, far more memory B cells than naive B cells of the same specificiry will be found. Moreover, these memory B cells remain viable for long periods of time to guard against subsequent infections. If the antigen reappears at a later time, generally as a reinfection, the memory B cells swing inro action and undergo another round of clonal expansion, rapidly producing new antibody-secreting plasma cells and new memory B cells. Thus, the memory or secondary response is faster, more profound, and more focused than the initial reaction. Such an tibody responses are known as humoral immuniry and were the basis of von Behring and Kitasaro's initial observations, discussed earlier (46,47). Antibodies are only part of the immune response. Cellular immuniry resides principally with the T lymphocytes. These lymphocytes are classified according to protein surface markers. T cells with C D4 markers are called C D4 lymphocytes, whereas those with C DS markers are referred to as C DS lymphocytes. Although the CD4 and C DS cells are commirred ro react with specific antigens, naive T cells do not recognize their antigens unless the antigen has been processed and binds in the peptide binding groove of the MHC molecules. Such antigen processing, in association with the MHC self-markers, is the primary means of preventing the immune system from reacting against one's own cells. Antigen receptors on C D4 cells will only recognize antigen presented to them in association with class I I MHC molecules. This means that APCs must first phagocytose and break down the antigen into strings of amino acids (referred to as antigen process ing), complex it with M HC class II molecules, and then present it to CD4 lymphocytes. Once this happens, the activated C D4 cells will differentiate into either Til l or T112 cells. BrieAy, armed Til l cells are responsible for inAammatory-rype reactions in that they secrete various proinAammatory cytokines and are involved in defending against intracellular pathogens. T 11 2 cells are in volved with B-cell activation, and like TH I , produce a variery of cytokines. Also, some of the members of the expanded clone of CD4 cells become memory T cells.
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Like the C D4 cells, C DS lymphocytes cannot recognize anti gens unless the antigen has been presented in association MHC markers of the class I, rather than the class II variery. Antigens that are processed in this manner arise within somatic cells. Thus, antigens from intracellular pathogens, cancer cells, and foreign cells (organ transplants), are the primary targets of C DS-cell re sponses. Once the CDS cells have been stimulated by their re spective antigens in association with M HC class I markers, they too undergo clonal expansion to produce cell-specific cytoroxic T lymphocytes (CTLs) and appropriate CTL memory cells. These CTLs do not produce antibodies like the B cells. They are, how ever, killers of cancer cells and foreign tissue cells, such as organ transplants and cells which harbor intracellular pathogens. CTLs destroy their target cells by secreting a substance called perforin that lyses the target cell membrane. Thus, the antibodies from the B cells (plasma cells) generally target extracellular pathogens, bacteria, parasites, or viruses found in blood or body tissues. The initial appearance of a pathogenic organism will require activation of the naive lymphocytes through antigen recogni tion and clonal expansion ro produce the effector cells, plasma cells, T helper cells, and CTLs and their respective effector molecules-antibodies, cytokines, and perforin. This primary immune response requires 5 to 12 days before it can make a significant impact on the pathogenic microbe, and this time lag often has fatal consequences. However, once the memory cells have been put in place by the primary response, a subsequent appearance of the pathogen triggers a rapid secondary immune response in I to 3 days. Such expeditious protective immuniry is the basis for vaccines that implement a primary immune response, generally without the pathogenic consequences, and set up the immunologic memory mechanisms for a rapid and intense pro tective secondary response. Humoral immuniry in women can partially protect their neonates by passive transfer of antibody via the placenta and through breast milk. Thus, effective vac cination or previous exposure to pathogens may offer vertical protection between generations by way of these passive immune mechanisms. The New Englandjournal o/Medicine recently published sev eral review articles on basic science and clinically relevant topics in immunology that physicians and medical students will find es pecially useful (54-69). The series has an easy-to-read sryle with colorful illustrations, and can be downloaded from the Internet
(www. nejm. or[j .
NUTRITIONAL AMMUNITION: PLEASE PASS THE VITAMINS AND MINERALS The Importance of a Healthy Diet
The pathogenesis of many infectious diseases (e.g., pneumonia, diarrhea, measles, TB) are notably magnified by malnutrition (70). This negative impact on infectious diseases is due chieAy to its effects on immuniry. Cell-mediated immuniry, the comple ment system, the phagocytic response, and cytokine and antibody production are all adversely affected (50). Vitamin A deficiency is associated with impaired phagocytosis and reduced humoral and cellular immuniry, and it is believed to worsen measles in children,
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which in some African countries kills more children than malaria. Likewise, nuuitional deficiency noticeably increases the risk of respiratory and diarrheal illnesses (70). A vitamin E deficiency impedes Tcell function, whereas a lack of calcium is linked to a low fibrinogen level, exacerbating numerous bacterial infections. Finally, a zinc deficiency adversely affecrs cytokine production and is a predisposing factor for a variety of infections (50). In addition to the negative impact that malnuuition has on immunity, a healthy diet plays a more direct role in modulat ing the devastating effects of infectious disease. Furthermore, it is obvious that microbes are capable of compromising a person's nuuitional status. In their monograph on nutrition, eI Lozy and co-workers describe this concept as a synergy of malnutrition and infection (7 1 ). To illustrate this concept further, Koski and Scott point out that heavy Ascaris infections will likely have a delete rious effect on the nutritional status of the infected person and, concomitantly, malnuuition is believed to increase or intensify susceptibility to other parasitic infections (72). They appropri ately describe this as the "negative spiral." In our experience in Africa and Latin America, children with pathogenic bacterial or parasitic infections often present to clinics with loss of appetite as the most predominant symptom. This finding seems somewhat predictable, however, since a sick child, especially one who is vomiting profusely or suffering from severe diarrhea, will proba bly be anorexic. The duodenal protozoan Giardia lamblia usually produces watery diarrhea and malabsorption in children. Some times an infection will, in time, spontaneously clear. If a chronic infection does occur however, there is a risk of long-term growth retardation (73). Intestinal helminths may also negatively impact the nuui tional status of the host. Necator americanus and Ancylostoma duodenale, the two human hookworm species, are linked to iron deficiency anemia. Hookworms apparently are avaricious feeders and if the worm burden is heavy enough, appreciable blood loss will result (35). To a more serious extent, the chronic loss of serum protein markedly worsens protein malnuuition, common in rural tropical regions where hookworm infections are abun dant. Another example, well known to students of parasitology, is tapeworm pernicious anemia, a potential complication resulting from an infection with the broad fish tapeworm Diphyllobothrium latum. The condition, characterized by the presence of mega loblastic anemia, is directly linked to a deficiency of vitamin B 1 2 . Apparently, the tapeworm simply sops up this important vitamin, producing a marked deficiency. Ingestion of the dried pulverized worms, expelled in the person's feces, was once believed to be a useful remedy to reverse the anemia (74).
THERAPY AND ANTIMICROBIALS: THE ENDLESS BATTLES The Osteopathic Approach in Treating Influenza Patients in 1 9 1 8
During the 1 9 1 8 influenza epidemic most American physicians, DOs and M Ds alike, understood the benefits of isolating their sick patients, instituting appropriate hygiene measures, and dili gently regulating adequate fluid intake. According to Gevitz, these were fundamental and universal concepts in medicine at
the time (75). But instead of prescribing calomel (a mercury compound) and Dover powder (ipecac and opium mixture) to the patient with influenza for the purpose of relieving pain and inducing perspiration, the unswerving osteopathic practitioner rejected the orthodox pharmaceurical regimen completely. The results proved to be remarkable, especially for patients with pneu monia. While 1 2% to 1 5% of the patients n·eated by MDs died, only 1 % of those ueated by DOs succumbed. Ir was a defining period in osteopathic medicine, and patients inevitably came to realize that DOs had the medical skills not only to manage chronic diseases but to provide additional ueatment choices for acute illnesses like influenza and bacterial pneumonia (76). The Principles of Chemotherapy and Present-Day Worries
Admittedly, the ueatment of influenza and other infectious dis eases during the 1 9 1 8 flu pandemic was primitive by today's stan dards. In recent years, the pharmaceutical industry has provided many options to battle influenza and its complications. There are neuraminidase inhibitors-an effective medication that, if started early enough, will reduce the number of days a person is symp tomatic (77)-and several antibiotic choices to fight the deadly bacterial pneumonia that often accompanies influenza-weakened lungs. Without question, the use of antibiotics-those antimi crobial agents developed from natural effusions of certain bacteria and fungi-has made a significant impact on human health by reducing malaise, attenuating postinfectious sequelae, and often currailing mortality. But there are qualifiers and issues to be reck oned with in future years. The antibiotic age we live in is a falla cious utopia. The continual emergence of new antibiotic-resistant suains of pathogenic organisms (e.g., staphylococci, pneumo cocci, enterococci, mycobacteria) is an alarming but nor unex pected consequence of natural evolution, coupled with unwise overuse of these powerful tools. Now we face multiple-drug re sistance, the ultimate equalizer from the microbe's perspective. All this, of course, raises concerns about human prospects and medical practices in a postantimicrobial era (78). Antibiotics (microbial by-products) did not evolve for the ben efit of humans. Antibiotics evolved because they enhance lever age in the struggle for space and nuuients with other microbial species. This should come as no surprise since microbes have competing interests. A toxic substance secreted by one species may provide the necessary competitive advantage for coloniza tion by keeping the other species at bay (Fig. 1 0.9). Humankind is merely an unintended benefactor of this microbial struggle for survival. In this vein, many microorganisms have evolved countermeasures-mechanisms that impede antibiotic efficacy. Unfortunately these mechanisms also undermine modern medi cal uses of these therapeutic agents. Most of these anti-antibiotics are enzymes like ,B-Iactamase and other antibiotic-destroying en zymes. The genes for these enzymes are often located on plasmids, self-replicating extragenomic DNA circles that are often trans ferable to other bacteria, even if the species is unrelated (79). Conjugative uansfer of vancomycin-resistant genes from a strain of Enterococcus foecalis to S. aureus has been demonstrated in the laboratory (80). The significance of this suggests that "superbugs"
J O.
FIGURE 10.9. An example of com petitive i n h i bition. Note the zone of inh ibition. (Photo by L.A. Jensen.)
or bacteria that are resistant to all known antimicrobials will be a realiry in the future. Mechanisms by which bacteria resist antimicrobial drugs include: 1. Loss of antibacterial activity. Beta-lacramases hydrolyze the ,B-Iactam ring of penicillin and cephalosporins and other en zymes that destroy aminoglycosides. 2. Loss or modification of a receptor. An altered receptor of penicillin-binding proteins (PBPs) in the methicillin-resistant S. aureus (M RSA) and an altered receptor on the 50S riboso mal subunit. 3. Bacterial permeability changes. Bacterial resistance to tetracy clines and polymyxins are represented in this caregory. 4. Altered metabolic pathways. Some organisms that are resistant to the sulfonamides are able to utilize preformed folic acid and do not require p-aminobenzoic acid (PABA). 5. Altered enzyme fimction. Some bacteria wirh reSistance to trimethoprim have reduced dihydrofolic acid reductase in hibition (79). Many reasons exist as to why antibiotics should be used wirh caution and discretion. Antibiotics, especially broad-spectrum drugs, often eliminate the normal microbiota-collareral dam age of sons-creating secondary problems, such as oral or vaginal candidiasis. The yeasr replaces the normal flora. More serious is the potentially life-threatening diarrhea of pseudomembranous colitis, caused by a marked overgrowth of Clostridium difficile aFter robust and prolonged antibiotic use. For some infections, antibiotic therapy has absolutely no relevance and may acrually hinder clearance of rhe pathogen (80). Case in point, antibiotics are generally contraindicated for uncomplicated cases of intesti nal salmonellosis or campylobacteriosis. These infecrions almosr always resolve without treatment, and the use of anribiotics would only disrupt the normal flora, allowing an unresrrained prolifer ation of the pathogen. Furthermore, the possibiliry always exists that inappropriate use-possibly based solely on faulry empiric assessment-will hasren the development of drug resisrance. The responsibiliry of prudent use of antimicrobials, of course, does not rest with physicians alone-dentisrs, nurse practitioners,
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and other medical professionals compound the problem. More over, there is a crirical problem of patient self-medication. Often patients fail to comply with the regimen prescribed because of a lack of understanding of their responsibilities. It is incumbent that physicians and midlevel health care providers also function as health educators. Many patients horde medications to be used without medical approval in the future. The unfortunate ten dency is to avoid the physician whenever possible, even borrow ing medicines, or clandestinely purchasing them via the Interner or just over the U.S. border in Mexico, where many medications can be obtained wirhout prescription. Of course, the long-term stockpiling of antibiotics is pointless and may even be counterpro ductive since most drugs will lose porency if stored improperly, and many (e.g., penicillins) have short shelf lives. The parient should at least be informed of rhe problems associated with these practices. One of the most serious influences on the emergence of antibiotic-resistance involves the use of antimicrobials as growth promoters in animal feed. Penicillins, cephalosporins, tetracy clines, fluoroquinolones all have been used for this purpose. It has been estimated that 50% of rhe antimicrobials produced in rhe U.S. are used for subtherapeuric purposes in animals (81). The possibiliry exists rhat vancomycin-resistant enterococci, as sociated with avoparcin (a glycopeptide) , have already evolved in livestock; circumstantial evidence points to this conclusion in Europe (82). Furthermore, ground meats (poultry, pork, and hamburger) are potential sources for antibiotic-resistant salmonellae (83). Similarly, other resistant pathogens that nor mally reside in animals (e.g., Campylobacter jejuni, hemorrhagic E. coll) are often passed to humans in foods. In conclusion, the feeding of antibiotics to healthy domestic animals for growth promotion is an unsound practice, one that will only complicate therapeutic options for people in the future. Likewise, indiscrim inate use of antibiotics in any form will most assuredly lead to an increase in resistant organisms.
CONTROL EFFORTS: KEEPING A SAFE DISTANCE The Importance of Hygiene
Several years ago, one 'of us (LA]) observed a surgeon examining a patient for an inguinal hernia. The physician was not wearing gloves during the examination and did nor immediately wash his hands when he left the room to check a postsurgical case. Un doubredly, a basic medical school lesson was forgotten. Maybe handwashing seems jusr too simple a procedure to be of any value to the average physician (84), bur, the facr still remains, handwashing prevents the transmission of disease. lr is rhe prin cipal means of preventing nosocomial infecrions and to reduce the spread of anribioric-resisrant organisms from one parient to another (85). It is simply the cardinal rule: physicians must wash their hands berween patients. Such has been rhe case since rhe 1840s when rhe Hungarian physician Ignaz Semmelweis, in an effort to control puerperal fever ( s. pyogenes) in the materniry ward of a Vienna hospital, required rhat all medical students and student midwives wash rheir hands before examining obstetric patients (86). Correspondingly, diligent handwashing by food
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handlers after using the toilet prevents the spread of GI viral and bacterial foodborne pathogens (87). Caregivers who wash their hands between diaper changes will prevent the spread of Shigella in day care centers (88), and salmonellosis can be averted if chil dren will wash their hands after playing with pet reptiles (89) and chicks or ducklings (90). A nother important control procedure includes the changing of gloves between patients. Gloves protect both the patient and the health care worker. Moreover, wearing latex gloves should not be considered a substitute for proper hand hygiene. Physicians and n u rses should wash their hands whether they wear gloves during procedures or not (84). It has been proven that in countries where personal hygiene and communiry public health practices-like the inspection foods, sanitation of waste, and filtration of drinking water-are regularly practiced, there are considerably fewer problems with infectious diseases than in countries where food and water sources are microbiologically suspect. It has even been suggested that the purification of drinking water is the most important preventive measure for intestinal disease in humans and saves more lives than antimicrobial therapy and immunizations combined (22). The History of Vaccines and the "Snuffing Out" of Smallpox
As mentioned throughout this chapter, our present era of relative good health has been due to improvements in n utrition, personal and community hygiene, antibiotics, and vaccines. The basis for vaccines has been underscored in the discussion on immunity. However, the chronicles of vaccination begin in the occult his tory of smallpox, a disease so dreaded that even the founder of osteopathic medicine, Dr. A.T. Still feared contracting it and referred to smallpox as his "dread by day and by night" (91). Over recorded time and probably long before, smallpox was one of the most feared and detestable of all diseases. Not only was its death toll appallingly high, but survivors were often horribly scarred. The normal portal of entry for the variola virus, the etiologic agem of smallpox, is the respiratory tract, but ir was discovered that a cutaneous route was not nearly as lethal (mortality rate of 1%) and conferred complete protection against any future as sault. This technique was referred to as variolarion (rhe practice of inrroducing purulent matter extracted from an open small pox lesion into the skin of another person). It was employed in India prior to 1 000 B.C. Ir was a dangerous practice since too deep a scarification would result in a full-blown smallpox attack. Nonetheless, it became widely p racticed, and since vario lation required a fresh source of infecrious pus, some emerprising "professional" variolators would pick scabs from smallpox pa tients and grind them imo a powder. The marerial could be stored for momhs in quills. These early practitioners would travel from village to village just ahead of predicted epidemics and offer the powdered smallpox scabs as a snuff to the fearful public for a price. This practice was especially harmful because the normal route of transmission of the virus was through rhe nasal mucosa and, as one would expect, it led to far more epidemics than it prevented. [n 1796, the English physician Edward Jenner discovered a safer way to prevem smallpox. Jenner noted that milkmaids of ten had sores resembling smallpox on their hands and rarely, if
ever, contracted smallpox. I nterestingly, they were often enlisted to nurse those with the disease. He surmised that the sores on the milkmaid's hands, which came from similar lesions found on the udders of cows, provided protection. He extracted pus from a cowpox lesion on the hand of a dairymaid and inoculated it jusr under the skin of an 8-year-old boy (parental consent was obtained). Complete immunity evidently resulted because, when challenged with "variolous matter" (i.e., variolation), smallpox or isolated pox lesions at the inoculation site did not develop (9294). Jenner recon firmed these results several times. The word "vaccination" (after vacca for cow, a Larin etymology) was origi nally coined by Jenner to describe this procedure, although Pas teur later enlarged rhe basic meaning to include all like protective measures for infectious diseases. Jenner's remarkable success led to the developmem of a large scale vaccination program for the prevention of smallpox. The last known case of naturally acquired smallpox occurred in Somalia in 1977, but just 10 years earlier, 2 million people had died from the disease (93). Smallpox has now been eradicated; thus, vaccina tion, with all its potential side effects is no longer relevant. If only humankind could be as lucky with other infectious diseases. With regard to smallpox, the war has almost been won. Elimi nation of the variola virus will be completed when remaining stocks maintained by the United States, the Russian Federation, and possibly other countries are totally destroyed-not before (95). As it stands now, the victory is incomplete. [mentional release of the smallpox virus, considering that most people currently lack immunity, could be disastrous. An MMWR editorial noted in 1997: "Some things need be done only once in the entire history of the world" (96). The smallpox virus as a biological warfare threat is real. Modern-Day Vaccines and Safety Issues
The vaccine used by Jenner was made from pus and lymph from i nfected cows, an impure concoction by modern standards. Also, arm-to-arm vaccination was often employed. Human-to-human vaccination was convenient but ir was not without risk. Some times, presumably because of a co-infection, the variola virus was transmitted to the u nwitting vaccinee. Poxviruses are anri genically related and, therefore, immunity induced by Jenner's cowpox virus was protective against variola-at least for a while. The cowpox vaccine was different from the traditional vac cines of today. Lived-attenuated or chemically inactivated mi crobes and microbial components (e.g., capsular polysaccharide conjugated with protein and bacterial toxoids) currently em ployed provide a much purer and safer product. The hepatitis B recombinant-DNA vaccine, for example, is based on a surface antigen. With regard to safety issues of vaccines, serious adverse re actions associated with licensed vaccines are rare. Some serious complications of the vaccinia vaccine (for smallpox) are eczema vaccinatum, generalized vaccinia, progressive vaccinia, and posr vaccinial encephalitis. These occur more often among primary vaccinees than revaccinees. Fatal complications, as a result of postvaccinial encephalitis or progressive vaccinia, occur at a rate of 1 death per 1 million primary vaccinations or 1 death per 4 million revaccinations. As with other live-viral vaccines, vac cinia is contraindicated for pregnam women (97). Rare adverse
1 0.
complications of other vaccines occur, including intussuscep tion for rotavirus, demyelinating encephalopathy for measles, Guillain-Barn� syndrome for inAuenza, and paralysis for oral po liovirus. Anaphylaxis, of course, is always a possibility with any injecrable preparation (55). Many present-day vaccines are cur rently being redesigned as subunit or even D NA-based vaccines that reduce potential complications even further. With regard to vaccinarions, a moderate and a conservative approach is probably best.
Microbiologic Considerations and Infectious Diseases
1 77
7. Colley DG, LoVerde PT, Savioli L. Medical hel m i n t hology i n the 2 1 st century. Science. 200 1 ;293 : 1 437-1 438.
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892. 9. Mouton CP, Bazaldua OV, Pierce B , Espino DV Common i n tections in older adults. Am Fam Physician. 200 1 ;63 :2 57-268.
1 0. Ebell M H , Sm ith MA, Barry HC, et al. Does rhis patient have mep throat? }AMA. 2000;284:29 1 2-29 1 8 .
1 1 . Loesche
W),
Grossman, N S . Periodontal d isease as a specific, al
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SUMMARY
Although some infectious diseases have been virtually contained or eradicated altogether because of aggressive vaccination and control programs, newly identified microbes, antibiotic-resistant strains, and reemerging pathogens represent formidable chal lenges for physicians and midlevel health care providers. For a microbe to be classified as a pathogen, virulence determinants factors of toxicity and invasiveness-must be expressed. These factors, which evolved for the singular purpose of giving the microbe a selective advantage, oftentimes work in conjunction with inAammatory mechanisms to produce morbidity. As a re sult, cells and tissues are damaged and the patient experiences clinical symptoms like fever and diarrhea. Evidence suggests that a positive nutritional health srarus will strengthen the immune system (nonspecific and adaptive immunity) and mitigate the ef fects of disease. And finally, to avoid encouraging the evolution of resisrant microbes, antibiotics and antimicrobial agents should be employed only when other therapeutic options do not otherwise exist.
1 2. Cates W J r. Esti mates ot the incidence and prevalence o f sexually trans m itted d iseases in the U n i ted States. American Social Health Association Panel. Sex Transm Dis. 1 999;26:[4 Suppll :S 2-7.
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1 5 . Centers for D i sease Control. Giardiasis. Surveillance Uni ted States, 1 992- 1 997. MMWR. 2000;49(SS-7): 1 - 1 7. 1 6. Neu HC, The crisis in ant ibiotic resistance. Science. 1 992;257: 1 0641 073. 1 7. Cetinkaya Y, F al k P, Mayhall CG. Vancomycin-resistant enterococci. Clin Microbiol Rev. 2000: 1 3 :686-707. 1 8 . Whitney CG, Farley M M , Hadler J, et al. I ncreas i n g prevalence of m ul t i d rug-resistance Streptococcus pneumoniae in rhe U n i ted States.
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ACKNOWLEDGMENTS
We wish to thank Douglas R. Rushing, professor of biochem istry at The University of Health Sciences (U HS), for reviewing the manuscript. We also grateful for the suggestions on the im munology sections by Bonnie A. Buxton, associate professor of microbiology ( UHS).
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ENDOCRINE SYSTEM A ND BODY UNITY: OSTEOPATHIC PRINCIPLES AT A CHEMIC AL LEVEL RONALD PORTANOVA
ENDOCRINOLOGY KEY CONCEPTS
A rev iew of the general chemical types of hormones (amines, peptides/proteins, and steroids) and for each chemical type of hormone a discussion regarding: Biosy nthesis, storage, and release Characteristics of transport i n the blood • Mechanism of action (receptor, signal transduction, and effector mechanisms) • Metabolism/degradation • "Classic" endocrine glands, the hormone(s) secreted, the mechanisms that control the rate of hormon e secretion , including feedback (positive, negative) mechanisms, and the principal biologic action(s) of the hormone(s) •
•
A review of the integration of hormone action with regard to the regulation of: Reproduction Growth and development • Energy management • P reservation and stabilization of the internal e nv i ro n ment • I ntimate relationship between the principles that underlie endocrinology and the principles that guide the study and p ractice of osteopathic medicine • •
The endocrine system is a whole-body com m unications sys tem. Endocr i ne infor mation is transmitted in the for m of struc turally specific chemical messengers, the hormones, and received by equally specific chemical structures, the cell receptors. The endocr ine system participates in the control and i ntegration of bodily processes that are fundamental to human l i fe: Reproducrion, growth, and development E nergy management • Preservation and stabil ization of the inter nal env ironment
•
•
Terms and Definitions
The traditional v iew of hormones and endocrine glands dates from the work of Baylis and Starling in the early part of the 20th century. A hormon e is an i n formation-carry i ng molecule, secreted in small amounts by a specific glan d and transported in the blood to a distant site, where it exerts its biologic effect. These ideas pertain to what m ight be called the tradi tional or clas sic hormones and endocrine gla nds. It is now clear that cer tain hormones and hormonelike substances (e.g., prostagla ndins, var ious growth factors) do not fit this descriptio n . These non classic hormones have two key characreristics: 1. They are produced in orga ns not normally though t of as en docrine glan ds; for exa mple, atrial natr i uretic peptide (ANP) is secreted by the heart. The k idney produces renin, erythro poieti n , and the hormonally active metabolite of vitamin 0 (l,25-[O HJ2-D3). 2. They may act locally, without transport i n the blood, on con tiguous cells or even o n the cells that produce them , functions that are referred to , respectively, as paracr ine and autocrine.
Chemical Structure of Hormones
E ndocrine i n formation is encoded in specific chem ical structure. Every hormone is structurally unique; seemi ngly minor differ ences in chemical strucrure can dramatically affect the activity of the molecule. Nevertheless, chemically, all of the hormones co n sidered below fal l i n to one of three broad str uctural categor ies (Table ILl): 1. Amino acid derivatives
2. Peptides and proteins 3. Stero ids These strucrural categories are associated with typical physi cal and chemical character istics that have i mportant functional implications.
180
If.
Osteopathic Considerations in the Basic Sciences
TABLE 11.1. CLASSIC ENDOCRINE GLANDS AND HORMONES BASED ON STRUCTUREa
Chemical Structure Amines
Hormone
Gland Adrenal medulla
Epinephrine, norepinephrine
MajoJ Target and/or Function Whole-body adaptation to stress, including regulation of cardiovascular system (CVS) and energy flux
Thyroid
Thyroxine (T4), triiodothyronine (T3)
Whole-body including central nervous system (CNS); growth and development, organ system performance, energy metabolism
Peptides and proteins
Neurohypophysis
Vasopressin (AVP, antidiuretic hormone [ADH])
Nephron, water metabolism; CVS, regulation of blood flow/pressure
Oxytocin
Smooth muscle; milk let down,
Hypophysis, pars intermedia
Melanocyte-stimulating hormone (MSH)
Melanocytes in lower vertebrates;
Adenohypophysis
Adrenocorticotropic hormone (ACTH),
Adrenal cortex; regulation of growth
uterine motility however, role in humans unknown corticotropin
and functional status (especially steroidogenesis)
Prolactin (PRL)
Mammary; growth of gland and milk
Growth hormone (GH) (somatotropic
Whole body; growth and
synthesis hormone [5TH), somatotropin) Thyroid-stimulating hormone (TSH, thyrotropin)b
development, organic metabolism Thyroid; regulation of growth and functional status (especially thyroid hormone secretion)
Follicle-stimulating hormone (FSH)b Luteinizing hormone (LH)b
Gonads; regulation of reproduction including gamete production and development and gonadal steroidogenesis
Hypothalamus
Corticotropin-releasing hormone (CRH) Thyrotropin-releasing hormone (TRH)
adenohypophysial hormone
Gonadotropin-releasing hormone (GnRH,
secretion; also found at other sites
FSH/LH-releasing hormone) Growth hormone-releasing hormone (GH-RH, somatocrinin) Growth hormone-inhibiting hormone (somatostatin) Blood (via hepatic precursor), CNS
Adenohypophysis, regulation of
Angiotensin
(extrahypothalamic regions of CNS, pancreas, others) and may serve neurotransmitter, neuromodulation, or other local (paracrine) functions Adrenal cortex; regulation of steroidogenesis (aldosterone); CNS, neurotransmission/modulation
Parathyroids
Parathyroid hormone (PTH, parathormone)
Bone/kidney; regulation of calcium
Pancreatic islets, !'I-cells
Insulin
Liver, adipocyte, muscle, other;
and phosphate metabolism regulation of energy metabolism, plasma levels of glucose and other metabolites; widespread anabolic actions Pancreatic islets, a-cells
Glucagon
Liver, adipocyte, regulation of energy metabolism, mobilizes glucose and other oxidative substrates
Steroids
Thyroid, C cells
Calcitonin
Bone, calcium metabolism
Adrenal cortex, zona fasciculata
Cortisol
Liver, adipocyte, muscle, other; energy metabolism, widespread catabolic actions; adaptations to a wide variety of whole-body noxious insults (stresses)
Adrenal cortex, zona glomerulosa
Aldosterone
Nephron, sweat glands, salivary glands, other; promotes sodium retention and potassium loss Reproductive tract, mammary;
Ovary
regulation of growth, development, function; tissue-specific anabolic effects Progesterone
Reproductive tract, mammary; regulation of reproduction, lactation
(continued)
11.
Endocrine System and Body Unity
181
TABLE 11.1. (continued)
Chemical Structure
Gland
Hormone
Testes
Testosterone (T)
T-sensitive tissues (via T as
Dihydrotestosterone (DHT)
precursor)'
Major Target and/or Function Reproductive tract; regulation of growth, development, function; tissue-specific and general somatic anabolic effects
aThe information contained in this table is not intended to be all-inclusive. A given hormone may be produced at multiple sites and may be known by additional synonyms. Certainly, with regard to hormone-responsive targets and function, the information summarized here is grossly incomplete; many targets and biologic actions, indeed important biologic actions, are not included. It must also be stressed that only those glands and substances "classically" recognized as primarily endocrine in nature are included. Indeed, a comprehensive tabulation of the large and growing list of hormones (or hormonelike substances) would include, at least, the following: the pituitary endorphins and lipotropins, the placental hormones (human chorionic gonadotropin [hCGI and human placental lactogen [hPLJ), additional pancreatic and gastrointestinal hormones (gastrin, vasoactive intestinal peptide [VIPI. pancreatic polypeptide, cholecystokinin [CCKI. gastric inhibitory peptide [GIPI. and secretin), as well as a number of hormones produced in organs traditionally considered to be nonendocrine, such as heart (atrial natriuretic peptides [AN PsI. kidney (cholecalciferol metabolites, erythropoeitin [ESFI. renin), lymphocytes (interleukins), liver (insulinlike growth peptides [lGPs, somatomedinsJ), platelets (growth or transforming factors, including platelet derived growth factor [PDGFI and tumor growth factor [TGF-tJ]), and other sites (various growth and/or transforming factors, including epidermal growth factor [EGFI and TGF-a). bTSH, FSH, and LH contain a carbohydrate moiety attached to the protein component and are thus glycoproteins. 'Testosterone is converted to DHT in various peripheral tissues; both metabolites, T and DHT, are biologically active.
ENDOCRINOLOGY AND OSTEOPATHY
This cha pter discusses the basic elemenrs of endocrine physiology, The information is presenred in summary form and is meanr ro serve as a guide for further study. I The information is orga n ized with reference ro principles t hat guide the study and practice of osteopathic medicine. This arra ngemenr is didactic and natural since body unity is the focus of endocr i nology and osteopathy.
STRUCTURE AND FUNCTION
Structure and function are not only interrelated but are inseparably linked at aff levels ofthe biologic spectrum. The inrerdependence of str ucture and functio n , a basic pr in ciple of osteopat hic medicine, is also a fundamenral pr i nciple of endocr inology. I ndeed, the specific biologic activity of a hor mone origi nates in the str uctural characteristics of the molecule. Endocrine physiology is most usefully studied and undersrood in terms of molecular str ucture. In t he following discussio n the inr errelation of hor mone structure and funct ion is co nsidered in relation ro endocr ine processes that underlie the actions ofall hor mones. In this regard, it is useful ro view the hor mone as part of a simple endocrine system (Fig. 1 1. 1), consisting of the following: 1. An endocrine gland and the hormone it produces
2. A transport system ro del iver the hormone from its site of production ro its site(s) of action 3. An effecror organ (target) that undergoes a biologic change in respo nse co the hor mone The biochemical events t hat occur in the endocr i ne gland are referred ro as cellular processing. They incl ude the biosy nthesis, srorage, and release of the hor mone. Transport of the hor mone in the plasma depends on the physical and chem ical character ist ics of the hormo ne. The nature of the transport process is an importanr deter minant of the metabolism of the hormone a nd
lin [his [ext, [he reader will find Chapters 7 (by Pa[[erson and Wurster), 8 (by Willard), 9 (by Sparks), and
useful.
10 (by Jensen and Jensen) especially
its rate of removal from the plasma, that is, the metabolic clear ance rate (MeR) of the hor mone. The biochemical evenrs that accounr for the biologic change in the target are referred ro as the mecha nism of action of the hor mone. These three fundamenral componenrs of an endocrine system-cell ular processing, tra ns port, and mecha nism of action-are co nsidered in t he following sections with reference ro the inexorable link between str ucture and funct ion. Cellular Processing
The cellular and subcellular evenrs involved in the biosynr hesis, srorage, and release of hormones are generally differenr iated and grouped on the basis of t he chemical structure of t he hormone (pept ide/protein, steroid, and am ine). Peptides and Proteins
The biosynrhesis of peptide and protein hormones is basically co nsistenr with the typical patter n ofeukaryot ic protein synthesis. That is, specific messenger RNAs are transcribed in the nu cleus on DNA and carry t he genetic message ro the cyroplasm, where it is translated inro the specific sequence of amino acids t hat co nstitute t he hor mone. In t he case of proteins ro be ex ported from the cell, including hormones, peptide bond forma t ion occur s on membrane-bound ribosomes, that is, the rough endoplasmic reticulum (RE R) . As peptide bond formation oc curs, the polypept i de is extruded t hrough the lipid membra ne of t he endoplasmic reticulum, sequestered within the lumen of the R E R, and transported ro the Golgi apparatus, where it is packaged inro secrerory vesicles. D uring this entire process, t he polypeptide is effect ively segregated from other cell ular pro teins and co nstituenrs of the cell cyrosol. This feature has the
Hormone
FIGURE 11.1, A simple endocrine system consisting of the endocrine cell and the hormone it produces, the transport system to deliver the hormone from its site of production to its site of action, and the tar get (effector) cell that undergoes a biologic change in response to the hormone.
182
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Osteopathic Considerations in the Basic Sciences
advantage of simultaneously protect i ng and concentrati ng the nascent polypept ide. The molecule that is initially synthesized on t he RE R is not the hor mone per se, but rather o ne oftwo l arger precursor molecules, referred to as a prohor mone or a pre-prohormone. The authentic ( mature) hor mone is for med by sequential proteolyt ic cleavages of the precursor as it is transported through the RER and packaged into secretory vesicles in t he Golgi apparatus. In response to an adequate stimul us, the secretory vesicles fuse with the cell mem brane and release their contents, including the hor mone, into the extracellular perivascul ar space. This bulk transport process is known as exocytosis, or reverse pinocytosis, and character isti cally involves these processes: Expendirure of energy (adenosine tr iphosphate) Mobilization of calcium io n • Part icipation of the contr act ile microtubul ar system •
•
In most cases, as a means of rapidly respo nding to demands for increased hor mone secretion, polypept ide hor mone-secreti ng cells store ample amounts of hor mone-filled secretory vesicles. That is, the hor mone has been presy nthesized and prepackaged and is held in the cell in a for m ready for release. Steroids
Just as polypept ide hor mone-secreti ng cells are able to respond rapidly to circumstances that require increased secret ion of the hor mone, so too are cells that secrete stero id hormones. The strategy employed by these cells is different from that already de scribed. The cells that secrete steroid hor mones (adrenocortical, ovar ian, testicular) all originate fro m a common embryologic site, the primitive urogenital r idge. As such, it is not surprising that these fu nctio nally d ist i nct cells are not o nly strucrurally similar but also employ basically similar pathways for stero id hor mone biosynthesis (stero idogenesis). In all cases, stero id hormones are produced from a common precursor, cholesterol, via sequential enzymatic modifications of the steroid nucleus. The stero id-secret i ng cells store large amounts of ester ified-cholesterol (in the for m of fat droplets) . The intra cellular pool of the precursor is maintained by cholesterol b iosyn thesis in the cell and also by taking up prefor med cholesterol fro m the blood. Ring modifications t o the stero id nucleus are catalyzed by enzymes associated with specific subcellular structures (e.g., mitochondria, endoplasmic reticulum). The enzyme profile of the cell deter mi nes the nature and location of the r i ng modi fications. In so doi ng, it determ ines whether the final steroid product is cortisol, aldosterone, androgen , or estrogen . Steroid hor mones are highly li pid-soluble and are released from the cell by simple diffusion across the plasma membrane. U nlike pep tide and protein hormo nes, the steroids are not packaged into secretory vesicles and are not stored within the cells in significant amounts. I ncreasing the rate of steroid synthesis meets demands for increased secret ion of the hormones. Amino Acid Derivatives
The amine-type hormones are secreted by the adrenal medulla (catecholami nes, including epinephrine and norepi nephr i ne) and
t he t hyroid gland (tr iiodothyron ine and thyroxine). In both glands, the active hor mones are derived from a precursor, the amino acid tytosine, supplied via the blood. Once for med, the catecholamines are packaged into secretory granules and stored within the cell. Release of the hor mones occurs by means of an ex ocytotic process simil ar to that described for peptide and protein hormones. The biosynthesis and release ofthe thyroid hor mones is closely t ied to the metabolism of a large glycoprotein, thyroglobulin. Thyroid hormones are derived from the iodination and linkage o f two residues of the amino acid tyrosine. During the entire biosynthetic sequence, however, the tyrosine molecules are not free within the cell but instead are incorporated into thyroglob uli n via peptide bonds. After the thyroid hor mones are for med, they remain covalently linked to thyroglobulin. This macro molecule, thyroglobulin with its attached hormo nes, comprises the major const ituent of a gelatinous mater ial known as the thy roid colloid. Large amounts of the colloid are stored in the lumen ofthe thyroid follicle, that is, outside ofthe thyroid follicular cell . Release of the t hyroid hor mones i nvolves the exquisite inter play of several subcellular organelles. I n brief, follicular cells take up droplets of colloid (by endocytosis) . In the cell, Iysosomes (containing hydrolytic enzymes) merge with the colloid droplets, and proteolysis ofthe thyroglobulin molecule frees the active thy roid hormones that then diffuse across the cell membrane and enter the bloodstream. It is difficult to imagine that A.T. Still would not consider the subcellular ballet i nvolved in production and release of the thyroid hormones to be a graphic representation of the interrelationship of structure and funct ion . Transport and Metabolism
Once the hor mone is released at its site of production , it is trans ported in the blood to a distant target site, where it produces a biologic change. The magnitude of the change in the target, the biologic response, is proportional to the concentration of the hor mone in the blood. This, in turn, is a fu nction not only of the rate at which the hor mo ne enters the blood (rate of secret ion), but also of the rate at which it is removed from the blood, that is, the M CR. The char acter istics of a particular hormone's transport process have a significant effect on the MCR and therefore on the biologic actio n of the hor mone. In general, hor mones circulate in the blood in one of two ways, depending on the chem ical structure and sol ubil ity char acter istics ofthe molecule. Amine and polypeptide hor mones are readily soluble in the aqueous phase of the plasma and circulate in a free, unbound for m . In contrast , steroid and thyroid hor mones are hydrophobic and travel in the blood in association with carrier proteins. The carr ier, or transport, protein may be a specific plasma globulin with high-affin ity binding sites for a par ticular hormone (e.g., testostero ne-binding globulin, or TeB G ) . It can also be a nonspecific plasma protein (e.g., al bumin) that associates loosely with a number of hor mones. Several aspects of the binding of hormones to carrier proteins are of part icular importance and again underscore the not ion that for m i ndeed gives r ise to function. First, only the free, unbound fr act ion of the hormo ne is biologically act ive. F unctionally, the transport protein-hor mone complex serves as a circulating
11.
hormone reservoir that can be used ro augment or replenish the free, biologically active, hormo ne pool. Second, changes in plasma levels of binding proteins occur both physiologically (e.g. , cortisol-binding globulin levels in crease during pregnancy) and pathologically (e.g., liver disease). Such changes are reRected in the rotal (bound plus free) hormone concent ration, but not necessarily in the concent ration of free, biologically active hormone. This is of practical importance ro the osteopathic physician, since diagnostic p rocedures may measure rotal plasma hormone, an unreliable index of the actual activity of the hormone. Third, t he MC R of a circulati ng hotmone is directly related ro its binding characteristics. Hormones that are tightly bound ro carrier proteins have a longer lifetime in the plasma than hor mones that circulate in a free or loosely bound form (e.g., respec tively, thyroxine, days versus vasopressin, minutes). Mechanism of Action
The mechanism of action of a hormone refers ro the sequence of chemical and morphologic events that mediate the specific biologic action of the molecule on a particular target tissue. At minimum, these intermediary processes must account for certain general characteristics of hormo ne action. That is, hormones are dist ributed (via the blood) indiscriminately throughout the body, but only certain tissues (targets) respo nd ro t he hormone. A par ticular tissue may respond ro only one hormone or ro several different hormo nes. Some hormones act on only a si ngle tissue or tissue type, whereas other hormones act at numerous, distinct sites. Finally, a particular hormone may elicit widely differing responses in diFFerent target tissues. Hydrophilic Hormones
Peptide hormones and catecholamines act on target cells thro ugh a Four-stage process.
Endocrine System and Body Unity
183
cell membrane, G-protei ns, which, in turn, regulate (increase or decrease) the generation of substances reFerred ro as seco nd messengers. Stage 3. Second Messengers
Stage 3 is that of the seco nd messengers. The hormone (first messenger) initiates the biologic response, but the respo nse is mediated by int racellular second messengers. Cyclic adenosi ne monophosphate (cAMP) was t he first of the intracellular media rors ro be recognized, but it is now clear that other substances also fill this ro le, including, For example, cyclic guanosine monophos phate (cGMP ) , calcium io n , and phospholipid metabolites such as diacylglycerol and inosirol triphosphate. Stage 4. Biologic Response
Stage 4 occur s when the second messenger int eracts with the chemical machinery of the cell ro produce the biologic response. The interaction normally involves a change in the activity of a protein, oFten an enzyme. It is t his p rotei n (enzyme) t hat deter mines t he characteristics of the biologic response. For instance, in the heparocyte, cAMP generated in response ro glucagon sti m ulates the phosphorylase enzymes and glycogen breakdown. I n t h e adipocyte, glucagon increases t h e production o f cAMP, acti vation of an enzyme known as hormone-sensitive lipase, and the hydrolysis of triglyceride. One characteristic feature of peptide and protei n hormones re quires f u rther discussion. A particular hormone may elicit widely differing respo nses in different target tissues. For example, the same posterior pituitary hormone that produces antidiur esis in t he nephron produces vasoconstriction in t he vasculature and t h us is known, respectively, as antidi ur etic hormone (AD H ) and vasopressin. I n the case of the parathyroid hormone (PT H ) , even a partial list of biologic actions and respective targets would i nclude: P hosphaturia and bicarbo naturia in renal proximal t ubules I ncreased calci um reabsorption in renal distal tubules • Bone resorptio n i n osteoblasts • I ncreased thymidine incorporation in osteocytes •
Stage 1. Hormone Receptor Interaction: Signal Generation
Stage 1 occurs when t he interaction of the hormone with a spe ci fic, high-aFfinity recepror on the cell membrane signals the ini tiation of t he response sequence. It is the presence or absence of the recepro r that determines whether the cell responds ro the hor mone. A particular cell may have receprors fo r one or more ho r mones. Fasciculata cells in t he adrenal cortex respo nd selectively ro adrenocorticotropic hormone (ACTH), whereas adipose cells respond ro several hormones, including glucago n, epinephrine, ACTH, and vasopressin. Both t he number of receprors and the affinity of the recepro rs are physiologically regulated and signiF icantly affect the biologic response. Moreover, abnormal recep ror structure and/or f unction is an important component of the pathophysiology of endocrine disorders (e.g., diabetes mellitus). Stage 2. Signal Transduction
In stage 2, signal t ransduction , hormone recepror interaction inRuences the guanine nucleotide-sensitive co mponents of the
•
The presence of multiple disti nct biologic actions wit hin a si n gle molecule gives rise ro the notio n t hat some hormones may con tain m ultiple distinct st ructural features (amino acid sequences); that is, that some hormones are in fact polyhormones. Lipophilic Hormones
Steroid hormones and thyroid hormones enter the target cell and bind ro specific recepro r proteins, localized primarily wit hin the n ucleus. The hormone-recepror co mplex regulates the t ran scriptio n of specific genetic segments in DNA and ulti mately the synthesis of specific messenger RNAs and cellular protei ns. In cont rast ro the hydrophilic hormones that regulate the activity of existing cellular proteins (enzymes), the response ro lipophilic hormones is mediated by changes in the amount of new pro tein (enzyme). The final biologic response is characterized by the chemical activity (function) of the protein (s) synthesized in
184
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Osteopathic Considerations in the Basic Sciences
response to the hormone. It can range from the i ncreased synthesis of a particular enzyme or functionally related group of enzymes, such as increased hepatic synthesis of gluco neogenic enzymes i n response to cortiso l, to cellular differentiation and tissue growth, such as prostate hypertrophy in response to androgens.
THE BODY FUNCTIONS AS A WHOLE
The body fu nctions as a whole. It is regulated, coordinated, and integrated through multiple interactive systems. Hormones play a major role i n the o rchestration of body u niry. In this endeavor, the endocrine system does not operate in isolation but is i nterdependent with other body systems. The following discussion deals with the i nterrelation of endocrine, cardiovascular, and neural function. Cardiovascular System
E ndocrine fu nction is dependent on cardiovascular function. This is most obvious in that hormones rely on the cardiovas cu lar system (CVS) as a means of transport to distant sites. The transport fu nction of the CVS usually involves the systemic circu latio n , bu t other specialized vascular networks are also employed to great advantage (discussed subsequently) . The circulatory sys tem also participates i n controlling the secretio n of hormones and in determ ining the magnitude of their effect at the site of action (target) . That is, alterations in blood flow to the endocrine gland co ntribute to alterations in secretion rate. For example, hyper emia often accompan ies increased secretion, and changes in blood flow ro the target affect the rate of delivery and the effect of the hormone. Commensurate with the role of the CVS in endocrine fu nction, endocrine glands are rypically highly vascu larized. For example, throughout the mammalian k ingdom, blood su pply to the pitu itary (mL per mg of tissue weight) is greater than that of any other tissue. In the adrenal gland, cells of the zon a fasciculata are arranged in bicellular colum ns separated by capillaries; that is, each cell is in direct co ntact with a capillary. While the endocrine system clearly depends on cardiovascular fu nction, hormones have a major i n fluence on the CVS: Catecholami nes have well-known actio ns on the heart and vasculature. Adrenergic cardiac fibers influence myocardial co ntractiliry and rhythm. Adrenergic vasoco nstrictor fibers are a dominant influence on systemic vascu lar resistance. Catecholamines of adrenal medullary origin and a number of other hormones also i n fluence the CVS: Vasopressin and angiotensin are vasoconstrictors. Thyroid hormones affect heart rate. Thyroid hormones and aldostero ne increase the fo rce of ven tricular contraction . In addition to these direct actions, endocrine mechanisms (the renin-angiotensin-aldosterone system, antidiuretic hor mone, ANPs) are an important co mpo nent in the regulatio n
of whole-body fluid and electrolyte metabolism, the extracellu lar fluid (ECF) and blood volume and, indirectly, cardiovascu lar fu nctio n . The endocrine mechanisms serve to maintain fluid homeostasis and cardiovascular function under normal co ndi tions and to protect cardiovascular fu nction against the conse quences of challenges such as water deprivation or hemo rrhage. Nervous System
A wide variery of external sti muli, or changes in the external en vironment, alter the activiry of the endocrine system by means of multisynaptic neural pathways. Fo r example, auditory stim uli activate the hypothalamic-pitu i tary axis and increase cortisol secretion. Light cycles i n fluence endocrine rhythms, and groups of females living together may develop synchronous periods of go nadotropin secretion and ovarian function. Changes in the i nt ernal environment, such as the chemical co mposition of the blood, directly affect hormone secretion without the necessiry of neural i n tervention (discussed su bsequently). Nevertheless, even in cases like this, neural influences may play a role. In sulin secretion is a rypical example: Although glucose and other metabolites stimulate release of the polypeptide, ,B-cell innerva tion (sympathetic and parasympathetic) modulates the secretory response. Just as the nervous system influences endocrine activiry, hor mones have significant effects on neural activiry. The endocrine effects can range from actions on single neurons ro alterations of complex mental activiry and behavior. Peptides
A number of peptide hormones have been fou nd to alter central nervous system (CNS) activiry. For example, vasopressin acts in the CNS to decrease body temperature and to improve memory. I n some cases, peptide hormones have been found not only to act in the CNS but also to be produced in the CNS. Examples of these hormones i nclude the ANPs and angiotensin, which, respectively, i nhibit and stimulate the sensation of thirst. Steroids
Gonadal and adrenoco rtical steroids affect the activiry of the hy pothalamic neurons that co ntrol the anterior pituitary. They thus play a major role in regulating pituitary-gonadal and pituitary adrenocortical activiry. Moreover, both rypes of steroids influence complex patterns of neural activiry; fo r example, androgens stim ulate libido (sex drive) i n both males and females. Cortisol de ficiency (adrenal insufficiency, Addison disease) is accompanied by an abnormal electroencephalographic pattern and behavioral and emotional disturbances, including anxiery and depression. The cortisol deficiency is corrected by administering the steroid, but caution must be exercised since cortisol excesses also lead to behavioral disorders. Amines
The actio ns of the thyroid ami nes on the development and fu nction of the CNS are especially profound. Thus, infantile
11.
hypothyroidism (creti nism) is associated with retarded menral development. The earlier the condition appears and the longer it goes untreated, the more severe the effects, culmi nating in ir reversible damage to the brain. Congenital hypothyroidism is a current leading cause of preventable mental deficiency. Even af ter the developmental period, thyroid hor mones influence neural activity. In the adult, thyroid status is related to gross behavior such as alertness, mental acuity, and irritability. I n some cases the interaction of endocrine and neural f u nc tion is so complete that the distinction berween the rwo sys tems is in fact blurred. Nowhere is this more evident than i n the hypothalamic-pituitary complex, where neural and endocrine activity are combined in the same neuroendocrine cell . The pep tide hormones oxytocin and vasopressin are secreted by neurons having their cell bodies located in the hypothalamus and send ing their axons into the neurohypophysis (posterior pituitary). I nstead of ending on another nerve or effector, such as a m uscle, the neur oendocrine cells terminate on pituitary capillaries and re lease their hormones i nto the system ic circulation. Another group of hypothalamic neur oendocrine cells deliver their hor mones not to the systemic circulation, but rather to a specialized (portal) vas cular system that supplies blood to the adenohypophysis (anrerior pituitary) . These cells, referred to as hypophysiotropic neurons, regulate the secretory activity of the anterior pituitary. Final Common Path
Neural influences predominate in the regulation of anrerior pitu itary hormone secretion. It is well known that ACTH secretion is related to photoperiod. Growth hormone secretion is associ ated with sleep stages. Light, odor, auditory, and tactile sti muli as well as emotional disturbances infl uence gonadotropin secre tion and reproductive function. For a time, the relationship be rween anterior pituitary and CNS f unction presented a concep tual difficulty, since the adenohypophyseal secretory cells are not in nervated. (The anterior pituitary is innervated by vasomotor fibers.) Indeed, the (older ) endocrine literature refers to the ante rior pituitary as a gland under neural control, but lacking a nerve supply. The physical link berween the CNS and the anterior pituitary is not neural but vascular, consisting of a specialized arrangement of vessels, alter natively known as the pituitary portal vessels or the hypothalamic-hypophyseal portal vessels. I n brief, the ante rior pituitary is regulated by neurohormones that are produced i n the hypothalamus a n d transpor ted to the pituitary in the portal venous blood. The por tal vessels originate in a capillary nerwork (primary plexus) located in the hypothalamus. The capillaries coalesce to form the pituitary portal veins, which enter the ante rior pituitary and give rise to a secondary capillary plexus. The hypothalamic neurohor mones, hypophysiotropic hormones, are produced by neurons that ter minate in the hypothalamus in close contact with the primary capillary plexus. The neurohormones enter the por tal venous blood and are delivered to the anrerior pituitary. This exquisite interrelationship of neural, vascular, and endocrine f unction is sometimes referred to as the fi nal com mo n path. Sir Geoffrey Harris postulated the f unctional significance of the pituitary por tal vessels about 40 years ago. It is a credit to
Endocrine System and Body Unity
185
A.T. Still mat he recognized the i mportance of such relationships almost half a century earlier.
SELF-REGULATING, SELF-HEALING
The body is inherently self-regulating and self-healing. Responses to internal and external events are modulated through feedback mech anisms with homeostasis of the internal environment, the internal milieu, as a major goal. Homeostasis of the internal enviro nmenr is a primary goal of endocrine physiology. To accomplish this goal , the rate of hormone secretion is modulated according to changes in the in ter nal environment. The relationship berween hormones and the internal environment is completely i nteractive: Changes in the i nter nal environment affect hor mone secretion, and changes in hormone concentration i n fluence the composition of the in ternal environment. Regulation of Hormone Secretion
The rate of hormone secretion is controlled by specific chemical signals that increase or decrease me rate of hor mone biosynthesis and release. The chemical signals include neural transmitters (e.g., acetylcholine, norepinephrine), supplied at a synaptic j unction , a n d n u merous constituents of the blood a n d extracellular fl uid, such as: Various substrates (e.g. , glucose, amino acids) Ions (e.g., sodium, potassium, calcium) • Other hor mones •
•
Regardless of the chemical nature of the signa l (s), in all cases the rate of hor mone secretion is tightly coupled to demands for the hormone. This is in response to changes in the i n ter nal en vironment, which in turn are, of course, responsive to changes in the exter nal environment. The control mechanisms are de signed to ensure that the rate of hor mone secretion is, in fact, appropriate to environmental conditions. When these mecha nisms succeed, as they usually do, the hor mone plays a vital role in the self-regulating and self-healing aspects of the body. On the other hand, failure of these mechanisms leads to hormone imbal ances and the creati o n of an inter nal environment hostile to the health, well being, and even the very survival of the individual. Control Mechanisms
The secretion of a hor mone is typically controlled by a self regulating servomechanism designed to match circulating con centrations of the hormone to the momentary needs of the in dividual. Two essential features of the control scheme are readily apparent. First, the systemic concentration of the hor mone, or of some variable related to the hormone, such as a metabolite, must be monitored. Second, this information must be returned or fed back to the endocrine organ. The secretion of the hormone is adjusted u p or down according to me nature of the information returned: inhibitory, negative feedback or sti m ulatory, positive feedback.
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f - - 1 - - -(-
-
-
-
-
+-
-
1 - - - - -(- - - - - -(- - - - t -
I CNS I Hypothalamus � C R H �I Adenohypophysis � ACTH ---+ I Adrenal f-- Cortisol - FIGURE 1 1 .2 . Cortisol feeds back at several sites to dampen activity of hypothalam ic-pitui tary-adrenal axis and ultimately to limit its own secretion. CNS, central nervous system; CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropic hormone; solid arrow, sti mulates; dashed arrow, inhibits.
Negative feedback mechanisms are more common than pos itive feedback mechanisms throughout the endocr ine system. Negative feedback mechanisms are inherenrly self-limiting. I n their most basic for m they operate as follows: I. The hormone produces a response in a target cell. 2. Some fearure of that response acts back on the cell that pro duces the hormone to decrease (limit) its secretion.
For example, the adenohypophysis secretes ACT H , which then acts on fasciculata cells in the adrenal cortex ro stimulate the production of cor tisol. Cor tisol has widespread effects through out the body. One important action of the steroid is ro act back on the adenohypophysis to i nhibit ACTH secretion. This closed-loop infor mation pathway is diagra mmed in Fig. 1 1. 2 as one component of a multifaceted control scheme that regulates the hypothalamic-piruitary-adrenocortical axis. This complex control scheme i ncludes several hormones and m u l tiple negative feedback loops. The first hor mone, cor ticotropin releasing hor mone (CRH) , is produced in the hypothalamus and del ivered to the pituitary in the portal venous blood. The hy pothalamic peptide stimulates the secretion of a second hormone, ACT H , that enters the systemic circulation, and activates the adrenocortical secretion of sti l l another hor mone, cor tisol. The adrenal steroid feeds back o n the anterior pituitary, the hypotha lamus, and on other sites in the CNS. Negative feedback effects at these several loci all con tribute to dampen the activity of the hypothalamic-pituitary-adrenal axis and ultimately to l i m i t the secretion of cor tisol. Since negative feedback mechanisms are in herently self-limiting in narure, it is per haps not apparent that this mechanism is equally important as a means of increasing hormone secretion. For example, inadequate circulating levels of cortisol are accompanied by decreased negative feedback that leads to activation of the hypothalamic-piruitary-adrenal axis and increased secretion of the steroid. As noted, positive feedback mechanisms are also employed ro control endocrine systems. Here, two hormones (or other var i ables) change in the same direction, so that an initial increase in the activiry of the system leads to further increased activiry. This rype of mechanism does not l i m it, but rather, amplifies the mag nirude of the effect and produces an abrupt, explosive change in the activiry of the system. AJthough positive feedback mechanisms are rather uncom mon, they never theless play a vital role in regulating certain as pects of endocr ine fu nction. A par ticularly noteworthy example is the role of positive feedback in regulating reproductive f unc tion. The pituitar y gonadotropins, fol licle-stimulating hormone and luteinizing hormone (FSH and LH, respectively), stimulate the production of estrogen. The steroid acts back on the ovary to promote growth and development of the ovar ian follicle and
additional estrogen secretion. As a consequence, plasma concen trations of estrogen r ise dramatical ly. Near the midpoint of the menstrual cycle, the high-circulating levels of steroid tr igger a sud den, marked increase in LH secretion, which , in turn, induces ovulation. Ovulation depends on the preovulatory LH surge, and LH secretion is driven by the positive feedback effects of estrogen at two primary sites: the ovary and the pituitary. The importance of these events to normal reproductive f unction is underscored by the fact that contraceptive steroid regimens are expressly de signed to create steroid imbalances that prevent the preovulatory LH surge. Temporal Patterns
As descr ibed, the rate of hormone secretion is tightly controlled and responsive ro physiologic demands. AJthough it is clear that secretion rate (the amount of hormone delivered to the blood per unit time) influences the circulating concentration and ac tiviry of the hor mone, hormone activiry is not a simple func tion of concentration. That is, the temporal patter n of changes i n secrerory rate and circulating concentration of the hor mone also i n fluence hormone activiry. Many, perhaps all, endocrine glands secrete hormones in a repetitious stop-and-go fashion, a quiescent per iod followed by a burst of secretory activiry. This leads ro small but physiologically significant oscillations in plasma hormone concentrations. This secretory pattern, re ferred to as pulsatile or episodic secretion, has two important character istics: 1. The rate of hormone secretion (amountlrime) is the prod uct of the frequency (episodeslrime) and amplitude (amount/ episode) of the secrerory episodes. 2. Changes in secretory rate are produced by corresponding changes in both parameters; for example, negative feedback signals decrease both the frequency and amplitude of the secretory episodes.
Episodic secretion is character istically associated with high frequency oscillations in secretory activiry: Release episodes are separated by only brief intervals of time (minutes). I n some cases the high-frequency secrerory episodes are superimposed upon other lower frequency temporal patterns or rhythms having per i odicities of hours, days, or even months. For example, ACTH and the pituitary gonadotropins are secreted episodically and display high-frequency oscillations in plasma concentration. At the same time, plasma levels of ACTH (and also cor tisol) are well known to cycle on a daily basis, in the classic diurnal rhythm. In repro ductively competent females, pituitary gonadotropins (and also the gonadal steroids) cycle rhythmically within approximately a I - month per iod.
11.
The cellular and molecular mechanisms that generate pat terned or rhythmic hormone secretion are not well understood. The implication of phasic hormone release also requires further study. Nevertheless, it is clear in a few cases that the oscilla tions are physiologically significant. For example, inadequate se cretion of hypothalamic luteinizing hormone-releasing hormone (LH-RH) leads to reproductive fai lure. This condition is cor rected by adm i nistration of the peptide, but only if the LH-RH is given in a pulsatile fashion that approximates normal endogenous secretion. Processes Regulated by Hormones
Hormones are i nvolved in regulating the most fundamental as pects of human life. I ndeed, hormones play a vital role with regard to the survival of the species. That role includes: Reproduction Growth • Development to reproductive maturity •
•
Hormones also play a vital role with regard to the survival of the individual: • •
Maintenance of the internal environment Energy metabolism
Reproduction
Hormones produced by the hypothalamus (gonadotropin releasing hormone, or G n RH ) , the pituitary (FSH, LH, prolactin (PRL), growth hormone), and the gonads (androgens, esttogens, progestogens) interact to regulate reproductive function. Repro ductive competence requires the ability to produce gametes (ova, sperm) and the ability to unite the gametes by attracting and mat ing with members of the opposite sex. There are several aspects of this process: Gamete formation (e.g., spermatogenesis, oogenesis) • Mating ability (e.g. , growth, development, maintenance of the reproductive tract) • Mutual attractiveness (e.g., male and female phenotype, pattern of sexual behavior) •
All are infl uenced by or totally depend on the reproductive hormones. After conception, maternal support for the developing fetus (pregnancy) is hormone-dependent, and in mammals, even after birth, hormones continue to play a role in nurturing the infant during lactation. Growth and Development
The regulation of intrauterine growth is poorly understood. Sur prisingly, hormones that have dramatic effects on the neonate (growth hormone, thyroid hormone) appear to have l ittle i n fl u ence on fetal growth. Somatomedins and other growth factors undoubtedly play a role in prenatal growth, but much research must be done to clarify that role.
Endocrine System and Body Unity
1 87
The regulation of postnatal growth is better understood. I n addition t o a n umber o f nonhormonal factors, such as nutrition, hygiene, and general health, normal growth and development depend on the interplay of several hormones, including: Growth hormone and the somatomedins Thyroid hormone • Insulin • Cortisol • Gonadal steroids •
•
Imbalances in the secretion of these hormones, excesses as well as deficiencies, dramatically affect growth, especially if the imbalance occurs during the normal growing period. For exam ple, hyposecretion of growth hormone produces dwarfism. Hy persecretion of the hormone leads to giantism. Thyroid-hormone deficit i mpairs growth of the body and also has devastating effects on the development of the CNS and mental capacity. Cortisol or the gonadal steroids in excess slow or even arrest growth and lead to short adult stature. Internal Environment
Many, and in a broad sense all, hormones participate in the de fense of the internal environment. Although no aspect of the i nternal environment is unimportant to health and well being, certain features are regulated and guarded especially closely by functional groups of hormones. These include: 1. Ionic composition (Na+, K+, and H+) of the body fl uids, most notably the blood and cerebrospinal fluid (the renin angiotensin-aldosterone system, ANp, insulin, and other hormones) 2. Volume of the body fl uids, especially the ECF volume and the blood volume (ADH , the renin-angiotensin-aldosterone system, ANp, cortisol, and others) 3. Plasma level of calcium and phosphate ions (PT H , 1,25[OHJ 2-D3), calcitonin, and others) 4.
Structural i n tegrity and function of body tissues, including bone, muscle, and adipose tissue (growth hormone and the somatomedins, PTH , 1 ,25- [OH J 2-D3, gonadal steroids, in sulin, glucagon , cortisol, and others)
5. Direction and rate of flow of metabolic energy Energy Metabolism
The hormonal regulation of energy metabolism allows the body to meet i ts need for a constant supply of energy in spite of the intermittent intake of food. Even at rest, vital bodily p rocesses must be maintained. There is a significant metabolic "cost of living," the basal metabolic rate. On the other hand, the intake of energy (calories contained in food) is sporadic; the consump tion of excess food (caloric i ntake exceeds momentary needs) is i nterspersed with periods of fasting. To resolve this problem, excess energy is stored i n a form that is readily mobilized and available for use when necessary. The metabolic flow in both directions, storage and retrieval, is d irected and controlled by hormones.
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Osteopathic Considerations in the Basic Sciences
During the period when exogenous fuels are available, i nsulin is of primary importance. The polypeptide stimulates the uptake and metabolism of glucose (glycolysis) and promotes the storage of small metabolites in their respective macromolecular forms (i.e., glucose as glycogen , amino acids as protein, and free fatty acids as triglyceride). When exogenous fuels are not available, sev eral hormones, most notably glucagon and cortisol, collaborate to mobil ize energy from endogenous storage sites. Glucagon stimu lates the hydrolysis of glycogen (glycogenolysis) and triglyceride (lipolysis). It increases the formation of new glucose from noncar bohydrate sources (gluconeogenesis). Cortisol stimulates gluco neogenesis and mobil izes amino acids (gluconeogenic precursors) from protein depots. The precise physiologic role of newly (since the previous edition of this text) discovered hormones, such as ghreli n and leptin-shown to i n fl uence energy balance, fuel uti lization, and body weight-remains to be determined. The importance of the hormonal controls is dramatically il l ustrated in clin ical conditions such as diabetes mellitus and Ad dison disease (cortisol deficiency) . The absence of insulin leads to a metabolic profile that in many respects resembles that seen in long-term food deprivation (starvation) and, if left u ntreated, death. In the absence of cortisol, gluconeogenesis is so seriously impaired that short periods offood deprivation, even an overnight fast, pose a serious threat to life.
information was available at the time osteopathy can1e i nto being. The future surely holds stil l more, and even unexpected, infor mation concerning not only endocrinology but all body systems. However, the conclusion is inescapable: Osteopathic philosophy is so deep-rooted in an u nderstanding of the fabric of life that this new information, too, will be embraced.
SUGGESTED READINGS Friedman JM, Halaas ] L. Leptin and the regulation of body weight in mam mals. Nature. 1 998;395 :763-770.
Frohman LA, Felig P. In trod uction to the endocrine system. In: Felig
P, Frohman LA, eds. Endocrinology and Metabolism. New York. NY: McGraw- Hili; 200 1 :3- 1 7. Greenspan FS, Gardner DG, eds. Basic and Clinical Endocrinology; 6th ed. New York, NY: Lange/McGraw- Hili; 200 1 . Griffin JE, Ojeda SR, eds.
Textbook of Endocrine Physiology, 4th ed.
New York, NY: Oxford University Press; 2000. Horvath TL, Diano S, Sotonyi P, et al. G h relin and the regulation of energy balance-a hypothalamic perspective. Endocrinology. 200 1 ; 1 42:4 1 634 1 69.
Kahn CR, Smith RJ , Chin WW. Mechanism of action of hormones that act at the cell s urface. I n : Wilson JD, Foster DW, Kronenberg H M , Larsen PR, eds. Williams Textbook of Endocrinology. Philadelphia, PA:
WB Saunders Co; 1 99 8 : 5 5-94. Kelly RB. Pathways of protein secretion in eukaryotes. Science. 1 985 ;230: 2528.
M in-Jer T, Clark ]H, Schrader WT, O' Malley BW. Mechanism of action
CONCLUSION
of hormones that act as transcription-tegulatory f'lctors. In: Wilson J D, Foster DW, Kronenberg H M , Larsen PR, eds. Williams Textbook ofEn doerinology. Philadelphia, PA: WB Saunders Co; 1 998:55-94.
This chapter reviews the endocrine system with reference to osteo pathic philosophy and concepts. The picture that emerges is that osteopathy embraces endocrine physiology. The principles that direct the study and practice of osteopathic medicine might well have been formulated on the basis of a through understanding of endocrine physiology. Yet A.T. Still never studied endocrinology, for this is a new science, evolvi ng entirely during the 20th cen tury. Almost all of the endocrine information presented here is a product of the last few years of research and virtually none of this
Molitch M E. Neuroendocrinology. In: Felig P, Frohman LA, eds. Endocrinol ogy and Metabolism. New York, NY: McGraw-Hili; 200 1 : 1 1 1 - 1 7 1 . Sayers G, Portanova R. Regulation of the secretory activity of the adrenal correx: cortisol and corticosterone. In: G reep RO, Asrwood EB, eds. Handbook ofPhysiology, Section 7: Endocrinology. Vol 2. Baltimore, M D :
Williams & Wilkins; 1 975:4 1 53. Themmen APN, Huthaniemi, IT. M utations of gonadotropins and go nadotropin receptors: elucidating the physiology and pathophysiology of pituitary-gonadal function. Endocr Rev. 2000;2 1 : 5 5 1 -583. Theofilopoulos A N . The basis of autoimm unity. Part 1 : Mechanisms of aberrant self-recognition. Immunol Today. 1 99 5 ; 1 6:90-98.
PHARMACOLOGIC AND OSTEOPATHIC BASIC PRINCIPLES ROBERT J. THEOBALD, JR.
KEY CONCEPTS •
• • • •
Appreciate the development of pharmacology as a biomedical discipline, its importance in the history of medicine, and its relevance to A.T. Still's position on drug use Appreciate similarities between basic pharmacologic concepts and the basic principles of osteopathic medicine Understand and explain the differences of a reductionist view and a holistic view of biomedical science List several intrinsic and extrinsic factors that influence drug responses of an individual Be able to list and describe the pharmacologic phases of drug responses
This chapter is designed to provide the reader with appreciation of the relationship between the biomedical science of pharmacology and osteopathic medicine. The foundation of all medicine is a solid basic science education in which medical students learn the fundamental concepts of biomedical science. These concepts allow them to build on this foundation with clinical courses and training. During their basic science education, and while students learn about the concepts of osteopathic philosophy, structure function relationships, and the importance of homeostasis and body unity, they should begin to realize that the concepts of pharmacology and the concepts of osteopathy are similar. These concepts complement each other and other medical modalities. The concepts of osteopathy are concepts crucial to the practice of good medicine, to making sound clinical decisions, and to the integration of basic science and clinical science in the treatment of patients. For the reader to have a perspective of the relationship of phar macology and osteopathic medicine, it is necessary to provide some historical background of both disciplines and definitions of some basic terminology. The detailed history of both phar macology and osteopathic medicine would be better found in other volumes. References to both can be found in any library in any osteopathic medical school, or by visiting the website for the
Kirksville College of Osteopathic Medicine (www.kcom.edu) and the American Society for Pharmacology and Experimental Ther apeutics (ASPET, www.aspet.org). Pharmacology is a biomedical science that encompasses the study of substances that have po tential therapeutic and/or toxicologic activity in biological sys tems. There are subsets of the discipline of pharmacology in which studies are focused on specific classes of substances, such as chemotherapeutic agents, or on specific arenas, such as phar macokinetics. Pharmacokinetics is the study of how an organism affects substances, including absorption, distribution, biotrans formation, and excretion of the substance. Pharmacodynamics is the study how drugs affect an organism, how the drugs interact with receptors and second messengers, mechanisms of action, and other parameters of drug-organism interaction. Pharmaceutics is the science of drug preparation, including factors such as physical and chemical characteristics of a specific chemical entity. The scientific discipline of pharmacology is relatively new when considering the history of disciplines such as anatomy and physiology. The use of various plants and other natural substances in the treatment of disease has been occurring for millennia; how ever, an organized study of pharmaceutical agents by a discipline was an important advance. Historically, discovery and develop ment were based on folklore or observation, but today new drugs are mainly developed by organic chemists working with phar macologists using basic knowledge of molecular targets. Early scientists laid the groundwork for modern pharmacologic stud ies. A more complete listing is available on the Internet from ASPET. Among those notable scientists listed on the website are: Rudolph Bucheim (1820-1879), who established the first lab oratory dedicated to experimental pharmacology in Dorpat (now renamed Tartu, Estonid); Oswald Schmeideberg (1838-1921), who set up an institute of pharmacology in Strasbourg, France; J.N. Langley (1852-1925) and Sir Henty Dale (1875-1968), two scientists in late 19th century England, who pioneered phar macology using a physiologic approach; and John J. Abel (1857-1938), who established the first chair of pharmacology in the United States in 1891 at the University of Michigan. Abel, known as the "Father of American Pharmacol ogy", trained many U.S. pharmacologists.
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Modern research in pharmacology was accelerated during World War II, when the U.S. government established several programs, such as the wartime antimalarial program, and the ini tiation of strong analytical and synthetic chemical approaches in the discipline. Since then, biomedical science has expanded to encompass studies in many other areas, including neuropharma cology and cardiovascular pharmacology. In the era of medicine when A.T. Still was formulating and implementing his philosophy and principles of osteopathic medicine, the use of pharmaceuticals was routinely irrational and heroic. Mercurial compounds, quinine, and many other toxic compounds were commonly used for treatment of a variety of diseases with little or no basis in science (1). Still's distrust and disdain for drugs was a decision of safety and preservation for his patients because, in many instances, the treatments used were worse than the disease. As pharmacologic advances occurred, based on scientific study and thought, Still embraced therapy based on these studies and allowed a course in pharmacology to be presented in the osteopathic curriculum (1). As stated earlier, the basic concepts or tenets of osteopathic medicine are the foundations of the practice of good medicine. These tenets were recently readdressed in the Louisa Burns Lec ture presented by Felix Rogers, DO, at the 2001 American Osteopathic Association Convention (2). In his presentation, Dr. Rogers restated the tenets as follows: 1. A person is the product of dynamic interaction between body, mind and spirit; 2. An inherent property of this dynamic interaction is the capac ity of the body to maintain health and recover from disease; 3. Many forces, both intrinsic and extrinsic to rhe person, weaken this inherent capacity and contribute to the onset of disease; and 4. The musculoskeletal system significantly influences the body's ability to maintain this inherent capacity and to resist disease processes. From these Dr. Rogers espoused four principals of patient care. These principals revitalize and reemphasize the basic concepts of osteopathic medicine, refocusing them on the holistic approach to patient care. It is not in the scope of this chapter to provide a forum for discussion of the restatement of Still's basic tenets; therefore, this chapter will restrict focus to the original basic tenets of osteopathic medicine. Still's original basic concepts of osteopathic medicine were dis cussed in a paper by Korr (3) in the 1990s, in which he emphasizes the need to redirect basic biomedical research from a reduction ist view to a view more suited to investigation of the body as a whole unit. Korr states, "the reductionist paradigm is not unpro ductive . . . but it is incomplete" and "reductionist, mechanistic medical research fails to see that when illness occurs, whatever the affected part, it is illness of the person" (3). The logical corollary to this is the need for clinical medicine to treat the whole person, not just the diseased part. Korr further states that this "mechanis tic biomedical philosophy" believes "that the way to understand anything, including humans, their illnesses, and the origins of their vulnerability, is to take them apart; that is, to reduce them to their components, and to study these and their interactions as
minutely as possible" (3). The major problem with this view is the lack of appreciation of the effect of illness and treatment of illness on the whole organism, the total human body. This reduction ist view, held by many practicing clinicians, is contrary to basic concepts of pharmacology, and to the concepts of osteopathy. As Korr's paper implies, whatever the physician does to any parr of the patient, the physician also does to the whole body because the body is a unit whose parts respond to anything done to any parr. The osteopathic principles, body unity, homeostasis, and the relationship of structure and function, are mutually supportive of the basic principles of pharmacokinetics and pharmacodynamics. These pharmacokinetic and pharmacodynamic principles pro vide the basic foundation of our understanding of how the body deals with these drugs and how drugs work in the body. These principles complement osteopathy and the role of osteopathic manipulative treatment (OMT) similar to the way they comple ment other medical modalities. Use of drugs to treat an illness does not, and should not, preclude the use of OMT any more than it should preclude the use of other modalities, such as surgery. The role of the physician is to orchestrate the use of all appro priate interventions to the best advantage of the patient, always basing decisions on fundamental principles of osteopathy and of all good medicine. This chapter focuses on the basic principles of pharmacology, providing a basis for the student's understand ing of the similarities of pharmacology and osteopathy, and how pharmacology, OMT, and other medical modalities can be mu tually complementary. This chapter also discusses the interaction of these principles, illustrating that they are intertwined and must be considered together during any decision-making process. The most important pharmacologic concept to remember when considering the use of drugs is that of individualization of therapy. A major point in this concept is that physicians rrear people, whole people, and wharever rhey do to any part of a per son, they also do to the whole person. The body, as a unir, is comprised of many components and factors, some of which are intrinsic and some extrinsic, which affect responses to drugs and other medical interventions. To individualize drug therapy, one must be fully aware of these factors, both intrinsic and extrinsic, that are part of each person and inAuence any response to drugs. The intrinsic factors include characteristics such as age, sex, genet ics, health, race, and other factors inherent in a person's makeup. The extrinsic factors include characteristics such as occuparion, lifestyle (smoking, alcohol consumption, physical activity, erc.), diet, home environment, and other factors that may be altered, if necessary. These factors, found in Table 12.1, determine who rhe
TABLE 12.1. FACTORS RESPONSES
Intrinsic Factors
THAT
INFLUENCE
DRUG
Extrinsic Factors
Body weight and size
Diet
Age
Smoking
Sex
Occupation
Body composition
Lifestyle
Genetic factors
Physical activity level
Somatovisceral factors
Home environment
Physical health Psychological health
12. Pharmacologic and Osteopathic Basic Principles
patient is and inAuence how the patient will respond to any drug prescribed. These are the factors a physician must consider when choosing medication for any patient because that person is the composite of the exrrinsic and intrinsic factors. In other words, the body is a unit (one osteopathic principle) made up of these factors, each of which will be affected by whatever the physician does to the patienr. A second osteopathic principle states that the body has in herent self-regulatory, defensive, and recuperative powers. This principle is very similar to the phenomenon called homeostasis. Homeostatic mechanisms are a system of conttol mechanisms that use feedback loops to maintain stability of bodily functions. These mechanisms help the body self-regulate, provide defense against anything that triggers an untoward response, and help maintain a stable internal environment in which injured tissues can utilize the natural recuperative powers inherent in the body, described so well by Still (4). Many diseases, in fact probably all diseases, may be considered disruptions of homeostasis; that is, they are disruptions of the stability of activity or function of some system in the body. Discussion of homeostatic mechanisms is vital to understanding the effects of many drugs on the systems of the body. Drugs produce many effects throughout the body, changing levels of activity in organ systems; changes that stimulate reAex responses in the body, or sometimes blunt these responses. Drugs can also alter the environment in which an organ functions such that the body's reAex mechanisms, homeostatic mechanisms, can reclaim control of a malfunctioning system, reinforcing the con cept of body unity. The third osteopathic principle states that structure and func tion are reciprocally related. This principle is analogous ro the structure activity relationship described for many drugs. In the mid-19th century an English physician, James Blake, established the principle that the chemical structure of drugs determines their effect on the body (5). Fraser, another English physician, and Brown, a chemist, further defined the relationship between functional groups of drugs and the characteristics of the drugs (5). The concept of structure-activity relationships for drugs and their effects is vitally important to the understanding of the pharma cokinetics and pharmacodynamics of a drug, including adminis n'ation, distribution, biotransformation, excretion, and effect at specific receptor sites. The processes occurring with the adminis tration of a drug and the production of effects in a living system can be divided into three phases: (a) the pharmaceutical phase, (b) the pharmacokinetic phase, and (c) the pharmacodynamic phase. These phases are shown in Table 12.2. The pharmaceutical phase is the study of the relationship be tween the nature and intensity of the biologic effects observed and the different factors related to the nature of the drugs, such as the physical state, particle size, which salt is used, and so forth. These factors are important and affect the dissolution and disintegration of a drug after oral administration. In order to be absorbed into the body from the gastrointestinal (GI) tract, a drug must be dis solved in the aqueous contents of the stomach. For this to occur it must disintegrate from the tablet or capsule form. The impor tance of this area for pharmacology involves the assumption that drugs dissolve completely in the GI tract upon oral administra tion. The validity of this assumption involves consideration of differences in various commercial preparations. This factor must
191
TABLE 12.2. DRUG ADMINISTRATION AND EFFECTS Administration of drug
.j. Disintegration and dissolution of drug
I-Pharmaceutical
.j. Absorption Distribution Biotransformation Elimination
.j. Drug receptor interaction
.j. Drug effects
]
-Pharmacodynamic
be considered when choosing preparations for administration to patients. It is important in determining bioavailability of drugs that can be critical in certain clinical situations. Pharmacokinetics is the study of factors that determine the amount of drug at sites of biologic effect at various times after application of the drug to a biologic system. These factors deal with the concentration of drugs in the body as a function of time. Phenomena of absorption, distribution, biotransformation (metabolism), and elimination are considered by pharmacokinet ics; in other words, what the body does to the drug. In order to have any effect on the body, a drug must have access to the body and appropriate sites of action within the body, usually receptors. It must be absorbed in sufficient amounts to produce effective con centrations at the sites of action. Age, diet, blood Aow through the site of administration, and pH of body Auids at the site of administration are some of the factors inAuencing absorption. Distribution of the drug from the site of administration to the site of action is inAuenced by factors such as structure of the drug, binding of the drug to plasma proteins, pKa, and other factors. One important fact to remember is that only the portion of drug that isfee (not bound to or stored in some biological tissues, such as plasma proteins) is active and capable of producing an effect, of distributing and equilibrating in the body, of being biotrans formed and excreted. Termination of drug effects in the body occurs several ways, through redistribution to nonsites of action, biotransformation, and/or excretion. Remember that just because the effects of a drug are no longer apparent, the drug is not neces sarily excreted from the body, and that the clinical manifestation of effects that are expected are not the only effects of the drug. Pharmacodynamics is the study of biochemical and physio logical effects of drugs as they interact with the body at various levels of organization and systems in the body. Attention is fo cused on the characteristics of drugs; in other words, what a drug does to the body. The effects of a drug are the consequence of the interaction of the drug with structures in the body called re ceptors. This interaction occurs through the attachment of the drug to the receptor via some type of chemical binding, such as hydrogen or ionic or covalent binding. The interaction can oc cur because the structure of any given drug determines if it will bind to a specific receptor and if it binds, what type of effect it will have-agonistic or antagonistic. An agonist is a drug whose structure allows it to bind to its receptor and produce some action or effecr. An agonist is said to possess intrinsic activity. An an tagonist is a drug whose structure allows it to bind to its receptor
192
JJ. Osteopathic Considerations in the Basic Sciences
without producing an action or effect; it possesses no intrinsic ac tivity. This phenomenon of drug-receptor interaction exemplifies the osteopathic principle of structure-function relationships. The structures of the drugs and receptors determine their function. The student should also remember that many drugs are structural analogues of endogenous substances that have been isolated from the body and identified. Still strongly encouraged this when he said in his autobiography, "Man should study and use the drugs compounded in his own body" (6). In effect, that is what has been done. Structural analogues of endogenous substances have been synthesized and altered to have agonist or antagonist effects on specific receptors. Alteration of structure, for example, addi tion of an OH group or a methyl group, can produce an altered function, again exemplifying the basic osteopathic principle that structure and function are intimately related. Recent examples of this include immunologic agents, such as the interferon ana logues, and the prostaglandin-based antisecretory/cytoprotective agent, misoprostol. Most drug effects, but not all drug effects, are mediated through receptors. Receptors are proteins or protein-related struc tures in membranes that link drugs to intracellular functional sys tems through signal transduction mechanisms. The interaction of receptors and signal transduction mechanisms are varied and include receptors coupled to ion channels, receptors coupled to G-proteins, receptors linked to tyrosine-kinase, and intracellular steroid receptors interacting with specific target DNA elements. Nonreceptor-mediated drug actions include mechanisms such as drug interaction with small molecules (e.g., chelation, or gastric acid neutralization) and inhibition of enzymes (e.g., inhibitors of angiotensin-converting enzyme). It is important to remember that although drugs are classified by a major mechanism of ac tion, such as a-adrenergic receptor antagonists, drugs may have other mechanisms of action and all drugs have multiple effects. It may be best to address the interactions of osteopathic and pharmacologic principles individually. For example, when con sidering treatment for a patient with a central nervous system (CNS) disorder that requires medication that will enter the CNS, the physician must consider the structure-function relationship of the tissues involved and the structure-activity relationship of any drug being considered. The blood-brain barrier, a barrier that restricts polar molecules from entering the brain readily, protects the brain from severe toxic effects of drugs like peni cillins or tubocurarine. The structure of the cerebral capillaries has an essentially continuous layer of endothelial cells with tight gap junctions that form the barrier. The blood-brain barrier is neither absolute nor invariable. Very large doses of drugs, such as penicillin, will cross the barrier. In addition, inflammation of the barrier lessens its effectiveness. Also by knowing that the barrier allows small molecules and lipid-soluble molecules to enter the CNS much more readily, the physician can choose a drug with those characteristics. A drug like succinylcholine, a neuromus cular blocking agent used as an adjuvant in surgery, possesses a charged ion in its structure, is not very lipid soluble, and therefore, does not readily cross the blood-brain barrier. However, a drug like thiopental, a barbiturate that is highly lipid soluble, enters the CNS so rapidly that it produces effects within seconds after an intravenous administration of sufficient dose. Subsequently, be cause of its lipid solubility, thiopental rapidly leaves the CNS and sequesters in other lipid tissues that are not sites of action, such as
adipose tissue. This termination of effects is due to redistribution of the drug away from the site of action. Structure-activity relationships are also important when con sidering drugs that readily sequester in certain tissues for clinical effect. In treating a patient with a lower urinary tract infection, several factors must be considered when choosing an appropri ate antimicrobial agent. First, the antimicrobial agent must be effective against the infecting organism. Second, and of key im portance here, any pharmacologic agent used must concentrate in the urine in large enough levels to provide adequate antimicro bial activity. Structural characteristics of pharmacologic agents influence mechanisms of termination of effects and clearance of the drug from the plasma. Agents such as sulfonamides and trimethoprim are rapidly cleared into the urine, providing ample concentrations in the urine for antimicrobial activity. Drugs such as minocycline and doxycycline do not concentrate in the urine and therefore would not be appropriate choices for treatment of lower urinary tract infections. Considering the interactions of osteopathic and pharmaco logic principles in this manner should help the student un derstand the interrelationship; however, the student should remember that these principles need to be integrated so that as a physician, one can provide a comprehensive approach to caring for each individual patient. It is the intention of the author that the following discussion of hypertension will provide an example of the interrelationships of the principles. The etiology of primary hypertension, although not clearly understood, apparently involves an initial increase in cardiac out put (7). This increase in cardiac output increases blood flow to tissues, which, in turn, causes a compensatory autoregulation at the tissue level. The autoregulation involves a twofold action; a functional autoregulation produces a vasoconstriction that will decrease flow to the tissue while a structural autoregulation causes hypertrophy of the vessel wall that amplifies any vasoconstric tor activity or stimulus, such as sympathetic nerve stimulation. The structural change, hypertrophy, contributes and amplifies the functional change, vasoconstriction, producing an even greater elevation of blood pressure (8). This interaction of structure as an amplification of the functional change provides support for the osteopathic tenet involving structure and function relationships. The structural change, vascular hypertrophy, is not solely re sponsible for the elevation of blood pressure, but it is an important contributor and, in fact, may be the autoregulatory component responsible for the chronic elevation of blood pressure seen in hypertension (7). Understanding this chronic role of hypertro phy may lie in consideration of the concept of down-regulation of receptors that are under chronic neurotransmitter stimulation. However, that may be a tangential issue here. The basic concept is that some trigger, unknown perhaps, creates a change that pro duces a structural/functional alteration in vascular smooth muscle resulting in an abnormal homeostatic level of blood pressure. Treatment of hypertension with pharmacologic agents alters this abnormal state and attempts to return blood pressure to a "normal" level, that level which would be maintained by the body's own homeostatic mechanisms, if they were functioning properly. The pharmacologic intervention provides several ben efits. During the time of pharmacologic maintenance of blood pressure, there is some evidence that the hypertrophy of vascular smooth muscle regresses, leading to a decrease in blood pressure
12. Pharmacologic and Osteopathic Basic Principles
(7). This again supporrs rhe osreoparhic rener rhar srrucrure and funcrion are relared. A decrease in muscle mass leads ro a decrease in muscle rension and a decrease in blood pressure. Evidence is also emerging rhar afrer some period of rime, pharmacologic in rervenrion may be decreased or sropped complerely because rhe parienr's own homeosraric mechanisms become capable of nor mal regularory conrrol of blood pressure, eliminaring rhe need for pharmacologic inrervenrion. Therefore, rrearing hyperrension wirh pharmacologic agenrs is nor in conrrasr ro rhe osreoparhic rener rhat describes rhe body's self-healing porenrial, it acrually supports this and may provide benefit similar ro OMT, where a rreatmenr regimen, in addition ro other benefits, provides an opporruniry for rhe body ro heal irself. In this insrance, the body's homeosraric mechanisms are allowed ro regain proper conrrol of blood pressure because rhe pharmacologic agenrs mainrain blood pressure ar rhe appropriare level while rhe self-healing actions of rhe body occur; in this insrance, rhe decrease in vascular smoorh muscle mass. Addirionally, OMT has been shown ro decrease hypersymparhetic rone, decrease roral peripheral resisrance, and affecr rhe renin-angiorensin-aldosrerone sysrem (9). Therefore, appropriare OMT in conjuncrion wirh pharmacologic rherapy could hasren rhe rerurn of normal funcrion of rhe body's au roregularory sysrems. Prior ro iniriarion of pharmacologic rrearmenr of hyperren sion, several poinrs musr be considered in lighr of rhe principles of viewing rhe body as a unir and individualizarion of rherapy. Firsr, the cause of rhe hypertension should be fully invesrigared, determining if rhe hypertension is primary or secondary. If any facrors are presenr rhar rend ro raise blood pressure, such as smok ing, rhen rhese facrors should be eliminared or ar leasr modified ro lessen rheir inAuence. Second, when rrearing very high blood pressure, rrearmenr should begin wirhour delay; however, overag gressive rrearmenr may be risky and should be done wirh exrreme care. Ir is importanr in trearing parienrs wirh very high blood pressure ro lower blood pressure gradually so rhar hyporension does nor result. Third, trearmenr of hypertension requires a long rerm, perhaps lifelong, relarionship berween rhe parienr and rhe physician. Physicians need ro reassess parienrs periodically ro de rermine if pharmacorherapy is srill necessary and, if so, is srill effecrive. The reassessmenr should be an evaluarion of the rotal parienr, wirh rhe aim being ro find a rherapeutic regimen, includ ing a drug or combinarion of drugs, thar lowers blood pressure effecrively, rhat is not conrraindicated in any way, and rhat may be posirively helpful in orher ways. These poinrs have been adapted from EO. Simpson's chaprer on hypertensive disease in Averys Drug Treatment (10). Drugs used ro trear hypertension fall inro several classes, including diurerics, ,a-adrenergic recepror blocking drugs, a-adrenergic recepror blocking drugs, adrenergic neuron block ing drugs, cenrrally acting a-adrenergic agonists, calcium channel blocking drugs, direcr acring vasodilarors, angiorensin converting enzyme inhibirors, and ganglionic blocking agenrs. Choice of which agenr ro use depends upon fully evaluaring rhe parienr, including all facrors listed here. For example, use of a ,a-adrenergic recepror blocking drug, such as propranolol, would be effecrive in lowering blood pressure. However, consid eration must be given ro mher facrors, such concurrenr diseases. Blockade of ,a-adrenergic receprors can exacerbare symproms of orher diseases, such as congestive heart failure, peripheral vascular
193
disease, bronchial asrhma, or chronic obsrrucrive pulmonary dis ease. Some of these agenrs could also inrerfere with the conrrol of diabetes because of blockade of ,aradrenergic receprors, while other agenrs with inrrinsic sympathomimeric activiry could ag gravare anginal symproms or increase risk for parienrs wirh a previous myocardial infarction. These agenrs are also known ro cause sexual dysfunction in some men. This indicates the need ro consider sex and age facrors in clinical decisions, as well as making counseling available prior ro and during the use of rhese agenrs in male parienrs. Orher antihypertensive agenrs, such as the adren ergic neuron-depleting agenr, reserpine, cross the blood-brain barrier and can cause CNS side effecrs like depression and seda tion. Considerarion of lifesryle musr be made when agenrs such as rhese are parr of rhe clinical armamenrarium. If a patient lives alone and must be self-sufficient, such as in rhe case of many older adulr patienrs, then agents rhar cause depression and seda tion may be parricularly dangerous. Prescribing other agenrs with no or less CNS side effecrs would be a bener choice. It should be apparenr that in making pharmacologic decisions, the total patienr must be considered. The physical, menral, and spirirual aspecrs of rhe parienr musr be known because rhe physician does not rreat just rhe hypertension, rhe physician trears the whole pa tient. The inrrinsic and extrinsic facrors listed in Table 12. J are jusr a checklisr, a beginning for rotal patienr evaluation. In summary, the physician musr remember rhat pharmaco logic rherapy does not preclude rherapy with orher modaliries, especially osteoparhic modaliries, and can be effectively inregrared inro an osreoparhic approach for rhe rrearmenr of disease and dysfunction. Ir must be undersrood rhar rhe principles of os reoparhy and pharmacology are murually supporrive and are, in realiry, very similar. Individualization of rherapy and undersrand ing body uniry, should be rhe framework of all clinical decisions. Do what is besr for rhe parienr, rhe whole parienr, and remember rhar wharever drug you give, or rreatmenr you apply ro any parr of the body, you are administering to the whole body.
REFERENCES J. Lane MA. In: A. T Still Founder of Osteopmhy. Kirksville, MO: The Journal Printing Company; J 926:7-8;52. 2. Rogers, FJ. Building on rradition. Louisa Burns Lecrure, Oerober 23, 2001. 3. Korr 1M. Osteopathic research: the needed paradigm shifr. jAOA. 1991;91 (2):156-17 J. 4. Still AT. In: Schmucker RV, ed. Early Osteopathy in the Word.. of A. T Still, 36. Kirksville, MO: Thomas Jefferson Universiry Press, Northeast Missouri State Universiry; J 99 J. 5. Levine RR. Pharmacology: Drug Actions and Reactions, 4rh ed. Bosron, MA: Litrle, Brown and Co; J 990: J2. 6. Still AT. Autobiography of Andrew T Still. Published by the author, Kirksville, MO; J 908:89. Reprinted J 98 J, by American Association of Osteopathy, Indianapolis. 7. Onrot J, Rangno RE. Treatment of cardiac disorders: hypertension. In: Melmon KL, Morrelli HF, Hoffman BB, Nierenberg OW, eds. Melmon and Morrelli's Clinical Pharmacology: Basic Principles in Therapeutics New York: McGraw-Hili, 3rd ed. 1992:52-83. 8. Folkow B. Early structural changes. Brief hisrorical background and principale nature of process. Hypertension. 1984;6[Suppl 3]: J -3. 9. Mannino JR. The application of neurologic reAexes ro the treatment of hypertension. jAOA. 1979;79( I 0):225-23 J. J O. Simpson FO. Hypertensive disease: In: Speight TM, ed. Avery's Drug Treatment, 3rd ed. Oxford: Blackwell, J987:676-73 J.
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OSTEOPATHIC CONSIDERATIONS IN THE BEHAVIORAL SCIENCES
INTRODUCTION JOHN A. JEROME
During the last century, the leading causes of death were diseases such as influenza, tuberculosis, pneumonia, diphtheria, and gas trointestinal infections. "Since then, the yearly death ratefrom these diseases per 1 00, 000 people has been reducedfrom 580 to 30!" (1) . Today t h e major causes of premature death a n d disability resul t from behavioral factors, such as accidents and violence, or long standing habi ts, such as smoking, high-fat diets, lack of routine exercise, stress, and alcohol abuse (2) . The World Health O rgani zation and Harvard School of P ublic Health both predict that by 2020 , in the developing countries where four-fifths of our planet's people will l ive, seven out of ten deaths will be traced to lifestyle factors setting the stage for ischemic heart disease, depression, and chronic obstructive pulmonary diseases. In fact by 2020 tobacco alone is expected to cause more premature death and disability than any single disease (3) . Future improvements in health will come from managing the effects of unhealthy behaviors (4). From an osteopathic perspective, the behavioral sciences are the clin ical and scientific application of biophysical knowledge to the understanding and treatment of health and illness. Signs and symptoms of various types represent behavioral and physiologic imbalances and breakdowns in a patient's effort to adapt to and cope with change. Osteopathic philosophy is deeply rooted in the belief that balances of physical, mental, and social systems are necessary for health. When one system is stressed or altered, the structure and function of other systems are stressed and altered as well. T he primary care physician sees the repercussions from this imbalance as the signs and symptOms of physical and behavioral illness. Somatic dysfunction and neuromusculoskeletal changes are common examples. All patients with physical illness of any kind have an emo tional reaction to the illness. Over half of all patients in the United States with emotional problems are treated solely by a pri mary care provider (5). During treatment, they use approximately
twice as much routine medical care as those without psychological problems. The goal of this section on behavioral sciences is to add cl ini cal and scientific knowledge to the understanding and treatment of the patient as a unit of body, mind, and spirit. These chap ters present some behaviorally based strateg ies for helping pa tients manage their physical health, thinking patterns, emotional condition, and levels of functioning in relationships within the context of the patien ts' social and cultural environment. Osteopathically oriented patient care bases parr of its phi losophy on the understanding that these biophysical factOrs are interrelated and interdependently li nked with disease and illness; a patient's health should be an optimal balance of physical, men tal, emotional , and spiritual well being. This balance is achieved through a collaborative partnership based on truSt and active communIcation.
REFERENCES
I.
Cenrers for Disease Conrrol and Prevenrion. Ten Leading Callses ofDeath
in the United States, 1977. Washingron, DC: Governmenr Publishing Office; 1994. 2. Narional Cenrer for Healrh Statistics.
Health of the United States.
Hyansville, MD: Public Healrh Service; 1990. 3. World Health Organization. Murray J L, Lopez AD, cds. The Global Bur
den of Disease and Global Health Statistics. Cambridge, MA: Harvard University Press; 2000:389-940. 4. Shapiro S, Skinner EA, Kessler LG, et a1. Utilizarion of health and men ral healrh services: rhree epidemiologic catchment area sires. Arch Gm
Psychiatry. 1984;41 :971.
5. Hankin J, Oktay JS. Mental Disorder and Primary Medical Care: An Analytic Review of the Literature. Rockville, MD: Government Printing Office; 1979. Narional Insritute of Mental Healrh, Series 0 No. (ADM) 78-661.
HEALTH PROMOTION AND MAINTENANCE CERALD C. OSBORN
KEY CONCEPTS • • • • • • • • • • •
Impact of lifestyle and behavior on hea l th and illness The importance of nutrition and health, i ncluding food pyramid P hysical activity, and effects on disease a nd weight O besity and disease, weight control and fi tness Substance use, abuse, and treatment, including tobacco, a lcohol, and illegal drugs Personal safety, es pecially i n a utomobiles and homes Safe sex ua l practices Healthy families a nd work satisfaction Str ess anticipation and self-regulation Importance of personal suppor t s ys tems Doctor-patient relationship, a nd s trategies for communication and change
Historians of medicine describe in detail the dramatic changes that have taken place in medical education, practice, r esearch, and technology in the 20th century. All agree that these changes in our system of health care have traded shor t-term mortaliry for long-term morbidi ry. It is ironic, however, that o ur moder n high- technology advances in acute medical care have done little to improve overall human survival. At the beginning of the 20th century the average life ex pectancy was 47 years . By 1994, life expectancy dramatically increased to 7 1.4 years for men and 78.4 years for women (1). A recen t epidemiologic study, the C lobal Burden of Disease (C B D ) , based upo n a very sophisticated ana lysis and more ega li tarian princi ples , sets life expectancy standards at 82.5 years for women and 80 years for men (2) . These increases are mostly attributa ble to a drastic reduction in infant mortaliry. Overall mortaliry has decreased because of effective public health meas ur es aimed at disease prevention for large populations, not beca use of high technological medical procedures aimed at individuals. These fundamental preventive meas ures include those tha t provide us with clea n air and wa ter, high-qualiry affordable food, and safer
wor k environments. Addi ng to this i ncreased s urvival expectancy is a pharmaceutical industry providing us wi th immunizations to prevent the most common acute infectious diseases and wi th anti bioti cs to treat those infections we fail to prevent. Further strides in improving the long-term hea l th of our patients depend on unders ta ndi ng the major impact of lifes tyle and behavior on health and illness . This i nvolves educating o ur patients, encour agi ng their active par ticipation in and cooperation with hea lth maintenance, and motivati ng them to make choices that promote healthy, vigorous, and enjoyable lives. Aging is i nevitable, but for most people, ill health is not. Assisting patients to live long a nd live well does not mean em phasizing prevention while neglecting high technological research and practice. Research and the development of new technologies are permanent and vital components in the conti nuum of health care. Helping patients to live longer and better does mean, how ever, tha t new preventive health care m us t be given at leas t eq ual status i n the medi cal educa tio n and practice of the future if os teopathic physicians are to make a significant di fference in the overall health of the population. The C B D represents the most current and profo und study surveying health, injur y, and illness worldwide. This i nvestiga tion is a long-term collaborative effor t by the Harvard School of Public Health, the Wor ld Health Organizatio n, and the World Bank Croup. Mortaliry data are very im por tant but epidemiolo gis ts have always known that mortality s tatis tics a lone provide an i ncomplete picture of the impact o f illness . Mortaliry is easy to defi ne a nd meas ure; mor bidi ty is not. The C B D study has come closest to providing the more com plete picture health policy plan ners need by developing the co ncept of " Disability-Adjusted Li fe Years" ( DALy) . This ma nner ofstudying the impact ofillness goes beyond the factOrs that contribute to death a nd adds a method to determine which illnesses rob people of fulfi lling and productive lives . The C B D i dentifies and confirms a number ofs tartling and dramatic shifts i n the patterns o fdisease worldwide, allowing clear comparisons to be made between mature market-economy "de veloped" and developing nations. Since the C BD's data sets begin i n 1990 and project to 2020 and its current data are so accurate, it provides a reliable road map i ntO the future. One of the s ur prising trends clear ly shows that developing nations are movi ng more tOward the patter ns o f developed o nes today. Noncommu nicable diseases s uch as depression and hear t disease are ecli psi ng
II! Osteopathic Considerations in the BehavioraL Sciences
198
pas t threats like infectious disease and malnutrition. Consider i ng disability as well as mor tality, the G B D also demonstr ates the formerly underes timated burden of mental illness. Even back i n 1990, the data show that psychiatric conditions (unipolar depres sion, alcoholism, bipolar disorder, schizophrenia, and obsessive com pulsive disorder) accounted for fiv e of the top ten leadi ng causes of disability wor ldwide. The burden of mental illness is even higher in developed nations and the trends con ti nue in an alarmi ng direction. It is also s triking to note the complex inter locki ng nature of behaviora l risk factors and many diseases. The most common behaviors i nvolved with disease and ill health are tobacco use, alcohol use, and unsafe sexual practices. The G B D predicts that b y 2020 the burden o f illness b y tobacco use alone will out weigh any single disease. Complicating things fur ther, some diseases predispose to others (e.g., hyper tensio n and dia betes i ncrease the risk of hear t disease and peripheral v ascular disease). These noncommunicable diseases are highly infl u enced by li fes tyle and health habits. Osteopathic physicians committed to comprehensive care m us t place more focus upon effective behavioral change to improve upon the health care we deliver. G enetic therapies offer exciting possibilities to correct basic de fects involved wi th noncommunicable diseases, but these treat ments remain far i nto the future. For the foreseeable future we m ust continuously improve our present model of treatment, and this i ncludes li festyle a lter ations . We simp l y m ust pay more atten tion to self-imposed behavioral risks. Focusing upon "the basics" proven by com pelling data will assis t our patients to live long and live well.
TABLE 13.2. CHANGE IN THE RANK ORDER OF DISEASE BURDEN FOR 1S LEADING CAUSES, WORLDWIDE 19902020
Disease burden measured in Disabil ity-Adjusted Life Years (DALYS)
1990
2020 (Baseline Scenario)
Disease or injury
Disease or injury
Lower respiratory infections
Ische m i c heart d isease
Diarr heal diseases
2 Unipolar major depression
Conditions arising during the perinatal period
3 Road traffic accidents
Unipolar major depression
4 Cerebrovascular disease
Ischemic heart disease
5 Chronic obstructive pulmonary d isease
Cerebrovascular disease
6 Lower respiratory infections
-+--¥-��7'
Tuberculosis
Tuberculosis
Measles
8 War
Road traffic accidents
9 Diarrheal diseases
Congenital anomalies Malaria
11 Conditions arising during the perinatal period
Chronic obstructive pul monary d isease
12 Violence
Falls
13 Congenital anomalies
Iron-deficiency anemia
14 Self-inflicted injuries
Protein-energy malnutrition
15 Trachea, bronchus, and lung cancers
16
NUTRITION
Science verifies Oscar Wilde's aphorism: "You are what you eat. Issues regardi ng nutrition need not generate the contr oversy and confusion so often portrayed i n the popular media. Al though controversies do exist, scientific nutritionists agree far more often than they disagree abour what consti tutes a healthy diet. Re search consistently demons tr ates that what people choose to eat is key to their general well being as well as to specific illnesses, especially cardiovascular disease, neoplasti c disease, diabetes, and osteoporosis (3 ,4) (Tables 13 .1 and 13.2). A diet consisting of the most currently determined proportions of protein, carbohydr ate, and fat can r adically improve one's over al l level of health.
"
TABLE 13.1. THE LEADING CAUSES AND PERCENTAGES OF ALL DEATH IN THE UNITED S TATES
1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Heart d isease Cancer Stroke Bronchitis and emphysema Accidents Pneumonia and influenza Diabetes m e l l itus HIV infection Suicide Chronic liver diseases
Reprinted with perm ission from Report on Nutrition and Health,
32.1% 23.5% 6.8% 4.5% 3.9% 3.6% 2.4% 1.6% 1.4% 1.1%
The United States Surgeon General's
1994.
More useful than the former " Four Food Groups," which most patients lear n in elementary school, is the more up-to-date " Food P yramid" ( Fig. 13.1). The food pyramid helps clarify the newer and healthier proportions of proteins, carbohydrates, and fats in a more unders tandable visual constr uct. The typical American diet after World War I I has been about right in the amount of protei n, overly generous i n simple carbohydrates and fats, and too meager i n com pl ex carbohydrates. The food pyr amid helps guide patients toward these newer and healthier proportions (Table 13 .3). A simple readj ustment of these proportions to current recom mended levels offers significant protection from the development of cardiovascular disease and neoplas tic i llness (5). Fur ther read j ustment, encouraging foods lower in sodi um and richer in cal ci um and potassium, offers protection agai nst osteoporosis and hyper tension. Even patients who develop hyper tension despite following these dietary recommendations experience better control with m ul timodal treatment, whi ch i ncludes becomi ng more aerobi cally fit and moderating alcohol use, along wi th the most current pharmacologic care (6 ) .
13. Health Promotion and Maintenance
199
Food Guicle Pyramid A Guide to Daily Food Choices
Fats, Oils
Be
KEY • Fat (naturally occurring '" Suga/s and added) (added) TheW aymbolt Ihow fat., 0111 and added sugars In foods.
Sweets
USE SPARINGLY
Meat, Poultry, Fish,
Milk, Yogurt
Be
Dry Beans, Eggs,
Cheese
Be Nuts Group 2-3 SERVINGS
Group
2-3
SERVINGS
FIGURE 13.1.
Use the Food Guide Pyramid
to help you eat better every day ...the Di Fruit
Vegetable Group
3-5
2-4
SERVINGS
Group SERVINGS
etary Guidelines way. Start with plenty of Breads, Cereals, Rice, and Pasta; Vegeta bles; and Fruits.Add two to three servings from the Milk group and two to three serv ings from the Meat group. Each of these food groups provides some, but not all, of the nutrients you need. No one food group is more important than another
Bread, Cereal, Rice
Be
Pasta
on fats, oils, and sweets, the foods in the
Group
(Reprinted with permission from U.S. Department of Agri culture. H u m a n Nutrition Information Ser v i ce, Aug u st 1992. Leaflet No. 572.)
6-11 SERVINGS
PHYSICAL ACTIVITY
Modern science cons is tently shows that a healthy life is an ac tive life. Although the popular media prov ide many s rories abom people who compulsively exercise, these s rories teach us noth ing beyond the obvious consequence of fanaticis m in any health endeavor. Health researchers in this area agree that higher levels of physical activ i ty delay all-cause mortality primarily because of lower rates of cardiovascular disease and cancer. Thei r research also shows that physical activ i ty is inversely associated with mor bidity as well as mortali ty. A comprehensive prospective s rudy of physical activ ity and its relations hip ro health and specific illnesses demons trates that the risk of all-cause and cause-s pecific mortal i ty decli nes across physical fi tness qu i nti les from the leas t fit ro the most fit in both sexes (7) . These trends remain even after s ta tistical adjus tment for facrors such as age, s moki ng, cholesterol levels, paren tal hisrory of heart disease, and follow-up i nterv als.
TABLE 13.3. PERCENTAGE OF DAILY CALORIES CONSUMED
P ro te i n Complex carbohydrates Simple carbohydrates Unsatu rated fats Saturated facts Ada pted from Pfeiffer
GJ.
Typical American Diet (%)
Recommended Diet(%)
15 20 25 25 15
15 40 15 10 20
Taking Care of Today and Tomorrow. A Resource
Guide for Aging and Long- Term Care. Reston, VA: The Center for Corp orate Health Promotion,
1989.
for good health you need them all. Go easy small tip of the pyramid.
Like nu trition, the basic princi ples of exercise are s traightfor ward and easy to u nders tand for most people. Becoming more fi t through exercise prov ides many benefits, which include reduc ing risk of cardiovascu lar disease, os teoporos is , and non i nsu lin dependent diabetes. General benefi ts of regu lar moderate exercise also i nclude a reduction in feelings of anxiety and depress ion and even Improvement 111 I m mune res ponses. The most important principle to emphasize regardi ng exer cise is fu n and enjoyment. If all physicians wou ld encourage their patients to pursue enjoyable physical activ ities , these ac tiv i ties wou ld more likely become a component of a health ier lifes tyle. Most people find exercise more enjoyable when paired with a social activity. Therefore, phys i cal activ i ties that can be shared with fam ily, friends, and colleagues are more likely to be conti nued as a part of ordinary social lives. The other i m portant general pri nci ples include common sense, bal ance, and variety. The most sys temically healthfu l types of phys i cal activity are those that are aerobic. Aerobic exercise gen erally i nvolves sus tained, comfortable, su bmaxi mal effort as op posed to anaerobic, short-burst, quickly exhausti ng, "spri n t s tyle" aC( Iv I tles. Patients beginning an exercise program are encou raged to s tart slowly, regardless of i n i tial level of fi tness , and then i ncrease thei r activity gradually. Most patients d o n o t need cardiac s tress tes ts o r expensive, highly technical sports medici ne evaluations prior ro s tarting an exercise regimen. Patients should begin at a comfort able point cons istent with their age and overall fitness level. They should then gradually i ncrease ro their self-determined level of m aximal fu n and enjoyment. Gentle srretching before warming u p and after cooling down will prevent inju ry, speed u p pos t exercise recovery, and decrease the probability of delayed muscle
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III. Osteopathic Considerations in the BehavioraL Sciences
soreness. It will also i ncrease the likelihood of patients continuing their fi tness programs. Amer i cans s pend appr oximately $8 billion per year on health s pas and exercise clubs (10). While this may add ro their so cial enjoyment, becom i ng more fi t need not be ex pensive. The most impor ranr ex penses for any exercise program i nvolve h av ing proper shoes and safery equipment (such as a helmet for bicycling and wris t braces and elbow and kneepads for inline skating) rec ommended for the patients' selected activiry. Careful arrention m us t be paid ro clothing when exercising in hot or cold weather. This is es pecially tr ue for o lder patients because of the increased r isk of heat s troke, heat exhaustion, and hypotherm ia. Functional and protective cloth i ng are essential . Sryle is optional. Other pro tective equipment impor rant for safery involves protection from the sun. Good qualiry s unglasses and sun block should be a par t of most outdoor exercise equ i pment kits. L i kewise, adequate hydra tion is extremely impor tant. For aerobic exer cise lasting less than one hour, cool water is gener ally sufficient. For longer periods of exercise or in hot, h um i d condi tions , any of the popular "spor ts dr inks" provide im por rant additional glucose and electrolyte r e placement, preventi ng dehydration and speeding up pos texercise recovery.
OBESITY
It is ironic that, along wi th the current emphasis on health and fi tness, an increas i ng number of Americans are obese (11). Health researchers and physicians engage in vigorous debate over the relative r is ks of being mildly ro moderately over weight. They agree, however, that as patients become increasingly over weight, their health risks also incr ease. Both cross-sectional and cohor t s tudies s how associations between obesiry and hyper lipidemia, hyper tension, and hyper i nsuli nemia. These lead co the increased prevalence of coronar y artery disease and noninsulin-dependent diabetes melli tus (12-15). Some rypes of cancer, degenerative j oint disease, s leep apnea, gout, and gallbladder disease also more prevalent wi th increas i ng obes i ry (16-18) . An addi tional irony is that the caloric-res tr iction dietary treat ments for obesiry so often recommended are i neffective over time. Surveys of current literature indicate that dietary treatm en ts alone do not work; some are detr imental and even dangerous . Recent s urveys illus tr ate the complex iry of the dilemma (10-19). The definitive cr i ter i a for a r isk/benefit analysis of the r is k of obe siry and the risks of weight loss diets are yet ro be determined. The current approach co the problem is co suspend the singular concern for weight alone and focus on the over all level of fitness regardless of weight. When patients ask about weight loss, the physician should include a com plete discussion about physical fi tness. The detri menral and ultimately i neffective res ul ts of caloric-res triction di ets should also be em phasized. Patients should be frequently r e minded that nutr i tious food in the propor tions shown in the food pyram id is the necessary fuel for healthy phys ical activiry and basic body functions. Healthy eating, not caloric restr iction, and daily aerobic activ iry are the cornersrones ofliv ing long and living well. In the U.S., weight-loss i ndustry estimated at nearly $30 billion is s uppor ted more by the widespread An1erican social s tigma
roward obesi ry rather than by a concern for health. Confronting Out own aes thetic prejudices and those of our patienrs is an ex cellent place ro s tar t when it comes ro weight management. The aesthetic ideal most often promoted by the adver tisement and fashion indus tries is sim ply unrealistic for most people (J 0). Following scientifically corroborated principles related co fit ness is the best adv ice for the foreseeable future. Exciting research into the genetic controls i nvolved i n hunger, satiery, and lipid metabol ism continues, but new clinically applicable treatments remain far in the future (20). In the meantime, physicians who deem phasize weight and em phasize fi tness wi ll serve their patients best. Literature wri rren by exercise physiologists for laypeople emphasizes these points and is available co augment physicians' advice and counsel (21).
SUBSTANCE USE AND ABUSE
Popul ar media arrention and rancorous political debate tend co focus on i llegal s ubstance abuse. Yet two legal subs tances , cobacco and alcohol, contribute more co the miser y and ill health of our patients than do all the illegal s ubs tances com bined. Focusi ng on those legal s ubstances that constitute the most significant health hazards co our patients is central co primary care practice. Public heal th research on the marrer is clear, despite political debate clouding the iss ues about the dangers of subs tance abuse. Tobacco
The 1989 United States HeaLth and Prevention ProfiLe, published by the Centers for Disease Control (CDC), does not equivocate: Cigarette smoking is the singLe most preventabLe cause of death in our society." The firs t Surgeon GeneraL's Report on Smoking was
"
published in Januar y 1964 . It created ins tantaneous, j ustifiable worldwide shock. The second report was issued in Januar y 1979 . What the Secretary of Health, Education, and Welfare, Joseph Califano, wrote in that repor t's preface was even more forceful: "[TJhis document reveals with dramatic clarity, that cigarette smok ing is even more dangerous-indeed, far more dangerous-than was supposed in 1964." Smoking cessation is so cr itically importanr
that the predictions of the G B D need co be repeated here. " By 2020 cobacco is expected co ki ll more people than any si ngle disease, s urpassing even the H IV epidem ic." The message co our patients m ust be clear, consis tent, and firm: " I f you don't smoke, please don't ever s tarr; if you do, pLease stop!" This is clearly more easily said than done, but acting as an agent of change co promote smoking cessation among our pa tients, might be the bes t thing we, as physicians, ever do for our patients and their families. The vast major iry of those who have scopped smoking have done so on their own, without for mal or profess ional help of any ki nd (mos tly by the "cold turkey" tech nique). The rest have required some level of professional guidance or a specific program. The following are some useful methods the physician can s ugges t co help patients scop smoking (22) . 1 . Declare a date co scop and make it publ ic. A wr itten statement, including a request for the supporr and encouragement offam i l y, friends , and co-wor kers , is a good idea. An advertisement
13. Health Promotion and Maintenance
declar ing one's intent to stop smoking can even be taken out in a local newspaper. 2. Prepare to quit by making effor ts to mini mize s tress , eat health ier than before, and begin a gradual and systematic ptogram of physical fi mess. 3. Attend to nicotine withdrawal by smoking fewer cigarettes per day, or only smoking a portion of each cigarette before extin guishing it; switching to a different low-tar and n icotine brand of cigarettes after each pack; never buy i ng more than one pack at a ti me; and conti nuing the gradual weaning process . 4. Stop learned smoking behavior patterns by waiting at least 10 minutes before lighting up when the crav ing begins; dis tracting attention from the crav ing to light up by us i ng only the non dominant hand to hold a cigarette and setting the cigarette down berween puffs; lock up the pack of cigarettes berween smokes . 5. Think in terms of one-day-at-a-time. Rather than thinking that smokingwill never again be an option, concentrate simply on not smokingfor one day. O ne day is easier to manage than a lifetime. 6. Stay pos itive and think of the endeavor as life enhancing rather than as a sacr ifice. On the quitting date and thereafter : 1.
Make sure all cigarettes are gone.
2. Build in rewards: money that would have been s pent each week on smoking can be placed into a s pecial savings ac coun t. Spin-off savings can be banked, too, if one considers the replacement/repair cos ts of clothes, fur niture, and car in ter iors damaged by cigarettes. The cost of at leas t one v is i t to the doctor for a smoking-related health problem can also be added to the account. 3. Prepare for ti mes of crav ing by keeping subs ti tutes handy, s uch as sugarless gum, sl iced fr uit, carrot or celery sticks . 4 . I ncrease fl uid intake. 5. Keep a calendar or diary of the day-to-day progress. Even with physician adv ice, some patients may require med ications to ass ist their smoking cessation progr am. Medications useful for attenuating nicotine craving and the effects of with drawal include n icotine polacrilex chewing gum and n icotine transder mal patches. O ther medications include doxepin, a tr i cyclic antidepressant, bupropion, a newer antidepressant, and c1onidine, a centrally acting antihyper tensive agent (23 ,24) . O ther agents under investigation include cor ticotropin and citric acid aerosols (25 ,26) . The most current comprehensive metaanalysis of s moking cessation interventions reveals that the most effective progr ams employ more than one modality for motivating behav ioral change and involve both phys icians and non physicians in an indiv idu alized face-to-face effort. These programs also prov ide a motiva tional message on multiple occasio ns , over the longes t possible time per iod (27). Smokers have a death rate 30% to 80% higher than non smokers, and they cons ume a dispropor tionate share of health care resources . In 1985, the direct health care cos ts of s moking-
201
related illnesses exceeded $ 16 billion . Calculations for the indirect cos tS, such as lost productiv i ty and earn ings from excess mor tality, disability, and premature death, totaled more than $37 billion. Promoting s moking cessation for patients is one of the most im por tant primary prevention effor ts physicians can under take. Alcohol
The excessive use of alcohol accounts for a wide spectr um of health and social problems. Alcohol plays a cas ual or contr ibuting role in deaths res ulting from accidents, homicides, and su icides, as well as diseases s uch as cirrhosis and cancer . Beyond the nega tive effects on i ndiv iduals with alcoholis m , the disorder also has been es timated to negatively affect the liv es and health of many other people. Alcohol abuse is implicated in 50% of all divorces, in 45% to 68% of spouse abuse cases , and in up to 38% of child abuse cases . Alcohol abuse is especially har mful dur i ng pregnancy. Fetuses can be serious ly harmed by alcohol. Fetal alcohol sy n drome is now one of the three leading causes of prenatal mental retardation i n the U ni ted States , and it is completely preventable. A person who abuses alcohol rarely changes this maladaptive behavior without s trong, consistent, systematic, and long-term treatment. The first step involves accur ate diagnosis so that the appropriate treatment can fol low. A num ber of useful examiner and self-admi n is tered ques tionnaires are available, but the most useful diagnostic screen consists of four si mple questions . The screen's acrony m , CAGE, comes from the cr itical word in each q ues tion (28): I. Have you ever tr ied to Cut down on your dr inking? 2 . Are you Angry or Annoyed when people ask you about your dri n ki ng? 3 . Do you ever feel Guilty about your dri nki ng? 4. Do you ever take a morning Eye opener? One positive response s ugges ts the poss ibility of alcoholism and mer its fur ther exploration. Two positive answers make the l i kelihood extremely high. Three posi tive responses to q ues tions 1 through 3 , or a s ingle positive response to q ues tion 4 , is most likely diagnos tic. The helpful featur es of these q ues tions are their simpl icity, sens itivity, and efficiency. These q ues tions take under rwo minutes to ask and they should be included in every initial ambulatory and hospital admiss ion workup. O ne of the most recent s urveys of treatment options for alcoholism indicates that compulsory inpatient treatment followed by close monitor ing for incipient relapse y ields the bes t r es ults (29). Alcohol abuse often is a symptom of psychiatric illness , most commonly anxiety and mood disorders . The ubiquity, social ac ceptance, and relative low cos t of alcoholic beverages make dr ink ing an effective s hort-ter m and maladaptive long-ter m manner of self-medication. If the alcohol problem is a primary disor der (alcohol-related disorder, Diagnostic and Statistical Manual ofMental Disorders, Fourth Edition [O SM-IV]) (30) , subs tance abuse treatmen t alone suffices . If the alcohol problem is secondary to a psychiatric disorder (dual-diagnos is), s pecific attention to the under ly i ng i l lness must be addressed si multaneously wi th the sub stance abuse d isorder. The most useful recent method to diagnose psychiatric disor ders efficiently and accur ately in an ambulatory
202
//f. Osteopathic Considerations in the Behavioral Sciences
care setting is the Pri me-M D ( Pr i mary Care Evaluation of Men tal D isorders) (31 ) . Pri me- M D is a well-validated and highly reliable question naire that screens for psychiatr ic disorders. Pa tients fi ll out a ques tionnaire and the phys ician then follows up any posi tively endorsed target sym ptoms. It is s peci fic for the most common psychiatric disorders present ing to pri mar y care practice , i ncluding mood, anxiety, somatoform concer ns , and alcohol-related problems. If a psychiatric disorder is coexis tent with alcohol is m , refer ral for psychiatr ic cons ultation and co-management is s trongly recommended.
of all issues; rather it represents si gni ficant areas where simple attent ion can make a major difference in household safety. The general nature of these recommendations do not minimize their i mportance for the health of patient s . • • • •
Illegal Substance Abuse
The effects of illegal s ubstance abuse range from har mful to deadly; prevention is par amount. E ffor ts must be made on a s pectr um of fronts , fro m gover nmental to personal, to discour age illegal substance use. Early diagnosis is i m perative and in most cases treatment i nvolves a l i felong r ecovery process . Self help groups are useful and the most successful ther apy usually in volves multi modal treatment efforts by a multidisciplinary team. The primary care physician generally is the coordi nator of the team-oricnt ed treatment program.
•
•
•
PERSONAL S AFETY
Attending to personal and family safety is a major component of a preventive health program. Educating patients by prov iding the best and most current infor mation is key. Addressing personal safety iss ues ca n be i ncorporated i nto new patient screen i ng and provided for current patient s in the for m of pamphlets. Some satety vi deos are also avai lable. Automobiles
Approximately 50,000 people i n the Uni ted States die every year in automobile accidents. The automotive industry has made sig nificant stri des in making cars safer with the advent of air bags and anti lock brakes . Laws that make the use of seat belts manda tory and call for infants and s mall children to be secured in the rear seats in protective seating have also helped reduce deaths from automobile accidents . Physicians can help patients better understand automobile safety iss ues by encouraging patients ro: • • • • • • •
Purchase ve hi cles wi th the latest safety dev ices (i.e., air bags , 3nt i lock brakcs) Keep automobiles safer through proper m ai n tenance, es pecially of brakes and tires Obey s peed l i m i ts and all traffic regulations Follow all regulations when operating recreational vehicles Wear an approved helme t and protective clothing when oper ati ng a bicycle , moped, or motorcycle Avoid drivi ng while taking sedative medications Never dr ink alcohol be fore dr iv ing
Home
Provi de patient s with infor mation on how to maint ai n a safe env i ronme nt in their home. The following list is not i nclusive
•
Keep medici nes , har mful chemicals, and cleaning products secure and especially out of reach of children. Prevent fires by j udicious use ofauxiliary home heating devices and by proper use of electrical appliances and outlets. If fire should occur, m i n i mize danger and damage by the use of smoke detectors and fire extinguis hers . Develop and practice an escape plan from the home in the event of fire or other disas ter (i.e. , ear thquake, hurr icane, tor nado) . Most local fire depar tment s and electr ic companies will inspect your home and make safety recommendations at l i ttle or no cos t. Patients who choose to own guns should keep them in a secure place, unloaded, with appropr iate locki ng mechanisms on the tr iggers . L ikewise, ammunition should be kept in a secure place , separate from the weapons. Keep power tools and lawn care equi pment in good repair, es pecially their safety guards, and wear safety glasses and ear plus during their operation. Falls are a major cause of injury to older adults. Keep ba th rooms and s tairways free of obstacles and install appropr iate lighting, handles, and banis ters . Secure the edges of throw r ugs to minimize tr ips and fal ls . I n wint er, keep sidewalks a n d outdoor s tairs clear of snow and ice. This can be a component of a family's fitness plan.
The home health checkl ist in Table 13.4 was speci fically de veloped for older adult patient s (32 ) .
SEXUALITY
Sexual behavior is a ce ntral component of healthy human func tioning and a source of pleasure, comfor t, and intimacy. Unfor tu nately, lack of knowledge about human sexuality can result in more than an unwanted pregnancy; it can res ult in illness and death. As well as providing the bes t poss ible counsel and in for mation about contraception and family planning, physicians must also infor m sexually active patients about safe sex practices . Female patients s uffer far more than male patients in the area of sexually tr ansmitted diseases (STDs) due to their more compli cated and lengthy reproductive roles. Again, ironically, ill health, disability, and death from unhealthy sexual practices are almost comple tely preventable. High-risk pr actices should ilil mediately be cur tai led. These include: Sex with an intravenous substance abuser Sex wi th a prosti tute, stranger, or person whose sexual his tory is unknown • Sex without the use of a condom • Sex wi th any person who engages in any of the above behaviors •
•
Fur ther, patients should be adv ised that absti nence or main tai n i ng a mutually monogamous relationship wi th one par tn er are the bes t methods for preventing all types of STDs. For many
13. Health Promotion and Maintenance TABLE 13.4. HOME HAZARD CHECKLIS T
Stairs Adequate i l l u m i nation Top and bottom steps painted Nonskid treads Handra i l : detached, graspable, end of rail shaped to sign ify bottom of stairway Risers pai nted i n easily visible color Living areas-Carpets Edges tacked down completely Wal l·to·w a l l with thick, shock-absorbent pads No throw rugs
• • • •
Other E m phasis on control of pets and small chi ldren to avoid causing trips No low couches, sharp-cornered furniture, or chairs on casters Light switches easi ly accessible to door or room Lighted switches Bathroom Nonskid rubber mats i n shower or bath Handrails in bath and by toilet Adequate l ighting in bath and n ight l i g ht on access path Water temperature reg u l ated at 43 C (110 F) or lower Clearly marked h ot a nd cold faucets, preferably with separate con trols Seat i n tub Kitchen Adequate i l l u m ination Stove controls large and clearly marked Large, easi ly grasped, protected hand les on pots and pans Stored items easily accessible Miscella neous Smoke detectors with reg ularly checked, working batteries Adequate access and escape doors and windows Consider personal alarm system keyed to emergency system to be worn by h ig h risk patient Reprinted with permission from Snipes GE. Acc iden ts i n the elderly. 1982;26:117-22.
problems or who are in turmoil should be encouraged to seek help, whether it be support from caring relatives and friends, suppOrt groups, or professional fam ily therapy. The primary care osteopathic physician should engage patients in constructive discussions about family health. A recent guide for health and long-term care (4) lists five qualities shared by healthy fam ilies:
•
Living areas-Fl oors No highly polished floor surfaces Nonskid wax Thresholds removed No extension cords Access pathways free of low-lying furniture or other objects Baseboard l ighting in halls
Am
Fam Physician.
people, however, this advice is not acceptable. In such cases, the physician should instruct patients to minimize high-risk behav iors. Although not 1 00% effective, consistent and correct use of condoms and other barrier contraceptives decrease risk of pregnancy and STDs and should be encouraged. Studies reveal that using contraceptives containing the spermicide nonoxynol-9 with condoms offers further projection if the barrier should fail.
FAMILY AND WORK
A healthy family life has long been known to be a source of com fort, joy, and inspiration. The family is the basic unit of sociery and needs the support of all. Fragmented, blended, or single parent families need even more support. Families experiencing
203
A clear undemanding of each member's role and responsibilIties An equitable distribution of power Support and encouragement Effective communication A shared system of values or beliefs
Ie should become routine in osteopathic, family-oriented health care to inquire about these characteristics in medi cal history taking and to promote them at every therapeutic opportuniry. Doing work that one finds meaningful is a source of pride and personal fulfillment. The most tragic work situation is for one to feel trapped in a work circumstance one despises. Many people, however, fai l to take the steps necessary to make their work more meaningful or to prepare themselves to change j obs or careers. I f patients fi n d that, despite thei r best efforts, they are unhappy i n their work, they should b e encouraged t o survey their situation and develop a plan of change. Opportunities for alternative edu cation and training are more abundant and accessible now than ever before. Even i n the most difficult economic circumstances, education is the best investment a person can make. Many people unhappy with their work never take full ad vantage of what the situation offers. Most large employers have tuition-reimbursement plans for educational courses that go un used by employees. Patients should also be encouraged to cul tivate friendships at work. If a workplace does not provide ac tivities, patients can become agents of change who organize and develop work-related social or sports activities. Work need not be daily tedium and loathing and even planning for a change can be the activiry that lifts a patient's spi rits and gives them hope and comfort. Work should not be a constant endeavor of joyless striving, but rather an undertaking that provides meaning and satisfaction.
STRESS
No life is without stress. There are, however, adaptive and mal adaptive manners ofcoping, even under the most stressful circum stances. Although there are many events that can happen in our l ives that are completely unexpected, many ofl i fe's difficulties can be anticipated and managed effectively. Many people accept h igh levels of stress in their lives but do not appreciate the high price they pay. Medical research has shown that a life lived in chronic stress can trigger and activate psychophysiologic disorders such as hypertension, peptic ulcer disease, and coronary artery disease (33). More recent research in psychoneuroimmunology shows a relationship between stress and anenuation of immune responses (34) . Mental health researchers have long known that stress plays a strong role in various forms of anxiery and depressive disorders, as well as in many forms of substance use and abuse.
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111. Osteopathic Considerations in the Behavioral Sciences
TABLE 13.5. SOCIAL READJUS T MENT S CALE
Holmes Points
Life Events 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 1 7. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 3 1. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43.
Death of spouse Divorce Marita l separation J a i l term Death of c l ose fa m i ly member Personal i nj u ry or i l lness Marriage Fired from job Marital reconci lation Retirement Change in health of family member Pregnancy Sex d ifficulties Having a baby Busi ness readjustment Change in financial state Death of c l ose friend Change to d i fferent line of work Change i n n u m ber of argu ments with spouse Mortgage large i n relation to income Foreclosure of mortgage or loan Change i n respons i b i l ities i n work Son or daughter leaving home Trou ble with in-laws Outstanding personal achievement Spouse beg i ns or stops work Beg i n or end school Change i n l iving c on d itions Change i n personal habits Trou ble with boss Change in work hours or conditions Change i n residence Change i n schools Change i n church activities Change i n recreation Change i n social activities S m a l l mortgage i n relation to i ncome Change i n sleeping ha bits Change i n n u m ber of fam i l y get-togethers Change i n eating ha bits Vacation Christmas M i nor violations of the law
1 00 73 65 63 63 53 50 47 45 45 44 40 39 39 39 38 37 36 35 31 30 29 29 29 28 26 26 25 24 23 20 20 20 19 19 18 17 16 15 13 13 12 11
Reprinted w i t h permission f r o m H o l m e s TH, R a h e R H . The s o c i a l readjust ment rating scale. J Psychosom Res.
1967;7: 1 7-20.
Most recently, stress has been conceptualized as an organ ism's nonspecific response in an attempt w adapt w demands. Those demands can cover the spectrum of psychological, so cial, and physiological functioning. Even ordi nary day-w-day events, whether seen as positive or negative, involve adaptation w change. The concept of adaptation w change now dominates current thinking about stress. In 1 967, Holmes and Rahe verified the stress of adaptation (35 ) . They developed a scale and assigned poi n ts w 43 common life events w develop a stable and objective poin t of reference. They were not concerned with how people interpreted or felt about these events but merely with whether they happened. They demonstrated that the greater number of points a person scored over a I-year period, the greater the proba bility of ill ness occurring within the next 2 years. The preventive implications are clear. Although a number of stress scales are now
available, the Holmes & Rahe Social Readj ustment Scale remains one of the most highly validated and widely used (Table 13.5) (35) . This scale can be easily incorporated inw medical prac tice and used liberally w help patients j udge their own vulner abilities and develop increasingly effective antici pawry coping strategIes. Stress can also be self-generated. The "type A personality" first described by Friedman and Rosenman has now become a house hold word (36 ) . Although it has been argued excessively as w whether the "type A personality" is a feature of cownary artery disease, the adaptive style of a person with type A characteristics can hardly be envied. Research beyond Friedman and Rosenman's seminal work indicates that competitiveness, impatience, and dif ficulty dealing with anger and hostility are the core characteristics of people prone w coronary artery disease. It might be difficult w completely alter these maladaptive styles, bLlt counseling and education can modifY them w the point where a patient's risks are significantly lowered (37).
SUPPORT SYSTEMS
One of the major facwrs attenuating stress is an effective system of psychosocial support. The physician should conceptualize a patient's support system as a network of expanding concentric circles with the patient's closest confidant at the center. The im portance of having person (s) in whom we can confide cannot be overemphasized in buffering the effects of life stress. Most times this central confidant is a spouse or best friend, or it could be any one who demonstrates care, concern, and respect for feeli ngs and opinions. This confidant serves the preventive role of ensuring that all burdens and troubles can be shared. A system of support ranges from the confidence of having trusted advice available when plann i ng a predicted transition w the comfort and nurtur i ng of friends, neighbors, and community during an unforeseen tragedy. Confidants also help professionals, such as the clergy or physicians, w provide assistance. Last, but certainly not least, re ligious faith provides the opportunity for a spiritual confidant. Patients for whom a spiritual dimension w life is important derive great comfort and benefit from their bel ief in power and meaning beyond what can be known in life in the world. Physicians should not underestimate the positive healing power of spiritual belief systems.
DOCTOR-PATIENT RELATIONSHIP
The doctor-patient relationship remains the si ngle most pow erful heali ng wol of the physician. Technology is obviously im portant, but the power of the doctor-patient relationship allows "high-tech" medicine w be used most wisely and to the greatest benefit. Primary and secondary prevention are two of the most i mportant goals of the osteopathic physician, especially those in primary care practice. Physicians can do the most w encourage patients w become partners in their health care by using the power inherent in the docto r-patient relationship. Most physicians agree that counseling is one of their most important tasks; paradoxically, most feel i neffective in this role.
13. Health Promotion and Maintenance
Many physicians Feel generally pessimistic about their abil i ty to motivate patients toward positive change. This pessimism exists pardy due to a lack of eFFective training about behavioral change during medical school and in postgraduate medical education. Physicians generally underestimate the diFficulty i n changing be havior, even their own . Most wrongly believe thei r only duty is to provide information and end up preaching to or lecturing their patienrs, rather than inForming them. Because this approach alone usually Fails, physicians can become discouraged and stop trying to change patient behavior or begin to provide information in a cursory manner, never really expecting patienrs to cooperate. Behavioral scienrists investigating change as a process have proposed both general and specific approaches that are realis tic, practical, and broadly applicable in health care settings. One of the most helpful models is that proposed by Prochaska and DiClemente (38,39). This approach divides the process of change into stages. The duty of osteopathic physicians is then to assist their patients to idenriFy the stage they are in and to move suc cessFully into the next. This approach is useFul in three important ways because it:
Attending to emotional responses Ask about and label fee l i ngs Legitimize fee l i ngs Support and encourage patient Be nonj udgmental Generate respectful statements
1. Acknowledges that change is diFficult and requires planning.
Reprinted with permission from Stoffelmayr B, Hoppe RB, Weber N.
2. Minimizes discouragement on the part of patienr and physi cIan.
Care.
3. Continually encourages positive work toward lasting or per manent change. The stages of change include: I. Precontemplation: I n this first stage patients are unaware of or perhaps deny the negative consequences of their behavior. This can include, For example, rationalizations l ike: "I know lots of people who smoke who are healthy." The task of the physician in this stage is to make patienrs aware of the Fallacy of such rationalizations by providing good i n Formation and/or by in troducing therapeuric tension into the patienr's belief systems. 2. Contemplation: At this stage, patienrs spend variable lengths of time reflecting on their behaviors and assessi ng both negative consequences of continuing a behavior and the probable benefits of positive change. 3 . Preparation: Patients acknowledge that change is desirable. The physician's task is to negotiate a plan aimed at the higher likelihood of success. 4. Action: The patienr and physician implement the plan For behavioral change with clear outcome measures to monitor progress. 5. Maintenance: Patients have experienced the reinforcing effects of their action plan to the poinr where the change becomes an ordinary part of their l i Fe. The Prochaska/DiClemente model allows For the possibility and probabil iry relapse, especially with difficult changes like smoking cessation. I F or when relapse occurs rather than abandoning the process, the physician and patienr move back to a prior stage to troubleshoot the problem beFore moving ahead again. Continuous attention and incremental improvement are far superior in the long run to giving up in frustration or demoralization.
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TABLE 13.6. COMMUNICATION S T RATEGIES FOR BEHA VIOR CHANGE ENCOUNTERS
I nforming a patient Establ ish a base l i n e Explain and instruct Be clear, avoid jargon Check understanding Obta i n i n g a com mitment to behavior change Make clear statement about desired behavior Explore read iness for change Obta i n a comm itment Negotiating and tailoring reg imen Identify congruence between physician's and patient's expectations Work toward plan that patient can agree to Ta i l or plan to patient's circu mstances; d isrupt routines m i n i mally Consider a written contract
Faci l itating patient participation: the doctor-patient encounter. Primary
1989; 1 6:265-278.
A review of doctor-patient relationship literarure proposes four specific sequenrial strategies for motivating patient cooper ation and encouraging patienrs to take more personal responsi bility for their health (40). These strategies are grounded in the patienr compliance l i terature and have been expanded and in tegrated to include relevant social influences and psychotherapy research. A major conrribution of this research has been the iden tification of the patient's health beliefs as a powerful predictor of cooperation with treatment. The review focuses on the critical importance of the doctor-patienr relationship and interaction and then expands to the patient's relationship with the enrire integrated primary care health team. Patients who are not clear about what they are expected to do are unlikely to follow recom mendations. A n umber of srud ies show major patient dissatisfaction with not receiving enough i nFormation from physicians! Dissatisfied patienrs are less likely to cooperate and may not even rerum (Table 13 .6) (40 ) . Strategy 1 : Inf ormi ng the Pati ent
The physician should never make assumptions about a patient's knowledge and understanding, regardless of socioeconomic class or level of education. A confident level of baseline knowledge should first be established. The physician can implement this by allowing the patient time to explain thei r understanding of health problems and then identify any i ncorrect or idiosyncratic perceptions. The cultural belief system of patients should also be explored. Verbal i nstructions should be clear and can be sup plemented with pictures and printed materials if necessary. The physician should avoid jargon whenever possible. The physician can check the patienr's level of understanding by asking the pa tient to repeat i nstructions or demonstrate how they might share the i nstructions with a third party.
206
111. Osteopathic Considerations in the BehavioraL Sciences
TABLE 13.7. P RIMARY CARE-BASED HEALTH PROMO TION
Activity
Outcome
Agent
Screening
Identification of risky behavior
Inform ing (Table 1 3.6)
K n owledge
Counse l i n g (Table 13.6) Tra i n i ng/education
Comm itment to behavior change Sk i l is to make sh ort-term behavior change
Emotional support P l a n adjustment/motivation
Motivation Long-term
Reprinted with permission from Stoffelmayr
265-278.
B,
Hoppe
RB,
Physician Nurses Other staff Physician Nurse Health educator Physician Physician Nurses Other staff Health educator Nutrition ists Entire PHCO team Entire PHCO team
Adjunct Questionna i res Interactive Computer Written materials Video station Written contract Written materials
Telephone cal is/letters Telephone cal is/letters B i ologic measurement
Weber N . Facilitating patient participation: the doctor-patient encou nter. Primary Care.
S trategy 2: Obtaini ng Commitment from the Patient
This involves the use of referent power, social power bestowed on a significant figure whose acceptance and approval are highly regarded and desired. The use of this referent power involves making direct and clear statements about a desired behavior change and eliciting the patient's com mitment to cooperate. Using the example of smoking, this would involve stating in a nonj udgmental bur direct and authoritative manner the detri mental effects of smoking, and then asking the patient directly for a commitment ro stop. Physicians' success in eliciting this com mitment is revealed in higher patient smoking cessation rates. Strategy 3: Negoti ating and Tailoring a Regimen
All treatment recommendations require a change from the pa tient's ordinary lifesryle. The more complex the changes recom mended, the more difficult for the patient to cooperate. The goal of negotiation is to arrive at an agreement. Through negotiation and exploration of lifesryle and belief system issues, a regimen can be tailored to the individual life circumstance of each pa tient. When the negotiated agreement is written up as a mutually binding contract, it is more likely to be kept. A verbal agreement may also suffice. Strategy 4: Attending to the Patient's Emotional Resp onses
The qualiry of the doctor-patient relationship is crucial at this point. Patients often complai n , even bitterly so, about not be ing listened ro or not having the opportuniry ro tell their story. Stories abound about technically competent but cold and aloof physicians. Research i nto doctor-patient relationships has shown that patients' j udgments about physicians are made on the basis of the physician's abiliry to recognize and respond to emotional con cerns. Positive behavior change occurs more often in the presence of a high-qualiry doctor-patient relationship. Patients in distress
1 989; 16:
and suffering anxiery are not in the best condition to attend to the cognitive components of their instructions. When physicians attend ro a patient's emotions and set the patient at ease, they facilitate and promote the patient's understanding and coopera tion. Physicians also need to communicate their i nterest and con cern for their patients nonverbally. Several tactics com municate care and interest i ncluding smiling, sitting down, using appro priate eye contact, and not appearing to be rushed. The osteopathic physician has a distinct advantage over other health care professionals through the medium of touch and "the laying on of hands." Through the i n tegrated verbal and nonverbal communication of care, truSt is promoted, cooperation is max im ized, and the doctor-patient relationship is further strength ened. The use of the integrated primary care team in this process is summarized in Table 13.7 (40) . CONCLUSION
Most of the task of providing the highest qualiry, cost-effective care involves teaching and motivating patients. The place to be gin in creating the desired behavior we wish to see in our patients is to make them clearly reflected in our own. Many physicians have been successful in altering their personal health behavior habits for the better, but there is always room for improve ment. Docror means teacher, and the old maxim remains sounds: " Example isn't the best way to teach, ulti mately it is the only way to teach."
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Factors in 1990 fllltl Projected to 2020. Cambridge, MA: Harvard Un i 3. The UllitetlStates SlIrgeon Gmeml 's Report on Nlilrition anti Health, 1988. Washingron, D.e.: U.S. Deparrmem of Healrh and Human Services, 1 988. 4. Pfeiffer GJ. Taking Care ofTotiay and Tomorrow; A Resource Guidefor Ag
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376. 24. Franks P, Harp J, Bell B. Randomized conuolled rrial of c10nidine for
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27. Korrke TE, Barrisra R N , er al. Arrribures of successful smok i ng cessarion i n rervenrions in medical pracrice. A mera-analysis of39 con rro lied rrials.
7. Blair S N , Kohl W H I I I , Paffenbarger RCJr. Physical firness and all-cause morraliry. }AMA. 1989;262:2395-240 I .
}AMA. 1 988;259( 1 9) :2883-2889. 28. Ewing JA. Derecring alcoholism, rhe CAGE Quesrionnaire. }AMA.
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1 984;2 5 2 :1905 - 1 907. 29. Walsh DC, H i gson RW, cr al. A randomized trial of rrearment oprions
9 . Pyne DB, er al. Train i ng srraregies ro mai nrain immu nocomperence i n
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Kuczmarski RJ. Prevalence of overweighr and weighI' gain in rhe U nired Srares. Am } Clin Nlitr. 1 992;55:4955-5025.
1 2. Arkinson RL, er al. Weighr cycling. Narional Task Force on rhe preven rion and rrearmenr of obesiry. }AMA. 1994;272( 1 5) : 1 1 96-1202. 1 3. Narional l nsriwres of Healrh. Healrh impl icarion of obesiry: consensus
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Overweight Patiem. 71'earmmt ofthe Seriomfy Obese Patient. New York, NY: Guilford; 1 992:3-32. 18. WilliI' We. Assessmenr ofMorbitlity and Momlity Risk ill the Overweight
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INTRODUCTION TO PSVCHONEUROIMMUNOLOCiV DAVID A. BARON
their basic function. Specifically, the immune response can be KEY CONCEPTS • The effects of stress on health and disease, and the field of
psychoneuroimmunology • The role of the hypothalamic-pituitary-adrenal (HPA) axis
in stress medicine • Conceptualization of the brain and immune functioning
as an interactive system • Integration and similarity of the functioning of the central
nervous, immwle, and neuroendocrine systems • Historical perspective of mind-body medicine • Altered immune function with mood disorders • The relationship between emotional stress and altered
immune response • Differentiating the biomedical and biopsychosocial models
modulated by input from the nervous and neuroendocrine sys tems. The high degree of similarity and integration between the immune, central nervous, and neuroendocrine systems is teleo logically sensible due to the fact they have a common task, to persevere homeostasis and assure the consistency and integrity of body cells and tissues, for which integration and regulatory redundancy is an obligation (I). In many ways, this hypothesis is similar to osteopathic phi losophy. In addition to musculoskeletal integrity, it emphasizes the importance of rotal body homeostasis in maintaining health and treating disease. The basic principles of PNI, like Engle's
(3) biopsychosocial model, stress the interconnectedness, or hard wiring, of emotions to the body's physiologic functions. Despite centuries of interest, clinical observation, and anecdo tal reports, research on the complex interactions between the cen tral nervous system (CNS) and the immune system has only taken place in modern medicine. This in part, is due
to
the lack of un
derstanding of the complexities of immune functioning and the
PSYCHONEUROIMMUNOLOGY This chapter introduces the field of psychoneuroimmunology (PNI). PNI conceptualizes the brain and immune functioning as an interactive system. As Rubinow (I) points out, the im mune, neuroendocrine, and central nervous systems are stimulus response systems that are similar in the functions they subserve and tighrly integrated in their actions. The reciprocal regulatory effects of these systems provide a basis (but not proof ) for the belief that brain-immune interactions are clinically relevant and not reducible
to
characteristics of component systems.
limited availability of biologic probes to observe and measure the impact of one system on another. George F. Solomon, MD coined the term psychoimmunology as recenrly as 1964, in his classic paper, "Emotions, Immunity, and Disease: A Speculative Theo retical Integration" (4) . In this paper, Solomon offers a theoretical explanation of how emotional states can diminish immunocom petence, ultimately resulting in physical disease. These specula tions were of significant interest to the mental health communiry, particularly psychologists and psychiatrists. However, they did not enjoy a similar level of acceptance by the medical commu niry at large, and especially not by immunologists. Without data derived from well-controlled research studies, the consensus was that something as imprecise and variable as emotion could not
Research
have an impact on a seemingly hard-wired physiologic response like immune functioning. No reasonable explanation existed re
Research from the past decade confirms the tighrly integrated and
garding how these systems could communicate with each other.
surprising similarities between the functioning of the central ner
There was no reason why they should.
vous, immune, and neuroendocrine systems. Pert and colleagues
Despite repeated reports of illness following a significant emo
(2) suggest that the intimate integration of these three systems
tional stressor, nothing more substantial than observational or
warrants their consideration as a single system. All three systems
anecdotal reports existed to convince the nonbelievers. It was
can function as sensory and effecter organs, recognizing foreign
Adds (5) accidental finding that immunosuppression could be
antigen (immune) or incoming physiologic signals (endocrine or
classically considered in mice, by pairing taste aversion (saccharin)
nervous). All three transmit signals and information as part of
with an immunosuppressive medication (cyclophosphamide),
14. Introduction to Psychoneuroimmunology that ignited research interest in PNl. For the first time, direct evidence demonstrated the potential for external manipulation of the immune system. Intriguing questions followed. If im munologic response could be behaviorally conditioned to turn off, could it be conditioned to turn on? Could this help explain why the patient who, shortly after giving up the will to live, dies, or conversely, why some patients refuse to succumb and ulti mately defY the odds to survive life-threatening illnesses. These and related questions stimulated human PNI research. In the early 1980s, Kiecolt-Glaser published a series of prospective studies examining the effects of emotional stress on the function of the immune system. Kiecolt-Glaser (6) measured natural killer (NK) cell activity, y-interferon (IFN-y) production by lymphocytes, stimulated with concanavalin A (Con A), and mitogen responses in medical students prior to important exam inations. The results of this study demonstrated that emotional stress did in fact have a measurable negative effect on the immune system. In an important follow-up study, students who were taught relaxation training had a significant increase in NK cell ac tivity compared to students who had not received stress-reduction training. This was the first well-controlled clinical human study that demonstrated evidence of immune enhancement resulting from a psychological intervention (6). Not only did stress reduc tion improve immune response; students who were not taught stress-reduction techniques self-reported an increase in infectious illness symptoms around exam time (7 ). These provocative ex periments clearly demonstrated an effect in otherwise healthy subjects. Would the results be similar in a study of patients with underlying chronic illness? Castes and colleagues (8 ) conducted a prospective study of35 asthmatic children to evaluate the impact of a psychosocial inter vention (PSI) on immune functioning. The immune measures studied included NK cell number and activity, interleukin (IL)-2, (9) and leukocyte affinity for immunoglobulin E (lgE) receptors (an important marker related to asthmatic attacks). Clinical out comes assessed included the number of asthmatic attacks, use of bronchodilators, and overall pulmonary function. The psychoso cial intervention consisted of a 6-month training program in self relaxation, guided imagery, and enhanced self-esteem. The results of the study demonstrated a significant reduction in the number of asthmatic attacks, decreased used of bronchodilator medica tions, and overall improvement in pulmonary functioning during the psychosocial interventions, as compared to the 6 months be fore entry into the study. In fact, surface markers for IgE in the children receiving the PSI became similar to nonasthmatic chil dren. Smyth and colleagues (10) report similar findings in adults with asthma and rheumatoid arthritis. These well-designed clin ical trials offer preliminary data supporting the hypothesis that psychosocial stress can, and does, affect immune functioning and ultimately wellness. Mood Disorders
A merry heart doeth good Like a medicine but a broken spirit dries the bones. -GaLen In addition to stress-induced immune suppression, altered im mune functioning has been reported in patients with mood dis-
209
orders. The Greek physician, Galen, reported the relationship between clinical depression and physical illness in the 2nd cen tury C.E. He observed that melancholic (depressed) women were especially susceptible to breast cancer. In an effort to replicate and further explain this observation, Levy and colleagues (II) mea sured NK cell activity (a measure of immune competence) and psychological stress in women with breast cancer. They found NK activity to be a reliable and valid predictor of the patient's prog nosis relative to their lymph node status. In a separate study, these same authors reported that 51 of baseline NK activity changes could be accounted for by assessing a patient's adjustment to diag nosis, depressive symptoms, and perceived lack of social support. They concluded, based on multiple clinical trials, that differ ences in NK activity and overall prognosis could be predictably determined by assessing baseline stress as measured by emotional adjustment, depression or fatigue, and lack of social supports. A more recent review of the relationship between PNI and cancer by Kiecolt-Glaser (12) reports: "substantial evidence from both healthy populations under stress as well as individuals with cancer associated psychological stress for immune deregulation and that stress may also enhance carcinogenesis through alter ations in DNA repair and or apoptosis." The study concluded that psychological and behavioral factors could inAuence the inci dence and progression of cancer through psychosocial inAuences on immune function. Other studies over the past decade have explored the relationship between emotional stress and altered immune response. Stein (13) reports behavioral pathology and neuropsychiatric impairment of patients with autoimmune and viral conditions associated with systemic lupus erythematosus (SLE) and multiple sclerosis (MS). Early studies in the 1970s reported an increase in the prevalence of herpes simplex virus in patients with a psychotic depression when compared with age matched nondepressed controls. Unfortunately, these studies did not monitor any specific immune parameters. Schleifer and colleagues (14) demonstrated that depressed pa tients have a decreased number of peripheral T cells compared with those of nondepressed control subjects. Their data suggest that the functional activity of lymphocytes, as well as the num ber of circulating immunocompetent cells, is reduced in patients with clinical depression. They also speculate that the altered im mune functioning in patients with depression might be related to the severity of their depressive symptoms.
Implications for Medical Education
The primary goal of medical educators in the United States is to train medical students to diagnose and treat organic patho logic conditions. Much of what takes place in the practice of clinical medicine and surgery is based on conventional wisdom and long-standing patterns of practice. Mental health issues are often ignored and viewed as unimportant for treating physically ill patients. Too often psychiatrists are considered experts only in mental illness, rather than medical specialists. In the biopsychoso cial model, psychosocial issues are seen as separate and distinct from biologic concerns. Yet consider the following facts: • Emotionally distressed patients visit the doctor and are hospi
talized more often than nondistressed patients.
210
iil. Osteopathic Considerations in the Behavioral Sciences
• People with emotional distress commonly visit their docrors
• • • • •
with physical symptoms and complaints (dizziness, headaches, fatigue, pain, etc.) and never report mood symptoms. Nearly two-thirds of all physician visits fail to confirm a bio logic diagnosis. Medical illness can precipitate emotional distress, which com plicates medical treatment and increases medical costs. Emotional distress often goes unrecognized and untreated in medical encounters. Appropriate mental health treatment reduces emotional dis tress, medical utilization, and costs. Savings from reduced medical costs can offset the cost of pro viding mental health treatment and stress-reduction training, which may result in lower overall health care costs.
Unfortunately, these facts are often ignored, leading to a strik ing mismatch between the true needs of patients and the health care services offered. The result is often less effective care, frus tration for both patient and physician, and the waste of ever shrinking health care resources. If nothing else, PNI research underscores the need to assess patients' emotional distress. Elicit ing information on stress levels and recommending appropriate stress-reduction strategies might have a positive impact on a pa tient's overall health. For patients suffering from ongoing illness, attending to these issues may improve response to other somatic treatments.
Despite [he general acceptance of this concept by health care providers, it is difficult to define stress, let alone the impact it has on disease and wellness. Early concepts focused on stress being a force of universality, acting on a passive body, with all people reacting in a similar way to a disruption. The modern concept emphasizes that stress is not what happens, but rather how a person reacts to a stressful event. Distress arises when a person perceives that imposed demands (stress) have exceeded their ability to cope with them. There is a physiologic response to stress. This response involves activation of the hypothalamic-pituitary-adrenal (HPA) axis; it is modulated by the autonomic nervous system (ANS). The ANS maintains balance through its two primary components, the sympathetic branch, regulating arousal, and the parasympathetic branch, in ducing relaxation. How stress and other noninfectious stimuli affect the body's defenses against disease are not yet completely understood. Although significant advances have been made (15-17 ) , key questions need to be answered to better understand the clinical implications of stress on health and disease. These include: • How does everyday emotional stress affect the immune system? • What are the actual health consequences of stress-induced im
munologic changes? • Does chronic psychological stress promote long-term deregu
lation of the immune function? • Can stress management and alteration of immunologic and
endocrine effects alter or cure disease? Treatment Recommendations
The physician should emphasize the importance of lifestyle alter ations such as cutting down on caffeine, maintaining a healthy diet, quitting smoking, and exercising regularly. Other stress reduction strategies can be tailored to the patient's lifestyle and can be a key component in disease prevention. It is the responsi bility of physicians to educate their patients about the importance of maintaining a healthy lifestyle. Make patients aware of target organs and areas particularly vulnerable to stress, such as the heart, kidney, gastrointestinal tract, and musculoskeletal system. Osteopathic physicians with special training in musculoskeletal dysfunction are likely to encounter a disproportionate number of patients with stress-induced musculoskeletal complaints. The education process should include protecting patients from claims of miracle cures or unsound, porentially dangerous interventions, such as unproven megavitamin therapies. The physician should be cautious not to overinterpret or overgeneralize clinical ob servations. A laboratory finding demonstrating a decrease in an immune parameter does not necessarily predict a change in health status.
• Is there, to some extent, well-controlled, valid, and reliable
research that can address these clinical questions' (18 )
CONCLUSION
Our understanding of the intricate complexity of immunology and neuroscience is growing rapidly. Since the first edition of this text (1997), significant advances have been made in under standing the basic molecular mechanisms of PNI. Early clini cal observation is rapidly becoming scientifically proven fact. As with osteopathic concepts, the key to continued acceptance in the medical community, and ultimately the enhancement of the wel fare of patients, is adherence to the principles of methodologically sound scientific research. PNI researchers can be proud of their accomplishments to date. Research has demonstrated that the CNS is in direct and constant communication with the immune system. The goal of future investigation is to better understand their "language" and how to manipulate it to promote health. The challenge to the next generation of osteopathic researchers and clinicians is to continue, and to expand on, the work in progress in this exciting and important field.
THE EFFECTS OF STRESS ON HEALTH AND DISEASE
The arrivaL oja good cirClls consisting ofdowns is a greater benefit upon the health ofa town than that oftwenty Asses Laden with drugs. -Dr. Thomas Sytfellham Throughout history, medical researchers and clinicians have ob served and reported the effects of stress on health and disease.
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J 977(Apr 8); J 96: J 29- J 36.
14. Introduction to PsychoneuroimmunoLogy
4. Solomon GF, Moos RH. Emotions, immunity, and disease. Arch Gen
Psychiatry. 1964;11:657-674. 5. Ader R, Cohen N. Behaviorally conditioned immunosuppression.
Psychsom Med. 1975;37:333-340. 6. Keicolt-Glaser, jR. Stress, personal relarionships, and immune funcrion: healrh implications. Brain Behav Immun. 1999;13:61-77. 7. Keicolr-Glaser j R, Garner W, Speicher C, er al. Psychosocial modifiers of immunocomperence in medical srudenrs. Psychsom Med. 1984;46: 714. 8. Casres M, Hagel I, Palenque M, et al. Immunological changes associated with clinical improvement of asthmaric children subjecred to psychoso cial intervention. Brain Behav [mrnun. 1999; 13:1-13. 9. Glaser R, Kennedy S, Lafuse W, er al. Psychological srress-induced
211
13. Srein M. Future direcrions for brain, behavior, and rhe immune system.
Bull NYA cad Med 1992;68(3):390-410. 14. Schleifer Sj, Keller SE, Siris SG, er al. Depression and immunity. Arch
Gen Psychiatry. 1985;42:129-133. 15. Hassed, C. Psychoneuroimmunology: A platonic view of rhe immune sysrem. Austral Fam Physician. 1999;28 (9):950-951. 16. Warkins A. Mind-Body Medicine: A Clinicians Guide to Psychoneuroim
munology. London, England: Churchill Livingstone; 1997. 17. Keicolr-Glaser j, Glaser R, Gravesrein S, er al. Chronic srress airel'S rhe immune response ro inAuenza virus vaccine in older adulrs. Proc Nati
Acad Sci. 1996;93:3042-3047. 18. Trilling, jS. Psychoimmunology: validation of rhe biopsychosocial model. Fam Pract. 2000;17(1):90-93.
modulation of IL-2 receptor gene expression and IL-2 producrion in peripheral blood leukocytes. Arch Gen Psychiatry. 1990;47:707712. 10. Smyrh M, Stone A, Hurwitz A, et al. Effecrs of writing about srressful
SUGGESTED READINGS
experiences on symptom reducrion with asthma or rheumatoid arthriris, a randomized rrial. JAMA. 1999;281:1304-1309.
II. Levy SR, Lippman M, d'Angeio T. Correlarion of suess factors wirh sustained depression of narural killer cell acrivity and predicted prognosis in patients wirh breast cancer. J Clin OncoL 1987;5:348-353. 12. Kiecolt-Glaser j, Glaser R. Psychoneuroimmunology and cancer: facr or fiction? EurJ Cancer. 1999:35(11):1603-1607.
Ader R, Felton DL, Cohen N, eds. Psychoneuroimmunology. San Diego, CA: Academic Press; 1991. Trilling ]S. Psychoneuroimmunology: validation of the biopsychosocial model. Fam Pract. 2000;17(1):90-93. Warkins A. Mind-BodyMedicine: A Clinicians Guide to Psychoneuroimmunol
ogy. London, England: Churchill Livingstone; 1997.
PAIN MANAGEMENT JOHN A. JEROME
KEY CONCEPTS
Histo ry and theories of pain management Different types o f pain, including acute and chronic • Areas o f i n formation flow w ith chro n ic pain , central control process cognitive/emotional appraisals • Use o f med ications and anesthetics in pain management • Osteopathic approach to pain management •
•
Pain is the most common complaint for which individuals seek medical attention (1) . Persistent pain is associated with large decrements in psychological health and daily functioning (2). When successful, pai n treatment that relies on the trad itional medical model can be gratifY i ng for both physicians and patients. Relief of discomfort can be accomplished safely and easily with nonprescription medications and/or osteopathic manipulation. However, effective treatment using this model depends on two factors: 1. Clearly identifiable and correctable biologic mechanisms un derlying the pain 2. A straightfo rward treatment strategy that i nterrupts the pain signal Unfortunately, only a small subset of pain cases meets these c riteria. For the vast majority of patients the pain persists and becomes chronic. The underlying causes cannot be clearly iden tified o r medically corrected and numerous attempts to surgically or biochem ically dec rease the pain signal fai l to provide significant long-term relief. The founding princ iples of osteopathic medici ne are based on the observations that the body possesses a natural heal ing power and that there are inherent recuperative, restorative, and reha bilitative powers. As Irvin Korr writes in Chapter 1 of this text: 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 ro undergo spontaneous remission.
Chronic pain is unique in that the organized, i ntegrated unity and collaboration of body com ponents are not functioning in a restorative manner. The person in pain has a wonderfully evolved
endogenous opioid system built to relieve pain, and yet this nat ural ability to adj ust and adapt has somehow failed in the patient w i th chronic pain. Such pain problems are so remarkably resis tant ro conventional medical therapies that chronic pain is one of the most frequent causes of disability in the United States today (2). For the osteopathically trained physician, the musculoskeletal system is the primary means of pain expression. In the muscu loskeletal system, unique sensory, affective, and evaluative ex pressions of pain and its related behavior are made possible by the coordinated contractions and relaxations of striated mus cles. It is inevitable that continuous or chronic pain causes both structural and functional d isturbances in the m usculoskeletal sys tem. In turn, chronic pain causes repercussions elsewhere in the body and has an i m pact on the total functioning of the person. The osteopath recognizes that the person in pain is more than a biologic event. He or she is a thi n king, feeling problem solver. That person, when confronted with pain, actively seeks informa tion, makes decisions, and attempts to put forth his or her best effort possible in adapting to the painful condition. Osteopathic treatment i s aimed at the person in pain, not the pain in the m us cle or the pain in the head. The d ualistic separation of mind and body, which currently is un iversally rejected in osteopathic phi losophy, is still unfortunately the basis of much clinical med ical practice and biomedical research (3) .
HISTORY OF PAIN THEORY
The modern history of pain theory began w ith Descartes ( 15961650) , who considered the brain, rather than the heart or some other organ, as the site where pain sensation was recognized. He described the sequence of a pain event in three stages: I.
Onset of tissue damage
2 . Movement of a signal up a transmission l ine 3. Conscious experience of, and behavioral response
to
the pain
Descartes wrote (Fig. 15.1): IHor example fire (A) comes near the foot (B), the minute particles of this fire, which as you know move with great velocity, have the power ro set in Illotion the spot of the skin of the foot which they rouch, and by this means pulling upon the delicate thread (c, c) which is
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Specificity theory argues that pain results from excessive sti m ulation of touch sensors. It asserts that any sensory st imulus is capable of producing pain if it reaches sufficient intensity. Pattern Theory
Pattern theory suggests that all nerve endings at the periphery are fundamentally alike. A parricular pattern of impulses produces pain through the overst i m ulation of sensory nerves. Central Summation Theory
Cent ral sum mation theory asserrs that reve rbe ratoryactivity in the spinal cord , which projects signals to brain mechanisms, is the process underlying the perception of pain in response to intense sti m ulation or tissue damage. Fourth Theory of Pain
FIGURE 15.1. Descartes' (1664) concept of pain pathway. Fire (A), foot (B), thread (c, c), pore (d, e). (From Me/zack R, Wall PD. Pain mechanisms: a new theory.
Science. 1965; 150:971, with permission.)
The "fourth theory of pain" proposes that pain can be separated inro rwo components: perception of pain and psychologic reac tion to pain . It assumes a one-to-one relationship berween the intensity of the incoming noxious signal and the resultant expe rience of pain. The psychologic reaction to the pain is assigned a minor role. This theory is another version and refinement of the earlier specificity and summation theories of pain. It d iffers from earlier theories in that the psychological perception of pain is recognized as a component of the pain experience. Sensory Interaction Theory
artached to the spot of the skin, they open up at the same instant the pore (d, e) against which the delicate thread ends, just as by pulling at one end of a rope makes to strike at the same instant a bell which hangs at the other end.
Conrinuous pain that could not be linked to such a t issue damaging event was considered a mystery, a punishmenr, or a menral problem. As a result, the first systematic studies of pain did not take place until the early 19th cenrury, when physiology emerged as a true experimenral science. These early studies provided evidence that Descartes' theory of pain transmission lines and other mech anisms responsible for adverse pain signals were overly simplistic. Since that time, rather than focusing on the unity of m ind and body, pain research has focused instead on mapping and describ ing the pain transmission (nociceptive) pathways. Consequently, the evolution of pain theory has closely paralleled the increasing knowledge of sensory physiology. Since current concepts of pain managemenr are based on historical transmission theories, a brief outline of those theories follows.
Specificity Theory
Specificity theory asserrs that pain is an independent sensation. Pain has its own specialized sensory transmission apparatus that is associated with touch and temperature, which conveys infor mation from the sensory organ to t he brain cenrer responsible for that sensation.
The sensory interaction theory idenrifies the existence of rwo transmission systems involved in the movemenr of pain and other sensory information: 1 . A slow system that involves the thinly myelinated fibers 2. A fast system that involves the large myelinated fibers Accord ing to this theory, both systems transmit signals into the spinal cord . The cord sums the inputs and produces a neural pattern that is t ransmitted to the brain, where it is perceived as pam. Gate-Control Theory
The gate-control theory of pain (4,5) blends the scienrifically agreed on elements of the earlier signal transmission theories and emphasizes signal modulation at the spinal cord . Th is theory predominates today. The model is heuristic and incorporates ev idence of subcortical information ptocessing mechanisms that can inAuence the experience of pain. This includes specializa tion, cenrral summation, pattern ing, and modulation of inputs (Fig. 15.2) . These mechanisms were all cornerstones of earlier theories. The gate-conrrol theory also includes the inAuence of psychological evenrs on the perception of pain . A l imitation of the gate-control theory of pain is that psycho logical evenrs are not defined or differentiated from each other. All the brain's mechanisms and psychosocial factors involved in pain perception are placed under the umbrella term "cent ral conrrol
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Central control processes (cognitive control)
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I
I I
Medial Ascending pathways L
S
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Descending inhibition system
Lateral Ascending pathwa ys
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ivational-affecti ve
system
I I I
I
(central intensity monitor)
I
I I I I I I
Motor mechanisms
� (action system)
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Senso ry
Discriminative system (spatio-temporal analysis) -
FIGURE 15.2. Conceptual model of sensory, motivational, and central control determinants of pain according to Melzack and Casey. Output of T cell in the dorsal horn projects to the sensory-discriminative system via the lateral ascending system, and to the motivational-affective system via the medial ascending system. Central control "trigger" is represented by the heavy line running from the large system to the central control processes. Interaction between motivational-affective and sensory-discriminative systems is indicated by arrows. (Slightly modified from Bonica JJ, sec. ed. The Management of Pain, I. Philadelphia, PA: lea & Febiger, 1990:90.)
processes." Since the advent of gate theory, research on the spinal thalamic tracts and gat ing mechanisms in the spinal cord has increased and added to the development of this theory.
PSYCHOLOGICAL COMPONENTS
Signal transmission is the main focus of all these earlier pain theories. The consequence of this preference for t ransmission models of pain is that the central control processes become an inconsequential repository for the mind and the psychosocial factors associated with the experience of pain. The psychological factors includes: • • • • • • • • •
Memory for pain Attention and distraction Cogn ition and affect Meaning of the pain Personality traits and disorders Early pain experiences and learning Social context and cultural background Informat ion-processi ng style M i nd and conscious awareness
The organizat ion, let alone function, of the central control processes must be at least as complex as the physiologic pain transmission systems studied thus far (4) . Bonica took a significant step toward incorporating psycho logical component s into chronic pain models. He i ncluded the brainstem pain inh ibitory systems i nto the evolving blueprints of pain signal transmission within the brain. Accord i ng to
Bonica (5) , one structure of the descending inhibitory system, the periaqueductal gray, "receives important input from such rostral structures as the frontal and insular cortex and other parts of the cerebrum that are involved in cognition." As un de rstand ing of the brain's involvement in pain perception grows, a complete blueprint of the transmission system must include a description of how the conscious human mind processes pain informat ion. For the osteopathic physician, the mind and body are in separable. Osteopathic philosophy is rooted the belief that the experience of pain as displayed in the musculoskeletal system is i nfluenced by: Genetics Lifelong learn ing and conditioning • Use and abuse of the body • Social and cultural factors that shape the individual's percep tion of pain
•
•
DEFINING PAIN
In 1979, the Subcommittee on Taxonomy of the International Association for the Study of Pain redefi ned pain by integrating both physiological and psychological component s . This modifi cation was published in Pain ( International Association for the Study of Pain) (6) as well as in the Proceedings of the 3rd World Congress on Pain (7). Pain: An unpleasant sensory and emotional experience associated with acrual or potential tissue damage, or described in terms of such damage.
15. Pain Management
Note: Pain is always subjecrive. Each individual learns rhe appli carion of the word rhrough experiences relared ro injury in early life. Pain is rhe experience rhar we associare wirh acrual or porenrial rissue damage. lr is always unpleasant and rherefore an emorional experi ence. Many people report pain in rhe absence of tissue damage or any parhophysiological cause; usually rhis happens for psychological reasons. This definirion avoids rying pain ro rhe stimulus. Acriv iry induced in rhe nocicepror and nociceprive parhways by noxious srimulus is nor pain, which is always a psychological srare.
Acute Pain
Acute pai� is usually associated with a well-defi ned biologic cause and a rapid onser. Ir vanishes after healing has occurred. Acute pain follows an inj ury to the body and implies a natural healing process of short duration. It is only expected to persist as long as the tissue pathologic condition itself. Acute pain is also often , but not always, associated with objective physical signs of: • • • • • • • • •
Increased cardiac rate Increased systolic and diastolic blood ptessure Increased pupillary diameter Striated muscle tension Decreased gut motility Decreased salivary flow Decreased superficial capillary flow Changes in bronchiole diameter Releases of glycogen, adrenali ne, and noradrenaline
These changes in dynamic activ ity are assumed to be roughly proportional to the intensity of a noxious stimulus. The enor mous biologic value of acute pain is a rapid orientation to the noxious stimulus and reaction to minimize or escape the damage being done by the noxious stimulus. Some acute pain during the healing process fosters rest, protection, and care of the i njured area and thereby promotes healing and recuperative processes. The overall behavioral signs of acute pain are agitation and the emerging flight-or-fight reaction. Patients with acure pain are anxious about the pain's intensity, meaning, and impact on themselves and their l ifestyles. Drug therapy and allowing the natural healing processes to occur are the mainstay of treatments for the management of acute pain .
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At the biochemical level, when noxious stim ulation of muscle afferent C fibers i s prolonged and persistent, excitatory amino acid and peptide neurotransmitters are released in greater amounts and for longer periods (8). The resulting activation of N-methyl-D aspartate ( N M D A) receptors and the release of substance P leads to hyperexcitability of central nervous system (CNS) neurons and expansion of the size of the painful area beyond the original site of damage. This central sensitization and enlargement of peripheral pain receptor fields (9) allows nonnoxious sensations such as light touch to be experienced as painful (allodynia) and noxious stim uli to be perceived as more painful (hyperalgesia) (0). These biochemical changes add to the suffering and misery associated with chronic pain. A pattern of objective signs also emerges as the patient in chronic pain now reports: • • • • • • • •
Sleep disturbance Decreased libido Irritability Depression Decreased activity level Deterioration in i nterpersonal relationsh i ps Change in work status Increased preoccupation with health and physical function
Over time, patients in chronic pain become hypervigilant to all i ncoming stimuli, their behavior regresses, and they demand pain control from the medical community at any cosr. The envi ronment around the p atient i n chronic pain also often reinforces these ongo ing pain behaviors. The pain behaviors are expressed through the m usculoskeletal system and are i ntegrated into the patient's l ifestyle. The result is that pain becomes the focal point of the ind ividual's life. This leads to demoralization and sufferi ng. The outcome of these structural and functional disturbances is the refractory, enduring pain experience commonly referred to as the "chronic pain syndrome." The person in pain expresses all these structural changes, f unctional disturbances, thoughts, feelings, and pain behaviors through the m usculoskeletal system . Much visceral, metabolic, and endocrine activity is also responding to the moment-by moment changes of the musculoskeletal system in response to prolonged pain. With this rich afferent input of the musculoskele tal system i nto the CNS , it is inev itable that continuous red un dant pain has profound consequences to the patient's mind, body, and spirir.
Chronic Pain and Suffering
Unfortunately, and rather often, pain persists after healing. It also persists after all conventional medical treatments and drugs have been tried. A constant barrage of erratic nociceptive impulses into the brain provide no new or useful information, but the adverse signal continues to reach consciousness. As an example, a pa tient with a failed back surgery 2 years postoperatively does not need to experience pain every time he moves his spine to rem ind him that he has scar tissue, adhesions, and functional changes in the structure of his back. Since he is no longer in the acute heali ng phase, the information provided by this type of repetitive noxious stim ulation leads to center sensitization, neuroendocrine abnormalities, and abnormalities of regional cerebral blood flow.
NEUROPATHIC PAIN
Convincing arguments exist for the stance that chronic pain in some cases is caused, or at least set in motion, by chronic patho logic conditions and/or damage to the CNS. Neuropathic pain mechanisms that can be self-sustaining produce complex, erratic nociceptive data that continually activate the biological and psy chological systems involved in the perception and expression of pain (5) . Examples i nclude: 1. An abnormal neural hypersensitiv ity that results from pro longed nociception, such as when wide dynam ic range neu rons (WD RNs) of the dorsal horn are activated in response
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to repeated intense stim ulation. Once activated, the W D RN s will respond t o non noxious stimuli a s strongly a s they had to noxious stimuli. 2 . Ton ic sensory inputs that originate in scar tissue, damaged nociceptive fibers, collateral sprouting, and peripheral neu ropathies. 3. Phasic sensory inputs that are brief, fast-rising ( i . e., quickly reaching maximal intensiry), intense, novel, or complex. 4. Visceral and sympathetically maint ained somatosensory and nociceptive inputs. 5. All other sensory end-organ inputs, particularly thermal sensory and mechanical-sensory inputs that have become con ditioned stimuli through repeated pairing with nociception. 6. A lack of descend ing inhibi tory tonic and phasic down-flow from the brain. NOCICEPTORS
Pain begins when a poten tially tissue-damaging stimuli activates specialized sensory receptors called nociceptors. These nocicep tors are found mostly in the skin, subcutaneous tissue, and muscle fascia and j o ints. When activated , nociceptors, l ike other end organ receptors generate i mpulses that are transm i tted along pe ripheral fibers to the C N S . Some characteristics that d i fferentiate nociceptors From other somatosensory receptors are: 1. Small receptive fields 2. High-response thresholds 3 . Relatively persistent d ischarges without rapid adaptation 4. Location restricted to the end ings of small afferent fibers NOCICEPTION
Nociception is a neurochemical process by which a noxious stim ulus creates a pain signal that is transmitted from the periphery to the brain. It begins with noxious stimulus that distorts or damages tissue releasing the endogenous inflammatory chemi cal by-products of tissue damage such as prostanoids, serotonin, cytokines, h istamine, and b radykinin. These chemical by-products of tissue damage activate rwo classes of peripheral nociceptors that cause subjectively d i fferent noxious inputs. The A8 fibers produce sharp, well-localized, d is tinct pain associated with the injury i tself. In contrast, C fibers produce a dull, poorly localized, surprisingly persistent signal that evolves aFter injury. At the time of injury, pain is fi rst created by A8 fibers, and later by unmyelinated C fibers. Activation of these primary aFFerent neurons leads to a release of excitatory amino acids, such as glutamine and asparagine, which act on N M DA receptors. Substance P is then released ( 1 1) which leads to Long fastingdepolarization of the cell membrane and initiates continu ing transmission of the noxious signal straight to the brain, which explains why pain may continue long aFter inj ury. The final subjective pain experience is only weakly correlated with the degree of injury, the extent of damage, the number o f receptors afFected, or t h e energy of t h e noxious stimulus that provoked them. It is not the noxious input i tsel f but rather how
i t is interpreted by the brain and conscious mind that determines an individ ual's unique pain perception and behav ior.
SPINOTHALAMIC PATHWAYS
The spinothalamic system consists of rwo parts: the neospinotha lamic tract and the paleospinothalamic tract. Both contribute in d iFFerent ways to the perception of pain. In addition to nociception, other sensory information is trans mitted along these pathways, contributing to the inFormation and raw data entering the brain in response to nociception. The neospinothalamic tract rapidly delivers noxious impulses that give rise to the perception of sharp, well-localized pain, and an imme diate warning of possible progressive inj ury. The slower paleospinorhalamic tract is composed of both long and short fibers projecting to the thalamus, insula, and cingulate and p reFrontal cortices. Its pain perception is one of dull, aching, poorly localized pain sensations. Impulses arriving from the pa leospinothalamic pathways synapse with neurons that reach the l imbic forebrain structures. They then profusely project to many other parts of the brain. This pathway transports large amounts of general in formation that produce the long-term motivational and emotional d imensions of pain. Although the spinothalamic transmission systems appear to correlate well with A8- and C-fiber pain, one cannot assume that these structures simply represent subjective di mensions on a one to-one basis. There are many interactions and feedback loops be rween them. Nor should it be assumed that the A8 and C fibers contribute solely to neospinothalamic and paleospinothalamic pathways, respectively. Pain transmission can be closely approx i mated by such a model, but it is a comparatively simple trans mission schematic. Although nociceptors can faithfully detect, transduce, and sig nal tissue inj ury, the afferent barrage is modulated at all levels of the nervous system by a multitude of neurochemical pro cesses, spinal cord excitabiliry, and brain reorgan ization. Long term changes in sensory neurons create self-perpetuating neu ronal activiry even before the noxious stimuli reach higher brain centers. Much of this modulation is activated by sympathetic and somatic efferent neurons, which cause vasoconstriction and skeletal muscle spasm. In the brain, the synthesis of a complex pain perception From the incoming sensory information is fur ther modified by anxiery and brain chemical changes following persistent noxious input. F unctional brain imaging studies indi cate that there are brain chemical abnormalities in chronic pain patients and that pain perception is linked to specific neurochem ical changes resulting in long-term cortical reorganization ( 12). Specifically, there is a depletion of N-aceryl aspartate and glu cose in prefrontal cortex. N-aceryl aspartate is localized within the neurons and involved in synaptic processes and functions as a neural axonal marker ( 13). More important, the breakdown of N-aceryl aspartate has been documented in various cond itions of neuronal cell damage and losses including stroke, multiple sclerosis ( M S) , Alzheimer disease, and epilepsy (14) . Persistent noxious input alters brain chemistry in the prefrontal cortex, which is i mportant to sensory learning (I5). Changes in pre frontal cortex chemistry also disrupts overall cognitive processes
15. Pain Management (16) contributing to the suffering experienced with continuous noxious sensory input (17,18) . Functional imaging stud ies also support the idea that pain is processed and experienced within a d istributed and intercon nected network or neuromatrix of cortical and subcortical struc tures. This complex synthesis of chem ical and b iopsychosocial factors into a network of interconnected causal agents helps to explain why chron ic pain often persists. It also explains why the osteopath ic emphasis on the musculoskeletal system and t reat ing the whole person is critical to the effective management of chron ic human pain. Central Control Processes (the Mind)
Central control processes is the term for the brain's mental t rans formation of a nociceptive signal into cogn itions, emotions, and behavior responses. The patient's responses to pain also are either reinforced or punished by the env ironment. That information is then fed back through the central control processes. Th is syn thesis of nociceptive information across a series of cognitive and emotional appraisals allows the individual to surv ive, adapt, and learn. The suffering associated with ch ron ic hu man pain reflects ongoing challenges to the pain information-processing system. The suffering and agony occurring in the patient's m ind i s of ten a consequence of prolonged and erratic noxious sti m ulation. The end product is the patient's inability to integrate additional incoming noxious data into adaptive information-processing rou tines or to elicit effective strategies for coping with pain. For the osteopath ic physician, already well versed in the philosophy and practice of manual medicine, the realization comes quickly that the patient in pain has a mind (or central control processes) insep arable from the body and that the pat ient actively thinks and has feelings about their pain. Becoming versed in how the pain infor mation is psychologically o rganized in the human mind allows the osteopath to bring their medical practice to fruition.
PAIN INFORMATION FLOW AND THE MIN D
Information Row implies that humans have the capacity co iden tify and incorporate potentially useful stimuli, co translate and transform the information received from the stimuli into mean ingful patterns, and co use these patterns in forming an optimal response (19,20). The pain informat ion contained in Ao-fiber input immediately accesses and activates precise central control processes, wh ich then rapidly and efficiently respond co a poten tial tissue-damaging stimulus. In contrast, C-fiber pain informa tion supplies an ongoing status report after the inj ury and brings into focus all conditions that s ur round the inj ury. As the individual thinks about the particulars of the t issue damaging event, learning takes place. The individual antici pates damaging events and makes adjustments co optimize their chances for adaptation, learning, and long-term surv ival (21). Historically, the basic need co anticipate and avoid potential tissue-damaging events has set the stage for considerable com plex higher-ordered thinking and innovative problem solving. Th rough evolution, humans have become good at anticipating, avoiding, or minimizing pain. When these skills are augmented
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with the ability co create symbols for communication, and co use language, reasoning, and abstract thinking, the result is the capacity for maximal adaptation. Persistent pain can lead co spinal cord excitability, brain reor ganization, and self-perpetuating neuronal activity. The cellular and neurobiologic consequences are anxiety, depression, and re duction in quali ty o f l i fe (21) . Behaviorally, the patient continu ally seeks medical attention in search of t reatment that will either interrupt the pain signal or help manage the i mpact of the pain on l i festyle. As a result, the patient begins co suffer, and the suffer ing continues unti l the threat has passed. Information processing models of pain assert that a specific series of mental events occurs at the central control level, following prolonged noxious stimula t ion (19) . F igure 15.3 illustrates the Row of somatosensory data through an interconnected network or cortical and subcortical structures, as a noxious sti m ulus i s transformed inro information that facil itates pain perception, cognitive-emotional appraisals, and musculoskeletal/behav ioral responses. The consequences of these responses are remembered and fed back through the cen tral control processes. Thi s results in a dynamic-plast ic system; dynamic in that the information-processing systems continually respond to nociception, and plastic in that they also continually change as a result of nociception. The synthesis of pain infor mation, coupled with the cognitive-emotional appraisals, allows individuals to survive, learn, and adapt. The osteopathi c profession has a h istoric opportunity to help suffering patients because of its philosophy of whole-person, health-oriented care. Osteopath ic physicians al ready recogn ize the relationshi p between the m usculoskeletal system and pain expression. Osteopathic physicians understand and expect the interaction of mind and body systems. Osteopath ic physicians know that systems both influence and are inRuenced by mental information-processing systems, the manifestation of wh ich-a patient's pain and suffering-is shaped by a hiscory of learning experiences, pain perceptions, and appraisals. Pain Perception
The noxious sensory input is in itially d i rected to the medial and lateral thalamus, anterior cingulate cortex, somatosensory, and perifrontal cortex. The noxious sti mulus is consciously registered along with many other sensory inputs surrounding the painful event. Conscious attention i s d irected quickly toward noxious, damaging, or th reatening sensory events . The m ind's central con trol p rocesses scan this pain information for recognizable patterns in an effort to attach meaning, affect, and (eventually) a label to the nociceptive event. The ability to focus selectively on noxious stimuli in the perceptual field, while ignoring others, is extremely i mportant. If h uman beings did not quickly focus on pain, we would be overwhelmed by the many extraneous events present at the point of the t issue-damaging event and not protect ourselves, fight, run, or tend to the wound. If the noxious signal is very intense or the damage very seri ous, the central control p rocesses will stop the pain processing to devote all resources to coping and survival. We are built to survive first and have pain second. Descending pain inh ibitory pathways from the brain modulate the t ransmission of the noci ceptive signals to form an endogenous, anti-nociceptive system.
ENVIRONMENTAL RESPONSE
/
� SUFFERING
PAIN
/
� BEHAVIORAL RESPONSES
BRArN STEM REFLEXES
·Startle reflex
•
Vocalizations
·Fight or Flight
·Emotional expressions
·Immune system
·Musculoskeletal reactions
·Endogenous antinociception
·Problem solving routines
system
PREFRONTAL CORTEX ·Mediating complex behavior ·Long term planning ·Reasoning, reflection ·Abstract thinking •
Long-term memory
ANTERIOR CrNGULATE CORTEX
SOMATOSENSORY CORTEX INSULA
Area
"PAIN
24
NEUROMATRIX" ·Integrates cognition, affect,
·Precise detailing of pain
response selection, pain memory
sensation, localization, intensity •
•
Alerting, orienting
LA TERAL THALAMUS
Emotional appraisals
MEDIAL THALAMUS
·Registers incoming pain
·Integrates surrounding pain
intensity and location
information
SPINAL MODULATION •
Substantia
•
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FIGURE 15.3. Central control flowchart for the series of cortical activations and mental events that occur following noxious sensory input. Pain and suffering are an emergent property of the human brain as the noxious stimulus is processed in an interconnected , parallel neuronetwork ("pain neuromatrix") composed of cortical and subcortical brain structures.
15. Pain Management Components of this system are found in the m idbrain periaque ductal gray matter, the nucleus raphe magnus, and the locus caeruleus. The chemical spinal mediarors involved in descending anti-nociception include seroronin, norepinephrine, and acetyl choline 8. When activated, these brain systems can dampen pain sensation and inhibit behavior reactions typically evoked by nox ious stimuli (22). Cognitive/Emotional Appraisals
When the nociceptive signal reaches h igher brain centers and true consciousness, thoughts, feeli ngs, and words are put ro the event, memories form, and plans of action are made. The cog nitive/emotional appraisals occur at the anterior cingular correx, parricularly the Brodmann areas (23,24). The anterior cingulate correx is an extensive area of the limbic correx overlying the cor pus callosum which is involved in the integration of cognition, affect, and response selection. Projections ro the prefrontal correx activate th inking about the pain and rev iew of past memories of pain (24) . Cont inuous pain and activation of pain memories encourage the assignment of global labels ro pain experiences, lumping a large variety of pain experiences inro a single pain construcr. Memories that are associated with the nociceptive signal are srored ro form an expansive nerwork, or neuromatrix, of pain-related information (25) . A pain neuromarrix can be thought of as a cognitive srructure that forms the basis for all furure beliefs abour pain and for the problem-solvi ng strategies employed in response ro pai n. As pain becomes chronic, the pain neuromatrix expands and becomes more rigid in a self-perperuating process. I n trying ro find a way ro cope with the pain, individuals begin focusing more on the pain, ignoring i nformation or explanations that do not fit the pain neuromarrix. Over t i me, pain memories and appraisals are rev ised ro fit the pain neuromarrix, furrher expanding and solidifying ir. Emotional appraisals of the noxious sti m ulus be come "hot" or emotionally charged when the current pain event is perceived as hav ing a sign i ficanc personal impacr. A number of appraisal steps are involved in this process. The outcome of each appraisal can set the stage for the next appraisal. T he entire ap praisal process rriggers significam emotional linkages ro the pain . The emotional appraisal process begins with orienci ng and startle reflexes, and subsequent feeli ngs of surprise or interest, preparing the individual ro engage in more focused detailing. For example, furrher appraisals m ight determ ine that the noxious stimulus is harmful, generati ng fear and hyperv igilance. If the noxious stimulus is appraised as damaging, the i ndividual would feel anxious and likely avoid the sti mulus. If the noxious stimulus is appraised as benign, the individual might experience some interest or cur iosity and even decide ro approach and learn more about the noxious i npur. In either case there is generalized auronomic arousal and moror responses, such as those that would be called on ro fight o r flee. If a person is unable ro take any action, they often feel anger when their actions are blocked or sadness from a sense of loss of control. Over t ime, the loss of concrol over the noxious sti m ulus leads ro depression. The patient begins ro reporr feeling rrapped, helpless, or frusrrated with the i nability ro overcome pain.
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Eventually the patient makes a global appraisal in an efforr ro understand the painful event, especially why it happened and its long-term i m pacr. Emotions attached ro the ourcome of global appraisal include shame, fostered by a sense that one has failed ro reach an ideal standard for mastering and living with chronic pain. Emotions also include guilt, fostered by a sense that one has t ransgressed personal, family, and/or cultural expectations for adequately coping with pain. As a result of these perceptual and appraisal processes, behaviors are selected, emotions are la beled and linked ro painful musculoskeletal sensations, and the experience of pain and suffering reaches full expression, often th rough the m usculoskeletal system. Pain Information-Processing Summary
Processing the pain information contained in a noxious stimulus requi res that a person: 1. Selectively review all information at the onset of pain. 2. Retain various aspects of the i nformation ro be analyzed and organized i n ro meani ngful patterns (i.e., "pain neuromatrix"). 3. Compare this noxious sti m ulus i nformation ro pain i nforma tion already catalogued in memory. 4 . Transmit recognized pain patterns ro specific pain information appraisal systems, including those responsible for attachi ng affect and meaning ro the experience, and those responsible for translating the pain information inco behav io rs, muscu loskeletal reactions, and problem-solvi ng routines. 5. Selecting and executing various problem-solving srrategies i n an effort ro adapt and cope with p a i n and learning. These pain strategies both influence and are influenced by the pa t ient's m usculoskeletal environmenr. A majo r p layer in the pa tienc's musculoskeletal environmem is the osteopathic physi cian, who often only sees the end p roduct of musculoskeletal reactions, pain behaviors, and the patient's demand for im mediate pain management.
PAIN MAN AGEMENT
Convenc ional treatment of chronic pain is often complicated by a patient's beliefs about medical science and the expectations that they consequently place on physicians. For example, many pa t iencs believe that complete pain relief is not only obtainable but is their right, and they expect physicians ro provide that relief. Unforrunately, the underlying biopsychosocial mechanisms of chronic pain are not fully undersrood. As a result, convent ional treatments fail, leading ro frustrat ion for the patient , whose ex pectations are unfulfilled, and for the physician, whose goals are blocked . A large part of a physician's practice involves treating patients who have chronic pain. Treatment begins with a biopsychoso cial pain hisrory. A simple mnemonic for that hisrory is found in Table 15 . 1. Convencional approaches ro pain t reatment rely primarily on: 1. Medications 2. Anesthetic blockade
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TABLE 1 5 . 1 . S I MPLE MNEMONIC TO COLLECT BIOPSY CHOSOCIAL PAIN H I STORY P A
Palpatory evidence; motion that provokes pain
I
Intensity
N
Name (how it feels in sensory, affective, and evaluative terms)
S
Suffering and stress (pain's impact on quality of life, mood,
Area (location, radiation, dermatomes)
(0- 1 0 score)
relationships, and family)
3. Physical therapies 4. The osteopathic mission to restore function Medications
Medications are an important management strategy, particularly for acute pain. The three main categories of medications are: 1. Nonopioid analgesics: aspirin, salicylate salts, acetami nophen, and nonsteroidal ant i i n flammatory drugs (NSAl Ds) 2. Opioid analgesics 3. Analgesic adjuvants These drugs are prescribed accordi ng to the World Health Organization's analgesic ladder. I t i nvolves choosing among these th ree groups based primarily on pain i n tensity. Many m ild-to moderate acute pains readily respond to nonopioid analgesics alone; they are the obvious first choice. Some moderate-to-severe pains may require combining the nonopioid analgesics with a low-dose opioid preparation, the second step in the analgesic ladder. The third step is the addition o f a h igh-dose, time-released opioid preparation to the nonopioid analgesics. At any of these three steps, analgesic adj uvants might also be useful. The American Pain Society (APS) and the I n ternational As sociation for the Study o f Pai n (IASP) outline a number of i m portant concepts to remember when choosing drugs to manage paIn: l.
Individualize route, dosage, and schedule
2. Administer analgesics on a regularly predetermined time schedule 3 . Recognize and treat side effects 4. Do not use p lacebos to assess nature of pain 5. Watch for development o f tolerance 6. Use analgesic adjuvants
intermuscular route, which has the d isadvantages of painful ad ministration, fluctuations in the absorption from muscle, an up to 60-minute lag to peak effect, and a rapid fall-off. Intravenous bolus adm i nistration provides the most rapid onset, with shorter time to peak effect. Repeated boluses can be llsed to load concen trations providing pain relief, followed by mai ntenance infusion for severe pain. Continuous i nfusions provide steady blood levels with fewer side effects. Patients can also be given active responsibility and a sense of control over their medication by selF-administering an analgesic bolus with a microprocessor controlled by infusion pump. The opioids can also be administered intraspinally (epidural or in trathecal). Described as patient-controlled analgesia (PCA), the patient can activate a demand switch that delivers a preset dose of opioid into an intravenous l ine, if a predetermined time (often called the "lock out" i nterval) has elapsed since the previous dose. In some of the most severe and long-term chronic pain cases, the entire system can also be implanted in rhe individual and pro grammed to deliver medication across a preset daily schedule. An implanted morphine pump is for severe, long-term chronic pain cases, such patients with cancer or who are terminally ill, or when all other treatments have fai led. Another advance in the route of administration is transder mal patches that allow the medication to be absorbed through the skin. These patches provide contin uous opioid infusion with out pumps, needles, or internally implanted devices. Children, in particular, would rather endure pain than have a shot or pai nFul procedure. Fortunately, opioids in lollipops, nasal sprays, and rectal suppositories are now available. New, longer-acting topo graphical preparations such as a lidocaine patch are also available and can be applied to the skin an hour beFore a painFul injection. It is crucial not to create pain during the attempt to re l ieve pain. The old adage that "something has to hurt or taste bad to work" is archaic. PainFul injections and procedures run the risk of provoking i n flammation and muscle spasm in the vicinity of the injection, thereby generating central sensitization and even more pai n. Similarly, sympathetic reflexes can occur, which decrease microcirculation in the injured tissue and adja cent m uscle, producing some degree of ischemia and smooth muscle spasm. Because pain is a complex perception, many painFu l procedures performed to relieve pain can, over time, al ter how pain i nformation is processed mentally. This can lead to pain avoidance behaviors such as inactivity and/or Fear in an ticipation of pain leading to excessive autonomic arousal and analgesic use.
7. Block pain trans mission These organizations are a constant source of updated i n for mation on the rapidly changing pharmacologic knowledge base regarding pain control with drugs. See the " Resources" section at the end of this chapter for contact i n formation.
INDIVIDUALIZATION
The oral route of medication adm i nistration is optimal because of its convenience, safety, flexibility, and the relatively steady blood levels produced. It i s especially optimal when compared with the
AN ALGESICS
When pain medications are given on an as-needed basis, it can take several hours and h igher doses of opioids to relieve pain, leading to a cycle of undermedication alternating with periods of overmedication and drug toxicity. Administering opioids on a scheduled, around-the-clock basis leads to fewer side effects. Al though morphine i s a strong opioid and often is a drug of choice, it is important to be Familiar with the dose and time course of a variety of opioids. Patients must be followed closely, particularly when begin n ing or changing an analgesic regimen. Monitoring
15. Pain Management pain relief and side effects frequen tly, and adjusting the regimen accordi ngly, is crucial.
SIDE EFFECTS
The mosr common side effecrs of opioids i nclude sedarion, con sripation, nausea, vomiting, itching, and respiratory depression. These side effecrs can escape recogn irion unless rhe parient is asked directly abour them. Several ways to treat side effecrs are to: 1.
Change the dose, regimen, or route on rhe same drug
2. Try a different opioid 3. Add anorher drug thar counteracts the adverse effecr 4. Use a route of admi nistration rhat minimizes drug concentra rions ar rhe sire producing the side effect When choosing drugs, one should also be aware of rhe poren rial hazards of mixed agonist-antagonisrs.
PLACEBOS
The analgesic effecr from intramuscular saline (or anorher placebo) provides little i f any useful informarion about the gene sis or rhe mechanisms of pain. In fact, many parients who have a documenred organic basis for their pain obrai n remporary relief from sal i ne injecrion. A recent sysremaric review of 130 studies involving 3,795 patients wirh physical parhology indicared a con sisrent reducrion in pain i nrensity for rhose assigned ro placebo groups (25) . There are many sufficient biochemical and psycho logical reasons to explain a person's favorable response to placebos. The brain produces a variety of morphi nelike pepride subsrances, the mosr prevalenr of which are enkephalins and endorphins. Derivatives of these compounds, metencephalon and endorphin, are derived from pituitary-lipotropin and have opioid-agonist properties. Binding of enkephalins to specific receptors appears to inhibit the transmission of noxious impulses via peripheral unmyelinated fibers to the higher cenrers of the brai n. These en dogenous opioids have also been found in higher centers o f the CNS, such as the hypothalamus, periaqueductal gray maner, and nucleus raphe magnus. Pain-relieving, morphinelike peptides are produced in response to a person's feelings and beliefs about the treatment. These naturally occurring pep tides act l i ke morphine, with the exceptional advanrage of being produced endogenously. A positive placebo response simply speaks to the strength of an individual's central control processes (i.e., mind) to recruit their descending inhibitory system to block pain. The osteopathically trained physician knows that pain relief occurs both i n the m ind and in the body.
PHYSICAL TOLER ANCE/DEPENDENCE
Tolerance means that a larger dose of medication is requi red to maintain the original effect. This is an especially common oc currence in patients in all age groups who regularly use opioid analgesics. To delay rhe development of tolerance, and to pro vide effective analgesia for the tolerant patient, opioids can be
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combined with nonopioids or switch can be made to an alternate opioid. B e aware of the development of physical dependence. Physical dependence means that an abrupt cessation of the opi oid will lead to withdrawal symptoms. Opioid use is limited by legitimate concerns such as m isuse, addiction, and possible di version for nonmedical uses (26) .
PSYCHOLOGICAL A D DICTION
It is difficult to compete with morphi ne for i ts analgesic efficacy. Opioids are very reinforcing as they relieve pain. Morphine, l ike alcohol or caffeine, easily passes through the blood-brain bar rier and goes directly to the brain . Behaviors on the patient's part that secure a continuous flow of opioids are quickly rein forced. Addictive behaviors, including excessive medication de mands or prescription misuse, are often determined and shaped by the reinforcement, or consequences o f the patienr's request for pain-relieving drugs and the powerful relief they bring. In ad dition drugs that appear to stim ulate brain reward mechan isms, such as opioids, sedatives, stimulants, anxiolytics, and can nabi noids, are particularly prone to addictive behaviors. The patient in chronic pain exhibiting drug-seeking behaviors and becoming overwhelmingly involved with using and procuring pain-relieving drugs may be demonstrating learned addictive behaviors, some of which are i nadverten t1y learned in the doctor-patienr relation ship. I n the usual medical setting, these learned behaviors take the form of: 1. M issed office appointments with subsequent o ff-hour calls for prescription renewals 2. Forgery of prescriptions, or solicitation of prescriptions from multiple physicians 3. Securing drugs from other patienrs, family members, or off the street 4. Loss of control, craving, and compulsive use despite negative consequences 5. Novel dosing, timing, or route of administration, such as oral to mucosal or i n travenous Ie is i m portant to be alert to these cues. Remember, the patienr with physical pathology who i s undermedicated will also be ex hibi t i ng addictive behaviors, and the diagnosis in that case will be "pseudo-addiction." Patients with legitimate chronic pain will re spond to opioids admi nistered on a scheduled around-the-clock basis.
AN ALGESIC ADJUVANTS
A number of other classes of drugs can either enhance the ef fect of opioids or aspirin l i ke drugs, have independent analgesic activity in certain s ituations, or counteract the side effects of analgesics. The most common o f these are the tricyclic antide pressants and the newer seroton i n reuptake inhibi tors (SSRls) . In controlled trials, these drugs have relieved pain related to neu ropathy, postherpetic neuralgia, and chronic pain syndromes, regardless of whether the patienr was depressed. The analgesic
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effect of tricyclics begins at lower doses. In animal studies, tricyclics potentiate opiate analgesia, possibly by blocking the reuptake of serotoni n and norepinephrine at CNS synapses. However, there is no evidence to support the use of tri cyclics in acute pain treatment. Interestingly, tricyclic antide pressants, which block the reuptake of norepi nephrine and sero tonin, are largely used for the treatment of neuropathic pain. Noradrenergic-2 agonists are popular bur they can produce side effects, especially hypotension and sedation. They are primarily l i mited to patients with long-term chronic pain. The following have all been prescribed as analgesic adjuvants with varying and limited degrees of success: • • • • • • • • •
N SAlDs Cyclooxygenase (COX)-2 inhibitors Antihistami nes Benzodiazepines Hypnotic agents Muscle relaxants Steroids Opioid agonist/antagonists/extenders/antiemetics Anticonvulsants
patterns that help in coping with the pain. There are several anesthetic blockades that attempt to intercept the noxious in put and thereby prevent its entry into the perceptual field. These i n clude:
Facet Injection:
Facet rhizotomy:
Dry needling of trigger points:
Local infiltration oftrigger points with anesthetics:
As with all medications prescribed as analgesic adj uvants, these should provide an opportunity for: Increasing activities of daily l iving Participating i n physical therapy • Decreasi ng pain behaviors • Developing long-term behavioral changes and pain-coping strategies •
temporarily decreases small fiber afferent activity by injection of a local anesthetic into the articular branches of Luschka, which innervate the zygoapophyseal joint capsules. eliminates small fiber afferent activity through thermocauterization of the articular branches of Luschka. produces a volley of small fiber afferent activity that causes brainstem inhibi tion of the ascending spinoreticular, spinothalamic, and spinocortical pathways. causes a biphasic effect that initially decreases pai n by the same mechanism as dry needling. Infiltration of the anesthetic decreases small fiber input from the trigger sites and central facil itory states. This decreases afferent activity associated with pain.
•
The patient given drugs for pain control should be actively partici pating in rehabi l i tation aimed at restoring functioning. Goals should be outlined for the patient that include a phar macologic interruption ofthe pain to allow behavioral changes and new cognitive and behavioral strategies for pain control. Discuss treatment goals with the patient prior to and conti n uously during the adm in istration of any drugs for pain control.
Counter Irritants
Counter irritants flood the perceptual field with many complex somatosensory stimuli, preventing the noxious input from be i ng fully recognized and channeled into the higher levels of the central control processes. These treatments, prescribed by the physician, are often carried out by a physical therapist sensitive to the osteopathic model of treating the biopsychosocial aspects of pain.
Hot Packs PAIN TRANSMISSION BLOCKING
To control acute pain, anesthetic blockade of neural transmis sion to vi rtually any part of the body can temporarily be achieved by di rect application of local anesthetics (nerve blocks) , such as procaine, lidocaine, tetracaine, or bupivacaine. In some severe cases, substances that destroy neural tissue can be i n jected ( neu rolytic block) in an effort to permanently obliterate the neural transmission mechanisms. Diagnostically, nerve blocks determine specific pathways to aid in the differential diagnosis of the site or transmission mech anisms of a given pain. Prognostically, they partially predict the probable effectiveness of neurolytic or neurosurgical procedures. Interestingly, the pain-relieving effects of local anesthetics can often exceed the duration of the chemical blockade of neu ral transmission. The reason for this is not completely under stood. It might be a result of decreasi ng sympathetic reflexes and skeletal muscle tension. Perhaps it results from the cre ation of pain-free time during which the patient can restructure the pain information-processing routines or learn new behavior
Hot packs promote local and reflexive decreases in sympathetic tone. Locally, this increases blood flow and washes out nociceptive metabolites. In general, it decreases segmental reflexes and sym pathetic tone, decreasing afferent activity and promoting muscle relaxation. Transcutaneous Nerve Stimulation
Transcutaneous nerve stim ulation (TNS) involves peripheral nerve stimulation with small amounts of electric current. The mechanisms underlying the therapeutic effect are not clearly un derstood, but three theories have been proposed: 1. Electrical stimulation p referentially activates large myelinated fibers in the spinal cord, i nterfering with pain perception and increasing pain tolerance. 2. Electrical stim ulation results in local axonal fatigue of A 8 fi bers, reducing small fi ber afferent (nociceptive input) activi ty. 3. Electrical stimulation activates the descending inhibitory sys tem, which is i nvolved in endogenous opioid production.
15. Pain Management Ice
Ice causes a sudden increase in smail fiber activity that Roods the afferenr pathways, causing the brainstem to inhibit further nociceptive inpur from the affected area.
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subjective and objective pain measurements in patients with fibromyalgia (29). I ncreased aerobic activity can also reduce headache (30). Proprioceptive Neuromuscular Faci litation
Vibra tion
Vibration differentially stimulates large proprioceptive afferent fibers. This action is thought to interfere with pain perception. Ethyl Chloride
Ethyl chloride Roods the ascending nerve pathways with small fiber input. When inrense, it can result in supraspinal descending inhibition of small fiber afferents.
OSTEOPATHIC PAIN MAN AGEMENT
Currenr osteopathic thinking is far more than structural diagno sis and pharmacologic management. The m ission of osteopathic pain management is to restore both physiologic and psychologi cal function through multiple avenues of intervention (27) . The magnitude and vision of treatment m ust go beyond the conven tional medical models of obstructing and/or flooding nociceptive pathways. The art and science of osteopathic medicine i s best expressed in the treatment of the musculoskeletal system. Os teopathic manipulative diagnosis and treatment are extensively reviewed in Section VII. The focus in this chapter is on other medical and psychological restorative treatments that comple ment the structural and functional management of the muscu loskeletal system. Stretching
Poorly conditioned muscles tend to be sore after exercise. Stretch ing produces relaxation ofhypertonic m uscles by increasing Golgi tendon-organ discharge and reflex i nh ibition. Stretching the hy pertonic muscles causes an i ncrease in y -afferent discharge that elicits brainstem- descending i nhibition, thereby faci l i tating m us cular relaxation. Simple stretching exercises reduce both the n um ber and intensity of myofascial trigger points (28) . Strengthening
Strengthening exercises hypotonic muscles. Muscle activity in creases blood Row and produces a trophic response. Patients are encouraged to begin a regular fitness program of simple Rex ion and extension exercises with the ultimate goal of establish ing a mainrenance program of walking, runni ng, or aquatic exercise to achieve muscle conditioning and cardiovascular endurance.
Proprioceptive neuromuscular facilitation ( P N F) involves the use of dynamic and static muscular contractions in the reacquisition of joint mobili ty and general Rexibility. PNF stimulates proprio ceptive and efferent i mpulses that promote more efficient muscle use, relaxation, and n u trition through i mproved neurocircula tory effects. PNF range-of-motion exercises use reciprocal i nhi bition concepts to relax muscles. The goal is to rehabil i tate muscle groups and rei n force appropriate motor unit patterning. Gait Training
Patients in pain will develop limps and move in guarded ways to obtain short-term pain relief. Gait training is used to improve patterned motion behaviors (ga i t) through synergistic muscular activities that im prove complex motor behavior. Biofeedback and Muscular Relaxation
Biofeedback therapy trains the patient to modify physiologic pro cesses that are monitored by some i nstrument or device. Tension headaches appear to originate with sustained contraction of the musculature of the neck and possibly the scal p. I nvestigators have developed biofeedback techniques for tension headache therapy using electromyography to evaluate tension in frontalis and other m uscles. For pain relief, the patient is also taught general relax ation techn iques, such as diaphragmatic breathing and p rogres sive relaxation. Patients are taught how to relax their muscles and to manage i nsomnia and anxiety associated with chronic pain. Relaxation techniques alrer sympathetic activity as i ndicated by decreased respiratory and heart rate, oxygen consumption, and blood pressure. Counseling
Counseling uses i n terpretation to identify unrecognized factors underlying maladaptive pain-processing routines. Some patients might unearth early t raumas that are played out in their chronic pain experiences. For example, an individual might begin to un derstand that pain perceptions are triggered or amplified by feel ings that originated in childhood but that later came to be labeled as pain. Counseling also actively reinterprets the associations be tween pain and other feelings-especially depression, shame, and guilt that sometimes arise our of the experience of pain i tself. The primary purpose of counseling is to foster coping mecha n isms through conscious awareness of feel i ngs, behaviors, and consequences. Behavior Modification
Cardiovascular Fitness
Research indicates that more that 80% of patients with mus cular pain are not physically fit, as determined by maximal oxygen uptake ( 28) . Cardiovascular fitness training decreases
Behavior modification incl udes classic and operant condition ing, desensi tization, and direct rein forcement for modifying pain behavior to alter the patient's perception and report of pain. For example, children and adolescents who are reinforced to
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[[I. Osteopathic Considerations in the Behavioral Sciences
attend school, despite having a headache, not only mai ntain their class progress, but have a significant reduction in their headache activity (3 1) . The osteopathic physician strongly rei n forces pai n coping strategies.
TEACHING PAIN COPING STR ATEGIES
Osteopathic physicians encourage adaptive coping mechanisms and mature defense mechanisms that are common among the mentally healthy.
Distraction: Sublimation: Suppression:
Problem solving:
Humor:
Volunteerism:
redirecting attention to reduce subjective distress associated with nociception. indirectly solving a problem by doing someth i ng else that gives you pleasure. a conscious decision ro postpone paying . attention to nociception and its consequences. anticipating future dangers l i nked to nociception and setting strategies i n motion t o deflect t h e danger. which perm its continuing emotional expression without individual discomfort or unpleasant effects on others. being altruistic involves getting pleasure from giving and supporting others, rather than being a victim to pai n.
SUPPORT GROUPS
Pain support groups rely on developing a strong therapeutic al l iance among group members and the physician or psychologist leading the group. These groups are an extremely powerful and low-cost strategy for managing large numbers of patients with chronic pain (32) . The goal is to help patients cope with and adjust to their pain and condition. In support groups, patients reconceptualize the meaning of their pain, their cognitive and emotional appraisals, and problem-solving strategies. They re view how their pain i mpacts themselves and their l i festyle and identi fy the events in the environment that rei n force their pain behaviors and musculoskeletal reactions. If not taught in a group therapy model, the following concepts form at least an outline for teaching coping strategies within the doctor-patient relation ship. These concepts are also the foundational ideas for the advice given to the pain patient on how to th i n k about and manage their pain (20) . 1. My pain is real. I will reject any notion that what I a m feeling is a l l in my head. 2. I accept that I might need outside help to control my pain, and I refuse to quit o r give i n to the pain and the deterioration it causes. 3. At times my pain has had an overwhelming influence on my l i fe, but I believe that I can choose how I react to it. 4 . My best efforts and those o f the medical community have not stopped my pai n. This is not necessarily a fault of mine or
a shortcoming of medicine. I will no longer fight with myself about this or blame medicine. No figh t, no blame. 5. I w i ll start by taki ng an inventory of the price I pay for pain, and the rewards I get from pai n. This inventory must be done honestly and without fear of the findings. I will recognize some aspects of my coping with pain that I am doing well, and will also admit to myself mistakes that I have made in trying to cope with the pain. G . I will forgive myself unconditionally for the past mistakes I have made while trying to adjust to the pai n, and forgive others whom I perceive are responsible for my pain and troubles. 7. I will discuss my pain-driven behaviors, feelings, and thoughts openly with those I trust and when appropriate, be willing to make amends for any harm that I might have done. 8. I will hold two ideas in my head: (a) something might come along to relieve my pain and (b) at this time, I have to cope with the pain I have. I will accept myself as a worthwh ile and fallible person who is l iving with pain at this point in my life. I will then move forward, with hope and courage, toward my primary goals of intimacy, bonding with others, and healthy interpersonal relationships. 9. I can choose to seek additional help at each step by devel oping a spi ritually based program directed toward acceptance of my pain . I can then live by whatever spiritual principles promote wellness. 10. After gaining a reasonable level of functioning and pain control, I will recognize that there is still more to life than a con stant struggle to live with pai n . Then, I will gradually separate myself from my pain management program or doctor, with the complete understanding that I may return at any time. I under stand that I have more important primary goals in l i fe, and that coping with pain is a secondary issue-something I do ro get ro these primary goals.
CONCLUSION
Pai n management options run along a conti nuum from noni nva sive and low-risk to i nvasive and high-risk alternatives. Low-risk choices center on the osteopathic philosophy of compassionate care regardi ng the whole person in pai n, with the primary em phasis on factors originating in the muscu loskeletal system. In addition to osteopathic manipulative treatments, further low-risk choices include: Medications Exercise • Relaxation training and biofeedback • Counseling and support groups
•
•
M ild-risk options i ncorporate nerve blocks, and nonopioid and opioid analgesics. Moderate-risk alternatives incl ude im plantable therapies, particularly spinal cord stimulation and in traspinal drug-infusion systems. The high-risk treatments consist of surgeries and nerve-destroying procedures. The most prudent overall treatment starts out and stays low-risk and noni nvasive. Fortunately, osteopath ic manipulative treatments and the other low-risk pain management options are also the most cost-effective and the most user-friendly to the patient. Patients in pain can be
15. Pain Management sedentary, deconditioned, overweight, tense, underexercised, and depressed. With encouragement from the physician, they can be come physically fit, receive osteopathic manipulative treatmenr, be rrained in relaxation rraining, and be enrolled as members of a chronic pain suppor( group that will l i kely lead co adjustmenr co the pain condi tion. Most patienrs with chronic pain can be m anaged effectively when the rreating physician uses a combination of mese low-cost, conservative creatmenrs. For the most difficult cases, nerve blocks and/or opioid analgesics might be necessary. With a pain that is severe and disabling, i mplantable therapies and neurodestructive procedures are always the last resorr. They should only be carried our in consultation with other physicians and psychologists, as an orchestrated team effon. The choice of i nvasive therapeutic i n rervenrion for pain is determined largely by the severiry of the patient's pain problem, resources available, comparative risk of the procedures under consideration, and emotional and physical state of the patient (33). Finally, it is of great importance for osteopathic physicians ro distinguish between acute and chronic pain in their daily prac tice. Chronic pain can conri n ue in an unrelenting fash ion without ongoing evidence of tissue damage. Its persistence does not nec essarily mean that the original organic damage has failed co heal or that the patient has significant psychiarric problems. Chronic pain behavior might reAecr:
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Pain is the most common element i n the sympcoms presented co physicians. But as so eloquently stated by John Loeser (41) : It is suffering, not pain, that brings patients into doctor's offices in hopes of finding relief. Astounding developments in our under standing of the mechanisms of nociception should not cause us to lose sight of our patients' goals. Chronic pain is far more than a sensory process. We must maintain the biopsychosocial model of chronic pain if we are to provide effective health care to our patienrs. Understanding the componenrs of pain facilitates this goal. Suffering is an emergent property of the human brain and is dependent upon consciousness. It roo is worthy of study by scienrists and of concern to clinicians.
Successful managemenr of chronic pain depends on much more than knowledge. Knowledge m ust be teamed with keen obser vation, patience, and compassion. Many physicians have come co believe that treating chronic pain and suffering, with all its b iopsychosocial elements, reflects both the rrue art and the true science o f osteopathic medicine.
R EFERENCES 1 . Schappert M. National Ambulatory Medical Care Survey: 1 992 sum mary, Wash i ngton, DC: National Center for Health Statistics, 1 99 2 . 2. Elliorr AM, Sm it h B H , Penny K l , et al. T he epidemiology of chronic
• • • • • • • • • •
Allodynia Hyperalgesia Spinal cord excitability Sleep disturbance Depression or anxiery Brain reorganization as a result of continuous noxious input Preoccupation with health and physical function Personal i ry disorder Job srress Dysfunctional family environment
Such high-risk chronic pain patients require psychological and social management in addition co medical care. There are a variery of craps (34) i nro which the well-intenrioned but unwary primary care physician can fal l when managing high-risk chronic pain patienrs. Such patients should be referred co a multidisciplinary pain service when a complex problem is encountered. These complex problems are more often the exception than the rule, and the vast majoriry of patients with chronic pain can be treated easily by using the least invasive, conservative rreatments (35,36). In summary, the physician's goal is co rescore both physical functioning and adaptive musculoskeletal responses through the simultaneous use of physiological and psychological i nterven tions (37). When managing chronic pain, it is routine co use osteopathic manipulative techniques (38) , medications. and psy chological counseling. Combini ng these elemenrs i n to a comprehensive rreatmenr approach increases the chances of a successful outcome (39). I n tervention srrategies, which simultaneously address t h e biolog ical, psychological, and social faccors of chronic pain, are more likely co succeed and modify chronic pain perception and behav ior (40 ) .
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North Am. 1 998;6: 1 -20. 1 4. Salibi N , Brown MA. Clinical MR Spectroscopy: First Principles. New York, NY: Wilcox, 1 998. 1 5 . McI ntosh AR, Rajah MN, Lobaugh NJ. I n teractions of pre frontal cortex in relation to awareness in sensory learning. Science. 1 999;284: 1 53 1 1 533. 1 6. Grachev JD, Fredrickson BE, Apkarian AV. Chronic pain is associated with abnormal brain chemistry. Soc Neurosci Abstr. 1 99 9 ; 2 5 : 1 4 1 . 1 7 . Talbot J D , Maret S , Evans AC, et al. Multiple representations o f pain i n human cerebral cortex. Science. 1 99 1 ;25 1 : 1 35 5- 1 3 5 8 .
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1 8 . Casey KL, Monoshima S, Berger KL, et a1. Positron emission romo graphic analysis of cerebral structures activated specifically by repetitive noxious heat stimuli. ] Neurophysiol. 1 994;2:802-807. 1 9. Jerome JA. I n formation processing theory of chronic pain [ B ulletin] .
Am Pain Soc j. 1 99 2 ; 1 : 7- 1 0. 20. Jerome JA. Life after pain. Clin ] Pain. 1 99 1 ;7: 1 67- 1 68 . 2 1 . Hunt SP, Manyh, PW. The Molecular dynamics o f pain control. Nat
Rev Neurosci. 200 I ;2 (2) 83-9 1 . 22. DavidoffRA. Trigger points and myofascial pain: roward understanding how they affect headaches. Cephalgia. 1 99 8 ; 1 8:436--448. 23. Vogt BA, Derbyshire S, Jones AKP. Pain processing i n four regions of the h u man cingulate cortex localized with co registered PET and M R imaging. Eur} Neurosci. 1 996;8: 1 46 1 - 1 473. 24. Devinsky 0, Morrell MJ, Vogt BA. Contributions of anterior cingulate ro behavior. Brain. 1 99 5 ; 1 1 8:279-306. 25. H robjarrsson A, Gotzsche Pc. An analysis of clinical trials com paring placebo with no treatment. N Engl } Med 200 1 ;344(2 1 ) : 1 594- 1 602. 26. Savage S , Covingron Ee, Heit HA. Definitions related ro the use of opioids for the treatment of pain. Consensus document. Am Acad Pain
34. Hartwick CT. Turorial 1 7 : ho w ro manage a difficult pain patient. Pain
Digest. 1 99 5 ; 5 :93-95. 35. Wal l P D , Melzack R. Textbook ofPain, 3rd ed. New York, NY: Churchill Livingsrone; 1 994. 36. Acute Pain Management Guideline Panel. Acute Pain Management: Op
erative or Medical Procedures and Tim, rna. Clinical Pmctice Guideline. Rockville, M D : Agency for Health Care Policy and Research, Public Health Service; February 1 992. U.S. Dept. of Health and Human Ser vices publication 92-2. 37. Aranoff G M . Pain Centers-A Revolution il7 Health Care. New York, NY: Raven Press, 1 988. 3 8 . Anderson G B , Lucente T, Davis AM, et al . A comparison of osteopathic spinal manipulation with standard care for patients with low back pain.
N Engl} Med. 1 999;34 1 ( 1 9) : 1 426- 1 43 1 . 39. Seaman D R, Cleveland C. Spinal pain syndromes: nociceptive, neu ropathic, and psychologic mechanisms. } Manipulative Physiol TIler. 1 99 9 ; (7):458-47240. JeromeJA. Transmission or transformation) I n formation procession the ory of chronic human pain. Am Pain Socj. 1 993;2(3): 1 60- 1 7 1 . 4 1 . Loeser J D . Pain and suffering. Clin } Pain. 2000; 1 6 [Suppl 2 ] :S2-6.
Med, Am Pain Soc, Am Soc Addict Med. 200 I . 27. Elkiss M , Jerome J . Chronic pain syndrome: a n analysis o f current ther apies. Mich Osteopath j. 1 978;43:8. 28. Bennett RM , Clark SR, Goldberg, et al. Aerobic fitness i n patients with fibrositis. A controlled study of respirarory gas exchange and 1 33 xenon clearance from exercising muscle. Arthritis Rheum. 1 989;32(4):454460. 29. McCain GA, Bell DA, Mai FM, Halliday PD. A controlled study of the effects of a supervised cardiovascular fitness training pro gram on the manifestations of primary fibromyalgia. A rthritis Rheum. 1 988;3 1 (9) : 1 1 35-1 1 4 1 . 30. Lockert D M , Campbell J E The effects o f aerobic exercise o n migraine.
Headache. 1 992;32: 50-54. 3 1 . Lake A I I I I . Behavioraland Nonpharmacological Treatmentsfor Headache. Philadelphia, PA: WE Saunders; 200 I .
RESOURCES International Association for the Study of Pain ( www. iasp-pain.org) Headquarters Office 909 N E 43rd Street, Suite 306 Seattle, WA 98 1 0 5-6020 USA Phone 206-547-6409 Fax: 206-547- 1 703 E-mail:
[email protected] American Pain Society ( wwlU.ampainsoc. oriJ Corporate Office 4700 West Lake Avenue
32. Turk De, Meichenbaum D , Genest M . Pain and Behavioral Medicine:
Glenview, IL 60025 - 1 485
A Cognitive Behavioral Perspective. New York, NY: Guilford; 1 983. 33. Turk De, Melzack R. Handbook of Pain Assessment. New York, NY:
Phone: 847-375-47 1 5
Guilford; 1 992.
Fax: 877-734-8758 (roll free) E-mail: info@ampainsoc. org
LIFE PHASES AND HEALTH JED MACiEN
A useful definition of development is "a sequential increase in the structural or functional complexity of a system" (1). His torically, the understanding of human development has also led ftom the less to the more complex. For example, infants were once thought of as being almost "blank slates." Early environ mental experiences, especially with the primary caretaker, were assumed to result in the formation of the personality, and bi ologic influences were discounted. Individual development was thought of as a smooth upward reaching line that had a some what inevitable progression. The logical extension of this model was that very early experiences and behavior should predict later behavior. In fact, early experiences do not seem to predict later behavior in any simple way (2). Instead, it appears that human development is characterized by periods of time when behaviors change radically, then relative stability unril the next period of change. This discontinuous view of human development along with rapid advances in the neurosciences has helped to alter our clinical approaches to behavior disorders in both children and adults. Tr is now as important to understand how the central nervous system responds to various environmenral inputs as it is to understand behavioral responses. Maternal depression and child abuse and neglect are the best-studied examples of adver sity in humans and other primates. These phenomena will be used throughout this chapter as paradigms for understanding neurobiologic responses to adversity.
CONTINUITIES AND DISCONTINUITIES IN DEVELOPMENT
Considerations of the process of developmenr must take into account biologic influences, environmental effects, and the paradigm of discontinuous development. It appears that rather than shifting smoothly from one phase to another, transitions are characterized by "biobehavioral shifts" (3). These times of rransition involve fairly sudden reorganizations of the biologic, cognitive, affective, and social characteristics of the organism. The end result is new, more complex behaviors (4). The tim ing and genesis of these shifts relates to repression and dere pression of genes, both due to internal timing factors and to environmental influences. Furthermore, it is becoming appar ent that the organism is busily attempting to manipulate the environment in ways beneficial to the organism. The move
from childhood to adolescence is a paniculariy cogent exam ple of a biobehavioral shift. Puberty is associated with an up surge in sexuality with very different behaviors toward the oppo site sex, an increase in aggression, and striking physical changes (5). Teenagers develop very different relationships with parenrs and peers than were present as children. The epidemiology of various disorders changes. For example, the sex ratio for de pression changes from 1: 1 to a large predominance in females. These kinds of shifts in behavior are characteristic of growth and development.
PRENATAL PERIOD
Brain growth and development in utero and in infants and chil dren proceeds from the brainstem to the cortex (6). Infanrs in urero respond to environmental influences in terms of both physical and behavioral development. A long list of factors can influence intrauterine growth and development (7). Cigarette smoking and malnutrition are associated with decreased fetal growth. Alcohol use can result in fetal alcohol syndrome. The effects of these and other substances on later development are much less clear. The literature on later effects of intrauter ine exposure to substances of abuse reveals no compelling evi dence that illicit substances result in long-term deficits. Rather, it appears this risk is probably related to the adverse environ mental circumstances to which many of these children are ex posed (8). Just as the fetus grows and develops, the mother and other family members are likely to go through developmental steps in preparation for childbirth and caring for a new child. Mothers specifically are said to become more preoccupied with the self and with the neonate, especially after perceiving fetal movement. Fathers may also experience a beginning attachment when move ment is palpable through the abdomen. When this developmental process is not allowed to proceed to completion, parents may not be ready to interact with their infant in helpful ways. For exam ple, parents of very premature infants may not be ready to feed, nurture, and otherwise care for their infant. They may have dif ficulty in feeling as if the baby is responding to them in any way. This may lead to further difficulties with growth and develop ment. Thus, various behavioral difficulties may have their genesis in this period.
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INFANCY
At birth, the brainstem is almost fully functional. However, fore brain limbic structures are very immature (9). Infants come into the world with certain preprogrammed capabilities that have evolved to help maximize their chances for survival. For those who wonder why human infants do not come into this world with more developed capabilities, consider that there is a limit to the capacity of the female pelvis to accommodate an infant head. Given this limit on brain size, infants are equipped with only those capacities needed for survival. Rooting, sucking, grasping, and the Moro reflex are all adaptive in that they help the infant feed or maintain contact with the primary caretaker. Less obvious capabilities are also present. It turns out that newborns engage in complex visual activities. They scan patterns by means of eye movements going back and forth across edges (l0). By the age of I to 4 months, they are able to discriminate many speech sounds ( 1 1). These innate preprogrammed behaviors and capabilities are critical to the ability of the infant to develop and participate in the dyadic interaction between it and the primary caretaker, a phenomenon often termed "attachment." Attachment can also be defined as "an enduring emotional bond uniting one person with another" ( 12). In their very influential work, Bowlby and Ainsworth (J 3) suggest that all of these preprogrammed behav iors and predispositions serve to help develop a secure attachment between the infant and caretaker so that optimal psychosocial de velopment can take place. In fact, a secure base for attachment has at least three characteristics: 1. it is reliable, 2. it shields the infant from environmental threats, and 3. it is sustaining and provides the infant with resources ( 13). Klaus and Kennell (14) used the term "bonding" for the first manifestation of this phenomenon because it occurs immediately after birth. They theorized that infants who were separated from their mothers and cared for in the newborn nursery did not bond as well as infants who were allowed to stay with their mothers. Although this particular notion has not been substantiated, a process of bonding does take place and is promoted by a variety of behaviors in which infants and parents engage. Holding infants at a distance that maximizes face-to-face contact, exaggerared greeting behaviors, and parental imitation of newborn facial and vocal expressions are all part of this process (15). For the new born's part, eye contact with the primary caretaker, vocalizations, and the appearance of a social smile at about eight weeks are all behaviors that will engage the caretaker and help promote re ciprocal interaction. These behaviors that elicit stimulation from caretakers are incredibly important for brain growth and devel opment. The human brain grows more through the first year of life than at any other time. Glucose use by the cerebral cortex rises from birth to 4 years; at age four, it is twice that of adults. There is also tremendous growth and proliferation of neurons and the production of axons, dendrites, and synapses during the first 2 years of life. These networks are actually pruned as time goes by based, in part, on how active they are (16). This "use it or lose it" phenomenon partly accounts for the smaller brain growth seen in deprivation. Failure to thrive is a diagnosis made
in infants who do not grow and who do not achieve developmen tal milestones such as the development of a social smile. This is often the direct result of the failure to achieve a relationship with a caretaker when they rarely handle or interact with the infant. There is experimental evidence that touch, in part, operates as a soothing mechanism in animals by activating brain opiates ( 17). This mechanism may be operative in the therapeutic effect of osteopathic manipulative therapy. In summary, human infants are born with predispositions and tendencies to grow and learn in particular directions. This selective seeking of specific types of activities promotes brain growth and development. Evidence in rodents shows that rats raised in complex group environments have 20% ro 25% more synapses per neuron in the upper visual cortex than rats reared socially or individually in standard cages ( 18). This same phenomenon is likely operative in humans. A further issue of importance is that of adaptability. The abil ity to modulate and change behaviors to match what might be happening in the environment is an important attribute. For instance, a parent who is unable to become calm and to sooth an irritable, cranky infant is likely to have an infant who is, in fact, irritable and crying much of the time. The situation, some times labeled as colic, may be the result of a mismatch between what a parent is able ro provide and what a particular child needs. Given at least average parenting ("the ordinary devoted mother"), most infants are able to obtain the stimulation and nurturance needed from the environment to progress developmentally ( 19). Competent caretakers are able to modulate their infant's arousal caused by displeasure, fear, or frustration by calming the infant and returning him or her to a tolerable emotional state ( 18). A large and rapidly growing literature now exists documenting the interaction between neurobiology and environment in in fants and children. Clearly, infants respond to their environment behaviorally and their central nervous systems respond as well. Decreases in the normal expected amount of stimulation can have profound effects. For instance, infants whose mothers are depressed exhibit dysregulated neurobiologic rhythms including elevated norepinephrine and cortisol levels, decreased vagal tone, and increased right frontal EEG activation. They show lower scores on the Bayley scale of infant development and grow ' th delays up to the age of 12 months (20).
AGES ONE TO FIVE
Many changes occur during the ages of one to five. Brain growth and development continues. As noted previously, the number of synapses in the one- to two-year-old is greater than the number in the adult brain. Around the age of one, children begin to walk. A sense of one's own body also begins ro emerge in a coherent way. Gender identity seems to be set by about age two and a half (2 1). Expressive language becomes evident. Babbling is present from about age 6 months to age 18 months. Words first appear between 8 and 18 months, after which there is rapid acquisi tion of words (22). Receptive language usually exceeds expressive language until the age of four to five. With increasing indepen dence and a developing ability to understand and evaluate social situations comes the appearance of behavior different than that desired by parents. Some parents will begin to have oppositional
16
batrles with their suddenly not so compliant two- to three-year old. Talking with parents about consistent and calm limit-setting will often help parents through these difficult times. Other common problems in this age group include toilet train ing and problems with the birth of siblings. Most children will become interested in toilet training between two and a half and four years of age. There are many good texts and videos avail able on this subject. It is important not to develop battles of will around this issue. The birth of siblings is a time when children will feel displaced by a new intruder. They will often oscillate between excitement and anger at the new arrival. Opportunities to be with parents without the sibling and to engage in pleasur able activities are helpful, as are opportunities to vent anger in protected settings. A child who begins to throw dolls around the room after a new sibling arrives home is expressing anger in a way that will not hurt the sibling. Some regressive behavior can also be expected. Bedwetting, thumb sucking, or more oppositional behavior might be seen. Children who are abused and/or neglected in early life do suf fer long-term behavioral and neurobiologic consequences. At a minimum, they appear ro have increased vulnerability for psychi atric disorders ( 18). Abuse is correlated with a host of behavior and psychiatric difficulties in young children including inter personal and academic difficulties, aggression, suicidal behaviot, risk taking, and diagnosable psychiatric disorders (23). A vari ety of studies demonstrate that children who are abused and/or neglected have either hyperreactive or blunted hypothalamic pituitary-adrenal axis responses ro various stressors (24-29). Per sistent changes in corticotropin releasing facror neuronal systems are seen in many primates who experience stress, as well as in depressed humans (30-32). Overall, there is a great deal of evi dence for long-lasting changes in the central nervous systems of individuals who have been abused and neglected in childhood.
SCHOOL-AGE CHILD
Generally, children from kindergarten to puberty are considered to be school age or latency-age children. The major tasks of this period are cognitive development and socialization. Cognitively, young school-age children are said to be dominated by "centra tion." They tend to view events as happening to them or in some way being affected by them. For example, children in this age group who experience parental divorce usually think that they, in some way, caused the divorce. It is not unusual ro see increases in depression, oppositional and angry behavior, and declines in school performance as a result. Objects also tend ro be measured and defined by only a few of several possible dimensions and may be classified in idiosyncratic ways. Children may measure the vol ume of a column of water exclusively by its height or width with out taking into account changes in both parameters (33). Cog nitive psychologist Jean Piaget (33) termed this preoperational thinking. When the school-age child achieves the ability to con serve, that is, ro recognize constant qualities or quantities of ma terial even when the material undergoes changes in shape or color, he is said to have achieved the concrete operational level (33). School is a central experience for children. For some, this is the first time they spend the majority of the day with other children.
Life Phases and HeaLth
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School may be the first experience with adults other than par ents in authority roles. Thus, a premium is placed on the ability ro interact in socially appropriate ways with other children and adults. Rapid advances in interaction abilities take place. Chil dren begin to learn strategies for continuing interactions and for reengaging after rejection and failure in groups. The development of self-concept as well as further internalization of a self-identity is heavily dependent on these early experiences in school. Many children are likely ro have daycare experiences either beginning in the preschool or early school years. Although this is a controversial subject because non-parental daycare can certainly be harmful, high-quality, non-parental daycare is very likely to be beneficial. The most important variable is probably the quality of care, which is highly dependent on the sensitivity and warmth of the caretakers (34). Much more research needs ro be done on this subject ro understand optimal types, length of care, and how such care interacts with parental care. Pediatricians and family practitioners are likely to see chil dren with common problems such as aggressive behavior, separa tion anxiety when going ro school, academic problems, and the appearance of attention-deficit hyperactivity disorder. Because school is a central experience and the family is still a center of activity, in order ro evaluate these difficulties, physicians will need information from the parents, child, and the school.
ADOLESCENCE
As noted previously, adolescence marks a time of profound biobe havioral shift with reorganization of cognitive, emotional, and biologic functioning. Adolescence generally coincides with the onset of puberty. In females, breast budding precedes menarche by about 1 year (35). In males, the onset of puberty is marked by pubic hair and penile growth. Hormonal increases tend ro begin before these secondary sexual characteristics appear (35). One of the triggers for the pubertal process may be related ro a particular fat ro lean body mass ratio (36). Cognitive and social-emotional changes are extremely impor tant during this time period. Cognitively, in Piagetian terms, the adolescent moves from the stage of concrete operations ro for mal operational processes (33). The individual begins to grasp highly abstract concepts and to manipulate them. The ability to formulate hypotheses and the use of deductive reasoning are formal operational processes that have obvious applications in school. Perhaps the hallmark of adolescence is the process of separation-individuation (37). During this period, it is said that the "final" crystallization of the adult personality is taking place along with a gradual separation from the family of origin. Many facrors contribute ro and interact in this developmental process. Cognitively, the adolescent can now conceive of a larger world and others outside the family as having importance and rele vance. The peer group begins ro overtake parents in importance regarding matters of dress, opinion, and in numerous other ar eas. Relationships with the same and the opposite sex become of overwhelming concern. In short, the adolescent uses these rela tionships and the ability ro think independently in order ro sepa rate from the family, build an increasingly independent lifestyle,
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and develop a character structure capable of self-regulation and independent action. Some conAict with parents seems to be an inevitable result of and may enhance this process to some extent. However, the traditional view of adolescence as a developmen tal period of turmoil does not seem to be true for a substantial number of adolescents. Offer and colleagues (38) documented a large group of male adolescents who seemed to go through this period of time in a "continuous growth" mode. Little evidence of conAict or turmoil with family members was found, and this group was able to integrate various experiences of adolescence and to accept cultural and societal norms without conAict. Adolescents may also choose to separate in maladaptive ways. Individuals who engage in delinquent acts may be choosing an al ternate path of separation from the family. In a chronic disease sit uation such as diabetes, adolescents may need more care and may not be able to become as independent as their peers. In reaction, they may become neglectful of diets or insulin injections. The adolescent diabetics with repeated ketoacidotic episodes might be engaging in a maneuver to express independence in the only effective way they know. The opposite also occurs; that is, adolescents who never re ally separate and remain childish and enmeshed with parents. In Western and especially American culture, adolescence is pro longed. College and professional education can extend into the late 20s or early 30s with continuing financial dependence on parents. This pattern may be particularly pertinent to medical students who undergo long periods of training, at first without any and then with minimal remuneration. Other patterns of progression through adolescence do occur. That which we consider normative is, in part, culture-bound. In some cultures, preadolescent and early adolescent male homosex uality is normative and does not seem to result in large numbers of homosexual adults. In a number of cultures, a sharp demarca tion takes place between adolescence and adulthood with rites of passage. Hamburg (39) comments that the fundamental requirements for healthy adolescent development are: I.
finding a valued place in a constructive group,
2. learning how to form close, durable human relationships, 3. feeling a sense of worth as an individual, 4. achieving a reliable basis for miling informed choices, 5. knowing how to use the support systems available to them, 6. expressing constructive curiosity and exploratory behavior, 7. believing in a promising future with real opportunities, 8. finding ways to be useful to others, 9. learning to live respectfully with others in circumstances of democratic pluralism, and 10. cultivating the inquiring and problem-solving skills that serve lifelong learning and adaptability. For practitioners caring for adolescents, it is important to be supportive of the normal developmental process of the age group. Seeing the adolescent with parents for at least part of the medi cal visit is helpful, but teenagers will often have concerns about confidentiality that will need to be discussed and respected.
ADULTHOOD
Although some personality development and change continues to occur in adulthood, for the most part, research in this area demonstrates that personality is fairly stable (40,41). Based on this viewpoint, drastic personality changes in adulthood or old age should be viewed with a high index of suspicion. Similarly, cognitive changes should not be attributed to "aging" but should be investigated as a sign of possible pathology (42). As he did for childhood and adolescence, Erik Erikson (37) outlined a series of stages, including young adulthood, adulthood, and old age. He assigned a number of developmental tasks to each stage. In young adulthood, he contrasts competing drives of intimacy and isolation. Intimacy involves the development of a sharing mutual relationship; whereas, isolation is a sense of being separate and unrecognized. The most important relationships are those that develop with potential partners. Developing a sharing, intimate relationship is of paramount importance. In adulthood, the core task is generative, meaning creativity, procreativity, and productivity. There is a drive to have children, to succeed at one's career, and to be productive. One of the driving forces of adulthood is that of caring for and raising children. Passing on values and resources is a prime motivation. However, as a consequence of increasing life spans, a compet ing dynamic seen in increasing frequei1cy is that of the need to care for aging parents. Middle-aged adults may find themselves responsible for the financial and perhaps physical care of elderly parents as well as their own children (43). The stress and burden of this kind of situation can be significant. Clinically, younger and middle-aged adults may presenr wirh depressions and anxiety disorders. Even more common, somatic symptoms as an expression of various stressors are seen.
ELDERLY
In most cultures, advanced age has been highly regarded but rarely encountered (44). Improved medical care is resulting in lengthening life spans. Formerly lethal disorders may now result in longer-term chronic illnesses with morbidity and disability. It is appropriate that Erikson (37) has included a stage of old age in his schema. In old age, the competing drives are said to be integrity vs. despair. Despair and depression can be related to the knowledge that the life span is increasingly limited and to the loss of a spouse, friends, and career. Erikson does propose the competing drive of integrity, a SOrt of wisdom and perspective that comes with experience. In the Berkeley older generation study, when asked what periods of their lives brought them the most satisfaction, "right now" was named most often (45). This set of coping mechanisms will be extremely helpful in old age when changes occur in many areas of social and individual functioning. As individuals age, they may begin to expect to slow down and to develop some infirmities and disabilities. If expected, these problems may be taken in stride without too much upset or turmoil. Dietz (46) reports that older adults generally experi ence higher levels of self-efficacy and self-esteem compared with
16. Life Phases and Health younger individuals. This finding may be explained by a con rinuing process of marurarion in older age in which elders begin to look inward for a sense of meaning and accepr rheir accom plishmenrs in life as adequare. On rhe orher hand, unexpecred or catasrrophic life evenrs are especially srressful and less likely to be handled well (47). In many culrures, the elderly are viewed as carriers of culture and memory and repositories of wisdom and judgment. This viewpoinr comes close ro rhe Eriksonian concept of an ideal old age. However, old age can degenerate into despair over conrinual losses of funcrion, spouse, and friends. Good healrh is particularly imporranr for good morale and coping skills (48). Thus, one of the primary concerns of elderly individuals is rhe quality of rhe physical and psychological care rhey receive. They may be increasingly demanding of healrh care professionals for care that promores rhe besr possible funcrioning. Among the problems becoming more frequenr in rhe very old is dememia. The Swedish Cemenarian Srudy esrimated rhar at leasr 27% of rheir cohon of individuals aged 100 had symptoms of dememia (44). Older individuals have a justified concern wirh rhe quality of rheir final days. The avoidance of discomfon and long, drawn out dearhs while anached ro various life suppon devices creares concern and should become a topic of discussion. Physicians are often nor comforrable with ralking aboL![ dearh and will acrively rry ro avoid such discussions. Pain especially deserves panicular anenrion, not least because rhe Joim Commission on Accredita rion of Health Care Facilities require health care facilities ro I.
recognize rhe right of patienrs ro appropriate assessmem and managemenr of pain,
2. idenrify pain in patienrs during rheir inirial assessmenr and reassessments, 3. documenr acceprable ourcomes of rreatmenr, and 4. educate providers, patients and rheir families abour pain man agemenr (49). Pain scales are a useful means of measuring pain severity. Qual ity, location, durarion, and phenomena that might increase or decrease pain are also important ro assess. A number of sources discussing medication approaches ro pain relief are available. In general, mild pain may be treated with as pirin, acetaminophen, or nonsteroidal, antiinAammarory drugs. Moderate pain may be (I'eared with these agenrs plus opiates such as codeine or oxycodone. More severe pain is treated with mor phine and similar opiares plus orher analgesics. End-of-life care is not truly complete wirhout the componems of advance care planning, clear discussions of palliative care, and the use of hospice care with irs ream approach. Finally, relatives and others close ro dying individuals also need care and often need help with grieving. CONCLUSION
The course of human development is characterized by an ever increasing level of complexity with a series of biobehavioral shifts ro new levels of organization. Although individual early expe riences are important, it is not likely that any single incident
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will produce a radical alteration in personality. What seems to be important is consistent parenring and an adequate environ mem in which the individual can grow and develop. What is carried forward, what is continuous, is the pattern of consistent relationships that develops. Human developmem is a complex process that has no singular determinam of behavior or disorder. Development is truly a biopsychosocial process.
REFERENCES l. Yates TT. Theories of cognitive development. In: Lewis M, ed. Child and AdoLescent Psychiatry: A Comprehensive Textbook. Baltimore, MD: Williams & Wilkins; 1991. 2. Kagen J. Conrinuiry and change in the opening years of life. In: Emde RN, Harmon RJ, eds. Continuities and Discontinuities in DeveLopment. New York, NY: Plenum Publishing; 1984: 15-39. 3. Zeanah CH, Anders TF, Seifer R, et al. Implications of research on infant developmenr for psychodynamic theory and practice. J Am Acad Child AdoLesc Psychiatry. 1989;28(5)657-668. 4. Emde RN, Easterbrooks MA. Assessing emotional availability in early development. In: Frakenberr WK, Emde RN, Sullivan JW, eds. Early Identification of Children at Risk. New York, NY: Plenum Publish ing; 1985. 5. Runer M. Conrinuities and disconrinuities in socio-emotional develop menr: Empirical and conceptual perspectives. In: Emde RN, Harmon RJ, eds. Continuities and Discontinuities in DeveLopment. New York, NY: Plenum Publishing;1984:41-68. 6. Nelson A, Bloom E. Child developmenr and neuroscience. Child Dev. [997;68:970-987. 7. Smotherman Wl� Robinson SR. Prenatal inAuences on development: behavior is nOt a rrivial aspect of fetal life. J Dev Behav Pediatr. 1987;8(3):I 7I-I 76. 8. Hans S. Prenatal drug exposure: behavioral functioning in late childhood and adolescence. NIDA Res Monogr. 1996;I64:26I -276. 9. Joseph R. Environmenral inAuences on neural plasticity, the limbic sys tem, emotional developmenr and arc3chment: a review. Child Psychiatry Hum Dev. 1999;29(3):I 89-208. 10. Haith MM. RuLes that babies Look by Hillsdale, NJ: Erlbaum; 1980. 1[. Eimas PO, Siquelend ER, Josczyk p, et al. Speech perception in infanrs. Science. 197I;I 7I:303-306. 12. Thompson RA. Anachmenr theory and research. In: Lewis M, ed. ChiLd and AdoLescent Psychiatry: A Comprehensive Textbook. Baltimore, MD: Williams & Wilkins; [991:100-108. 13. Kraemer GW. Psychobiology of early social anachmenr in rhesus mon keys. Ann N Y AcadSci. [997;807:401-4I8. 14. KJause MH, Kennell JH. Mothers separated from their newborn infants. Pediatr Clin North Am. 1970;17: I 0[5-1037. 15. Emde RN. Developmenr terminable and interminable: innate and mo tivational factors from infancy. Int J PsychoanaL. 1988;69:23-42. 16. Singer W. Development and plasticity of cortical processing architec tures. Science. 1995;270:758-764. 17. Kuhn CM, Schanberg SM. Responses to maternal separation: mecha nisms and mediators. lnt J Dev Neurosei. 1998;I6(3-4):261-270. 18. Glaser D. Child abuse and neglect and the brain-a review. J Child Psychol Psychiatry. 2000;4I(I):97-I16. 19. Winnecon OW. Primitive EmotionaL DeveLopment. New York, NY: Basic Books; 1945. 20. van der Kolk B, Fisler R. Childhood abuse and neglect and loss of self regulation. BulL Menninger Clin. 1994;58:145-168. 2 I. Money J, Hampson JG, Hampson JL. An examination of some basic sexual concepts: the evidence of human hermaphroditism. Johns Hopkins HospitaL Bulletin. [995;97:301-3I 9. 22. Baker L, Cantwell DP. The development of speech and language. In: Lewis M, ed. Child and AdoLescent Psychiatry: A Comprehensive Textbook. Baltimore, M 0: Williams & Wilkins; 1991:I 00-108.
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III. Osteopathic Considerations in the Behavioral Sciences
23. Kaplan SJ. Pelcovitz D. Labruna V. Child and adolescenr abuse and neglect research: a review of the past 10 years. Part I: physical and emotional abuse and neglect. } Am Acad Child Adolesc Psychiatry. 1999;38( I 0):1214-1222. 24. Hart J. Gunnar M. Cicchetti D. Salivary cortisol in maltreated chil dren evidence of relations between neuroendocrine activity and social competence. Dev Psychopathol. 1995;7:11-26. 25. Ladd C. Owens M. Nemeroff C. Persistent changes in corticotropin releasing factor neuronal systems induced by maternal deprivation.
Endocrinology. 1 996;137:1212-1218. 26. De Bellis M. Chrousos G. Dorn L. et al. Hypothalamic-pituitary-adrenal axis dysregulation in sexually abused girls. } Clin Endocrinol Metab. 1994;7:249-255. 27. Hart J. Gunnar M. Cicchetti D. Altered neuroendocrine activity in maltreated children related to symptoms of depression. Dev Psychopatho!. 1996;8:201-214. 28. Kaufman J. Birmaher B. Perel J. et al. The corticotropin teleasing hor mone challenge in depressed abused. depressed nonabused. and normal control children. BioI Psychiatry. 1997;42:669-679. 29. De Bellis M. Baum A. Birmaher B. et al. Developmental traumatology Part I: biological stress systems. BioI Psychiatry. 1999;45:1259-1270. 30. Heim C. Owens D. Plotsky P, et al. The role of early adverse life evenrs in the etiology of depression and post-traumatic stress disorder. Ann N
YAcadSci.1996;813:1-14. 31. Johnson EO. Themis C. Kamilaris C. et al. The biobehavioral conse quences of psychogenic stress in a small social primate. BioI Psychiatry. 1996;40:317-337. 32. Heim C. Newport D. Bonsall R. et al. Altered pituitary-adrenal axis responses to provocative challenge tests in adult survivors of childhood abuse. Am} Psychiatry. 2001;158:575-581. 33. Combrinck-Graham L. Development of school age children. In: Lewis M. ed. Child and Adolescent Psychiatry: A Comprehensive Textbook.Bal timore. MD: Williams & Wilkins; 1991:I 00-108. 34. Lamb M. Effects of nonparenral child care on child development: an update. Cart J Psychiatry.1996;41:330-342. 35. Brook CG. Endocrinological control of growth at puberty. Br Med Bull.
1981;37:281-285.
37. Erikson EH. Elements of a psychoanalytic theory of psychosocial devel opment. In: Greenspan SI. Pollock GH. eds. The Course ofLift: Psycho analytic Contributions Toward Understanding Personality Development. 11 Latency. Adolescence. and Youth. Washington. DC: National Institute of Mental Health :357-372. 38. Offer D. Adolescent Development: A normative perspective. In: Greenspan SI. Pollock GH. eds. The Course of Lift: Psychoanalytic Con tributions Toward Understanding Personality Development. fl Latency. Adolescence. and Youth. Washington. DC: National Institure of Men tal Health :357-372. 39. Hamburg D. Toward a strategy for healthy adolescent development. Am} Psychiatry. 1 997;festschrift supplemenr. 40. Douglass K. Arenberg D. Age changes. cohort difference and cultural change in the Guilford-Zimmerman Temperament Survey. } Gerontol. 1978;33:737. 41. Costa Jr. PT. McCrae RR. Personality in adulthood: a six-year longitu dinal study of self-reports and spouse ratings on the NEO personality inventory. J PmSoc Psycho!. 1988;54:853. 42. Costa Jr. PT. McCrae RR. Personality and aging. In: Hazzard WR. Andres R. Bierman EL. et aI. eds. Principles of Geriatric Medicine and Gerontology. New York. NY: McGraw-Hill; 1990: I 01-107. 43. Brody EM. Parent care as a normative family stress. Gerontologist.
1985;25:19-29. 44. Samuelsson SM. Alfredson BB. Hagberg B. et al. The Swedish Cente narian Study: a multidisciplinary study of five consecutive cohorts at the age of 100. Int J Aging Hum Dev.1997;45(3):223-235. 45. Field D. "Looking back. what period of your life brought you the mOSt satisfaction." Int} Aging Hum Dev. 1997;45(3): 169-194. 46. Dietz B. The relationship of aging to self-esteem: the relative ef fects of maturation and role accumulation. 1m} Aging Hum Dev.
1996;43(3):249-266. 47. Neugarten BL. Social and psychological characteristics of older per sons In: Cassel CK. Riesenberg DE. Sorenson LB. et al. eds. Geriatric Medicine. New York. NY: Springer-Verlag New York; 1984:28-37. 48. Adkins G. Marrin P, Poon LW. Personality traits and states as predictors of subjective well-being in centenarians. octogenarians and sexagenarians.
36. Friach RE. McArthur JW Menstrual cycles: fatness as a determinanr of
Psychol Aging. 1996;11(3):408-416. 49. Michigan State Medical Society. et al. The Michigan Physician Guide to
minimum weight for height necessary for their maintenance or onset.
End-Of-Life Care. East Lansing. MI: Michigan State Medical Society.
Science.1974;185:949-951.
2000.
STRESS MANAGEMENT IN PRIMARY CARE JOHN A. JEROME
CONCEPTUALIZING STRESS KEY CONCEPTS • Empathy for stress-related problems and their many
manifestations • Suess and related somatic complaims, including those
related to somatic dysfunction • Signs and symptoms of depression • Signs and symptoms of anxiety • Signs and symptoms of alcohol abuse • Signs and symptoms of insomnia • Adaptive methods for coping with stress • Overview of treatmem techniques • Impact of the doctor/patient relationship
In primary care, suess-induced somatic complaints are the mech anisms underlying the symptoms for 20% to 35% of all pa tients seeking treatment from physicians (1,2) . [n the United States, more than 33% of the population is susceptible to acute or chronic stress and the physical and psychological disorders caused by stress (3) . The effects of suess include the following changes: Biochemical Physiologic Behavioral Psychological Many of these changes are directly related to health. This chap ter reviews the major theories of suess and presents a framework for understand ing and treating the causes of stress. It includes guidelines for the cognitive/behavioral management of the ef fects of stress related to: Anxiety Depression Alcohol abuse Insomnia
Physicians often speak of suess as i f it explains many unusual patient behaviors, signs, and symptoms. The term stress is also used as a catch-all term for emotional reactions (such as anger, fear, and depression) or as an explanation for drug and alcohol abuse. Lay defi nitions are primarily concerned with the notion of environmental pressu res and the belief that such pressu res are aversive. I nstead, osteopathic physicians learn to use palpation and ma nipulative treatment to aide in physically managing stress-related effects. A narrow psychosocial focus occurs when patients and physicians talk about stress as an exclusive problem. Discussion often centers on stress-inducing environmental variables or on their biologic/psychological consequences. Suess is both. Treating symptoms such as depression, anxiety, drug abuse, and insom nia does not alrer environmental stressors or their un derlying mechanisms. The ueating physician is not able to di rectly control or change these psychosocially complex processes.
STRESS AS PROCESS
Stress is an i nteractive process in which the patient responds in predictable biopsychosocial ways to certain environmentally or internally mediated stressors. The process unfolds as a sequence of feeli ngs, thoughts, and actions i nvolving many i nteracting biopsychosocial factors. Stress is not a single precipitating event or the resulting biologic consequence(s). Stress involves: Environmental stimuli Psychological appraisals Feelings Behavioral and physiologic consequences Physiologic responses to stressors are often linked to b iochem ical measurements of stress and tension in the musculoskele tal system. An osteopathically oriented examination for stress related somatic dysfunction is one such measurement. Several objective measurements a llow the physician to form i mpressions about the patient's emotional status and biologic condition and identifY markers for the bodily systems most affected by stress.
234
[JJ. Osteopathic Considerations in the Behavioral Sciences
For example, catecholamines and corticosteroids secreted by the adrenal medulla and cortex, respectively, can be measured from urine and plasma levels. The secretion of catecholamines reRects sympathetic arousal because the adrenal medulla is i nnervated by the sympathetic nervous system. Secretions of epi nephrine and norepinephrine are also part of the sympathetic arousal process. The secretion of catecholamines leads to systemic reactions in the body such as increased cardiovas cular reactivity and changes in cognitive, emotional, and behav ioral functioni ng. These changes are often expressed as chron ic muscle tension. Little doubt exists in the mind of the osteopath i cally trained physician that stress is reRected in the musculoskele tal system (4,5). By considering function along with structure, osteopathic con cepts emphasize the role of the body's commun ication systems ( nervous, ci rcularory, and endocrine) in facilitating somatic dys function caused by stress. The term facilitation means the en hancement or rei n forcement of otherwise subthreshold neuronal activities that stim ulate effector units to inappropriately carry out whatever action they normally do (6). Examples of effector sites are: Muscle bundles Muscle groups Viscera Other neural units and networks Osteopathic treatment is designed to raise stimulus thresholds so that stressors are less l ikely to induce or maintain somatic dysfunction-related problems.
THEORIES OF STRESS
In 1932, Cannon (7) was the first to write that the release of cat echolami nes and musculoskeletal arousal i n i tially faci l i tate adap tation. Being aroused by stress provides a biologic advantage that enables the individual to rapidly respond to danger. H istorically, these stress-related increases of catecholamines enhanced survival and adaptive responses. We ignored a pain, fought back, ran to safety on broken bones, and scrambled to the top of the food chain. We have survived as a species, but now survival depends on how we relate to our cortically driven society. That first described in Cannon's early work as our "fight-or-Right" strategy no longer serves us adequately in our ambiguous and increasingly complex world. Now we i nternal ize the stressors and become distressed. We experience somatic dysfunction then present ourselves to the primary care physician requesting treatment for symptoms and problems. Damaging stress levels are reached when perceived threats or dangers upset the biopsychosocial balance. When prolonged stress reaches critical levels, chronically increased concentra tions of antii nRammatory corticosteroids and proinRammatory prostaglandins can negatively alrer immune responses, with in creased vulnerability to immu ne-related problems. Damaging stress levels are reRected in the neuromusculoskeletal system as d isruption of the body's homeostasis that exhausts the patient. Chron ic d iseases, impai rments, and disabilities are apt to follow under certain circumstances.
Osteopath ic philosophy teaches that structure and function are i nterdependent; that form follows fu nction. Thoughts, emo tions, and behaviors in response to stressors are in a blended and complex relationship that can affect both anatomy (structure) and physiology (function). Selye (8) fi rst described the interdependent processes of re spond i ng to stress as the general adaptation syndrome (GAS). Selye believed that our response to stress was a specific syndrome following certain patterns and affecting specific organs. Stress itself could be induced by a variety of i nternal or external stimuli. When patients are contin ually stressed, they move through three response stages. Fi rst, there is a startle response and orienti ng reflex as the patient becomes aware of the stress and is biologically alarmed. Adrenal, cardiovascular, respi ratory, and musculoskele tal functions increase. Next is an attempt to cope and problem-solve biologically, psychologically, and socially. The patient mobil izes all resources to meet and resist the stressor. [f the patien t is successful, mastery and learni ng occur. If the patient fails, he or she becomes exhausted physiologically, mentally, and emotionally. The third stage, exhaustion, is what the osteopathic physician sees clinically as a variety of dysfunctional signs and symptoms affecting any and all organ systems, including the neuromus culoskeletal network. As coping responses fail, the exhaustion depletes adaptive reserves and resistance disappears. Common consequences of this failure to adapt include: Fatigue Depression Anxiety Insom n ia Musculoskeletal complaints Drug-seeking behaviors When emotional and biologic reserves become depleted, pa tients often seek medical attention. Careful questioni ng is needed to uncover such ptoblems as: Family disruptions Job d issatisfaction Chronic overstimulation Feel ing overwhelmed Poor nutrition Lack of exercise Abuse-physical, emotional, verbal, sexual I nqui ries to the pri mary care physician are not about coping with stress, but more often requests for a quick fix: "I need something for my stomach." "Can I have some time off work?" "1 need something for depression." "Give me something to sleep." "What should I do about my teenager?" Because osteopathic theory emphasizes the interdependence of body structure and its overall fu nction, osteopathic physicians commonly use palpatory diagnosis and osteopath ic man ipulative treatment in the primary care setting to help diagnose and manage somatic components of this syndrome.
17. Stress Management in Primary Care
Clinically, two approaches are possible: 1. Change rhe srressor.
begins by accurarely reviewing Four of rhe mosr common behav ioral consequences of srress (12,13): Depression Anxiery Subsrance abuse Insomnia
2. Help rhe parienr respond in healrhy ways ro rhe srress. Change Stressor
BeFore seeking medical rrearmenr, rhe parienr probably has al ready rried ro change rhe srressor wirhour much success. More quick advice usually doesn'r work. Many srudies illusrrare rhar compliance wirh physician advice is low (7), parricularly i n rhe currenr c1imare of healrh care delivery where rhe pace is hecric and oFren impersonal. As parienrs shih between physicians and insurance plans in a managed care environmenr, rhe personal relarionships once forged between physician and parienr disap pear. Trusring relarionships are d i fficulr ro esrablish under rhese circumsrances, increasing rhe likelihood rhar professional advice will go unheeded. Many parienrs who come ro a primary care serring are looking For help wirh srress-relared symproms. A primary care osreoparh ically orienred approach assesses all rhe disrurbing psychosocial and organic problems, including rhe neuromusculoskeleral ele menrs, so rhar a long-rerm rrearmenr sn'aregy can be developed. In such cases, afrer a derailed h isrory is raken and complere physi cal examinarion, rhe rrearmenr srraregy incorporares all elemenrs of rhe osreoparhic philosophy. Ir includes: Palparory diagnosis Manipularive rrearmenr Exercise, dier, smoking, alcohol, drug cessarion Appropriare medicarion Coping srraregy educarion When hands-on procedures are used ro idenrify srress-induced somaric dysFuncrion, rhe experienced osreoparhic pracririoner can derermine wherher rhe observed parrern of somaric dysfunc rion is associared wirh primary neuromusculoskeleral dysfunc rion, conrriburion from somarovisceral or viscerosomaric com ponenrs, or a more complex behavioral dysfuncrion. D irecring all aspecrs of rrearmenr roward modifying rhe biopsychosocial causes and maladaprive responses ro srress is i m porranr. The pri mary care physician musr consranriy be aware rhar clinically evi denr srress reAecrs rwo realiries: 1. A parienr's immediare response ro srress-inducing environ menral evenrs produces b iopsychosocial consequences. 2. A parienr's long-rerm srress managemenr sryle is an imporranr process in which rhe physician musr inrervene for long-rerm adaprive change. Change Response to Stress
As previously menrioned, srress-relared condirions are Found in ar leasr 20% of primary care ourparienrs (9-11). By changing rhe response ro srress, one i mmediately trears some of the au ronomic componenrs of stress-related somatic dysFunction and rheir anrecedenrs. Success is more l i kely when physicians educate parienrs, guide and menror rheir adaprarion, and reach rhem cop ing and srress-masrery skills. In a primary care pracrice, diagnosis
235
When rhe exacr diagnosis i s made, careFully inForm rhe pa rienr and rhen guide h i m or her rhrough a process of problem idenrificarion and problem-solving designed ro eirher rel ieve or cope with rhe srress. The remainder of rhis chaprer reviews rhese four srress-induced p roblem areas fro m a cognirive behavioral standpoinr. Emphasis is on rapid rechniques for diagnosis and on specific srrategies ro be employed wirhin rhe docror-parienr relarionship.
DEPRESSION
Feeling "down" is a universal experience. Being sad or "bl ue" accompanies disappoinrmenrs, serbacks, or losses in l i fe. The de pressed mood usually lasts a shorr rime and passes. For some people, however, rhe sadness becomes inrense and long lasring, coloring every aspecr of rheir exisrence. The furure seems hope less. They feel: Powerless Consumed by rheir helplessness Overwhelmed Unable ro concenrrare, sleep, or solve the rourine problems of l i fe In rhe Unired Stares, clinical depression resulrs in rhe hospiral ization of 6% of all women and 3% of all men (14,15), with 15% of all who are severely clinically depressed evenrually comm i rring suicide (16). The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edirion (DSM-IV) (17) and the Guidelines for Derec rion and Diagnosis in Primary Care (18,19) caregorize menral healrh diagnoses. The word depression refers ro a syndrome in which a variery o f signs and symproms occur. Typically, rhere is a change from previous adequare emmional funcrioning ro a depressed mood and a loss of pleasure in l i fe's usual acriviries. The depressed person feels sad or empry mosr of the rime and ofren experiences impairmenr in inrerpersonal, social, or occupational Funcrioning. Associared symproms include: Farigue Feelings of worrhlessness Excessive guilt Agiration D im i nished abilities ro problem solve or concenrrare Indecisiveness Insomnia or hypersomnia Possible suicidal rhoughrs If five or more of rhese symproms are presenr for more rhan 2 weeks, a diagnosis of major depressive disorder is considered. IF
236
//1. Osteopathic Considerations in the Behavioral Sciences
over the last 2 years the patient reports h aving fel t these symptoms and says that for more than half o f that time it was hard to work, take care o f simple thi ngs at home, or get along with people, the diagnosis is dysthymia.
TABLE 17.2. M E D I CAL ILLNESSES AND CON DITIONS WITH INTRINSIC SYMPTOMS OF DEPRESSION Park i nson disease Normal pressure hydrocephalus Mult i p l e sclerosis/stroke Brain tumors (temporal lobe)
Measurement of Depression
Adrenal insufficiency syndrome
There are many self-admin istered i nventories, such as the Zung Depression Scale (20,21), the Beck Depression Inventories (22,23), and the M M PI Depression Scale (24,25) . These in ventories provide rel iable and valid measures of the severity of depression. The patien t can i n i tially be tested for a baseline mea sure and then repeatedly tested with the same i nstrument to measure progress. More recently developed structured interviews such as the P Rl M E- M D (26,27) allow one to q uickly (i.e., i n 8.4 m i nutes) determ i ne the presence of pivotal signs a n d symp toms (Table 17.1) . Medical disorders with i nt rusive symptoms of depression must be ruled out (Table 17.2). Depression has also been reported as a serious adverse effect o f more than 100 commonly prescribed d rugs (Table 17.3). Tricyclic antidepressants and seroton i n reuptake inhibitors are the gold standards for ini tiating management of many serious, possibly organic, depressions (28,29) . Recoveries are often dra matic as the patient reverts to predepression levels o f functioning. Primary care physicians are exposed to a tremendous amount of publicity and marketing from drug companies to manage the symptoms of depression with various pharmacologic products.
TABLE 17.1. STRUCTURED DEPRESSIONa
I NTERVIEW QUESTIONS
FOR
Hypercalcemia Cancer Metal (thal l i u m , mercury) intoxication Ch ronic pain and d isease ( i .e., fibromyalgia, d i abetes m e l l itus) A common symptom i n geriatric populations
20%-24% of medical i npatients N e u ro l og i c disorders (i.e., related to abnormal catecholamines or i ndoleam i ne metabo l ism) Cardiac d isease Serious medical injury (i.e., s p i nal cord, end-stage renal d isease) Dementia, head trauma, seizure d i sorders
From Derogatis LR, Wise TN. Anxiety and Depressive Disorders in the Medical Patient. Clinical Practice NO.4. Washington, DC: Americ an Psychiatric Press; 1989:121, with permission.
TABLE 17.3. DRUGS WITH KNOWN I N D UCE CLIN ICAL DEPRESSION Antihypertensives
G u anet h i d i ne Clonidine
YES
NO
Feeling tired o r having l ittle energy?
YES
NO
Poor appetite or overeating?
YES
NO
Little i nterest or pleasure i n doing t h i ngs?
YES
NO
Corticosteroids
Feeling down, depressed, or hopeless?
YES
NO
Progesterone
Feeling bad about yourself, or that you
YES
NO
i ng too m u c h ?
are a fai l u re or h ave let yourself o r your YES
NO
read ing the newspaper o r watching teleYES
NO
moving around a lot more than usual?
YES
NO
that you wou l d be better off dead or of h u rting yourself i n some way? (Te l l me about it.)
#1 to #9 are yes, one of which i s #4 or #5,
then consider major depressive disorder. If the condition has
2
Benzodiazepines B arbiturates
Neuroleptics
Cardiovascu lar agents
could have noticed?
persisted over the last
Estrogen
Fl u phenazine
or speaking so slowly that other people
SCORING: If five o r more of
Hormones
Haloperidol
If No: What about the o p posite-moving
9. In the l ast 2 weeks, h ave you had thoughts
Hyd ralazine
Alcohol
vision?
8. Being so fidgety o r restless that you were
Propranolol
Central nervous system depressants
family down?
7. Trouble concentrating on t h i ngs, such as
PROPENSITY
Reserpine
nearly every day?
2. 3. 4. 5. 6.
Serum sod i u m or potassium reductions
a-methyldopa
For the l ast 2 weeks, have you had any of the fol l owing problems
1. Trouble fal l i ng or staying asleep, or sleep-
Hyperparathyroidism Vitam i n B12 or i ron deficiency
years and the patient reports that it was
D i g ital is Procai namide Anti-parkinsonian drugs L-Dopa Am antad ine Antimicrobials
hard to do their work, take care of t h i ng s at home, or get along
Cycl oserine
with other people, then consider dysthymia.
Gram-negative agents S u l fonamides
aprim ary care eva l uatio n fo r m e nta l diso r d e rs ( P ri me-M Dl . From Spitzer RL, Williams JB. PRIME-MD Clinical Evaluation Guide.
New York, NY: Biometrics Research, New York State Psychiatric Institute; 1994, with permission.
From Derogatis LR, Wise TN. Anxiety and Depressive Disorders in the Medical Patient. Clinical Practice, NO.4. W ash ington , DC: Am erican Psychiatric Press; 1989:125, with permis sio n .
TO
17. Stress Management in Primary Care
The belief is that as the symptoms are relieved, the patient's phys ical complaints and general adaptation will improve. More com monly, however, problems do not subside entirely. When this i s the case, other interventions can b e used. General osteopathic care uses multiple strategies, such as:
237
TABLE 17.4. FAULTY REASONING PATTERNS NOTED I N DEPRESSION-PRO N E PATIENTS Arbitrary inference-draw i n g a specific conclusion i n the absence of evidence to support the conclusion. Selective a bstraction-draw i n g a conc l u sion based on a deta i l taken out of context.
Counseling Drug therapy Exercise Osteopathic mani pulative treatment designed to decrease the effects of stress-related d isorders and somatic dysfunction
Overgeneralization-drawing a broad, globa l conclusion o n the basis o f one o r more isolated pieces o f i n formation. Magnification and minimization-exaggerati n g the signi ficance o f negative events a n d m i n i m i z i n g the sign i ficance o f positive events. Persona lization-relating external events to oneself when there is no realistic basis for m a k i n g such a connection. Absolutistic, dichotomous thinking-placing all experiences i n one o f two opposite categories.
Cognitive Behavioral Factors in Depression
Depression can be understood in many ways within the frame work of learning theory (30,31) . Deficits in social skills can set the stage for unrewardi ng social, vocational, and personal rela tionships causing subsequent feelings of depression. Studies with animals and humans exposed over time to inescapable stress have shown that the subjects failed to demonstrate s imple behaviors to escape or avoid the stress and subsequent punishment (32) . In a laboratory setting, when exposed to inescapable electric shock, dogs and humans fel t helpless and both suffered from naturally occurring depression. Human and an i mal groups showed similar response patterns of: Passivity Slowed learning Impaired problem solving Loss of appetite Their inability to stop the stressor or to escape from the stressor initiates cogn itive processes that lead to a sense of powerlessness. Victims of inescapable stress lower their future expectations for control over stress and have measurably lower self-esteem and lower motivation (33-35). Beck (23,30) describes negative schemas as a learned maladap tive thinking process that often leads to depression. When faced with stressful events, some patients routinely employ negative views of themselves and their abili ties (i.e, negative schemas) and are dominated by themes of failure and personal inadequacies. They have learned to expect their performance to be worse than that of others (36,37), and view the world as an overwhelming place, laden with burdens, and filled with excessive demands and daily defeats (38). Over time, negative depression schemas become stable, long standing thought patterns. People with these panerns both or ganize experiences as depressing and selectively direct anention to the negative aspects of current and future srressors. These depression-prone personalities perceive the present as depress ing, remember the past the same way, and respond to the future in a fixed, negative manner, independenr-of what occurs in their environments. There are six basic cognitive errors in logic that a patient learns over time (Table 17.4) . Insight into these faulty reasoning patterns is helpful for some depressed patients. Osteopathically trained physicians routinely work with their patients' cogni t ive coping styles in addition to pharmacologically managing meir de pressive symptomatology. Obviously, drug therapy and cognitive
From Beck. AT. Rush AJ. Shaw BF. Emery G. Cognitive Therapy of Depression: A Treatment Manual. New York. NY: Guilford: 1979. with permission.
behavioral treatments augment and complement one another. With major clinical depression, admi n istering these strategies si multaneously often yields a superior result (39,40).
ANXIETY
Chronic anxiety is a generalized state of fear or apprehension in response to a perceived threat. The chronically threatened i ndividual will eventually begin to experience anxiety and d istress i n everyday si tuations that would not normally have elicited such reactions in the past. An anxious reaction is a basic, genetically programmed h uman response to a real or i magined threatening stressor. The biologic changes elicited by an anxious reaction have specific adaptive survival value. They represent alertness and arousal responses for bener behavioral and biologic focusing and coping with me threat. An anxious reaction represents one of several built-in stress programs that patients can use to adapt to and cope with new threats in their environment. Physically, anxiety is a generalized state of fear with especially strong manifestations in the hypotha lamic, sympathetic, autonomic, adrenal, and reticular neuroen docrine networks. Physiologically, the symptoms reRect height ened autonomic arousal, including: Elevated heart rate Occasional heartbeat irregularities Blood pressure changes Sweating Intestinal distress Blood sugar changes Generalized muscle tension Decreased pain tolerance The last two are readily observed during an osteopathically oriented examination of the m usculoskeletal system. Anxious in dividuals also report general symptoms such as: Insomnia Excessive worrying Forgetful ness Irr i tability Difficulty concentrating
238
lfJ. Osteopathic Considerations in the Behavioral Sciences
Experienced osteopathic physicians soon learn that chronic exposure to anxiety-inducing scenarios without adequate coping strategies often involve irrational cognitive appraisals of threats that, in turn, can lead to further and commonly excessive antici patory anxIety. Anxiety disorders occur in 15.4% of the patient population and accoun t for 11% of all physician visits (13) . A study of 350 primary care physicians rated anxiety disorders as the most com mon psychiatric problem seen in their clinical practice (41) . Anxi olytic benzodiazepines are among the most commonly prescribed medications in the Un ited States, and primary care physicians write 85% of these prescriptions. The diagnosis of anxiety is compl icated by the fact that anxiety is often not the patient's chief complaint. Rather, patients experiencing anxiety generally com plain of physical problems. Primary care physicians often fo cus exclusively on physical symptoms, failing to note that the patient's complaints are really created by unteported or unrecog nized anxiety and chronic autonomic arousal including disturbed sleep-wake cycles. Hypervigilance is apparent with expressions of apprehensive expectations and generalized unfocused fears. Re member that there are medical problems that magnify anxiety. Table 17.5 lists medical disorders and conditions associated with high amounts of anxiety. Anxiety is also identified by diffuse and often severe panic attacks and general agitation that m ight not be related to any one particular situation or immediate stressor. The pani c usually lasts anywhere from a few seconds to more than a n hour. These dreaded feel ings of being overwhelmed and out of control appear suddenly and climb to high i n tensities. The attacks are accom panied by i n tense feel i ngs of apprehension over some presumed or pending d istress or catastrophe. During panic attacks, one will experience: Sweating Trembling Choking Shortness of breath Chest pain Heart palpitations Dizziness Paresrhesia
Measurement of Anxiety
Anx.iety inventories such as the state-trait anxiety invenrory (STAl) (42) and anxiety subscales of the M M PI-2 (24,25) mea sure individual differences in anxiety susceptibility and the pa tient's tendency ro perceive a wide range of situations as threaten i ng. The i nvenrories also measure the patient's reported response ro these situations with a�sociated activation and arousal of the auronomic nervous system. Physiologic measurements of anxiety focus on: Skin conductance Heart rate Blood pressure Respirarory rate Gastric motility symproms Pupillary diameter M uscle tension These measuremenrs can also be routinely collected in the pri mary care setting. Structured i nterview questions ro elicit infor mation from the anxious patient seen in family practice settings are another rool (Table 17.6). Anxiety Treatments
An osteopathically oriented approach for managing anxiety in volves treating both the physical symproms of chronic arousal and the mechanisms oflearned and reinforced maladaptive arousal in response to prolonged stress. Benzodiazepines can be prescribed
TABLE 17.6. STRUCTURED INTERVIEW GEN ERALIZED ANXIETY D I SORDERa
QUESTIONS FOR
1. Have you felt nervous, anxio u s, or on edge on
YES
NO
more than h a l f the days in the l a st month? In the last month, have you often been bothered by any of these problems?
4 . Muscle tension,
2. Feel i n g restless so
aches, or
that it is hard
soreness?
6. Trouble concentrating on t h i n gs, such as rea d i n g a book or watc h i n g TV?
to sit sti l l ?
5. Trouble f a l l i n g
3. Getting tired very easi ly?
7. Becoming easi l y
asleep or stayi n g
a n n oyed or irritated?
asleep?
TABLE 17.5. MEDICAL DISORDERS AND CONDITIONS AS SOCIATED WITH D I SPROPORTIONATELY H I G H AMOUNTS OF ANXIETY Hyperthyroidism Cardiac d i sease (e.g., arrhythmias, paroxysmal tachyca rd i a s) Mitral valve prola pse Pernicious anemia Respiratory d i sease Endocrine d isorders (e.g., hypoglycemia) Porphyria Depressive ill ness Pre-se n i l e o r sen i l e dementias E ffects of drug or alcohol use/withdrawal Caffei ne/tobacco use Hypoglycemia Pheochromocytoma E p i l e psy
8. Are three or more of #2 to #7 checked? 9. In the last month, have these problems made it
YES
NO
YES
NO
YES
NO
YES
NO
YES
NO
h a rd for you to do your work, take care of thi ngs at home, or get along with other people?
10. I n the last 6 months, have you been worryi n g a great deal about different things, and has this
been on more than half the days in the last
6 months? (Count a s yes o n l y if yes to both.) 1 1. When you are worrying t h i s way, do you find that you can't stop?
12. These current anxiety symptoms
are not due to
the b i o l ogic effects of a physical d i sorder, medication, or other drug? SCORING: Yes to
1, 8, 9, 10, 1 1, and 12 constitutes a probable
d i a gnosis of generalized anxiety disorder.
aprimary Care Evaluation for Mental Disorders (PRIME-MD). From S p i tzer RL, Williams JB. PRIME-MD Clinical Evaluation Guide. New York, NY: Biometrics Research, New York State Psychiatric Institute, 1994, with pe rm i s sio n .
J 7. Stress Management in Primary Care
to reduce the paralyzing anxiety associated with a clear external stressor. These are most effective if prescribed on a temporary emergency basis with the goal of preventing dependence and ia trogenic withdrawal anxiety when medications are stopped. One should avoid chronic use. Physical symptoms can also be con n·olled by relaxation, controlled diaph ragmatic breathi ng, and biofeedback (43,44). Anxiety-generating thoughts can be identi fied and techniques to counter them explored. These treatments attempt to reduce anxiety by enhancing coping abilities, pro viding interpersonal support, and trai ning the patient to reduce learned anxiety associated with environmental stimuli . All of these treatment modalities can be effectively used to gether or separately according to patient needs. Also, general measures to improve coping ability such as a healthy diet, mod erate exercise, weight control, and mobilizing a support system of family and friends can set the stage for effective long-term anxiety management (45). Positive outcomes of the proposed treatment will result when the primary care physician enters collaborative management relationships with anxious patients. The goal of these relationships is to alleviate overly aroused patients' fears as they learn new coping styles.
ALCOHOL USE AND DEPENDENCE
Medical care for alcohol abuse has become routi ne work in pri mary care practice. The use of alcohol as a coping strategy is uniquely human. As our society becomes more complex and am biguous, more parients use and alcohol to manage stress. The reported use and abuse of intoxicating chemicals that alter the physiology of the body and the central nervous system dates back to rhe ancient Egyptian papyri and rhe Greek amph ithe ater at Delphi. Alcohol abuse and dependency have become a self-medication strategy for stress that is socially tolerated and modeled for our children. Alcohol abuse adversely affects the lives of 10 m illion Amer icans and their families, and is involved i n 10% of all deaths in the Un ited States. Alcohol abuse and dependence are often prevalent in both partners where spousal and child abuses occur (46,47) . Physicians in primary care settings recognize only about hal f the problem drinkers they encounter and are even less l i kely to identify problems in women and the elderly (48-51). At one end of the drinking spectrum, alcohol is used in mod eration without adverse consequences. At the other end of the spectrum are those drinkers who suffer medically, vocational ly, and psychosocially from repeated abuse of alcohol. Most of the dri nkers with varying consumption patterns and risks of a1cohol related problems lie in the middle. Only 5% of the th ree-fourths of all Americans who drink acquire the d isorder of alcoholism (48). Many people drink while under stress to anesthetize them selves and to experience the numbing effects of alcohol as a strat egy for managing their anxiety or depression. Excessive problem drinking, in and outside the work place, costs U . S . industry ap proximately $ 15 billion a year (49). Besides the significant eco nom ic consequences, alcohol also presents a sign ificant health hazard and challenge to the osteopathic physician attempting to help his or her patients manage stress. Alcohol overuse is both a response to stress and a cause of further stress.
239
Alcohol as Response to Stress
It is important to distinguish between the effects of alcohol and the disease of alcoholism. Alcoholism is the consequence of the overuse of alcohol in people who are predisposed to addiction by genetic, physiologic, psychological, sociologic, and other factors. The disease of alcoholism, regardless of the cause or whether the onset is acute or insidious, will eventually take over the l i fe of the patient and his or her fam i ly. I n low concentrations, alcohol depresses the brain's neuronal and synaptic transmission systems, including inhibitory centers (52). These depressant effects creare three self-reinforcing psy chological and behavioral patterns (53): Euphoriant effects Disinhibiting effects Anxiety-rel ieving effects I n itial euphoriant effects reRect central nervous system seda tion, temporarily increasing self-esteem, cou rage, and confidence. To the alcoholic, these disinhibiting and anxiety-rel ieving effects seem almost magical. For example, alcohol's effects often allow a person to: Tal k to the opposite sex Speak up at school or parties I n teract with the boss Have fun playing with the children Dance well Be less sexually inhibited As with any mood-altering drug, the magic ends and the in dividual returns to previous functional levels after he or she stops drinking. A clear understanding of the drinking pattern is necessary to detect whether the problem is harmful or abusive or repre sents alcohol dependency. The DSM-IV (17) is the most widely used diagnostic framework for alcohol-related disorders. Ques tions used in the PRlME- M D structured interview for alcohol use are also useful (Table 17.7). The CAG E questionnaire (54) is another simple diagnostic screen that consists of four questions: I. Have you ever tried to Cut down on your drinking?
2. Are you Annoyed when people ask you about your d rinking? 3. Do you ever feel Guilty about your d ri nki ng? 4. Do you ever take a drink as a morning Eye opener? Positive answers on three or four questions are diagnostically significant. Alcohol as Cause of Further Stress
Once alcohol use becomes a primary stress management strat egy, further stress follows (Table 17.8) . Alcohol might have been i n itially used to manage stress, but disruption in work, personal, and social relationships, and isolation are the final consequences. The urgent need to drink concentrates the patient's remaining en ergies on securing and i ngesting alcohol. Denial, minimization, and self-deception are used to explain the alcoholic's deteriora tion, especially when d iscussing alcohol use with the primary care physician. When the patient's self-esteem or prominence in the
240
ff! Osteopathic Considerations in the Behavioral Sciences
TABLE 17.7. STRUCTUR E D INTERVIEW TO ELICIT I N FOR MATION O N PROBABLE ALCOHOL ABUSE/DEPE N D E NCEa Opening I n q u i ries: Have . . . . you thought you should cut down on your d r i n k i n g ? Why? Has . . . . someone complai ned about your d r i n k i n g ? Who? Why? Do . . . . you feel g u i lty or upset about your d r i n k i n g ? Why? Have . . . . you had five or more d r i n ks in a s i n g l e day i n the past month? How often have you had that much to d r i n k i n the past
6 months?
The tasks of the physician are to: Develop a strong relationship built on trust Make the diagnosis of alcoholism compassionately Elicit the support of fam ily and friends Refer the alcoholic to a recognized recovery program Rei n force the stress management techniques
Has that caused a n y problems?
1. Has a doctor ever suggested that you stop d r i n k i n g
YES
NO
because of a problem with you r health? (Count as yes if patient has continued to drink i n the last
Social Support
6 months after doctor suggested sto p p i n g . ) H a v e any of the f o l l o w i n g h a p p e n e d to y o u more than one time in the last
6 months?
2. Were you d r i n k i ng, high from a l cohol, or hung over
YES
NO
YES
NO
YES
NO
YES
NO
while you were work i ng, g o i n g to school, or ta k i n g care of other respo n s i b i l ities?
3. What about missing or being late for work, school, or other responsi b i l ities because you were d r i n k i n g or h u n g over?
4. What about having a problem getting along with other people while you were d r i n k i n g ?
5. W h a t about driving a car after h a v i n g several d r i n ks
STRESS MANAGEMENT TECHNIQUES
or after d r i n k i n g too much? SCORING: Yes to most questions. (Consider responses to ope n i n g
i n q u i ries and other information known about the patient, s u c h as information obtained from a f a m i ly mem ber.)
' Primary Care Evaluation for Mental Disorders (PRIME-MD). From Spitzer RL, Wil liams J B . PRIME-MD Clinical Evaluation Guide. New York, NY: Biometrics Research, New York State Psychiatric Institute; 1994, with permission.
The most powerful tool in the management of the patient's stress is h i s or her support network. This social network gives a per son the feeling that he or she is valued and cared about. The idea that people need to be surrounded by groups of people who provide love and a sense of belonging is not new. The patient needs help to identify mentors and significant others in his or her environment whom he or she can trust and with whom he or she can share feelings . The osteopathic physician assumes an important role by providing this help and counseling the stressed patient. Referrals to self-help groups in the community such as A1anon and Recovery, I nc. can help to reduce the patient's self absorption. Participation in these groups also leads to the develop ment of outside interests that are compatible with a lifesty le free of addictions. Spiritual Support
commun ity is at risk, lying, evasion, and other manipulative be haviors emerge as strategies to avoid admitting the problem to the primary care physician and ro others. At the point of threatened or actual loss of job, fami ly, home, or health, the physician may intervene and encourage the patient to enter an alcohol treatment program. Primary care physicians normally refer patients with alco holism to special ized treatment programs. Alcohol abuse is a chronic, relapsing d isease, and these patients often require more consistent and i nvolved treatment than primary care physicians can provide (55) . The recovering alcoholic will need a physician's guidance and family support to learn to face l i fe's stressors with out the use of intoxicants. With support from the physician, the fami ly, and a peer suppOrt group, the patient can change his or her maladaptive stress management style and abstain from alcohol.
TABLE 17.8. ALCOHOL-RE LATED STRESS-I NDUCED FAC TORS AFFECTI N G SOMATIC DYSFU NCTION Increased central nervous system excita b i l ity
For patients undergoing elective open heart surgery for coronary artery disease, those experiencing strength or comfort from their spiritual feelings are three times more likely to survive than are those without spiritual support. Those who partici pate in social and community groups (such as local school programs, senior centers, h istorical societies, etc.) also have three times the sur vival rate of those who do not take part in social activity. A 1995 study (56) involving 232 patients over age 55 found that seniors who had both "protective factors," i .e., spiritual and social sup port, enjoyed a 1O-fold increase in survival. The amount or type of spiritual Ot social activity did not matter as much as the partic ipation, comfort, and support derivedfrom the activity (56). Why and how spiritual feel ings and social support extend life after open heart surgery is not understood. There are over 200 studies corroborati ng this health-enhancing, l i fe-prolonging effect in a variety of ci rcumstances and population groups. It is well doc umented, for example, that Mormons (both clergy and devout members) have extremely long life expectancies. The physiologic mechanisms behind longevity, health, and social support are not well understood, however.
Associated vita m i n and nutritional deficiencies Cirrhosis Wernicke-Korsakoff syndrome A lcoholic dementi as F u nctional gastrointest i n a l changes with a n d without gastrointest i n a l bleeding Pancreatitis Esophageal varices B lackouts; brief a m nesic periods Ataxia and poor coord i nation
Sense of Control
A sense of control is a powerful mitigator of stress. Patients can be given a sense that they can cope by learning to anticipate a potential stressor. The perception that a stressor can be accurately anticipated or stopped i ncreases one's range of problem-solving possibilities and consequent feeli ngs of control. By giving a pa tient i n formation about stressors before the patient's exposure to
17. Stress Management in Primary Care
them, researchers have reduced the threatening appraisals made when the stressor is experienced. Studies have determ ined that the stress of surgery or of common medical procedures can be reduced by giving patients accurate expectations, particularly i n terms o f pain and recovery time. Perceptions of Risk
Assessment of risk is inAuenced by certain biases and perceptions brought into the stressful situation by the patient and the health care provider. Many patients need to construct simplified models of the complex i nteraction of stressful factors i n theit environ ment to effectively cope with stress. The physician must provide the patient with simplified models of how the world works and which risks must be taken to put the patient at ease. Many pa tients like to use simple models to i ncrease their understanding of health problems and the subtle and complex factors surround ing the risks posed by a stressor. Setting the stage for decreased anxiety and adaptive coping is as easy as taking a moment to listen to the patient's conceptual model of the stressors in his or her life. From there, the physician can offer concrete expla nations of the stressors and the risks imposed on the patient. One example is tel ling a patient with back pain that he or she has degenerative disc disease and osteoarthritis. This can sound intimidating and hopeless. To help the patient understand the diagnosis, the physician can describe the condition from the pa tien t's perspective. In this example, the patient's diagnosis could be described as "an aging back with stiffness that can be treated in many ways." Observational Learning
Observational learning occurs without any apparent d i rect rein forcement. Many coping behaviors for stress can be learned if the patient observes another person model ing the behavior. Learn ing occurs without the i ndividual patient making a response or receiving tangible external reinforcement for the behavior. This suggests the importance ofour i nternalizations and cognitive abil i ties, which allow us to transform what has been observed into many new patterns of behavior. Encourage your patient to become i nvolved in setti ngs and groups of people who are coping with stress. This can lead to new patterns of coping behaviors. For example, patients with intractable pain fear physical movement. Having them attend a group aquatic exercise program lets them observe others, per haps older or in poorer health than themselves, moving without damage or injury. This vicarious learning lessens the patient's apprehension when the painful area is moved. Progressive Rel axation
Progressive relaxation is based on the premise that muscle tension is closely related to anxiety. Individuals feel a significant reduction i n experienced anxiety as their tense muscles are made to relax. The teaching of progressive muscular relaxation skills fol lows a standard procedure. The individual practices m uscle relaxation after he or she decides which muscle groups are tense. For ex ample, tell an i ndividual to tighten h is or her jaw and notice a
241
pattern of feel i ng strain i n these muscles. After maint aining the tension for approximately 10 seconds, tell the subject to let the muscle group completely relax, and then to notice a d i fference in sensation as the p laces that were previously tense and strained relax. After a few minutes of relaxation, repeat the sequence. The main goal of the train i ng program is to teach individuals what it feels l i ke to relax each m uscle group and to provide practice in ach ieving greater relaxation. Once the i ndividual can discrimi nate the pattern of tension i n a particular muscle group, omit the i nstruction to tense before relaxing. I nstead, the i ndividual must relax the muscle from the present level of tension. The original relaxation procedure required months of trai ning with hundreds of trained muscle s i tes. Cli n ical practice employs a much more abbreviated form of train i ng and is easy to teach to the patient in a primary care setting. Systematic Desensitization
This treatment procedure employs a graded h ierarchy of stress ful scenes and images. It incorporates the patient's perception of the least stress-provoking s ituations to the most stress-provoking situations. Using imagery, the individual is fi rst taught to relax individual muscles. When the i magery and muscle relaxations are mastered, work begins on an increasingly complex hierar chy of i magery and learning that moves gradually from low- to h igh-stress situations. Successful deep muscle relaxation inhibits stress-i nducing anxiety as both nonthreaten ing and threatening scenarios are i magined. As skills improve, i nstruction helps the learner tolerate i ncreasingly d i fficult scenes during the relaxation process. As tolerance increases for anxiety-related i magery, the pa tient learns tolerance for anxiety-induced l i fe situations. The ther apeutic effectiveness of systematic desensitization has been shown with many anxiety-related disorders, such as phobias (including medical procedures), i nsomnia, and stress-related psychophysio logic d isorders such as ulcers, asthma, and hypertension (57) . Behavioral Rehearsal
Allowing indiv iduals to act out or role-play their problem-solving strategies of behavior i s a method used in many d i fferem forms in primary care settings. The physician observes, l istens to, and models or encourages the appropriate behaviors the patient m ight try. The physician o ften teaches assertiveness and problem-solving tech niques. These techn iques are most effective with individuals who experience stress as a result of difficul ties i n self-expression. A lack of appropriate i nterpersonal skills exacerbates stress-related physical symptoms. For example, an overwhelmingly demand ing boss or spouse i s a common cause o f stress-related symp toms and health care seeking in a pri mary care setting. By teach i ng verbal strategies to more effectively deal with excessive and unfair demands, patients learn new and more effective coping behaviors. Cognitive Restructuring
I n cogn itive restructuring, the physician determ i nes and chal lenges specific thoughts or self-verbalizations that comribute to
242
111. Osteopathic Considerations in the Behavioral Sciences
the stress-related d isorder. Treatment is designed to help the pat ient modify negative, self-doubting statements by replacing them with self-enhancing declarations (58) . One cognitive re structuring method is called thought stopping. Thought stop ping is used when patients experience distress because o f ob sessive thoughts about stressors they have di fficulty conrrolling. This also occurs with insom niacs, who cannot stop th i n king long enough to fal l asleep. The patienr is asked to concentrate on the anxiety-induced thought and, after a short period, the physi cian suddenly and em phatical ly says, stop. After this procedure has been repeated several times, the patient will report that the thoughts were interrupted by the word stop. The physician then shifts control back to the patient. Specifically, the client is taught to utter a subvocal stop whenever he or she begins to engage i n a self-defeating ru mination.
Biofeedback
Using physiologic monitoring equipment, the patient can be taught to inA uence physiologic processes such as: Blood pressure Heart rate Sweat gland activity Skin temperature Neuromuscular activity Sphi ncter control Pen ile tumescence By receiving aud i rory or visual feedback, one learns about the close relationsh ip between mind and body. The availabil i ty of sensitive recording devices for home use has made i t pos sible to work on these skills in a more organized and regular man ner. There is a lack of systematic and well-controlled out come studies that concl usively show the clin ical effectiveness of some new monito ring devices. H owever, supportive l i terature for biofeedback-related m uscle relaxation is slowly and cautiously ap pearing. Temperature biofeedback, which is also receiving pos itive support in the literature, has been shown to control Ray naud's phenomena and m igraine headaches. From an osteopathic perspective, biofeedback makes it possible to extend voluntary control over some elements of somatic dysfunction by decreas ing arousal responses affecti ng somatic and viscerosomatic reAex activities. Learning to master these responses helps develop a sense of control and im proves confidence in one's self-healing abili ties.
experience more (61,62): Hosp i tal izations Anxiety Depression Fibromyalgia Propensity for alcohol and other substance abuse An i nability to remain asleep is most common, followed by d i fficulty fal l i ng asleep, and abnormal early morning awaken ing. Contributing factors appear divided among the following (60): Psych iatric (35) Psychophysiologic (15) Drug and alcohol dependency (12) Periodic limb movemenrs (12) Medical, roxic, environ mental (4) Various other (15) Typical ly, insomn iacs are chronically aroused autonomically (anxious), or cogn itively depressed and unable. to stop thinking and worrying at bed time. They worry about not getting to sleep and then are too aroused at bedtime to sleep. This worrying leads to fears that they will have poor daytime performance if they cannot make themselves sleep. I nsomnia begets more insomnia and leads to poor learned sleep habits and routines. Insomnia lasting more than 3 weeks requi res specific behavioral strategies to counteract rhe learned aspects of the insomnia. It also requi res relaxation techniques and, if needed, interm ittent use of sedatives or hypnosis. I nsomnia can be managed effectively by teaching sleep habit techniques that employ a variety of strategies (Table 17.9). These techniques form the foundation for the guidance that the osteo pathically trained physician gives to the patient. When sleep is restored, the patient feels more alert, and there are fewer vegetative and clinical signs of depression and anxiety during waking hours. Patients practicing good sleep habits report improved concentra tion, better problem solving, and more effective management of rhei r stress. Augmenting sleep habit strategies with medication for sleep during short i ntervals is another method used to manage insomnia. A prescription for exercise and a muscular relaxation
TABLE 17.9. GOOD SLEEP HABITS Get u p about the same time every day, regardless of when you go to bed. Go to bed only when sleepy. Esta blish rel axing pre-sleep rituals.
Psychophysiologic Insomnia Management I n the United States, approximately 10 million people consult
their heal th care provider ann ually for sleep disorders, with half receiving prescriptions for sleeping medications (59) . Epidemi ologic studies suggest that 20% to 35% of respondenrs describe sleep problems as severe or constant for as long as 14 years; however, other health problems are commonly identi fied as the primary complaint (60) . Persistent i nsomnia is not l i fe threaten ing. When com pared with good sleepers, however, insomn iacs
Exercise reg u l a r l y and keep active. Org a n ize your day around reg u l a r times for eating and outdoor activities with reg u l a r exposure to bright l i ght, which synchronizes circad i a n cycles. Avoid caffeine, n icotine, alcohol, excessive warmth, and h u nger at bed time. If you nap, try to nap at the same time every day. When laying down to sleep, relax a l l your muscles, particularly your face and jaw, and breath slowly and evenly. If you don't f a l l asleep i n when s leepy.
20 m i n utes, get back u p and return to bed
17. Stress Management in Primary Care
training tape to be used i n the evening hours will also p romote better sleep. All th is, coupled with encouragement by the physi cian who functions both as educator and guide, will alleviate II1somnla.
243
1 5 . Beck AT. Depression: Clinical, Experimental, and TheoreticalAspects. New York, NY: Harper & Row; 1 967. 1 6. Copas ]B, Robin A. Suicide in psychiatric patients. Br } Psychiatry. 1 982; 1 4 1 : 503-5 1 1 . 1 7. American Psychiatric Association. Diagnostic and Statistical Manual of
Mental Disorders, Rev. 4th ed. Wash i ngton, DC: American Psychiatric Association; 1 987. 1 8. Depression Guideline Panel. Depression in Primary Care. f. Detec
CONCLUSION
tion and Diagnosis. Clinical Practice Guideline No. 5. Rockvi l le, M D :
The osteopathically trained physician has many available tools to employ a broad approach to stress-related problems, i ncluding varieties of somatic dysfunction. Anxiety, depression, i nsom nia, and drug and alcohol abuse are common symptoms seen in pri mary care offices. Osteopathic management can be practiced i n three ways: 1 . By treating symptoms as they are reported and observed.
US Dept of Health and H u m an Services, Public Health Service, Agency for Health Care Policy and Research publ ication 93-0 5 5 0 ; A p r i l 1 993. 1 9. American Psychiatric Association. Diagnostic and Statistical Manual of
Mental Disorders. Primary Care Version. Was h i ngton, DC: American Psychiatric Association; 1 996. 20. Zung WWK
.
A self-rating depression scale. A rch Gen Psychiatry.
1 96 5 ; 1 2:6370. 2 I . Zung WWK A rating instrument for anxiety disorders. Psychosomatics. .
1 97 1 ; 1 2 : 1 64- 1 67.
2. By giving advice on managing stressors.
22. Beck AT. Depression: Clinical, Experimental and TheoreticalAspects. New
3. By guiding and mentoring stress-related responses toward pos i tive coping behaviors and strategies (the most rewarding) .
23. Beck AT. Cognitive Theory and the Emotional Disorders. New Yo rk, NY:
Successful diagnosis depends on understanding the i nterac tions of the biopsychosocial factors that lead to stress-i nduced problems. Successful treatment depends on giving clear explana tions so that the patient understands the mechanisms that perpet uate his or her distress. The long-term goal i s to assist the patient toward self-mastery and self-healing.
York, NY: Harper & Row; 1 967. International Universities Press; 1 976. 24. H athaway S R, McKinley JC, MMPI Manua!. M i n neapolis, M N : Psy chological Corp; 1 943. 2 5 . Dahlstrom WG, Welsh G S. A n MMPI Handbook. M i n neapolis, M N : University of M i n nesota Press; 1 972. 26. Spitzer RL, Williams ]B, et al. PRIME-MD Clinical Evaluation Guide. New York State Psychiatric Institute, B i o metrics Research Dept. 722 West 1 68th Street, U n i t 74. New Yotk, NY; J 994. 27. Spitzer RL, Williams J B . Utility of a new procedure for diagnosing mental d isorders in primary care. }AMA. 1 994;272(22): 1 749- 1 756. 28. Cameron OG . Presentations of Depression. New York, NY: John Wiley and Sons; 1 987.
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DC: Government Printing O ffice; 1 988. 4. Korr 1M. The sympathetic nervous system as mediator between somatic and supportive processes. I n : American Academy of Osteopathy Yearbook. I nd ianapolis, I N : American Academy of Osteopathy; I 970: I 70-1 7 5 .
5 . Korr 1 M . Sustained sympathicotonia a s a factor in d isease. I n : A merican Academy of Osteopathy Yearbook. Indianapolis, I N : American Academy of Osteopathy; 1 978:207-22 I .
33. Abramson LY, Sackheim HA. A paradox in depression: unconrrollability and self-blame. Psychol Bul!. 1 977;84:835-85 I . 34. Abramson LY, Seligman M E P, Teasdal e ] . Learned helplessness i n hu mans: critique and reformulation. } Abnorm Psychol. 1 978;87:4974. 35. Seligman M EP Helplessness: On Depression, Development, andDeath. San Francisco, CA: Freeman; 1 97 5 .
6. Ward R. Manual healing methods. I n : Report to the National Institutes of
Health on Alternative Medical Systems and Practices in the United States,
3 6 . Hollon SD, Beck AT. Cognitive therapy of depression. I n : Kendall PC, Hollon SD, eds. Cognitive-Behavioral Interventions: Theory, Research and
Procedures. New York, N Y: Academic Press; 1 979: I 53-204.
pub. no. 1 294; 1 995: 1 1 3- 1 1 9. 7. Cannon WB. The Wisdom ofthe Body. New York, NY: Norton; 1 932. 8 . Selye H. The Stress ofLife, rev. ed. New York, NY: McGraw-H ili; 1 976. 9. Anderson SM, Harthorn B H . The recognirion, diagnosis and treatment of mental disorders by pri mary care physicians. Med Care. 1 989:27;869-
37. Hollon SD, Kendall Pc. Cognitive self-statements in depression: de velopment of an auromatic thoughts questionnaire. Cognit Ther Res. 1 980;4:383-395. 3 8. Funabiki D , Calhoun J . Use of a behavioral-analytic procedure in eval uating two models of depression. } Consult Clin Psycho!. 1 979;47: I 83-
886. 1 0. Schulberg HC, Burns BJ. Mental d isorders i n pri mary care: epidemio logic, diagnostic, and treatmenr research directions. Gen Hosp Psychiatry.
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Clinical Intervention. New York, NY: Spri nger-Verlag; 1 986.
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40. D'Zurilia TJ , Nezu AM . Development and p re l i m i nary evaluation of the social problem-solving inventory (SPSI). Paper presented at the meeting of the Association for the Advancement of Behavior Therapy. New Yo rk,
1 1 06. 1 2. Robins L N, Regier DA, eds. Psychiatric Disorders in America. New York, NY: Free Press; 1 99 I . network: treatment of mental ill ness by non psychiatrist physicians. A rch
NY: Elsevier Science; 1 990. 42. Spielberger CD, Gorsuch RC, Lushene RE. Manual for the state-trait
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November 1 98 8 . 4 1 . Noyes R, Roth M , B urrows G D . The Treatment ofAnxiety, rv. New York,
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43. Keabie D . The Management ofAnxiety. New York, NY: Church i l l Liv i n gstone; 1 989.
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44. Kennerley H . Managing A nxiety. Oxford, U K: Oxford University Press; 1 990. 4 5 . Morris CG. Psychology: An Introduction. Englewood Cliffs, N J : Premice Hall; 1 993.
eds. The Biology ofAlcoholism, /I: Physiology and behavior. New York, NY: Plenum Publishing; 1 978. 54. Ewi n g JA. Detecting alcoholism. The CAGE questionnaire. JAMA. 1 984;252: 1 90 5- 1 907.
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J Cen Intern Med. 1 992;7 : 5 1 7-52 1 . 50. Curtis J R, Geller G , Stokes EJ, et al. Characteristics, diagnosis and rreat ment of alcoholism in elderly patiems. J Am Ceriatr Soc. 1 989;37 : 3 1 03 1 6. 5 1 . Dawson N V, Dadheech G, Speroff T, et al. The effect of patient gender on the prevalence and recognition of alcoholism on a general medical service. J Am Intern Med. 1 992;7:38 1 5 . 52. Kissin B. The pharmacodynamics and natural h istory of alcoholism. In: Kissin B, Begleiter H, eds. The Biology ofAlcoholism, III: Clinical
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Pain. New York, NY: Brun ner/Mazel; 1 976. 5 9 . Lacks I� Morin CM. Recenr advances in the assessmenr and treatment of insomnia. J Consult Clin Psycho!. 1 992;60:5 86-594. 60. Rosekind MR. The epidem iology and occurrence of insomnia. J Gin
Psychiatry I 992;53(suppl 6):46. 6 1 . Lesch DR, Spire J-p Clin ical electroencephalography. In: Thorpy MJ , ed. Handbook of Sleep Disorders. New York, NY: Marcel Dekker I nc; 1 990: 1 33 1 . 62. Buysse DJ, Reynolds I I I CF. I nsomnia. I n : Thorpy MJ , ed. Hand
book of Sleep Disorders. New York, NY: Marcel Dekker Inc; 1 990: 375-433.
OSTEOPATHIC PSYCHIATRY RONALD H. BRADLEY GERALD G. OSBORN JOHN A. JEROME MARY C. WILLIAMS
EPIDEMIOLOGY KEY CONCEPTS • • • • •
History of osteopathic psychiatry Psychiatric diagnosis and multiaxial assessment Depression, anxiety, and somatoform disorder identification and care Considerations when treating various psychotic disorders and substance abuse disorders Assessment and management of personaliry disorders
Osteopathic philosophy and its practices are organized around the belief that everyone is basically healthy and that the dis ease processes are superimposed. We also know that genetic and constitutional variables deeply affect these processes. In this con text, the goal of structural diagnosis and osteopathic mani pulative treatment is to correct neuromusculoskeletal changes in such a way that natural homeostatic mechanisms become more efficient at mainraining health. Importantly, this belief system affects the way osteopathic psychiatrists work with patienrs. Collaborative care that respects an individual's natural restorative processes is a core concept. As a specialty, osteopathic psychiatry systematically inregrates individual, biologic, psychological, and social e1emenrs to bet ter understand mental health and illness. Fundamentally, its area of expertise is to care for the mentally ill. In contempo rary terms, osteopathic psychiatry believes that mental illness arises from complex interactions among genetic and constitu tional vulnerabilities as inAuenced by interpersonal, environ mental, and societal srressors. An objective multiaxial diagnos tic and reporting system is used to communicate investigational and treatment information to patients, their families, and ptofes sional colleagues. Comprehensive treatment plans focus on the whole person-mind, body, and spirit. The origins of osteopathic psychiatry begin early in the 20th century with the establish ment of the Still-Hildreth Sanitarium in Kirksville, Missouri (see below).
Current United States population studies estimate that approxi mately 20% of the U.S. population is affected by menral disorders during any given year. In total, about 26% have either a mental or addictive disorder. Six percenr have addictive disorders and 7% to 10% suffer from a variety of depressive syndromes. Many deal with more than one disorder at the same time (1-4). Impor tantly, these individuals are more likely to experience a variety of chronic, long-term physical and psychiatric illnesses. In 1996, the direct cost of menral health services in the U.S. totaled $69 billion. This figure represents approximately 7.3% of total health care spending during that fiscal year. An additional $17.7 billion was spent on Alzheimer's disease and $12.6 billion on substance abuse disorders (5). History of Osteopathic Psychiatry
Psychiatry became one of the earliest osteopathic specialties. A.T. Still strongly believed his methods were most beneficial when used to treat the whole person-body, mind, and spirit. He worked diligently for the establishment of the first osteopathic sanatorium and kept a close eye on its progress. Shortly before his death in 1917, his last dictated note to mem bers of the osteopathic profession was: Dear Boys and Girls,
[ know you are keeping your eyes on the progress that is being made at Macon, Mo., in the treatment of mental and nervous diseases. We have a great deal of experience. My personal experience covers a period of something over fifty years in the treatment of mental cases, but until Arthur and the boys Charlie, and Harry, became interested in Macon sanarorium, we never had a place where we had a chance ro look after this class of patients. 1 have always contented that a majority of the insane patients could be treated successfully by osteopathy, and [he success that the boys have been having in the last three and one-half years bears out my faith, and I am very anxious for the entire profession ro know of the work that is being done.'
The above message was enclosed with the following letter ftom Dr. Charlie Still:
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The above is the Christmas Greeting that Father intended sending out to all of the boys and girls in the field practicing osteopathy. He has been so interested in the work at Macon; he felt that it was the crowning sheaf in his life's work. He, however, had a stroke of paralysis that terminated fatally before the greeting was sent.
A.G. Hildreth, D.O. , Charles E. Still, D.O., and Harry M. Still, D.O., founded what was ro become the Still-Hildreth Sanaro rium. A.G. Hildreth served as its president and superintendent until his death in 1941 (6). Shortly after opening, they hired Lynn van Horn Gerdine D.O., M.D., who was the fi rst chief psychi atrist. When the Still's approached him with their offer, he was already teaching physiology at Harvard medical school under the guidance of the renowned Walter Cannon, M.D. Dr. Gerdine taught psychiatry, osteopathic therapeutics, pathology, and phys ical diagnosis at the American School of Osteopathy in Kirksville from 1903 until 1914. Dr. Gerdine obtained his A. B. from Johns Hopkins in IS95 where he studied political science under Woodrow Wilson. He received his master's degree from H arvard University in IS99 during its "golden age" when William James, Ph.D., the father of modern psychology, was achieving fame. Dr. James encouraged Dr. Gerdine ro seek his training in osteopathic medicine at the MassachusettS College of Osteopathy. He did so, obtaining his D.O. degree in 1901 and his M.D. degree from Rush medical school in Chicago in 1905. Subsequently, he spent his entire career practicing as an osteopath and was the only clinician at Still-Hildreth Sanitarium with formal postdocroral training in psychiatry. Sanitarium patients were a diverse group, both as ro diagnosis and time spent in the hospital. Some came for diagnostic evalua tion while others stayed for months. In general, a firm diagnosis was not fully established until the patient had been there for at least 6 weeks. Prior ro arrival, many had been diagnosed elsewhere and were found ro be beyond hope of recovery (6). These early osteopaths noted that psychiatric patients had considerably less freedom of cranial suture motion, especially around the cranial base and temporal bones. They also reported less cranial vault resiliency. Diagnostically, there seemed ro be more inherent movement restrictions involving the following: Occipital sites in schizophrenia Sphenobasilar symphysis in manic-depressive cases • Fronrosphenoid articulations in "involutional dementias" (6) •
•
In the I 950s, Floyd Dunn, D.O., a professor of psychiatry at both the Philadelphia College of Osteopathy, and later at the Kansas City College of Osteopathy and Surgery, spoke of the association of auronomic dysfunction with psychiatric disorders. He cited data from 1,000 psychiatric patients. More than 50% demonstrated palpable sites of somatic dysfunction at C2 and T4-6 paravertebral regions of the spine (7). Far in advance of his peers, his classroom lectures routinely connected neuroendocrine activities with a variety of mental disorders. Of several osteopathic sanitariums, the Still-Hildreth oper ation opened first and stayed open the l ongest. Several similar operations emerged during the early 1900s. These included the Dufur Osteopathic Hospital in Ambler, PA, which opened in
1921, Merrill Osteopathic Sanarorium in Venice, CA, in 1923, the Edgehill Sanarorium in Knoxville, TN, in 1924, and the Brooklawn Osteopathic Sanarorium and Clinic in Syracuse, NY, in 1932. The American College of Neuropsychiatry, now called the American College of Osteopathic Neurologists and Psychiatrists, was founded in 1939. Many of its early members combined neu rology, psychiatry, and internal medicine. Some practiced each specialty separately while others combined their work with inter nal medicine. Grover Gillum, D.O., a founding member of the College, and professor of internal medicine and neurology at the Kansas City College of Osteopathy and Surgery, was a prominent example. Another example was Wilbur Cole, D.O., who com bined neurology and basic science research. Among his many accomplishments was the 1940s publication of his discovery of moror end plates on striated muscle. The Still-Hildreth Osteopathic Sanarorium's holistic prac tices, fi rst instituted by Arthur Grant Hildreth, D.O., initially emphasized nutrition and diet along with its neuromusculoskele tal osteopathic work. Consuming large quantities of milk was a central tenet because it was considered a "natural food." The insti tutional environment was upbeat and socially positive, a marked contrast ro the stark and punitive atmospheres of most other psy chiatric institutions. For example, patients were encouraged ro use the boathouse, beaches, music room, and library, as well as many other social activities (6).
MENTAL HEALTH AND ILLNESS: "T HE BRAIN-BODY DILEMMA"
Most themes of modern osteopathic psychiatry began with an cient Greeks. Almost 3,000 years ago, Homer marveled at the range of personality and emotional variables. He stated that "ro one man a god has given deeds of war, ro another the dance, ro another the lyre and song, and ro another the wide-sounding Zeus puts a good mind. " The Greeks treated depression as some thing the body could overcome by using strong emetics, purges, rest, and counsel. Hippocrates, the father of medicine, wrote that mental illness had natural causes and that the brain was the seed of emotions and thought. Much of modern science and psychia try amplifies Arisrotle's assertions that the human brain is capable of reason and moral choice (i.e., mental health). What distinguishes the human brain from other brains is the relative size of the cerebral cortex, the one-fourth inch thick cover ing of gray matter on the lobes and hemispheres of the cerebrum. Only in human beings is the cerebral cortex so large in relation ro general body size. Its many folds and convolutions, the gyri, which increase the surface area of the brain and allow the body ro pack a maximal amount of neural tissues inside the skull, further distinguish the human cortex. Scientists roday agree that the unique abilities of the human mind are directly attributable ro the cerebral cortex. These abil ities go hand in hand with thinking, observing, analyzing, and integrating experiences and feelings ro solve problems and plan ahead. Within this biophysical context, the mind, body, and spirit are tightly integrated. This has led ro the development
18.
and evolution of the biopsychosocial model, developed by George Engel, which emphasizes the unity o/mind, body, andspirit within the context of one's social and cultural environment. Clinically, complex interactions among these areas influence both the pa tient's level of distress and mental health, as well as disease and illness-related responses.
EARLY TREATMENT HURDLES: ASYLUMS
In the Middle Ages, European psychiatric treatment took a huge step backwards when mental illness was generally viewed as "pos session by the devil," a penalty fOf moral depravity or as punish ment for wrongdoing. Asylum inmates were routinely restrained and treated like dangerous animals. Some were tortured, beaten, or burned at the stake. Skulls were analyzed to look for lunacy stones. Asylum keepers often thought that a sudden shock would restore reason. As a result, inmates were commonly dropped without warning into tanks of icy water or strapped into chairs and rotated rapidly to induce shock. Bloodletting was also a fa vorite treatment. Abandoning both adults and children whose intelligence or behavior did not measure up to society's stan dards was common. This was often a death sentence. In rare cases, the mentally disturbed were treated well. This was particu larly true when they were seen as divinely blessed and spiritually enlightened. The idea of humane therapy began several centuries later when Phillippe Pinel (1745-1826) became director of the Bicetre Asylum in Paris. He rejected the notion that the mentally ill were possessed by demons. He set new precedents by un chaining inmates and beginning programs of "kindness, reas surance, and counsel." His therapies included discussions with patients about their problems. His radical and "enlightened" acts helped lay the foundation for modern psychiatry as a branch of medicine. In the 1860s, Charcot became interested in patients display ing neurologic deficits without organic findings. Routinely, these patients were dismissed as hysterical and malingering. Insight fully, Charcot understood that these patients were truly suffering and treated them with combinations of hypnosis and counseling. Since then, patient care has steadily improved through combi nations of expanding psychological and behavioral knowledge coupled with better understanding of cultural and fundamen tal humanitarian concerns for the fights and feelings of the mentally ill.
LACK OF UNIFORM DESCRIPTIONS AND NOMENCLATURE: A MAJOR PROBLEM
An early major and fundamental communication hurdle was a lack of uniform descriptions for mental disorders and their treat ment. This changed in 1883 when the German psychiatrist Amil Kraepelin published the first uniform classification of mental illnesses. He created categories based on the onset, symptoms, development, and outcome of illness. Over the next 40 years, Kraepelin expanded and revised his lists. Eventually, his system
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became the foundation for l ater psychiatric taxonomies and an indispensable guide for the diagnosis and treatment of mental illness through the first half of the 20th cenrury. Since the 1950s, the American Psychiatric Association has published additional diagnostic guidelines referred to as the Di agnostic and Statistical Manual 0/ Mental Disorders (DSM). The DSM-IV is the current revision (8). The manual describes and categorizes more than 200 mental conditions. It is beginning to look at outlines and protocols for the use of specific medications and counseling techniques.
DOCTOR/PATIENT RELATIONSHIPS
One of the most important clinical tasks that any osteopathic physician, including a psychiatrist, should perform is a mean ingful biopsychosocial history. When done well, this foundation becomes a framework for insightful diagnosis. After developing essential demographic data, the reason for seeking psychiatric help is explored. For example, ask the patient "why are you seeking (psychiatric) treatment right now?" Un derstanding that most people are resistant to ask for help, the physician needs to empathize with the patient's plight. Three im portant interview characteristics are essential: clinicaL congruence, empathic understanding, and unconditionaL positive regard for the patient. When done well, these characteristics create a safe, non judgmental clinical environment that allows the patient to speak freely. Clinical congruence demonstrates a clear, consistent, and or ganized way of probing, inquiring, and sorting out issues, signs, and symptoms. Empathic understanding implies genuine accep tance of all of the patient's feelings and concerns about his or her situation. Unconditional positive regard means the clinician is nonjudgmental, regardless of how self-defeating or irrational particular behaviors appear to be. A chronologic narrative history of events leading to the first visit are explored using the who, what, when, and where inquiry model. As the process unfolds, family members and other treat ing sources are gleaned for essential information. This includes obtaining previous medical and mental health records.
PAST PSYCHIATRIC HISTORY
Past history includes exploration of psychological and biologic vulnerabilities, including environmental and social factors. Ex amples are substance abuse history and evidence of previous illegal or illicit activities. Previous pathologic diagnoses are documented and should include presenting symptoms, extent of incapacity, type of treatment, and names of treating physicians and hospitals.
PSYCHIATRIC DIAGNOSES, DATA COLLECTION, AND MEDICAL RECORDKEEPING
The DSM-IV is an official international numerical coding sys tem that classifies mental disorders. The system facilitates data
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collection and reponing procedures for insurance carriers, as well as both governmenral and nongovernmenral organizations. Diagnostically, the multiaxial assessmenr system evaluates five axes using the following: DSM-IV Classification
Axis I Axis II
Axis III Axis IV Axis V
Clinical Disorders and other conditions idenrified as primary focus of clinical attention Personality Disorders and Menral Retardation developmentally longstanding and typically predate onset of Axis I symptoms General Medical Conditions that are linked to presenring somatic dysfunction Psychosocial and Environmenral Problems that may affect diagnosis, treatmenr, and prognosis Global Assessmenr of Functioning across all areas of biopsychosocial functioning
This multiaxial system approach forms a systematic structure for organizing, reponing, and conveying clinical information. Each axis represenrs a simplified assessmenr for that particular area. Selected common Axis I disorders, signs, symptoms, and treatmenr options are described below.
AXIS I DIAGNOSIS Depression and Anxiety Disorders
Major depressive disorders (MDD) and anxiety disorders com monly occur together (9). Fifty percenr to 60% of individu als with MDD over a lifetime also report one or more anxiety disorders. The anxiety disorder predates depression in the ma jority of cases (10). The combined evidence of several studies demonstrates that co-morbid depression and anxiety disorders are associated with greater symptom severity and persistence, more severe social impairmenr, increased help-seeking behavior, and higher incidence of suicidal thinking and attempts (11-13). Multidimensional treatmenr is generally more effective than sin gle inrervenrions alone. In general, they combine pharmacologic approaches with psychotherapy, cognitive restructuring, and, in some cases, social effectiveness and relaxation training (14,15). Factors affecting both neurophysiologic and pharmacokinetic principles are importanr to successful treatment. For example, a working knowledge of serotonin, norepinephrine, and dopamine systems is essenrial. Many patienrs who are anxious or depressed report great com fon and tension relief from basic osteopathic manipulative tech niques. Simply being touched and thoughtfully cared for is very powerful treatment. As osteopaths, we know that much emo tional tension is stored in muscles. Releasing that tension is at the core of treating anxiety and musculoskeletal symptoms. Bipolar Disorders
Bipolar disorder is a recurrent mood disorder. More than 90% of the individuals who have a single manic episode have fu ture occurrences. A manic episode is characterized by periods of abnormally and persistently expansive and irritable moods that last at least 1 week.
The manic episode needs to be sufficiently severe to cause marked impairment in social or occupational functioning or to require hospitalization, and may be characterized by the presence of irrational behaviors and speech. The episode must not be due to the direct physiologic effects of drug abuse, a prescribed med ication, or somatic treatmenrs for depression (e.g., electrocon vulsive therapy, light therapy, or toxin exposure). The episode must not be due to the direct physiologic effects of a general medical condition (e.g., multiple sclerosis, brain tumor). Manic speech is typically pressured, loud, rapid, and difficult to inrer rupt. Individuals often talk nonstop, sometimes for hours on end without regard for others' wishes to communicate. Speech is sometimes characterized by joking, punning, and amusing ir relevancies. Theatrical behavior with dramatic mannerisms and singing is not unusual. Thoughts may race, often at a rate faster than can be aniculated. Distractibility is evidenced by an inabil ity to screen out irrelevanr external stimuli (e.g., the interviewer's tie, background noises, conversations, or furnishings in the room). Goal-directed activities involve excessive planning and dispro portionate panicipation in wide-ranging multiple activities (e.g., sexual, occupational, political, and religious). Increased sexual drive, fanrasies, and behavior are often present. Decreased need for sleep is a hallmark. Early waking and feel ing full of energy is common. Sometimes the sufferer goes sleep less for days without feeling tired. Treatment for bipolar disorder requires long-term medication management and supponive counseling. Osteopathic manipula tive therapies alone have not proved helpful. Lithium carbonate, carbamazepine, and vaIproic acid are medications used to treat acute mania. Lithium's effects are usually delayed for up to 1 to 2 weeks, but 85% of patienrs usually respond well. Because of lithium's slow response, anti psychotics and benzodiazepines are also imponanr in the initial treatmenr (16-18). Lithium also has been used in the strategy to treat resistanr depression. Carba mazepine may be used in rapid-cycling bipolar illness if either lithium or valproate is ineffective or poorly tolerated. As of this writing, carbamazepine therapy is not approved for acute ma nia by the Food and Drug Administration (FDA). The F DA approved valproic acid as an alternative for nonresponders to carbamazepine or lithium.
GENERAL ANXIETY DISORDER
General anxiety disorder (GAD) is a vety common DSM-IV diagnosis in primary care. Essenrial features are excessive anxiety and worry (apprehensive expectation) occurring more 'days than not for at least 6 monrhs. The individual finds it impossible to control worry, which is accompanied by at least three additional symptoms: restlessness, easy fatigability, difficulty concenrrating, irritability, muscle tension, and disturbed sleep. Benzodiazepines are a frequently over-prescribed treatment mainstay. Antidepressanrs for GAD are also surprisingly effec tive because co-morbid relationships occur with depression in approximately 95% of this population (19-21). Antidepressanrs have a real advantage because of their lower potenrial for abuse and dependency. In general, they are also better tolerated than benzodiazepine for long-term use.
18.
A most striking and prominent symptom of GAD is a full blown panic attack (8). The essential feature of a panic arrack is a discrete period of intense fear or discomfort that is accompanied by at least four of 13 somatic or cognitive symptoms. Too often needless laboratory testing and unnecessary treatment goes into chasing down the biology of these symptoms when GAD is the real underlying mechanism. Symptoms include: I.
palpitations or pounding heart/accelerated heart rate
2. sweatlI1g 3. trembling or shaking 4. sensations of shortness of breath or smothering 5. feelings of choking 6. chest pain or discomfort 7. nausea or abdominal distress 8. dizziness or lightheadedness 9. derealization or depersonalization 10. fear of losing control or "going crazy" I I.
fear of dying
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the diagnosis. At least two gastrointestinal symptoms other than pain must be present. Most sufferers also report chronic nausea, abdominal bloat ing, diarrhea, or constipation. Gastrointestinal complaints (some times caused by medications taken to treat other symptoms) can lead to frequent x-ray examinations. Sometimes inappropriate ab dominal surgery occurs if clinicians are not alert. Irregular menses, menorrhagia, and vomiting throughout pregnancy are common. Men often experience erectile or ejaculatory dysfunction. Often conversion symptoms suggest a neuroLogic condition, such as impaired coordination or balance, paralysis, localized weakness, difficulty swallowing, aphonia, urinary retention, numbness, dimming vision, blindness, hearing impairment, unexplained seizures, amnesia, or loss of consciousness other than fainting. The adages of "first do no harm" and "don't make a thick chart out of a thin chart" are particularly appropriate when working with somatoform disorder patients. Management should employ insight-oriented psychotherapy, appropriate osteopathic manip ulative care (to relieve symptoms), support groups, and exercise physiologist training programs.
12. parasthesias (numbness or tingling sensation) 13.
chills or hot Aashes
Schizophrenia
The hallmark of osteopathic treatment should include relaxation training, breathing exercises, establishing a thorough differential diagnosis, reassurance, and routine osteopathic manipulative therapy (OMT) for the musculoskeletal display of emotional tension. Pharmacologic treatments for panic arracks include combinations of selective setotonin release inhibitors (SSRls) such as paroxetine and serotonin-norepinephrine release inhibitors (SNRls) such as venlafaxine. Symptom relief is almost immediately obtained with high-potency benzodiazepines such as a1prazolam (22,23). Antidepressants are the first-line agents because of their doc�mented efficacy, safety, and tolerability be fore use of long-term benzodiazepines. Sometimes high doses of alprazolam (up to 10 mg/day) are needed to relieve the initial anx iety. Low doses should be used initially (alprazolam 0.5 mg two or three times daily) with subsequent dose increases as needed (24).
Schizophrenia is a psychotic disorder characterized by disturbed thinking, blunted/Barrened affect, poor concept of self, and psy chomotor agitation/retardation. Conceptually, the term is de fined as the loss of ego boundaries and gross impairment in re ality testing, with accompanying loss of one's sense of self. Both auditory and visual hallucinations and delusions are prominent (8). Because of their presentation, delusions are sometimes difficult to judge, especially across cultures. In general, however, when poor psychosocial functioning appears in the history, it is related to unusual thinking parrerns. Some are relatively unimpaired in their subculture, interpersonal relations, and occupational roles. Others ex.hibit substantial impairments, including deteriorating occupational functions and social isolation. Usually, their families seek help before the patient does.
Somatoform Disorders
Brief Psychotic Disorder
The essential features of somatoform disorders are patterns of vague, expansive, and recurring multisystem somatic complaints. A somatic complaint is clinically significant if it results in medical treatment (e.g., taking medication) or causes significant impair ment in social, occupational, or other important areas of func tioning. Multiple somatic complaints cannot be fully explained by any known general medical condition or the direct effects of a substance (8). These patients typically overuse emergency room visits, osteopathic and chiropractic treatment, massage therapy, or other similar systems. Multiple somatic complaints generally begin before age 30 and occur over several years. Importantly, symptom reports cannot be fully explained by any known medical, genetic, constitutional, or drug-related diagnosis. At least four different sites (e.g., head, abdomen, back, joints, extremities, chest, rectum) orfunctions (e.g., difficulties with men struation, sexual intercourse, urination) are needed to establish
Brief psychotic disorder is a disturbance involving the sudden on set of at least one of the following positive psychotic symptoms: delusions, hallucinations, or disorganized speech (e.g., frequent incoherence, grossly disorganized, or catatonic behavior). A typ
ical episode lasts at least 1 day, but less than prior levels offunctioning is the rule (8).
1
month. Recovery to
Both schizophrenia and brief psychotic disorders respond well to antipsychotic medications. Typical antipsychotics depress or reduce maladaptive behavioral responses and emotional tension. They also decrease auditory hallucinations and delusions. In some, they induce generalized sedation. They are not universally effective and many have significant side effects involving one or more organ systems, which tends to limit patient compliance. Os teopathic manipulative therapies are of limited value with these primary brain chemistry/organization conditions. Even when sta bilized on medications, touch is often confusing and misinter preted.
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SUBSTANCE ABUSE
The first step to effectively treating substance abuse or depen deJ1Ce is to conduct a complete biopsychosocial evaluation to be sure there is not an underlying medical or psychiatric problem contributing to the situation. Even when medical and psychiatric problems are identified and managed, outpatient trearment for substance abuse is often indicated for a minimum of 2 years. This should include long term support groups for relapse prevention and 12-step recovery model programs such as Alcoholics Anonymous (AA) or Nar cotics Anonymous (NA). Continuing drug screens on an outpa tient basis and overall psychiatric monitoring are essential. Man aging somatic complaints with OMT is often beneficial once the addictive behaviors are stabilized. Substance abuse related disorders include: 1. disorders related to the taking of a drug of abuse, including alcohol 2. misuse of prescribed medications 3.
over-the-counter medications taken improperly or excessively
The diagnosis is made by biopsychosocial history and urine drug screen. Differentiation should be made between tolerance, pseudotolerance, physical dependence, addiction, and pseudoad diction. •
•
•
•
•
Tolerance is the need for an increased dosage of a drug to produce the same level of analgesia that previously existed. Tolerance also occurs when a reduced effect is observed with a constant dose. Pseudotolerance is the need to increase dosage that is not due to tolerance, but due to other factors such as disease progression, new disease, increased physical activity, lack of compliance, change in medication, and drug interaction. Physical dependence can be described as the occurrence of withdrawal symptoms after drug use is stopped or quickly decreased withour tin·ation. It is not addiction. Physical de pendence " . . . is not a clinical problem if patients are warned to avoid abrupt discontinuation of the drug and a tapering regimen is used. " Addiction is "psychological dependence on the use of sub stances for their psychic effects and is characterized by com pulsive use . . . " Addiction should be considered if patients no longer have control over drug use and continue to use the drugs despite harm. Pseudoaddiction is drug-seeking behavior that seems similar to addiction but is due to unrelieved pain. T his behavior stops once that pain is relieved, often through an increase in opiod dose. "Misunderstanding of this phenomenon may lead the
TABLE 18.1. EFFECTS
OF COCAINE BASED
clinician to inappropriately stigmatize the pain patient with the label 'addict. ' In the setting of unrelieved pain, the re quest for increases in drug dose requires careful assessment, renewed efforrs to manage pain, and avoidance of stigmatizing labels. " Neither tolerance nor withdrawal is necessaryor sufficient for a diagnosis of substance dependence. Some individuals show a pat tern of compulsive use without signs of tolerance or withdrawal. Some use larger quantities for longer periods than intended, and virtually all daily activities revolve around the substance and great amounts of time spent obtaining, using, and recovering from its effects.
COCAINE ADDICTION
Cocaine is one of the most commonly abused pharmacologic agents. Table 18.1 outlines use patterns for various cocaine preparations. Addiction is the most common complication of cocaine use. Because the drug "high" is so pleasant, compulsive drug seeking quickly takes over the victim's life. Family, social, work, and recre ational withdrawal is the rule rather than an exception. Chronic use results in tolerance of its many effects. This is particularly likely to occur with usage at high doses or in conjunction with binges. Because of its alleged ability to produce prolonged and in tense orgasms, early cocaine use is often linked with compulsively promiscuous sexual activity. In the long term, however, reduced sexual drive and complaints of sexual problems are common. Table J 8.2 outlines some of the effects. T here is no standard protocol or recognized pharmacologic treatment for cocaine dependency at the present time. Substance abuse treatment discussed earlier yields mixed results at best. Os teopathic medicine is truly challenged by this chemically induced, often total, breakdown in mind, body, and spirit (Table J 8.3).
Benzodiazepine Abuse
Benzodiazepines are the most widely prescribed medications for anxiety disorders and insomnia in the United States (25,26). Ac tions of each type are listed in Tables 18.4 and 18.5, and with drawal is very difficult. The most common treatment approach is slow withdrawal over 6 to12 weeks. To prevent seizures, phenobarbital is some times used to control the clinical course. The phenobarbital ap proach calls for assessment of the total amount of daily benzodi azepine use that is then converted to a phenobarbital equivalent. Carbamazepine is another useful agent (27-29).
ON
TYPE
AND ROUTE
OF
ADMINIS
TRATION Cocaine Preparation
Route of Administration
Cocaine
Intranasal
Hydrochloride (powder)
Intravenous
Crack cocaine (alkaloidal, free base)
Inhalation (smoking)
Onset of Action
Peak Effect
2-3 min 30-45 s 8-10 s
30-45 min 10-20 min 5-10 min
18.
TABLE 18.2. EFFECTS OF COCAINE AT VARYING DOSES
Osteopathic Psychiatry
TABLE 18.4. CATEGORIES
OF
2S 1
BENZODIAZEPINES
BY
HALF-LIFE Low doses Heightened sense of well-being, alertness, energy, and
Ultrashort-acting
Short- or Intermediate-acting
Long-acting
Modest elevation in heart rate and blood pressure
Estazolam
Alprazolam
Chlordiazepoxide
Enhanced performance on mental and physical tasks
Midazolam
Lorazepam
Clonazepam
Temazepam
Oxazepam
Clorazepate
self-confidence
Increasing doses Intense euphoria, agitation, impulsivity
Triazolam
Diazepam Flurazepam
Heightened aggressive and sexual behavior
Prazepam
Paranoia
Quazepam
Headache Chest pain Severe overdoses Hallucinations Delirium Seizures Severe hypertension Tachycardia Cardiac arrhythmia Hyperthermia Coma Respiratory arrest Death Seizures and intense muscle activity contributing to hyperthermia; and rhabdomyolysis resulting in acute renal failure
Protocols for the withdrawal process can be found in many references. Table 18.6 outlines phenobarbital/benzodiazepine equivalencies. Recovery, lapse, and relapse are common ele ments of substance abuse rehabilitation. Benzodiazepines are no exception. Recovery in the initial stage of abstinence is affected by many factors, including: a. b. c. d. e.
patient's motivational level, severity of abuse, related medical, psychiatric, and psychosocial problems, age, gender, and ethnicity, social support (30).
Because detoxification alone is rarely adequate, many relapse without suitable aftercare. Relapse prevention should be part of the long-term plan. Steps that help maintain abstinence include: a. b. c. d.
supportive individual psychotherapy, joining a self-help recovery group, joining a 12-step program, anxiety management techniques such as biofeedback and ex erCIse, e. learning to anticipate, identify, and cope with risks that in crease relapse risks. (31,32).
ALZHEIMER'S DISEASE
Symptoms of Alzheimer's disease include memory loss that affects everyday living and overall quality of life, difficulty performing fa miliar tasks such as naming common objects, getting lost easily in familiar places, poor and decreased judgment abilities, problems with abstract thinking, frequently losing or misplacing items, a general loss of interest, and changes in mood, behavior, and per sonality (8). Patients are often symptomatic for as long as 5 years before a clear diagnosis is made. Three stages characterize Alzheimer's disease (33). 1. Stage one is mild and usually lasts 2 to 4 years. During this stage, the victim often says the same thing over and over, gets lost easily, and loses interest in previously enjoyable activities. As time passes, personality changes are clearly evident. 2. Stage two usually lasts 2 to 10 years. This stage is characterized by increasing difficulty dealing with recent events, dressing, feeding, and personal hygiene. With progression, argumen tativeness, paranoia, and assaultive behavior are increasingly common. 3. Stage three usually lasts 1 to 3 years. At this point, the victim is no longer physically or mentally capable of speech or cog nition, and general coordination steadily deteriorates. Loss of bladder and bowel function is common (34). There is no cure for this devastating problem. At the time of this writing, two or three brain-selective pharmacologic agents are available. Donepezil hydrochloride is the oldest of the group and has been shown to slow the deterioration processes by several months. Osteopathic care centers provide active planning and supportive counseling for both the family and caregivers who themselves suffer the musculoskeletal and emotional stress of this disease.
DELIRIUM TABLE 18.3. DETERMINANTS OF HOSPITALIZATION FOR COCAINE ABUSE Chronic crack smoking or intravenous use Concurrent dependency on other addictive drugs or alcohol Serious concurrent medical or psychiatric problems Severe impairment of psychological functioning Insufficient motivation for outpatient treatment Lack of family and social support Failure in outpatient treatment
Delirium may occur in individuals with normal brain function ing, bur it is actually more common in those with underlying brain disease, such as dementia. It is more common in the el derly, probably due to changes in neurotransmitters because of age and disease-related loss of neural tissues. Delirium may be due to primary brain disease or diseases else where in the body that affect the brain. Metabolic, toxic, struc tural, or infectious processes are most common. Physiologically,
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Osteopathic Considerations in the Behavioral Sciences
TABLE 18.5. BE NZODIAZEPINE WITHDRAWAL SYNDROMES Syndrome H igh-dose withdrawal
Low-dose withdrawal (slow taper)
Signs/Symptoms
Time Course
Anxiety, insomnia, nightmares,
Begins 1-2 days after a short acting
Response to Reinstitution of Benzodiazepine Signs and symptoms reverse
major motor seizures,
benzodiazepine is stopped;
2-6 hours following a hypnotic dose of a
psychosis, hyperpyrexia,
3-8 days after a long-acting
benzodiazepine
death
benzodiazepine is stopped
Anxiety, agitation, tachycardia,
Signs and symptoms emerge
Signs and symptoms reverse
2-6 hours
palpitations, anorexia, blurred
1-7 days after discontinuation of
following a sedative dose of high-potency
vision, muscle cramps,
the benzodiazepine or after
benzodiazepine
insomnia, nightmares
arousal mechanisms of the thalamus and reticular activating sys tems of the brainstem are physiologically impaired. Sleep disrup tion and superimposed stress often worsen symptoms. Symptoms of delirium flucruate rapidly, often within a matter of minutes and worsening late in the afternoon to early evening, which is commonly called sun downing. Consciousness clouds with increasingly prominent disorientation as to time, place, and person. Attention deficits are the rule, with frequent confusion regarding day-to-day events and daily routines. Personality changes and altered affect are common. Symptoms include irritability, inappropriate behavior, fearfulness, or overtly psychotic fearures, such as delusions, hallucinations, or paranoia. Some may be withdrawn, quiet, or apathetic. Others become hyperactive, excitable, and physically restless (35,36).
ADULT ATTENTION DEFICIT DISORDER
Adult attention deficit disorder (AD H D) is a common but con troversial syndrome characterized by inappropriate hyperactivity, impulsivity, and inattention dating from childhood (8). It is char acterized by excessive physical and mental activity. Limited abil ities to control daily behaviors are the rule, even when adjusted for age. The most prominent childhood and adolescent symptoms and signs are poor social performance, hyperactivity, tantrums, drug and alcohol use, antisocial personality, depressed mood, and general anxiety. Significant controversies surround the best treat ment strategies. Combinations of centrally acting stimulants such as methylphenidate along with lifestyle education and support group activities are commonly used. TABLE 18.6. DE TERMINING BE NZODIAZEPINE/PHE NO BARBITAL EQUIVALE NCIES Dose Equivalent of Benzodiazepine Alprazolam Chlordiazepoxide Clonazepam Clorazepate Diazepam Flurazepam Lorazepam Oxazepam Temazepam Triazolam
30 mg Phenobarbital (mg) 1 25 2 15 10 30 1 30 30
AXIS II DIAGNOSES Personality Di sorders
The term personality disorder refers to longstanding patterns of disordered (often chaotic) behavior and emotional activiries. Learning rhe behavioral features of personality disorders can im prove management and rrearment plan ning. Primary care physi cians are apt to miss rhe diagnosis, particularly if unaware of Axis II disorders, because rhe disorder ofren underlies persisrent chronic illness. Importantly, personality disorders are persistent, develop early, and endure for life. In stressful siruarions, under lying generic and environmental srressors ofren express them selves through personality disorders. Frequent reactions are re portS of vague, nonspecific whole-body pain, intrapsychic and emotional pain, worsening of preexisting problems, and reporting the life-long effects of physical, verbal, sexual, and psychological abuse. I.
Cluster A: asocial personality cluster consisting of paranoid, schizoid, and schizotypal personality disorders.
2. Cluster B: dramatic/emotional personality disorder cluster con sisting of borderline, histrionic, and narcissistic personality disorders. 3. Cluster C Anxious personality disorder cluster consisting of avoidant, dependent, obsessive-compulsive, and passive aggressive personality disorders Assessment of Axis II Personality Di sorders
The most common assessment tool is the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) (37,38). Over 50 years old, it is one of the oldest and research-validated personality evaluarion rools, and it is often used to evaluate fundamental personality characteristics associated with chronic physical and mental dis orders. From an osteopathic perspective, it is imporrant to know rhat the MMPI-2 results are valid. Only valid testing delineares parients who present with ambiguous funcrional and organic neu romusculoskeletal complaints (39-41). Of the three clusters, patients fitting into cluster B (dra matic/emotional) are rhe most troublesome for the primary care physician. This is because borderline histrionic and narcissistic personality disorders represent a pervasive pattern of instabil ity in interpersonal relationships, affecting self-image and affec tive/emotional relationships. Patients with musculoskeletal com plaints that de£}r trearment spend a lot of time visiting many primary care physicians.
18.
These cluster B individuals show marked impulsivity begin ning in early adulthood. Four psychosocial areas are affected: 1. Continual efforts are made ro avoid real or imagined aban donment by the physician or his staff. 2. Patterns of unstable and intense interpersonal relationships are characterized by alternating extremes of idealization and devaluation of the docror/patient relationship. 3.
Typically, there is a persistent identity disturbance with markedly dis(Urbed and/or disrorted self or body image.
4. Persistent impulsivity also occurs in at least two outside areas that are potentially self-damaging: a. spending b. sexual activities c. reckless driving d. substance abuse e. binge eating f. recurrent suicidal behavior, gestures, and threats g. affective instability, particularly strikingly apparent mood shifts and overreactivity h. chronic feelings of loneliness and emptiness I. inappropriately intense anger and lack of control over anger J. transient-related paranoid ideation or severe dissociative symproms Behaviorally, cluster B personality disorder patients enter your office in the following ways: 1. They think you're wonderful and claim that all other physi cians before you did not understand them. 2. They 'make scenes ro fill needs' for attention, disrupting both your practice schedule and private life. 3.
They fight with the staff and are never satisfied.
Typically, they are demanding, and treatment failure or regres sion is the rule. Negative counter-transference complexities are also common. In some, self-mutilation tendencies and manipula tive suicidal efforts occur. They also demonstrate abandonment, engulfment, and annihilation concerns that do not respond ro medications. The most difficult differential diagnosis is sorting out person ality disorder and its many manifestations from depressive disor der. Depressive disorder is characterized by pervasive guilty feel ings, agitation, suicidal tendency, remorse, and withdrawal. Stable (as contrasted with unstable) relationships are present along with more severe vegetative signs. Personality disorders, on the other hand, speak of loneliness and emptiness. Repeated suicidal ges(Ures, persistent rage, cre ation of demanding relationships, and delusionary self-sufficiency are other traits. The best way ro treat personality disorders includes concur rent treatment with a psychiatrist or psychologist. The goal is ro help strengthen ego and self-concept defenses so the patient can more effectively rolerate anxiety while gaining greater con trol over counterproductive impulses and manipulative counter transferences. Counter-transference effects are common with these patients. Typically, they want frequent visits, cannot rolerate separation,
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and are easily angered with you and your staff. Boundaries must be set between you, your staff, and the patient. Manipulative behavior, such as missing appointments, must be addressed im mediately in order ro establish a stable treatment framework. A passive therapeutic approach is counterproductive with these patients. Osteopathic manipulative therapies are always misinter preted, never productive, and complicate an ever-increasing com plex docror/patient relationship. Instead, the active approach is confronting self-destructive behaviors, establishing connections between feelings and actions, and setting limits while maintaining focus on the here and now.
IMPORTANCE FOR PRIMARY CARE PHYSICIANS
The need for the primary care physician ro understand and use this multiaxial diagnosis system is of utmost importance in devel oping an overall treatment plan that sets realistic and obtainable goals. A multiple biopsychosocial approach is apt ro be most effective. Medication, psychotherapy, and healthy lifestyle mod ifications that focus on strengthening mind, body, and spiritual aspects are fundamental management strategies. Important "here and-now" considerations are diet, exercise, focusing on healthy re lationships, and use of appropriate osteopathic manipulative care.
CONCLUSION
Thoughts, feelings, and behaviors are influenced by complex combinations of genetic inheritance and cultural influences. Re alistic and reasonable diagnostic and treatment planning should always incorporate these complexities within the capacity of the patient. At best, this is a difficult task. This chapter describes a widely accepted, multiaxjal diagnostic system that identifies treat able Axis I behavioral/psychological problems. It also focuses on the Axis II personality disorders that complicate routine treat ments of Axis I and a myriad of Axis III general medical disor ders. Osteopathic manipulative techniques covered elsewhere in this text address the musculoskeletal management of many psy chiatric signs and symproms. The patient needs ro experience a nonthreatening environment that encourages open self expres sion and long-term mental health. Osteopathic psychiatry is based on the assumption that peo ple have within themselves the resources ro understand their thoughts, feelings, and the environmental forces surrounding them. With that understanding and physician support, they can change their behavior and mood. Empathic understanding, non judgmental acceptance, and genuine caring about the patient are an osteopathic hallmark for psychiatry.
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23. Owens MJ , Nemeroff CB. Role of serotOnin in the pathophysiol ogy of depression: focus on the serotOnin transporter. Clin Chem. 1 994;40:288-295. 24. Smith DE, Wesson DR. Benzodiazepines and other sedarive-hypnotics. I n : Galanter M, Kleber H, eds. American Psychiatric Press Textbook 0/ Substance Abuse Treatment. WashingtOn, DC: American Psychiatric Press; 1 994: 1 79- 1 90. 25. Wesson DR, Smith DE, Seymour RB. Sedative-hypnotics and tricyclics. I n : Lowinson ] H , Ruiz P, Millman RB, et ai, eds. Substance Abuse: A Comprehensive Textbook, 3rd ed. Baltimore, MD: Will iams & Wilkins; 1 997:27 1 -279. 26. O'Brien CPO Drug addiction and drug abuse. In: Hardman jG, Limbird LE, eds. Goodman & Gilmans The Pharmacological Basis o/Therapeutics, 9th ed. New York, NY: McGraw-Hili; 1 996: 557-577. 27. Klein E, Uhde TW, POSt RM . Prel iminary evidence for the utility of car bamazepine in alprazolam withdrawal. A m } Psychiatry. 1 986; 1 43:235236. 28. Ries RK, Roy-Byrne PP, Ward NG, et a!. Carbamazepine treatment for benzodiazepine withdrawal. A m } Psychiatry. 1 989; 1 46:536-537. 29. Pages KP, Ries RK. Use ofanticonvulsants in benzodiazepine withdrawal. A m } Addict. 1 998;7: 1 98-204. 30. Daley DC, Marlatt GA. Relapse preven tion: cognitive and behavioral interventions. In: Lowinson J H, Ruiz P, Millman RB, et ai, eds. Substance Abuse: A Comprehensive Textbook, 3rd ed. Baltimore, MD: Williams & Wilkins; 1 997:533-542. 3 1 . Daley DC, Salloum I. Relapse prevention. In: Ott Pj, Tarter RE, Ammerman RT, eds. Sourcebook on Substance Abuse. Needham Heights, MA: Allyn & Bacon; J 999:255-263. 32. Alling FA. DetOxification and treatment of acute sequelae. In: Lowin son j H, Ruiz P, Millman RB, et al, eds. Substance Abuse: A Comprehen sive Textbook, 3rd ed. Baltimore, M 0: Williams & Wilkins; 1 997:4024 1 5. 33. Morris Jc. Differential diagnosis of Alzhei mer's disease. Clin Geriatr Med. 1 994 ; 1 0:257-276. 34. Small GW, Rabins PV, Barry Pp, et al. Diagnosis and treatment of Alzheimer's disease and related disorders: consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer's Associ ation, and the American Geriatrics Society. }AMA. 1 997;278: 1 3631 37 1 . 3 5 . Wise MG. Delirium due to a general medical condition, delirium due to multiple etiologies, and delirium not otherwise specified. I n : Gabbard GO, ed. Treatment o/Psychiatric Disorders, 2nd ed., volume I . Washing tOn, DC: American Psychiatric Press; J 995:423-443. 36. MarcantOnio ER. Delirium. In: Rake! RE, Bope ET, eds. Conns Current Therapy. Philadelphia, PA: WB Saunders; 200 I : I 1 44- 1 1 47. 37. Dahlstrom WG, Welsh GS, Dahlstrom LE, eds. An MMPf Handbook. Volume I: C/inical lnterpretation, revised ed. Minneapolis, M N : Un iver sity of Minnesota Press; 1 960. 38. Hathaway SR, McKinley j . Minnesota Multiphasic Personality Inventory. Min neapolis, M N : University of Minnesota Press; 1 930. 39. Hanvik LJ . M MPI profiles in patients with low back pai n . } Consult Clin Psychol. 1 9 5 1 ; 1 5 :350-353. 40. McCreary C, Turner j, Dawson E. Di fferences between fu nctional versus organic low back pain patients. Pain. 1 977;4: 73-78. 4 1 . Sternbach RA, Wolf SR, Murphy RW, et al. Traits of pain patients: the low-back "loser." Psychosomatics. 1 973; 1 4 :226-229.
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CLINICAL PROBLEM SOLVING SARAH A. SPRAFKA
Personal Data KEY CONCEPTS •
•
•
Four approaches to data gathering and synthesis, including pattern recognition, hypothetico-deductive method, problem-oriented perspective, and clinical decision analysis Problem-solving practices, including therapeutic rouch, musculoskeletal pain, osteopathic manipulative treatment and medication, patient as a whole, and integrative thinking Osteopathic approach to clinical problem solving
in (he long term, the osteopathic concept will survive because true
Name: Richard Johnson Age: 5 5 Ethnicity: White Reason for visit: "I was raking leaves on Sunday and I got an aching sensation in my left shoulder. It still bothers me today." Vital Signs
Height: 6' I" Weight: 203 Ibs. Blood Pressue: 1 60/ 1 1 0 mm Hg Pulse: 75 regular Respirations: 1 6
principles never die. They may be averted, submerged, even denied, but they will emerge again, stronger than ever. They have only to be applied every day in patient care to show how jimdamental and timeless they tire
(1).
This chapter discusses clinical problem solving from an osteo pathic primary care perspective. It begins by looking at four dif ferent approaches to clinical problem solving and discussing how each can be incorporated in the osteopathic family doctor's iden tification and explanation of a patient's problem. The second section discusses case vignettes to report and analyze an inquiry into osteopathic practitioners' self-reported problem solving pro cesses. That inquiry is the source for the illustrative quotations used throughout this chapter. The third section summarizes a case illustrating application of the osteopathic approach to clini cal problem solving. EXAMPLE CASE
Consider the following case.lr is a Wednesday in mid-November. The setting is the office of A.B. Marrin, DO, an osteopathic family practitioner. Mr. Johnson has made an appointment to see the physician. At the time of the patient's visit, Dr. Marrin looks at the chart and notes that this is the patient's first visit to the office. One-half hour has been allocated for the appointment. Based on preliminary examination, the following data have been entered in the chart:
Discussion
Ifyou were Dr. Marrin, what might you be thinking? At this point you have just the slightest bit of information about M r. Johnson. He complains of shoulder pain. His weight is high relative to his height. You picture a large man. His blood pressure is elevated. At this stage of your interaction with this patient (you have not met him yet), your first priority is clearly to conduct a thorough history and physical examination including a diag nostic palpatory examination, and to become acquainted with the patient as a person. As you plan for what you would like to learn from M r. Johnson, you begin to consider some pos sible mechanisms for his presenting problem. These may be wide-ranging and include trauma to the shoulder or somatic dysfunction in the shoulder. He may have viscerosomatic re Hex activity associated with cardiovascular and/or pulmonary disease. At this point we leave the actual visit with Mr. Johnson, and consider some approaches you might take with this patient: How you organize your data gathering and data synthesis How you view this patient as an individual and as a member of a group How you plan a short-term as well as longer-term strategy for your interaction with M r. Johnson
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IV Os teo pa thic Co ns ideratio ns in Clinic al Pro blem So lv ing
DATA GATHERING AND SYNTHESIS
Data gathering and synthesis are at the heart of the problem solving process for the clinician. The following sections elaborate on four major forms of data gathering and synthesis, and apply them to the example of Mr. Johnson. Pattern Recognition
For the clinician, pattern recognition (also called pattern match ing) is often invoked on those occasions when there is a clear (almost textbook) picture, often of a diagnostic or causal nature, seen in the patient's presentation. For example, a clinician who is of a mind to consider a pattern for M r. Johnson might think: Aha' White male, in his 50s, overweight, high blood pressure, presents with a variant on chest pain. Coronary artery disease, I'll bet you. And to complete the picture, I'll bet he smokes, has high cholesterol, and has a high-stress, sedenrary job. I'll even bet you he has a positive treadmill test result.
Most of what we know about pattern matching comes from the work of Patel and colleagues (2-3) and Norman and colleagues (4-7). The former have compared the diagnostic thought pro cesses used by expert physicians with those of nonexperts, and those used with more and less complex problems. For example, expert physicians are described as employing a type of "forward reasoning" in solving straightforward problems; it involves going from highly selective data gathering directly to diagnostic con clusions. This process appears to be analogous to a sophisticated form of pattern recognition or pattern matching. It contrasts with what is called "backward" reasoning. Backward reasoning is employed when the diagnostician does detective work by con sidering possible diagnoses and then checks back in the data to see whether supportive cues are present and uses the diagnos tic hypotheses to guide further data gathering. Novice problem solvers use backward reasoning (what others often refer to as the hypothetico-deductive method) much more than expert problem solvers do. Norman and others have concentrated their research on re call and use of visual patterns such as those found in dermato logic problems and x-ray study interpretation. Problem solving by osteopathic primary care physicians corroborates and expands on this research. The following examples illustrate this type of reasonll1g. VISUAL PATTERNS
Three types of visual patterns are common. One is the visual distinction of the presence of illness. Clinicians have described situations in which they walk into the examining room and the first thing they note is that the patient "looks sick." They use cues such as the patient's: Coloring Dullness of the eyes Lethargy Change in appearance since the last visit
Clinicians express the importance of visually assessing the ap parent severity of the patient's illness or "how sick" the patient looks. They note that this initial assessment often sets rhe tone for the subsequent workup. The assessment guides whether the workup is directed at identifying potentially serious physical ill ness or something that may be less serious or possibly lifestyle related, and whether it is more or less urgent for the physician to reach a preliminary conclusion and initiate treatment. A second visual pattern particularly meaningful for osteo pathic primary care physicians is that of the musculoskeletal sys tem. On the first observation of the patient, the physician notes the patient's posture and movements. He or she notes structural asymmetries (such as in levels of key bilateral landmarks) and observes symmetry, asymmetry, and any apparent restriction of the patient's natural spontaneous movements. A third visual pattern noted by primary care physicians is identification of skin lesions. The experienced physician can tell by looking at a patient whether he or she has a disease such as chicken pox, whether there is a skin injury such as a burn, and whether there is a common dermatology problem such as psoriasis, squamous keratosis, or tinea crura. SEASONAUENVIRONMENTAL PATTERNS
Common diagnostic patterns occur seasonally, and may be asso ciated with the patient's living environment. Such problems are usually respiratory, for example: Sore throat Upper respiratory infection Bronchitis Sinusitis In addition to visual and auditory cues such as runny nose, red eyes, and a distinctive cough, part of the diagnostic pattern is the season in which the presentation occurs. These problems are frequent in children in the fall and winter months when they are at school in an enclosed room with poor air circulation. Another common pattern is seen in a child who presents with signs and symptoms of bronchitis and who is known to live in a home where members of the household smoke. AB DOMINAL PAIN
Abdominal pain is a frequent reason for visits to the family physi cian. It can occur in many forms, and some family physicians feel they have seen enough of certain distinctive presentations that they have become a diagnostic pattern. Two common presema tions are: 1. The patient complains of colicky lower abdominal pain with radiation to the flank or groin, and feels more comfortable moving around than sitting or lying still. This pattern suggests a kidney stone. 2. The patient is a woman between the ages of 30 and 50, often with several children, who presents with right upper quad rant pain that radiates to the right side and often to the right
19. Cl inic al Pro ble m So lv ing
shoulder, and with nausea, vomiting, and bloating. This pat tern suggests gallbladder disease.
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its occurrence has diminished co the point that it is now con sidered rare. Nonetheless, our awareness that it is potentially life threatening does not allow us co forget about it.
ESTABLISHED PATIENT
Patients often tell the physician what their problem is and what treatment is needed. This is particularly true for patients with chronic illnesses or for elderly patients with numerous health problems that are being managed by the physician. Here, the panern is not so much a visual or diagnostic one as it is the panern of the individual patient as he or she has interacted with the physician over time. When such a patient presents with a complaint, with Ot without his or her own explanation of the problem, the physician asks, "Does this problem fit the panern for this patient? Would I expect this patient ro have this problem given what [ have learned about him or her over the years?" The answers to those questions help guide the interaction with the patient.
CAVEATS
Although quick co admit that evoking a diagnostic panern for common problems is hard co avoid and tends co increase with experience, clinicians often offer warnings against being trapped. Two examples are pertinent: 1.
MUS CULOSKELETAL PATTERNS
Osteopathic physicians recognize panerns for musculoskeletal problems. Examples are: l. The patient experiences sharp, h ighly localized pain in the thorax with inhalation that worsens with a deep breath. This pattern suggests a rib restricted in inhalation. 2. The patient experiences low back pain with walking. This pattern suggests sacral rorsion, or other pelvic somatic dys function. 3. The patient experiences headaches that start in the shoulder girdle or neck and progress upward to envelop the head. There is a feeling of the head being in a vise, or being squeezed by a stocking that is coo tight. This pattern suggests a tension (or musculoskeletal) headache. UNUSUAL BUT DISTINCTIVE PROBLEMS
At the opposite end of the spectrum for pattern recognition is the panern formed for the uncommon problem. When patterns are formed for these problems, it is often because they are serious, even life-threatening, and should not be missed under any cir cumstance. A salient example ofsuch a problem is Reye syndrome, which is a potentially life-threatening condition that occurs in some children as a consequence of aspirin ingestion (usually for a viral illness). As the pattern of signs and sympcoms became clearer (i.e., as it cook on the characteristics of a syndrome) , health care providers as well as parems were encouraged co "think Reye's." Reference lists outlining the signs and sympcoms of the syn drome were posted in emergency departments, physician offices, and other patient care areas. In a reasonably short time, the pat tern of this rather rare illness was internalized well enough by physicians and other providers that coday it rarely goes unrecog nized. In recent years, thanks co improved parent and provider awareness of the causes of and treatments for Reye syndrome,
2.
The patient is an elderly man, somewhat overweight, who presents with pain on the right side of his face, dizziness, and left ear pain. Examination reveals elevated blood pressure and infla mmation of the left ear. The diagnostic panern con sidered was otitis media for which ear drops and antibiotics would be prescribed. The patient subsequently suffers a cere brovascular accident (eVA). The physician realizes there has been a mistake as a result of incomplete data gathering and interpretation. The significance of the elevated blood pressure had not been considered nor had the fact that the patient felt more light-headed when he lay down. In his data interpreta tion, the physician included only the cues that obviously fit the common panern and did not give adequate attention co those cues that might have been indicative of another prob lem. The physician jumped co a convenient conclusion and fell inco a rather serious trap of erroneous or at least incomplete diagnosis. The patient's chart lists several complaints as the reason for the visi t. Exanlpies are: Headache Dizziness Dry mouth Double vision Emotional lability Shortness of breath Occasional muscle spasms This patient expresses not only varied complaints but also complaints representative of several systems. The number and multisystemic nature of the complaints is a typical pattern for the patient who may be perceived as a hypochondriac. The physician can easily fall into the trap of treating this patient superficially without gaining an understanding of his or her underlying problems.
Although practical instances of problem solving by pattern recognition reflect research findings, practitioners' experiences suggest a much more complex scenario than that created in the laboracory. The practitioner sees the pattern of the COtai patient in life's environment. The experience of the primary care prac titioner with many patient encounters, as well as with several encounters with the same patient, allows him or her to develop pattern recognition habits not readily discovered in the controlled psychological study. First is the pattern of perceived illness. Over numerous pa tient encounters, the seasoned practitioner learns co distinguish the visual and behavioral panern of a patient who is ill. Primary
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care practitioners have a pattern for a patient who "looks sick." Key factors facilitating developmem and application of this pat tern recognition skill that are particularly useful to the primary care physician (and awkward to effectively represem in psycho logical studies of clinical problem solving) are repeat visits and time. Especially in the instance of the established patiem, any change from the patient's expected appearance raises a flag for the physician: "This patiem looks sick." Time and repeat visits also contribute to expecting and rec ognizing seasonal illness patterns. The primary care practitioner develops caveats around pattern recognition. A sixth sense, based on years of experience, warns against jumping ro conclusions from recognition of a pattern. AJthough pattern matching is an efficient problem-solving method in primary care and is used fre quently with success by family practitioners, there is always the feeling of "Yes, but what if . . . " or "This solution seems decep tively simple. I sense something more complex." The potential dangers of pattern matching or instant diagnosis were summa rized as follows by an osteopathic fam ily practitioner: "Where you get imo trouble is when you walk in (to the examining room) with the diagnosis already made. You can really get nailed." Hypothetico-Deductive Method
We think about complex and not-so-complex problems in every day life using a hypothetico-deductive method. Clinical problem solving is a specialized application of this method. Imagine one evening you come home after dark, let yourself into the house, flip on the kitchen light switch, and nothing happens. What do you think? Probably your fi rst thought is that the bulb is burned out. The problem situation has presented itself with your identifi cation of an abnormal fi nding (no light at the Aip of the switch). You then immediately generate a hypothesis about the cause of the abnormal finding (burned out bulb) . One possible next step would be to replace the bulb and see if that solves the problem (test the hypothesis, in this case with an intervemion). Another more conservative step would be to try other lights in the house see whether they work (gather more data to further defi n e the problem). You might even pause to consider whether there is a his tory of this or a similar malfunction occurring in the past. When did you last replace that bulb? Just recently? That would make "burned out bulb" a less likely hypothesis. Is this on the same cir cuit as the dehumidifier? Perhaps the surge from the dehumidifier coming on overloaded the circuit and tripped the breaker? That would suggest hypotheses in an entirely different area and involv ing the fundamentals of how the house is wired and/or where cer tain appliances are located. However, the probability is high that it is the bulb and not something more eX[ensive like an overload or a short circuit or a power outage affecting the emire house. You can combine the high probability that it is the bulb with the knowledge that changing the bulb can do no harm. It can only solve the problem or fail to solve the problem. The thought processes we invoke are multiple and h ighly varied even for some thing as simple as a darkened kitchen. Now let us go back to M r. Johnson's case, identify the signifi cant abnormal and normal findings, generate the hypotheses, and logically apply this hypothetico-deductive reasoning. Even before to
your imeraction with Mr. Johnson, you have enough information to set you thinking. Based on the cues of the presenting complaint (gender, age, height, weight, and blood pressure), you probably generate some preliminary diagnostic hypotheses regarding the mechanism of the patient's illness. You are able to do this before you meet the patient. Two major components of the hypothetico-deductive method are cue acquisition and hypothesis generation. Problem solving for a complex problem like this involves the early generation of several diagnostic hypotheses. Often the physician begins to con sider diagnostic possibilities based on just a few cues, as you have done with M r. Johnson. Frequemly, several diagnostic hypothe ses come to mind or are retrieved from the physician's long-term memory based on between one and five cues. How many hypotheses? During the diagnostic workup, hy potheses are carried i n short-term memory while they are being evaluated, so the number is limited. Usually the physician can expect to keep track of between three and seven diagnostic hy potheses during a complex clinical encoumer. What kind of hypotheses? Hypotheses can be general, such as the "cardiovascular problem" or "gastrointestinal problem" that you might be considering for M r. Johnson. Or they can be spe cific, such as "pleurisy" or "myocardial infarction." The level of definition depends on several factors, such as the specificity of the data, how life-threatening the problem is, and the sophistica tion of the problem solver. With more detailed information, the physician can entertain more focused hypotheses. For a patiem presenting with diarrhea and abdominal cramping, a physician might differentiate between ulcerative colitis and Crohn disease rather than simply hypothesizing a problem in the bowel. That is nor to say that clinical problem solving is predictably logical, going from general to specific. Specific hypotheses can be generated based on an extremely small data set, or the physician might have a substamial set of cues and still entertain global hy potheses. The sophistication of the physician is based on his or her knowledge base. The clinician who has been in practice longer has a larger knowledge base of problems (including more complex re lationships) than the clinician with less experience has. AJthough it would not appear that clinical problem solving in general is a learned skill, the ability to solve clinical problems increases with experience and the building of the clinical knowledge base. Whether the problem is life-threatening is a variable that often comes into play in clinical problem solving. It especially affects hypothesis generation when the physician realizes that the pa tient's symptom complex suggests a serious acute illness such as myocardial infarction. The physician's first duty is to ascertain the presence of a life-threatening condition and treat it (or at least stabilize the patient). Those situations can involve the immediate recognition of a sign-symptom pattern or the generation of a spe cific diagnostic hypothesis for which there might be a standard treatmem protocol or algorithm. After generating one or more diagnostic hypotheses, the physi cian proceeds with additional cue acquisition (which can be guided by the hypotheses) . As with the example of the kitchen light, one expects certain findings be present or absent if one or another hypothesis is true. For example, if the burned out bulb hypothesis is accurate, then the cue of nonfunctional bathroom light is unlikely (unless, of course, the bulbs had burned our in to
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both rooms). However, if the hypothesis of tripped circuit breaker is true and the bathroom and kitchen lights are on the same cir cuit, then one might test that hypothesis by trying the bathroom light. We return to Mr. Johnson. As you elicit more data from the patient, you can relate the new cues to your working hypotheses, a process known as cue interpretation. Cues are usually interpreted as: Positive (tending to support a hypothesis) Negative (tending to refute a hypothesis) Noncontributory (not helpful for the evaluation of a hypothesis) M r. Johnson was raking leaves when he experienced pain in the shoulder. If you later learn that Mr. Johnson's pain is not repro duced with movement of his arm, that cue may be interpreted as negative for trauma. If you learn that he does not experience pain when climbing stairs, that cue could be interpreted as negative for exertional angina resulting from coronary artery disease. If you learn that he does not experience pain with deep breathing, that cue could be considered negative for a pulmonary hypothesis. It must be noted that a negative cue (or even several negative cues) does not rule out a hypothesis. Negative cues might cause the physician to move the hypothesis lower on his or her probability list; however, it takes substantial negative evidence or confirma tion of a competing hypothesis for a diagnosis to be ruled out. In conjunction with cue interpretation, an orderly data gath ering process allows you to generate new diagnostic hypotheses. With the iterative process of data gathering, hypothesis genera tion, and cue interpretation, you begin prioritizing hypotheses. If all possible causes of the patient's problem are equally serious, give top priority to the most likely diagnosis, lower priority to the next most likely, and so on. Prioritizing diagnostic hypotheses is usually a much more complex process. When the physician is making the transition from the preliminary phases to hypothesis evaluation and prioritization, considerations such as treatability, severity of the illness (whether it is life-threatening) , and methods to be used for further hypothesis testing enter into the decision making process. In Mr. Johnson's case, a high priority might be given to the hypothesis of coronary artery insufficiency. Even though you dis cover cues in Mr. Johnson's data set negative for that hypothesis, experience suggests that given this patient's risk factors and d:e seriousness of the illness, it is a top-priority hypothesis. The pn mary care osteopathic physician can make creative use of the hypothetico-deductive model beyond what has been elaborated on in ongoing studies of clinical problem solving. Most of the studies involve only one extensive (simulated) patient encounter. The primary care physician can plan multiple encounters with the patient (cue acquisition and interpretation opportunities) that might include implementation and assessment of the various phases of a management plan (hypothesis testing and hypotheSIS evaluation opportunities). The hypothetico-deductive model for clinical problem solving typically involves four major steps: Cue acquisition Hypothesis generation
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Cue interpretation Hypothesis evaluation There are some caveats for the osteopathic primary care practi tioner in applying the hypothetico-deductive model in its purest form. Chief among those is that the model is oriented toward cause and effect. In a sense, the cues the physician elicits from the patient are the effects of some disease or dysfunction, which may be viewed as the cause. Using the hypothetico-deductive model puts the clinician in the role of detective or analyst who draws from long-term memory hypotheses (such as normal anatomy, physiology, pathophysiologic states, specific disease entities, s� n dromes, etc.) that account for most, if not all, of the cues belllg offered by the patient. The ultimate objective, of course, is to use identification and solution of the diagnostic problem as the basis for development of a management plan that helps restore the patient to a healthy state. The goal is to resolve the patient's clinical problem. There are other disadvantages or limitations to using this ap proach exclusively in considering diagnostic problems. In addi tion to being disease-oriented, the hypothetico-deductive model is extremely focused. In applying the model, the clinician is not encouraged to consider the whole patient. The model is highly cognitive and almost impersonal at times. Invoking the model does not necessarily prompt the clinician toward exercise of ef fective interpersonal skills or skills i n patient education. If not supported by other effective clinical practices such as always keep ing an open mind and listening carefully to the patient's entire story, the hypothetico-deductive model can put blinders on the clinician, resulting in potentially serious errors. As Hunter (8) notes in her book, Docto rs 'Sto ries , the clinician who brings to the patient encounter his or her own perspective different from that of the patient runs the risk of transforming the patient's story into the doctor's story. Through selective questioning, listening, and examination, the doctor risks gathering data that fit his or her preliminary impression of the patient's problem. Under those circumstances, data can be missed or, worse, the doctor can make up cues that were not part of the patient's presentation. Even with thorough, orderly data gathering, cues can be over- or underinterpreted (interpreted as too strongly or not strongly enough related to a hypothesis), or they can be totally misinterpreted. The hurried physician who relies too heavily on the hypothetico-deductive model can be led down a primrose path. Properly applted, the hypothetico-deductive model of clinical problem solving can help the physician solve complex, difficult diagnostic pr?blems. It is a method often seen in the hospital or consultatlon set ting as well as used by the primary care practitioner face� wi.th a complex diagnostic dilemma. For a thorough, academiC diS cussion of the hypothetico-deductive problem solving model, see Medic al Pro blem So lv ing: An Analys is of Clinic al Reaso ning (9). Problem-oriented Perspective
In the 1950s, development of the problem-oriented medical sys tem was begun by Lawrence Weed, MD. The system had sev eral components, a key one of which was the problem-oriented
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medical record ( PO M R). A major goal of the problem-oriented medical system was to focus on the patient's problems and the interrelationships among them. The system was intended for use by primary care practitioners as well as specialists. The system places heavy emphasis on: Establishment of a patient database Problem identification Patient education Record keeping Patient records, especially hospital charrs, are usually source oriented. The sections of the charr are organized by the source of rhe data. There is a section for physician's nores, for nursing notes, for laboratory nmes, and others. In developing rhe POMR sysrem, Weed sought to reorder the record keeping system so rhar it was organized around problems. If M r. Johnson's chan conrained a repon of a chesr x-ray srudy, it m ight be included under a shortness of breath on exerrion problem (if one had been idenrified for him) rarher rhan under radiology. The POMR has four components: Defined database Complete problem l isr Initial plans Progress notes Narrative progress notes contain the following information: Subjective data Objective data Assessmenr Plan The acronym SOAP makes rhe four secrions easy to remem ber. Subjecrive dara are rhose provided by rhe patient or another source of informarion (e.g., a parent) abour rhe progress of the problem being addressed. These are usually historical data. Ob jective dara are those elicited by the physician and are usually physical examination data. They can also be results of labora tory or imaging tests, or standardized tests such as the Menral Starus Examination and the Geriatric Depression Scale. In the assessmenr, rhe physician records his or her interpretation of the subjecrive and objecrive dara. I n the plan, rhe physician records any one or all of rhe following: Diagnostic plan: whar funher diagnosric data are needed to undersrand rhe parienr's problem Therapeuric plan: whar rhe physician intends to do ro manage rhe problem Patienr education: what information needs to be discussed with the patienr regarding rhe problem The progress note or SOAP note has proved to be one of rhe most functional aspects of the problem-oriented sysrem as well as one of the leasr cumbersome to implement in a busy primary care practice. In the 1 960s and early 1 970s, when the POMR sysrem had irs grearesr visibiliry, physician accountabiliry (in patient care as well as educarion) was a high prioriry. The problem-oriented system with its strong emphasis on comprehensiveness, avoidance of
speculation about diagnoses, and parienr education provided a merhod for audit and accountabiliry thar seemed ideal. How does clinical problem solving relare to rhe problem oriented system? Thar question has been a source of con([o versy since Weed introduced rhe system. Our narural tendency when confronred with a problem is often to formulare rhe prob lem and then immediately starr generating hyporheses abour its cause. Thar kind of cognitive speculation does nor fir in well with the careful building-block process prescribed by rhe problem orienred approach. Parr of the reason for developing rhe problem oriented sysrem in rhe firsr place was Weed's and orhers' concerns that physicians were making diagnosric and therapeutic errors i n approaching clinical problems because they were jumping to conclusions too quickly based on incomplete dara. Through rhe problem-oriented system, Weed hoped to influence the develop ment of orderly clinical problem-solving skills in student physi cians. Parr of his goal was to educare medical students and resi dents in rhe use of a highly structured rhoughr process for clinical problem solving. The process begins wirh the establishmenr of ar leasr a parrial (if nor complete) darabase for rhe patient from which rhe problem lisr and inirial plans emerge. This approach provides a standard method for addressing each patient's problem complex. Shorrcuts are not encouraged, and sreps should not be skipped in problem identificarion and problem solving. A record is developed for rhe parient rhar is a direct reflecrion of rhe student's reasoning, and is used in evaluarion of rhe srudent's clinical learning progress. As researchers began to gain grearer insighr into rhe cogni rive processes involved in clinical problem solving, ir became clear that what Weed and the problem-oriented sysrem were ad vocaring involved a major rransformarion of age-old habits of diagnosric rhinking. Physicians do nor usually gather a complere database for a patient before forming impressions. Rarher, they use preliminary impressions or hyporheses to guide dara gath ering. Physicians tend to see parterns, problem complexes, and interrelationships among problems rhar are centered on prioriries (e.g., is rhis life-threarening, is it treatable) and parhophysiologic processes (whar is rhe cause of rhis ser of signs and symptoms). They mighr have trouble seeing problems as separare entiries, only possibly to be combined larer. As clinical rrainers, rhey may have rrouble teaching learners to rhink in ways rhat they find alien and inefficienr. Resistance to the wholesale adoprion of rhe problem oriented sysrem has been heavily influenced by rhe pragmatic stance thar "if it is nor broke don'r fix ir." For decades, a rra dirional combinarion of approaches to clinical problem solving, record keeping, and accounrabiliry has been used rhar is effec tive and efficienr. This new system would nor only revolutionize thinking about clinical problems bur would also turn the entire organization of record keeping systems and hospital audit systems on irs ear. Even third-parry payers and medical education would be affecred. Although seemingly logical, rhe problem-oriented medical sysrem proved difficult to implemenr. Several components are still frequenrly used, however, especially in family physicians' of fice records. For example, one m ight expect to see a numbered problem l ist at the front of the patient charts in some offices. The problem-oriented influence most likely to be seen in conrempo rary physicians' chans is the progress note or so-called SOAP note.
19. Clinical Problem Solving
Some medical education programs are problem-based rather than academic discipline Ot system-based. Although a wholesale trans formation of clinical reasoning did not take place, the impact of the problem-oriented system is still felt. For a detailed explana tion of the problem-oriented system, see Your Health Care and How to Manage It ( 1 0) and Applying the Problem-Oriented System ( 1 1 ). Clinical Decision Analysis
The clinical decision analytic approach ro diagnostic problem solving involves appreciating and using probabilities and their relationships in the diagnostic process. Looking back at our pre liminary presentation for Mr. Johnson (even with the scant data we had before we met him), we could formulate a hypothesis of pain as a result of coronary artery insufficiency. One test of the accuracy of that diagnostic hypothesis is a treadmill test or stress electrocardiogram (ECC). Our pattern matcher was already speculating about the anticipated outcome of that test before even meeting M r. Johnson. Before performing the test, consider what we would learn from the results and how much it would help us diagnostically. At the most basic level, we can interpret the results of the test as positive or negative, nor mal or abnormal. As with all tests, there are degrees of abnormal, but for now we stick with just the two categories. A positive OLlt come tends ro confirm the diagnosis and a normal oLltcome helps refute it. Cost is also associated with the test. Although minimally in vasive, the stress ECC involves not only patient and health care provider effort and time bur also monetary cost. How much do we learn from the test, and does what we learn justify the cost? How much further hisrory and physical examination data do we need before we feel comfortable deciding whether ro order this test? First, we will consider the diagnostic perspective. Laboratory tests commonly used for diagnosis have predictive statistics asso ciated with them based on the probability that a person with a certain disease will have a positive outcome on the test, as well as the probability that a healthy person will have a negative outcome on the test. The stress ECC is commonly used to test the diag nostic hypothesis of angina pectoris as a result of coronary artery insufficiency. Based on studies of large numbers of patients, we know the following about the test associated with coronary artery disease (CAD): The probability that a patient with CAD will have a positive test result The probability that a patient who does not have CAD will have a normal test result For a given patient sample, we can ascertain the probability that a patient with a positive test result has CAD as well as the probability that a patient with a normal test result does not have CAD. Using these probabilities helps us decide whether our pa tient should undergo the test. Section 1 of the Appendix provides statistical properties of the stress ECC as it relates to CAD, details on definitions of terms, and an example. In addition to applying our knowledge of test characteristics in judging the value of a test as it relates to a certain problem, we
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also use this probabilistic method to help us revise our thinking abour a diagnostic hypothesis. We can assign a probability to the hypothesis of pain as a result of coronary artery insufficiency for Mr. Johnson. For example, on the basis of fi n dings from the history and physical examination, we may be 70% sure that the hypothesis is true for this patient. Under these circumstances, we ask Mr. Johnson to undergo a treadmill test. What do we learn if the test result is positive? If the result is negative? How do the test results help us evaluate our primary working hypothesis? To relate the general information we have about the stress test to Mr. Johnson's special case, we use a method called the Bayes theorem, which is a formula for combining and revising prob abilities based on new information. It was devised by Reverend Thomas Bayes in the 1 700s. Section 2 of the Appendix gives an illustration of how Bayes theorem is applied in thinking about M r. Johnson's problem. There are several schools of thought regarding the use of clinical decision analysis, even at this simple level in diagnos tic problem solving. Some clinicians, especially in fields such as cardiology where there is an extensive database on statisti cal properties of tests, frequently use cli nical decision analy sis to help decide whether to order tests. Clinicians also use it, with the inclusion of utility estimates, ro help in choosing management plans. An added benefit of decision analysis in the high technology fields is thar it can help control costs if used conscientiously. Another perspective, held more widely by primary care physi cians, is more utilitarian. It states that regardless of the increment by which I m ight be able to improve my diagnosis with the result of a test whose statistical properties I know, I am (or am not) going to do the test anyway, because there is more to a test result than just diagnosis. For example, an argument in favor of doing a stress ECC for a patient with a high likelihood of CAD (meaning that I would learn little diagnostically from a positive test result) is that I can use the ourcome to establ ish a target exercise heart rate for this patient, and therefore, a basis for developing a man agement plan. Similarly, an argument for doing such a test to assess a hypothesis with a low subjective probability ("I am quite sure this is not the patient's problem, but 1 don't want to miss it") is if the test proves positive and the patient does indeed have the disease ( not a necessary relationship, but it could happen), then it was worth doing the test. As one family physician put it: "If there are 95 negative tests out of 1 00, and of the five posi tive ones, one results in saving a patient's life, the other 99 were worth it." A third perspective is what one might call the common sense approach. Here, the clinician is aware of probabilistic relation ships between test results and diagnoses. However, he or she uses them in an informal way. The clinician's reasoning might be: "1 know this test helps me with the diagnosis. However, if it's neg ative, it won't tell me anything. A negative test result won't rule out this diagnosis. I'm quite sure this is not the patient's problem, so rather than risk wasting time and money on something that might have low yield, I'll do some other cheaper, less invasive
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tests to try to confirm another hypothesis and use this test only if all else fails." I n this argument, the physician is considering several facrors (cost and invasiveness as well as the potential value of alternatives) in addition ro diagnosis ro reason against using a particular test. We have considered the decision analytic approach ro clin ical problem solving from the perspective of how it can help the primary care physician use diagnostic tests effi c iently and effectively in the problem-solving process. To use this method, the diagnostician must know a minimum of the statistical prop erties of the test he or she wishes ro order as well as, ideally, the prevalence in his or her patient population for the disease or problem being tested. Knowing that information and ap plying Bayes theorem also allows the physician ro estimate the change in probability of a diagnostic hypothesis under consid eration and, thus, ro have an idea of how the results of a test contribute ro further understanding the patient's problem. Two references on clinical decision analysis are Medic al Dec is io n Mak ing ( 1 2) and CLinic al Ep ide m io logy: A B as ic Sc ie nce fo r Clinic al Medic ine
( l 3).
You have probably recognized many of the terms and con cepts discussed above as the same concepts used in discussions of evidence-based medicine (EBM). And rightly so: EBM has emerged in recent years as a way ro understand and apply sta tistical principles and findings from clinical research (which had often been associated principally with epidemiology and public health) ro the evaluation and management of an individual pa tient. A definition of EBM is: "Evidence-based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients" ( 1 9). Those who regularly use and teach the EBM approach ro di agnostic and management decision making outline a series of specific steps for the process. First, identify the patient's prob lem or some key aspect of the problem where the application of external evidence should prove useful (this will usually be a di agnostic or management question). Second, formulate a focused clinical question. A well-formed question may have four parts: identification of a group of patients similar ro yours; identifica tion of the intervention or test you are considering; comparison with another test or intervention; and outcomes. An example of a question regarding intervention might be "When compared with standard therapy alone, would adding anticoagulants with warfarin ro standard heart failure therapy lead to lower mortality or morbidity from thromboembolism in patients with heart fail ure from dilated cardiomyopathy who are in sinus rhythm, and is this enough ro be worth the increased risk of bleeding?" ( 1 9) . The third step in the process is ro identify a source of evidence (often a randomized clinical trial) that will hopefully answer your question. Fourth, critically appraise the study or studies you find to ensure they are appropriate for your needs and, particularly, to ascertain that the study group(s) and your patient were both from similar populations. Fifth and last, synthesize the evidence you gain from your research and apply it ro your patient. As you can see, this is a very highly structured and rigorous approach ro clinical problems in patient diagnosis and management. As with other prescriptive approaches to clinical problem solv ing such as the problem-oriented approach and clinical decision analysis, evidence-based medicine has its avid proponents: those
clinicians who use it regularly and teach their students and resi dents to apply it in the evaluation and management of their pa tients. Although most primary care clinicians have not adopted the evidence-based approach ro the exclusion of other models for clinical problem solving, many are familiar with its tenets and incorporate them into their day-ro-day patient evaluation and managemen t. We have presented several models for clinical reasoning. None of these models is used exclusively by clinicians in pondering di agnostic problems. However, all are used ro some extent. The next part of this chapter presents some examples of osteopathic primary care physicians' reasoning about patient problems ac companied by a discussion of their possible application to the problem-solving models we have discussed. OSTEOPATH I C PHYS I CIANS' CLINICAL PROBLEM SOLV ING
After considering several models of clinical problem solving, the reader may wonder if osteopathic physicians think that way. We conducted an inquiry into osteopathic physicians' impressions of their own problem solving processes. The subjects were primarily family practitioners, as well as specialists and generalists who were not family docrors. Data from 1 3 family docrors were used in the study. Non-family practitioners were from the following practlce areas: Surgery Pediatrics General internal medicine Cardiology SportS medicine Three academically based family practitioners were included. The experimental method was a face-to-face interview with each subject i n which three major questions were posed and elaborated: 1.
2.
3.
"Please tell me about a case or cases you have seen recently (of a type of case) where as soon as the patient presented you believed you knew the nature of the patient's problem." This question was intended to elicit a discLl5sion of pattern matching problem-solving processes. "Please describe a case or cases you have seen recently (or might still be working on) that have been a real diagnos tic dilemma." This question was intended ro elicit discus sion of more complex problem-solving processes such as the hypothetico-deductive and decision analytic methods. "Please discuss a case or cases you have seen recently where you were able ro say: I handled that case the way I did because I am an osteopathic physician. There was something particularly osteopathic about the way I approached that patient." This question was intended to elicit subjects' perspective on what is distinctive about osteopathic physicians and how what they perceive as osteopathic is expressed in their clinical approach to their patients.
We analyzed the subjects' responses in an attempt ro answer the question of whether practicing physicians actually use problem
1 9. Cli nic aL Pr obLem S oLvi ng
solving methods such as: Pa'ttern matching Hypothetico-deductive thinking Decision analysis/EBM Problem-oriented process Subjects' use of pattern matching is summarized in the ear lier discussion of that model. This section focuses on diagnostic challenges or dilemmas, and what physicians saw as distinctively osteopathic about their thinking. Quotations are taken directly from physician interviews. Complex Diagnostic Problem Solving
What are diagnostic dilemmas for osteopathic primary care prac titioners? What problem-solving processes do they use in resolv ing the dilemmas? Clinician problem solvers used the cyclical processes of data gathering, hypothesis generation, and cue interpretation (the hypothetico-deductive method) clarify diagnostic problems and try to reach conclusions. They used probabilistic thinking in two major ways. First, they used it to prioritize hypotheses to investigate based on their under standing of problem/disease prevalence combined with perceived cost of investigation. Second, they used probabilities to prioritize hypotheses for ruling out, or hoping to rule out, based for the most part on the perceived gravity or life-threatening potential of the disease or illness. On occasion, clinicians called on knowledge of basic biologic principles (usually structure and function, occasionally biochem istry and microbiology) to trigger generation of diagnostic hy potheses as well as interpret cues in light of the hypotheses. The following sections discuss a series of cases that illustrate physi cians' application of these three major forms of reasoning: Hypothetico-deductive thinking Probabilistic reasoning for purposes ofprioritizing hypotheses based on prevalence, and gravity of illness Application of basic biologic principles to the analysis of com plex clinical problems There are some contributors to the problem-solving process that are especially applicable in ambulatory care and that are not addressed in major psychological studies of clinical prob lem solving. The one key operating factor that separates the primary care practitioner's experience from that of an experi mental subject is the return visit. The practitioner has an op portunity to interact with the patient on several occasions over a protracted period, thus introducing the variable of time into the problem-solving process and, with it, the natural course of an illness. The ambulatory care physician can use response to treat ment as a key diagnostic variable. He or she can consider and assess more environmental, social, and psychological hypotheses as the underlying causes of a patienr's illness than can the physi cian/researcher who sees the patient only once or for a short time period. Examples of our interviewees using these variables were frequent. The most common diagnostic dilemma for the primary care physicians that we interviewed was abdominal pain and,
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more speci fically, abdominal pain in women. Abdomi nal pain as dilemma (what might be considered the opposite end of the diag nosis spectrum from pattern matching) attests to the frequency of abdominal pain as the reason for a visit to the physician. Statis tics show that stomach pain, cramps, and spasms are rhe 1 0th most common reason for visits to U .S. physicians ( 1 4) . Of the problems mentioned by our study group, abdominal pain was menrioned 1 0 times, and eight of the complaints came from women patients. Other diagnostic dilemmas and the num ber of times they were mentioned include: Fatigue (4) Headaches (3) Multisystem complaints (2) Chest pai n ( I) Tremor ( I ) Back pain ( I) Leg swelling ( 1 )
to
CASE ONE
The patient is a 33-year-old woman complaining of abdominal pain, bloating, and diarrhea. This is an established patient, and the physician noted she had undergone a dramatic change in appearance since her last visit. She was clearly sick. After physi cal evaluation, which did not help reveal a particular cause, the physician entertained a hypothesis of viral gastritis using the rea soning that the hypothesis explained the findings reasonably well and it was a common underlying cause for this sign/symptom complex. The patient was n'eated conservatively with Auids and dietary management. In the first round of clinical problem solving with this patient, the physician was able to recognize a change in the patient's ex pected pattern of appearance. He began using the hypothetico deductive approach, probabilistic reasoning (a common cause for the sign/symptom complex), and time in developing and testing a diagnostic formulation. The patient returned in one week. On return visit, upper ab dominal pain, bloating, and diarrhea as well as ankle edema were noted. The physician now entertained a hypothesis of cardio vascular dysfunction as the cause for the edema, which might also explain the gastrointestinal problems, or which might be an additional underlying problem. This is the second round of problem solving for the physi cian. There is a continuation of the problems seen on the first visit, plus a new symptom: ankle edema. The physician is still us i ng hypothetico-deductive thinking understand the patient's problems. He is generating hypotheses that together or separately might explain the findings. However, there is no indication that the physician was feeling able to resolve the problem. Rather than coming together, the problem was becoming more complex and diffuse. And rhe patient's condition was worsening. As ti �le passed, the patient became more seriously ill to the point where she was showing clinical and biochemical signs of severe malnourishment. An upper GI evaluation revealed a badly damaged small bowel, caused, as it turned out, by a to
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gluren enreropathy that had progressed ro rhe poinr of being life-threatening before ir was discovered. It rook three rounds of clinical problem solving, plus time, ro assess response ro trearment and observe the development of the illness before the physician was able ro generate rhe requi site hypotheses. The hyporheses combined with the gravity of the patient's illness indicated ordering the upper GI test that evenrually revealed her underlying disorder. Technology did not diagnose rhe problem, however, as is often implied, particularly in specialty-oriented practice. Had the physician not reasoned rhe problem rhrough rhe point where he knew the test was indicated, he would not have had rhe opportunity ro learn what the rechnology eventually revealed. ro
CASE TWO
The patienr is a 34-year-old woman presenting with multiple complaints rhat are centered in the abdominal area and lower back. The principal complainr on the first visit is episodic mide pigastric pain. The parienr also complains of occasional lower abdominal pain, low back pain, and constipation. The patient is obese. Exam ination reveals decreased bowel sounds but no re bound tenderness or guarding. No other abnormaliries are found. There is a family hisrory of gallbladder disease thar, rogether with rhe patient's complainrs and appearance, triggered a general diag nosric hyporhesis of gastroinrestinal dysfunction. I ncluded were rhe specific hypotheses of gallsrones, along wirh possible reflux esophagiris, and irrirable bowel syndrome. The physician did not assign a high probability ro the hypothesis of gallsrones, rhink ing rhar rhe orher two were much more likely, as well as less costly ro treat. She chose ro treat rhe symproms cOllservarively (and, in part, use response ro trearment ro test hypotheses) wirh medication and diet. The patienr did not respond ro trearment. Th is is anorher case where more than one round of prob lem solving is required. Here, rhe physician starts by using hypothetico-deducrive reasoning ro generare diagnosric hyporhe ses based on a complex of signs anL symproms. She also uses prob abil istic rhinking ro assign likelihood ro her hyporheses, which helps with decision making about trearmenr. Although nor dis cussed as one of our fundamental problem-solving approaches, rhe physician also calls on conceprs of cosr-effectiveness when she considers COSt of resring and rreatment in developing a manage ment plan. Before her nexr scheduled visir, the parient called the physi cian complaining of bloating, incapacitaring pain, and no bowel movement for 5 days. Ulrrasound of the gallbladder revealed no abnormality. The urgency of the patienr's complaints suggested a more serious hyporhesis, such as large bowel obstruction; how ever, rhe patient did nor appear physically ill enough ro support that hyporhesis nor was it supported by x-ray or laborarory find IIlgs. The physician continues ro rhink hyporhetico-deductively. She feels she needs ro dig deeper, be more invasive in her in vesrigarions, and incur more expense ro undersrand rhe parienr's problem. The physician generared ar leasr one new hyporhesis. She did nor feel ir was supported by enough dara ro be a strong contender. The physician appears ro be balancing seriousness (if
this is bowel obstruction ir is extremely serious, and I had betrer nor m iss it) with likelihood (the hypothesis was not supported wirh sufficient cues, and although rhe patient expressed urgency abour rhe problem, she did nor appear ill enough to suggesr that the problem was life-threatening). On a subsequent visit, the patient revealed she was at rhe rop of rhe lisr for job cuts in her department. This was a rurning poinr for rhe physician. She refrained from ordering addirional expensive resrs and chose rarher ro discuss rhe relarionship of rhe parient's signs and symproms wirh her job anxiety. The patient agreed there m igh r be a relationsh ip. The physician saw rhe patient's realizarion of the relarionship between stress and physiologic symproms as rherapeuric. The patienr improved once she undersrood how rhe rhrear of job loss could be rhe basis for physical illness. In rhis case, rhe physician used rime, failure ro respond ro rrearmenr, and her knowledge from previous acquaintance wirh rhis esrablished parienr as triggers for new diagnosric hyporheses and further dara garhering. These eventually revealed whar rhe physician rhoughr ro be rhe underlying problem. The case also exemplifies the primary care physician's ability ro use repear visirs, rime, and failure ro respond ro rrearment as a basis for generar ing diagnostic hyporheses involving the parienr's psychological and social environment as rhe underlying cause of physiologic complainrs. Physicians who discussed cases wirh us relared several instances where the apparenr underlying problem was social or environ mental. These types of problems and rhe primary care osreo parhic physician's role in assessing and developing management plans wirh parients are discussed elsewhere. We offer two com posire scenarios discussed by several physicians. In rhe fi rsr scenario, the parienr is a woman in her 30s or 40s who is married or in a significanr relarionship. She comes ro see the physician wirh a complainr or brings her child with an illness. The complaint presented on any individual visir does nor usually require the complex problem-solving process bur rarher calls on rhe physician's pattern recognirion skills for common problems. The cue this prorotypic parienr presents thar requires complex problem-solving skills is rhar of mulriple visirs wirh resolurion of short-term problems and lingering evidence of an underly ing long-rerm problem. For rhis complex parienr presentarion, rhe mosr common underlying causes are clinical depression and physical or psychological abuse. If rhe primary care physician can see rhe big picture and generate one of rhese hyporheses, he or she is well on rhe way ro appropriare assessment and managemenr of rhe parient's major problem. One study subject (a woman physician) relared an extensive discussion of her discovr.ry of rhis symprom complex and her subsequenr realizarion of jusr how prevalent abuse and depression are among women patienrs. In rhe second scenario, rhe patient presents wirh multisysrem complaints. The patient is usually a woman. She has seen several physicians without a satisfacrory outcome. She mighr or mighr not be married or in a relationship. She is usually in her 30s or 40s. The hisrory may be rarher complex, and usually involves pain. For example, the parient might have a hisrory of migraine headaches for which she is taking medication, hypertension for which she is also taking medication, abdominal pain, and chronic diarrhea. She mighr also have episodes of back pain for which she rakes medicarion. The abdominal pain might be inrense and
J 9. Clinic al P ro blem So lving
highly localized, e.g., in the right upper quadranr. On hearing this history, the physician in question focused her complex problem solving process on the abdominal pain, entertaining hypotheses such as gallbladder disease or common bile duct stone, as well as abdominal distress of functional origin based on a h istory of abuse as a child, a failed marriage, and current involvement in a lesbian relationship. The patient was vague abom her extensive past medical and surgical history, prompting the physician to request her medical records from previous providers. The records revealed that the patient had been and is currently in a drug rehabilitation program. At this stage, the physician's perspective on the case changes dramatically because it is now apparent that the problem underlying the patient's physiologic complaints is the complex sociobehavioral problem of long-term, unresolved substance abuse. CASE THREE
The patient is a 1 9-year-old woman presenting wirh acute pelvic pain. She is sexually active. Physical examination reveals diffuse, nonlocalized lower abdominal pain on palpation. Pelvic and rec tal examinations revealed no abnormalities. The physician further analyzed the problem by considering basic anatomic structure, asking himself what is in the right and left lower quadrants of the abdomen. In women, the major structures in the lower quadrants of the abdomen are part of the uterus (which can be palpable if enlarged), the Fallopian rubes, and the ovaries. The cecum, ap pendix, and a portion of rhe ascending colon are on the righr. Portions of the descending colon are on the left. The physician generates a diagnostic hypothesis set that includes primarily in fectious and inflammatory processes because the onset of pain was acute: Pelvic infection Urinary tract infecrion Inflammatory bowel disease Appendiciris is also considered, but wirh low probability be cause rhe clinical cues did not support that hyporhesis but did support the others. The patient is treated wirh a preliminary trial of antibiotics on the justification that not only might the treat ment be appropriate for her problem but also that the response to treatment would provide diagnostic information. Once the treat ment regimen was completed, the patient's pain recurred and she rerurned to the physician. This initially apparently straightforward infectious problem becomes complex when the patient fails to respond to treatmenr. The physician initially uses hypothetico-deductive reasoning (ap parently successfully) only to learn his standard medical approach to the problem has not brought resolution. When the patient rerurned after completing the initial treat ment regimen, the physician chose to seek a second opinion and referred the patient to a specialist in gastroenterology who could not find signs of significant treatable pathophysiologic processes. The patient rerurned to the primary care physician. In this third round of problem solving, the primary care physi cian was able to use his unique perspective to further assess the patient. Unlike the specialist, the primary care physician had seen
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the patient on several occasions over many years. Thanks to the factor of time and rerurn visits, he believed he knew the patient and believed her complaints were sincere. On a subsequent visit, after exhausting all other logical pos sibilities, the physician sought a third opinion from a gynecolo gist who performed a laparoscopic investigation that revealed a chronically inflamed appendix. Surgical removal of the appendix resolved the problem. The physician was clearly perplexed going into the last round of problem solving for this case. What had seemed to be an almost simple diagnostic and management problem had not resolved. Referral had not yielded sarisfactory results. The problem's man ifestarion did not suggest any reasonable causes beyond those he had already considered. The physician's acquaintance with the patient as well as his need for resolution led him to pursue an other avenue (that of structure and function) that finally proved fruitful, and he will probably never forget this extremely atypical example of an inflamed appendix. CASE FOUR
The patient is a woman in her 30s who presents to the emergency department with multiple acute complaints. The primary prob lems are severe headache and abdominal pai n as well as chest pain and palpitations. The headache and abdominal pains were so in tense that narcotics were administered in the emergency room to relieve them. The patient was admitted, and an attempt was made to ascertain whether the multiple symptoms were the re sult of multiple problems or one problem. For the headache, the physician first entertained the hypotheses of subdural hematoma or rumor. Although on physical examination there were no neu rologic signs to suggest either of those diagnoses, a computerized axial tomography (CAT) scan was done to be sure. It did not show any abnormalities. The patient complained of palpitations, and physical examination in the emergency room showed sinus tachy cardia. A treadmill ECG showed no abnormalities. The physician hypothesized that the cardiac symptoms and headaches were the result of stress or anxiety. The patient was treated with a shon term regimen of benzodiazepine (alprazolam), which relieved the headache and palpitations but did not affect the abdominal pall1. At that point, the physician believed he was dealing with two separate problems. One was the basis for the headaches and car diac symptoms, which responded to treatment with an anxiolytic agent, and the other was an undiagnosed abdominal problem. The patient's pain was localized in the upper abdomen, which triggered hypotheses of gallbladder disease or common bile duct obstruction, among others. The former was quickly ruled out be cause the patient's gallbladder had been surgically removed. Ab dominal ultrasound showed a suspicious dilatation of the hepatic duct, which was confirmed by contrast dye radiographic evalua tion to be a common duct stone. Removal of the stone resolved the abdominal pain. The complex presentation in this case is what some might see as an internist's delight, even though part of the solution was surgical. The complex presentation triggered a variety of hy potheses, some of which were potentially life-threatening, which
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the physician hoped to rule out early on. The hypothesis set for this case included solutions that explained the combined data set (headaches, cardiac problems, and abdominal pain) and others that separated the problems. Response to the short-term treat ment confirmed the hypotheses for more than one problem. This case is an excellent example of successful complex hypothetico deductive reasoning in which hypothesis generation and evalua tion from a single problem as well as a multiple-problem perspec tive yield resolution on essentially the first round. I t is becoming more and more likely that primary care osteopathic physicians will see cases like this one. When they do, the cases should be cognitively satisfying. CASE FIVE
The patient is a man in his 50s employed as a fire fighter who states he experienced an acute episode of chest pain approximately I week ago while fighting a house fire. The first and most likely hypothesis the physician generates is angina pectoris as a result of coronary artery disease. The patient has risk factors for CAD such as: Age Weight Smoking A stressfu I job The patient does not appear in acute distress at the time of presentation. The physician prescribes sublingual nitroglycerine as needed to relieve the pain and has the patient undergo a stress treadmill ECGs (one on being re ECG . After not one but ferred to a cardiologist) , no abnormality is found. Neither tread mill test triggers the pain. An echocardiogram performed at a ter tiary care center is interpreted as showing a valvular abnormality. The pri mary care physician is not satisfied that it is the cause of the patient's chest pain. During the testing period, the patient experi ences the pain occasionally without relieffrom the nitroglycerine (failure to respond to treatment). Until now, the physician has avoided asking the patient to undergo cardiac catheterization in favor of less costly, less invasive tests. Eventually cardiac catheter ization reveals severe coronary artery disease requiring four-vessel bypass surgery. In this case, the physician expected a straightforward hypothetico-deductive reasoning sequence to yield the antici pated solution. This was almost a case for pattern recognition. The physician was tripped up in the hypothesis testing phase. The patient's failure to respond to treatment and successful execution of two treadmill tests constituted evidence against the hypothesis of angina pectoris as a result of CAD. Nonetheless, the physician would not rule out that hypothesis and insisted on performing a more definitive (and much more costly) evaluation: the results of which confirmed the hypothesis he had held all along. The physician considered the negative treadmill test resulr as evidence against the hypothesis of coronary artery disease as the basis for the patient's chest pain. Nonetheless, the physician stuck by his original hypothesis using what appears to be intuition that he was on the right track. This is a perfect example of where probabilistic reasoning could have helped the physician resolve his ambivalence about the test results. Take a moment to consider twO
the results using Bayes theorem. Section 3 of the Appendix out lines how information about this case m ight be analyzed. We can readily see from that illustrative analysis that our physician's intu ition was correct. Going through the formalities of probabilistic reasoning tells us that for a patient whom we are so sure has a diagnosis of coronary artery disease that we can assign a prob ability of 90%, even a negative stress ECG result only reduces our probabiliry to j ust below 80%. In fact, for this patient, we probably didn't need the stress test to establish the diagnosis. I f the result had been positive, it would not have helped that much either. This is a highly atypical case. In most cases like this, the pa tient's presentation and course of illness are typical for the most likely diagnostic hypotheses, and diagnosis and management can proceed in an orderly fashion. The good primary care physician is alert to the atypical case and is able to use a combination of intuition and trust in the patient's sincerity to tell him or her when a case cannot be resolved "by the numbers." SUMMARY
The primary care practitioner's thought processes reflect and ex pand those found in the controlled studies of clinical problem solving. Primary care osteopathic physicians regularly make in formal use of hypothetico-deductive reasoning as well as prob abilistic thinking. They also analyze problems using principles of structure and function. The primary care physician experi ences a unique form of the complex problem-solving process as a re�ult of his or her patient encounter pattern. In contrast to a specialist who might see the patient on a consultation or in the hospital setting during an intense period of a brief hospital stay, the primary care physician sees the patient for multiple compar atively short episodic visits. This encounter pattern allows the primary care physician to assess the patient's short-term response to treatment as well as his or her long-term health/illness pattern. The primary care encounter pattern provides the physician the unique opportunity to reasonably consider diagnostic hypotheses that are time dependent (e.g. , depression, physical and psycho logical abuse, and hidden substance abuse) as part of a complex problem-solving methodology. The physician's problem-solving process is expanded to include the variables of repeat visits, time, and response to treatment, enabling him or her to place the problem-solving process for each patient in the context of the patient's life experience as well as that of the physician's practice experience. Osteopathic A pproach
The definition of what is osteopathic is different for every osteo pathic physician. For some, primary care is a key factor in being osteopathic. Others may focus on the musculoskeletal system, palpatory diagnosis, and manual medicine as uniquely charac terizing the osteopathic approach. In this text, the authors have agreed on four basic biologic principles particularly applicable in the practice of osteopathic medicine. The principles were formal ized and related to osteopathic practice in a document produced by the Kirksville College of Osteopathic Medicine ( 1 5) and subse quently discussed in a report of a survey of osteopathic physicians
19. Clinic al Problem Solving
( 1 6). The principles are as Follows: I . The body is a unit. 2. The body possesses seiF-regularory mechanisms. 3. Structure and Function are reciprocally interrelated. 4. Rational therapy is based on an undersranding of body unity, self-regularory mechanisms, and the in terrelationshi p of struc ture and function.
These principles are Furrher articulated in Chapter I , Osteo pathic Philosophy. Primary care practitioners in this study showed their aware ness of osteopathic principles in a few i nstances by quoting ver batim precepts they used as a Foundation for some aspect of their practice. More frequently, appreciation of osteopathic tenets was expressed through discussion of the role of the musculoskeletal system in diagnosis and treatmenr. By far the most prevalenr theme was the more global ability of the osteopathic physician ro consider the whole patienr from functional, structural, sociobe havioral, and other perspectives. OSTEOPATHIC PRECEPTS
Physicians quoted two precepts that aFFected their thinking: "The rule of the artery is supreme" and "The body heals itself" (a refer ence ro the precept ofself-regulation). A third precept, applied but not clearly articulated, was the interrelationship between struc ture and function as exemplified by the DO's use of visceroso matic and somarovisceral reA exes in diagnosis and treatment. Examples were given of applications of the self-regulation pre cept. First, the osteopathic physician's awareness that the body is a unit and is capable of selF-regulation and selF-healing helps him or her ro gain a deeper understanding of the illness or dysfunction that might be the underlying reason for the patienr's overt signs and symproms of disease. The osteopathic physician is aware that there might be a more Fundamenral deviation from health that has compromised the patient's inherenr functional dynamic equilibrium and allowed an illness or disease ro develop. Second, with regard ro the resroration of health, the osteo pathic physician's awareness of the body's capacity ro heal itself helps him or her give more serious consideration ro the treat menr option of "do nothing," or ro "try managing this problem by supporring the body's Function and avoiding medication for a while." The physician's understanding of the body's capacity for self-regulation and self-healing allows him or her to be comfort able with avoiding overmedication. The osteopathic physician is aware of the role of structural treatment in enhancing the body's self-regulatory capabilities. Third, the physician respects the patient's (perhaps inruitive) understanding of the body's capacity for self-regulation and heal ing. One physician related a brief story about patients with a com mon cold. He noted, "Most people are competent." When dealing with an upper respirarory infection, most use over-the-counrer medications, rest, and Auids to enable the body to heal itself. The physician understands that treating the somatic compo nenr lets the patienr's body heal itself with or without medication. Expanding on the role of viscerosomatic reAexes in diagnosis and treatment, salient examples follow.
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CASE SIX
The patient is a woman in her 30s or 40s who is employed as a secretary, a type of work that involves sitting in the same position for long hours doing repetitive tasks such as keyboarding. The patienr presents with hand numbness. There are no other symptoms. Palpation of the neck reveals bilateral changes in the musculoskeletal system From T 1 -4. Treatmenr of the cervical and thoracic areas resolves the hand numbness. There are several possible interpretations of the struc ture/function relationships in this case. One interpretation has to do with the anatomic relationship of the first rib, the clavicle, and the brachial plexus. Another has to do with the fact that the arm receives primary sympathetic innervation from T2-S. The relationship m ight have to do with possible fascial tension at the thoracic inlet preventing good lymphatic drainage for the affected arm and hand. Another physician described her evaluation of patients' backs. When she first performed the physical examination, she looked for asymmetries (such as whether one side of the rib cage was more pronounced than the other) and for convexities or scoliosis. She noted how findings in patienrs' backs affect how they walk and how they do their jobs and the impact these findings have on their health. She was then able to use these initial cues in evaluating subsequenr complaints the patient brings to her. In these instances, osteopathic physicians apply their under standing of the interrelationship of structure and function to diagnose and treat patienrs osteopathically. MUSCULOSKEL ETAL SYSTEM IN DIAGNOSIS AND TREATMENT
Osteopathic physicians have an important diagnostic and thera peutic tool in the musculoskeletal system. Clinicians cali on it in several ways. From the patient evaluation perspective, palpatory diagnosis of musculoskeletal problems is a skill unique to the osteopathic physician. There are numerous examples of patients with mus culoskeletal problems reFerred to osteopathic physicians by non DOs who could not arrive at a satisfactory diagnosis with x-ray studies or EMGs and could not resolve the patient's pain with medication such as analgesics or muscle relaxants. The osteo pathic physician is able to diagnose the patient's problems using palpatory skills and treat the problems with osteopathic manip ulative treatment (OMT). The patient's pain is resolved with a simple noninvasive diagnostic and treatment approach. The next cases illustrate the osteopathic physician's special skills in muscu loskeletal diagnosis. CASE SEVEN
The patient is a domestic worker in her 40s. She presents with low back pain, which she attributes to an injury she sustained on the job. She states she fell backward into a bathtub and hurt her back. The physician is able to diagnose the problem as a sacral torsion. She treats the patient and relieves her pain. The patient seeks compensation, and the physician is called on for
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r v Os te opathic Consi de rati ons in Cli nic al Proble m Solving
a deposition. Her abiliry to describe the palpatory findings and their relationship to the patient's story helps make the patient's case. The next case is a counterexample. CASE EIGHT
The patient is a woman in her 30s who presents with low back pain. The physician generates several hypotheses suggested by the acuteness and severiry of the pain, including the patient's chief complaint that she is passing a kidney stone. That hypothesis is supported not only by the patient's history (acute onset, localiza tion of pain, family history of kidney disease), but also by phys ical examination (patient moving around on examination table, low back tender to palpation) and preliminary laboratory results (trace of blood in urine) . The physician takes abdominal x-ray views with and without contrast medium, none of which shows an abnormaliry. She srarts the patient on a regimen of antibiotics. The pain, still present, is localized on the right side, suggesring possible gal lbladder disease. Ultrasound of the gallbladder reveals no abnormaliry. To quote the physician: "Finally it occurred to me that maybe the pain in her back is because she's got pain in her back." Palpatory diagnosis revealed somatic dysfunction ar L l -2, which the physician treated, relieving the patient's pain. "She skipped out of the office." The lesson here for the physician was that as a DO, she should nor forget her unique perspective. She needed to always remember to include the musculoskeletal system in her diagnostic formulation and treatment plan. Musculoskeletal (osteopathic manipularive) treatment is seen by many osteopathic physicians as the si ne qua nonof osteopathic distinctiveness. For most primary care DOs, it is a unique part of their treatment methodology and, though characterized as ad junctive by some, plays a key role in parient management. The following cases are examples. CASE NINE
This case illustrates osteopathic manipulative treatment and re lief of stress. The patient is a woman in her 30s who is being treated by a non-DO for hyperthyroidism. She suffers intractable headaches for which the physician cannot ptovide relief. The pa tient is referred ro the osteopathic physician, who describes her as a rypical patient with hyperthyroidism: extremely thin, intense, slighrly bulging eyes, quick birdlike movements, and rapid heart beat. Musculoskeletal evaluation reveals the patient be "stiff as a board." The DO treats rhe somatic dysfunction in the pa tient's neck and shoulders using osteopathic manipulation, with liule effect. After several visits, however, the patient's headaches ease and she gains movement in her neck and shoulders. The patient lives in a stressful family environment that includes her terminally ill husband. The burden of family mess as well as the hyperthyroidism is reRected in her musculoskeletal system. Regular manipulative treatment in combination with ongoing medical therapy for the hyperthyroidism addressed the patient's disease process, increased the patient's comfort, and facilitated her abiliry to manage her life. ro
CASE TEN
The patient is an adult with SIl1USltls. The physician describ ing this case sees many of these patients, especially in the fall and winter when people spend more time in an enclosed environment. The physician has established a routine in her office for managing a patient with this problem. She starts by doing a complete eval uation, including a structural assessment, especially checking the thoracic and cervical spine, and thoracic inlet. She treats those areas of the cervical and thoracic spine that need it with manipu lative medicine and performs a lymphatic pump technique. She notes the osteopathic manipulative treatment usually produces rather dramatic relief of symproms and seems to improve rhe effectiveness of the medication she prescribes. In her patient edu cation, she includes instructions for administering saline solution nose drops, drinking a lot of Ruids, keeping the eustachian rubes clear if the ears are involved in the infection, and refraining from or minimizing smoking. She says, "[ feel nice and osteopathic with cases like that." She notes that because these cases are not usually diagnostic challenges, she can focus during her time with the patient on structural diagnosis, manipulative rreatment, and patient education. CASE ELEVEN
The patient is a healthy man in his 30s. He works as a salesper son. Although his job requires him to be on his feet, he is not particularly active in his work. He m ight be characterized as a "weekend sportsman" who, though exercising litrle during the week, exercises vigorously on weekends. As a result, he experi ences back discomfort, which is then exacerbated by his work. The physician takes a focused history reveal ing no arthritis, in jury, or underlying disease process that would express itself as back pain. The chief diagnosis is "musculoskeletal problem due to overuse." The patient's somatic dysfunction in the pelvis, lum bar, and thoracolumbar regions is treated with osteopathic ma nipulative treatment with good results. THERAPEUTIC TOUCH
Osteopathic manipulative medicine, although useful in its own right as a treatment modali ry, is further effective as a form of therapeutic touch. This is particularly important to the primary care physician who seeks to know and rreat the whole patient. Whether the patient is an elderly woman who comes in regularly for treatment of her stiff neck, or a postaccident patient with neck pain, the act of touching the patient to evaluate and rreat the m usculoskeletal system is therapeutic. One physician noted that her patients thought she listened to them better than another physician, and that m ight be because she touches them where it hurts rather than, for example, looking at x-ray films. MUS CULOSKELETAL PAIN
Palpatory diagnosis and osteopathic manipulative treatment are particularly effective in evaluating and rreating musculoskeletal
J 9. Clinica l Pro blem So lv ing
pain, ·.g., in post-accidem patiems. The vignettes ourlined in cases seven and eight are just two instances of the value of palpa rory diagnosis in cases of musculoskeletal pain. The osteopathic physician's ability ro put his or her hands on the patiem and tell them where it hurts is not only a form of therapeutic rouch but is also meaningful ro patiems, as well as being cost effective. The patiem is comforted by diagnostic rouch applied ro a painful musculoskeletal area and perceives it as a form of listening ro their body. Furthermore, the abiliry ro accurately imerpret pal parory findings from the musculoskeletal system is perceived as a uniquely osteopathic skill. In one comparison between himself and a non-DO, a physician discussed referrals. He noted that the referral letters from non-DOs tended ro focus on the immediate problem, such as a car accidem or work injury. The osteopathic physician considers the injury in the comext of the patiem's rotal body mechanics: Is the patient right or left handed? Is this a woman with a young child? What hip does she carry the baby on? What is the patient's posture like? What is the overall body condition? Following treatmem, further consideration ofbody mechanics can be used ro assess its effectiveness.
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most distinctively osteopathic traits for the primary care physi cian, however, are the perception of the patient as a whole in an environmem and the capacity for integrative thinking. Examples are the best illustrations. One woman physician had many women patients in her prac tice. Not infrequently they asked her about the pros and cons of hysterecromy. Her advice in nonmalignant cases was often ro discourage them after considering the short- and long-term con sequences of surgical removal of the uterus. In the short-term the patient must recover from the traumatic invasion of her body and likely experiences post-hysterectomy depression. In the long term, the woman experiences permanent loss of reproductive function as well as loss of an important organ. The body is not simply a container for parts. The uterus is an integral part of a woman's bodily identity; its removal constitutes a partial loss of that personal identity. A physician who practiced in an economically depressed area had many children in his practice who suffered frequent respi ratory infections and sore throats. He saw the children as part of an unhealthy environment. They were usually poor, with a poor diet. They often did not have clean clothes, had not bathed recently, or did not have proper shoes (e.g. , children who wore canvas sneakers without socks in the winter) . The physician saw these characteristics of their life environment as contributing his understanding of their illness and his abiliry effectively treat them and restore them to health, or at least more optimum functioning. A woman physician managed many pregnant patients, includ ing their deliveries. Her whole patient approach ro the manage ment of pregnancy and delivery involved awareness of the patient in her environment. On the in itial encounrer, the physician con sidered wi th the patient the social context of her pregnancy and asked these questions: to
to
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OSTEOPATHIC MANIPULATIVE TREATMENT AND MEDICATION
One last category where palparory diagnosis and especially osteo pathic manipulative medicine are particularly helpful is in rela tion ro medication. In case 1 0, we offered a brief vignette where OMT was thought ro relieve symproms of upper respirarory in fection (sinusitis), and enhance the effectiveness of medication. OMT may also help a patient avoid medication. Several physi cians cited instances when they used this reasoning, particularly with elderly patients suffering from arthritis pain. One physician noted regular visits by elderly patients who sought manipula tive treatment for neck and shoulder stiffness, enabling them ro avoid medication. Another rold of elderly women patients with osteoporosis who are hospitalized with a cardiac problem but who also suffer musculoskeletal pain. Gentle osteopathic ma nipulative treatment ro the spine makes them more comfort able. A thi rd physician specifically insrructs his elderly patients in exercise and stretching techniques ro maintain mobility and avoid arthriric pain and sriffness. The physician treats these pa tients regularly wirh osteopathic manipulation. In his words: "It helps them avoid antiinAammarory medications rhat cause gas trointestinal problems. It's better for them ro spend their money on a visit ro the docror for a manipulative treatment than on drugs." PATIENT AS A WHOLE
The role of the musculoskeletal system in health and illness or injury and the osteopathic physician's skills in evaluating and treating the musculoskeletal system are important. By far, the
Is the patiem married ro the father of the baby� Is this her first pregnancy? What is the fam ily's reacrion to the pregnancy? What is the father's reaction? If the patiem is not married to the father, did he end their relationship when he found out she was pregnant? What are the patient's expectations? The physician emphasizes patient education on the first en coumer. During prenatal care, the physician treats musculoskele tal complaims with manipulative treatment. She finds that back pain, leg pain, stress at the pubic symphysis, and sacral somatic dysfunction seem to be the most common problems. During la bor and delivery, the physician is presem. She finds that being there is therapeutic, especially if the patient is struggling. The physician provides coaching and companionship during this in tense experience, sharing what she calls "a real space" with the patient. She is able to perform osteopathic manipulative tech niques that are helpful, including a cranial technique (CV4) and sacral traction. Post parrum, the physician feels better able manage the patiem and her infam knowing she is thoroughly acquaimed with the circumstances of the pregnancy. In addition to being there and actively facilitating the delivery, she has gained the patiem's confidence. to
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IV. Os teo pathic Considera tions in Clin ic al Prob le m So lv in g
INTEGRATIVE THINKING
ExemplifYing the osteopathic physician's distinctive capacity For inregrative thinking, one physician expressed her approach liter ally: "You diagnose with all of your senses," she said. The physi cian looks, feels, and smells while listening to the patienr. You look at the patienr's body language, For evidence of skin lesions, and personal hygiene, and relate that ro what the patienr is telling you. She said, "The body doesn't lie. The patienr may, but the body doesn'r." I Fyou question a patienr's credibility, the use oFall of your senses in patient evaluation helps elicit the patienr's true hisrory. CASE T WELVE
A physician described a particularly troublesome case wherein the impact of the patient's environmental context was a signifi c ant Facror in diagnosis and treatmenr. The patienr is a 27-year-old man presenting with abdominal pain on exertion. He is a basketball player, tall (6'8"), thin, usually healthy, and in good physical condition, who practices basketball three or Four times a week. The abdominal pain occurred while playing basketball. The onset of pain was gradual, characterized as a cramping type of pain. It did not occur in association with eating or other activities. There was no hisrory or evidence of sports injury. On learning of the reason For the visit, the physician considered the patienr in his life conrexr. This was a healthy individual with a complainr who was seeing a physician for the first time on the advice of his father. Even before examining the patienr, the physician, knowing the family, believed the patienr was legitimately, potenrially seriously ill, or he would not have sought help. The physician attributed his ability ro make those preliminary assessments ro the Fact that he was an osteopathic family practitioner in a relatively small community. Physical examination revealed a large mass on palpation of the abdomen with no other abnormalities. The physician sought ro Further characterize and localize the mass with a Rat plate of the abdomen, and a CAT scan. The Rat plate showed accumulated srool in the left side of the large bowel, but no mass. Furthermore, the patienr stated the pain was on the right, and he reported having a bowel movemenr every day. The data did not fir. At this point, the physician's thinking ran along two lines. First, he believed there was a serious problem but did not wanr ro alarm the Family. He was aware that the patient's father-in-law, who was in his 50s, had passed away only three weeks before and the Family was grieving his loss. The physician considered several hypotheses ro explain the anomalous data set, including the possibility of a hemaroma on the muscle wall that had developed from an inadvertent or Forgot ten injury during basketball practice. The physician ordered an ultrasound of the abdomen that revealed a solid mass. It was now incumbenr on him ro inForm the patienr's family of his thinking. He was aware of the potenrial fear of cancer, especially because a family acquaintance (not a relative) had had a son (perhaps near the patient's age) die From cancer. The physician made a poinr of using probabilities ro assure the family that the likeli hood of a benign process was much higher than the likelihood of a malignancy. Surgical laparoromy was done, revealing a benign
tumor approximately 5" in diameter that was removed, Followed by unevenrful recovery. The physician described his problem-solving process for this case as occurring on two planes. One was the diagnosis and man agemenr of the medical problem; the other was the managemenr of the interaction with the patienr's family. He saw his ability ro effectively integrate those two lines of thinking into eFfective overall patienr managemenr as particularly osteopathic. SUMMARY
Osteopathic thinking is many things ro many people. Osteo pathic primary care practitioners seem ro agree that there are a few key things about how they view patient care that make them par ticularly osteopathic. The first is their ability ro effectively use the musculoskeletal system in patient evaluation and managemenr. They are able to bring those skills to bear in a range of areas, all the way from the most Fundamental diagnosis and rreatmenr of musculoskeletal complainrs to relating musculoskeletal inrerven tion to the use of medications, to the realization of the power of therapeutic touch. They also show a keen awareness of the body's inherenr capacity for regulation and self-healing through their understanding of the inreraction of different therapeutic inter ventions and their ability to use support of the musculoskeletal system to restore the patient ro health. Even more meaningful to those osteopathic primary care physicians, however, is their special understanding of the patient as a whole who exists in an environment and their unique ability to think integratively about the patient in his or her life circumstance. This global sense of the whole person is for them far and away the greatest physician attribute that makes them distinctively osteopathic. ILLUSTRATIVE CASE
We return ro Mr. Johnson. We conclude this chapter by first recalling the information we presented about the patient earlier in the chapter, and then analyzing the case using an osteopathic approach to clinical problem solving. Description
The patient is a white male, age 55, presenting with a complaint of aching in the left shoulder that he experienced while raking leaves. Other pertinent data are that the patient is overweight and hypertensive. You may wish to turn back to the initial patient presentation ro recall the specific statement of the reason For the visit, as well as the vital signs. STOP: If you were Dr. Martin, what might you be thinking as you are planning to conduct a thorough history and physical examination including a diagnostic palpatory examination' What possible mechanisms might you be considering for his presenring problem? The picture presented by the preliminary data suggests a liFe pattern that might have led to enough deterioration in the pa tient's ability to maintain homeostasis that it has culminated in this acute problem of pain. The pain could be of musculoskeletal
J 9. Cli nic al Problem Solving
origin, perhaps a strained ligament, muscle spasm, swollen ten don, a myofascial trigger point, or even referred pain from the cervical or thoracic spine. Segmental facilitation (in this case in rhe thoracic spine) lowers the response threshold for many poren rial shoulder complainrs. These are your mosr likely considera rions ar this poinr. However, other more porenrially serious causes must be considered such as a problem of cardiovascular origin in volving ischemia, venous and lymphatic congestion, or referred pain from the arreries of the hearr. The pain might also be re ferred from dysfunction of the gastrointestinal system, or perhaps be a problem of pulmonary origin, such as pleurisy. Less likely possibilities include immunologic disorders such as arthritis, con nective tissue disease, or cancer. You also consider that there could be more than one mechanism that would explain most or all of the findings. For example, the elevated blood pressure may be a consequence of the pain experience or the patient's anxiety re garding his illness or his first visit to a new doctor, or it could be part of the same underlying problem that is causing the pain. As you enrer the examination room and greet M r. Johnson, you note he is, as you expected, a large, heavy man who appears in no acute distress. You note an odor of cigarette smoke on the patient's clothing and hair. He is draped for examination, so you are unable to note whether he has a pack of cigarettes in his shirt pocker. As he shakes your hand you note he has a firm grip. H is shoulders are level and he holds his head upright in the midline position. His coloring appears normal for a man his age. There is no evidence of hypoxia (bluish skin) or Aorid coloring. As he speaks, you note he does not have difficulty breathing at rest. He describes his problem. The shoulder discomforr occurred while he was raking leaves last Sunday afternoon. It was of gradual onser. He characterizes the discomforr as a heavy aching feeling. He indicates the frontal aspect of the upper chest on the left, and the left shoulder when you ask him to show you where the pain is. The pain does not seem to go anywhere outside of the left shoulder and upper chesr. Specifically, it does not move to the sternal area or into the back. He has had pain like this before on two occasions. The first one occurred last summer when he was using a posthole digger to help his son put in a new fence. The other occurrence happened approximately 2 months ago when he was helping a neighbor push her car out of the mud. On both occasions, the pain sub sided with rest and was completely gone by the following day. When the current episode happened, he rested, with relief after approximately 1 0 minutes. The pain recurred when he resumed the exerrion of leaf raking. The discomforr seems to be more as sociated with exerrion than with simple motion of the left arm and shoulder. The patient cannot reproduce the pain by moving the arm and shoulder while at resr. He has not noticed pain with any other form of exerrion that does not involve the arms and shoulders, such as climbing stairs. During the history of the presenting complaint, you ask him to take a deep breath and fully exhale. This does not reproduce the pain. The patient rates the pain when it was at its strongest as approximately a seven on a scale of one to 1 0. It has not completely gone away, and he would currenrly rate the discomfort as a two or three on the same scale. Before continuing with a more detailed health history, you ask Mr. Johnson what it was that prompted him to seek help at this time. He responds that he has had aches
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and pains before that always went away. He sought help for this episode because it has not resolved as previous episodes had. Furthermore, he recalls a couple of years ago when a co-worker told him her husband had pain in his left shoulder and arm while raking leaves, and it turned out he was suffering a hearr attack. He admits he is concerned. STOP: Review what you know about M r. Johnson. First and foremost, consider the impact the patient's life pattern has had on his health . His lifestyle, which has brought him to his current health status, has involved a steady challenge and deteriora tion of his body's capabilities for self-regulation. The pain he has experienced on this most recent occasion as well as several previous ones is probably the manifestation of an acute medical problem. The problem results from a steadily decreasing ability on his parr to mainrain structural and functional balance and sustain a healthy dynamic equilibrium. The pain itself involves the musculoskeletal system but might not originate within these elements. Because moving the arm and shoulder at rest does not reproduce the pain, the joints of the shoulder are probably not the cause. Absence of pain with nonexerrional active motion of this region suggests that the pain probably does not originate with the muscles of the shoulder girdle. The fact that other forms of exertion such as stair climbing do not bring on the pain makes a cardiac problem such as coronary arrery disease less likely as well. Deep inhalation and exhalation while at rest did not reproduce the pain, which would tend to weaken a pulmonary hypothe sis. Further investigation is needed to evaluate the more remote possibility of a gastroinrestinal problem. You continue the health history, guiding Mr. Johnson through a past medical history and review of systems. to
Past Medical History
Mr. Johnson has not seen a physician In almost 1 0 years. His only significant past health problems have been gastrointestinal. Approximately 1 1 years ago, he experienced periodic abdominal discomfort and intolerance to certain foods. After attempts at conservative management were unsuccessful, his gallbladder was removed with uneventful recovery. He has experienced no sig nificanr health problems since then. He has not had any further abdominal discomforr or problems with diarrhea, constipation, or bloody stools. H is diet and weight are essentially unchanged since his surgery 1 0 years ago. Family History
Mr. Johnson is the third oHour children. H is father died 20 years ago at age 68 after a myocardial infarction. His mother is still living, age 85, and in relatively good health. His oldest brother died 3 years ago at age 60 after a myocardial infarction. He has one other brother, age 58, whom he has not seen in several years and about whose health status he knows little. His sister, age 52, lives nearby, and is in good health. Cardiovascular
He has had no difficulty breathing and has not experienced di aphoresis or shortness of breath with the chest discomforr. He
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IV Os teo pathic Co nsi dera tio ns in Cli nic al Pro blem So lvi ng
sleeps on his back or side and does not recall ever awakening feel ing shorr of breath. He continues to smoke approximately rwo packs of cigarettes a day. Musculoskeletal
He experiences occasional joinr stiffness and low back pain, which he attributes to old age and being overweight. The back pain comes and goes and has not changed in the last several years. The joint stiffness has worsened somewhat in the last year.
evidence includes: History of a high-fat diet Lack of exercise Stressful sedentary work Smoking Alcohol consumption The presenration is an acute problem of pain suggesting a serious medical problem. Musculoskeletal Pain
Endocrinologic
He has not experienced increased hunger or thirst in the last year. He has not experienced any night sweats, tremor, or intolerance of temperature changes. Genitourinary
He has not had any urinary urgency, hesitancy, difficulry starting the stream, or change in force of the stream. He and his wife have inrercou rse approximately once a month. He has no difficulry achieving and maintaining an erection and orgasm. The chest discomfort does not occur during intercourse. Pulmonary
He has not experienced hemoprysis, cough, phlegm, or pain with respiration. Ears, Nose, and Throat
He has occasional headaches that are relieved by ibuprofen. He does not have difficulty hearing or ringing in the ears. He has had no loss or blurring of vision. He wears glasses for reading, which he purchased at a local department store. He has not had his eyes examined since the complete physical examination associated wi th his gasrroi n testi nal problems several years ago. Social History
Mr. Johnson tells you he is employed in a rather stressful, seden tary job. He has been married 25 years and has rwo grown chil dren who no longer live at home. His wife also works outside the home. Berween them, they have a reasonable standard of l iving and health insurance through his employer. M r. Johnson smokes approximately rwo packs of cigarettes a day. He drinks berween two and three 1 2-ounce beers a day during the week and approx imately rwice that many a day on weekends. M r. Joh nson does not exercise regularly and his diet is high in fat. STOP: Before conrinuing to the physical examination, es tablish some priorities for possible ways to explain the patienr's deviation from health, as well as possible diagnostic hypotheses explain his acute presenting problem. You see your most likely considerations and related cues as follows. There is long-tetm compromise of the body's ability maintain health to the point that the patient's problem is now acute, and the health behav iors are significant risk factors for further damage. Supporting to
to
He has musculoskeletal pain, possibly costochondritis, from thoracic, cervical, and/or shoulder somatic dysfunction, with possible radiculopathy or arthritis. The supporring evidence includes: Pain located in upper chest and shoulder Associated with exertion during use of associated muscles and jOlll ts Patient is 55, overweight, has stressful job, sedentary lifesryle Patient has experienced pain and stiffness in other joints Controverting evidence includes: Character of pain is heavy and aching Rest does not completely relieve pain Deep breath with complete exhalation does not reproduce palll Movement of arm and shoulder does not reproduce pain Patienr describes pain as differenr from previous episode Cardiovascular Referred Chest Pain
The supporting evidence is: Character of pain is heavy and aching Association of this and previous episodes with upper body exertion Failure reproduce pain with simple movemenr Acute phase of pain relieved by rest Male, age 55, BP 1 60/ J J O Stressful job Sedentary lifesryle High-fat diet Smokes Family history of cardiovascular disease Conrroverting evidence includes: Location of pain Pain not associated with coitus, climbing stairs, or other exerrion Pain not accompanied by shortness of breath or diaphoresis to
Gastrointestinal Referred Pain
The supporting evidence includes: Location in upper chest and shoulder Patien t is 5 5
19. Clin ic al Pro blem So lvin g
Overweight High-fat diet Controverting evidence includes: Partially relieved by rest No apparent association with eating or foods Gallbladder has been surgically removed Pu lmonary Referred Pain
Supporting evidence includes: Location in upper chest and shoulder Brought on by upper body exertion Patient smokes The controverting evidence is: Deep breath does not reproduce pain Acute phase relieved by rest You decide to order your preliminary differential diagnoses as follows (from most likely to least likely): Chest pain as a result of coronary artery insufficiency Primary musculoskeletal pain Gasttointestinal pain Pulmonary referred pain Although the pain is highly atypical for angina, your reasoning is that Mr. Johnson has several risk factors for heart disease and it would be a serious error to miss a cardiovascular problem in this patient. Phys ical Examination
Repeat vital signs: unchanged. Heart: regular rate and rhythm withour S3 or S4 murmurs. Chest and lungs: normal to percussion; auscultation of lungs reveals scanered rhonchi; bruits heard over both femoral arteries; no carotid bruits. Musculoskeletal findings that would aid in the diagnosis: ten derness to local palpation of paraspinal tissue at T2-5 on the left; tissue texture ropiness in that area; no pain on direct palpation of shoulder; active and passive motion of shoulders and arms is symmetrical without restriction; passive motion of shoulders and arms does not elicit pain on either side; direct pressure applied over left glenoid fossa does not elicit pain; range of motion of the cervical spine is full; muscle strength testing in the upper extrem ities is symmetric, 5+/5+, and does not reproduce the pain; no trigger points are identified in the pectoral muscles; costochon dral joint pressure does not elicit pain or discomfort; no cyanosis or edema STOP: After completing the physical examination, take time to explain your thinking to the patient. What will you tell him? Take a few minutes to think through a possible explanation that he would understand. Your explanation may include the following information: 1 . Expression of empathy for the patient's concerns about his problem, and reinforcement for seeking care.
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2. Outlining of short-term and long-term plan based on your assessment of his immediate problem and your concerns about his overall health. Based on history and physical examination, possible sources of his acute medical problem are: 1 . Coronary artery disease, which is supported by a history of pain with exertion as well as his lifestyle, smoking, and other risk factors. Although this seems like a problem of possible musculoskeletal origin, the facts that he could not reproduce the pain with motion and that you did not reproduce it with passive motion or direct pressure on the area suggest that the musculoskeletal component of the pain is secondary to some other underlying process. 2. Gastrointestinal and pulmonary causes for the pain have not been completely ruled out, but they are much less likely at this time. Your discussion oflong-term considerations could include the following. Based on information about his lifestyle and data such as his weight and blood pressure, you are concerned that he is at risk for more serious health problems. It appears that his life pattern over the years has continuously challenged his body's ability to stay healthy. Once his immediate problem is managed, you wish to work with him to develop some life habits that will improve his body's ability to return to and sustain optimum function, thus reducing further health risks. You decide to do the following additional tests: Chest x-ray CBC Urinalysis Cardiac enzymes Cholesterol ECG Stress test Your reasoning is that this is a new patient with significant health risks. These are low-cost, high-yield sources of baseline data. Ordering these tests for this patient is in keeping with the standard of care for your community. If you need to refer this patient to a cardiologist, for example, these data would be needed at a mlllimum. You ask your office assistant to prepare M r. Johnson for an ECG to be done in your office directly following the completion of the physical examination. You ask Mr. Johnson to schedule the other tests and another appointment for 2 weeks from today, indicating that you will call him if results of the tests suggest he should see you sooner. In the meantime, you ask him to consider long-term management of his health, specifically how you and he can work together most effectively to begin to return him to a status of greater health and reduce his risks of subsequent illness and dysfunction. The test results are as follows: Chest x-ray film, ECG, and stress test show no abnormalities Blood count, urinalysis, cardiac enzymes, and cholesterol are all within normal limits
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STOP: I n our presentation of M r. Johnson's case, we have intentionally placed the clinician in a listening rather than ques tioning role. [n a scenario portraying the physician as an active hypothesis tester, he or she asks numerous questions to elicit information specifically relevant to the hypotheses under con sideration. Furthermore, the physical examination could have focused on only the region of the complaint and on those regions that would yield data positive or negative for favored hypothe ses. That pattern of data gathering is not usually functional for the osteopathic primary care physician, so we have elected not to emphasize it here. Now we have a reasonably complete preliminary data set for Mr. Johnson. A thorough evaluation of his illness is in order. The two major possible mechanisms for his presenting problem are chest pain atypical for angina with secondary musculoskeletal pain (probably as a result of coronary artery disease), and primary musculoskeletal pain. The first explanation has the strongest support. The patient's pain could likely be of cardiac origin. It is a heavy, aching pain that is brought on by exertion and relieved by rest. It is not reproduced by direct pressure on or movement of the affected area. It does not seem be related to eating (i.e., exacerbated by certain foods, or associated with gas or bloating) , or breathing (e.g., brought on by taking a deep breath). The patient has many health risk factors for coronary artery disease. He is male, age 55, has a sedentary stressful job, does not exercise, is overweight, and smokes. Although the patient has few pertinent physical findings, those you did el icit are telling: elevated systol ic and diastol ic blood pressure, femoral artery bruits, and tenderness and tissue texture abnormalities at T2-5, which have been shown to be associated with viscerosomatic reAexes from coronary artery disease ( 1 7, 1 8) . There are four characteristics used to establish a diagnosis of typical angina pectoris: I . Chest discomfort brought on by exertion and/or stress. 2. Location substernal or anterior chest wall. 3. Pain feels heavy, like pressure or squeezing. 4. Pain is soon ( 1 0 minutes or less) relieved by rest, or immedi ately with nitroglycerine. This patient has three of the four characteristics. Last, a normal chest x-ray film and ECG do not rule out coronary artery disease. At this point, you can assign approximately 70% likelihood to a diagnosis of coronary artery insufficiency, with the diagnosis of primary musculoskeletal problem at a 20% likelihood, and other diagnostic possibilities combined in the remaining 1 0% probability range. You are now able to develop a management plan for the patient. to
Self-regulation Rational therapy The application of those precepts by any given clinician prob lem solver to any given patient problem is not only idiosyn cratic to the patient but also to the problem solver. The following considerations seem to be fundamental to osteopathic problem solving. In considering a patient's problem, the osteopathic physician must be able to perceive the problem as evolving from a compro mise in the body's ability maintain a healthy dynamic equi librium or homeostatic state. Under circumstances of adequate nutrition, exercise, and physiologic and anatomic balance, the body's normal state is one of health. Whether they are amenable to labeling as disease processes, health problems constitute devi ations from that normal state of health. The goal of osteopathic problem solving is to ascertain the nature and source of the de viation from health. The major problem solving models articulated here, which, in various forms, comprise most of what we know about clini cal problem solving, can be considered to represent a subset of osteopathic problem solving. The problem-solving models and the osteopathic approach are far from being mutually exclusive. Rather, the osteopathic problem solver is seen as calling on the more restricted, reductionistic models to incorporate into his or her more global, holistic, conceptualization of health and ill ness, to achieve a more complete understanding of a patient's problem. Not all osteopathic primary care physicians use osteopathic problem solving or are even cognizant of it. Therefore, it would be inaccurate to say that osteopathic problem solving is just what osteopathic physicians do. It is more than that. With further understanding and investigation, we can characterize osteopathic problem solving to the point of articulating a model that is as applicable and teachable as the more allopathic models we have now. to
REFERENCES 1 . As rei I L. Reflecrions and a fo recast.
The DO. 1 98 1 ; 2 1 ( 5 ) : 1 5 5-1 59.
2. Groen GJ , Parel VL. The relarionship between comprehension and rea
son i n g in medical expertise. I n : Chi M T H , er aI., eds. The Nature of
Expertise. H illsdale, NJ : Erlbaum; 1 98 8 : 287-3 1 0. 3. Parel VL, Groen GJ, Norman GR. Reason i ng and instrucrion in medical
curricula. Cognition and Instruction. 1 993; 1 0:335-378. 4 . Schmidr HG, Norman GR, Boshu izen H PA. A cogn irive perspecrive
on medical expertise: rheory and impl icarions. Acad Med. 1 990;65 :6 1 162 1 . 5 . Norman G R, B rooks LR, Allen SW, er al. The dcvelopment of expertise
in dermatology. Arch Dermato/. 1 989; 1 2 5 : 1 062-1 065.
CONCLUSION
As we leave Mr. Johnson, consider what we have learned from his case and the many other brief cases presented here that could comprise an osteopathic approach to clinical problem solving. Osteopathic problem solving is loosely couched in the four basic precepts of Body unity Structure-function interrelationship
6. Brooks LR, Allen SW, Norman G R . Rule and insrance-based i n ference
in medical diagnosis. J Exp Psychol Gen. 1 99 1 ; 1 20 : 278-287.
7. Sch m i d r H G , Boshuizen H PA. Encapsularion ofbiomcdical knowledge. I n: Evans D, Parel VL, eds. Advanced Models of Cognition for Medical
Training and Practice. New York, NY: Spri nger-Vcrlag New York; 1 993. Doctors' Stories: The Narl'lltilJe Structure ofMedical Knowl edge. Princeton, NJ : Princeton University Press; 1 99 1 . 9 . Eistein AS, S h u l man LS, Sprafka SA. Medical Problern Solving: An Anal ysis of Clinical Reasoning. Cambridge, MA: Harvard University Press; 8 . H u n ter KM.
J 978. 1 0 . Weed LL.
Your Health Care and How To Manage ft. Essex Junction, VT:
Essex Publishing Co; 1 97 5 .
19. Clinical Problem Solving
I I . Walker H K, Hursr J W, Woody M F. Applying the Problem-Oriented Sys
tem. New York, NY: Medcom Press; 1 973. Medical Decision Making.
Boston/London: Burrerworrh's; 1 988. 1 3 . Sackerr D L, Haynes RB, Tugwel l P.
Clinical Epidemiologv: A Basic Science for Clinical Medicine, 2nd ed. Bosron/Toronro/London: Lirrle, Brown and Company; 1 99 1 .
National Ambulatory Medical Care Survey: 1 990 Summary.
Hyansvi l le, M D: US Deparrmenr of Healrh and Human Services, Public Healrh Service, Cenrers for Disease Conrrol, Narional Cenrer for Healrh Srarisrics; 1 992. 1 5 . Special com m i rree on osreoparhic principles and osreoparhic rechn i c of
rhe Kirksville Col lege of Osreoparhy and Su rgery. A n inrerprerarion of rhe osreoparhic concept: renrarive formularion of a reaching guide for faculty, sraff, and srudenr body. journal ofOsteopathy Ocrober 1 95 3 : 81 0. 1 6. Sprafka SA, Ward RC, Neff D. Whar characrerizes an osreoparhic prin
ciple? Selecred responses ro an open quesrion. j Am Osteopath Assoc. 1 98 1 ;8 1 (2): 29-33. 1 7. Beal Me. Viscerosomaric reAexes: a review.
j Am Osteopath Assoc.
1 985;85( 1 2): 786-80 I . 1 8. Kuchera M , Kuchera WA.
Osteopathic Consideratiom in Systemic Dys function. Ki rksvil le, M O : KCOM Press; 1 990.
1 9. Sackerr DL, Rosenberg WMC, Muir Gray JA, er al. Evidence-based
medicine: Whar ir is and whar ir isn't. bttp:llcebmjr2.ox.ac. uklebmisisnt.
htlll i.
APPENDIX TO CHAPTER 1 9 Section 1 . Statistical Properties of Stress ECG as it Relates to Coronary Artery Disease
Diagnostic statistics for the stress ECC: a common method for displaying statistics is shown in Table 1 9. 1 below, known as a 2-by-2 table. We can analyze the table step by step as follows. I magine that we conducted an experiment on a sample of 500 patients. Fur thermore, imagine that half (250) of our patients had CAD as determined by the gold standard, an objective verification of the presence or absence of the disease in our patient sample. That is our defined disease prevalence for this purpose. It is clearly unrealistically high; a change in prevalence to a more realistic level can change what we learn from test results. We have now established the values at rhe bottom of our "CAD present" and "CAD absenr" columns. Now, say all 500 of our patients un derwent a stress ECC. We would find that approximately 1 72 of them had positive test results and that test results for 328 of our patients would be normal. That would establish the values for the "Stress ECC +" and "Stress ECC - " rows of our table. We would also learn that, of the patients who had CAD, ap proximately 1 50 had a positive stress test result. Those are our true positives. Furthermore, approximately 228 of our healthy patients would have normal test results (true negatives). Clearly, the test is not perfect, but it does identify a fair number of true positives and a large proportion of true negatives. To allow us to TA BLE 1 9 . 1 . DIAGNOSIS O F CORONARY ARTERY D I S EASE
Stress ECG + Stress ECG Total
generalize from this study of 500 patients to other populations, we convert the number of true positives and tfue negatives proportion. I n the first instance, we divide true positives by total number of patients with CAD ( J 50/250 0.60). That gives statistic expressing the probability that a patienr with CAD will have a positive stress ECC result, which is called the true positive rate or sensitivity of the test. Similarly, we divide the true nega tives by the total of non-CAD patients (228/250 0.9 1 ) . That statistic tells us the probability that a patient with no CAD will have a normal stress ECC result, which is the true negative rate or specificity of the test. Sensitivity and specificity remain con stant for a test over time and with changes in disease prevalence. They would only change if, for example, the quality of the test changed to increase or decrease its association with the presence or absence of this disease process. Two other values of even greater interest to physicians than sensitivity and specificity are positive predictive value and nega tive predictive value. Those are the values that tell us for a known disease prevalence what the probability is of the disease being present given a positive test result (positive predictive value) and, conversely, what the probability is of a patient being disease free given a normal test result (negative predictive value). In our ex ample above, these can be found as follows: to a
1 2. Sox Jr HC, Bla(( MA, H iggins M C, er al.
1 4 . Schappert S.
277
Present
Absent
Total
1 50 1 00 2 50
22 228 2 50
1 72 328 500
a
=
=
Positive predictive value or 1 50/ 1 72 .87
=
True positives/AJI positives
=
Negative predictive value or 228/328 .70
=
True negatives/ AJI negatives
=
Thus, in a patient population where approximately half of the patients actually have coronary artery disease, any given patient with a positive stress ECC result will have an 87 probability of having the disease, and a patient with a normal stress ECC result will have a 70 probability of being disease free. However, unlike sensitivity and specificity, positive and negative predictive values are strongly affected by changes in disease prevalence. Consider the following example in Table 1 9.2. As in the first example, we have a total patient sample of 500. However, we have revised the disease prevalence to 1 0, or 50 out of 500 patients who have CAD, a level much more likely to be seen by the primary care physician. We know thar the true positive rate or sensitivity of the stress ECC is 0.60, so we can establish that for this patient population, 30 of our patients who have CAD by the gold standard will have a positive stress ECC result. We also know that the true negative rate or specificity of our test is 0.9 1 , so we can establish that approximately 430 of our healthy patients in this group will have a normal stress ECC result. Now, what if a patient in this group whose health status we didn't know had a positive stress test result? How sure could we be that he or she had CAD? We can ascertain that as TA BLE 1 9. 2 . DIAGNOSIS OF CORONARY ARTERY DISEASE
Stress ECG + Stress ECG Total
Present
Absent
Total
30 20 50
40 410 450
70 430 500
278
IV Os teopathic Consi derati ons in CLi nic al Problem Solvi ng
follows: Positive predictive value True positives/Total positives or 30/70 .43 Note how strongly the positive predictive value is affected by prevalence of the problem. In our previous examples where we arbitrarily decided that half of the patients had the target disease, our stress ECG had a positive predictive value of .87. However, if we decrease the disease prevalence to a more realistic level of 1 0, we find that the positive predictive value of the test decreases also, to just over half of what it was in the previous example. Let us look at what happens to negative predictive value: Negative predictive value True negatives/All negatives or 4 1 0/430 . 9 5 Thus, the negative predictive value of the stress test is also strongly affected by change in disease prevalence, only in the opposite direction. Its predictive power improves. =
p( + 1 "' D) Which reads "the probability of a positive test result given no disease" that we determined earlier was the false-positive rate.
=
=
=
The formula version of Bayes theorem we use in the example reads as follows: p(D) x p(+I-'-D) p ( D / t) ( p--;- ) ) +-{( -)-x-p-(-( +-:-( "' 0-))) x-p+ 1 0rvDp-
D
I
What does it all mean? First, a brief introduction to the sym bols we have used Symbol
Meaning
Example
Probability p(A) probability of A Not P("'A) probability of not A p(AI B) probability of A given B Given Looking first at the equation's numerator: p(D I +) This is what we are trying to find. For this example, it reads the probability of the diagnosis given a positive test result. Or, what is the probability that M r. Johnson has CAD given that he has a positive test result? Conceptually it is the same as the positive predictive value, and could be calculated using a 2-by-2 table. In this instance, it is being applied to a specific case rather than a patient population, and we are calculating it using Bayes theorem. p(D) The probability of the diagnosis. In this case, consider a 70 probability of CAD for M r. Johnson. p( + 1 D) The probability of a positive test result given the diagnosis. We also know that. It is the sensitiviry of the test, equal to 0 .60 for the stress ECG. I n the denominator of the equation, we repeat the numerator (the probability of disease times the true positive rate) and add the following: p ( '" D) Probability of no disease, or our subjeC[ive probability that M r. Johnson's chest pain is not the result of coronary artery disease. p
=
=
=
a. We have setried on a tentative diagnostic probability of coro nary artery insufficiency of 0 . 70 for Mr. Johnson. So, for us, p(D) 0.70 b. We know the sensitivity or true positive rate of the test to be 0.60. p(+ 1 D) 0.60 c. By subtracting, we can establish the probability that Mr. Johnson's pain does not result from CAD: p("'D) I p(D) or, in our case, 1 -.70 or 0.30. d. Last, we can look back at Table 1 9. 1 and find the false-positive rate of our test to be 22/250 or 0.09. p(+ I "'D) 0.09. =
=
=
=
Substituting the numbers in the formula, we obtain the ex pression:
Section 2 . Revising probabilitie s: Bayes theorem
=
How do we determine the appropriate numbers to fill into Bayes theorem for M r. Johnson?
p(D I +)
0.7 x O .6 =
(0.7 x 0 . 6)
+ (0.3
x 0.09)
0.42
=
0.42 0.94
+ 0 . 027
Then uSll1g Bayes theorem and starting with a diagno sis to which a probability of 0.70 was assigned (called the prior probability) and knowing the sensitivity and specificity of the stress ECG, we have learned that we can improve our prediction of CAD for this patient from 70 to 94 if the result of the stress test is positive. Another way of say ing this is the posterior probability of CAD for this patient is 94. That is a reasonable improvement, and many diagnosti cians would probably justify asking the patient undergo the test. to
Section 3. A Firefighter in his 50s with Chest Pain
In sections 1 and 2, we obtain the necessary values for our formula. First, we try to determine the probability that the patient has the disease given a negative test result (or the negative predictive value of the test). To do that, we use a combination of the following elements: The probability that he does have the disease; [P(D)] which, given the strength of his risk factors, we could set rather high, like at 0.90 (or 90% probability) . The probability of a negative test result given the disease (or the false-negative rate), which in this case is 1 - the sensitivity, or 0.40 The probability that we think the patient does not have the disease, which is 1 - the probability that he does, or 0. 1 0. The specificity of the test, which we know be 0.9 1 . to
1 9. Clinica l Pr ob/ern S olvi ng
Putting those numbers in our formula, we get the following expression: p(D) p( - I D) p(D I ) { p(D) p(- I D) } + { p( � D) x p(- I � D) } 0.9 0.4 (0.90 0.4) + (0. 1 0.9 1 ) = 0.798 x
-
=
x
x
x
x
279
We see from this illustrative analysis that our physician's inru ition was correct. Going through the formalities of probabilistic reasoning for a patienr whom we are so sure has a diagnosis of coronary artery disease that we can assign a probability of 90% tells us that a negative suess fCG result only reduces our prob ability for that diagnosis just below 80%. In fact, for this patient, we probably did not need the stress test establish the diagnosis. (Q
(Q
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OSTEOPATHIC CONSIDERATIONS IN FAMILY PRACTICE AND PRIMARY CARE
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INTRODUCTION RICHARD L. VAN BUSKIRK ROBERT E. KAPPLER
Primary care in the osteopathic profession exists as an orientation in modern medicine that emphasizes a personal and sustained or longitudinal healing relationship between the p hysician and the patient. The osteopathic primary care physician helps patients cope with both episodic declines in health and chronic health problems with maintaining health by integrating the genetic, physiologic, anatomic, behavioral, familial, social, cultural, and economic issues that affect a person's ability to sustain and, in some cases, regain health . This approach differs significantly from the limited problem- and system-specific orientation that typifies the medical and surgical specialties. Thc focus in osteopathic primary care is on a breadth of know1edge and skills that encompasses most of modern medicine. As such, the osteopathic primary care physician tends to be a gen eralist, recognizing and acknowledging the importance of the details, but always attempting to integrate the whole picture. I n this regard, osteopathic primary care physicians probably d o not differ significantly from MD primary care physicians. In both cases the gencralist orientation seems to be an issue of personality and personal preference. Patients generally present to a primary care physician regard ing a new complaint. As well, the classic general health screening performed by most primary care physicians often becomes the occasion for the early discovery o f a medical problem like hyper tension or diabetes that has not yet become symptomatic. Thus, in many cases the primary care physician is the fi rst to diagnose a patient's new health problem. As long as the problem does not demand a procedural intervention that is too complicated, the primary care physician can capably manage most preliminary care for any diagnosis. When a patient's health problems become sufficiently ad vanced or complicated or require complex therapeutic interven tion and specialist care, the primary care physician often becomes the bridge between the primary care setting and that of the spe cialist. Patients expect that the primary care physician will be able to optimize their care by referring them to the best special ist for their particular problem. Where multiple problems exist, the primary care physician will continue to provide care in those areas beyond the specialist's purview, and make sure that the pro posed treatment plan does not compromise other aspects of the patient's care. Finally, when the specialist completes their aspect of the patient's care, the patient is generally returned to the care of the primary care physician. For many patients the primary care physician is their fi rst and perhaps only contact with the U.S. health care system. The primary care physician often provides the primary diagnosis for
the patient's health problems and, in many cases, the majority of management for those problems. Health screening and health maintenance, routine care, and care for acute, time-limited dis ease are generally considered the purview of the primary care physician. Referral to special ists is reserved for those cases in which the diagnosis is incomplete, the management is beyond the individual physician's knowledge or skills, or procedures are required for which the family physician has insufficient train ing. [n some cases the medical insurance industry has attempted to formalize these roles as externally imposed standards coupled with obligatory referral approval by the insurer and penalties for noncompliance. This "gate-keeper" concept has not been well received by the medical community or by patients. However, mi nus the sanctions and the obligatory approval by the insurer, it does define in part the complex role the primary care physician plays in the health care system. In geographical areas where the number and diversity of spe cialists is large relative to the patient population and there is a paucity of primary care physicians, it is not uncommon fo r a patient to end up seeing four IiIr five different specialists in their attempt to obtain a diagnosis and treatment for a medical prob lem. This is definitely not cost-effective nor does it encourage a patient's belief that the medical care system is very effective. Where there are adequate numbers of primary care physicians, the initial diagnosis is likely to be made by the primary care physician and a well-focused referral is made to the appropriate specialist, saving time, effort, and money. The primary care provided by an osteopathic physician differs significantly from that of the M D's in its interpretation of some of the factors affecting health and disease. Both versions of primary care would freely acknowledge the fi rst two statements of the os teopathic concept: that the body fu nctions as a whole in both a biologic and social context and that it is inherently self-regulating and self-healing (see Chapter 1 ). Again, M D primary care physi cians would at least philosophically accept the idea that structure and function are interrelated. However, the osteopathic impli cation of that concept, that the musculoskeletal system plays a profound integrating role in everything from behavior, social, and interpersonal interactions to cellular, organ, and system-level in tegration in health and disease, is unique to osteopathic medicine. From this unique perspective arises the fourth principle, that ra tional diagnosis and treatment is based on the implications of body unity, self-regulation and self-healing, and the interrela tionship of structure and function. Thus all osteopathic care, including that from primary care physicians, includes the use of structural diagnosis and osteopathic manipulative treatment.
Introduction
From this perspective, osteopath ic primary care has developed with the following defining characteristics. First, it is an approach that views the patient as a unique, i ntegrated, self-regulating in dividual, united in mind, body, and spirit. No disease and no attempt to maintain health can be understood i n less than the complete context of the i ndividual, including the neuromuscu loskeletal system. Second, disease is viewed as an unnatural state, the natural state being a healthy dynamic balance. Thus when a fundamentally healthy organism is confronted with disease, it heals itself. The source of healing is within the patient. It is not the physician who does the healing, but rather the physician helps provide a context in which healing can occur. Third, when disease is present the osteopathic p hysician is charged with the task of discovering, wherever possible, the source or underlying cause of the apparent disease. Treating the patient symptomatically, while possibly useful in self-l imiting diseases, is not the desired goal for either the patient or the physician. Fourth, the osteopathic primary care physician uses all rational and scientific diagnostic and treatment methods available in the service of developing and sustaining health. This i ncludes palpatory diagnosis and osteo pathic manipulative treatment, medications, surgery, and lifesryle modifications, as appropriate. Osteopathic primary care physicians tend to focus on devel oping and sustain i ng health in their patient populations rather than more narrowly focusing on eradicating disease. This empha sis on health recognizes that healthris-l�ot a fixed state. Rather i t i s a dynamic positive i nteraction with all aspects o f one's life and circumstances. Criteria for a healthy life include: 1 . Adequate food, shelter, education, and income 2. Adequate rest and exercise 3. Adequate strength, Aexibili ty, and endurance 4. A mechanically and dynamically balanced neuromuscu loskeletal system 5. The ability to maintain functional social and interpersonal relationships
6. Freedom from or healthy control of mental impairments and i l lnesses 7.
Emotional and spiritual stability
8. Successful coping strategies that can withstand psychological, interpersonal, and biological stresses
9.
283
Strong immune responses to biological and psychosocial challenges
1 0. Good compensation for l ong-term genetic, mental, emo tional, and disease-related health issues. The uniquely osteopathi c contribution to helping the patient restore health lies i n the recognition that the musculoskeletal system is intimately involved in all of these criteria. As a result, musculoskeletal diagnosis and treatment is a fundamental and i ntegral part of the methods used by osteopathi c primary care physicians to help the patient find and maintain health. One of the common tasks for osteopathi c primary care physicians is the development of a rational exercise program that helps the patient maintain good musculoskeletal dynamic stability. One such program is that developed by Dr. Kappler (see the following section). There are fou r specialties that make up osteopathi c primary care. They are family medicine, i n ternal medicine, pediatrics, and geriatrics. Each of these specialties focuses on the longitu dinal care of the individual in their complete context, i nclud ing family, social, economic, and cultural factors along with the medical/biological factors commonly accepted as the purview of medicine. In each of these primary care specialties the osteo pathic physician seeks to estab lish a long-term relationship that involves truly getting to know the patient in order to help the patient restore and maintain health. Some specialties, like pe diatrics and geriatrics, are focused on the special problems of specific age groups. But in all four areas of specialty, the care pro vided to the i ndividual is long term and not l i m i ted to specific disease p rocesses or organ systems. Under some circumstances obstetrics/gynecology is also considered a pri mary care specialty. However, even among practitioners of that specialty, there is dis sension as to whether they are able to focus on both the general medical and the birthing and sutgical aspects of their practice i n a consistent enough fashion t o consider that they are providing a form of primary care. Finally, emergency medicine straddles the line berween being a primary practice discipline and a specialty. Its practitioners are generalists in that they deal with all aspects of disease i n all ages and both sexes. They differ from most of the other primary care specialties in that they focus on episodic acute care and, as a result, do not develop the kind of i n teractions over the long term that are typical of primary care.
284
V Osteopathic Considerations in Family Practice and Primary Care
EXERCISE PRESCRIPTION ROBERT KAPPLER
WRITING THE EXERCISE PRESCRIPTION
A complete exercise p rescription should contain the following elements: 1 . Goals of the exercise: What is to be accomplished? Assess i n i tial strength, endurance, and mobility. 2. Mode of exercise: flexibility, strength training, etc. Examples include weight l ifting, games, and swimming. 3. I ntensity: How much load or resistance? How fast or slow? 4. Duration: How many repetitions? How long do they last?
FIGURE 2. Pelvic tilt.
5. Frequency: number of sets, times per day, times per week.
6. Progression: incremental i ncrease of intensity, duration, and/or frequency. Principles and Terms
Exercises should i nvolve the patient's cerebral cortex controlli ng the muscle activity. Ballistic or uncontrolled motions must be avoided. Keep the cortex attached to the m uscle. The following principles of exercise are illustrated by examples shown in Figs. 1 through 8. To be effective, these exercises must be performed slowly so that the intersegmental m uscles of each segment are requi red to participate. Fast exercises will actually skip over the stiff areas, and the objective of the exercises will not be achieved.
FIGURE 3. Torso curl.
1 . Position to obtain relief: the constant rest position (Fig. 1 ) or bringing the thighs toward the chest to reduce a lumbosacral hyperextension. 2. Passive stretching: the physician stretches the muscle. 3. Active stretching: the patient stretches the psoas by extending the hip. 4. Use motion to promote circulation of tight, congested mus cles: getting out of bed and walking around the room. 5. Use exercises to mobilize tight, stiff, restricted areas: activate muscle contraction to provide shoulder rolls and mobilize the shoulder girdle area. FIGURE 4. Reverse torso curl.
FIGURE 1. Constant rest position.
FIGURE 5. Torso (back) extension.
Introduction
�
...-"
�
--------�
,,
, ,,
,,.
285
�
FIGURE 6. Hip hyperextensions (psoas resets).
6. Use exercises to strengthen weak areas: curls or sit-ups strengthen abdominal muscles. 7.
Use exercises to im ptove spinal motion so that all segments of the spine contribute to total motion. The objective is to provide for smooth, coordinated spinal motion: core exer cises focusing on the trunk include torso curl, reverse torso curl, and torso (back) extension.
8. Use exercise to provide stability, strength, and endurance throughout the range of motion. This type of exercise re quires multiple repetitions with a moderate significant resis tance. 9.
There is a continuum within the spectrum of exercise. Es tablish an acceptable range of motion fi rst. This i nvolves eliminating specific restrictions as well as achieving an over all range of motion. Strength, stability, and endurance fol low. The trophic stimulus of active exercis(si:?engthens all tissues involved (bone, connective tissue), not j ust muscle.
1 0. Group activity has a much higher compliance rate than does individual effort. The body is no stronger than its weakest link. Many well conditioned patients have a back or musculoskeletal problem that severely limits their function. The physician should direct treatmem to strengthen the weak l ink. The proper dosage o f exercise may b e mini mal. An overdose w i l l cause harm a n d worsen the condition. Physically active patients instinctively look for an exercise program tailored to the strong parts of their body without regard for the weak link. Pursuing exercises with type A aggressive behavior will usually make a condition worse, not better. It is
A
B FIGURE 7. A: Angry cat (raise chin and sway back). B: Angry cat (tuck chin and arch or raise back).
...._--
--_ ....
.,,
, ,.
�
,
t
FIGURE 8. Cervical isometrics.
impossible to know what exercises are right for any given patient without the patient actually trying them. Exercises must stop short o f pain. Pain is an indication that the joint i s being stressed or overloaded. The object is to find ways to strengthen the muscle and tissues without causing more in j ury o r stress to the joint. Discomfort, as with stretchi ng muscles, is acceptable. Avoiding inj ury or stress to joints often requires an exercise program specifically tailored for the patient. For pa tients who compulsively exercise, the exercise prescri ption may decrease their activity level from excessive to appropriate. Giving healthy patients a pamphlet containing a series of standard exer cises is acceptable, but this is not sui table for patients with health problems. The dose o f exercise may vary from day to day. One day, a patient may be able to do an exercise easily. On another day, the exercise may cause pain and the patient cannot tolerate the exercise. Patients should be instructed to reduce the intensity of an exercise when appropriate and always told to stop short of pam. Flexion and extension should be performed in the same ex ercise session. Flexion and extension exercises for the spine must p recede exercises i nvolving rotation and side bending. This order comes from the following biomechanical concept: Aexion and extension are pure and uncoupled motions. If free Aexion and extension motion can be obtained, rotation and/or side bending will i ntroduce group motion rather than single segmental mo tion. Most spinal motion i nvolves neutral or type I mechanics. This type of motion is group motion, defined as a number of contiguous spinal segments contributing to an overall positional change. By contrast, local spi nal dysfunctions often produce non neutral mechanics (type II). This effect localizes force to a single segment. A strong, functional extremity m ust be attached to a strong trunk. A strong limb is no better than the trunk to which it is attached. Programs to strengthen extremities, therefore, should i nclude the trunk. Osteopathic diagnosis and osteopathi c manipulative treat ment (OMT) to relieve somatic dysfunction or fascial tension of the spine and/or extremities may be the key to a successful
286
V Osteopathic Considerations in Family Practice and Primary Care
exercise program for the patient. OMT can provide improved motion of the spine, which makes it possible for the body to compensate, mobilize, and strengthen. Patients often ask if it is acceptable to perform certain exercise activities. If it does not hurt, the activity is probably acceptable. If the patient develops d iscomfort later, such as the next day, the dose of activity should be reduced. While there is a proper time for rest following inj ury, bed rest and inactivity do not increase muscle strength. The rehabil i tation phase requires active work on the patient's part. Continued inac tivity will only lead to a progressive cycle that incl udes weakness, reduced resistance, and increasingly severe clinical consequences resulting from minor stresses. We sometimes refer to these pa tients as deteriorating. The osteopathic philosophy encourages physicians to get involved with their patients. Physicians must be prepared to help patients fully recover or be rehabilitated through physician i nstruction and monitoring of a good exercise program. All physicians are encouraged to seek health with their patients. SPECIFIC PROBLEM AREAS OF SPINAL DYSFUNCTION Extended Somatic Dysfunctions of the Spine
tends to restrict extreme hyperextension ofL5 so that the patient can tolerate the spinal extension exercises. Lumbar Disc
Lumbar disc problems usually will not tolerate a Aexion load of the lumbar spine. Flexion exercises are, however, usually indicated in these patients. I f the patient's head is elevated to reduce the gravitational load and a slant board is used for sit-up or curl ab dominal exercise, lumbar exercises are much easier for the patient to tolerate.
ILLUSTRATED EXERCISES FOR PATIENTS
The illustrated exercises for patients that follow each include a series of instructions directed to the patient's perspective. Constant Rest Position
The purpose of the constant rest position is to reduce lumbar and cervical lordotic curves and relax paraspinal and psoas muscles. This position reduces lumbar intradisc pressure. Instructions:
The motion restriction is flexion (forward bending) with in creased freedom o f extension. Extension exercises are essential for treatment of extended somatic dysfunction of the spine. Flexed areas (extension restriction) above and below the extended dys function will mai ntain the area of dysfunction. Extension ex ercises address the flexed areas that maintain the segment with extended dysfunction. Hyperextension, however, is pain fu l for these patients. I f the upper thoracic interscapular area is involved and the patient must perform a prone spinal extension exercise, excess extension can be controlled by limiting extension of the head and neck. This is accomplished by keeping the patient's chin roward the chest.
The purpose of the pelvic tilt is to strengthen lower abdominal muscles and reciprocally inhibit lower lumbar paraspinal muscles.
Neck Pain
l.
Neck pain is often associated with instability of some of the cervi cal j o i nts. Active exercises are necessary to strengthen and stabilize those weakened segments of the cervical spine. First, find a dose of strengthening exercises that will work without causing pain. Mild isometric exercises with the neck in a comfortable neutral position often fit this starting point. The circumduction neck exercises (neck rolls) that were often recommended by physicians in the past have been found to localize the forces to the unstable area and compound the instability that is present. Lumbosacral Pain
The L5 is the most mobile of the lumbar segments, and it is of ten unstable. Patients with backache need extension exercises to strengthen paraspinal extensor muscles, yet it is common to find L5 extended (backward bent) while the upper lumbar region is flexed. In this position, extension movement of L5 will produce subjective pai n . The extension exercises can be performed com fortably if you position your patient prone on the table and place a pillow or pillows under the pelvis to flex L5. This positioning
l.
Place your lower legs on a chair or on a similar device.
2. Position your torso so that your thighs are perpendicular to the Aoor or even at a 45-degree angle with the abdomen (Fig. 1). 3. Place a pillow under your head. Remain in this position 15 to 20 minutes. Strengthening Exercises
Pelvic Tilt
Instructions:
Start from the constant rest position or, alternatively, lie with your thighs Aexed and feet on the Aoor.
2. Attempt to curl your buttocks off the ground, Aattening the l umbar curve to the Aoor (Fig. 2). 3. Hold for a few seconds, then return slowly.
Torso Curl (Crunches) The purpose of the torso curl is to strengthen the upper abdom inal muscles and inhibit the paraspinal muscles. Instructions:
1. Start from the constant rest position or supine with thighs flexed. The psoas muscles must be relaxed and not used in the exercise. 2. Place fi ngers on abdominal muscles. 3. Tuck chin down and in. 4. Slowly curl head and then shoulders off the Aoor (Fig. 3). 5. Continue to ascend upward, with each vertebra moving off the Aoor individually rather than as a group.
Introduction
6. Hold top position. 7. Rerurn slowly to starring position. The slow approach can be accomplished with a counr of four-four-four: four counrs up, hold for four counts, four counrs down.
Reverse Torso Curl The purpose of the reverse rorso curl is to srrengthen the lower abdominal muscles. This exercise is a progression from the pelvic tilr. Instructions: I.
Lie supine on the Aoor.
2. Rest your hands at your sides or grasp the end of the table over your head. 3. Draw your knees to your chest, Aexing knees and hips as far as possible. 4. Using your lower abdominal muscles, slowly curl buttocks off the ground to the approximate level of TI2 ( Fig. 4). 5. Hold this position for a few seconds, then return slowly. Use the four-four-four counr.
Torso (Back) Extension The purpose of the torso extension is to stre,(grhen the paraspinal muscl es. Precaution:
This exercise can increase low back pain, especially in the acute state. Hyperextension ofL5 can be painful in some patienrs. The patienr must be cautioned to stop shorr of pain. I f back pain be comes worse by doing this exercise, even i f it does not hurr at the time, it should be stopped or the number of repetitions and/or duration of each repetition should be decreased. Sometimes plac ing one or more large pillows under the pelvis will Aex L5 and allow the exercise to be done without pain. Instructions: I.
Lie prone on the Aoor.
2. Place your hands at your sides with your thumbs poinring our. 3. Keep your chin tucked in, mainraining your head in line with your torso. 4. Slowly raise your head and torso off the Aoor (Fig. 5). 5. Hold the position; return slowly to the Aoor. Use the four four-four counr.
287
Instructions:
1 . Lie prone on the Aoor, hands under the anrerior superior i liac spine (ASIS). 2. Keep your chin rucked in. 3. Slowly raise one leg, keeping the knee locked and the ASIS pressed into the hand (Fig. 6). Note: Once hip
extension is maximized, additional movemenr of the thigh (upward) is achieved by rotating the pelvis, which is not desired. By keeping the ASlS pushed into the hand, pelvic rotation is avoided.
4. Hold the position for a few seconds; return slowly to rhe Aoor. 5. Repeat for both legs.
Angry Cat The angry cat exercise is designed to relax the low back muscles and to relieve the spasm or cramp that causes pain in the lower lumbar region. This exercise eases tired backs and minor aches and pains caused by bad posture. It will help a person stand erect withour pain, even after a rough day. Instructions:
I. Get on all fours on the Aoor. 2. Keep knees and hands apart. 3. Arch the back and l i ft up the chin ( Fig. 7A). 4. Arch as much as you can. Lift the chin as h igh as you can. 5. Raise your back and tuck in your chin (Fig. 7B).
6. Raise your back as high as you can. 7. Tuck in your chin as close as you can. 8. Combine these movemenrs inro one smooth exercise; do not pause.
Cervical Isometrics The purpose of cervical isometrics is ro strengthen the neck by performing isometric exercises. Instructions:
I. Flexion: place the hand on the forehead, push the forehead inro the hand, but do not allow the head to move ( Fig. 8). 2. Extension: place the hand on the back of the head. 3. Side bending: place the hand on the side of the head.
Hip Hyperextensions (Psoas Resets)
4. Rotation: place the hand on the side of the head, sl ightly more anteriorly than when doing the side-bending exercise.
The purpose of hip extensions is to stretch (lengthen) and recip rocally inhibit the psoas muscle.
5. Amounr of force: starr with a mild amounr (35 pounds), and increase as needed.
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OSTEOPATHIC FAMILY PRACTICE: AN APPLICATION OF THE PRIMARY CARE MODEL RICHARD L. VAN BUSKIRK KENNETH E. NELSON
The role of the primary care physician, ro a significant degree, has defined osteopathic medicine for over 100 years. As recendy as 30 years ago, more than 70% of osteopathic physicians pracriced primary care medicine (1). Most of these were general pracri tioners, the precursors ro roday's fam ily practice physicians (see Chapter 2). The percenrage of primary care physicians in osteo pathr: medicine at the start of the 21st cenrury hovers berween 56% and 58% (1), and the American College of Osteopathic Family Physicians is the largest componenr group of the American Osteopathic Association. The reason for this is pardy due ro the fundamenral narure of osteopathic philosophy and pardy a result of the social-political environmenr in which osteopathic medicine evolved. The facror that most i nfluenced the osteopathic focus on pri mary care was the osteopathic philosophy itself (2,3; see also Chapters I and 2). With the osteopathic emphases on the dy namic uniry of the i ndividual human being and the i nrerlocki ng aspects of form and function, there was little room ro consider the individual organs as having meani ngful function indepen denr from the whole bei ng. Dr. A.T. Still's diagnosric merhods involved examining the whole of human anaromy for areas of dysfunction that could be caus i ng a problem thar presenred as "disease," even ar sites well distanr from the local manifestation (2,3). Likewise, focus on "sysrems" rhat span the whole body, such as the circularory/lympharic and neural nerworks, as the i nregra rors of health and disease, tended ro reinforce rhe osreopathic propensiry ro treat the whole person. Other hisrorical facrors merely served ro rein force this na tive osteopathic orienrarion roward primary care. These i nclude the predomi nandy rural and small rown narure of early osreo pathic pracrices and the unfortunate half cenrury of exclusion of osreopathic physicians from allopathic residencies and research programs. This hisrory is well detailed elsewhere (see Chaprer 2). Today's osteoparhic family physicians are trained and cerrified ro pracrice as primary care physicians in the fields of osteopathic medicine and surgery. They are one of rwo osreopamic specialry groups whose cerrification specifically includes osteopathic ma nipulative treatmenr (OMT). They assume the responsibiliry of their patienrs' comprehensive and conrinued health care and act
as a coordinaror of the patienr's health services. They accept the rotal conrinuing responsibiliry for the patienr and/or the fam ily as a whole. The osteopathic family physician recognizes the need for and uses qualified consultanrs when medical or surgical conditions warranr such professional expertise. The osteopathic family physician may devote particular arrenrion ro one or more other fields of specialry practice, such as addiction, geriatric, and adolescent and young adult medicine (1).
OSTEOPATHIC FAMILY MEDICINE AND PRIMARY CARE
Osteopathic medicine has always used the inrerdependenr knowl edge and skills o f generalists and specialists working rogether: the generalist with broadly developed skills and knowledge of many differenr disciplines and the specialist with substantial in-depth knowledge and skills in more narrowly defined areas. Conrem porary fam ily medicine represents a unique development in the evolution o f health care delivery. The fam i ly physician must be a generalist ro effectively deal with the broad spectrum of problems encountered in practice. However, the family physician is i ndeed a specialist in the longirudinal coordination of multiple diverse problems inro a holistic (in the individual, fanlily, and greater social conrext) patient-oriented system of health care. The fam ily medicine model i m plies the presence of personal accessibility, availabiliry for a variery of medical and b iopsychosocial prob lems, and willingness ro coordinate most aspects of conrinuing personal and fam ily-related health care (4,5). Because primary care physicians' skills and i nformation base need ro encompass the breadth of medical knowledge, there is a tendency on the part of some ro assume that the lesser degree of focus and depth of knowledge relative ro a specialist equals less qualiry in medical care delivery. This is unrrue. Several out come studies exami n i ng the medical care delivered by primary care physicians versus that of specialists suggest that there is no significant qualiry difference (6,7). Osteopathic fam ily physicians work with patienrs from cradle ro grave. This broad acceptance of patienrs of all ages produces
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V Osteopathic Considerations in Family Practice and Primary Care
several of the unique focuses of family medicine: (a) longitu dinal care; (b) care of the individual in the family and social context; and (c) care of multiple generations of the same family. In fact these longitudinal, holistic, patient-oriented aspects of os teopathic family medicine more easily lend it to the application of classic osteopathic principles than possibly any other specialty area of medical practice. It is in these contexts that this chapter will evaluate osteopathic family medicine. Many of the concepts to be explored are shared by the other osteopathic primary care specialties and as well by nonosteopathically trained family physicians. I t is beyond the scope of this chapter to evaluate all components of family prac tice in detail. Textbooks of family medicine are available for the reader who wishes to pursue this subject in depth (4,5). This chapter is intended to provide a general overview o f the nature of family medicine in an osteopathic context and, where appropri ate, emphasize those aspects of osteopathic family medicine that are distinctive in contemporary medicine.
THE WHOLE PERSON AND DISEASE
To find health should be the object of the doctor. Anyone can find disease (2). -AT Still, Philosophy o/Osteopathy A tendency to consider disease the appropriate focus of health care exists in both popular thinking and in the generally used medical model. While some attention is given to "preventive medicine," the focus is on the diagnosis, treatment, and man agement of disease. It is as if disease were the natural state of human beings. [n the general osteopathic model and in osreo pathic family medicine the focus is on the development and maintenance of health. In the osteopath ic model the normal, balanced, and integrated human o rganism can generally avoid infection, even though pathogenic organisms colonize the body. A person can avoid most other disease as well, and those ill nesses that cannot be avoided often can be recuperated from readi ly, provided a healthy environment is maintained and stres SOl'S are controlled in the context of structural integrity and balance. Disease, when it occurs, is considered to be a disturbance of the innate dynamic balance of health. Genetic predisposition, inappropriate immune response, dietary insufficiencies or in discretions, emotional upheavals, familial-social-economic stress, environmental stress, and/or musculoskeletal disturbances can perturb the body's dynamic balance. Many of these factors can co exist. Disease occurs when such perturbations, particularly those of a long-term nature, overwhelm the body's natural compen satory mechanisms. The body's abi lity to compensate is such that most individuals maintain what they would characterize as "good health" for most of the time, even in the presence of chronic disease. It is the objective of the physician to restore and maintain the patient's balance of health. The primary care objectives of the osteopathic family physician extend beyond acute episodes and interventions into the longitudinal maintenance of health and stabilization of disease where it cannot be eliminated.
It is clear that most disease has widespread effects. Although it may be convenient to classifY a particular disease as being focused in a particular organ, it is rare that a disease does not have effects throughout the body. An obvious example is seen in cardiovascu lar disease where effects are found from the smallest capillaries to the heart itself, thereby affecting the whole body. A similar exam ple is seen in diabetes where an endocrine disorder has vascular, neural, renal, and immunologic effects. A less obvious example that will further illustrate this point can be seen in pharyngitis. Typically, pharyngitis produces both local pain in the throat and a more generalized body ache and malaise. These symptoms require both nociceptive neural activa tion and a general alteration of central and autonomic neural ac tivity. Inflammation arises due to local ized and systemic immune activation, with altered macrophage, lymphocyte, and monocyte responses. Fever develops from altered temperature control mech an isms as a method of weakening the invading organism. Fatigue and loss of appetite are mediated by glucose-insulin, glucocorti coid, and tumor necrosis factor activity. Local pharyngeal pain and inAammation is associated with congestion and lymphedema of the pharyngeal and anterior cervical soft tissues. Neural reAex mechanisms mediated through the trigeminal and sympatheric nerves produce viscerosomatic reAexes in rhe upper cervical and upper thoracic regions (8,9). Similar to this example, based upon the experience of generations of osteopathic physicians, there is local, general, and segmentally related spinal musculoskeletal in volvement in virtually all disease.
OS TEOPATHIC DIAGNOSIS AND TREATMENT OF DISEASE
Despite the impressive strides that have been made in the pqgt 60 years, contemporary medical methods of diagnosis and thera peutics remain significantly less than perfect. Modern laboratory studies and noninvasive imaging have significantly improved our ability to diagnose disease. Yet, false posi tives and equivocal re sults continue to raise questions as to the correct diagnosis. The best diagnostic tools are often very expensive or the diagnostic al ternatives are too diverse for the patient or the health care system to be able to afford all of rhe tesrs available. Established traditional methods of h istory taking and physical examination still provide the best foundation for clinical decision making and often al low the physician to Iimir the number of addi tional procedures necessary to attain a diagnosis. Tradi tionally, the best treatment plan was based on patterns learned from mentors and/or one's experience with patients. The current move toward what is termed "evidence-based medicine" would appear to be a useful additional tool in as much as it pro vides some guidance as to what is or is not an effective treatment for a specific disease. On the other hand, even in rhe face of the most rigorous diagnostic criteria and a trearment plan based on the most rigorous scientifically proven data, patients con tinue to confound us with their individual variation in response and tolerance to our treatments and their side effects. Therefore experienced family physicians often use multiple strategies. Os teopathic family physicians have a special advantage when using palpatory diagnosis and manipulative treatment.
20. Osteopathic Family Practice
THE ROLE OF PALPATORY DIAGNOSIS AND MANI PULATIVE CARE
A basic osteopathic principle states that the neuromusculoskele tal system is functionally and inextricably linked with all body systems. A corollary of this concept is the explicit statement that disease and musculoskeletal dysfunction are also i nextrica bly linked. This is the fundamental principle behind somatic dysfunction. Somatic dysfunction is functional impairment with its primary manifestation i n the neuromusculoskeletal and fascial systems. Although somatic dysfunction may exist in the presence of pathology, it is not in itself pathology. As noted in Section I I , the basic science section o f this text, somatic dysfunction has the potential for negatively affecting both the i mmune and endocrine systems as well. When treati ng a patient with any health problem, one can determine how to int egrate the treatment of somatic dysfunction into the therapeuric protocol by asking the following questions: I . How is musculoskeletal dysfunction affecting the ability of the person to function? Whether one is dealing with activ ity restrictions as the result of pai n or gait and other body use disturbances, this is the most obvious manifestation of somatic dysfunctiPn and the one that becomes the occasion for almost universal musculoskeletal treatment by osteopathic physicians. 2. How are musculoskeletal and fascial dysfunctions affecting the patient's abi l i ty to respond to disease processes? The mechan ical component of somatic dysfunction results in restriction of motion. The compromising effect of thoracic cage somatic dys function upon the patient with chronic obstructive pulmonary disease is an example. 3. How is ci rculatory stasis affecting the patient? Efficient movement of the thoracic i nlet, thoracic cage, abdom inal di aphragm, mesenteries, and pelvic diaphragm i s necessary for op timal low-pressure fluid (lymphatic and venous) dynamics and tissue perfusion. Inefficiency of this mechanism further adds to the tendency for tissue congestion. Somatic dysfunction of the extremities can compromise arterial, venous, and lymphatic flow. 4. What sympathetic somatovisceral mechanisms are present? Spinal facilitation associated with thoracic and upper lumbar so matic dysfunction results in increased sympathetic tone to seg mentally related structures. 5. What parasympathetic somatovisceral mechanisms are present? Spi nal facil itation associated with high cervical and sacral somatic dysfunction results in increased parasympathetic tone to segmentally related structures. 6. What organ level dysfunctions are manifesting in muscu loskeletal and fascial restrictions and tissue texture changes?
The first three questions address predominantly the mechan ical effect of somatic dysfunction upon the patient. The fourth and fifth questions deal with the impact of somatovisceral reflexes upon the patient. The sixth question relates to what have been termed the viscerosomatic reflexes. Each of the first five questions focuses on direct effects of pri mary somatic dysfunction on the general functional level of the individual. Each represents part of the most obvious clinical manifestation of the effects of the musculoskeletal system on the function of the body as a whole. All five of these questions are
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consi dered valid reasons for treating the musculoskeletal system. While it may be tempting to restrict musculoskeletal treatment to only those manifestations oriented around the first question, the other four are equally valid. Thus OMT is i n dicated for the specific treatment of the neu romusculoskeletal man ifestations of somatic dysfunction. OMT is used to i ncrease available motion, modi fy activity of the ner vous system, and increase tissue perfusion. The experience of the osteopathic profession is that OMT is often sufficient for recovery from a variety of conditions, including many that are not specifi cally musculoskeletal in nature. Part of this effect i s undoubtedly due to the interactive effects of the musculoskeletal system on the fascia, circulation, and the autonomic nervous system. D iseases are often the result of structural disorders relati ng to both the viscera and the somatic system. I n current terms, there is close interleaving of visceral, autonomic, neural, immunologic, and musculoskeletal systems (see Chapters 7, 9, 1 0, and 1 3). As fi rst propounded by A. T. Still with the founding of the profession, the key to restoration of health is to enable the body's own restora tive mechanisms (2,3). For example, based on the experience of the osteopathic community in the 1 9 1 8 i nfluenza epidemic ( 1 0), and on the general experience of osteopathic physicians over the past 1 00 years, OMT should have some added benefit in the recovery from at least some viral i l lnesses ( J 1 - 1 8). However, i t should b e noted that formal outcome studies supporting the use of OMT in the treatment of nonmusculoskeletal disease is sparse 0 3-22). Finally there is the viscerosomatic relationship between dys functions in the viscerae and the musculoskeletal system. Palpa tory evaluation of viscerosomatic reflexes has been used as a diag nostic tool by the osteopathic profession for at least a century. As demonstrated both clinically and in the laboratory (8, 1 2, 1 3-32), viscerosomatic reflexes are present with a wide variety of disease. They develop in response to visceral pathology. Although there is considerable overlap in the presentation of these reflexes for var ious viscera, they can help the osteopathic physician distinguish between various potential diagnoses (Table 1). Viscerosomatic reflexes are identifiable as tissue texture abnormality and tender ness in the dermatomes and myotomes that are embryologically and neurologically related to the viscera that sti mulate them. They are most easily palpable i n the paravertebral soft tissues. A pure viscerosomatic reflex, withour concomitant mechanical spinal somatic dysfunction, generally will demonstrate tissue tex ture abnormality and tenderness proportionate to the degree of visceral pathology in the absence of definitive restriction of mo tion. The tissue texture abnormali ty may or may not demonstrate leftlright asymmetry, but there will not be vertebral positional asymmetry. One of the dilemmas of osteopathic musculoskeletal medicine is the differentiation between a viscerosomatic reflex and pri mary somatic dysfunction. Johnston and Golden, however, have recently suggested that there are significant differences in the patterns that can help disti nguish the two (33). Viscerosomatic reflexes, like primary somatic dysfunction, cause muscle spasm, tissue tenderness, and pain. For i nstance, the pudendal nerve (S2-4), a branch of the pelvic splanch n ic nerves, innervates the pelvic diaphragm. Pain in the pelvic floor may be viscerosomatic (pelvic parasympathetic) in origin , or it may simply be the result
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V Osteopathic Considerations in Family Practice and Primary Care
TABLE 20. 1 . VISCEROSOMATIC REFLEXES Card iovascular
Respiratory
Gastrointestinal
Urinary
Reproductive
Endocrine
Cardiac rate/rhythm
T 1 -2, C2 left (vagus)
Myocard ium
T3-S left (T3-T4 right)
Nasopharynx
T 1 -4, occiput-C2
Larynx and trachea
T 1 -4
Lung parenchyma
T3-4 Iateralized
Bronchomotor
T 1 -3 lateralized (T2 left)
Bronchial mucosa
T2-3 lateralized
Vagus
C2 more common left
Oropharynx
T 1 -2
Esophagus
T2-4 right
Stomach cardiac area
T4 right
Stomach fundus
TS l eft
Stomach pylorus
T6 left
Duodenum
T6-S right
Small intestine
TS- 1 0 right
Cecum and appendix
T l 2 right (tip of 1 2th rib)
Ascending colon
T l 2-L 1 right
Descending colon
L2-3 l eft, 52-54
Pancreas
T6-S bilateral
Liver and gallbladder
T l O right
Kidney
T 9- 1 1 lateralized
Ureter
T l 1 -L3 lateralized
Bladder
L2-3 (T 1 1 -4), 52-4
Gonads
T l 0 lateralized
Uterus
T l O-L2 bilateral, 52-4
Fallopian tubes
T 1 1 -L 1 lateralized, 52-4
Prostate
T l 2-L2, 52-4
Pituitary
C 1 -2 (midcervical and
Thyroid
T2, C2 vagus, upper
upper thoracic), cranial thoracic "flexion hump " Thymus
Upper thoracic, C2 vagus
Pancreas
T6-S bilateral, C2 vagus
Adrenal
Adrenal
of a primary sacropelvic somatic dysfunction. Proper application of O MT should resolve primary somatic dysfunction. Although viscerosomatic reflexes can be affected by O MT, typically vis cerosomatic findings will not resolve until the underlying visceral condition is treated. T herefore failure of somatic dysfunction to respond to properly applied OMT should lead to the consid eration of a viscerosomatic etiology. I ndeed, evaluation of any somatic dysfunction should include inquiry about segmentally related viscera. Example: A 53-year-old man presents with a chief complaint of substernal chest pain with some pain i n his left shoulder. He is a building contractOr who continues to " keep h is hand in" as a carpenter. He denies shortness of breath, diaphoresis, o r nau sea. He has an absolutely benign medical histOry and no histOry of trauma. Both maternal and paternal grandfathers, his father, and one of three brothers had cardiovascular disease. Primary differentials would include cardiac disease, esophageal disease, musculoskeletal dysfunction or disease, and the remote possibil ity of pulmonary disease. Physical examination reveals no sig ni ficant cardiac or pulmonary findings. Epigastric tenderness is noted without guarding, organomegaly, or masses. The muscu loskeletal examination reveals somatic dysfunction involving the left cervical spine, thoracic spine, fi rst and third ribs on the left,
and a bilateral area of tissue fullness and edema (23, 25) present at T7 but none at T l th rough T4. The patient also shows ten derness of the left third costOchondral junction, bur it does not reproduce his pai n . Additional findings include Chapman reflex tender points for the cardia of the stOmach and esophagus (34) (see Chapter 67). An electrocardiogram demonstrates normal si nus rhythm without any ST elevation or depression. Even with such findings physicians traditionally have been forced to instigate an emergent full cardiac workup given similar complaints and h istOry. However, with musculoskeletal diagnos tic tOols, an osteopathic physician would be fairly comfortable reassuring the patient that his chest pain is probably from reflux esophagitis. Treating his somatic dysfunction relieves parr of his thoracic discomfort as well as diminishing vagal and sympathetic inputs that may be affecting the general functional level of the viscera. Dietary and lifestyle changes suggested by the physician should contribute to diminishing h is esophageal symptOms. As well, the physician might consider a prescription of a peptic acid secretion inhibitOr as a functional test and treatment for the pa tient's gastroesophageal reflux. Finally, because of his family his tOry and age it would be prudent to obtain a lipid profile and in stigate a cardiac stress test to ensure that there is no cardiac disease. These tests do not need to be performed emergenrly but rather as an expectant evaluation of the patient's general health risks. It is well established that musculoskeletal dysfunction at some level is the rule, rather than the exception, even in the healthy pop ulation. Denslow and Korr first demonstrated this in their pub l ished work with the sympathetic nervous system (26,27,35 ,36). Even though neuromusculoskeletal complaints might not be the chief complaint or mentioned in the histOry, knowledgeable pal patOry examination commonly identifies tender and painful mus culoskeletal sites associated with classically defined somatic dys function. Because these findings are so common, their origins and significance require careful thought. It is common to have patients present with visceraJly related findings and associated asymptOmatic sites of somatic dysfunction. It is reasonable to suppose that similar asymptOmatic somatic dysfunction sites ex ist in the general population without clinical symptOms. For such a group, one assumes that the somatic dysfunction represents a potential disease trigger, a somatOvisceral reflex, or a signal that latent or subclinical disease or impairment is present (a viscero somatic reflex). This offers opportunity for early diagnosis or the i n itiation of preventive efforts. In either case the presence of such somatic dysfunction is more l ikely to be recognized in the primary care setting by the astute osteopathic family physician. Musculoskeletal treatment and palpatOry diagnosis are fun damentally safe. There are few specific conrraindications for the use of OMT, although some OMT techniques are relatively con traindicated in some specific circumstances (see Chapter 72). There are three other reasons why an osteopathic physician might not use OMT on a patient. First, if the physician is uncomfort able performing OMT because of a perceived lack of skill, it is probably better to refrain from using OMT for complex cases until further training has been obtained. Second, an absolute con traindication for the use of OMT would be a patient's refusal. Third, in some circumstances the patien t's culture may prohibit or limit such treatment, for instance, some religious beliefs pro h ibit patients from being treated by physicians of the opposite
20. Osteopathic Family Practice
sex. It is very imporrant that the osteopathic family physician be sensitive to an individual's psychological, social, and cultural beliefs and orientations in such cases.
TREATING THE WHOLE PERSON
It is a fundamental philosophic commitment of the osteopathic profession that we should be treating the whole person: body, mind, and spirit. Certainly, few thoughtful students of mod ern medicine would entertain the idea that the physician's job is only to treat the patient's body. However, l ike medical students throughout the world, osteopathic students are often taught i n such a way that individual organs and body systems seem to function as discrete entities. This reductionist teaching strategy makes it easier to communicate fact-based concepts and ideas. Its weakness, however, is in the lack of explicitly stated systems integration, which is left to the student to figure out on their own. Osteopathic education is at its best when integrative think ing and problem solving are emphasized. This is accomplished by highlighting the importance of i nterdependent structure and function concepts. The recognition of the role that the nervous system plays in integrating the body into a holistic mechanism, and the significance that somatic function and dysfunction play in that mechanism, greatly facilitates such integrative thinking and problem solving (27). During family medicine residency and thereafter in the pro fessional life of the osteopathic family physician, the emphasis on treating the whole person is expanded upon and stressed. Patient care includes many strands including the physical care of the in dividual, emotional health and healing, the family context, and the social, ethnic, work, and economic context of the individual. This often extends beyond the individual patient to include deal ing with the whole family, and in many cases, the community context in which the patient and the physician reside. As in most of the rest of medicine, the osteopathic fami ly physician often deals with the acute manifestations of disease. Beyond the necessity to treat the current disease, these episodes offer the opporrunity to evaluate and manage long-term health risks. Because family practice often includes care for more than one generation of a given family, the physician may possess a greater awareness of patients' genetic and lifestyle risk factors than patients are aware of themselves. Exam ple: A 22-year-old woman develops episodic anxiety, palpitations, and fatigue, chronic myalgia, and inability to lose weight after giving birth to her fi rst child. The physician has treated her grandmorher, morher, one uncle, and one aunt and an adulr child. The grandmother, mother, and the aunt all have Hashimoto thyroiditis. The physician is aware of this informa tion even though the patient herself does not know or understand that aspect of her family's health. This h istory is taken as adequate ground for investigation of the thyroid gland for palpable irreg ularities and evaluation of antithyroid antibodies to determine whether the patient may have developed Hashimoto thyroiditis. Of course, other potential etiologies must be considered, includ ing viral infection, postpartum depression, musculoskeletal dys function, or persistence of gestational diabetes, if that had been present.
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When the patient's genetic and lifestyle risks are not known, the osteopathic family physician will engage i n a h istory taking process that will help determine contributing causes for the cur rent episode. Example: A 38-year-old woman presents as a new patient with a complaint o f weight gain, low back pain, and urinary frequency and urgency. The osteopathic family physician eval uates not only the patient's urine, but her personal and family history as well. This patient's history i ncludes multigenerational adult-onset diabetes mellitus and heart disease and a personal h istory of hypertension, excessive thirst, and frequent urinary tract infections over the past 8 months. The prudent and appro priate evaluation and treatments will include obtaining a urine specimen for immediate dipstick evaluation and for culture and sensitivity. If i ndicated by physical examination and the urine dipstick evaluation, empiric antibiotics may be prescribed while awaiting urine culture results. Whether or not a urinary tract infection is present, somatic dysfunction will be found with in volvement of at least the thoracolumbar and sacral regions. This will be treated with OMT both to imptove the patient's comfort and to ameliorate any somatovisceral reflexes (frequency and ur gency). Theoretically, additional benefit is derived from somatic modulation of the immune functions (see Chapters 1 4, 20, and 26) although this has not been empirically demonstrated in the case o f a urinary tract i n fection. Laboratory studies will evaluate possible diabetes and/or thyroid d isease. Obviously the long-term consequences of diabetes would be much more clinically significant than the short-term p roblems o f weight gain, a urinary tract infection, a n d lumbosacral somatic dysfunction. Whether the patient should p tove to have diabetes or merely have a strong genetic propensity for it, the appropri ate treatment would include such lifestyle modifications as a diet restricting simple carbohydrates and an increase i n exercise. Thy roid and antihypertensive treatment will be initiated i f clinically indicated. Long-term plans for the patient should include peri odic monitoring of her blood pressure and body weight along with laboratory tests for fasting serum glucose, l ipids, and possi bly thyroid-stimulating hormone. When the current episode of d isease has presented multiple times in the patient's past, focus may be on potential underlying disease processes and lifestyle issues that have not been addressed heretofore. Example: A 43-year-old man, the father o f rwo school-age children, who is a known smoker, presents with his third episode ofacute btonchitis i n as many years. It would be appropriate to ask about any viral illnesses in his family and to get a chest radiograph and complete blood count, as well as perform a flow-volume-loop pulmonary function test. Additionally, it would be appropriate to review h is personal h istory for any childhood asthma (very o ften adults will fai l to report this or minimize it as having no rele vance to the present) and inquire as to fami ly history of asthma. Treatment could involve the use o f bronchodilators and possible inclusion of a penicillin-derivative cephalospori n, or macrolide antibiotic i f the episode has been prolonged. Any somatic dys function should be identified, particularly in the cervical and tho racic spine, the ribs, thoracic i n let, respiratory diaphragm, and accessory muscles of respiration. OMT will be useful to allevi ate musculoskeletal d iscomfort that inevitably accompanies acute
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V. Osteopathic Considerations in Family Practice and Primary Care
bronchitis, as well as to i mprove depth o f respiration, vascular and lymphatic function, and the immune response (11,12,14,20,21; see also Chapter 10). Additionally, the episode becomes an oppor tunity for the physician to reemphasize to the patient the need to stop smoking both for his short-term and long-term health and that of his children. Should the acute episode of bronchitis lead to a diagnosis of asthma, that diagnosis would h ave obvious long-term implications for the patient's health. These three examples demonstrate the principles of multigen erational care, genetic/famil ial and lifestyle risk assessment, some aspects o f disease prevention, and i ndividual counseling for long term restoration o f health. As well, the osteopathic fam i ly physi cian must often deal with questions involving patients' personal and social expectations, economic status including affordability o f the care proposed by the physician, i nsurance coverage, and at times religious and health beliefs that are d ifferent from those of the physician.
PHARMACOTHERAPEUTICS IN OSTEOPATHIC PRACTICE
Early in its h istory osteopathic practice minimized the use o f drugs. A t that time most available drug treatments consisted of toxic, ineffective, or addictive chemical compounds such as calomel, morphine, digitalis, whiskey, and laudanum. To his credit, Dr. Still found the use of such drugs repugnant ( 2,3,37). His own experience as a physician using the available drugs o f t h e day convinced him that drugs were inevitably harmful. Os teopathy was in troduced as an alternative. Dr. Still emphasized that restoration of musculoskeletal, neural, and circulatory bal ance would provide the body with adequate resources for recov ery from disease. I n extreme situations the osteopathic physician could resort ro surgery (2,3). Other early osteopathic emphases included appropriate diet, correction of psychological dysfunc tion, and physical work. During the first 20 years of the 20th century this parsimonious attitude among osteopathic physicians toward p harmacothera peutics shifted (see Chapter 2). Osteopathic hospitals were emerg ing and medical care in general was changing. Pharmacotherapeu tics was being developed on a scientific basis. By the mid-1920s pharmacology courses were included in all osteopathic curricula offered in the United States. Today, medications are i ntegral and valued elements of Amer ican osteopathic care. However, we should be ever mindful of the limitations of all medications, including their side effects and, in the case of antibiotics and antiviral agents, the tendency of drugs to induce resistance in their proposed targets. I t is crucial from both theoretical and practical standpoints that the osteo pathic family physician encourages lifestyle modifications, re moves structural and functional impediments from the patient's normal ability to function, and otherwise avoids the use of med ications whenever possible (38). Much of the abuse of pharmacotherapy at the beginning of the 21st century stems from the physician's attempts to ameliorate the symptoms of functional conditions. Even many recognized pathologic conditions, like hypertension, may be thought of as symptoms of underlying pathophysiology. Osteopathic medicine
seeks to affect the underlying physiology through the use of lifestyle modifications, OMT, and pharmacotherapeutics, when necessary. It is in these instances that the osteopathic physician's patient-centered, rather than disease-centered, approach to pa tient care offers advantage. Many functional symptoms are re duced by the appropriate use of OMT and lifestyle change, thereby decreasing the need to prescribe symptom-suppressing medications. Conceivably, the underlying pathophysiology may also be affected by reducing drug dosage requirements or enhanc ing the efficacy of appropriately prescribed drugs. DISEASE MANAGEMENT AND HEALTH RESTORATION
The osteopathic family physician's role is to provide the context and opportunity in which the parient can recover health. The physician recommends and in some cases performs appropriate interventions. The physician also needs to proactively minimize negative side effects and complications by carefully weighing risks and benefits of potential therapies. However, the physician should always recognize that the ultimate decisions to participate in this care are the patient's and further, that healing is not an act per formed by the physician. It is in fact the act of the patient's body, mind, and spirit. The ultimate purpose of osteopathic medical intervention is to help the patient with the restoration of healrh. To this end the physician will take measures to 1. Relieve symptoms. 2. Remove, or at least diminish, the population of pathogenic organisms where there is infection. 3. Remove or repai r diseased pieces of the body surgically where necessary. 4. Replace substances no longer produced or absorbed. 5. Desensitize the body to or remove from the body substanc6 that are producing an imbalance. 6. Sensitize the body to necessary substances that are being un derutilized. 7. Rebalance the dynamic stability of the body. 8. Restore emotional and psychosocial stability. LONGITUDINAL CARE
The general population considers that the role of the physician is to diagnose and treat disease. In contemporary society dis ease is thought of as a condition of relatively acute onset that is responsible for distressing symptoms. The osteopathic family physician, however, will deal not only with specific acute disease episodes, but also with chronic illnesses that may last for decades. Longitudinal care is one of the aspects of all primary care that distinguishes it from the medical and surgical specialties. Primary care physicians typically see their patients over many years and under a variety of health care-related incidents. Specialist care is often episodic and focused on a particular disease, although with some long-term diseases the specialist may see the patient for many visits over a number of years. Even in this latter case the
20. Osteopathic Family Practice
specialisr generally focuses on a single disease or organ sysrem. On rhe orher hand, rhe family physician may see rhe same pa rienr from birrh co rhe end of l i fe. Admirredly, rhis is rare given rhe grear mobiliry of our sociery. However ir is nor uncommon for rhe osreoparhic family physician co provide obsrerric care co rhe parienr, and years larer co rhe parienr's child. As nored earlier rhis can provide a unique perspecrive on fami l ial risk faccors. The family physician will deal wirh nor only specific disease episodes bur also wirh chronic illnesses rhar may lasr for decades. Such longirudinal care also provides an inrimare knowledge of b iopsy chosocial and medical problems rriggered by problems i nside rhe family and irs immediare environmenr. Ir can also go a long way co undersranding fam ily dynamics and rhe culrural m i l ieu in which rhe fam ily funcrions. Osreoparhic family physicians are commonly rrained in a wide variery of minor surgical procedures, colonoscopy, and obsrerric and gynecologic procedures. Their pracrice serring and personal preferences will dererm ine how many of rhese procedures rhey will perform. Mosr are also rrained co do basic procedures in whar i s now being rermed orrhopedic medicine, incl uding arthrocentesis, j oinr injecrions, local nerve blocks, and uncompli cared casring, procedures rhar complemenr rhe use of OMT. Finally, when awienr is nearing rhe end of his or her l i fe ir is rhe primary care physician who mosr ofren m usr provide end-of-life counseling and palliarive care. Generally the osteo parhic family physician has been wirh rhe parienr for a long time and knows rhe parienr's fam ily milieu. This makes it easier and more narural for rhe physician co discuss end-of-life issues i n a sensirive manner, allowing for appropriare decision making and subsequenr suppOrt in a manner rhar respecrs rhe parienr's aucon omy and bel iefs.
PREVENTIVE HEALTH AND HEALTH MAINTENANCE
All diseases and dysfuncrions fal l inco four classes: imm unologic, anaromic, generic, and l i fesryle. I m munologic dysfunctions are discussed in Section I I . Anacomic dysfuncrions and/or rrauma, i n cluding sprains, srrains, fracrures, amputarions, and organ dearh from rraumaric ischemia, accounr for many family practice visirs. Generic problems are becoming increasingly h igh profile, as are lifesryle and self-defeating culturally based and b iopsychosocially inAuenced behaviors. In all classes of disease rhere are mulri pie possibili ries for long-range ameliorative and p reventive/health maintenance inrervenrions. Ir is in these conrexts that osteopathic family physicians can be particularly effecrive. As noted previously, family physicians tend co emphasize pre venrive medicine and mechanisms that will maintain a patient's healrh (4,5). This is in accordance wirh the general osteoparhic concept rhar disease is rhe effect of a fai lure co mai ntain normal compensarory mechanisms both in rhe body and the environ menr. This concept specifically suggesrs rhar treatment of disease is besr effecred by resroring rhe body's compensarory mechanisms and balance, while reducing or el iminaring stresses within the per son's environmenr. More ro the point, it i mplies that disease i s prevenrable, making i t i s the osreopathic physician's fundamenral role co help patienrs understand and implemenr healthy l i fesryles.
295
PSYCHOSOCIAL CONSIDERATIONS IN FAMILY P RACTICE
Tradirional basic and clinical science education emphasizes rhe physiologic, biochemi cal, anacomic, and genetic bases for health and disease. Modern osteopathic fam ily practice explicitly incor porates psychosocial and cui rural i n A uences ( 1 ,4,5). Some aspecrs are obvious, such as the i nreraction between patienrs' and physi cians' personaliries and i nrerpersonal skills. The patient's ability ro undersrand physician explanations and discussion depends on a variery of subrle communication cues and socially and cultur ally defined inrerpersonal i n reracrion sryles (see Chapter 19 and Section III). The pri mary care physician o fren deals wirh clearly defined psychological problems such as personaliry d isorders, subsrance abuse, eating disorders, anxiety and depression, and rhe disrup tive and stressful effects of personal, family, and j ob-relared stres sors. In fact, there are data that s uggest rhar, with rhe exceprion o f psychoses, primary care physicians treat more psychological problems rhan do psychiarrists (4,5,7). Nor only do fam ily physi cians prescribe appropriate medicarions for psychologically based problems, bur rhey ofren provide significant amounts of personal and family counseling. Even the seemingly simple decision ro seek healrh care is often complicated by marginally underscood i n teracrions between the patienr's personal, fam ily, cultural, and work-relared elements. Economic factors, parricularly the availability of insurance, fur ther complicate the patient's decision making. The individual's response co psychological, social, and economic faccors can lead co significant differences in the decision co seek or not ro seek medical care. Some esrimares suggesr rhar as many as 60% of a sympcomaric population for many diagnosable diseases, such as m igraine headache and back pain, may never see a physician for the complainr (38). Orher varianrs i n these psychosocial elements produce medical over-urilizarion, Munchausen syndrome, failure co seek medical care until a condirion has escalared ro emergency srarus, over-reliance on or i nappropriate demand for medication, frank refusal co rake medicarion, and noncompliance. Another psychological varianr is rhe i n famous medicarion "allergies" rhar lead a parienr co reject each medication tried while demanding the physician come up wirh rhe "right" drug. Many patients, some with diseases and many without, com plain of problems relating ro the body when the core issues may relate more co l i fe stresses, incl uding psychological and interper sonal problems. If the physician overlooks the role of personaliry and srress-related faccors in the patienr's complainrs, sympcom conrrol and even disease cure may lead co new sympcom forma rion and complainrs . Multisystem somacoform disorders, fatigue, and chronic pain often involve such personaliry and srress-relared faccors. These disorders often i nclude sympcoms i nconsistent with known dis ease or may not demonsrrate objecrive findings rhar are com patible with the complainrs. People who exh ibit rhese problems have very often seen multiple physicians. In fact, one of the most telling signs i ndicating a strong psychological componenr is the denigration of the previous physician's efforts. Often these disor ders include a significant complainr of musculoskeletal pain that on close evaluation by the osteopathic physician demonstrates
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V Osteopathic Considerations in Family Practice and Primary Care
little , if any, relevant somatic dysfunction. F inally most of these d isorders are resistant to accepted medical treatment. A num ber of studies have demonstrated that a significant component of such complaints includes significant psychological factors, such as chronic stress, anxiety and depression, sleep disturbance, and per sonality disorder (see Chapters 1 4 , 1 5 , and 1 7). The osteopathic primary care physician can help the patient understand these naturally occurring body-mind-spirit interactions and thereby develop better coping strategies. Finally, most physical disease, particularly chronic d isease, can lead to psychological and social disturbances for the patient and the family. The role of multiple and chronic srressors in the de velopment of psychological disturbances and physical disease has been a recognized component of medicine since Selye's studies in the 1950s (38). That disease, whether acute or chronic, plays the role of stressor i s well demonstrated (see Chapters 15 and 19). Failure to recognize this body-mind connection can lead to such problems as poor compliance with treatment, acceleration of the disease process, and development of co-morbidities.
FAMILY PHYSICIAN AS OMBUDSMAN
The osteopathic family physician's role is appropriately that of an ombudsman: a health care coordinator and facilitator for the complex i nteractions between the patient, specialists, hospitals and other care facilities, and i nsurers. The complexity of the cur rent health care system, coupled with a similar complexiry in medical diagnosis and treatment, often leaves the patient bewil dered and lost. An additional role for the family practice physician in the physician-as-ombudsman model i s as an interpreter for the pa tient. In the face of the complex nature of disease, the complex ities of diagnostic tests, and the options facing the patient for treatment, the patient has a h igh probab ility of being confused. All the additional information now available to the patient with I nternet access and computerized databases only adds to the con fusion. The osteopathic fami l y physician can interpret all this information for the patient and , through effective dialogue with the patient, assist in a decision-making process that will provide a road map to achieve optimal treatment. The primary care physician can often expedite the i nteraction with the specialist by acting as a go-between. Where there i s a need for interpretation of the options presented by the specialist, it often falls to the primary care physician to put things in plain everyday language and lay the options out in a fashion that can be understood by the patient.
COMMUNITY OUTREACH AND PUBLIC HEALTH
The osteopathic family physician's commitment to helping patients develop and maintain health often extends beyond office- and hospital-based medical care. Teach ing patients signs and symptoms of potentially important d isease manifestations , proper diet and exercise regimens, proper ergonomics on the job and in everyday life, appropriate immunizations and private and public hygiene measures often easily segues into transmis-
sion of the same information to the public at large. The breadth of knowledge required of the osteopathic family physician and the h ighly developed communication skills that are demanded in family medicine make the osteopathic family physician uniquely qualified for both private and public health education. Partici pation in public clinics and medical outreach programs provides similar extension of the osteopathic physician's reach beyond rhe confines of private practice. One of the most troubling aspects of the modern American health care system is that it leaves a large portion of the popula tion "medically underserved." A recent model of family practice (39) suggests that family practice is in a unique position to help the medical profession find a way to extend health care to the whole population. This new model suggests that this maldistri bution of medical services is due to the tendency of the public to demand and the physician to provide inappropriate medical services. A prime example is the use of antibiotics to trear self limiting infections that are generally vi ral in nature. Not only does this expend limited resources that migh t be better used elsewhere , but it also tends to ptomote antibiotic resistance in pathogenic bacteria. While this model has been promoted in the defense of "evidence-based medicine" (39), the more general point is that family physicians are in a strong position to pro mote a more thoughtful , resource-sparing approach to medicine. This approach balances the needs of the individual against the ultimate needs of the population as a whole. Finally, the osteopathic family physician can provide valuable service to the osteopathic communiry and to the general pop ulation by participating in the education of future osteoparhic physicians. Whether in the classroom, in hospital training pro grams, or in-office one-on-one training, the unique strengths of osteopathic family practice need to be passed on to furure gener ations of osteopathic physicians.
CONCLUSIONS
(
This chapter has examined the nature of osteopathic family prac tice at the beginning of its second century of l ife. Osteoparh ic family physicians are uniquely positioned to deal with a wide spectrum of health and disease-related problems, including bi ologic, social, economic, and cultural i nfluences. The emphasis is on resource mobilization to promote health and healing, in cluding medical and surgical care, osteoparhic manipulative care, and psychosocial and general family care. Through appreciation for the osteopathic philosophy and its principles, the osteopathic physician is able to provide a uniquely powerful take on fam i ly medicine. This includes emphasizing the importance of self healing and the interdependence of the biological , psychological, and social factors that are so potent in the development of disease and the recovery and maintenance of health.
REFERENCES I . Membership Directory: Americall College ofOsteopathic Family Physicians and American Osteopathic Board ofFamily Physicians. Arli ngwn Heights, I L; 2000-2001 :3 1 9 .
20. Osteopathic Family Practice
2. Still AT. Philosophy of Osteopathy. Published by the author, Ki rksville,
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2 1 . Noll DR, Shores J H, Gamber RG, et al. Benefits of osteopathic ma
MO; 1 899. (Reproduction published by the American Academy of
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(Reprinted by Easrland Press, Seatrle, WA; 1 992). 4. Rakel RE. Textbook of Family Practice, 5th ed. Philadelphia, PA: W B Saunders; 1 995. 5. Taylor RB, et al. Family Medicine: Principals and Practice, 5th ed. New York, NY: Springer-Verlag; 1 998. 6. McGann KD, Bowman MA, Davis SW. Morbidity, mortality and charges for hospital care of the elderly: a comparison of internists' and family physicians' admissions. j Fam Pract. 1 995;40:443-448. 7. Greenfield S, Nelson EC, Zubkoff M, et al. Variations in resource utilization among medical specialties and systems of care. JAMA. 1 992;267: 1 624- 1 630.
8. Beal M . Viscerosomatic reflexes: a review. jA OA. 1 985;85 :786-80 I .
22. Radjieski JM, Lumley MA, Cantieri M S . Effect of osteopathic manip ulative treatment on length of stay for pancreatitis: a randomized pilot study. jAOA. 1 998;98:264-272. 23. Beal Me. Viscetosomatic reflexes: a review. jAOA. 1 98 5 ; 8 5 : 5 3-68. 24. Beal MC, Moriock JW. Somatic dysfunction associated with pul monary disease. jAOA. 1 984;84: 1 79- 1 84. 25. Beal MC, Kleiber G E. Somatic dysfunction as a predictor of coronary artery disease. jA OA. 1 98 5 ; 8 5 :302-307. 26. Korr 1 M . Sustained sympathicotonia as a factor in disease. I n : Korr 1 M , e d . The Neurobiological Mechanisms i n Manipulative Therapy. New York, NY: Plenum Publishing Co; 1 978:229-268. 27. Korr 1 M . The spinal cord as organizer of disease processes: some pre l i minary perspectives. jAOA. 1 976;76:35-45.
9. Sumino R, Nozaki S, Kato M. Central pathway of trigemino-neck reflex
28. Johnston WL, Kelso A F, Babcock H B . Changes in the presence of a
(abst). I n : OraL-fociaL sensory and motor functions. InternationaL Sympo
segmental dysfunction pattern associated with hypertension. Part I: A
sium on OraL PhysioLogy. Tokyo, Japan: Rappongi; 1 980:28. 1 0. Smith RK. One hundred thousand cases o f influenza with a death rate
short-rerm longitudinal study. jA OA. 1 99 5 ;95 :243-2 5 5 . 29. Johnston W L , Kelso AF. Changes in t h e presence of a segmental dys
of one-fortieth of that reported under conventional medical treatment.
function pattern associated with hypertension. Part I I : A long-term lon
jA OA. 1 920; 1 9: 1 72- 1 75 .
gitudinal study. jAOA. 1 995;95 : 3 1 5-3 1 8 .
I I . MilierCE. The mechan ics oflymphatic circulation: lymph hearts.jA OA. 1 923;22:397-398, 4 1 5-4 1 6.
1 2. Pearson WM, Hines N H , Polovich CA, et al. Symposium on Respira tory Diseases-Etiology, Pathology, Diagnosis, and Treatment. jA OA. 1 938�6:307-33 1 . 1 3. Purse
FM.
Clinical evaluation of osteopathic manipulative therapy in
measles, jAOA. 1 96 1 ;6 1 :274-276. 1 4. Rumney Ie. Osteopathic manipulative treatment of infectious diseases. Osteopath Ann. 1 974;2: 29-33. 1 5 . Blood HA. I n fections of me ear, nose and throat. Osteopath Ann. 1 978;6:465-469. 1 6. Harakal J H . Manipulative treatment for acute upper respiratory disease. Osteopath Ann. 1 98 1 ;9:253-2 57. 1 7. Schmidt Ie. Osteopathic manipulative therapy as a primary factor in the management of upper, middle, and pararespiratory infections. jA OA. 1 982;8 1 :382-388. 1 8. Kaluza CL, Sherbin M . The physiologic response of the nose to osteo pathic manipulative treatment. jAOA. 1 983;82:654-660. 1 9. Whiting CA. I nvestigation of the phagocytic index. Bull. no. l . AT Still
30. Johnston WL, Hill ]L, Elkiss M L, Marino RV. Identification of stable somatic findings in hypertensive subjects by trained examiners using palpatory examinarion. jAOA. 1 98 2 ; 8 1 :830-836.
3 1 . Johnston WL, Kelso A F, Hollandsworth DL, Karrat J . Somatic manifes tations in renal disease. A clinical research study. jA OA. 1 987;87:22-35. 32. Kuchera M , Kuchera AW. Osteopathic Considerations in Systemic Dys fUnction. Kirksville, MO: Kirksville College of Osteopathic Medicine Press; 1 990. 33. Johnston WL, Golden W) . Segmental definition-Part I V. Updati'ng the differential for somatic and visceral inputs, jA OA. 200 1 ; 1 0 1 :278-283.
34. Chapman F. An Endocrine Interpretation of Chapman's Reflexes. Indi anapolis, IN: American Academy of Osteopathy; 1 956.
3 5 . Denslow J S , Hassett. The central excitatory state associated with postural abnormalities. j Neurophysiol 1 944;5 :393-402. 36. Korr
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37. Still AT. Autobiography of A ndrew T Still Publ ished by the author, Kirksville, MO; 1 908. ( Reprinted by the American Academy of Os teopathy, Newark, O H ; 1 989).
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38. Selye H. The Stress ofLife, 2 n d ed. New Yo rk, NY: McGraw- H ili; 1 978.
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39. Slawson DC, Shaghnessy AF. Becoming an i nfo rmation master. j Fam
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Pract. 200 I ;50: 5 1 -56.
GENERAL INTERNAL MEDICINE DONALD R. NOLL JOHN M. WILLIS TERRI TURNER
KEY CONCEPTS • Applications of osteopathic philosophy and principles in
internal medicine practice • Managing the patient with complex problems • Applications of palpatory diagnosis and manipulative
treatment in patients with systemic dysfunction or disease
Editor's Note. This clup[er lays our many osteopathic concepts [hat fir very well with clinical problem-solving concepts found in Chapter 19.
INTRODUCTION
Inrernal medicine is dedicated to both [he primary and specialty care of adul[ pa[ienrs ( J ,2). Many inrernal medicine specialists provide primary care services, while others, especially [hose who have subspecialized, provide consultative services. Examples in clude preoperative medical clearance, postoperative in-hospital medical care, and office consul[a[ion with a family practitioner for an individual with mul[isystem problems. Internal medicine also includes an array of subspecial[ies, such as cardiology, pul monology, gas[roenrerology, nephrology, endocrinology, hema tology, oncology, infectious disease, geriatrics, immunology, and rheumatology. The term "in[ernis[" refers to a physician who is a special is[ in [he field of inrernal medicine. In[ernis[s have a minimum 3 years of postgraduate training in [he managemenr of pa[ienrs with inrernal organ and systemic diseases. They practice in virtu ally all pa[ienr care serrings, including office, hospi[al, and long term care facili[ies. An inrernis[ who manages pa[ienrs primarily in [he hospital is of[en referred to as a "hospi[alis[" or "inren sivis[," if specializing in [he care of patients in [he intensive care unIt. [nrernal medicine specialists are dedicated to disease preven [ion, diagnosis, and managemenr of bo[h acure and chronic disor ders. A distinctive featLlre of in[ernal medicine specialty practice
is the emphasis on [he diagnosis and managemenr of pa[ienrs with complex medical or multiple-organ system disorders. This requires an in-depth knowledge of diagnostics, pa[hophysiologic processes, and how disorders and treatmenrs inreract with one another. The American College of Osteopathic Internists (ACOI) was founded in 194 1 to regulate and improve the standards of ed ucation and training of osteopathic internists. The allopathic counterpart to the AC O I is the American College of Physicians American Society of Internal Medicine,which claims to represenr more than 115,000 inrernists (2). This number dwarfs the esti mated 3,36 J primary care osteopathic internists known to be in active practice in the United States a[ the beginning of the 2 1s[ century. Although [he number of osteopathic general internists is small, [hey are experiencing rapid growth, increasing by 85.6% over [he past 10 years, which is faster [han [he 68.7% growth rare experienced by [he osteopathic profession as a whole over the same period of rime (3). Bo[h allopathic and osteopathic residency programs las[ three years. Today, doctors of osteopathy ( DOs) are training in both allopa[hic and osteopathic programs. For [he 1999-2000 aca demic year, [here were estimated to be 293 residenrs [raining in 44 American Osteopathic Associa[ion (AOA)-approved general internal medicine programs. At [he same rime, [here were 856 DOs in programs approved by the Accredi[a[ion Council for Gradua[e Medical Educa[ion (ACGME). For subspecialty in[er nal medicine [raining, [here were 104 DO residents in AOA approved versus 258 in ACGME-approved programs (4).
DISTINCTIVENESS OF OSTEOPATHIC INTERNAL MEDICINE
Osteopathic internists have much in common with [heir MD colleagues. They see the same types of pa[ienrs, read [he same textbooks, journals, and medical literature; [hey use [he same laboratory and radiologic diagnostic procedures, and prescribe [he same medications. With increasing frequency, DO internists practice alongside as well as in collabora[ive practice arrange ments with M D inrernis[s. There are, however, distinctions [hat set [hem apart.
21. General Internal Medicine One is that graduates of osteopathic medical schools are more likely to choose a primary care specialty (i.e., general inrernal medicine). On the other hand, those who decide upon furrher subspecialty rraining generally have a strong background in gen eral medical care. Culrurally, the osteopathic profession often asserts that any good specialist must first be a good generalist who can readily deal with "whole-person" concepts. Another distinction is the application of osteopathic philoso phy and principles in patient care. " Osteopathic principles" refers to a body of ideas or principles that comprise osteopathic philoso phy, while "osteopathic practices" usually refer to one's additional training and education in the use of osteopathically orienred palpatory diagnosis and osteopathic manipulative rreatmenr (OMT). Both palpatory diagnosis and manipulative treatment used in a conrext of total patient care are long-standing practices used by the osteopathic community-at-large. When knowledge ably applied, they reflect the practitioner's sensitivity for both the osteopathic philosophy and its concepts (see Chapter 1). Using this same analogy, applications of convenrional medical practices can be reasoned to be "osteopathic" when the philo sophic principles of osteopathic medicine are applied with sim ilar "whole-person" sensitivity. This includes awareness of any neuromusculoskeletal manifestations associated with a parricu lar disease or other related problem (s), the so-called "somatic component." How "osteopathic" a particular inrernist might be is assessed not only by how often OMT is used, but also by the manner in which osteopathic principles are applied to the breadth and scope of medical practice. Key principles that distinguish an osteopathic approach within the specialty include: 1. The individual is viewed as a dynamic and evolving prod uct of psychosocial, physical, behavioral, mental, and emotional influences that affect mind, body, and spirit along with all human relationships. Dysfunctions in any part of any system inevitably and interdependently affect all others. 2. Structural and functional changes are interdependent (i.e., anatomically, physiologically, behaviorally, and psychosocially). Dysfunction in any component calls for careful assessmenr of all others. 3. Everyone is born with an inherent capacity for self regulation, self-healing, and fundamenral health mainrenance. Some are better at it than others. When both short- and long term srructural alterations occur in any system or in rerdependent network, dysfunction and disease often follow. Some problems require sophisticated medical care, while others call for a wide va riety of other rreatments, including, for example, interventional OMT, surgery, or psychiatric care. 4. All treatment plans consider the patient as a whole. En abling patients to successfully care for themselves as indepen dently as possible is a primary treatment goal. Palpatory diagnosis and OMT are designed to identifY and correct s([ucrural ban'i ers that interfere with mechanical, neurocirculatory, lymphatic, and general metabolic functions. Appropriate use of exercise and behaviorally oriented rreatment plans are parrs of a successful ap proach. Additionally, both patient and family education for care givers is essential if success is to occur, parricularly when dealing with long-term care.
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MANAGING PATIENTS WITH COMPLEX PROBLEMS
In the clinical setting, patients often present with signs and symp toms that are neither obvious nor classic (i.e., they are not found in the textbooks). From an osteopathic principle perspective, complex health breakdowns occur when health-enhancing regu latory mechanisms fail. For example, one set of symptoms and signs often represents more than one disease process. For the internist, this is the rule rather than an exception. A common example: An individual with hyperrensive cardiovascular disease often presents with diabetes, emphysema from smoking, and a va riety of readily identifiable neck and shoulder-related complaints that osteopathic physicians often refer to as the latter as part of an osteopathically important "somatic component." In this clinical scenario, each condition interdependently affects the others. The osteopathic internist's role is to understand and knowledgeably . deal with these relationships. An internist also needs to understand the interrelating ef fects of rreatment, how the treatment alters the condition be ing treated, and how the rreatment interacts with the other conditions. The osteopathic approach to such complexity is to understand the broad picture and how the various parts relate to the whole. To do this, one must systematically break the ptoblem down into its component parrs, generating a hierarchic problem list. A determination is then made as to how each element relates to the total picture. Some problems carry more weight than others (see Chapter 19). First and foremost, one must understand the primary reason (i.e., the chief complaint) that brings the patient to the doctor. Each patient has personal agendas that need to be respected, recognized, and addressed. Second, the internist is looking for an underlying cause for the various pathophysiologic processes, even as the patient provides the history of the present illness. Often there are multiple causes, and sometimes problems are in surmountable and irreversible. If there is a unifYing etiology, it is obviously more appropriate to address the cause rather than just its effects, even though depression and anxiety are common accompaniments. From a whole-person point of view, all are ad dressed in some way. What distinguishes a successful internist is persistent atten tion to detail (i.e., looking for impor rant, sometimes overlooked information). The first question is perhaps the most imporrant: " Why is the patienr ill?" The more one understands the solution to the question, the more rational the treatment plan becomes.. The second question is " How does the problem affect the whole patienr?" This explores how interrelated the human body's systems are and how structure and function relate to one another. AT. Still described his thought process while evaluating a patient as follows: When
a
patient comes ro me for examination and begins
ro
talk ro
me about symproms ... while listening, [ am seeing in my mind's eye the combinations of sysrems which go ro make up rhe whole of that body structure. I am concentraring on her srory, rrying
ro
derermine
through rhe descriprion given ro me rhe structural alrerarions, which have occurred ro produce rhe symproms described. I am seeing firsr the bony framework and the joints, which hold it rogerher as one
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Osteopathic Considerations in Family Practice and Primary Care
sysrem, rhe foundarion upon which all orher srrucrures in rhe human body are builr. I am seeing, especially, rhe posirions of rhose bony
Many of the concepts discussed above are best highlighted by way of two case illustrations below.
pans and rheir relarionships, one wirh rhe orher. Then I see rhe liga ments .. . rhe muscles . . . rhe nervous sysrem in all irs relarionships, in every funcrion of rhe body ... conrrolling rhe funcrions of rhe internal organs, rhe circularion of body Auids, and nurririon of rhe various body parts . .. I furrher see rhe arterial sysrem. .. .rhe venous sysrem .. . rhe Iympharic sysrem (and rheir funcrions) . .. and lasr bur nor leasr I sec rhe glandular sysrem of rhe body and wonder how ir brings abour irs effecr in each particular case (5).
Notice the systematic approach as he moves through each body system, thinking about how they relate to the patient's symptoms and how he "keeps" in his "mind's eye the combinations of systems that make up the whole." A series of circumstantial questions should always be kept in mind: 1. How is each probLem afficting the others? This is of greatest significance when an individual has multiple medical and psy chosocial problems. In a laboratory experiment, scientists strive to create simple or "perfect" problems, in which all the variables are eliminated, except the one under study. In clinical practice, physicians struggle with "imperfect" problems with many con founding and interacting variables For example, an acute wors ening of chronic renal failure will promote Auid retention and trigger congestive heart failure in an individual with preexisting left ventricular dysfunction due to prior myocardial infarction. The worsening congesrive heart failure often leads to cardiogenic shock and further renal failure, setting up a fatal feedback loop. Another example is the patient with well-controlled diabetes mel litus who experiences a loss of glucose control during an acute infection. 2. How does treatment affict each problem? It is rare for a medication to have only one local effect. Clinically, it is common for a useful drug effect to be detrimental because of adverse effects in other systems. For example, a drug in the thiazolidinedione class may be an appropriate choice for the management of diabetes mellitus. However, this class of drugs is also known to cause Auid retention. If the patient has congestive heart failure, the addition of this medication could cause the heart failure to worsen and the patient may decompensate. While the drug is quite appropriate for a diabetic, it might not be the best choice for a diabetic with congestive heart failure. 3. How does the treatment affict the patient? Treatments of all rypes do more than alter biologic systems and modify faulry physiology. They also have physical and emotional impacts upon both the patients and, in many cases, their caregivers. Effects that may be acceptable to one person may be totally unacceptable to another. 4. How does the patient affict the treatment? Treatment must be acceptable on both a personal and cultural level, because pa tient confidence and trust are essential for both compliance and successful treatment outcomes (i.e.,in the case of potentially toxic treatment, are the side effects and complications at risk?). The issues that surface surrounding this question are often difficult and ethically complex. Strong, empathic, and insightful commu nication with the patient and affected family members is essential in order for acceptable decisions to be made.
Case One
G.H. is a 68-year-old man who presents with burning pain from his epigastrium radiating to his back. His pain began this morning about 2 hours after he took his daily medications. He describes the pain as a 5 on a scale of 10, with 10 being the most severe pain he has ever had. He admits to being light-headed upon standing up and reports having a black tarry bowel movement. He has no shortness of breath sitting up in bed and denies orthopnea or pal pitations. Allergies: Penicillin causes a rash. Medications: He is taking atenolol, for coronary artery disease; atorvastatin for hypercholesterolemia and coronary artery disease; lisinopril for hypertension; daily mononirrate for angina, and sublingual nitroglycerin as needed for chest pain; metformin for rype 2 diabetes mellitus; naproxen as needed for backache; and ibuprofen (over the counter) as needed for headache. Past Medical History
Coronary artery disease was diagnosed 4 years ago, documented by coronary angiogram after an episode of unstable angina. Last cholesterol level 2 J 0,2 months ago. Exertional angina better with resr, but patient has refused surgery (coronary artery bypass). Hy pertension for 15 years, well controlled, monitored at home by his wife three times per week. Diabetes mellitus for J 0 years,con trolled with diet and medication. Last HgBAIC 6.9,2 months ago. Family History
Father died of a heart attack at age 60. Mother died of heart failure at age 80. Brother has colon cancer. Social History
No history of alcohol or tobacco use. Review of Systems
Patient is remarkable for headaches, which have been bothering him for the past 3 or 4 weeks. He also had several episodes of chest heaviness last month, brought on by exertion and relieved by rest and sublingual nitroglycerin. His physician added the mononitrates to his routine medications and the episodes of chest heaviness resolved. He is not presently having chesr pain. He has had mild epigastric discomfort for the past few weeks, but not severe until today. Appetite has been poor and he has been nauseous today. Today was the first time he noticed his stool being black. Physical Examination
The patient is alert and appears well oriented. His supine blood pressure is 120/70 and pulse is 70 beats/minute. Upon standing,
21. General Internal Medicine he becomes dizzy, his blood pressure drops ro 90/50, and pulse increases ro 100 beats/minute. Skin appears pale. Mouth moist, neck supple, heart rate regular, lungs clear ro auscultation, ab domen soft with hyperactive bowel sounds, extremities without edema, and no gross focal neurologic deficits. Paraspinal muscu lature at the sixth thoracic vertebra level on the left is tender and the tissue texture is "boggy." Rectal examination reveals a good sphincter rone, no prostate nodules, no rectal polyps or masses, and black malodorous srool. A nasogastric tube is placed in the patient in the emergency room and returns red blood from the sromach. Laboratory Evaluation
Remarkable laborarory findings: hemoglobin 8 g, blood urea ni trogen (BU N) 40, and serum creatinine (Cr) 2.3 mg/d L. Baseline tests from a routine office visit several months ago: hemoglobin 12 g/dL, BU N 15, and serum Cr 1.0 mg/dL. Random serum blood sugar is 230 mg/d L and srool is strongly hemo-occult pos itive. Electrocardiogram shows sinus rhythm with nonspecific ST wave changes. Impressions
1. Acute upper gastrointestinal (GI) bleed with acute anemia 2. Orthostatic hypotension 3. Recent episodes of anginal type chest pain 4. Acute deterioration in renal function 5. Uncontrolled type 2 diabetes mellitus 6. Hisrory of coronary artery disease 7. Recent headaches 8. Hisrory of hyperlipidemia 9. Hisrory of hypertension 10. Viscerosomatic thoracic somatic dysfunction Discussion
The patient obviously has an acute upper GI bleed as evidenced by the findings of new epigastric pain, black srool,hyperactive bowel sounds, frank red blood from nasogastric suctioning, acute 4-g drop in his hemoglobin levels, and hemo-occult positive srools. He has somatic dysfunction at T6, which also points ro a prob lem in the upper Gl tract. Orthostatic hypotension is established by the greater than 10 mm Hg drop in his sysrolic blood pres sure measured when he went from a supine ro standing position. The rise in pulse and dizziness upon standing also supports the finding of orthostasis. This finding is worrisome since it indicates significant loss of blood volume, hemodynamic instability, and highlights the life-threatening nature of the patient's problem. Unless stabilized, the patient may deteriorate inro hypovolemic shock and bleed ro death. The initial focus of management will be ro ensure that the patient has an airway, is being oxygenated adequately, and that his vital functions are stabilized. In this occurrence, the patient is losing a significant amount of blood and the system has ro be brought back inro balance, first with intravenous (i.v.) Auids that primarily stay within the in travascular space (normal saline, lactated Ringer solution), then
301
with transfused blood. These are often referred ro as "volume expanders" because they primarily stay within the intravascular space (inside the blood vessels) and will therefore more rapidly correct the loss of blood volume. Normal saline or lactated Ringer solutions are given immediately because they are readily avail able. It will take some time ro type and cross-match the blood for transfusions. Ultimately, large volumes of i.v. Auids and mul tiple units of blood may be needed before the blood pressure is stabilized and the bleeding srops. True ro assertion that the body is self-regularory and self-healing, most episodes of GI bleeding spontaneously srop on their own without external intervention. The strategy, like many modern acute care interventions, is sim ply ro resrore some degree of balance (homeostasis) back into the system long enough for the body ro heal itself. If bleeding persists or if blood loss is at a faster rate than can be replaced, further in tervention will be necessary. This is usually endoscopy ro find the source of the bleed and the utilization a "heater probe" ro cauter ize and srop the bleeding. Failing this, surgical intervention may be necessary. While addressing the immediate life-threatening problems and stabilizing the patient, the internist asks: " Why did this pre viously stable person become acutely unstable?" In this era in which patients are on multiple medications, any change in con dition that coincides with a medication change should be con sidered iatrogenic. In this case the first medication change was the addition of nitrate therapy. The effect of the nitrates on the disease process (coronary artery disease) promoted sympromatic relief of anginal chest pain. Adding a nitrate medication would not likely induce an upper G I bleed. However, a well-known side effect of nitrate therapy is headache. Upon further questioning, the patient said he was experiencing headaches for the past sev eral weeks, and began taking over-the-counter ibuprofen. It is reasonable ro conclude that the combination of two nonsteroidal antiinAammarory drugs (naproxen and ibuprofen) caused the pa tient ro develop peptic ulcer disease, resulting in the GI bleeding that led ro a decreased volume status due ro blood loss. In cases of this type, blood loss often causes a decrease in avail able oxygen in the bloodstream, aggravating myocardial perfusion problems with an accompanying increase in anginal symproms and, in some cases, inducing an acute myocardial infarction. Ad ditionally, decreased blood volume results in an increase in the sympathetic auronomic outAow, a classic stress response. Blood glucose levels increase and loss of diabetic control is common. The decrease in renal function can be explained by a decreased renal perfusion due to a decrease in circulating plasma volume coupled with the loss of the protective effects of renin due to the angiotensin-converting enzyme inhibiror (Iisinopril). Case Two
A 75-year-old woman presents to the emergency room with acute shortness of breath. Her dyspnea started abou I' 8 hours ago and has gradually worsened. Several days ago, she developed a sore throat, muscle aches, and a productive cough. Her cough has worsened and roday she reponed a fever of 102° F. She normally has some dyspnea with exertion, but now is acutely dyspneic, even at rest. She gets some relief by sitting up. Her past medical history is remarkable for severe chronic obstructive pulmonary
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disease (CO P D) From years of smoking tobacco products and restrictive lung disease From a severe burn injury affecting both the lung and skin, which occurred years ago. She also has type 2 diabetes mellitus. Current medications include glipizide (an oral hypoglycemic agent), chronic home oxygen, and oral prednisone. She also takes albuterol (a bronchodilator) in a metered dose inhaler, two puffs four times a day. She has no known allergies. Social History
She has a 50 pack-year history, but quit smoking 5 years ago. On review of systems she reports acute anxiety and air hunger. Physical Examination
The patient's respiratory rate is 35 breaths/minute, pulse 90 beats/ minute, blood pressure 120/80 mm Hg, and temperature 102°F. Remarkable physical findings include the extensive skin burn scars on the upper body, barrel chest wall consistent with obstruc tive pulmonary disease, and bilateral diminished breath sounds with wheezing. She has some crackles in the right lower lung field. She has increased paraspinal muscle tenderness on the right 4th through 6th venebral level. Chest x-ray confirms emphysema with a new right lower lobe pulmonary infiltrate. Laboratory Findings
Remarkable laboratory findings are a 20,000 white blood cell count, and a serum blood sugar of 280 mg/dL. The admitting impressions are: 1. Acute right lower lobe pneumonia 2. Exacerbation of C O P D 3. History of restrictive pulmonary disease secondary ro an old burn injury 4. History of smoking tobacco products 5. Uncontrolled type 2 diabetes 6. Viscerosomatic-somatic dysfunction related to the pneumo nIa. Supportive care is initiated (i.v. fluids, oxygen) along with bronchodilator treatments every 4 hours, i.v. methylpred nisolone, and i.v. antibiotic therapy. The patient is put on an insulin sliding scale to cover her hyperglycemia. She receives ad junctive OMT to mobilize the rib cage, diaphragm, and bal ance autonomic tone. She reports subjective improvement in her breathing and anxiety after her O MT sessions. Her medical prob lems improve and she is evenrually discharged from the hospital. She follows up as an outpatienr with her osteopathic internist for periodic O MT and management of her medical problems. Her oral steroids are successfully weaned off, promoting better conrrol of her serum blood sugars. The number of yearly hospitalizations is decreased.
pneumonia increased her serum blood sugars. The diabetes it self is associated with diminished immune function, which made her more vulnerable to the respiratory infection, and also im paired her ability to heal. From an osteopathic perspective, the cause of the pneumonia was not primarily the exposure to the microbial pathogen (although it is understood she would not have pneumonia without a pathogen), but it is a failure of the body's host defenses against the pathogen. While the antibiotics are greatly beneficial, they basically help the body fight infection. If an individual has severe immune dysfunction, even high doses of multiple antibiotics may not save the patient. This case also illustrates how OMT can be used for dealing with respiratory problems. In general, the goal is to improve thoracic spine, rib cage, and diaphragmatic movement, as well as improve the general circulation including venous and lymphatic drainage. It may also improve autonomic nervous system function in a variety of ways. While the success of antibiotic therapy is dependent on matching an antibiotic to a sensitive pathogen, OMT is designed to improve host defense mechanisms.
OSTEOPATHIC MANIPULATIVE TREATMENT FOR VISCERAL AND SYSTEMIC DISORDERS
The concept that manual methods can be use to treat systemic diseases has been around for most of recorded history (6). A number of clinical studies support the use of OMT for non musculoskeletal problems. In a review of chiropractic medicine, five randomized controlled clinical trials of nonmusculoskeletal problems (menstrual pain, hypertension, and C O P D), were re viewed. Three out of the five studies were actually of osteopathic manipulation (7). Other groups, including chiropractors, have published outcome studies using their own methods (see Chap ters 6 through 9 and 74 through 76). To date, there have been few randomized O MT-related clinical trials. Recently, the authors reviewed 50 Journal of the American Osteopathic Association abstracts published between 1997 and 2001 under the osteopathic manipulative treatment/osteopathic principles (OMT/ O P P) category. Just under 42% of the papers discuss visceral or systemic problems, 32% relate to musculoskele tal disorders, and 26% could be classified as "other." The latter are mostly mechanistic and methodologic studies (authors' un published data). (See Section 8, Chapters 74 through 77.) Interest in OMT effects on systemic disorders is long standing, beginning with Dr. Still's earliest work, which empha sized its use for not only visceral and systemic disorders, but also for a wide variety of somatic disorders. While developing his ap proaches, Dr. Still often referred to the use of drugs as "a system of blind guess work" (8). He taught that a physician knowledgeable in anatomy and physiology reasons back to the cause (8,9).
USE OF OSTEOPATHIC MANIPULATIVE THERAPY FOR VISCERAL DISORDERS
Discussion
BY OSTEOPATHIC INTERNISTS
This individual is hospitalized for an upper respiratory problem that progressed to pneumonia due to her impaired pulmonary system (she has both restrictive and obstructive disease). The in crease in systemic glucocorticoids from solumedrol and stress of
For what visceral or systemic disorders has OMT been ad vocated? Kuchera and Kuchera, in their textbook Osteopathic Considerations in Systemic Dysfonction, review the use of OMT for
21.
the common cold, pneumonia, obstructive lung disease, asthma, myocardial infarction, essential hypertension, congestive heart failure, upper and lower GI disorders, irritable bowel syndrome, urinary tract infections, and dysmenorrhea (9). All of these dis orders are clinical problems internal medicine specialists com monly manage. A wide variety of opportunities remain for addi tional OMT-related clinical research in relation to each of these conditions. Although few surveys have been conducted, it is generally be lieved that many osteopathic internists do not use O MT. Yates surveyed Oklahoma DOs and found that the percent of patients DOs report using O MT on was highly associated with the physi cian specialty, but not with the school they attended, practice setting, or years in practice ( 10). He found that four out of five Oklahoma DOs used OMT, but the frequency varied greatly. Osteopathic manipulative specialists used OMT the most, fol lowed by family practitioners, pediatricians, internists, sutgeons, rehabilitation specialists, and those described as "others."
EVIDENCE SUPPORTING THE USE OF OSTEOPATHIC MANIPULATIVE THERAPY FOR PNEUMONIAS
The largest study ever conducted on OMT was by Smith dur ing the 19 18- 19 19 influenza epidemic ( 1 1). This study is still referenced today. Smith gathered data from 2,445 osteopathic physicians, from every section of the country, who reported treat ing 1 10, 120 cases of influenza, with 257 deaths from influenza, a very low mortally rate. He also reported 6,258 cases of "epi demic pneumonia," which had 635 deaths, a mortality rate of 10%. These mortality rates were compared with national average mortality rates, estimated from 142 health commissioner reports, and estimates from the National Census Bureau and several in surance companies. The mortality under medical treatment of the day was estimated to be 5% for influenza (versus 0.002% for DO-treated group) and 30% for pneumonia (versus 10% for DO-treated group) during the epidemic. Smith also asserted that the duration of illness under osteopathic care was shorter. Although this study has great historical significance to the profession ( 12), its scientific value today is limited. The study was conducted before the age of antibiotics during a time when conventional drug treatments for pneumonia may have done more harm than good. For example, a medical handbook from the period advocates using such treatments as subcutaneous adrenalin, blood letting in robust individuals, vaporized creosote, and strychnine as a cardiac stimulant, to list just a few (I3). In con trast, osteopathic treatment consisted of manipulative treatment sessions of perhaps 15 minutes' duration, one to three times a day. The focus was on mobilizing the thoracic cage, cervical spine, encouraging expectoration of pulmonary secretions, sometimes manipulation to the kidneys, hydration, ensuring regular bowel movements with enemas, use of cold compresses, warm poultices, encouraging sweating, and shunning the use of drugs (14- 16). A 1920 editorial published in the Journal of the American Medical Association dismissed claims of superior outcomes by various "drugless healers" on the premise that anyone who really had influenza would forsake "the quack as soon as they realized their danger and invoke the aid of medicine" ( 17).
General Internal Medicine
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TABLE 21.1. COMPARISON OF OSTEOPATHIC MANIPULA TION TREATMENT (OMT) AND "LIGHT TOUCH" SHAM PROTOCOL GROUPS IN OLDER ADULTS HOSPITALIZED WITH PNEUMONIA (1996-1998 STUDY) OMT Group (n
=
28) Mean
(± Standard
Duration of i.v.
Light Touch
30) Mean (± Standard
(n
=
Deviation)
Deviation)
p-value
5.3 (± 2.2)
7.3 (± 2.8)
0.002
6.6 (± 2.9)
8.6 (± 2.9)
0.014
antibiotics (days) Length of hospital stay (days)
Several studies in this era of antibiotic therapy have been con ducted to evaluate the role of adjunctive OMT in the hospital setting. In the early 1960s, Kline studied 47 pediatric pneumo nia patients hospitalized for respiratory tract infections ( 18). The time period to recovery was 9.2 days in the O MT-only group, 8.3 days in the antibiotic-only group, and 6.4 days in the O M T plus antibiotic group. Stiles reported that those who received OMT during their hospital stay for asthma, low back pain, pe diatric pneumonia, gallbladder surgery, appendectomy, or hys terectomies, had shorter average length of hospital stays relative to those who did not. However, the study appears to be based on a retrospective chart review, and was not a prospective randomized controlled study (I9). In 1999, Noll and colleagues published results of a pilot, ran domized, controlled trial of 21 older adults hospitalized with pneumonia that showed shorter mean length of hospital stays and duration of i.v. antibiotic use in the group treated with O MT. However, the differences between groups did not reach statistical significance (20). The authors then conducted a larger, more refined prospective study (2 1). In this prospective trial, 58 older adult patients were randomized to a "light touch" sham protocol group or an OMT protocol group. Subjects received a standardized protocol treatment session consisting of seven ma nipulation techniques or a light touch protocol twice a day for up to 15 minutes duration for the length of their hospital stay, or until respiratory failure requiring a ventilator, or death. All subjects received at least one consultation with an osteopathic manipulation medical specialist, which, for the treatment group, included O MT for specific somatic dysfunction. The sham group received a structural examination only. An acute pathophysiology score was used to establish that both groups had similar severity of illness upon entry. The attending physicians responsible for determining the duration of i.v. antibiotic use and length of hos pital stay were blind to patient group assignment. The outcome was that the O MT group stopped i.v. antibiotics 2 days sooner than controls, and also were discharged 2 days sooner than the control group. (Table 2 1. 1).
CONCLUSION
The use of osteopathic principles and OMT are important com ponents of osteopathic medicine's heritage. Evidence emerg ing from carefully controlled clinical trials is beginning to
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demonstrate that these principles and their practices are useful in both acute and chronic care settings. Osteopathic physicians are uniquely able to quickly implement these methods as newer evidence supporting their use emerges.
10. Yates HA. Opinions toward the use of OMT by Oklahoma DOs responding to survey in 1984 and 1999.
j Am Osteopath Assoc.
2000;8:514(abst). II. Smith RK One hundred thousand cases of influenza with a death rate of one-fortieth of that officially teported under conven[ional medical
Osteopath Assoc. 1920; I: 172-175. The D.o. s, Osteopathic Medicine in America. Baltimore,MO:
treatment. jAm 12. Gevitz N.
Johns Hopkins University Press; 1982:71-72.
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13. Fitch WE.
The New Pocket Medical Formulory. Philadelphia, PA: �A
Davis Co; 1927:245-245b. 1. American College of Osteopathic In[ernists. Available at:
www.acoi.
14. McCole, GM. Spanish or epidemic influenza from the treatmen[ side.
I n[ernal
15. �raser JM. Warning against giving too prolonged exhausting general
www.doctorsfomdults.comPhtml. Accessed April
treatmen[ in flu: A plea for shorter treatments and more of them.
orglGeneralWhat.html. Accessed April 25, 2002. 2. American
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Medicine. Available at:
Phy sicians-American
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25,2002.
Osteopath Phys. 1919;6:1-6.
Osteopath Phys. 1919;6:14.
3. AOA �act Sheet.
The DO. january 200 I: 12-15.
4. Singer AM. 2000 Annual Statistical Report. Chevy Chase, MO: Amer
16. McConnell CP. T he treatmen[ of influenza, [EditoriaIJ. jAm
Osteopath
Assoc. 1918(Oct):83-85.
ican Association of Colleges of Osteopathic Medicine; March 200 I:
17. �igures never lie. JAMA. 1919:731.
(Table XXIX):38.
18. Kline CA. Osteopathic manipulative therapy,antibiotics, and supportive
5. Hildreth AG.
The Lengthening Shadow of Dr. Andrew Taylor Still. Pub
lished by Mrs. AG Hildreth and Mrs. AE Van V leck, Macon, MO; 1942; 181-183. 6. Northup G.
I L: American Osteopathic Association; 1966. cOn[ributions. Arch
Intern Med. 1998;158:2215-2224. Philosophy of Osteopathy. Published by the author, Kirksville
MO; 1899. 9. Kuchera M, Kuchera AW.
jAm
Osteopath Assoc. 1965;3:278-281. 19. Fitzgerald M, Stiles E: Osteopathic hospitals' solution
Osteopathic Medicine: An American Reformation. Chicago,
7. Kaptchuk Tj, Eisenberg OM. Chiropractic origins, cOn[roversies, and 8. Still AT.
therapy in respiratory infections in children: Comparative study.
OMT. 20. Noll
to
ORG's may be
The DO. 1984(Nov):97-101.
DR, Shores j, Blyman PN, Masterson EV. Adjunctive os
teopathic manipulative treatment in the elderly hospitalized with pneumonia: a pilot study.
j Am Osteopath Assoc. 1999;(3): 143-
152. 21. Noll DR,Shores j, Gamber RG,et al. Benefits of osteopathic manipu
Osteopathic COnJiderations in Systemic Dys
function. Kirksville, MO: KCOM Press; 1990.
lative treatment for hospitalized elderly patients with pneumonia.
Osteopath Assoc. 2000;(12):776-782.
jAm
GENERAL PEDIATRICS SHAWN CENTERS MARY ANNE MORELLI COLLEEN VALLAD·HIX MICHAEL A. SEFFINGER
KEY CONCEPTS
Osteopathic pediatrics as primary care Osteopathic evaluation of children • Osteopath ic approaches to pediatric patients with systemic dysfunction; common examples from the musculoskeletal, respiratory, gastrointestinal , and neurologic systems. •
•
Pediatrics is the arr and science of health care for children. Unril the beginn ing of the 20th cenrury, very few physicians treated children exclusively. As physicians focused on infanrs and chil dren, it became more obvious that children are not simply minia rure adults, but that they have differenr anatomic proportions, physiology, biochem istry, and pathology. Osteopathic pediatric specialists are trained to approach the whole child from the phys ical, menral, nutritional, social, and parenral viewpoinrs. All the available and appropriate medical modalities and specialists are utilized. The osteopathic approach to the pediatric patient is founded upon osteopathic philosophy and principles as outli ned in Chapter I. Additionally, neuromusculoskeletal eval uation and manipulative treatment which identifies, treats, and attempts to alleviate inefficient structural mechanics is another distinctive modality osteopathic pediatricians utilize in disease prevenrion and recovery. The osteopathic pediatrician is, through awareness of the in terdependence of strucrure and function, constantly observi ng for evidence of somatic dysfunction that can affect healthy growth and developmenr. The ill child is not alone in having somatic dysfunction problems; the well child may also be strucrurally ill and, by a complete whole-patienr approach, these problems may be corrected. The main goal in treating the pediatric patienr who has a disease is maximizing the child's health potenrial and returning the patienr to a homeostatic base ( 1 ) . Before being established as a specialty, pediatrics was taught to osteopathic physicians-i n-trai ning as a branch of obstetrics and obstetricians treated newborns and older children. I n the late 1 920s and early 1 930s, however, osteopathic physicians across
the counrry began to take inrerest in specializing in the treatmenr of children. The demand for formal training and certification increased as new medical technologies and pharmaceuticals bur geoned and pediatric textbooks and j ournals became established. In 1 939, Watson, Percival, and Whittell founded the American College of Osteopathic Pediatricians. This provided necessary standards for osteopathic pediatric medical education, procedures for review and credential ing, and conr i nuing education of osteo pathic pediatricians (1). Currently, qualifications for specialty certification requires 3 years of postgraduate residency training in an accredited training program and successful completion of required competency evaluations and standardized exam inations. The fact that a child is a dynamically changing organism with differenrial rates of growth and maruration of component parts demands conrin uous reevaluation of i nrerrelationships. Funda menral diagnostic and therapeutic principles applied to adults do not hold true for pediatric patienrs. Organ systems are at differenr levels of maturation at the time of birth and grow and develop at significantly differenr rates. As the child matures, inrerrela tionships between systems and their regulatory mechanisms vary over time. The child must therefore be approached and observed longitudinally. Because infanrs and small children are totally dependenr on their parenrs or caretakers and the environment for sustenance and nurturing, they must be considered as part of a complex biopsychosocial system. During early years of development, the parenr-child dyad functions as a single unit, although the child and the parent remain individuals. Early parent-infant bonding is vital to healthy child development. When bonding is i ncomplete or dysfunctional and jeopardizes the child's health and survival, appropriate inrervenrion by health and social services profession als is warranted.
OSTEOPATHIC PEDIATRICS AS PRIMARY C ARE As the twig is bent, so doth the tree incline. -AJexander Pope
Since its inception, osteopathic medicine has focused on pri mary care. Care of children was an integral part of the general
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V Osteopathic Considerations in Family Practice and Primary Care
osteopathic physician's practice. [ n his Autobiography and Os teopathy: Research and Practice, A.T. Still presented case studies and principles of osteopathic treatment of children with a wide variety of afAictions, including infectious diseases (2,3). Allevia tion of spi nal joint restriction and fascial tensions found through out the body in ill children hastened their recovery. In add ition to applications for musculoskeletal injuries and disorders, osteo pathic manipulation was used as an integral part of treatment for children suffering from common epidem ic infectious diseases such as diphtheria and polio. Children under osteopathic care had improved outcomes (2). I n 1 9 1 8, Mil lard wrote a text on the treatment of poliomyelitis in children with osteopathic meth ods, including osteopathic manipulative treatment (OMT) (4) . [n 1 939, Watson and Percival , attending physicians at the Los Angeles County Osteopathic Hospital pediatric unit, designed the first prospective clinical trial of disti nctly osteopathic care com pared with no nosteopathic care of children admitted to the hospital with pneumonia. In a prelimi nary report, they presen ted data in support of decreased morbidity and mortality of children treated with complementary OMT along with standard medical care compared to similar cohorts at other hospitals where OMT was not offered ( 5 ) . [ n addition to complementing standard measures in treating infectious diseases, osteopathic physicians have made sign ificant contributions in the understanding of the mechanical component of a variety of disorders and conditions challenging children of all ages (see "Systemic Dysfunction" later in this chapter) . Special at tention, however, has focused on the newborn . Deleterious effects of uteri ne forces upon the fetus during labor and delivery were documen ted by Little in 1862 (6). [n 1 9 1 3, Wh iting stressed the im portance of treating the pregnant mother's somatic dysfunction before delivery based on her data showing decreased labor and delivery time in 223 patients treated with OMT thtoughout preg nancy to alleviate somatic dysfunction (7). In a recent metaanal ysis of data regard ing osteopathic care of obstetric patients, King found that prenatal OMT improved postnatal outcomes (8). Arbuckle, among others, advocated correcting the mechani cal component of neuromuscular problems, such as those found in patients with cerebral palsy, by treating somatic dysfunction found in newborns as a result of traumatic birth forces upon the cranium (9). She treated patients from around the world at her Osteopathic Cerebral Palsy Institute from 1 9 53 to 1 967. One example of the magnitude of the effect of the osteopathic approach in addressing somatic dysfunction with OMT in this critical period of development was found in a twin who suffered severe prenatal birth trauma from being lodged in his mother's pelvis for several months before delivery. At 1 0 months he was diagnosed with cerebral palsy and was so stiff that he was unable to sit. His mother was in tears, having been given little hope or suggestions for remedying the condition. With weekly OMT his Aexibility increased markedly. He was soon able to sit without aid, crawl, and creep, and by 1 8 months he began to walk. Barnes described applications of osteopathic principles and manipulative treatment in the management of com mon newborn problems such as asphyxia, atelectasis, emesis, brachial plexus in jury, colic, bowel problems, and clubfoot ( 1 0) . Children with psychological disturbances, concentration problems, learning dis abili ties, and poor performance at school were found to have an
increased incidence of cranial somatic dysfunction and a history of an obstetrically complicated delivery (I 1 , 1 2) . Woods noted demonstrable improvements in behavior in children suffering from these conditions upon resolution of somatic dysfunction with OMT ( 1 3, 1 4) . Sutherland lectured o n birth trauma and vomiting i n the new born ( 1 5) . His description of how birth trauma to the occiput could affect the vagus nerve led Frymann to methodically ex amine 1 ,250 newborns to investigate this proposed relationship between cranial structure and neurologic dysfu nction (16) . This survey suggests that strain patterns of the developmental parts of the occiput are involved in nervous system dysfunctions, such as vomiting, tremor, irritabil ity, hypertonicity, and hyperactive peri stalsis. Frymann went on to participate in several clinical research studies, lecture worldwide, and founded the Osteopathic Center for Children and Osteopathy's Promise to Children foundation in San Diego, California ( 1 7) . Major areas o f concentration i n pediatric practice are health maintenance, health promotion, and disease prevention. Recom mended schedules of health maintenance for the pediatric patient can be found in most pediatric textbooks ( 1 8) . Exam inations of wel l children are more difficult to perform than those of sick chil dren because the initial hypothesis set is not guided by a specific complaint. Problem prevention and health maintenance are of prime importance in well-child care. The history, physical exam ination, and clinical problem solving are instead guided by an extremely wide range of hypotheses related to disease states or disorders that are subclinical and not manifesting obvious signs or symptoms at the time of evaluation. The pediatrician focuses on primary, secondary, and tertiary prevention. Primary prevention refers to prevention of a disease process so that it will not affect the child. Dietary guidance and immunizations are one example of this approach. Secondary pre vention is aimed at identification of subclinical disease before the development of overt symptoms (e.g., at the time of the interim history, physical, and structural exam ination) . In this way, inter vention can be provided to arrest cli nical progression or eliminate the disease. Tertiary preventive practices consist of identification of cli nical disease or disorder and alleviation of the disease or disorder through therapeutics and/or rehabilitation. OMT is ef ficacious as primary and secondary intervention of asymptomatic somatic dysfunction as well as tertiary i ntervention in the symp tomatic child. Well-child care and regularly scheduled pediatri cian visits provide sufficient time for primary and secondary pre vention of pertinent lifestyle disease. The osteopathic physician should take time to discuss issues of: Child development Accident prevention • Nutrition • Discipline • Parenting
•
•
Too often, the suggestion for children with developmental de lay or structural issues is to "watch and wait." Treating structural problems of children should be done early to facilitate develop ment and prevent problems at a later date ( 19) . "Wait and see" is not an effective approach to structural and developmental issues
22. General Pediatrics
in children. Children should enjoy osteopathic treatment at reg ular intervals to optimize their potential in health, growth, and development. Infants should be examined shortly after birth to evaluate the effects of any birth trauma. Some infants need no treatment after birth, but most of those who do will benefit from early treatment. Infants and children should be treated at rhe first sign of illness to facilitate their healing. During times of rapid growth and development, as children learn to climb, walk, and run, periodic treatments are needed. When behavioral or academic issues surface, there is often a struc tural component. Before orthodontic care, OMT can help free any structural restrictions in the face, palate, and jaw. Correct ing the underlying structure first makes relapse less l ikely and a straightened smile easier to maintain. During orthodontic care, OMT can help prevent headaches and scoliosis from worseni ng and minimize mood changes (20). OMT is obviously warranted to alleviate somatic dysfunction arising from sports inj uries (see Chapter 37).
OSTEOPATHIC EVALUATION OF CHILDREN Osteopathic Pediatric History
In the evaluation and treatment of children, the osteopathic physician must consider the medical, structural, social, psycho logical, and spiritual needs of each young patient, as well as the child's age and developmental level. Much, if not most, of this information is elicited during the history, requiring careful atten tion to the past medical and surgical history, current medications, allergies, birth and trauma history, and a thorough review of sys tems. Social issues should also be addressed, paying particular at tention to the stabil ity of the child's home and family life as well as any h istory of substance, physical, or emotional abuse among family members. When evaluating adolescents, the osteopathic physician should also inquire about sexual activity, as well as drug and alcohol use. Often, many features of a patient's history can be ascertained by reviewing the patient's previous medical records, if available. The salient details of the history are then reviewed by the osteopathic physician and combined with data from the physical and osteopathic structural exami nation, as well as laboratory tests, if indicated, to create a clinical impression of the patient. These data then form the foundation for further diagnosis and treatment of the pediatric patient. The evaluation and treatment of a pediatric patient begins with the utmost respect and consideration of the needs of the child. If the child has had negative experiences with health care providers in the past, then takinga thorough history with the child present may be difficult. Young children often become i mpatient during the history-taking process. In older children, repetition of previous diagnoses given by other health care providers, whether accurate or not, may reinforce the feeling in these children that they are being negatively labeled by the health care system. Fur ther, parents of pediatric patients may divulge traumatic personal or family histories during the initial history taking. In many cases, being confronted with traumatic family stories may not be in the best interest of the child, especially early in the therapeutic re lationship. Therefore, the in itial pediatric history is often best
307
elicited from the child's caregiver(s) without the child present in the room. Conversely, it is often beneficial to obtai n a history from older children without the child's caregiver present. Preteens and ado lescents will often reveal critical pieces of history that may not otherwise have been revealed if the caregiver were present, such as sexual activi ty, a history of abuse, or use of ill icit substances. Osteopathic physicians are trained to search for the underlyi ng cause of an illness, or, at a minimum, the anatom ic, structural, and functional contributors, i ncluding the presence of somatic dysfunction, to a disease process. Thus, the importance of an accurate, detailed h istory, with special attention paid to trauma history, i ncluding birth trauma and associated physical, environ mental, and emotional events that lead to such trauma, cannot be overstated. Childhood traumas tend to have far-reaching and long-term effects as structures are in their formative stages of growth and development. I nitially, the chief complaint should be addressed. The timing of the in itial symptoms of the chief complaint should be noted with reference to any preceding h istory of trauma. Note any falls, environmental exposures, or whether the family or child were under undue stress, including fam ily disagreements, moves, vacations, or death. A detailed history of the course of pregnancy, including any trauma that the mother may have sustained during the preg nancy, should be obtained. The emotional and mental state of the mother during and after the pregnancy is important, as well as whether the mother used medications, alcohol, or illicit drugs. The physician should also inquire as to whether the pregnancy was planned or not. Unplan ned pregnancies may have placed rhe fetus at higher risk for drug and alcohol or other environmental exposures. A detailed birth h istory should be obtained, including gesta tional age, duration of labor, mode of delivery, and use of anes thesia. Any complications during delivery should be noted. The Apgar score, color of the infant, presence of caput succedaneum, or any cranial molding, as well as any abnormalities found during the newborn examination, should also be noted. Certain situa tions place the newborn at higher risk for somatic dysfunction i ncludi ng: • • • • • • • • • • •
Breech, transverse l ie, face presentations Cephalopelvic disproportion Firstborn infants Labor augmentation with oxytocin Long or difficult labor Multiple birth (twins, triplets, etc.) Postterm infants Prematurity Use of epidural or general anesthesia Uterine anomalies (e.g., fibroids, septa) Vacuum extraction , forceps Answers to the following questions are also helpful:
Was Was • Was • Was •
•
there need for a cesarean section? there a period of uterine inertia? there meconium aspiration? the fi rst breath vigorous?
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V Osteopathic Considerations in Family Practice and Primary Care
Did the baby require stimulation or resuscitation? Did the baby have a lusty cry? • Was the baby able to establish nursing in the fi rst 24 hours? •
•
H istory of any of the following behaviors can i ndicate cranial base somatic dysfunction: Difficulty in latching on to the nipple or learning to suck Excessive crying or inconsolability • Arch ing of the back or repeatedly throwing the head back in early infancy • Excessive vomiting or spitting up
•
•
In the older child, a detailed h istory of previous illness, aller gies, and surgeries should be made. A careful h istory of accidents and trauma should be taken including the force involved, velocity, direction, and area of impact. Document the type of forces, the treatment, and whether any changes in behavior or personal ity occurred. Obtain a complete developmental history with empha sis placed on the ages at which the patient attained milestones. Dental history including extractions and any other procedures should be documented.
sphenobasilar articulation that has carried the head into a par allelogram distortion is suggested if one temporal bone is more anterior than the other without medial or lateral motion. A lateral strain can be related to transient tachypnea of the newborn, and other respiratory irregularities ( 1 7,2 1 ). The sacrum of the infant should be examined for i nterosseous and lumbosacral compression and torsion patterns. Strain pat terns in the sacrum are clin ically related to strain patterns in the cranium. This is hypothesized on the basis of anatomic contiguity of the dura mater, which attaches to the foramen magnum, C2, and C3, as well as 52. Sitting next to the infant or child and plac i ng two fingers or a hand under the sacrum allows for assessment of the motion of the sacrum while steadying the pelvis anteriorly with the other hand. Restrictions in regional motion evidenced by abnormal static position should be noted. As the child grows, the amplitude of the primary respiratory mechanism increases and can be more easily palpated. The tiny in trinsic motion (not postural) of the sacrum in relation to the ilia should be symmetric around a transverse axis at 52. Check for symmetry between the two sides of the sacrum. One side may feel lower, indicating ro tation around an anterior-posterior axis. If the base of the sacrum feels anterior on one side, it is rotated on a vertical axis.
Osteopathic Pediatric Structural Examination
The osteopathic pediatrician incorporates a thorough osteopathic structural exam ination as part of the overall evaluation and treat ment of pediatric patients. While the content and goals of the pediatric structural examination differ little from the osteopathic structural examination used when evaluating adult patients, there are often differences in how the structural examination in children is approached. Generally, children are best evaluated by examin ing range of motion regional ly, rather than segmental testing of individual vertebral units. The clin ician should perform the structural examination in a manner that is min imally threatening to the child. Often , it is helpful to build trust in and rapport with the child before the examination begins, usually by engaging the child in nonthreat ening play and smiling often. Much useful information about the child's structural and fu nctional status can be gained by simply observing the child sitting, lying, nursing, crawli ng, and walking. The cranium is first assessed visually, checking for signs ofgross structural asymmetry, and then assessed manually for asymmetry or restriction of motion . In newborns, placing a gloved fi nger into the mouth to encourage sucking often aids i n evaluating cranial motion with the other hand. The infant's cranial motion can of ten be difficult to feel. However, if the physician can palpate the motion from the infant's sucking movements equally in all areas, this is generally a sign of symmetry in the cranial mechanism. The physician should cradle the occiput in the hands and gen tly place the tips of the index fingers on the mastoid process of the temporal bones. Because there is no bony mastoid process at birth, the attachment of the sternocleidomastoid (SCM) muscle can be used as the palpatory landmark. Note if there is symmetry or if one fingertip is posteromedial to the other. The temporal bone is externally rotated if the tip of the mastoid is posterome dial, or less prominent, and i nternally rotated if the tip of the mastoid is anterolateral, or more prom inent. This asymmetry in dicates the position of the occiput as the temporal bone moves in relation to the occiput (see Chapter 62). A lateral strain of the
SYSTEMIC DYSFUN CTION Musculoskeletal System Musculoskeletal Development
Children are born with mostly cartilaginous articulations. Their bones have maximum flexibility at birth. The spine has a minimal C-curve in the cervical region that increases as the infant becomes able to support the weight of their head. By 8 to 9 months of age, most infants begin to sit up and develop a thoracic kyphosis. At 1 3 months to 5 years of age, the toddler begins to ambulate and completes the development of the lumbar lordosis. In later child hood and adolescence, there is rapid growth of the long bones. Some children and adolescents may develop a leg length discrep ancy during this period. The vertebral bodies may continue to ossifY until 25 years of age. The infant cranium is a complex structure at birth; the bones of the infant skull are composed of small areas of ossification formed within cartilage, with fibrocartilaginous articulations at the base and within membrane at the vault. The cartilaginous and mem branous portions of the cranium and their articulations permit maximum compressibility to allow the infant to pass through the birth canal with less resistance. Initially, the infant cranium com prises 50% of the infant's body surface area and doubles in size during fi rst year oflife. By 6 years of age, the skull reaches 90% of adult size. The cranial bones are enveloped in fascial membrane; i ntracranially, there are the dura and pia mater and arach noid. The dura mater has reflections that form the falx cerebri and tentorium cerebelli. The dura is firmly attached at the occipital atlantal (O-A) joint , the inner aspect of the sacrum at 52, and is continuous with the spinal nerve root sheaths. According to the osteopathic cranial concept, these membranous attachments determine how the cranial bones move in relation to each other and the sacrum (see Chapter 62). As the infant matures, the cranial bones ossifY and the flexible articulations of the occiput and parietal bones interdigitate, lim iting motion (Table 22. 1 ).
22. General Pediatrics
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TABLE 22.1. STAGES OF OSSIFICATION OF THE CRANIAL BONES: CRANIAL BONES FROM BIRTH TO AGE 6 YEARS
1 Year
Birth
3 Years
6 Years
Temporal Three parts; petrosal, squamous, and mastoid
Bones fused, mastoid
Mastoid enlarged, sagittal serrations
formation
Petrous full size, jugular surfaces appear
Occipital Four parts; base, squama, two lateral,
Four parts
Condylosquamous junction
condylar parts
ossifying
Foramen magnum full size, condylosquamous junction fused
Sphenoid Three parts; central body with lesser
Bones fused, pterygoid
Well ossified
wings; two greater wings; pterygoid
process assume right angle
processes
to centra I body
Sphenoid sinus well developed
Frontal Two parts; metopic suture present
Open metopic suture
Metopic partially closed
Metopic suture either closed or patent for lifetime, frontal sinuses growing
Parietals Large in proportion to other bones; cover parietal lobes of brain; no venous sinus
Remain larger proportionately
Remain larger
Ossified
proportionately
grooves Atlas Three parts
Three parts
Three parts
Completely fused
Maxilla Two parts
Increase in height
The ribs begin primarily as cartilage and are oriemed hori zontally in infants. As the child grows and ambulates, the ribs slowly progress toward their final "bucket handle" and "pump handle" motions. They continue to ossify and grow i n length as the child matures. The sacrum is composed offive modified verte brae with cartilaginous articulations at birth. These articulations have maximum mobility in the i nfant and progress toward their final motions as the bones ossify in late adolescence. At birth the ilium is composed of three bones; the il iac bone, ischium, and pubis. These are partially cartilaginous at birth with fibrous articulations. The ilia fuse by 20 years of age. The extremities in infants are Aexible and are composed mostly of cartilage, par ticularly at the articulations. Growth plates are present at joints and in the long bones comprising a minimum of the body sur face area in the infant but becoming more significant as the child grows. A normal range of motion in the joint s should be present in the neonate unless an abnormal neuromuscular condition eXists. Cranium
The success of spontaneous, unassisted birth is dependent on the maternal pelvic size, shape, and Aexibility. In the primigravida, the infant cranium may be engaged in the pelvic outlet for days or weeks. The infant often presents with the right occiput, Aexed posture, and as the head descends below the symphysis pubes, it rotates from an oblique to an anterior-posterior axis and the neck extends. After delivery of the head, the neck de-rotates and the right shoulder is delivered. As the i nfant's head descends, the cranial bones "mold" to accommodate the pelvis. This may result in a palpable corkscrew restriction in the imracranial membra nous attachments to the cranium, which require adjustment with OMT in order to reestablish normal cranial mechanics.
The infant cranium is designed to accommodate the tremen dous forces of the delivery process. A traumatic delivery can result in somatic dysfunction that can have long-term effects on the child if not corrected. Restrictions in motion of the bones with dural membranous attachments may affect the process of nor mal growth and development. The unrestricted mobility of the cranial bones and membranes is essential in the normal develop mem of the primary respiratory mechanism (see Chapter 62). The bone most commonly susceptible to somatic dysfunction from the birthi ng process is the occiput. Incidence of cranial somatic dysfunction i n newborns is estimated at 88% ( 1 6) . Through their sucking and crying, most i nfants will self-colTen most cranial so matic dysfunctions acquired at birth; however, sometimes there will be cranial dysfunction that conti nues throughout childhood and even int o adulthood (22). A baby or child with plagiocephaly (a misshapen skull) from a traumatic birth may suffer from a variety of disorders related to intracranial membranous strains, cranial nerve entrapments, or central nervous system i rritation or compression (6, 1 2 , 1 6) . Man ifestations of these mechanical dysfunctions can be general, as in developmental delay or behavioral disorders, or more specific, as in difficulty with tongue movement in suckling (cranial nerve [CN] XI I ) , excessive vomiting (CN X), colic (CN Xl) , or opistho tOnic posturing (corticospinal pyram idal tracts) (21-2 5 ) . A sin gle somatic dysfunction, like occipital condylar compression, can cause several signs or nerve entrapment due to impingemem of CN I X, CN X, and CN Xl at the j ugular foramen and CN X I I at t h e hypoglossal foramen. Facial nerve trauma may result from a difficult delivery, especially when forceps were needed. This is the result of trauma to the peripheral branch of the facial nerve or nuclear agenesis. It results in flaccid paralysis of the face with loss of the nasolabial fold and in the case of central involvement, an
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V Osteopathic Considerations in Family Practice and Primary Care
eye that cannot completely close and a smooth forehead. There is often an associated CN VI palsy with lateral rectus weakness and nystagmus. Nerve entrapments l i ke these can be treated with cranial OMT (22-2 5 ) . Residual dysfunctions can have serious consequences in relation to neurobehavioral development. Sphenobasilar lateral strain patterns produce the appearance of a "parallelogram"-shaped head. Sphenobasilar and i ntracra nial membranous strains can cause abnormal tension on the ten torium cerebelli. Cranial somatic dysfunction affecting CN III, CN IV, and CN VI is thought to play a role i n disorders of abnor mal position and movement of the eye. Cranial OMT has been noted empirically to facil itate restoration of normal eye position and movement (21,22) . Some strain patterns are believed to affect brainstem functions and respiratory drive. Apnea and bradycar dia can be manifestations of these somatic dysfunctions (22). Cranial strain patterns in children do not necessarily manifest as neurologic deficits. Patients may be asymptomatic or have gener alized complaints, ranging from allergies to severe head pai n . The most common presentation is the child with chronic or recurrent upper respiratory tract disorders (discussed later in this chapter) . Research int o the effects of cranial somatic dysfunction is in its infancy. Though there are as yet no prospective randomized clini cal trials investigating this clinically apparent relationship, expert panels of osteopathic physicians recommend that cranial somatic dysfunction in the neonate or infant, whether symptomatic or asymptomatic, warrants OMT (26) . Treatment of cranial traumatic birth inj uries involves rib rais ing at delivery to calm the sympathetic nervous system and im prove efficiency of breathing and body A uid movement, O-A and condylar decompression, sacral traction, and affected cranial bone decompression. Treatment involves releasing the restric tions as soon as the infant is physiologically stable. The sacrum is treated with gentle traction and can facilitate release of intracra nial membranous strain patterns. The O-A and condylar parts are decompressed with gentle posterolateral traction. Treatment of each restriction involves gentle, but firm direct action OMT that involves distracting and guiding the cranial bones into their respective restrictive motion barriers and maintaining them in that position until a release is felt. This requires very little force. Costal Cage
Costal cage somatic dysfunction may be the result of a direct trau matic force to the area or an indirect result of muscle imbalance or spasm secondary to a non rhythm ic breathing mechanism. The history may reveal asthma or chronic cough, but particularly, an episode of severe coughing or wheezing related to this i ncident is most common. In normal breathing, air movement is accom plished by unrestricted movement and mobiliry of the diaphragm. The coordinated contraction of the diaphragm is mediated via the phrenic nerve and nerve fibers that exit from the midcervical area (C3-5 ) . Thus, cervical or thoracic somatic dysfunction can predispose to rib dysfunction. It is rare for children to sustain rib fractures since their ribs are Aexible and well calcified with good cartilaginous articulations. Infants with posterior rib fractures should always be suspected of having suffered abuse. Fractured ribs have nodular calcified areas at the costotransverse articulation adjacent to the spi nal column. Rad iographically, the fractures are often at various stages of cal cification. Posterior rib fractures are the result of the infant being
held and shaken. The cartilage absorbs the force anteriorly, but posteriorly the ribs have bony articulations with the transverse processes and are relatively i n Aexible. Such infants present with severe to moderate pain with breathing. They have tenderness and fullness over the affected rib that becomes worse with either inhalation or exhalation. The upper ribs are best palpated an teriorly and the lower ones are best palpated in the midaxillary regions. There are usually associated thoracic segmental somatic dysfunctions that need to be treated. Children with cystic fibrosis or a- I -antitrypsin deficiency are at the greatest risk for rib somatic dysfunction. These children present with severe chest pain that is worse with i nhalation. Chil dren and adolescents with scoliosis and asthma are predisposed to developing rib somatic dysfunctions as well. These children should be screened and treated after a thorough structural exam ination at each visit. First, the physician should relieve muscle spasm with i nhibition, countersrrain, or muscle energy OMT. Next, the segment/rib is treated with indirect OMT. The physi cian mon itors the rib movement while the child takes a deep breath, then moves the rib further i nto the direction of ease of movement. Attempting direct positioning often elicits guarding due to aggravation of the intercostal muscle spasms. High veloc iryllow ampli tude ( H VLA) is a useful technique with the patient supine or sitting. The child will immediately be able to breathe without pain, although some residual tenderness to palpation will remain. The physician must remember to also relieve any associated diaphragm motion restrictions. Vertebral Spine
Torticollis ("wry neck") can present shortly after birth or at any time during childhood. It is defined as shortening or con tracture of the SCM on one side with the head tilted toward and rotated away from that side. There may be irritation of the spinal acces sory nerve (CN Xl) from somatic dysfunction of the cranial base affecting the j ugular foramen and its contents. In congenital cases, the SCM becomes shortened and ropy. In acute cases, a lymph node may be irritating the SCM or trauma has occurred that re sults in SCM spasm. [n acute torticollis, the SCM is exquisitely tender. The differential diagnosis incl udes a cervical dislocation of the vertebra or spinal cord tumor which would have other structural and neurologic fi ndi ngs including sensory deficits. In chronic torticollis, there is often a pattern of long-standing O-A dysfunction with a cranial lateral and possibly vertical strain patterns. These are the result of abnormal intrauterine position ing or an abnormal birth event/position. There may be a h is tory of a shoulder dystocia at birth. The differential diagnosis of chronic torticollis includes a cervical malformation or K1ippel Feil anomaly. The best treatment outcomes are obtained by addressing the underlying cranial and cervical somatic dysfunction. These chil dren respond to i ndirect, followed by direct, action OMT pro cedures. The physician should begin with in hibition of tender points via counterstrain and indirect techniques. This requires good com mun ication and a level of understanding that, upfor tunarely, many children have not yet achieved. I n these cases, the techniques must be modified so that the area is positioned until a tense fascial area of palpation softens. Indirect muscle energy tech niques (reciprocal inhibition) can also be helpful. In some cases, the use of antiinAam matory medication and muscle
22. General Pediatrics
relaxanrs may be necessary, with the child returning I II 24 to 48 hours for definitive OMT. Muscle energy, with infanrs and children, works well and can be devised like a game. Addressing other related vertebral and sacral dysfu nctions is often necessary as wel l. The physician can teach parenrs tech niques to stretch the SCM and the child is seen and treated on several visits over a period of weeks. Scoliosis is most often fi rst diagnosed in childhood. It can show up in the neonatal period but is rare. Congenital scoliosis is caused by anomal ies of the spine involving fusion or abnormal development of the spine. These infants may have other organ involvement. Scoliosis seen in childhood is defined as an abnormal curvature of the spine in the coronal and sagittal planes. It is categorized as structural or nonstructural. The structural curves have an axial rotation on forward bending. Defi ni tive diagnosis is by stand ing postural radiographs. Nonsrructural scoliosis is the result of poor posture, muscle spasms, or a shorr leg. In the i nstance of structural curves, the spinous process rotates toward the concav ity and is seen as a promi nence of either the ribs or paraspinal muscles on that side with forward bending. The etiology of most abnormal spinal curves is idiopath ic. Patienrs must be managed with careful observation, sequenrial radiographs, balanced muscle strengthening/fascial mobilization, and bracing. Many cu rves classified as idiopathic are actually secondary to "shorr leg syndrome." These children present with scoliosis, chronic lu mbar or sacral somatic dysfunction, and/or hip pai n . Standing postural radiographs show unequal i liac crest heights and sacral base and femoral head heights that are not level. The lumbar convexity is toward the short leg side often with a com pensatory curve in the opposite thoracic side. Correction of the short leg with a heel or sole lift (orrhotic device) along with OMT, leads to improvement or alleviation of the scoliosis. Lumbosacral somatic dysfunction is often symptomatic if in duced from a fall or hyperextension inj ury. It can be the result of "overuse" with a preexisting structural problem, such as a shorr leg, scoliosis, or spondylolysis/spondylolisthesis. Patienrs present with pain in the low back or h ip. They complain of pain with forward bending and experience a "catch" in their low back or hip. Palpatory fi ndings include L5-S 1 side-bending somatic dys function associated with a sacral rotation or shear. Children with lumbosacral dysfunction will have a positive standing Aexion test on the affected side. When neurologic findi ngs are present, radio graphs should be taken and must include oblique lumbar views. When the x-ray results are available and normal, treatment is begun and directed toward relieving the acute problem. I nitial relaxation of muscle spasm using counterstrai n, soft-tissue re laxation, trigger-point inhibition. and muscle energy will allow defi nitive treatmenr. Physiological sacral n utation (anterior movemenr of the sacral base) occurs along a transverse axis at 52. The sacrum may engage a restriction with rotation around an axis or shear. The sacrum undergoes nutation, then counternutation during the birthing process. There is a torsion componenr as well, since the oc ciput presenrs anrerior or posterior and undergoes rotation i n the birthing process. When the toddler sits and then ambulates, the sacrum assumes the normal position. Toddlers have an accenru ated lumbar lordosis due to i nadequate abdominal musculature. This induces bilateral sacral nutation. As growth and develop-
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ment conri n ue i n to adolescence, the sacrum undergoes unusual stresses secondary to rapid phases of growth and physical activi ties. Lumbar dysfu nction and restriction of motion of the ilium affect sacral motion. Conversely, there is often an il iac rotation to compensate for the sacral im balance. This is corrected using mus cle energy and positioning. Sacral and lu mbar somatic dysfunc tions respond well to both direct and indirect OMT procedures. An associated pubic shear may be present that can be treated using muscle energy tech nique. When the child has recurrent problems, exercises and stretch ing can help. Unequal leg lengths also affect sacral mechanics. Consider a lift for the shorr leg in the older adolescent to prevent sacral somatic dysfunction from recurri ng. Upper Extremity
Shoulder dystocia and fractured clavicles from a traumatic birth are common in the newborn period. Motion testing will reveal crepitance, with palpation over the clavicle. There may be an as sociated brachial (Erb) palsy with the arm lying extended by the side and hand i n ternally rotated. This is the result of injury to C5-6 nerve roots. A rarer injury occurs to C7-8 and T l nerve roots. These infanrs will have additional paralysis of the hand and ipsilateral ptosis and miosis. Prognosis is better if the upper arm is involved and, un less the nerves are severed, 90% resolve spontaneously within the first year. These are treated with gentle handli ng, avoidance of placi ng the infant on the fractured side, and splinting the hand in physiologic position when the lower arm is affected. Indirect manipulation of spinal somatic dysfunc tion may help, but direct H VLA should be avoided. Children are at i ncreased risk of inj ury of their extremities secondary to i ncreased range of motion of joinrs, growth plates, participation in competitive activities and, due to their immatu rity, relative i nability to make safe decisions. Because the child's long bones are in the process of mineralization during this highly competitive period, they may suffer from overuse injur i es . Shoulder inj uries i nclude strains of t h e rotator cuff, clavi cle fractures, and acromioclavicular separation or strain. Rotator cuff injuries involve overuse tendon itis or forces of torque on the forearm. These may occur to such an extent that an avulsion frac ture occurs at the tendon inserrion site. The child presents with pain and achi ng with rotation of the arm, particularly when the forearm is benr 90 degrees at the elbow. Acromioclavicular and clavicle fractures result from blunt injuries to the lateral aspect of the shoulder. Rotator cuff and acromioclavicular inj uries are treated with counrerstrain, ice, and nonsteroidal anriin Aamma tory medication. Physicians must remember to consider underlying visceral dis ease in patients with persistent shoulder pai n , pain unexplained by the structural findings, or in those patients who do not re spond to treatment. Referred pai n to the right shoulder occurs with gallbladder disease. Duodenal inAammation refers pain to the left shoulder. Tender poinrs found over the anterior shoul der could be a manifestation of Chapman reAexes from upper respiratory tract infections and can be treated with inh ibition. Clavicle fractures are diagnosed with a defect to the lateral aspect of the clavicle, with palpable crepitance upon elevation of the shoulder. These fractures are treated ini tially with immobi lization in a clavicle restraint, then after 3 to 4 weeks, range of motion (Spencer technique) and counterstrain. Children rarely
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V Osteopathic Considerations in Family Practice and Primary Care
suffer from a "frozen shoulder" since they are eager to use their arm and will do so despite pain. The elbow is an area of vulnerability for the child because of the conAuence of growth plates. Children are at risk of supra condylar fractures with residual growth and functional problems. The radial head is vulnerable to dislocation secondary to a sud den jerk to the arm resulting in a "nursemaid's" elbow. These injuries are treated with pronation/extension to a sudden supina tionlAexion position with pressure over the radial head at the antecubital area. Children may sustain overuse inj uries with re sulting lateral or medial epicondylitis. These are best treated with rest, ice, and antii nAammatory medication. Counterstrain and treatment of trigger points works well. In all cases, assessment of the mechanism of injury and modification of the mechanics will help resolve the problem. Supracondylar fractures are the result of significant forces and involve the growth plates. The arm m ust be i m mobilized above and below the elbow. This leaves residual somatic dysfunction that responds to range of motion and counterstrain OMT. Spiral fractures of the long bones are indicative of child abuse unless the history of injury is sufficient to explain the fracture. Wrist inj uries present with pain over the wrist with Aexion. They are usually the result of repeated forces on the Aexed hand. They are seen in gymnasts, volleyball players, cheerleaders, and stringed instrument/piano players. The wrist pain results from a dropped scaphoid or stress fracture of a carpal bone. These children present with a catch or pain in the wrist with Aexion. They may have a continuous ache. Fractures have cont i nuous pai n with tenderness to percussion or vibration directly over the fractured carpal bone. Treatment includes ice, rest, modification of the precipitating behavior, and OMT. If a fracture is suspected by history or testing, a radiograph should be obtained prior to attempting manipulation. The dislocated scaphoid responds to H VLA: rotation in a figure of eight, then sudden Aexion with pressure over the scaphoid with the thenar eminence. The same results are accomplished with gentle traction and pressure over the scaphoid, dorsum of the wrist. Some children develop chronic pain in this area and benefit from sleepi ng with "cock-up splints." [ f median nerve entrapment/inAammation occurs, counterstrain, myofascial release, stretch ing exercises, and nocturnal splinting help. Fingers and toes are prone to jamming inj uries. These inj uries are the result of a sudden force to the end of the digits resulting in pain and swelli ng over the proximal or distal joints. The clin ician should always perform motion testing to ensure that the tendons are intact and not avulsed from the bone at their points of insertion. Once it has been established that there is no fracture via examination or radiograph, the inj ury can be treated with simple tech niques. Gentle traction , rotation, and movement into Aexion will restore range of motion. I f the original force results in an extension inj ury, these can be gently taken into Aexion . It is helpful to mobil ize Auid from the joint via efAeurage. Lower Extremity
Most commonly, leg length inequality is due to unequal develop ment (27). Incidence in the asymptomatic pediatric population is berween 8 5 % to 90% (27) . It is not known which children will develop problems related to a short leg; however, it is prudent
to consider treatment with a heel lift and OMT if it causes an unlevel sacral base, scoliosis, and/or somatic dysfunction. The restrictions in motion of the ilium involve anterior or pos terior rotations. This rotation may be associated with unilateral sacral shears. A short leg may produce an ileal rotation poste rior on the same side. Pubic shears may be present secondary to trauma. Arthrogryposis is a congenital condition involving reduced range of motion of j oints. I n fants with this condi tion are born with fixed joint contractions due to abnormal intrauterine forces and/or i nnervation of muscles. Treatment involves physical ther apy for range of motion and treatment of trigger points. In fants may be born with hip dysplasia that occurs more com monly with those born from a breech position . The hips will dislocate with Onolani and Barlow testing. These infants should have hip ultrasounds performed by experienced radiologists at 2 weeks of age. If the hips can be dislocated, they should be placed in a Pavlik harness and referred to an orthopedic surgeon (see Chapter 33). I n children who present with pain in the lower extremity, the source can be from any area below the waist. They often cannot localize the pain specifically. Pain in the hip may be the result of trauma to the sacrum as the result of a fall. The clin ician must be sure there is no joint effusion or fever ro establish that there is no septic or rheumatoid arthritis. Children and adolescents who have significant hip abnormalities will have restricted range of motion. If motion testing produces pain, crepitance, and reduc tion in motion, the physician should consider a sli pped capital femoral epiphysis or Legg-Calve-Perthes disease. These condi tions can be excluded with radiographs of the hips, including the frog leg view. These children benefit from counterstrain OMT, treatment of trigger points with inh ibition, and range of motion exercises. Children and adolescents with sim ple somatic dysfunction present with pain over the lateral aspect of the hip and full Aex ion and external rotation of the hip joint . They have tenderness over the sacroiliac articulation on the affected side. The joint has no crepitance to palpation with motion testing. In chronic hip pain , the pain may be the result of abnormal posi tioning for a sport/dance activity. The most com mon problem is caused by exaggerated external rotation of the hip. Pain i n the hip joint may be referred pain from the gastroi ntestinal tract. Treatment begins with de-rotation of any i liac rotation, followed by OMT to correct any sacral somatic dysfunction . The sacral dysfunction responds to HVLA, muscle energy, counterstrain, and indirect OMT. Radiographs are helpful if the pain is continuous, severe, and not relieved with gentle treatment. Pain may be referred from the lumbar area to the hip. Treatment includes elim inating somatic dysfunction in the l umbar region. Stretches and modi fication of the offending behavior will help make the treatment permanent. Pain i n the knee is often the result of nerve impingement of the peroneal nerve at the fibular head. Knee pain is commonly associated with sports activities and is due to overuse traunp or abnormal body mechanics. Gym nasts tend to overextend the knee joint; ballet dancers tend to externally rotate the knee. Par ticipants in contact sports may have trauma to the knee resulting in a lateral/medial or an anterior/posterior force being applied.
22. General Pediatrics
The child's knee is a dynamic area of growth and developmenr that is especially prone to srress injuries. The lateral aspect of the knee may be affected by abnormal or excessive stresses placed on the fibular head as the result of leg crossing. It may be the result of restriction or trauma to the distal fibula at the ankle. It is important to assess the mechanism of injury or overuse to determine a treatment plan. Pain can be referred to the knee from the colon. Young chil dren with fever, knee pain, and effusion can have septic arthritis. I f this i s suspected, aspiration and culture of the fluid, blood counrs and cultures, and radiographs should all be obtained. Antibiotics are warran-red if the condition is determined to be septic. Chil dren suffer from overuse/srress injuries such as Osgood Schlatter disease and have pain and swelling over the patellar tendon in sertion site. Treatmenr is rest, ice, anriinflammatory medication, modification of the insuJting behavior, srretching before and after activity, and traction/gentle range of motion exercises. Restrictions in the gliding motion of the proximal fibular head can be relieved with slightly flexed positioning and gentle gliding anterior/posterior of the fibular head. M ild trauma of the knee with minimal effusion may benefit from gentle traction on the lower leg and counterstrain OMT. Elevation and relief of prox imal lymph flow obstruction at the inguinal area will promote drainage. Prior to treatment, the knee must be motion tested to assess for stability of the l igamentous attachments. In the child, growth plates and the physiologic srresses of growth complicate the knee dynamics. When pain and swelling are present, the knee should be elevated and immobilized. Treatment of pelvic somatic dysfunction will i mprove circulation to the joint. Ankles are commonly injured in sports activities. These in juries are usually the result of eversion of the ankle with result ing effusion in the joinr and associated tears of the ligaments of attach ment. There may be a fracture of the distal fibula that can involve the growth plate. The child presents with pain and swelling over the lateral aspect of the ankle and h istory con sistent with the injury. If vibration over the distal fibula elicits pain, a radiograph should be obtained prior to manipulation, including a stress view, to rule out fracture. If the radiographs are negative for fracture, treatment includes motion testing for stability assessment, ice, elevation, antiinflammatory medication, and lymphatic drainage OMT techniques. Once the effusion has resolved, the ankle should be rehabilitated with retraining of the proprioceptor response with the " Baps" board (a round board with a variable-sized ball underneath) . Other injuries of the an kle can result in hyperextension at the calcaneaJ/rarsal area. I n children, the ligaments are very flexible and the joints that are stable in adults have motion in children. There may be a congen ital minor malformation such as a calcaneonavicular coalition. Tight heel cords can lead to ankle pain and abnormal mechanics. Pain in the feet is usually the result of poor arches and anatomic variations. Ballet dancers employ abnormal positioning and "toe shoes" that exaggerate the arches and stress the growth plates. Most instructors will not let dancers wear toe shoes until their growth plates have fused. Runners and jumpers will often get stress fractures and may get tendonitis of the Achilles insertion site. These are treated with ice, elevation, rest, stretching (especi ally after the activity) , and OMT. Manipulation will correct a nav icular somatic dysfunction. These somatic dysfunctions present
313
as pain in the arch of the foot that worsens with pointing the toes. Fullness can be palpated over the medial aspect of the arch. The patient is positioned prone with the leg bent at the knee. The physician's thenar eminence is positioned over the fullness. Trac tion, rotation in a figure of eight, then hyperextension with a sudden snap over the fullness will reduce the navicular somatic dysfunction. Stress fractures will have pain with vibration over the fractured area. These are treated with rest, wearing of a hard-soled shoe, and antiinflammatory medication. Injuries may be prevented with stretchi ng exercises and orthotics when structural problems are identified. In children, sportS inj uries are complicated by the presence of growth plates and hyperflexible joints. They may sustain permanent damage if they are not treated appropriately. Most areas can be treated with range of motion and stretching, but opposing muscle group development may help to prevent further inj ury. Physical therapy rehabilitation should be offered to the competitive child athlete for complete healing and protection from further inj ury. Growing pains occur i n children from 3 to 6 years of age and are defined as aching in the lower legs, usually at night. The pain awakens the child from sleep and is relieved by acetam inophen, gentle massage, and heat. No joinr swelling or restriction in range of motion is associated with these pains. The pain may be worse after a day of vigorous activity. The etiology is thought to be similar to "shin spli n ts;" fascial strain due to rapid growth and activity leading to tight fascial sheaths. This is worsened with any structural problem and resrriction in normal movement. When evaluating for this problem, a good history will exclude the pos sibility of a serious issue such as osteomyelitis or osteosarcoma. Ie is i mportanr ro watch the child walk and correct any srruc tural problems of the feet with orthotics. Evaluation for sacral somatic dysfunctions and leg length differences, and rreatment of any lower extremity restrictions in motion, may relieve the fascial tension. The definitive treatment is fascial mobilization using counterstrain and i nstruction on stretching. Modification of activities that exacerbate this condition will also help. Juvenile Rheumatoid Arthritis
Juvenile rheumaroid arthritis O RA) is a group of diseases that involve chronic joint i nflammation and extraarticular symproms. The etiology is thought ro be auroimmune and may follow a viral infection. Infections and emotional distress trigger exacerbations of this condition. The disease causes swelling of the synovial membrane and joint effusion, followed by bony desrruction. In the polyarticular type of J RA, the small joints of the hands are affected. The joints have effusion and warmth, but no ery thema. This occurs bilaterally and can affect the cervical spine and temporomandibular jaw. H i p and sacroiliac involvement occurs later in the disease process. Mfected joints are tender ro rouch and motion, but not severely. In the pauciarticular type of J RA, the onset of arthritis occurs in a few large joints and those affected are usually asymmetric. Systemic manifestations include i ridocy clitis, rash, heparosplenomegaly, generalized lymphadenopathy, and pleuritis or pericarditis. Treatment goals are ro preserve joint function and support normal psychosocial development. Physical therapy and manip ulation using gentle techniques will help improve structure and
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function and maximize circulation to the joints. Keeping lymph Aow going via lymphatic pumps, and gentle joint pumping, will maximize the circulation of nutrients to the joi nts and the re moval of waste. Ba.lancing the sympathetics and parasympathetics via CV4 and rib raising will ensure good circulation to the joints and the synovial membranes that are al ready i n flamed. H VLA should b e avoided since the joint s are i nAamed, b u t muscle en ergy and the use of i ndirect or counterstrain work well and are tolerated. Maintai n i ng range of motion to T2-8 and T 1 0-L2 will help reduce associated visceral symptoms from facilitated seg ments associated with upper and lower extremity involvement. Diaph ragm mobil ity and removal of restrictions at the O-A j unc tion will optim ize Auid mobilization. Remember that ankylosing spondylitis can be associated with joint pain and is experienced as pain in the sacroiliac joint, hip, and back. The inAammation of the spine over time results in a rigid spine and starts in the lumbar spine and works its way up. This is opposite of J RA, which starts in the cervical spine. Treatment includes OMT to maintain range of motion, good posture, and max i m izing circulation of n utrients to and removal of wastes from the joint spaces. Untreated, the spine becomes stiff and i m mobile with loss of the normal curves. OMT can help to maintain segmental mobility but should be gentle. Indirect muscle energy and counterstrain techniques are most helpful. Chi ldren with J RA should be encouraged to maintain activi ties including non-weight-bearing activities such as swimming. Pain can be relieved by treatment of trigger points with inhibition and posi tioni ng. Special attention should be given to relieving any fascial restrictions to promote maxi mum range of motion and circulation. Daily CV4 cranial tech nique has been helpful in controlling symptoms.
RESPIR ATORY SYSTEMIC DYSFUN CTION Mechanics of Pediatric Respiratory System
An infant or small child is not a m i n iature adult in respiratory terms. The upper airway and nose account for the majority of airway resistance in adults. In children younger than 5 , the lower ai rway resistance is 2 . 5 times greater, accounting for the greater th reat to infants and young children from viral infections of the lower ai rway. Infant tissues are softer and the tissue planes are looser and more compressible than those in the adult. An infant with diffi culty breathing may recruit accessory muscles of the neck, tho racic cage, and abdomen to aid breathing. The increase i n force may cause ai rway collapse. Changes in ai rway resistance play a major role in pediatric pulmonary diseases such as asthma, pneu monia, and bronchiolitis. Because the muscles in the small air ways are incompletely developed during the fi rst years of life, young infants may be less responsive to bronchodilator therapy. Their sympathetic nervous system is well developed however, and they respond well to rib-raising tech niques. The genioglossus m uscle is innervated by the hypoglossal nerve and is the principal muscle maintaining the patency of the upper airway. It pulls the base of the tongue and hyoid bone anterior when it contracts, dilating the upper airway and oppos ing the negative pressure exerted by the diaphragm. Suppression
of upper-airway muscle activity may occur with sleep or severe esophagea.l reAux. Com pared to adults, the thoracic volume of a child is small due to short, narrow ai rways. Therefore, mucosal edema profoundly decreases the radius of the ai rway and increases the resistance. The cartilaginous ribs of the infant and young child are rwice as compliant as the bony ribs of the older child or adult. Infants' ribs are oriented i n a more horizontal di rection than those in adults because they articulate li nearly with the spinal column and sternum. There is anterior-posterior displacement during inspi ration. The intercostal muscles primarily stabilize the chest wall in the fi rst years oflife because they do not have the leverage to lift and expand the ribs. Therefore, though the diaphragm is the chief muscle of respiration in all patients, it is especially important in the child for i ts role i n generating changes in tidal volume. The diaphragm muscle fibers insert horizontally on the inner surfaces of the ribs in the infant instead of obliquely as in the adult. Ideally, breathing, vigorous crying, and nursing re-expand the overlap ping cranial bones. If this does not occur as nature planned, free ing any restrictions in the newborn's body helps establish optimal respiration. An infant who suffers more severe birth trauma, or other insult, may not have the vitali ty to self-correct. Newborn Diaphragm Dysfunction
A restriction or rwist i n the thoracic diaphragm, which can be caused by the rotation of the baby passing through the bi rth canal or by in utero positioning may also cause problems. Respiration may be irregular and the infant may be irritable or prone to the h iccups. For example, a rwin who was in a transverse lie throughout pregnancy conti n ued to have irregular breathing and grunting in his 3rd month of life. In addition, he was quite i rritable and never smiled. Examination showed a rwist through the thoracolumbar area and thoracic diaphragm. He also had marked lumbosacral compression, restricted temporal bones, and an O-A compression. Though he was born via cesarean section, the tight quarters of the uterus shared with his brother caused marked compression throughout his body. As he was treated and his diaphragm released, he began to visibly relax. His breathing became more regular and within a week he began to smile. H is parents were thrilled to have a happier, more relaxed baby. Newborn Temp oral Bone Somatic Dysfunction
At birth, the neonate's first breath must overcome the resistance of the lungs and the surface tension of the Auid in the lungs. The fi rst forceful contraction of the inspiratory muscles must be deep and accompanied by large transpulmonary pressures to overcome the surface and viscous forces. If the neonate has suffered trauma, infection, or the effects of drugs, the fi rst breath may not contain the force needed to establ ish effective respiration. Infants with respiratory difficulties have a higher incidence of temporal bones that are not moving in a symmetric, physiologic pattern. This type of strain may most commonly result from unilateral com pression of the condylar parts, or the occipital-mastoid area or the frontal-sphenoid area. When the temporal bones have restricted or asymmetric motion, the newborn or infant may have poor res piratory effort or uneven respiration. This may occur when the
22. GeneraL Pediatrics
sphenobasilar symphysis is compressed due to birth trauma as is seen in cephalopelvic disproportion. Release of restricted tempo ral bones and condylar decompression can aid the development of quiet, easy respiration, emphasizing once again the i mportance of structure and function. Osteopathic Approach to the Pediatric Patient with Respiratory Tract Infections
An inj ury, lack of sleep, poor nutrition, and/or social stress can predispose a child to be more susceptible to viral infections. Symptoms often start with activation of the immune system. In the upper respiratory tract, there would be signs of erythema, fever, or cough, signaling an immune response to a presumed infection and can also include wheezing, rales, retractions of ac cessory muscles of respiration, nasal flaring, and an increased respiratory rate. Treatment may include OMT, a variety of phar macologic agents, fluids, and in the case of airway swelling, home treatment with warm steam for about 1 0 minutes, cool outside air, and oxygen mist, if hospitalized. Otitis Media
Otitis media is the most common reason for a child to visit a pediatrician in the first 5 years of life. It is the most prevalent disease after respiratory illness in children, affecting nearly 20% of all infants in the United States. It is responsible for nearly 30 m illion physician visits per year. Acute otitis media is characterized by the sudden onset of in flammation of the middle ear, which is accompanied by fever, pain, and irritability. There is a loss of anatomic landmarks, ery thema, and bulging of the tympanic membrane. Chronic otitis media with effusion is a chronic inflammation of the inner ear that persists for 3 or more months. In this condi tion, the middle ear may be frequently retracted or concave and the child may present without signs of acute infection. Since the early 1 950s, the mainstay of medical treatment of middle ear infections has been antimicrobial therapy. Although antimicrobial therapy is shown to be about 20% more effective than placebo, studies show that once therapy is initiated the like l ihood of reinfection is high. Bacterial organisms most commonly involved in otitis media infection include Streptococcus pneumo niae, Haemophilus influenza, and Moraxella catarrhaLis. However, these organisms are rarely cultured from the middle ear even i n acute infections. Pathogenic bacteria can b e culrured from the middle ear in only 1 1 % to 22% of children presenting with acute infection. Viral etiology may play a role and is found in about 20% of symptomatic children. Thus, it is important to remember that any infection is a result of a combination of in fluences: degree of virulence and quantity of an infecting agent, along with host susceptibility. The osteopathic approach favors measures that improve host resistance and recovery concurrent with weakening, or eradicating the infecting agent. Allergens also seem to be important in both chronic and acute infection. It has long been known that exposure to tobacco smoke, wood-burning stoves, and airborne allergies are associated with increased frequency of otitis media. However, in recent years, food allergies have also been i mplicated. The most prevalent of these are allergies to dairy, wheat, and egg white.
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Regardless of the source, nearly all authorities on the subject refer to the key role the eustachian tube plays in the development of otitis media. The eustachian tube is a short canal found on the lateral wall of the pharynx connecting the middle ear to the nasopharynx. Like the respiratory tract, it is l ined with ciliated epithelial cells. These cells function to move secretions from the middle ear to the nasopharynx. The tube also functions to equil ibrate m iddle ear pressure with atmospheric pressure. The child who is less than 3 years of age has a relatively short eustachian tube and it is prone to collapse, especially during swallowing. At birth to about 3 to 4 years of age, the eustachian tube has a horizontal orientation. This changes to a more downward slant in children over the age of 4 and accounts for the dramatic decreased incidence of otitis media after this stage of development. When one approaches otitis media from a structural point of view, i t is clear that any structure placing tension on the eu stachian tube will increase the likelihood ofobstruction. Certainly hypertonicity of the posterior pharyngeal muscles, especially the medial pterygoid, the digastric m uscles, and dysfunction of the hyoid bone, may play an important role in eustachian dysfunc tion. Yawning, sucking, and swallowing aid the eustachian tube in equilibrating atmospheric pressure with middle ear pressure. However, uncoordinated, inefficient sucking and swallowing may worsen eustachian tube dysfunction and cause reflux. Irritation of the glossopharyngeal (CN IX) and the hypoglossal (CN XI I) nerves resulting from compression of the j ugular foramen and hypoglossal canal are the most common osteopathic findings as sociated with sucking and swallowing difficulty. This may also be yet another benefit of breast-feeding. I t is well known that infants who are breast-fed have a much lower incidence of otitis media. The i mmunologic makeup of breast milk certainly p l ays a m ajor role. However, the actual sucking process itself may also be involved. Infants who are breast-fed use an entirely separate muscular sequence compared to those who are bottle-fed. Breast-fed infants tend not to tongue thrust and therefore widen the arch of the hard palate. Bottle-fed infants, on the other end, tend to tongue thrust, pushing the rigid bottle nipple superiorly which results in a narrow hard palate reducing the relative space between the eustachian tube and the adenoids in the fossa of Rosenmuller. This predisposes the eustachian tube to reflux and obstruction. The use of pacifiers and chronic thumb sucking essentially causes the same process and may account for the i ncreased rate of otitis media reported in these children. Perhaps the most common structural finding in children with otitis media, however, is the association with impaired mobility of the petrous portion of the temporal bone. Prior to birth, the tem poral bone is i n three developmental parts, each of which moves physiologically relative to the others. The petromastoid portion, which develops i n the cartilaginous cranial base, contains the structures of the m iddle and inner ear. The squamous portion, developing i n membrane, forms a large part of the lateral wall of the skull. The tympanic portion, resembling a tiny horseshoe applied laterally to the petromastoid-squamosal j unction, pro gressively develops after birth into the external auditory canal. In the healthy child the temporal bones have a slight inter nal and external rotation movement, about 8 to 1 4 times per m inute. This physiologic motion aids in mucociliary transport and drainage of the middle ear. If this motion is impeded, then
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drainage of the middle ear will be impaired. The resulting fluid stasis may result in middle ear fluid accumulation and inflamma tion. When the temporal bone is i nternally rotated and its mo tion is restricted from moving into external rotation, eustachian tube blockage can occur. This can be further complicated by a hypertonic sternocleidomastoid muscle (SCM) , which will pull the petrous portion of the temporal bone i nto i n ternal rotation and prevent its motion i nto external rotation. A primary cause of such a restriction is direct trauma to the temporal bone from birth trauma or from a blow to the head. Birth trauma resulting in cranial somatic dysfunction predisposes the infant to otitis media. Hypertonicity of the SCM may also result from direct trauma, impaired mobility secondary to impaired diaphragmatic respira tion, or hyperirritability of the spinal accessory nerve. The spinal accessory nerve exits though the j ugular foramen at the base of the occiput. As has previously been discussed, this area is a common area of birth trauma. The goal ofOMT is to obtain unimpeded physiologic motion of the temporal bones, diaphragm, and lymphatic system along with a coordinated, efficient swallowing cycle that allows appro priate drainage of m iddle ear fl uid through the eustachian tube. OMT addresses somatic dysfunction found in the surrounding myofascial structures including the medial and lateral pterygoid muscles, the digastric m uscles, and the SCM on the side of the dysfunction. The O-A area should be addressed and any spe cific cranial strain patterns should be ameliorated. Several spe cific treatments can be used to address temporal bone motion dysfunction. Pharyngitis
Pharyngitis is one of the most common complaints of children, representing about 5 % of all pediatric visits. These children may present with i n flammation of the pharynx, adenoids, and ton sils. The lymphoid ring in the posterior pharynx, known as the Waldeyer ring, serve as a defense against infections of the mouth and throat. The most common cause of pharyngitis is susceptibility to a viral pathogen, primarily rhinovirus. Adenovi rus, which often additionally presents with rhin itis and a posterior cervical lymph node, is another common virus. Less commonly, bacterial etiology is an infectious agent, ac counting for less than 1 5% of cases. Group A ,B-hemolytic Strep tococcus is the most common bacterial pathogen. The tonsils may be covered with an exudate and the child may present with high fever, strawberry tongue, and scarlatiniform rash. If a bacterial pathogen is suspected, a culture and rapid antigen test should be obtained. Culture-positive disease requires antibiotic treatment to prevent rheumatic fever. Therapy must be initiated within 9 days of the stan of the symptoms. Therapy, however, does not decrease i ncidence of poststreptococcal glomerulonephritis. Structurally, there is i n flammation of the posterior pharyn geal muscles. The hyoid may be markedly restricted in motion on one side. There may be cervical lymphadenopathy and poste rior cervical somatic dysfunction. The medial pterygoid may be hypertonic. The child may have a narrow arched palate, which may be related to pacifier use, chronic thumb sucking, and mouth breathi ng. Restriction in the physiologic motion of the clavicles, tho racic outlet, and diaphragm may result in decreased lymphatic
drainage. This may be accompanied on the side of the dysfunc tion by hyperton icity of the SCM and elevation of the fi rst rib. Treatment. It is i mportant to increase fluids, and a wholesome diet free of processed, mucous-forming foods, especially dairy and sugar, should be encouraged. The underlying structural is sues must be addressed. The clavicle and first ribs should be free in their motion and the diaphragm should be released if re stricted. Somatic dysfunction of the anterior cervical fascia, the medial pterygoid muscles, and the hyoid bone should also be addressed. Last, techniques to enhance to the body's own inher ent immunity should be used. This may include lymphatic and splenic pump, compression of the fourth ventricle, and lymphatic drainage techniques. Anterior cervical fascial release and muscle energy techniques can be very beneficial. OMT can be helpful in the resolution ofpharyngitis. A simple, non invasive manual procedure is anterior cervical fascia stretch ing as outlined below:
The patient lays supine. The hands are placed beneath the cervical spine while the thumbs are gently introduced posterior to the SCM between the anterior fascial planes. • Extremely gentle stretchi ng of the soft tissue is performed until free motion is restored to the area. •
•
Muscle energy OMT can be used to release tense pharyngeal musculature as follows: • • • • • •
The child is in a sitting position. The cornu of the hyoid bone is held by the thumb and index finger, while the opposite hand stabilizes the cervical spine. The hyoid is grasped and moved to the right side and the left side, away from the midline. The hyoid is then held away from the midline on the side of greatest ease, while the child swallows several times. The procedure is then repeated on the opposite side. This results in relaxation of the pharyngeal musculature and often provides signi ficant relief from pain.
Croup
OMT is a great help in alleviating symptoms in children suffer ing from an illness such as croup. Physicians who are skilled with their hands can hasten comfort and recovery in mild croup and often eliminate the need for hospitalization in moderate to mod erately severe croup. Croup (acute laryngotracheal bronchitis) is common in young children and results from a viral infection of the subglottic area of the upper airway that causes acute in flammation and edema. Because a child's airway is small and the cartilage of the trachea soft, upper ai rway narrowing during inspi ration occurs more often in chi ldren than adults. The narrowest segment of a child's airway is the solid cricoid cartilage in the subglottic region, the origin of the characteristic hacking cough and often a hoarse voice. If there is a greater degree of airway obstruction, children may have inspiratory stridor and respira tory distress. Occasionally, respi ratory distress is so severe that endotracheal i ntubation is needed. Accurate diagnosis from history and physical examination is the fi rst step. Croup is a viral ill ness dut must be di fferentiated
22. General Pediatrics
from several more serious bacterial i nfections such as bacte rial tracheitis, acute epiglottis (supraglottis), and retropharyngeal abscess. , Osteopathic treatment of children with croup is directed at supporting normal physiologic processes and counteracting dele terious pathophysiologic processes. Because of the i nflammation and the edema, stimulating the sympathetic nervous system will help. I n contrast [0 the airway edema found in asthma due [0 bronchoconstriction, in croup, it is the vasodilation. Vigorous stimulation of the sympathetic chain ganglia in the upper tho racic region will aid vasoconstriction. Drug therapy follows a similar approach. Nebulized epine phrine rapidly ameliorates moderate [0 severe symp[Oms, but because its effects last only 1 [0 2 hours, i t is usually only used when a child is admitted [0 the hospital.
Bronchiolitis
Bronchiolitis is an acute viral infection of the lower respira[Ory tract in children up [0 age 2. It can cause mild to severe respi ra[Ory distress. The organism invades the epithelial cells of the bronchioles causing sloughing of the cells, edema, and increased mucus. Narrowing and overdistention of the small airways, un even air trapping, and the m ismatching of ventilation and blood flow (ventilation perfusion mismatch) can lead [0 hypoxemia. The diagnosis is based on clinical presentation, age of the child, and the time of year (28). The incidence of bronchiolitis increases i n winter and spring and can be caused by a number of viruses. The most common cause is respira[Ory syncytial virus (29) . Other viruses i nclude parainfluenza, adenovirus, rhinoviruses, influenza viruses, and Mycoplasma. Some symp[Oms may be more prominent depend ing on the viral cause. Each virus can cause different signs of dysfunction. For instance, rhinovirus can cause much nasal con gestion. With influenza virus, cough, diarrhea, and myalgias may be more prominent symp[Oms. Adenovirus may cause erythema and congestion in the pharynx. Mycoplasma can cause bullous myringitis (air behi nd the tympanic membrane) . In children under 5 years, lower airway resistance is 2 . 5 times greater than in adults. These changes in airway resistance make bronchiolitis a challenge in the young infant. In addition, the muscles in the small airways in very young infants and children may not be developed enough [0 make bronchodila[Or therapy helpful. However the sympathetic nervous system is well devel oped, making osteopathic techniques, such as rib raising, effec tive. As the heads of the ribs are raised, it is postulated that the thoracic sympathetic chain ganglia are stimulated. I n T l -6 this stimulates efferent activity [0 the airways, which i ncludes the re lease of epinephrine. Along the same lines, nebulized epinephrine has been found i n some studies [0 be helpful in infants hospi talized with bronchiolitis (30). In a child not needing hospital ization, stimulating the body's own supply of epinephrine avoids the possible rebound effect of the drug epinephrine. How long this effect lasts depends on the severity of the illness and the effectiveness of the physician perform i ng OMT. In using OMT co enhance effective physiology in any con dition, one must treat the physical fi ndings of that particular patient. Somatic areas important ro assess for somatic dysfunc tion and treat with OMT in patients with bronchiolitis include:
317
1 . Cervical region: The phrenic nerve (C3, C4, C5) provides mo[Or i n nervation co the thoracic diaphragm. Parasympathetic innervation co the vagus nerve can be addressed at the O-A and atlantal-axial (A-A) j unction. Techniques include O-A decom pression and myofascial release. 2. Rib cage: The work of breathing can be reduced by as suring that the thoracic cage has free motion. Optimizing rib cage motion will facilitate blood flow [0 and from lungs as well as enhance lymphatic drainage, improve i mmune response, and prevent accumulated bronchial secretions. Tech n iques include rib raising, scapula release, i ntercostal fascial release, thoracic diaphragm release, and clavicular release. Rib raising in an i n fant or small child can be done by encircling the rib cage with both hands; the fingerpads are placed bilaterally on the posterior inferior rib angles. Lateral and cephalad traction are applied. Be sure [0 note that the ribs are more horizontal in children than in adults. 3. Sympathetic nervous system: The sympathetic nervous sys tem can be addressed at the coscovertebral j unction. Rib raising i n itially stimulates sympathetic outBow, but ultimately will re duce sympathetic outBow. 4. Thoracic diaphragm: Free diaphragm motion is important in generating changes in tidal volume. Note the more horizontal i nsertions in infants. A seated or prone diaphragm release can be used in infants and small children . The posterior crural attach ments can be treated with lateral traction of the heads of ribs 1 1 and 1 2 . 5 . Sacrum: Free motion i s essential for efficient functioning of the respiracory system because of the dural tube which attaches at the foramen magnum, C2, and second sacral segment. In an infant or small child the sacrum can be gently decompressed; the physician p laces two fingers under the sacrum and uses caudal traction. 6. Temporal bones: Respiration is influenced through the ten corium cerebell i attaching [0 the petro us portion of the temporal bones. I f the temporal bones are restricted in i n ternal rotation, breathing will be shallower. The temporal bones are balanced co free motion . The sooner osteopathic treatment is ini tiated, the faster the re sponse. The respiracory rate can be counted before and after treat ment co assess the effectiveness of treatment. The lungs should be auscultated before and after treatment co assess the changes [0 see if secretions h ave cleared, whether or not there are fewer rhonchi and wheezes, and if the airflow has improved. Parents can be taught [0 do rib raising at home co continue treatment. Rib raising can be done once or twice a day for a m ild illness, and more often if i ndicated. Certainly, m uch research needs co be done co document the efficacy of OMT in i nfants with upper respira[Ory tract viral illnesses. The parents in our practice know the effectiveness of OMT i n respiracory illnesses. Belcastro and colleagues developed a research pro[Ocol for bronchiolitis (3 1 ) . The i nitial respiracory score was based on respiracory rate, retractions/nasal flaring, and cyanosis. The OMT included scapular release, rib raising, i nter costal fascial release, anterior and posterior diaphragm release, and cervical fascial release. Although the study was inconclusive due co a small number of patients and extremely short treatment time (60 [0 90 seconds), it provides a useful model.
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V Osteopathic Considerations in Family Practice and Primary Care
InFants and children develop respiratory problems for a num ber of reasons. As noted earlier, children's airways are smaller, magnifying distress caused by foreign invasion or structural issues. The following is a case h istory of a child with both issues. The patient was i n itially seen at 2 weeks of age. Labor began spon taneously 1 0 days early. Maternal medications included oxytocin, pain medication, and epidural anesthesia. There was some brady cardia. After a spontaneous vaginal delivery, the baby was gray and the cord was wrapped around his neck three times. Apgar scores were 3 and 7, and the newborn's muscle tone was low. He had a pectus excavatum with much drawing in of the chest with breathing. Upon examining h i m the following day, sacral compression, temporal bones held in internal rotation, and tight periscapular and intercostals muscles were noted. Using direct ac tion myofascial release O MT, rhe sacral compression was released, and temporal bones were released so they could move freely i n external a n d i n ternal rotation . Scapulae a n d i ntercostal muscles were released. Feedi ng improved after the first treatment. The baby received soy formula and Fed well without any problems. At 8 weeks of age he developed nasal congestion without fever, and a cough. Upon auscultation a few diffuse expiratory wheezes were heard. The infant's rib cage showed mild retractions but there was no nasal flaring. He was alert and feeding well despite a respiratory rate of 60. Due to h is age, the season (winter) , and the presentation of the illness, this child's distress was most likely related to a vi ral inFection and diagnosed as bronchiolitis. Osteopathic structural examination found a restricted costal cage and upper thoracic spine, especially at T2-4 on the left, i ncluding restriction of the left second to fourth ribs. OMT to address restricted areas in cluding rib raising was done initi ally on a daily basis for 2 days, then every 2 to 3 days until the baby's ill ness resolved. This infant avoided hospitalization as a result of OMT and reliable parents who knew how to count his respiratory rate and look for signs of respiratory distress. H e continued to receive regular osteopathic treatments directed at i mproving compliance ofh is musculoskele tal system and quality of motion of respiratory structures (i.e., sacrum, ribs, spine, cranium) , and by 6 months, his pectus ex cavatum was significantly reduced. He had one other episode of wheezing before he was a year old. The child is now 7 years old and has not gone on to develop reactive airway disease. Because bronchiolitis may lead to recurrent airway obstruction symptoms and many pharmacologic agents have limited effective ness, the search continues for the most effective treatment (32). The osteopathic approach of addressing the pathophysiology and somatic dysfunction can be of great assistance to patients with bronchiolitis. The authors (SC, MAM) have found that infants and children treated aggressively with osteopathic manipulation improve their respiratory status faster and are less likely to develop reactive airway disease. Osteopathic App roach to the Pediatric Patient with Asthma
Asthma is the most common chronic disease i n children and the most frequent admitting diagnosis in children's hospitals. The incidence of childhood asthma has dramatically i ncreased i n the last decade. Many external causes have undoubtedly contributed:
i ncreased environmental and chemical toxins, subcl inical nutri tional deficiencies from processed diets and devitalized soil lack ing trace minerals in commercial farmi ng, in addition to assaults on the human immune system. Asthma is a lung disease char acterized by (a) airway obstruction or narrowing that is usually reversible, (b) airway inflammation, and (c) bronchial hyperre sponslveness. Asthma is a prevalent disease in children that Favors boys ( 1 0% to 1 5%) over girls (7% to 1 0%)-a number that equal izes in adolescence as boys tend to outgrow their asthma more quickly than girls. Eighty to ninety percent of children who de velop the disease are symptomatic by 5 years of age and 30% are symptomatic as early as 1 year. A number of factors may precipitate an asthma attack: •
• • • • • • • •
emotional stress including anxiety, fear, anger, and suppressed feelings that may be caused by such Factors as a dysFunctional family exerCise gastroesophageal reflux inhaled and ingested allergens (e.g., pollens, mold, spores, house dust, mites, animal dander, food) inhaled i rritants (e.g., tobacco, smoke, air pollution, aerosol sprays, strong odors) medication (e.g., aspirin, nonsteroidal antiinflammatory drugs, ,Bblockers) poor diet or mucogenic foods (e.g., dairy products) viral respiratory infections weather changes (including wind and changes in temperature and humidity)
Additionally, mechanical inj ur ies can precipitate an asthma attack. This is especially true of injuries to the head or sacral regions. The authors (SC, MAM) have Found that a hard fall on the sacrum will often precipitate an asthma attack. It is essential to be sure the sacrum is fully released. One patient who had many hospitalizations for asthma had been under good control for several years, with the need for only occasional medication, suffered an exacerbation when he ran head-on into a railing, h itting his nose and bruising his Face. When the eFfects of the injury were removed, h is symptoms subsided. The clinical manifestations of asthma-wheezing, dyspnea, cough-are the result of airway obstruction that may develop grad ually or abruptly. The diameter of the airway lumen determines the amount of obstruction and is influenced by a number oFfac tors including airway smooth muscle contraction and hypertro phy. Bronchial smooth muscle is in nervated by the vagus nerve (CN X) and vasovagal reflexes can cause bronchoconstriction. Therefore, in asthma bronchial spasm and increased bronchial se cretions can be caused by overactivity of the bronchial branches of the vagus nerve. On a cellular level many changes also take place. Action of the sympathetic nerves innervating the bronchi are diminished and the normal equilibrium with the vagus nerve is disturbed. Physical Examination
<
Though wheezing is a characteristic breath sound in asthma, it may not be heard in the most severe cases in which all breath sounds will be markedly reduced. The physician should look for
22. Gen era! Pediatrics
TABLE 22.2. PHYSICAL SIGNS OF POTENTIAL AIRWAY OBSTRUCTION •
A prolonged forced exhalation
Decreased mobility of the
phase
thoracic cage, especi ally during exhalation
Whispering or inability to talk
N asal polyps, rhinitis, s i n usitis,
signals severe respiratory
tonsillitis
distress Evidence of l ung hyperinflation
Increased kyphotic spinal curve
(barrel chest) Use of accessory muscles (e.g.,
Mouth breathi n g, malocclusion, drool i ng
intercostals, scalenes, and sternocleidomastoid muscles) Pectum excavatum or
Allergic shiners, nasal crease
carinatum Agonal or anxious facial
Eczema, often in flexor creases
expression
the signs and symptoms outlined in Table 22.2 when examining the patient. To optim ize the effects of OMT these specific areas should always be checked for evidence of somatic dysfunction: I . Upper thoracic vertebrae, ribs, and sternum. 2. T I -5 to address sympathetic innervation to the lungs. 3. O-A j unction and the course of the vagus nerve to address parasympathetic responses. 4. Accessory muscles of respiration. 5 . Anterior cervical fascia. 6. Thoracic diaphragm (used in all phases of breathing, the pumping action of the diaph ragm also assists the adrenal glands. The phrenic nerve ftom the cervical plexus [C3-5J enervates the diaphragm. Its mobility is inAuenced by the lower six ribs, L l -2, and the sternum . ) . 7. Chapman reAexes for the lungs, sinuses, a n d adrenal glands. 8. Evaluate the cranial-sacral mechanism. Is there a sphenobasilar compression? Treat the sacrum and temporal bones to enhance the primary respiratory mechanism. 9. T I O L2 (significant for the relationship with the kidneys, adrenal glands, diaphragm, and ribs I I and 1 2) . -
In considering the differential diagnosis in patients with signs and symptoms of obstructive airway disease, search for the un derlying cause (Table 22.3). TABLE 22.3. DIFFERENTIAL DIAGNOSIS OF OBS T RUCTION IN INFANTS AND CHILDREN
AIRWAY
Obstruction of Large and Obstruction of Large Airway Foreign body in trachea, bronchus, or esophagus
Small Airways Asthma Viral bronchiolitis
Vascular rings
Bronchopulmonary dysplasia
Laryngotracheomalacia
Aspiration from swallowi n g
Enlarged lymph nodes or tumor
mechanism dysfunction or
Laryngeal webs
gastroesophageal reflux
Tracheostenosis or bronchostenosis
Vascular engorgement Pulmonary edema Croup Tuberculosis Pneumonia
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Osteopathic Management of Patients with Asthma
The most effective apptoach toward treating the child with asthma is mul tifaceted and involves treating the underlying pathophysiology and structural resrrictions, medications, diet, environmental control, breathing exercises, emotional support, and allergen reduction. It is evident that for heal th, there must be a balance of the sympathetic and parasympathetic nervous systems. During an acute attack, it is important to reassure and calm the child and the mother. Shortness of breath is very frightening. Acute treatment of asthma includes beta-sympathomimetic drugs to bronchodilate constricted bron chioles. In addition, osteopathic manipulation can aid the body in producing similar chemicals. The physician should focus on vigorous stimulation of the sympathetic nervous system, partic ularly T l -6, to aid in bronchodilation and rib raising to ease breathing. When a patient is too uncomfortable to lie down, initial treat ment can be performed with the patient seated or standing. After an acute attack, it is important to treat all aspects of the primary and secondary respiratory system. For healing, the imbalance in the nervous system must be corrected. The hands-on osteopathic approach involves the following: (a) aiding the body in balancing the parasympathetic and sympa thetic response of the nervous system; (b) optimizing blood Aow to and from the lungs; (c) lymphatic drai nage; (d) maintaining adrenal and glandular fun ction; and (e) assisting i n free motion of the rib cage, diaphragm, sacrum, temporal bones, etc., based on the physical findings. OMT ofchildren with asthma has several objectives. The most important is correcting the structural component of the illness. Often this addresses the underlying pathophysiology and leads to reduction of medication as well as a reduction of the frequency of asthma attacks. The patient and their parents also benefit from an i ncreased awareness of the body's ability to heal itself, leading to earlier, wiser, and more consrructive intervention. The authors (SC, MAM) have found that most children who receive early and regular osteopathic care, and whose parents are compliant with a healthy diet and early i n tervention, do not require maintenance medication. AT. Still had great success relieving asth ma and hay fever. He attributed his success to correcting spinal somatic dysfunctions, especially of the th ird and fourth thoracic vertebrae (2,3) . The presence of somatic dysfunction at this spinal segment is most l ikely due to a viscerosomatic reAex. It is also one of the spinal segments from which the sympathetic nervous system innervates the lungs. The most useful techniques for treating asthma patients in clude: thoracic stimulation while the patient is either seated or lying down; rib raising; scapula release; diaph ragm release; lym phatic pump via the feet and thoracic cage; evaluation and treat ment of the sacrum and head; and cervical, thoracic, and l umbar manipulation with myofascial release, muscle energy, counter strain, or HVLA, if appropriate for the patien t's age. A child unable to lie down can be treated in a seated position. The entire body should always be examined, as a somatic dysfunction in a distant extremity may be the cause of a fascial strain affecting the thorax or elsewhere. It has been our experience (SC and MAM) that if a child can receive a vigorous OMT with i n 1 2 hours of the
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V Osteopathic Considerations in Family Practice and Primary Care
onset of an asthma attack, the attack can often be broken without the use of medication. Medications for Asthma
Drug therapy For asthma focuses on treating the bronchospasm and inAam matory components of asthma. Many new drugs are being developed to address specific receptor sites. However as an osteopathic physician , we m ust not overlook the underly ing pathophysiologic cause of the problem. Bronchial asthma is presently regarded as a chronic inAammatory disorder with re versible airway obstruction and increased airway responsiveness to many stimuli. This suggests there is an altered response of the target organ and not a single i n Aammatory process (33). I t is important to be aware of all side efFects of any medication prescribed. Although inhaled corticosteroids are Far safer than systemic steroids, 80% of the i nhaled steroid passes through the gastrointestinal tract. Steroids adversely afFect the normal Aora of the intestine, contributing to "leaky gut" syndrome. This in tensifies allergic tendencies, which are usually already present. A diagnosis of asthma or allergy presupposes a stress on the adrenal gland. This stress is compounded by the use of steroids, which suppress adrenal function. When antiinAammatory medications are used, probiotic support for the i ntestinal tract is needed as well as nutritional support for the adrenal gland. Steroids are life saving and should be used when needed. However, they can cause side efFects such as immune suppression, shortened stature, weak ened bones, and cataracts. The physician must search deeper for causes and not rely on constant medication. Popular medications to treat asthma include: • • • • • • •
Beta-agon ists Mast cell stabil izers Corticosteroids (inhaled or systemic) Theophylline Anticholinergics Antibiotics (if bacterial infection) Leukotriene inhibitors
Environmental Concerns
Parents should be i nstructed on how to reduce dust, especially in the child's bedroom. Allergy covers should be used on mattresses and pillows. If carpets cannot be removed, they can be treated For dust mites. Sheets should be 1 00% cotton and washed i n hot water. Decorating that encourages dust collection should be avoided. In a damp climate, a dehumidifier may be needed. In a dry climate, a hum idifier can be helpful; however, it m ust be kept clean and Free of mold. The use of toxic chemicals, cleaners, and pesticides near the child should be avoided. Diet
When parents want to change the health of their child, it is es sential that they understand, quite simply, that we are what we eat. Parents must be to sustain a healthy diet For their child. Such a diet consists primarily of fresh vegetables, fruits, nuts (if toler ated) and seeds, brown rice, and whole grains. They must take a firm stand against their child's desire to i ndulge i n fast foods, sweets, processed foods, and artificially Aavored, preserved, or colored products. The importance oHresh foods to avoid chemi-
cals, allergens, and trans-Fats routinely cannot be overemphasized. Parents should be taught to read labels on all Foods because Food colorings, sulfites, preservatives, and other modifications oHood can trigger allergic reactions and asthma. For instance "modified wheat starch," a thickener used in many processed foods, is "mod ified" by six different chemicals, all of which can trigger asthma and allergic reaction. A "hypoglycemic diet" should be followed. Sufficient protein is important. Mucous-producing foods, such as milk, ice cream, excess cheese, white Aour, and sugar, should all be avoided. It is important to support adrenal gland health with adequate vitami n C plus bioAavonoids and a natural source of B vitami ns. Patients with asthma with a h igh dietary intake of magnesium have better lung function and a reduction in wheezing. Mag nesium deficiency increases the amount of h istamine released in the blood. Encouraging breast-feeding exclusively in the first 3 months of life decreases the incidence of children developing reactive ai rway disease (34) . Breathing Exercises
Breath ing is the only subconscious vital function that can be raised to a conscious level. Proper breathing helps the nervous system relax while shallow, spasmodic breathing signals alarm (35). Breathing exercises help strengthen peripheral and acces sory muscles that aid breathing. Many breath ing exercises can be adapted into games for children . Games are more Fun than "exercise" or "therapy." Since asthma is an air-trapping disease, expi ratory exercises are useful. For instance, a game can be cre ated out of blowing a ping pong ball across a table. Many children with respiratory problems use their diaphragm incorrectly, rais ing it with i nspiration i nstead of allowing it to descend. With the physician's hands cupped around the costal margins, the child "pushes the hands away" with a deep breath; the diaphragm is then allowed to rise on exhalation. The osteopathic approach to asthma provides a unique and effective treatment opportunity that addresses the structural com ponent of the illness, which reduces the need for medication and the frequency of attacks. In addition, OMT i ncreases awareness of the body's ability to heal itself and therefore encourages timely, more effective intervention. OMT is designed to balance the sym pathetic and parasympathetic responses, reduce mechanical im pediments to optimal thoracic cage motion, enhance lymphatic and venous drainage, improve arterial blood supply, and opti mize the primary respiratory mechanism. In addition, the osteo pathic physician can use such tools as medication, environmental change, breathing exercises, nutrition, and psychological support to enhance the effects of OMT. Parents and patients alike need to be taught to act immediately at the first sign of an impending illness or asthma attack. Most children with a h istory of asthma who are on a wholesome diet and receive excellent osteopathic manipulative medicine management do quite well with reduced or no medication. The Pediatric Gastrointestinal System
The gastrointestinal system is one of the most important sys tems in physiologic maintenance of health in children. It is fun damental for proper growth and development. Gastrointestinal
22. General Pediatrics
complaints are among the most common reasons a cbild is seen by a pediatrician. AT. Still and the early osteopathic physicians regarded tbe gastroi ntestinal system second only to the brain in its importance in well functioning of the body. In fact, it was often referred to as tbe second brain or abdominal brain. The enteric nervous system parallels the central nervous system in density and quantity of neurons. The system can be surgically separated from the central nervous system and still maintain physiologic function. Still attributed many childhood diseases to dysfunction of this system (3). Gastroesophageal-Reflux Disease
Gastroesophageal-reflux disease (GERD) presents as frequent emesis shortly after feeding associated with failure to thrive, apnea and bradycardia, or wheezing. These children may have signif icant i ncrease in their gag reflex. They often have a history of abnormal delivery events i ncluding vacuum extraction, augmen tation with oxytocin, and prolonged labor. Somatic dysfunctions found include sphenobasilar lateral strain or torsion, O-A com pression, and sacral torsions. These infants may have compres sion of the fourth ventricle due to foramen magnum asymmetry. These somatic dysfunctions produce abnormal stimulation of CN IX, C N X, and CN Xl. The i ncreased vagal tone is respon sible for bronchospasm, bradycardia, and delayed gastric emp tying. This is best treated by releasing the O-A restriction but may require treating the sacral base restriction simultaneously. The clinician should place the pads of the middle fingers over the condyles at the base of the skull, then apply gentle traction i n a n outward and upward direction until the tissue softens. Gen tle sacral traction may help facilitate release of the O-A somatic dysfunction. Constipation
Constipation in young children is a common com plain t and re sponds readily to OMT. An appropriate history and physical examination is an essential fi rst step in all cases. The history should especially focus on the dietary intake including noncom plex carbohydrates, and water i ntake. Psychosocial issues should be addressed in older children. Osteopathically, the physician should be careful to examine for autonomic imbalance and pay close attention to the A-A and O-A joints as vagus nerve involvement can contribute to auto nomic imbalance. Both the pelvic and abdominal diaphragms should be examined and treated since ptosis of the viscera may be a problem. The patient assumes the prone knee-to-chest posi tion and the practitioner gently lifts the intestines from the pelvis, thus restoring free uni mpeded motion and blood flow. This often brings immediate results. Treating the child with fascial release of the colon can be extremely helpful. Diarrhea
Diarrhea in the inFant and child is common and responds to OMT. The underlying cause must fi rst be addressed. Acute diar rhea, most often caused by viruses, must be differentiated from chronic diarrhea, which could have multiple causes. InFectious
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diarrhea should be difFerentiated from the noninfectious type. Regardless of cause, somatic dysfunction is often found. Decreasi ng hyperparasympathetic activity may be very benefi cial. The use of deep inhibitory pressure from Tl 0 to the sacrum is indicated. Deep pressure over the sacrum may result in de creased tenesmus. Correction oflumbar somatic dysfunction and rib raising will also be helpful.
NEUROLOGIC DYSFUN CTION IN CHILDREN
The nervous system of the child is a dynamic, expanding, and i nt egrated system that ulti mately affects all other vital systems of the child's body. Function of this system is dependent upon an unimpeded, physiologic, and integrated structure. This structure includes the osseous case that surrounds the brai n and spi nal cord, the delicate fascial and membranous coverings that lie beneath the osseous covering, the arterial, venous, and lymphatic chan nels, and the ligamentous and articular structures that check and allow motion. Impairment of this delicate suucture will impair Function. Evaluation of children from a neurodevelopmental approach can give valuable clues in developing a management plan, includ ing the utilization of OMT. It can serve as a guide to evaluate the success of ueatment of developmentally delayed children un dergoing osteopathic ueatment. In some instances, restoration of lost reflexes to cultivate i ntegrated arm, leg, and head movement and visual uacking may be needed. These exercises, when part of an overall osteopathic treatment program, can be very beneficial. Sensory neural developmenralists reFer to neurologically dis organized children as those children who are i nefficient in their ability to receive, process, store, and utilize inFormation through their five senses. They may exhibit hyperesthesia or hypoesthe sia. Hyperesthesia is defined as an abnormal increased response to sensory stimulation. Hypoesthesia is defined as an abnormal decreased response to sensory stimulation. For example, a child with tactile hypoesthesia may have an exuemely increased pain threshold, may exhibit selF-mutilating behavior in order to receive tactile pain stimulation, may constantly run their hands across the carpet to receive deep joint stimulation, and may seek and be contented with various Forms of vibration. Children with tactile hyperesthesia may refuse to wear certain types of clothing, exhibit exueme irritability from tags on clothing, may reFuse certain tex tured food or in some cases all solid food, and may be adverse to any type vibratory stimulation. These developmental i nefficiencies are thought to be the result of a disorganized nervous system. A number of studies show that brain growth and development occur at predetermined chrono logic ages. These predetermi ned times of rapid growth occur be tween 3 months oHetai life to about 2 to 3 years postnatally. The Fundan1ental cause of neurologic disorganization results from a child i nefFectively passing through or missing milestones at cer tain critical stages of neurologic and neuronal development. This may occur if there is prolonged i n terruption of normal inFant development and stimulation. As an osteopathic physician it is especially important to evalu ate children who have known somatic dysfunction for problems related to neurologic disorganization. Neural disorganization can
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V Osteopathic Considerations in Family Practice and Primary Care
be from organic or ex�ernal causes. A child who is seriously ill (i.e., a serious bacterial i l lness, seizures, chronic i l lness) during a rime of rapid neuronal growrh may nor receive adequare sensory moror srimularion i n a given area. Myofascial srrain and somatic dysfuncrion may also be a causative facror in l i m iting the child's active range of morion and opporruni ry for sensory stimulation and developmenr. The child never reaches rhe specific develop mental m ilesrone, yet the myelination associared wirh rhar mile srone continues to develop. The neural parhway is developed but the neurologic skill is never realized. External causes i nclude forced deprivation as seen in orphan children placed in cribs unril lare infancy with l irrle social or i ntellectual srimulation or the so-called border babies who are housed i n i nner ciry hospital nurseries and do not receive normal parent-child bonding and srimularion. I n neurologically compromised children manipularion di rected roward the auronomic nervous system may posirively affect rhe sensory responses and disorganization of the central nervous sysrem. Borh neurologically compromised and uncompromised children show marked im provement in srandard neurodevelop mental profiles upon receiving OMT compared with a control group (36) . Osreopathic treatment may improve the functional resrrictions or disabiliry, but because thar functional restricrion has been present during crucial periods of development, neuro logic disorganization may occur. In these cases it may be neces sary ro re-parrern the specific neurologic sequences thar may have been m issed. This is the focus of neurodevelopmental therapy. Al though osteopathic manipulation appears ro help in overall neu rologic development, if a child, because of funcrional disabiliry, does nor receive adequare neurologic stimulation, disorganization wi 11 often persist. Disorgan ization is the result of discrepancies in moror-sensory organization and the level or age of neuronal developmenr. The child may progress from a sirri ng position ro standing position or walking without ever crawling. The vestibular stimulation from side-ro-side turning of the head, ventral tactile stimula tion, ocular-foveal far and near vision stimularion, acousric spa rial srimularion, and cross-lateral hemispheric stimulation of the cenrral nervous system thar occur as rhe child crawls is never experienced. Wirhour this previous stimularion the child walks. However, the child may have deficits in coordination. The gair cycle may be abnormal. The child may have difficulry with deprh perceprion and orientarion in space. Because of the dispariry be rween neuronal growrh and developmental sti mularion and de pendi ng on rhe child's age and which level or levels of the brain are involved, the child may exhibit a number of problems in areas of learning, social izing, and behaving. Four principles govern sensory neural development. Firsr, de velopment is a conti nuous process that proceeds in a caudad cephalad direction. Therefore, rhe i n fant will inirially present with the mosr primirive reAexes at rhe level of the medulla and spi nal cord, such as rhe srartle reflex, Babinski reAex, and lighr re Aex. As neuronal developmenr proceeds, rhe well-organized new born will inirially have an aronic neck reflex and fencing pose ( 1 ro 4 months), which will lead ro rhe abiliry of rhe i n fant ro roll back ro front at 5 months. From 6 ro 8 months, as progressive neuronal development occurs, the infant will begin ro first crawl, and then creep. The myelinarion and developmental sti mulation
in the areas of rhe pons and midbrain mediare this. Sranding and walking begins at 9 ro 1 2 months as rhe correx develops. Second, the sequence of development is the same in all children. However, rhe rare of development may vary. Developmental rare is referred ro as superior, average, or slow. If given proper srimularion and neurologic feedback, slow children may increase rheir rate. Third, primirive reflexes musr be exringuished before corresponding vol untary movements can be obtained. This is parricularly imporranr in children who present with developmental delay and neurologic d isorganizarion. Persisrenr reAexes and persisrent hypersensiriv i ry or hyposensiriviry musr be overcome before proper neuro logic organizarion can occur. Fourrh, rhe rare of milesrone de velopment in one area may nor parallel rhe rare in anorher area. This is especially apparenr in children who are neurologically disorganized. Ir is imporranr rhar every child receive a developmenral screen i ng (Table 22.4) . Those wirh suspecred neurologic or develop mental issues may benefir from a more derailed profile of devel opment. The presence of primirive reAexes such as rhe srartle, rooting, Perez-Galant, and aronic neck reAexes should be evalu ared even in rhose children who are older and do nor appear ro have gross neurologic damage. Children with significanr deficirs can be given an exercise program thar effecrively re-parterns rhe nervous sysrem leading ro improved neurologic organizarion. Neidner worked with children who had muscular dysrrophy. H e developed an effecrive myofascial OMT procedure beneficial ro many children wirh rhis disease (Table 22. 5 ) . From rhe os teopathic point of view, structural inregriry permits freedom of physiologic motion allowing the in herent therapeutic capaci ry of the nervous system ro stimulate neurologic development, inte gration, and organization. Even a slight change in this structural integriry may alrer function. Osteopathic rrearment of the neurologic system involves diag nosis and treatmenr of the whole body si nce ligamenrous, mem branous, or fascial srrain within any part of the body can affect any orher part. We do not assume or confine treatmenr ro the cranium but evaluate the body as a unit focusing on areas that i m pair inherenr physiologic motil i ry. Colic
Colic, irritabiliry, and sleeplessness present with lateral and verti cal strain parrerns (parallelogram heads). They exhibit impinge menr of the accessory nerve (CN X I ) . This occurs in the foramen magnum but may be the result of the rorsion of rhe falx and tentorium. These infants often have sign ificant membranous re srrictions with poor cranial morion. They may have sacral base restriction. They have obvious abnormally shaped heads with one eye appearing "more shallow" than the other, and placed inferi orly. They may have a rorticollis (tilt rheir head and rotate ro the same side). These i n fants respond best ro release of rhe sacral re srrictions, then treatmenr of the srrain parrerns, rhe verrical rhen lateral. The strains are [I'eared by direcr, gentle remolding of any parietal and frontal abnormalities, and carrying the grearer wings of the sphenoid inro normal position. The O-A should be de compressed. Treatment of any trigger poinrs on the SCM i"s by palpation of tight fascial areas with the head benr ro the side and rotation unril the area softens.
22. General Pediatrics
323
TABLE 2 2 .4. DEVELOPMENTAL PROFILE Scale/Age Range
Mobility
36 mas 72 mas Satisfactory: 96 mas
Able to do skilled
22 mas Average: 48 mos Satisfactory: 67 mos
Walks and runs in
Excellent:
Average:
Language Uses first-grade
activities, evidences
vocabulary with
laterality
good sentence
Manual Writes on first-grade level
structure Excellent:
cross-pattern
Speaks five- to eightword sentences
Performs bimanual tasks efficiently
with good articulation
1 3 mos 24 mos Satisfactory: 45 mos Excellent:
Average:
Walks with arms held below waist
Speaks
25 words and
Capable of cortical
uses several
opposition
two-word couplets
b ilaterally and simultaneously
8 mas 1 2 mos Satisfactory: 26 mos
Excellent: Average:
Walks unassisted without pattern for
Spontaneously uses words
ten steps, arms
Capable of cortical opposition, either hand
elevated
4 mos 8 mos Satisfactory: 1 3 mos
Creeps in
1 mo Average: 2 . 5 mas Satisfactory: 4.5 mos
Crawls in
Excellent:
Average:
cross-pattern
Makes meaningful, and goal-directed
Has volitional prehensile grasp
sounds with good tonality
Excellent:
cross-pattern
Consistently has vital cry i n response to
Able to release grasped object
threatening sounds or events
Birth
Randomly moves arms and legs
Birth cry present
Reflexly able to grasp object
(Adapted from "Profile of Development." American Academy for Human Development. Piqua, O H ;
Apnea
In children with apnea, there is a marked reduction in the primary respiratory motion. They may have a cranium held in extension. Their head may appear long, from front to back, and narrow, from side to side. This is commonly seen in infants who were born prematurely who tend to have a high, arched palate. The temporal bones are fixed i n internal rotation. The sphenoid is fixed in extension. The foramen magnum is narrowed and the fourth ventricle is compressed. The brainstem modulation of homeostasis is abnormal which results i n high vagal tone causing apnea and bradycardia. Treatment includes release ofany cranial base dysfunction with restoration of the parasympathetic tone. This is accomplished with release of cranial base restrictions and any i ntraosseous re strictions in the sphenoid, if present. Associated sacral restrictions must be released. The major focus of treatment is to restore phys iologic brainstem activity. Closed Head Injuries
I njuries to the head and neck tend to be sudden accelera tion/deceleration i nj uries and to involve the soft tissue. Chil dren have flexible necks and relatively large heads. Their neu rologic system is still developing and the membranes are h ighly vascular. I nertial inj uries can result in concussion and whiplash. They present with the history of a blow to the head or a sudden change in directional forces, resulting in a brief period of loss
1 989.)
of consciousness or disorientation, with or without neck pai n . The palpatory findings i nclude cervical spasm a n d somatic dys function, cranial dysfunction, and a greatly diminished primary respiratory mechanism. These are treated with counterstrain or indirect/muscle energy OMT to the cervical somatic dysfunc tions. This is followed by cranial OMT for correction of any abnormalities and a CV4 to enhance the primary respiratory mechanism. The younger the child, the more significant the po tential for cranial dysfunction due to the susceptibility to strain of the membranous attachments.
Learning Disorders/Hyperactivity
Learning disorders are increas ingly common among children of all ages with few long-term or effective treatments. I n one study, 209 children between the ages of 4 and 1 4 diagnosed with learn ing difficulty were evaluated by osteopathic structural examina tion ( 1 2) . Seventy-two percent of the children with a learning difficulty diagnosis had a significant past history of birth trauma compared to only 28% i n the control group. Labor lasting more than 24 hours was highly associated with learning difficulty. Eye motor coordination and visual perception i mbalances were highly associated with children experiencing difficulty. Lateral strains of the sphenobasilar symphysis may be espe cially implicated in oculomotor disturbances. These dysfunc tions may be a result of intrauterine pressure or early postnatal or perinatal trauma displacing the axis of the orbit. This can cause
V Osteopathic Considerations in Family Practice and Primary Care
324
TABLE 2 2 . 5 . NEIDNER TECHNIQUE William Neidner, DO, recognized that in health, viewing the human body from above the head, there is a clockwise fascial rotation. This is a profoundly relaxing treatment and should be considered at the conclusion of a treatment program after more local strain patterns have been resolved.
1 . Patient Supine • • • •
Stand at the head of the patient with a hand over each shoulder, the fingers spread over clavicles and upper ribs. Test the ease of diagonal motion anterior and inferior of right shoulder and then left shoulder. In the counter-clockwise pattern the right shoulder will move more freely. Apply a direct fascial release (i.e., attempt to carry the left shoulder anterior to the patient's right shoulder and inferior while restraining the right shoulder posteriorly).
• Hold until the release occurs, and the left moves freely. • At the moment of release the resistance to the anterior-inferior motion of the left shoulder melts away. 2. Stand on the Left Side of the Table for All of the Following Five (2-6) Steps • Take patient's left arm, abduct it at the shoulder about 75 , flex it at the elbow 90 . • The operator slips their right arm posterior to the patient's left upper arm and rests their right hand on the patient's forearm. • Encourage internal rotation of the shoulder girdle by slightly lifting the upper arm toward the ceiling and depressing the forearm toward the floor.
• Wait for release and ease of motion to occur. 3. Place Each Hand on Either Side of the Lower Half of the T horacic Cage • Spread the fingers to encompass as wide an area as possible. • Evaluate ease of rotation: counter-c lockwise (right hand will carry right thoracic cage anteriorly and inferiorly more easily) clockwise when left thoracic cage moves anteriorly to right and inferiorly more freely.
• Apply direct action into the restrictive barrier until left side moves more freely anteriorly and inferiorly. 4. Assess Pubic Tubercles • In counter-clockwise pattern, left tubercle will be superior to right. • Apply direct action fascial release to move the left side inferiorly. 5. Place Hands over the Innominate Bones Bilaterally with T hu mbs over Anterior Superior Iliac Spine • Test for anterior-inferior medial motion of each side. • If counter-clockwise, right side will move more freely. • Apply direct action fascial release to bring left side into anterior, right, and inferior directions. 6. Left Lower Extremity • Flex hip about 45° and knee about 80 , adduct, internally rotate, and hold the thigh until there is fascial release of pelvic girdle into direction of clockwise motion.
7. Patient Prone with Face Turned to the Right • Stand at the head of the table with hands placed over the shoulders. The fingers are spread over the scapulae. • If counter-clockwise motion predominates the operator's right hand will carry the patient's left shoulder posteriorly, inferiorly, and medially more easily than the operator's left hand will move the right shoulder posteriorly, inferiorly, and medially.
• Apply direct fascial release through the left hand (i.e., to the patient's right shoulder, until the softening and ease of motion occurs). 8. Stand on the Left Side of the Table (i.e., the right side of the patient for all the following steps) • Take the patient's right shoulder to 80' of abduction and external rotation by lifting the hand toward the ceiling, and elbow with the upper arm posteriorly, medially.
• Turn to face toward the patient's feet. Grasp the lower thoracic cage with both hands spreading the fingers over the ribs and laying the thumbs beside the vertebral column.
• In counter-clockwise motion the physician's right hand will move the patient's left rib cage posteriorly, medially, and inferiorly more easily than is possible on the opposite side.
• Apply direct action fascial release to move the right rib cage (i.e., the operator's left hand posteriorly, medially, inferiorly). • Hold until softening and melting of the resistance occurs. 9. Facing the Child's Feet from the Head of the Table, Place Both Hands on the Iliac Crests, T humbs toward the Posterior Superior Iliac Spine • If counter-clockwise motion predominates, the operator's right hand will carry the patient's left innominate bone more easily into posterior, medial, inferior direction.
• Apply direct fascial release into the restrictive barrier. • Hold the pressure until release is palpated. 1 0. Place Right Hand over the Sacrum with the Heel of the Hand at the Base and Fingertips over the Coccyx • Reinforce with the left hand. • To encourage clockwise motion apply direct fascial release to the sacrum inferiorly on the patient's right side (i.e., with the operator's thumb) and anteriorly on their left side (i.e., with operator's little finger).
• Hold the pressure until release is palpated. 1 1 . Stand beside the Right Lower Extremity Facing toward the Head • With right hand under the knee and the left hand on the ankle, carry the hip to 45 of flexion with external rotation and abduction. • To encourage clockwise motion lift the knee toward the ceiling with a posterior, inferior motion while depressing the foot toward the floor. • Hold this direct fascial release until the softening and increased freedom of motion occurs.
22. General Pediatrics
changes of rension in exrraocular eye muscle resulring i n eye mus cle imbalance. These disrorrions would also change membranous, fascial, neural, and venous relarionships. Children wirh arrenrion deficir wi th hyperkinesis often p resenr with findings similar ro rhose wirh learning issues. Visual track ing and lareral strains of the sphenobasilar symphysis are often seen. However, rhe child with hyperactivity ofren has more severe findings. Compression of the sphenobasilar symphysis is often an issue. The occipiral condyles and rhe foramen magnum are often compressed, resulting in pyramidal and auronomic disrurbances. Cranial dysfuncrion may arise in these children from sacral com pression or orher disranr areas of rhe body. Frequently, condylar decompression and release of basilar compression will resulr i n immediate a n d dramaric improvements i n sympromarology. Clearly, regardless of diagnosis, treatmen t of rhe underlying cause of rhe child's symproms is essential. Cerrainly, attenrion ro diet and a nutririon program rhar is wholesome (in its whole stare) , unprocessed, and free of pesricides and insecricides can be helpful. In some cases neurodevelopmenral rherapy or develop menral optomerric rraining may be necessary once rhe underlying somatic dysfunctions are corrected.
CONCLUSION
New challenges are arising in pediatrics. More infertility issues have led to a myriad of inrervenrions. The n umber of mulri pIe births has risen, producing challenges rhar resulr from two or more fetuses sharing rhe small space in rhe urerus. The next decade will conrinue to produce new challenges for rhe osteo parhic physician working wirh children. In addition to infec tious disease, auristic spectrum disorders and developmental de lay, learning difficulries and behavioral issues, and environmenral and lifestyle-relared diseases are all on rhe rise. Major adulr dis eases, such as arherosclerosis, coronary artery disease, and hyper rension, l ikely have roors in childhood. Improving the healrh and well being of rhe general population requires attention during the earliest years of life. Osreoparhic srrucrural diagnostics and OMT used for chil dren can be significant modaliries for primary, secondary, and rertiary prevention. In general, children respond well to direct anion, articulatory rreatments, such as myofascial release, and mobilizarion. Older children also respond to a combination of muscle energy and mild thrust or HVLA. Cranial OMT is i nvalu able in the newborn period and rhroughout childhood. Counrer srrain rech niques are helpful if there are render poinrs related to the somatic dysfuncrion. Somatic dysfunctions related to acute inj ury often respond to indirecr rechniques. In many instances children are Aexible enough for somaric dysfuncrions to resolve spontaneously. Relieving mechanical stresses and strains palpable throughout rhe body wirh OMT has benefited children wirh neurologic and behavior problems, academic and perceptual problems in school, an increased susceptibility to disease, such as ear infections, fre quenr colds, reactive air disease, and gastroinrestinal problems. Unforrunarely, lirtle research on rhese modaliries has been at rempred. Osteopathic pediatrics provides a complete discipline
325
of healrh care for children; the furure requi res the expertise of osteoparhic pediatric specialists conducring scientifically based, randomized, and blinded clinical trials. The future of pediatrics will focus heavily on primary care and preventive medicine. As a primary care discipline, the pe diatrician is in an ideal posirion to affect health and well being. Lifestyle diseases rhat affect the majority of the popularion can be prevented or minimized by providing anticiparory guidance, es pecially during adolescence, in epidemiologically i mportant areas such as: Dietary counseling for conrrol of obesity and hypercholes terolemia • Drug, alcohol, and tobacco avoidance • Accidenr prevention •
Osteopathic pediatricians are responsible for systematically investigating and documenring applications of osteopathic con cepts and principles during the early stages of child develop men t. Early i nrroduction of osteopathic care can affect and improve neurodevelopmenral outcome significantly. Osteopathic treat ment of the child will conrinue ro be comprehensive, including osteopathic manipulation, nutrition counseling, strengthening and stretching exercises, and anricipatory guidance and preven tion.
REFEREN CES 1 . Bomboy RP. The Colden Anniversary History of the A merican College of Osteopathic Pediatricians, 1940-1990. Trenwn, N J : American College of Osteopathic Pediatricians; 1 990. 2. Srill AT. A utobiography ofA. T Stiff. Indianapolis, IN: American Academy of Osteopathy; 1 908. 3. SriiJ AT. Osteopathy: Research and Practice. Seattle, WA: Eastland Press; 1 992. Originally published in Kirksville, MO: Journal Printing Co; 1 9 1 0. 4. M illard FP, ed. Poliomyelitis. Kirksville, MO: Journal Printing Co; 1 9 1 8 . 5. Watson JO, Percival, E N . Pneumonia research in children at Los Angeles County Osteopathic Hospital. A prel iminary report. jA OA. 1 939;39(3) : 1 5 3- 1 59. 6. Arbuckle BE. Effects of Uterine Forces Upon the Fetus. jA OA. 1 9 54;5 3:499-508. Also in The Selected Writings of Beryl E. A rbuckle, D. o., FA. C. 0. P. The National Osteoparhic Institute and rhe Cerebral Palsy Foundation; 1 977: 1 2 1 - 1 4 1 . (Original reference: Little W) . On the inAuence of abnotmal parturition, difficult labors, premature births, and asphyxia neonawrum, on the mental and physical conditions or the child, especially i n relation w deformities. Trans Obstet Soc [ Londo n ] . 1 862;3:293-344 .) 7. Whiting 1. Can the length of labor be shortened by osteopathic treat ment. jA OA. 1 9 1 3:9 1 7-92 1 . 8. King H H . Osteopathic manipulative treatment in prenatal care: evi dence supporting improved outcomes and health policy implications. MOj 2000; 1 0:25-33. 9. Arbuckle BE. The Selected Writings ofBeryl E. Arbuckle, D. 0., FA. C. o. P The Narional Osreoparhic Institute and the Cerebral Palsy Foundation; 1 977. 1 0 . Barnes M. Osteopathic treatment of infants. jA OA. 1 94 1 ;40:242-243. I I . Upledger JE. The relationship of craniosacral examination find ings i n grade school children with developmental problems. jA OA. 1 978; 77: 738-754. 1 2. Frymann VM. Learning d ifficulties or children viewed in the light or the osteopathic concept. jAOA. 1 976;60-6 1 .
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1 3 . Woods R. A physical finding related w psychiatric disorders. jA OA. 1 96 1 ;60:988-993. 1 4 . Woods R. Structural normalization in infants and children with par ticular reference w disturbances of the central nervous system. jAOA. 1 973;72:903-908. 1 5 . Wales AL, ed. Teachings in the Science ofOsteopathy. Transcribed Lectures of WiLliam Carner Sutherland, D. 0. Portland, O R: Rudra Press; 1 990. 1 6. Frymann VM. Relation of disturbances of craniosacral mechanisms w sympwmawlogy of the newborn : study of 1 2 50 infants. jA OA. 1 966;65: 1 059-1 075. 1 7. King H , ed. The Collected Papers of Viola M. Frymann, DO: Legacy of Osteopathy to Children. Indianapolis: I N . American Academy of Os teopathy; 1 998. 1 8. Behrman RE, KJiegman RM, Jenson H B, eds. Nelson Textbook ofPedi atrics, 1 6th ed. Philadelphia, PA: WB Saunders; 200 I . 1 9. Greenman PE. Structural abnormalities o f children. jAOA. 1 97 1 ;7 1 : 1 57. 20. Magoun H I Sf. Osteopathic approach w dental enigmas. jAOA. 1 962;62: I I 0- 1 1 8. 2 1 . Frymann, VE The expanding osteopathic concept. AAO Yearbook, 1 967;67 : 5 0-62. Reprinted in King H H, ed. The Collected Papers of Viola M. Frymann, DO: Legacy of Osteopathy to Children. Indianapolis: I N . American Academy of Osteopathy; 1 998. 22. Magoun HI, ed. Osteopathy in the Cranial Field, 3rd ed. Kirksville, MO: Journal Printing Co; 1 976. 23. Magoun HI Sr. Entrapment neuropathy in the cranium. jAOA. 1 968; 67:643-652. 24. Magoun H I Sf. Entrapment neuropathy of the central nervous sys tem, part I I . Cranial nerves I-IV, Vl-Vl I l , X l I . jAOA. 1 968;67:779787.
25. Magoun H [ Sr. Entrapment neuropathy of the central nervous system, part I I I . Cranial nerves V, IX, X, X l . jA OA. 1 968;67:889-899. 26. Educational Council on Osteopath ic Principles Core Curriculum. Washingwn, DC: American Association of Colleges of Osteopathic Medicine; 1 988. 27. Beal Me. A review of the shorr-leg problem; and the shorr leg problem. I n: Peterson B, ed. Posture Balance and Imbalance. Newark, N J: American Academy of Osteopathy; 1 983:26-42. 28. Panitch H B . Bronchiolitis in infants. Curr Opin Pediatr. 200 I ;Jun 1 3 (3):256-260. 29. Oski FA, DeAngelis CD, Feigi nm RD, et ai, eds. Principles and Practice ofPediatrics, 2nd ed. Philadelphia, PA: J B Lippi ncott Co; 1 994. 30. Bertrand P, Aranibar H, Castro E, Sanchez I . Efficacy of nebul ized epinephrine versus salbutamol in hospi talized infants with bronchiolitis. Pediatr Pulmono! 200 1 ; 3 1 (4) :284-288. 3 1 . Belcastro M R, Backes CR, Chila AG. Bronchiolitis: a pilot study of osteopathic manipulative treatment, bronchodilawrs, and other therapy. jA OA. 1 984;83(9):672-676. 32. Kartan M. Epidemiologic evidence of increased airway reactivity in chil dren with a hiswry of bronchiolitis. j Pediatr. 1 999; 1 3 5(2 Pt 2):8- 1 3 . 33. Brusasco V, Crirnini E, Pellegrino R. Ai rway hyperresponsiveness in asthma: nOt just a matter of airway inAammation. Thorax 1 998;53:992998. 34. Gdalevich M , Mimouni D, Mimouni M. Breast-feeding and the risk of bronchial asthma i n childhood: a systematic review with meta-analysis of prospective studies. j Pediatr 200 I ; 1 39(2) :26 1 -265. 35. Firshein RN. Reversing Asthma. New York, N Y: Warner Books; 1 996. 36. Frymann VM, Carney RE, Springall P. Effect of osteopathic med ical management on neurological development in children. jA OA. 1 992;92: 729.
GERIATRICS THOMAS A. CAVALIERI
KEY CONCEPTS
H istorical perspective on geriatric medicine Theories and physiology of aging • Comprehensive geriatric assessment, i n cl ud i ng medical, functional, psychological, and social components • Special clinical concerns with the elderly: confusion, urinary incontinence, fall i ng, and iatrogenesis • Special contribution of osteopathic medicine to the elderly
•
•
The elderly require a special approach in medical care and treat ment; they are not j ust older adults. Elderly individuals have needs stemming from aging physiology, the psychosocial i mpact of aging, and age-related diseases. The approach to the care of the elderly must be multidisciplinary and holistic; it m ust be driven by the goals of health maintenance and optimizing func tion. Osteopathic medicine is ideally suited to provide an ap proach to cli nical care of the elderly aimed at achieving these goals.
HISTORICAL PERSPECTIVE
The National Institute of Aging promulgated the geriatric imper ative in the 1 970s and 1 980s. It called for health care professions to respond to unmet clinical needs of the elderly (I), and of fered academic, attitudinal, demographic, and economic reasons to j ustify this concept. Academic reasons for the geriatric i mper ative centered on the absence of clin ically relevant i n formation on geriatrics and gerontology in the curricula of health p rofes sional schools and training programs. Attitudinal reasons for the geriarric imperative focused on negative stereorypes o n aging be lieved to result in prejudice against the elderly and thought to be commonplace in our health care system. Demographic and economic aspects ofthe geriatric imperative focused on the rapidly rising number of people who were 65 years and older in the United States and the i mpact of this population on health care costs. Representing over 1 2% of the total U . S . population today, this group i s projected t o i ncrease t o more than
18% of the population by the year 2030. The mean life span by the year 2040 will conti nue increasing and is projected to be well into the eighth decade o f l i fe for both sexes. The "old old," those over age 8 5, are the most rapidly growing segment of the U . S . population . By the year 2040 i t is projected that there will be 1 million centenarians in the United States. With the elderly as the highest users of health care resources, these demographic changes will have an i mpact o n the cost of health care (2). The past two decades have witnessed the impact of the geri atric i mperative o n the development of geriatric medicine in this country. While it is generally believed that we are still far from meeting the health care needs of the elderly, the geriatric im perative has succeeded in spawning much-needed research in geriatrics and gerontology, influenced changes in medical edu cation, and significantly altered our approach to the clinical care of the elderly. Osteopathic medicine has contributed greatly to the development of geriatrics in the U n ited States.
AGING PROCESS
The aging process itself is far fro m being completely understood. Recognizing the i nterrelationship among structure, function, and homeostasis with regard to the aging process is critical to the clinical care of the elderly. While aging and disease are distinctly different, the effects of the aging process on various organ sys tems are believed to reduce the organ's capacity to respond to increased demand. This has been called impaired homeostasis; it has significant clinical impact.
Theories of Aging
Various theories of aging have been proposed. The immu nologic theory for aging attributes the decline in organ reserve seen with aging to the diminishing effects of the immune system. Thus, the thymus gland m ight be the master gland of the aging pro cess, beginning with its i nvolLltion at a young age. Numerous cell ular theories of aging are still actively being investigated . The transcription theory attributes aging to the cell's limited abiliry to repair errors in transcription that occur in all cells. The oxidative stress theory is a widely acceptable explanation of the aging process. This theory claims the oxygen converted
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V Osteopathic Considerations in Family Practice and Primary Care
TABLE 23.1. PHYSIOLOGY OF AGING AND CLINICAL IMPACT
Clinical Predisposition
Age·Related Change Body Composition and Conformation Decreased height Decreased lean body mass
Changes in pharmacokinetics
Decreased body water Increased body fat Aging Skin Thinning and sparseness of hair
Baldness
Hair follicles produce less melanin
Graying hair
Thin, fragile, wrinkled skin
Propensity to injury
Capillary fragility
Senile purpura
Decreased subcutaneous fat
Pressure sore
Atrophy of sweat glands
Difficulty in body temperature regulation
Decreased response to pain sensation and temperature
Accidents
Aging Eyes Loss of elasticity of lens
Presbyopia
Increased density of lens
Cataracts
Change in aqueous kinetics
Glaucoma
Decreased pupillary size
Falls and accidents
Sluggish light reflex Decreased color vision Increased glare sensitivity Aging Mouth and Teeth Loss of lingual papillae
Loss of interest in food
Poor taste sensation
Malnutrition and weight loss
Atrophy of olfactory bulbs and decline in sensation of smell
Decreased appetite
Resorption of gum and bony tissue surrounding teeth and bone of mandible
Loss of teeth and periodontal disease
Increased risk of gas poisoning
Aging Ears Decrease in cerumen glands
Drier cerumen
Atrophy of cochlear hair cells
Presbycusis
Loss of auditory neurons
Presbycusis
Aging Cardiovascular System Increase in blood pressure
Hypertension
Aorta and large arteries lose elasticity and systemic vascular resistance increases
Left ventricular hypertrophy
Decreased baroreceptor reflex activity
Orthostatic hypotension
Calcification and sclerosis of heart valves
Valvular stenosis, endocarditis
Calcification and sclerosis of conduction system
Conduction abnormalities
Altered cardiac output
Decreased hemodynamic response to stress
Decreased heart rate
Decreased response to stress
Aging Respiratory System Calcification of costal cartilages
Decreased secretion clearance
Decline in alveolar surface area
Effects of hypoxemia
Alteration in pulmonary function tests Decreased vital capacity
Increased risk of pulmonary complications
Decreased maximum breathing capacity Increased residual volume Decreased Pa02 Aging Renal System Progressive loss of renal mass
Alteration in drug pharmacokinetics
Decrease in renal blood flow Decreased tubular function
Greater tendency toward dehydration
Decrease in creatinine clearance
Increased risk of adverse drug reactions
Aging Nervous System Decrease in brain weight
Drug toxicities, delirium
Alteration in CNS neurotransmitters Decrease in memory
"Benign senile forgetfulness"
Decreased reaction time
Decreased
Altered sleep with decreased deep sleep and increased wakefulness
Increased sleep disturbances
Decreased vibratory sense
Altered gait
Decreased righting reflex
Falls, accidents
10 scores
Increased postural instability
Falls, accidents
Altered gait
Falls, accidents (continued)
23. Geriatrics
TABLE 23.1.
329
(continued) Age-Related Change
Clinical Predisposition
Aging Musculoskeletal System Loss of muscle mass
Decreased strength
Loss of bone mineral density
Osteoporosis
Osteoarthritis
Symptomatic arthritis
Fractures
Aging Hematologic System Decreased lymphocyte production Decreased bone marrow cellularity Decreased hematopoietic functional reserve
Predisposition for anemia
Aging Endocrine System Impaired glucose tolerance
Diabetes mellitus
Increased insulin resistance Decreased estrogen
Menopause, predisposition to osteoporosis and coronary artery disease
Aging immune System Decreased T-cell function
Predisposition to infections and malignancies
Decreased antibody production to new or old antigen
Predisposition to infection
Increased autoantibodies
Predisposition to autoimmune disorders
Aging Gastrointestinal System Decreased gastric HCI production
Altered drug absorption
Colonic motility diminished
Consti pation
Decreased calcium absorption
Osteoporosis
Decreased hepatic biotransformation
Altered pharmacokinetics
Decreased hepatic albumin synthesis
Altered pharmacokinetics
Aging Genitourinary System Decreased bladder capacity
Urinary incontinence
Alterations in pelvic support Enlarged prostate gland
Prostate obstruction
Diminished vaginal and cervical secretion
Pruritus, dyspareunia
Decrease in sexual response
Fear of impotence
during metabolism inro superoxide anions, hydrogen peroxide, and hydroxyl radicals causes damage overtime. Researchers have proposed that antioxidants, such as vitamin E, block the· effect of free radicals, thus slowing the aging process, but there is evidence to show that an rioxidants such as vitamin E can enhance the average life span in animal models. Other cellular theories of aging i nclude the error theory, redundancy failure, and the cross linkage theory (3,4). Physiology of Aging
The aging process itself is characterized by significanr inrerindi vidual variation, manifested by the concept of chronologic age versus physiologic age. Thus, an individual can have a chrono logic age of 75 but a physiologic age of 5 5. Another basic concept of physiologic aging is that the changes with age are l inear (i.e., occurring at the same rate over time). Also, these changes are cumulative and actually begin at a young age, usually in the third decade. As such, an SO-year-old is not aging faster than a 40-year old but has the cumulative effects of the aging process over three or four decades (Table 23. 1 ). Later sections in this chapter review age changes that have pro found clinical impact. Understanding the relationship between structure and function, and taking into accounr age-associated altered homeostasis are vital to geriatric clinical care. With ad vanced age the body composition changes, causing a decrease i n
height, lean body mass, and body water, along with an increase in body far. These changes, which alter the vol ume of distribution of certain drugs, have signi ficanr effects on pharmacokinetics with age and must be considered in prescribing drugs for the elderly. Dermatologic changes such as a decrease in subcutaneous fat, loss of sweat glands, and capillary fragiliry predispose the elderly to easy bruising, pressure sores, skin tears, and difficulry in body temperature regulation (5). Ophthalmic changes consist of a loss of e1asticiry of the lens, causing presbyopia, an i ncrease in the near poi nr of vision. Thus, with age, abil i ry to read fine prinr dimin ishes. Loss of auditory neurons and cochlear hair cells results in presbycusis, a dimin ished abiliry to hear high-pitched sounds. Changes i n the cenrral nervous system (CNS) i nclude: Loss of brain weight Diminurion of many neurotransmitters • Decline in memory • I ncreased postural i nstabiliry • •
These changes have been linked to the increased prevalence of deliriu m and falls in the elderly. Although these changes may result in some cognitive losses with age, demenria is not a normal concomitant result of these neural changes. Changes in the m usculoskeletal system due to aging include a loss of m uscle mass and a decrease in bone mineral densiry. These effects o n bone predispose the elderly to osteoporosis and
330
V Osteopathic Considerations in Family Practice and Primary Care
fractur es. This factor m ust be considered i n the selection of certain osteopathic manipulative techniques in this age group. Various changes take place in the cardiovascular system with age. Systolic blood pressure and, to a lesser extent, diastolic blood pressure increase with age, contributing to increased hyperten sion in the elderly. Calcification and scletosis of the heart valves predispose the elderly to valvular stenosis and endocarditis. The cardiac output at rest is unaltered, b ur with increased exertion there is a decreased hemodynamic response. Pulmonary changes consist of a decl ine in alveolar surface area, a decrease in vital capaci ty, and a decrease in the partial pressure of arterial oxygen. These changes are believed to predispose the elderly to postoper ative pulmonary complications. With age there is a considerable decl ine in the number of nephrons of both kidneys, causing a significant decline in crea tine clearance which may vary among individuals. This has an im portant clin ical impact on the prescribing of drugs for the elderly because many drugs are eliminated through renal excre tion. Caution must be used in prescrib i ng such medication to the elderly in view of diminished renal function. [mmunologic changes consist of a decrease in Tcell function, a decrease in antibody production, and an increase in autoantibodies. These changes might account for the higher i ncidence of infections, ma lignancies, and autoimmune disorders in the elderly, as reflected in the imm unologic theory of aging (5).
COMPRE HENSIVE GERIATRIC ASSESSMENT
Most medical care provided for the elderly is adm inistered in primary care settings, an arena in which osteopathic physicians have been at the forefront. Primary care physicians skilled in the care of the elderly should recognize the importance of continu ity of care and manage their patients, if possible, in all clinical sites where the elderly receive care, including the office, hospital, home, and other long-term care settings. The physician skilled in geriatric med icine should be comfortable providing care in all these sites. Care is multidisciplinary. No one health care pro fessional can meet all the mul tidimensional needs of the elderly. The physician must be willi ng to collaborate with multiple health care providers, such as nurses, social workers, physical therapists, psychologists, pharmacologists, other medical specialists, and clergy. At the heart of geriatric care is the goal of optimizing fUllction for the elderly, avoiding institutionalization, and maintaining the patient, as much as possible, in the comm u n i ty. This can be achieved through careful multidimensional evaluation coupled with a plan that stresses health maintenance and d isease preven tion. This approach has been rooted in osteopathic philosophy for decades. The multidimensional evaluation of the elderly consists of a medical, social, functional, and psychological assessment. This has been called the comprehensive geriatric assessment and in geriatric assessment programs is performed by a geriatric mul tidisciplinary team often consisting of a geriatr ician, geriatric nurse, gerontologic social worker, and other healthcare profes sionals. The beneficial effects of this team approach have been well documented, and include accuracy in diagnosis, decrease in
unnecessary medications, avoidance of institutionalization, and increased longevity (6) . Comprehensive geriatric assessment usu ally incorporates the use of assessment tools to measure various aspects of the evaluation, such as function, cognition, and affect (7). While not all elderly patients can or need to be evaluated in a comprehensive geriatric assessment program, this multid imen sional approach to eval uation of the elderly can be incorporated i n to the primary care physician's practice. Medical Assessment
The medical component of the comprehensive geriatric assess ment i ncludes the history, physical examination, and review of the baseline laboratory screening tests. There are significant differ ences berween assessmen t of the elderly and assess men t ofyounger adults. Common obstacles should be kept in mind when assess ing the elderly. For instance, atypical presentations of diseases are common. If this dimension is not considered, important cli nical problems can easily be overlooked in the elderly. For example, delirium might be a manifestation of pneumonia, or a patient might appear to have dementia when the problem is actually depression. V isual and hearing losses commonly contribute to commu n ication problems. Practitioners should see their elderly patients in a quiet, well-lit room and speak slowly in a deep voice while facing the patient, when necessary. It is a common myth that older people overreporr problems. Actually, the elderly tend to underreport symptoms, possibly be cause of fear, embarrassment, misconceptions about normal ag i ng, or cognitive i m pairment. Older persons might fail to report impotence because they believe it to be normal for their age or fai l to report urinary incontinence because of fear of institution alization . While the patient is the prime source for the history, other sources for history taking can be invaluable. This might be particularly necessary when the patient has cognitive distur bances. Sources can include family, other physicians, past medical records, and visiting nurses, among others. Because the elderly often have multiple concurrent problems, the history might be associated with multiple complaints. Pa tience and clin ical skill should be exercised to prioritize and sort out each complaint. A careful medication history is vital in the assessment of the elderly and should include both prescribed and over-the-counter preparations. The elderly use more medications than any other segment of the population, using over 40% of all medications while representing over 12% of the population. The elderly have the highest incidence ofadverse drug reactions; which means the physician should view new complaints as possible drug reactions. Elderly patients should be asked to bring all prescribed and over-the-counter medications to appointments periodically to be evaluated by the primary care physician. This has been re ferred to as the "paper bag test" because it often results in a bag ful l of medications for the physician to review. Also, it is impor tant when asking about allergies to differentiate true allergy from medication side effects; older people often report a histo ry of a drug side effect as an allergy. The review of systems for the elderly is different becaus� it must focus on questions that reAect common problems for which
23. Geriatrics
the elderly are not likely to report. Examples include: Falling Impotence • Depression • Change in bowel habits • Urinary incontinence • •
Because nutritional problems are so common in this age gtoUP, particularly for elderly men living alone, a dietary assessment is important. The history should also address ethical issues such as patients' views on advanced liFe suppOrt, their relationships with their families, and the presence of advance directives. The physical exami nation can take longer with the elderly be cause ofdecreased mobility. Patience is required. Parts of the phys ical exami nation may be performed in an order different from the usual to accommodate special situations, such as wheelchair bound or bed-bound patients. Because the elderly are oFten em barrassed about their situation in life or reluctant to undress for a physical, the physician should exert care to avoid un necessary exposure. Be aware of age-associated changes in physical findings that differentiate age and disease. Blood pressure evaluation should include both supine and standing measurements because of the frequency of orthoscasis in the elderly. Because visual distur bances and hearing disorders are common in the elderly, it is important to assess vision and hearing. Weight should be mon itored carefully because nutritional problems are common. Gait should be observed; gait disturbances are common and often lead to Falls. CareFul assessment of the carotid arteries for bruits is important because of the increased Frequency of carotid artery disease. The cardiac examination often reveals a grade I or I I systolic ejection murmur as a result of age-related changes of the aortic valve. Bibasilar rales on exami nation ofthe lungs might not reflect pulmonary disease or heart failure but could indicate atelectasis, particularly in immobile, bed-con fined patients. The abdominal examination should include deep palpation for the presence of an abdominal aortic aneurysm. Leg edema is commonly found and is usually the result of chronic venous stasis rather than heart Failure. The neurologic examination should include a careFul assess ment of cognitive status, using a standardized assessment dis cussed in a later section of this chapter. It should be kept in mind that ankle j erks are oFten absent bilaterally in the elderly without clinical significance, and there is a diminution of vibratory sense of the lower extremities with age. Because musculoskeletal dis orders increase significantly with age, predisposing the elderly to functional disability and immobility, the importance ofthe struc tural examination cannot be overemphasized. It is important to assess For somaric dysFunction, ranges of motion, postural dis turbances, and abnormalities of gait. Developmental structural changes of the spine such as kyphosis and scoliosis are common in the elderly and should not be overlooked. Because of physiologic changes with age, interpreting stan dard laboratory data is different for the elderly. Knowledge of age-associated alteration of various laboratory parameters is im portant to prevent overdiagnosis or underdiagnosis (8). The
TABLE 23.2. LABORATORY
VALUES
THAT
331
DO
NOT
CHANGE WITH AGE Hepatic Function Tests Serum bilirubin AST ALT GGTP Coagulation Tests Biochemical Tests Serum electrolytes Total protein Calcium Phosphorus Serum folate Arterial Blood Tests pH Paco2 Renal Function Tests Serum creatinine Thyroid Function Tests T4 Complete Blood Count Hematocrit Hemoglobulin RBC indices Platelet count
(F rom Cav al i eri lA, Ch opra A, Bryman PN. Wh en outsid e th e norm is normal: interpreting lab data in th e aged . Geriatrics. 1992;47(5) : 6 6 -7 0, wi th permission.)
erythrocyte sedimentation rate and blood glucose i ncrease with age, For example, whereas creatinine clearance and serum albu min decline. Serum electrolytes and hemoglobin are unchanged with age (Tables 2 3 . 2 and 23.3) (9). Functional Assessment
At the heart of comprehensive geriatric assessment is a deter m ination of the patient's physical Functioni ng. This consists of an evaluation of the patient's ability to perForm the activities of daily l iving (ADLs) and the instrumental activities of daily living (lA DLs) . The ADLs include: • • • • • •
Bathing Toileting Feeding Dressi ng Grooming Ambulation
The lAD Ls involve a higher level of functioning and include such tasks as: • • • • • • •
Housekeepi ng Meal preparation Telephone use Financial management Shopping Transportation Medication administration
This i nFormation is essential to aid the physician in deter mining recommendations for patient placement such as the need
V Osteopathic Considerations in Family Practice and Primary Care
332
TABLE 23.3. LABORATORY
VALUES
THAT
DO
CHANGE
WITH AGE
TABLE 23.4. MINI-MENTAL STATE EXAMINATION Maximum
Degree
Value
of Change
Score Orientation
Alkaline phosphatase
I ncreases 20% between 3rd and Bth decades
Biochemical tests Serum albumin
Slight decline
Uric acid
Slight decline
Total cholesterol
Increases 30-40 mg/dL by age 55 in women and age 60 in men
HDL cholesterol
Increases 30% in men; decreases
Triglycerides
Increases 30% in men and 50%
Serum B12
Slight decrease
Serum magnesium
Decreases 15% between 3rd and
30% in women in women
Bth decades Decreases 25% between 3rd and Bth decades Creatinine clearance
Decreases 10 mUmin/1.73 m2 per decade
T3
Possible slight decrease
TSH
Possible slight increase
Glucose tolerance tests Minimal increase (within normal range) 1-h postprandial blood sugar
Increases 10 mg/dL per decade after age 30
2-h postprandial blood sugar
Increases up to 100 mg/dL plus age after age
White blood cell count
5 Where are we (state) (county) (hospital) (floor)? Reg istration 3 Name three objects: one second to say each. Then ask the patient to repeat all three after you have said them. Give one point for each correct answer. Repeat them until he or she learns all three. Count trials and record number. Attention and Calculation 5 Begin with 100 and count backwards by 7 (stop after five answers). Alternatively, spell "world" backwards. Recall 3 Ask for the three objects repeated above in #3. Give one point for each correct answer. Language 2 Show a pencil and a watch and ask patient to name them. 1 Repeat the following: "no 'ifs', 'ands: or 'buts'"
Thyroid function tests
Fasting blood sugar
5 What is the (year) (season) (date) (day) (month)?
40
Decreases
3 A three-stage command: "Take a paper in your right hand; fold it in half and put it on the floor." Read and obey the following: (show subject the written item). CLOSE YOUR EYES Write a sentence. Copy a design (complex polygon as in Bender-Gestalt). 30 Total score possible
(From Fol stein MF, Fol stein 5, McHugh PRo Mini-Mental State: a practical method for grad ing the cognitiv e state of patients for the cl inician. Psychiatr Res 197 5;12: 189- 198. El sev ier Science Ltd , Oxford , E ngl and with permission.)
(From Cav al ieri TA, Chopra A, Bryman PN. When outsid e the norm is normal: interpreting l ab d ata in the aged . Geriatrics. 1 992;47(5) :66-7 0, w ith permission.)
for home care, a nursing home, or a residenrial care facility, The funcrionaJ assessmem can be obtained by quesrioning the parienr or family or by di rect observation. Direct observation is probably superior bur is rime consuming. W i dely used srandardized assess menr tools enable rhe clin ician to perform a functional evaluation ( 1 0,1 I). Psychological Assessment
The psychological assessmenr of the elderly evaluates both cog n irion and affect. Srandardized, vali dated assessmem tools are widely used both to screen for and measure dememia and de pression . A careful assessmenr of cognirion is an essemial aspecr of geriarrics. Oriemation, regisrrarion, arremion, recall, and lan guage should all be tesred, The mosr widely used cognitive assess mem tool, the M i ni-Memal State Examination, is easily admin isrered and reproducible, and enables rhe clinician to measure and follow rhe pariem's memaJ starus (Table 23.4) ( 1 2 ) . Demen ria can easily be m issed in rhe elderly if the cli nician does not perform a cognirive assessment. Depression, which has its high esr incidence in rhe elderly, can presenr arypically and be easily misdiagnosed. Assessing affect by quesrion i ng rhe parienr abour signs and symptoms of depression is important. The use of a stan dardized assessmenr tool, rhe Geriarric Depression Scale, aids i n recognizing a n d quanrifying depression (Table 2 3 . 5 ) ( 1 3 ) .
TABLE 23.5. GERIATRIC
DEPRESSION
SCALE
(SHORT
FORM) Choose the Best Answer for How You Felt Over the Past Week 1. Are you basically satisfied with your life?
yes/no
2. Have you dropped many of your activities and
yes/no
interests? 3. Do you feel that your life is empty?
yes/no
4. Do you often get bored?
yes/no
5. Are you in good spirits most of the time?
yes/no
6. Are you afraid that something bad is going to
yes/no
happen to you?
7. Do you feel happy most of the time?
yes/no
B. Do you often feel helpless?
yes/no
9. Do you prefer to stay at home, rather than going
yes/no
out and doing new things? 10. Do you feel you have more problems with memory
yes/no
than most people? 11. Do you think it is wonderful to be alive?
yes/no
12. Do you feel pretty worthless the way you are now?
yes/no
13. Do you feel full of energy?
yes/no
14. Do you feel that your situation is hopeless?
yes/no
15. Do you think that most people are better off than
yes/no
you are?
Negativ e responses for questions 1, 5, 7 , 11, and 13 i nd icate d epression. The remaind er of positiv e responses ind icate d epreSSion. (From Yeasav age JA, Brink TL. Dev elopment and v alid ation of a geriatric d epression screening scal e: a preli minary report.) Psychiatr Res 1983;17 : 1, 37-49. E l sev ier Science Ltd . , Oxford , E ngl and , w ith permission.)
23. Geriatrics
333
Social Assessment
TABLE 23.6. DIAGNOSTIC CRITERIA FOR DEMENTIA
Assessmenr of the patienr's socioeconomic siruation is essel1[ial [0 comprehensive geriatric care. Knowing the family strucwre and the patiem's relationship with their family is importanr, as fami lies are still the most prevalel1[ caregivers in a com munity. Understanding the patiel1['s values and attiwdes roward various therapies is also importanr. Idel1[ifying the patiem's suppon sys tem, whether it is informal, such as the family, or formal, such as community agencies, is likewise essel1[ial. The physician should be aware of the patiel1['s fi nancial resources ro determine the feasibility of access ro certain services. The physician must be aware of and actively il1[erface with var ious community agencies or programs that provide vital support services for the elderly. These include the local Area Agency on Aging, visit i ng n urses' associations, Meals on Wheels, and Adult Protective Services.
A. The development of multiple cognitive deficits manifested by both: (1) memory impairment (impaired ability to learn new information or to recall previously learned information);
(2 ) one (or more) of the following cognitive disturbances: (a) aphasia (language disturbance) (b) apraxia (impaired ability to carry out motor activities despite intact motor function) (c) agnosia (failure to recognize or identify objects despite intact sensory function) (d) disturbance in executive functioning (i.e., planning, organization, sequencing, abstracting). B. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
e. The course is characterized by gradual onset and continuing cognitive decline.
(Adapted from Diagnostic and Statistical Manual of Mental Disorders. DSM-IV. 4th ed. Washington, DC: American Psychiatric Association; 1994.)
SPECIAL CLINICAL CONCERNS
Geriatrics spans a broad spectrum of clinical concerns addressi ng issues ranging from prevel1[ive care for a healthy active elderly individual [0 the managemel1[ of a frail 90-year-old person with multi ple problems. Certain cli nical problems for the elderly are of extreme importance because of both their profound clinical impact and increased prevalence. These problems i nclude: Confusion Incominence • Falling • Iatrogenesis • •
Umil recen tly, these problems received linle anenrion either from a clinical or a research perspective, yet they accoul1[ for high morbidity and mortality in the elderly.
chorea, inoperable brain rumors, and Parkinson disease. The re maining 1 0% result from treatable causes such as the effects of various drugs, brain tumors, v i tamin BI2 or folate deficiency, de pression, thyroid disturbances, and CNS infection ( 1 6) . Once demenria is diagnosed, a careful workup is needed [0 maxim ize treatmel1[ options and aid in prognosis. It is importam [0 rule o u t the presence of a treatable dementia. A comprehensive geriatr ic assessment is necessary [0 evaluate the multidimensional needs of the patiel1[ with dementia. The diagnostic workup involves a series of blood tests includi ng: • • • • •
Confusion
Disrurbances of cognirion consisr of demel1[ ia and del irium and are common in the geriarric population. While cognirion remains relatively inract with normal aging, demel1[ia affecrs more rhan 25% of those over the age of 80. Signs of demel1[ia i ncl ude: gradual onset; dysfunction of mulriple spheres of il1[ellecr such as memory, abstract thinking, and j udgmenr; unaltered state of consciousness; and inability [0 perform ADLs (Table 23.6) ( 1 4) . Unlike dementia, delirium is a potel1[ially life-threatening ill ness thar is sudden in onset and is associated wi th a clouded state of consciousness and a disturbance of the sleep-wake cycle (Table 23.7). I r is often a result of a [Oxic or metabolic disturbance ( 1 5) . Because delirium is a potel1[ially life-threaten ing disorder, i t i s im ponam thar the clin ician differel1[iate demel1[ia from delirium (Table 23.8). In addition [0 an increased prevalence in the elderly, demel1[ia has a tremendous impacr because it is a common reason for in stitutionalization and is one of the leading causes of monality af fecting the elderly. Alzheimer d isease accoul1[s for approximately 50% of the causes of dememia; multi-infarct demel1[ia accoul1[s for another 25%. Fifteen percen t of demel1[ias are caused by irre versible disorders of the CNS, such as Pick disease, H Ul1[ing[On
•
Complete blood coum Blood urea n i trogen Serum creatinine Thyroid function tests V itam i n BI2 and folate levels Serologic test for syphilis
I f indicated, a serologic test for human i m m unodeficiency virus ( H I V ) should be considered. Computed [Omography (CT) or magnetic resonance imaging ( M R I ) of the head should also be ordered. At t i mes, an electroencephalogram, neuropsychological testing, and a l umbar puncture are useful in the workup. Because
TABLE 23.7. DIAGNOSTIC CRITERIA FOR DELIRIUM
A. Disturbance of consciousness (i.e., reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shih attention. B. A change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia.
e. The disturbance develops over a short time (usually hours to days) and tends to fluctuate during the course of the day. D. There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by the direct physiologic consequences of a general medical condition.
(Adapted from Diagnostic and Statistical Manual of Mental Disorders. DSM-IV. 4th ed. Washington, DC: American Psychiatric Association; 1994: 132-133.)
334
V Osteopathic Considerations in Family Practice and Primary Care
TABLE 23.8. DIFFERENTIATING
DELIRIUM
FROM
DE
MENTIA
incontinence: Urge Stress • Overflow • F u nctional •
Delirium
Dementia
Onset
Sudden
Insidious
Consciousness
Reduced
Clear
Attention
Globally disordered
Normal
Cognition
Globally disordered
Globally impaired
Hallucinations
Usually visual
Often absent
Delusions
Fleeting, poorly
Often absent
systemized Psychomotor activity
Increase or decrease
Usually normal
Speech
Often incoherent
Word-finding
Involuntary movements
Asterixis or coarse
Often absent
Physical illness/drug
Present
difficulty tremor Often absent
toxicity
the problems of the patient with dementia span the dimensions of medical, behavioral, n ursing, ethical, and social needs, man agement should be multidiscipli nary. The physician m ust be an effective team leader to access and i mplement the plan of care. Osteopathic physicians, with their emphasis on holistic primary care, are well suited for this role. Skillful management can con tribute significantly to the well being of the patient and their family ( 1 7) . While the precise cause o f Alzheimer disease is still unknown, recent clin ical and basic science research have expanded our un derstanding of rhis devastating disorder. Data suggest a genetic link to Alzheimer disease probably related to chromosome 1 4 , 1 9, or 2 1 . Diagnosis requires careful clinical assessment and the exclusion of other causes for dementia. Cholinesterase i n hibi tors are now available as cognitive enhancing agents for the treatment of Alzheimer disease. Donepezil is most widely used. These agents are best used for mild and moderate disease. Their long-term effect is still being studied. Other agents being as sessed as possible cognitive enhancers include estrogen , non steroidal anti-inflammarory agents, gingko biloba, and vitami n E ( 1 8 , 1 9).
Urinary Incontinence
Urinary incontinence is a common disorder that is referred to as a hidden ill ness in the elderly because it is often overlooked by clinicians and because the elderly often do not report i t out oHear of institLltionalization. In fact, urinary i ncontinence is of ten the last event to occur before n ursing home placement. This problem afflicts approximately 1 0% of the com m u n i ty-dwelling elderly, 30% of the elderly i n acute care settings, and approxi mately 50% of n ursing home residents. Its i mpact is seen in the psychological effects of isolation and depression, the potential for skin breakdown and infection, and the economic i mpact of institutionalization and costs of care. Although i ncontinence can occur acutely as a result of drugs or infection, the focus here is on persistent inconti nence. An u nderstanding of normal m ic turition is essential to understand the mechanisms and manage ment of this problem. There are four types of persistent urinary
•
Urge i ncontinence, the most common type in the elderly rep resenting approximately 65% of cases, is the result of an unstable bladder with uninhibited bladder contractions. Patients with this type of inco nt inence have the sudden urge to void but simply can not make it to the bathroom in time. I t is commonly the re sult of CNS conditions such as stroke, dementia, and multiple sclerosis. It can be successfully treated with anticholi nergic drugs to relax bladder contractions and biofeedback to aid in bladder relaxation . Stress i ncontinence occurs primarily in women and accounts for 1 5% of cases. It is manifested by incontinence with coughing or laughing and is related to weakness of the pelvic musculature and urethral incompetence. Treatment can be accomplished by estrogen cream to enhance the integrity of the urethra, exercise, biofeedback to improve strength and tone of the pelvic muscu lature, and beta-adrenergic agonists to improve urethral tone. At ti mes, surgical i ntervention is needed. Overflow i ncontinence represents approximately 1 0% of cases and is often described as being associated with a dimin ished stream and leakage of small amounts of urine. It might be the result of urethral obstruction because of prostatic enlargement or a urethral stricture. It m ight also be the result of a distended acontractile bladder such as occurs in diabetes mellitus or as a complication of anticholinergic drugs. A urologic evaluation is essential to rule out obstruction. Cessation of anticholinergic medications is important, and if obstruction is ruled out, a trial of cholinergic agonists may be i nitiated. F unctional incontinence accounts for the remaining 1 0% of cases. This type is the result of the patien t's physical inability to reach the toilet in time. It is usually a result of a problem with mobility, such as advanced arthritis, muscle weakness, or strokes. Treatment centers on making toilet facilities more readily available or obtaining a bedside commode. The role of the primary care physician in the recognition and management of this i nconti nence is essential, and particularly in volves coordinating the involvement of the multiple disciplines of nursing, social work, and urology (20). An indwelling Foley catheter should be avoided except in rare circumstances, such as with the presence of severe pressure sores. Significant advances have been made in clinical research in the treatment of i nconti nence. Once believed to be a disorder surgically treated by the urologist with l ittle success, new data suggest that modalities ini tiated by the primary physician, coupling medical treatment with exercise and behavioral management, can result i n improvement of most community-dwelli ng, cognitively intact elderly i ndividu als with incontinence (2 1 ) . While many osteopathic clinicians re port increased efficacy when manipulative management is added to this regimen, studies are underway to document its efficacy. Falling
Gait disorders and instabiliry o ften result in falls in the elderly, and have a profound impact on the clinical care of older individ�lals.
23. Geriatrics
Accidents are the fiFth leading cause of death in the elderly; ap proximately 70% of accidenrs resulr From Fal ls. Considering the decrease in bone mi neral densiry with age, Fractures of the hip, femur, wrist, and humerus are not uncommon. H i p fracrures lead ro hospitalization, complications of surgery, and complications of immobiliry. There is a significant risk of instirutionalization after hip fracture; some clinicians report mortaliry rates as high as 20%. Until recently, l ittle attention has been focused o n why the elderly Fal l and what measures can be taken ro prevent falls and their consequences. Changes in postural control such as a decrease in proprioception and m uscle tone, a slower righting reAex, and an increase in postural sway are all thought ro con tribure ro Fal ls. The increased incidence of various disorders with age, such as degenerative j o i nt disease, strokes, peripheral neu ropathy, muscle weakness, and impaired vision, are all believed to contribute ro the increased Frequency of Falls. The causes For falls in the elderly are classified as either extrinsic or i n trinsic. Extrinsic causes account For approximately 50% of Falls and are largely a result of environmemal Factors such as poor l ighting, throw rugs and frayed carpets, unstable Furn i rure, and inappropriate bed or roilet heights. I n trinsic causes For Fal ls include such problems as syncope, drop attacks, cardiac dysrhythmias, strokes, transient ischemic attacks, seizures, Parki nson disease, and orthostatic hy potension (Table 23.9) (22). Drugs such as antihypertensives, sedatives, anti psychotics, and hypoglycemics are also common causes of Falls in the elderly. Evaluation of the fall ing patient should include a careful h is rory of prior falls, a review of the patient's medical starus, and a list of all current medications. The review of systems should include questioning the patient regarding symptoms suggesting transient ischemic attack, dysrhythmia, seizure, and so on. A careful physical examination should include supine and stand ing blood pressures For onhostasis, an assessment of visual acuiry, evidence of joint or limb deformiry, disorders of the feet, and evidence of muscle weakness or sensory deficits found in the neurologic examination. Gait should also be observed. A careFul structural examination can reveal m usculoskeletal abnormali ties that might be conrriburory. Depending on the results of the his rory and physical, various laborarory studies such as a complete blood count, electrolytes, and blood urea nitrogen might be in order. Other srudies that might be appropriate include an elec troencephalogram , CT of the head, electrocardiogram, 24-hour Holter moniror, or carotid Doppler. An evaluation by a physical therapist and a home environmental assessment for hazards by a visiting nurse or occupational therapist are often necessary. Management consists of treating the primary underlying dis order iF discovered. Physical therapy for gait training and use of an assistive device such as a walker or cane might be in order. En vironmental manipulation such as improving lighting, increasing roilet height, and installing saFery bars m ight also be necessary. The team approach ro care of the Fall ing patient, incorporating the nurse, physical therapist, occupational therapist, and others, can contribute significantly to the outcome. Recent research has revealed that this approach can reduce the frequency offalling for elderly individuals who have a high risk of falling by 30% (23). Research is under way ro demonstrate the im pact of osteo pathic manipulative treatment (OMT) on prevention of Fal ls in the elderly. Specialized assessment programs For falls have
335
TABLE 23.9. INTRINSIC CONDITIONS LEADING TO FALLS AMONG OLDER A DULTS
Condition Orthostatic hypotension
Symptoms Along with Fall Lightheadedness with postural change Palpitation or postural sway along with postural change
Diabetes mellitus
Reduced sensation of lower extremities
Vitamin
B 1 2 deficiency
Cardiac arrhythmia
Reduced proprioception Palpitation,
shortness of
breath,
dizziness, or syncope Transient ischemic attack or cerebrovascular accident
Unilateral weakness, visual disturbance, or speech changes
Seizure
Aura, urinary or bowel
Osteoarthritis of hips or knees
Weakness in quadriceps or knees
Hyperthyroidism/
Proximal muscle weakness of lower
incontinence, or syncope (or both) hypothyroidism
extremities
Polymyalgia rheumatica
Pelvic girdle weakness or quadricep
Norma I pressu re
Ataxic gait, urinary incontinence,
muscle weakness (or both) hydrocepha I us Central nervous system lesion
and dementia Mental status change Focal neurologic deficit
Meniere's syndrome, labyrinthitis, or benign
Poor balance, ataxia, vertigo, dizziness
positional vertigo Hypoglycemia
Acute onset of mental status change, tremors, dizziness, weakness, or diaphoresis
Alcohol intoxication
Ataxic gait, mental status change, slurred speech
(F rom Cav al ieri TA, G ray- Mic el i D. Eval uati ng and prev enti ng f al l s among the eld erl y popul ation. JAOA. 1 994; 94(7):6 1 0-6 1 4, w ith permission.)
contribured ro m uch needed clinical research relevant to this important clinical syndrome i n the elderly (24). latrogenesis
The elderly are particularly prone to iatrogenic disorders. Altered homeostasis coupled with the Failure of physicians to recognize the special needs of the elderly contribute ro the increased fre quency of iatrogenesis in this age group. Common iatrogenic problems in the elderly include polypharmacy, immobi l i ry, and unnecessary hospitalization. The elderly have a high Frequency of adverse drug reactions; studies show that the incidence of ad verse drug reactions i ncreases sign ificantly with age. It has been reponed that approximately 40% of hospi tal ized elderly patients develop an adverse drug reaction. Studies have also demonstrated that approximately 3% of all hospital admissions are the result of drug-induced disease, and the majoriry of these patients are el derly. Srudies show that adverse drug reactions increase with the n umber of medications taken . These observations are believed to occur because of a decrease in the therapeutic window with age. Both pharmacokinetic and pharmacodynamic changes occur that predispose the elderly to adverse drug reactions. Changes in body composi tion, such as a decline in serum albumin, altered hepatic metabol ism, a decline in renal function, and changes in absorption, all contribute to the pharmacokinetic al terations.
336
V Osteopathic Considerations in Family Practice and Primary Care
Changes in receptors with age result i n altered sensitivity to cer tai n drugs. All of these changes are compounded by the problem of polypharmacy, common with the elderly. Elderly people take approximately fou r to five medications; nursing home patients av erage eight medications. [t is estimated that approximately 25% of medications prescribed for the elderly are u nnecessary. Re Aex drug prescribing has led to unnecessary medications. Ap propriate and rational drug prescribing for the elderly is essen tial. Effective non pharmacologic treatment modalities, such as OMT, are particularly preferred for the care of the elderly when indicated. Unnecessary bed rest and i mmobility are common iatrogenic problems for the elderly patient, particularly in hospitals and nursing homes. Physicians often fail ro recognize the complica tions of i mmobil ity for their patients and neglect orders such as appropriate ambulation, rotating the patient, or physical therapy consultations. Consequences of prolonged immobility and bed rest include: • • • • • •
Pressure sores Pneumonia Venous thro m boembolism Constipation Contrac[Ures Urinary inconti nence
Manipulative treatment m ight prevent many of the complica tions experienced by i mmobile geriatric patients. The rib-raising techn ique is easily performed and has a beneficial effect on the circulatory, respiratory, and nervous systems. The integral rela tionship of struc[Ure and function is the osteopathic concept most applicable to the consequences of i m mobility. M usculoskeletal activity is essential to maintain homeostatic mechan isms. Admission to the hospital can result i n significant dangers to the health of the elderly, unnecessary hospitalization should be avoided. Aside from the potential complications of medication and bed rest, hospital ized patients experience increased hazards as a result of diagnostic and therapeutic procedures and nosocomial infections. Diagnostic procedures that incorporate contrast me dia, such as arteriography, cardiac catheterization, or intravenous pyelography, are potentially risky procedures for the elderly be cause of a higher incidence of contrast-induced renal disease in the aged kidney. Elderly patients with diabetes mellitus and dehy dration have an even greater risk of developing contrast-induced renal disease. Hospitalized elderly patients are also at high risk of developing virulent nosocomial i n fections as a result of po tential i m m unosuppression related to their underlying illness as well as age-related changes in immune function. M icroorgan isms such as Staphylococcus or G ram-negative rods rapidly col on ize the oropharynx, ski n , or urinary tract and predispose the elderly to hospital-acquired pneumonias, urinary tract i n fections, and wound infections. The physician treating geriatric patients should consider every attempt to avoid hospitalization of the patien t in their management approach. Specialized acute care for the elderly units have been shown to be more effective for the management of elderly patients requiring admission to the hospital. Management is provided by a m ultidisciplinary team of health care professionals specially trained in the care of the elderly
patient. Beneficial outcomes have included: Decrease in medication use Avoidance of n ursing home placement • Improvement in functional status • I mproved survival rate • •
More research is needed to determine the effectiveness of geri atric units in acute care hospi tals (9) .
GERIATRICS AND OSTEOPATHIC ME DICINE
The past few decades have seen enormous growth and develop ment of the discipline of geriatric medicine in the United States. This has been an o utgrowth of recognized unmet needs of the elderly within our health care system. Osteopathic principles and practice mesh n icely with basic concepts of geriatric medicine and offer osteopathic medici ne a unique role in the growth and development of geriatrics in this country. I ncorporation of manipulative treatment into the clinical care of the elderly is an important modality of treatment that os teopathic physicians have as part of thei r therapeutic approach. Physicians often approach these patients with the use of phar macologic treatment and fail to i ncorporate other modalities of treatment such as physical therapy or manipulative treatment. Medications such as nonsteroidal antiinAammatory agents often have adverse effects on the elderly, heightening the imporrance of including nonpharmacologic means of treatment. Manipulative techn iques are beneficial to the elderly; as with any therapeutic modality, there m ight be a need to adj ust certain approaches to fit the special needs of the elderly patient. The increased frequency of osteoporosis and decline in bone m ineral density with age should d iscourage the use of cerrain high-thrust, high-velocity techniques in the elderly. Soft-tissue manipulation using muscle and fascia-stretching techn iques is particularly effective for many of the m usculoskeletal complaints of the elderly. Range of motion, respiratory, muscle energy, and craniosacral techniques are all beneficial approaches for geriatric patients. Al though O M T is a valuable tool in the management of geriatric patients, controlled, randomized studies are under way to docu ment its efficacy and expand its acceptance ( 2 5 ) .
CONCLUSION
M any principles that have guided osteopathic medicine for decades are the same principles that are at the hearL of geriatric medicine. The whole-person approach of osteopathic medicine is essential to geriatric care and involves a multidisciplinary, multi dimensional approach to the evaluation and management of the elderly that considers the medical, socioeconomic, psychological, and functional aspects of the patient. The primary care setting is the best forum in which to i mplement this comprehensive care program. Primary care, stressing health maintenance, has been a true strength of osteopathic medicine and is vital to holistic geriatric care. The integral relationship of structure to function has been at the core of osteopathic medicine and is epitom ized in the philosophy of geriatric medicine that has as its goal the
23. Geriatrics
maintenance of function. Osteopathic physicians are uniquely qualified to meet the health care needs of the elderly.
337
method fo r grading the cognitive state of patients for the clinicia n.
} Psychiatr Res. 1 975; 1 2: 1 89- 1 98. 1 3. Yeasavage JA, B r i n k TL.
Development and validation of a geri
atric depression screening scale: a prel iminary report. } Psychiatr Res.
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I . Buder R N . Geriarrics and inrernal medicine. Ann Intern Med. 1 979;9 1 : 903-908. 2. National Center for Health Statistics. Health, United States, 1 999, with Health and Aging Chartbook. HyattSville, MD: US Department of Health and Human Services, 1 999; D H H S Pub. no. (PHS) 99- 1 232. 3. Yates FE. Theories of aging: biological. In: Encyclopedia o/Gerontology, vol. 2, 1 996:545-5 5 5 . 4. HayRick L. HolV and Why We Age. New York, NY: Ballanrine Books; 1 994. 5. Kenney A. Physiology 0/Aging. Ch icago, I L: Yea r Book Medical Publish ers; 1 989.
1 5 . Cavalieri TA. Acute confusional states i n the geriatric population. }A OA. 1 984;83( I I ) : 80 1 -805. 1 6. Barry pp, Moskowitz MA. The diagnosis of reversible dementia in the elderly. A rch intern Med. 1 98 8 ; 1 48: 1 9 1 4- 1 9 1 7. 1 7. Cain T, Jurivich DA. Primary care guidelines for the evaluation of con fusion in the elderly. }A OA. 1 994;94(7) :60 1 -605. 1 8 . Small G W. Treatment of Alzheimer's disease: current approaches and ptOmising developmen ts. A m } Med 1 998; 1 04(4A) :32S-38S. 1 9 . Small G W, Rabins TV, Barry PP, et al. Diagnosis and treatmenr of Alzheimer d isease and related disorders. Consensus statement of the American Association for Geriatric Psychiatry, the Alzheimer's Associa
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7. Cavalieri TA, Chopra A, Gray-Miceli D, et a l. Geriatric assessment teams in n u rsing homes: do they work) }A OA. 1 993(Dec);93( 1 2). 8. Cavalieri TA, Chopra A, Bryman E When outside the norm is normal: i n terpreting lab data in the aged. Geriatrics. 1 992;47(5):66-70. 9. Kane R, Ouslander J, Abrass I. Essentials o/Clinical Geriatrics. New York, NY: McGraw- H i li Co; 1 999. 1 0. Kane RA, Kane RL. Assessing the Elderly: A PraeticaL Guide to Measure
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2 1 . Scientific Committee of the First I n ternational Consultation on In continence. Assessment and treatmenr o f uri nary inconti nence. Lancet 2000;3 5 5 : 2 1 53-2 1 5 8 . 22. Cavalieri TA, Gray-Miceli D. Evaluating and preventing falls a m o n g the elderly population. }A OA. 1 994;94(7) :6 1 0-6 1 4. 23. Tinetti M E, Baker D L, McAvary G, et a l . A multifactorial interaction to reduce the risk o f fa l l i ng among elderly people l i v i ng in the co mmun iry.
N EngL} Med. 1 994;33 1 ( 1 3 ) : 8 2 1 -827. 24. Close J, El lis M, Hooper R , et a l . Prevention of falls in the elderly trial (PROFET): a random ised controlled trial. Lancet 1 999;353:93-97. 25. Dodson D. M a n i p ulative therapy for the geriatric patient. Osteopath
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N
OSTEOPATHIC CONSIDERATIONS IN THE CLINICAL SPECIALTIES
INTRODUCTION MICHAEL A. SEFFI NGER
Although predom i nantly primary care oriented, osteopathic physicians have engaged i n a wide vari ety of specialty disciplines si nce the early years of the profession. Incl uded a mong th ese are gen eral and orthopedic surgery, ophthalm ol ogy, otorh i n olaryn gol ogy, and obstetrics and gyn ecology. Barred from allopath ic h ospitals, early DOs founded th ei r own h ospitals and specialty training programs (see Chapter 2). Several mixed staff U .S. i n stitutions offer both Am erican Osteopath ic Associati on (AOA) and Accreditation Cou ncil for Graduate M edical Education (ACG M E ) accreditation. Gradu ates of th ese programs are eligible to sit for both the osteopathi c a n d allopathic specialty boards, and b ecom e m embers of each organization . A s of 2000, AOA records indicate t h e fol l owing:
62% of its m embership l i st them selves in a primary care field 29% are in n on primary care specialti es, including subspecialty in ternal m edicine 3% practice ob stetrics and gynecology 0.85% l i st themselves as osteopathic manipulative m edici n e (OM M ) special i sts Th i s edi tion of Foundations for Osteopathic Medicine presen ts a number of changes in th i s section . B oth geriatrics and pedi atrics are n ow lin ked with the Primary Care section (Secti on V ) . Three chapters-nephrology, hypertensi on, gastroenterol ogy were dropped, chapters on em ergency m edici n e, n euromuscu l oskeletal m edicin e and osteopathic manipulative m edicin e have been added, and chapters dev oted ro physical m edicin e and re habil itation, sports m edicine, and surgery have been expanded.
CARDIOLOGY
Chapter 24 has been updated and expanded. Felix Rogers uses a m ore current interpretati on of osteopathi c tenets that i ncludes osteopathically oriented pati ent care guidel i n es for com m on ly oc curring cardi ovascular problems, i ncluding angina p ectori s, coro nary artery disease, and congestive heart failure.
and n eck structures and associated path ophysi ologic changes are concisely reviewed.
OSTEOPATHIC MEDICINE IN THE PRACTICE OF EMERGENCY MEDICINE
Peter Adler-M ichaelson, B ernadette Peters, and Raul Garcia pro vide this n ew chapter (Chapter 26) with an osteopathic per spective for patients seen i n the em ergency departmem (ED) . Although emergency care i s fairly well standardi zed, the po tential benefit associated with assessm ents of m echanically re lated n eurom u sculoskeletal problem s is not commonly addressed either diagn ostically or therapeutically. Thi s i s particularly true for problems that respond well ro osteopathic manipulative treat m ent. In this offering, the authors u se com m on ch ief complaints of pati ents presenting to the ED, such as, h ead, ch est, or abdom i nal pain, to h igh l ight ways in which osteopathically ori ented thinking and management can make a real difference.
GENERAL SURGERY
In th e first edition of this text, Syd n ey Ross covered the h i story of the gen eral surgery discipli n e, the osteopathic approach to chest and abdom inal surgery, and the appropriate use of osteopathic manipu lative treatm ent (OMT) in treating and preven ting post operative compl icati on s. I n thi s edition , Chapter 27 has been expanded by Con stance Cashen to i nclude selected examples of osteopathically oriented surgical evaluation and management of pati ents presenting with acute abdominal pain. As the author dis cusses a variety of imerdependent relation ships among visceral , n euroanatomic, and path ophysiol ogic processes, she also presems the use of adjunctive OMT for the prevention of postoperative i leus and atelectasis.
GYNECOLOGY AND OBSTETRICS OSTEOPATHIC MANAGEMENT OF EAR, NOSE, AND THROAT DISEASES
[n Chapter 25, Harri et and M ichael Shaw offer osteopathi c ap proaches, incl uding manipulative treatment, to the m ost com mon ear, n ose, and throat (ENT) problems such as si n u sitis, oti tis m edia, and pharyngitis. Anaromy and physiology of the h ead
M elicien Tenambel has updated and refi n ed her excel l em chap ters (Chapters 28 and 31) from the first edition . Women's h ealth care has always been i ntegral to the phil osophy of osteopathy. Th ese two chapters are i mended to ill ustrate the application of osteopathic principles to some of the m ore com m on h ealth care i ssues of wom en , i ncluding their neuromuscul oskeletal compo n ents (see Chapter 1).
Introduction NEUROMUSCULAR MEDICINE AND
341
PULMONOLOGY
OSTEOPATHIC MANIPULATIVE MEDICINE
Raymond J. H ruby has contributed this n ew specialcy chap ter (Chapter 29) . Osteopathic palpawry diagnosis and ma ni pulative creatment are th e hallmarks of th e osteopathic physician. The osteopathic physician who specializes in n eu romuscular m edicin e and osteopath ic manipulative m edicin e (NMM/OMM) i s uniquely qual i fi ed w manage primary care problems or consuh as a specialist on both h ospitalized and am bularory patients. Dr. H ruby presents an excell en t overview of this n ew fi el d.
Gilbert D'Al onzo and Sam u el Krachman have made Chapter 34 a defi n i tive treatise on the osteopathic approach w pati ents with p robl em s of the p u l m onary system. An excel lent discussi on of the m echanics of pulmonary function is presented. The auth ors pro vide a th orough rev i ew of the osteopathic research literature on palpawry diagnosis a n d OMT for pati ents with pulmonary dys fu nction as published i n th e JournaL ofthe American Osteopathic Association over its l Oa-year h istory. They concisely summari ze the evi dence i n support of osteopathic manipulative m eth ods appl icable to this patien t p opulati on . OSTEOPATHIC PHYSICAL MEDICINE
NEUROLOGY
AND REHABILITATION
Unchanged from the fi rst edition, in Chapter 30 M i tchel l Elkiss and Louis Rentz l ook at the com mon neurol ogic disorders of h eadach e, various spinal disorders, entrapmen t n europathies, carpal tunnel syn drome, and chronic pain syndrome i n l ight of osteopath ic evaluation and management, includi ng the use of OMT.
In a rewritten a n d expan ded chapter (Chapter 35), Michael Wieting a n d Jam es Lipton focus on the OMM aspects of os teopathic physical m edicine a n d rehabi l i tati on (OPM&R) . A concise h istory of the discipl i n e is offered al ong with a review of the current evi dence-based research literature related w ma ni pulative m edicine. Rehabi litation of the pat i ent with com m on m uscul oskeletal problems, such as chronic l ow back pain , carpal tun n el syn drome, a n d sports i n j ur i es are used ro dem onstrate an osteopathic approach i n evaluation and managem ent.
ONCOLOGY
First edition authors M ichael Opipari, Augustine Perrotta, and David R. Essig-B eatcy have updated and reorgan i zed their ma terial, emphasizing an osteopathically ori ented, patient-centered approach for this large pati ent population (Chapter 32). Physi cians n eed w be aware of m usculoskeletal manifestations of pri mary tum ors and m etastasis. I t is particularly important for the osteopathic physician who uses palparory diagnosis and manip ulative treatment w recogn i ze manifestations of cancer and the potential benefits and risks of applying man ual procedures w pa tients with oncologic disease. A discussion of appropriate utiliza tion of OMM in this patient population in the light of com m on sense, experience, and evi dence-based research l iterature review makes this chapter especially valuable.
RHEUMATOLOGY
Chapter 3G has been updated and expan ded by Michael Fi n l ey, who provi des consi derable revi ew of perti n ent li terature related ro a m odern osteopathic approach w rheumawlogic probl ems a n d clearly defi n es the tole ofOMT i n t h i s pati ent populati on . H e also provi des a clear and concise osteopath ic h istory and physical eval uation process for the pati ent suspected of, or already diagn osed as havi ng a rheu matol ogic disease. In addi tion w h ighlighting osteo pathic principles i n t egral to th e treatm ent of rheumatic diseases, th e chapter provi des a gen eral overvi ew of the knowl edge and ad vances in treatmen t devel oped since th e fi rst edi tion of this text. SPORTS MEDICINE
ORTHOPEDICS
Richard Scott, Michael Kuchera, and Jeff Patterson expan ded Chapter 33 w i nclude osteopath ic orthopedic approach es w the patient with shoul der i nstabilicy, i ncluding concepts and pri nci ples of orthopedic m edicine and prol oth erapy. This complem en ts the examples i n clu ded in the first edition of osteopathic orthope dic approaches w com m on problems of the knee, hip, and lower back.
As specialists in the care of the m uscul oskel etal system, osteo pathic physicians have been h el d in high regard by ath l etes for m ore than a century. Per G u n nar Brolinson, Kurt H ei n king and Albert Kozar have rewritten and expan ded Chapter 37 ro give a comprehensive osteopathic perspective on th e discipl i n e of sports m edicin e. I ncluded is osteopath ic evaluati on and management of the inj ured athlete, s i deli n e care as a team physician, pathologic m echan ics of sports and exercise-related injuries, and appropriate utilization of O M T.
342
VI. Osteopathic Considerations in the Clinical Specialties
INTRODUCTION TO THE FIRST EDITION FELIX J. ROGERS
Osteopathic m edicine is a comprehensive, i ntegrated approach to patient care. Although the tradi tional strength of osteopathic m edicine has been in primary care m edicine, osteopathic physi cians now provide h ealth care within all specialties and most subspecialt i es of m edicine and surgery. The chapters that follow focus on dim ensions of clinical prac tice that characterize or eluci date aspects of osteopathic philos ophy or practice. Each chapter also revi ews current and past research within th e osteopathic profession . In som e cases, ad di tional scientific l iterature is incorporated because i t directly pertains to issues central to osteopathic m edici n e. Each chapter provi des a brief overvi ew of the fi el d of m edicine described or discusses pertinent topics within the fi el d; none are inten ded to represent a com prehensive description of th e discipline.
clinical specialties. Other distinctive features of the osteopathic profession include: Characteristics of students s el ected for admission to medical schools The osteopathic educational process An emphasis on pri mary care, especially in un derserved areas An orientation to clin ical service as opposed to research and academ ic growth A rel iance on th e patient-physician relationshi p as a key el e m ent i n h ealth care These disti nctive features are addressed in other sections of this textbook.
OSTEOPATHIC MANIPULATIVE TREATMENT DEFINING DISTINCTIVENESS
AND CLINICAL PRACTICE
This section has 14 chapters representative of the clin ical disci plines. Many subjects are not included, esp ecially in th e subspe cialty areas of m edic i n e and surgery. The topics included were chosen as examples of the manner in which osteopathic princi ples have been applied to these clinical areas . Other fi el ds of study may not b e included because of a paucity of osteopathic research in that area, because the implem entation of osteopathic ten ets is more complex or difficult to express, or because the osteopathic approach is so sim ilar to another fi eld that its inclusion wou l d be redu n dant. Medici n e functions as a m ix ofclin ical experience, expert opin ion, and scientific evi dence. Yesterday's expert opinion is regularly overturned by today's scientific evi dence. More precise scientific evidence supersedes more gen eral scientific evidence. Sometim es scientific evi dence catches up with accepted clinical practice. It would be pleasant to th ink that we coul d defi n e as scientific what we do every day in patient care, but this is not the case. Osteopathic m edici n e, as a m inority profession with certain phi losophic emphases, is especially pressured to prove i ts el f i n the scientific arena. There are i n h erent difficulti es in this endeavor, however, because of the global nature of osteopathy's philosophic emphases. lt is hard to defi n e even small, m easurable hypotheses to test such tenets as structu re-function i nterrelationships, or the full nature of viscerosomatic or somatovisceral reAexes. At the same time, osteopathic m edicine is obligated to defi n e its disti nctiven ess. O n e aspect of our profession i s that we have defin ing characteristics; we en deavor as a group to establ ish guid ing pri nciples to represent a phi losophic a n d scientific basis for health care. The following chapters describe the extent to which these principles can be applied to the practice of medicine in the
Osteopathic specialists m ust consi der how osteopath ic manip ulative treatm en t (OMT) , a modality distinct in this profes sio n , m ight fit i n with current clin ical practice. Several clinical outco m es a n d related basic science research proj ects have sug gested how a n d un der what con di tions manipulative interven tions m ight work, but more extensive study is needed. B ecause all m edical practice is based on a sign ificant pro portion of clinical experience and expert opinion, osteopathic thought a n d, when appropriate, manipulative treatment are in cluded in this introductory survey of clin ical specialty correla tions. The chapters i n this section represent a variety ofapproaches to osteopathic specialty practice and are different from o n e another. Each represents o n e or more tenets of traditional osteopathic phi losophy: structure-function interrelationship, self-healing, and integration of systems. Some discipl i n es involve more obviously m usculoskel etal problems than others; in other chapters other ten ets are emphasi zed. In practice, osteopathic m edicine is a m ethod of h ealth care delivery implem ented by an i n dividual physician's approach to patient-physician relationships. In some cases, the relationship concentrates on th e musculoskel etal system , either as the pri mary expression of disease or because of its integral relationsh ip to health an dlor a disease process. I n this case, muscu loskeletal palpatory diagnosis and OMT represent issues of such central importance that they are both n ecessary and sufficient for pa tient care. Oth er circu mstances within the fi el d of m edici n e are such that, whi l e the musculoskeletal system might play a role in the patient's well being, the application of palpatory diagnosis and OMT might be considered adjunctive rather than primary.
introduction For example, in obstetrics, spons m edicine, p sych iarry, and pain managemenr, there are clear i ndication s for OMT that allow for the most complete expression of comprehensive patienr care man agem ene. Conversely, although OMT can b e significanrly ben eficial in rhe rreatmenr of the patient during pregnancy, labor, and delivery, the indications for O MT m ight be less frequently found in a gen eral gynecology practice or i n some of the m edical special ties. Recogn izing the central rol e of the n euromusculoskel etal sys tem in di sease and healrh maintenance, osteopathic physicians have u sed OMT as a m eans to implem en r their philosophic prin cipl es. Rem ember that OMT i s a tool for applying a philosophy, not the philosophy itself. Various approaches are now used to in terven e with the n euromusculoskel etal system , i ncluding exerci se, yoga, biofeedback, transcutaneous electrical nerve sti mulation, acupuncture, and tai chi. Because each of th ese modal i t i es, in cl uding manipulation, i s used by health care practitioners outside the osteopathic profession, one m ight conclude that a defin ing characteristic of osteopathic m edici n e is not found in practice pat terns that are in exclusive u se. The key feature is the philosophic orientation behind the application o f th ese m ethods of h ealth care, with an emphasis on the rol e of the n euromusculoskeletal system. The evolution of m edici n e in the 20th century has also changed the way in which OMT i s used. With the d evelopmenr of new technologi es, including imaging techniques, new pharma cologic agents, and the growth of molecular m edicine, palpatory diagnosi s and O MT might play a proportionately smaller rol e in some fields than they d i d in t h e recenr pase. These facts do not deny their hisrorical or presenr i m portance. If OMT did in fact save ten s of thousands of lives during the i n A u en za epidemic after World War I ( 1), we would concede that it represented the best therapy available at that time. If genetic engineering were to provide a breakthrough to create specific antiviral agents to treat a sim i lar inA uenza epidemic, we would all rejoice that more effective therapy i s now available. The development of effective antihypertensive agents has moved OMT ro an adjunctive rol e in the treatm ent of hyper tension, in contrast to a l egiti mate interest i n srudying the ef fectiven ess of this modality a few decades ago. l ron ically, the technological advances in heart transplantation m ight be seen as causing the opposite reaction. When patients on the waiting l i st for a heart transplant are enrolled in a program of cardiac rehabil itation exerci se, a sign i ficanr number show such improvemenr in
343
their functional status that they are removed from the transplant l i se. Thi s is because of enhanced m u sculoskeletal functio n, not because of a change i n their cardiac starus. I n those ·c1i n ical sci ences in which highly tech nical devel opments have com e to the forefront, the osteopathic physician might have the greatest rel evance because they can provi de the comprehensive perspective and integrated philosophi es that char acterize the best o f m edical care. For example, diagnostic m eth ods and therapies for patients with heart di sease have proli ferated dramatically in recent years. U n fortunately, so has the gen eral tendency to apply all m ethods ro all patien ts, even without scien tific rationale. A clinical managem ent strategy based on concepts of the u n i ty of body, structure-function relationships, and the in tri n sic abi l i ty of the body ro heal still constirutes the most ration al m eans of diagnosis and th erapy a s descri bed i n the following chapters. The degree to which palpatory diagnosi s and OMT are applied in each specialty varies considerably depending o n the nature of that special ty, the appl icabil i ty o f manual m edicine, and the sci enti fic research to support u se of these m ethods. Non ethel ess, each chapter i s based on the basic tenets of osteopath ic m edici n e as defined more than 100 years ago.
CONCLUSION
Both th e gen eralist and the specialist are obliged to u se the best in formation available for the care of the pati enr. 1n som e i n stances, this remains clin ical experience, the tradition that has worked for osteopathic physicians throughout the profession's history. To make the best u se of this experience, we rely on expert opin ion. When sci entific evidence i s di rectly or indirectly available, it should be u sed. All th ree types of authority are reAected in these chapters. Each author has attempted to make clear the strength of the sci en tific evidence that underli es recom m endation s for treat m ene. The goal i s always that of whol e patient care, in itsel f one of the traditional val ues o f the osteopathic profession.
REFERENCES 1 . Smirh RK. One hundred rhousand cases of inAucnza wirh a dearh rarc of one-fortieth of thar officially reponed under conventional medical treatmenr. jAOA.
1 920;2 1 : 1 72- 1 75.
THIS PAGE INTENTIONALLY LEFT BLANK
AN OSTEOPATHIC PERSPECTIVE ON CARDIOLOGY FELIX J. ROGERS
of this chapter is to present a brief review of these two parts of the field of cardiology to clarify the application of osteopathic con
KEY CONCEPTS • It is appropriate to consider the cardiovascular system in
terms of a modern interpretation of the basic tenets of osteopathic medicine and principles for patient care. • The growth of technology and scientific discovery in the
field of coronary atherosclerosis has led to two contrasting developments. On the one hand, acute coronary syndromes are now understood in terms of local cellular and molecular mechanisms, for which highly specific, technical interventions are appropriate. On the other hand, the vast majority of cases of coronary heart disease are preventable, since the cause of coronary atherosclerosis is primarily related to diet and lifestyle. • The muscle hypothesis represents a model for heart failure
that supplements the traditional approaches to heart failure
cepts; important subjects such as arrhythmias, valvular heart dis ease, hypertension, and congenital heart disease are not discussed. It is appropriate to consider the cardiovascular system in terms of a modern interpretation of the basic tenets of osteopathic medicine and principles for patient care ( 1). Because this is a text book primarily aimed at medical students, each of these tenets and principles will be listed in the overview, to provide a context for the discussion of pathophysiology and natural history and treatment of coronary heart disease and heart failure. It is hoped that medical students will incorporate these tenets and principles as benchmarks against which they can evaluate the medical lit erature in a critical manner, assess the relevance of osteopathic principles, and verify the applicability of the material that they read and study.
and highlights the emphasis of the osteopathic profession on the musculoskeletal system. •
OVERVIEW
A comprehensive approach to the patient with
Tenet I: A Person Is the Product of Dynamic
cardiovascular disease requires the incorporation of evidence based guidelines and an emphasis on primary and secondary disease prevention through lifestyle modification. The osteopathic profession has an historical mandate to provide emphasis to both components.
Interaction between Body, Mind, and Spirit The heart is a remarkable organ. It can be removed from one person and transplanted into another and it still maintains its basic function and rhythmic activity. In fact, isolated strips of heart muscle can be placed in a physiologic bath, and these char acteristics prevail. However, the optimal function of the heart occurs when it is in its appropriate context, in an intact person, with a complex control system and multiple inputs. There are
Cardiology
represents
the
largest
component
of
internal
an astounding array of interactions for the heart, including auto
medicine, and heart disease is the leading cause of mortality in
nomic control of the heart, the hypothalamic-pituitary-adrenal
the United States. Screening for heart disease is an essential com
axis, hormonal modulation, and interactions between the heart
ponent of every comprehensive evaluation performed by a family
and the brain, cognitive and neuropsychiatric function, and cir
practitioner, surgeon, anesthesiologist, or internist. The compo
cadian and ultradian function.
nents of a cardiovascular screening evaluation are the history,
Consider further that the heart needs to pump every minute
physical examination, electrocardiogram (ECG), and chest x-ray
of every day and every year. It needs to respond appropriately to
film. In this chapter, these components are starting points for the
the activities of daily living, to sleep, and to sudden strenuous
evaluation of patients with ischemic heart disease and congestive
exertion. It needs to participate in instantaneous control of the
heart failure. These two categories represent more than 75% of the
blood pressure in spite of challenges of posture, temperature, and
patients with heart disease that practicing osteopathic physicians
psychological stress.
see. The pathophysiology of these disease processes is discussed
Heart disease is the most common cause of death in United
along with the natural history, diagnosis, and therapy. The goal
States, and chronic heart failure and coronary heart disease
346
VI. Osteopathic Considerations in the Clinical Specialties
III
ft :r: =: v4 i¥ V
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3
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aVL
aVF
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jJ. .. .
.ttlt ..
.
.:,
;
: . IT:
:- �
�::� �':'i£=' ::L:h
� v6 �A FIGURE 24.1. T h is patient presented with subdural hematoma and was shown to have evidence of acute a nterior w a l l myocard i a l i nf a rctio n on electrocardio g ram (P anel A). Subsequently, card iac catheterizatio n showed normal co ro n a ry arteries. Left ventriculography demo nstrated a l a rge area o f a pical a k i nesia that is most evident when the d iasto l ic (Panel B) and systo l ic (P anel C) images a re com pared. The w a l l motion a b no rm a l ity reso lved com pletely within 3 days. ( F rom Ohtsuka T, H am ada M, Ko dama K, e t a l . Neurogenic stunned myoca rd i um . Circulation 2000; 1 01 : 2 1 22-2 1 24, w i t h perm issio n.)
represent cwo of the m o st common chronic diseases i n our so ci ety, especially in the geriatric population. Although it may be a chronic, slowly progressive d i sorder, cardiac deaths occur sud denly, and approximately one-fourth of all cardiac deaths occur without any warning or any premonirory signs. Th e heart is well inn ervated and participates in a broad range of reA exes ( 2- 1 2), i ncluding the viscerosomatic reAexes that are a major feature of classic osteopathic theory. The h eart has extrinsic efferent (sympathetic and parasympathetic) and afferent i n n er vation and also possesses an i n trinsic ( i ntracardiac) n erve supply ( 1 3-1 5) . The extri n sic and intrinsic n erve supplies i nteract with one another and this intri n sic n ervou s system may even function a s a "mini-brain" within the heart, to provide a "fine-tuning" of cardiac dynam ics ( 13) . The classic transmitters are adren ergic and chol i n ergic, but other important neurotran smi tters coex i st with these in the same n erve fibers, i ncluding adenosin e, cardiac n europeptides, somatostatin , and n i tric oxide (13) . A s we have a l l experi enced, o u r emotional state i s accompani ed by alterations of heart rate and blood pressure. Anger and stress have been associated with the occurrence of cardiac d i sorders like sudden death, arrhythmias, and myocardial i n farction (MI). Cardiovascular activity i s regulated by a system comprised of various tightly connected d i encephalic, m i db rain , brainstem, and
spi nal structures, i n which the hypothalamus i s fu nctioning as the highest l evel of com mand ( 1 6) . Regional damage to the central n ervou s system may also affect emotions and the fu nctioning of the cardiovascular system. Figure 24. 1 shows an example of extensive myocardial stun ning that occurred i n a patient with normal coronary arteries and a subd ural hematoma ( 1 7) . A definite circadian pattern o f o n set o f MI was demonstrated in the Myocardial Infarction Limitation Study ( 1 8) . Th e increase in morn i ng i ncidence of acute i schemic coronary even ts has been attributed to an i ncrease i n catecholamines and sen sitivity of vascular receptors, i ncreasing coronary vasomotor tone, and an i ncreasing myocardial oxygen demand, all of which lower th e threshold for i schemia ( 1 9) . The autonomic n ervous system i s also organized according to circadian i n A u ences, and important physiologic changes occur in the l evels of circulating corticosteroids, vasopressin , and other compon ent s of the hypothalamic-pituitary-adrenal axi s as well (20). Other biologic rhythms have also been demonst rated for cardiovascular events. For example, the l ikelihood o f Ml i s greater on a Monday than any other day of the week (21). More MIs occur in the winter than in the summer. Thi s holds true for areas i n which i t i s warm i n the winter (the southern United States) a s well as those areas with a cold winter. Thi s i ncrease in winter mortality
24. A n Osteopathic Perspective on Cardiology
347
occurs in infants and dogs as well, and in both the Northern and
quite different than other disease processes. Unlike chronic renal
Southern hemispheres. The common denominator appears not
failure, diabetes, or metastatic cancer, in which there appears to be
to be the stress of cold or the holidays, but the shorter days of
a relentless deterioration in the patient's condition, the clinical
winter, mediated by decreased daylight which is sensed by the
course of many patients with heart disease is characterized by
suprachiasmic nucleus
(22).
exacerbation and remission. Many patients return to a virtually
There are other well-defined examples of the interaction of the heart with other systems of the body. These include the cardio vascular response to stress, the hypothalamic-pituitary-adrenal system and the heart
(23) , the renin-angiotensin-aldosterone sys
(24) and systemic inflammation in patients with coronary artery disease (CAD) (25). Some of these will be discussed in
tem
more detail in the subsequent sections of this chapter. The link between the heart and spirit goes back thousands
normal functional status, even after catastrophic experiences with MI or decompensation of left ventricular dysfunction. CAD provides a clear example of inherent self-regulating and self-healing properties
( 64,65) . A century ago, the rule of the
artery was supreme. The dramatic role of revascularization ther apy for acute MI makes this rule no less true today. The mech anism of atherosclerosis and the regulation of vascular smooth muscle tone are best understood in terms of the natural ability of
of years. [n Hebrew psychology, the heart is primarily the seat
the human organism to resist and combat harmful influences in
of the mind and will, together with a whole range of cyclical
the environment. Knowledge of self-regulation and self-healing
spiritus) ( 26) .
forces at the arterial and arteriolar level forms the rational basis
Our language still contains many expressions in which the
for the treatment of MI, angina pectoris, and congestive heart
heart is used as a metaphor to express emotion, even though
failure, as discussed in the following sections.
emotions (Hebrew
ruah,
Greek
pneuma,
Latin
Western culture places emotional life in the brain, and not in the
As more information is gathered about the pathophysiology
heart. Several non-Western societies place emotions in the heart
of coronary atherosclerosis, and of left ventricular dysfunction,
(27,28) .
physicians are encouraged to adopt a long-term strategy of rever
Religion and spirituality are among the most important cul
sal, remodel, and regenerate. The past two decades have seen re
tural factors that give structure and meaning to human values,
search that demonstrates lifestyle modifications, with or without
behaviors, and experiences. Spirituality is a concept broader than
medications to lower cholesterol, can halt or reverse the progres
religion and is primarily a dynamic, personal, and experiential
sion of atherosclerosis (66-68) . It appears that the level of exercise
94% of patients regard their spir itual health and their physical health as equally important ( 29) .
intensity
process. One survey found that
(69) , diet ( 70) , and antioxidants (71) are variables in
dependent of serum cholesterol, which can have favorable effects
The implications of this for clinical practice have recently been
on coronary events or regression of atherosclerosis. Patients with
reviewed (30) . Studies have found that religious involvement is as
CAD and normal serum cholesterol gain significant benefit from
sociated with less cardiovascular disease. Of
16 studies examined 2001 review (31), 12 found that religious involvement was
further lowering of serum cholesterol
in a
of this knowledge is shown by a recent study that found the com
associated with less cardiovascular disease or cardiovascular mor
bination of simvastatin plus niacin led to regression of coronary
( 72) . The evolving nature
tality. Religious involvement is associated with health-promoting
atherosclerosis, but this effect was attenuated when antioxidant
(32), proper nutrition ( 33) , reg ular seat belt use (34) , smoking cessation (32) , and greater use of preventive services (35) . The role of intercessory prayer on cardiac
vitamins were added to this treatment
patients is less clear: A randomized, controlled trial conducted on
normal endothelial function
behaviors, such as more exercise
( 73) . In most studies, the
rapid reduction in coronary events clearly precedes regression of atherosclerosis and is believed to represent a reestablishment of
( 74-76) .
799 coronary care unit parients showed no significant effect (36) .
Other dynamic aspects of arteries include angiogenesis and
Apart from the field of CAD, research in the last two decades
remodeling in response to the development of atherosclerosis.
demonstrates the complex nature of neural regulation of cardio
Although the development of collateral blood vessels
vascular function and the components of the systemic effects me
the recannulation of occluded arterial segments have a beneficial
(77) and
diated by cardiac receptors. Integration of cardiovascular function
effect in terms of improving blood flow, angiogenesis itself has
and interactive mechanisms with other body systems is mod
been broadly linked to cancer
ulated by local and systemic neuro-effector, humoral, and im
proliferating vasa vasorum has been postulated to be a possible
munologic responses (37-42) . Research has shown that these fea
cause of plaque rupture
(78,79) . The neovascularization of
( 80) .
tures have clinical significance in congestive heart failure (43-48) .
Vascular remodeling is the phenomenon of compensatOry
As well, research in therapy focuses on neuroendocrine modula
enlargement in the presence of atherosclerosis to preserve near
tion through exercise
( 49-52) and pharmacologic therapy (53-
normal lumen diameter (Fig.
24.2) . Initially described in mon
63) as an intermediate outcome, in addition to assessing health
keys fed an atherogenic diet, this biologic response has now been
related outcomes, such as functional status and mortality.
demonstrated in human coronary (81) , carotid (82) , and femoral (83) arteries. Functionally important lumen stenosis may be de layed until the lesion occupies 40% of the internal elastic lamina
Tenet II: An Inherent Property of This Dynamic Interaction Is the Capacity of the Individual for the Maintenance of Health and Recovery from Disease
area. The preservation of a nearly normal lumen cross-sectional area should be taken into account in evaluating atherosclerotic disease with angiography
(81) . Lack of remodeling may be a ma
jor determinant in whether a person with coronary atherosclero
As physicians care for patients with heart disease over a period
sis develops any complications
of years, they observe that the natural history of heart disease is
intravascular ultrasound (IYUS) has provided clinicians with a
(84) . The clinical application of
348
VI. Osteopathic Considerations in the ClinicaL SpeciaLties 40%
Stenosis
FIGURE 24.2. Po ssible sequence of changes in atherosclero t i c arteries lea d i n g event u a l l y to lumen narro w i n g . Artery e n l a rges i n itia l ly (left to right in diagram) in asso ciation with plaque accum u latio n . (From
G lagov S, Weisenberg E, Zarins CK, et a l . Com pensatory e n l a rgement o f h um a n atherosclerotic co ro n a ry arteries. N Engl ) Med. 1 987;3 1 6: 1 37 1 1 375, w i t h perm issio n.)
practical tool to study coronary arterial remodeling, in addition to the benefit it provides in terms ofprecise assessment of atheroscle rotic plaque (85). Remodeling is also a critical component in the management of the patient with left ventricular dysfunction. I n some patients, the cause of primary left ventricular m uscle dysfunction may be spontaneously reversible, such as peripartum cardiomyopa thy, alcoholic cardiomyopathy, or viral myocarditis. I n patients with ischemic heart disease, while the left ventricular dysfunc tion itself may be i rreversible, therapy may halt or retard the progression of coronary atherosclerosis and the subsequent de velopment of additional myocardial damage. Further, the use of angiotensin-converting enzyme (ACE) inhibitors may prevent or retard deleterious left ventricular remodeling (86) and thereby reduce mortaliry and morbidiry (87, 88). A recen t repon demon stJ'ates the surprising result that left ventricular myocytes can i n fact regenerate following acute M I (89). While the clinical signif icance of this is presently uncertain, i t raises the hope that gene therapy may be able to take advantage of this process, with the ulri mate outcome of significant myocyte regeneration following acute M l . Tenet III: Many Forces, Both Intrinsic and Extrinsic to the Person, Can Weaken This Inherent Capacity and Contribute to the Onset of I llness
A useful perspective on CAD comes from the h istory of the home opath ic profession in the first systematic study of nitroglycerin in the Uni ted States. By using selected i ndividuals as "provers," nitroglycerin was evaluated for its efficacy i n treating headaches and palpitations. However, i n spite of a very careful, systematic approach, it was never learned that nitroglycerin could be bene ficial for the treatment of angina pectoris. Medical historian W. Bruce Fye ( 90) concluded that there simply were not enough people in the U . S . who had coronary heart disease for this diag nosis even to be considered. As recently as the 1 896 Textbook of InternaL Medicine by Sir William Osler, angina pectoris was con sidered to be rare. We might therefore view CAD as an epidemic confi ned to the 20th century and to the early part of this century. The prevalence of ischemic heart disease peaked around 1 967 and has been falling ever since. The death rate from heart dis ease has dropped by an astounding 60% in j ust the past 30 years (91 ). The National Heart, Lung and Blood I nstitute called for a further 20% reduction in coronary heart disease deaths over the
TABLE 24. 1 . RISK SCLEROSIS
FACTORS
FOR CORONARY ATHERO
Major Independent Risk Factors Ciga rette smo king E l evated blood pressure E levated serum total (and LDL) cholestero l Low serum H D L cholestero l D i a betes m e l l itus Advancing age Obesity' Physical i nactivity Predisposing Risk Factors Abdom i n a l o besityb Fam i ly histo ry of prem ature CAD Ethnic cha racteristics Psychoso c i a I factors Conditional Risk Factors E levated serum trig lycerides Sm a l l LDL particles E l evated serum homocysteine E l evated serum l i po protein(a) Prothrom botic factors (f i brinogen, etc.) Inflammatory m a rkers (e.g., C-reactive protein) ' Obesity is a body mass index
> 30 kg/m 2.
bAbdom i n a l obesity is defined by waist circumference: men > 1 02 cm women
(40"),
>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
VI. Osteopathic Considerations in the Clinical Specialties
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
VI. Osteopathic Considerations in the Clinical Specialties
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
VI. Osteopathic Considerations in the Clinical Specialties
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
'<..Y TIlERAPY
- Treat hypertension
"'\
TIlERAPY - All measures under stage A
- Encourage smoking cessation
- ACE inhibitors in
THERAPY - All measures under Stage A - Drugs for routine use:
- Treat lipid disorders
appropriate
Diuretics
- Encourage regular
patients
ACE inhibitors
- Beta-blockers in
exercise
appropriate patients
- Discourage alcohol intake. illicit drug use
Beta-blockers Digitalis - DietaI)' salt restriction
TIlERAPY - All measures under stages A. B. and C - Mechanical assist devices - Heart transplantation - Continuous (not intermittent) IV inotropic infusions for palliation - Hospice care
- ACE inhibition in appropriate patients
"-
359
./ FIGURE 24_ 1 0 . New model of four stages of heart fa i l u re as recom mended by the American Col lege of Cardiology and the American Heart Association. Stage A refers to i ndividuals at high risk for heart disease, but without structural heart disease. Stage B represents patients with structural heart d isease, but without symptoms of heart f a i l u re. (Modified from H u nt SA, B a ker DW, C h i n MH, et a l . ACCIAHA g u ideli nes for the eva l u ation and management of chronic heart f a i l u re in the a d u lt : Executive S u m m a ry. Circulation 200 1 ; 1 04:2996-3007.)
360
VI. Osteopathic Considerations in the Clinical Specialties
is characterized by specific symptoms (dyspnea and fatigue) and signs (fluid retention). There is no diagnostic test for heart failure because it is largely a clinical diagnosis that is based on a careful history and physical examination ( 1 95). Clinically significant left ventricular dysfunction activates neurohormonal mechanisms that promote fluid retention and that may perpetuate or worsen heart fai lure. Typically, these rep resent examples of compensatory mechanisms that are an exagger ated long-term response of a mechanism designed for short-term control. For example, the immediate hemodynamic response to hypotension caused by blood loss is i n tense vasoconstriction, ele vation of systemic vascular resistance, and salt and water retention by the kidneys. The neurohumoral activation in heart fai l u re in cludes alterations in the autonomic nervous system, i ncluding baroreceptor and peripheral adaptation (37, 44, 1 98, 1 99), adren ergic receptors (200,201), ren in-angiotensin-aldosterone system (202), atrial natriuretic factor (203,204), and endothelial func tion (205,206). The degree of activation of neurohormonal mechanisms ap pears to depend on the severity and acuteness of cardiac i mpair ment as well as the status of extracellular fluid volume (207). Local autoCl'ine and paracrine systems i n blood vessels and my ocardium may also contribute to the long-term regulation of vascular tone and play a role in the pathogenesis of ventricular remodeling, dilation, and progressive heart fai lure (47). Besides these neurohormonal effects, heart fai lure also affects the kidneys, gastrointestinal system, and skeletal m uscle. Heart failure is a symptomatic disorder that occurs as a conse quence of m ul ti ple influences on a patient with structural heart d isease. Decompensation of heart fai lure is a clinical considera tion of considerable relevance to the management of the patient with heart failure; i t often occurs because of progressive wors ening of structural heart disease. Sometimes decompensation of heart failure can be attributed to extracardiac features such as depression (208), malnutrition (209), anemi a (210), and socioe conomic status (21 1 ). The most common cause of decompensa tion leading to re-admission to the hospi tal is non-adherence to recommendations in regard to diet and medications (212, 2 1 3) (Table 24.2). Natural History
The natural h istory of heart failure is affected primarily by the underlying d isease process that causes lefr ventricular dysfunc tion . I n some cases, this is idiopathi c and irreversible. Some causes of primary m uscle dysfunction may be spontaneously reversible, such as peripartum cardiomyopathy, alcoholic car diomyopathy, or viral myocard itis. In other cases, the relent less deterioration of function may be i n terrupted by therapy for the underlying condition. For example, the treatment of sys temic arterial hypertension, especially with ACE inhibitors, may not only control hypertension but also enhance cardiac perfor mance and lead to regression of left ventricular hypertrophy. In the case of ischemic heart disease, although left ventricu lar dysfu nction may be i rreversible, therapy may halt or retard the progression of coronary atherosclerosis and the subsequent development of addi tional myocardial damage. Furthermore, ACE inhibitors may prevent or retard deleterious left ventricular
remodeling (86), and thereby reduce mortaliry and morbidity ( 87,88). Typically, heart fai lure is a progressive disorder, even without a new identifiable source of cardiac damage. The most common manifestation of this progression is a deterioration in left ventricu lar geometry, associated with chamber dilation, hypertrophy, and an alteration in ventricular shape to become more spherical. These myocardial changes increase the hemodynamic stress on the wall of the heart, and also decrease its mechanical performance; this i ncreases the magnitude of functional mitral regurgitation. In addition, fibrosis of the extracellular cardiac matrix has major adverse effects on the heart's electrical and mechanical fu nction and coronary vasodilator reserve, which can be prevented by the admi nistration of spironolactone (21 4). Patients with heart fail ure have a poor prognosis, with aver age mortali ty rates of at least 10% at J year and 50% at 5 years. The i m portant predictors of survival are: (a) the cause of heart failure, (b) patient's symptomatic and functional status, (c) hemo dynamic and pathologic findings, (d) neurohumoral activity, and (e) the presence of cardiac arrhythm ias (2 J 5). Diagnosis
The standard screen of history, physical exami nation, ECC, and chest radiograph are helpful to establish the diagnosis of con gestive heart failure. These modalities are best used to develop a composite assessment of the patient's status because pulmonary rales, j ugular venous distension, and peripheral edema may be presen t in a m inority of patients (21 6). Likewise, the ECC is usually nonspecific ( 2 1 7). In addi tion, complete blood count, serum electrolytes, creatinine, albumin, liver function tests, and urinalysis should be performed for all patients with suspected or clinically evident heart fai lure ( 189). Thyroxine and thyroid stimulating hormone levels should be checked in all patients older than 65 years ofage with heart fai lure and no obvious cause and in patients who have atrial fibrillation or other signs and symptoms of thyroid disease (189). To assess the patient's status, more specific data are needed concerni ng left ventricular systolic and diastolic function. Two di mensional ECC imaging with Doppler is the diagnostic method of choice to assess patients with suspected heart fail ure. These studies provide the most information about the heart, i ncluding left ventricular size and wall motion and function, in addition to providing information about the cardiac valves, atrial chambers, right ventricle, and pericardium ( 2 1 8). An estimation of ejection fraction is also possible from an ECC study. The diagnosis of left ventricular diastolic dysfunction has been well established using Doppler ECC criteria (21 9,220). Exercise test i ng is an emerging modality used to define the functional status of patients with heart fai l ure (221 ). Brain natriuretic peptide ( B N P) is a cardiac neurohormone secreted from the cardiac ventricles as a response to ventricular vol ume expansion and pressure overload. BNP levels have been shown to be elevated in patients with left ventricular dysfunction and correlate with the NYHA classification as well as prognosis ( 222, 223). A rapid point-of-care test for BNP has recen tly been shown to be beneficial for the diagnosis of heart fail ure in an urgent care setting (224,225).
24. An Osteopathic Perspective on Cardiology Because heart failure is the end point in a diverse group of clin ical disorders, effore should always be made to establish a specific diagnosis. The calise is often reversible or treatable. I t i s unacceptable si mply t o use heart fai lure a s the fi nal diagnosis without reference to possible causes. Approximately two-thirds of patients with heart failure have underlying CAD. Treatment
Goals of therapy for heart failure are to enhance survival, im prove the quality of life, and improve symptoms. These therapies have been well described in important practice guidelines and consensus statements ( I 89 , 1 95, 226) . Heare failure is the epidemic of largest magnitude within the field of internal medicine and the most important cardiovascular entity from a health care and economic standpoint. Therefore, the appropriate perspective is to identify those conditions and behav iors that are associated with an increased risk of heart fai lure before patients show any evidence of Structural heart disease (stage A) . Because early modification of these factors can often reduce the risk of heare failure, working with patients on these risk factors provides the earliest opponunity to reduce the i mpact of heart fai lure on public and individual health ( I 95) . Specific risk factor modification should be directed to the treatment of hypertension and d iabetes, and the management of atherosclerotic d isease. In creased systolic or diastolic blood pressure is a major risk factor for the development of heart fai lure ( 227,228) . The presence of diabetes markedly increases the likelihood of heart fai lure in pa tients without structural heart disease (229) and adversely affects the ourcome of patients with established heart failure ( 230,231 ) . In patients with diabetes, the target level of blood pressure should be 1 30/85, lower than that of nondiabetic patients. Patients with known atherosclerotic disease are likely to develop heart fai lure, and physicians should control risk factors for atherosclerosis in these patients. Other conditions that cause cardiac inj ury include cigarette smoking, alcohol or cocaine use, cardiotoxic anticancer chemotherapy, and prolonged tachycard ia (232,233). The most common situation to diagnose left ventricular dys function in patients who do not have symptoms of hean failure (stage B) is in the setting ofM l . These patients are at considerable risk of developing subsequent hean failure. They should all re ceive treatment with an ACE inhibitor and ,B -blocking agent. Pa tients with a h istory of M f and preserved left ventricular function will also benefit from an ACE inhibitor (234) . Patients with se vere valvular heart disease should typically undergo valve surgery before symptoms occur, especially with regurgitation of the aortic and mitral valves. Patients with left ventricular systol ic dysfunction and current or prior symptoms (stage C) are routinely managed with a com bination of four types of drugs: a diuretic, an ACE inhibitor, a ,B-adrenergic blocker, and (usually) digitalis. The value of these drugs has been establ ished in numerous large-scale clinical trials. Even if a patient symptomatically improves with diuretics alone, the cl inical evidence clearly indicates that both an ACE inhibitor and a ,B-blocker should be given and maintained in all patients who tolerate them. In particu lar, physicians are encouraged to use ,B-blocking agents in the management of patients with heart failure, even though these drugs were previously thought to be
361
relatively contraindicated in heart fai l ure management. Three major clinical trials demonstrate the efficacy of these agents in patients with moderate and severe heart fai lure (235-237). One new approach to the patient with heart failure looks not only at the enhanced activation of endogenous vasoconstrictor neurohormonal substances (such as the renin-angiotensin system) but also looks at i nadequate response to endogenous vasodilator systems, such as kinins and natriuretic peptide. Current investi gation is under way regarding vasopeptidase inhibitors that block not o n ly the ACE, but also the neutral endopeptidase, which leads to enhanced activities of endogenous vasodilators. One vasopep tidase inhibitor, omapatrilat, is being developed for the treatment of hyperrension and for the treatment of heart fail ure ( 238) . Ne siritide, a B N P produced by recombinant gene tech nique, has beneficial hemodynamic effects in patients with decompensated heart failure (239). Patients with end-stage, refractory heart failure (stage D) typi cally have symptoms at rest or with m i n i mal exertion, and cannot perform most activities of daily l iving. They represent the most advanced stage of heart failure and should be considered for spe cialized treatment strategies such as mechanical circulatory sup port, continuous intravenous positive i notropic therapy, referral for cardiac transplantation, or hospice care ( I 95) . They will need meticulous control of Auid status, and they should receive ACE inhibitors and ,B-blockers given with caution. Exercise and Heart Failure
The mechan isms responsible for the exercise i ntolerance of pa tients with chronic heart fai lure have not been clearly defined. Many studies show a poor relation between cardiac performance and the symptoms of heart fai lure. Patients with a very low ejec tion fraction may be completely asymptomatic, and patients with preserved left ventricular systolic function may have severe dis abi l i ty. The apparent lack of agreement between the severity of systolic dysfu nction and the degree of functional impairment is not fully understood. It may be related to alterations in ven tricular diastolic function, valvular regurgitation, pericardial re straint, and right ventricular function. I n ambulatory patients, noncardiac factors may contribute to exercise intolerance. These include changes in peripheral vascular function, skeletal mllscle physiology, pulmonary dynamics, and neurohormonal and reAex autonomic activity. These noncardiac factors may explain why the hemodynamic i mprovement produced by therapeutic agents in patients with chronic heart failure may not be immediately or necessari ly translated i n to clinical improvement. Although phar macologic interventions may p toduce rapid changes in hemody namic variables, signs and symptoms may improve slowly over weeks or months, or not at all. The Muscle Hypothesis
The "muscle hypothesis" proposes the possibi l i ty that abnormal skeletal muscle in heart failure results in activation of m uscle ergoreceptors, which in turn leads to an enhanced signal to ven tilation, and results in sympathetic activation (Fig. 24. 1 1 ) (51 ) . The afferents fro m skeletal muscle are sensitive t o metabolic ef fects of muscular exercise. They then modulate hemodynamic,
362
VI. Osteopathic Considerations in the Clinical Specialties
FIGURE 24. 1 1 . The muscle hypothesis. (Modified from Coats AJS. Clark AL. Piepoli M. et al. Symptoms and q u a l ity of l ife i n heart fail ure: the muscle hypothesis. Br Heart J . 1 994;72[Suppl] :S36-S39.)
venrilawry, and auwno m ic responses. These are small myelinated and un myeli nated aFferents, of group [ I I and IV aFferents. They arise From "Free" or "naked" nerve term i nals, associated with col lagen structure and skeletal m uscles or with blood and lymphatic vessels. They are presumed w be engaged i n Feedback control, where m uscle work regulates energy supply. The cenrral reflec tion of these pathways is in the venrral lateral medulla, i ncluding the lateral reticular nucleus. These recepwrs are overactive during exercise, and play a larger role in responses w exercise in patients with chronic heart failure with respect w conrrol subjects. The overactivated m uscle signal in heart Fail ure due w abnormal i ties in exercising m uscle causes an i ncreased ventilawry drive (239) . The m uscle aFFerenrs are hiswlogically i nseparable From pain fiber aFFerenrs, so they may serve sensory as well as reflex function, mediating the sensation oFFatigue and the exaggerated ven t ilawry and cardiovascular responses to exercise ( 240) . This system could mediate a sympatho-excitawry and vasoconstricwr response w exercise. However, the subnormal blood flow response w exercise and pharmacologic vasodilation is complex, and may i nclude persistenr vasoconstricwr drive, edema of resistance vessel walls, a relative paucity of peripheral blood vessels, a deficienr n itric oxide vasodilawr, and enhancement of the vasoconstricwr endothelin (24 1 ) . The neural l i n k w explain the m uscle hypothesis of exercise in wlerance in chronic heart failure was investigated in 92 stable parienrs with heart fai l ure, compared w 28 age-matched con trols. Exercise w lerance was measured by bicycle ergometry; the ergoreflex activity was evaluated with two dynamic handgrip tests. Three m i n utes o F l ocal circulawry occlusion was used during the second study, w isolate the neural componenr w the ergoreflex (as opposed w circulating metabolites) . Isometric handgrip was as sociated with a prolonged i ncrease in systolic and diaswlic blood pressure, an i ncrease in ven ti lation, and i ncrease in leg vascular re sistance. The inrensity of the reflex was higher in N YH A class I I and I I I heart Fai lure patienrs than i n class I patients (242) . The Role of Exercise Training in Chronic Heart Failure
It is estimated that at least one-Fourth of patienrs with chronic heart Failure are l i m ited by skeletal m uscle changes rather than decreased cardiac output and underperFusion. This may explain
why certain patients do not respond w inorropes or vasodi la tors, and establishes the role of cardiac rehabilitation exercise in patients with heart failure. Random ized, controlled tria.ls have assessed the eFfects of ex ercise tra i n i ng i n patients with sympwmatic heart Failure (243250) . Studies have demonstrated i mprovemenr i n exercise capac i ty ( measured by peak exercise duration or peak oxygen consump tion) ( 243-250) and also show Favorable changes in auwnomic nervous system function (249), regional blood flow (246), en dothelial Function (251), and skeletal m uscle Function (252,253) . During long-term moderate exercise train ing, heart Failure pa tients random i zed w the exercise group experience an increase in their peak exercise oxygen consumption and an improvement in the myocardial thal l i u m score. Measures of their quality of liFe improved parallel to the i ncrease in peak oxygen consumption (250). Exercise tra i n i ng has also been shown to lead to atten uation of the harmFul process of leFt venrricular remodeling in postin Farction patients, perhaps through a chronic decrease in sympathetic nervous system tone (254). With exercise train i ng of 1 to 6 months, a significanr i ncrease in exercise duration has been demonstrated in the trained sub jects. The observed i ncrease of 26% to 37% is al most double that which has been reported with ACE inhibiwrs or digoxin ( 255,256). The i mprovement with exercise is additive w the ben efits of ACE inhibitors and ,B-blockers ( 246,257) . Some of the skeletal abnormali ties are due to deconditioning, and they are partly reversed by exercise trai ning. Training has also been shown to reduce the exaggerated ergoreflex activi ty, thereby im proving the response to exercise (258) . The exercise prescription For patients with heart failure is sim i lar w other types of heart d isease-the patient should engage i n aerobic activity that allows them to accu mulate 30 minutes of exercise three times each week. OFten these patienrs do not wlerate their fi rst week of exercise well . They may need addi tional rest or may need to delay other household or leisure time activity. Because of co-existing disease, or exacerbation of symp tOms, patients with heart Failure may experience interruption of their exercise program. The patient should be encou raged that the person who is most unfit has the mOSt to gai n From an exercise program (Fig. 24. 12) . An expert panel of the Agency for Health Care Policy and Re search recom mends exercise For patients with heart failure (163). Exercise needs to be i ncorporated i nt o a comprehensive program of outpatient management For heart Fail ure. Today, such a pro gram i ncludes more than the standard therapy of ACE inhibitOrs, di uretics, digitalis, ,B -blockers, and spironolactone. Additional components of a comprehensive program i nclude diet instruc tion, salt restriction, nurse-di rected telemedicine Follow-up, and occasionally freestan d i ng heart Failure clin ics. Osteopathic Implication
Si nce the m uscle hypothesis of chronic heart Fai lure places a cen tral role on peripheral mechanisms (51), especially i nvolving mus cle ergoreceptOrs, this model of heart fai l ure is appropriate For evaluation and testing by members of the osteopathic proFession. The obvious question that arises is: what is the most ap propriate intervention inro the derangements of m usculoskeletal
24. An Osteopathic Perspective on CardioLogy �
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2. Linden RJ. ReAexes from the heart. Prog Cardiovasc Dis. 1 97 5 ; 1 8: 20 1 -22 l . 3 . Paintal AS. Vagal sensory receptOrs and their reAex effects. PhysioL Rev. 1 973;53: 1 59-227. 4. Malliani A, Peterson OF, Bishop VS, Brown AM. Spinal sympathetic cardiovascular reAexes. Circ Res. 1 972;30: 1 58- 1 66. 5. Malliani A, Lombardi F, Pagani M . Functions of afferenrs in cardio vascular sympathetic nerves. } Auton Nerv Syst. 1 98 1 ;3:23 1 -236. 6. MarkAL. The Bezold-Jarisch reAex tevisited: clinical implications of in h ibitOry reAexes originating in the heart.} Am CoLf CardioL. 1 983; I :901 02. 7 . Wurster RD. Cardiac autOnomic control interaction of somatic and vis ceral afferenrs. I n : Panerson M M , Howell I N , eds. The CentraL Cormec
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function associated with chronic hean fai l ure? The obvious an swer is those i nrervenrions that are most effective! Alrhough it would be a[[ractive ro say that the most appropriate is ro apply OMT, at the presenr time, the i nrervenrion with proven efficacy is cardiac rehabi litation exercise tra i n i ng and localized m uscle group training as described above. On a theoretical basis, other i nrervenrions inro the musculoskeletal system such as yoga, tai chi , and dietary approaches are wonhy of srudy. Ir is i ntriguing ro consider the possibiliry that OMT could play a role i n rhe management of patienrs with chronic hean fai lure. Very few srudies have been conducted (259). However, the developing l iterarure concerning rhe m uscle hypothesis of heart fai lure and the effects of exercise rraining provide a road map that could lead ro the developmenr of a conceptual model for testing the efficacy of O MT. Manipulative rreatmenr would be di rected at the paraspinal muscularure, the appendicular sys rem , and the resp irarory diaphragm. The magnirude of effect of OMT would be compared ro orher i nrervenrions such as car diac rehabilitation exercise. The inrermediate outcomes would be changes in palparory findi ngs of the m uscularure, the peak oxygen consumption wirh exercise, exercise duration, the slope of venrilation ro carbon dioxide production, and measuremenrs of auronomic nervous sysrem rone such as hean rate variabiliry. The health outcomes would be improved qual iry of life, NYHA classification, and functional starus. Because of the delayed time course of improvemenrs i n musculoskeletal function i n response ro i n rervenrion, rhe response ro O MT would have ro be followed over an interval of 4 ro 8 weeks, or possibly longer.
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myocardial infarction. Final report of the Lyon Diet Heart Study. Cir culation. 1 999;99:779-7 8 5 . Rogers Jl� Rogers Jc. T h e role of osteopathic manipulative therapy i n t h e treatment of coronary heart disease. }A OA. 1 976;76:7 1 -8 1 . Konstam M , Dracup K, Baker D , et al. Heart railure: Evaillatioll atld Care o/Patients with Left Venrricular Systolic Dysfunction. Clin ical Prac tice Guidelines No. I I . Rockville, M D: Agency For Health Care Policy and Research; June 1 994. Public Health Service. US Department of Health and H uman Services. AHCPR publication 94-06 1 2. O'Connell J B , Bristow M . Economic impact of heart failure in the United States: Time for a different approach. } Heart Lung Transplant 1 993; 1 3:S I 07-S I 1 2. Haldeman GA, CroFt J B, Giles W H , Rashidee A. Hospitalization of patients with heart failure: National Hospital Discharge Survey, 1 98 5 to 1 995. Am Heart}. 1 999; 1 37:352-360. National Heart, Lung, and Blood I nstitute: Morbidiry and Mortal iry Chartbook on Cardiovascular, Lung, and Blood Diseases/ I 992. Rockville, M D: U S Department of Health and Human Services; 1 992. Kannel WB, Belanger AJ . Epidemiology of heart failure. Am Hearl }. 1 99 1 ; 1 2 1 :95 1 -957. Massie B M , Shah N B. Evolving trends i n the epidemiologic facrors of heart failure: rational for preventive strategies and comprehensive disease management. A m Heart}. 1 997; 1 33 :703-7 1 2. Hunt SA, Baker DW, Chin M H , et al. ACCIAHA guideli nes for the evaluation and management of chronic heart failure in the adult: executive summary. A report of the American College of Cardiol ogy/American Heart Association Task Force on Practice Guidelines (Commirree ro revise the 1 99 5 guidelines for the evaluation and man agement of heart failure.) Circulation. 200 I ; I 04:2996-3007. Ho KK, Pinsky J, Kanne LWB, Levy D. The epidemiology of heart fail ure: the Framingham Study. } A m Coli Cardiol. 1 993;22[Suppl AJ:6A1 3A. Stauffer JC, Gaasch W H . Recognition and treatmen t ofleft ventricular diastolic dysfunction. Prog Cardiovasc Dis. 1 990;32: 3 1 9-332. Creager MA. Baroreceptor reAex funerion in congestive hearr failure. A m } Cardio/. 1 992;69[Suppl] : I OG- 1 5G. Ferguson DW, Abboud F M , Mark AL. Selective impairment of baroreAex-mediated vasoconstrictor responses in patients with left ven tricular dysfunction. Circulation. 1 984;67:4 5 1 -460. Bristow MR, Ginsburg R, M inobe W, et al. Decreased catecholamine sensitivity and beta-adrenergic receptor densiry in fail i ng human hearts. N Engl} Med. 1 982;307:205-2 1 I . Anderson FL, Port J D , Reid BB, et al. Myocardial catecholam i ne and neuropeptide Y depletion i n failing ventricles of patients with idio pathic dilated cardiomyopathy: correlation with beta-adrenergic re ceptor down regulation. Circulation. 1 992;85:46-53. Lee W H , Packer M. Prognostic importance of serum sodium con centration and its modification by converting enzyme inh ibition in patients with severe chronic heart failure. Circulation. 1 986;73:257267. Cody RJ . Atrial natriuretic faeror i n edematous disorders. Annll Rev Med 1 990;4 1 :377-382. Wei CM, Heublein DM, Perrella MA, et al. Natriuretic peptide system in human heart failure. Circulation. 1 993;88: I . Treasure CB, Alexander RW. The dysFunctional endothelium in heart failure. } Am Coli Cardiol. 1 993;22[Suppl] : 1 29A- 1 34. Stewarr DJ, Cernacek P, Costello KB, et al. Elevated endothel i n - I in heart failure and loss ofnormal response to postural change. CirCil/ation. 1 992;85:5 1 0-5 1 7. Benedict CR, Johnstone D E, Weiner D H , et al. for the SOLVD Inves tigators. Relation of neurohormonal activation to clinical variables and degree of ventricular dysfunction: a report from the registry of studies oflefi: ventricular dysfunction. JAm Coli Cardio/. 1 994;23: 1 4 1 0-1 420. Vaccarino V, Casal SV, Abramson j , Krumholtz H M . Depressive symp toms and risk of functional decline and death in patients with heart failure. } A m Coli Cardiol. 200 1 ;38: 1 99-20 5 . Wine KKA, Clark AL, Cleland JGF. Chronic heart failure a n d m i cronutrients. } A m Coil Cardiol. 2 0 0 I ; 3 7 : 1 765-1 774. Kannel WE. Epidemiology and prevention of heart failure: Framing ham Study i nsights. EliI' Heart}. 1 987;8 [Suppl F J : F23-F29.
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VI. Osteopathic Considerations in the CLinicaL SpeciaLties
2 1 1 . Philbin EF, Dec W, Jenkins PL, DiSalvo TG. Socioeconomic sratus as an independenr risk facror for hospiral readmission for hearr failure. Am} Cardiol. 200 1 ;87: 1 367- 1 37 l . 2 1 2. Opasich C, Rapezzi C, Lucci D, er aI, on behalf of the Italian Ner work on Congesrive Hearr Failure (l N-CH F) I nvesrigarors. Precipirar ing facrors and decision-making processes of shorr-rerm worsening of hearr failure despire "oprimal" trearment (from rhe IN-CHF Regisrry). A m } Cardio!. 200 I ;88:382-387. 2 1 3. Happ N B, Naylor M D , Roe Prior P. Facrors contriburing ro rehos piralizarion of elderly parients wirh hearr failure. } Cardiovasc Nurs. 1 997; I I :75-84. 2 1 4. Weber KT. Aldosrerone in congesrive hearr failure. N Engl } Med. 200 I ;345: 1 687- 1 697. 2 1 5 . Edwards BS, Rodeheffer RJ . Prognosric fearures i n parienrs wirh con gesrive hearr failure and selecrion crireria for cardiac transplantarion. Mayo Clin Proc. 1 992;67:485--492. 2 1 6. Harlan WR, Oberman A, Grimm R, er al. Chronic congesrive hearr failure in coronary arrery disease: clinical crireria. Ann intern Med. 1 977;86: 1 33- 1 38. 2 1 7. Srapleron J F, Segal J I� Harvey WP. The elecrrocardiogram of myocar dioparhy. Prog Cardiovasc Dis. 1 970; 1 3:2 1 7-239. 2 1 8. Echeveria H H , Bilisker MS, Myerburg RJ , er al. Congesrive hearr fail ure: echocardiographic insighrs. Am} Med. 1 983;75:750-7 5 5 . 2 1 9. Nishimura RA , Abel M D, Harle L K , e r a l . Assessment of diasrolic Funcrion of rhe hearr: background and current applicarions of Doppler echocardiography, I I . Clinical studies. Mayo Clin Proc. 1 989;64: 1 8 1 204. 220. Nishim ura R, lajik AJ . Evaluarion of diastolic filling of rhe lefr ventri cle in health and d isease: Doppler echocatdiography is the clinician's Rosetta stone. } Am Coli Cardio!. 1 997;30:8- 1 8. 22 1 . Lipkin DI� Scriven AJ, Crake T, et a1. Six-minute walking tesr for assess ing exercise capacity in chronic hearr failure. Br MedI 1 986;292:653655. 222. Madda K, Takayoshi T, Wada A, et al. Plasma brain natriuretic pepride as a biochem ical marker of high lefr ventricular end-diastolic pressure in parienrs wirh sympromaric lefr-ventricular dysfunction. Am HeartI 1 998; 1 35:825-832. 223. Clerico A, lervasi G, Chicia M, er al. Circularing levels of cardiac natriureric peprides (AN P and BN P) measured by highly sensirive and specific immunoradiometric assays in normal subjecrs and in parients wirh different degrees ofhearr failure . } Endocrinolfnvest. 1 998;2 1 : 1 701 79. 224. Dao Q, Krish naswamy P, Kazanegra R, er al. Urility of B-type natri ureric pepride in rhe diagnosis of congesrive hearr failure in an urgenr care setting. } Am Coli Cardio!. 200 1 ;37:379-385. 225. Cheng V, Kazanegra R, Garcia A, et al. A rapid bedside resr for B-type [ narriureric] peptide treatmenr outcomes in parients admir ted for decompensared hearr failure: a pilor study. } Am Coli Cardio!. 200 I ;37:386-39 1 . 226. Packer M , Cohn I N , on behalf of the Steering Committee and Mem bership of the Advisory Council to I mprove Ourcomes Narionwide in Hearr Failure. Consensus recommendarions for rhe management of chronic hearr failure. Am} CardioL 1 999;83 [SuppI 2AJ : I A-38A. 227. Levy D, Larson MG, Vasan RS, er al. The progression from hyperren sion to congesrive hearr failure. JAMA. 1 996;275: 1 5 57-1 562. 228. Wilhelmsen L, Rosengren A, Eriksson H , Lappas G . Hearr failure in the general popularion of men-morbidiry, risk facrors and prognosis. } Intern Med. 200 I ;249:253-26 1 . 229. He J , Ogden LG, Bazzano LA, er al. Risk factors for congesrive hearr failure in US mcn and women: N HA N ES I epidemiologic follow-up srudy. Arch Intern Med. 200 I ; 1 6 1 :996-- 1 002. 230. Krumholz HM, Chen YT, Wang Y, er al. Predictors of readmission among elderly survivors of admission wirh hearr failure. Am Heart I 2000; 1 39:72-77. 23 1 . Shi ndler D M , Kosris J B , YusufS, er al. Diaberes mellitus, a predictor of morbidity and morrality in rhe Studies of Left Ventricular Dysfunction (SOLVD) Trials and Regisrry. Am} Cardiol. 1 996;77: 10 1 7- 1 020. 232. Perers KG , Kienzle M G . Severe cardiomyoparhy due to chronic rapidly conducred arrial fibrillarion: complere recovery afrer restorarion of sinus rhyrhm. Am} Med. 1 988;85:242-244.
233. Grogan M, Smirh HC, Gersh BJ, Wood DL. Left ventricular dys funcrion due to atrial fibrillation in parients i nirially believed to have idioparhic dilared cardiomyoparhy. Am} Cardiol. 1 992;69: 1 5701 573. 234. Yusuf S, Sieighr P, Pogue J, er al. Effecrs of an angiorensin-converring enzyme inhibitor, Ramipril, on cardiovascular events in high-risk pa tients. The Hearr Ourcome Prevenrion Evaluarion Srudy l nvesrigarors. N Engl} Med. 2000;342: 1 45-1 53. 235. Packer M , Bristow M R, Cohn I N , er al. The effecr of carvedilol on morbidity and morrality i n patients wirh chronic hearr failure. N Eng! } Med. 1 996;334: 1 349- 1 3 5 5 . 236. M E R l T- H F Srudy Group: Effect of metoprolol CRlXL in chronic hearr failure: metoprolol CRlXL randomized intervention rrial in con gesrive hearr failure (MERlT-HF). Lancet. 1 999;353:200 1 -2007. 237. Packer M, Coars AJS, Fowler MB, et al. Carvedilol Prospecrive Randomized Cumularive Survival Study Group. Effecr of carvedilol on survival in severe hearr failure. N Engl } Med. 200 I ;344: 1 65 1 1 658. 238. McClean DR, lham H, Garlick AH, er al. Clinical, cardiac, renal, arrerial and neurohormonal effecrs of omapatrilar, a vasopepridase inhibiror, in parients wirh chronic hearr failure. } Am Coli Cardiol. 2000;36:479--486. 239. Piepoli M . Central role of peripheral mechanisms in exercise intol erance i n chronic hearr failure: rhe muscle hypothesis. Cardiologia. 1 998;43 (9):909-9 1 7. 240. Abboud FM, Heisrad DD, Mark AL, Schmid, PG. ReAex control of the peripheral circularion. Prog Cardiovasc Dis. 1 976; 1 8:37 1--403. 24 1 . Drexler H. Reduced exercise tolerance i n chronic hearr failure and irs relarionship to neurohormonal factors. Eur Heart I 1 99 1 ; 1 2[Suppl C] : 2 1 -28. 242. Piepoli M , Ponikowski P, Clark AL, er al. A neural link ro explain rhe "muscle hyporhesis" of exercise i ntolerance in chronic hearr failure. Am HeartI 1 999; 1 37: 1 050- 1 056. 243. Jette M , Heller R, Landry F, Blumchen G . Randomized 4-week exercise program in patients wirh impaired left ventricular funcrion. Circula tion. 1 99 1 ;84: 1 65 1 - 1 667. 244. Koch M, Doward H , Brousrer J-P. The benefir of graded physical exercise in chronic hearr failure. Chest. 1 992; 1 0 1 :23 1 S-234S. 245 . Kosris J B, Rosen RC, Cosgrove N M , et al. Nonpharmacologic therapy improves funcrional and emorional srarus in congesrive hearr failure. Chest. 1 994; 1 06:996- 1 00 I . 246. Hambrechr R, N iebauer J , Fiehn E, er al. Physical rraining i n parients wirh stable chronic hearr failure: effecrs on cardiorespiratory firness and ulrrastructural abnormalities of leg muscles. } Am Coli Cardio!. 1 995;25: 1 239-1 249. 247. Kiilavuori KM, Toivonen L, Naveri H, Leinonen H. Reversal of au ronomic derangements by physical training in chronic hearr failure assessed by hearr rare variabiliry. Eur Heart I 1 99 5 ; 1 6:490--495 . 248. Kereyian SJ , Levine A B , Brawner CA, er a l . A randomized controlled trial of exercise rraining in parients wirh heart failure. Ann Intern Med. 1 996; 1 24: 1 05 1 - 1 057. 249. Giannuzzi P, Tavazzi L, Temporelli PL, er al. Long-rerm physical rrain ing and lefr ventricular remodeling afrer anterior myocardial infarcrion: resulrs of rhe exercise in anterior myocardial infarcrion (EAMI ) trial. } Am Coli Cardiol. 1 993;22: 1 82 1 - 1 829. 250. Belardinelli R, Georgiou D, Cianci G, Pucaro A. Randomized, con trolled rrial of long-rerm moderare exercise rraining in chronic hearr failure. Circulation. 1 999;99: 1 1 73-1 1 82. 25 1 . Hambrechr R, Fiehn E, Weigl C, er al. Regular physical exercise correcrs endothelial dysfuncrion and improves exercise capacity in patients wirh chronic hearr failure. Circulation. 1 998;98:2709-27 1 5. 252. Gordon A, Tyni-Lenne R, Persson H, er al. Markedly improved skeleral muscle funcrion with local muscle training in parients wirh chronic hearr failure. Clin Cardiol. 1 996; 1 9: 568-574. 253. Ohrsubo M, Yonezawa K, Nishijima H, er al. Merabolic abnormaliry of calfskeletal muscle is improved by localized muscle training wirhour changes in blood Aow in chronic hearr failure. Heart. 1 997;78:437443. 254. Gianuzzi P Arrenruarion of unfavorable remodeling by exercise training in posr infarcrion parienrs wirh lefr ventricular dysfuncrion: Resulrs of
24.
the Exercise in Left Ventricular Dysfunction (ELVD) Trial. Circulation. 1 997 ;96: 1 790-1 797. 255. Meyer TE, Casadel B, Coats A)5, et al. Angiotensin-converting en zyme inhibition i n physical training and heart fai lure. j In! Med. 1 99 1 ;230:407-4 1 3. 256. Riegger GA) . The effects of ACE inhibitors on exercise capacity in rhe treatment of congestive heart failure. j Ca"diovasc PhamacoL 1 990; 1 5 1 5uppl 2J :54 1 -546. 257. Meyer K, 5chwaibold M, Westbrook 5, et al. Effects of exercise training
An Osteopathic Perspective on Cardiology
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and activity restriction on 6 m i nute walking tesr performance in pa tients with chronic heart failure. Am Heart). 1 997; 1 33:447-453. 258. Piepoli M , Clark AL, Volterrani M, et al. Contriburion of muscle afFerents to the hemodynamic, autonomic, and ventilatory responses to exercise in patients with chtonic heart failure. Effects of physical rraining. Circulation. 1 996;93:940-952. 259. Rogers F), Glassman ) , KaviefF R. Effects of osteopathic manipula tive treatment on autonomic nervous system function in patients wirh congestive heart failure. jA OA. 1 986;86:605(abst).
OSTEOPATHIC MANAGEM EN T OF EAR, NOSE, AND THROAT DISEASE HARRIET H. SHAW MICHAEL B. SHAW
KEY CONCEPTS
Structure and function of the ear, nose, and throat (ENT) region • Pathophysiology, diagnosis, and treatment options for com mon ENT problems seen in primary care settings, including sinusitis, allergic rhinitis, otitis media, and acute ronsi l litis and pharyngitis • The osteopathic approach to the diagnosis and treatment of ENT problems •
The ears, nose, and throat are not a system u nto themselves; they are parts of at least three d i fferent systems. Their grouping together as a specialty is l i kely due to their sharing of several facrors, including having a respirarory mucosal l i n ing, contain i ng organs of special senses, having internal connections to each other, and being located in the head and neck. The nose, paranasal sinuses, mouth, and throat function in the respirarory system as passageways for inspired and expired air. I n addition, the nose and paranasal sinuses play an important role in conditioning and filtering the i nspired air. Olfaction is the special sense of the nose. The special senses of hearing and balance are housed in the ears. The mouth and throat function as part of the digestive system i n chewing, swallowing, and the special sense of taste. The throat and mouth also aid in speech. Due to the diverse nature of this area, numerous and very different clinical problems are associated with treating the ears, nose, and throat. They range from i nfectious processes to vertigo to difficulty swallowing or talking. Preventing and treating many of these problems depend on an appreciation of the physiologic functions and anatomical relationships that exist. Several problems of the ear, nose, and throat are com monly encountered i n the primary care setting. These i n clude allergic rhinitis, si nusitis, otitis, and tonsillitis. Treating this area from an osteopathic perspective uses the basic concepts of structure function relationship and the body's in herent heali n g capacity.
These common problems serve as examples of how to approach the ENT patient osteopathically. The respiratory system demonstrates the remarkable health mai ntenance systems within the body. With an understanding and appreciation of normal anatomy and function, the physician can effectively treat ENT patients to enhance the abil ity for re covery and the natural resistance to disease. It is the responsibility of the osteopathic physician to consider the specific needs of the patient and design a management plan deemphasizing interven tion in favor of promoting the body's ability to regulate itself toward health. Patient education plays an im portant role in the treatment and prevention of ENT problems. I ncreasi ng patient awareness of medication abuse, pollutants, humid ification, and allergies is a critical aspect of management. Osteopathic manipulative treatment has been used empiri cally to treat ENT problems commonly encountered in primary care (1,2,3). This treatment is based on the musculoskeletal sys tem's i mpact on circulatory Aow to and from all the tissues of the body and its effects on physiologic function by way of the auto nomic nervous system. Promoting lym phatic circulation plays an important role in reducing swell ing and inAammation, as well as in stimulating the immune system . Studies have shown physio logic function of various organs to be affected by noxious somatic afferent stimulation (4,5). Clinical experience has shown that in corporation of musculoskeletal treatment in the management of ENT patients i m proves recovery time and reduces incidence of recurrence and complications (6,7). Medical intervention can be accompl ished in the most ben eficial way when consideration is made of the natural forces at work to maintain homeostasis. Medications, surgery, and allergy desensitization can be most effective when based on specific di agnoses and combined with patient education and appropriate musculoskeletal treatment. General knowledge of myofascial anaromy, lymphatic circu lation, and autonomic nervous supply ro the head and neck can enhance osteopathic treatment of patients with ear, nose, and throat problems. Specific attention to each organ's unique aspects of anatomy, built-in mechanisms for health, and predisposing factors for disease will enhance treatment of specific conditions.
25. Osteopathic Management of Ear, Nose, and Throat Disease MYOFASCIA OF THE HEAD AND NECK
As in other areas of the body, connective tissue forms covering and padding around the structures in the neck. It is denser im mediately next to organs and muscles and looser between organs. The looser areas form potential spaces where fluid may collect, including infection, swelling, and blood. Fascial relationships become important because of the struc tures that transverse or are enclosed by fascia and because of the location of fascial spaces. It is characteristic of fascia to split to surround muscles or organs and unite again on the other side. In places, it attaches firmly to bone as it blends into periosteum. This creates a situation of unl i mited connectedness and relationship to various and d istant structures. Fascia serves both a compart mentalizing and connecting function. It defines muscles, muscle bundles, and organs while connecting them to each other. It lim its the spread of infection and swell ing but allows it to fol low the channels of fascial spaces. Fascial sheaths form around nerves and vessels, providing passageways for neural supply, blood, and lymph flow. As in many other areas of the body, fascia in the head and neck is identified in layers (Fig. 25.1). The superficial fascia en ci rcles the neck and contains variable amounts of fat but, unlike other parts of the body, encloses voluntary muscles, such as the platysma and the muscles of facial expression. Several arrange ments of deeper fascia are deep to the superficial layer. Preverte hral fascia encloses the vertebral column and associated muscles, forming a vertebral compartment. Bilateral neurovascular com partments, the carotid sheaths, are formed by fascia surrounding and enclosing the great vessels and vagus nerve. In the anterior neck, the visceral compartment, formed by the pretracheal fas cia, contains the trachea, esophagus, and associated structures. The superficial layer of fascia attaches to the hyoid bone. In ferior to the hyoid, it courses downward and attaches both to the anterior and posterior surfaces of the sternum and the clavicle. Above the hyoid, the superficial fascia passes below rhe muscles of the floor of the mouth, around the submand ibular and parotid
371
glands, and encloses the masseter and medial pterygoid muscles; it then attaches to the mandible, pterygoid plate, and the zygo matic arch. The prevertebral layer begins on the cervical spinous processes and l igamentum nuchae, forms a circle around the back muscles deep to the trapezius, and then courses around the transverse processes of the cervical vertebrae and in front of the vertebral bodies. In some places, it l ies in d i rect contact with the superficial fascia, and in others, it separates from it to provide passage for nerves and vessels. The preverrebral fascia specifically fol lows the scalene muscles and forms a sleeve for the brachial plexus and the axi llary artery. Near the t ransverse processes, the preverrebral fascia embeds the cervical sympathetic trunk. The pretracheal fascia encircles the trachea, esophagus, and thyroid gland. It is continuous with the superficial layer of cer vical fascia that encloses the infrahyoid muscles. Following these muscles inferiorly behind the sternum, it fuses with the fibrous pericardium in the superior mediastinum. Superiorly, the pre tracheal fascia fuses to the hyoid bone and the thyroid cartilage. Above the hyoid bone, this fascia remains well developed around the esophagus and the pharynx.
LYMPHATIC CIRCULATION IN THE HEAD AND NECK
The lymphatic system of the neck consists of numerous lymph nodes connected by lymphatic channels that eventually end in the thoracic and right lymphatic ducts. The thoracic duct receives drainage from the left side of the head and neck while the right lymphatic duct drains the right side. Each empties independently into the junction of the internal jugular and subclavian veins on their respective side of the body (Fig. 25.2). Cervical lymph nodes are generally divided in groups submandibular, submental, superficial cervical, deep cervical, and paratracheal (Fig. 25.3). The submandibular and submental nodes are intimately connected with the superficial fascia covering
Pretracheal fascia layer
Sternocleidomastoid m. -------..L1
Trachea Deep cervical lymph nodes
Carotid sheath Prevertebral fascia layer
Scalene m. I I
!
Trapezius m.
/
/
/
/ FIGURE 25. 1 . Fascia I layers of neck.
Superficial fascia layer
Vi. Osteopathic Considerations in the Clinical Specialties
372
Sternothyroid m.
-----::!l
Deep ceNical lymph nodes
r---Transverse ceNical a.
���� ���� �
__ _____
Internal jugular v. --F�iii:!'f:-7:..r.:�
_-"..;;....;,.;�;:;;;:;--- "Omohyoid
fascia"
Phrenic n.
Thoracic duct
...... .
r-::��i7::-""";+-::---� Prevertebral fascia
--
;.,;;:;r----.,.=....�� .. ..
--
Suprascapular a.
Sternohyoid m.
=.;.,-- Subclavius m. Ant. sterno clavicular IIg.
FIGURE 25.2. Deep cervical lymphatics. (From Moore
MD: W i l l i a ms
& W i l k i ns; 1985, with permission.)
the digastric and mylohyoid muscles. The superficial cervical nodes lie along the external jugular vein and on the external sur face of the sternocleidomastoid m uscle. The paratracheal nodes are irregularly located and, as do all the aforementioned groups of nodes, drain into the deep cervical lymph nodes. These promi nent, deep nodes form a chain embedded in the connective tissue of the carotid sheath around the internal jugular vein (Fig. 25.1). The intimate association of the lymphatic channels to the myofascial structures in the neck makes lymphatic Aow partic ularly susceptible to changes in myofascial tone. Hypertonia in the cervical myofascial tissues can impede lymphatic Aow. Free dom of motion in muscles of normal tone improves lymphatic circulation.
AUTONOMIC NERVOUS SUPPLY IN THE HEAD AND NECK
Sympathetic fibers to the head arise from the upper thoracic segments of the spinal cord ( Fig. 25.4). Preganglionic fibers as cend from there to the superior cervical ganglion in the upper
KL. Clinically Oriented Anatomy, 2nd ed. Balti more,
cervical area, where they synapse. Postganglionic fibers from the superior cervical ganglion join the internal carotid plexus. Sym pathetic supply to the nose and paranasal sinuses passes through the sphenopalatine ganglion, which lies posterior to and slightly above the posterior end of the middle nasal concha (usually be low the Aoor of the sphenoid sinus). Sym pathetic fibers from the carotid plexus also reach the ear, by inferiorly penetrating the tympanic cavity. Sympathetic fibers are presumably vasomotor and are most often vasoconstrictors. Somatic inAuence on the sympathetic nervous supply to the head and neck, in the form of somato-visceral reAexes, would most likely occur in the upper thoracic area, where the sympathetic fibers originate, or the upper cervical area, related to the superior cervical ganglion. Parasympathetic supply to the nose is from the facial nerve (cranial nerve VlI). Irs preganglionic fibers form part of the greater petrosal nerve, synapsing in the sphenopalatine ganglion. These include both vasodilator and secretory fibers. Postgan glion i c fibers are distributed from the sphenopalatine ganglion with the sensory and sympathetic fibers. The glossopharyngeal nerve (cranial nerve IX), which exits the cranium with the vagus and accessory nerves through the jugular foramen, also carries
25. Osteopathic Management of Ear, Nose, and Throat Disease
373
some parasympathetic fibers. These synapse in rhe otic ganglion and mostly supply the parotid gland.
x---- Submandibular r-----
Superficial parotid
)
FIGURE 25.3. Superficial cervical lymph nodes. (From Moore Kl. Clin ically Oriented Anatomy, 2nd ed. Baltimore, M D : Williams & W i l k i ns; 1985, with permission.)
To glands and vessels of mucous membranes
Geniculate
NOSE AND PARANASAL SINUSES Healthy Structure and Function
The nose, an organ of respiration and olfaction, functions to fil ter, humidifY, and regulate the temperature of i nspired air. The paranasal sinuses in the maxillary, frontal, sphenoid, and ethmoid bones are air-filled extensions of the nasal cavities and serve sim i lar functions to that of the nose. Regardless of the temperature of outside air, the temperature of i nspired air is changed to ap proximate body temperature during its passage through the nose. Similar changes are made in moisture content of i nspired air so that it reaches the trachea at almost ambient humid ity. The su perior, m iddle, and i n ferior turbinates, or conchae, are elevations on the lateral nasal walls. Heavily endowed with blood vessels, they help control the tem perature of the i nspired air. The nose filters particulate m atter in the air: Much of the smoke, dust, pol lens, and bacteria are trapped and removed before the air enters the lungs. The nasal septum and the turbinates help create an air Row pattern in the nose that can m aximize the air-conditioning function of the nose and paranasal sin uses. The nasal cavity and paranasal sin uses are covered by pseu dostrat ified, columnar, ciliated epithel ium. Goblet cells and sub m ucosal glands contribute to the m ucous blanket that covers and protects the epithelium. This mucous film has two layers. The cilia beat withi n the i n ner, serous (sol phase) layer. The outer, more viscous (gel phase) layer is moved by synchron ized cil iary action (Fig. 25.5). Secretions from the sinuses pass i nto the nasal cavity through the various ostia or ope n i ngs in the sinuses. The outer layer of mucus traps dust and other particles and moves
ganglion Gel phase of -------.....,. mucous blanket Sol phase
Carotid plexus
--
� S uperior
o
"
" L
cervical ganglion Middle cervical ganglion
I
, PNS:
I I
,'-TI I
/-T2
---
Deep petrosal nerve
SNS: - - - - - - - .
Activates secretory
Vasoconstriction of
glands
vessels (drying of mucosa)
FIGURE 25.4. Autonomic nerve supply to upper respi ratory tract.
FIGURE 25.5. C i l iated respi ratory epith e l i u m .
VI. Osteopathic Considerations in the Clinical Specialties
374
TABLE 25.1. COMMON DISORDERS OF THE NOSE AND PARANASAL SINUSES Disorder Epistaxis Nasal fractures Acute r h i n itis
Posterior
A l lergic rh i n itis
ethmoid
Non-a llergic vasomotor r h i nitis Atrophic r h i nitis
Sphenoid
Polyposis
sinus
Deviated nasal septum U n i l ateral nasal d ischarge Foreign body Choana I atresia M a l i g nancy Head tra u m a
Maxil l ary ostium
Auditory tube
orifi ce FIGURE 25.6. Paranasal s i n u s drainage patte rns.
them through the ostia i nro the nasal cavity, where mucus is transported inro the nasopharynx and swallowed. The process is referred ro as mucociliary clearance. Pathogens may be incorpo rated i nro the cells of the mucosa or destroyed by Iysozymes and secrerory immunoglobul i n A with i n the mucus. Normal function of the paranasal sinuses depends on the ef fectiveness of mucociliary clearance. There are rwo basic drainage patterns of the sinuses. The anrerior ethmoid, fronral , and max illary sinuses are part of the anrerior parrern drain i ng ro the os tiomeatal unit under the middle turbinate. The posterior ethmoid and sphenoid si nuses are in the posterior parrern and drain ro the sphenoethmoid recess (Fig. 25.6). The ostiomeatal unit is located superior ro much of the maxillary sinus, making it necessary ro actively move the mucous blanket "uphill" for effective drainage. This nondependenr drainage situation exists with the sphenoid and, in some instances, with the ethmoid sinus as well . Condi tions that create obstruction ro the normal flow of air and mucus predispose the sinuses ro disease and are described i n standard ENT references. The lymphatics from the anrerior portion of the nose drain inro the lymphatics of the ski n . Of the larger, posterior lymphat ics, some drain directly ro the deep cervical nodes, but most drain behind the throat ro the retropharyngeal nodes before con tinuing ro the deep cervical nodes. Proper balance of the auronomic nervous system is necessary for healthy mucosal functio n . Blood supply ro the nasal mucosa is regulated through the sympathetic nervous system. Sympa thetic preganglionic fibers arise from the Tl-4 cord level, and postganglionic fibers from the superior cervical ganglia join the internal carotid plexus. Fibers reach the sphenopalati n e ganglion via the deep petrosal nerve and the nerve of the pterygoid canal.
S i n usitis
Unopposed sympathetic stimulation leads ro vasoconstriction ac companied by drying of the mucosa. Nasal mucus production is predominantly regulated by parasympathetic nerve fibers, but sympathetic fibers also reach the glands. Stimulation of parasym pathetic fibets generally increases goblet cell secretions. The parasympathetic, secreromoror i nnervation comes from the fa cial nerve (cran ial nerve V1I) and synapses in the sphenopalatine ganglion (Fig. 25.4). Tobacco smoke and other pollutants ad versely affect mucus flow by inactivating cilia (8). The quantity and composition of the mucus is i nfluenced by various facrors, such as temperature, humidity, oxygen concentration, pollution, and irritants. Neuromediarors, such as substance P, also appear ro i nfluence the function of the mucosal glands (9). Common Pathophysiology
I nflammation is a common cause of disease 111 the nose and paranasal sinuses (Table 25.1). The inflammarory process can be initiated by i n fections (viral or bacterial), allergies (food or inhalants), and irritants (chemical or mechanical). Inflammation is accompanied by swel ling of the mucosa, excessive mucus pro duction, and decrease of cil iary motility. Symproms include ob structed breathi ng, pai n , rhinorrhea, and sometimes epistaxis. Prolonged i nflammation predisposes ro recurrent infection and changes, such as thickening of the mucous membranes and inhi bition of cilia. These conditions impede the normal airflow and functioning of the mucosa. Poor venous and lymphatic circula cion from the area can cause inflammarory mediarors ro remain i n the tissues longer and prolong the i nflammatory reaction. Nasal obstruction and abnormal airflow may be due ro venous and lymphatic congestion causing engorgement of the mucosa, as occurs with allergic rhinitis or upper respirarory i n fections. It may also be caused by structural defects, such as polyps or a deviated septum. Changes in the mucosa and in airflow patterns have an adverse effect on the cleaning, humidifYing, and temperature con trol of the air, as well as on the oxygen concentration in the si nuses. Sinusitis may result from prolonged derangement of airflow. Obstructions due ro mucosal changes are responsive ro ac tivities that alter sympathetic nerve d ischarge. Vigorous physical exercise has been shown ro improve nasal function for up to
25. Osteopathic Management of Ear, Nose, and Throat Disease 60 minutes by reducing nasal airAow resistance and nasal blood Aow (l 0). In a group of 12 subjects serving as their own controls, osteopathic man ipulation resulted in significant improvement of nasal function, as measured by nasal pressure curves (11). Ad dressing somatic dysfunction with osteopathic manipulation adds to patient comfort and aids the normal heal ing process (6,7). Tis sue changes in the upper thoracic and upper cervical areas would be expected to accompany sympathetic motor dysfunction of the nose and paranasal sinuses. Chronic conditions and progression of d isease can be prevented by decreasing congestion and pro moting good airAow.
SINUSITIS Diagnosis
Acute sinusitis is one of the common mani festations ofi nAamma tion and obstruction in the upper respiratory tract. Patients often present with nasal congestion, pain in the face or head, a feeling of full ness around the eyes, and, occasionally, fever. Other signs and symptoms i nclude a foul taste or smell, postnasal drai nage, and fa tigue. Physical exami nation reveals tenderness to percussion over the sinuses. Nasal mucosa is often red and congested with either clear or purulent dra i nage. Structural abnormalities, such as sep tal deviation or hypertrophied turbi nates, are sometimes noted. Transillumination of the sinuses may reveal decreased light trans mission, but is not a defin itive test. Edema and tenderness are frequently evident in the periorbital area. Numerous studies de scribe accompanying cervical soft tissue hypertonia with varying degrees ofmotion dysfunction (1,12,13). Local ized, small areas of tenderness and tissue tension corresponding to Chapman's reAex points have been noted in the suboccipital area and i n ferior to the clavicle, over the first rib (14). Various other somatic dysfunctions occur unique to the individual patient. Computed tomography (CT) of the si nuses is replacing standard x-ray films for evaluation of sinusitis. [n recurrent sinusitis, CT can delineate an anatomic blockage at the ostiomeatal complex, which suggests the need for functional endoscopic surgery. Chronic sinusitis can develop if the cause of inAammation is not removed and steps are not taken to restore the condi tions favoring good physiologic function . It is important to determine whether i n fectious agents, allergens, or irritants are the primary etiology. Local structural deform ities causing poor aeration of the sinuses may be predisposing to persistent infection. Decreased venous and lymphatic return can contribute to continued con gestion and poor healing. Treatment/Management
Treatment falls under several categories-patient i nstruc tion/participation, musculoskeletal , medical, and surgical. Once the underlying pathophysiologic process has been determi ned, management in the four areas can be tailored to the patient's particular needs, keeping in mind the general goals of reducing edema and inAammation, promoting s inus drainage, and con troll i ng infection (15). [ n all cases, promoting mucociliary clearance is essential to the overall treatment and prevention of complications. Patients
375
should be i nstructed to drink warm, clear Auids to hydrate the mucous membranes and i ncrease mucocil iary clearance (10). M i l k is believed to thicken secretions and is not recommended. No controlled cli n ical trials of antihistam ines in si nusitis exist, nor is histami ne known to play a role i n this disease (10). Antih is tamine side effects of overdrying the mucosa and slowing cil iary motion should be considered before use of these medications. For patients with concomitant allergic disease, the availabiliry of nonanticholinergic antih istami nes, such as astemizole and terfe nadine, has made it possible to avoid some of these compl ications. Mucoactive agents, such as guai fenesin, hyperton ic sal i ne, and saturated solution of potassium iodide (SSKI), that alter the char acter, production, or movement of mucus may be helpful (10). When medications are used, they should be selected for spe cific reasons. I nAammation due to i n fection should be treated with appropriate anribiotics. The most common pathogens in volved in si nusitis are Streptococcus pneumoniae, Haemophilus in jluenzae, and MoraxeLla catarrhalis. [ n chronic sinusitis, Staphylo coccus aureus may also be encountered. Oral decongestants may be helpful in treating congestion and swelli ng, but they are not usually recommended in ch ildren . Topical decongestants are of ten overused and lead to rebound swelling of the mucosa, which is known as r h i n itis medicamentosa; therefore, they should be used short term in acute si nusitis. Topical corticosteroids may be helpful i n reducing edema and i nAammation, thus promot ing sinus drainage. They are not, however, considered first-line therapy i n sinusitis. The rationale for the use of osteopathic man ipulation in si nus disease is to affect myofascial constraint on venous and lym phatic Aow and to alter somato-visceral reAexes to the si nuses (15). Muscle activiry is a recognized mechanism of increasing lymphatic A ow. Osteopathic man ipulative treatment (OMT) to the neck, specifically those techniques involving muscle action (such as muscle energy and myofascial techn iques), should con tribute ro i ncreased lymphatic Aow from the head . Because lym phatic channels are embedded in the cervical fascia, soft tissue technique treatment (see Chapter 54) ro the cervical area may also serve ro promote lymphatic circulation. The expected result would be reduced swelling of the si nus and nasal mucosa. Direct and indirect pressure tech niques over the si nuses and sphenopala tine gangl ion are described for assisting drainage of the sinuses (16). With some of the lymphatic drainage leaving the nose and entering the lymphatics of the skin , d irect pressure in this area would be expected ro encourage lymphatic circulation. Rhyth mic motion of the cranial bones as part of the cranial rhythmic impulse may be a significant facror in promoting si nus drainage. Following this l i ne of th inking, treatment of dysfunctional mo tion patterns, particularly involving the max il lae, sphenoid, eth moid, and frontal bones, should be part of sinusitis treatment (see Chapter 62). Ultimately, lymphatic Auid from the head and neck must en ter the central circulation in the area of the subclavian and int er nal jugular veins. Somatic dysfunction of the structures in th is area, includ ing the upper ribs, upper thoracic spi ne, and clavicles, should be considered as a potential impediment ro lymphatic Aow (Fig. 2 5 .7). The observation of somaro-visceral reAexes by Sata and Schmidt (4,5) suggests the modulation of visceral function with
VI. Osteopathic Considerations in the Clinical Specialties
376
Internal jugular vein Thoracic duct
Clavicle
Subclavian vein
Rib 1 FIGURE 25.7. Thoracic i n let a n d lymphatic relationships.
various somatic stimuli . Somatic stimuli associated with somatic dysfunction of cervical and upper thoracic areas could impact the sympathetic vasomotor tone to the sinus area. One of the goals of O MT to this area would be to improve blood Aow by altering the somatic component of this somato-visceral reAex. Chemical irritants (tobacco smoke as the most prevalent) also cause inAammation of the respiratory mucosa. Smokers suffer from frequent inAammatory conditions of rhe nose and paranasal sinuses. Children l iving in a home where tobacco smoke is present are at high risk for develop i ng respiratory disorders (17). Patient education is essential and o ften needs to be o ngoing. Judicious use of n icotine supplements and smoking cessation programs are helpful for some patients. History is helpful in identifying patients with hypersensitivity or overexposure to common chemicals, such as formaldehyde and petroleum products. I ncreasing awareness of potential exposure is often sufficient treatment; however, some cases require substantial l i festyle and occupation changes. Obstruction due to local structural abnormalities may exist and needs to be evaluated on physical examination and, at times, with further diagnostic tests (CT and endoscopy). I n the pres ence of structural abnormalities, such as deviated septum, nasal polyps, e n larged turb i nates, or obstruction of the sinus ostia, if conservative therapy fails to con trol recurrent infections, a surgi cal approach may be i n dicated. ALLERGIC RHINIT IS Diagnosis
Symptoms of rhinorrhea, sneezi ng, itchy eyes, and watery eyes are associated with allergic rhinitis. This condition usually shows seasonal variation and recurrence. On physical exam ination, it is characterized by engorgement of the turbinates, which appear pale or violaceous rather than erythematous, as in viral rhini tis. Nasal polyps are sometimes present and appear as yellowish, boggy masses of mucosa. It is also common to see signs of chronic rhinorrhea and postnasal drainage. Treatment/Management
I nAammation due to allergy, associated with allergic rhinitis, can be treated with antihistamines, steroids (inhaled or systemic),
' cromolyn sodium, hydration, and manipulative techniques that aid circulation. Reducing swelling by promoting venous and lym phatic circulation and decreasing the concentration of chemical, i nAammatory mediators in the i nterstitial tissues is particularly important. Antihistam ines are useful in countering the inAam mation and vasomotor symptoms associated with allergic disease. Their anticho l inergic side effects, particularly mucosal dryi ng, may complicate the treatment. Many patients do not tolerate the drowsiness associated with traditional antihistamine therapy. Selective H I antihistamines (nonanticholinergic) minimize these side effects and offer a safer option for treating the allergic compo nent ofENT problems (I 0). Nasally inhaled antih istamine prepa rations with minimal anticholinergic effect are also available. The inhaled steroids are effective in reducing the local inAammation and associated symptoms, and they are also indicated for prevent ing recurrence of nasal polyps. They may require from 3 days to 2 weeks of regular use for symptomatic improvement. Systemic steroids should be used cautiously and reserved for severe and/or resistant cases. Sodium cromoglycate (cromolyn sodium) serves as a mast-cell stabilizer and has a suppressive effect on other inAam matory cells. It is best used prophylactically for allergic rhinitis and may also require regular use over I to 2 weeks for benefits to become apparent (18). Addressing the specific allergic cause is essential to effective and lasting treatment. Responsible allergens may be foods or in halants (dusts, pollens, molds, animal dander). History is helpful in determining the offending allergens. Year-round symptoms that are worse indoors suggest animal dander, dust, or dust mite allergy. Pollens are most common in the spring, grasses in the summer, ragweed in late summer and fall. Allergy testing and elimination diets are often necessary for specific diagnosis and treatmen t . Environmental con trol, particularly for dust, molds, and animal dander, is an important part of treating ENT disease with an allergic etiology. This requires educating and encouraging the patient who may become discouraged with the demand ing lifestyle changes.
EARS Healthy Structure and Function
The ear is a complex organ of hearing and balance (Fig. 25.8). The temporal bone houses or provides attachmen t for all parts of the ear. The external ear consists of the pin na and external meatus. The pinna collects and localizes sound. The mcatus is an air-filled tube through which soun d waves travel to reach the middIe ear. The middle ear con ta i ns the tympanic membrane and three bones, or ossic1es-malleus, i ncus, and stapes. The middle ear is air-filled and transmits sound from the air media to the liquid media of the i nner ear. It is lined by ciliated, respiratory mucosa. The inner ear consists of the liquid-fillcd cochlea for auditory sense and the vestibular system for the sense of equilibrium. Also lined by respiratory mucosa, the auditory or eustachian tube connects the middle ear to the nasopharynx. The lateral one-third of the auditory tube lies in the temporal bone, and the medial two-thirds is cartilaginous, opening only with swallowing or yawning. Air enters or leaves the middle ear cavity through this
25. Osteopathic Management of Ear, Nose, and Throat Disease
Tympanic Isthmus Auditory tube
01
lube
orifice
Tympanic
of lube
cavity
377
Aditus ad antrum Mastoid antrum
Inferior concha
P h aryng eal
.".-_.....r __
orifice of tube
.;:-;:.r;=.;;;:-;"T!-
Styloid process
''II.16rr-- Exi.
carotid a.
Pharygeal recess
Soft palate ----':.-.,
••��-
Stylohyoid m.
iiiiijpo;;"';';;:::;r.--
Stylopharyngeus m.
FIGURE 25.8. Structures of the ear. (From Moore KL. Clinically Oriented Anatomy, 2nd ed. Baltimore,
MD: W i l l ia m s
& W i l k ins; 1985, with permission.)
tube, providi ng balanced pressure between the atmosphere and middle ear. Loss of this connection due to obstruction, which can occur with swel ling of the mucosa or hyperplasia of the adenoids, results in poor functioning of the auditory system. The result is Auid accumulating in the middle ear and subsequent infection. Children are often susceptible to middle-ear infections. Their auditory tubes are short and horizontal, and the supporting tensor veli palatini muscle is less efficient than in adults. The blood vessels and lymphatics supplying all the structures in the head are contained in the cervical fascia. The deep cervi cal lymph nodes lie in the reflection of the cervical fascia. The prevertebral fascia that invests many of the muscles of the neck lies over the sympathetic chain. The superficial lymphatics, as well as the external jugular vein, pierce the superficial fascia as they pass to join deeper structures. Along with lymph from the nose and upper pharynx, the lymph drai nage from the middle ear forms a plexus in front of the auditory tube before goi n g ro the retropharyngeal nodes. Obstruction o f this plexus is believed to be one of the causes of serous otitis media. The i ntimate relation ship of myofascial structures to the blood vessels, lymphatics, and ganglia serving the ear are evident (19). The influence of musculoskeletal manipulation in the treatment of ear problems is believed to exert some of its effect through these relationships ( 1 ,16,20).
Common Pathophysiology
The ear is subject to numerous types of disorders involving the external, middle, or i n ner ear (Table 25.2). It can be affected by i n fection and i n flammation, and by neurologic and vascular prob lems. Pain, hearing loss, vertigo, and tinnitus are some symptoms TABLE 25.2. COMMON DISORDERS OF THE EAR Disorder Hearing loss Sensorineural Cond uctive Externa l canal obstruction I m pacted cerumen Exostoses/chondromas Fore i g n bodies Externa I otitis Bacterial Fungal Otitis media Acute With effusion Mastoiditis Ti n n itus Vertigo/Dizzi ness
378
VI. Osteopathic Considerations in the Clinical Specialties
associated with these p rocesses. Because the sensory innervation to the ear is derived from the trigeminal, facial, glossopharyngeal, vagal , and upper cervical nerves, otalgia is frequently a result of referred pain from other areas of the head and neck. Temporo mandibular joint dysfunction and cervical dysfunction are com mon causes of ear pain. The external ear is subject to infections, especially if persis tently exposed to a moist environment. The vestibular function of the inner ear can be disturbed as a result of infection or of neu rologic or vascular im pairment. Heari ng loss can be due to various disturbances in the middle ear or to neurologic deficits. Chronic exposure to loud noise con tributes to hearing loss (sensorineural) by traumatic damage to the receptors in the cochlea. I n fectious and inAammatory processes in the auditory tube and middle ear are common causes of temporary hearing loss and ear pain. Upper respiratory infections and allergy, with mucosal inAam mation and lymphoid hyperplasia, may lead to auditory tube dysfunction . Persistent obstruction of the auditory tube pressure equalizing system results in increasing negative pressure and de creased ventilation in the middle ear. Under these conditions, nasopharyngeal secretions could be aspirated into the middle ear and drainage impaired. The lowered PA02 impedes granulocyte formation , and bacterial colonization frequently results. Factors such as enlarged adenoids can aggravate the pooling of secretions in the middle ear. ReAux of nasopharyngeal contents into the middle ear is more likely when swallowing occurs in the supine position . Bottle feeding has been associated with increased in cidence of otitis media, but evidence does not seem to warrant avoidance of bottle feeding (2 1 ). Evidence has been found that attendance at day-care p rograms and exposure to tobacco smoke increase the risk of middle ear infections (22). Middle ear effusion can accompany acute infections and per sist over several weeks or mon ths. It is usually associated with temporary hearing loss and, when present over extended periods, may lead to delays in receptive and expressive language develop ment (23).
OTITIS MEDIA Diagnosis
Otitis media (infection of the middle ear) is among the most common childhood diseases encountered in primary care. The incidence may be increasing with larger n umbers of children at tending day-care centers. Acute otitis media often follows an up per respiratory infection . The patient presents with earache, fever, and hearing loss. Small children who are unable to clearly com municate these symptoms may present with irritability, insomnia, or tugging at the ear. With the presence o f pus in the middle ear, the tympanic membrane appears bulging and erythematous, and has decreased mobility with pneumatic otoscopy. After resolution of the acute infection, effusion may persist in the middle ear. Patients complain of painless hearing loss. The tympanic membrane may appear dull, and is often retracted in chronic cases. Evidence ofAuid can be observed in the middle ear as bubbles or an air-Auid level; however, even though an effusion exists, these signs are not always presen t. Auditory tube dysfunction, often accompanying middle ear disease, may manifest as tenderness j ust below the pinna near
the angle of the j aw. Evidence of inAammation of the mucosa of the nasopharynx accompanied by postnasal drainage may also be noted in patients with otitis media. Lymphadenoparhy and tenderness in the cervical soft tissues are also common findings. Examination should include evaluation for cervical and upper thoracic somatic dysfu nctio n . Cranial dysfunction, particularly involving the temporal bones, is frequently seen (2,24). Treatment/Management
I n forming patients and families about practices that predispose to ear problems is part of total patient care. [ n the well-baby examination , the opportunity often exists to discuss infant feed ing and avoidance of bottle feeding in the supine position. It is appropriate to encourage parents to protect their children from passive tobacco smoke. There are conAicting views regarding treatment of acute oti tis media (25). It is generally held that prolonged hearing loss, especially in certain developmental stages, is detrimental to de velopment of language and, possibly, reading skills. Therefore, attention needs to be paid to otitis media that becomes chronic or recurrent. Guidelines have been published by the U.S. De partmen t of Health and H uman Services for uncomplicated oti tis media with effusion in children ages one to three (2 1 ). The recommendations for the first 6 weeks of the condition are ob servation or oral antibiotics, as well as environment risk control. At 3 months, if significant hearing loss is present, tympanostomy with tube placement is an additional treatment option. I f the con dition has been present for 4 to 6 months with hearing loss, tube placement is indicated. According to the report, treatment in this age group should not include decongestants, antihisramines, or oral steroids. Decreasing the edema in and around the auditory tube creates an environment for healthy fu nction. Several manipulative tech niques have been described to specifically address improved lym phatic and venous drainage from the head and neck ( 1 2, 16,20). Osteopathic manipulative tech nique, such as Gal breath mandibular drainage, is easily performed and may provide consid erable benefit in reducing the congestion that leads to a chronic condition ( 1 6,20). Normalizing cervical muscle tOne by treat ing specific cervical somatic dysfunction or using soft tissue techniques may allow for improved lymphatic drainage from around the auditory tube. I n fectious processes benefit from im proved blood Aow, which is necessary for healing and deliv ery of medications. Arterial blood Aow to the ears should be optimized by addressing the effect of somatic dysfunction in the upper thoracic and cervical areas on vasomotor tOne. Tech niques such as rib raising and lymphatic pump can provide a more general approach to increasing lymphatic circulation and reducing congestion and inAammation in the ears. Treatment of specific rib dysfunctions may offer a longer lasting improve ment in lymphatic Aow. Treatment of temporal bone dysfunc tion can allow for normal exit of the auditory tube from that bone. Recent studies provide evidence of clinical improvement in children with acute otitis media regarding decreased use of an tibiotics, decreased number of infections, decreased need for surgical tube placement, and improved tympanograms (3 1 ). Os teopathic manipulation for the treatment of respi ratory infections should include techniques to increase lymphatic Aow, address
25. Osteopathic Management of Ear, Nose, and Throat Disease
viscerosomatic and somato-visceral reflexes, and improve thoracic cage motion (27) . Recognizi ng causes of auditory tube dysfunction may be crit ical to the treatment and prevention of otitis media. Allergic manifestations, such as red, i tchy eyes and persistent, clear nasal discharge, suggest further allergic workup. Dietary questions re gard i ng food i n tolerances or i n fant colic may suggest the i nfluence of food sensitivities. Control of the allergic aspect o f inflamma tion needs to be considered and d iscussed with the patient or the patient's family. Enlarged tonsils or adenoids are a cause of poor auditory tube drainage. Swallowing and chewing open the auditory rube and can be suggested as exercises for patients to help clear middle ear effusion (26). A l lergy, as well as infection, may play a role i n the enlargement of these lymphoid organs. I f acute bacterial infection is the cause, i t should b e appropriately treated with antibiotics, considering the common pathogens S. pneumoniae, H. injluenzae, and Streptococcus pyogenes.
379
Pharyngeal tonsil Ostium of auditory tube
Lateral pharyngeal
---HrT\-\+ A
band of
--=::.,----l-- Tongue
lymphoid tissue Palatine tonsil Lingual tonsil
T HROAT / PHARYNX Healthy Structure and Function
The pharynx is divided i n ro the nasopharynx, which i ncludes the portion above the soft palate; the oropharynx, from the soft palate to the hyoid bone; and the laryngopharynx, from the hyoid bone to the lower border of the cricoid cartilage. The oral cav ity l ies immed iately amerior ro the oropharynx. The oral cavity and oropharynx are l ined by squamous epithel ium, whereas the nasopharynx and laryngopharynx are lined by pseudostratified ciliated columnar (respiratory) epithelium. A collection of lym phoid tissue, referred to as the Waldeyer ring, is located in the pharynx and plays an importanr role in immunity, especially i n the first few years o f life. The tongue and other structures i n the oral cavity have important functions in digestion and speech. The palatine (faucial) tonsils are masses of lymphoid tissue located on either side of the posterior oropharynx. The adenoids (pharyngeal tonsil) are found on the upper and posterior walls of the nasopharynx. The tonsils and adenoids comprise the major portion of the lymphoid tissue of the Waldeyer ring encircling the pharynx. These structures, together with the li ngual tonsil, an aggregate of lymph nodules on the posterior aspect of the tongue, and scattered lymphoid nodules beneath the mucous membranes of the pharyngeal wall, are the sites for B and T lymphocyte activ ity (Fig. 2 5 .9) . All major classes of immunoglobulins are produced here by the B lymphocytes while the T lymphocytes participate in cell-mediated immunity. With high demands for immune func tion placed on these lymphoid organs, hyperplasia can occur. Secondary obstruction of airflow through the nasopharynx and auditory tubes results from sign ificanr lymphoid hyperplasia. Blood supply to the tonsils is supplied by the external carotid system. Several arterial branches (typically th ree) go to the tonsils from the facial and l ingual arteries. Venous drainage is accom plished by a plexus around the tonsillar capsule, which drains into the tonsillar branch of the lingual vei n and connects with the pharyngeal plexus (28) . The pharyngeal mucosa is rich in lymphatics. Lymphatic drainage of the tonsils goes to the sub mandibular nodes and to the superficial and upper deep cervical nodes. A node behind the angle of the mandible is especially as sociated with i ncreased lymphatic activity from the tonsils (29).
W-H-- Larynx
FIGURE 25.9. Lymphoid tissue in the pharynx.
Common Pathophysiology
A variety of pathologic p rocesses can occur in the pharynx (Table 2 5 . 3 ) , but i nfection is the most common . Group A beta hemolytic streptococci and viruses are the common i n fectious agems. Neisseria gonorrhoeae, Mycoplasma, and Chlamydia tra chomatis are also considerations. Viral i n fections may cause ul cerative lesions o f the tongue, l ips, or buccal mucosa. Herpes simplex virus is responsible for herpes labialis o r cold sores. Oral candidiasis (thrush) is commonly encountered in demure wear ers, patiems on corticosteroids or broad-spectrum anribiotics, diabetics, and those immunocompromised, as by acquired im munodeficiency syndrome, chemotherapy, or local radiation.
ACUT E T ONSILLIT IS/PHARYNGIT IS Diagnosis
Sore throat is a common complaint, particularly in children. Edema, pain, and i n fl ammati o n are usually associated with TABLE 25.3. COMMON DISORDERS O F THE THROAT Disorder Pharyngitis Tonsi l l it i s E p i g lottid itis I n fectious mononucleosis Thrush Peritonsi l l a r abscess Laryngitis
380
VI. Osteopathic Considerations in the Clinical Specialties
pharyngitis. Often accompanied by fever, odynophagia, and ten der adenopathy, it is d i fficul t to d i fferemiate viral from bacterial i n fection on i nspection. Bacterial i nfection is typically exudative. Hoarseness, cough , rhinorrhea, and coryza are more often asso ciated with viral i n fection. The appropriateness of using certain tests to identify group A beta-hemolytic streptococci i n fections is being questioned (30). Latex agglLltination amigen tests and solid-phase enzyme i m m unoassays ( ELISA) p rovide quick, but only moderately sensi tive, screens for streptococcal infection. AJ though more sensitive, throat cultures take longer for results to become available. Because all group A beta-hemolytic streptococ cal pharyngitis cases should be treated to prevem more serious sequelae, i ndividual decisions for d i agnosis and treatmem should take i nto account the local p revalence o f resistant streptococ cal i n fections, patient h istory, potemial for compliance, and the availabi l i ty and reliability of the laboratory. Differential diagnosis i ncl udes infectious monon ucleosis, diphtheria, fungal i n fections, and pharyngeal manifestations of systemic disease.
racic areas not o n ly reduces swelling but also stimulates the im mune response. Removing i nRam matory mediators from the site of i nfection by promoting venous and lymphatic circulation al lows for a more favorable healing environment. Healing may also be enhanced by addressing sympathetic, vasomotor control af fected by somatic dysfunction of the upper thoracic and upper cervical (superior cervical gangl ion) areas. Presumably, i mproved arterial flow would also i ncrease the tissue levels of prescribed antibiotics or other medications.
MUSCULOSKELETAL APPROACH TO THE EAR, NOSE, AND THROAT PATIENT
The major principles to consider in treating ENT patiems in terms ofthe m usculoskeletal component of health and disease are: 1 . assisting venous and lymphatic circulation, 2 . promoting arterial Row,
Treatment/Management
G roup A beta-hemolytic streptococcal pharyngitis requi res a 1 0-day cOLltse of oral antibiotics or a single i mramuscular dose o f Benzathine Penicil l i n G. Penicillin V potassiu m and cephalosporins are effective. Erythromycin or azithromycin are reasonable alternatives for individuals who are allergic to peni cill i n . Ancil lary rreatmem to control symptoms and make the patient more com fortable i ncludes analgesics, ami inflammatory agems, salrwater gargli ng, and osteopathic manipulation. Viral i n fections requ i re only symptomatic treatmem. Osteopathic manipulation to reduce swell i ng and i m p rove lymphatic Row (probably stimulating the i mmune response) can be particularly helpfu l i n providing symptomatic relief (7,27). The Galbreath tech nique o f mandibular drainage reduces tonsil lar congestion and may o ffer pain relief and reduce the chance of lymphatic congestion around the auditory tube (Fig. 2 5 . 1 0). I m proving lymphatic circulation by addressi n g any somatic dysfunction o f the upper ribs, clavicle, cervical, and upper tho-
FIGURE 25.10. Superficial sinus drainage tech n ique.)
3. normalizing spinal reRexes affecting function of the ear, nose, and throat, and
4. relieving pai n . I t i s reason able t o expect that the use o f musculoskeletal di agnosis and treatment i n these patients will help the patiem feel better, assist in heali ng, and improve their overall resistance to d isease. As a guide, evaluate and treat somatic dysfunction from cen tral body areas to the periphery, allowi ng for free Row of ve nous and lymphatic fl u i ds. The rationale for treating somatic dysfunction in the upper thoracic and cervical spine is to de crease somatic stimulation in the area of the sympathetic outflow and ganglia supplying the head and neck. I mproving venous and lymphatic flow also provides the rationale for osteopathic manipulative treatment to the cervical and thoracic i nlet ar eas. An attempt is made to decrease myofascial tension in the
FIGURE 25. 1 1 . G a l breath technique for m a n d i b u l a r d ra i nage. (From Shaw HH, Dyer RR. One-Minute Osteopathic Techniques for the Busy Clinician, 1 st ed. Tu lsa, OK: Oklahoma State U n iversity College of Osteopath ic Medicine; 1 997, with permission.
25. Osteopathic Management ofEar, Nose, and Throat Disease
381
FIGURE 25.1 4. Ped a l lymphatic p u m p tec h n i q ue. (From Shaw HH, Dyer
FIGURE 25. 1 2 . Su boccipital i n h i bitory pressu re/cra n i a l base release
tech nique. (From Shaw HH, Dyer RR. One-Minute Osteopathic Tech niques for the Busy Clinician, 1 st ed. Tu lsa, OK: O k l a h o m a State U n iver sity College of Osteopathic Medicine;1 997, with permission.)
areas through which lymphatic and venous vessels pass from the head to where they enter the central circulation at about the level of the first rib. Superficial drainage techniques (effleurage) applied to the face from medial to lateral decrease tissue con gestion in the anterior sinus regions (Fig. 2 5 . 1 1 ). The mandibu lar drainage techn ique described by Galbreath (20) is an effec tive lymphatic drainage procedure for the ear, auditory canals, and throat (Fig. 2 5 . 1 0). Chapman reflexes are small, nodular, and tender areas that have been observed in relationship to in flammatOry d iseases of visceral structures. Used for diagnosis and treatment, they are believed to represent viscerosomatic re flexes and have been shown to be responsive to a rotary pres sure technique ( 1 4) (See chapter on Chapman reflexes). Cranial treatment, i nclud i ng suboccipital inhibitOry pressure, is espe cially i n dicated in sinus disease and m iddle- and i n ner-ear con ditions (Fig. 25. 1 2). Lymphatic pump techniques are i n tended to stimulate general lymphatic flow by affecting i ntrathoracic pressures (Figs 25.13 and 2 5 . 1 4). Their use is described in the
RR. One-Minute Osteopathic Techniques for the Busy Clinician, 1 st e d . Tulsa, O K : Oklahoma State U n iversity Col l ege of Osteopathic Medicine; 1 997, with permission.)
osteopathic l i terature regarding treatment of i n fectious disease 0 5, 1 6,27).
REFERENCES 1 . Blood HA. I n fections of the ear, nose and throat. Ost Ann. 1 978; 6( 1 1 ) : 1 4- 1 8 . 2. Woods DE. Management ofENT problems. OstAnn. 1 980;8(5) : 3 1 -4 1 . 3. Moser RJ . Sinusitis, the effective osteopathic manipulative procedures in the management thereof. Yearbook of Selected Papers. Academy of Applied Osteopathy; 1 953: 1 5- 1 6. 4. Sato A. ReAex modulation of visceral functions by somatic afferent ac tivity. The Central Connection: SomatoviscerallViscerosomatic Interaction. Proceedings of 1 989 American Academy of Osteopathy International Symposium: 53-72. 5 . Sato A, Schmidt RF. The modulation of visceral functions by somatic afferent activity. ]pn ] Physiol. 1 987;37: 1 - 1 7. 6. Pinta! WJ , Kurtz M E . An in tegrated osteopathic treatment approach in acute otitis media. ] Am Osteopath Assoc. 1 989;89(9): 1 1 39- 1 1 4 1 . 7. Schmidt Ie. Osteopathic manipulative therapy as a primary factor in the management of upper, middle, and pararespiratory infections. ] Am
Osteopath Assoc. 1 982;8 1 (6):382-388. 8. Wasserman SJ. Ciliary function and disease. ] Allergy Clin Immunol. 1 984;73 : 1 7- 1 9. 9. Wagen man n M, Naclerio RM . Anatomic and physiologic considerations in sinusitis. ] Allergy Clin Immunol. 1 992;90:4 1 9-423. 10. Zeiger RS. Prospects for ancillary treatment of sinusitis. ] Allergy Clin
Immunol. 1 992;90:478-495. 1 1 . Kaluza CL, Sherbin M. The physiologic response of the nose to osteo pathic manipulative treatment: prel i m i nary report. ] Am Osteopath Assoc. 1 983;82(9):654-660. 1 2. Harakal J H . Manipulative treatment for acute upper-respiratory dis eases. Ost Ann. 1 98 I ;9(7):30-37. 1 3. Hoyt WH o Current concepts in management of sinus disease. ] Am
Osteopath Assoc. 1 990;90( 1 0) : 9 1 3-9 1 9. 1 4. Owens e. An Endocrine Interpretation of Chapman's Reflexes. Academy of Applied Osteopathy; 1 963. 1 5 . Shrum KM, Grogg SE, Garton P, et al. S i n usitis in children: the impor tance of diagnosis. ] Am Osteopath Assoc. 200 1 ; 1 0 1 ( 5 ) : S 8-S 1 3. 1 6. Cathie AG. The sino-bronchial syndrome. Yearbook of Selected Papers. Academy of Applied Osteopathy; 1 968:9-1 1 . 1 7 . Charlton A. Children and passive smoking: a review. ] Fam Proct. FIGURE 25. 1 3. Thoracic lymphatic pump tech n i q u e . (From Shaw H H,
Dyer RR. One-Minute Osteopathic Techniques for the Busy Clinician, 1 st ed. Tulsa, OK: Oklahoma State U n i versity Co l l ege of Osteopath i c Medicine;1 997, w i t h permission.)
1 994;38(3): 267-277 . 1 8 . Naclerio RM. Allergic Rhinitis. N Engl] Med. 1 99 1 ;325 ( 1 2):860. 1 9. Greenman PE. Fascial considerations in treatment of the head and neck.
Ost Ann. 1 975;3 (2):34-42.
382
VJ. Osteopathic Considerations in the Clinical Specialties
20. Galbreath W. Manipulative srructural adjustive treatment i n middle ear
deafness. j Am Osteopath Assoc. 1 92 5 ;24:74 1 . 2 1 . U . S . Department of Health and Human Services. Managing otitis media
with effusion in young children. Arch Otolaryngol Head Neck Surg. 1 994; 1 20:793-796. 22. Froom J , Culpepper L. Otitis media in daycare children. A report from
the International Primary Care Network. j Film Pract. 1 99 1 ;32:289294.
26. Honjo J , Okazake N. Opening mechanism of the eustachian tube. Ann
Otol Rhinol Laryngol. 1 980;89(3 ) : 2 5-27. 27. Rumney [e. Osteopathic manipulative treatment of infectious diseases.
Ost Ann. 1 974;2: 29-33. 28. Krmpotic-Nemanic J, DrafW. Surgical Anatomy ofHead and Neck. New
York: Spri nger-Verlag; 1 988. 29. Hollinshead WH. Anatomyfor Surgeons: The Head and Neck. Harper &
Row; 1 968.
23. Updike C, ThornburgJ D. Reading skills and audirory processi n g abiliry
30. Wegner DL, Witte DL. lnsensitiviry of rapid antigen detection methods
in children with chronic oritis media in early childhood. Ann Otol Rhinol
and single blood agar plate culture for diagnosing streptococcal pharyn
Laryngol. 1 992; 1 0 1 : 530-537. 24. Magoun H. Osteopathy in the Cranial Field. Journal Printing Company;
3 1 . Mills MV, Henley CE, Barnes LLB, Carrero JE. The usc of os
1 976: 2 1 3-2 1 5 . 2 5 . Browning G, Bain B. Childhood otalgia: acute otitis media. BMj. 1 990;300: 1 005-1 007.
gitis.
JAMA.
1 992;267(5) :695-697.
teopathic manipulative treatment (OMT) as adjunctive therapy for acure otitis media 2002.
in children.
Submi tted for publication, June
OSTEOPATHIC MEDICINE IN THE PRACTICE OF EMERGENCY MEDICINE PETER ADLER·MICHAELSON BERNADETTE BRANDON RAUL GARCIA
KEY CONCEPTS • • • • •
The history of the profession of osteopa thic emer gency medicine The philosophy of the profession of osteopa th i c emergency medicine The logistics a n d demogra phics of emer gency medicine The a ppL ica tion of the osteopa thic philosophy a n d a ssessment i n the Emer gency Depar tment (ED) The a pplica tion of osteopa thic philosophy, pr i nciples, pa lpa tory dia gnosis, a nd ma nipulative trea tment i n the E D
phy sicia ns received their ABEM board cer t ifi ca tion ( 1 ) . This wa s (a n d still is today ) a 3-y ear tra ining pr ogra m leading to boa rd eligibility. A B E M board cer tifi ca tion is issued a fter pa ssi ng the wr i tten a n d ora l exa mi na tion. U n til 19 88, the so-ca lled " practice ca tegory" or " gra ndfa ther cla use" by which one could become boar d eligible a nd likewise cer tified a fter ha vi ng wor ked ma ny y ears within the fi eld of emer gency medicine wa s also r ecognized ( 2 ) . M Ds a n d DOs a like wer e (a nd still are) a ccepted for board eligibility and cer tifi ca tion by the ABEM. Today ther e are 1 2 5 medica l schools, both a llopa thic a nd osteopa thic, tha t ha ve for ma l depar tments of E M pr oducing r o ughly 600 board-eligible phy sicia ns ea ch y ear (2).
HISTORY AND DEVELOP M E N T OF OSTEOPATHIC E M E RG E N CY M EDICINE HISTORY AND DEVELOPMENT O F E M E RGENCY
AS A PROFESSION
MEDICINE AS A PROFESSION
Emer gency medicine (EM), in one for m or a nother, ha s existed si nce the begi nning of time. However, as a medical specia lty in the U nited Sta tes, it offi cia lly bega n in 1968 when a group of eight phy sicia ns for med the Amer i ca n College of Emer gency Medicine (l). It gr ew out of the rea l iza tion tha t ma ny of the clinica l lessons tha t ha d been learned in the Korea n a nd V ietna m wa rs could a lso be a pplied i n pea ce time a nd could help ma ny pa tients. A yea r la ter, these eight phy sicia ns held the fir st Scientifi c Assem bly in Emergency Medicine in the U ni ted Sta tes (1) . I n J 9 70, a t the U n iversity of Cincinna ti , the first residency i n emer gency medicine wa s star ted ( 1 ) . At first, EM wa s r egulated a s a subspe cia l ty under a coa lition of the Amer ica n Board of Fa mily Pra ctice, the Amer ica n Board of I n ter na l Medicine, the America n Board of Obstetr ics a nd Gy necology, the Amer i ca n Board of Otolary n gology, the Amer ica n Board of Pedia tr ics, the Amer ica n Board of Psy chia try a nd Neurology, a nd the Amer ica n Board Sur gery. I n 1979, a separate, sovereign r egula tory board, the Amer ica n Board of Emer gency Med ici ne (ABE M ) wa s r ecognized by the Amer ica n Boar d of Medica l Specia lties a nd the Amer ica n Medica l Associa tion as the 23rd medical specia l ty (2) . In 19 80, the fir st emer gency
Like its a l lopa thic counter par t, the Amer ica n College of Osteo pa thic Emergency Phy s icia ns (ACOEP) wa s founded by physi cia ns wor king i n the fi eld who fel t this emerging specia l ty needed its own voice. In 197 5, a sma l l gr oup of emer gency osteopa thic phy sicia ns sent a lett er of i nt ent to the Amer ica n Osteopa thic Associa tion (AOA) seeking a ffi liate sta tus with i n tha t orga n iza tion. At the following AOA convention, the first offi cer s were elected. The college wa s for ma lly r ecognized in 197 8 a nd held its fir st scientifi c a ssembly tha t y ear. Since tha t time, the ACOEP ha s gr own to become the second lar gest specia l ty col lege within the AOA, second only to the Amer i ca n College of Osteopa thic Fa m i ly Pra ctitioner s (3). I n 19 80, noti ng the gr owth and future of E M , the AOA crea ted a n osteopa thic board to r egulate the specia lty of EM within the os teopa thic profession, the Amer ica n Osteopa thic Board of Emer gency Medicine (AOBEM) (3) . Eligibility now requir es comple tion of a 3-y ear residency progra m. U ntil 1997, there was a lso a pra ctice ca tegory by which one could become AOB EM board eligible. Cer tifi ca tion requires the successful completion of wr it ten, ora l, a n d clinical exa mi na tions ( par ts J , I I & JU ) (3). The first osteopa thic emer gency medicine residency wa s esta blished
384
VI.
Osteopathic Considerations in the Clinical Specialties
In 1 979 at the hospital of the Philadelphia College of Osteo pathic Medicine (3) . Presently there are 27 residency traini ng pro grams in osteopathic emergency medi cine in this country, gradu ating roughly 150 EM board-eligi ble osteopathic phy sicians each y ear (3) .
PHILOSOPHY OF OSTEOPATHIC EM ERGE N CY M EDICIN E
The osteopathic philosophy, which is discussed in more detail in Chapter 1 of this text, can be described as the application of the osteopathic principles of: 1 . the u n i ty of body, mind, and spirit, 2. the self-healing capacity of the body, 3. the i nt errelatedness of the structure and function with i n the body, and 4. the creation of a ser. si ble treatment plan based on the fi rst three principles that most appropriately leads patients back toward their best achievable level of homeostasis. From the osteopathic perspective, the patient i n the ED has experienced a breakdown in some aspect of thei r body -m i nd spi ri t unity (e.g. , fractures, lacerations, other trauma, fear, anxi ety, depression, abuse, psy chosis, drug or alcohol abuse, chronic disease, loneli ness, alienation) , has lost their i nnate ability to heal and self-regulate, (e.g., poor nutri tion, chronic stress, chronic disease, aging, alienation within society ) , and has a disru ption of the structure-function i nterrelatedness principle, such that they present with a variety of fu nctional or structural dy sfunction that makes up their sy mptomatology. As described above, in the last 25 y ears, emergency medicine has developed into a separately regulated medical specialty for both the allopathic and osteopathic professions. T he philosophy of EM is the application of the principles of emergency medicine: diagnosing and treating emergent and urgent conditions, using a primary assessment to quickly recognize l i fe-threatening condi tions, treating appt opriately to stabilize the patient , completing a more detailed secondary assessment of the patient, and arranging defin itive care to create an overall treatment plan that will assure the best outcome. The sy nt hesis of these two philosophies and practices is what osteopathic emergency medicine is about, and it provides a won derful opportun i ty for us to help patients in emergent and urgent si tu ations. Osteopathic treatment i n the emergency room is not much different than in other clinical s i tu ations. The goal is to assist the patient to regai n their body - mi nd-spirit unification, to regai n or optimize their self-heali ng capacities, and return to a more effecti ve structu re-fu nction i nt errelatedness. One distinctly osteopathic approach that helps accompl ish this goal is the application of osteopathic palpatory diagnosis and treatment modalities. Many osteopathic students and phy sicians feel that i t m ust be difficult to apply palpatory diagnostic skills and manipulative treatment modalities in the ED. This is far from the t ru th. The main goal of this chapter is to provide an overview and some helpful guidelines as to when
and how osteopathic philosophy, princi ples, palpatory diagno sis, and manipulative treatment modalities can be appropriately employ ed in the E D . Of course, t h e priority i n t h e ED t o stabilize any poten tially l i fe-threateni ng illnesses takes temporal priority over the ac tu al application of osteopathic manipulative medicine (OMM). T here are periods of time in the E D when the osteopathic phy si cian will not have the time o r the in ner peace necessary to ap ply OM M . There are, however, times when it is relatively quiet and the application of O M M is possible. The problem is that it is impossible to know this ahead of time in order to schedule O M M treatments, which can be frustrating for physician and patient. The specific aspects of osteopathic assessment and treatment for a number of common p resentations to the ED will be dis cussed later in this section. We will focus on the specific additional aspects of osteopathic assessment and treatment modalities that can be very helpful in the ED. There was a time when ultrasound exam ination was not used very oft en in the E D . Later, after many of us became trai ned and competent i n this assessment modality or had in-house staff able to do these examinations, it was hard to imagine not having ultrasound to assist in the evaluation of the patient. Osteopathic assessment and treatment is much the same. Many of us have become very comfortable with this important form of assessment and treatment and can nor imagine not having this modality as an option i n the ED.
"EXTE N T OF THE PROBLEM" IN OSTEOPATHIC E M E RGENCY MEDICINE Logistics and Demograp h i cs wit h i n E mergency Med i c i n e
Table 26. 1 shows the breakdown by category of chief complaints leading to visits to the ED (4) . Cases of upper respiratory in fection, low back pain, and other musculoskeletal disorders are the most com mo n complaint s with which patients present to the ED (4). These conditions provide excellen t opportunities to apply O M M ( 5 ) . Chest pai n, asthma, abdominal pai n, pelvic pain, and, of course, other musculoskeletal complai nt s, such as joint pain and extrem ity disorders, are j ust a few other very com mon ED presentations for which O M M can and should be i mplemented either in the ED or later in the primary care setting ( 5 ) . The prevalence of m usculoskeletal disorders i n this coun try is enormous and growing. Table 26.2 shows a breakdown of the chief musculoskeletal complaints present ing to the ED (6) . The financial burden on society of all musculoskeletal condi tions has increased from an estimated $ 1 26 billion in 1 988 to an estimated $ 2 1 5 billion i n 1 99 5 (6). I n 1 997 and again in 1 998, the annual cost to treat r he more than 3.8 million ED visits due to m usculoskeletal sports inj uries i n the 5 to 24 y ear age range alone has been estimated to be $ 680 million (7) . We have shown that there are many patient s presenting to the ED that have a primary musculoskeletal com plaint. For these patient s , the application of O M M is often one of the most appropriate treatments (5 ) . The
TABLE 26.1. NUMBER AND PERCENT DISTRIBUTION OF EMERGENCY DEPARTMENT VISITS WITH CORRESPONDING STANDARD ERRORS, BY PRIMARY DIAGNOSIS: UNITED STATES, 1999
Major disease category and ICO-9-CM code rangea
Number of visits
Standard error
Percent
Standard error
(in thousands)
(in thousands)
distribution
of percent
All visits
102,765
4,493
100.0
Infectious and parasitic diseases
001-139
2,866
194
2.8
0.2
Neoplasms
140-239
346
63
0.3
0.1
Endocrine, nutritional and metabolic diseases, and immunity disorders
240-279
1,779
138
1.8
0.1
Mental disorders
290-319
2,903
215
2.9
0.2
Diseases of the nervous system and sense organs
320-389
5,863
388
5.8
0.2
Diseases of the circulatory system
390-459
4,397
273
4.4
0.2
Diseases of the respiratory system
460-519
12,991
765
12.9
0.4
Diseases of the digestive system
520-579
5,947
366
5.9
0.2
Diseases of the genitourinary system
580-629
4,372
249
4.3
0.2
Diseases of the skin and subcutaneous tissue
680-709
2,826
220
2.8
0.2
Diseases of the musculoskeletal system and 710-739
5,578
359
5.5
0.2
Symptoms, signs, and ill-defined conditions
780-799
16,377
888
16.2
0.5
Injury and poisoning
connective tissue
800-999
29,586
1,322
29.3
0.6
Fracture
800-829
3,676
216
3.6
0.2
Sprains
840-848
6,290
354
6.1
0.2
Intracranial
850-854
281
47
0.3
0.0
Open wounds
870-897
7,296
405
7.1
0.3
Superficial
910-919
1,601
134
1.6
0.1
Contusion
920-924
4,458
234
4.3
0.2
Foreign bodies
930-939
635
78
0.6
0.1
Burns
940-949
574
75
0.6
0.1
Complications
958-959
1,587
134
1.5
0.1
Poisoning and toxic effects
960-989
953
102
0.9
0.1
2,235
147
2.2
0.1
3,865
238
3.8
0.2
1,732
127
1.7
0.1
1,338
288
1.3
0.3
Other injury Supplementary classification All other diagnosesb
V01-V82
Unknown<
- Category not applicable. 0.0 Quantity more than zero but less than 0.05. aBased on the International Classification of Diseases, Ninth Revision, Clinical Modification (lCD-9-CM) (21). blncludes diseases of the blood and blood-forming organs (280-289); complications of pregnancy, childbirth, and the puerperium (630-676); congenital anomalies (740-759); and certain disorders originating in the perinatal period (760-779).
TABLE 26.2. NEW PROBLEM VISITS TO PHYSICIANS IN OFFICE-B ASED PRACTICE FOR MUSCULOSKELETAL CONDITIONS, BY PATIENT'S MOST FREQUENTLY MENTIONED PRINCIPAL REASON FOR VISIT: UNITED STATES, 1995a Visits (in thousands)
Reason for Visit Codeb
Male
Female
Total 3,700
5905
Back symptoms
1,757
1,942
5925
Knee symptoms
1,538
1,821
3,359
5940
Shoulder symptoms
1,075
1,469
2,544
5935
Foot and toe symptoms
901
1,477
2,378
5910
Low back symptoms
869
1,259
2,128
5900
Neck symptoms
750
1,218
1,968
5960
Hand and/or finger symptoms
780
720
1,500
5955
Wrist symptoms
401
825
1,226
5920
Leg symptoms
676
547
1,224
5050
Chest pain or related symptoms
430
668
1,098
5930
Ankle symptoms
532
466
998
5945
Arm symptoms
434
527
961
5950
Elbow symptoms
397
374
771
5055
Pain, other specified sites
497
219
716
1570
Finger/hand injury, unspecified
366
320
686
aReason for visit mentioned by patients with a musculoskeletal condition diagnosis. b Codes are based on Schneider D, Appleton L, McLemore T: A Reason for Visit Classification for Ambulatory Care. National Center for Health Statistics, Vital and Health Statistics 2, 1979. Source: National Center for Health Statistics. National Ambulatory Medical Care Survey, 1995.
386
Vi.
Osteopathic Considerations in the Clinical Specialties
osteopathic emergency phy sician is uniquely able to provide this kind of treatmenr as time allows i n the E D . Theoreti cal Aspects o f t h e Osteopath i c Med i c i n e Approach t o the Patient i n the E mergency Department
[t may seem that E M and osteopathic medicine are mutually ex clusive. This is far from the truth. Thr ough many y ears i n E M , [ (Adler-Michael son) have used osteopathic principles and prac tices during every emergency medicine shift I have ever worked. The unity of spirit, mind, and body, as well as the i nrerrelatedness of structure and function, is as evidenr in the ED as it is in an office or hospital practice. The body's capacity and attempts at self-regulation and self-healing are, at times, even more apparenr in the emergency departmenr than in an office or hospital prac tice. [ know of no presenr atio n to the ED for which there were no osteopathic considerations that could be helpful to the patient. For example, i n the assessment and treatment of headaches, vi ral upper respi ratory infections (U RIs) , si nusitis, whiplash i n j u ry, chest pai n, abdom inal pai n , pneumonia, py elonephritis, kidney stone, cy stitis, obstetrical complications, pelvic i nflammatory dis ease, arthritides, trauma to an extre m i ty, and so on, applications of distinctly osteopathic princi ples and treatmenr modalities can considerably assist the patienr s' recovery (8) . One important aspect of E M that is also helpful i n osteopathy is the need to alway s consider the larger picture, to be aware of the patient's primary ill ness or inj ury, and to move toward specific details as time allows. This is essenr ially the same as assessing the patienr osteopathically to determine the key somatic dysfunction or the primary restriction, treating this, and knowing that t he secondary somatic dy sfunction wil l subside (see Chapter 29) . Patienr history is imperative. Listening carefully to the pat ient' s description o f the pain o r discomfort will often give imporr anr clues as to the cause. The concept of typical patterns of referred pain F rom various stru ctures in the body is a crucial concept i n all o f medicine. For example, gallbladder disease often refers pain to the tip of the right scapula (9) . Heart disease with ischemia or inFarction ty pically refers pain up i n to the j aw, down t he i nside of the Ic ft arm, or i nr o the m idepigasr rium ( 1 0) . The ty p ical pain described by the patienr suffering from pancreatitis is a midepigas e ric pain that radiates straight through to the back ( 1 0) . This same concept applies when the problem is a somatic dy sfunction of a my ofascial structure. For example, the psoas muscle will ty pically cause pain in the low back and anr erior groin areas on the side of the dy sfunction ( 1 1 ) . A right psoas somatic dy sfunction will oFten present together with a left piriformis somatic dy sfunct ion: the so-called psoas sy ndrome ( 1 2) . A piriformis muscle dy sfunction ty pically causes buttock and/or posterior thigh pain due to its origin and i nsertion and proximity to the sciatic nerve. K nowing these "ty pical" sy m ptom distribution patterns for various d isease states or somatic dy sfunction allows the phy sician to more readily and rel iably arrive at the correct diagnosis. A screening structural examination that is done quickly and ef fi ciently and that includes ly mphatic, my ofascial, cranial, and so matic aspects can help the osteopathic emergency phy sician find the key lesions that, when treated, will provide the most assistance to the patienr in regaining homeostasis. This exami nation is per-
formed during the secondary sur vey and after any life-threatening condition has been addressed. See the "Practical Considerations" section below for an example. The concept offoci/itation can also help the emergency physi cian with his or her diagnosis in the ED. A visceral disease process will commonly cause Facilitation of spinal segments in a specifi pattern. For example, significant cor o nary artery disease (CAD) facilitates to the spine in the T I -6 re gion and often causes ty pical somat ic changes: bogginess or ropi ness of the paraspinal tissues and more diffuse palpatory changes (usually without hy peremic skin changes) . The segments often follow Fry ette ty pe 2 mechan ics, i.e., T2 F RL SL (8). This is an example of viscet osomatic reflex activity. Another important aspect of osteopathic medicine is the use of Chapman reflex poinr s, which can indicate the presence oF visceral disease and can be very helpful in the assessmenr of the ED patient ( 1 3) . To use the example of the patienr with CAD, he or she will display significanr ly painful reflex points bilaterally in the 2nd intercostal space close to the sternum ventrally and ber ween the 2nd and 3 rd transverse processes dorsally. We will give further examples of the application of these later in the section. For more details on Chapman reflex points, see Chapter 67. Another i mportant consideration of osteopathic medicine that applies to every patienr regardless of setting is improvement i n t he F unction of the ly mphatic sy stem. [n acute ureteral obstruction, it has been shown that renal hilar ly mph flow can i ncrease up to three times their original capacity in an attempt to compensate for t he illness ( 14 ) . I n addressing t h is very im porr anr self-regulatory sy stem, whether through t echniques to elimi nate or reduce ob structions to ly mphatic flow, techniques to actually i ncrease the flow of ly mphatic fluid, or both , we can significantly help the patient move toward homeostasis. Several examples of the ap plication of t hese techn iques are described later in the section. For more details on the structure and Function of the ly mphatic sy stem, see Chapter 68. In essentially every presenr ation to the ED, i t is possible to address the imbalance with i n the autonomic (sy m pathetic and parasy mpathetic) nervous sy stem. Achieving or moving toward balance will greatly assist the body in i ts selF-regulatory mecha n ism, regardless of the patienr ' s complainr (8). Several examples o f the application o f these techniques are given later i n this section. For more details on the structure and fu nction of the autonomic nervous sy stem (ANS) , see Chapter 6. Especially i n emergency medicine, it is important to be aware of the possibility of atypical presentations in patienr s. For example, chest pain with normal laboratory values, normal electrocardio gram, and even subjective improvemenr after an OMM treat ment can still be due to unstable angina or even a my ocardial infarction. This is one example of why t he m issed or incorrectly diagnosed acute my ocardial infarct (AM I ) is the highest mal practice pay ment situation in emergency medicine. Table 26.3 shows the leading causes of malpractice suits by category i n the ED ( 14 ) . The presenr medical-legal climate in this country, espe cially i n the E D , is such that an emergency phy sician is constanr ly aware of possible "traps" i n assessmenr and treatment and of situ ations where a missed diagnosis o r i ncorrect treatmenr could have grave consequences. As shown later in the section, using several of the concepts described in th is chapter gives the osteopat hic
26
Osteopathic Medicine in the Practice ofEmergency Medicine
387
TABLE 26.3. MALPRACTICE CLAIMS MADE, PAID, AND AVERAGE PAYOUT Total Claims
Number of
Average
Made Since 1985
Claims Paid
Payout(S)
Breast cancer
2,986
1,039
204,436
Brain-damaged infant
2,613
934
449,486
Reason
Pregnancy
1,953
530
128,978
Heart attack
1,770
563
190,347
Intervertebral-disc displacement
1,662
402
172,041
Lung cancer
1,639
504
149,823
Appendicitis
1,296
368
83,100
Femur fracture
1,290
365
85,255
Cataracts
1,151
269
96,603
Sterilization
1,119
349
46,770
Source: "The Cutting Edge: Vital Statistics." Washington Post, 12 September 1995, p. 5. Data are for the period 1985 through 1995 derived from Physician Insurers Association of America data. The organization insures 25% of the nation's doctors.
em ergency physician a significant advantage over his or her allo pathic counterpart.
saging m otion until the tissues begin to sof ten, was f ound by Chapm an nearly 1 00 years ago to im prove f unction and relieve clin ical sym p tom s ( 1 3) .
PRACTICAL OSTEOPATHIC CONSIDERATIONS
The Lymphatic System
IN EM ERGE NCY MEDICINE DIAGNOSIS AND TREATMENT
A num ber of im portant, practical osteopathic considerations i n em ergency medicine diagnosis a n d treatm en t are presented, f ol lowed by an exam ple of how to do a m usculoskeletal screeni ng exam ination i n the ED and a case exam ple. Several im portant considerations i n osteopathic m edicine can be specifically helpf ul i n diagnosing and treating patients in the ED. Signs of viscerosomatic reflex activity: typical tissue/segmental changes of f acilitation and/or the presence of Chapm an reflex points are im portant di agnostic signs. In addition, addressing lymphatic system consi derations and attem pting to balance the autonomic nervous system wi ll f urther assist the patient i n h is/her self -regulatory m echanisms. Vi scerosomati c Activity
An im portant sign of viscerosomatic activity is finding bogginess or ropiness of the paraspinal tissues on osteopathic palpatory exam ination, m ore dif fuse palpatory changes, and usually less warm th without hyperem ic skin changes in a spinal segment area appropriate f or the organ(s) i n questi on (37). These som atic dysf unction changes usually aff ect one or two segm ents, often in a Fryette type 2 orientation (i.e., T2 F RL Sd in cardiac d isease states (8) . A second im portant si gn of viscerosomatic activity is the pres ence of Chapman reflex poin ts ( 1 3) . In the above cardiac patient, the presence of anterior and/or posterior Chapm an reflex points i n the second i ntercostal space on the lef t, j ust lateral to the sternal border ventrally and between the transverse processes of T2 and T3 on the left dorsally, would be excellent support f or the diagnosis of significant heart disease. Research is currently under way to determ ine the diagnostic and therapeutic reliability of these points (Adler- Michaelson and Crow, u npublished re search) . Treatm ent of these points, through a fi rm circular m as-
A quick but eff ecti ve way of assessi ng the lym phatic system is to check f or signs of fluid congestion in key points on the body that correspond to larger body areas, e.g., supraclavicular area, posterior axi llary f olds, m idepigastrium , on so on. Based on the osteopathic physician' s knowledge of the flow of lym phatic fluid in the body, the practical considerations involving the lymphatic system are to first elim inate any m yof ascial restrictions to the lym phatic flow (release all diaphragm s) and then to i ncrease the flow f rom the area in question, as appropriate f or the patient. See Chapter 68 f or specific lym phatic techniques. The Autonom i c Nervous System
Attem pting to norm alize the autonomic nervous system is an im portant goal of osteopathic m edicine. The m aj ority of ill pa tients present in a hypersym pathetic state. It is tem pting to think i n term s of decreasing the sym pathetic tone or increasing the parasym pathetic tone, but i n true osteopathic f ashion (believing that the body has self -regulatory f aculties) , it is m o re appropri ate to think i n term s of norm al izing the two aspects of this very im portant hom eostatic system: the sym pathetic and parasym pa thetic nervous system s. Techniques applied to the craniosacral and upper cervical areas will tend to norm alize the parasym pathetic system . Techniques appl ied t o the thoracic and lum bar areas will tend t o norm al ize the sym pathetic system . See Chapter 6 and Chapters 4 8 through 50 f o r specific techniques. The Scree n i n g Exami nation
There are m an y f orm s that the screening exami nation in the E D can take, dependi ng on t h e ski l ls of the particular osteopathic physician and the tim e available. One f orm described here has been tested over m any years of practice. This screening exam ination can be com pleted in approxim ately 1 0 to 15 m i nutes. The physician m ay not need to perf orm all of the f ollowing steps during the assessm e n t of every patient.
388
VI.
Osteopathic Considerations in the ClinicaL SpeciaLties
First, the presenting compLaint will ofte n suggest the proble m . I t i s the re fore important (as me nt io ne d above ) t o know the ty p ical distribution o r patte rns of pain that most patie nts de scribe with various dy sfunctions ( 1 1 ) . Knowing the ty pical pain distri bution patte rns p re se n t i n m usculoske le tal dy sfunction, whe the r due to the primary unde rly ing dise ase p roce sse s o r only se condary change s, he lps the phy sician to more q u ickly and corre ctly arrive at the appropriate diagnosis. Se cond, e valuation of the patie n t in the E D, e spe cially one with a musculoske le tal complaint or compone nt, should be gin with observation of: the patie nt walking (obse rve asy mme tries in the gait cy cle ), the patie n t standing (static te sts: gross asy m me tries fro m the ante rior, poste rior, and late ral pe rspe ctive s, a short le g, sco liosis, conge ni tal abnormalities, e tc . ; motion te sts: standi ng fle xion and hip-drop te sts) , • the patie nt se ate d (static te sts: gross asy mme trie s, scol iosis, conge ni tal abnormalities; motion te sts: se ate d fle xion te st, trunk side be nding and rotation te sts, ce rvical spine fle xion, side be nding, and rotation te sts) .
•
•
T he se obse rvations and te sts will ofte n give i mportant clue s a s t o the location of the patie n t' s primary re striction. The scree ninge xamination should the n include visual and pal patory examination ofthe skin. The patie nt should be e valuate d for change s i n te mpe ratute (warme r i n are as of acute somatic dy s function, coole r in are as of chronic somatic dy sfunction), mois ture (m ay be incre ase d in are as of acute somatic dy sfunction), oiline ss (may be i ncre ase d in are as of acute somatic dy sfunction), te xture ( may be roughe r or have obvious skin changes, such as pimples, cafe -au-lait spots, rough or he avy hair growth patte rns in are as of somatic dy sfunction o r conge nital anomalies), and tur gor or conge stion (may be i ncre ase d in are as of acute or chronic somatic dy sfunction ) . Ne xt, a fasciaL Listeningsequence, base d on the obse rvations of Z ink and Lawson (15) (see Chapte r 4 1 ), may give valuable infor mation as to the pre se nce of compromise d homeostatic me cha nisms in the body. Asse ssing the body 's fascial p re fe re nce s, e spe cially at the four transition zone s (cranioce rvical, ce rvicothoracic, thoracolumbar, and l umbosacral), allows the osteopathic phy si cian to de te rm i ne whe re, i f at all, the patie nt is de compe nsated. I n a he althy pe rson, the re will e ithe r be no ide nt ifiable p re fe re nce or the re will be a patte rn of alte rnating pre fe re nce s ( L, R,L,R, or R,L, R, L) called compe nsatory patte rns. A re as of de compe nsa tion (non-alte rnating pattern ) corre late we ll with are as of somatic dy sfunction in the body. Ne xt, a more focuse d e xamination of specific muscle groups or individual muscles suspecte d, fro m the e arlie r e valuation, to be i n somatic dy sfunction can the n be pe rformed using the we ll known muscle trigger points.. Trave l l and S immons ( 1 1 ) have shown that the pre se nce of extre me ly painful, we l l-de marcate d are as in p re de scribed locations within a specific muscle corre late s we l l with somatic dy sfunction of that m uscle . I n j ust a fe w se conds, the knowle dge able oste opathic phy sician can de te rm i ne which m us cle s or m uscle groups are in dy sfunction by using this me thod. Examination of the strain/counte rstrai n "te nde r points" dis cove re d by J ones ( 1 6) (see Chapte r 63) can contribute valuable
information about the body's state of balance l imbalance (see Chapte r 63 for more on strain/counte rstrain ) . Ne xt, the Lymphatic system c a n be quickly asse sse d by e xam i n i ng the following are as for signs of bogginess or conge stion within the tissue s: the supraclavicular space, the poste rior axillary fold, the m ide p igastric area, the poplite al space, the i nguinal re gion, the wrist are a, the ante cubital fossa, and the Achilles te ndon area. Conge stion in the se are as can be an important clue to dy s function of the ly mphatic sy ste m in the re late d body are as. At an appropriate time i n the scree n i ng e xamination se que nce, the craniosacral me chanism can be asse sse d for rate, vitality, and quali ty ofthe cranial rhy thmic i mp ulse (CRI) and for the motions of fle xion, exte nsio n, and i nte rnal and e xte rnal rotation of the bone s of the skull and sacrum (see Chapte r 62). Anothe r appropriate scree n i ng e xami nation i n the oste opathic asse ssme n t of the patie n t is the asse ssme n t of the abdom i nal col late ral ganglia, and the ce liac, supe rior, and infe rior me se nte ric ganglia. The ce l iac ganglion i n ne rvates the stomach, duode n um, live r, gallbladde r, pancre as, and splee n . The supe rior me se nte ric ganglion i n ne rvate s the je j un um, i le um, the proximal half of the colon, the kidney s, adre nals, and the gonads. The infe rior mese n te ric ganglion i n ne rvate s the distal half of the colon and the pe lvic organs (e xce pt the gonads) . If a subjective re port of te nderness or an objective se nse of re striction is note d in the are a e xamine d, this can be a clue to visce ral dy sfunction in organs re late d to that ganglion (8) . As time allows, a focuse d asse ssme n t of the patie' nt for furthe r signs o f visce rosomatic re fle x activity can be quickly pe rforme d. Appropriate se gme ntal le ve ls and the pre se nce of Chapman re flex points can be he lpful in confirming the pre se nce of visce ral dise ase ( 1 3) . Last, a focuse d asse ssme nt of spinal se gme nts i n dy sfunction is comple te d while looking for te nde rne ss, asy mme try, range of motion diffe re nce s, and tissue te xture change s (the TART crite ria for somatic dy sfunction). A good oste opathic structural e xamination should be a part of e ve ry patie n t visit to the ED, e spe cially as part of the se condary survey for those with musculoske le tal complaints. That is, fol lowing the primary asse ssme nt survey with any ne ce ssary i n i tial stabilization and comple tion of any more urge nt priorities. A case e xample he lps to show the application of the above princi pIe s. A 34-ye ar-old fe male pre se nt s to the ED with sudde n on se t, e xcruciating, right low back, flank, and groin pai n, as we ll as le ft buttock pain , for the last 2 hours accompanied by nau se a and vomiting. He r pulse is 1 1 0 be ats/min and he r re spi rations are 1 4 pe r m i n . He r vital signs are othe rwise normal. She is unable to walk back to the e xami nation are a ( no obse r vation possible ) and is unable to fi nd a comfortable position in which to lie ( ty pical si tuation for a kidney stone or gallstone ) . She continue s t o vomit i n the E D and i s scre am i ng i n pain . She is pale, swe aty a n d be gins fee ling faint. She re ce ive s an i.v. with normal sali ne and oxy ge n at 1 00%. The cardiac mon itor shows sinus tachy cardia. Blood is drawn and se n t to the labora tory along with a urine sample (scree ned for stones) for a uri naly sis. She is give n an analgesic and an antie me tic by ve in and be come s quie te r. He r pe rsonal and family me dical/surgical his tory is ne gative . He r blood work is all within normal lim its. U rine
26
Osteopathic Medicine in the Practice of Emergency Medicine
shows gross blood and no signs of infection. She is feeling much better after the medication, which allows a screening structural exami nation. 1.
The natu re of her pain and presentation is classic for kidney stone. Low back pain and gr oin pain can also indicate psoas dy sfunction, a common complication of a passing kidney stone (the ur et er passes direct ly over t he psoas muscle) .
2. Static and motion tests reveal only a sidebending and rotation to the right in the lumbar area. 3. Examinat ion of the skin reveals only diffuse cool, sweaty changes consistent with her hy persy mpathet ic state (sec ondary to pain) on presentat ion. 4. Fascial preference examination reveals an decompensated L,R,R,R pattern (there could be a problem in the thora columbar region ) . 5. Evaluation o f her trigger points shows positive fi ndings i n the upper lumber paraspinal musculature o n the right. 6. Eval uation of the counterstrain tender point shows dy sfunc t ion of the right psoas and iliacus muscles, as well as t he left piriformis muscle (psoas sy ndrome) . 7. Evaluation of her ly mphatic sy st em shows no abnormalities. 8. Craniosacral evaluation shows only slightly i ncreased rate, normal vitality, and normal cranial bone motion. 9. Exam ination of her superior mesenteric ganglion is painful and shows significant restriction (the kidney is supplied by this gangl ion). 1 0. She has painful Chapman reflex points for the right kidney (anterior: 2 cm cephalad and 2 cm lateral-right of the um bil icus; posterior: bet ween the right transverse processes of Ll and L2), as well as boggy, cool, mildly swollen tissue in the T I 2-L3 area. 1 1 . We find the TART criteria for Ll -2 F RR SR segmental somatic dy sfunction. The diagnosis is nephrolith iasis wit h secondary psoas and pir iformis muscle somatic dy sfunct ion and viscerosomatic l umbar spine somatic dy sfunction. The patient receives addi tional, small doses of the narcotic analgesic and stabilizes well. As t he E D is relatively quiet, she receives OMM for her psoas, piriformis, and lumbar spine dy s function, as well as fascial release for her superior mesenteric ganglion, and Chapman reflex point treatment for the kidney. She feels better and prefers to not wait the 2 hours for the i ntra venous py elogram (IVP) to be done (the radiology techn ician is busy with other emergencies), but rat her to go home with med ications and instr uctions to screen her ur i ne, get the IVP in the morning (scheduled) , and to see her fam ily practitioner (an osteo pathic physician) the next day. The next day she does not present for the [ V P but del ivers t he stone to her fam i ly practit ioner, who continues the O M M for the remai n i ng somatic dy sfunctions. She is seen 4 day s later and again 8 day s later, at which time she is pain free. This case shows the use of the osteopathic screeni ng examina tion leading to an i ntegrated osteopathic management approach to the pat ient. As mentioned above, not all steps must be com plet ed in each pat ient . There are certainly cases where not all
389
steps will provide additional or even consistent information. With enough p ieces of the puzzle in place, however, we will be able to see the picture clearly! As in all areas of medicine, one has t o be cognizant of the situations in which O M M is relat ively or absolutely contrai ndi cated. A patient with extremely low vitali ty will oft en not tolerate O M M . A patient who refuses to allow y ou to touch them (i.e., a case of rape o r molestation, or post t raumatic stress sy ndrome) will be difficult to treat with O M M . As it is im possible to know which patient is i m munocompromised or cont agious at any one time, it is import an t to alway s take precautionary measures when handling body tissues, fluids, and contacting pat ient s in t he E D setting. I n acute trauma cases, the use of gent le, indirect O M M treatment techn i q ues is indicated. [ n the osteoporosis pat ient, avoid h igh-velocity, low amplitude ( H VLA) tech niques.
PATI E N T-ORIEN TED CLINICAL S C E NARIOS
The goal in this section is to present t he distinct aspects of t he application of osteopathic principles and practices regardi ng diag nosis and treatment t hat apply to given body regions or p resenting complain ts. A more detailed discussion of the underly ing specific pathology or description of the application of specific osteopat h ic man ipulative medicine (OMM ) t echniques is referred to i n t he various sections and can be found in other areas of this text . The Osteopathic Approach to the Patient with Com plaints in the Head and Neck Regions
The emergency phy sician encounters a variety of pathophysio logic p rocesses i n the head and neck region. U p to 50% of the i n j ur ies to t he body occur i n the head, and this is t he leading cause of death in persons y ounger t han 4 5 y ears of age ( 1 0) . Symptoms, Pathophysiology, and Epidemiology Cephalgia
Cephalgia is a very common chief complaint encou ntered in emergency medicine, and i t carries great potential for serious, adverse effects (J 7). Studies have shown that 69% of patients with subarachnoid hemorrhage reported headache on p resentation t o the E D ( 1 8) . Evaluation of the severe headache can b e difficult. M any patients that look generally ill do not frequently have life threatening ill ness ( 1 8) . Eye Pain
Three percent of patients presenting to the ED have an ey e-related chief complaint, and most of these patients can be treated by the emergency phy sician without consulting an ophthalmologist ( 1 9) . Otitis media is the most common diagnosis made in t h is coun try for children y o u nger than 1 5 y ears of age ( 1 9) . This is caused, in large parr, by developmental factors oft he eustachian tube. [n adult patients, t i n n it us and vertigo are frequent ly seen in the ED, as is ear t rauma (20) . I n flammatory processes, infection, foreign bodies, and ototoxic drugs contribute signi fican tly to a l ist of common etiologic factors leading to ear complaints in t he ED. Cranial somatic dy sfunction can play a role in the etiology
390
VI.
Osteopathic Considerations in the CLinicaL SpeciaLties
of se condary ver tigo and tinnitus (20) . Dire ct e a r trauma can be cause d by a numbe r of me chanisms, such as blast inj ury, che mical or ther mal e xposur e , acoustic trauma, and blunt trauma (20) .
the root of the pathologic proce ss. The phy s ician should e valuate the eye s, nose , e ars, and throat, as we ll as the muscles within the face and ne ck area.
Nosebleeds/Upper Respiratory Infection
Eye
Epistaxis is see n in 15 out of e very 1 0,000 patie nt visits re quir i ng me dical care , and more than 1 0% of the se re qui re hospital admission ( 1 9) . U ppe r re spiratory infe ction (U RI) and sinusitis are , by far, the most common pr oce sse s i n this parr of the body that are see n in the E D . Sinusitis has bee n re por te d to affect 14 % of the ge ne ral population ( 1 0) .
Trauma, fore ign bodies, infe ctions, i nflammatory proce sses, and se q ue stration of fluids in the eye s are commonly see n . Oste o pathic phy sicians must fi rst r ule out worse possible dise ase pro ce ss (e .g., acute angle glaucoma, acoustic e xposure , ce n tr al artery occlusion, re tinal de tachme nt, rupture d globe ) . Oste opathic pal patory skills will assist in the diagnosis of proce sse s like an incre ase i n i ntraocular p re ssure . With the e xce ption of a splash injury that nee ds i m me diate copious irrigation, the initial ste p in all eye e val uations is the asse ssme n t of visual acu i ty (2 1 ) . Every e mer ge ncy phy sician should be fam iliar with diagnostic instrume nts, such as the slit lamp, tonome te r, and ophthalmoscope ( 1 0) . The e val uation of cranial bone move me nt and tissue te xture changes in the orb i ts, maxillae , and vome r is also imporrant in ophthalmo logic pre se ntations. Se condary cause s of ey e dise ase proce ss like URI/sinusitis must be e nte rtained. Sinusi tis is the most common cause of orbital ce lluli tis (22) .
Neck Pain
Ne ck pain is a sy m ptom arising from a large numbe r of e tio logic factor s, i ncluding tr auma (watch out for abuse situations), de ge ne rative disorde rs, i n fe ction, ne oplasm, i nflammatory pr o ce sses, as we ll as musculoske le tal i n jury ( 1 0) . Acute trauma to the cer vical spine commonly follows automobile and motorcy cle accide nts, and falls of all kinds, as we ll as abuse situations ( 1 9) . Phary ngitis and U RI fre q ue ntly cause ne ck pain as part o f the i r sy mptomatology (through visce rosomatic activity ) . Pe ritonsillar and re tr ophary nge al absce sse s are infe ctious pr oce sse s p re se nt ing with ne ck pain that can quickly le ad to ai rway compromise and de ath. I nfe ctions, such as me n ingitis, fre que n tly p re se n t with ne ck pain and stiffne ss due to me ninge al i rritation. The knowl e dge able phy sician will re cognize that muscles will ofte n be hy poto n ic i m me diate ly afte r trauma, only to be come significantly hy pe rtonic se ver al hours late r. Furthe rmore , trauma that is se vere e nough to te ar m uscle or ligame n t tissue or to b re ak bone will ce rtainly be significant e nough to cause concomitant somatic dy sfunction locally, as we l l as e lse whe re in the body. I n case s of trauma, rare ly are chie f complaints focusing o n the ne ck isolate d . The so-calle d "whiplash of the ne ck" i nvolve s i ne rtial force s that affect the e ntire body, particularly the cer vical re gion but also having key site s in the ste rnum and pe lvis. Long-ter m ce rvical pr oble ms ty pically will be associate d with compe nsatory somatic dy sfunction i n the se are as, as we ll as e lse whe re i n the body. Diagnosis
Ear Pain
A fore ign body must always be conside re d in childre n pre se nting with ear complaints (23) . Fore ign bodies i n adults usually pre se nt i m mediate ly afte r the e nr ry of the fore ign body as oppose d to childre n (whe re rhe fore ign body may have bee n se lf-inse rred), and the time to pre se nr ation can be prolonge d (23) . The asse ss me n r of cr anial somatic dy sfunction can assist the oste opathic e mer ge ncy phy s ician i n the comple te asse ssme n t of the patie nt pre se nt i ng with an e ar complaint. The te mporal bone play s a vi tal role in ear pr oble ms, e spe cially in childre n . The distal parr of the e ustachian tube lies on the te m poral bone , and tissue te xture change s or abnormal move me n t of the te m poral bones can lead to e ustachian tube proble ms. Te mporal bone dy sfunction, occipito mastoid suture dy sfunction, me dial pte ry goid muscle spasm, and cranial tor sions have also bee n implicate d to cause e ar sy mptoms (8, 1 1) . Additionally, otalgia may be re fe rre d from othe r struc tures, such as tee th, tongue , tonsils, the esophage al area, and the te mporomandibular joint (24) .
Cephalgia
Ce phalgia may occur as a re sult of many dise ase pr oce sse s that fall under the cate gor ie s d iscusse d above . Three major gr oups of pathologic conditions affe ct the pain-se nsitive structure s of the he ad and ne ck ( 1 9) . They e manate from a vascular, te nsion, or i nflammatory proce ss. Te nsion le ads the list of e ti ologic fac tor s for he adaches, followe d by vascular origin and i nflammatory proce sse s ( 1 9) . The oste opathic phy sician must be astute and rec ognize that the ce phalgia may be re fe rre d from othe r structure s i n the he ad (eyes; ears; nose ; i n tr acranial, subarachnoid, subdural, e pidur al blee ds; mass le sions; hy per te nsive e me rge n cy ; me n ingi tis; toxic exposure ) . A carefu l ne ur ologic e mphasis in the clinical e valuation is cr itical in the diagnosis process ( 1 8) . A ne ur ologic de ficit can warn the phy s ician of a fast, pote ntially le thal proce ss that must be re ve rse d i n orde r to bring that patie nt's body toward i ts homeostatic state . The oste opathic clinical e valuation may also i nclude asse ss me nt of the articular mobility of the cr anial bones. The pr imary re spiratory me chanism can be asse sse d to he lp find
Nosebleeds/Upper Respiratory Infection
Blunt rrauma to the nose fre que ntly produce s nasal fracture s and e pistaxis. Epistaxis can be se par ate d into ante rior and poste rior varie ties, base d on the location of the blee d. The re is a long list of cause s of e p istaxis. Infe ction , fore ign bodies, rrauma, alle rgic rhinitis, hy pe rte nsion, tumors, and hereditary coagulopathies are se ve ral common e tiologie s ( l 0) . Sinus mucosal obstr uction is the most common cause of sinusitis. Cr an ial somatic dy sfunction can also play a large role i n the e tiology of sinusitis. Frontal and max illary bone fixations are be lieve d to impair drainage from the sinuse s by obstructing blood circulation, as we ll as maxillary sinus drain age pathway s (24) . Phy sicians must be quick to recognize e me rge n t proce sses, such as nasal rrauma, e pistaxis, and ce re brospinal fluid (CSF) rhinorrhe a, that may warrant immediate e ar, nose , and throat ( ENT) and ne urosurge ry consults. Childre n fre q ue ntly i nse rt fore ign bodies i n the nasal cavity ( 1 0) . Patie nt asse ssme nt is augme nte d by the use of osteopathic palpatory skills
26.
Osteopathic Medicine in the Practice ofEmergency Medicine
ro exam i ne For an increase i n pain or tension over specific sinuses or over the exit si tes of the supr aor bi tal and i n Fr aor bital br anches of the tr igem inal ner ves, and For cr anial bone r estr ictions. Cor recting secondary causes of the nasal disease pr ocess, such as oti tis media, should also be consider ed. Neck Pain
Em er gent pr oblems, such as air way com pr om ise and acute neck inj ury secondary ro tr auma, m ust be consider ed. Musculoskeletal hy per activity Fr om r o ITicollis, "whiplash," som atic dy sFunction, or other cer vical str ains and spr ains ar e commo n pr oblems that the osteopathic em er gency phy sician can d iagnose and tr eat. A str ai n or spr ai n diagnosis should not be m ade beFor e obtaining a good hisr ory and phy sical exam i nat ion that i ncludes an osteo pathic str uctur al exam ination and necessary r adiogr aphic studies ro r ule out m or e ser ious pr ocesses. My oFascial tr igger points ar e Frequently the r esult of over use or tr auma, and their evaluation can assist the ED phy sician in diagnosis. Integrated Osteopathic Treatment Cephalgia
The Am er ican College of Em er gency Phy sicians' clinical policies For adolescent s and adults pr esenti ng with headaches ser ve as a guide ro objectives of tr eatment ( 1 7) . The Four goals a re: J . To pr ovide eFFective tr eatm en t For pr im ary headache sy n dromes.
2. To diagnose and eFfectively tr eat patient s with gener ally benign and r ever sible secondary headache causes. 3. To appr opr iately select patients For emer gency i nvestigation and tr eatm ent of suspected cr itical secondary headache causes. 4. To pr ovide appr opr iate disposit ion and Follow-up for all d is char ged patients. With the suspicion of vascular headaches, the occipir om asr oid release, which is consider ed r o be a j ugular venous congestion r e lease techn ique, will be very helpFul. The j ugular veins and vagus ner ves pass through the jugular For am en that is located between the occipital bone and the petr o us por tion of the tem por al bones (26) . Eighty -five per cent of the venous dr ainage in the head passes thr ough the jugular For am en (8). Occipir oatlantal decom pr ession is also thought ro enhance the par asym pathetic ner vous sy stem by norm alizing vagus ner ve Function (8) . Com pr ession of the four th ventr icle (CY4) tech nique, used ro dissi pate cer ebr al spinal Auid and norm alize the vagus ner ve Function, is another cr aniosacr al technique useful in this setting (24) . As m ost of these patient s will have a hy per sym pathetic r one, norm alization o f the segm ents T I -4 will help ro balance the sym pathetic supply ro the head and neck ar ea. Once sym pathetic and par asym pathetic sy stem s ar e normalized, thor acic inlets can be r eleased, and venous r e tur n Fr om the head can be Fur ther enhanced. Thor acic lym phatic pum p techniques m ay then be used ro Fur ther the elim i nation of metabol ic waste pr oducts and other by -pr oducts of the un der ly ing pathophy siology thr ough the thor acic duct. Chapm an reAex poi nts can be used as a Fur ther adj unct i n the ther apy of cephalgia. These and other r eAex points can also be shown and taught ro the patient For selF-tr eatm ent.
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Medications ar e often used i n conj unction with other tr eat ment m odalities ro enhance r apid r ecovery. The use of appr opr i ate analgesics r o shor ten the tim e r o pain r esolution and m uscle r elaxants ro enhance the patient's r ecovery Fr om m uscular spasm s m ay be warr anted. However , the need For m edication is oFten de cr eased with the application of O M M . Im pr ovement of sleeping patter n and nutr i tion, corr ection of postur al im balance, r elax ation and r el ief of str ess, contr ol of cafFeine, alcohol, or other dr ug intake, and hom e str etching exer cises could enhance r ecov ery. Tim ely educational r ei n for cem ent by the em er gency phy si cian of the impor tance of ongoing car e by their pr im ary car e phy sician enhances futur e patient com pl iance i n these often sim ple, y et im por tant , adjunctive m easur es. Eye Pain
Acoustic exposur e, splash i n j ury, and centr al ar ter ial occlusion warr ant imm ediate tr eatm ent pr ior ro com plete clinical evalua tion ( 1 9) . The phy sician m ust fir st r apidly take charge of and con tr ol any em er gency, or der necessary ther apies and m edications, and/or secur e an ophthalm o logy consul t as r equired. Pr imary or adjunctive use of O M M is again directed r owar d enhanc ing the patient's ability ro self-heal. Healing fr om p rocesses of inFectious or i n Aamm ar ory etiologies r equir e optimal ANS, lym phatic, str uctur al, and imm une sy stem function. Im pr oving ve nous and lym phatic dr ainage with fam iliar techniques (see above) will help ro accom plish this. Norm alization of the sym pathetic and par asym pathetic ner vous sy stem function will also assist the patient. Ophthalm o logic lym phatic pum p consists of light per cussion over the affected ey e's closed ey elid. This has been shown ro be beneficial in decr easing intr aocular pr essur e in patients with chr onic open-angle glaucom a (8) . This is not r ecomm ended for patients with acute closed-angle glaucom a who need m edici nal tr eatm en t within 3 r o 5 day s ro pr event blindne ss ( 8 ) . M uscle ener gy of extr a ocular m uscles can be used to balance the my ofas cial tensions i n this r egion (8). Avoidance of a cigar ette sm oke envir onm ent that will irr i tate the ey es is warr ant ed. Glaucoma patient s should avoid sudden changes between dar k and br ight envir onm ents. Ear Pain
With r egar d to ear pain, the tr eatm en t pr ior ities in the ED ar e imm ediate r ever sal of any life-thr eaten ing pathologic pr ocess, r e pair of tr aum a, imm ediate r em oval of for eign bodies, and ad dr essing the etiology of a sudden hear ing loss. A for eign body that is irr em ovable in the E D should pr om pt an ENT r eferral. I t is unclear whether pharm acologic tr eatment of otitis m edia is warranted because evidence-based docum e nt ation shows that over 80% of the cases r esolve spontaneously (27) . H owever , the use of antibiotics has gr eatly r educed the r isk of com plications from bacter ial infection pr ocesses (27) . I nAamm ar ory pr ocesses m ay be tr eated with an appr opr iate antiinAamm ar ory agent. Cor r ecting cr anial som atic dy sfunction gr eatly benefits r ecovery by incr easing cir culation r o the ar ea and norm alizing str uctur e of ner ves and venous/lym phatic r eturn (24) . I nhibitio n or i nt erm i t tent tr action to the m ed ial ptery goid m uscle, ear lobe tr action, or hy oid bone r elease m ay be em ploy ed to enhance eustachian tube dr ainage (8, 1 1,28) . The " M u ncie tech n ique," r eferr i ng to Cur tis H. Muncie, who or iginally descr ibed the pr ocedur e i n the
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1 920s, can also be used. The technique requires the physician to intraorally place a fi nger posteroinferior to the tonsillar pillar, and to gently pump in the Rosenmuller fossa i n a cephalad direction to release the obstructed eustachian tube (29) . Lifesryle changes can also enhance recovery from ear problems. Avoiding cigarette smoke environments that may i ncrease frequency of disease pro cesses l i ke otitis media is i ndicated (8) . Be alert for disease p rocess breakouts in school or day-care. Nosebleeds/Upper Respiratory Infection
Racemic epinephrine can be used to decongest the nasal m ucosa and loosen a stuck foreign body ( 1 0) . I nabiliry to remove foreign objects in the ED should p rompt ENT referral. Displaced nasal fractures warrant plastic surgery referral ( 1 0) . Epistaxis should be tamponaded with anterior and posterior packing. Antibiotics, an tihistamines, and topical steroids are the mainstream therapy for sinusitis. ModifYing autonomic balance (parasympathetic stim ulation causes a thin mucus to be produced and sympathetic stimulation a thick m ucus) to affected tissues can i mprove im portant self-regulatory mechanisms in the patient. Another goal of O M M is to assist in reducing pain symptomatology result i ng from the disease process. This can be accomplished by nor malizing the ANS (hypersympathetic tone is usually present) , improving lymphatic drainage (reducing local congestion con tributing to pai n ) , and balancing the musculoskeletal structures involved in the pathology. The release of the upper cervical so matic dysfunction and the cervicothoracic j unction has been empi ricall y shown to create better circulation and improved ve nousllymphatic drainage (30) . Other manipulative treatments can be i mplemented to directly reduce tissue edema and facili tate sinus drain age, as well as to decrease m ucus viscosiry (3 1 ) . Intraoral stimulation of the sphenopalatine ganglia, inhibition of lateral pterygoid muscle trigger points, and CV4 and trigeminal nerve stimulation tech niques will produce parasympathetic stim ulation and production of thin nasal secretions (8, 1 1 ) . Frontal, maxillary, and nasal bone restrictions should be released for sig n ificant improvement of sinus drainage (24 ) . The most direct drainage enhancement is achieved through sinus drainage tech niques that create gentle intermi ttent pressure over the sinuses (32) . Lifestyle changes may lead to faster recovery. Avoidance of allergens is beneficial. Discussion of controlling alcohol con sumption and other drug use that may decrease i mmune system response is warranted in the ED to reinforce the importance of patient i nvolvement and compliance. Neck Pain
Any signs of airway compromise should be promptly treated with early airway management and anesthesia consultation. Neuro surgery consultation should be obtained if unstable cervical spine inj ury is suspected. I n fectious processes may be treated with i n cision and drai nage, antibiotics, or both. Systemic steroids can be used to decrease inflammation. Secondary causes of pharyn geal disease, such as otitis media and sinusitis, must be con sidered, assessed, and treated as appropriate. After assessment, treatment of any painful myofascial trigger points with a vari ery of manual or medical means (pressure, spray, i njection) can play a significant role in i mproving the subjective pain of the patient. Musculoskeletal neck pain, even i n an acutely painful
presentation, can often be effectively treated with counterstrain using cervical tender points ( 1 6) , indirect myofascial release to muscles and fascia of the neck and anterior cervical region, fa cilitated positional release (FPR), or even gentle muscle energy techniques (30) . Acute torticollis is often responsive to a rhyth mic muscle energy protocol first described by Ruddy (33) and designed to decongest the swelling in the i nvolved cervical muscle bellies. The Osteopat h i c Approach to the Patient with Chest Pai n
Any physician who has treated a patient presen ting with chest pain knows that the large component of fear and anxiery from the patient regarding their symptoms can significantly compound the problem. Nearly everyone i n our society has either known someone or heard a story about someone who had a heart attack and died or was seriously debilitated as a result. The patient often presents with tachypnea, tachycardia, mydriasis, and a cold sweat-all clear signs of a hypersympathetic state that, in most patients, will negatively impact the delicate supply and demand of perfusion balance to the myocardium. The first priorities i n the evaluation and treatment of the chest pain patient are the potentially life-threatening conditions: e.g., unstable angina, acute myocardial infarction (AM I ) , aortic dissection, pulmonary embolism, spontaneous pneumothorax, and esophageal rupture (Boerhaave syndrome) ( 1 0) . An unstable patient must fi rst b e stabil ized by the best methods available at the time. This usually means admi nistering oxygen, starting an i ntravenous ( IV) line and giving appropriate fluids, monitoring the patient for heart rhythm disturbances, and giving appropriate additional medications to treat his/her pai n, anxiery, dysrhythmia, and any hemodynamic instabiliry. A primary survey is then completed where any life-threatening problems are iden tified and treated. After this, a secondary survey is performed with a head-to-toe examination and fi ngers or tubes in every ori fice as appropriate. A structural examination is completed during this secondary survey. When this is completed, definitive care is then planned for the patient and undertaken. Please refer to an emergency medicine textbook for more detailed information on these interventions (ACLS Textbook, A TLS Textbook, refs. 1 0 and 1 9) . Diagnosis
When the patient is stable, the osteopathic approach to the chest pain patient should include such issues as detailed family and social h istory, identification of risk factors for coronary artery d isease (CAD) , strategies for reduction of alterable risk factors (table showing risk factors) (34; see also Chapter 1 3) , medications presently being taken (or not taken) , nutrition, exercise patterns (or lack thereof) , and O M M considerations. There are many common musculoskeletal conditions, such as scoliosis, i ncreased or decreased kyphosis, and so on, that can have a negative impact on the fu nction of the cardiovascular system either as a primary problem or as a compensatory mechanism for other ailments. There are a number of congenital conditions, for example Marfan syndrome, with obvious m usculoskeletal
26.
Osteopathic Medicine in the Practice of Emergency Medicine
findings that are known ro also have congenital cardiac anomalies present. An inspection of the patient ro determ ine if any of these con ditions are present is an important fi rst step. A leg length discrep ancy, for example, that leads ro compensarory posrural changes and facilitation of the upper thoracic segments can lead ro com promise of cardiovascular function. Regional range of motion abnormalities and uncompensated fascial patterns ( 1 5) in the cervicothoracic area can be a further sign of a compromised homeostatic mechanism , and might be creating somato-visceral reflex activiry that potentially weakens the cardiovascular system. In the case of the cardiovascular system, the T l -6 area is often facilitated. An additional example of a somato-visceral connection is the right pectoralis major trigger point that Travell ( 1 1 ) describes as causing or contributing to supraventricular dysrhythmias. (An arrhythmia is the absence of a rhythm, whereas a dysrhythmia is an abnormal rhyth m . ) This point overlies the right fifth i n tercostal space one-half the distance from the sternum to the nipple. I f this point is active and apparently playing a role in the generation or maintenance of the dysrhythmia, then treating this poi n t (pressure, spray, i njection, etc.) can help eli m i nate the problem. As mentioned above and shown by Schwarz and Stone ( 3 5 ) , there i s usually a hypersympathetic tone present i n chest pain patients. Rosero (36) has shown, however, that there are sirua tions where hyperparasympathetic tone is found, especially with inferior wall ischemia and infarction with hypotension and/or bradycardia. Both situations of abnormal ANS function are in appropriate responses and need ro be addressed. Assessment of the lymphatic system is also important. This is accomplished by first assessing the key areas of the body (e.g., supraclavicular space, posterior axillary folds, midepigastrium) for signs of fluid congestion, and then appropriately treating any somatic dysfunction in the following areas, for the given reasons: 1 . The T I -2 spinal area and the ribs 1 -2 left and right (these are important for the proper function of the thoracic i nlet and the entire lymphatic system); 2. The thoracic i nlet (the fi rst very i m portant central lymphatic diaphragm); 3 . The iliopsoas muscle group, the thoracolumbar spinal area, the quadrarus lumborum muscle, as well as the lower ribs (all important for the proper function of the respiratory di aphragm) ; 4. The respiratory diaphragm (the second very i mportant central lymphatic diaphragm ) ; 5. The piriform is muscle, innominate, a n d sacral areas ( a l l im portant for the proper function of the pelvic diaphragm); 6. The pelvic diaphragm (the third very important central lym phatic diaphragm ) . Ifyou are treating a patient that displays recurring somatic dys function in the upper thoracic area despite appropriate O M M , you should consider the possibil iry of cardiovascular pathology (or pathology in other viscera that faci l itates ro these segments). In addition, the Chapman reflex points can be helpfu l i n clari fying whether there is viscerosomatic reflex activiry. The anterior
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Chapman reflex points for the heart overlie the second i nt ercostal space b ilaterally near the sternum, and the posterior points are between the second and third thoracic vertebrae bilaterally j ust lateral to the spinous processes. In the patient with chest pain, we must be aware of the fact that the pain may be of musculoskeletal origi n , of cardiovascu lar origin, or both. We must realize that the presence of appar ent chest wall syndrome based on appropriate history, physical ( i ncluding structural examination ) , and negative laboratory/x ray/EKG fi ndi ngs, even with significant i mprovement after an O M M treatment, does not rule out cardiovascular disease nor the need for further cardiovascular workup. Costosternal syndrome, thoracic outlet syndrome, costochondritis, and i ntercostal neuri tis are common presentations that can m i m ic chest pain of cardiac origin ( 1 0) . Integrated Osteopathic Treatment
Rogers and Rogers (37) showed significant i m p rovement in symp tom !\ i n patients with coronary insufficiency after the application ofO M M . The goals of the application ofO M M for the chest pain patient are to maximally support the body's own self-regulatory, self-healing mechanisms through i mproving the perfusion ofoxy genated blood to the tissues at risk and i mproving venous and lymphatic return from these tissues. When both structural and functional elements related to the cardiovascular system are nor malized, the body will be i n a position to find i ts own best level of homeostasis. The form, t i m i ng, and manner of application of O M M will depend on the history, present status of the patient, and the diagnostic and therapeutic plan for the patient. The key concepts i n achieving these goals are addressing any somatic strucrural abnormalities with facilitation of spi nal seg ments, normalizing the autonomic nervous system fu nction as much as possible, improving the lymphatic system function , and addressing the issues of viscerosomatic reflexes with facilitation of spinal segments. The most appropriate concept for the treatment of the ANS in the chest pain patient is that of normal izing the two com ponents, the sympathetic and parasympathetic nervous systems. See Chapter 6 for the common ANS effects on the various organ systems. This is accomplished by exa m i n i ng and appropriately treating any somatic dysfunction i n the following areas, for the given reasons: The T 1 -6 region: normalizing sympathetic distribution to the heart (38). • The ribs i n this same region: "rib raising" tech nique ro inhibit the dorsal chain ganglia and reduce hypersympathetic tone; the T 1 0- 1 1 segments: sympathetic distribution to the kid neys and adrenals; the craniosacral, CO-2 region: normalizing parasympathetic distribution to the heart. • The C3-5 region: diaphragmatic irritation due to inferior wall pathology, by way of the phrenic nerve, can faci l i tate to these segments. •
The most appropriate concept for the treatment of the lym phatic system in the chest pain patient is that offirst removing any
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blockages to the appropriate Aow of lymphatic A uid, and then to specifically increase this Aow as the patient is able to tolerate it. [ n this way, we can best support the patient i n homeostatic self regulation. See Chapter 68 for more detail regarding lymphatic function. After the release ofany somatic dysfunction and normalization of the fu nctions of the above structures, any n umber of the fol lowing techniques can be applied in order to improve the general Aow of lymphatic A u id i n the body: • • • • • • •
Miller thoracic pump Other thoracic pump variations Pectoral rraction tech nique Abdomi nal pump techniques and variations Splenic and liver pump tech n iques Specific extre m i ty techniques Pedal pump tech nique and variations
Treating these points with either light vibratory pressure or firm massaging pressure until the tissue softens will assist the body in heali ng. An example from my (Adler-M ichaelson) ED practice may further encourage the reader to maintain an open mind regardi ng an i nt egrated treatment approach. A 50-year-old male was brought i nto the ER after driving in to a tree at about 45 mph. H is vital signs were unstable, he was moani ng in pai n , and he showed apparent supraven rricular cardiac dysrhyth m ias on the EKG monitor. He had a bleeding facial laceration and a significant thoracic contusion with ecchy moses; active bleeding had been controlled by the paramedics. With oxygen delivery, A uid resuscitation, bleeding control, and moderate pain control, the patien t stabil ized. The laboratory re sults came back showing elevated muscle enzyme levels. X-rays were negative, and the cardiac dysrhyth m ias remained nonlethal, requiring no further specific treatment. The patient was adm itted for monitoring with the diagnosis of thoracic/cardiac contusion, and facial contusion and laceration secondary to the motor vehi cle accident (MVA) . The next day, the patient was able to add the very important history that he had excruciating chest pain while driving and felt fai nt before waking up i n the ambulance on the way i nto the hospital. His enzyme levels stayed elevated and fol lowed the typical pattern for an A M I . H e continued to do well and was discharged to cardiac rehabi l i tation. In all probabil i ty, his MVA was a direct result of h is cardiac chest pain and AM I . I n medicine we have t o always b e able t o think beyond the obvious! By addressing, evaluating, and treating to normalize the so matic structural aspects, autonomic nervous system aspects, lym phatic system aspects, and viscerosomatic aspects of the patient, we can best assist the patient i n reestablishing h is or her best pos sible level of homeostasis. In this way, we are truly putting i n to practice the best of our osteopathic knowledge and wisdom. lhe Osteopathk A.pproa�h to Disorders of the Cardiopulmonary System
The emergency physician is called on everyday to exam i ne, diag nose, and treat patients who complain of difficulty breathing. The trained emergency physician is well prepared to determine the eti ology of dyspnea and provide ti mely and appropriate treatment.
For the most critical patients, the emergency physician must always be ready to intervene and take control of ven tilation and respiration through the use of artificial means. Community-acquired pneumonia accounts for several million visits to physicians and hundreds of thousands ofhospitalizations each year. It is the sixth leading cause of death, and it is often more severe in those patients at the exrremes of age. There are numerous reports detailing the success of osteo path ic treatment of pneumonia in the pre-antibiotic era, with the most famous being the great difference in morbidity and mortal i ty between those patients rreated with OMM versus those treated medically in the i n A uenza pandemic of 1 9 1 8 (39). More recently, a clinical trial showed that older adults with pneumonia who were rreated with O M M had a significantly shorter duration of i ntravenous antibiotic treatment and a shorter hospital stay when compared with patients who did not receive manipulation (40) . Congestive heart fai lure (CHF) is a syndrome of abnormal Auid retention secondary to the loss of the normal contractile srrength of the myocardium and manifested primarily by short ness of breath ( l 0) . The osteopathic emergency physician must be familiar with the multi ple etiologies of heart failure and be prepared to begin standard medical treatment with oxygen , di uretics, n itrates, and other therapies, as indicated by the underly i ng cause. Aggressive ai rway management should be anticipated and performed if necessary. I n C H F, the lymphatic load is i ncreased. [f the thoracic inlet is restricted or if there is somatic dysfunction of the thoracic cage or the respiratory diaph ragm with a reduction of the usual pressure gradient between the i ntrathoracic and i ntraabdom inal cavities, lym phatic pumping will be reduced and Aow will be impeded. O M M to these srructures and lymphatic pump tech niques will improve lymphatic Auid mobilization and assist in the clin ical i mprovement ofthe patient ( 8 ) . The astute physician must realize, however, that the ability of the CH F patient to deal with this extra Auid load (mobilized lymphatic Auid) is limited. Ir is detrimental to further overload the already overloaded heart, and so how much lymphatic Auid the patient can handle must be careful ly considered. Diagnosis
The ANS i n nervation to the lungs comes from the vagus nerves cranium, CO-2 levels (parasympathetic) , and the T I -6 thoracic trunks (sympathetic) . The right and left vagus nerves descend and pass through the thoracic in let on their respective sides, and each divides and branches to form part of the right or left pulmonary plexus. The thoracic sympathetic trunks are contributed from the posterior mediastinum and complete each pulmonary plexus. The fibers then form on the root ofeach lung and spread out along bronchial subdivisions (4 1 ) . Pulmonary dysfunction and m ucosal irritation result i n in cteased visceral afferent i mpulses to the spi nal cord, primarily in the 1' \ -6 \eve\s. 1'he tJaintu\ Cha?man re\\ex ?oints tor the \un'?,s can be palpated i n the third or fourth i ntercostal spaces anteriorly and at the T3-4 vertebrae posteriorly (8). Patients presenting with an acute exacerbation of asthma typ ically demonstrate one or more of a triad of symptoms, i ncluding coughing, wheezing, or dyspnea (42). The diagnosis of a reactive
26.
Osteopathic Medicine in the Practice ofEmergency Medicine
airway state is usually obvious with the history and physical exam ination of the patient, but the osteopathic emergency physician must exclude other causes of dyspnea that present with cough and/or wheezing. The mobility of the thoracic cage must also be addressed. Viscerosomatic reflexes can lead to thoracic vertebral somatic dysFunction, and vigorous coughing can ptoduce multi ple areas of exhalation rib somatic dysfunction, especially at the third or Fourth rib (8) . Assessment of thoracic i nlet and respi ra tory diaphragm Functions are critical in the context of pulmonary disease processes. Prior to releasing the thoracic i nlet i tself, the up per thoracic segments, upper ribs bilaterally, and the sternum are important structures to assess and treat if in dysfunction. BeFore releasing the respi ratory diaphragm, the thoracolumbar j unction is equally i mportant to assess and treat if i n dysfunction. I f the C3-5 region is i n dysfunction, i t should be assessed and treated to optimize the phrenic nerve function i n support of the respiratory diaphragm function. Clinically, pneumonia may present with obvious features, such as tachypnea, chest pain, rigors, inspiratory rales, bronchial breath sounds, rhonchi , and/or wheezi ng. Atypical pneumonia may present with any or none of the above symptoms, or with a variety of extra-pulmonary signs and symptoms. Some older pa tients may present with only a change in mental status (without respiratory complaints) ( 1 0) . A recent, as yet unpublished study by T. Crow, et al. showed a good correlation between Chap man reflex points in the 3rd and 4th i ntercostal space anteriorly and on T3-4 posteriorly and the diagnosis of pneumonia. Th is knowledge can assist the osteopathic physician in both making the diagnosis of pneumonia and i n beginning a helpFul therapy. Integrated Osteopathic Treatment
The osteopathic treatment plan for the acutely ill patient does not need to be elaborate or extensive. In fact, some believe that roo much manipulation early in a patient's course oFillness would be detrimental (8) . The osteopathic emergency physician should begin standard medical treatment for asthma with oxygen, beta agonists, and steroids as indicated. With the medical manage ment begun, the osteopathic emergency physician can address the ANS, lymphatic, viscerosomatic, and structural components of the disease process. Initially, the thoracic sympathetics in the area of the first six thoracic vertebrae may be stimulated for a bronchodilator response. The vagus nerve function can be nor malized at the occipitoatlantal j unction, the cervical spine, and the thoracic inlet. However, the osteopathic emergency physician must remember that these segments are probably already facili tated and care should be given not to over treat them. It m ight be preFerable to treat the parasympathetic in nervation to normalize the vagus nerve function. Consequently, rib raising and general lymphatic techniques can then be applied to improve rib motion, pulmonary Function, and lymphatic Function. I t is important to remember that many of these structural lesions are viscerosomatic in origin and probably do not respond well to high-velocity, low-amplitude techniques, so more gentle techniques, perhaps with activating forces, are likely to be more efficacious (8) . Treatment of asthma, pneumonia, or C H F can include, for example, the ANS, lymphatic, i mm u ne, viscerosomatic, and
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structural musculoskeletal systems in order to reduce congestion, reduce sympathetic hyperactivity, and mobil ize the thoracic cage (8) . O M M to the thoracic spine, rib cage, and diaphragm will i mprove the actual mechanics of breathing. Lymphatic flow can then be i mproved by applying m yoFascial tech niques to the tho racic inlets and then by using a pectoral lift or lymphatic pump technique to mobilize the lymph fluid. As mentioned above, treat ment of the C3-5 region in advance of normalizi ng the respiratory diaphragm Function will also greatly assist the patient. Osteopat h i c Cons iderations i n Patients w ith Abdom i n a l/Pel v i c Pa i n
Abdominal pain i s a com mon p resenting complaint among E D patients (43). Potentially life-th reaten i ng events, such as rup tured abdominal aortic aneurysm or ischemic bowel, do oFten present with abdomi n al pain, so a h igh level of suspicion must be maintained. More commonly, the patients presenting to the ED have a benign cause for their abdom inal pain, but oFten an extensive workup occurs before that determination can be made (44) . Approximately 20% of patients presenting to the E D with abdominal pain may require admission for observation or Further workup. Diagnosis
There are some historic clues that can help the osteopathic emer gency physician determine the etiology of pain. Pain in the right upper quadrant may originate from hepati tis or cholecystitis. Pain in the epigastrium is typical for gastric irritation from gastritis or peptic ulcer disease, but may also be seen with in trathoracic pathology, such as a lower lobe pneumonia or cardiac ischemia. Pancreatitis may also present with epigastric or left upper quad rant pain. Pain in the left lower quadrant may indicate col itis, diverticulitis, or in a female, problems with the fallopian tube or ovaries. Right lower quadrant pain suggests appendicitis, Meckel diverticulitis, or, again, fallopian tube or ovarian disease. Pain described as com i ng from the back or the side and radiating into the groin is typical of nephrolith iasis, but when abdom i nal aortic aneurysms are m isdiagnosed, it is commonly as a kidney stone (4 5 ) . Psoas spasm/dysfunction also frequently presents as pain in the flank or midabdomen radiating into the lower quadrants or groin area. Dysfunction in the lower extremities, especially the hip, may also present as abdomi nal pain. This is particularly true i n children. Males with testicular pathology may present with lower abdominal pain as well. The quality and onset of the pain can also give some clues to the diagnosis. Appendicitis typically develops over 1 to 2 days. The pain is described as dull, achy, begi n n i ng in the perium bilical region, and slowly moving to the right lower quadrant. The viscera of the abdomen respond to distension by producing discomfort in the associated soma; so i nflammation and disten sion of the appendix produces pain in the tenth thoracic nerve distribution-the periumbilical region. As the i n flammation in creases, the peritoneum also becomes irritated. The peritoneum does have pain fibers, so at that time, the patient senses pain at the region of irritation-the right lower quadrant. Pain origi nat ing ftom other hollow viscous presents similarly; a patient with
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VI.
Osteopathic Considerations in the Clinical Specialties
small bowel obstruction or diverriculitis may i n itially complain of an achy m idline pai n . Only as direct peritoneal i n flammation develops will they localize to the area of real pathology. These patients may also complain of waves of pain , often referred to as "colic," which are produced by the normal peristalsis against a fixed obstruction, such as a stone. Pain described as burning is rypically associated with peptic ulcer d isease. Abdominal pain in a female patient includes several other diagnostic possibilities, including ectopic pregnancy, salpingitis, mi ttelschmerz, ovarian torsion, or cyst. Any female of chi ldbear ing age who presents with abdom i nal pain must have a pregnancy test. Although a negative pregnancy test does not completely rule out ectopic pregnancy, i n the absence of other compelling symp toms it effectively does. If the patient with abdom inal pain is pregnant, physical exam i nation alone is not an adequate deter m i nant of whether the pregnancy is in the uterus. An ultrasound and a serum quantitative f3 H CG should also be performed. Certain conditions are more likely to occur at different ages. In a young, otherwise healthy individual, aortic abdominal aneurysm o r ischemic bowel is unlikely, but these must certainly be entertained in the older population. I n young children with ab domi nal pai n, i nt ussusception should be considered if the clinical picture of i n termittent severe pain , progression to depressed men tal status, and the late finding of "currant jelly" stool are present. Other conditions are more common in certain age groups, but certainly can occur any time i n life. These include peptic ulcer disease (perhaps with perforat io n ) , volvulus, intestinal obstruc tion, or appendicitis. Ectopic pregnancy is more often a disease of young women , but can occur i n any woman of childbearing age. Assessment of the abdominal collateral ganglia and the celiac, superior, and inferior mesenteric ganglia can assist the osteopath ic physician i n arriving at a diagnosis. The celiac ganglion i n nervates the stomach, duodenum, liver, gallbladder, pancreas, and spleen. The superior mesenteric ganglion i n ne rvates the jejunum, ileum, proximal half of the colon, kidneys, adrenals, and gonads. The inferior mesenteric ganglion innervates the distal half of the colon and the pelvic organs (except the gonads) . If a subjective report of tenderness, or an objective sense of restriction is noted in the area exam ined, this can be a clue to visceral dysfunction in organs related to that ganglion (8). The assessment of the fascial envelopes of the organs i n the abdominal area can assist the osteopathic emergency physician i n making a diagnosis. Restriction of fascial motion in a region of the abdomen or around a specific organ is a clue to the loss of com pensatory mechanisms in this area. Assessment for the presence of asymmetrically painful Chap man reflex points is a clue to the presence of viscerosomatic ac tiviry, indicating the likelihood of visceral d isease i n the related organs of the body. The facilitation of specific spi nal segments due to visceral organ pathology can tell the astute osteopathic physician which organ or organ system might be decompensated, that is, where the body's self-regulatory capaciry has been over whelmed. Assessment of the spine with this knowledge in m i nd will assist in the overall assessment of the patient. As with abdomi nal pai n, in any patient p resenti ng with pelvic pai n, the life- or organ-threatening conditions, such as ectopic pregnancy, ovarian or testicular torsion, or pelvic i nflammatory
disease must be considered fi rst. A common cause of pelvic pain is pelvic inflammatory disease. A patient may present in a fairly rypical positio n that has been sometimes referred to as the " P I O shuffle": a gait with the hip flexed and the lumbar spine extended. The i ntimate connection between the iliopsoas muscle complex and the pelvic organs makes this quite understandable. Integrated Osteopathic Treatment
To normalize the sympathetic nervous supply to the gastroin testinal system i n order to im prove excursion of the rib cage (Chapter 49), assess and treat any somatic dysfunction in the thoracic and thoracolumbar areas, as well as in the rib cage. To free-up and improve the function of the lymphatic system, release restrictions and i mprove the funcrion of the respiratory d iaphragm. The pressure gradients between the thoracic and ab dominal cavities are a primary driving force in the lymphatic flow within the body. I mproving the function of the respirarory diaphragn also improves the mobiliry of and sti mulation to the abdom i nal organs. Specific osteopathic abdominal/lymphatic techniques i nclude visceral techn iques, such as the treatment of the above-mentioned ganglia to free-up restrictions in the fascial sheaths around the abdom inal organs, mesenteric release tech n ique, colonic stimu lation technique, and techniques like the pedal pump that assist in lymphatic drainage. Chapman reflex points for the abdominal area can be assessed for asymmetrical tenderness and treated to assist the osteopathic physician in diagnosis and to assist the body in homeostasis. Splenic and liver pump techniques can release important hu moral and cellular agents into the circulation to assist the i mmune system . Non life-threatening causes of pelvic pain, such as dysmen orrhea, may be greatly helped by the addition of OMT to pa tient treatment. Im proved motion at the pelvic and thoracic di aphragms acutely decreases pelvic congestion, and these women would also greatly benefit from referral to an osteopath for longer term treatment. Treatment of the psoas would be beneficial in patients with primary muscle problems, as well as visceral problems causing somatic reaction. Treatment of the psoas should focus on release at both the origin and insertion. The psoas arises from the lateral aspect of T I 2 and the lumbar vertebra. l ts fascia th ickens to form the medial arcuate ligaments, a site of attachment for the diaphragmatic crura (46). The psoas continues its descent in the posterior abdominal wall; its fibers mesh with the il iacus muscle, which arises from the iliac fossa and lateral sacrum (46) . The iliacus and psoas converge deep to the i nguinal ligament and femoral vessels and i nsert into the anteromedia\ aspect of the fem u r (46) . Treatment with facilitated positional release (Chapter 64) , counterstrain, or muscle energy (Chapter 63) techniques can be particularly effective in this area. An i ndirect myofascial release method may also be used as follows: With the patient supine, the 1 2th rib/vertebral complex is carried inferiorly and slightly anteriorly. The i nsertion of the iliopsoas is then palpated at the lesser trochanter of the femur, j ust inferior to the inguinal ligament, which is usually a tender point for the patient. The hip
26
Osteopathic Medicine in the Practice ofEmergency Medicine
may then be flexed and slighrly externally rotated, or the m uscle simply released berween the treating hands ( H . Etrli nger, personal comm un ication ) . Patients with spasm of t h e piriformis m uscle a n d compression of the sciatic nerve often present with low back or buttock pain, but may complain of i nguinal, pelvic, or lower abdominal pain. Facilitated positional release (Chapter 64) is particularly useful in the emergency department because of its rapid result, bur if time al lows, counterstrain, muscle energy, or myofascial release techniques may also be employed.
397
6. The Economic B u rden of Musculoskeleral Complaints to the ER. National Cenrer for Healrh Srarisrics. Narional Ambulatory Medical Care Survey. Adanta: National Center for Healrh Srarisrics. 1 99 5 . 7 . Emergency visits for sporrs related inj uries. A n n Emerg Med. 200 I ; 37:3. 8 . Kuchera M L. Kuchera WA. Osteopathic Considerations in Systemic Dys
fimction. 2nd ed. Columbus. O H : G reyden Press; 1 994. 9 . Goroll AH, May LA. Mul ley
Jr
AG. Primary Care Medicine. Philadel
phia. PA: J B Lippincorr Co; 1 99 5 :328. 1 0. Tinr i nal l i . Emergency Medicine: A Comprehensive Stlidy Guide. New York: McGraw - H i l i ; 1 98 5 .
I I . Travell ) G , Si mmons D G . Myofoscial l'{/in and Dysfimction: A Trigger Point Manual. Baltimore: W i lliams & Wilkins; 1 983. 1 2. Psoas syndrome. I n : Ward R. ed. Foundationsfor Osteopathic Medicine. Balti more: Williams & Wilkins; 1 997.
SU MMARY
1 3 . Owens e. An Endocrine Interpretmion of Ch{/pman's Reflexes. American
We have described some of the important steps and dates in the history and development of the profession of allopathic and osteopathic EM. Important philosophical considerations i n the field of osteopathic emergency medicine have been discussed, and a number of theoretical and practical i nsights i n to the use of osteopathic principles and practices i n E M have been given. Several of the more important case scenarios i n EM have been presented, and concrete examples of how osteopathic principles and practices can be safely and effectively appl ied have been glven. The practices of osteopathy and EM are not inconsistent; in fact, they lend themselves very n icely ro a cooperation or syn thesis of assessment and treatment in the E D . Obviously, there are times in a busy ED when O M M cannot be appl ied as one would in an OMM practice. The specific osteopathic form of as sessment and treatment, including observation, skin assessment, palpatory structural exam i nation, referred pain patterns, facilita tion of spinal segments, assessment of abdominal col lateral gan glia, trigger points, tender points, ANS balance issues, lymphatic assessment and treatment tech niques, and the use of Chapman reflex points can significanrly help the osteopathic emergency physician in the diagnosis and treatment of the patient. The os teopathic treatment, given with the correct i ndication and ap plied in a genrle and respectful fashion, can and will, some times dramatically, im prove the patient's ability to self-regulate and achieve their most appropriate homeostatic level. These will often be applied as an adjunct measure in the E D and, when done correcrly, will assist i n significanrly decreasing the patient's morbidity.
1 4 . Malpractice suirs by category, "The Curring Edgc" Vital Statistics. The
Osreoparhic Association; 1 937.
Washington Post. 1 2 Seprember, 1 99 5 . 1 5 . Z i n k G . Lawson WB . An osreoparhic s rrucrural examinarion a n d func rional i n rerpreration of the soma. Osteopath Ann. 1 979; December. 1 6. Jones L . StrainlCounterstrain Tender Points. AAO; 1 96 1 . 1 7. American College of Emergency Physicians. C l i n ical Pol i cy for the I n i rial Approach to Adolescenrs and Adulrs Preseming to the Emergency Departmenr wirh a Chief Co mplaim of Headache. Ann Emerg Med. 1 996:6:. 1 8 . Shesser R. Headache caused by serious i l l ness. Evaluarion i n an cmer gency serring. Postgrad Med. 1 987; 8 1 :3. 1 9. Rosen P. Emergency Medicine. Concepts {/nd Clinical l'mctice. 4rh ed. Sr. Louis: Mosby-Year Book; 1 99 8. 20. Turbiak T. E ar Trauma. Emerg Med Clin North Am. 1 98 7 ; 5 : 2 . 2 1 . Garcia G E . Management of ocular emergencies and urgent eye problems.
Am Fam Physician. 1 996;53:2. 22. Melanson SW. C l i n ical pearls, headache and eye pa i n . Acad Emerg Med. 1 996;3 : 9 . 23. Frirz S. Foreign bodies of rhe exrernal audito ry canal . Emerg Med Clin
North Am. 1 98 7 ; 5 : 2 . 2 4 . Magoun H I . Osteopathy i n the CmniaL Field.
Ki rksville. MO: The
Journal Priming Company; 1 976. 25. Deleted i n page proofs. 26. Moore KL. Anatomy. 3rd ed. Was h i ngton. D.e.: Library or Congress; 1 98 5 . 2 7 . Hoyr W H . Osreopathic manipularion i n the trearmem of musclc conrraction headache. J Am Osteopath Assoc. 1 979;7 8 : 5 . 28. P i n ral W. An i nregrared osreoparhic rrearmenr i n acure o t i r i s media.
J Am Osteopath Assoc. 1 989;89. 29. Pran-Harringron D . Gal breath rech n ique: A manipulative rreatmenr for Otitis media revisited. J Am Osteop{/th Assoc. 2000; I 00.
30. Frank E Osteoparhic mani pularive rrearment applicarions for rhe emer gency department patienr. J A m Osteopatb Assoc. 1 996. 3 1 . Graig TJ . Srare of the an rherapy for s i n usitis. J Osteopath Assoc. 1 998. 3 2 . Digiovanna E. A n Osteopathic Approach to DiagrlOsis and Treatment. 2nd ed. Philadelphia. PA: Lippi ncorr-Raven Publishers; 1 997. 33. Ruddy TJ . Osreopathic rhyrhmic ducrion rherapy. I n : Barnes M W. ed. Yearbook ofAcademy ofApplied Osteop{/thy. I nd ianapolis. I N : AAO;
REFERENCES I . Vukich D. Emergency Medicine: Coming of Age. Jacksonville Medicine. March; 1 999. 2. American Board of Emergency Medicine. What is A B E M ? Available at: Imp:! I www. abem.org. Accessed 200 I . 3 . American Osreoparhic Board of Emergency Medicine. Available at: hrrp:! Iwww.aobem.org. Accessed 200 I . 4 . Centers for Disease Conrrol. The National Center for Health Staristics. Available at: hrrp:llwww.cdc.gov/nchs/. Accessed J uly. 200 I . 5. Paul F, Buser B. Osteoparhic manipularive rrearmenr applicarions fo r rhe emergency depanmenr patienr. J Am Osteopath Assoc. 1 996; 96(7 ) .
1 96 1 . 34. Heart D isease Risk Factors. Dallas: American Heart Associarion; 1 998. 35. Schwarz PJ , Srone H L. The role of the auronomic sysrem in suddcn coronary death. Ann N Y Acad Sci. 1 982;382. 36. Rosero H, et al. Correlarion of pal patory observarions wirh anaromic loclls of acure myocardial i nfarction. J Am Osteop{/th Assoc. 1 987; 87. 37. Rogers J1� Rogers J e . The role of osteoparhic mani pulative therapy in r h e trearment of coronary h ean disease. J Am Osteopath Assoc. 1 976; 76. 38. Beal Me. Viscerosomaric reA exes: a review. J Am Osteop{/th Assoc. 1 98 5 ; 8 5 . 39. Riley G W. Osteoparhic success i n r h c rrearmenr of i n A uenza a n d pneu monia. J Am Osteopath Assoc. 2000; I 00: 5 .
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Osteopathic Considerations in the Clinical Specialties
40. N o l l DR, Shores J H , Gamber RG, er a!. Benefirs of osreoparhic manip ularive rrearmem for hospital ized elderly parienrs wirh pneumonia. JAm
Osteopath Assoc. 2000; 1 00: 1 2 . 4 1 . Moore KL, Dalley AF. Clinically OrientedAnatomy, 4rh ed. Philadelphia: Lippi nco[[ Will iams & Wilkins; 1 999. 42. Cullison B, Emerman C. The clin ical challenge of acure asrhma: diagno sis, disposirion and o u rcome-effecrive managemem: Year 200 1 updare.
Emerg Med Rep, Am Health Consult. 200 I ;22: 1 1 . 43. Ciccone A, Allegra J R, Cochrane D G , er al. Age-relared djfferences
in d i agnosis wirhin rhe elderly pOPlllarion. Am J Emerg Med 1 998; 1 6. 44. Gold M , Azevedo D. The comem of adulr primary care episodes. Public
Health Rep. 1 982;97. 45. Bessen HA. Abdominal aorric aneurysms i n emergency medicine. Rosen, Barkjn, eds. Emergency Medicine: Concepts and Clinical Practice, 4rh ed. Sf. Louis: Mosby-Year Book, 1 998. 46. Clemenre CD. Anatomy: A Regional Atlas of the Human Body, 3rd ed. Balrimore, M D : Urban & Schwarzenberg; 1 987. Fig 225.
GENERAL SURGE.RY CONSTANCE CASHEN SYDNEY P. ROSS
KEY CONCEPTS • • • • • • •
Foundations of osteopathic concept in surgery Osteopathic principles in abdominal and chest wall surgery The relationship of neuroanatomy and pathophysiology in the evaluation of acute abdominal pain Diagnosis of the most com m on causes of acute abdominal pain requiring surgical treatment Management of postoperative complications using osteopathic meth ods Somatic dysfunction and the alimentary tract The use of osteopathic manipulative treatment as an adjunct in the prevention and treatment of postoperative i leus and atelectasis
One chapter representing the field of general surgery is necessarily selective; therefore, this chapter will provide a brief review of the development of general surgery as a discipline in osteopathic medicine. It will then focus on the essential area of diagnosis and treatment in general surgery, the acute abdomen, taking an integrative view to highlight relevant osteopathic concepts. The practice of surgery is almost as old as humanity. With the use of tOols, Neolithic men and women became craftspeople. They might have also used implements for surgical purposes, be cause examples of trepanation ( removal of a segment of bone from the skull) have been discovered in France dating to the Neolithic period. Signs that skull wounds healed indicate that a fair propor tion survived the operation ( 1 ) . Surgical procedures were highly devel oped among some of the pre-Columbian peoples. Wounds were cleaned and closed with an asrringent vegetable concoc tion or egg substances from diverse birds and then covered with feathers or bandages made of ski n. A mong the Incas and other pre-Columbian peoples, the surgeon was often a separate prac titioner who looked after wounds and performed bloodletting and other lesser surgical procedures (2). The ancient Egyptians employed cauterization and the fi re drill as surgical tOols. They made a type of adhesive tape by impregnating gums into linen strips used to pull gaping wounds together (3).
I n the early years of the 1 9th century, the principal therapies open to European and American physicians were general regi mens of: Diet Exercise Rest Baths and massage B loodlening Scari fication Cupping Blistering Sweati ng Emetics Purges Enemas Fumigations Many plant and m i neral drugs were available, but only a few rested on sound physiologic or even empirical fou ndati ons. For the m ost pan, practiti oners permined illnesses to run their course wirhout i nterference; careful observers noted little benefit from the therapies avai lable. When anesthesia became com mon place and the limi tations of pai n disappeared, surgical procedu res multiplied in number and complexity. The potential benefits of surgery were overshadowed, h owever, by the frequent, devastating infections that often resulted in death. Only when the bacterial origi n of infectious disease was discovered and the necessity for keeping germs away from the operative field was proved (notably by Lister) could surgery safely enter the i nterior regions of the body ( 4) . Surgery has been i ncluded i n the training of osteopathic physi cians since the fi rst school of osteopathy opened in 1 892. And rew Taylor Still addressed the field of surgery and reAected appropri ate concern regarding this training in the fol lowing statement from 1 90 1 : How much surgery should be raughr in an osreoparhic school is a very imporranr inquiry, and should be answered posirively ro rhe poinr. We claim under our chaner
ro
reach surgery, and if we fail
ro reach rhar branch we have nor lived up have failed ro honor our obligarion
ro
ro
our promise, and we
rhe srudenr. We have a chair of
surgery filled by a professor whose learning and pracrice have made him an able judge of rhe imporrance of rhis branch. In answer
ro
400
VI. Osteopathic Considerations in the Clinical Specialties
how much surgery the Osteopath should have taught ro him we will
thoroughly trained in the preoperative and posroperative care of sur
say, that he should be armed with a general knowledge of operative
gical patienrs, as well as in the technical performance of surgery. These
surgery ro the degree that the physician when in ordinary practice
principles of general surgery are the basis of all the surgical subspecial
will always be ready and sensibly qualified ro meet all emergencies in
ties. The core areas include surgery of the abdominal wall, alimentary
common practice; such as serring dislocated shoulders, elbows, wrists
rract, breast, endocrine organs, and trauma. In addition, the general
and fingers, the hip, knee, ankle, foot, and bone or bones of the arm
surgeon has knowledge and experience in gynecologic, oncologic, or
and leg. He should know how ro adjust fractured ribs and bandage
thopedic, pediatric, peripheral vascular, plastic, and urologic surgery.
the body ro keep such fractures in place unril the bones unite. He
The general surgeon is also trained and experienced in the manage
should be taught to explore and note all dislocations of the spine
menr of the critically ill patient with multiple organ system failure
from the head
the coccyx; and how ro adjust and keep in place
including but not limited ro cardiopulmonary resuscitation, nutr'i
the many divisions of the spine, the neck, the dorsal, the lumbar, the
tional suppOrt, endoscopic procedures, management of sepsis, and
ro
sacrum, and the innominates. He should be and is taught ro do all
coagulopathies. A comprehensive training (residency) is the basis for
operative surgery, with or withour council, that is generally done in
this definition (7).
small villages and in rhe counrry; such as amputations of a roe, a foot, a leg, or thigh. How ro operate to relieve watery and other deposits of the abdomen and the chest. To remove external growths that appear upon the body at any place, that is done by the ordinary surgeon in general practice. Then in obstetrics we teach thoroughly and impress good training in the use of instrumenrs in that branch of practice, as we wish him particularly trained for the responsible duties that an hour may throw on him. We teach the use and the administration of anesthetics, and how ro proceed in gunshot, knife, saw, and other wounds. In short, our school is prepared and inrended ro qualifY its graduates when called in council or ro lead that they may have the necessary information at that time so they will not be handicapped nor embarrassed (5).
The field of surgery advanced considerably in the ensuing decades and as the osteopathic profession grew, so did the surgical exper tise of i ts physicians. On January 26, 1 927, the American College of Osteopathic Surgeons (ACOS) was i ncorporated as a not for-profit corporation. The ACOS was founded to provide and maintain standards of excellence in the practice of surgery and i ts training programs. Until then, osteopathic physicians were almost exclusively primary care physicians. Though many had skills i n sururing wounds or perform i ng m i nor surgical procedures, those that desi red specialry training in surgery either became an ap prentice to an American surgeon who was trained in E urope, or went to Europe to obtain further training. The establishment of the ACOS enabled them to receive h i gh-qualiry surgical training in America. The founding members of ACOS wanted to i ncor porate osteopathic concepts i nto the practice of surgery. They all believed that Still's teachi ngs improved the care of surgical patients. Surgery is usually defined as that branch of medicine that treats d iseases, inj uries, and deformities by manual or operative methods (6) . Using this definition, no branch of the healing arts owns surgery. No surgical incision or procedure can be called os teopathic or allopathic. Sociery at large does not ask for a political definition of surgery but rather accepts it as a medical practice based on the sciences of anatomy and physiology. There is no os teopathic surgery; however, there are osteopathic physicians who are trained in surgical disciplines and perform surgical procedures within the context of osteopathic medicine. [n 1 983, the Board of Governors o f the American College of Osteopathic Surgeons approved the following definition of general surgery: General Surgery is a specialty that encompasses a wide field of prac tice. It requires cognitive and procedural skills for rreating a broad variety of diseases, injuries, and deformities. General surgeons are
The application of osteopathic philosophy in the practice of gen eral surgery is evident in i ts critical understanding of the anatomy of each organ system and how aberrations result in the pathologic function that we recognize as common surgical disease. It follows that the purpose of surgery is to set the stage for the body to heal i tself by structurally (surgically) altering or removing the source of pathologic function. The approach to the patient as a "whole" recognizes the i m pact of other organ system disease, as well as psychosocial factors on the presentation and treatment response of the patient. The osteopathic surgeon has been trained in a standardized residency program in which these precepts provide a critical perspective on patient management which encompasses the preoperative and postoperative care of the patient, as well as the application of surgical technique. As stated, although general surgery covers a wide range of dis eases, this chapter will focus on pathologic conditions that cause acute abdominal pain in which surgical treatment has been shown to provide the best o utcomes. The discussion wi ll include a re view of the neuroanatomy of abdominal pain and the pathophys iology of specific disease processes. It will focus on four diseases, namely: appendicitis, cholecystitis, diverticulitis, and small bowel obstruction. Finally, the prevention and treatment of several post operative complications will be considered from an osteopathic poi nt of view.
O S T EOPATHIC EVALUATION AND TREAT M E N T O F T H E PAT I E N T WITH ACUTE ABD O M I NAL PAI N
Acute abdominal pain is t h e most common reason that the gen eral surgeon will be called to the emergency department. An understanding of the presentation of acute abdominal pain re quires a critical appreciation of the neuroanatomy of nociception. Acute abdominal pain is both a somatic (peripheral nervous sys tem) and visceral (autonomic nervous system) phenomenon. A brief review of the neuroanatomy of abdominal viscera indicates that it is pri marily the autonomic nervous system that allows for the selective recognition of noxious stimuli, such as stretch, dis tention, infla mmation, and ischemia. Other damaging stimuli, such as cutting or burning, cannot be perceived by abdominal organs. The autonomic nervo us system is com posed of rwo divisions: the sympathetic nervous system and the parasympathetic ner vous system. Their end-organ effects are generally opposing and
2 7. Genera! Surgery
therefore provide adaptive balance ro organ responses. The affer enr nerves for nociception tend to follow along the same p ath ways as the sympathetic nervous system but are not specifically identified as either sympathetic or parasympathetic but simply as "vi sceral afferenrs." The autonomic nervous system is composed of a rich network of fibers that extends from the limbic structures of the brain through the spinal cord and cranial nerves to innervate most tissues and control organ functions. It is generally associated with non-volitional body processes. I n the abdomen, the sympatheti c componenr is conrributed by the thoracic, lumbar, and pelvic splanchnic nerves, and the parasympathetic by the paired vagus nerves arising from the tenrh cranial nuclei of the brainstem and the sacral splanchnic nerves arising from S2-4. The sympathetic nervous system begins as cell bodies in the lateral horns of spinal segmenrs TI-L2 with axon s extending through the venrral roots ro the paravertebral gangl i a. These paired lines of i nrerconnected ganglia l ie along each side of the spinal cord like two strings of pearls. The axons, al so called pre ganglionic fibers, converge to form the greater splanch n i c (T5-9), lesser splanchnic (T 1 0- 1 1 ) , and least splanch n i c (T 1 2) nerves. The final desti nation of the splanchni c nerves is the prevertebral gangli a ( celiac, superior mesenreric, inferior mesenreric) . From here, postganglionic sympathetic fibers travel to their target or gans. (Please see Chapter 6, Autonomic Nervous System, for a full discussion and multiple figures depicting these pathways.) The parasympathetic innervation structure i s more stream lined. Long, preganglionic axons from the vagus nerves extend through the prevertebraI ganglia as they pass directly to the vis cera. Their short, postganglion ic fibers form parr of the network in the visceral wall called the enreric nervous system. Both the sympathetic and parasympathetic nerves exert their effects through the enteric nervous system. This network offibers is composed oftwO layers. The outer myenreric (Auerbach) plexus controls gastroinrestin al motili ty. The inner plexus ( Meissner) controls gastroin restin al secretion and local blood flow. Percep tion of nociceptive stimuli results in alterations in gut fun ction mediated at th is level. For example, m arked reduction in gut motility-ileus-commonly occurs in perito n i ti s. The visceral afferenr system for nociception l argely follows along the pathway of the autonom ic (efferenr) nervous system described above. The axons of these nerves (first-order) originate in the mucosa and wall of a viscus. Transmi ssion extends along fibers that pass, without synapsing, through the prevertebral and paravertebral ganglia to the dorsal root gangli a where their cell bodies l ie. These neurons extend to synapse in the dorsal horn of the spi n al cord. The second-order neurons cross to the con tralateral spinothalamic and spinoreticular tracts to ascend to the thalamus and pons/medulla, respectively. From here, thi rd-order neurons carry information to the somatosensory cortex causing the conscious perception of pain ( spinoth al am i c pathway), as well as to the limbic system and fronral cortex causing the aversive re sponse to pain (spinoreticular pathway). Specific aspects of this anatomy explain why visceral pain is initially perceived as vague in location and quality. I t is generally described as aching in nature, rather than sharp or i n tense, and is perceived as originating in the one of three midline regions
401
versus a d iscrete uni lateral location. Th i s relates partly to the paucity of visceral afferenrs compared with the l arge n umber of som atic afferenrs originating in skin and m usculoskeletal struc tures. Equally imporranr i s that the tran smission of vi sceral pain occurs via slow nonmyelinated C fibers versus the fast conducting A-o fibers that transmi t somatic pain. Finally, the i n itial location of pain as regional versus specific relates to the embryologic developmenr of abdominal vi scera as m idline structures with midline neurovascular supply. They di vide i n to foregut (T5-9) , midgut (TS-ll) , and hindgur (T ll-LJ) areas. Foregut structures i n clude the distal esophagus, stom ach, and the proxi m al d uoden um, as well as the liver, biliary tree, and pancreas. M idgut structures i ncl ude the small intestine, appendix, ascending colon, and proximal two-thirds of the tran sverse colon. The h indgut incl udes the distal third of the transverse colon, the descending colon, and the rectosigmoid. They are loosely associ ated with the cel i ac, superior mesenreric, and inferior mesenreric ganglia, respectively. Thus, in general, pain from structures inner vated at these levels will be perceived as occurring in the epigastric, periumbilical, or hypogastric m idline areas, respectively. The somatic component of acute abdominal pain i s caused by the parietal peritoniti s that occurs adjacenr to the involved viscera as i n fl am m ation progresses. Also referred to as the "percutaneous reflex of Morley," it is conducted by A-o fibers following the associated dermatome to unilateral spinal segmenrs, which results in the localization and increasing i n tensity of acute abdom inal pai n , as �ell as the increased m uscle tone of the abdominal wall associated with guardi ng and rebound tenderness. The third component of acute abdominal pain, known as re ferred pain, is a clear example of how structure determ ines func tion. Referred pai n i s defined as discomfort occurring in a si te distant from the diseased viscus. The explanation of referred pain lies in the i nrricacies of the neuroanatomy previously described. The spinothalam i c tract is largely nondiscrim i n atory for visceral versus som atic pain. Because somatic nervous input far exceeds visceral, the central nervous system (CNS) is "fooled" and per ceives the pain as originating partly in the peripheral structures innervated by the same spinal segments as the diseased vi scus. For example, the pain ini tiated by gallbladder inflam m ation (T7-S visceral afferent i nnervation) is perceived as occurring in the right subscapular area (T7-S som atic afferent innervation). In a sim il ar m an ner, visceral afferents syn apse on interneu ron s in the spi n al cord that stim ulate somatic efferent neurons at the same level. Thi s local reflex activity i s referred to as a vis cerosomatic reflex. I t results i n somatosensory changes palpable in a paraspinal location as tissue tenderness, asymmetry, range of motion restriction, and ti ssue texture changes (TART). The find ing of specific somatic dysfunction i n a patient with acute ab domi n al pain can provide useful information as to the origin of the pain. The p araspinal location should direct one to con sider organs known to h ave sympathetic i n nervation at the same level, resulting from the fact that visceral afferents that trigger vis cerosomatic reflexes predictably follow the sympathetic efferent p athways. (See Section VIII, Chapter 4S, Thoracic Region, for organ innervation identification.) With this d iscussion of nociceptive anatomy as a backdrop, consider the more cli n ical aspects of acute abdominal pai n. A s stated previously, acute abdominal pain i s the most common
402
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reason for urgent surgical consultation. Four of the most common causes include acute appendicitis, acute cholecystitis, diverticuli tis, and small bowel obstruction. These entities share common mechanisms of pathophysiology. To appreciate the evolution of symptom s and physical signs, understanding these mechanism s is essential. In each of these diseases, the initiating factor is the obstruc tion of a hollow viscus or duct structure. Thi s results in luminal distention and stasis of organ contents. Because venous and lym phatic supply form l ow-pressure nerworks, the increasing back pressure causes obstruction of these outflow nerworks resulting in organ wall edema. Th i s progresses to arterial inflow obstruc tion and ischemia. "The law of the artery is supreme"-ischemia leads to wall gangrene, perforation, and peritonitis. Because the gastroi ntestinal tract is colonized with varying levels and rypes of bacteria, the stasis described above causes bac terial overgrowth. Transmural infection of the comprom i sed vis cus results and contributes to the peritonitis caused by gangrene and perforation. Bacterial liberation of endotoxins and the release of inflammatory mediators result in the systemic septic response. Left un treated, the systemic inflammatory response syndrome of multiple organ failure occurs with h igh levels of co-morbidiry and mortal iry. We will consider some individual case studies, reviewing his toric and physical fi ndings, laboratory and imaging studies, and principles of treatment. Case One
A 28 -year-old African -American male presents to the emergency department ( E D) with progressive abdominal pain occurring over the last 8 h ours. Previ ously well, he n oticed mild pain in the peri umbil ical area that became ptogressively worse, was unrel ieved by antacids, and is now more intense and focused in the right lower quadrant (RiQ). He has eaten no unusual foods, but i s nauseated and has vomi ted once since admission to the ED. H e den ies uri nary complaints. Previ ous medical h i story i s negative. He is married and works as a bank teller. Physical exam ination reveal s a temperature of 99.8° F, pulse of 95 beats/m in and blood pressure ( B P) of 1 1 0/70. Neurologic, cardiovascular, and pulmonary exam ination s are negative. Abdom inal exami nation demon strates a nondi stended ab domen wi th decreased bowel sounds. Light palpation reveals cutaneous hypesthesia in the TIO- 1 2 dermatome on the right. Tenderness at McBurney point and localized rebound are n oted. Rovsing, psoas, and obturator signs are positive. Rectal examina tion is negative and no inguinal hernias are appreciated. Struc tural exami nation reveals tissue texture changes and tenderness at TII-1 2 on the right, and right rib 1 2 tip tenderness. CBC shows a leukocytosis of 1 3 ,000/mm 3. Urinalysis and acute abdominal series are negative. What differential diagnoses are suggested by this clinical pic ture? Does the testing verify the likely cause? The temporal pattern and qualiry of the pain provide impor tant clues. As stated previously, the visceral component of acute abdominal pain cau ses i n i tial vague discomfort pointing to an organ derived from one of th ree embryologic gut segments based on neurovascular supply. I n this case, the periumbilical location
suggests an organ supplied by the superior mesenteric vasculature and ganglion (small bowel, right colon, appendix) . The subsequent somatic component localizes the pain, sug gesting the right lower quadrant position of the appendix. I n particular, McBurney point tenderness (located one-third of the distance from the anterior superior iliac spine to the umbilicus) reveals the localized peritonitis of progressive appendicitis. Rovs i ng sign (palpatory pressure of the left lower quadrant causing RLQ pain), a positive psoas sign ( RLQ pain with straight-leg raising on the right), and obturator sign ( RLQ pain with passive internal rotation of the flexed right thigh) confirm the peritoneal irritation. Somatosensory structural fi ndi ngs are consistent with the in nervation level of the appendix ( T l l - 1 2) , and other associated symptom s (e.g., nausea and vomi ting foll owing the occurrence of pain) strengthen the diagnosis. The l i st of differential diagnoses for appendicitis is long and is well presented in standard surgical textbooks (al so, see Emergency Medicine, Chapter 26). H i story and physical examination are the cornerstones of confirming or discarding this diagnosis, but certain tests that strengthen the clin ical impression are generally obtained. Leukocytosis of 1 0,000 to 1 8,000 per mm 3 with a left shift is common but n ot absolute. Other laboratory studies, such as urinalysi s, liver function studies, and amylase, may be obtained if the clinical picture is unclear. Elevated C-reactive protein with neutrophilia substantiates the diagnosis. I maging studies are useful in equivocal cases, especially with pediatric, older patients, and some female patients. Plain films of the abdomen are generally nonspecific, but may reveal an isolated loop of adjacent small bowel ("senti nel l oop") or an appendicolith ( l 0% to 20%) . Ultrasound showing a noncompressible appendix is diagnostic in about 90% of cases. Computerized tomography (CT) changes, including a dilated appendix and/or periappen diceal/cecal inflammati on or mass, are 90% to 1 00% sensitive and 95% specific for appendicitis. A strong clinical picture ob viates the need for these studies and they should n ot be ordered on a routine basis. Appendicitis remains the most common surgical emergency, affecting 7% of the population, both male and female, and peak ing berween ages 1 0 to 30. Treatment is straightforward and con sists of appendectomy, performed laparoscopically or via open technique. Preoperative antibiotic coverage for the usual bacteria in this area (Gram-negative aerobes, such as Escherichia coli and Klebsiella, and Gram-posi tive aerobes, such as Streptococcus fae calis, and anaerobes, specifically Bacteroides fragilis) is routine. Recovery is generally rapid (discharge in 24 to 48 hours) but may be delayed in cases of perforation and abscess. Case Two
A 44-year-old H i spanic female presents with complaints of upper abdominal pain, nausea, and vomiti ng. She states the pain started last evening after a fast food meal. It began in the epigastric region, accompanied by bloating. Because she has suffered similar mild "indigestion " recently, she generally avoids fried foods. She took an over-the-counter H -2 blocker and went to bed only to
27. General Surgery
be awakened by progressively severe upper quadrant abdo m inal pain, which was continuous and radiated to the right shoulder and subscapular area. She is a multi parous female with a positive family history of gallstones in two sisters and her mother. She works as a school counselor and "watches her diet" because she is mildly overweight. Her h istory is otherwise negative. Physical exami nation reveals a healthy-appearing female i n moderate distress from abdominal pain. She i n termittently changes position and grips her right subcostal area. Vital signs show a temperature of 1 00. 1 0 F, pulse of 1 10 beats/min and BP of 1 40/8 5 . Neurologic and cardiopulmonary examinations are negative. Abdominal examination reveals a rounded abdomen, which is silent on auscultation. Palpation confirms acute tenderness in the right upper quadrant (RUQ) with a palpable fullness and posi tive Murphy's sign (inspiratory arrest with RUQ palpation). TART changes at T7-9 on the right, and tenderness over the medial right seventh intercostal space (Chapman reflex) are noted. Laboratory studies show a moderate leukocytosis of 1 5 ,000. Bilirubin, alkaline phosphatase, serum glutamic-oxaloacetic tra nsaminase (SCOT) , and amylase are mildly elevated. U ltrasound confirms gallstones with a thickened gallbladder wall (greater than 4 mm). H IDA scan indicates cystic duct ob struction with nonfilling of the gallbladder after 4 hours. This patient presents with the classic p icture of acute calculus cholecysti tis. Her symptoms are di rectly correlative to the patho physiology of this disease. The early onset of epigastric pain is consistent with the gall bladder's foregu t origin. Due to cystic duct obstruction b y the offending calculus, mucus hypersecretion ensues, causi ng pro gressive gallbladder distention. Increasing wall tension results in small-vessel ischemia and wall edema. The other critical mech anism involves the toxic effects of altered, supersaturated bile (lysolethicin and platelet-activating factor are thought to be i n volved) i n patients with cholelithiasis. The resultant inflammation of the adjacent subcostal peri toneum (in nervated by T7-.8) explains the progression of clinical findings, i.e., focused RU Q pain and tenderness and the posi tive Murphy's sign. The referred pain pattern of the right subscapular area (T7-8) and shoulder (C4), as well as the viscerosomatic reflex changes at T7-9 on the right, are predictable based on the noci ceptive anatomy of the biliary system and adjacent diaphragmatic surface ( innervated by the phrenic nerve, C4) . Laboratory and imaging studies are toutinely ordered to con firm the diagnosis. The pattern of findings discussed above is typi cal. Ultrasound accuracy exceeds 95% in detecting cholelithiasis; hence, it is the study of choice to confirm the d iagnosis. A pos i tive ultrasound and consistent clin ical picture generally obviate the need for a H IDA scan, but its accuracy (greater than 90%) is excellent and it is useful i f the impression of acute versus chronic cholecystitis or other acute disease is unclear. CT is also used i f the diagnosis i s equivocal, because i t can demonstrate gallbladder distention, wall thickening, and pericholecystic fl uid, though not with the accuracy of ultrasound. About 20% of patients with symptomatic cholelith i asis will develop acute cholecysti tis. Females exceed males three to one in the development of gall stones, though this drops by half above
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age 50. Other risk factors i nclude obesity, multiparity, and a posi tive family h istory of gallstones. The indicated therapy for acure calculus cholecystitis is chole cystectomy. Treatment has h istorically questioned the value of early (wi th i n 48 to 72 hours) versus delayed surgery (medical treatment to resolve the acute episode with an "interval" chole cystectomy in 6 to 8 weeks). With the increasing expertise in laparoscopic cholecystectomy (the preferred surgical technique), the early approach is favored. Conversion to an open procedure is i ncreased in cases of perforation, abscess, or extreme edema. Antibiotic coverage for typical gut pathogens is routine, but cultures o f the bile are frequently negative. Uncomplicated acute cholecystitis treated in this manner gen erally results in rapi d recovery and discharge in 24 to 48 hours. Complicated disease (perforation, abscess, emphysematous cholecystitis) or severe co-morbid disease can be approached with vigorous medical therapy with or without cholecystostomy (drainage of the gallbladder) , and eventual cholecystectomy when the patient's medical condition perm i ts. Case Three
A 50-year-old white female is evaluated for diffuse abdomi nal pain and bloating that began 2 days ago. She s tates it began as i nterm i ttent cramping pain with nausea and two episodes of diar rhea. She thought i twas the flu. H owever, the colicky pain became more continuous and was accompanied by recurrent episodes of vom i ti ng, initially described as bilious but now feculent. She has had no further stools and her abdomen is "swelling. " Her past h istory is posi tive for a hysterectomy 6 months ago and for anemia due to recurrent u terine bleeding from uterine fibroids. She is an accountant who recently moved her office to a new location and was consequently moving heavy boxes. Based on the history, what aspects of the physical examina tion would corroborate a diagnostic i mpression o f small bowel obstruction? On examination, vital signs are stable, but she is obviously uncomfortable. Inspection o f the abdomen confirms moderate distention. Bowel sounds are h igh-p i tched and peristaltic rushes are heard. Palpation reveals generalized tenderness with minimal rebound in the mid to lower abdomen. A lower midline surgical scar is evident. No hernias or abdominal masses are appreciated. Pelvic and rectal examinations reveal no masses. Structural exam i nation demons trates paraspinal muscle spasm and tenderness at T8- 1 0 bilaterally. Laboratory studies i nclude complete blood cell count (CBC), basic chemistry profile, and urinalysis. A mild leukocytosis, and elevated blood urea nitrogen (BUN) and urine specific gravity are noted. Serum potassium is sligh tly decreased. Amylase is normal. An acute abdomi n al radiograph series is performed. Findings include d ilation of the small bowel, absence of gas in colon and rectum , and multi ple air-fluid levels in a "stairstep" pattern. CT scan is negative for free air but confi rms a small bowel obstruction wi th djlated, slightly thickened loops of s mall bowel. These findings are consistent with acute mechanical small bowel obstruction. The most l i kely cause is postoperative ad hesions (up to 70%) from the prior hysterectomy. Hernias and neoplasm are next i n frequency for causing obstruction.
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The ch aracteristic d iffuse panern of pain indicates a promi nent visceral component of nociception in most patients pre senting with small bowel obstruction. Development of more localized continuous pai n with prominent somatic signs (e.g, rebound, guardi ng, and rigidity) signal the development of i s chemia and gangrene at the si te of obstruction. Fever and leuko cyto sis strengthen this possibility and mandate early surgical i n tervention. Still, it should b e noted that none of these signs either alone or in combination can absolutely identify strangu lated bowel. Metabol ic acidosis and hyperamylasemia also suggest comprom i sed bowel. Fluid and electrolyte abnormalities are common. Dehydra tion, as evidenced by elevated BUN and urine specific gravi ty, occurs due to Auid losses through vom i ting and sequestration i n the obstructed bowel loops. Nasogastric suction to decompress the bowel and repletion of the Auid and electrolyte losses i s crit
o f 8 0 beats/mi n and a temperature of 1 0 1 0 F. Cardiopulmonary examination i s noncontributory. Abdominal examination demonstrates mild distention. A RLQ scar i s evident. Bowel sounds are present but diminished. M arked localized tenderness in the LLQ is present with a palpable m ass. Rebound tenderness and guarding are noted in thi s area. M ild tenderness is present in the RLQ and left upper quadrant (LUQ) . Some left flank concussion tenderness is noted. Rectal ex ami nation demonstrates a non nodular, slightly enlarged prostate, no rectal m asses, and a borderline positive hemoccult study. Structural exami nation reveals increased tissue texture changes with tenderness in the LJ-2 level on the left. Tenderness is al so noted along the superior th ird of the ilio tibial band of the left leg-the area of Chapman reAex for the sigmoid colon. Laboratory studies demonstrate a leukocytosis of 1 8,000. Electrolyte and chemistry profiles are wi thin normal limits. Acute
ic.aL Sur,?,ery is often delayed for several hours in c.ases of severe
abdominal series is \'lerfotmed. findin'?,s of mild, nons\'lecihc
volume depletion until vi tal signs and urine output are improved. Antibiotic coverage of gut bacteria is given perioperatively i n cases o f si mple mechanical obstruction requ i ring surgery. Patients showing signs of incomplete obstruction, such as small amounts of colonic air on abdominal film s or contrast p ass ing slowly into the colon on CT scan , are treated with n asogastric decompression and observation. Up to 80% will resolve sponta neously, with obvious improvement in 24 to 48 hours. Operative treatment of small bowel obstruction includes re lease of the obstructing element (e.g., adhesive band, hern i a en trapment , resection, or bypass of neoplasm). Judging viability of an ischemic portion of bowel requires experience, but can be as si sted by Doppler studies and Auorescein staini ng. Resection of all nonviable bowel is mandatory. If question remains, a second-look operation in 24 hours should be performed. With these strategies, the morbidity and mortal i ty h istorically associated with small bowel obstruction h ave been markedly de creased. Con tin ued efforts to prevent further adhesion formation, such as the appl ication of barrier agen ts (such as a bioresorbable membrane), will be the key to reducing the i ncidence of small bowel obstruction in the future.
small bowel distention are noted. Gas i s seen in the colon. The psoas stripe on the left i s obscured. No free air is evident. CT scan demonstrates marked i nAammatory change in the sigmoid colon with a pericolic abscess. Thi s patient presents with acute perforated diverticulitis, a complication of diverticulosis. Diverticulosi s affects greater than 50% of people over the age of 60, and 75% by age 8 5 . Fortunately, only about 1 0% to 25% will develop diverticulitis. The cause of diverticulosis is rel ated to the American low-fiber diet ( 1 0 to 1 5 grams per day), which creates firm stool that re quires high colonic pressure to propel. Thi s particularly affects the sigmoid colon with its intrinsically smaller lumen. Contin ued con traction again st firm stool promotes circular muscle hy pertrophy, which causes further luminal narrowing. The law of Laplace predicts that tran smural pressure increases as the radius of a cylinder decreases, so the weak points of the colonic wall, where nutrient vessels penetrate, develop the small herniations of mucosa and muscularis that we call diverticulosi s. Obstruction of the neck of the diverticulum by inspissated feces with resultant i schem ia and perforation leads to varying degrees of pericolonic inAammation and abscess. This spreading process can result in a reflex ileus or entrap adj acent smail bowel ( 1 0% to 30%) and cause obstruction . In either case, nausea and vom i ting resul t. Erosion into the bladder or vagina, causing fistu las (5% to 1 0%) is a long-term sequelae that causes pneumaturia and chronic infection. Evaluation of diverticulitis routinely involves CT scan, which is 90% to 9 5% sensitive and greater than 70% speci fic. Barium enema and colonoscopy should not be performed due to the risk of perforation. The H inche classification of clinical progression of divertic uliti s is helpful in planning treatment. Stage I (pericolonic in Aammation) often responds to medical therapy ( 70% to 80%), i .e., intravenous antibiotics to cover normal colonic bacteria, hy dration, and bowel rest. Iffever, leukocytosis, and LLQ pai n do not improve within 24 to 48 hours, surgery i s indicated. Sigmoid resection with primary anastomosi s i s possible in contained disease. Otherwise, the use of resection with end colostomy and closure of the rectal stump ( H artmann procedure) is performed. This "two-stage" procedure requires repeat laparotomy in 6 to 1 2 weeks for reanastomosis of the colon.
Case Four
A 70-year-old wh ite male is seen after presenting with lower ab dominal pai n, which began 4 days ago and is primarily i n the LLQ with radiation to the left lumbar area. The patient has not suffered from n ausea or vomiting, but h as no appetite and some fever and chills. He has been constipated for the l ast 3 days and states that he usually h as a bowel movement every 2 days. He de nies any rectal bleeding. He has had somewhat sim i l ar symptoms on one or two occasions in the past, but fel t that thi s was simply due to con stipation. He has no urinary tract complai n ts. Hi s history i s positive for mild hypertension, for which he takes a .B-blocker. He underwent an appendectomy at age 1 6. Medical hi story i s otherwise negative. He i s retired and lives with his wife. I f th i s patient were seen in the physician's office, what physical findings would prompt you to consider hospi talization? Exam ination of the patient demonstrates a well-nourished, well-developed 70-year-o ld white male with noticeable abdomi nal discomfort. Vi tal signs show a blood pressure of 1 52/8 7, pulse
27. General Surgery
Stage 2 (pericolic abscess) may be drained with CT-guided as piration and then treated as stage 1 disease if the abscess collection is accessible (70% to 90%). Otherwise, a Hartmann ptocedure is required. Stage 3 (generalized purulent periton itis) , and stage 4 (fecal peritonitis) are rou tinely treated with a H artmann procedure.
MANAG EMENT OF POSTOP E RATIVE COMPLI CATION S Ate lectasis
Major surgical procedures that involve the abdominal wall have a relatively h igh morbidity. Table 27. 1 lists the serious complica tions that can occur after a variety of major surgical procedures. Sabiston (8) stated that pulmonary complications can occur in 5 7 o f all major surgeries performed with general anesthesia. The i n cidence o f compl ications can double in abdominal surgery, triple for smokers, and quadruple for patients with chronic obstruc tive pulmonary disease. Atelectasis, a collapse of alveol i that ren ders them unable to be involved in gas exchange, is the most frequent pulmonary complication after surgery. This compli cation general ly sets the framework for subsequent pulmonary infections. In considering the problem of atelectasis, an appreciation of respiratory mechanics after abdominal surgery is required. Res pi ratory motion depends full diaphragmatic excursion, as well as unencumbered rib motion (see Chapter 49, Regional Exami na tion and Treatment: Rib Cage, for detailed discussion) . Unfortu nately, the natural response of the patient wi th incisional pain is abdominal wall splint ing and shallow breath ing, which increases the risk for this complication . Without this pumping action, full alveolar expansion, especially in the lung bases, does not occuI'. Because oxygen exchange in these areas is greatly dimin ished, an environment is created that encourages the development of pneumonia (a dreaded postoperative complication that inevi tably lengthens hospital stay and can precipitate other organ dysfunc tion in vulnerable patients). I n the United States, an incentive spirometer is the most popular mechanical method used for preven tion of postopera-
TABLE 27 . 1 . POSTOPERATIVE COMPLICATIONS OF MAJOR SURGICAL PROCE DURES W o u n d i n fections Intraabdominal sepsis (peritonitis) Subphrenic and s u bhepatic abscess Empyema Mediastinitis Pneumonia Acute respi ratory i nsufficiency [ i nc l u d i n g adult respi ratory d istress syndrome (ARDS)1 Renal f a i l ure Postoperative j a u nd i ce Postoperative i leus Bowel obstruction Acute gastric hemorrhage M u lt i p l e organ f a i l u re Myocard i a l infarction
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tive atelectasis. [t is used extensively because it encourages deep breath ing and requires minimal supervision and personnel to ad minister (9, 1 0) . The beneficial effects of incentive spirometry in the prevention of postoperative complications have recently been challenged, however ( 1 1 ,12 ) , because changing the angle of the patient's recumbency from 60 to 30 altered the effectiveness of postoperative incentive spirometry. This finding suggests features other than just lung mechanics involving the major ai rways. One suggestion for the alteration in ai rflow with a change in recum bency is fluctuating diaph ragmatic motion ( 1 3) . I n the presence ofdiaphragmatic dysfunction, incentive spirometry can have little effect on improving gas exchange. The change in recumbency an gie alone is bel ieved to result in an i mproved diaphragmatic link tension relationship and a shift i n compartment compliance as the patient reclines ( 1 4, 1 5 ) . The earliest osteopathic physicians incorporated their under standing of viscerosomatic and somatovisceral reflexes into their management of patients in the postoperative period. The visceral motor, visceral sensory, and visceral tropic reflexes that arise from stimuli originating in the lungs appear to manifest themselves in tissue supplied by nerves arising in most of the cervical seg ments; the reflexes are most marked in those tissues suppl ied by neurons arising i n the third to fifth cervical segments. Potti nger ( 1 6) stated that the visceral motor reflex caused by in flam mation in the lu ngs shows i tself in the con traction of the fibers of those muscles that receive their origin from the cervical portion of the cord and particularly from the third to fifth cervical segments. This manifests clinically as an increased tone or spasm in the paraspinal tissues involved. Osteopathic surgeons have presumed that this viscerosomatic reflex might be clinically significant and could have important impl ications for the possibility that modifying a somatovisceral reflex could be beneficial in the postoperative state ( 1 7-22). I n 1 963, Henshaw ( 2 3 ) publ ished the results of an i n terventional trial of surgical patients. A total of 1 ,03 1 surgical patien ts were studied from 1 96 1 to 1 963. Of this total, 1 09 ( 1 0.6%) had pre existing somatic dysfunction at the level of the third, fourth, and fifth cervical vertebra before surgery. This cohort formed the study group for i nvestigation. Seventy-five of the 1 09 patients were given osteopathic manipulative treatment ( O M T) for these somatic dysfunctions. I n this group, three patients (4%) devel oped postoperative pulmonary compl ications. J n the 34 patients who had cervical spine somatic dysfunction but did not receive O MT, 29 (85%) developed some form of pulmonary compl ica tion. U n fortunately, the external val idity of such a study is dimin ished in our era because the patients were not randomized. In ad dition, the defi n i tion of pulmonary complications was so broad that a high percentage of the defined entities (emphysema, pul monary edema, cough) are of such sufficiently vague end points that they do not represent meaningful outcomes. There would be considerable i n terest in knowing the outcome of the 922 pa tients who had surgery in the absence of preexisting cervical spine somatic dysfunction. The Henshaw study was conducted according to research methods and employed statistical methodology that was typi cal for that time period. Although the study does not withstand modern scientific scrutiny, the described results are so impressive that a current study to replicate these findi ngs is warranted.
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vr. Osteopathic Considerations in the Clinical Specialties
Another form of O MT that is described as effective i n the prevention ofatelectasis in the postoperative period is the thoracic lymphatic pump (TLP). The TLP is a ven ti lator-assist techn ique that uses passive and active rib excursion. The TLP technique is reported to have reduced the mortality from the 1 9 1 8 i n fluenza outbreak from 5% in the general population to 0.25% in 1 00,000 treated patients (24). A recent study indicated that TLP can be equally as effective as i ncentive spi rometry in reducing the postoperative occurrence of atelectasis ( 2 5 ) . This study also i ndicated that patients treated with the TLP had an earlier recovery and faster return to pre operative values for both the forced vital capacity and forced expi ratory volume at 1 second ( F EV l ) compared with patients who did not receive TLP. OMT has been recom mended in the postoperative median sternotomy patient to promote faster re turn to normal chest and diaphragmatic dynamics (26). This is particularly i m portant because there are more than 250,000 pa tients ann ually undergoing coronary bypass grafting through a median sternotomy incision. The postoperative addition of rib raising provides a means of directly assessing and enhancing respiratory motion. This artic ulatory technique is well described in Chapter 55, Articulatory Tech niques, and can be easily applied to the hospitalized patient.
VISCEROSOMATIC A N D S O M ATOV I S CE RAL R EFLEXES
M any osteopath ic physicians believe that treating the somatic component of a viscerosomatic reflex can improve a visceral pathologic condition. The diagnosis of a viscerosomatic reflex is based on a documentation of visceral disease and the objective findings of somatic dysfunction on palpatory exam ination. The finding of somatic dysfunction should lead to a review of the pa tient's cl in ical status to determine whether symptoms of a visceral disorder can be elicited. Beal (27) defines the somatic component of a viscerosomatic reflex as having the following findings: •
• • •
Two or more adjacent spi nal segments that show evidence of somatic dysfunction located within the specific autonomic reflex area A deep confluent muscle reaction Resistance to segmental joint motion Skin and subcutaneous tissue changes consistent with the acuity or chron icity of the reflex
However, the predictive value of palpatory fi ndings in the differential diagnosis of visceral disease has not been established for clin ical practice. The resu lts can be variable, depending on i nterobserver differences or issues related to the i nterpretation of musculoskeletal findings. At the same time that the clin ical util i ty of m usculoskeletal findi ngs is incompletely defined, the effectiveness of manipulative treatment fot somatic manifesta tions of chronic organ disease has not been established. Many osteopathic physicians have advocated manipulative treatment as part of the treatment regimen for organic problems of the heart and gallbladder. Although postoperative manipulative treatment has been recommended as promoting a shorter, smoother con-
valescence from the effects of visceral disease, prospective studies have not been conducted to test this hypothesis.
PRE- AND POSTOPERATIVE SOMATIC DYSFUNCTION
The process of surgery, i.e., lying on the rigid table under anesthe sia, can result in postoperative back pain and cephalgia. Similarly, many patients have chronic areas of somatic dysfunction that be come exacerbated during a surgical ill ness. Despite the surgical treatment of the visceral dysfunction, the somatic component may persist and even mi mic a recurrence of the original condi tion, such as causing a variant of post-cholecystectomy syndrome in cases of continued somatic dysfunction at T7. I l eus
One of the major postoperative problems that can affect any type of surgery is postoperative ileus. I leus is defined as the func tional inhibition of propulsive bowel activi ty, regardless of the pathogenic mechanism. This is differentiated from motility dis orders resulting from structural abnormali ties, which is called a mechanical bowel obstruction. I leus after surgery is further clas sified i n to postoperative and paralytic ileus. Postoperative ileus is the uncomplicated ileus that occurs after surgery and resolves spontaneously within 2 to 3 days. It most likely results from the temporary inhibition of extrinsic motil i ty regulation and is more severe in the colon. In contrast, postoperative paralytic ileus lasts for more than 3 days after surgery. It affects all segments of the bowel and probably results from further inhibition of local, intrinsic contractile systems. Patients who have this disorder ac cumulate gas and secretions in the intestinal system, leading to bloating, distension, emesis, and pai n . Despite major advances in many areas o f medicine, relatively few improvements have been made in the understanding of ileus. The most important advance was made over a century ago, in 1 884, with the i ntroduction of nasogastric suction (28). The earliest studies of bowel moti lity focused on mechanisms for re duction and stimulation of i ntestinal contractions. Early in this century, the role of inhibitory sympathetic reflexes mediating ileus was recognized. With the inhibitory reflex efferent limb clearly established, investigators searched for the afferent system. Many possibilities exist, including peritoneal or cutaneous stim ulation, release of inhibitory humoral agents, inhibi tion of smooth mus cle by inflammation, or muscle or nerve inhibition by anesthetic agents. Parasympathetic fiber stimulation increases motility, and stim ulation of sympathetic fibers inhibits it. Vagal nerve section in animals does not alter small intestinal motili ty, whereas splanch nic nerve division i ncreases con tractility. Sympathetic chronic inhibitor control predominates in the gut. Sympathetic activa tion occurs with stress and surgery and is thought to significantly alter bowel motil i ty during the postoperative period. The treatment for ileus has changed l i ttle in the last 1 00 years. Nasogastric intubation and suction is the only proven effective therapy. The medical regimen is modified so that medications diminishing motil i ty are minimized. Intravenous hydration is
27. General Surg ery
necessary unril the i leus resolves and the al imenrary rract can be used. Total parenreral nurrition may be necessary in cases of prolonged ileus. In 1 968, Herrmann (29) reporred the results of a study i n which h e performed a chart review o f 3 1 7 consecutive patients undergoing major surgery who received routine postoperative OMT compared with a subsequenr series of92 patienrs who did not receive postoperative OMT. In this study, the description of adynamic ileus used the following criteria: 1. 11. 111. IV.
Absence of bowel sounds Abdom inal distension Tympany to percussion of the abdomen Absence of Aatus being passed per rectum
For those patienrs in whom adynamic ileus was diagnosed, OMT was then performed in the followi ng manner. With the patienr supi ne, intermittent pressure was applied to the paraver tebral tissues of the lumbar and lower thoracic spine, ptoducing extension of those areas, in addition to deep pressure. This was done for approximately 2 min utes. The treatment was repeated every 2 hours. Each patienr was periodically reexamined to ob serve the effect, if any, that the treatment had on the criteria used for the diagnosis of postoperative adynamic ileus. Only one case of ileus was noted in the series of 3 1 7 patienrs who received OMT postoperatively. This represents an i ncidence of 0.3. Seven patients (7.6%) in the group of92 patienrs who did not receive postoperative OMT developed ileus. In these seven cases, the age range was ftom 9 to 73 years. After the adminis tration of OMT, six of these patients showed improvement, as manifest by a resumption of bowel sounds or passage of Aatus. This study was not a controlled, random ized rrial, and the reporr provides scanr details of the study design and methodology. I t suggests that postoperative O M T aids in prevention o f postoper ative ileus. Because this viewpoint is widely held by practitioners ofOMT, a randomized trial is warranted to investigate i ts efficacy in the treatment of this and other postoperative complications. OMT has been used in the management of postoperative ileus for years. It add resses the sympathetic effects on gut motility. In hibition of sympathetic hyperactivity allows the natural return of i nrestinal function as the balance with parasympathetic stim ulation is restored. Manipulative treatmenr of ileus is d irected toward in Auencing sympathetic outAow through the paraverre bral ganglia (sympathetic chain) of T5- 1 1 . The following are a few of the OMT tech niques that are used in treating postoperative ileus: 1.
11.
111.
IV.
Gentle inh ibition ofhyperronic thoracic and lumbar paraver tebral muscles to the point of tissue relaxation (2 to 5 minutes total time); this is most effectively di rected toward spinal seg ments that are associared with the surgical site via supplying sympathetic in nervation to the involved viscera. I ndirect method fascial release manipulation of the di aphragm, thoracic inlet, and mid-cervical spine. Treating Chapman reAex poinrs along the outer thigh and paraverrebral regions (30). Thoracolumbar counrerstrain tender poi nts can also be treated to facilitate recovery (3 1 ) .
407
CONCLU S I O N
Osteopathic principles are widely implemented In the surgical treatment of patients today. The formal development of this pro cess began with the establishment of regular surgical trai ning programs in the osteopathic profession in 1 926. The pl'lmary focus has centered on the osteopathic concepts of: 1 . The interrelationshi p between structure and function. 1 1 . The need to treat the patient as a regulated, integrared, and coordinated unit
The first precept represents the rationale for the application of osteopathic manipulative rreatmenr in the preoperative or pOSt operative period. The second precept is expressed in the surgeon's approach to the patient, the patienr's family and social suppOrt, and the patient's psychological state as critical features related ro the overall outcome of any surgical procedure. Understanding the approach to the surgical patienr requi res an appreciation of anatomy, with regard to both organ fu nc tion and nociception. The anatomic structure of the autonomic nervous system and the pathophysiology of organ dysfunction determ ine the nature of pain expression and clin ical presenra tion. This was furrher explored by presenring four cases of acute abdominal pai n. Surgery for these and any major ill ness can result in postoperative compl ications, most com monly atelectasis and ileus. An osteopathic approach can conrribute to the prevenrion and resolution of these problems. The osteopathic approach to the surgical patienr uses the diagnostic information provided by structural examination, as well as the added rreatmenr dimension provided by manipulative care. The addition of osteopathic manipulative treatmenr ro the postoperative care of the surgical patient is therapeutic and greatly appreciated by the patient. All patients should be rou ti nely screened for somatic dysfunction as parr of the basic surgical exam i nation. Although the acutely ill patient often cannot com ply with a full musculoskeletal exam ination in three positions, an appropriate screen i ng examination can be inregrated into the physician's usual approach to these patients. An excellent exam ple with diagrams is described in Chapter 44, Musculoskeled Examination for Somatic Dysfunction. Attenrion to possible viscerosomatic reAexes and assessing Jones and Chapman tender points (see Chapters 63 and 67, re spectively) can provide valuable information in formulating the surgical diagnosis and can indicate areas to be included in a ma nipulative rreatmenr plan . Com parative assessmenr in the postop erative patient and arrenrion to the patien t's structural complaints will guide an appropriate treatmenr program. Osteopathic manipulative treatment is underused in the rreat ment of surgical patienrs. The challenge for the osteopathic sur geon is to translate years of clinical experience with osteopathic palpatory diagnosis and rreatmenr into research protocols that determine the effectiveness of these methods for the surgical pa tienr. Specific areas for i nvestigation include the possibility that thoracic lymphatic pump or other techniques might reduce the overall i ncidence of pulmonary atelectasis, or that OMT might reduce postoperative adynamic ileus.
408
VI. Osteopathic Considerations in the Clinical Specialties
REFERENCES
20. Larson NJ. Manipulative care before and after surgery. Osteopflth Med. 1 977:4 1 -49.
I . Lyons A S . Prehisroric medicine. I n : Lyons A S , Petrucelli RJ , eds. Medicine, An flLustrated History. New York, NY: Harry N. Abrams; 1 97 8 : 27 . 2. Bosch J , Petrucelli RJ . Medicine in the p re-Columbian Americas. I n : Lyons A S , Petrucelli
RJ , eds. Medicine, An fLiustrated History. N e w York,
NY: Harry N. Abrams; 1 978:50- 5 5 . 3. Lyons A S . Ancient Egypt. I n : Lyons AS, Petrucelli RJ , eds. Medicine, An
JlLustrflted History. New York, N Y: H a rry N . Abrams; 1 978:98. 4. Lyons AS. The beginning of modern medicine. I n : Lyons AS, Petru celli
RJ' eds. Medicine, An IlLustrated History. New York, NY: H arry N .
Abrams; 1 97 8 : 523-533. 5 . Schnucker RV, ed. Early Osteopathy in the Wordr ofA. T StiLL. J(jrksville, MO: The Thomas Jefferson University Press; 1 99 1 . 6 . Dorland's MedicaL Dictionary. Philadelphia, PA: WB Saunders; 1 98 1 . 7 . Minmes of the meeting of the Board of Governors of the American Col lege of Osteopathic Surgeons; Ocrober, 1 983. Also, American College of Osteopathic Surgeons, General Surgery Discipline Bylaws, Article I I , 1 988. 8. Sabisron J r. DD. Essentials ofSurgelJ Philadelphia, PA: WB Saunders; 1 987. 9. Dohi S, Gold M I. Comparison of [wo methods of posroperative respi rarory care. Chest. 1 978;73 : 5 92-595. 1 0 . Jung R, Wight J, Nusser R, et al. Comparison of three methods of respirarory care following upper abdominal s urgery. Chest. 1 980;7 8 : 3 1 35.
2 1 . Sti les ET. Osteopathic treatment of surgical patients. Osteopath Med. September 1 976: 2 1 -23. 22. Young GS. Posroperative osteopathic manipulation. Academy ofApplied
Osteopathy Yearbook. Carmel, CA: American Academy of Osteopathy; 1 970:77-82.
23. Henshaw RE. Manipulation and posroperative pulmonary complica tions. The DO. September 1 963: 1 32- 1 33 . 24. S m i t h RK. 1 00,000 cases of inA uenza w i t h a death rate 1 /40th of that officially reported under conventional medical treatment.)Am Osteopath
Assoc. January 1 920: 1 72- 1 73. 2 5 . S leszynski SL, Kelso AF. Comparison of thoracic manipulation with incentive spirometry i n p reventing posroperative atelectasis. ) Am Os
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function, 2nd ed. Columbus, O H : Greyden Press; 1 994:96-97. 3 1 . Schwartz H R . The use of countersuain in an acurely i l l in-hospital population. ) A m Osteopath Assoc. 1 986;86:433-442.
1 1 . Schweiger 1 , Gamulin Z, Forster A, et al. Absence ofbeneht o f i ncenrive spi rometry in low risk patienrs undergoing elective cholecystecromy.
Chest. 1 986;89:652-656. 1 2. Srock MC, Downs JB, Gauer PK, et al. Prevention of posroperative
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human diaphragm. ) AppL
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2. Fischer J E, Nussbaum MS, Chance WT, et al. Manifestations of gastroin testinal d isease. I n : Schwartz S I , ed. Principles ofSurgery. New York, NY: McGraw-H i li ; 1 999: I 033-1 04 1 . 3 . G lasgow RE, Mulvihil SJ. Abdominal Pain, Including the Acute Ab
1 5 . Sharp J T, Goldberg N B , Druz WS, et al. Relative contribution of the
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1 7. Brock ww. Osteopathy and surgery. ) Osteopathy. April 1 905 : 1 1 1 1 1 3. 1 8. Down ing WJ . Osteopathic manipulative treatment of nonsurgical gall bladder. Academy ofAppLied Osteopathy Yearbook. Carmel, CA: American Academy of Osteopathy; 1 96 5 : 1 96- 1 99. 1 9. Koogler P. Osteopathic care of surgical cases. ) Osteopathy. April 1 94 9:2 1 -24.
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WB Saunders; 2000:720-727.
5. Klein KB, Melli nkoff SM. Approach ro the Patient with Abdominal Pain. I n : Yamada T, ed. Textbook of Gastroenterology. Philadelphia, PA: J B Lippincott Co; 1 994:660-664. 6. Netter F H . Atlas ofHuman Anatomy, 2nd cd. East H anover, NJ : Novartis; 1 999. 7. Sorkin LS, Wallace M S . Acute Pain Mechanisms. Sllrg eLill North Am. 1 999;79: 2 1 3-229.
GYNECOLOGY MELIelEN TETTAMBEL
KEY
CONCEPTS
Anatomy of the pelvis Somatic dysfunction and pelvic pain • Osteopathic evaluation of pelvic pain • Osteopathic approach to the treatment of pelvic pain
•
•
What diserlSes does woman have that man does not have' Such diserlSes as belong to the womb and its appendages ... It matters not whether the cause is for remote or in close proximity to the uterus; we must find it, or we will befound in the antediluvian tribe o/speculum cranks 0/all the blindftmale doctors' ages. -A. T. Still (1) The osteopathic obstetrician-gynecologist has the opportunity to integrate the influences of the musculoskeletal system into the management of a variety of health care concerns experienced by female patients. Knowledge of anatomy and physiology of the reproductive system is key to osteopathic management of related somatic dysfunction. Palpatory expertise of the female pelvis and its contents is a prerequisite for ancillary testing and patient man agement. Because of the broad scope of gynecology, this chapter does not address all diagnostic and treatment topics involving the female reproductive system. Instead, it focuses on two common women's health care issues frequently encountered by primary care providers-pelvic pain and pelvic organ disorders.
PELVIC PAIN Anatomy
Evaluation of pelvic pain requires extensive knowledge of the anatomy and physiology of the female pelvis. Although standard references (2-4) completely discuss the anatomy of the female pelvis, salient points helpful to osteopathic physicians are sum marized here to illustrate possible causes of somatic dysfunction. The pelvic floor consists of the levator ani muscles and pelvic diaphragm complex (5). It contains the visceral pelvic fascia and pelvic diaphragm, and the urogenital anal triangles with superfi cial and deep genital muscles. The sphincters of the urethra are also included.
The levator ani group forms the deepest layer of striated mus cles and is laterally bordered by the arcus tendineus, the piri formis muscle, and the obturator internus muscle. The fascia of this group is continuous with these pelvic diaphragm muscles. The anterior pubic portion of the levator ani muscles includes the pubococcygeus, with the puborectalis and pubovaginalis por tions. The iliococcygeus forms the posterior iliac portion. The ischiococcygeus muscle lies adjacent but more superior to the levator ani group and assists the levator ani in its supportive function. The perineum can be divided into the urogenital triangle re gions and the anal triangle regions (6) (Tables 28.1 and 28.2). Superficial external genital muscles form a figure eight around the vagina and urethra and around the anus (Fig. 28. 1). Deeper in the urogenital triangle is the urogenital diaphragm. It is an terior ro and more superficial than the pelvic diaphragm. It is also incorporated transversely with muscle and fascia that span bilaterally across the ischiopubic rami. The urogenital diaphragm consists of the striated urogenital sphincters. The female urethral sphincters include the striated sphincter urethrae and distal intrinsic and external sphincters. The levator ani and the compressor urethrae muscles assist the sphincters in urethral closing (7). The pelvic floor performs three important functions: sup portive, sphincteric, and sexual. The pelvic floor, in conjunction with the pelvis bones, muscles, and connective tissues, provides support of the pelvic organs against gravity and any increases in abdominal pressure. Support and tone for vaginal walls are also provided. Sphincteric function aids in control of perineal openings. Pelvic floor muscles prevent incontinence by increasing intraurethral pressure and stabilizing endopelvic fascia during sphincter contraction. The muscles also relax for defecation and contract to control flatus. They help prevent fecal incontinence by keeping the anorectal angle closed (8). A functional pelvic floor stabilizes the proximal urethra, improves severe lower tract symp tomatology, and assists in the ability to delay urination via bladder reflex inhibition (8). The sexual function consists of contraction of perivaginal muscles during coitus to enhance sexual activity. The muscles also respond reflexively during orgasm. Decreased pubococcygeal strength and awareness impede sexual response (9). The striated muscles of the vaginal introitus and skin of the perineum receive somatic motor and sensory fibers from the
V1. Osteopathic Considerations in the Clinical Specialties
410
TABLE 28.1. PELVIC
DIAPHRAGM
(THE
PELVIC
FLOOR
TABLE 28.2. UROGENITAL AND ANAL TRIANGLES
AND WALLS)
Action
Muscle Action
Muscle
Urogenital triangle region (superficial layer) Levator ani
Ischiocavernosus ischial tuberosity
Erection of clitoris
Anterior pubic portion:
Bulbocavernosus (bulbospongiosis)
Vaginal sphincter and
Pubococcygeus
assists in erection of
Supports the pelvic viscera
c Iitoris
(pubovisceral) Pubovaginalis
Sphincter of vagina and urethrae
Puborectalis
Loops around rectum, elevates and helps constrict anal canal
Superficial transverse perineals Deep layer/perineal membrane Striated urogenital sphincter muscles
Posterior iliac portion: Fibococcygeus
Assists in support of pelvic viscera
Coccygeus
Flexes coccyx, assists in support of pelvic
isch iococcygeus
Anchors perineal body
Upper portion Sphincter urethrae (rhabdosphincter)
Obturator internus
Lateral or external rotator of hip
Pyriformis
External rotator of hip, stabilizes hip joint
Constrict urethral lumen
Lower portion (deep transverse perineal)
viscera, and stabilizes the sacroiliac joint
Compresses ventral
Urethrovaginal sphincter
wall, assists
Compressor urethrae
incontinence mechanism
lumbosacral plexus. The pelvic viscera are supplied by the au tonomic plexuses, conveying sympathetic and parasympathetic nerves to these organs. Ventral roots of the lumbar and sacral nerves originate from the lumbosacral plexuses. The obturator nerve, the lumbosacral trunk (of the plexus), and the entire sacral plexus lie in proximity to the pelvic organs. Only particular branches of the plexuses are directly involved in pelvic innervation (Fig. 28.2). Muscular contraction and vasoconstriction are mediated by sympathetic innervation, whereas muscle relaxation and vasodi lation are caused by parasympathetic innervation. Most auto nomic fibers enter the pelvis via the superior hypogastric plexus, which runs from the fourth lumbar vertebra to the hollow of the sacrum. It descends into the base of the broad ligament to join the parasympathetic fibers from the pelvic plexuses. The motor fibers and accompanying sensory nerves arrive ar the pelvic plexus from 52-4 by way of the nervi erigentes. The sensory nerves from
Anal Triangle Region External and sphincter Voluntary sphincter of
Subcutaneous part
the anal canal and
Superficial part Deep part
assists the puborectalis
rhe urerus, which escort rhe sympatheric nerves to enter the cord ar Tll and Tl2, cause referred pain to the abdomen. Cervical afferenr nerves, 52-4, refer pain to rhe lower back and lumbosacral regions. Autonomic innervarion to rhe pelvic organs includes these sensory fibers: 5ympatheric Parasympatheric • Motor • Visceral • •
Right
Left Pubis
Ilium
Acetabulum (hip socket)
Transversus perinei profundus
Perineal body
Inferior layer of urogenital diaphragm (cut)
Obturator Sacrotuberous ligament Levator ani, pubic part (pubococcygeus) Levator ani, iliac part Coccygeus (ischiococcygeus)
Transversus perinei superficialis Sphincter ani externus Anus Anococcygeal body
FIGURE 28.1. Pelvic floor muscles as seen from below in the supine female. (From Travell J, Simons D. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol. 2. Baltimore, MD: Williams & Wilkins; 1992, with permission.)
28. Gynecology
____ --:'-
411
Greater splanchnic n.
--+_ Lesser
__
splanchnic n. t---C -+- eliac ganglion ___ _ L...-
Least splanchnic n.
Utu.
� Lumbar
_ __
sympathetic chain """,,--L.._ Ovarian plexus
Superior hypogastric plexus
FIGURE 28.2. Nerves of uterus and perineum. Pansky B. Review of Gross Anatomy,
(From
Sensory Nerves
Motor Nerves
The uterus, vagina, ureter, bladder, and rectum are supplied by the inferior hypogastric plexus. Visceral afferent pain pathways of the ovary, fallopian tube, uterus, and cervix connect with the spinal cord at the level of Tll- 12. Pain is referred to correspond ing skin dermatomes, usually from the lower abdomen. Sacral plexus injury can cause disabling changes of a motor or sen sory nature, as Beal ( 10) discusses in his review of viscerosomatic reflexes. The genitofemoral nerve (Ll-2) traverses across the belly of the psoas major muscle to the anterior thigh to supply the labia majora. Injury results in sensory changes. The obturator nerve (L2-4) supplies motor branches to the adductor muscles of the leg, hip, knee joint, and medial thigh. Injury results in loss of thigh adduction, loss of internal and external rotation, and sensory losses to these areas. Table 28.3 summarizes nerves that cause painful impulses from the pelvic organs. Circulation and lymphatic drainage of the female reproductive system are closely integrated. The blood supply to the ovary is derived from the ovarian artery off the abdominal aorta, and the ovarian branch of the uterine artery. Veins accompany the arteries as plexiform vessels. Those on the left converge to form the left ovarian vein that drains into the inferior vena cava. Lymphatic
5th ed. New York, NY: Macmillan; 1984:459, with permission .)
drainage of the ovary proceeds from the hilum of the ovary to the lumbar nodes. The fallopian tubes derive their blood supply from the ovar ian artery, as well as from the uterine artery. Venous drainage is into the ovarian or uterine veins. Lymphatic drainage is into the lumbar lymph nodes, accompanying the ovarian lymphatics. The blood supply to the uterus originates from the internal iliac arteries through the uterine arteries. Each uterine artery gives off a cervical branch. The vessel terminates by communicating with the ovarian artery. Venous return is from the uterine plexus, which communicates with the vaginal plexus and the ovarian plexus, forming the uterine vein that empties into the internal iliac vein. Lymphatic drainage is divided. The body of the uterus is drained by the lumbar nodes, superficial inguinal nodes, and external iliac nodes. The cervix is drained by the external and internal iliac nodes and the sacral nodes. The vagina is supplied by the vaginal branch of the uterine artery. Inferior vesical and middle rectal arteries send branches to the vaginal wall. The internal pudendal artery supplies the lower vaginal wall. Venous return is through a vaginal plexus, which joins the uterine plexus to form the uterine veins and empty into the internal iliac vein. Sacral nodes and superficial
TABLE 28.3. NERVES CARRYING PAINFUL IMPULSES FROM PELVIC ORGANS
T9-10
Organ
Nerves
Spinal Segments
Sympathetic via renal and aortic plexus and celiac
Ovaries
and mesenteric ganglia T9-10
Sympathetic via aortic and superior mesenteric plexus
Outer two-thirds of fallopian tubes, upper ureter
T 1 1- 12, L 1
Sympathetic via hypogastric plexus
Uterine fundus, proximal fallopian tubes, broad ligament, upper
S2 4
Pelvic parasympathetic
Upper vagina, cervix, lower uterine segment, posterior urethra,
bladder, cecum, appendix, terminal large bowel -
bladder trigone, uterosacral and cardinal ligaments, rectosigmoid, lower ureters S2-4
Pudendal, inguinal, genitofemoral, posterofemoral cutaneous
Perineum, vulva, lower vagina
412
inguinal nodes drain the lower portion of the vagina; the upper vault drains into the external iliac, internal iliac, or common iliac nodes.
PATIEN T EVALUATION : HISTORY AN D PHYSICAL EXAMIN ATION
Patient history should include description of pain with reference to: • • • • • • •
Localization Quality Intensity Radiation Duration Aggravation Alleviation
The relationship of the pain to the menstrual cycle, bowel movements, urination, sexual activity, physical activity, and trauma should also be discussed. Similar painful episodes in the recent or distant past should be explored, along with other pos sible related somatic complaints, such as anorexia, weight gain, or other gastrointestinal (GI) or urologic symptoms (11). Also note musculoskeletal complaints that may or may not accom pany pelvic pain, such as low back pain or headache. Ascertain the influence of pain and its ability to disrupt activ ities of daily living, as well as other concurrent events that may have occurred with the acute onset of pain. Examples include cramps with IUD placement, sexual trauma, falls, and/or strain from lifting heavy objects (12,13). Whereas acute pelvic pain may be of sudden onset and localize within 24 hours, chronic pelvic pain differs in both duration and location. As described by Glintner (14), chronic pain is pain that has been present for 6 months, is diffuse and intermittent in na ture, and involves no organic pathologic findings. Fifteen to 30% of women presenting with this complaint undergo laparoscopy and 10% to 15% undergo hysterectomy (15,16). Some women may have associated stressors, such as depression over pregnancy loss, employment issues, or personal relationships (17). The per ceptions that both the patient and her partner have about the illness are also important. Elicit information about medications or other attempts to relieve the pain. Psychological evaluation may become necessary, but should not preclude other diagnostic studies, especially when the pain itself becomes the disease rather than a symptom of the disease (11,18). Additional gynecologic history should include inquiries about: • • • • • • •
Osteopath
VI.
Infertility Infection Methods of contraception Endometriosis Gynecologic surgery Obstetrical procedures and deliveries Last pelvic examination
The surgical history should include not only pelvic procedures but also any other procedures, such as orthopedic, urologic, or neurologic operations. The medical history should include con-
ditions that could manifest as pelvic pain, such as colitis or inter stitial cystitis (19). To avoid guarding, the physical examination should focus on careful and gentle palpatory evaluation of the abdomen. Attempt to reproduce and localize the pain during the pelvic examination to discover findings that may correspond to specific pathology (20). Consider endometriosis if the uterus is fixed and if there is uterosacra.l nodularity that is also tender to palpation (21). Note if the cervix is laterally displaced on bimanual examination (22). Tender adnexal enlargement may suggest an ovarian cyst, torsion, ectopic pregnancy, or infection. A backache may be the result of uterine prolapse (23). Palpatory structural examination to evaluate spinal curves, un level sacral base or lower extremities, paravertebral muscle con tractions, and somatic dysfunction from the cranial base to the feet may guide the physician to address neuromuscular hyperac tivity or inappropriate somatovisceral reflex activity (24). Partic ular emphasis should be placed on the identification of somatic dysfunction of the sacrum, lumbar spine, and pelvic and respi ratory diaphragms. Localization of counterstrain tender points is used to treat pain caused by muscle imbalance. Identification of Chapman reflex points may render clues about pelvic organ dys function. A postural x-ray study may confirm palpatory findings of scoliosis or other structural imbalances. Osteopathic manipu lative treatment may alleviate distress that surgery cannot. Consider psychological evaluation if an obviously traumatic event is directly associated with the onset of pain or if there is concomitant neurosis, psychosis, or aberrant behavior (25). Table 28.4 summarizes some of the more common causes of pelvic pain.
TABLE 28.4. CAUSES OF PELVIC PAIN Gynecologic Endometriosis Pelvic inflammatory disease Abdominopelvic adhesions Severe pelvic relaxation Uterine myomata Benign ovarian neoplasms (solid and cystic) Ovarian remnant Cyclic pelvic pain (primary or secondary dysmenorrhea) Urologic Urinary tract infection Cystitis (interstitial and acute) Renal calculi Gastrointestina I Irritable bowel syndrome Crohn disease Diverticulitis Constipation Bowel obstruction Muscu loskeleta I Somatic dysfunction Hernias Muscular strains/sprains Herniated disk Fibromyositis (with or without trigger points) Pelvic bone tumors Psychogen ic Psychosexual trauma/abuse Depression Somatization
413
28. Gynecology
DIFFERENTIAL DIAGNOSIS OF PELVIC PAIN Dysmenorrhea
Painful menstruation, or dysmenorrhea, can be primary or sec ondary to organic pelvic disease. Approximately 50% of men struating women are affected by dysmenorrhea, of which 10% may require bed rest. The peak age of incidence is 20 to 24 years. Primary dysmenorrhea usually appears within 6 to 12 months of menarche and may be a feature of ovulatory cycles. Dysmenor rhea may be caused by uterine comractions or ischemia, psycho logical factors, and cervical factors (26,27). Psychological factors may alter pain perception. Cervical stenosis has been cited as a painful stimulus (28). Women with dysmenorrhea may have increased frequency or duration of uterine contractility. Cramping usually begins a few hours before menses and can persist for hours or longer. The pain is localized to the lower abdomen and back. It may also be associated with nausea, fatigue, dizziness, headache, or altered bowel habits. Treatment options include: • • • • • • •
Nonsteroidal antiinflammatory drugs (NSAIDs) (29) Cyclo-oxygenase-2 (COX-2) inhibitor drugs Oral contraceptive pills Calcium channel blockers Progestogens Osteopathic manipulative treatment (30-32) Gonadotropin-releasing hormone (GnRH) agonists (33)
Osteopathic treatment may reduce the severity of pelvic pain by treating Chapman points in the iliotibial band, or by address ing somatic dysfunction at the level of Tl 0-L2 (sympathetics) and dysfunction at S2-4 (parasympatherics). To relieve edema, lym phatic drainage should be enhanced at the abdominal diaphragm, thoracic inlet, and lower extremities (34). Self-treatment may include the knee-chest position to lift the uterus out of the pelvis. If a patient fails to respond to medical and/or osteopathic manip ulative treatment, consideration should be given to a secondary cause of dysmenorrhea. Laparoscopy and/or hysteroscopy with endometrial curettage may be performed to exclude pelvic disease. Secondary dysmenorrhea is not limited to menstrual pain, is less related to the first day of bleeding, develops in women 30 to 40 years of age, and may be associated with other symptoms. These symptoms may include dyspareunia, infertility, and/or ab normal bleeding (35). Table 28.5 summarizes possible causes of primary and secondary dysmenorrhea. Management focuses on treatment of specific underlying disease or somatic dys function. Some of these diseases are discussed in the following sections.
TABLE 28.5. CLINICAL
FEATURES
OF
PRIMARY
Primary Dysmenorrhea Initial onset-within 2 years of menarche. Pain-cramplike, lasting 48-72 hr after onset of menses; strongest in intensity over lower abdomen. May radiate to back or inner thigh. Associated symptoms-nausea and vomiting, fatigue, diarrhea, lower backach� headache. Pelvic examination findings-normal. Secondary dysmenorrhea Endometriosis-pain occurs in premenstrual or postmenstrual phase or may be continuous. Patient may experience dyspareunia, premenstrual spotting, or have cul-de-sac nodularity on examination. Age of onset in the 20s or 30s. Pelvic inflammation-initially pain may be menstrual, but may extend into premenstrual phase with subsequent cycles. Patient may have intermenstrual bleeding, dyspareunia, and pelvic tenderness. Fibroids, adenomyosis-pain is a dull, heavy ache in pelvis. Uterus enlarged on examination and may be tender. Ovarian cysts-unilateral tenderness, radiating into thigh. Adnexal enlargement on examination. Pelvic congestion-dull, ill-defined ache that worsens premenstrually but improves with menses. Patient may have history of sexual dysfunction.
Mood swings Depression • Fatigue • Difficulty concentrating
•
•
The term "premenstrual syndrome" (P MS), was first used by Greene and Dalton in 1953 (37) because many symptoms also occur around the time of ovulation, or midcycle. Approximately 5% to 10% of women experience severe PMS symptoms that interfere with normal daily life. Other women may have more se vere depression or mood swings that are mentally and physically debilitating. Premenstrual dysphoric disorder is a psychiatric di agnosis used to distinguish those patients who have augmented PMS signs or symptoms (38). The cause of P MS has not been entirely determined (39). Table 28.6 lists proposed hypotheses that attempt to explain the syndrome. Most healthy women report occasional symp toms before menses. The syndrome is associated with ovulation and, therefore, does not occur before puberty, during pregnancy, or after menopause. Nor does it occur in anovulatory women. Menstruation is incidental, as cyclic symptoms continue to be bothersome if the ovaries are still present in a woman who has
TABLE 28.6. PROPOSED
HYPOTHESES FOR CAUSES OF
PREMENSTRUAL SYNDROME Abnormal estrogen secretion Excess or deficiency of progesterone Excess or deficiency of cortisone, androgens, or prolactin
Premenstrual Syndrome
Excess or deficiency of prostaglandin Excess of antidiuretic hormone
Premenstrual problems have been formally described since 1931 by Frank (36). They include, but are not limited to:
Abnormality of endogenous opiates or melatonin secretion
Bloating of abdomen or pelvis Weight gain • Irritability
Hormone allergy
•
•
AND
SECONDARY DYSMENORRHEA
Deficiencies of vitamins A, 8"
86, or minerals such as magnesium
Hypoglycemia Menstrual toxin Psychological, social, evolutionary, and genetic factors
414
VI. Osteopathic Considerations in the Clinical Specialties
had a hysterectomy. Extensive metabolic and psychological stud ies have yet to identify a specific abnormality, but serotonergic neurotransmission dysfunction has been implicated (40). Treat ment options have included: • • • • •
•
Medication to suppress cyclic ovarian activity Psychotherapy to develop coping skills Diuretics to reduce bloating Diets with reduced fat, caffeine, or salt to reduce irritability or water retention Dietary or food supplements (pyridoxine or primrose oil), which may interfere with prostaglandin synthesis to lessen cramps (41,42) Osteopathic manipulative treatment (43)
Endometriosis
Endometriosis is a benign condition in which endometrial glands and stroma are present outside the endometrial cavity. Other locations include the ovary, bowel, bladder, peritoneum, and sites outside the pelvic boundaries. Endometriosis is a challenge to gynecologists because it is a diagnostic and surgical enigma (44). More than 15% of women have some degree of the disease. It is noted in approximately 20% of gynecologic surgical procedures and half the time, endometriosis is an unexpected finding (45). The characteristic triad of symptoms associated with en dometriosis is dysmenorrhea, dyspareunia, and dyschezia. Sec ondary dysmenorrhea first appears or escalates in the late 20s or early 30s. If the endometriosis is associated with obstructive genital anomalies, severe dysmenorrhea may occur at menarche (46). Dyspareunia is generally associated with deep coitus, which can irritate the endometrial implants located in the cul-de-sac, the uterosacral ligaments, or in portions of the posterior vaginal fornix. On pelvic examination, the cul-de-sac may feel gritty and be exquisitely tender to the touch (47). Dyschezia is experienced with uterosacral, cul-de-sac, and rectosigmoid colon involvement. AJ; stool passes between the uterosacral ligaments, the patient experiences pain. This symp tom is highly characteristic and is more common with en dometriosis than with chronic salpingo-oophoritis, a condition sometimes otherwise mistaken for endometriosis (48). If the ovarian capsule is involved with endometriosis, ovula tory pain and midcycle vaginal bleeding are reported by the pa tient. However, the nature of pelvic pain caused by endometriosis is variable. Some investigators have found that the degree of pain is inversely proportional to the extent of the disease (45). Mini mal endometriosis in the cul-de-sac may be more painful than a large ovarian endometrioma that can expand freely into the ab dominal cavity. Frequently, pelvic examination yields no signs of endometriosis. The diagnosis of endometriosis should be suspected in an afebrile patient with the previously mentioned characteristic en dometriosis symptom triad: a firm, fixed, tender adnexal mass and tender nodularity in the cul-de-sac and uterosacral liga ments. Pelvic ultrasound may indicate an adnexal mass of com plex echogenicity. The definitive diagnosis is made by the char acteristic gross findings of "blueberry" spots, chocolate cysts, or
"powder burns," or by histologic findings of endometrial tissue at laparoscopy or laparotomy (49,50). Management of endometriosis depends on the following con siderations (30): Certainty of the diagnosis Severity of symptoms • Extent of the disease • Preservation of fertility • Compromised function of the gastrointestinal and/or urinary tracts
• •
If reproductive capacity is not a concern, total abdominal hys terectomy with bilateral salpingo-oophorectomy should be con sidered. Menopause can be managed with hormone replacement therapy. If future fertility is a consideration, pursue conserva tive surgery, including resection of the disease, lysis of adhesions, ovarian resection, or ablation of small lesions (49). Medical therapy may be considered if the endometriosis is minimal in extent and the symptoms are tolerable. NSAIDs or COX-2 inhibitors are recommended to address dysmenorrhea. Oral contraceptive pills or hormonal manipulation may decrease the intensity and duration of dysmenorrhea and menses. Tempo rary suppression of menstruation and endometrial implant for mation can be achieved through short-term use of danocrine or GnRH agonists (51). Fertility is preserved by involution of im plants. However, when a palpable endometrioma is present, the likelihood of a complete response to medical therapy is small (51). Osteopathic treatment considerations for menstrual disorder pain include "rocking" of the sacral base for parasympathetic inhibition (34) and treatment of somatic dysfunction of the tho racolumbar spine, particularly TI0-L2. Mobilization of the res piratory diaphragm should improve respiration and circulation of body fluids. Treatment of the pelvic diaphragm relieves pelvic congestion and edema of the lower extremities. Because the men strual cycle is controlled by neuroendocrine system feedback, cra nial base or vertebral strain may interfere with endocrine function. Ovarian Pain
Ovarian cycts are usually asymptomatic, but pain may occur as a result of rapid distension of the ovarian capsule. Some women may develop recurren t hemorrhagic ovarian cysts that apparently cause pain and dyspareunia. Impaired blood supply to the ovaries has been implicated, especially after previous pelvic surgery, such as partial oophorectomy or hysterectomy (52). Bimanual examination reveals an adnexal enlargement with tenderness. Ul trasound may determine whether the cystic structure is complex or contains clear fluid. Resultant cyst formation may become painful. An ovary or ovarian remnant may become retroperi toneal secondary to inflammation or previous surgery (53). Osteopathic treatment considerations for ovarian pain include treatment of somatic dysfunction of the thoracolumbar junction, assessment of sacral imbalance and leg length discrepancy, and identification of Chapman reflex areas. Mobilization of the spine addresses aberrant somatovisceral reflex pathways. Additional treatment of the sacral base and leg length discrepancies may mechanically affect and improve blood supply to the ovaries and
28. GynecoLogy
the pelvis. Chapman reRex areas identify possible related somatic dysfunction of the reproductive system and gastrointestinal tract. Uterine Pain
Pelvic pain is not usually the result of variations in uterine posi tion in the pelvis. Deep dyspareunia may occasionally be assoCi ated with retroversion, whereby the pelvic nerves are irritated by stretching of the uterosacral ligaments, and pelvic veins become congested from uterine heaviness and position (54). A tender uterus that is noted on pelvic examination ro be fixed in retrogression should arouse suspicions of other intraperitoneal pathology, such as endometriosis or pelvic inRammatory diseas�. Laparoscopy is indicated to evaluate all pelvic structures. PelVIC heaviness and low back pain may be present with advanced de grees of uterine prolapse. Before deciding on hysterectomy as a course of treatment, some of these symptoms may be remedied by use of a pessary. Low back pain may respond to osteopathic treatment of the pelvic diaphragm or myofascial trigger points in the vaginal Roor or rectum. Application of deep inhibitory pressure may relieve back or pelvic pain in addition to identify ing and treating pelvic and lower extremity somatIc �ysfunctIon . (55). Under normal conditions, the chief characterIStiC of uterIne support is its mobility, and any loss of this mobility or chang�s associated with altered positional relationships are Important di agnostic signs. The structures involved in uterine suppor� are the levator muscle and fascia of the pelvic Roor, the paracervlcal and paravaginal tissues, which extend ourward from the vagina to the pelvic walls and which include the cardinal and uterosacral lIga ments, and the round ligaments, which assist in holding the uterus in its anterior position. Of these, the cardinal ligament is the most important. This structure consists of a loose meshwork of con nective tissue, which cannot be palpated when it is relaxed, but which forms a very firm ligament when the area is under tension. The concept of pelvic congestion syndrome has a variety of proponents. This syndrome has been described in multiparous women who have pelvic vein varicosities and congested pelVIC organs (54). Pain is worse premenstrually and is aggravate� by fatigue, standing, and sexual intercourse. In the clllllCal examlIla tion, the uterus is mobile, usually retroverted, soft and boggy, and slightly enlarged. There may be associated menorrhagia and uri . nary frequency (56). Dilated veins may be seen on venographic studies (57). Additional and independent factors other than ve nous congestion may be involved, as some women with pelvic varicosities have no pain. Surgery is not usually beneficial for this condition (58). There have been some uncontrolled observations of similar symptoms of pain and metrorrhagia occurring after tubal ligation, but no prospective studies have been perfor�ed (35). Structural and postural evaluation with palpatory examllla tion of somatic dysfunction of the lumbar spine and pelvis may elucidate areas for osteopathic treatment to relieve muscle distress and improve circulation to the pelvis. Uterine leiomyomas (fibroids) are smooth muscle tumors of the uterus that are the most common indication for major surgery in women. Twenty percent of women develop uterine fibroids by age 40 (3). Fibroids have the potential to grow to an enormous size but have low malignant potential. The majority cause no symptoms and may require no treatment other than careful ob-
415
servation. Occasionally, the patient may become aware of a lower abdominal fullness or mass above the pubic symphysis. Symp toms develop insidiously as the fibroid competes with neighbor ing organs for space in the pelvis. Symptoms include: Pressure Congestion • Bloating • Urinary frequency or retention • Dysmenorrhea • •
Other causes of pain are the result of fibroid infarction with degeneration, torsion on the fibroid's pedicle, or compression of pelvic nerves. Occasionally, a submucous leiomyoma may at tempt to protrude through the cervix, causing pain akin to that of vaginal childbirth. Management of this condition includes addressing the pa tient's desire for preserving future fertility, along with careful observation. Myomectomy may be performed to maintain the uterus for future pregnancy. Uterine curettage or endometrial ablation may control menorrhagia. GnRH agonists have been used to shrink myomas to enhance fertility, as well as reduce in traoperative blood loss. Oral contraceptives also reduce menstrual Row, preserve fertility, and control dysmenorrhea. Hysterecro�y is reserved for the symptomatic patient for whom reproduCtIve capability is not an issue. . Adenomyosis may cause dysmenorrhea and menorrhagia, but rarely does it cause chronic intermenstrual pain. Adenomyo�is is defined as the extension of endometrial glands and stroma lIlto the uterine musculature. Approximately 15% of women develop varying degrees of adenomyosis in their late 30s and early 40s, and they may have associated endometriosis (35). Patients ex press that their dysmenorrhea is of a colicky nature. In 30% to 40% of patients with adenomyosis, the disease is an unexpected pathologic finding in a hysterectomy patient who did not ex perience menorrhagia or uterine enlargement (45). In the case of a large adenomyoma, pressure on the bladder or rectum may be reported by the patient. On pelvic examination, the uterus IS symmetrically enlarged, but occasionally the uterus may enlarge asymmetrically, suggesting the presence of a fibroid. However, the adenomyomatous uterus is softer than a uterine myoma. !reat ment depends on the specific symptoms and on the exclUSion of other uterine pathologic conditions. Menorrhagia and dysmen orrhea, if not too severe, may be treated palliatively with NSAIDs, COX-2 inhibitors, oral contraceptives, or GnRH agonists (29). Osteopathic management consists of treating somatic dysfunc tion of the lumbar spine and pelvis, pelvic diaphragm, and mus cles of the anterior abdominal wall that may be inRuenced by posture. Otherwise, hysterectomy may be indicated. The ovaries . may be preserved if they are normal and if the patient IS not menopausal. Pelvic Inflammatory Disease
Pelvic inRammatory disease (PID) comprises a constellation of inflammatory disorders of the upper genital tract, including: • •
Endometritis Salpingitis
416
• •
VI. Osteopathic Considerations in the Clinical Specialties
Tubo-ovarian abscess Pelvic peritonitis
The two most common conditions of P ID in the non pregnant patient are salpingo-oophoritis and tubo-ovarian ab scess. The diagnosis of acute salpingo-oophoritis is often made inappropriately (59,60). The patient usually presents with lower quadrant abdominal pain that is frequently bilateral. She may have recently started her menstrual period. Additional symptoms may include nausea, dysuria, and purulent vaginal discharge. Ab dominal examination reveals generalized tenderness withour pal pable masses. Bimanual examination reveals cervical motion ten derness and bilateral adnexal tenderness. Usually there are no adnexal masses. Differential diagnoses must include (60): • • • • • •
Acute appendicitis Urinary tract infection Adnexal torsion Endometriosis Hemorrhagic corpus luteum cyst Ectopic pregnancy
The definitive diagnosis is confirmed by laparoscopy or la parotomy, especially when the patient is unresponsive to antibi otic therapy. If surgery is not indicated, empirical treatment with broad-spectrum antibiotics may be initiated on an outpatient or inpatient basis until the infectious agent is identified (61). Med ication alterations are then based on laboratory results. Patients with acute tubo-ovarian abscess experience: Severe pain in the low abdomen/pelvis High fever • Nausea and vomiting • Impending septic shock •
•
Abdominal examination reveals marked tenderness with mus cular rigidity, a pelvic mass, and rebound tenderness. Bimanual pelvic examination is extremely difficult because of the abdom inal pain. An adnexal mass may be discovered. It may be easier during a rectal examination to recognize a pelvic mass that may be directed inro the cul-de-sac. Differential diagnosis may include the following: • • • • • • • • •
Septic incomplete abortion Uterine rupture Acute appendicitis with possible rupture Peritonitis with or without abscess formation Diverticular abscess (in left-sided pain) Adnexal torsion Perforated peptic ulcer Pancreatitis Mesenreric artery thrombosis
Laboratory results of any vaginal cultures confirm the infec tious cause. Sonography may demonstrate adnexal pathology or cul-de-sac flocculation. The treatment plan includes hospitalization with intravenous hydration, analgesics, and systemic antibiotics. Abscesses may re solve without need for acute surgical intervention. Timing of sur gical intervention requires clinical judgment. Should the patient
not respond to 72 hours of multiagent broad-spectrum antibiotics and have persistent spiking fevers, urgent surgery may be neces sary to remove affected pelvic organs that have become infected by the ruptured abscess. Drainage and lavage of the peritoneal cavity may conserve pelvic organs. Chronic PID may cause pain because of recurrent exacerba tion that requires antibiotic therapy or because of hydrosalpinges and adhesion formation around the tubes, ovaries, and intestines. Endometriosis is the most frequently encountered differential di agnosis, particularly if there is no well-documented history of acute infection. Before ascribing pain symptoms to adhesions, one should note adhesions specifically in the area of pain local ization. Some patients with extensive pelvic adhesions may be asymptomatic. Laparoscopy or laparotomy may be required to identify the adhesions. Osteopathic considerations for treatment of PID include eval uation and treatment of somatic dysfunction at T 1 1-L2 to im prove circulation, and at the sacrum and related pelvic bones to balance the nervous system, as well as improve body fluid circu lationllymphatic drainage. Pel vic Floor Dysfunction
Pelvic floor muscle dysfunction can contribute to many condi tions, including: Urinary stress incontinence Fecal incontinence • Sexual dysfunction • Pelvic relaxation • Levator ani syndromes •
•
These problems are underreported, embarrassing, and under treated (62). Symptoms of these problems may limit a woman's activities of daily living. Pelvic floor dysfunctions are often pre ventable; emphasis should be placed on prevention through ed ucation and exercise before problems arise (63). Women are twice as likely as men to be incontinent (64). Denial is common because many patients believe that it is an inevitable result of childbirth and aging. Involuntary loss of urine during physical activity is called stress incontinence. Nygaard et al. (65,66) studied the relationship between exer cise and incontinence and found that 47% of regularly exercising women experience some degree of incontinence. Of 326 women, 22% were nulliparous. High-impact exercises (running and jumping) resulted in even more episodes of incontinence than did low-impact activities. Women who frequently exercised addressed their incontinence by wearing protective pads, staying. close to a toilet, and limiting fluid intake (67). Urogynecologic dysfunctions have multifactorial causes that require medical evaluation and urodynamic testing. When an evaluation indicates muscle dysfunction, an osteopathic physi cian may gain additional insight from understanding interrela tionship between structure and function of the pelvic structures. Successful manipulative treatment and exercise depend on the condition of the sensory and motor system of the patient. A rou tine pelvic examination may identify poor performance of pelvic floor musculature. Further examination should include visual
28. GynecoLogy
inspection of the perineum during a pelvic Aoor conrraction ro note whether the proper muscles are conrracting and relaxing, and digital palpation ro detecr muscle strength or pain. Note any cysrocele, recrocele, or poorly repaired episioromies. Uterine or vaginal prolapse should be noted. Pelvic relaxation with decrease in normal pelvic floor sup port can occur with congenital or developmental weakness of the supportive structures, or when pelvic structures (especially the pudendal nerve) are damaged during childbirth (68). Even if the pelvic Aoor muscles are not damaged in vaginal delivery, the muscles must accommodate the passage of the fetus through the pelvis. Scar tissue may limit muscle contractility (69). Postpartum patients are often afraid ro recondition the perineum because of pain, and they usually fail ro perform the Kegel exercises taught in childbirth classes (70,71). Manipulative treatment can be very beneficial in improving muscle rone and general nervous and circularory function; particularly in correcting associated postu ral imbalance. Nervous system dysfunction may be affected by uterine displacement and sacral base dysfunction (54). The fascia and supporr structures are also inAuenced by menopause and aging (72). Changes in the pelvic Aoor from chronic constipation and straining during defecation can lead ro anorectal incontinence with outstretched perineum and sphinc ter denervation (73). Chronic cough also strains the muscles of the pelvic Aoor (74). Kegel exercises, developed in the 1950s, were meant ro address early stages of pelvic relaxation, not to prevent the need for surgery (70). Although the mechanism by which these exercises alleviate dysfunction is not fully understood, the patient benefits from regular contraction and relaxation of iso lated muscle groups to increase motor recruitment abilities. Hypertonus dysfunctions of musculoskeletal and urogyneco logic systems are known as the levaror ani syndrome (75). Poorly localized pain is the primary sym·ptom. The pain may be located in perivaginal or perirecral areas, in lower abdominal quadrants, and in the pelvis. Vulvar or clitoral burning may sometimes be present. Pain can also be located in suprapubic or coccyx regions, even down the posterior thigh. More specific symptoms reported by women with hypertonus dysfunction include (76): • • • • •
Dysmenorrhea Dyspareunia Sexual dysfunction Voiding difficulty Urinary frequency/urgency
Tension myalgia of the pelvic Aoor is a spectrum of diagnoses of various syndromes of pelvic musculature, including piriformis syndrome, levator ani syndrome, coccygodynia, and vaginismus (77). Other diagnoses with a component ofhyperronus dysfunc tion include (78,79): • • • • • •
Chronic low back pain Endometriosis Chronic pelvic pain with negative surgical findings Interstitial cystitis Urethral syndrome Sphincter dyssynergia
417
Chronic pelvic pain is the second most common complaint in gynecologic practice. Musculoskeletal postural dysfunction has been implicated and can lead to levator ani syndrome by main taining inefficient holding patterns of muscles that conrribute to the persistence of pain (79-8 1 ). Somatic dysfunction of the pelvis, if untreated, may cause hyperronus as a result of restriction of motion of pelvic joints and their related structures. Myofascial pain syndromes create pain, tenderness, and auronomic phenom ena from myofascial trigger points. Travell and Simons (82) have identified trigger points in these muscles: Coccygeus Levator ani • Obturator internus • Adductor magnus • Piriformis or oblique abdominals • •
These pelvic muscle somatic dysfunctions may be treated wi th bimanual relaxation of muscle contractions. The vaginal palpat ing digits may apply inhibirory pressure, or use principles of counterstrain or myofascial technique to achieve release of ten sion or spasm. Identification of Chapman reflex points may also direct the osteopathic physician to treat related somatic dysfunc tion within the pelvis (83).
OTHER ORGANIC C AUSES OF PELVIC PAIN
Because the uterus and fallopian tubes share the innervation of the lower intestinal tract, pelvic pain can be nongynecologic in origin. Gastrointestinal sources of pelvic pain include: • • • • • •
Penetrating neoplasms of the GI tract Irritable bowel syndrome Parrial bowel obstruction InAammatory bowel disease Diverticulitis Hernia formation
Osteopathic consideration for treatment involves addressing somatic dysfunction of the thoracolumbar spine, pelvis, and lower extremities to improve circulation and enhance lymphatic drainage. Chapman reflex areas aid with differential diagnosis (83). Counterstrain tender point treatment relieves the somatic dysfunction component of GI pain. Low back pain of neuromuscular origin usually increases with activity and stress. Chronic low back pain without lower abdominal pain is seldom of gynecologic origin (84). Occasion ally, a pelvic mass accompanied by neuromuscular symptoms may be revealed during surgical exploration to be a neuroma or bony tumor (85).
CONCL USION
Although gynecologists are trained ro perform surgery on female patients, osteopathically trained gynecologists develop an appre ciation of the architecture and engineering of the pelvis. Through
418
VI. Osteopathic Considerations i n the CLinicaL SpeciaLties
use of skilled palpatory evaluation of a patient's internal and ex ternal body structure, they have the opportunity to both diagnose and prevent dysfunction that has been inAuenced by the muscu loskeletal system. Appropriately used osteopathic manipulative treatment offers relief of gynecologic pain that is not available by surgery or pharmacology.
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nical Bulletin 153: Antimicrobial therapy for gynecological injections. Washington, DC: The American College of Obstetricians and Gyne cologists; 1 99 1 . 62. Physicians hear about incontinence [editorial ] . }AMA. 1 990;264:238 1 2382. 63. Pope CS, Rabin J. Urinary incontinence: Evaluation and non-surgical management. The Female Patient. 200 1 ;26:4 1 -47. 64. Urinary Incontinence Guideline Panel. Urinary Incontinence in Adults.
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NEUROMUSCULOSKELETAL MEDICINE AND OSTEOPATHIC MANIPULATIVE MEDICINE RAYMOND J. HRUBY
KEY CONCEPTS • • •
• • • • •
The development of the earned fellowship in the American Academy of Osteopathy The evolution of certification in neuromusculoskeletal medicine and osteopathic manipulative medicine The development of the hospital-based osteopathic manipulative medicine consultation and treatment service The role of the osteopathic manipulative medicine specialist The examination and treatment of acutely i l l hospitalized patients The osteopathi c manipulative medicine consultation in the hospital Recording structural diagnosis and treatment of hospitalized patients A case study in cri t ical thinking for the osteopathic manipulative medicine specialist
In 1958, a meeting was held by a commi ttee comprised of representatives from the Academy of Applied Osteopathy (AAO, now called the American Academy of Osteopathy) and the Amer ican Osteopathic Association (AOA ) . T h is commi ttee met to study and to establish the fellowship ptogram of the Academy of Applied Osteopathy (FAAO) . The program was to recognize doctors of osteopathy (DOs) with special expertise in manipula tive skills and to encourage other DOs to improve their skills. In 1959, the following paragraph appeared in the directory of the Academy of Applied Osteopathy: A proposal was presented ro the Board of Governors of the Academy, and ro a special committee of the Advisory Board for Osteopathic Specialists for the formation of a new certifying board called the American Osteopathic Board of Manipulative Arts and Sciences. The proposal was made by a group of osteopathic physicians headed by Dr. T. F. Schooley, Phoenix, Arizona. Proposals for certification in the field of manipulative therapy have been studied for several years with no success in reaching agreement relative to the propriety and value of such a program. Those favoring such a step contend that there must be established a means of recognizing and accrediting the members of the profession who have developed a high degree of knowledge and skill in the field, and whose practices are based prin cipally upon the structural approach. Those opposed ro cerrification
Osteopath ic principles and philosophy (OPP) and the practice of osteopathic manipulative treatment (OMT) are part of the education of every osteopathic physician. These elements are in corporated inro the everyday practice of osteopathic medicine. Like other areas of medicine, over time a need developed for osteopathic physicians with special expertise in these distinctive elements of osteopathic medicine. Thus, the specialist in osteo pathic manipulative medicine (now called neuromusculoskele tal medicine, or N M M ) and OMT was born. These specialists are primarily responsible for the further expansion of osteopathic concepts and methods, and they contribute t h is expanded knowl edge to the profession through teaching, writing, and specialized cl inical practice. The need to recognize this special expertise i n NMM and O M T led t o t h e development of a primary certifica tion in this area through the American Osteopathic Association and to the development of an earned fellowship through the American Academy of Osteopathy.
in the field contend that the manipulative application of osteopathic principles is basic ro every osteopathic physician's approach ro the problems presented by his patien ts, and cerci fication of this basic and fundamental aspect of osteopathy would be improper and would limit the profession. All who have studied the matter are in agree ment that a means must be established for recognizing ability in the field
(1).
In 1960, the committee presented detailed recommendations for the functioning of the Board on fellowship, which was adopted by the Academy's Board of Governors and the AOA's Board of Trustees. The fellowship was described as an "earned" fellowship because i t required certain prerequisites, a 5 ,000 word written thesis, and oral, wri t ten, and practical examinations. The FAAO process was thus established. In 1971, a joint com m ittee of representatives from the AAO and the AOA met to discuss the steps necessary to convert the FAAO process to certification in osteopathic manipulative
29. Neurornusculoskeletal Medicine and Osteopathic Manipulative Medicine
medicine. A resolurion ro rhis effecr was presenred ro rhe AOA Board o f Trusrees bur was nor approved. However, in 1977, the AOA Board ofTrusrees did approve certificarion for the FAAO. The Board on Fellowship now became an AOA board directly responsible ro rhe Board of Trustees. Residency programs i n os reopathic manipularive medicine were developed by the Ameri can Osteopathic Board on Fellowship i n the American Academy of Osreoparhy (AOBFAAO ) . Over the years, the AOBFAAO underwen t several name changes. In 1983, rhe AOA asked for a name change for the board, and rhe Academy submitted rhe name "American Board on Osteoparhic Manipularive Medicine." This was approved by rhe AOA Board of Trusrees in July 1984, but because of subsequenr opposition ro rhis name by other consrituenrs of rhe profession, rhe name was later returned ro rhe AOBFAAO. In 1989, ro par allel sim ilar processes in other AOA specialry colleges, the AOA requested rhar rhe combined processes of certification in O M M and conferring of rhe FAAO b e separated. This was accomplished wirh the FAAO now being adj udicared by a Com m ittee on Fel lowship wirhin rhe AAO. A new certifying board was Formulated and named the American Osreoparhic Board on Special Profi ciency in Osteoparhic Manipulative Medicine (AOBSPO M M ) . The AOBSPOMM was a certifying board directly responsible ro the AOA Board of Trustees. In 1999, rhe AOBSPOMM was changed ro the "American Osteopathic Board on Neuromuscu loskeleral Medicine and Osteopathic Manipularive Medicine." Osteopathic physicians who successFully pass rhis Board's exam inarion are issued certificares indicating that rhey are certified in neuromusculoskeleral medicine and osteopathic manipulative rrearmenr. Tables 29.1 and 29.2 describe rhe currenr require menrs For certification in N M M and OMT, and rhe requirements for achieving rhe FAAO, respecrively.
THE DEVelOPMENT OF THE HOSPITAL-BASED
421
orher osreoparhic hospirals ro provide similar services. In addi tion, Dr. Stiles did much ro esrablish the role of rhe OMM spe cialisr in such a serting. H e described rhe elemenrs of this role as follows: As developed by Waterville Osteopathic Hospital, the duties of the direcror of osteopathic medicine are as follows: I.
The direcror is ro provide clinical consultation services for referred patients and ro document properly the osteopathic diagnosis and treatment utilized.
II.
The direcror is ro be an educaror and ro increase the staff's expertise and awareness of the applications and indications for osteopathic care. Creating a service of osteopathic medicine in a hospital setting provides a tremendous educational potential. The following edu cational rools can be utilized: (a) consultation reports; (b) courses in technique and principles; (c) committee reports on utilization of osteopathic manipulation; (d) departmental educational meet ings; and (e) staff educational meetings. Each of these rools pro vides an opportunity ro increase the awareness of the staff of the implications, applications, and indications for utilization of os teopathic care in a hospital environment. This naturally increases the awareness of the sraff as ro the types of patients who should be referred ro this service and offers a challenge ro staff members ro improve their own levels of expertise in the delivery of health care.
III.
The direcror of osteopathic medicine is ro fill a public relations role for the hospital
(2).
Docror Sriles also made note of the research potential aFForded by such a hospital-based service. In recen r years, a number of smaller osteopathic communiry hospitals in rhe Unired States have closed because of changes brought about by managed care and economic conditions. Other osteopathic hospitals have merged wirh allopathic i nsritutions. Despire rhese changes in rhe health care climare, a few hospiral based osreoparhic medicine services are srill in operarion.
OSTEOPATHIC MANIPULATIVE MEDICINE CONSULTATION AND TREATMENT SERVICE THE ROLE OF THE OSTEOPATHIC
As osteoparhic hospirals were developed in rhe early years of rhe proFession, OMT was an essential part of the rreatmenr of hospiralized parienrs. Wirh rhe developmenr of special ries and subspecialries within rhe osteoparhic profession, ir became more difficult For these DOs ro provide regular OMT ro their hos piral patients, due ro increasing patienr loads, time constrai n ts, and rhe overall demands of specialry pracrices. As a resulr, DOs who had more exrensive rraining in OMT and who dedicated much of their parienr care ro the use of disrinctive osteopathic methods were called on ro provide consultation and rreatmenr for hospiral parienrs. These DOs were viewed as specialisrs in OMM. This rype of practice gained Further impetus and an expanded role wirh rhe developmenr of a unique program ar rhe Waterville Osreoparhic Hospiral in Warerville, Maine, in 1973. This hospi ral esrablished the posirion of Direcror of Osreoparhic Medicine, a Full rime osreoparhic physician hired by rhe hospiral ro pro vide rhe basis For a consulrarion and rrearmenr service in rhe areas of OMT and OPP. The firsr direcror of rhis service was Edward G. Sriles. H is successful leadership of rhis program led
M ANIPULATIVE MEDICINE SPECIALIST
Today rhose DOs who have chosen ro special ize in NMM and O M M conrinue ro serve in expanded roles beyond rhose de scribed above. Some of these roles include: Providing outparient consultarion and rrearmenr services. The private practice of N M M and O M M . Ill. Serving as medical and legal experts i n N M M and O M M . IV. Teaching at colleges of osteopathic medicine, either a s fullrime or part-rime faculty. v. Serving in adm i nisrrarive positions, such as department chairs or deans, in colleges of osteoparhic medicine. VI. Direcring residency programs i n N M M and O M M . VII. Parriciparing in research projecrs i n N M M and O M M . VIII. Teaching in posrgraduate rraining programs and in contin uing educarion programs. IX. Participaring 111 inrernational programs on man ual medicine. x. Wriring scholarly works for journals and texrbooks. I.
II.
VI. Osteopathic Considerations in the Clinical Specialties
422
TABLE 29.1. CERTIFICATION AS A DIPLOMATE OF THE AMERICAN OS TEOPATHIC BOARD OF NEUROMUSCULOSKELETAL MEDICINE (AOBNMM) A Doctor of Osteopathy may be certified by the Board of Trustees of the American Osteopathic Association in recognition of his/her proficiency in neuromusculoskeletal medicine and the use of osteopathic structural and palpatory diagnosis and manipulative treatment in the total health care of patients. Osteopathic physicians who have completed a residency in neuromusculoskeletal medicine may establish board eligibility. Until December 31,2005, osteopathic physicians, whether in general practice or in any specialty practice, can also be so certified by fulfilling the appropriate eligibility requirements.
Minimum Requirements I. The applicant must be a graduate of a college of osteopathic medicine approved by the American Osteopathic Association. II. The applicant must be licensed to practice in a state, territory, province or country. III. The applicant must be able to show evidence of conformity to the standards set in the Code of Ethics of the American Osteopathic Association. IV. The applicant must have been a member in good standing of the American Osteopathic Association or the Canadian Osteopathic Association for a continuous period of at least 2 years prior to the date of certification. V. The applicant must have completed satisfactorily an internship of at least 1 year in a hospital approved for intern training by the American Osteopathic Association. VI. The applicant must have completed by AOBNMM application deadline: A. At least 2 years of an AOA-approved residency in neuromusculoskeletal treatment and osteopathic manipulative medicine and meet the AOA's criteria for board eligibility. B. Completion of the residency plus 1 year of neuromusculoskeletal medicine residency training option and who meets the AOA's criteria for board eligibility. C. If the board eligibility of a candidate who is a graduate of an neuromusculoskeletal residency program-either a 2-year AOA-approved residency program or if a residency plus 1 year of neuromusculoskeletal medicine residency training program has expired, the Academy will recognize the candidate as an applicant under the 5-year practice requirement under section D as follows: D. Until December 31,2005, osteopathic physicians who graduated from AOA-approved colleges of osteopathic medicine prior to December 31, 1999, may qualify via a "practice track", i.e., they must complete 5 years of practice, which may include an AOA-approved residency in other than a neuromusculoskeletal medicine residency. This training shall include active experience in the use of structural diagnosis and manipulative management in osteopathic medicine, with CME documentation: 1.
Five years CME credits based only on the last 5 years from an AOA printout, average of 50 hours per year (minimum of 250 hours total)
2.
150 hours (category 1-A only) must be programs sponsored by the American Academy of Osteopathy, or approved by the AOBNMM
and of these. certifying board. E. Four years of practice plus a college of osteopathic medicine approved pre-doctoral fellowship in osteopathic manipulative medicine. The continuing medical education requirements as stated in D1
& 2 above are applicable; or
VII. The applicant must document his or her qualifications in the formal application. VIII. The applicant must prepare and submit three case histories suitable for publication which document understanding of osteopathic sciences and their application in health and disease as it relates to his/her practice discipline. These cases should demonstrate breadth of knowledge, understanding and skills in various techniques, and paradigms, as well as will be expected on the written, oral and practical aspects of the certification exam. If a candidate's case(s) is(are) not approved, the candidate must submit an entirely new case(s) for the board's review. IX. The board shall establish individual eligibility of the candidate for examination. X. A written, oral, and practical examination will be required of each applicant. (From information posted on the American Academy o f Osteopathy website at
THE OSTEOPATH M ANIPULATIVE MEDICINE SPECI ALIST'S OSTEOPATHIC EXAMINATION OF THE HOSPITALIZED PATIENT History Taking and D ata Gathering
Begin the osteopat h ic h istory of the hospitalized patient with a review of the medical record, paying close attention to factors af fecting or affected by the neuromusculoskeletal system . Next, take the patient's history. If the patient is unable to give the history be cause of age, neurologic damage, intubation, or other causes, ask a family member to provide the h istory. The history for the neu romusculoskeletal evaluation includes the routine medical and surgical h istory, in addition to questioning the patient or fam i l y member about previous injuries and structural abnormalities. Typically, the following are included in the patient's h istory: Head trauma Motor vehicle accidents Pratfalls Fractures
http://www.academyofosteopathy.orglcertif.htm.
with permission.)
Episodes of loss of consciousness Presence of known shorr leg Scoliosis Previous experience with osteopathic manipulative treatment (OMT) Previous experience with other manual medicine modalities Response to previous treatments The h istoric data assist the physician in deciding which mus culoskeletal areas m ight contain primary somatic dysfunction and/or w hich m ight contain secondary somatic dysfunction pro duced by somatovisceral reAexes from related visceral dysfunc tion. The history also assists in deciding which manipulative techniques are most appropriate. P hysical Examination
Begin the examination with a review of the patient's original ra diographs. T h is is extremely important because bony and fascial abnormalities significant to the patient's disease process may not
29. NeuromuscuLoskeLetaL Medicine and Osteopathic ManipuLative Medicine
423
TABLE 29.2. REQUIREMENTS FOR FELLOWSHIP IN THE AMERICAN ACADEMY OF OS TEOPATHY (FAAO) Only AAO members may apply to the Fellowship Committee for examination pursuant to the earned Fellowship in the American Academy of Osteopathy (FAAO). Fellowship is awarded by the Academy's Board of Governors only upon the recommendation of the Fellowship Committee following successful completion of examination.
Purposes 1. To recognize continued and special achievement in the preservation and use of osteopathic principles and practices. 2. To acknowledge ability and service to the Academy and to the profession. Emphasis on the "categories"of activity as a gauge of achievement. 3. To maintain a group of leaders to encourage high standards of osteopathic medical practice with special emphasis on manipulative diagnosis and treatment, and to work for the integration of osteopathic concepts into all areas of practice. For this reason, physicians in other areas of practice or specialties are encouraged to qualify for this Fellowship. Such leaders would serve as resources and inspiration for the entire profession, but especially for those who have sought certification in manipulative medicine under the requirements of the American Osteopathic Association. Fellowship shall represent a second stage of high achievement in no way denigrating the importance of the first step which is Certification by the American Osteopathic Board of Special Proficiency in Osteopathic Manipulative Medicine or the American Osteopathic Board of Neuromusculoskeletal Medicine. It will represent an "earned" degree.
Requirements 1. Certification is a prerequisite, either in Special Proficiency in Osteopathic Manipulative Medicine or Neuromusculoskeletal Medicine and Osteopathic Manipulative Medicine. 2. Evidence of continued good standing in the American Osteopathic Association or the Canadian Osteopathic Association. 3. Membership in the American Academy of Osteopathy for a period of 5 years prior to application and to maintain Fellowship.
4. Practice requirement: Ordinarily, the practice requirements will be satisfied by the achievement of certification. At least 3 years of practice should intervene between the Certification and Fellowship application in the case of resident-trained candidates. 5. Scientific PaperfThesis requirement: A Scientific PaperfThesis (primary author) suitable for publication is required. Such papers shall not have been part of any qualification for another degree. The scientific paper/thesis will hopefully reflect originality and make some contribution to the body of osteopathic literature. A topic heading and brief outline and tentative bibliographyt (approximately 1-3 pages in length with appropriate explanatory statements) shall be approved prior to the writing of the scientific paper/thesis.
6. CME requirements shall include at least 30 hours of AAO-sponsored or Committee-approved training of each 50 hours per year as required by the AOA. The candidate will give evidence of this for the previous 3 years via the AOA CME printout. (There may be overlap here with the AOBSPOMM requirement.)
7. Case histories: ten case histories (not to include material supplied for certification) will be required. 8. Categories of service: the candidate shall supply evidence of fulfilling at least four of the six categories below: a. Contribution to osteopathic literature (specific publication, etc., should be listed). b. Development of osteopathic theory and/or manipulative method or procedure. c. Research related to osteopathic theory and practice. d. Contributions in the field of osteopathic education: Faculty (college, AAO, cranial, etc.) Visiting clinician Visiting scientist Preceptorship activity Clinical and/or hospital supervision and/or consultation e. AAO organizational activity (boards, committees, etc.) f. Public relations Community activity School physician Sponsor of health activity Public health service Other
Examinations No written examination will be given, but in-depth oral and practical examinations will be required. (From information posted on the American Aca demy o f O steo pa thy website at http://www.academyofosteopathy.org/certif.htm. with pe rm iss io n.)
(ME, continuing medical ed ucation.
have been mentioned in the radiology reporr. Only after review of the chart and the original radiographs, and recording of an integrated history is the physician prepared to perform a physi cal examination of the patienr. As with the h istory, integrate the osteopathic palpatory examination into the toutine medical ex amination of the patienr. The history and chief complaint dictate that some areas of the body must be more tho toughly investigated than others. It is generally easier to use a standard apptoach to the patient that can be modified slightly to fit each individual
patient's needs. Follow routine body Auid contamination proce dures during the examination of all patients. The following protocol is suggested, although alterations are necessary depending on the patient's needs and the physician's preference. This protocol is based primarily on the respiratory, circulatory, and neurologic models of osteopathic evaluation and treatment (4, 5 ) . Emphasize the major diaphragms of the body that i mpede normal Auid Row, and the bony and Fascial attach ments of those diaphragms. Emphasize rib function because of
424
VI Osteopathic Considerations in the Clinical Specialties
FIGURE 29.1. Anterior superior iliac spine compression test.
i ts relationship both to fluid movement w i th i n the body and to reflexes mediated by the sympathetic nervous system via the chain ganglia that lie anterior to the rib heads. Emphasize the paraspinal myofascial elements of the suboccipital, sacral, and thoracolumbar areas because of their i nvolvement with auto nomic reflexes that manifest in these areas. If the patient is ambulatory, the musculoskeletal examination is not significantly different from an outpatient structural evaluation. H owever, the routine outpatient musculoskeletal exami nation is not appropriate for acutely ill patients. A bedside osteopathic evaluation i n the supine position is necessary. A suggested examination begins with bilateral compression of the anterior superior iliac spines (ASISs), the ASIS compression test. This test indicates restrictions in i liosacral mobility that i nterfere with sacral and pubic motion, and pelvic diaphragm tension (Fig. 29. 1 ) . Evaluate and treat the sacrum and lumbar areas from the pa tien t's side. Generally, the patient is lying on an absorbent pad over a draw sheet and fitted mattress sheet. The sacrum and lum bar areas are easily approached by slipping the hands under the patient, palms up, between the draw sheet and the fitted mattress sheet. This is made easier by loosening the draw sheet from under the mattress and rol l i ng it up parallel to the patient on either side of the bed (Fig. 29.2). This rolled-up draw sheet serves as a sli ng with which the patient can be gently l i fted and rolled away, en abl ing the physician to place a hand under the pelvic or lumbar area without any effort required by the patient. Although this treatment procedure requi res palpating and treating through the thickness of the absorbent pad and draw sheet, it becomes easy with practice. This approach also protects the patien t's modesty, and the physician is less l i kely to come i n to contact w i th any discharge, drainage, urine, or feces i n the bed. Next, place the fi ngertips of one hand at the i n ferolateral angle of the sacrum and the fi ngertips of the other hand at the ipsilateral sacral base (Fig. 29.3). Exert alternate pressure in a n anterior direction w i th the fi ngertips, ascertai n i ng the ability ofthe sacrum to rock on i ts L-shaped articulation. This procedure reveals sacral motion restrictions. Next, place one or both hands under the patient's lumbar spine, and assess the tissue texture changes and motion restrictions of the lumbar spine according to the protocol suggested by Larson ( 3 ) . This is carried out by pressing anteriorly on the paraspi nal elements. First note tissue texture changes, then note any ease i n
rotatory motion induced b y using an alternating anterior pressure on the transverse processes. The characteristic texture changes resulting from viscerosomatic referral are most easily discerned with the patient sup ine, and with the examiner execU[ing anterior palpatory pressure. With the patient relaxed as much as possible, estimate the degree of lumbar lordosis. If the patient is not in the i mmediate postoperative period after abdo m inal or pelvic surgery, palpate the abdomen for vis ceral dysfunction. Assess restrictions of the thoracoabdomi nal diaphragm by placing one hand under the patient at the T I O-L2 area posteriorly, and the other hand anteriorly, just i n ferior ro the xiphoid process. One hand gently twists the underlying fas cia clockwise while the other hand twists counterclockwise; then , reverse the direction of testing. The abdominal diaphragm dys function is named according to the direction of preferred fascial movement sensed by the abdominal hand. Assess the excursion of the lower and upper ribs by having the patient breathe deeply. Lightly palpate the rib cage at the midaxillary l i ne for the lower ribs. Palpate over the midclavicular line lateral to the sternum for the upper ribs. If the patient has a chest tube i n place or is on a respirator, follow the motion present by lightly resting hands on the rib cage. Gently rest the palpating hand on the sternum and follow i ts motion, noting any fascial pulls and any costosternal articular restrictions (Fig. 29.4). Perform a screen of the anterior Chapman (6) and Jones points (7) in the thoracic and abdominal areas. Note any specific rib restrictions so that they can be treated later. Note the symmetry of the thorax and tension of the accessory muscles of respi ration. Adjust the bed to place the patient i n the Fowler position (approximately 1 5 degrees of head elevation), elevating the mat tress until i t is even w i th the top of the headboard. Move to the head of the bed and remove the patient's pillow. This positioni ng allows treatment with m i n i mal stooping and without removing the headboard. If the Fowler position is contraindicated, the en tire bed may be elevated. The bed may need to be pushed away from the wall ro permit access to the head of the bed. Be care ful not to disturb peripheral and central l i nes, suction tubing, urinary catheters, and other bedside obstacles. Follow this same procedure in the i n tensive care unit as well. If the patient is on a respirator, treat h i m or her in the position dictated by the life support systems. Standing and l eaning over the head of the bed, place a hand on each side of the patient's head, palms facing upward, and glide them between the draw sheet and the bed, or between the bed sheet and the mattress, down to the T 1 2-L2 area of the patien t's back (Fig. 2 9 . 5 ) . With elbows leaning on the head of the bed for support, place the fi ngertips over the transverse processes. Push anteriorly with the fi ngertips of both hands, first assessing the tis sue texture changes. Then, push alternately to assess the rotarory motion of the paraspinal elements. This is the same assessment used for the lumbar area. Move the hands more cephalad and repeat the process until the entire thoracic spine has been evalu ated. Also note fascial restrictions of the thorax and further defi ne rib somatic dysfunction noted on the rib motion screening ex amination. Place the fingertips of the anterior hand agai nst the costochondral junction, and those of the posterior hand at the rib head of the same rib (Fig. 29.6). Next, evaluate the thoracic inlet for fascial restrictions (Fig. 29.7) . I f the patient has any central venous l ines, the hand
29. Neuromusculoskeletal Medicine and Osteopathic Manipulative Medicine
425
FIGURE 29.2. Draw sheet sling for posterior palpation and treatment of the patient. A: Loosen draw sheet from under the mattress. B: Roll draw sheet parallel to the patient. C: Place hands between the draw sheet and the mattress to contact lumbar areas.
on that side must be placed more laterally, near the acromioclav icular joint. The presence of these lines does not contraindicate evaluating and treating this area but m akes it even more impera tive that it be evaluated. Evaluate the cervical area for the presence of somatic dysfunction. Assess the suboccipital area for condylar compression and occipito-atlantal (O-A) and adamo-axial (A-A) somatic dysfunc tion (Fig. 29.8) . Gently cradle the head and upper cervical area with the fingertips and hands. If craniosacral diagnosis is to be performed, the cranium is now palpated for somatic dysfunction. The cranium can be evaluated with many hand positions. I n one position (Fig. 29.9), the palms and fi ngertips gently rest on the
head with thumbs at the vertex or off the head, i ndex fingers at the area of the great wing of the sphenoid bone, m iddle and ring fingers on either side of the ear, and little fingers on the occiput. The bed is in Fowler position, and the physician is resting his or her elbows on the head of the bed for support. At this point, the neuromusculoskeletal system of the patiem has been assessed, including: I.
Sympathetic nervous system: Evidence of somatic dysfunc tion associated with the sympathetic nervous system is in dicated by palpation of the thoracic and upper lumbar area (spinal levels of origin of the sympathetic nervous system )
426
VI Osteopathic Considerations in the Clinical Specialties
FIGURE 29.4. Sternal palpation.
FIGURE 29.3. Sacral rocking.
for viscerosomatic and arricular restrictions, and palpation of the rib cage for restrictions affecting or being affected by the sympathetic chain ganglia. II. Parasympathetic nervous system: Evidence of somatic dys fu nction associated with the parasympathetic nervous system is ind icated by palpation of the sacral, suboccipital, and cra n ial areas (its central nervous system site of origin). III. Lymphatic system : Evidence of dysfunction affecting lym phatic Row is i ndicated by assessing the four major di aphragms of the body (pelvic, thoracoabdominal, thoracic inlet, and foramen magn um) and rib motion. I V . Visceral dysfu nction: Visceral dysfunction is reAected by pos itive anterior Chapman poi nts, visceral palpation (when pos sible) , and spinal somatic dysfunction that may be related to facilitated segments. v. Structu ral component: Asymmetries and abnormalities of the cervical, rhoracic, rib, and pelvic areas affect optimal func tion ing of the autonomic and lymphatic systems.
and the body's ability to heal i tself. Each intervention performed requires energy from that patient to incorporate the changes in duced i n to their body by the manipulation. Therefore, treat only those dysfunctions that impede the homeostatic processes. Leave long-standing or unrelated problems for outpatient care. There
TRE ATMENT OF THE HOSPITALIZED PATIENT General Consid erations
When treating the hospitalized patient, remember that the pa tient is acutely ill. The treatment goal is to promote homeostasis
FIGURE 29.5. Palpation of posterior thoracic area.
29. NeuromuscuLoskeLetaL Medicine and Osteopathic ManipuLative Medicine
FIGURE 29.6. Individual rib evaluation and treatment position.
FIGURE 29.7. Thoracic inlet evaluation and treatment position.
FIGURE 29.8. Suboccipital evaluation and treatment position.
427
FIGURE 29.9. Cranial evaluation with vault hold position.
is consensus among experts in hospital O M T that the acutely ill patient may only be able to tolerate short periods of treatment at any given time, so manipulative efforts may need to focus on areas of the body that require immediate a[[ention. For exam ple, a short leg and m ild functional scoliosis may not need to be addressed during a hospitalization for pneumonia unless they contribute to i mpaired homeostasis during the acute ill ness. The shorr leg, though it may be a contributing factor in lowering the patient's resistance to i n fections and trauma, can usually be evaluated after recovery from the acute incident. Alterations in tissue texture changes are helpful in following the patient's medical progress. The presence of new tissue texture changes at a given level alerts a physician to possible early organ dysfunction. Likewise, resolution of the viscerosomatic reRex in dicates i mproved health i n that area. One notable exception oc curs when treating extremely compromised patients. The severely ill patient whose v ital resources or i m mune system has been ex hausted will fai l to show tissue texture changes that should, in fact, be present considering the site of the organ dysfunction. In these patients, the presence of new tissue texture change in areas that are appropriate for that patient's i l lness may be a favorable sign. When formulating a man ipulative prescription (8) for an in patient osteopathic treatment, determ ine the frequency and dura tion. This varies according to the patient's condition. [n general, for very i l l patients, it is be[[er to provide frequent treatmenrs over shorr time i nrervals and to use less forceful techniques. This usually means treating the patient once daily, although some l iterature suggests more frequent application (9,10,11). As the patient i mproves, the i nterval between treatments and the treat ment duration may be lengthened if needed. The patient may also be able to tolerate the use of more direct techniques. Treat only those areas most l i kely to i mpair the recovery ptocess, con sidering both lymphatic Row and autonomic balance. When a hospitalized patient can tolerate 3 or 4 days between treatments, the manipulative treatmenrs may essen tially be provided on an i ntensive outpatient schedule. Psychiatric inpatienrs and those in drug and alcohol inpatient treatment programs may require a different schedule and are d iscussed separately. If the patient is unfamiliar with osteopathic treatments, espe cially those given at the bedside, brieRy explain the philosophy and reason for the OMT. A simple explanation seems to work
428
VI. Osteopathic Considerations in the Clinical Specialties
best, such as: "There are nerves from your spine that go ro both the back m uscles and the organs i nside. When an i nrernal organ is sick, a reAex is created that causes your back m uscles ro get tense. By treating your back, the reAex is calmed so that the organs can heal faster." Or you might say: " When you have pneumon i a (or congestive heart fai l ure, etc.) , the A uids in your body pool in your lungs, making your ill ness worse. Your ribs don't move normally either, making it more difficult to get rid of this A uid. The os teopathic treatmenr will help your ribs work more normally, and help pump the A uids our of your lungs." Further answers may be provided if the patient expresses an in terest. Usual ly, however, the patient simply relaxes with the physi cian's sooth ing rouch , and no further explanations are needed. For any medically ill, hospitalized patient, the presence of somatic dysfunction i n areas that impede normal auronomic or lymphatic fu nction ing can and should be treated. T he patient's disease process dictates the areas ro treat and the techniques ro use. Treatment P rotocol
Decide which areas most impair the patient's homeostatic bal ance, wh ich techniques are best suited for the patient, and how much treatment the patient can rolerate. In other words, create a man ipulative prescription ( 5 ) . A general rule of thumb is ro se lect at least one or two principle areas for treatment that are most relevant ro the patient's recovery. Additional areas may be added, depending on the response of the patient. In this way, the patient is not overtreated, and no i mportant areas are m issed. One should give consideration ro treatment approaches rhat would i mprove any or all of the following: Auronomic nervous system function Lymphatic Aow Respirarory excursion Biomechanics Visceral function Using this approach, important auronomic, lymphatic, vis ceral, and structural components relevant ro the patient's recovery are evaluated and treated. Some manipulative techniques appropriate in one situation may not be appropriate in another. For example, for a parient with fractures, avoid any treatment positioning that could desta bilize the fracture site. A patient in the intensive care unir with a myocardial infarction generally should not receive techniques using isometric patient contractions. The decision of where and why ro treat the patient l ies with the physician and is parr of the medical decision-making process. Sp ecial C onsid erations Acquired Immunodeficiency Syndrome Patien ts
Persons with acquired immunodeficiency syndrome (AIDS) who are hospitalized should be treated manipulatively with the same rational and system ic approach as all hospitalized parients. The nature of the disease process for which they have been hospitalized dictates wh ich areas should be treated manipulatively, as well as rhe in rensiry, d u rarion, and frequency of rhe treatment. As with
all parients, rourine body fluid precautions should be taken. [f the patient is i n isolation, special precautions are necessary, as discussed below. Drug and Alcohol Detoxification and Rehabilitation Pa tients
During drug or alcohol deroxification, the patient is not usually responsive ro OMT. After the deroxification has been completed, OMT has been noted by experts ro be helpful in aiding the recov ery process. Most parients undergoing drug or alcohol treatmenr have a long h isrory of trauma and/or abuse. OMT should address the lasring effects of that trauma on the musculoskeletal, emo tional, and cranial systems. Any medical or surgical conditions are treared according ro the guidelines described earlier. OMT in the inpatient psychiatric or drug/alcohol treatment setting seems ro be generally more effective than treatmenr of the same patient as an outpatient. Presumably, the i n tensive set ti ng, where n utrition, medication, exercise, peer support, situ ation control, and counseli ng are structured i nro the patient's existence, allows an increased recovery rate in the entire person ( m i nd, body, and spirit) . Experts have reported that OMT is extremely effective in this optimal setting. Intensive Care Unit and Respira tor Patients
When moving a patient in the bed or changing the bed posi rion, request assistance so as not ro endanger the stability of any drainage, i ntravenous, arterial, endotracheal, or feeding rubes. Patients on respirarors can and should be treated manipulatively. Avoid techniques that interfere with the respirarory rate, such as the pedal pump or classic lymphatic pump. Isolation Patien ts
If the patient has been placed in some form of isolation, require ments for gloves, gown, and mask m ust be followed. Palparory examination and O MT with gloves are not ideal, but protection is necessary. For patients with profuse secretions, it is wise ro use gloves even if no isolation prorocols are ordered. During the rreatmenr, position yourself and the patient in a manner that will reduce your chances of becoming infected. Pedia tric Pa tients
Newborns occasionally need treatment in the nursery for cranial entrapment neuroparhies that result i n colic and feeding disorders ( 1 2) . These conditions can often be relieved by simple, gentle, condylar decompression . Treatment of pediatric patients for medical i l lnesses (such as pneumonia) and posroperative OMT for infants involve the same processes used for treari ng adults. The techniques recommended, however, are usually articular, balanced I igamenrous tension, bal anced membranous tension, or myofascial approaches. One treat menr for children described by Max Gutensohn (personal com munication) enables the physician ro simultaneously articulate vertebral levels and encourage lymphatic Aow while seemingly playing a game w i rh rhe child. T h is is especially n ice for assisting recovery from respirarory disease. The child is held i n the air with the physician's hands encircling the chi ld's chesr under the axillae.
29. Neuromusculoskeletal Medicine and Osteopathic Manipulative Medicine
The legs are then gently swung in a circle, thereby mobilizing the area j ust distal to the hands on the torso. To articulate other areas, hold the child higher or lower on the torso. Gentle rib raising and spinal articulatory procedures in the lateral recumbent, supine, or seated positions are also well tolerated. Postoperative or Posttra uma Pa tien ts
When treating postoperative patients who are in the hospital, avoid excessive j iggli ng and overhead arm techniques. Some tech niques, such as the lymphatic pump with arms overhead or vig orous pedal pump, may endanger the stab i l i ty of the operative site or injury. Psychia tric Pa tients
The osteopathic premise states that the body is a unit, with mind, body, and spirit as i nterwoven parts of one being. T h is supports the concept of treating a patient with psychiatric i l lness to im prove function i ng of the rest of the body. I f the psychiatric patient is hospitalized for a medical or surgical condi tion, he or she is rreated for that condi tion following the guideli nes described ear lier. Patients who are hospital ized for their psych iatric disease also deserve an osteopathic structural evaluation and manipula tive treatment if indicated. The structural exami nation should closely evaluate the cra nial sacral mechanism and the upper thoracic regions, looking for evidence of somatic dysfunctions that could be produced by autonom ic reflexes. Older l i terature makes a strong case for dysautonomia as a significant factor in psychiatric disease, based in part on cli nical observations at the Still-Hildreth Osteopathic Sanitorium. Dunn ( 1 3) discusses the association of autonomic dysfunction with psychiatric disease and supports this associa tion with data from J ,000 psych iatric patients. More than 50 of these patients demonstrated palpable somatic dysfu nction at C2 and T4-6 paravertebral regions of the spine. In 2,288 exam inations, Woods ( J 4) demonstrated an altered rate o f the cran ial rhythmic im pulse in various psych iatric diseases, as compared with controls. In addition to affecting autonomic reflexes, OMT appears to have a calming effect on the psychiatric patient. Psychiatric patients generally do not tolerate h igh-velocityllow-ampl itude techniques wel l . Use a sooth ing treatment apptoach and a slow, gentle touch ( I S) . When psych iatric patients are receiv i ng elec troconvulsive shock treatments (ECTs), OMT withi n 24 hours of a treatment event does not appear to be productive. Provid ing OMT on the day after ECT, however, has been observed to be extremely effective. Osteopathic treatment of the cranial and pelvic areas is especially important for these patients ( 1 6) . OMT may be contraindicated for some psychiatric patients. A paranoid schizophrenic patient may interpret a hands-on treat ment modality as threatening and usually does not tolerate i t well . Touch may b e misinterpreted b y patients having difficulty differentiating fantasy from reali ty. For patients with a history of abuse, the manipulative treatment may be seen as a sexual ad vance or assault. In rare cases, the physician may decide against the manipulative treatment because ofconcerns of personal safety. As with all patients, the benefits of osteopathic treatment for psychiatric patients must be weighed against i ts potential adverse
429
outcomes. Most psychiatric patients in i npatient settings tolerate the treatment extremely well and quickly respond to treatmenr. R ecord ing O st eop at hic Diag nosis and Treat ment on t he H ospital C hart
After a session with a patient, the following must be recorded in the hospital chart: H istory Physical examination (including the osteopathic diagnoses) Treatment plan Treatment provided A protocol for adequately recording an osteopathic structural exami nation is outlined by the American Osteoparhic Associa tion in the Accreditation Requirements for Acute Care Hospitals ( 1 7) and is used in hospi tal credentiali ng. Each hospital may also have individual guidelines for the recording of osteopathic structural examinations. The American Osteopathic Association has also approved a standardized form for use in record ing neu romusculoskeletal exam i nation findings on hospital ized patients (Fig. 29. 1 0) . In general, the following should be incl uded in the recorded neuromusculoskeletal exam ination: Position {s) i n w hich the patient was exam i ned Notation of asym metries of the spine, ribs, head, shoulders, and extremities noted by visual examination or palpation Results of screening the range o f motion of the spine and extremities Location of tissue texture changes Any other relevant positive or negative findi ngs from the neu romusculoskeletal examination, as described above Correlation of the musculoskeletal exam i nation with the ch ief complaint{s) Follow-Up Eva lua tion and Trea tment
Begin the fol low-up exami nation with a review o f any new ra diographs, followed by a review of the medical record si nce the last evaluation. Take an i nterval h istory. Perform the physical ex amination following the protocol described above, noting any changes i n response to the previous treatment or i n the disease ptocess. The areas to be treated may change at every visit and are de termined by the i nterval h istory and physical examination. The tolerance for a longer treatment generally increases as the pa tient improves. The intervals between treatments are also usually i ncreased as the patient improves.
THE OSTEOPATHIC CONSULTATION
A l l osteopath ic physicians are trained to provide osteopathic di agnosis and treatment for their patients. Some osteopathic physi cians, with addi tional trai n i ng and skill, elect to provide this service on a consultation basis for other physicians. In this case, the physician becomes a consultant in osteopathic manipulative medicine ( O M M ) to the patient's attending physician. Most hos pitals require that physicians serving as consultants go through
Osteopat h ic M usculosk eletal Examination of the H ospita lized Patient I/ Examiner: (PrI"
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FIGURE 29.10. Recommended neuromusculoskeletal examination form for hospitalized patients.
29. Neuromusculoskeletal Medicine and Osteopathic Manipulative Medicine
a credentialing process and be granred privileges in their area of specialry. This credenrialing also applies ro O M M .
The Co nsu lt
The OMM consultant becomes involved with a patienr's care when the attend i ng physician writes an order requesting an OMM consult. The order should state the reason for the consult, specifying ei ther the specific patienr complainr (e.g., headache) or the organ systcm or disease ro be evaluated. This order may be written as a consultation only, or as an order ro consult and trear man�pulatively as indicated ("Consult regard ing left lower lobe pneumonia with OMT as indicated"). If the order does nor also specify for the consultanr ro treat the patienr if indicated, the consultant provides only an exam ination and recommendations for treatment. I n most cases, the attending physician also specifies that rreatmenr is requested. The attending physician may some times specify a certain number of treatments, essentially dictating part of the manipulative prescription. However, the consultant is the one performing the procedure (OMT), and the burden of actually formulating the mani pulative prescription is the respon sibiliry of the consulti ng physician. As i n the process described earlier, the O M M consult begins with a review of the patien t's radiographs and medical record, with special notation of findings that relate ro the neuromuscu loskeletal, fascial, and visceral systems. The osteopathic physician then evaluates the patient for the presence of somatic dysfunction of the neuromusculoskeletal, fascial, and visceral systems, and de termi nes its relevance ro the disease process for which the patient has been hospital ized. I f the attending physician does not request treatment, the consultant is ready ro write the consultation. I f the attendi ng physician also orders treannent if indicated, the consultant is obl iged ro determ i ne i f rreatmenr is ind icated. If so, the consultant proceeds with the OMT of the patient, following the treatment protocol described earl ier. After the exam ination and treatment ( i fordered and indicated) are completed, a consult is written in the medical record. Usu ally, a specially designated sheet is provided for the consultanr's written sum mary, which includes impressions and recommenda tions. A summary is written so that it can be i m mediately used by the attending physician, and the ful l report is then dictated. A written note should also be made in the progress note section stat i ng that a consult was completed, i ncluding the date and time. If the results of the examination or treatment i ndicate a clini cal need for i mmediate information, the consultant should also contact the attending physician directly and d iscuss the patient's case. The dictated O M M consultation should contain the following: I. II.
Ill.
IV.
Date and time of the consult. Name of the attend ing physician, reason for consult request, and whether the patient's chart and radiographs were re viewed. Statemenr that a h isrory was taken from the patienr (or family member), and a written summary of those fi ndings . Statemenr of t h e positions in which t h e patient was exam ined (was examined in the sitti ng, supine, and lateral recum-
43 1
bent position, or exam i ned i n the supi ne position only due ro presence of an endotracheal tube), and the results of the patient's physical exam i nation. v. I m p ressions. Generally, the consultant l i m i ts his or her di agnoses ro somatic dysfunctions. Also include any other di agnoses that are directly related ro the somatic dysfunction and the disease process, and the viscerosomatic and somaro visceral reAexes. The consultant is fu nctioning as an O M M specialist, n o t assuming other parts of t h e patienr's medical management. V I . Recommendations. This includes the manipu lative prescrip tion if OMT is ind icated, and recommendations for radio graphs, further evaluations, and rreatment modal ities rele vant ro the consult. V I I . Treatment given, i f any. Areas treated, techniques used, and the patient's response ro treatment are recorded here. Use standard nomenclature as defi ned in the G lossary of Os teo pa!'hic Terminology (see G lossary). VIII. Follow-up recommendations. IX. An expression of thanks ro the requesting physician for the consult. x . Request that the original consult be placed i n the medical chart and that phorocopies of the consult be senr ro the attending and consulting physicians. Fol l ow - U p
Follow-up consultations are performed at the request of the at tendi ng physician or i f the consultant feels that a reevaluation is indicated. The prorocol is essentially the same as the initial con sultation, with the exception that radiograph and chart reviews are only necessary from the date of the i n i tial consultation. Follow-up rreatment is provided at the consultant's d iscretion i f he or she has been asked ro participate in the patient's care. In this case, the consultanr is then seeing the patient as an estab l ished patient and no longer as a cons u l tant. The prorocol for fol low-up treamlenr is described in the Follow- Up Eval uation and Ti'eatment section above.
A CASE STUDY IN CRITICAL THINKING FOR THE OSTEOPATHIC M ANIPULATIVE MEDICINE SPECI ALIST
The following case study ( 1 8) provides an example of how the specialist i n N M M and OMM applies osteopathic theory, meth ods, and though t processes i n the care of the patient. Case P re se nt at io n
A 48-year-old man was adm itted ro the hospi tal with a diagnosis of acute myocardial i n farction ( M I ) and congestive heart fail ure. A t this time, he states he is worried about his outcome. He complains of slight chest pressure and slight nausea. He has a hisrory of hypertension and hypercholesterolcmia. He has known coronary artery disease from electrocardiogram (ECG) and stress treadmill evaluations, as wel l as angina on ex ertion, but refuses i nvasive studies or rreatments and agrees ro
432
VI. Osteopathic Considerations in the Clinical Specialties
rake medications for chest pain, hypertension, and hypercholes terolemia. Present medications are aspirin, atenolol, atorvastatin, and p.r.n. use of subli ngual nitroglycerin for chest pai n . H e had been shoveling snow, developed chest pain, left arm pain, and then nausea that did not respond to subli ngual n itroglycerin. The chest pain persisted, but he waited 1 6 hours before tell i ng his wife. He had emergent medical care on admission to the emergency room that i ncl uded aspirin, oxygen admi nistration, heparin , and appl ication of n itropaste on the chest. He was sta bil ized and adm i tted to the hospital . The NMM and OMM specialist is asked to do a structural eval uation and provide appropriate osteopathic manipulative treatment (OM T) for this patient.
P hysical F ind ing s
He is 6 feet tal l, and weighs 230 pounds. He appears anxious, pale, and sl igh tly diaphoretic and is resti ng i n the bed i n a sem i-Fowler position. A nasal cannula is in place, a large-bore i .v. is i n fusing into left forearm, and a right subclavian line has been placed. A cardiac mon i tor is attached. He is having sl ight chest pressure, but no respiratory distress. There is an S3 gallop rhythm, rales in the l ungs, the liver is enlarged and soft, and there is grade 2 pretibial edema. Osteopathic evaluation reveals: OA FSLRIl, A-A rotated left Left fi rst rib elevated T l ERLLSL T2-4 N S J( RL with tissue texture abnormalities i n paraspinal soft tissues along T2-4 left, i nclusive of the rib angles T7- 1 0 NSL RIl, Diaph ragm motion restriction on the left with ribs 7- 1 0 ex halation restriction (inhalation somatic dysfunction)
V I1 I .
The N M M and OMT specialist would consider the following points about the patient's pathophysiology: He has both backward and forward cardiac failure. Coronary thrombosis secondary to platelet aggregation with antecedent coronary artery disease is the most common mech anism. I I I . Compensatory responses i nclude i ncreased sympathetic tone, i ncreased blood pressure and hean rate, increased myocardial contracti l ity, and i ncreased myocardial work load. IV. These mechanisms contribute to a "supply and demand" im balance for perfusion of the myocardium. v. Arrhyth mias are commonly associated with hean disease and myocardial ischemia. Sympathicotonia encourages tach yarrhythmias and i nappropriate i ncreased parasympathetic tone encourages bradyarrhythm ias and heart blocks. VI. Visceral faci l i tation of the spi nal cord from the visceral afferent fi bers from the myocardium in the region of the myocardial i n farction faci l i tates its spi nal cord segments and produces the deep severe pressure. This then refers to the correspond ing somatic efferents and enhances the palpable tissue texture changes. I.
II.
Cenai n poin ts about functional anatomy are also considered. This incl udes knowledge of structure and physiology necessary to properly carry out the osteopathic man ipulative treatment support: Chtonic viscerosomatic tissue changes are palpable in the paraspi nal deep soft tissues of related spinal cord segmenrs (i.e., T I -5 ) . Chronic segmenral somatic dysfunction, acring over time, can produce a hyperexcitable or "facilitated" spinal segment. This irritable segmenr responds abnormally (usu ally excessively) to minimal stimuli and can cause an increase in the sympathetic outAow to related visceral organs, e.g. , the heart and coronary arteries. II. Research studies have documented viscerosomatic reflexes in the left upper thoracic area of patients with myocardial infarction. 1 1 1 . Some osteopathic physicians describe the cardiac reAex as sidebenr left and rotated right (group mechanics) i n the upper thoracic spine. This long-term positional change is produced by chronic hypertonicity of the left upper thoracic muscles. IV. Somatic dysfunction at T 1 -2 is often associated with patienrs that develop tachyarrhythmias. v. A right pectoralis major rrigger point has been associated with some cardiac arrhythmias, many of which are resistanr to antiarrhythmic drugs. VI. Scientists have identified dorsal root ganglion cells with a visceral projection to the heart and a somatic projection to the left arm. A si ngle cell has twO projections: one to the periphery, and one to the viscera. This cell reports to the I.
D iag nostics
The ECG shows ST segment elevation , and laboratory results reveal that C K enzyme ( M B fraction) is elevated. Troponin- l is elevated. Chest radiograph is reported as normal. G iven the above i n formation, the N M M and OMM specialist considers the fol lowing questions: Of all the specific structural findings l isted above, which are the most sign ificant ones? Which are the next most signifi cant ones? I I . What is the rationale for why each of the somatic dysfunc tions l isted above might be related to this patient's condition? I I I . What would be the goals for providing osteopathic manip ulative treatment (OMT) for this patient? I V . Will the structural exami nation need to be modified for th is patient? If so, how� v. Are there mani pulative techniques that would be appropriate for each of the somatic dysfunctions l isted above? Will they need to be modified to be appl ied i n this case? If so, how? VI. Are there any OMT tech niques that are contraindicated in this patient? V I I . What is the evidence base for the use ofOMT i n conditions l i ke th is? Where would such information be found? I.
Our osteopathic principles state that the body is a unit and that the body has sel f-healing and self-regulatory ca pabilities. Does doing OMT address these principles? What other things might be considered for this patient that would demonstrate that he is being treated holistically and being helped to "self-heal" and i mprove his health?
29. NeuromuscuLoskeLetaL Medicine and Osteopathic ManipuLative Medicine
VII.
spi nal cord. The central nervous system is not accustomed to the nociceptive input From the hearr, so the pain is interpreted as coming From the arm. I n i tial pain From an MI is visceral in nature and is usu ally a severe deep pressure Feeli ng. This then often begins to disappear, but is Followed by developmen c of severe sharp chest pain with arm and neck reFerral as the viscerosomatic reflex takes over.
Goals For osteopath ic manipulative management include a general plan For manipu lative treatment of this patient and a discussion of treatment options, contraindications, and plans For Follow-up evaluation and treatment. I nitial M anag ement
Treat viscerosomatic reflexes with inhibitory pressure or re lease tech niques directed toward upper thoracic and O-A so matic dysFunctions. 11. Th is reduces viscerosomatic chest pai n . 1 1 1 . Improvement of chest p a i n relieves anxiety, w h i c h reduces central nervous system Facilitation. I V . Treat the musculoskeletal (O-A, cervical, upper thoracic, rib) components associated with arrhythmias. This reduces detri mental somatic infl uence to the facilitated segment and the heart. v. For tachyarrhythmias, treat the upper thoracic somatic dys functions that encourage inappropriate sympathetic outflow to the heart. These areas are usually located at T I -2 and their correspond ing ribs. V I . For bradyarrhythm ias and hearr block, normal ize the vagal response. This i ncl udes treatment of O-A/A-A and cervical region somatic dysfunctions. Some useful techniques for th is include suboccipital i nhibition and indirect approaches to cervical somatic dysfunction. I.
Do not put the patient in treatment posi tions that restrict respiratory efforts. I V . Liver pump, liver flip, and classic thoracic p um ps may be too vigorous for this patient. The liver and spleen may be friable, so be careful to avoid undue sudden compression or decompression changes in the abdomen or undue abdo m i nal pressure v. Continue to treat to provide optimal lymphatic flow to reduce the amount of scarring from the healing process.
Ill.
Fu rther T hou g hts
This man had signi ficant antecedent hearr problems. One would, therefore, expect to find chronic upper thoracic changes (usually left). Often, this type of patient would have a group upper left thoracic curve (type I ) . It usually takes about 24 hours for a cardiac viscerosomatic reflex to develop, so this should be present in this patient by now. As the viscerosomatic reflex takes over, the chest pressure becomes sharper in nature. A viscerosomatic reflex change develops at the T3-T5 region un less the i n farct is posterior. In a posterior M I , the reflex is usually at T5, and this usually spills over into the stomach area producing G [ symptoms in the patient. This viscerosomatic visceral reflex begins to affect upper GI sympathetic innervation. Upper G I symptoms are also influenced through the C2 connection with the vagus nerve. Nausea, vomi ting, or other upper GI complaints are a common clinical problem. There are two basic rhythm problems: I.
11.
Long- Term Manag ement
Treat chronic motion restrictions of the upper thoracic region iF present. This type of treatment is best performed once the patient is ambulatory. 1 1 . Treat as necessary to maintain proper diaphragmatic function. Technique selection may involve direct or indirecr methods, such as myoFascial release or thoracoabdomi nal diaphragm release using the indirect method. 111. Treat the cervical spine with su boccipital inhibition and re l ieve any midcervical somatic dysFunction. This may help with diaphragm Function via the phrenic nerve. IV. Use thoracolumbar soFt tissue release, arriculatory treatment, or myoFascial release; all can improve diaphragm Function. v. Normalize Fascias at the thoracic i nlet and re-dome a flat tened thoracoabdominal diaphragm. Congestion of the my ocardium has been associated with an i ncreased amount of myocardial damage From similar coronary arrery blockage. I.
Contraindications and cautions regarding treatment: I.
11.
Do not use forceful direct method treatments. Do not overrreat and tire the patient.
433
Bradyarrhythmias and heart block are l i kely i f vagal nerve i r ritation dominates. Somatic dysfu nction in these patients is usually found in the neck. Right-sided O-A and C2 somatic dysfunctions are more l i kely to i n i tiate o r predate cardiac brad yarrhythmias. Left-sided O-A and C2 somatic dysfunction are more l ikely to i n i tiate or predate cardiac bradyarrhythmias or hearr blocks. Tachyarrhythm i as are l i kely i f sympathicotonia domi nates the clinical picture and T l -2 is the usual site of the somatic dys function
I nitial OMT
This i nvolves i n itial use of paraspinal i n h ibi tory pressure and my ofascial release technique to the T l -2 region and then treatment of the T3-5 regions. Clinical experience has shown that i f C3-5 is treated first before i nhibition of the T l -2 and T4-5 regions, arrhythmias i ncrease. Apparently the treatment of C3-5 fu rrher faci l i tated the cord segments at the T l -2 region. Somatic dysfunctions at the O-A, A-A, C2, and/or the occip i tomastoid suture are treated to reduce or e l i m i nate i nappropriate vagal cardiac response. If there is a tachyarrhythm ia, check for a right pectoralis m us cle trigger point and if tender, spray and stretch to relieve it. This type o f tachyarrhythmia is often u n responsive to amiarrhyth m ic drugs. If this trigger poim is etiology of the arrhyth mia, the ar rhythmia responds almost i nstantaneously. The patient m ust be treated i n a comfortable position in bed u nless the cardiologist allows the patiem to sit up. Be careful not to disturb the patiem's tubes, i .v. l i nes, and other monitoring equipment.
434
Osteopathic Considerations in the Clinical Specialties
VI.
CONCLUSION
2. Sti les EG . Osteopathic m an ipulation i n a hospital environment. J Am
The specialist in neurom usculoskeletal medicine and osteopathic manipulative medicine is a valuable addition to the osteopathic profession. The role of this important specialist i s to provide clin ical expertise when requested, and to expand the ever-evolving osteopathic concept. The NMM and OMM specialist plays a crucial role in the development and application of osteopathic theory and practice in the areas o f education, research, and service.
3. Larson N. Sum mary o f sire and occurrence of paraspi nal soft tissue
Osteopath Assoc. 1 976;76: 1 7-32. changes in the i n tensive care u n i t . J Am Osteopath Assoc. 1 976;75:840842. 4 . H ruby RJ . Pathophysiologic models: aids ro the selection of man i pula tive techniques. J A m Acad OSfoepath. 1 99 1 ; I (3 ): 8- 1 O. 5 . Zi nk J G . Respirarory and c i rcu larory care: the concepmal model. Osteopath Ann. 1 987; I 0 : I 08- 1 I I . 6. Owens C . A n Endocrine Interpretatioll of Chapman! Reflexes. Carmel, CA: American Academy of Osteopathy; 1 963. 7. Jones L. Strain Counterstrain. Newark, OH: American Academy of Osteopathy; 1 98 1 . 8 . Kuchera WA, Kuchera M L . Osteopathic Principles in Practice, 2nd ed. Col umbus, O H : G reyden Press; 1 994: 297-302.
ACKNOWLEDGMENTS
9 . Herrma n n E P. Posroperative adynamic ileus: I ts preven tion and treat
The author wishes to express appreciation to John P. Goodridge, DO, FAAO, for his valuable advice and information regarding the development of the certification process for NMM and OMT and the FAAO, and to Karen M. Steele, DO, FAAO, for the use of material regard ing hospital evaluation and treatment. In addi tion, the following acknowledgements from the previous version of this chapter are gratefully extended: M r. Lowell Jackson for al lowing photography o f an actual in patient osteopathic treatment for educational pu rposes; Richard Koss, DO, for assisting i n the treatment and photography; Ross Carlson, DO, fo r his assis tance i n the research and writing of this chapter; and Will iam A. Kuchera, DO, FAAO, for his invaluable critique of this chapter.
ment by osteopathic m a n i pulation.
I 9 6 5 ; ( Ocrober): I 63- 1 64.
The DO. Preceprs & Practice.
1 0. You n g GS. Post-operative Osteopathic M a n i pulation. Academy of Applied Osteopathy Yearbook. Colorado Spri ngs, CO: American Academy of Osteopathy; 1 970:77-82.
I I . Rum ney IC. Osteopathic m ani pulative treatment o f i n fectious d isease. Osteopath Ann. 1 97 4 ; (Julyl:29-33. 1 2. Magoun H I . Osteopathy ill the CraNial held, 2nd cd. K i rksv i l le, MO: Journal Pri nti ng Co; 1 966:234, 263. 1 3 . Dunn FE. Osteopath ic concepts i n psych iatry. J Am Osteopath Assoc. 1 9 50;49(7)March: 3 54-3 57. 1 4. Woods jM, Woods RH . A physical fi nd i ng relared ro psychiatric disor ders. J Am Osteopath Assoc. 1 96 1 ;60:988-993. 1 5 . B radford, SG. Role of osteopathi c manipu lative therapy i n emotional disorders: A physiologic hypothesis. J A m Osteopath Assoc. 1 965 ;64:484493. 1 6. Upledger J E, Vredevoogd J D .
Cralliosacral nl'rapy. Seattle, WA:
Eastland Press; 1 983: 268. 1 7. Accreditation Requirements, Acute Care Hospitals. Chicago, I L: American
REFERENCES
Osteopa thic Association; 1 992:75-76. 1 8 . Adapted from : Kearns C. ed. Clinical Osteopathimlly Integrated Learn
I . Egglesron , A. Directory. 1 959.
Pres iden t's
I nd ianapolis,
Report. IN:
A cademy of Applied Osteopathy
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of Osteopathy;
iNg Scenarios. Chevy Chase, M D : The Educational Council on Osteo pathic Princi ples, A Council of the American Association of Col leges of Osteopathi c Med icine; 200 I .
NEUROLOGY MITCHELL L. ELKI55 LOUI5 E. RENTZ
KEY CONCEPTS
Overview of neurologic structures Headaches, including m i graine, cluster, and tension-type • Treatment for headache • Spinal d isorders • Peripheral nerve entrapments, including carpal tunnel syndrome and chronic pain syndrome • •
The specialty of neurology deals with the structure, function, disease, and dysfunction of the neuromusculoskeletal system. The neuromusculoskeletal system includes the brain, spinal cord, and peripheral and autonom ic nervous systems, as well as the m uscu lar system. The early development of osteopathi c medical con cepts emphasized the role of the nervous system as an integrator of function between the various systems of the body ( 1 ) . This chapter provides an overview o f neurology as practiced by osteopathic physicians, focusing on some common neuro logic disorders in which the application of osteopathic concepts is straightforward. The syndromes of headaches, spinal disorders, peripheral nerve entrapments, and chronic pain are described in more detail.
OVERVIEW
The central nervous system (CNS) is particularly unique in the human animal. It allows us the potential to pursue ratio nal thought, experience the deepest emotional states, perform complex motor functions with l i ttle or no conscious attention, and have mechanisms for integrating a multitude of bodily func tions. The system includes segmental mechanisms for regulating sensory and motor functions. It includes primitive brain centers responsible for posture and locomotion, more evolved systems of personality and feel ing, and the most evolved system of the capac ity for human mindfulness. All functions of the human organism are under some form ofneural control; therefore, the maintenance of normal nervous system activity is essential for health. Relevant to the osteopathic physician is the intimate relation between the
nervous system and manifestations of somatic dysfunction (2). As we dissect the nervous system into i ts component parts, we must remember that the subtotal of nervous system activity is a complex of electrophysiologic and neurochemi cal phenomena, demonstrating features of instability superimposed on tonic ac tivity at multiple l evels of the nervous system and resul ting in the complex neurobiology of humans. The structure of the nervous system can be clinical ly divided into reasonably circumscribed areas that correspond to specific neurologic functions. For purposes of d iscussion, these d ivisions are the: Brain, including the cerebral cortex, basal ganglia, cerebell um, and brainstem Spinal cord Peripheral nerves and muscles These areas are discussed more comprehensively in other texts (3). The cerebral cortex contains the primary motor system for the initiation of conscious motor activi ty, the pri mary sensory system for the appreciation of conscious sensory input, and the centers for memory, speech, and visuospatial integration. Lesions in these areas produce contralateral defects in motor and sensory functions. Compromise of the dominant hemisphere distu rbs speech and l anguage functions while nondominant hem ispheric disruption influences visuospatial processing and the potential for visual imagery. The basal gangl ia are intermediate nuclear structures that act as relay stations between the other sensori motor control systems. The primary c l in i cal functions of the basal gangli a include the inhibition of segmental reAexes, such that resting muscles can remain at rest. They control automatic and associated movements that occur without conscious p rocessing (e.g., swinging the arms while walking, or smiling while tal king) . Disorders of the basal ganglia typically produce tremors at rest, rigidity, loss of associated movements, and posture d isturbances. The cerebellum functions to match proprioceptive input (state of the muscles and joints) with cortical output (motor intent) to control m uscles du ring movement to ensure smooth motor tran sitions and to maintain posture and balance. Clinical d isorders of the cerebellum manifest as tremor d uring movement, postural abnormalities, i mbalance, and ataxia.
436
VI. Osteopathic Considerations in the Clinical Specialties
The brainstem acts as a connection berween the cerebral cortex, the basal ganglia, the cerebellum, and the spi nal cord. Through it, all impulses traveling i n to or out of the CNS are trans mi tted to the spinal segmental level. The brainstem also contains the nuclei of the cranial nerves and the autonomic centers. The spinal cord extends in segments from the brainstem. The segments ex ist in relation to each nerve root and contain the an terior horn cells from which the peripheral motor nerves arise and the dorsal horns where sensory neurons enter. I n essence, the motor toots supply all the muscles related to that segment (myotome) and similarly receive the sensory input from that seg ment (dermatome). The peripheral nerves transmit impulses to the muscles for movement and contain the sensory fibers for pain, temperature, touch, and proprioception. The autonomic nervous system, sympathetic and parasympa thetic, con trols the visceral functions of the body. With rapidity and int ensity, the autonomic nervous system can i n Auence vis ceral fu nctions. Each autonomic pathway comprises a pregan glionic and postgangl io n ic neuro n . Preganglionic sympathetic neurons originate in the i ntermediolateral column of the tho racolu mbar spinal cord and exit through the ventral toots and spinal nerve to pass i nto one o f the chain ganglia. There they either synapse or pass thtough to o ne of the outlying sympathetic ganglia. From the sympathetic chain ganglia or the outlying gan glia, postgangl io n ic neurons originate and course to their organ of destination. The parasympathetic division originates in the brainstem and the sacral cord. Their preganglionic neurons pass unin terrupted to the organ that is to be controlled. The postgan gl ion ic neu rons are located in the wall of the target organs. These summary descriptions of the anatomy of the nervous system ill ustrate that each of these systems is i nt erdependent and exerts its ulti mate effect in either the facilitation or i nhibition of the spinal cord segments (4). The nervous system continually receives information about the organism's i nternal and external enviro n ment through the afferent sensory system arising from the musculoskeletal system and the viscera. This i n formation is processed central ly, transmitted i n the CNS in some form, and stored as learned or retained i n formation. The nervous system output is transmi tted through the efferent limb to the somatic and visceral com partments of the body. I t is through the motor unit that the domi nant effects of the motor system are manifest and through the peripheral autonomic system that efferent nervous functions are played out on the viscera. Through this ptocess, the neutomuscular system helps to preserve and maintain total body fu nctional integrity. Practically speaking, the assum ption of the upright stance in volves an i n tricate i n teraction of the basic neurologic centers, with particular reference to the descendi ng supraspinal pathways, the cooperation of the basal ganglia and cerebellum, the l i mbic system, and the lobes of the neocortex. This evolutionary ac compl ishment frees the human hands for manipulation of i ts environ ment and for fu rther development. Biomechanical dys fu nction can be a consequence of an imperfect adaptation to a contin ually chang ing center of gravity in the upright stance. The neuromusculoskeletal system provides the human with i ts behav ioral repertoi re; dysfunction of the neuromusculoskeletal system results in the c l i n ical phenomenon of somatic dysfunction. The next section elaborates on the concept of the osteo pathic lesion and common neurologic disorders that illustrate
osteopathic concepts in the genesis of symptoms and signs, as well as in therapeutic management.
CONCEPT OF SOMATIC DYSFUNCTION
Theoretical mechanisms of the i nterrelationsh ip berween the spi nal cord and m usculoskeletal abnormalities known as somatic dysfunction are largely based on the concept of segmental fa cilitation. J. Stedman Denslow originally defined this concept in the early 1 940s using a new investigational techn ique of the time: electromyography. The concept of segmental facil itation, as described by Denslow (5), was that motor neuron pools in spinal cord segments related to areas of somatic dysfunction were maintai ned i n a state offacilitation . That is, they were chronically hyperirritable and therefore hyperresponsive to impulses reach ing them ftom any source in the body. The source of input in cluded proprioceptive and nociceptive stimuli from the periphery under the influence of the supraspinal centers desc ribed above. Denslow (6) went on to conclude that muscles i n nervated from these segments are, therefore, kept in a state of hypertonus much of the day with i nevitable impediment to spinal motion and with structural and functional consequences to the m uscle and person over a period of rime. Stated another way, the facilitated segments are bel ieved to be related specifically to somatic dysfunction such that areas of lo calized pai n , tenderness, increased muscle tension, or limitation o f motion in a spinal segment influence that part of the nervous system to which they are con nected. Conversely, the muscu loskeletal phenomena can be i nAuenced by the segmen tal nervous system behavior i tself, which can be produced by facilitation orig i nating from peripheral, central, and visceral parhways (7) . The concept of segmental facil itation is an extension of gen eral concepts of neuronal facil i tation. In segmental facilitation, a spinal segment receives exaggerared input from either a so matic or visceral srructure. The efferent motor and autonomic components of the spi nal segment are maintained in a state of exci tement, such that further stimulation results i n additional ac tivation with somatomotor and sympathetic manifestations that are clinically recognizable. The segment is hyperirritable and, like a lens, shows qualities offocusing the input. In this way, ascending or descending i n put tends to converge and locally increase the ac tivity at the faci l i tated segment. A decreased threshold to stimuli is applied above or below the segment and can resul t i n increased efferent somatic ( muscle contraction) and autonomic (sweat, va somotor) activity at this level. I n this way, the spinal cord can be seen as an organizer and active participant in the disease process (8-1 1 ) . The involved m uscles can be maintai ned in a hypertonic state and thereby affect spinal motion, contributing to the re strictive m usculoskeletal pattern typical of somatic dysfunction. Likewise, excess sympathetic segmental efferent activity can af fect related somatic and visceral structures. The pathophysiologic consequences of local sympathetic hyperactivity are documented ( 1 2) and could play a role in the signs and symptoms of somatic dysfunction. Segmental dysfunction of the neuromusculoskeletal system becomes visible when it manifests signs of somatic and/or sym pathetic hyperactivity. A fferent stimuli from i n ternal and ex ternal sources are organized by spinal cord mechanisms and
30. Neurology
manifest clin ical features un ique to the individual. I n dividuals have uniquely different responses to a general i ncrease i n psychic or physical stress. The common presence of i ncreased somatic and sympathetic activity results in tissue texture abnormalities (TTA) , one of the cardinal features of osteopathic palpatory di agnosis ( 1 3) . It is the pattern of somatic dysfunction and its relationship to visceral disease that becomes particularly relevant as a diagnostic tool ( 1 4, 1 5) . Manipulative treatment influences the neural mechanisms responsible for the aforementioned reac tive tissue changes; therapeutic success can be assessed thtough changes in these same factors. I mpulse-based electrical activity is not the only mechanism whereby the nervous system can infl uence bodily functions. The presence of trophic substances produced by the nerve cell and transported along its axon and microtubular structures are criti cal in maintain i ng the vitality of the organism (16). These sub stances transsynaptically affect a variety of target end organs. The antegrade and retrograde flow of axoplasm suggests that the com munication is bidirectional . This normal axoplasmic flow is dis turbed by primary disease of the neuron (motor neuron disease) or in those cond itions that produce mechanical deformation of the nerve by entrapment, stretch, angulation, or pressure ( 1 7) . Perceptions a n d feeli ngs can i nfl uence the state of the body's muscular activity, autonomic activity, and the capacity of its homeostatic mechanisms to respond to exogenous i nfluences including the ability to respond to osteopathic manipulative treatment (OMT) . Neuroendocrine mechan isms allow the affec tive tone of individuals, their feeling state, and their personali ty to have an impact on their neuromusculoskeletal system. These mechanisms can be localized to the limbic system, the hypotha lamus, the pituitary gland, and the neutoendocri ne c i rcuits. In the early stages, continued afferent barrage (nociceptive, proprioceptive, autonomic) and a wideni ng zone of i nvolvement maintains the state of chronic facil itation. With chronic somatic dysfunction, a more lasting mechanism m ust be at work. Sus tained patterns of excitability and synaptic trans mission become learned behavior in the spi nal cord and brain ( 1 8) . The facili tated segment is the focus of efferent neuronal hyperexcitability. Metaphorically speaking, the zone of somatic dysfunction con tinues to represent the squeaky wheel. Additional local o r general afferent stimulation results in an i ncreased somatic and sympa thetic efferent outpouring to those tissues i n nervated through the facilitated segment, manifesting as increased signs and symptoms of somatic dysfunction. See also Chapters 7, 8, and 73. The osteopathi c point of view considers wel lness or health a positive state. It appreciates the organizational uni ty, i nherent healing capaci ty, and self-regulating ability of the human body. Concern for the i nterrelationship between structure and function is crucial.
HEADACHES
Headaches are one of the most frequent presen t i ng com p la ints to both the general practi tioner and the neurologist. Table 30. 1 rep resents the current I n ternational Headache Society classification of headaches ( 1 9) . This classification is useful for establishi ng a clinical diagnosis of headache type; good scientific models exist for only some of the headache types, and there could be overlap
437
TABLE 30.1. INTERNATIONAL HEADACHE SOCIETY CLAS SIFICATION OF HEADACHES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Migraine Tension-type headache Cluster headache and chronic paroxysmal hemicrania Miscellaneous headaches unassociated with structural lesion Headache associated with head trauma Headache associated with vascular disorders Headache associated with nonvascular intracranial disorder Headache associated with substances or their withdrawal Headache associated with noncephalic infection Headache associated with metabolic disorder Headache or facial pain associated with disorder of other facial or cranial structures
12. Cranial neuralgias, nerve trunk pain, and deafferentation 13. Headache not classifiable (From International Headache Society. Classification of headaches.
Cephalgia.
1988;8(suppl
7).
with permission.)
between categories of headache i n a given patien t. Most headaches are m ixed tension-type and m igrai ne. This presentation is com p l icated by the multifactorial nature o f headache, i ncluding these features: Physical Psychological Familial Ethnic Cultural The osteopathic physician i s uniquely situated to evaluate the headache patient and to manage d iagnostic and therapeutic resources. Pai n can result from noxious stimulation of the eyes, ears, mouth, and nasal cavities. Pain-sensitive i nt racranial structures i nclude the venous sinuses and thei r tributaries, the dura (par ticularly at the base of the brai n ) , and the arteries of the pia arachnoid and dura mater. Some extracran ial structures are also pain sensitive, including the: Skin Subcutaneous tissues Fascia Muscles Arteries Cranial periosteum Regional articulations Acute h e ad pain is often the resul t of dysfunction, displace ment, or e ncroachment on one of the above structures. Cranial nerves V, V II , IX, and X, and upper cervical nerve roots II and III convey i m pulses from the head and face. The afferent sig nal is carried along A and C fibers of the peripheral nervous system, predo m i nantly with the cells in the spinothalamic and trigeminal spinal tracts in laminae I, II, V, and X. The nocicep tor fibers transmit synaptically using glutamate, substance P, and other neuropeptides (20) . A description of the quali ty and location of the headache is useful in establishing a cause. I nvestigate these questions: •
Does i t pound l i ke a vascular headache or squeeze like a tension headache?
438
•
• • • • •
VI. Osteopathic Considerations in the Clinical Specialties
Does it localize to the regIOn o f the extracranial arter ies, sin uses, teeth, tendinomuscular attachments, temporo mandibular joint, or cervical vertebrae? What are the severity and the time course of the pain? Is there an acute, severe onset, as is typically seen in subarach noid hemorrhage? [s it chro n ic and nagging, more typical of tension-type headache? Does it tend to reoccur like migraine? [s it a once in a l i fetime eve n t like most CNS i n fections?
For example, migraines often occur in the morni n g and rarely last more than a day or two. Cl uster headaches typically occur at nigh t and rarely last for more than 30- 1 20 m i n utes. Tension headaches can last for weeks o r months. The associated features o f a headache include its relation to: Menstruation Activities Head position Ti me o f day Exercise Sleep habits Environmental toxicity Food and drink int ake It is i m portant to know the age of onset, relevan t family h istory, and exacerbating and relieving facrors. A psychosocial assessment and thorough history and physical exam ination can reveal the symptoms and signs of anxiety, depression, and anger that can increase and heighten pain awareness. The physical exa m ination of these patients i ncludes a thor ough general examination and a comprehensive neurologic ex amination, i ncludi ng: Mental state Cranial nerves Strength ReAexes Coord i nation Sensation Appropriately detailed m usculoskeletal assessment The m usculoskeletal assessment is most rewarding for patients with chro n ic or acute recurring headache. The neurolTIuscu loskeletal assessment includes active and static body analysis. Observe and palpate the facial and mandibu lar attachments, the temporomandibular joints, and the tempo ralis, masseter, occipi to-frontalis, bucc i nator, and pterygoid m us cles, eval uati ng levels of m uscle contraction and local tenderness with direct superficial and deep cervical palpation from the skin to the synovial j o i n ts. Assess rotational characteristics of the head, cervical, and upper thoracic regions, as well as the basioccipital at tachments at the atlas for anterior, lateral, and posterior asymme try. In addition, carry out a scree n i ng of the total m usculoskeletal system . The screening can i nclude evaluation of: Leg length and lower extremity symmetry Sacropelvic base analysis
Cranial rhythmic activity Suture mobility analysis In clinical practice, the relationsh ip between symptoms and signs and the abil i ty to reproduce the pai n ful symptoms during the examination are helpful i n clinical localization. This is par ticularly true for the biomechan ical syndromes, such as (21-23): Temporomandibular joint syndrome Malocclusive dental syndromes Cervical spine syndromes (spondylosis, disc degeneration, facet dysfunction) Cra n ial neuralgias Cranial suture syndrome Short leg syndrome Nerve encroachment syndrome Myofascial pain syndromes This type of evaluation suppl ies i nformation that can be es sential to form ulating comprehensive therapeutic objectives. Therapeutic success can be optim ized by multimodality eval uation and treatment. The psychosocial model can suggest whether cognitive, behavioral , or psychotherapeutic i n terven tion is needed. The pharmacologic model attem pts to describe the problem neurochemically and offers a logical i n tervenrional pro tocol based on differential pharmacotherapeutic profiles (such as serotonergic, dopaminergic, noradrenergic, GABA-ergic, cholin ergic). The biomechanical model provides a rational basis for choosing among manipulative treatment methods ( i .e., direct ac tion, indirect action , or myofascial techniques). Furthermore, therapies directed at enhancing the self-healing capacities of an i ndividual are im portant in the overall therapeu tic formulation . These therapies include nutritional evaluation and counseling, evaluation and education in sleep hygiene, in struction and p rescription of appropriate relaxation and stress reduction therapies, the use of therapeutic exerc ise, and the pro motion of a positive attitude through education about the nature of headaches, the realistic objectives of management, and the use of positive visual i m agery (24). Migraine Headaches
I n m igraine headaches, disordered neurogenic con trol of the cran iocerebral circulation accompanies the attack (25). The trigemi nal vascular system (the trigeminal neuron whose un myeli nated axon surrounds a cephalic blood vessel) fu nctions in pain trans m ission and in promoting inAalTImation in the affected blood ves sels via the neurochemical activity of substance P (26) . Cerebral, meningeal, basilar, and vertebral arteries can be affected through the trigeminal, vagal, and upper cervical axons, which all con verge in the trigemi nal nucleus caudal is of the brainstem (27,28 ) . T h e i n A am matory response is associated with norepinephrine and serotonin release of brain stem origi n, and histamine, adeno sine, and bradykin i n of local origi n . When t h e m igraine i s triggered, the in trinsic brainstem nora drenergic system (from the locus ceruleus) is activated and triggers enhanced neuronal firing in the susceptible cerebral cortex. This fi ring in the cerebral cortex originates a spread ing wave of cor tical depolarization that ultimately reaches pain-sensi tive blood
30. Neurology
vessels, resulting in depolarization of the associated [rigemino vascular axon. This depolarization [riggers a sterile inflammatory reaction th rough the release of substance P and the activation of mast cells and prostaglandin synthesis (25 ,26). Migraine can be accompanied by an aura consisting of neu rologic changes, typically in a vascular distribution, lasting from 10 to 90 mi nutes, that m i m ics and sometimes results i n transient cerebral ischemia. In rare cases, the neurologic aura resolves and the migraine becomes complicated as the patient suffers cere bral infarction. The most common auras are ocular and can i n volve sci ntillating scotomata or flashing l ights, often occurring i n jagged lines-the so-called forti fication spectrum (29). T h e vi sual phenomena can be multicolored and typically changes size, shape, and distribution during the evolving aura. The aura usually precedes the acrual headache but can occur dur i ng and even after. On occasion, the aura is separate from the headache component or the headache can be absent (30). Multi focal neurologic symptoms can occur in the basilar artery distribution (the Bickerstaff syndrome) and i nclude (3 1 ) : Cranial nerve changes Dysarthria Facial paresthesia Ataxia Vertigo [n the middle cerebral artery distribution, m igraine can have manifestations of hemiparesis, hemisensory loss, or aphasia. I n general , the aura presents with visual phenomena, atypical for cerebrovascular insufficiency. A clue to m igraine symptoms is a gradual progression of symptoms, unlike the rapid march of a focal seizu re or the sudden onset of cerebral vessel thrombosis or embolism. M igraine can begin i n childhood, adolescence, or adulthood. In women, it can be associated with hormonal fluctuation. Mi graine is typically a thtobbing pain, fol lowing a vascular distri bution of the superficial or deep cerebral vessels and lasting for several hours. It is often associated with nausea or vom iting, and sensitivity to bright lights, loud noises, or strong smells. For some patients, tenderness, tightness, pain, and l i mitation of motion i n the suboccipital and cervical musculature accompanies m igraine. Character istical ly, m igraine is relieved by sleep. On i n itial presentation of migraine, it is not always possible to be certain of the diagnosis, and a well-designed differential diagnostic process is appropriate (Table 30.2). AJthough the risk of aneurysm, brai n tumor, arteriovenous malformation, or vas culitis is sl ight, enhanced brain com puted tomography, magnetic resonance imaging ( M R I ) , or cerebral angiography is useful to exclude these possibilities and should be used if the diagnosis is uncertain (32). M igraine can acutely respond to vasoactive drugs, such as sumatriptan, other triptans, dihydtoergotam i ne, ergotam i ne, isometheptene, and even caffeine. The serotoni n I-d receptor agon ists (sumatriptan, dihydroergotamine) are particularly effec tive in aborting a m igraine. Simple agents l i ke aspirin or ac etami nophen are often combi ned with barbiturates and/or nar cotics. Other nonsteroidal antiinflammatory drugs (NSAI Ds) are also used with variable success. The parenteral use of phenoth-
439
iazines is helpful; but unfortunately, they are frequently associated with unacceptable side effects (33). When m igraine headaches are frequent or severe, the pro phylactic use of medications is i ndicated. Medications used reg ularly to help prevent m igraines i nclude beta-blockers (e.g., propranolol) , calci u m channel blockers (e.g., verapamil), tri cyclic antidepressants (e.g., am itriptyline) , seroto n i n a ntagon ists (e.g., cyproheptadine, fluoxeti ne) , ergot derivatives (e.g., methy sergide), and anticonvulsants (e.g., valproic acid) . Nonpharmacologic approaches, i ncluding OMT, are often valuable. Osteopathic management of m igraine can incl ude O MT. I n the active phase of m igraine, vigorous treatment can, theoretical ly, i ncrease blood flow to an already i nflamed vascular bed, thereby expl ai n i n g the clin ical exacerbation that can follow [reatment. Gentle therapy with i ndirect techniques, and venous and lymphatic drainage tech niques are likely more helpful dur ing the attack. Because ofthe prom inent autonomic i n volvement, evaluate and treat at the sympathetic sites of lower cervical and upper thoracic vertebrae, associated ribs, and myofascial attach ments. Treatment can be di rected at joints of the head and neck, m uscles, and myofascial restrictions of the head, neck, and shoul ders. Behavioral tec h niques li ke biofeedback, relaxation therapy, and ptograms that teach stress reduction and coping ski lls have also been successfully used to reduce the frequency and severity of m igraine attacks (34). For some patients, m usculoskeletal triggers or prodromes exist for their m igraines (35,36). The possible role of m usculoskeletal [riggers is further sug gested in posttraumatic migraine. I n such cases, trauma to the skull, cervical spine, or myofascial elements is followed by a uni lateral, throbbing migraine (21,37). These headaches can recur for days, weeks, and months. OMT can be used in an attempt to modify triggers that arise from bony, l igamentous, and my ofascial s[ructures. I n practice, O M T is especially useful between migraine events, when the patient is more tolerant of mani pula tion. Applications of local heat, cold, massage, acupressure, trigger poi n t therapy, acupuncture, traction, or local anesthetic blockade can be used i n these regions that typically harbor tender points referri ng pain to the headache zone. These applications might help to decrease the afferent activity from the painful site and reduce the primary and secondary muscle spasms. Cluster Headaches
Cluster headache is a distinctive vascular syndrome character ized by attacks that tend to occur daily for weeks at a time only to van ish again for months or years. Approximately 20% of pa tients develop a chro n ic form, called chro n ic paroxysmal hemi crania or hemicrania continua (38). Cli nicians believe that cluster headaches are the result of neurogenic i nflammation affecting the vascular plexus of the cavernous s i n us, its triburaries, and its au tonomic nervous supply (39.40). The headaches tend to occur at certai n times of the day; most notably, they develop 2-3 hours after goi ng to sleep. Like m igrai ne, cluster headaches o ften occur when the individual i s switchi ng from rapid eye motion (REM) sleep to non-REM sleep. This is accom pan ied by a shift from parasympathetic, cholinergic activity to sympathetic, ami nergic (catecholamine, serotonin, and norepinephri ne) activity (41).
VI. Osteopathic Considerations in the CLinical Specialties
440
TABLE 30.2. HEADACHES RESULTING FROM SYSTEMIC DISEASE OR PRIMARY NEUROLOGIC DISORDER Paraclinical Features (lab, Clinical Features
Pathophysiology
Disorder Glaucoma (61)
Increased intraocular
Dilated pupil, disturbed
pressure Berry aneurysm,
Cerebral aneurysm,
Treatment
Abnormal tonometry
Medication, surgery
Blood in the (SF, abnormal
Neurosurgery
vision, general headache Explosive headache, nuchal rigidity, abnormal
hypertension
ruptured or
x-ray, etc.)
angiogram
neurologic signs
unruptured (62) Temporal arteritis (63)
Inflammation
T hrobbing headache, > 55
years old, tender
Elevated ESR, positive
Glucocorticoids
biopsy for arteritis
temporal artery, blurred vision, jaw claudication Optic neuritis (64)
Inflammation,
Orbital pain, loss of vision, worse with eye motion,
demyelination
Abnormal visual evoked
Glucocorticoids
response, abnormal MRI
papillitis Dissection of carotid or
Drugs, trauma
Severe, local pain, tender artery, Horner syndrome
vertebral arteries
Angiogram, ultrasound,
Surgery, anticoagulants
MRI, MRA
(65-67) Temporomandibular joint syndrome, internal
Joint degeneration,
Pain in jaw, click in joint,
muscular imbalance
derangement,
Dental, physical therapy, exercise
with lateral or vertical
myofascial (68) Trigeminal neuralgia
Abnormal MRI
locking of joint, pain movement, tight muscles
(69)
Irritation of CN-5, vascular
Sharp, stabbing pain in
loop, mechanical Infection
Herpes zoster Meningitis encephalitis
(anticonvulsants), neurosurgery Virus identification
Antiviral therapy
(+)(SF pleiocytosis, low
Antibiotics,
rash/vesicles Usually infection bacterial
Nuchal rigidity acute headache, fever, signs of
viral, etc.
glucose, high protein
infection Infection
Sinusitis, facial
Traction, displacement of
Recent onset, headache,
painful structures, block
worse at rest
of CSF, hydrocephalus
papilledema
Leukocytosis, abnormal
Antibiotics
(T/MRI
bone, fever
from a mass
corticosteroids, supportive therapy
Nasal obstruction, tender
osteomyelitis (70) Intracranial hypertension
Medication
wind, eating, chewing Burning pain hypersensitive
trigeminalis cervicalis
Rarely abnormal MRI
trigeminal zone, triggers:
Abnormal (T/MRI
Glucocorticoids, furosemide, mannitol, neurosurgery
Benign intracranial
Altered CSF dynamics
Young, female, obesity,
hypertension (71)
Increased (SF pressure,
Glucocorticoids,
hormone fluctuating,
small ventricles,
acetazolamide, (SF
sight papilledema
enlarged blind spot
removal, neurosurgery
Posterior fossa mass, Chiari
Exertional headache, strain, lift, cough,
malformation, migraine
exercise, coitus (72)
variant Communicating, block in
Normal pressure
Abrupt, severe, lasts 15-20 minutes, men> women Ataxia, incontinence,
(SF absorption
hydrocephalus
Trauma
Myofascial pain
dementia
c erebrospina l fluid;
points, poor sleep
If no mass, precede activity with NSAIDs
Hydrocephalus, cisternography
Bands, nodules, trigger
syndrome (23) (SF,
(T/MRI
Ventricular shunt, (SF removal OMT, spray/stretch, needling
ESR, erythrocyte sedimentation rate; MRI, magnetic resonance imaging; CT, computed tomography; NSAIDS, nonsteroidal
antiinflammatory drugs; OMT, osteopathic manipulative treatment.
Cluster headaches tend to be periorbital in location and char acteristically develop rapidly and reach severe intensity within minutes. They are associated with auronomic vasomoror features including: Prosis Miosis Conj u nctival injection Unilateral lacrimation Rhinorrhea Nasal stuffiness Distinct from migraine, cluster headaches are much more common in men. They can occur several times a day and can
even awaken the sufferer from sleep. Cluster headaches can be seen after trauma and, ar rimes, can refer pain ro the cervical and upper thoracic paraspinal region, as well as ro the suprascapular . region (42,43). The carotid-cavernous vascularure is involved along with its auronomic innervation . This includes the pterygopalatine gan glion and the cervical sympathetic ganglia. Patiems often have a tender carotid artery, called carotidynia. Anempts ro anesthetize the pterygopalatine ganglion with cocaine or lidocaine have been somewhat successful. Cluster headaches might respond acutely ro paremeral sumacriptan or dihydroergotamine, both of which are seroronin I-d recepror agonists (44 ) . Many respond ro inhaled oxygen via facial mask (5-7 Llminute for 5-10 minutes). Prophy lactically, beta-blockers, calcium chan nel blockers, and tricyclic
30. Neurology
antidepressants are used along with short courses of high-dose steroids or NSAIDs. For the more chronic cluster, l ithium is a potent therapy. Not surprisingly, O MT is best directed to the upper ribs, the cervicothoracic spine, the associated soft tissues, and the relevant craniofacial structures. Tension-Type Headaches
Tension-type headaches are classified by the I n ternational Headache Society as episodic or chro n ic. They are further divided by the presence or absence of involvement of the pericranial mus-' cles. I nvolvement can be demonstrated by electromyography or palpation (45 ,46). Tension-type headache is the most frequent headache type. It is characterized by mild-to-moderate intensity pain , described as pressing or tighteni ng, typically bilateral, and usually occipital in location. In distinction from migraine, it i s not aggravated by exercise or routine physical activity. L i ke migraine, it runs in fami lies, is more common in women, and can be affected by hormonal cycles. It is episodic if i t occurs less than half the days of the month and chronic if it occurs more than half the days o f the month (47). The International Headache Society distinguishes between tension-type and migraine headaches. Many believe, however, that these headache types are related disorders. I n fact, most pa tients with migraines have tension-type headaches, and many patients with tension-type headaches have migraines. Both mi graine and tension-type headaches might be the result of abnor malities i n central pain control mechanisms, as well as trigemi nal neuronal hypersensitivity. Both might be associated with mus cle tenderness, electromyographic abnormalities, and abnormal platelet serotonin levels. When severe, they both can be associ ated with depressed cerebrospinal fluid; ,B-endorph i n s (47). Clin icians theorize that there might be a vascular, supraspinal, and myogenic integrated model for migraine and tension-type headache (48). The trigeminal nucleus caudalis is a major relay nucleus for head and neck pain . Nociceptive i nput from the peri cranial muscles and the cephalic arteries converge at this nucleus, which has excitatory and inhibitory output. When the afferent nociceptive signal is i n tense, sensitization of the entire pain path way, peripheral and central, can occur. This faci litation creates a painful sensitivity to typically non noxious stimuli. I n the mi graine, the nociceptors are vascular and the n o nnoxious stimuli are vascular pulsations. I n the tension-type headache, the noci ceptors are myofascial and the nonnoxious stimuli are muscle contractions. In either case, supraspinal faci l i tation is l i kely to be present and neuronal sensitization can occur. Some neurologists would modifY the classification of the I n ternational Headache Society to incl ude chro nic daily headache, which is further differentiated as a daily or near-daily type of headache with superimposed migraine. Patients with chronic headaches are prone to overusing multiple drugs and have a high rate of treatment failure. The headaches can be primary, as a trans formed migraine, a chronic tension-type headache, a new daily headache, or hemicrania conti n ua. Secondary causes of chronic daily headache can exist, i ncluding posttraumatic headache, cervical spine dysfunction, vascular disorders, and nonvascu lar i ntracranial disorders (35 ,49-51). Frequently, an episodic
441
problem becomes chronic as a result of analgesic medication overuse. Treatment begins with a close look to identifY any medication overuse, drug dependency, or depression, which require specific i n tervention. I n quire for a past history o f emotional, physical, or sexual abuse and i ncorporate that i n formation i n to the treatmen t rationale. Every effort is made to identifY and eliminate potential sources for triggers, such as the: Teeth Jaw Sin uses Cranial and cervical bones Join ts Ligaments Associated myofascial structures These, too, demand specific i n terventions. Physical, psycho logical, and pharmacologic therapies can operate concurrently ( 5 2). Treatment
In headache management, the presence of somatic dysfunction is systematically identified and handled with OMT. Cervical verte bral segmental disorders, focal and regional myofascial disorders, and craniosacral d isorders are common (53,54). Exercise par ticular care with regard to manipulation of the cervical spine. I n frequently, cervical mani pulation has been reported to aggra vate a herniated i n tervertebral disc or a spinal cord injury ( 5 5); most critically, cervical manipulation has been associated with vertebral artery laceration, i ntimal dissection, thrombosis, and thromboembolic i n farction i n the vertebrobasilar distribution of the posterior circulation (56-58). Most o f the complications have been seen with hyperextension and hyperrotation of the upper craniocervical segments, often in the course of a thrusting tech n ique ( 5 9). Pharmacologic therapy is best served with a clearly l imited (symptomatic) regimen to prevent drug-induced headaches. Pre ventive therapy is usually begun with a tricyclic antidepressant, especially useful when there is an associated sleep disturbance. More recently, sodi um valproate has been found to have prophy lactic value in chronic daily headache. Nonpharmacologic therapies are also prescribed. Patients can be evaluated and educated regardi ng proper sleep hygiene. A ther apeutic exercise program should be customized to the patient. Nutritional evaluation and recommendations can be given. Re laxation strategies and visual i m agery techniques can be taught to each patient. I t is important to involve the patient as an active participant i n his or her own therapy. Being able to assess the patient more completely permits a more comprehensive diagnosis. Multifactorial problems allow the formulation of a more thorough and multifaceted treatment program, i n creasi ng the potential for success. The osteopathic approach offers a successful model for an i ntegrated multidimen sional treatmen t with the patient as the focus and the physician as the facilitator (60). I n addition to primary headache syndromes, a wide variety of neurologic and systemic disorders present with headache. These
442
VI. Osteopathic Considerations in the Clinical Specialties
disorders must be considered when evaluating the patient en route to establishing a wotking and d i fferential d iagnosis, before pro ceed ing with any therapeutic intervent ion. Table 30.2 is a collec tion of some of those conditions, h ighl ight i ng clinical, d iagnostic, and therapeutic features. In general, less specific sym ptoms indicate a greater suspi cion that something more than benign headache is present. Con sider further diagnostic studies, M Rl, computerized tomography, electroencephalography, cerebral angiography, blood and cere brospi nal Auid analysis, and neurologic consultation when the patient does not respond promptly and appropriately to osteo pathic medical management.
SPINAL DISORDERS
The practice of neurology frequently involves problems affecting the spine. This can i nvolve the spinal col umn and i ts structural elements (spondylopathy), the nerve roots (rad iculopathy), and even the spinal cord (myelopathy). The spinal colu m n i ncludes the vertebtal body, the i nterver tebral disc, the facet joints, the l igaments, and the myotendinous structures. The pathophysiology of spinal col u m n d isorders often involves a degenerative process, such as spondylosis (osteoarthri tis) of the vertebral body, wh ich is frequen tly seen in association with degeneration of the i nt ervertebral disc. The degeneration ulti mately affects the adjacen t related facet joi nts and results i n strain in ligaments and myotendinous structures. Ti'auma com monly underlies this process (73). The spinal col umn can also be affected by mal ignancy arising in the bone or, more com monly, from secondary metastasis of systemic cancer. I n fection of the spi nal col u m n can result from systemic infection, such as mycobacterial, fungal, or bacterial sep sis. Spi nal pathologic conditions can also occur with osteoporosis and other metabolic abnormal ities o f bone, or from less common arth ritic d iseases, such as ankylosing spondylitis or rheumatoid arth ritis. Disease processes adjacent to the spine can also result in spinal col u m n destruction, including paraspi nal tumors and abscesses (74-77). A common pathophysiologic process affecting the spi nal col umn is the process of somatic dysfunction. Somatic dysfunction can affect si ngle segments o r m ultiple spinal segments and ac company any of the aforementioned spinal colu m n pathologies. The spinal nerve roots are affected by their location withi n t h e spi nal canal. They are exposed t o trauma from (78-80): Extruding d iscs Fractu red bone fragmen ts Spinal and paraspinal rumors Degenerative changes in the vertebral elements I n traspinal ligaments Frank avu lsions I n add ition, the nerve roots lack the tight endothelial j unc tion of the blood-brain barrier; the result is lowered protection from infection (e.g., herpes zoster, syph ilis), neoplastic i nvasion, inAam matory demyel i nation (e.g., G u i l lain-Barre syndrome) , or toxic expos u re to chemotherapy agents, myelographic contrast agents, or anesthetic agen ts. The nerve roots are also suscepti-
ble to vascular i nsufficiency in the form of vascul itis, diabetes mellitus, and radiation exposure (81). Spinal cord syndromes can result from an in trinsic patho logic condition or from i n j ur y to the spinal cord from extrinsic compression. I nt ri nsic spinal cord pathologic conditions include myel itis, typically as a result of a vi rus, vasculitis, or multiple scle rosis, and neoplasms of the glial elements of the cord. Nutri tional deficiencies can also result in degeneration of the spinal cord typically subacute combined degeneration from cobalamin de ficiency. CNS degenerative d iseases affecti ng the spi nal cord in clude motor neuron disease and multisystem degeneration. The spinal cord is vulnerable to ischemia if there is disruption in the anterior spi nal artery c i rculation . Severe spinal trauma can result in hemorrhage or laceration of the spinal cord. Extrinsic compres sion of the spinal cord can result from the same conditions that cause nerve root compression, typically tumors that are primary or metastatic in the spi nal canal, and from epidural infection or hematoma. Compression fractures of the vertebral bodies can re sult in subluxation and spinal cord compression. When the spi nal cord is compressed from epidural tu mor or infection, the spi nal cord symptoms are preceded by vertebral pain (82-85). The symptom of vertebral bone or l igament d isease is usually pain. Typically, patients complain of deep and ach ing pain in the affected region of the spine. Often. the pain is worse i n certain positions or with certain activities. For example, patients with in tervertebral d isc disease commonly complain that their back pain is worse with prolonged sitting or stand ing, whereas acute prob lems are made worse with activity and improved with rest. The pain can refer locally to paraspinal segments. This referral pattern most likely has to do with nociceptors converging on a common dorsal horn projection neuron (86). I n the cervical region, the pain can involve the upper arm, shoulder, and scapulothoracic regio n . In the lumbar regio n . it involves the low back, hip, and upper leg. Numbness, weakness, and other neurologic symptoms are notably absent when only the bone and l igamentous vertebral elements are affected. Patients with radiculopathy might complain of pai n. numb ness, ti ngl ing, or other sensations that typically are described as ra diating from proximal to d istal. I n the cervical region (C-2-T-2), the radiation is i n a dermatomal pattern i n the posterior cranial regio n , neck, upper torso, and upper extremi ty. In the lum bosacral region (L- J -S-5), i t is i n a dermatomal pattern in the low back, buttock, and low extremi ty. I n the thoracic region, the radiation is in a dermatomal pattern i n the chest or abdomen. Because the pain is generated in the nerve root, patients describe a variety of pain sensations, including electric, burni ng. stabbing, dull, sharp, or tearing pain. Patients also describe impulses of pain with cough i ng, sneezing, lifti ng, or moving the bowels. The pain is often worse with positions that either compress the nerve root (side-bending of the spi ne) or stretch the nerve root (forward bending of the spine) . The pain can be relieved by maneuvers that take the pressure or stretch off of the nerve root. Spi nal steno sis can produce radicular symptoms on the basis of intermi ttent ischemia to the nerve roots, typically related to walking. When the motor fibers are affected, patients with radiculopa thy can complain of weakness local ized to the muscles i n nervated. I n the lumbosacral region, the nerves supplying bladder, bowel, and sexual function can be affected; patients might complain of uri nary hesitancy or retention, constipation, or impotence.
30. Neurology
The pain of spi nal tract origi n is diffuse and referred several segments below the level of the lesion. The location of motor and sensory complaints depends on the area of the spinal cord involved. Unilateral lesions of the spinothalamic tract cause con tralateral numbness to pain and temperature, whereas lesions of the posterior columns cause ipsilateral loss of position sense, l ight touch, and vibration. Bilateral lesions of the sensory fibers result in bilateral sensory disturbances below the level. Limb weakness results when there is an abnormality in the anterior horn cells or corticospinal tracts. The weakness can be accompanied by atro phy if it is in the lower motor neurons or spasticity i f i n the upper motor neurons. Bladder, bowel, and sexual functions are often compromised. On physical examination, test sensation with pain , temper ature, and touch. With radiculopathy, the sensory loss i s der matomal, and the margins of sensory loss m ight not be as de marcated, as seen in peripheral nerve lesions. The motor deficits are in muscle groups with a common myotomal i nnervation. The weakness of i ndividual m uscles is usually partial rather than complete. Because the ventral roots contain the lower motor neu rons, radicular weakness is often associated with fasciculations, decreased m uscle tone and bulk, and decreased reflexes. In the upper extremi ties, the root i nnervation i s checked by the deep tendon reflexes of the biceps (predominantly C-5) , brachioradi alis (predomi nantly C-6), triceps (C-7), and the fi nger flexors (C-8) . In the lower extremities, the root i nnervation is checked by the deep tendon reflexes of the quadriceps (predominantly L-4) , biceps femoris (L-5), and gastrocnemi us (predominantly S- 1 ) . Unilateral sacral root lesions can cause numbness but usu ally do not affect muscle control. However, when bilateral sacral roots are involved, the rectal sphincter becomes weak. Test m us cle strength for all of the major muscle groups of the upper and lower extremities. Provocative maneuvers can be of great diagnostic value i n patients with radiculopathy. In cervical or l umbar nerve root compression syndromes, side-bending of the involved spine can narrow the i ntervertebral foram i n a and i ncrease radicular com plaints (Spurling sign ) . Conversely, applying manual traction to the cervical or lumbar region usually oFfers relief. Stretching the nerve roots of the sciatic nerve with straight leg rai s i ng can pro voke radicular symptoms ( Lasegue sign ) . Man ual compression of the external j ugular veins can cause an i ncrease in i ntraspinal pressure. Compression aggravating radicular symptoms i n either the upper or lower extremity (Naffiiger sign) can be a sign of nerve root compression (87). Many diagnostic tools are available for evaluating the func tional and structural aspects of nerve roots. M RI o ffers the best noninvasive view of the nerve roots and surrounding structures. Computerized tomography has some value when bone details are needed. I nvasive myelography, with the instil lation of i ntrathe cal contrast, contin ues to have a role diagnostically, especially when combined with post-myelogram computerized tomogra phy. Sometimes it is i m portant to evaluate the cerebrospinal fl uid for signs of infection, i nflammation , neoplasia, or hemorrhage by determining the cell count along with protein, glucose, and mi crobiologic studies (88-90 ) . The functional status of nerve roots c a n be tested w i t h nerve conduction studies that i nclude antegrade and retrograde re sponse to stimulus (F responses and the H reflexes). Nerve con-
443
duction studies and electromyography can reveal the presence of radiculopathy, but the abnormalities detected are a function of the chronicity of the lesion. Electrophysiologic testing o f the nerve roots can also be done with somatosensory evoked poten tials (9 1 -93) . The physical findings i n myelopathy classically reveal a sen sory level. Spinothalamic-mediated pain and temperature, and dorsal column-mediated touch, vibration, and position sense are disturbed below the level of spinal cord disturbance. Typically, this affects p a i n and temperature begi n n i ng several segments be low the actual level of the lesion. Usually both s i des are affected. Because primarily upper motor neurons are involved, the motor exa m ination reveals a spastic i ncrease i n tone and an i ncrease i n the muscle stretch reflexes below the level o f the lesion. Weakness is diffuse and can be mild or severe. The distribution of weak ness reflects the pathologic condition i n the anterior horn cells or corticospinal tracts. Depending on the level o f the les ion, the patient can have positive Babinski signs and ankle clonus in the lower extremities and positive Hoffman signs i n the upper ex tremities. Sphincter tone can be i ncreased. Gait can be disturbed by spasticity, weakness, or sensory ataxia. Patients with dorsal col umn sensory loss lose their balance and fall when asked to stand unaided with their eyes closed (Romberg sign). If the patient's neck is flexed, he or she could experience an electric sensation traveli n g the spinal cord and the extremities (Lherm itre sign), which is the result of stretc h i ng the long dorsal colu m n fibers (87). When specific disease of the spi nal colu m n is identified, in stitute appropriate treatment. When there is structural weakness, supportive bracing can be used. Physical therapies are often valu able. Therapeutic exercise regimens are an essential component to all comprehensive treatment plans. Consider n utritional as sessment and supplementation when necessary. Use medications with analgesic, antiinflammatory, and bone supportive proper ties. Anesthetic blocks of locally irritable structures (or facets) can be effective (94). OMT is useful in a wide range of vertebral col u m n disorders, i ncluding those of somatic dysfunction ( 9 5- 1 00 ) . M acDonald ( 1 0 1 ) demonstrated responses to osteopathic mani pulation For low back pain of 1 4 to 28 days' duration on the basis of outcome studies. In 1 995 the Agency for Health Care Policy and Research (AHC P R) concluded manipulation to be saFe and effective For patients in the fi rst month of acute low back pain symptoms with out radiculopathy ( 1 02 ) . Osteopathic treatment is derived from the more comprehensive nature of the osteopathic neurologic evaluation. The exa m ination can yield i n formation local to the area o f chief complaint, as well as more general i n formation on the effects of i n terrelated problems. For example, a person with mecha nical low back pain could have an associated visceral d isease (such as endometriosis) that can contribute viscerosomatically to the physical fi n d ings that the patient presents. Likewise, a similar low back pain could be related to a problem with the foot or leg. By identifyi ng contributing elements, a more complete diag nostic understanding can be reached and a more comprehensive treatment undertaken . Standard tteatment of radiculopathy is appropriately directed to the specific pathologic condition i nvolved. For example, an tiviral agents are used for herpes zoster i n fection, or antineoplastic agents for carcinomatous radiculopathy. For degenerative spine
444
VI. Osteopathic Considerations in the Clinical Specialties
conditions causing radiculopathy, physical measures to reduce compression and deformation with traction, physical therapy, and therapeutic exercise are beneficial. Attempt to decrease i n flammation with o r a l corticosteroids o r nonsteroidal antiinflam matory medicatio n . Sometimes the corticosteroids, along with anesthetic agents, are i n t roduced i n to the epidural space, usually lumbar but occasionally thoracic or cervical ( 1 03, I 04). Patients are given extensive education about provocative aspects of their l i festyle, work, and habits with a goal of m i n i m izing aggravating factors. If pers isrent radiculopathy causes progressing sensory or motor findings or pain that cannot be controlled, surgical de compression is advisable. When the cauda equina is affected, a particular urgency exists to diagnose and decompress. I n these cases, a delay in treatment can be associated with a marked i n crease i n morbid i ty and with l in gering bladder, bowel, sexual, and lower extremity dysfunction. Specific i ntervention with OMT has to be undertaken cau tiously, if at all, for patients with radiculopathy. Any manipu lative procedures that i ncrease nerve root compression o r de formation can be potentially i n j u rious. Nonetheless, i n careful hands, the use of knowledgeably applied gentle manipulative forces m ight improve conditions for the nerve root and could potentially affect arterial, venous, and lymphatic circulation, as well as improve local biomechanical factors. At the least, OMT can be useful i n alleviating some of the secondary m usculoskele tal reaction that develops in the face of nerve root pathologic conditions.
PERSONAL APPROACH TO NEUROLOGIC DIAGNOSIS
When patients present with variable complaints of pain, sensory disturbance, or weakness, it is the neurologist's job to answer three questions. These are: L. IL. III.
Is there a neurologic abnormali ty? Can the neurologic abnormal i ty be localized? Can a differential d iagnosis be generated for the abnormali ty in question?
For example, if a patient presents with neck or back pain , the physician attempts t o localize t h e symptom b y h istory. A n effort is made t o differentiate spinal cord disorders, nerve root syndromes, or vertebral disorders. In the general h isto ry, it is necessary to know the patient's past personal history of i l lness, trauma, and surgery. Knowing the fam i ly history is valuable a s a potential source of hereditary or consti tutional susceptibility. The general history i n cl udes a search i nto the history for abuse (substance, physical, sexual, and emotional ) . A t the same time, explore t h e psychosocial background of the pa tient and his or her fam ily. Inquire into the patient's nutrition, work, and exercise habits , sleep patterns, and potential risk expo sures. A mental status exami n ation to evaluate the h igher cortical functions and arousal system should be fol lowed by a complete neurologic exami nation. This exa m ination i ncludes evaluation of the cranial nerves and the motor and sensory system. Test coor dination and gait. Motor exa m ination i n cl udes an assessment of
muscle tone, muscle strength, muscle bulk, and the activity of the associated myotendinous reflexes. Sensory exami nation i ncludes tests o f l ight touch, pain, temperature, vibration, and propriocep tion. I n addition to a routine neurologic exam ination, perform a m usculoskeletal structural examination for patients with spi nal com p laints, i ncluding ( 1 05 ) : I nspection of t h e patient walking a n d standing, from a n anterior, posterior, a n d lateral view, looking for static and k inetic structural asymmetries. 1 1 . Performance o f the standing flexion test. I I I . Performance of the standing lateral flexion test. IV. Performance of the seated flexion test. v. Assessment of seated trunk rotatio n . VI . Assessment of seated lateral flexion. V I I . Seated cervical assessment for flexion, extension, lateral flex ion, and rotation. V I I L . Sup i n e rib testing. LX. Supine upper extremity testing. x. Supine and prone lower extremity testing. L.
The m usculoskeletal structural exam i nation provides struc tural signs of asymmetry (e.g., scoliosis, an increase in kyphosis or lordosis, or sign ificant deviation from balanced gravitational centering) . In addition, the l imbs and vertebral complex can be assessed for characteristics of motion by adding a palpatory exam i nation of the soft tissue ( muscles, l igaments, tendons, deep and superficial fascia, and the subcutaneous structures ) . The site of the primary musculoskeletal problem can often be determi ned. It is possible to know what biomechanical problems are helping to create, maintain, and aggravate the primary problem. I n the areas of clinical i nterest, make the soft tissue examination, the motion testing, and the static structural examination precise to identify the local elements of dysfunction. The musculoskeletal findings are often secondary to another disease of the musculoskeletal system, a reaction to internal dis ease, or a compensatory response to the presence of pai n . Assess i n g the patient more thoroughly allows a more i n clusive diagnosis with the possibility of a more extensive treatment program, in creasing the potential for success. The ability to exclude the more unusual and potentially m o rbid conditions can only result from such an osteopathic evaluatio n . Additionally, this approach of fers the ability to choose among mul tiple and costly diagnostic possibilities.
ENTRAPMENT NEUROPATHIES
Entrapment neuropathies represent a localized inj ury or i rritation to one of the peripheral nerves. They are caused by the mechani cal effects of the i mp i nging adjacent tissues. The typical anatomic causes i nclude entrapment withi n the osseofibrous tunnels where the nerve changes course against fibrous and muscular bands. En trapment can be precipitated by trauma; once the trauma occurs, the local anatomic configuration often causes a repetition of a mechanical i njury. This local anatomic configuration can result in local comp ressive i nj ury to the neural elements. The neural elements at risk i nclude both the axon and the associated myeli n . I t c a n compromise local circulation, i ncluding arterial, venous,
30. Neurology
TABLE 30.3. SITES OF NERVE ENTRAPMENT AND TREAT MENTS Nerve Median
Site of Entrapment Carpal tunnel, pronator teres, anterior
Treatment OMT, splint, exercise, surgery
interosseous syndrome Ulnar
Elbow, cub ital tunnel,
OMT, exercise, s urgery
canal of Guyon, thoracic outlet Radial
Supin ator muscle
OMT, exercise, s urgery
Brachial
Thoracic outlet
OMT, exercise, s urgery
scalenes, pectoralis
445
reversed by restoring proper circulation . As things get worse, the capillary circulation is sufficien tly slowed to create endoneurial edema, epineural edema, and i n rratunnel edema. This edema can still be reversed if adequate decompression is obtained. I n the final stages, there i s arterial insufficiency a n d i ncreasing me chanical deformation , resulting in nerve fiber destruction and u l ti mate fibrous replacemenr. Carpal tunnel can be caused by trauma to the wrist, hy pertrophic arthritides, or thickeni n g of the flexor retinaculum. Hypertrophic neuropathy, local edema, ganglion cysts, and tenosynovitis can all compromise the carpal tunnel. Some sys temic diseases are predisposing, such as:
minor, cervical rib Sciatic
Pelvic outlet piriformis
OMT, exercise, surgery
muscle Posterior tibial
Tarsal tunnel
OMT, exercise, surgery
Common
F ibular head
OMT, exercise, surgery
Obturator
Obturator foramen
OMT, exercise, surgery
F emoral
Pelvic brim inguinal
OMT, exercise, surgery
peroneal
ligament Ilioinguinal
Abdominal wall
Intercostal
Rib cage
OMT, exercise, surgery
Trigeminal
F oramen ova Ie,
OMT, surgery
OMT, exercise, surgery
foramen totundum, petrosphenoid ligament, Meckel's cave Cranial nerves
Orbital apex, exit
1I, II1, IV, V,
foramina, reciprocal
VI
tension membrane,
OMT, surgery
cavernous sinus Cranial nerves VIII, IX, X, XI, XII
Basisphenoid,
OMT, surgery
basiocciput, jugular formina, hypoglossal canal
Cranial nerves VII, VIII Cranial nerve I
Temporal bone, internal
OMT, surgery
aud itory meatus Ethmoid, cribriform
OMT, s urgery
plate, sphenoid, lesser wing OMT, osteopathic manipulative treatment.
and lymphatic i n fluences. Table 30.3 represenrs specific sites o f nerve enrrapmenr ( J 06, 1 07). Carpal Tunnel Syndrome
Carpal tunnel syndrome is the result of enrrapmenr of the dis tal branches of the median nerve as it passes through the carpal tunnel. The tun nel is formed by the carpal bones and the carpal l igaments. The contents of the tun nel are flexor tendons and the median nerve. Either strong flexion or extension of the wrist can impact the median nerve. There can be acute compression with mechanical deformation and ischemic change. Chronic pro gressive compression can result in vascular compromise. The first effect ofincreased compression is an obstruction ofvenous return from the nerve, which leads to i ncreased capillary distension and further i ncreases i n i n tratun nel pressure. This conrinues to self amplify in a cycl ic fash ion, i mpairing n utrition to the nerve. The large, myeli nated fibers are most vulnerable. At this stage, symp toms appear with pain, and paresthesia is usually transienr and
Hypothyroidism D iabetes mellitus Pregnancy Leukem i a Paraproteinemia Gout The diagnosis depends on a careful h istory to d i fferen riate local disease from systemic disease. With systemic d isease, the symptoms are frequently bilateral. The h istory is i m portanr i n understanding predisposi ng biomechanical factors. These factors are often related to work, hobbies, or chronic behaviors. The patienr complains of pain and paresthesias in the thumb, i n dex, and l o ng fi n ger. Ach i n g can spread prox i mally to the arm and forearm. Early, the pain i s transienr; later, i t becomes permanent. Commonly, i t is worse at n ight o r during provocative activities. In the earliest stages, a shake of the hand can restore circulation and relieve symptoms. Later, i m mobilization with a spl i n t can be relieving. Vague weakness, often described as dropping thi ngs, is common. Physical examination reveals a sharply demarcated median nerve sensory deficit, confined to the palm, often splitting along the long fi nger or ring finger. M o tor exa m ination reveals a weak ness of the thumb abductor, thumb opposer, and distal th umb flexor. I n the more advanced stages, atrophy of the thenar emi nence i s evidenr. Tinel sign i s often positive, with percussion of the nerve at the wrist producing a tingling i n to the hand. Phalen test, forced wrist flexion, can reproduce the pain and paresthesias. Even a reversed Phalen test, forced wrist extension, can be provocative. Electrodiagnostic tests are helpful in corroborating the diag nosis and quanrifying the degree of abnormality. The fi n d i ng of prolongation of the distal motor and/or sensory latencies is an early sign o f demyeli nation. Axonal i nvolvemenr and degenera tion are demonstrated by the appearance of neurogenic atrophy on electrom yography. The electromyogram can be useful to rule out more proximal lesions, such as a radiculopathy. The carpal tunnel itself may be demonstrated on plain radiogram, computed tomogram, and even better with M RI , wh ich can reveal the struc tural consequences of an anatomic compression. The standard treatmenr has consisted o f i m mobilization with wrist splints and avoidance of the provocative activities related to the carpal tunnel syndrome. Paraneural infiltration wi th local anesthetics and corticosteroids is sometimes used. When conser vative measures fai l , surgical decompression is the appropriate treatmenr ( 1 08).
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VI. Osteopathic Considerations in the Clinical Specialties
The osteopathic neurologist begins with a more thorough evaluation. Not o n ly is the biomechanical function of the wrist exami ned but the biomechanics of the fi ngers, hand, forearm, elbow, arm, shoulder, cervical and thoracic spine, and rib cage are also assessed. This assessmenr is performed i n rhe conrext of a complete osteopathi c structural exami nation. Restrictive le sions along the upper extrem i ty and shoulder girdle can i n A uence circulation (venous, lymphatic, and arterial) and mechanical de formation of the median nerve that begi ns at the nerve root, runs through the brachial plexus, and termi n ates in the median nerve that ru ns through the arm and forearm before passing through the carpal tunnel. Whole body mechanical issues, l i ke slumped posture, can i n A uence the local conditions at the carpal tun nel. The veins and lymphatics drain proxi mally i n to the supe rior vena cava and thoracic duct. Mechanical dysfunction i n the rib cage and cervicothoracic region are as relevant as the me chanics of the arm i tsel f. Arterial i nsufficiency can be affected similarly at multiple levels. The sympathetic componenr, often understated, can be i n A uenced from the root of the neck, where the sympathetic gangl ia are found, through the upper extremity itself. The treatmenr, then, is to treat general structural problems with OMT and exercise. D i rect man ipulation to the functional releasing of biomechan ical barriers at the: Neck Upper back Shoulder Rib cage Thoracic i n let and outlet Upper ann Forearm Wrist Hand Fi ngers The techn iques can be d i rect or indirect, and n umerous ex am ples of osteopathic rreatmenr approaches have been proposed. These i ncl ude myofascial release, muscle energy, thrusting, and fu nctional techniques (97, 1 00, 1 09). Sucher ( I 09) has demon strated a model for clinically, electrophysiologically, and graphi cally evaluating carpal tunnel syndrome. H e has shown the patho logic changes on neurologic exami nation, through distal nerve latency studies, and by obtain i ng M R I i m ages of the carpal tun nel to measure its vol ume. H e has then proceeded to treat these patienrs with O MT. He retests his patienrs and demonstrates objective changes in neurologic findi ngs, distal nerve latencies, and carpal runnel volume, as measured by M R l . Sucher ( 1 1 0) presenrs strong evidence for the therapeutic value of osteopath ic management techniques. Another syndrome o f nerve en rrapmenr is thoracic outlet syn drome. This is a syndrome affecting the brachial plexus at the level of the cervicobrachial j unctio n . It is associated with abnormal cervical ribs and most often with disturbed myofascial relations. Thoracic outlet syndrome most typically affects the lower trunk of the brach ial plexus. Compression can occur over the slope of the fi rst rib, i n the triangle made by the scalenus anrerior and medius, along fibrotendinous attachments of any of the scalenes,
along fibrosseous cervical rib rud iments, or under the pectoralis mmor. Patients m ight also complain of pain and numbness of the upper extremity typically extending along the ulnar aspect of the hand. The pain is usually worse with the arm elevated or ab ducted. Thoracic outlet syndrome can be associated with pai n, weakness, and a variety of sensory complai nts. Physical fi nd i ngs i nclude sensory loss, particularly in the ul nar distribution. Weakness of i ntrinsic, ulnar i n nervated muscles is an unusual late finding in thoracic outlet syndrome. Provocative tests are help ful to diagnose and localize the syndrome. Depending on the site of entrapment, there m ight be local ized tenderness. For ex ample, with symptoms elicited on isometric scalene contraction, the entrapment can be localized to the scalene triangle and is associated with localized tenderness of the brachial plexus at this site. When hyperabduction with extension is the culprit, the site of entrapment is often the tendon of the pectoralis minor and local pectoral hypertonicity; tenderness is typical. Sometimes a bruit of the subclavian artery can be auscultated at the site of its compression ( I 1 1 ) . Electrodiagnostic confi rmation is frequently difficult. Pro longed nerve conduction velocity across the thoracic outlet can be demonstrated; in more advanced cases, axonal i nvolvemen t might be encountered on electromyography. Somatosensory evoked po tentials of the upper extremity can be localizing ( l 1 2) . I maging of the region in question is best attempted with M RJ ; however, M RI findings are frequently i nconclusive. Sim ple cervical spine radiograms m ight reveal the presence of cervical ribs. Standard management i ncludes exercises to improve posture, reduce mechanical stress, lengthen shortened muscles, and avoid ing symptom-producing c i rcumstances. Analgesics, antii nAam matory agents, m uscle relaxants, and physical therapies are used. Progressive stretching exercises are i ncluded when i ndicated. When conservative measures fai l , surgical i ntervention remains. Osteopathic management of thoracic outlet syndrome in cludes appropriate structural evaluation with particular attention to the cervical, thoracic, costal, scapular, and brachial mechani cal relationships. In comparison with carpal run nel, the thoracic outlet syndrome involves a more widely affected area. It is there fore more d ifficult to defi ne the i nciting event and to establ ish targeted therapy. Evaluation of posrure reveals a high incidence of posture with head forward and with rounded, upward, and anterior displaced shoulders. Evaluation of the work station and of the habits of the patien t can reveal a subset of behaviors that are dysfunctional. OMT consisti ng of myofascial-releasing maneu vers to the restrictive m usculoskeletal structures can be useful. When they are o n ly temporarily useful and symptoms return when the patient resumes h is or her unal tered l i festyle, efforts to modify the patient's l i fe circumstances are employed. These ef forts i nclude modification and elimination of occupational and avocational mechanical stressors and the promotion of postural awareness with train i ng in postural modification. The most im portant long-term asp�cts are the identi fication of the specific b iomechanical restrictors and the prescription and training of the patienr i n the performance of self-adm i n istered stretch i ng exercises ( I 1 3- 1 1 6) . As a general concept, the temporary benefi cial response to manipulative therapies can be understood using this model. When the pathologic process i nvolves chronically
30. Neurology
447
acquired, well-learned maladaprive somaric behaviors, ir is nor surprising rhar a single manipularion does nor eradicare such a process. Mulriple srraregies are necessary. Parienr educarion, in srrucrion, and performance in a prorracred rherapeuric exercise program is ofren mosr useful. I n rhis way, rhe neuromusculoskele ral sysrem can be reeducared. A parricularly osteopathic approach to the cranial neu roparhies can be based on rhe writings of Surherland as our li ned by Magoun ( 1 07). In this rexr, rhe anatomy o f rhe nerves and their relationship to dural i nvestmenrs, nearby vasculature, bony forami nae, and osseol igamentous structures are elaborately described. The naturally mobile aspect of rhese cranial and in tracran ial structures was appreciated. Sutherland and Magoun recognized the potential for vul nerabi l i ry to mechanical distor tion and compression with rhe resu!ranr production of symp toms, ofren direcrly local ized to individual cranial nerves. Such symptoms can be relared to rrauma, developmenral phenomena, inAammarion, or ischemia.
cause pain to be referred to distant sites. These patterns of refer ral have been meticulously derailed by Travell and Simons (23). The muscles can harbor pai n ful nodules and bands thar acr as rrigger poi nrs and are associared wirh pai n, stiffness, l i m itation of morion, and weakness. Idenrified appropriately, the muscles are responsive to a variety of differenr rreatments direcred ar rhe acrive trigger point. When these rrigger points are deactivared by deep pressure, dry need l i ng, local i n fil tration, stretchi ng, or OMT, rhey no longer serve as a source for pain generation ( 1 1 8) . Nonpharmacologic therapies focused on enhancing the self heal ing capacities of an i ndividual are particularly i m portanr in rhe overall therapeutic formulation . These non pharmacologic rherapies i n clude:
Chronic Pain Syndrome
•
• • • • • •
There is a difference between parienrs suffering acure pain and those suffering chronic pain (see Chapters 8, 1 5 , and 35) . Patienrs with acure and subacute pain syndromes rypically have some degree of tissue i n j ury with nociceprive activarion. These can be recurring evenrs, as in rheumatoid arrhri ris, migraine headache, or trigem inal neuralgia. Ongoing aCLne pain is usually rhe resulr of continued nociceprive i n pur from a desrrucrive rype of lesion, such as a mal ignant neoplasm. Conversely, chronic benign nonmalignanr pain syndromes last for more rhan 6 months wirhour obvious signs of ongoing rissue damage. These chronic pain syndromes can be associared wirh adequare or i nadequare coping by the patient. When coping is insufficient, the pain becomes the central focus for rhe patient. Pa tients with rhis problem are bel ieved to have conri nuous low-level nociceprive barrage or alreration of central processing pathways. This nociceprive barrage can be rhe result of musculoskeleral or orher peripheral pathologic processes wirh nociceptor acrivarion . Ir can also reAecr a pathologic condirion of rhe nociceptors, rheir axons, and their cenrral connecrions ( 1 1 7) . Cl in ical experience demonsrrates a h igh i ncidence of biome chanical dysfuncrion in rhe patient with rhe chro n ic pain syn drome. It is nor uncommon thar patients wirh rhis rype of pain syndrome are under recognized as havi ng a sign ificant srrucrural parhologic cond irion. In facr, significant biomechan ical dysfunc rion can be presenr, representing eirher a primary or secondary process. This information can go unrecogn ized by the major iry of evaluators who use only standard neurologic and medical evaluarion. Patients can begin with one pathologic problem and over ti me develop secondary somatic dysfuncrion. Conversely, pa tients can begin with a pri mary biomechanical i nsult that el udes recognition. In either event, the recogn ition of somatic dysfunc tion and its appropriate management are helpful i n rhe global management of the patienr with chron ic pain. One outcome of a good srructural exami narion is rhe diagnosis of the common and ofren overlooked myofascial pain syndrome (see Chapter 66). This syndrome requi res rhe palpatory identi fication of tender trigger poin rs in muscles rhar, when palpated,
•
Nutritional evaluation and counseling Evaluation and education i n therapeutic sleep hygiene l nsrrucrion and prescri ption of appropriate relaxation Srress reduction techniques Therapeutic exercise Positive visual imagery Promorion of a positive attitude through education about the nature of their pain problem Formation of realistic objecrives of managemenr
AJI of these techniques i nvolve the patienr as an acrive parric ipant in his or her own therapy.
CONCLUSION
It is clear that assessing the patient more completely generates a more comprehensive diagnosis. This fosters the prescription for a multifaceted rreatmenr program that i ncreases the poten rial for success. An addirional advantage i ncl udes an abi l i ry to exclude more unusual yet potentially morbid causes of chronic pai n. Furrhermore, it offers the osteopathic neurologisr the tools to rationally choose among rhe multiple and cosrly diagnostic and rherapeuric possibiliries. The osteopathic approach offers a successful model for i ntegrated multidimensional rreatment wirh rhe patient as the focus and the physician as the facil itator ( 1 9) .
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OBSTETRICS MELIelEN TETTAMBEL
KEY
CONCEPTS
• Somatic dysfunction in normal pregnancy,
• • • •
including low back pain, other musculoskeletal problems, fluid circulation, and hormonal changes Indications and contraindications for osteopathic manipulative treatment during pregnancy Examination, viscerosomatic reflexes, skeletal changes, and biomechanical changes in each trimester of pregnancy Evaluation of lumbosacral spine and pelvis for labor and birth; possible rupture of pubic ligaments Somatic dysfunction and treatment in the postpartum period
that may respond particularly well to osteopathic manipulative treatment (OMT) or that may be relative contraindications to such treatment are of special interest.
SOMATIC DYSFUNCTION IN NORMAL PREGNANCY
Three broad areas of somatic dysfunction effect changes in both mother and ferus. These include: • Changes in maternal suuc(Ure and biomechanics as a result of
the developing fetus • Changes in body fluid circulation • Hormonal changes
An up-to-date osteopath must have a masterfuL knowledge ofanatomy and physioLogy. He {sic} must have brains in osteopathic surgery, osteopathic obstetrics, and osteopathic practice. -A. T StilL (1)
Osteopathic management of an obstetric patient requires knowl edge of the influence of the maternal structural framework on the pregnancy and the effect of the pregnancy on the patient's strucrure. Somatic dysfunction, as defined in the American Os teopathic Association's glossary, is "impaired or altered function of related components of the somatic (body framework) system; skeletal, arthrodial, and myofascial structures, and related vascu lar, lymphatic, and neural elements" (2). Evaluation and treat ment of somatic dysfunction enhances homeostasis, facilitates maternal adaptation to structural and hormonal changes, and may alleviate maternal discomfort caused by an enlarging uterus. During the process of evaluating and treating somatic dys function, the osteopathic obstetrician monitors fetal well being and addresses potential stresses in the mother's body that can oc cur as a result of pregnancy, labor, and birth. Physical changes and stresses in maternal structures, even apart from psychological aspects, are common. More than half of all pregnant women re port some kind of musculoskeletal pain during pregnancy (3,4). There are several aspects of the changing maternal-fetal struc tural relationships that may cause somatic dysfunction at any time from conception to postpartum. These relationships can be organ ized, like pregnancy, into tri mesters. Obstetric condi tions
These are listed in descending order of our ability to treat os teopathically. AJthough most of these changes are reversible, wide variability exists among patients in the time interval after birth before complete reversion to the pregravid condition. The most obvious changes that occur during pregnancy are in the mus culoskeletal system. The nongravid pelvis assumes a new angle when filled with a gtowing fetus, and must be able to support the weight and volume of the enlarging uterus and fetal suuc tures (often up to 6 kg). During fetal growth, the mother's center of gravity shifts forward. In compensation, the lumbar spine as sumes an increased lordotic posture, with a resultant increased pelvic tilt. This tilt is defined by the angle between the horizon tal and the posterior superior and posterior inferior iliac crests (angle theta in Fig. 31.1) (5). The thoracic spine also increases its kyphotic posture. The changes in body Auid circulation and hormones during pregnancy are generally less obvious, less well srudied, and more controversial regarding their origins than are the changes in the musculoskeletal system.
Low Back Pain
One of the most common complaints and complications of preg nancy is low back pain, which has been traditionally accepted as inevitable by women and their physicians (6). The majority of published reports regarding its cause are either anecdotal or re flect data taken from patient questionnaires. Only two studies have employed a traditional detailed physical examination of pa tients to properly diagnose the source of back pain (7,8). Several
31. Obstetrics
FIGURE 31.1. Spinal and pelvic changes in pregnancy. (Adapted from DiGiovanna EL, Schiowitz S. An Osteopathic Approach to Diagnosis and Treatment. Philadelphia, PA: JB Lippincott Co; 1992.)
srudies have found that heavy manual labor and smoking are risk facrors for the developmenr of low back pain symproms dur ing pregnancy (7-12). Pariry, age, and previous hisrory of low back pain have also been associated with such symproms in most srudies, but other reports have not supported these conclusions, perhaps because of limitations in study design, methods, and/or statistical power. The following have not been found ro corre late with the development of low back pain symproms during pregnancy (4). • Race • Occupation • Fetal weight • Pre-pregnancy maternal weight • Weight gain • Exercise habits • Sleeping posture • Mattress rype • Shoe heel heights (13) • Previous epidural anesthesia • Previous hisrory of low back pain
The gravid uterus and the compensatory lordosis that it causes create a tremendous mechanical burden on the lower back ( 1 4,15). This altered posture increases stress across the vertebral facets of the lumbar spine, and increases shear forces across the intervertebral disc spaces. The paraspinal muscles shorten poste riorly, and are unbalanced by overstretching abdominal muscles anteriorly. Fast and colleagues clinically illustrated the abdominal weakness in pregnancy by comparing the abilities of rwo groups
4S 1
(a 36-week pregnanr cohort and an age- and weight-matched group of nonpregnant women) ro perform a sit-up. Of the preg nanr patients, 86% could not perform a si ngle sit-up, compared to just II % of the nonpregnanr controls (I 6). This major difference in abiliry to perform a simple exercise involving the abdominal musculature is thought ro be indicative of the major change in both normal structure and function during pregnancy. Hyperlordosis is often implicated in the etiology of low back pain. While radiographic studies have nOt verified this to date, Bullock and associates used an inclinometer to measure the pro gression of kyphosis, lordosis, and pelvic tilt in 34 pregnancies (17). In their study, thoracic kyphosis increased an average of 6.6 degrees, lumbar lordosis 7.2 degrees, and pelvic tilt only 1.9 degrees throughout the course of pregnancy. These small degrees of increase and tilt did not correlate with developmenr of low back symproms in their study group. Snijders and co workers studied 16 pregnant women, using a combination of reflecrometers and mathematical modeling ro measure curvature of the spine in the weeks just before and just after delivery (18). Their patienrs were an average of 10-mm taller before delivery and kyphosis and lordosis were less marked before delivery than after. They postulate that these findings are a result of a relaxation of the psoas muscle, which allows the normally presenr lordosis to flatten. Ostgaard and colleagues have concluded that pregnant women compensate for intrapelvic changes by subrle lumbar lor dosis. These investigators postulate this lordosis comes about by extension of the upper trunk and neck and hip joint extension, rather than lumbar spine extension (19). Pain in the sacroiliac region has been suggested to result from excessive connective tissue stretch and microtrauma, as a con sequence of the trunk extensor muscle forces that balance the anterior tilt of the pelvic brim caused by the growing uterus (20). Distention of the pelvis further increases mobiliry of the sacroil iac joints (Fig. 3l.l). The transition berween physiologic and pathologic pelvic relaxation, resulting in pain, is indistinct. At first, the main symptoms of pelvic relaxation are spontaneous pain and tenderness of the sacroiliac joints elicited by direct or indirect pressure (21,22). Later, sacroiliac relaxation results in lumbar backache that radiates down the back of the thighs. Oc casionally, pain may radiate over the anterior aspects of the lower part of the abdomen and thighs (23,24). Another rype of back pain that commonly affects a large group of pregnant women is located in the posterior part of the pelvis, distal and lateral ro the lumbosacral junction. Pain radiates ro the posterior part of the thigh, may extend below the knee, and thus may be interpreted as sciatica or posterior joint syndrome. A study of 436 pregnant women by Ostgaard and colleagues revealed that this condition, given the name "posterior pelvic pain," is different than sciatica, in that it is less specific than the nerve root syndrome in distribution and does not extend down inro the ankle and foot (25). This pain is different from posterior joint syndrome because it does not emerge from the lumbar area. Additionally, it does nor include muscle weakness or sensory impairment, and reflexes are unchanged. Therefore, posterior pelvic pain associated with pregnancy should not be rreated as low back pain or sciatica because it is not the result of nerve compression. The patient should be evaluated for postural imbalance and possible spinal segment facet problems.
452
VI. Osteopathic Considerations in the Clinical Specialties
Radicular symptoms ofren accompany low back discomfort associared wirh pregnancy (6). Despite increased shear placed across the disc space (which varies among individuals), herniated nucleus pulposus during pregnancy is uncommon, having an in cidence of only 1: 10,000 (26). It has been posrulated that direct pressure on nerve roots/plexi by the gravid uterus is responsi ble for many of the radicular symptoms (27). " Parietal neuralgia of pregnancy" was first described by Bushnell in 1949 (28). He proposed that mechanical pressure of ligamentous structures of the spine on nerve roots (resulting ftom increased lordosis of pregnancy) was responsible for radicular pain of pregnancy. The symptoms present primarily as paresthesias in the distribution of the ilioinguinal and iliofemoral nerves. Also occasionally as sociated with radicular symptoms is "lightening," an event that generally occurs during the final 4 weeks of pregnancy. The pre senting part of the ferus settles into the pelvis, thus "lightening" the pressure against the diaphragm and upper abdominal caviry (29). Breathing becomes much easier for the mother, but she may also experience radicular symptoms, which have been arrributed to direct pressure of the gravid uterus on components of the lum bosacral plexus that coalesce into the sciatic nerve. A recent study using magnetic resonance imaging demonstrated that bulges or herniations of lumbosacral discs are common in women of child bearing age and that pregnant women do not have an increased prevalence of disc abnormalities (30). Pregnancy may cause preexisting scoliosis to progress. Berman and co-workers ident ified an increased ptogression of the curve in three of eight patients who had idiopathic scoliosis (31). They proposed a link between the effects of the hormone relaxin and the mechanical stress of pregnancy that causes scoliotic curves of more than 25 degrees to progress. In contrast, in a large ret rospective review of 355 women who had idioparhic scoliosis (175 of whom had been pregnant and 180 of whom had not), Betz and associates concluded that pregnant scolioti c patients are not at risk for an increase in the progression of spinal cur vature (32). Scoliotic curves tend to progress in adulthood, but pregnancy does not seem to aggravate the rate of increase. In addition, mild-to-moderate idiopathic scoliosis does not appear to create problems with pregnancy. The rate of successful preg nancy outcomes in women who had scoliosis did not differ from those without scoliosis (32). However, one review suggests that patients with scoliosis had more premature births than were ex pected (33). Women with previous posterior spinal fusion for idiopathic scoliosis have also been shown to have no increased risk of development of low back pain during pregnancy (32). Other Musculoskeletal Problems
Although certain musculoskeletal changes occur during preg nancy, pregnancy itself may affect some preexisting muscu loskeletal conditions such as rheumatoid arthritis and ankylosing spondylitis. Pregnancy may have ameliorating effects on most women who have rheumatoid arthri tis, usually beginning as soon as they become pregnant and continuing until about 6 weeks after delivery (34). The signs and symptoms of the disease may recur with a Aare-up in the postpartum period. Some investigators have speculated that rheumatoid arthritis tends to improve in preg nancy because of increased cortisol secretion (35). Others have
proposed that increased a-glycoprotein in the maternal serum decreases inAammation (36,37). Some researchers also assert that substances derived from the fetal tissues alter the severiry of this autoimmune disease, perhaps through secretion of cortisol or other substances (38). Whereas rheumatoid arthritis generally improves with pregnancy, ankylosing spondylitis is often aggra vated by pregnancy, perhaps because of the increased stresses on the sacroil iac joints duri ng enlargement of the nearby uterus (39). Overall, the course of the disease (over decades) is not affected positively or negatively by one or more pregnancies (39). Even though ankylosing spondylitis ofren limirs motion of the pelvic joints, it is usually not a hindrance to vaginal delivery (40-42). Changes in Body Fluids and Circulation
Increased circulation to the pelvic organs is necessary to meet the merabolic needs of fetal development. Unfortunately, this in crease is sometimes accompanied by insufficient return of Auid into maternal systemic circularion. Either of these can result in congestion or edema of maternal organs and tissues. Fluids in crease an average of 6.5 L over the course of pregnancy (43). Hemorrhoids or varicosities of the vulva or lower extremities may occur as a result of sluggish venous return inAuenced by pressure of the uterus on the venous plexi in the pelvis. Back pain may also be related to development of varicosities (43-45). Some women complain of nighr back pain 1 to 2 hours after lying down, which may awaken the patient from sleep. Fast and others note that dependent edema accumulates when a pregnant woman is in the upright position during the day (43). When she lies down at night, the changes in osmotic forces allow some of this Auid to return to the intravascular space, resulting in increased ve nous retUrn. This increased venous return, coupled with venous blockage that occurs by pressure of the fetus on the vena cava, results in decreased blood flow through the pelvis. A delayed, stagnant hypoxia of the neural tissue and the vertebral bodies ensues, producing the delayed low back pain (and, somerimes, radicular symptoms) that awaken the patient (45). Physical factors of pulse and respiration changing pressure gradients between the abdomen and the thorax alter venous Aow dynamics, causing congesrion (Fig. 3 1 .2) (46). Because of this flow alteration, a change in volume of abdominal organs (e.g., liver, pancreas) also occurs, which tends to increase abdominal caviry pressure. This reversal of venous Aow into vertebral and spinal membranes causes central nervous system congestion, re sulting in complaints of headache, nausea, and light-headedness. Because the venous system of the spine is valveless (47), blood from the spinal cord, membranes, and spine passes through com municating veins to the azygous and hemiazygous systems (which do not have individual veins for all rhoracic and lumbar spinal lev els). Venous blood from these areas usually drains into the heart via the superior vena cava. Decreased efficiency of this closed system may decrease oxygen and cardiac ourput as arterial blood volume is influenced by cardiac contractions "pushing" venous blood, and as respiration "pulls" venous blood with breathing ef forr. Nausea, headache, and congestion of the liver and pancreas may result from venous stasis also caused by rhe gravid uterus on the vena cava, as well as the venous plexi emanating from the spine (48).
3 J. Obstetrics
Back/Spine: Backache � Axoplasmic Flow
CNS: Malaise Confusion Headache Irritability Dizziness Nausea/Vomiting Lightheadedness
Pelvis: Hemorrhoids Vulvar Varicosities � Maternal Nutrition IUGR, SGA Legs: Varicosities Edema Cramps
Chest:
� 02 � Cardiac Output
Abdomen: Constipation Liver Congestion Pancreatic Congestion Vasomotor Instability
453
Anorher major change during pregnancy related to hormonal alterations occurs in the respiratory system. During pregnancy, there are relatively large changes in the mechanical configura tion of the thoracic cage, most of which occur before the uterus enlarges sufficiently to account for such increases. The chest cir cumference increases 5 to 7 cm, the subcostal angle increases from 68 to 103 degrees, and the diaphragm is pushed superiorly by about 4 cm, but increases in excursion by 1 to 2 cm (53). These changes lead to a 30% to 40% increase in tidal volume, and a similar increase in minure ventilation, since the respiratory rate is essentially constant. These changes are usually arrribured to the effects of higher levels of circulating progesterone in pregnancy (based on physiologic studies of progesterone-treated, nonpreg nant animals), but relaxin possibly also plays an important role. Elevations in steroid hormonal levels (especially progesterone) may promote Auid retention, which enhances congestion in both local tissues (e.g., periuterine) and distant sites (e.g., pedal edema, exacerbated by gravity). This congestion may decrease oxygena tion and metabolism at the cellular level, leading to accumulation of metabolic waste products in soft tissues, as well as in the gas trointestinal tract (54).
F IRST TR IMESTER
FIGURE 31.2. Diagram of pathophysiology of congestion during preg nancy. (Adapted from Kuchera M, Kuchera W. Osteopathic Considera tions in Systemic Dysfunction, 2nd ed. Kirksville,
MO: KCOM Press; 1992.)
Hormonal Changes
During pregnancy, alterations in hormonal levels cause physical changes in many parameters. One of the most dramatic of these changes is the widening and increased mobility of the sacroiliac joints and the symphysis pubis, which begins at the 10th to 12th week of pregnancy. The increased width of the symphysis pubis can be detected radiographically as early as the first trimester and reaches its maximum near term. The hormone relaxin has been identified as a major contributor to these changes in joint laxity during pregnancy (15). Relaxin is secreted by the ovarian cor pus lureum during pregnancy (49,50). Concentrations of relaxin are elevated during the first trimester and then decline early in the second trimester to a level that remains stable throughout the rest of the pregnancy until labor (49). Interestingly, the level of relaxin is not increased with [Win gestations. Lower concen trations have been found, however, after 43 weeks of gestation, and in women in premature labor (50). Primary target tissues are the cervix, uterus, and ligamentous structures of the pelvis. In preparation for passage of the felLls during the birthing pro cess, pelvic articulations are relaxed by the hormone relaxin (51). MacLennan and colleagues report that women who have been incapacitated by low back pain during pregnancy have extremely high levels of relaxin (52), suggesting that excessive relaxin is not Il1nocuous.
At the initial prenatal visit (usually after the first or second missed menstrual period), the obstetrician obtains a full health inventory and performs a complete physical examination (54). In addition to performing a traditional pelvic examination, the osteopath ically trained obstetrician may also perform further palpatory structural examination to identify somatic dysfunction that could affect the outcome of pregnancy. Asymmetry of bony landmarks, joint motion tests, tissue texture changes, and local tenderness are used to confirm areas of somatic dysfunction. Palpatory ex amination of the paraspinal tissues is performed to identify areas of tissue texture changes that represent viscerosomatic reAex sites (55). Special attention is given to evaluation of any tissue texture change at the costotransverse area because of the belief that au tonomic nerve effects on segmental muscles are specific. Spinal segmental sites for somatic dysfunction associated with visceral disease are related to the autonomic nervous system supply for various organs (47,56-62). Hansen and Schliak have identified spinal reAex sites at thoracolumbar levels T 10-L2 (Fig. 31.3) (63) affecting: • Large bowel • Appendix • Kidney • Ureter • Adrenal medulla • Testes • Ovaries • Urinary bladder • Uterus
Woods reports that presurgical palpatory findings of a vis cerosomatic reAex correlated with the diagnosis in 10 of 13 pa tients who had acute abdominal disorders (64). Palpatory diag nosis of viscerosomatic reAexes should assist the physician in the
VI. Osteopathic Considerations in the CLinicaL SpeciaLties
454
() I I
I I I I Sympathetic T10 T11 T12 L1 L2
;;
Para. sympathetic I S2 / /. Pelvic nerve S3 ��------�� S4/
1/ II FIGURE 31.3. Sympathetic and parasympathetic innervation of the fe male pelvis. (From DiGiovanna EL, Schiowitz S. An Osteopathic Ap proach to Diagnosis and Treatment. Philadelphia, PA: JB Lippincott Co; 1992, with permission.)
differenrial diagnosis of somatic pain. When combined with other historical or physical evidence, a positive reflex may enhance the predictive value of the diagnosis of visceral disease. OMT of viscerosomatic reflexes has been advocated on the basis that it is designed to reduce residual effects in the somatic structures following a visceral disorder, or to influence the viscus through stimulation of somatovisceral effects (65). Osteopathic physicians have advocated manipulative treatmenr as a part of the treatmenr regimen for organic problems, as well as for preop erative and postoperative managemenr of patients with organic disease (66-69). In the first trimester of pregnancy "morning sickness," or hy peremesis, is a common complainr. The precise cause of the nau sea and vomiting remains unclear (54). Viscerosomatic reflexes may be idenrified on structural examination and often respond to OMT (61). Chapman reflexes (70) are anrerior and posterior myofascial tender points related to organ function, which have been "geographically charted" on the body (Fig. 31.4). Evalua tion of C2 and T5-9 may idenrify digestive disturbances (71). Tenderness of a Chapman anrerior poinr can be used for diag nosis, as well as an indicator to evaluate the degree of success in relieving organ dysfunction. Posterior poinrs are less sensitive to palpation and are usually used for treatmenr. Anterior points should be used for treatmenr when attempts at a posterior ap proach are unsuccessful. The indications and contraindications for OMT during pregnancy are summarized in Table 31.1. Pregnanr women often inquire about exercise at the first pre natal visit. Selection of exercises should reflect a consideration of the changes in the patienr's weight, body habitus, and balance
to minimize the risk of injury to the patienr and fetus (3,23,72). Mainrenance of good abdominal tone should be encouraged (73). Currenr recommendations from the American College of Obste tricians and Gynecologists are that pregnanr women exercise for no longer than 15 minutes at a time and that they maintain a pulse rate of less than 140 beats per minute and a core body tem perature of less than 38°C (74). It has been shown that the second stage of labor lasts only half as long in athletes as in nonathletes (75). Of course, regimens should be individualized. High-risk patienrs, such as those who have diabetes, hypertension, defects of the cervix, or a h istory of miscarriage may not be able to ex ercise (76). In addition to exercise, weight gain has been advised to be limited to a total of 9.1 to 13.6 kg (approximately 1.4 kg per monrh) during the course of pregnancy.
SECOND TRIMESTER
In the second trimester of pregnancy, the uterus is emerging from the pelvis inro the abdomen. The patienr may become aware of fetal motion, as well as stretching pains above the pubic sym physis. If the patient has had abdominal or pelvic surgery, pain may be augmented by stretch ing of previously formed adhesions. Fascial release (direct or indirect) treatmenr may provide some relief in this situation. Round ligament pain may correspond to anterior counterstrain poinrs L3-5 (Fig. 31.5). Suuctural examination of the pelvis at this time may address restrictions of motion of the sacrum and related ligamentous and muscular structures that could result in backache, sciatica, cramps, or posterior pelvic pain (25). The patient may be treated in the sitting, standing, prone, or supine position-whichever po sition she can best tolerate. Almost any type of treatment modality (both direct action or indirect method) can be used, depending on operator skill and patient acceptance. Although complainrs related to skeletal changes continue in the second trimester, the second most frequent area of musculoskeletal symptoms during pregnancy is pain in the hands and wrists (3). Carpal tunnel syn drome (CTS) occurs most frequently in the second uimester, and is the cause of these symptoms for many women. Symptoms of CTS often include the classic triad of numbness, tingling, and pain at night, usually bilaterally (28,77). CTS probably results from localized edema and swelling in the carpal tunnel. It occurs rwice as commonly in pregnant patients who have swelling of the fingers as in those who do noc. It also occurs more commonly in those women with preeclampsia and hypertension (78). In one study, CTS occurred in 2% of 2,358 pregnant women (79), and in another study, 25% of 1,000 women had median nerve com pression at some time during pregnancy (78). These symptoms are somewhat more common in older primiparous women who have generalized edema (79). CTS in pregnancy virtually always resolves completely soon after delivery (80). Palliative management is indicated for pa tients who are sufficiently symptomatic to warrant any ueat menc. Nighttime splinting of the wrist to support it in neuual or slight dorsiflexion has been reported to be successful (79). Sucher has demonstrated improvemenr of nerve conduction studies and magnetic resonance changes resulting from osteopathic ueatment with myofascial technique (81,82).
3 J. Obstetrics
455
Retina. Conjunctiva --__
---.....,��!Ji:4=---- NASAL SINUSES
Middle Ear
Pharynx. Tongue
�.smu�' � . : �
��:J����::�---CEREBRUM
____
������ _ARMS � (aI&o pectoralis minor) z.;��--.:�r-;��_ NEURASTHENIA (also pectoralis major)
-E��
----
Stomach (pe1'ista!&is:I�) l.Mtr. \i8I� D �iKKll8I'(
...-
___
Spleen(0. P8I1Q"eas
r-r---- PYLORUS@ i'H--i--- OVARIES �t---_ INTESTINES
(peir stalsis)
Small Inte&tiA86 --_:::;;...--= AdrenaI&-----!
APPENDIX@ ��-------��� -
Abdomen. Bladder
-U
---
Urettva Ubwus--
___ �
,.......��
�--ir--- LARGE INTESTINES
���
__
Vagina. Prostate Uterus. Broad Ligament Glands---Rectum. Fallopian Tubes Seminal
Groin
-»+--...r-i:"'---.."..,_ SCIATIC NERVE
(posterior)
Yo
.....
Vesicles
Clitoris Vagina
HEMORRHOIDAL PLEXUS -+.
____
I:'J:.=::====::;� SCIATIC NERVE (anterior)
points are bilateral exce@whereindi cated R All as
for right and
@ or left
A
FIGURE 31.4. Diagram of Chapman reflexes.
THIRD TRIMESTER
In the last 3 months of pregnancy, gravitational effects on the uterus and its contents accentuate abdominal fascial drag on in guinal tissues, causing pressure on the venous and lymphatic re turn Row from the lower extremities, and also on the inferior vena
cava. Leg edema and hemorrhoids are common complaints. The pregnant woman may find it difficult to lie in a supine position without experiencing nausea or dizziness from hypotension that results from vena caval compression. During the third trimester, the mechanical and structural changes in the woman become maximal. As a result of these
456
Vi. Osteopathic Considerations in the Clinical Specialties
Middle Ear Nasal Sinuses Phcuynx Tonsils Tongue =:�_---- Esophagus. Bronchus Thyroid. Myocardium IF-:-;i----- Upper Lung. Upper Umb .,...;--+ Lower Lung
Retina. Conjunctiva ----T�.
_____
Larynx PyIoris
-----�
___ __
__ _ _
Small Intestines -----....==--;--;;;:�r Appendix
Stom�
...- ;r�---- Uver R (acidity>C0 .... ..... _��MStoma (peristaisiRCD liver. G allbladder � -,. \ ��7...,.:\� Sp�en(1). P�eas� .. ---- L. Adrenal .----L. Kidney •• ----- Bladder ___
___ -
Area
Intestine: peristalsis
}
These are on the anterior abdominal around the umbilicus
wall
Ovaries
�::;;;;:;;:::;:;::;---- Urethra t.4Ih�:----- Uterus
Prostate or Broad Ugament
r-----��--___ Rectum
\4--+--- Colon
All points are bilateral Pt where ind�t� �for � right and�or
B FIGURE 31.4. (continued)
changes in biomechanics, complaints attributable to loss of bal ance, changes in gait, and especially low back pain are very com mon. Constipation and reflux esophagitis are also frequent, again due to near-maximal changes in structures, fluids, and/or hor mones. Myofascial or soft tissue osteopathic treatment may be utilized to mobilize fluids from extremities to the systemic cir culation. Specific palpatory structural examination to identify gastrointestinal viscerosomatic reflexes for treatment may also be
helpful. Treatment of the pelvic diaphragm to lift pelvic contents may relieve constipation. Treatment of somatic dysfunction in the midthoracic spine may relieve gastrointestinal complaints, such as esophagitis or gastroesophageal reflux symptoms. Osteopathic treatment to relieve somatic dysfunction should focus on spinal segmental levels of Tl O-L2. the sympathetic nerve supply that influences adrenal and ovarian function, as well as uterine contractility. Gitlin and Wolf (83) have provoked uterine
31. Obstetrics
457
TABLE 31.1. INDICATIONS AND CONTRAINDICATIONS FOR OSTEOPATHIC MANIPULATIVE TREATMENT DURING PREGNANCY
-0-
Indications: •
Somatic dysfunction during pregnancy
•
Scoliosis or other structural condition associated with pregnancy Edema, congestion, or other pregnancy-associated condition amenable to osteopathic manipulative treatment
•
Gynecoid
Gynecoid/Platypelloid
Contraindications: Undiagnosed vaginal bleeding Threatened or incomplete abortion • Ectopic pregnancy • Placenta previa • Placental abruption • Premature rupture of membranes (preterm) • Preterm labor (relative contraindication) • Prolapsed umbilical cord • Eclampsia and severe preeclampsia • •
•
--0-- e
Surgical or medical emergencies (other than those listed above)
Anthropoid
contractions in a small group of women with term pregnancies following use of osteopathic cranial manipulation. Additional case hisrories pertaining ro osteopathic management of preg nancy, with discussion of treatment techniques, may be found in Osteopathy in the Cranial Field (84).
Anthropoid!Android
\j
--
--
LABOR AND DELIVERY
After the 36th or 37th week of gestation, prior ro active labor, pelvic examination is performed ro evaluate fetal size, presen tation, and pelvic outlet accommodation for the fetus. An as sessment of the patient's chances for delivering vaginally can be made by interpreting the examination of the "true pelvis" (inlet, midpelvis, and ourlet). The pelvic inlet is bounded anteriorly by mentally constructing a line from the iliopectineal lines along the pectineal eminence and pubic crest ro the symphysis. Posteriorly, the inlet is bounded by the sacrum at the level of termination of the iliopectineal lines. The sacral base is not included, as it is superior ro this terrirory. The plane of the pelvic inlet is a flat surface bounded similarly, but usually inclined horizontally (with the patient in a standing position) at a 40- ro 60-degree angle. The pelvic outlet is bounded by the pubes, ischial tuberosities, and coccyx. The midpelvis contains all structures berween the pelvic inlet and outlet. Caldwell-Moloy classification of pelvic types provides the stan dard for learning the identifying features oHour basic pelvic types (85): • Gynecoid • Android • Anthropoid • Platypelloid
This classification is based on normal variation in the following pelvic features (Figs. 31.5 ro 31.7): • Shape of inlet • Splay of pelvic sidewalls • Prominence of ischial spines
Android/Anthropoid
Android
-0- V Platypelloid (or Flat)
PlatypellOid!Android
FIGURE 31.5. Pelvic types. The four "classic types," as defined by Caldwell-Moloy classification of pelvic types are shown in the left col umn. The shapes of the pelvic space for each type are shown in the center column. "Mixed" pelvic types are shown in the third column; these are named by the posterior shape first, followed by the anterior shape.
• Height of pubic symphysis • Transverse diameter of pelvic outlet • Width of pubic arch • Curvature and inclination of the sacrum
Early pelvic typing may become necessary if there is a past hisrory of trauma or fracture, or if the baby's size seems greater than that indicated by menstrual date. Definitive pelvic typing is not clinically helpful prior to 32 weeks of gestation. If delivery occurs before this time, the baby may be so small that bony architecture may not be a major factor in the labor and delivery process. The closer to term the pelvis is evaluated, the less patient
458
Vi. Osteopathic Considerations in the ClinicaL SpeciaLties
\ \
FIGURE 31.6. Evaluation ofthe transverse diameter. The lateral motion of the gloved finger is limited by the transversely narrowed pelvis (as indicated by the arrows). (From Steer eM. Maloy's evaluation of the pelvis. In: Steer eM, ed. Obstetrics. Philadelphia, PA: WB Saunders; 1959, with permission.)
discomfort there is likely to be, as pelvic tissues become more softened and relaxed as a result of hormonal and physiologic effects of pregnancy on the musculoskeletal system. [n individuals, "pure" pelvic rypes are unusual. Despite a great variation in individual features of the bony pelvis, the birth canal is curved anteriorly in nearly all women (Fig. 31.8). To be born,
FIGURE 31.7. Estimation of width of subpubic arch. Panels A and B indi cate the method of examination to determine the narrowed diameters in the mid- and lower pelvis. Panels C and 0 indicate the estimation of the wide diameters of the mid- and lower pelvis. (From Steer eM. Maloy's evaluation of the pelvis. In: Steer eM, ed. Obstetrics. Philadel phia, PA: WB Saunders; 1959, with permission.)
FIGURE 31.S. Axis of the pelvis, seen on sagittal section. Note that the curve is relatively straight throughout the inlet, but curves ante riorly in the midpelvis. The dashed lines indicate planes of the pelvic inlet, midpelvis, and outlet, top to bottom. (From Scott JR, DiSaia P. Danforth's Obstetrics and Gy necology, 7th ed. Philadelphia, PA: JB Lippincott; 1994: 105-128, with permission.)
the fetal presenting part must negotiate both the pelvic curve and any narrow areas that may be present in the pelvis. Other maternal and fetal variables to contend with during labor are the qualiry of uterine contractions, head molding abiliry, and head flexion capabiliry. Most normal labors require minimal intervention. Osteopathic structural evaluation of the patient in labor should focus on the lumbosacral spine and pelvis, especially on mobiliry of the sacrum. Manipulative management considera tions might include gentle techniques (such as soft tissue or my ofasciaI stretching) that cooperate with natural forces of labor; pregnant patients do not tolerate active or aggressive manual procedures at this time. Treatment of the thoracic spine with soft tissue techniques may regulate L1terine contractions via sympa thetic influence (86). Treatment of sacral base dysf�lIlction may influence cervical dilation. Osteopathic treatment of the cranium has been shown to influence uterine contractions (83). A posterior sacral base provides ample space throughout the coLltse of fetal descent; however, the fetal occiput may maintain the posterior position at delivery. If the sacral base is restricted anteriorly in its lower portion, the occiput tends to rotate into the anterior pelvis, usually maintaining the occiput anterior position for delivery. If the entire sacrum persists in an anterior position throughout its long axis (i.e., a flat pelvis), the head descends through the midpelvis in the transverse position. Sometimes a cesarean section becomes necessary for delivery because the head
31. Obstetrics
cannot descend any furrher or cannot rotate for a vaginal delivery. OMT of the maternal pelvis with the objective of addressing sacral motion resrrictions may assist the labor and birrh process. Despite the variery of pelvic rypes and disrorrions, the fetal head may rraverse the pelvis unevenrfully, if the pelvis is large enough ro accommodate the size of the infanr (87). The most deleterious conditions are those encounrered when an average sized head attempts ro squeeze through an average-sized android, or "funnel" pelvis in which the spines are prominenr, sidewalls convergenr, lower sacrum anrerior, and subpubic arch narrow. When the subpubic arch is wide, the occipur may position i tself with ease. If the arch is narrowed, the occiput remains posterior, in the area of the sacrum. With prolonged maternal pushing, in addition ro possibly unsatisfacrory placemenr of the maternal legs in stirrups, iliac dysfunction, sacral base restriction, back and leg pain with resultanr neuropathy, and even pubic symphysis separation may occur (88,89). True ruprure of the ligamenrs supporring the symphysis pubis during labor does occur. Lindsey and Leggon believe that rupture is caused by the wedge effect of the forceful descenr of the fetal head against the pelvic ring, usually during delivery, creating a separation of more than 1 cm (90). Normal physiologic separa tion has been reported not ro exceed 10 mm, and this amounr of separation causes only slight symproms or no symproms at all (91). Characteristically, when the pubis ruptures, there is an often audible "crack" with acute pain in the region that may radiate ro the back or thighs. Walking and bending aggravate the pain, and the patienr develops a waddling gait. On examination, a distinc tive gap may be palpable at the symphysis. There may also be soft tissue swelling and tenderness over the area. Treatmenr usually consists of conservative measures: bed rest in the lateral decubi rus position and a restrictive pelvic binder ro reduce the separa tion and ro maintain the reduction (3). Additional osteopathic srrucrural evaluation of the spine and pelvis, and manipulative treatmenr of additional areas of somatic dysfunction, may help ro stabilize the pelvis and ro reduce soft tissue swelling. Although subsequenr pregnancies are generally unaffected (92,93), some patienrs may experience pain in the suprapubic region during subsequenr pregnancies, especially in the third trimester.
459
Another frequently encountered cause of pain in the hand and wrist is de Quervain tenosynovitis, which results from compres sion and irritation of the extensor pollicis brevis and abducror pollicis longus tendons as they pass through the first dorsal com partment of the wrist near the sryloid process of the radius (3). Fluid retenrion has been suspected as an initiaror of this prob lem, which is inrensified by the use of the hand and fingers and by movemenr of the wrist (97,98). Patients who have persistent symproms have reporred that infant care activities (97), as well as breast-feeding (98,99), aggravate the condition. Al though back pain is the most common complainr of expec tanr mothers, persistenr back pain can also become a problem during the postpartum period. Russell and associates have inves tigated facrors associated with long-term backache after child birrh in 299 patienrs, especially those facrors that may have been associated with epidural anesthesia during labor (100). They con cluded that, although new long-term backache was reported by the women given epidural analgesia in labor, the pain tended ro be posrural and not severe. Also, no differences existed in the narure of the backache between those who did or did not receive epidurals during labor. Although back pain during or after preg nancy may be common, it should not be dismissed on the basis that it is a normal accompaniment of pregnancy. The lumbosacral spine should be evaluated for extended segmental dysfunction. Back pain can also be addressed by normalizing structures passing through the obturaror canal.
CONCLUSION
A systematic approach by the osteopathic obstetrician who has been rrained ro idenrify and treat somatic dysfunction may reveal underlying sources of discomfort. In this si tuation, OMT may be used ro effect a more comfortable and enjoyable childbearing experIence.
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The osteopathic physician can maximize a successful experience for the mother. She may also need treatmenr of residual somatic dysfunction in the postpartum period. The most obvious chal lenge is to assist the postpartum patienr in returning her pelvis, axial skeleron, and the supporring soft tissues ro their pregravid state; this often calls for OMT. King and H itchcock have demon srrated the benefit of OMT in the reduction of morbidiry and morraliry due ro complications of labor and delivery (94,95). Although CTS usually occurs in the second or third trimesters, Wand reports i ts developmenr in 1 8 patienrs, not during preg nancy but while they were nursing (80). These symproms re solved when breast-feeding ceased. Snell and co-workers reporr similar findings in 5 patients in the puerperium and attribute the problem ro Auid retenrion caused by the hormone prolactin (96).
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ONCOLOGY MICHAEL I. OPIPARI AUGUSTINE L. PERROTTA DAVID R. ESSIG-BE ATTY
KEY CONCEPTS • •
• •
•
• • •
• •
Philosophic principles of care of the patien t with cancer Malignancies that appear as disease involving bone and soft tissue structures, the central nervous system, or the peripheral nervous system, including renal cell cancer, lung carcinoma, and plasma cell neoplasm Manifestations of malignancy in musculoskeletal system, including back pain, joints, m uscle, and skin Manifestations of malignancy in the central nervous system, including cerebral and i ndirect paraneoplastic malignancies Manifestations of malignancy in peripheral nervous system, including remote peripheral manifestations, spinal cord compression, and other causes of peripheral neuropathy Viscerosomatic-type oncologic responses Presenting diagnostic and treatment options to patients Supportive care of patien ts with cancer including symptom and pain relief, blood and blood products, and general supportive care Stress and treatment Osteopathic approach, including indications and contraindications for osteopathic manipulative treatment
Osteopathic physicians do not treat disease, they treat patients
(1). -Philip
E. Creenman, DO Care more particularly for the individual patient than for the special
featum ofthe disease (2).
-Sir William Osler
INTRODUCTION
Medical oncology is a subspecialty ofi nternal medicine and repre sents that branch of medicine dealing with the incidence, preven tion, diagnosis, and medical management of malignancy. Cancer is the second leading cause of mortality in the United States. The field of study surrounding oncology is constandy chang-
ing due to progress of cancer research in diagnosis and treat ment over the past 30 years. Medical oncology has grown as a specialty over these years with the advent of subspecialty fel lowships since the mid-1960s. This 3-year training program is taken after completion of 3 years of training in general internal medicine. Primary care physicians or surgeons generally refer patients to oncologists when they either suspect or have diagnosed malignant tumor disease. In most cases, the oncologist will serve as the guide for a patient's care through the maze of cancer diagnosis, surgical and radiation treatment and/or delivery of chemotherapy and, when necessary, through end-of-life and palliative care. Significant advances leading to cure and long, functional disease-free intervals are now commonplace.
ONCOLOGY
The patient with a cancer diagnosis presents a complex series of events for the primary care physician. The clinical manifestations of this family ofdiseases are many and may be secondary to al tered structure or function at the primary site of tumor involvement or due to involvement of a secondary site with metastatic disease or remote tumor effects such as paraneoplastic syndromes. Often the malignant process may present with signs or symptOms unrelated to the primary site, and without any clinical evidence of metas tasis. Metastasis may occasionally be present and subclinical, yet produce symptOms, or indeed metastasis may be tOtally absent with the primary tumor manifesting itself through a paraneo plastic mechanism. Through this mechanism a malignancy may affect a hormonal cytokine or metabolic process to exert effects at distant sites or within other organ systems without metastasis being present. Patients with cancer, as in all persons with chronic disease, are still people. They are human beings with families, with thoughts, feelings, hopes, and dreams. They have parents and children, friends and colleagues. These are not cancer patients but people with cancer. They are not interesting cases with great physical findings but are living and breathing people. Therefore, discus sion concerning their disease and plans and options for treatment m ust be carefully individualized. These persons must be offered choices and options that are neither right nor wrong but may be
32. Oncology
correct for one person while not for another. The oncologist and primary care physician should always care for the person , even if rreatmenr for the d isease is unavailable. There must always be optimism. These patients must always be offered the comfort of care even if treatment is unavailable. This care will include pre vention of and meeting needs for pain and other symptoms if necessary. This will include supporting the person's fullest level of functioning at home with family and loved ones, or traveling or even working. In many cases there arrives a time in the course of a disease when no further treatment is available. At that time it is es pecially im porrant that the treating physician tefocus attention from the incurable disease ro the person who has to l ive with the disease. This treatmenr involves treatment of mind, body, and spirit including the individual's belief system or spirituality. Often, l istening is all that is needed. Lack of emotional and phys ical abandonment is essential in spite of i nability to treat disease. Healing a person can occur while losing a batrle ro disease. This is a significant opportunity for the caregiving physician. Although treatment of the whole person is the foundation of the physician's interactions with the patienr, it is especially importanr to empha size this aspect of the relationship when you can no longer treat the disease.
THE WHOLE PATIENT: DEFINITION
Throughout this chapter, the reader will see reference several times ro the ph rase" whole patient." The conrext in which this is used refers to a person or human being together with a disease, and not only an ill ness to be diagnosed and managed. That hu man being presents a constellation of potenrial issues related or unrelated to the disease. They may be represenred as personal, social, financial, or spiritual in natu re. The treating oncologist needs to be aware and, at various ti mes, involved in any or all of these aspects, together with the diagnosis and managemenr of the malignancy. This defines the "whole patienr," and although a humanistic qual ity to be strived for by all physicians, is especially linked to the osteopathic, "holistic" philosophy associated with treating a fully integrated/interrelated system.
OSTEOPATHIC PHILOSOPHIC PRINCIPLES OF CARE OF THE PATIENT WITH CANCER
Traditional cancer therapy includes surgery, radiation therapy, and drug therapy. We must continue to use each and all of these modalities. However, we must never forget that we are caring for a person rather than a tumor. Patient decisions and actions are often based on their thoughts, feeli ngs, and perceptions. To Treat or N ot To Treat
Many physicians assume that all cancer must be treated, whethet or not there is anything effective to offer. Remember, we must treat every patient, but have no need to treat every cancer. In many cases more benefit can be provided to the patient with care ful understandi ng, supportive therapy, and meeting the needs of
463
the patient than with defini tive antineoplastic therapy. There fore, honesty with the patient is necessary; honesty regard ing the availability of effective treatment modalities and regarding cure. A life-th reatening disease, such as metastatic renal cell cancer, can be discussed in a positive and optim istic fashion. The patient can be i nformed regarding the unpredictable natural history of the disease, which can have long-term stable control in some pa tients. l m munotherapeutics such as interferon and interleukin (IL)-2 can be d iscussed and offered if the patienr is an appro priate candidate. The patient, however, must be reassured that the physician will be available throughout the treatment course. Patients must be reassured that they will not be permi tted to re main uncomfortable and that multiple modalities are available for relief of d iscomfort. They are reassured that the physician will discuss all decisions regarding therapy with them and assist them in decision making. The physician must inform and support the family if the patienr wishes. Throughout the d iscussion, which may become more repetitious and personal as the relationship develops, touching of the patient is important. The patient must leave the physician after each visit confident that a partnership has developed. Touching as C ommunication
Some patients complain that the only time a physician has touched them i n the past was i n the process of physical exami nation or the placing of a stethoscope on a chest. Patients with cancer feel comforted by an appropriate touch of a hand or even, on occasion, a tear shed with theirs. Touch ing is a nonverbal communication with the patienr that says, [ recognize you as a whole person, not only a diseased body or organ or an interesting case. Recognition of the whole person encompassing the cancer is to recognize the i ntegration of all of the body systems. This offers the consideration that no system can alone become diseased or healthy without impact or benefit to the whole person or other systems. They must all get well and survive together. The basic osteopathic philosophy emphasizes the need to treat the person as a whole. This approach must consider the patient with the disease as well as the patient's environment. This full embodi ment of supportive care can facili tate patient care and provide patient benefit to a greater degree than trad itional anticancer therapy. Osteopathic physicians are known for thei r respect for the role of the neuromusculoskeletal system i n health and disease. Palpa tory diagnosis and treatment of neuromusculoskeletal dysfunc tions have been hallmarks of this profession from its inception. Within this chapter, the disease of malignancy as a whole will be discussed with an emphasis on its manifestations/effects on the neuromusculoskeletal system. The relationship of the neurostructural presentation of a patient with malignancy ver sus a nonneoplastic structural lesion can be interesting and deceiving. Three separate malignancies are presented as index tumors, and serve as prototypes for the variety of neuromusculoskeletal presentations to be d iscussed. All three of these malignant diseases have the potential to present as disease involving bone and soft tissue structures, the cenrral nervous system (eNS), or peripheral nervous system.
464
VI. Osteopathic Considerations in the ClinicaL SpeciaLties
RENAL CELL CANCER
This disease (hypernephroma, Grawitz tumor) is an elusive, un predictable one, accounti ng occasionally for prolonged delays in diagnosis. Renal cell carcinoma makes up only 2% to 3% of all malignant disease (3) . The classic triad of presentation including hematuria, flank pain, and abdominal mass is infrequent, occur ring in less than 10% of cases (4,5). The presenting symptOms, however, are more commonly associated with distant manifesta tions, either metastatic or paraneoplastic. As many as 34% of pa tients have metastasis at the time of diagnosis (6) . When presenr, metastases occur most commonly in lung, bone, liver, and lymph nodes (6,7). This tumor is com monly referred to as the "internist's tumor" due to its presentation with humoral or systemic signs and symptoms of a medical nature rather than a urologic nature. The systemic manifestations may include anemia or erythrocyto sis, fever of unknown origin, weight loss and hypercalcemia, all of which may occur in the absence of metastatic disease. The hyper calcemia is often related to elaboration of an ectopic parathyroid hormonelike substance from the tumor (parathyroid hormone related peptide, or PTH rP) . In addition, a hepatic dysfunction syndrome may occur in up to 15% of patients without metastasis mani festing as significantly altered hepatic enzymes (8) . The natural history of renal cell carcinoma is unpredictable. Patients with metastatic d isease may remain stable for months to years and suddenly develop progressive metastasis leading to death. Patients with progressive disease may likewise suddenly stabilize for prolonged periods of time. Renal cell carcinoma is one of the most common tumors to be reported to undergo spon taneous regression after removal of the primary site (9). However, the majority of these cases have not been histologically confirmed. Neuromusculoskeletal metastasis may occur to the spine pro ducing back pain, to soft tissue areas as a mass, a compression of spinal cord, or nerve root producing peripheral neuropathic symptoms, or can produce CNS signs and symptoms due to di rect metastasis or paraneoplastic effects (hypercalcemia) . The diagnosis of renal cell cancer is most com monly accom plished by radiologic techniques (computed tomography [CT) scan, magnetic resonance imaging [MRl], intravenous pyelo gram, and ultrasonography) . Treatment with surgery is most effective when the disease is localized. I f metastatic disease is present, the extent and location will d ictate whether surgery is appropriate. Radiation and chemocherapy are palliative and of limited benefit. Immune-modularing therapy with IL-2 and/or a-interfeton hold some promise.
LUNG CARCINOMA
Lung cancer is the most common cancer and most common cause of cancer death in both men and women. The use of cigarettes and tobacco products accounts for over 30% of cancer deaths and is responsible for 80% to 85% of lung and laryngeal can cers. A rapid rise in lung cancer incidence and death in women is due to an increase in smoking among women. In men, the rate has stabilized and may be showing early evidence of reversal due to smoking discontinuation. At the time of diagnosis, the dis ease generally has spread to regional lymph nodes or distant sites. Small cell lung cancer (oat cell cancer) is one of the four major cell
types oflung cancer arising from the bronchial surface epithelium and originating as a submucosal growth. Epidermoid (squamous cell) cancer, adenocarcinoma, and large cell car�inoma make up the other major varieties. Small cell lung cancer is generally an aggressive, rapidly growing neoplasm making up approximately 20% to 25% of lung cancers. Once, the most common variety of lung cancer, epidermoid carcinoma now has a 25% to 30% incidence, with adenocarcinomas comprising 40%, and large cell cancer 15% of lung tumors (10). Traditionally survival has been believed to be the best in epidermoid cancers. However, with the recent advent of intensive combi nation chemo/radiation ther apy, small cell lung cancer has shown an improvement with up ro 20% long-term survivals. Due to its aggressive behavior, small cell lung cancer has approximately a 70% incidence of regional lymph node involvement at the time of surgical resection (II). At autopsy, lung cancer metastasis has been shown to be presenr in every body organ with small cell cancer having absolute like lihood of extrathoracic metastasis. Common clin ical problems relate to distant metastasis i ncluding CNS metastasis with neu rologic deficits; bone metastasis presenting with bone or back pain and pathologic fracture; l iver metastasis; adrenal metastasis; and lymph node and skin metastasis. Bronchogenic carcinoma may present as a Pancoast syndrome with pain in the neck, axilla, anterior lower ribs, and scapular region, with thoracic paraspinal muscle spasm and paresthesia in the upper extremity (12). Significant relief of pain may be achieved with osteopathic manipulative therapy (OMT) while undergoing defi n itive radiation therapy and/or chemotherapy. Paraneoplastic syndromes occur commonly with lung can cer. Some occur more specifically with individual histologic va rieties of lung cancer. These may represent presenting symp toms, without metastasis, or even prior to the diagnosis of the primary lung cancer. Paraneoplastic syndromes seen include Cushing syndrome, syndrome of inappropriate anridiuretic hor mone (SIADH), non metastatic hypercalcemia (PTH rP), sub acute cerebellar degeneration, dementia syndromes, peripheral neuropathies, and polymyositis, as well as dermatomyositis. Any of these syndromes may present as al tered CNS function and may create difficulty in discussing appropriate rreatmenr options and decisions. A frequent musculoskeletal para neoplastic mani festation is hypertrophic pulmonary osteoarthropathy. While the previously noted endocrine syndromes, except for PTHrP pro duction, are particularly common with small cell carcinoma, the osteoarthropathy is most commonly seen with adenocarcinoma. Lung cancer should be included as a part of the differenrial diag nosis in all patients with paraneoplastic syndromes. A type of paraneoplastic syndrome occurring with lung can cer i nvolves the ectopic production of bombesin, a multiple amino-acid neuropeptide hormone. Since bombesin was first iso lated from amphibian skin the mammalian equivalent, gastrin releasing peptide (GRP) or human bombesi n, has been found in tumors of neuroendocrine and some non-neuroendocrine ori gins (13). Bombesinlike immu noreactivity has been found in human brain, spinal cord, gasrrointestinal (GI) mucosa, and pul monary neuroendocrine cells. H igh levels of this immunoreac tivity are noted in up to 50% of pulmonary carcinoid tumors and in many small cell (oat cell) lung cancers (I4). This sub stance is particularly interesting because of its apparent autocrine growth-enhancing ability imposed on the tLImors.
32. Oncology
The diagnosis of lung cancer requi res tissue confi rmation by biopsy, surgical resection, or cytology of sputum or selected bronchial washi ngs. Therapy varies with the specific cell type and stage but commonly involves a combination of surgery, ra diotherapy, and/or chemotherapy. Overall survival at 5 years after surgical resection for all resectable stage cell types varies berween 30% and 80%, although the previously noted negligible survival rates for small cell cancer are improving due to the use of intensive combination chemotherapy (15).
PLASMA CELL NEOPLASM (MULTIPLE MYELOMA)
This is a neoplasm of B-lymphocytes of monoclonal origin that progresses to a large cellular population. The plasma cells pro duce immunoglobulins or immunoglobulin fractions that can be distingu ished and detected in blood and urine as monoclonal or M protein on a protein electrophoresis pattern. The diagnosis of this neoplasm is made by the demonstration of bone marrow plasmacytosis, monoclonal immunoglobulin detection, anemia, and bone pain (16) . This disease is the most common primary tu mor to involve medullary bone and may often be overlooked in a patient presenting with back pain . Often the symptoms are vague and nonspecific. Typical lytic "punched out" bone lesions may be absent and a diffuse osteoporosis pattern may be seen on radio graph. The incidence of myeloma is reported to be berween rwo to four per 100,000 population with a h igher rate i n blacks than whites. Plasma cell tumors may originate in extramedullary sites as well. They have been known to arise in almost any organ with the upper air passages (nasal sinuses, nose, nasopharynx, tonsil) being the most frequent extramedullary sites. These tumors may also arise in skin and subcutaneous tissue, thereby presenting as soft tissue masses. At least rwo-thirds of patients present with the skeletal symptom of bone pain, especially in the spine and ribs. Pathologic fractures are very common. Spinal cord compression and nerve root compression are common complications of this disease and may produce radicular pai n. Peripheral neuropathies may occur as a result of amyloid deposition in nerves or perineural vasculatu re. Other clin ical problems common in the patient with myeloma include hypercalcemia, which is reported in up to 35% ofpatients at presentation (17). The progressive confusion and drowsi ness in these patients may resemble CNS disease. G I symptoms of nausea, vomiting, and constipation together with polyuria may signal the onset of hypercalcemia. A hyperviscosity syndrome is also a complication of myeloma, especially immunoglobulin A ( IgA) myeloma, and is due to a change i n concentration, size, and shape of the monoclonal globulin. If the serum viscosity rel ative to water rises above 4, symptoms occur. These may include cephalalgia, visual disturbance, fatigue, vertigo, nystagmus, pare sis, and eventually confusion and coma. This combination of symptoms may closely resemble CNS metastasis. Hyperviscosity is treated by plasmapheresis and speci fic chemotherapy i ncluding steroids and alkylating agents. Attempts should be made to diagnose myeloma earlier than presentation with pathologic fracture. Anemia, proteinuria, and rouleaux formation on a peripheral smear report, or a report of bone demineralization may be early clues.
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Myeloma usually enters a chronic phase that is easily respon sive to steroids and alkylating drugs. Pathologic fractures may be surgically treated with pinning for long bone d isease. I mpend i ng fractures and spinal cord/nerve root compression should be irradiated. Maintaining activity and ambulation is essential in treatment of this disease. Fluid hydration is beneficial for the re nal complications and in preventing hyperviscosity. Eventually the patients enter an acute phase characterized by packing of the marrow with plasma cells producing pancytopenia leading to infection. Infection and renal failure are often term inal events. We have evaluated rwo relatively com mon malignant diseases and one extremely com mon malignant tumor. All three were selected due to their frequent ability to present with signs or involvement of the nervous, muscular, or skeletal system. The impact of these tumors may affect soft tissue and bone simul taneously, sequentially, or not at all. Any physician following or treating a patient with malignancy must be aware of the natural history potential of such presentations.
UNIQUE NEUROMUSCULOSKELETAL MANIFESTATIONS OF MALIGNANCY
The manifestations discussed within this section will be divided i nto musculoskeletal, central nervous system, and peripheral ner vous system. Metastasis can often inAuence the presentation within these systems. Metastasis is often overlooked because of the site of i nvolvemen t. The major mechan isms of metastasis i n volve direct tumor extension and lymphatic and hematogenous dissemination. The specific vasculature i nvaded in the process of metastasis may determine the site that will be i nvolved in the distribution of the bloodborne metastasis (14,15). This is typi fied in prostatic carcinoma and other pelvic tumors by metastatic spread to the vertebral spine, or in carci noma of the breast by spinal metastasis in the absence of pulmonary spread (18,19) . Th is metastatic pattern to vertebral bone may occur as a result of the vertebral venous plexus, a system of valveless vessels extending along the spine and forming anastomoses with veins extending from the brain to the pelvis. Batson, who described the anatomy of this system that now carries his name, demonstrated exten sive retrograde-antegrade vascular Aow potential in this venous system as related to posture and abdominal pressure (18,19) . Musculos keletal System
Back Pain
The bony skeleton is the second most common metastatic site of malignancy in terms of frequency (20). Over 80% of the metastatic tumors originate within breast, prostate, lung, kid ney, and thyroid gland (21). Microscopically, at autopsy, a much h igher rate of metastasis to bone is present than is noted clini cally, with i n excess of 80% i n breast and prostate cancer, 50% in thyroid cancer, and 40% in lung and kidney cancers (21). The spine is involved most often with a reducing order of fre quency extending from lumbar to dorsal to cervical areas of the spine (22-24) . Back pain is often the fi rst i ndication of metastatic disease. Metastatic bone disease is much more common than pri mary bone tumors. Metastatic bone disease in the spine may
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VI. Osteopathic Considerations in the Clinical Specialties
be lytic (clastic or destructive) or blastic (sclerotic) or a mixture of both, depending on the predominant process of Formation or destruction of bone which occurs in metastases. Back pain may be present For varying periods of time beFore the onset of neurologic signs or symptoms, which usually occur secondary to compression of a nerve root or the spinal cord. The origin oFback pain may be diFficult to localize in the skeletal system due to the vagaries of diagnostic tests available. Radiographs do not visual ize osseous changes as early as radionuclide scans. Scans depend on osteoblastic activity For demonstration of abnormalities (25) . Actual loss oF bone density of at least 50% is required to demon strate metastasis by radiograph. Without the osteoblastic process and in purely lytic bone disease, a False-negative bone scan may thereFore occur. In the older adult patient, a reactive or inflam matory process such as arthritis or degenerative vertebral disease can mimic the metastatic process and create a False-positive bone scan. ThereFore, bone scan abnormalities require radiographic, C"C or M Rl confirmation of metastases. Two procedures are oFten indicated For comparison prior co a definitive diagnosis and initiation of treatment. CT and M Rl , which have a greater degree o f resolution, are oFten helpFul in detection of otherwise silent lesions. OFten, with a h igh index of clinical suspicion and without imaging documentation, localiza tion by specific sensory or dermatomal level can Focus an area to permit treatment by radiation therapy. In evaluation of the patient with back pain, one must always consider malignancy, es pecially prostate cancer in a man over 55 years of age. Additional systemic maniFestations may include weight loss, pain unrelated to motion or position, and pain unresponsive to analgesic med ications. Oftentimes there is an urgency in considering spinal metastasis so that appropriate therapy and maintenance of neu rologic function can be maintained in patients with spinal cord compression. Leptomeningeal carcinomatosis is seen most often in small cell lung cancer, breast cancer, and leukemia. In these patients, a variety of diagnoses may precede the diagnosis of leptomeningeal disease. These include cerebral tumor, meningitis, psychoses, hys teria, and polyneuritis (26). This manifestation of systemic ma lignancy may occur as a presenting symptom. The presenting sympcoms often include low back pain, nonspecific leg pain (radicular), headache, and mental status change in addition to extremity weakness, neck pain, and nuchal rigidity (27). The diagnosis is confirmed by finding malignant cells in the cere bral spinal fluid (CS F) as well as elevated CSF protein and low CSF glucose levels (27) . The evaluation of these patients, without knowledge of the presence of a related malignancy, can easily lead to mistaken diagnosis for the back and leg pain resulting from a "m usculoskeletal somatic lesion" rather than mal ignancy. Joints
The joints may be involved with malignancy by either a pri mary tumor or metastatic process to the bone or synovium. This presents as a picture of asymmetric arthritis, or diffuse artiCLI lar changes caused by an indirect, humoral-related process as in hyperrrophic osteoarthropathy. Leukemia in children has been reported to present as localized or diffuse bone pain associated with joint swell ing and pain (28) . Bronchogenic carcinoma has
likewise been reported to present with symmetric painful swell ing of the digits resembling early rheumatoid arthritis as a result of metastasis (29) . Undiagnosed renal carcinoma has been reported by Ritch and colleagues in three cases to present and be treated as shoulder arthritis, prior to discovery of metastasis to the clavicle or upper humerus (30). Hypertrophic pulmonary osteoarthropathy (H POA) is a para neoplastic syndrome presumed to be due to secretion of estrogen, growth hormone, or neurogenic faccors in patients with intratho racic tumors (31). This syndrome produces a symmetric clubbing of fingers and toes, periostitis of long bones, and polyarthritis re sembling rheumatoid arthritis (32) . The joints most frequently involved are the knees, ankles, and wrists. The clinical presenta tion is pain, tenderness, and swelling of the affected joints. In volvement of the metacarpal-phalangeal and proximal interpha langeal joints has been reported. A classic finding is periosteal ten derness and radiographic evidence of periosteal elevation. Lung cancer is the most frequent malignancy associated with H POA, which occurs in 12% of patients with adenocarcinoma and less often in squamous cell cancers (32) . Osteoarthropathy is negligi ble in small cell cancer of the lung. Upon synovial fl u id analysis, generally a noninflammatory fluid finding is noted (33,34). In ruling out rheumatoid involvement, the rheumatoid factor is ab sent in H POA. Perhaps the most characteristic finding is the dramatic symptom relief that may occur within hours of primary tumor resection (28). Muscle and Skin
A wide spectrum of skin, muscle, and connective tissue manifesta tions are associated with previous, current, or as yet undiagnosed malignancy. These may be secondary co direct or metastatic in volvement or due to a paraneoplastic effect. Adenocarcinoma of bronchial origin has been discovered as a mass of the calf (35). Previously undiagnosed renal carcinoma has been reported as a large, growing vascular mass of the biceps muscle (7). Metastatic soft tissue or muscle masses can occur and have been reported in any anatomic area. These may produce pain and affect func tion due to compression of muscle or to nerve invasion. These masses may occasionally be small, deep-seated, and not readily detectable. Therefore, they may be overlooked and treated inap propriately (36). A malignancy incidence of up to 50% has been reported with dermatomyositis and polymyositis (32). These conditions may precede the malignancy by days or years. The skin manifestations when present include a purplish erythema. The predominant clinical complaint is a progressive prox imal muscular weakness developing over weeks to months. Muscle biopsy, elevated ery throcyte sedimentation rate and muscle enzymes, and abnormal electromyogram (EMG) all play a role in the diagnosis. This syn drome, more common in men, is often labeled carcinomatous myopathy or neuromyopathy due to the dim inished to absent deep tendon reflexes. The predominant associated malignancies are lung and gastric cancer. Acanthosis nigricans, a hyperpigmented, hyperkeratotic skin lesion in intertriginous or flexor areas ofaxillary, neck, or anogen ital areas is often associated with gastric carcinoma or other ab dominal mal ignancies.
32. Oncology
Asymmetric shoulder girdle and arm pain may occasion ally present as a structural problem simulating cervical nerve root irritation or brachial plexopathy, as i n thoracic ourlet syn drome. This may be seen in lung cancer with apical involvement and brachial plexus compression by a superior sulcus (Pancoast) tumor. Occult Malignancy Presenting with Musculos keletal Symptoms
Children
Cancer in children is more insidious than in adults and may mimic musculoskeletal disease, developmental processes, or childhood psychological problems (37) . Occult cancer in chil dren presenting with musculoskeletal symptoms is an especially poignant example of why a h igh index of suspicion should be triggered when a child presents with disproportionate pain lev els or an "atypical" pattern of arthritis that is not characteristic of a specific rheumatic disease. Although underlying neoplasm is found in less than 1% of such patients complaining of mus culoskeletal symptoms (39), cancer kills more children than any other disease (37). In 10 of1,254 such children, there were 6 acute lymphoblastic leukemia; 2 lymphomas; 1 Ewing sarcoma; and 1 neuroblastoma (38). I n a retrospective survey of29 children ultimately diagnosed with malignancy and referred to a pediatric rheumatology clinic, provisional diagnoses included: juvenile rheumatoid anhritis (12 children); nonspecific connective tissue disease (4 children); disci tis (3 children); spondyloarthropathy (3 chi ldren); systemic lupus erythematosus (2 children); Kawasaki disease (2 children); and Lyme disease, mixed connective tissue disease, and dermato myositis (1 child each) (39) . The final diagnoses were 13 cases of leukemia; 6 neuroblastoma; 3 lymphoma; 3 Ewing sarcoma; and 1 each of ependymoma, tha lamic glioma, epithelioma, and sarcoma. The children, between the ages of 1 to 15 years (19 boys and 10 girls), had symptoms or signs of musculoskeletal pain (82%); fever (54%); fatigue (50%); weight loss (42%); hepatomegaly (29%); and arthritis (25%) . Features that suggested malignancy i ncluded nonanicular "bone" pain (68%); back pain (32%); bone tenderness (29%); severe constitutional symptoms (32%); and features "atypical" of most rheumatic diseases (48%) . The "atypical" features were consid ered to be night sweats (14%); ecchymoses and bruising (14%); abnormal neurologic signs (l0%); abnormal masses (7%); and ptosis (3%) . Adults
Malignant neoplasms in the adult are associated with a wide variety of paraneoplastic hematologic syndromes. The most fre quently recognized are hypertrophic osteoarthropathy, carcino matous polyanhritis, dermatomyositis/polymyositis, and para neoplastic vasculitis (40). Lesser-known associations are fasciitis,
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panniculitis, erythema nodosum, Raynaud phenomenon, digital gangrene, erythromelalgia, and lupuslike syndromes (40). Paraneoplastic musculoskeletal manifestations of malignancy may coincide, follow, or antedate the diagnosis ofcancer or herald i ts recurrence. The clinical course parallels that of the primary rumor, and treatment of the underlying malignancy often results i n the regression of the rheumatic d isorder. Rheumatic mani festations suggesting a hidden cancer include: rapid onset of an unusual i nfl a mmatory arthritis; clubbing or diffuse bone pain in a patient 50 years or older; chronic unexplained vasculi tis; refractory fasciitis; Raynaud syndrome unresponsive to vasodila tor therapy; rapidly progressing digital gangrene; or Lambert Eaton myasthenic syndrome (40). Managemen t of paraneoplastic rheumatic syndromes consists in control of the underlying cancer; symptomatic treatment of the rheumatic syndrome with a non steroidal antiinfl a mmatory disease modifier, cyclo-oxygenase-2 inhibitor, or glucocorticoid; and appropriate osteopath ic muscle energy and manipulative techniques. Central Nervous System
Although the eNS is a composite of both brain and spinal cord, only those manifestations related to the brain will be discussed here. This will i nclude mal ignant disease involvement of the brain and those manifestations associated with pri mary malignancy that give rise to eNS symptoms without a direct metastatic rela tionship. Direct Cerebral Malignancy
Malignant disease may occur in the brain either as a primary tumor or as metastasis from an extracran ial primary site. The symptoms noted are referable to the region of the brain involved. Of the extracranial tumors that often spread to the brai n, the most common are lung and breast. Autopsy studies have shown that of all cerebral metastasis, approximately 65% are multi ple in occurrence (41) , thus the rationale for utilizing whole brain irra diation as therapy rather than surgery. Surgical therapy is limited to selected situations (true solitary lesions) in metastatic brain disease. In most circumstances, adequate control of symptoms, as well as main tenance of eNS function, will be attained with whole brain irradiation until the primary d isease progresses. Indirect Paraneoplastic
Various syndromes have been described that may indirectly af fect the eNS. These syndromes affect the CNS less often than the peripheral nervous system (42). One of the most common syndromes is subacute cerebellar degeneration. This man ifests as a progressive symmetric disabling cerebellar failure and clin ically includes ataxia and dysarthria (43). Other cerebellar features may also occur. Demen tia is often associated with the cerebellar degen eration. There is generally progressive clin ical deterioration with an occasional report of cli n ical improvement with removal of the primary tumor (42) . The most frequent malignancies associated with subacute cerebellar degeneration are lung, prostate, and col orectal cancer. Other dementi a syndromes can also occur and are often associated with hematologic malignancies (progressive multi focal leukoencephalopathy).
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VI. Osteopathic Considerations in the Clinical Specialties
A number of endocrinologic manifestations of malignancy occur in which there are indirect CNS signs. These are not a result of metastasis, but due to polypeptide hormonelike substances or cytokines produced by the pri mary tumor. These hormones are autonomous in their production and not regulated by normal hormonal feedback control. The three most frequent of these syndromes are Cushing syndrome, SlADH, and non metastatic hypercalcem ia. The ectopic ACTH syndrome (Cushi ng syndrome) is most commonly associated with lung cancer, especially small cell (oat cel l) lung cancer. In small cell cancer of the lung, 25% of pa tients have either the clinical syndrome or signifi cant elevations of ectopic-produced ACTH (32) . Cli nical manifestation is by signs of corticoid excess, which include muscle weakness, hypokalemia, edema, hyperglycemia, hypertension, and neurologic syndromes of altered mental status. The same syndrome may occur i n other tumors as wel l. The most effective therapy is treatment of the primary tumor. The syndrome of inappropriate antidiuretic hormone also oc curs most commonly in lung cancer, especially the small cell variery with 8% to 10% of these patients having the clin ically ev ident syndrome (32). The hormone arginine vasopressin (AVP) is produced in high quantities by the tumor. The major labora tory features are hyponatremia, reduced serum osmolaliry, and increased urine osmolaliry relative to serum. The significant cli n ical symptoms include altered mentation, confusion, lethargy, psychosis, seizures, and coma. This may mimic a primary CNS tumor. Hypercalcem ia is the most frequent metabolic complica tion associated with malignancy. It occurs commonly with breast, lu ng, renal carcinomas, head/neck cancers, and multi ple myeloma. This entiry occurs in approximately 10% of all patients with cancer. Approximately 15% to 20% of this group of patients will not have evidence of bone metastasis (32). Hyper calcemia associated with breast carcinoma and multiple myeloma is usually secondary to bone metastasis with calcium release from bone into the serum. Lung cancer, especially of the epidermoid and large cell varieties, and kidney cancer are most frequently as sociated with non metastatic hypercalcemia. Both of these tumors account for over 50% of the cases of tumor produced PTH rP. It is not unusual for either of these tumors to present cli n ically with symptoms due to hypercalcemia before a diagnosis of malignancy has been made or suspected. The major clin ical signs and symp toms of hypercalcemia occur with serum calcium levels in excess of J 4 microfarad (J-l-F) per dL. Serum calcium levels measured as ionized calcium or total calci um must be adjusted by formula based on serum albu min levels. It is only the ionizable (free or unbound) portion that is clin ically significant. The clin ical effects of hypercalcemia are predominant on four systems. The GI system effects include nausea, emesis, anorexia, and constipation. The renal manifestations are polyuria, and polydipsia, with a late effect of nephrocalcinosis. Cardiovascu lar effects include significant echocardiographic alterations, ar rhyth mias, hypertension, and a marked i ncrease in digitalis sen sitiviry. The neurologic effects, which not uncommonly resem ble metastatic CNS disease, i nclude depression, lethargy, hypore Aexia, progressive stupor and eventual coma, and possibly death. Treatment should begin promptly and include intravenous hy dration and avoidance of calcium administration. Selected use of
drugs includes osteoclast inhibitors such as mithramycin, calci tonin, and b isphophonates. In addition, definitive treatment of the primary tumor by surgical resection, radiation, or chemother apy is essential. Peri pheral N ervous System
This section will d iscuss the direct and remote effects of the malignant process from the standpoint of symptoms related to peri pheral motor or sensory nerve involvement in the extremities. Although it is acknowledged that many of these problems have their origin within the CNS, oftentimes the end effects mani fest themselves peripherally in the extremities. Therefore, these considerations will occur from the point of signs and symptoms rather than origi n. Remote Peripheral Mani festations
Peripheral neurologic problems are common in many patients with cancer. The most frequent etiology of these problems is direct invasion by primary or metastatic tumor. However, neu ropathic symptoms (carcinomatous neuropathy) due to remote effects of the malignancy on the peripheral nervous system can occur but are quite uncommon. Therefore, in addition to the dis cussion of the myasthenic syndrome and sensory motor polyneu ropathy, this section will describe spi nal cord disease with nerve root and plexus involvement. Myasthen ic syndrome, also known as Eaton-Lambert syn drome, is especially associated with small cell lung carcinoma. This disorder is characterized by proximal pelvic girdle muscle weakness. Other muscle symptoms may occur and other tumors may be associated. This syndrome is unlike myasthenia gravis in that the E M G muscle potential and clinical strength improve with repeated stimulation or with exercise (44,45). The Tensilon test (diagnostic for myasthenia gravis by instant relief of muscle weakness after Tensilon admin istration) is not responsive as it is with myasthenia gravis. Treatment of this disorder rests essen tially with treatment of the primary malignancy (small cell lung cancer with chemotherapy) . M ixed sensory-motor polyneuropathy is most com monly seen associated with malignancy. This entiry is most often seen with lung, breast, and GI malignancy (46) . The involvement produces distal extremity muscle weakness and wasting of muscles asso ciated with distal sensory loss and areAexia. EMG studies have shown denervation of muscle and slowed nerve conduction time, while, histologically, axonal degeneration and demyelination are noted (42). Recovery appears to be rare. Spinal Cord Compression
Epidural metastasis and spinal cord compression occurs in 5% to 10% of patients with cancer (47). The vertebrae are the most common sites of bone metastasis, which may lead to vertebral collapse and compressive involvement of the spinal cord and nerves. This subject is of importance because of the frequency with which it occurs and the devastating effects that result if the signs and symptoms are not recognized in time to intervene. It is common for patients with vertebral metastasis to present to emergency rooms or primary care physicians with low back pai n
32. Oncology
and have this approached as a structural or somatic problem. I t is of ultimate importance that spinal cord compression, which is a true oncologic emergency, be considered clinically and evaluated carefully. Of course, certain signs may exist which should di rect one's attention to th is consideration. These include age over 50 years, recent weight loss, presence of lymphadenopathy, pain nonresponsive to previous treatment measures, and neurologic deficits in a patient with a history of malignancy (47) . Constans and colleagues reporr on a review of 600 cases of spi nal metastases with neurologic manifestations and note that 53% had thoracic spine localization, 32% lumbosacral spine localization, and 15% cervical spine localization (48). Therefore, it appears appropriate to recommend radiographic evaluation for patients with thoracic back pain without a known etiology. This recommendation how ever does not apply to patients with lower back discomfort, the most common back pain complaint seen by primary care physi cians. In Constans' review, the most common primary rumor in men was in the lung (19. 1 7%), and in women was in the breast (53.31%) (48). Tumor metastasis to the vertebrae occurs most com monly due to a system of valveless, small veins known as the Batson plexus. These are richly connected to other venous systems with the pelvic, retroperitoneal, extraabdom inal, and thoracic areas allowing freedom of movement of tumor cells to implant and metastasize within the spine. However, blood Aow alone does not account for the osteotropism of some tumors-notably prostate and breast cancers. The primary presenting symptom of spinal cord compression is back pai n, which in most cases is local ized to the involved area of verrebral damage. In reported series in which radiographic and surgical findings are noted, osteolytic lesions are usually present (71%), with osteoblastic lesions in 21% and mixed lytic-blastic lesions in 8% (48) . The back pain may have been present for days to weeks or longer and seldom, by itself, is it a major reason to seek attention. The progression of symptoms to motor weakness, numbness (sensory loss), and finally bladder or rectal dysfunction (autonomic loss) will create concern for the patient. The entire process may have a variable rate of progression. The significant pathophysiologic process is related to spi nal cord and nerve in farction due to arterial or venous occlusion by the compression process. As the progression of neural compression occurs, the symp tom focus shifts from that of back pain to localization of neuro logic symptoms in the extrem ities with pain, weakness, or numb ness. Radiculopathy, identified by pain referred from the primary spinal site, dermatomal sensory changes, and altered deep tendon reAexes, is common, especially in the lower extremities. This pro cess may be bilateral or un ilateral. If bilateral, it is not unusual for one side to progress more rapidly than the other side. Occa sionally, an entire nerve plexus (cervical or lumbar plexopathy) may be involved, producing pain or ach ing in a si ngle extremi ty only, without a dermatomal pattern. The anatomic site of the radiculopathy or plexopathy may be determined by the primary tumor. Most cervical spinal cord compression is noted with lung cancer (40%), followed by breast cancer. Brachial plexus involvement occurs most often in associ ation with lung cancer. Apical or superior sulcus rumors of the lung commonly predispose to brachial plexopathy resulting i n arm and hand symptoms o f pai n, swelling, and loss o f function.
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Lumbar plexopathy is most often associated with pelvic tumors, especially colorectal cancer and sarcomas (49) . The symptom complex presented is generally the same as with spinal cord com pression, with pain the first and predominant symptom. The pain is radicular in approximately 85% of cases (49). Plexopathy in the lumbar area can also present as unilateral or bilateral lower extremity symptoms. Specific areas of paresis, paresthesia, or pain can help to localize rumor involvement to a specific portion of the plexus. Diagnostic tests beyond the plain x-ray film are needed to local ize the tumor and plan therapy. M RI is the modality of choice in spinal cord compression and can often provide the necessary information for treatment planni ng. When suspicion exists for spinal cord or plexus compression, diagnostic imagi ng studies should be done quickly. Treatment is initiated for suspected spi nal cord compression with corticosteroids such as high-dose dexamethasone. It is ad ministered as soon as the diagnosis is suspected and before di agnostic studies are completed. The beneficial effect of steroids may be only short term and may result in pain relief by relieving inAammatory edema. Steroid adm in istration is usually continued th rough the i mmediate therapy period and then tapered. Defini tive therapy requires surgical lami nectomy and/or rad iotherapy. Surgery is preferred i n radioresistant tumors (renal carcinoma) or in cases of rumor recurrence after previous radiation. Thus far, most radiation results are comparable to surgical results. The responses are variable and must be j udged by the degree of symp toms and neurologic deficit with which the patient presents at diagnosis. Most patients with signi ficant paresis or paraplegia at diagnosis will not regain neurologic function. Patients who maintain neurologic function at diagnosis will generally retain function after therapy. Spinal cord compression must be consid ered in any cancer patient with back pain and/or lower extremity symptoms. Other Causes o f Peripheral Neuropathy
Other phenomena may produce peripheral neuropathy with direct tumor or paraneoplastic involvement. Neurotoxic chemotherapy (Vinca alkaloids, cisplatin, taxanes) may produce paresthesia, muscle weakness, and hyporeAexia. Other neu ro path ic effects have been reported such as neuronal deposition of amyloid in multiple myeloma, or hemorrhage into nerves in leukemia. I n conclusion, it is not uncommon for malignant tumors to present at onset or through the course of disease progression with neurologic, muscular, or skeletal symptomatology. Often the symptoms may mimic osteopath ic musculoskeletal lesions with or without accompanying neurologic components. An overview of many of the most frequently encountered central or peripheral neurologic and musculoskeletal findi ngs has been presented here. A P ossible Visceros omatic-Type Oncol ogic Response
Tumor Necrosis Factor (Cachectin)
A variety of cytokines can act as immune system modulators and have been shown in vitro and in vivo to have anti tumor effects.
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VI. Osteopathic Considerations in the Clinical Specialties
These include the interleukins, i nterferons, and tumor necrosis factor (TNF). TNF can serve as an example of a potential vis cerosomatic antineoplastic response. TNF is a polypeptide hor mone secreted principally by macro phages (50). This substance is produced in the body in response to various stimuli including neoplasms and infection. After attack of an organ or system i t i s speculated that the body responds i n a self-protective manner by signal between cells involved in i mmunity and i nflammation (5 1 ) . Multiple biologic responses may occur which may be either beneficial or harmful to the body. The responses are dependent on the level of TNF released, the duration of the exposure, and other factors (52). It is believed that excessive production and exposure associated with infection may lead to tissue destruction and endotoxic shock (52) . Cachexia, frequently associated with mal ignancy, infection, and other processes, is believed to be sec ondary to TNF, hence the name cachectin. Anti neoplastic activity ofTNF has been noted against a wide variety of tumors (53) . The cytolytic effect ofTNF is directed toward tumor cells but not on normal cells (50). The mechanism of action may be related to a direct cellular attack as well as an indirect attack through tumor vascular damage (53) . In addition to the antitumor effects noted, TNF may also exert mitogenic properties as well as inflamma tory properties such as fever induction. TNF appears to be a prime mediator of the i mmune system interacting with i mmune responses, such as enhanced cytolysis when combined with inter feron, enhanced macrophage and neutrophil function, activation ofT cells, and control of some leukocyte precursor differentiation (50) . In addition, evidence now exists that TNF has antibacterial and antiviral properties. Cytokines create potential treatment opportunities. Combi nations with immune modulators, or even chemotherapeutic agents, are being attempted for possible enhanced synergistic re sponse (52). Burgess and colleagues report an i ncreased antitumor activity against renal cell carcinoma metastasis i n an animal model by combining recombinant human TNF plus VP- 1 6 chemother apy (53). TNF represents an excellent model in oncology of a somatic response to stimulation of a viscera or organ system by invasion of tumor or infection. The response provides evidence for the self-regulatory and self-protective healing capacity of the somatic structu reo
ETHICS OF PRESENTATION OF DIAGNOSTIC AND TREATMENT OPTIONS TO THE PATIENT
When discussing the finding of malignancy or the effectiveness of treatment, the cardinal rule m ust always be to tell the truth. A patient must never be deceived. It may not be unusual that protective fam ily members or a spouse will request that the pa tient not be informed of the presence of malignancy, but it is often themselves that these families are protecting since the pa tient usually does far better in accepting information. When a patient asks a question they m ust be answered truthfully. How ever, additional information need not be offered all at one time unless requested. Patients handle information better when it is given over ti me, rather than all at one time. Patients and fam ilies need truth and honesty and should always be left with optimism.
Optimism may not always relate to effectiveness of treatment or longevity, but must offer assurance of comfort, symptom con ttol, and lack of physician abandonment if no further disease treatment is available. Therefore, the physician must 1. Tel l the tru th, never l ie. 2. Remember that all of the truths are not necessary unless asked specifically. 3. Offer optimism and reassurance. Relating the diagnosis of cancer to the patient and discussing the disease, prognosis, and diagnostic and treatment options must be done with knowledge and understanding of the perceptions of the patient. This aspect of patient care is extremely significant. As an osteopathic physician, one has a distinct advantage in these discussions because of the osteopathic phi losophy of treating the whole patient rather than only the disease. Most patients continue to perceive a future with cancer as a short, lonely, painful, and helpless prospect. The initial discussion with the patient may be by the oncologist or the primary care physician. The phi losophy used when presenti ng a cancer diagnosis to the patient and family is based on hope, realistic goal setting, honesty, integrity, and the knowledge that the i ndividual is more than their disease. It is important to inform the patient and family that the di agnosis is malignancy or cancer. Use of the term tumor should be avoided, as it is often confusing and may be deceiving. The patient should be asked whether or not to include their spouse or family in the initial discussion. In most instances, a strong suspi cion already exists and the patient may prefer support from spouse or family. It is important to sit with the patient and discuss the diagnosis in a supportive, unhurried fashion. The understanding and support offered at this time will set the tone and pattern for the remainder of the treatment relationship with the patient. A fully informed, trusting, and cooperative patient will, in most cases, remain cooperative and trusting. After informing the patient about the diagnosis, a distinction should be made for the patient about cure of disease and control of d isease based on realistic expectations of what is possible. Pa tients and families need an opportunity to th ink, ask questions, d iscuss, and express feeli ngs. They may feel abandoned if they are hurried through a brief one-sided discussion, informed they will be referred to an oncologist, and sent on their way before they can ask a question. The physician should ask the patient and their family what they have been told before beginning a discussion. Speal< in lay language no matter what the educational level of the patient. Stress that something positive can be done for the patient. The greatest fear of the patient is that they will be told there is nothing that can be done. Even in the case of a medically untreatable cancer, the patient can be given hope of support, comfort, and caring. A supportive attitude is some times difficult for the patient to accept from a family member, therefore, this attitude must be conveyed from the physician. If surgery, radiation, or chemotherapy is available and to be offered, the patient is informed, but always with the knowledge that gen eral supportive care will be available at the same time if needed. In the even t of metastatic disease that cannot be cured, stress the potential long-term control of the chemotherapy or radiation to be utilized. I ndicate that the purpose of the systemic therapy is to
32. Oncology
at least stabil ize the disease at present levels and prevem furrher growth or spread, if not shrink disease. Throughout the enrire in teraction, an atmosphere is ro be created of concern for the whole patient rather than only i nrerest i n the disease. The patienr is ro be cared for whi le the disease is attacked. Throughout the course of the conversation, do not hesitate ro hold the patienr's hand, arm, or shoulder or ro pat thei r hand or arm. Patienrs and families have indicated that this seems ro convey even more sincerity in caring about the whole patient than any level of discussion. Often when discussing therapy, especially chemotherapy, a patient may be very resistanr ro discuss treatment options due ro previous unfounded " horror srories." It is appropriate ro be aggressive in encouraging chemotherapy when it has a known good outcome in a particular malignancy and the likelihood is high of a beneficial effect. Otherwise, therapy, including inves tigational or cooperative group prorocols, can be offered in an objective manner wh ile i nforming the patienr of al l benefit and risk potentials. I f the patienr is strongly opposed ro the uncerrain benefit ora treatmenr program, reassure the patient and allay any guilt. This can be done by informing the patient, and especially the family that, in many malignancies, there is no definite right or wrong therapy. This is the reason investigational treatment prorocols are available. The right choice is the choice that leaves the patient and family comfortable with thei r decision and does not create conAict between patient and family, especially i n the later phases of the disease process. The physician must supporr the patienr's choices, unless proven benefit is being deprived by the choice made by the patient. This may not apply at the time of initial discussion and therapy presentation, but later when search ing for a subsequent therapy or when choosing ro disconrin ue an i neffective or roxic therapy. The supporr by the physician of the patienr's choices reaffirms the care and importance of the patiem in the rotal treatmenr of the disease. The patienr's needs must be met. Discussion of prognosis is generally avoided at the i n itial con sultation with the patienr. Address this question by a statement indicating the need ro wait ro observe the response of the planned treatment. The presence or absence of a response and type of re sponse will inAuence and may change prognosis. Often during the initial presenration, it is helpful ro sit beside or across from the patienr, without a desk in the middle, or at the side of the hospital bed. Closeness ro the patienr, body language, and verbal communication consistenr with empathic discussion of support and concern, and the agreement ro work as a partner in treating the patient, all help ro create an i n tegral relationship between patient and physician. The key elemem throughout the entire future relationsh ip with a patient must be the treatmenr of the whole patient rather than a diseased organ. The patienr must Imow that throughout the course of the d isease and treatment, the less that can be done for the disease, the more will be done for the patien t. At the initial consultation or at subsequent visits after discus sion of response or suggested changes in treatment prorocol, the patienr will often have a desire ro take the physician's hand or embrace the physician in gratitude. One may partici pate in this gesture with the patient. Patients who have been treated with the holistic philosophy discussed have been observed ro have improved longevity and
471
function over comparable patients who have been treated with only an objective, rigid, scientific philosophy of an i nvestigational study without personalization.
SUPPORTIVE CARE OF THE PATIENT WITH CANCER
The supportive care that the patient may require at certain times during their illness carries an equal weight ro the specific anti neoplastic therapy used. In the event of a patient who declines specific antitumor therapy or who term inates such therapy after a trial, supportive care becomes of paramount importance during the patient's remaining life with the disease. Supportive care consists predominanrly of th ree categories: symprom control and pain relief, blood and blood products, and general supportive medical care. The latter category includes in fection prevemion and treatment, nutrition support, and reha bilitative support and may also incl ude psychosocial, legal, and pasroral care support, all of which are components of hospice care. The discussion on medical management of pain control, use of blood and its products, n utrition, and infection therapy will be limited here. These subjects are well reviewed and documen ted in the medical literature. Rather, these subjects will be reviewed from the philosophic viewpoinr of a medical oncologist with an osteopathic background and experience. Symptom and Pain Relief
Symproms other than pain and discomfort are important ro ad dress for the cancer patient. Anxiety and apprehension may be addressed by spending time in discussion with the physician, so cial worker, nurse, psychiatrist, or psychologist. Simple treatment program adj ustments may be made ro correct the symprom. Pain should always be treated. This seems the least a physician can do for a patiem, especially if cure of disease is not possible. The patient must not be forsaken in favor of the disease process. A large n umber of traditional modal ities are available ro treat pain including analgesics and various delivery methods ro improve ef fectiveness (intrathecal or i nrravenrricular injections, conrinuous infusion pumps, self-delivery pumps, etc.). In addition, neurosur gical procedures such as cordoromy and rhizoromy are available as well as anesthetic blocks. H owever, although no scientific data are yet available, another modality is also useful in selected pa tienrs ro alleviate anxiety and pain symproms. Simple, gentle, soft tissue manipulation without any pressure or thrust can be effec tive, especially in late stage, inactive, and bed-bound patients. The procedure permits the physician ro rouch the patient and commit time to care for the patienr in addition ro the disease. B lood and B lood P roducts
Red blood cell transfusions ro correct anemia, granulocyte trans fusions during prolonged suppression in sepsis, and platelet trans-' fusions ro prevenr bleeding during bone marrow suppression, are all supportive measures that are occasionally needed. These may be needed during periods of disease complications or during
472
VI. Osteopathic Considerations in the CLinicaL Specialties
toxicity from systemic therapy. This support is often lifesaving. However, continued support with expensive or scarce blood prod ucts must be balanced with the benefit to be attained in end-stage patients in the terminal phase of the d isease process. General Supportive Care
Nutritional support of the patient with malignancy is essential whether the patient is actively being treated or not. Malnutri tion is part of a general failure-to-thrive syndrome commonly associated with cancer. The patient may need other supportive care such as antibiotics, blood products, and psychosocial sup port in order to assist with nutrition. In addition, n utritional counseling with a dietician may be helpful as well as nutritional supplements, which are available as commercial products for high-protein enteral support. Total parenteral nutrition admin istered through percutaneous or surgically placed venous access may also be used for hospital ized patients for whom the enteral approach is not possible due to small intestinal or other specific circumstances. Anti-infective therapy may be lifesaving during periods of in creased risk, such as granulocytopenia after chemotherapy. It may also be provided as combination antibiotic therapy to treat docu mented infection, sepsis, or fever during granulocytopenia. Spe cific antimicrobial therapy is guided by culture and sensitivity results. Mobility and bowel or bladder functions are areas of general supportive care not only for the patient with cancer but also for any geriatric patient or patient who is critically ill. All patients can be encouraged to be mobilized out of bed as much as possible. A positive attitude on the part of the patient can be maintained to a greater degree with i ncreased mobility. This may lessen stress and anxiety and even support the immune system i n its attack on the d isease. In addition , mobilization enhances venous blood return and reduces the risk of venous thrombosis, decubirus ul ceration, edema, and constipation. Many patients with cancer have prolonged periods of bed rest due to bone pain, pathologic fracture, or paraplegia due to spi nal cord compressive disease. I n these patients, mobilization i s essential to maintain even minimal functional ability. If assisted ambulation is possible, it should be encouraged. If ambulation is impossible due to pain, fracture, weakness, or neurologic deficit, sitting in a chair may be possible. For the totally bed-bound patient, side-to-side moving with mild soft tissue manipulation can be offered. Bowel function can be maintained with appropriate hydra tion, nutrition, and activity. Stool softeners and other medications or maneuvers such as manual (suppository or digital) stimulation can be used. Constipation can ptovide significant d iscomfort to an i mmobile patient especially one with bone pain or fracture. Bladder function and control is also essential for patients con fi ned to bed. If i ncontinence is present, an indwelling catheter can be useful. However, every attempt should be made to remove the catheter and resume normal function if possible. If it is not necessary, a catheter will only keep patients in bed and inactive for ptolonged periods and i mpair the benefits of physical activity. Rehabilitative care is often an essential element in symp tomatic and supportive management of the patient with cancer. Rehabilitation may include physical, occupational, and speech
therapy. This may be indicated after management of spinal cord compression syndrome, cerebral metastasis, and head and neck malignancies. Often rehabilitative care assists with functional pal l iation in patients who may have 6 or more months of life ex pectancy. Hospice care is becom ing widely recognized and used as an effective modality in the care of terminally ill persons. Hospice focuses on meeting the needs of the patient and the family after effective therapy for the disease is no longer available. The hospice philosophy is focused on effective pain and symptom manage ment while also meeting other physical, social, emotional, and spiritual needs with the aid of a multidisciplinary team of special ists in each area. The patient is maintained in an environment of warmth and caring with family, in the home, except when this is not possible or is unavailable. Dealing with pain and preparation for death is very diFficult or i mpossible for some physicians and represents a deficiency in medical train ing. Hospice meets this need, so death can be accepted as a natural phase of life.
STRESS OF DISEASE AND TREATMENT OF T HE PATIENT AS MODULATORS OF BIOLOGIC RESPONSE
Psychoneurobiology refers to the interrelationship between emo tions, the CNS, and somatic cellular biologic responses. There is l ittle argument that the immune system plays a signi ficant role in the i nitiation and course of malignant disease. The role oFT and B-celi lymphocytes and helper, suppressor, and natural killer (NK) cells together with i nterferons have all been extensively re viewed in the literatute. It appears that the connection between the CNS and the systemic response to ill ness is often mediated by the endocrine system with the assistance of cortisol, the endoge nous opiates (endorphins and enkephali ns), and other steroids and hormones that can regulate some aspects of cellular biologic response (54). Nerve endings have been demonstrated within lymphoid organs (nodes and spleen) . I n addition, receptors have been demonstrated on the surface of lymphocytes for hormones such as ACTH (54) . Thus, it is conceivable to believe that cer tain stresses on the h uman body can alter the biologic response in terms of enhanced or suppressed output or function of sub stances i ncluding i nterFeron, NK cells, and so forth (55,56). One can then speculate on the effect of the cancer process, which can produce Further suppression of an already suppressed immune system. Although i n teresting to speculate, the concept of immuno logic surveillance has not been able to be confi rmed in clinical or human research definitively, particularly as applied to the ef fect of stressors. Stress and anxjety may lead to i ncreased out put of cortisol and catecholamines th rough pituitary ACTH . The cortisol then may initiate a n i mmune suppressive response (54,57) . Glaser and colleagues have demonstrated depressed in terferon production by leukocytes concomitant with a reduced interferon regulation of NK activity at times of increased stress (58) . The endogenous opiate polypeptides, B-endorphin, and the enkephalins have been demonstrated ro enhance N K cell produc tion and activity as well as inhibit metastasis in laboratory animals (59,60) .
32. Oncology
Although no definitive scientific evidence yet exists, it ap pears possible that alterations i n the emotional state and spirit of the patient with cancer, assisted by the physician through opti mism, support, and empathy, can tesult i n an enhanced biologic response. Recognition and treatment of the whole person can pro duce this alteration in the patient's emotional status. The oncol ogist often encounters a patient with advanced metastatic d isease who, without specific antitumor therapy, is able to continue to live and function while wai ting for i m portant life event to occur (i.e., a child to graduate, a marriage, the b irth of a grandchild) . The emotional state and the will to l ive seem to have the ability to affect the biologic behavior of the disease and the well being of the patient.
OSTEOPATHIC MANIPULATIVE TREATMENT FOR THE PATIENT WITH CANCER
Many osteopathic physicians have mistakenly believed that ma nipulative treatment is contraindicated for the patient with can cer. While this may be true for some techniques or for some pa tients, other techniques can be helpful for relieving pain, improv ing visceral function, reducing tension and stress, and i mpn;)Ving the doctor-patient relationship through touch. This section will review the contraindications, indications, and specific techniques for OMT in the patient with cancer. Contraindications f or Osteopathic Manipulative Treatment
While OMT i n general is not contraindicated (Table 32.1), treatment of the area immediately surrounding a cancer is con traindicated because of the risk of hematogenous spread. This is particularly true for the vertebral column where the Batson ve nous plexus, a system of valveless vessels anastomosing with brain and pelvic veins, provides a two-way route of metastasis. There fore, OMT for the entire vertebral column is contraindicated when there is known or suspected vertebral rumor. A primary or metastatic vertebral cancer should be suspected when there is acute back pain associated with systemic symptoms such as fever, chills, n ight sweats, fatigue, and weight loss. Persistent back pain despite adequate treatment also raises a possibility of vertebral tu mor. And, of course, back pain in a patient with another known cancer or a suspected cancer at a site that commonly metasta sizes to the spinal column should raise the index of suspicion (Table 32.2) . Two types of mani pulative techn iques do pose some risk when used for the patient with cancer. High velocity low amplitude (HVLA) techniques have been reported to cause pathologic rib fractures in patients with osteoporosis. Presumably, these thrust TABLE 32 . 1 . MANIPULATIVE TECH N I QUES BEARING CON SIDERATION AND POTENTIAL CAUTION Thrust near bone/j o i nt cancer Lymphatic p u m ps Effleurage Any techn ique in i m mediate vicin ity of cancer
TABLE 32.2. PRI MARY
MALIGNANCIES
WHICH
473
COM
M O N LY M ETASTASIZE TO THE VERTEBRAL COLUMN AND SPINAL CORD, LISTED I N DESCE N D I N G ORDER OF FRE QU E NCY
Vertebrae Breast
Spinal Cord Lung
Prostate
Breast
Lung
Colon
Kidney
Sarcoma
Thyroid
techniques could result in fracture of a rib or other bone weakened by primary or metastatic tumor. Therefore, HVLA technique is contraindicated for joints associated with bones that have known or possible cancer (61) . Thrust technique can be safely applied to the oncology patient as long as metastasis to the area being considered for treatment has been ruled out by MRI, CT scan, or bone scan. Other techniques, such as muscle energy or indirect techniques, can be safely applied for joint somatic dysfunction even when there is documented bony involvement, as long as there is no direct extension of tumor i nto the area being treated. Other potentially risky techn iques for patients with known or suspected cancer are lymphatic pumps and effleurage. Since one route of metastasis is lymphogenous spread, these techniques could contribute to spread of cancer. Factors known to contribute to lymphogenous spread i nclude passive limb exercise, prior cor tisone therapy, extent of local d isease, and lymphatic i nvasion and obstruction (62-64) . This potential for lymphatic metasta sis appears to be due to normal lymphatic transport of cells and lymph node efficiency at filtering and disseminating such cells (65-67) . While lymphatic pumps have never been demonstrated to i ncrease lymphatic transport, their purported mechanism sug gests a potential contribution to lymphogenous spread of cancer cells. Tissue m assage has been demonstrated to stimulate lymph transport and to reduce lymphedema (68,69) . Conversely, there is increasing evidence that physical exer cise can reduce risk for breast and colon cancers (70-75) . While the mechanism for this decrease i n cancer risk with exercise is uncertain, there is some support for a hypothesis that moder ate exercise improves i m mune function (76). A short-term en hancement of antibody response has also been demonstrated for lymphatic pumps (77-80) . Soft tissue massage has been shown to i ncrease N K cell number in human immunodeficiency virus ( HIV)-positive patients (81,82) . Massage has also been shown to reduce pain and anxiety in cancer patients (83-87) . The balance of evidence cited here suggests that lymphatic pumps and effleurage should be applied with caution in patients with cancer. Passive lymphatic treatment can be substituted for active lymphatic pumps and effleurage when lymphatic metastasis is a concern. Myofascial techniques for the thoracic inlet and abdominal diaphragm as well as pectoral traction can be safely applied in patients with cancer with pneumonia, lymphedema, or other problems for which a lymphatic pump or effleurage m ight have otherwise been considered (88,89) . Soft tissue techniques other than effleurage (see Chapter 56) may be helpful in reducing pain and anxiety in patients with cancer when not applied in proximity to tumor sites.
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VI. Osteopathic Considerations in the Clinical Specialties
INDICATIONS FOR OSTEOPAT HIC MANIPULATIVE TREATMENT IN T HE ONCOLOGY PATIENT
OMT, if judiciously applied, can be a very valuable tool for the care of oncology patients, who have the same potential for non cancerous somatic dysfunction and pain as anyone else but with more psychosocial stress (Table 32.3) . In addition, the patient with cancer may be saddled with postsurgical pain as well as cancer pai n. Furthermore, the terminally ill patient may have im mobili ty-related visceral dysfunction amenable to OMT. For patients with known cancer, the pri mary indication for OMT is musculoskeletal pain associated with somatic dysfunc tion but not directly related to the tumor. The somatic dysfunc tion can be unrelated to or secondary to the cancer or its treat ment. For instance, a patient who underwent median sternotomy and resection of a l ung cancer may develop thoracic and i nter costal pai n from a preexisting somatic dysfunction made worse by the su rgery, a viscerosomatic reflex from the lung to the thoracic spine, or surgical trauma to the costovertebral or costochondral joints. The choice of techniques for treating somatic dysfunction in the patient with cancer and musculoskeletal pain is h ighly ind ividual ized and depends on age, severity of ill ness, previous inj uries, other diseases, and time si nce surgery. In general, indirect methods, such as myofascial release and counterstrain techniques, are more appl icable when there is acute or severe illness, and with advancing age. Direct methods such as thrust and muscle energy should be reserved for the stable patient and when metastasis to the area being treated has been defi ni tively ruled out. OMT is also indicated for prevention or treatment of immobi lity-related complications in the bedridden patient who is term inally ill with cancer. Prolonged im mobility can cause at electasis predisposing to pneumonia or constipation, which may al ready be present as a side effect of narcotic analgesics. To prevent and treat atelectasis or constipation, thoracolumbar soft tissue and rib-raising treatment can be appl ied daily, in many cases by fam i ly members instructed to do these tech niques at home. The i n i tia tion of rib raising should be preceded by treatment of sign ificant vertebral and rib somatic dysfunction to prevent exacerbation of . visceral facilitation. Extremity lymphedema with swelling and pain, especially com mon after radical mastectomy for breast cancer, can be helped by OMT. Ini tial ly, the fascial diaphragms are treated to reduce tension around proximal lymphatic vessels, thereby facilitating lymph drainage from the extremity. If the cancer is cured or the risk for lymphogenous metastasis is insignificant, effleurage to the involved extremity or a lymphatic pump can be appl ied im mediately following diaphragm treatment. If helpful, effleurage
TABLE 3 2 . 3 . I N D ICAT I ONS
FOR
OSTEOPAT H I C
LATIVE TREATMENT I N PATIE NTS WITH CANCER
Indications Pa i n and somatic dysfunction Constipation Atelectasis Pneumonia Postsurgical lymphedema
MANI PU
and lymphatic pumps can be taught to a family member to be appl ied once or twice a day for lymphedema. Pain, immobility and its consequences, and postsurgical lym phedema are common problems in patients with cancer that can be readily treated with OMT. An additional benefit of treatment is an improved sense of well being which many patients report. It is enti rely possible that this period of well being is due to en hancement of the i mmune system wi th elevated outpu t of cellular im mune substances, NK cel ls, or endogenous opiates. It has been demonstrated that prognosis may be predicted in patients with breast cancer by the sustained level of NK cell activity (90). A future study to measure serum and CSF levels of various immune substances in response to OMT would be an invaluable addition to the osteopathic literature.
COMPLEMENTARY AND ALTERNATIVE MEDICINE IN ONCOLOGY
AJthough little objective research has yet been accomplished in the use of alternatives in cancer treatment a number of modalities have been used anecdotally for discom forr or symptom control and general immune enhancement. These include acupuncture and static magnets for control of discomforr and better rest and reduced need for analgesics. M assage and other relaxation tech niques may assist in stress reduction. Herbal products are often considered to enhance the immune system as well as for cancer prevention but must be used with caution, considering poten tial drug interactions with prescribed pharmaceuticals. Perhaps a more studied technique has been visual ization or guided imagery to aid in stimulating immune response to assist with trad itional chemotherapy or radiation therapy benefit.
CONCLUSION
The osteopathic physician has a special opporrunity and obli gation to treat the patient with cancer as a whole patient, not j ust a disease. Practitioners of the osteopath ic approach, with its emphasis on touch and healing, can provide patients with cancer and their families with the information and support they need.
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3 59. 39. Cabral DA, Tucker L B . Malignancies in children who i n i tially p resent with rheumatic complaints. j Pediatr. 1 999; 1 34 ( 1 ) : 53-57. 40. Fam AG. Paraneoplastic rheumatic syndrome. Best Pract Res Clin Rheumatol. 2000; 1 4 (3):5 1 5-533. 4 1 . Sugarbaker PH, D u n n ick N R, S ugarbaker E. Diagnosis and staging. Tn DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principals and Practice of Oncology. Philadelphia, PA: J B Lippincott, 1 982; 1 1 : 232. 42. Riddoch D . Neurological manifestations of cancer. Practitioner 1 9 8 1 ;225:8 1 9-826. 43. Btain WR, Wilkinson M. Subacute cerebellar degeneration associated with neoplasms. Brain. 1 965 ;88:465. 44. Lambert E H , Eaton LM, Rooke E D . Defect of neuromuscular condition associated with malignant neoplasms. Am j Physiol. 1 9 56; 1 87:6 1 2. 45. Lambert E H , Rooke E D . Myasthenic state and lung cancer. I n : Brain WR, Norris FH ] r. eds. The Remote Efficts of Cancer on the Nervous System. New York, NY: Grune & Strarron ; 1 96 5 : 67-80. 46. Croft PB, Urich H , Wilkinson M. Peripheral neuropathy of sensorimo tor type associated with malignant disease. Brain. 1 967;90:3 1 -66. 47. Bates OW, Reuler ) B . Back pain and epidural spinal cord compression. j Cell Intern Med. 1 988;3: 1 9 1 - 1 97. 48. Contans JP, de Divitiis E, Donzelli R, et al. Spinal metastasis with neu rological manifestations. j Neurosurg. 1 983;59: 1 1 1 - 1 1 8. 49. Jaeckle KA, Young OF, Foley, KM. The natural history of lumbosacral plexopathy in cancet. Neurology. 1 985;35:8 1 5 . 50. Van Der Merwe PA. Tumor necrosis factor. S Aft Medj. 1 988;74:4 1 1 4 1 7. 5 1 . Abraham E. Tumor necrosis factor. Crit Care Med. 1 989; 1 7: 590-59 I . 52. Tracey KJ, Vlassara H , Cerami A . Cachecti nftumor necrosis factor. Lancet. 1 989; 1 : 1 1 22- 1 1 26. 53. Burgess ] K, Marshall F F, Isaacs ]T. Enhanced anti-tumor effects of re combinant h uman rumor nectosis factor plus VP- 1 6 on metastatic renal cell carcinoma in a xenograft model. j Urol. 1 989; 1 42: 1 60- 1 64. 54. Glaser R, Kiecolr-Glaser] . Stress-associated immune suppression and ac quired i m m une deficiency syndrome ( A ID S) . Adv Biochem Psychophar macol. 1 988;44 :203-2 1 5 . 5 5 . Glaser R, Kiecolt-Glaser ] F, Stout K, et al. Stress-related impairments in cellular i mm u nity. Psychiatry Res. 1 98 5 ; 1 6(3):233-239. 56. Glaser R, Kiecolt-Glaser JK. Stress and immune function. CLin Neu ropharmaco!' 1 986 ; 9 [ Supp l 4] :485-487. 57. Southam CM. Emotions, immunology and cancer: how mighr the psy che influence neoplasia? Ann NY Acad Sci. 1 969; 1 64(2) :473-47 5 . 58. Glaser R, Rice ] , Stout ]C, Kiecolr-Glaser ) K. Stress depresses interferon production by leukocytes concomitant w i th a decrease in natural killer cell activity. Behav Neurosci. 1 986; 1 00(5) :675-678.
59. Faith RE. I n h ibition of pul monary merastasis and enhancement of nat ural killer cell activity by methionine-enkephal i n . Brain Behav immun. 1 988;2: 1 1 4- 1 22. 60. Will iamson SA, Knight RA, Lightman SL, Hobbs J R . Differential ef fects of B-endorp h i n fragments on h uman natutal killing. Brain Behav lmmun. 1 987; 1 :329-335. 6 1 . Kuchera WA, Kuchera M L . Osteopathic Principles in Practice, 2 n d ed. Kirksville, M O : KCOM Press; 1 992:295. 62. Schmidt JD, McLaughl i n AP, Saltzstein SL, Garcia-Reyes R. Risk factors for rhe development of distant metastases in patients undergoing pelvic lymphadenectomy for prostatic cancer. A m j Surg. 1 982; 1 44( 1 ) : 1 3 1 -
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79. Measel ] W. The effect of the lymphatic pump on the immune response: I. Preliminary studies on the an tibody response to pneumococcal polysac charide assayed by bacterial aggl utination and passive hemagglutination. jA OA. 1 9 82;82:59-62. 80. Mesina ] , Hampton 0 , Evans R, et al. Transient basophilia following the application of lymphatic pump techniques: a pilot study. jA OA. 1 998;98(2) : 9 1 -94. 8 1 . D iego MA, Field T, Hernandez-Rief M, et al. H IV adolescents show improved i m m u ne function following massage therapy. Int j Neurosci. 200 1 ; I 06( 1 -2):35-45. 82. lronson G , Field T, Scafidi F, et al. Massage therapy is associated with enhancement of the immune system's cyrotoxic capaci ty. In t j Neurosci. 1 996;84( 1 -4):205-2 1 7.
83. Ferrell-Torry AT, Glick OJ. The use of therapeutic massage as a nursing i n tervention to modify anxiety and the perception ofcancer pain. Cancer NuTS. 1 993; 1 6(2):93- 1 0 1 . 84. Grealish L, Lomasney A , Whiteman B . Foot massage: a nursing i n terven tion ro modify the distressing symptoms of pain and nausea in patients hospi talized with cancer. Cancer Nurs. 2000;23(3):237-243.
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78. Jackson K M , Steele TF, Dugan EP, e t al. Effect of lymphatic a n d splenic
ORTHOPEDICS RICHARD A. SCOTT MICHAEL L. KUCHERA JEFF J. PATTERSON
KEY CONCEPTS • • •
• •
Value of orthopedic training to osteopathic physicians Elements of an osteopathic orthopedic examination Osteopathic orthopedic approach to developmental dysplasia of the hip, hip fracture in the geriatric population, osteoarthritis of the knee, low back pain, and shoulder instability Osteopathic approaches to ligamentous laxity and tendonosis Specifics of history and physical examination, pathophysiology, differential diagnosis, and management
and more functional adult. The etymology of the term orthope dics reflects this perspective as well: ortho means to straighten, and pedic refers to the pediatric population. The osteopathic or thopedic physician, with their emphasis on structure-function interrelationships, understands and respects this perspective. The field of orthopedics has subsequently been divided into orthopedic medicine and orthopedic surgery. Beginning in the 1930s, James Cyriax, MD, a British orthopedist, applied the concept of interrelated structure and function and developed a diagnostic and treatment system that is now known as ortho pedic medicine, in contradistinction to orthopedic surgery. He authored a series of original papers and the definitive text, Text book o/Orthopedic Medicine, which describes the importance of making a precise anatomic diagnosis based on: • •
The study of orthopedics is an integral part of osteopathic ed ucation. After residency, osteopathic orthopedic surgeons make up one of the specialty colleges in the osteopathic profession. Or thopedics is the specialty of medicine concerned with the preser vation of the health and restoration of function of the skele tal system and its associated structures (i.e., spinal and other bones, joints, and muscles) (1). Orthopedic training is essen tial to the osteopathic physician; orthopedic knowledge extends the ramifications of somatic dysfunction into the structural and anatomic-pathologic arena. Orthopedic knowledge is vital in the differential diagnosis of patients presenting with musculoskele tal complaints; it offers unique insights into the diagnosis and treatment of traumatic and nontraumatic diseases of the muscu loskeletal system. Many osteopathic orthopedic physicians spe cialize in sports medicine or devote a portion of their practice to this field. They have skills and a special perspective in treating the structural and functional problems arising from sports injuries. Through prevention and rehabilitation, they want to encourage maximum function within the athlete's structure. The emblem of the orthopedic society is based on an 18th century drawing by Nicholas Andry (Fig. 33. 1) that depicts a tree curved and twisted by the winds and weather, held upright by a series of ropes and splints (2). This image continues to influ ence the orthopedic community. By molding the growing skele ton, orthopedic physicians help a child grow into a straighter
• •
Joint range of motion patterns and their end-feel Referred pain patterns Differentiation of contractile and inert structures Understanding of selective tension
He also created his own system of manual techniques to be incorporated into treatment. Until his death in 1989, Cyriax believed that the intervertebral disc was the source of almost all spinal pain. While alive, his in fluence and his dogmatic teaching did not allow alternative ideas to compete (3). Since his death, however, orthopedic medicine in the United States has expanded its paradigm to embrace an un derstanding of myofascial and ligamentous pain. The American Association of Orthopedic Medicine (AAOM) consists of MDs and DOs who find value in Cyriax's commitment to make a spe cific anatomic diagnosis using standardized physical examination of the somatic system and who wish to emphasize conservative management of orthopedic cases. This organization embraces the diagnosis of somatic dysfunction and uses manipulative tech niques in their treatment regimens; it is also the North American representative of the international organization of fully licensed physicians interested in manual medicine. AAOM has officially adopted the Glossary of Osteopathic Terminology to maintain consistency in their discussions of diagnoses amenable to manip ulation. Treatment tools in orthopedic medicine include: • •
Manipulation Prolotherapy
478
VI. Osteopathic Considerations in the Clinical Specialties
FIGURE 33. 1 . An i mportant basic orthopedic principle is embodied i n the f i g u re o f t h e tree. The b o n e is n o t a n i n e rt, calcified, fibrous mate r i a l . It is a g rowing, plastic, dynamic structure with a n active metabolism that responds to a wide var i ety of sti m u l i, and is as truly a l ive as any other structure i n our bodies. " J u st as the twig is bent, the tree's i n clined," wrote Alexander Pope. (From Peltier LF. Orthopedics: A History and Iconography. San Francisco, CA: Norman P u b l i s h i n g ; 1993. Art from Andry N . L'Orthopedie. Paris: La veuve Al ix, 1741, with perm ission.)
• • • •
Trigger point therapy Orthotics Exercise prescription Commitment to an orthopedic perspective
Orthopedic surgery in the osteopathic profession is almost as old as the profession itself. At the American School of Os teopathy (ASO) in Kirksville, Missouri, at the beginning of the 20th century, George Laughlin, DO, was gaining acclaim as an orthopedic surgeon by applying European techniques to perform bloodless surgery on congenital hip dislocations and in other
orthopedic cases. The surgical team at the ASO at this time also included Andrew Taylor Still, MD, DO, who is credited with rev olutionizing the practice of surgery by osteopathy by employing osteopathic manipulative treatment (OMT) in preoperative and postoperative care (4). Research on the efficacy of the osteopathic approach for reducing postoperative surgical complications with OMT was carried out many years later by another Kirksville or thopedic surgeon, Edward Herrmann, DO (5). The osteopathic orthopedic specialist has been influenced by adherence to the principles of osteopathic medicine. Even if most of the time in orthopedics is spent in busy mechanical pursuits, equally important moments.are spent practicing as an osteopathic physician. In this sense, the orthopedist approaches patient care wi th a keen awareness that the orthopedic problem is but one part of an entire medical and social paradigm. It is in these moments of interaction with internists, family practitioners, and patients' family members that the orthopedist brings into play much of their osteopathic orientation. One of the goals in osteopathic orthopedics is to inculcate this attitude of wholeness in treatment, lest the specialist in training take the easy route and forget that their area of expertise is only part of the whole. An osteopathic physician treating an orthopedic problem ad justs or modifies their approach in a manner different from that of a nonosteopathic physician. Osteopathic orthopedic surgeons are in the subsection of orthopedic surgeons who have been trained osteopathically, but they are essentially surgeons. The thought processes of surgeons, different from that of nonsurgeons and in ternists, involve an approach to problem solving that has an im mediacy based on the need for urgent decision making. Farmer has studied the educational process and methodology used in training physicians to become surgeons and has noted differences in affect and approaches from that of general internal medicine, where the educational process has been studied more thoroughly ( J.A. Farmer, unpublished work, 1992). One of the aspects that may make orthopedics alluring today is the tremendous advance in the ability of physicians to diagnose and surgically treat and thus modify diseases and problems that, in the past, could only be watched as they progressed. What dif ferentiates the orthopedist from other physicians and surgeons includes often lengthy technical procedures using saws, drills, and metallic implants, as well as the activities associated with fracture reduction and casting, juxtaposed to delicate repairs of tendons and nerves under magnification. Before a surgical pro cedure, the orthopedic surgeon performs appropriate diagnostic examinations and tests and formulates a treatment protocol. Af ter surgery, prevention of complications, education about post operative nutrition, and rehabilitation necessitate a wide range of physician knowledge and skill. One aspect of orthopedics, both surgical and nonsurgical, deals with the diagnosis and treatment of traumatic and non traumatic diseases of the musculoskeletal system. Many health professionals address these issues today. Who should examine and who should treat the injured or aching skeleton? Among the many who offer health care are: • • •
Physician's assistants Nurse practitioners Specialty-trained registered nurses
33. Orthopedics
Chiropractic doctors Physical therapists • Massage therapists ' [n the h number of possible procedures and i mplants with differing mate rials and engineering designs. The surgeon must also work closely with the medical managers and hospital administrators who con trol the expenditures for this technology. Ultimately, these proce dures and tests are done for and on people who are not growing properly, have suffered traumatic injury, have developed arthritis, or have intractable pain. •
•
•
•
INTEGRATED OSTEOPATHIC ORTHOPEDIC EXAMINATION
The integrated osteopathic examination is detailed in other chap ters, but certain principles bear summary here. Recognition of re ferred pain patterns from nerve roots, peripheral nerves, myofas cial trigger points, and ligamentous structures is a prerequisite for the integrated osteopathic orthopedic examination. A neurologic screening examination is also important for differential diagnosis and prognosis in patients referred for orthopedic evaluation. Use of selective tension in the examination relies on the ob servation that normal structures are painless and/or strong when stressed; inAamed or strained structures are painful or weak. Orthopedic examination employs selective tension to evaluate muscle, meniscal, tendinous, and ligamentous structures and functions, looking for evidence of inflammation or strain. The physician isolates somatic structures and gently but specifically stresses them, looking for pain, weakness, and crepitus. The McMurray meniscal test and Yergason test are examples of this form of examination. The orthopedic physical examination of the somatic system evaluates specific joint characteristics, including range-of-motion and the end-feel associated with major and m inor joint motions. Often the same test of joint motion allows for structural and dysfunctional interpretations: excessive motion and/or a sloppy end-point to the motion may suggest a ligamentous laxity, while a restrictive barrier at the end of motion testing may suggest a somatic dysfunction. It is important to recall that, in somatic dysfunction, the restrictive barrier appears in one combination of directions and is absent in the opposite combination of directions; the barrier is also reversible with manipulation. Restriction in all directions is characteristic of a capsular pattern seen in pathologic conditions such as arthritis or the fibrotic reaction to trauma or overwhelming stress. In such structural diagnoses, somatic dys function is also often secondarily present and can be appropriately treated to the patient's benefit. After the secondary somatic dys function is treated, the primary structural barrier characteristics remalI1. This chapter is intended for generalists and primary care physi cians and reviews a few types of orthopedic diseases while dis cussing how the orthopedist sees these problems biologically, mechanically, and socially. The chapter discusses what may be distinctive aspects of an osteopathic practitioner's approach to six commonly seen orthopedic problems:
• • • •
479
Developmental dysplasia of the hip Geriatric hip fractures Osteoarthritis of the knee Acute low back pain Instability of the shoulder Ligamentous laxity and tendonosis
DEVELOPMENTAL DYSPLA SIA OF THE HIP
The osteopathic physician, in examining the child at the time of birth and afterwards, first evaluates the whole child. In so doing, the physician looks for dysmorphic features that may be associated with multiple anomalies: the child who has cardiac or gastrointestinal abnormalities, failure to thrive, supernumerary digits, or the inability to bend limbs after delivery (6). A child with multiple congenital anomalies may have abnormalities of the musculoskeletal system that occurred at the same moment in embryogenesis. Instability of the hip is one of the more common problems in newborn children (7). To evaluate hip stability, the physician observes any abnormalities in skin creases or gluteal folds, leg lengths, and inequalities, and watches for spontaneous motion and activities. The physician evaluates the hip while passing it through a range of motion, checks to see if there is easy and full abduction, and feels the placement and Auidity of motion of the femoral head in the acetabulum (the ball in the socket). An abnormality discovered in any of these observations or tests points to a problem. Most physicians know the Ortolani sign, which is a palpable sensation of a rapid motion of the femoral head or a "clunk" felt as the dislocated head is reduced into the hip socket from its dislocated position. Here, as Figure 33.2 shows, the femoral head is gently lifted over the labrum and into the socket. In the case of a reduced hip that is unstable, the Barlow test dislocates the hip as the femur is gently adducted with the hip Aexed. The physician gently applies pressure over the medial proximal fe mur and, while doing so, can feel the femoral head slip out of the socket. As the hip is dislocated, gentle pressure on the thigh or knees gives the feeling that the head is not articulating with the socket but that there is a soft end point as the pressure is applied. Moreover, the thigh appears shorter. A positive result in any of these tests, performed routinely in the neonatal ex amination, suggests further studies or treatment. These tests are performed easily and simply by the osteopathic physician and are examples of the preeminence of a physical examination and the significance of palpatory findings in the evaluation. In the early period of neonatal development, these physical examina tion tests are more significant than are most imaging modalities, although the recent use of diagnostic ultrasonography has in creased the accuracy and sensi tivity of the diagnosis of the dysplas tic hip. Ultrasonography is especially useful with abnormalities in the develop ment of the soft tissues of the acetabular region, which are not visualized on x-ray films (8) . During treatment, various i mages such as x-ray studies and computed tomogra phy (CT) scans can be used to assess the accuracy and adequacy of the treatment as the child grows or to confirm the physical diagnosis.
480
VI. Osteopathic Considerations in the Clinical Specialties
Normal hip
Deficient dysplastic acetabulum
FIGURE 33.3. Pavlik h a rness.
Subluxed
Reduction With abduction, head clunks i nto socket (Ortolani sign)
Dislocated hip FIGURE 33.2. Ortol a n i s i g n .
Treatment of developmentally dysplastic and dislocated hips involves the application of a fundamental osteopathic precept: that growth and maturation of the skeleton follows function. A properly positioned joint with good, easy motion and adequate blood supply and muscle balance grows and develops normally. The orthopedist's goal in the treatment of the dysplastic hip is to place that hip in a position whereby normal stimulation for growth of the acetabulum and proximal femur occurs. One can use external position devices such as casts or braces, internal fix ation devices, or structural changes operationally to change the alignment of the bones so that they are allowed to grow and mature in an improved position. In most cases, a dislocated or dislocatable hip can be either reduced shortly after birth or, if not reducible, held in a position
in which the proximal femur is heading or pointing toward and centered over the triradiate cartilage, the middle portion of the acetabulum. Many orthopedists today use the Pavlik harness to hold such a hip in a position of flexion and abduction while allowing the child to flex the hip and kick at will (Fig. 33.3). The position utilizes a safe zone whereby the femoral head is securely placed and at low risk of dislocation while the patient is harnessed. The pressures on the shaft are such that there is less risk for avascular necrosis of the femoral head than in those patients fixed in a rigid cast, which was the older method of treatment. The position in which the hips are placed is termed the human position, in contradistinction to older forms of immobilization in which the neonate's hip might be held in a position more akin to an amphibian or a frog. The principle is of essential importance: placing the hip within the socket in a stable position allows the body to continue to nourish the hip socket and allows its normal growth over a period of time. Pavlik himself stated, "with the help of stirrups, we want to achieve suitable flexion of the hips, and non-violent unforced abduction of the hips with simultaneous facilitation of movement in the hip joints. Centralization of the femoral heads in the acetabulum results spontaneously." While this has proven successful in most cases, there is still controversy regarding when to apply and how to define if the treatment is successful. One may use ultrasonography or magnetic resonance imaging (MRl) as well as CT scans to help determine adequacy of reduction and position. The risk of complications such as femoral palsy from tight straps over the femoral nerve above the knee or of avascular necrosis from constriction of the epiphyseal blood supply are rare (9-11). The second form of treatment of the growing child involves the realignment of the proximal femur and acetabulum to cen ter the growing femoral head within the acetabulum. A typical case of a late, unrecognized dislocation presents in a child of early walking age, at approximately J year. Such a toddler presents with a shortened leg or a waddling gait. As the child has grown with the hip in a dislocated position, the femur has progressed inro a more valgus position at the femoral neck shaft angle (Fig. 33.4). The acetabulum is deformed and shallow, and the cartilaginous
33. Orthopedics
ffl'»---
-ff----
Shallow acetabulum Valgus neck angles
481
Bone graft
Opening shelf
Closing wedge osteotomy Restoring normal neck shaft angle FIGURE 33.4. Long-sta n d i n g h i p dislocation.
lip, or labrum, is defective. The axis of the femur has anteverted, or rotated anteriorly, and developed into a straighter than normal, or valgus, axis. The femur is now roo long relative ro the mus cle and capsular tissues surrounding the hip, thus forced manual reduction of the head into the acetabulum places too much ten sion on the growing bones and results in avascular necrosis of the femoral head. A serious insult to the blood supply of the articular surface of a joint results in collapse of the underlying subchondral bone with fractures that cannot heal because of the lack of nutrition. In lay terms, this is a dead head, lifeless and unable to carry on its normal biologic function. Moreover, the acetabulum, which has not been stimulated by the femoral head acting within its cartilaginous tissues, has grown dysplastic with a deficient outer anterior and lateral rim. The cells for growth of the acetabulum have migrated proximal to the area of the true socket. The operative treatment for this condition is shown in Fig. 33.5. This operation requires that the superior and inferior sides of the hip joint, the femur and the acetabulum, be addressed simul taneously. In the femur, a shortening, varus osteotomy allows the femoral head to be reduced without undue pressure and changes the neck-shaft angle to a more normal degree from its valgus po sition. In the acetabulum, a more horizontal socket is formed by either placing a bone graft at the rim or performing an osteotomy above the rim and bending the growing cartilage. If the femoral head is kept reduced into the acetabulum and held there while the tissues heal, it stimulates joint growth and encourages continued normal development over time. Bones and joints are plastic and develop as a result of the forces that are applied to them. One of the joys of treating young people is to watch the growing child mature over time. The physician
FIGURE 33.5. Open correction of late deform ity.
can guide this development in many ways. The old saying, "As the· twig is bent, so grows the tree," implies a molding of the whole person. This image continues to influence the orthopedic community: by molding the growing skeleton, orthopedists help children grow into straighter, more functional adults. The term dysplastic hip is used for the abnormality in appear ance and congruity of the child's hip. The proper terminology is developmental dysplasia of the hip, which implies that dyspla sia may occur not only at birth but also after birth. Congenital dysplasia implies that all dysplastic hips are present at birth. If that were the case, then all should be recognizable at birth. Some hips, however, are normal at birth but become dysplastic in the extrauterine environment. It is important that the physician rou tinely examine the well baby's hips at regular office visits. The physician should check the child's hips for symmetry, leg length, and equality of abduction at the first postpartum office visit, at 6 weeks of age, and at 6 months of age. The final examination is at 2 years of age, when standing ability and balance are included (7). The physician who treats the child with a dysplastic hip is treating not only a mechanical problem in a child but also a child in a family, a small member of a complicated social structure. For the young child, nutritional, educational, and emotional support are paramount. The physician needs to encourage the parents to provide the child with sufficient protein, minerals, and vi tamins for growth. The physician also needs to encourage the parents to continue to supply intellectual stimuli or the school system to provide homebound instruction, since these children will have difficulty attending classes. Ensure that parents, siblings, and other nurturing family members provide emotional support to the child in a cast or in bed. A family with a child with hip dysplasia worries that the child will not walk and be active in life.
482
VI. Osteopathic Considerations in the Clinical Specialties
They need encouragemenr that the child will probably be able ro enjoy a lifestyle not unlike that of his or her friends. HIP FRA CTURE IN THE GERIATRIC P OPULATION
One of the drawbacks of aging is the progressive loss of bone min eral universally noted in men and women after they enrer their mid-70s. Weight-bearing bones develop osteopenia and have a resultanr structural weakness, panicularly in the hip, which must withstand heavy forces. When the structural inadequacy of the hip bone is joined with diminished visual acuity, balance, and coordination, falls and fractures are common. [n treating an ag ing population, the physician will encounter geriatric fracture problems. The patienr with a hip fracture presents with not only a me chanical problem to solve but also a personal and social problem. The personal upheaval in lifestyle and abilities as well as the se vere economic hardships to the injured person and their family profoundly influences all caregivers, illustrating a major problem for public health providers. The number of aging persons with hip fractures is huge, and the costs of treatment for the fracture and its associated morbidity are staggering. It is estimated that 280,000 Americans suffered hip fractures in 1994. The cost in 1994 was nearly $10 billion. If a disease becomes a public health problem when it affects a significant portion of the population, it is incumbent on the public and on physicians to attempt to prevenr or control the disease rather than simply treat the disease as I I' occurs. In the aging population, fractures of the hip are of multi ple types and are somewhat dependent on the forces that act through the hip. These fractures are described according to their location. There are subtrochanteric and intertrochanteric frac tures and subcapital fractures. Each particular type of fracture has its own treatment approach. Those fractures that are within the cancellous bone of the inrertrochanteric region, if not com minuted or broken inro many fragments, generally heal rapidly with stable internal fixation. Fractures in the subcapital region have multiple treatment protocols, and the approach is more dif ficult. The younger the patient, the more the physician should attempt to bring the bones to a physiologic healing. The blood supply to the femoral head is precarious. Simply aligning the bones and holding them together does not necessar ily ensure healing. JUSt as in the growth of the immature skeleton, healing of fractures requires adequate oxygenation, nutrition, and blood supply. For any patient with a subcapital fracture, the risk of avascular necrosis is high; nevertheless, with adequate protec tion and limited weightbearing, union can occur. The surgeon may try to reestablish circulation to the femoral head through a revascularization procedure in which a pedicle of bone attached to a blood supply is rotated into the proximal femur. One method one of the authors (RAS) has used with success is the transfer of a pedicle of bone from the trochanteric region attached to the quadratus muscle along with its large artery. This pedicle is im planted into the femoral head and neck. For younger patients, the surgeon tries to avoid prosthetic hip joint replacemenr, which is the alternative to internal fixation of the fracture. The younger the patient, the more likely it is that a prosthesis will fail before
the patienr has completed their active weightbearing life. To reca pitulate, fractures in the subcapital region should be treated with inrernal fixation in the hope that healing will occur. However, if the fracture is severely displaced or if there appears to be a high risk of diminished blood supply to the femoral head, a prosthetic replacement is indicated. As a person ages and the bone becomes more porotic, sub capital fractures become more impacted or displaced, and the treatmenr protocol separates those that are stable or minimally displaced from those that are displaced. For the first group, in ternal fixation with cannulated screws is recommended; in the laner group, prostheses are recommended. As a person ages more and the ability to ambulate or even get out of bed disappears, the protocol again becomes more complex because the physician needs to weigh the costs of hospital and surgical treatment and the high mortality rates against the possible alleviation of the acute fracture pain. A period of immobilization with traction may be sufficient for a fibrous healing in very old or cognitively impaired patients because it allows turning and protection from bed sores. For others, a replacement with an endoprosthesis may allow an earlier discharge from the acute care hospital to the extended care facility with a lessened incidence of contractures, decubitus ul cers, heart failure, and pneumonia. In the treatmenr of the older adult patienr with hip fracture, the osteopathic physician needs to address the respiratory, cardiac, and alimentary systems, as well as take steps to decrease the incidence of thrombophlebitis. The physician must realize that after a trauma, such as a fracture and fracture surgery, derangements occur in all of the body systems. The physician must be vigilant and treat these derangements as they occur rather than simply pay attenrion to the hip alone. Mo bilization of the thoracic spine often increases cardiorespiratory function and stimulates activity. Osteopathic physicians need to use their skills and knowledge to help society as a whole in its efforts to increase the quality and quantity of life. Hip fractures occur pardy because of bio chemical changes associated with aging. The physician should understand how they can help older adults mainrain their bony Stl ucture and integrity. The basic substrates needed for bone pro duction include protein and calcium. Physicians understand that the absorption of calcium through the gastrointestinal tract pardy depends on the inreraction of vitamin 0 and its various active hydroxylated forms with circulating hormones such as calcitonin and estrogen. In nonsmokers, 5 years of estrogen use may reduce annual hip fracture rate by more than 50%. Bone mineral production also is influenced by the basic prin ciple that if an organ or structure is not used, it wastes away. If bone is not used or stressed, calcium is not deposited. A limb at rest or not stressed by gravity, as in a space station astronaut or in a person on bed rest, quickly becomes osteopenic. A physician can help patients maintain bone production by ensuring dietary and supplemental conrrol of essential vitamins, minerals, and hor mones. Patients should be encouraged to exercise, particularly in a weightbearing or an anrigravity mode. Regular loading of the ap pendicular and axial skeleton is the best way to enhance sustained mineral production. To decrease the incidence of hip fractures in older adults, the orthopedic osteopathic physician should begin by encouraging middle-aged female patients to monitor their es trogen levels, replacing the estrogen particularly in those who
33. Orthopedics
are prematurely estrogen-depleted or who have proven acceler ated bone loss. All bone will not be maintained strong enough not to fracture, despi"te these measures. The home and workplace must be made safer. Obstacles that may cause one to trip and fall should be removed. Finally, the balance and agility of the older adult should be evaluated regularly and appropriate steps taken to control seizures or to prevent vision loss. The incidence of hip fractures is increasing as the population is aging. This is a population that is nutritionally and hormonally depleted. Moreover, it is a population that has forgotten to walk. Regulation of these factors as well as decreasing the extrinsic risk factors in the environment helps decrease the numbers of hip fractures. One of the ways in which the physician can decrease the risk of fractures is to decrease the amount of sedatives and drugs that can impair balance. A novel method for increasing stamina and balance has been proposed by Wolf. Based on a study performed by the National Institute of Aging, Wolf recommends that older adults practice the ancient Chinese exercise, tai chi (12). The osteopathic physician has a major role in helping the indi vidual patient as well as the population at risk for these fractures. In the treatment of a patient with a hip fracture, the goal is to con trol pain and return the patient to a nonhospital environment. How the physician treats or recommends treatment depends on the anatomic type of fracture as well as on the physiologic status of the patient. Figure 33.6 represents the types of fracture and the treatment options. Fractures of the proximal femur are generally classified as intracapsular (occurring within the joint) or extracapsular (which are usually intertrochanteric), in which the fracture line goes be> 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
VI. Osteopathic Considerations in the Clinical Specialties
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 <3 months of activity i ntolerance due to low back pain and/or back-related leg symptoms.
Search for " A E D FLAGS" (see text ) . Examination i ncludes neurologic screening and straight leg raising (SlA).
\
Yes
/
""\ AED FLAGS for spine fracture
1
/
No
Any AED FLAGS?
I'
AED FLAGS for cancer/infection
�
""\
AED FLAGS for cauda equina syndrome or rapidly progressing neurologic deficit .
'Plain x-ray of lumbosacral spine. If, after 1 0 days , fracture still suspected, or multiple sites of pain , consider bone scan and consultation before defining anatomy with CT.
-'- ...1..1
"" �1r � ' ,",' ·W; lI ·
�
...." CSC, ESA, U/A.
Immediate consultation for emergency studies and definitive care.
If still suspicious, consider consultation or seek. further evidence with bone scan, x-ray, or other lab. Negative x-ray alone does not rule out disease. If positive, define anatomy with M Al .
+
...."
)
,... Evidence of serious disease?
Yes
�
Arrange appropriate treatment or consultation
No
I.. r
In the absence of A ED FLAG , diagnostic testing is not clinically helpful in first 4 weeks of symptoms.
E,;de'" of nonspinal medical problem causing referred back complaints?
No
Yes
+ Exit Algorithm
Go to Algorithm 2
FIGURE 33.S. I n itial assessment of acute low back p a i n symptoms. CT, computed tomography; CBe. complete blood count; ESR, erythrocyte sed i mentation rate; utA, u r i n e analysis. (From Bigos S, Bowyer 0, Braen G, et al. Acute Low Back Problems in Adults. C l i n ical Practice G u i d e l i ne, No 14. Rockv i l l e, M D : U S Department o f Hea lth and H u m a n Services; December 1994. P u b l i c Hea lth Service, Agency for Hea lth Care Policy and Research A H C P R publ ication 95-0642, with permission.)
487
488
VI. Osteopathic Considerations in the CLinicaL SpeciaLties
the examiner include: When did the pain begin? When is it worse? What aggravates the pain? What relieves the pain? Have other family members had similar problems? Was the onset associated with a traumatic episode? Is litigation pending? Although many of the tests are essential to confirm a diag nosis, the physical examination is crucial. Physical examination includes: Observation Palpation and manual motion testing Neuromuscular examination Vascular assessment Although additional tests may later be employed, these four aspects of examination are essential. Many can be performed quickly and concurrently while distracting the patient. All require that the patient be gowned so that their back and legs can be observed and palpated. Examination of a fully clothed patient is inadequate. Observation requires a keen eye. Watch the patient while they move from chair to examining table and note their ability to get off and on the examining table with or without assistance. Note the gait to ascertain if limp, foot drag or drop, or lurch exists. Note the use of an assistive device, cane, or walker, as well as any alteration of muscle mass, tone, or atrophy, and the presence of any scars. Palpation of the back and limbs can be performed in multi ple positions. Note the tone of the muscles and the turgor of the skin in the extremities. Examine the spine in standing and supine positions, noting areas of discomfort, pain provocation, asymme tries, or muscle spasm. As the spine is placed through ranges of motion, note individual segments with abnormal findings and make measurements of the ranges of rotation, side bending, and flexion. Perform percussion of the spinous process and palpation of contiguous areas such as ischial tuberosity, greater trochanter, and groin. The neuromuscular examination tests motor power, particu larly the strength of the ankle and toe flexors and extensors, hip flexors, gluteal muscles, and rectal tone. The ability to stand on toes or heels unassisted is a sensitive evaluator of leg strength and the presence of intact S 1 or L5 nerve roots. Test for ab sent, present, or hyperesthetic sensation in legs, thighs, back, and perineum. Check deep tendon reflexes as well as the presence of clonus or a Babinski reflex. Assess the presence or absence of pressure on the nerve roots in the lumbar spine through the use of the straight leg-raising maneuver, which can be performed with the patient sitting and supine. This maneuver is performed as the patient flaxes the h ip while keeping the knee extended. Record symptom provocation in the form of back or ipsilateral or contralateral thigh and leg pain. Vascular assessment includes palpation of peripheral pulses and auscultation of abdominal, iliac, and femoral vessels. Multiple tests and signs can elicit symproms and help in the diagnosis. Examination of contiguous joints, such as the hip,
may elicit a cause of referred pain. Frequently, the examiner finds patients with exaggerated complaints. Sometimes the patient may appear hysterical, to magnify the symptoms or to be a malingerer. Careful recording of these findings will help the examiner arrive at a meaningful conclusion. Waddell and colleagues have listed tests and suggested evaluation for those with atypical findings (16). Pathophysiol ogy
The study of low back pain begins with an anatomic and patho logic consideration of the basis for pain. The basic structural el ement of the spine is the functional spinal unit (FSU). The FSU is the motion segment and is the smallest segment of the spine that exhibits biomechanical characteristics similar to those of the entire spine. It consists of two adjacent vertebrae and the con necting ligamentous tissues ( 1 7). How an FSU behaves depends on the structure of each of the elements and its characteristics, strength, flexibility, and responses to stress. Each FSU is part of the entire axial skeleton from the inion to the coccyx, and each has a mechanical role to support the mass of the body as it moves in space and time. The anatomic basis for disease encourages our understand ing of the FSU. Disease can emanate from the bony structure, the synovial joints, and the ligaments constraining the adjacent verrebra. Moreover, disease can be caused by problems of the interverrebral disc. F igure 33.9 shows the anatomic basis of the FSU. The FSU contains the elements to contiguous spinal ver tebrae, their connecting discs, and the associated ligaments and muscles. The posterior elements consist of the spinous processes, ligaments, muscles, and facet joints. The middle segment con tains the bony spinal canal and its contents, the neural elements, fat, and vasculature. The anterior elements include the vertebral bodies and the disc. In thinking about the spine as a source of pain, remember this anatomic image. Figure 33.10 describes the type of motions the FSU undergoes in response to applied forces. This is a three-dimensional image. Over the last century, most physicians have relied on two-dimensional imaging such as ra diograph and other modalities. Newer technology, such as real time three-dimensional computerized technology scans, allows us to better define the normal ranges for each of rhe motions. At present, definitions of measured abnormalities or segmental instability are unclear. The American Academy of Orthopedic Surgeons offers this definition: "Segmental instability is an ab normal response to applied loads, characterized by movement in motion segments beyond normal constraints" (18). Concrete numbers based on an x-ray study or on goniometric measurement to define a pathologic instability and prove that it is associated with a painful problem are lacking, except in cases of gross luxa tion or angular change as seen in fractures. Palpatory diagnosis, in which the end point of vertebral motion is ill defined and either restricted from normalcy or lacking uniformity, offers meaningful data to the examining physician. The stability of the osseous spine depends on three zones, consisting of the anterior, middle, and posterior elements. This model, devised after a retrospective analysis of spinal fractures in the thoracic and thoracolumbar spine, has been widely adapted for use by spinal surgeons to arrange the thought processes in a more logical manner (1 9). This diSCUSSion centers on the
33. Orthopedics
489
Facet
Facet joint I ntervertebral disk Vertebral body
Middle: ------'r---+ spinal canal neural elements
B
Anterior elements: vertebral body disk
FIGURE 33.9. Functional spinal u n it (FSU) seen from oblique projection (A) and end-on project ion (B).
problems of the bony and soft (issue srrucrures. The three columns as described by Denis include the posterior column formed by the posterior bony complex alternating with the pos terior ligamentous complex (supraspinous ligamem, imerspinous ligamem, capsule, and ligamemum flavum). The posterior longi-
F Force
)
M Moment T TranSlation
y
� ,- '\
R
. Rotatlon
Load
)
Display
FIGURE 3 3 . 1 0 . Three-dimensional coordinate system fixed in space. Twe lve-load components (forces or torques) are depicted. Appl ication of any one of load's components produces displacement of upper ver tebra with respect to lower vertebra, consisting of translation and ro tation, further divisible with respect to coordinate axes.
rudinal ligament, the posterior annulus fibrosus, and the posterior wall of the vertebral body form the middle column. The longi tudinal ligamem, the amerior annulus fibrosus, and the anterior part of the vertebral body form the amerior column ( 1 9). Denis designed his classification in an attempt to better un derstand the biomechanical changes found in the common and often devastating thoracic and thoracolumbar fracrures. In his retrospective srudy, he described fractures at risk for neurologic compromise based on injury of the middle column. Although fracrures of the low back or lumbar and lumbosacral spine are uncommon, the risk of damage to neural eiemems from middle column disruption in the lumbar spine is less because the cord usually stops above this area. The bony spinal canal is larger, and the cauda equina can be remarkably resistant to compressive dam age from fracture fragmems. For the anatomic basis of low back pain, the arbitrary separation of the spine into three segmems is helpful. It allows the physician to focus on the anatomic element that is the pain generator. Gunnar Andersson has divided the spine into amerior and posterior segmems for ease in isolating causes of disease (20). This author has labeled the central spinal canal as the middle column to isolate those emities that can cause back pain and may be presem in the spinal canal alone (Fig. 33.98). Emities that may cause acute back pain in the amerior spine include fracrures and invasive diseases of the vertebral body and disc, which include rumor, infection, and traumatic disc disrup tion. The Schmorl node or herniation of the disc through the vertebral end plate often characterizes traumatic disc disruption. The disc has often been implicated as the major source of spinal pain. Certainly, as the disc ages, undue stresses may be placed on the facet joims and arthritic spurs may compress into the spinal canal. However, in the normal spine, the disc under load bulges as a viscoelastic shock absorber (Fig. 33. 1 1) . The normal disc behaves in a viscoelastic manner under pressure. During bending (flexion, extension, lateral bending), one side of the annulus is subjected to compression while the other side is put under tensile load. Although it is normal for the disc to bulge in a degener ated state or with a deficient annulus, the disc can herniate or
490
VI. Osteopathic Considerations in the Clinical Specialties
Endplate
Endplate Disk under compressive force-normal. Disk pushes, "bulges" annulus outward and compresses end plates.
Eccentric load
.1. T
Te nsion
With bending, eccentric loads cause te nsile forces or unloading on one side and higher compressive loads on the flexion side. FIGURE 33. 1 1 . Disc stresses. F, force.
protrude through the ligament and irritate, compress, or damage the neural srrucrures. Diseases of the middle column include those that compress the contents of the spinal canal; these can be either inrrinsic or extrinsic to the canal. Examples of the latter are fragments of bone or disc that are herniated into or compress the thecal sac and neurofibromas or metastatic rumor masses that have entered the canal through the neural foramina and caused compression of the canal. Intradural tumors, meningeal infections, or the se questered disc when free within the spinal canal can cause intrinsic compression of the spinal cord, as can extradural benign tumors or fibromas. Any narrowing of the spinal canal causes stenosis, a constricting and narrowing of the space available for the spinal nerves and the cauda equina (21). Most often, spinal stenosis is a problem caused by bony changes, which are usually developmen tal and associated with aging and degenerative changes. These changes of stenosis rarely occur because of genetic problems, as in the case of the achondroplastic dwarf whose ossification has prevented the development of a large enough spinal canal. The cauda equina syndrome is a syndrome of low back pain, char acterized by involvement of the sacral nerves causing numbness around the perineum and loss of bladder and bowel function (20). Changes in the posterior column are common and often re lated to age or activity. The posterior elements contain the major motion segments of the spinal column including the apophyseal joints and the spinous processes. Fracrures of the posterior ele ments may be associated with severe trauma; most often, severe sprains of the posterior elements are associated with rotatory and
translational forces. Fracrures, sprain, and somatic dysfunction are part of a spectrum of derangements of the FSU. Mechanical means such as manipulation or rraction provide proper realign ment of the FSU in these conditions. The patient with acute low back pain often has a combination of preexisting problems associated with aging (22). Such changes involve desiccation of the disc with loss of disc height and elas ticity, the development of spurs at areas of excessive rraction, and inAammation of the apophyseal joint with the production of synovial hypertrophy. For many patients, combinations of factors work together to summate the pain load at each of the areas that generate low back pain. Often, bearable, yet constant, low back pain caused by the inevitable aging process may be increased by a mechanically minor twisting in the posterior elements. When the threshold is reached, the resulting pain drives the patient to see the physician. More often than not, attention to the poste rior elements with the use of manipulative techniques spares the expense of multiple diagnostic procedures and surgeries. Spondylolysis is the most common structural problem found in the pediatric population; it often is not diagnosed until radio logic examination is performed on the adult patient. Spondyloly sis is a defect in the pars intraarticularis, the bony bridge between the two facet joints; it is most often developmental or caused by a structural weakness. It may also be caused by an acute fracture, as in the case of the gymnast who repetitively stresses the area in hyperextension activities or in the contact athlete who acutely loads the spine in lordosis. Although the radiologic findings in the oblique, lumbar spinal x-ray view might suggest a more serious problem, most patients with acute low back pain and spondylol ysis do get better. W ith progressive motion, a vertebra can move or slip on the inferior vertebra; this is called spondylolisthesis. In the vertebra ·above the lumbosacral segment and most often in the aging spine, this is called pseudospondylolisthesis because it is nor associated with a traumatic, developmental, or congenital weakness of the pars intraarticularis. D i fferenti a l Diagnosis
The thought processes involved in diagnosis require separating into definable groups the different known entities with which acute and chronic back pain are associated. One of the ways to separate the different types of back pain is to ask a few elementary questions: 1. Is the pain intrinsic or extrinsic to the spine? 2. Does the pain emanate from some deranged structure in the spine or i? it directed to the spine from a distant or contiguous area? 3. Is the nature of the pain related to an injury, an inAammatory condition, an infection, a congenital anomaly, or compression of a neurologic structure? The extrinsic causes of back pain are associated with viscero genic and vasculogenic causes. Any visceral disease can manifest as back pain. The pain associated with pancreatitis is classic for irresolvable, unrelenting paroxysms of back discomfort. Prostati tis, renal colic from infection or an obstructed ureter, colitis, or perforated viscus and metastasis of cancer from the colon, ovary, or other contiguous organs may all present as back pai n. Most
33. Orthopedics
ofren a quick bur deliberare palparory examinarion of rhe ab domen and recrum differenriare these enrities. Vasculogenic causes of back pain are associated with claudica rion. Usually claudicarion presenrs with leg pain after or during exertion. Ir is uncommon bur not rare for the ischemic spine ro present with pain. The vasculogenic cause of low back pain that is rhe mosr urgent is rhat of the abdominal aortic aneurysm. Re membering rhar rhis is nor an uncommon enrity in the elderly popularion prone to arherosclerosis leads rhe physician to palpate and auscultare the abdomen. Of rhe myriad orher causes of back pain, those that are sys remic in origin rend ro acr directly on the spine rather than from a distant focus. There are sysremic diseases of inflamma tion, infection, and metasrasis that cause back pain. Of the in flammatory diseases, the arthrirides are mosr important; rhar which presenrs most insidiously is ankylosing spondyliris, one of rhe spondyloarthropathies. The diagnosis is difficult in the pa rient who has not developed the classic, lare radiologic changes bur who presenrs with severe episodic non traumatic low back pain and sriffness in bending. For this parienr, the appropriate blood studies may help confirm rhe diagnosis. The other seroneg arive spondyloarthroparhies and the inflammatory bowel diseases present with back pain for which the trearmenr is nonsurgical. Infecrions of rhe spine have been rare, bur rhey may become more prevalent in the near furure as viral diseases increase in a popularion wirh primary and secondary immunosuppression. In rhe proper hosr, any organism, if unchecked, is able to invade the paravertebral rissues, disc, or vertebral body. The paravertebral plexus of veins of Barson, for example, drains rhe organs of the pelvis and has been implicated as the conduit down which clusters of rumor cells or aggregares of bacrerial organisms pass. These cells may then grow as a metastatic site in a vertebral body or in the epidural space. An awareness of the problem leads to appropriare differenrial diagnosis followed by controlled biopsy, aspiration, and culrure. Mulriple myeloma is an example of a rumor that spreads to bone, particularly the marrow-rich vertebral body. Myeloma and all the myeloproliferative diseases are systemic diseases that tend to grow in the vertebral body, rendering it strucrurally weak and ready to fracture even wirh minimally applied force. The more common rumors to spread to bone are: Breast Prostare Kidney Thyroid Lung If faced with a middle-aged parienr wirh low back pain and radiographic suggesrions of a metastatic bone tumor, first ascer rain whether the more common rumors have become merasraric. There are multiple rumors, benign and malignant, primary and metastatic, that can cause back pain. Figure 33. 1 2 is an algorithm for diagnosis of spine tumors as proposed by James Weinstein, DO, a tertiary spine specialist (23). The physician and orthopedist evaluating the patienr with low back pain must include rumor as a possible cause of the pain, realizing that it is an uncommon cause. All of the following
491
should alert the physician that rhere may be a remote source of the low back pain: Malaise Fevers Weight loss Increased incidence of infections Change in stool character Blood in urine, spurum, or feces A history of night or resr pain greater than pain with acrivity also is suggestive of rumor spread to bone. Of the various tests performed in physical examination, the most importanr is that of percussion. In rumor and infection of the spine, percussion of the spinous process of the affecred vertebra causes severe pain out of proportion to that which might be expected. The physician who meets a patient whose low back pain is a sign of metastatic disease may not find [he diagnosis unexpected, although such a diagnosis usually startles the patient and the fam ily. The parienr with a somatoform disorder or psychogenic pain is not rare. Sometimes there are clues indicating a hysterical or hypochondriac pain pattern, such as frequent trips to the hospi tal or multiple operarions, which may suggest some nonorganic cause of back pain. Hysterical paralysis, reputed to be common in Freud's time, is rarely encountered today. Nevertheless, we all see patients for "execurive back pain" or back pain caused or am plified by the messes of life. The terminology used by people to describe their symptoms is often suggestive of nonorganic pain. " My fellow worker gives me a headache," " My job is a pain in rhe buttocks," or "] feel like I'm carrying the weight of the world on my shoulders" are all examples of the kind of metaphors used by patients in describing their somaric complaints. These may sug gest there are additional factors in back pain not associated with structural lesions. It is helpful to include in the patient history form a pain drawing in which the patienr pencils in the anatomic site of their pain (Fig. 33. 1 3). For those who are hysterical, char acteristic patterns of nonanatomic pain radiation are presenr (24). Just as it is important for the examining orthopedist to remem ber that metastatic disease is an omnipresent possibility and rhat a careful history and physical examination directs them to rhar possibility, it is equally important to remember that the sick pa rienr can have disease. Patienrs with psychoses and neuroses also have infections, rumors, fractures, and discogenic disease (25). M a nagement
Most often, the orthopedist is encouraged to believe that the refer ring generalist has evaluared rhe possibility of nonlocalized origin of back pain. Although the orthopedist runs through a checklist of nonlocalized possibilities during the interview and examina tion of the patient, the thoughts cenrer on the kinds of problems that are mechanical or strucrural and might require some form of operative intervention. Most acute low back pain improves over a period of rest or over time. Many patients can be assisted by manipulative treatment. Certainly many of the acute episodes of low back myositis and fibromyalgia are amenable to fascial massage and mobilization, counseling, and antidepressants. Over the last 1 5 years, there have been major efforts to under stand the nature of back pain. What are the sites or pain generators
492
VI. Osteopathic Considerations in the Cfinical Specialties
Yes
Neurologic Deficit
_11---
N o -------,
Spine CT-Enhanced Myelogram/M R I Chest X-ray
Spine Staging Spine CT-Enhanced Chest X-ray Metastatic Evaluation
Biopsy Most Accessible Lesion
Treatment of Systemic Disease and Symptomatic Spine Problems
Decompression, excision, and stabilization as indicated ± Radiation ± Chemotherapy
Systemic Staging Chest CT Spinal M R I
Observe
Excision and stabilization as indicated
Excision and stabilization as indicated ± Radiation ± Chemotherapy
FIGURE 3 3 . 1 2 . Algorith m of approach to spine tumors. (From Weinstei n J. D i fferential d i a g nosis ·and surgical treatment of primary benign a n d m a l i g nant neoplasms. In: Frymoyer JW, ed. The Adult Spine. New York, NY: Raven Press; 1991;41 :851, with permission.)
that transmit nociceprive impulses (26). Operating orthopedists are attempting to develop surgical designs to srabilize the unstable spine, as well as to define what stability is (27). They have also been refining approaches and tools to decompress the stenotic spine or entrapped nerve root. New technologies and materials are expanding the physician's abiliry to manage back pain and spinal conditions both surgically and nonsurgically. For parients with chronic low back pain with our spinal nerve impingement, the pain generator is rhoughr to be pain receptors innervating rhe disrupted annular fibers of the intervertebral disc. This "discogenic" back pain, confirmed by a provocative diagnostic injection into the disc i rself, has eluded a surgical therapy short of removing the functioning bur painful disc or fusing the functional spinal unit to obliterate irrirant mo tion. Nevertheless, there are ongoing biologic and biomechanical studies to design and build appropriate implants, which might en able the maintenance of stability and normal spinal uni r motion. Long-term studies on human implants, in which the implants reproduce srability and the normal viscoelastic behavior of the
human intervertebral disc, are lacking. A recent therapy has de veloped where a catheter, similar to thar used in discography, is placed into the disc percutaneously allowing heat to be delivered to the disc by a radiofrequency probe. The mechanism of how heating the disc reduces pain is elusive, though neurolysis of the free nerve endings has been suggested. The IOET procedure (In tra Oiscal Electrothermal Therapy) is now being performed by thousands of orthopedists, neurosurgeons, and pain management physicians. The long-term effects of the procedure, especially how IOET affects the stiffness of the disc and its implications for disc functional integrity are unknown at this time (28-30). Disc herniations resulting in sciatica that do not respond to conservative measures often drive a patient who is suffering to seek a surgical alternative. Removal of the offending disc material that is compressing nerves concordant with the patient's symptoms is generally accepted to bring short-term pain relief to 90% of properly selected patients (31). A variety of surgical techniques for open discectomy, microdiscectomy, percutaneous, and endo scopic techniques exist. W ith current technology, success rates
33. Orthopedics
Mark the area on your body where you feel the described sensations. Use the appropriate symbol. Mark areas of radiation. Include all affected areas.
Numb ness Constant, throbbing Ache
Increased Sensitivity
0000
Sharp Twinge
////1/1
xxx
FIGURE 3 3 . 1 3 . Pa i n drawing used by patient to depict severity, type, and location of p a i n . (From B i gos SJ . Acute Low Back Problems in Adults. C l i n ical Practice G u i d e l i ne, No 14. Rockvi l l e, M D : U S Department of Health and H uman Services; December 1994. P u b l i c Health Service, Agency for Health Care Policy and Research A H CPR publ ication 95-0642, with permission.)
decline and recurrence increases with the invasiveness of the pro cedure. Currently open discectomy or microdiscectomy is consid ered the standard, with microdiscectomy edging out open discec tomy in randomized trials for shorter hospital stay and return to work. In the foreseeable furure, image-guided stereotactic percu taneous surgical procedures will be the accepted mode for remov ing small offending tissues from the offended nerve root (32,33). The vertebral bodies are among the most common sites of osteoporotic fractures and, hence, back pain in older adults, par ticularly in postmenopausal women of European descent. Rates of vertebral fracture approaching 25% in women over 80 have been reported (34). Increased back pain and the resulting func tional limitations are a significant cause of medical visits. Two therapies have emerged in the prevention and treatment of these causes of back pain.
493
The bisphophonates (like alendronate) increase bone mass by inhibiting the normal bone resorptive process. It has been proven that alendronate can reduce the risk of a new vertebral fracture by 50% in postmenopausal women with osteoporosis. At least one study has shown that a1endronate therapy is effective in reducing back pain and improving functional status in patients with already existing vertebral fractures (35). Surgical treatment of int ractable back pain from vertebral compression fractures has previously necessitated major open pro cedures. Anterior surgical approaches to the spine are necessary to attempt to restore height to the vertebral body thus restoring the normal contour to the spinal column. The morbidity associated with this type of invasive procedure, especially in the patient age group associated with osteoporotic fractures, has limited it as a feasible option for treating pain alone. Kyphoplasty has developed as a reasonable treatment for in tractable pain secondary to osteoporotic vertebral compression fractures. Considered to be a minimally invasive surgery, the oper ation is performed percutaneously under Auoroscopic guidance. Catheters placed through the back into the crushed vertebra al low the passage of balloons into the vertebral body. The balloons are inAated under pressure, restoring height to the fractured ver tebra. The vertebra is then injected with cement, stabil izing its height. Many centers allow patients ro return home the same day. Previous techniques (vertebroplasty) have not provided restora tion of vertebral height, only stabilization with cement. Initial studies indicate pain relief to be significant and long lasting in these types of vertebral fractures (36). A variety of degenerative spinal conditions causing pain and neural comprom ise (i .e., degenerative disc disease, spi nal arth ri tis, degenerative scoliosis, spinal stenosis, degenerative spondylolis thesis) are often refractive to other therapies and are amenable only to surgery to relieve pain and improve function. Most pro cedures involve fusion of the involved functional spinal units as the common final step. Similar to other procedures to cease mo tion actoss a joint, spine surgeons have tried a variety of methods to achieve a bony fusion and remove pain by obliterating motion. Basics of spinal fusion necessitate removing cartilage from the opposing facet joint surfaces, holding the segments in a relatively motionless position by external bracing or internal hardware, and waiting months for transplanted bone to complete the osseous bridge across the motion segments, achieving fusion. The dif ficulty of obtaining a solid fusion in the best of circumstances is best appreciated in light of confounding factors. These in clude patient compliance with an uncomfortable brace, preex isting medical conditions that hamper bone graft incorporation, corticosteroid use, and smoking (a proven detriment to the local environment necessary for fusion to occur). The intervertebral surfaces have become another potential site for fusion. Traditionally the posterolateral bony surfaces of the vertebra (transverse process, pars, lamina) have been exposed and bone graft applied over successive levels to create the fusion mass. By removing a portion or all of the already degenerated disc and applying bone graft into that potential space, a greater surface area for fusion is available, increasing the likelihood of achieving the arthrodesis. Recently developed prosthetic devices, known collectively as "cages," are applied into the disc space in place of the degenerated disc, maintaining or even restoring the disc
494
VI. Osteopathic Considerations in the Clinical Specialties
space height, while awaiting bony growth to bridge the space. The largest multicenter trial of one rype of cage device reported fusion rates in J 96 patents with 4-year follow-up to be 95% (37). These procedures most often involve supplemental internal hardware to stabilize the spine, which may have reduced the necessiry of bulky braces to reduce unwanted motion during healing. Srrides are being talml to establish objective data regarding the efficacy of manipulative medicine. The osteopathic profession is challenged to perform objective studies carried out in a blinded prospective scientific manner. Accurate and reproducible data are difficult to obtain. More information that exemplifies current re search in manipulative medicine, the majoriry of which supports a beneficial effect of manipulative treatment in the management of low back pain, is available from various sources (38-56). Spinal surgeons who deal with complex curves in major ado lescent and adult scoliosis must approach the skeleton as a whole as they plan their surgery to balance the weight of the body over the sacrum with an instrumented spinal fusion. The geometric designs require four-dimensional analyses using the x, y, and z axes as well as vector and torsional forces over time (57). The approach to an 1 I -year-old with a paralytic curve and hydrocephalus is dif ferent from that of a 40-year-old with a 60% thoracic scoliosis resulting from Scheuermann disease, a developmental disorder with progressive localized kyphosis. Most osteopathic physicians have been well trained in the palpatory diagnoses of the small curves, rotations, and compensatory changes found remote from the primary lesion of somatic dysfunction. Osteopathic physi cians should find the three-dimensional aspects of scoliosis easy to conceptualize. Summa ry
Despite the exciting approaches and materials now available, surgery is only useful to try to stabilize or decompress the spine. Most of the time, surgery is unnecessary. Just as treatment for disorders of the growing skeleton is directed toward helping the patient's body mature under guidance, in most cases of acute low back pain, restoration of nutrition, srrengrh, and normal inter segmental morion alleviates pain. The use of algorithms or Row charts, although not foolproof, offer the clinician and the parient the greatest opportuniry not to miss causes of back pain that are dangerous and life-threatening, such as fractures or tumors, or are unusual, such as aneurysm or spondylitis. Mosr ofren, based on the history and presentation, these life-threatening diseases that can be associated with back pain are ruled out. Nonopera tive treatment consists of encouragement that the body will heal, medications to accelerate the healing, and manipulation and ex ercise to restore segmental normalcy and strength. IN STA BILITY OF THE SHOULDER
Injuries to the ligamentous structures of the major joints are com mon. The average layperson and general practirioner understand that a sprained ligament is painful and causes swelling and edema. All respect the need for ice, compression, and elevation (ICE) and protection of the injured joint until healing has occurred. This section of the chapter discusses injuries of rhe shoulder joint as
a model for sprains, or ligamentous injuries, the biomechanical changes that occur with sprains, and recognition of laxity of lig aments with instabiliry or tightness of joint strucrures causing adhesions. The spectrum Rows from rhose joints unable to be maintained within normal physiologic ranges and those unable to have normal physiologic motion. The goal of this section is to introduce the student to the osteopathic approach to the joint, to understand the biomechanical aspects of joint stabiliry, and to review possible mechanisms of treatment. The osteopathic physician needs to be able to recognize the un stable and the dislocated shoulder. Many physicians see parients with shoulder problems soon after a rraumatic episode, such as an auto accident or spons-related injury. Other times, weeks may pass after an injurious event before rhe patient presents to the physician with pain and instabiliry. Physicians also need to be able to recognize the unusual dislocation that occurs after seizure or electric shock. Sprains are either acute or chronic. The acute injury is asso ciated with tearing of strucrures; rhe chronic with strerched or inadequate structures. Instabiliry is also characterized by degree: complete dislocation versus subluxation or subtle instabiliry, such as is found in the "dead shoulder" of baseball pitchers who have pain associated with the overhead pitching motion. Instabilities are also diagnosed by direction: anterior, posterior, inferior, and multidirectional. A most interesting case of fracture-dislocation was recently reported in which rhe humeral head was not seen on radiograph and was found in rhe retroperitoneum. This was a case of intrathoracic dislocation following massive rrauma. While this incomplete list of classification may seem daunting it should not, as the physician should cover these aspecrs in rhe history and physical examination of the patient (58). As in orher areas of the orthopedic structural examination, the physician should listen, look, and feel. One can often learn more about the structure from finding our how and when rhe inirial in jury occurred, how often it has happened, and what the shoulder or joint looks or looked like when it was injured than from so phisricated images. Imaging, such as MRI and ultrasonography, is helpful to confirm a clinical diagnosis. In our sociery a con:obora tive image may be necessary prior to invasive treatment. Imaging, however, often lacks in specificiry and sensitiviry. Somerimes rhe readily obtained radiographs are nor helpful. As a case example, a common presentation to the emergency room is of a middle-aged, cachecric alcoholic man with seizure history and multiple co-morbidities. He presents posticrally com plaining of pain over the front of his shoulder and holds his arm protectively. Radiographic examination is negative. The physical examination is diagnostic. If the shoulder is posteriorly dislo cated there is a palpable hollowness anteriorly, and as the elbow is brought posterior to the midaxillary line with gentle pressure on the humeral head, the examiner can feel rhe shoulder return to its normal position. Often the reverse exanlination in the shoul der thar has spontaneously reduced will allow the physician to feel the head slide our of the joint. The patient examined long after the original injury will often have symptoms when the arm is circumducted. Posterior dislocarions account for 5% of all acute disloca tions. Nearly half are missed at initial presentarion. We men tion them because the examination is diagnosric jusr as in rhe
33. Orthopedics
FIGURE 33. 1 4. Typical appearance of a d is l ocated shoul der.
other directions of instability. The inrerested reader can read more about these problems in a textbook that details shoulder problems (59) (Fig. 33.14). Many factors are associated with joint stability. Problems with the osseous structures are common static factors. These include abnormal version of either glenoid or humerus, crushed glenoid, in which the defect in the structure allows the humeral head to slide out of the joinr, and the Hill-Sachs lesion, wherein a defect or grooved fracture in the humeral articular surface induces recurrent instability. The ligaments are thickenings of the capsular structure, which provide stability in the multiple positions in which the shoulder can be moved. The ligaments are mostly type 1 collagen. The strength, aging characteristics and repair mechanisms of torn ligamenrs are important factors in the healing process. Thickening of the capsule on the periphery of the joinr re sults in the formation of the labrum, or lip. The labrum has an essential stabilizing force for the shoulder in increasing i ts depth, as the joint is inherently unstable. Arthroscopic visualizations, anatomic dissections, and MRI imaging have helped us under stand the anatomy and function of the ligamenrous structures. The small amount of Auid within the joinr acts as a Auid mem brane allowing sliding or slipping, but inhibiting separation. This force is analogous to that of two wet glass plates that will slide on each other easily but are difficult to separate (60). The study of what makes the shoulder stable continues but the answers are elusive. The inrerested reader is referred to the studies of Soslowsky and colleagues on contact areas of the glenohumeral joinr, and to the recent analysis of the role of the labrum in centralization of the humeral head by Halder and others (6 1 ,62) . The many muscles around the shoulder are essential to stabili ty and important in dysfunction. The biceps, the rotator cuff, and
495
the scapulothoracic musculature are secondary stabilizers. If rorn the shoulder may displace. [f healed and tightened too much they can cause adhesions. The osteopathic examiner should palpate and test the function of the various muscles of the shoulder gir dle. Treatment then can be directed toward stretching the fibrosed muscle and exercising the weak or lax muscle. Electromyographic studies may help to ascertain if there is a neuromuscular etiology to dysfunctional shoulder girdle. In a high-performance, throw ing athlete these can be augmented with video of the throwing motion that can help in planning treatment. The goal of treatment of the unstable shoulder is to bring the patient to a painless, stable state in which they can carry out normal life functions. Most people who have dislocated their shoulder have learned how to protect themselves from recurrent dislocations. Strengthening of weakened secondary stabilizers will often assist this. Older people have fewer recurrent dislocations than younger people. In the noncompetitive athlete it is often prudent to assist the body in healing itself. Practitioners should beware of the voluntary recurrent dislo caror who can show you how they can actively, Houdini-like, dislocate the shoulder. Treatment for these individuals may not be rewarding. Abnormal collagen structure or a neuromuscular abnormality may be the cause. If the acute dislocation is a result of a tearing of fibers, the goal of rreatmenr is ro hold the joint in a position of protection. Keeping the rorn fibers approximated allows them ro heal with the least amounr of scar or laxity. Apply the principle ro our cast of seizure with posterior dislocation by holding the arm in a thoracobrachial cast or brace in which the elbow is posterior ro the chest wall and the arm is externally rotated. lr is intuitive to maintain the shoulder in this unusual position. Practice mov ing the arm around and reduplicate the position of dislocation; a posterior dislocation occurs often when the arm is extended for ward and a large force directs the humeral head out the back of the joint. It is then obvious that reversing these positions would tend ro keep the shoulder in a "reduced" position. Recent in formation has demonstrated that the position that approximates the rorn fibers of the joint capsule in an "anrerior" dislocation (the most common type of dislocation seen) is not what we most commonly use. Normally a "reduced" anrerior dislocation is kept in an arm sling with the arm inrernally rotated. froi and co researchers found, with the use of MRI, that the rorn anterior capsule was most closely approximated with the ai'm held at 90 degrees of external rotation (63). This can be a difficult position ro hold the patient in. Protection while healing is the precaution ro take to allow the body ro heal its injured tissues in the best way. Athletes can be protected from reinjury with braces. Hockey players may benefit from scraps that inhibit the checking oppo nent from lifting their arm overhead, which may be the unstable posmon. A tear of the labrum may not heal. A tear of the labrul11 at the anterior portion of the glenoid is called a Bankarr lesion. If this is found in a recurrent dislocaror or in a young athlete with an acute dislocation then surgical repair may be necessary. Surgery of the shoulder to repair instability is either open, through incisions, or endoscopic. More roo Is for minimally invasive repairs are be coming available. The results of acute repair of Bankart lesions are promising. In recurrenr instability the goal of treatment is
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VI. Osteopathic Considerations in the CLinical Specialties
to strengthen weak structures and stretch tight structures. Non operative means are preferred. If surgery is necessary there are multiple means for reconstruction of joints. We can divide the means of surgical reconstruction into sim plistic categories. Surgery is either open or endoscopic. Bones can be osteotomized where the angle or version is incorrect or grafted where there is a defect. Tissues torn from their origin are sewn, nailed, or screwed back into position. Tucks or plication is used to tighten up lax structures. Energy sources such as heat, thermal, electrical, or light and chemical are used to scar or shrink loose collagen srructures. Orthopedic surgeons enjoy the challenges and excitement of these varied innovative procedures. These techniques, however, are beyond the scope of this text. Of more importance is recogni tion of what the practitioner can do to help the injured joint. In brief summary, the practitioner must, with careful attention to palpatory skills, define the position of stability, and begin a pro gram to strengthen the rotator cuff muscles that will help hold the joint in a reduced position. More commonly, we are faced with a tight joint. The disease known as adhesive capsulitis is poorly understood. Some link it to an inflammatory condition of the synovial lining of the joint. In diabetics it may be part of the diabetic cheiropathy where changes in the collagen structure occur because of metabolic changes in glucose merabolism. OSTEOPATHIC APPROACHES TO LIGAMENTOUS LAXITY
Soft tissue injuries and diseases are important aspects in the eval uation and treatment of patients with problems in the muscu loskeletal system. While the orthopedic examination focuses on the joints and skeleton, the examiner must be aware of the tis sues that envelop the skeleton. Myofibrositis and fibromyalgia are two terms regularly used by rheumatologists to describe in flammatory and painful conditions related to these periarticular structures. Tendons and ligaments can also be stretched or be come fibrotic, leading to dysfunction of rhe involved joints. These alterations are usually not as amenable to antiinflammatory med ication, manipulation, or exercise. However, they may well be the underlying cause of the myofascial pain that so often drives the patient to seek medical care. The understanding of the pathophysiology of myofascial and ligamentous disease (enthesopathies) is rapidly evolving. Since the fascial system is integral to the support and normal function ing of the body, it follows that dysfunction of that system through weakness and improper healing of ligamentous structures will in time cause other common manifestations of orthopedic disease such as osteoarthritis and degenerative disc disease. If the sup portive structures are nor providing the proper tension in the tensegrity system, then the compression components begin to fail. Thus such problems as the failed herniated disc may well be preceded by a lengthy period of stress due to weakened supportive ligamentous structures. These problems are extremely common in modern society in the form of repetitive motion injuries, work injuries, athletic injuries, and accidents. In 1991 it was noted that 50,000 new chronic whiplash patients are added to the U.S. patient population yearly (64). Many of these conditions can be recalcitrant to treatment, thus an understanding of their patho-
physiology is important in order to ptovide the patient with a comprehensive and effective management plan. While the cause of chronic myofascial pain may well be multifactorial in many cases, it is clear that the commonly ascribed mechanism of inflammation of tendons and ligaments is not generally the cause. Because of recent research we must now reorient our thinking regarding the etiology of chronic soft tissue injuries and pain, and thus adjust our treatment approaches accordingly. Several studies have now described the pathologic changes in the Achilles and patella tendinitis, and lateral and me dial epicondylitis (65-69}. The tissue pathology is consistent in showing a loss of collagen continuity with an increase in ground substance, fibroblasts, and myofibroblasts (70). However, in flammatory cells are simply not present. Thus we are dealing with tendonosis and not tendonitis. The term tendinosis is not new in that German researchers in the 1940s used it. The term was pop ularized by Puddu and colleagues (71 ) and Nirschl and Perrrone (67). However, the common usage by the public and the medical profession of " itis" to describe what is really an "osis" or improper healing of collagen fibers, has led to much treatment aimed at reducing inflammation with little evidence that it is helpful. [n particular, the use of corticosteroids, which are widely used to "reduce inflammation" in patients with chronic tendonopathies, should be more carefully considered. Animal studies have shown that intratendonous injections adversely affect the biomechanics of tendons (72-74). Steroids have significant negative effects on healing tissue such as inhibiting the formation of adhesions, granulation, and connective tissue, the reduction of tendon mass and the decrease in biomechanical integrity and load before failure of the tendon (74). Amom found prior steroid injections to be the predictive factor in rupture of Achilles tendons (75). In lateral epicondylosis, Hay and associates found that when comparing steroid injection with nonsteroidal antiinflammatory drugs (NSAIDs) and simple analgesics, there was an advantage of steroids at 3 months, bur at 1 year all three groups were equal (76). Another popular therapy is the use of NSAIDs. In .the acute situation, inflammation is an integral part of the normal healing cascade. eyclo-oxygenase, which is blocked by cyclo-oxygenase inhibitor properties of NSAIDs, is involved in an early step in the normal healing cascade that breaks down arachidoni� acid. Arachidonic acid is released from cell walls and serves as a chemo tactic agent for fibroblasts, which are in turn necessary for the replacement of damaged collagen in connective tissue (77). The ability of NSAIDs to inhibit the healing response has been ex perimentally well documented and observed clinically (78). Thus, the interruption of the normal healing cycle may well make people feel better, bur may leave tissue improperly healed and weakened, thus leading to long-term pain, disability, and further injury. While most of the research on the effect of cor ticosteroids and NSAIDs has been done with tendons, because of the similarity in microstructure, it is reasonable to assume the same pathophysiology occurs in ligaments. Since these structures are rich in pain and proprioceptive fibers at the tendon-periosteal and ligamentous-periosteal junctions, these are the areas to which special attention must be paid in the trearment of chronic ren donosis and chronic ligamentous injuries. One of the integral osteopathic concepts is that of the body as a harmoniously functional unit in which alterations in one
33. Orthopedics
part affect the economy and function of the entire unit. Another fundamental concept is that the body tends to be self-regulatory, self-healing, and capable of self-maintenance. This latter con cept is often referred to as homeostasis, or homeostatic potential. The connective tissues of the body not only physically unite all the structures so they can perform harmoniously, but also aid in the homeostatic activities of the organism. Connective tissue is the largest "organ" of the body and if we were to remove ev erything but the connective tissue, we would appear basically the same. The majority of connective tissue is arranged as fascia. This facial envelope surrounds. invests, and supports the soft tissues through muscular attachments, supporting membranes, inter muscular septa, visceral ligamentous attachments, and investing sheaths for blood vessels and nerves. Attachments to bone in turn allow the intricate and extensive connective tissue system to function through a system of tension and compression. Thus the integrity of the bony framework and the fascial connective tissue system· are not only interdependent, but are key to the body's normal functioning and complex homeostatic mechanisms. Al terations in bony architecture lead to variations in connective tissue tensions, which in turn can lead to many of the mani festations of disease through disruption of nerve, blood, lymph, and internal organ activity thus impairing critical self-regulatory functions. Conversely, alterations in fascial tensions may also alter bony architecture over time. These fundamental principles regarding the importance of the musculoskeletal system have been further enhanced by the introduction of the concept of tensegrity (79). This concept was popularized with the geodesic domes of Buckminster Fuller and the intricately balanced sculptures of Nelson (80). The basic unit or triangular-shaped "truss" consists of tension and compression units, which are always in balance. This allows forces to be applied in any direction and yet maintain the balance of tension with compression, which changes throughout the unit to maintain the integrity of the structure. A bicycle wheel is a familiar example of such a tensegrity structure where the hub and rim function as the solid compression elements and the Aexible spokes are the tension elements. When you ride a bicycle, the forces are spread equally around the wheel at all times and altering one tension element alters the forces throughout the unit. As described by Levin, "the compression elements in tensegrity structures 'Aoat' in a tension network just as the hub of a wire wheel is suspended in a tension network of spokes" (8 1 ,82). The tensegrity icosahedron is the extension of the simple trian gular truss. The outer shell of this structure is the Aexible tension element held apart by internal compression struts that "Aoat" in the tension network much as the hub of the bicycle wheel. The icosahedron in repetitive form turns out to be the basic building block or structure of such things as carbon-GO organic molecules (83), viruses, and other organic structures (8 1 ,84). The very building block of bone, hydroxyapatite, is an icosahedron. The principle of tensegrity is applied to the human body from the molecular to the cellular to the macro level. At the cellu lar level, mechanical stresses are focused on signal transducing molecules that physically associate with cell surface molecules that anchor cells to the extracellular matrix (85). One cannot alter the tension or compression in one area without altering the tension, structure, and thus the function throughout the body. This brings us full circle to AT. Still's descriptions of the impor-
497
tance of fascia (8G). On the macro level, icosahedra may be linked in a hierarchical pattern with the muscles, ligaments, tendons, and fascia serving as the tension elements and the compression elements, the bones, suspended within this dynamic network. The spine is also modeled in the same fashion. This leads to a functioning unit that is omni-directional, essentially universally mobile with a continually changing tension compression distri bution (82). This allows for movement with the lowest energy costs and the least wear and tear. However, it is important to re member that disruption of one part of the system has a rippling effect throughout. The diagnosis of such injuries is made based upon the patient's history and upon physical examination that puts stress on the in volved ligaments, joints, and tendons. The history is often classic in that the patient will complain of pain while at rest or when having been in one position for a length of time. These patients cannot sit for long periods or wake up frequently at night with pain and must therefore change positions often. This is because in a static position, ligaments are put on stress because muscle tension is often lessened. Thus pressure on the ligament-bone junction causes a typical aching pain. Ligamentous laxity is also tested with the use of mobility test ing of various joints. It is important to remember that the joint capsule is simply specialized ligamentous tissue and really an ex tension of other ligaments surrounding the joint. Thus capsular laxity often is seen in combination with laxity of other ligaments around a joint. These tests check for hypermobility of ligaments and also for subjective pain when the ligaments are stressed. It is important to remember that palpation of ligaments is another form of stress testing by placing pressure on the ligament-osseous junction just as mobility testing does, and can thus be extremely useful in pinpointing areas that need to be treated to alleviate the patient's pain. Many practitioners find that "trigger points" in muscles can be symptomatic of deeper ligamentous involve ment and that when trigger points recur after injection therapy or other modalities, one should reexamine the patient with the appropriate ligamentous structures in mind. Once again, ortho pedic medicine specialists need to elevate the importance of the fascial system in diagnosis and treatment. As AT. Still described the fascia, he stated: " I know of no part of the body that equals the fascia as a hunting-ground. . . . By its action we live and by its failure we die" (8G). Multiple techniques are available to accelerate and maximize healing of tendonosis and ligamentous laxity. These include ther mal modification of tissues, surgical approximation of tissues, im mobilization and bracing, as well as chemical stimulation. Among the useful therapies for the treatment of the very common chronic pain due to ligamentous laxity is prolotherapy. This has been for merly termed sclerotherapy, but the term prolotherapy derived from proliferative therapy is now favored. Prolotherapy involves the injection of irritant solutions in small amounts directly into the osseous-ligamentous junction. This process then recreates the injury and promotes the strengthening and proper healing of the painful ligament or tendon. The strengthening of ligaments in this manner has been well documented in animal models by Liu and colleagues, who showed that rabbit ligaments were thick ened and strengthened by proliferating solutions (87). Human studies have included two randomized, double-blind, low back prolotherapy studies, one of which showed statistically significant
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VI. Osteopathic Considerations in the Clinical SpeciaLties
improvement (88,89). A double-blinded study on prolotherapy in knee osteoarthritis revealed statistically significant improve ment in joint pain, subjective joint swelling, flexion range of mo tion, and knee buckling. There was also anterior cruciate ligament tightening by objective measures in the prolotherapy group (90). Further information on this approach to soft tissue prob lems can be found in "Prolotherapy in the Lumbar Spine and Pelvis" (91). Internet resources can be located easily by logging onto the American Osteopathic Association website ( www. aoa net. org) and following the links to the American Academy of Sclerotherapy, which contains multiple links that provide more information.
1 3. Loniewski E G , W i l l iams J L, Jarski R, e t a l . The effectiveness o f osteo pathic m a n ipulative treatment after hip or knee arthroplasty: a prospec tive, conttOlled, randomized, single-bl i n ded outcome study. jA OA. 1 995;95 :492 (abst). 1 4. H erzog RJ . Magnetic resonance imaging of the spine. In: Frymoyer J, ed. The Adult Spine. New Yo rk, NY: Raven Press; 1 99 1 :475. 1 5 . Bigos S, Bowyer 0, Braen G , et al. ACllte Low Back Problems in Adults. Clinical Practice G u i deline, No. 1 4 . Rockville, M D . : US Department of Health and Human Services; December 1 994. Public Health Ser vice, Agency for Health Care Policy and Research. AHCPR publication 95-0642. 1 6. Waddell G , McCulloch JA, Kummei E, et al. Non-organic physical signs of low back pain. Spine. 1 98 0 ; 5 : 1 1 7- 1 2 5 . 1 7. White AA, Panjabi M M . Clinical Biomechanics of the Spine, 2nd ed. P h i ladelphia, PA: ) . B . Lippincott Co; 1 990:45. 1 8 . American Academy of Orthopedic Surgeons. A glossary on spinal termi
CONCLUSION
This chapter is not meant to discuss in any detail the surgical aspects of orthopedic treatment, even though these are the more exciting avenues for the surgeon. Acknowledgment and respect for the whole person and their inherent healing capacity, the interdependent relationship of structure and function and the need for rational therapeutic approaches form the foundation of the osteopathic approach to orthopedic medical and surgical problems. And so the reader is led back to the first illustration in this chapter, in which Andry likened the orthopedic surgeon to the gardener who nurtured his fruit trees so that, by gentle, steady guidance, they grew strong and straight. Andry espoused prin ciples of orthopedic medicine that will always stay in favor (92) . John Spears, D. 0. , helped update the section on Low back pain.
nology. Quoted in: Frymoyer J, Pope M H . Segmental instability. Semin Spine Surg. 1 99 1 ;3(2): 1 09. 1 9 . Denis F. The t h ree-col u m n spine and its significance in the classification of acute thoracolumbar spine i n j u ries. Spine. 1 9 83;8 : 8 1 7-83 1 . 20. Andersson G B , McNeil T. Lumbar Spine Syndromes, Ellfllufltion and Treatment. New Yo rk, NY: Springer-Verlag, 1 989. 2 1 . M i rkovic S, Garfin SR. Spi nal stenosis: history and physical examination. I n: Schafer M, ed. Instrllctiollal COllrse Lectures. Vol 43. Ta unton, MA: American Academy of Orthopedic Su rgeons; 1 994:435-439. 22. Frymoyer JW, Gordon SL. New Perspertives on Low Back Pain. Park Ridge, I L : American Academy of Orthopedic Surgeons; 1 989:2 1 7-24 1 . 23. Wei nstein J . D i fferential diagnosis and surgical treatment of primary benign and maligna n t neoplasms. In: Frymoyer JW, ed. Tbe Adult Spine. New York, NY: Raven Press; 1 99 1 :4 1 :8 5 1 . 24. Ransford AO, Cairns D , Mooney V. The pain drawing as an aid to the psychological evaluation of patients with low-back pai n . Spine. 1 976; 1 ( 2 ) : 1 27-1 34. 25. Stein D , Floman Y. Psychologic approaches to the management and treatment of chronic low back pai n . In: Wei nstein IN, Wiesel SW, eds.
The Lumbar Spine. Phi ladelphia, PA: WE Saunders; 1 990: 8 1 1 -827. 26. King AI, Cavanaugh J, Fairbank J , et a l . Diagnosis and neuromecha nisms. I n : Weinstein IN, Wiesel SW, Eds. The Lumbar Spine. Philadel ph ia, PA: WE Saunders; 1 990:74- 1 62.
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33. Orthopedics
39. Andersson GB, Lucente T, Davis A M , et al. A comparison of osteopathic spinal manipulation with standard care for patients with low back pain. N Engl} Med 1 999;34 1 ( 1 9} : 1 426- 1 43 1 . 40. Atchison J W. Manipulation for the treatment of occupational low back pain. Occup Med. 1 998 ; 1 3 ( 1 } : 1 85-1 97. 4 1 . Brodin H . I nhibition facilitation technique for lumbar pain treatment. MarlUri/ Med. 1 987;3:24-25. 42. Bronfort G . Spinal manipulation. Current state of research and its indi cations. Neurolog Clin North Am. 1 999; 1 7 ( 1 } : 9 1 - 1 1 1 . 43. Carey TS, Garrett J , Jackman A, et al and the North Carolina Back Pain Project. The outcomes and costs of care for acute low back pain among patients seen by primary care practitioners, chiropractors, and orthopedic surgeons. N Engl] Med 1 995;333: 9 1 3-9 1 7. 44. Chrisman 00, Mittnacht A, Snook GA. A study of the results following rotatory manipulation in the lumbar intervertebral disc syndrome.) Bone joint SlIrg. 1 964;46: 5 1 7-524. 45. peyo RA. Non-operative treatment of low back disorders: d ifferentiat ing useful from useless therapy. I n : Frymoyer J W, ed. The Adult Spine: Principles and Practice. New York, NY: Raven Press; 1 99 1 : 1 567- 1 579. 46. Greenman PE. Syndromes of the L-spine, pelvis and sacrum . In: Stan ton 0 , ed. Manllal Medicine. Physical Med Rehabil Clin North Am. New York, NY: WB Saunders; 1 996;7(4}:733. 47. Haldeman S, Phillips RB. Spinal manipulative therapy in the manage ment of low back pain. I n : Frymoyer J W, ed. Adult Spine: Principles and Practice. New York, NY: Raven Press; 1 99 1 : 1 5 8 1 - 1 60 5 . 48. Koes .BW, Assendelft W) , v a n d e r Heijden GJ , Bouter L M . Spinal manipulation for low back pai n . An updated systematic review of ran domized cli nical trials. Spine 1 996;2 1 (24} : 2860-2873. 49. MacDonald R, Bell CMJ. A n open controlled assessment of osteopathic manipulation in nonspecific low back pai n . Spine. 1 990; 1 5 :364-370. 50. Mannion AF, Munrener M, Taimela S, Dvorak ] . A randomized clin ical trial of three active therapies for chronic low back pain. Spine. 1 999;23:2435-2448. 5 1 . Mein E. Low back pain and manual medicine. A look at the l iterature. I n : Stamon 0, ed. Manual Medicine. Physical Med Rehabil Clin North Am. New York, NY: WB Saunders; 1 996;7(4 } : 7 1 5-729. 52. Pope M H , Phillips RB, Haugh LD, et al. A prospective randomized three-week trial of spinal manipulation, transcutaneous muscle stimu lation, massage and corset i n the treatment of subacute low back pain. Spine. 1 994; 1 9(22} : 2 5 7 1 -2577. 53. Powel l FC, Han igan WC, Ol ivero We. A risk/benefit analysis of spinal manipulation therapy for relief o f lumbar or cervical pain. Neurosurgery. 1 993; 33( 1 } : 73-78 (commentary: 78-79). 54. Seferlis T, Nemeth G, Carlsson AM, G i llstrom P. Conservative treatment in patients sick-l isted for acure low-back pain: a prospective randomised study with 1 2 months' follow-up. Eur Spine}. 1 998;7(6}:46 1 -470. 55. Shekclle I� Adams A, Chassin M, et al. Spinal manipulation for low back pain. Ann Intern Med. 1 992; 1 1 7: 590-598. 56. Van Tu lder MW, Koes BW, Bouter LM. Consetvative treatmem of acute and chronic nonspecific low back pain. A systematic review of random ized controlled trials of the most common interventions. Spine 1 997; 22( 1 8} : 2 1 28-2 1 56. 57. Asher MA, Strippgen W, Heinig C, Carson W. Isola instrumentation. In: Weinstein SL, ed. The Pedit/tric Spine. New York, NY: Raven Press; 1 994: 1 6 1 9- 1 657. 58. Andrews J R, Zarins B, Wilk KE. Injuries in Baseball. P h i ladelphia, PA: Lippi ncott-Raven, 1 998. 59. Norris T, ed. Orthopedic Knowledge Update: Shoulder and Elbow. Rose mont, 1 L: American Academy of Orthopedic Surgeons, 1 997. 60. Cole BJ , Warner JJ P. Anatomy, biomechanics, and pathophysiology of glenohu meral instabiliry. In: lanotti Jp, Williams G R, eds. Disorders of the Shoulder: Diagnosis and Management. Philadelphia, PA: Lippincott, Will iams & Wilkins, 1 999:207-232. 6 1 . Soslowsky LJ , Flatow EL, Bigliani LU, et al. Quantitation of in situ conract areas at the glenohumeral joint. ] Shoulder Elbow Surg. 1 998;74: 46-52. 62. Halder AM, Kuhl SG, Zobirz M E, et al. Effects of the glenoid labrum and glenohu meral abduction on stabi l i ty of the shoulder joinr through concavity compression . } Bone joint Surg. 200 1 ;83-A(7}: 1 0621 068. 63. I toi E, Sashi R, Mi nagawa H , et al. Positions of immobil ization after
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67. 68.
69. 70. 71. 72.
73. 74. 75. 76.
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82.
83. 84. 85. 86. 87.
88. 89.
90.
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dislocation of the glenohu meral joint. A study with use of magnetic resonance imaging. } Bone]oint Surg. 200 1 ;83-A(5}:66 1 . Chester J B . Whiplash, postural control, and the inner ear. Spine. 1 99 1 ; 1 6(7):247. Astrom M , Rausing A. Chronic Achil les tendinopathy: a su rvey of sur gical and histopathologic findings. Clin Orthop. 1 995;3 1 6: 1 5 1 - 1 64. Khan KM Bonar F, et al. Patellar tendinosis (ju mper's knee): find ings at histopathologic examination. US and MR imaging. Radiology. 1 996;200(3 ) : 8 2 1 -827. Nirschl RP, Pemone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. ] Bone Joint Surg {Am}. 1 979;80( 5 ) : 832-839. Kraushaar BS, N i rschl RP. Tendinosis of the elbow (tennis elbow): clin ical features and findings of histological , immunoh istochemical, and electron m ictoscopy studies. ] Bone Joint Surg {Am}. 1 999; 81 ( 2 ) : 269278. Ollivierre CO, Nirschl RP, et al. Resection and repair for medial tennis elbow: a prospective analysis. A m ) Sports Med. 1 999;23(2) : 2 1 4-22 1 . Khan KM Cook JL, et al. Overuse tendinosis, not tendinitis. Physician Sports Med. 2000;28(5}: 38-48. Puddu G , Ippolito E, et al. A classification of Achi lles tendon disease. A m ] Sports Med 1 976;4(4} : 1 45-1 50. Kapetanos G . The effect of the local corticosteroids on the healing and biomechanical properties of the partially i nj u red tendon. Clin Orthop. 1982; 1 63 : 1 70- 1 79. Ketch u m LD. Effects of triamcinalone on tendon healing and function. Plast Reconstr Surg 1 97 1 ;47:47 1 . Speed CA. Corticosteroid injections i n tendon lesions. 8M}. 200 1 ; 1 : 532-536. Astrom M. Partial rupture i n chronic Achil les tendinopathy: a retrospec tive analysis of 342 cases. Acta Orthop Srand. 1 998;69(4):404-407. Hay E M , Paterson S M , et al. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BM}. 1 999;3 1 9:964-968. Banks, AR. A rationale for prolotherapy. } Orthop Med 1 99 1 ; 1 2(3): 54-59. Oates JA, Fitzgerald GA, et al. Clinical implications of prostaglandin and thromboxane A2 fo rmation. N Engl] Med 1 988;3 1 9 ( 1 1 ) :689-698. Fuller RB. Synergetics. New York. NY: Macmillan; 1 97 5 . Nelson KD. Continuous tension, discontinuous compression strUC!llres. 1 96 5 . Levin S M . T h e icosahedron a s the th ree-dimensional fi n ite element in bio-mechanical suppOrt. In: Proceedings ofthe Society of General Systems Research Symposium on Mental/mages, Values, and Reality. St. Louis, MO: Society of General Systems Resea rch; 1 986. Levin SM. The i mportance of soft tissues for structural support of the body. In: Dorman T, ed. Spine: State of the A rt Reviews. Phi ladelphia, PA: Hanley & Belfus, I nc. 1 995;9:357-363. Kroto H. Space, stars, C60, and soot. Science. 1 988;242 : 1 1 39- 1 1 45. I ngber DE. The archi tecture of life. Scientific American. Jan uary 1 998;48-57. Chen CI. Tensegrityand mechanoregulation: from skeleton to cytOskele ton. Osteoarthritis and Cartilt/ge. 1 999;7( 1 ) : 8 1 -94. Still AT. The Philosophy and Mechanical Principles of Osteopathy. Kansas City, M O : Hudson-Kimberly Publishing Co; 1 902. Liu YK, TiptOn CM, et al. An in silll study of the inA uence of a sclerosing solution in rabbit medial col iateral ligamcllls and its junction strength. Connect Tissue Res. 1 983; I 1 :95- 1 02 . Ongley M J , Klein R G , e t a l . A new approach t o the treatmem o fchronic low back pai n . Lancet. 1 989; 1 43- 1 46. Klein RG, Eek Be, et al. A random ized double-blind trial of dextrose glycerine-phenol injections for chronic low back pain. ] Spinal Disord. 1 993;6:23-33. Reeves KD, Hassanein K. Random ized prospective double-blind placebo-controlled study of dextrose prolotherapy for knee osteoarthri tis with or without ACL laxity. Alter Ther Health Med 2000;6 ( 1 ) : 68-80. ,
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PULMONOLOGY GILBERT E. D' ALONZO, JR. SAMUEL L. KRACHMAN
KEY CONCEPTS • • • • •
Tight in teraction between respiratory structure and function Viscerosomatic and somatovisceral reflexes and l ung disease Thoracic lymphatic drainage Osteopathic manipulatory effects o n pulmonary function and lymphatic drainage Prevention and treatment of l ung disease, including pneumonia, chronic obstructive pulmonary diseases, respiratory distress syndrome, and postoperative pulmonary complications
Pulmonology is the study of l ung diseases and it is a subspecialty of i nternal medicine. Having its beginnings in the diagnosis and treatment of tuberculosis, pulmonary medici ne accelerated wi th the use of spirometry, flexible bronchoscopy, and the use of the mechanical ventilator outside of the operating room. Advances in cardiology and cardiothoracic surgery further supported the need for pul monologists who have, for the most part, dominated the area of critical care medicine. Most recently, pulmonologists have become intimately involved in sleep medicine. Osteopathic pulmonologists have been involved i n the entire evolu tionary process of pulmonary med icine. Osteopathic physi cians who practice pulmonary, critical care, and sleep medicine are growing i n number. The respiratory system is an absol utely ideal model to learn and explore osteopath ic medicine and i ts practice and princi ples. Furthermore, the practice of both critical care and sleep medicine requ ires a keen knowledge of the body as a whole, with all of i ts in tegrative and communicative mech anisms. Osteopathic physicians are conceptually well prepared for these areas. The lu ngs are totally dependent on the thoracic pump, which is influenced by the entire m usculoskeletal system and controlled by a large variety of neural and h u moral signals. This makes the respiratory system, in both health and disease, a prime target for osteopathic research. The respiratory system includes all of the components of the upper ai rway; the tracheobronchial tree, l u ngs, and pul monary circulation which are enclosed in the thoracic cage and
diaphragm; and the central nervous system with its peripheral connections. The central nervous system performs as a system controller, regulating the activity of the respiratory muscles and the thoracic cage, which functions as a pump. The pumping ac tion of this organ system is essential for the lung's mechanism to exchange oxygen for CO2 but it also assists in the retu rn of venous and lymphatic fl uids to the chest. Th is system provides adequate oxygenation, which is vital to end-organ function, re leases at least one major end product of metabol ism, CO2, and participates in the homeostasis of acid-base metabolic balance on a moment-to-moment basis. The l ungs are also involved in the elimination of various toxins and drugs, vocalization, and with pressurization of the abdomen, defecation, urination, parturition, and physical work. Malfu nction of an individual component of the respiratory system or alterations of the relationships among various componenrs can lead to disturbances in end-organ func tion and, evenrually, in total body performance. The respiratory system is completely dependenr on the musculoskeletal system for optimal performance. The respiratory system, l i ke other body componenrs, is con structed to preserve function and mainrain health. It depends on the proper function of other systems, and, of course, other systems depend on the process of respiration. Additionally, the l u ngs are organs that interface with the environ menr through the exchange of air that occurs with each breath . Each day, the l ungs are exposed to more than 10,000 L of ambient air that may conrain microorganisms, dusts, and chemicals. The expo sure to these noxious substances is l i kely responsible in part for a wide variety of diseases, including infections, inflam matory con di tions, and malignancies. However, the l ungs possess certain defenses that reduce the l i kelihood that injury and disease "w ill develop. The l ungs and the entire breathing process participate in the body's self-regulatory, self-healing, and health maintenance processes. Ptoper respiratory function depends on a delicate harmony with other systems, notably, but not exclusively, the cardiovascu lar, neuromuscular, and skeletal systems. Disease cannot occur in one system without affecting other body systems. The eventual extenr generally depends on the severity of the initial disruption. In essence, the body attempts to function as a unit with a cadre of p urposeful inrerrelationsh i ps and interdependencies between structure and function. Its goal is to enhance optimal function, ensure health, and prolong survival.
34. Pufmonofogy RESPIRATORY F U N CTION Ventilation
Venrilation consists of the movemenr of air from outside the body through the upper air passages and the subdivisions of the con ducting ai rways inro the terminal respiratory units, and back out again. The amounr of inspired air that reaches the sites of gas ex change is determined by many factors, including l ung parenchy mal distensibility and the way in which air moves or flows through the tracheobronchial tree. A pumping action, requiring a neuro m uscular and skeletal effort, is necessary to expand the l ungs and to cause air to flow through the respiratory system. Therefore, venrilation chiefly depends on the capabilities of the fol lowing: Thoracic cage including the respiratory muscles Mechanical properties of the airways Lung parenchymal respiratory units Respiration occurs at the level of the terminal respiratory u nit, which includes the alveoli, and it is defined as the process of gas exchange between the body and its environment. This exchange of gases depends on: •
Vol ume and distribution of blood flow thtough the pulmonary circulation • Volume and distribution of ven tilation within the l u ngs • Diffusion characteristics of oxygen and CO2 across the air blood barrier • Regulation of breathing influenced by a variety of neurologic and metabol ic factors The lungs can be expanded and contracted in two ways: 1 . By downward and upward movemenr of the diaphragm to lengthen or shorten the vertical diameter of the chest cavity 2. By elevation and depression of the ribs to increase and decrease the anreroposterior and lateral diameters of the chest cavity Normal breathing at rest is accompl ished almost entirely by the first of the two above methods. During inhalation, contraction of the diaphragm pulls the lower surfaces of the l ungs downward. During exhalation, the diaphragm relaxes and the elastic recoil of the lungs, chest walls, and abdominal structures compresses the lungs. When ventilation has to i ncrease, as with exercise or disease, rapid exhalation is necessary, and the elastic forces of the respiratory system are not sufficienr enough to meet the demands of respiration. Abdominal muscle conrraction occurs, forcing the abdom inal contenrs upward against the bottom of the diaph ragm. Additionally, when minute venrilation increases, recruitmenr of the accessory respiratory muscles raises the rib cage. Raising the rib cage, in turn, expands the l ungs to a greater degree than that found at rest and augments i nhalation . Proper functioning of the thoracic pump without restriction is essential. The major accessory muscles that raise the rib cage include the: Sternocleidomastoid muscles Anterior serrati Scaleni External intercostals Sternocostals
501
The m uscles that pull the rib cage downward during exhala tion are the abdominal recti and the i n rernal intercostals. The l umbar spinal curvature with the quadratus l umborum muscle can also be an important mechanical influence during active exha lation. However, all of this movement of m uscles requires proper m usculoskeletal i nteractive harmony. The cervical and thoracic spinal column and the cervical fascia which is continuous with fascia in the thoracic region, diaphragm, and eventually the m us culature of the l umbar spine acts as the foundation for this enrire respiratory movement process. Somatic dysfunction at any spinal segmenral level, whether due to a primary structural disturbance or neurologic or visceral disease, disrupts proper function. An example of this concept is found in a patient who has an acute myocardial infarction and experiences dyspnea or shortness of breath. The dyspnea could be due to associated heart fail ure, but it could also be due to high thoracic somatic dysfunction from the infarction with associated restriction of rib cage movement as resulting fro m this viscerosomatic relationship. In our prac tice, we have seen how a somatovisceral reflex disturbs the costal cage, and therefore l ung mechanics and pulmonary gas exchange, and contributes mechanistically in the patienr's perceived dysp nea. Treatment of somatic dysfunction by appropriate osteopathic manipulative i n tervention helps rel ieve dyspnea. Upper extremity m usculoskeletal structure and fu nction af fect respiration. Com mon myofascial attachments of the upper extremity cross the shoulder joint and attach to the thorax. Up per extremity m uscles, i ncluding the latissi m us dorsi, are active during forceful exhalation, especially with coughing and sneez ing. Pectoralis major and m inor and the serratus anterior muscles are active during deep and forceful in halation . Therefore, ful l myofascial structural mobility of t h e upper extremities enhances respiratory mobility and function, especially duri ng exercise and in disease, such as emphysema. As mentioned previously, the abdominal m usculature partic ipates in respiratory motion and along with the u rogenital di aphragm, helps establish an essential pressure gradient between the thorax and abdomen. Lumbar and sacral spinal motions play a role in the respiratory process. The diaph ragm is attached to the upper lumbar (Ll-3) spine, the lower six ribs, the xiphoid process, and the fasciae covering the quadratus l umborum and psoas muscles. The abdomi nal m uscles, includi ng the rectus ab dominus, insert on the pubis and act as accessory muscles of respiration. Abdominal, quadratus lu mborum, psoas, and shoul der girdle muscles and lumbodorsal fascia assist the diaphragm in respiratory motion. The quadratus l umborum anchors the J 2th rib, providing a stable base for diaph ragmatic contraction during inhalation and depresses the 1 2th rib during exhalation. Dur ing exhalation, the abdominal m uscles compress the abdominal contents, depress the lower ribs and assist in talki ng, si nging, sneezing, coughing, defecation, and parturition. Fascia from the thoracic region is continuous with the ab dominal and pelvic fascia, including the mesentery, retroperi toneum, and peritoneum. Respiration, therefore, affects viscera via fascial attachments and the resultant changes in thoracic and abdominopelvic pressure gradienrs and lymphatic and venous drainage from these regions, centrally to the heart. These move ments are synchronous and i n rerdependent. Osteopathic manip ulative treatment (OMT) is aimed at enhancing all respi ratory
502
vr. Osteopathic Considerations in the Clinical Specialties
mechanics and conversely, respiratory motion may be utilized to optimize OMT. In order to accompl ish this, OMT should be directed at somatic dysfunctions of the entire spine, rib cage, thoracic inlet, diaphragm, and all muscles of respiration. The l ungs have a continual elastic tendency to collapse, pulling away from the chest wall ; whereas the chest wall tends to recoi l outward. These movements i n opposite directions are responsible for the development of negative pleural pressure when the res piratory system functions in the i ntact state. The expandability of the lu ngs and thoracic cage is called compliance. Compliance is expressed as the volume i ncrease i n the l u ngs for each unit i ncrease in alveolar pressure, or for each unit decrease i n pleural pressure. Because compliance is an expression of the distensibility of the elastic respiratory system, measured values of compliance depend on the elastic recoi l properties of the l u ngs and chest wall . T h e lungs of patients with emphysema are more distensible, and the lungs of patients with diffuse l u ng fibrosis or other i nfil tJ'ative i nflammatory diseases are less distensible, or stiffer, than normal l ungs. Vol u me-pressure curves from adults with normal l ungs, with emphysema, and with l ung fibrosis are shown in Fig. 34. I. All th ree patients are assumed to be of similar age and body builds, so they would have thoracic cages with simi lar vital capacities. Note that emphysematous l ungs are larger than normal and fibrotic l ungs are smaller than normal. The curve from the patient with em physema is shifted to the left and above that of the normal curve, whereas the curve fro m the patient with fibrosis is flatter and sh ifted downward. When expressed at any given l u ng volume as a percent of the vital capacity (VC) , compliance is lower with fibrosis. There is also chest wall compl iance to consider since every l ung disease adversely affects the thoracic cage. Total tho racic compl iance involves both lung and chest wall components. Again, spi nal somatic dysfunction can negatively disturb chest wall and l ung compl iance and, hence, lung ventilatory function. Another factor that m ust be considered during breathing is resistance to airflow i n the respiratory system. Resistance is com puted from simultaneous measurements of the airflow and the
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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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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
VI. Osteopathic Considerations in the CLinical Specialties
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
VI. Osteopathic Considerations in the Clinical Specialties
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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
CO
the parenchyma of
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
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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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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
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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
93. Pratt-Harrington D , Neptune-Ceran R. The effect of osteopathic ma
the management of upper, middle, and pararespiratory infections . jADA.
nip ularive treatment in the POSt abdominal surgical patient. MDl
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1 99 5 ;Fall: 9- 1 3.
dren. jADA. J 966;65:964-972.
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
35. Osteopathic Physical Medicine and Rehabilitation
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-
519
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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VI. Osteopathic Considerations in the Clinical Specialties
(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
35. Osteopathic Physical Medicine and Rehabilitation
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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VI. Osteopathic Considerations in the Clinical Specialties
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
35. Osteopathic Physical Medicine and Rehabilitation
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
523
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.
524
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
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35. Osteopathic Physical Medicine and Rehabilitation
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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1 993;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.
1 4 . Hurwitz El, Aker P O , Adams AH, Ct al. M a n i p ulation and mobil iza
40. Prokop LL, Wieting J M . The Use of Manipulation i n SpOrtS Medicine
tion of the cervical spine: A systematic review of the l i terature. Spine.
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1 5 . G ross AR, Aker P, Quardy C , et al. Musculoskeletal medicine: Man
4 1 . Stanton O F, Mein EA. Preface. In: Kraft G H , cd. Physical Medicirle and
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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
527
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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VI. Osteopathic Considerations in the CLinical Specialties
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.
529
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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VI. Osteopathic Considerations in the Clinical Specialties
(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
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ACKNOWLEDGMENTS
1 9 . Scorr D L. Symmons D P M . Coulron
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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
536
VI.
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
An Osteopathic Approach to Sports Medicine
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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.
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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.
An Osteopathic Approach to Sports Medicine
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.)
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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.
An Osteopathic Approach to Sports Medicine
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
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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
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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
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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
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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
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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 <5 min OR posttraumatic amnesia > 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.
2 (moderate)
3 (severe)
No loss of consciousness; 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 <15 min; second grade-1 in same contest: disqualify athlete , return in 1 week if asymptomatic.
May return after 1 fully asymptomatic week; second grade-2: return to play after 2 weeks symptom free. Brief (seconds) grade-3 concussion: no play until asymptomatic for 2 wks; second grade-3: withold from play for a minimum of 1 asymptomatic month.
"All asymptomatic periods mean asymptomatic both at rest and with exertion. Asymptomatic means no headache, dizziness, or i m p a i red concentration plus the a b i l ity to fully reca l l the events occurring
before injury.
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treatments, such as appropriate conditioning and warm-up, avoidance of triggers, osteopathic manipulation, and physical therapy, as well as drug treatment which might include antis eroronergic and nonsteroidal antiinflammatOry medications, beta blockers, calcium channel blockers, and judicious use of narcotics as rescue medication. The sports medicine clinician must always be aware of special considerations regarding drug therapy when treating athletes and being aware of banned substances, as well as the ergolytic effects of certain medicines on athletic performance. Convenience and ease of use of medication is also a considera tion when they are to be used at or around the time of athletic competition.
RETURN-TO-PLAY CONSIDERATIONS
There is not a simple algorithm that determines rerum to play af ter sport injury. Medical factOrs are paramount, although a variety of non-medical factOrs (e.g., age of the athlete, level of competi tion, psychosocial issues) can influence rerurn-tO-play decisions. Although the decision to rerum to play can be complex, some medical sequelae of sports injuries do represent absolute con traindications to rerum to contact sports. Some specific examples would include neck injuries resulting in permanent central nervous system (i.e., spinal cord) dysfunc tion, permanent and significant peripheral nerve (i.e., nerve root) dysfunction, and certain infectious diseases in the active stages. Some other conditions, for example concussions and some heart conditions, represent relative contraindications to return to play, even in the setting of full recovery. Community physicians are asked to make rerurn-tO-play decisions regarding a wide vari ety of musculoskeletal conditions. Carefully designed symptOm directed functional testing can be invaluable in assisting the clin ician in making these sometimes challenging decisions. A typical example would be returning an athlete with an ankle sprain to his/her sport. One can design a series of progressive functional tests that simulate the loads and motions of the sport and evaluate the athlete's performance. Physical therapists and athletic trainers can provide assistance in this regard. Long-term health and prevention of secondary injury to the athlete should be the only concerns that guide return-to-play timing and permission from the team physician. A licensed, well trained sports medicine physician who is then responsible for making the final return-tO-play decision should evaluate each case individually and completely.
PERFORMANCE ENHANCEMENT
Today's athletes are bigger, stronger, and faster than ever before. This is accomplished by aggressive off-season training through physical, nutritional, and psychological means. As a team physi cian, it is important to evaluate those athletes with injuries during the season to be sure they have been maximally rehabilitated dur ing the off-season. Today's athletes improve performance by working specifically on flexibility, speed, strength, and endurance. Integral compo nents ro improved performance that are often overlooked are
balance and functional strength. As discussed earlier in vari ous sections, training the body in various neuromuscular pat terns that are sport specific is the key to performance enhance ment. Improved neuromuscular coordination is achieved through removal of somatic dysfunction and postural and muscle im balances while repetitively training to improve balance, energy transfer, and functional strength throughout sport-specific joint motions. Static pure strength is unimportant without balance and provides minimal advantage to the athlete. An athlete's ability is enhanced through a combination of improved flexibility, propri oception, strength, and practiced movement patterns, which all aim to build better neuromuscular coordination. The Use of Performance-Enhancing (Ergogenic) Drugs
The term ergogenic means any method to enhance athletic per formance. Its Greek root " Ergon" means "to work. " Historically, the ancient Greek Olympic athletes are believed to have used both herbs and mushrooms to enhance their performance. Drug abuse in the modern era of athletics became a recognized prob lem in the 1 950s when the use of stimulants was reported during the 1 9 52 winter Olympics in Oslo, Norway. Philosophically, ath letes will always look to gain an edge. Genes, nutrition, training techniques, and mental discipline best predict athletic success. Categories of ergogenic aids include pharmacologic, nutri tional, and physiologic, such as blood boosting. Recently, there has been increased emphasis on the psychological aspect of sportS performance, with many elite athletes using mental imagery and a number of other relaxation techniques to enhance performance. We must also not forget about the various technological and me chanical aids that are available, including such things as oversized tennis racquets, titanium materials used in golf clubs, lightweight racing shoes, and a host of other developments specifically related to each specific sport. In general, here in the United States, there seems to be a cultural bias toward the use of medication to "solve" problems. The American public is inundated with television and print ads encouraging the public to solicit prescription medications from their physicians to treat medical problems and enhance their quality of life. Superimposed on these issues are the use and abuse of alcohol and recreational drugs that are defined as non prescription drugs used for mood altering purposes. With respect to pharmacologic aides, the most commonly used substances include creatine, anabolic steroids, and human growth hormone. Regarding anabolic steroids, the mechanism of action is felt to be related to increased protein synthesis, increased red blood cell production, and central nervous system effecrs that include increased aggressiveness. Incidence of use has been var iously reported in the 3% to 1 2% range. Anabolic steroids are considered a controlled substance (class [II) with a. multitude of potential side effects on the cardiovascular system, the reproduc tive system, and the endocrine system. Research is limited and difficult to carry out due to the fact that these are banned sub stances; it is difficult to get athletes to participate in these types of studies. Human growth hormone is another commonly used er gogenic aid that cannot be detected using current drug testing
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methodology. It is produced using recombinant DNA technol ogy, and its high cost does in some ways limit its abuse. Proposed mechanisms of action include increased transport of amino acids inco tissue, as well as stimulation of mobilization of fat as an energy source. Potential side effects include those mentioned for anabolic steroids, as well as possible acromegaly, diabetes melli [Us, hearr faill1re, and osteoporosis. As with any injectable drug, the risk of infectious disease secondary to needle sharing must also be taken into consideration. Amphetamines have been used for over 50 years. They were initially used in World War [ l to prevent "battle fatigue." Mech anism of action includes central nervous system stimulation, speeding of reaction time, and masking of symptoms of fatigue. Potential of serious side effects include cardiovascular collapse, hypertension, hallucinations, irritability, and restlessness. All are currently banned substances. Caffeine is a special subclass of stimulant that may enhance performance in endurance athletic evencs. A mechanism of action is not clearly understood, but may be related to central nervous system stimulation and en hanced energy utilization. Caffeine is widely considered to be one of the safest, most effective, and extensively studied ergogenic aids. Incidence of use is estimated at approximately 60%, and it is legal for use in low doses (5 to 1 0 mg per kilogram). This dose represents about three to four cups of strongly brewed cof fee (about a 300 mg dose) . Potential side effects can include GI intolerance, dehydration, cardiac arrhythmia, tremor, and headaches. Blood doping is also em ployed by endurance athletes. Initially, the technique was to donate two units of autologous blood ap proximately 8 to 1 2 weeks prior to the athletic event and then reinfuse this blood about 1 week prior to competition. The mech anism of action was to increase oxygen-carrying capacity. More recently, athletes have used erythropoietin, which is an injectable medication that stimulates red blood cell production by bone marrow. Potential side effects of these techniques include stroke, blood clots, sudden death, transfusion reaction, headache, and hypertension. Proper nutrition is one of the most important contributing factors to enhancing athletic performance. Deficiency of key nu trients will impair performance; however, in a non-deficiency state, the effect of supplementation is often unclear and over stated. Several reports suggest that the two factors leading to im provement in athletic records over the last few years are improved diet and enhanced training techniques. A com prehensive discus sion of nutrition is beyond the scope of this chapter, bur the consumption of a diet balanced in carbohydrate, protein, and fat is extremely important. Probably the most often overlooked nutrient is water, and athletes must cOllSume more water than the general population to replace sweat losses. There are a number of "sports dri nks" that are commercially available that do an excel lent job of replacing Auid electrolytes and carbohydrates. Several s[Udies have indicated enhanced performance in endurance ath letics. It is important when using sports drinks to make sure to use them in practice prior to using them in competition, as they may cause gastrointestinal distress. With regard to technological aids, great strides have been made in many SpOrts to enhance an athlete's mechanical advantage. The use of oversize tennis racquets and titanium woods and graphite
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shaft golf clubs are just a few of the more commonly used techno logical aids. Lightweight and aerodynam ic bicycles and compo nents can result in significant time savings during racing. Regard ing running shoes, a 200 gram reduction in shoe weight improves running efficiency by about I %. For an elite marathon runner, this can result in as much as a minute and a half in time savings over the course of a marathon race. I n summary, genetic endowment is the key to high perfor mance. There is no substi[Ute for hard work and good nutri tion. Technology may be of benefit. Mental imagery and relax ation techniques are an emerging area. Nutritional technology has advanced, and research, although limited, does support the ergogenicity of some nutrients, but more work in this area is needed. The International Olympic Committee doping legisla tion states that any physiologic substance taken in an abnormal quantity with the intention of artificially and unfairly increas ing performance should be construed as doping and is illegal. One must always understand and appreciate the ethics of sports performance when considering the above issues.
SIDELINE AND EVENT MEDICAL MANAGEMENT ISSUES
A physician with an interest in sports medicine is often called on to provide medical services or coverage for an athletic event. This involvement may be limited to providing medical coverage or services as part of a medical team or a more comprehensive role with a commitment to assisting in planning, organizing, and administering the event medical team. The primary responsibility remains the health and safety of the athlete. The event physician may also have an implied role to protect the event organization from medical liability. Acute injury management during a mass partici pation event is often more complex, because the athlete will often present without an available medical database to the physician. As a result, appropriate medical management may require interaction with coaches, athletic trainers, and parents. The event physician should evaluate the athlete, treat if required, and make recommendations regarding re[Urn to play or further evaluation in the emergency room or with the athlete's primary care physician. The event physician must not only be knowledgeable in mus culoskeletal medicine, but must be prepared to deal with envi ronmental concerns, as well as injuries specific to the event being covered. This is especially true of mass participation endurance events, such as m arathons and triathlons. Specific recommen dations for event equipment and protocols can be found in the ACMC Handbook for the Team Physician (33) . In general, the physician at every event should initially and periodically assess the environment when appropriate, introduce all medical per sonnel to one another, and review an emergency response plan, including the chain of command. At least one physician and four medical personnel per 250 participants and one physician and two medical personnel per 1 0 ,000 spectators should be present and planned for. Available equipment, including communication equipment, should be evaluated prior to the event. The closest emergency room should be notified ahead of time of potential injuries that might be anticipated.
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CONCLUSIONS
rhe young), American Heart Associarion. Circulation. 1 996;94:8 50-
8 56.
From its beginnings, osteopathic medicine has taken an active role in promoting participation in athletics as a means to a healthy lifestyle and providing specialized treatment of athletes. Osteopathic principles and practice, including the use of man ual medicine, have a large role in the treatment of the athlete. Each athlete should be evaluated and treated on an individual ba sis, including a comprehensive evaluation of both structure and function when appropriate. Because of the wide variety of po tential injuries and medical maladies that can affect the athlete, the sports medicine physician must be comprehensively trained. Finally, physicians m ust always keep the health of the athlete as their primary goal when considering return-to-play decisions.
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N
OSTEOPATHIC CONSIDERATIONS IN PALPATORY DIAGNOSIS AND MANIPULATIVE TREATMENT
INTRODUCTION JOHN M. JONES, III ROBERT E. KAPPLER
The fol lowing chapters contain detailed descriptions of m uscu loskeletal exa m ination and various treatment techn i ques com monly taught at osteopathic medical colleges in the United States. We would l i ke to gratefully acknowledge the contributions made by the faculties o f those colleges. Andrew Taylor Still never taugh t what he called techniques and explicitly recom mended against teaching osteopathy in that fashion. He fel t that i f the physician knew anatomy, i t was unnecessary to teach techniques, because the method to be used for a particular patient's problems should be obvious. So why do we teach techniques at our col leges today? In 1892, when Still fou n ded the American School o fOsteopa thy, he established a curricul u m dominated by anatomy. This was partly because he discarded much of the standard medical cur ricul u m ; it was o f l ittle use to the physician and largely harmfu l t o the patient. There has been an explosion o f knowledge i n both the basic and clinical sciences since that time. To the medical stu dent, it often seems that all the knowledge accumulated i n the last century h as been retained in the curricul u m , without the deletion of a si ngle element of medical m i n utiae. This may be true to an extent. Currently, o n ly about 10% of the curriculum i n the first 2 years o f osteopathic education is reserved for teaching the phi losophy, pri ncip les, and mechanics of osteopathic manipulative diagnosis and treatment.
FORMS OF TREATMENT
There are many forms o f osteopathic manipulation . O n ly the ba sic rypes taught d uring the first 2 years at United States col leges of osteopathic medicine are presented i n the fol lowing chapters. Other forms o f osteopathic manipulation, such as visceral ma n ipulation, are left for later work. Also, not every possible for m of a particular technique is incl uded. For example, there are at least six ways to do high-velociry/low-amplitude (HVLA) thrust tech n i q ue on a rypical cervical vertebra. Only representative samples o f the techniques are i ncluded. These samples of treatment can be classified as soft tissue techn i q ues, articulatory techniques, or d i rect and indirect meth ods of treatment. Techniques named accordi ng to the activating forces used are muscle energy, springing, or h igh-velociry/low ampl i tude thrust. Those referring to a concept of treatment are called strain/counterstrain, myofascial release, or osteopathy i n the cranial field. Related topics o f release b y positioning are dis cussed, as well as Simon and Travel l 's system of trigger points. Though trigger point diagnosis and treatment is not classified as osteopathic, it fits wel l i n to the practice o f m usculoskeletal medicine and is used by many osteopathic physicians.
MODELS
In each of these classifications of treatment tech niques, the di agnosis and treatment are based on a mental model, a cognitive system of reference that is workable when applied to patients with somatic dysfunctions. Models have limitations. They can not ex plain everyth ing; that is not their purpose. They are designed to correlate certain gathered i n formation with a diagnosis and to relate this diagnosis to a successful treatment. The m uscle energy model of sacral torsion does not delineate the exact biomechan ics o f the sacrum or which specific muscle(s) are i nvolved in the treatment. However, if the physician collects data, arrives at a diagnosis, and treats the disorder as i ndicated, the somatic dys function should resolve. The m uscle energy model relates to the body i n terms of simplified biomechanics. Many physicians use the muscle e nergy model not because it is perfect but because it works and they are pragmatic. Models that survive the test of time and propagate are those that have empi rically proven themselves by benefiting the pa tients. The models in the fol lowi ng chapters are examples of ways to accom plish biomechanical changes and achieve treatment goals. They are not the only way. If you u nderstand anatomy, you can use a variety of ways to achieve the same objective. If you do not u n derstand anatomy, fol lowing a protocol may do the patient no good; the patient's physique may not conform to the 5' 10", 170-pound model on which the protocol was based. Knowing anatomy, however, is not enough by itself. You may, for i nstance, adapt a technique by using muscle energy activation on a posi tion normally followed by HVLA. You base this on what you palpate and sense happening with the patient and o n the patient's unique response to past or cur rent treatment. You may use treatment in two planes rather than three, because of positional l i m i tations imposed on the patient because of surgery, trauma, or the formation of osteophytes i n osteoarthritis. You m ight more appropriately make a completely different choice of treatment techn iq ue because of the pos itional l im i tation. For example, the m uscle energy model requires Aexion to confron t an extension lesion . If the surgeon wants the head to remain Aat, you may elect to use indirect myofascial release at the cervical segment level, requiri ng only a few degrees of motion, which would not raise the head off the pillow.
PHYSICIAN KNOWLEDGE AND EXPERIENCE
The choice of techn i q ue depends on the knowledge and expe rience of the physician, as well as the l i m i tations of the patient.
Introduction
553
When a patient has a diagnosable somatic dysfunction i n the cervical region, you have many treatment options. Some may be contraindicated, as illustrated by the case of a male septua genarian who was in the hospital for cardiac e1ectrophysiologic studies. He lost consciousness several times before admission when he turned his head. During provocative testing, his heart stopped beating for 6 seconds, until defibrillation was used to restart cardiac performance. Normally, one would think that use of strain/counterstrain techniques would be m uch easier on a patient than most other treatments. However, in this case, treat ment by strain/ counterstrain is contraindicated. Muscle energy, HVlA, or articulatory treatment would also be i nadvisable. Os teopathic diagnosis and treatment provide the alternatives of in direct segmental treatment or osteopathy i n the cranial field (with caution i n this case). Carefully consider your patient's l i m i tations, along with your own skill level, when choosi ng which technique to use. Clinical j udgment about "when to use what" is often d i ffi cult u ntil one acq ui res a certain body o f clinical experience. This is accompl ished largely by observing decisions made by other physicians.
of the i m pact of that procedu re on the total body. The body is constantly trying to maintain optimal homeostasis, using i ts self healing ability and self-regulatory mechanisms. By d i recting the osteopathic manipulation to a prime site, the body may be able to continue i mprovement. At the next visit, you can reevaluate body needs and administer further treatment as necessary. Begin ning physicians often hesitate to use manipulation on hospital patients. There i s the fear of treating an already debi li tated patient. Always bear in mind that a physician is expected not to use techniques that could hurt the hospital patient but to use common sense and cli n ical j udgment as to what the patient needs and is able to tolerate. Particularly i f you are working in a non-osteopathic i nstitution or with preceptors who learned only direct methods of treatment, there is the supposition on the part o f the preceptor that you would use H VLA without proper con s i deration. There may be many osteopathic techn iques; always discuss which techn i ques are best for the particular patient with the best risk:benefit ratio for treatment. The verbal ization of osteopathic manipulative treatment is al ways l i m i ted i n scope. We attempt to put i n to words an experience that i ncludes:
TECHNIQUE VERSUS TREATMENT
Palpatory assessment Other tactile and proprioceptive input Integration of those data o n a n onverbal level Kinesthetic response through our hands and/or other partS of the anatomy
Another problem is making the j u m p between performing a tech nique and doing an osteopathic treatment. Osteopathic manip ulation can be reduced i n scope to the point where i t appears to be a series of specific treatments for specific problems. If it is carried out in this fashion, however, it loses its identity as os teopathic manipulation and becomes merely manual medici ne. The term manual medicine i mplies a form of treatment applied by the hands. The term osteopathic manipulation indicates more than that; it indicates that the physician is applying the four basic principles of osteopathic philosophy. One of these principles is that the body is a unit. The true osteopathic approach cannot be broken down i nto isolated procedures specific for particular com plaints; the osteopathic approach treats the patient as a whole. It is often said that when you see an osteopathic physician for treatment of a low back problem, the doctor might check your feet, your knees, and your neck. The goal of osteopathic treatment includes consideration of the entire person, not a spe cific dysfunctional muscle. Though i ts success helps the patient overcome the dysfu nction or disease, the osteopathic treatment is performed to support the patient, in whatever way is indicated. That is the osteopathic ideal. Realistically, there are many times in medical practice where the dictates of time, resources, and energy d i rect you to apply this i deal i n l i m i ted form. The effects of applyi ng specific procedures to a specific dysfunction have far less profound effects than a total treatment. The de gree to which you apply osteopathic philosophy is determined by the degree to which you are practicing osteopathy. To offer an analogy, an engine sometimes needs an overhaul but sometimes only a minor adjustment or a si ngle part. I n the same way, time constraints may ind icate that a specific p rocedure should be pro vided today, with a more thorough treatment in the scheduled follow-up visit. A s ingle procedure that treats the body's needs may be preferable to no treatment at all, or to merely writing a prescription to treat the disease. At no time should you lose sight
We do all of this based o n cognitive knowledge. We do it to change the motion characteristics, fluid Aow patterns, and sensorimotor responses of our patients. It is not always possible to verbalize everything we do, partially because so many thi ngs happen s i multaneously. This makes it d i fficu lt to adequately de scribe each factor. Proprioception is d i fficult to describe, because the feel i n g of where one is in space is u nique to each individ ual. Because language is l inear and sequential, the description of two synchronous events m ight be perceived in a sequenced linear fashion. Because most mental processing is on a nonverbal level, it is often d i fficu l t to describe portions o f it at all. Korr ( 1) de scribed the experience of diagnosis and treatment as a nonverbal dialogue between the osteopathic physician and the patient.
ART OF OSTEOPATHIC MEDICINE
Osteopathic manipulative diagnosis and treatment are part of a complex process i nvolving three domains: Affective Cognitive Psychomotor The physician must have enough interaction with the patient to achieve relaxation and trust. The physician's brain m ust receive proper palpatory, visual, and auditory i n put, which is processed through previously gained cognitive knowledge. Reacting to this i n put, the physician's processing and kinesthetic output take place in a real-time, ongoing fashion. This all occurs s i multaneously, i n many forms of treatment, without stopping.
554
VII. Osteopathic Considerations in Palpator] Diagnosis and Manipulative Treatment
The an of med icine is not snicdy Faa-oriented. From initial observation and Facts, a diagnosis may appear accurate, bur fur ther observation can show otherwise. A diagnosis may be accurate For a l i m i ted time, aFter which diFFerent characteristics prevail. Pa tience and persistence help you adapt, accepting an i n medici ne, as well as science. Learning manual medicine skills is not l ike learning facts of biochem istry. Only a small ponion of the data can be grasped by memorization of facts. As with any psychomo tor skill, seeing or doing something once is only a begi n n ing. Repeated practice of the technique is necessary to gain ski l l . DiFferent patients also respond i n d ifferent ways t o t h e same tech nique. An individ ual also has a unique response to different techn ique types. Each practitioner becomes pan of this h uman equation and is also u n ique. The way you are taught a skill during trai ning may be d iFferent than the way you finally employ that ski l l . As you practice, you master the skill. An old story is told about an education professor who was approached by a teacher. '' I've taught second grade for 20 years," she told the professor, who repl ied, "Have you really taught second grade 20 years? Or have you taught 1 year 20 times'" Attenrion to variations in i n put From patienrs, as well as following the results of research, leads to constant refinement in skills. Merely learn ing treatmenr protocols and applying them in the same fashion never produces improvement. The human being who is you r patient is both your school and one of your teachers. In a simplistic way, each osteopathic techn iq ue system could probably be assigned to deal better with certain types of physi cal ailmen ts. However, this analogy ignores the complex h uman Factor. Physicians who use one type For all problems may have selected it because it is the one with which they are most com fonable or at which they are most adept. Their practices may be self-selecting for patients who benefit From what they do, with others leaving to find help elsewhere. A physician practicing the highest Form of osteopathy is one who uses the approach, method, tech niques, or plan that best matches the patient asking for help. I F the indicated osteopathic manipulative treatmenr is HVlA, that becomes the h ighest form of treatmenr For that patient. If i t is osteopathy in t h e cranial field, then that is t h e o n e that is most appropriate. Some may feel that OMT is si ngularly eFfective For a wide range of clin ical problems. Others are somewhat skeptical , often because they have not seen a patient who presented to a physician with a cl in ical problem. Some patients, oFten those with problems associated with mo tion loss from a non-recurring physical force or trauma, respond im mediately and d ramatically. Some resolutions take longer, as the body req u i res time to respond; heal ing takes t i me. Observe the eFfects of watering a brown lawn. Immediately aFter watering, the lawn is still brown, but it turns green with time. Sometimes somatic dysfunction is secondary to postural, me chan ical , or visceral disorders. I n these cases, 0 MT provides tem porary relieF, but the somatic dysfunction tends to return because rhe cause is still present. A psychic or emotional component is someti mes the major cause. These patients do nOt get better unril the emotional component is resolved. In some cases, OMT is used to provide mainrenance treat ment. The term mai ntenance is prejudicial, because i nsurance companies will nor pay for mai ntenance, even though this treat-
ment enables better function and qual i ty of liFe. The treatment is indicated and is proper. On occasion, patients j ust do not get bener despite rhe best efforts of the physician. The physician m ust constantly reexam i n e such cases, analyzing the data to see if a diFferent approach or type of treatment would be more efFective. The only way to know whar O MT does is to try it and gain cli nical experience by fol lowing the parients. Remember as you use this approach that you are promoting the eFficiency of natural Function in you r pa tienrs, enabli ng the h uman organism to function at its individual optimal level.
ANATOMY
To diagnose and treat a patient eFficiently and eFFectively, you m ust know anatomy. There are several ways to know anatomy. One way is by being able to locate and name every structure. Another is by being able to successfully palpate and mentally i n terpret the response of tissues from the proprioceptive input From your hands. All osteopathic techniques produce functional and physiologic changes in tissue, in the following ways: Lengthening Shortening I ncrease i n tone i n some m uscles Corresponding decrease in tone of their antagonists Increase in motion in one or more directions Decrease in other d i rections The effects of osteopathic manipularion go beyond their ob vious i m pact on the neuromusculoskeletal system, such as a de crease 111 pain or an increase in motion. Profound changes are seen Ill: Blood and lymphatic Auid Aow Neu ral sysrem Endocrine system Respi ration Au tonom ic balance I m p rovement of homeostatic mechanisms increases func tional efficiency of the tissues, enhances q ualiry of liFe, and in creases resistance to i l lness and i n j u ry.
ASPECTS OF LEARNING
When learning and practicing, remove as many distractions from the situation as possible. Ensure thar neither your own needs nor the environment distracts you. If you are trai ning the sense of touch, remove the distraction of sight and sound by closing your eyes and Focusing on palpation i n a quiet environment. IF you are Focusing on the need to go to the lavatory, you are not able to concentrate on sensory in put related to the patient, because you r brai n is directing attention to your own inrernal sensations. Hunger or rhirst can be tremendously distracting. An emotional upset may make it temporarily impossible For you to eFFectively receive i nput unless you can put the distraction out of your mind.
introduction
Thi nking about how much time you are taking or how much you have [Q do may block i mmediate proprioceptive i nterpretations. You may be learn ing a new field in an area rotally different from the cognitive skills at which you have excelled. Be patient with yourself and realize that your learning may not proceed at the same pace as the learn i ng of others. Sometimes it may be rapid; other times, slow. Continuous progress should be you r goal, but be patient with yourself as you learn this challenging integrative process. Is any one method or type of activation the most profound form of manipulative treatment in osteopathy? Which one gets the best results from the body? Is d i rect treatment superior ro indirect treatment? At times, l istening [Q one physician or a special interest group of physicians makes it seem as if this were so. However, the original q uestion makes as much sense as asking if the kn ife, fork, or spoon is the superior instrument for dining. Each has its place. Each has its function, [Q which the others are less well adapted. Can you use a kn ife [Q pick up peas? Certainly.
555
However, most o f us prefer one of t h e other instruments, because they are bener adapted [Q that function.
CONCLUSION
An osteopath ic physician looks at the study of osteopathic diag nosis and treatment as a lifelong d iscovery process that combines an and science. Your understanding and application of these prin ciples will, because of your commitment and receptivity ro new input, conti n ue ro develop and refine over your professional life.
REFERENCES 1. Korr
1M.
Somatic dysfunction, osteopathic manipul ative treatment and
the nervous system: a few facts, theories, many questions. J Am
Assoc.
1986;86:1 09-114.
Osteopath
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Part A. Overview: Evaluation and Management
PALPATORY SKILLS AND EXERCISES FOR DEVELOPING THE SENSE OF TOUCH ROBERT E. KAPPLER
KEY CONCEPTS • • •
• • • • • • • • • • •
An of palpation, including practice using hands and fingers Identification of dominant eye and hand in palpatory technique Present ptogressive exercises for developing palpatory skil ls to refine and i mprove begi n ning practitioners' sense of touch Perception of tactile differences i n tissue texture and motion Perception on palpation of layers and structures of the body Palpation of thoracic and l u mbar areas w i th passive Aexion Palpation for somatic dysfunction in cervical, thoracic, lumbar, and sacroiliac areas Development of finely tuned sensory perception and mental filters i n palpatory skill Motion perception Palpation of acute and chronic somatic dysfunction Perception of tactile d ifferences in tissue texture and motion Perception on palpation of layers and structures of the body Palpation of thoracic and lumbar areas with passive Aexion Palpation for somatic dysfunction in cervical, thoracic, lumbar and sacroiliac areas
This chapter in troduces the art of palpation. Being efficient and accurate with palpation is an asset for any physician regardless of specialization . Palpation is especially i m ponant to osteopath ic manipulative diagnosis and treatment because it is fundamental to functional and structural evaluation . Two of the essentials of effective practice are palpatory skill in locating and defi ning so matic dysfunctions and manipulative skill to appropriately treat them. T he Glossary oJOsteopathic Terminology ( I ) defines palpa tion as the application of variable man ual pressure to the surface of the body for the purpose of determining the shape, size, con-
sistency, pOSitIO n , in herent motiliry, and health of the tissues beneath. Another definition ( DiGiovan na E. New York Col lege of Osteopathic Medicine. opr course syllabus, 1992) putS it another way: Palpation consists of lighdy placing the hands or fi ngers on the patient's body to discover changes in rhe normal condition of soft tissues, bones, or organs beneath the su rface of the skin, as well as the s kin itself. Still another definition incl udes rhe descriptive words "gentle handling," an im portant point to remember when applying this skill. Skill in recognizing normal tissue movements along with changes rhat signal dysfu nction or disease can be acquired wirh contin ued practice.
ART OF PALPATION
The art of palpation requires discipline, rime, parience, and prac rice. To be most effective and productive, palpatory fi ndings must be correlated with knowledge of functional anatomy, physiology, and pathophysiology. It is m uch easier to identify frank parho logic stares (
558
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
PALPATION WITH FINGERS AND HANDS
Palpation wirh rhe fingers and hands provides sensory informa tion (Frymann V. Syllabus for workshop on palparion, 1990) rhar the brain interprers as: Tem perature Texture Surface h umidiry Elasticity Turgor Tissue tension Thickness Shape Irri rabiliry Morion
analysis and interpretation. This last step translares palpatory findings into meaningful anatom ic, physiologic, or pathologic states ( Frymann V. Syllabus for workshop on palparion, 1990). Fami liarity with osteopathic terminology permits description of palpatory findings in consistent rerms. Effective palpatory technique cannot be learned by obser vation. Watch i ng another physician palpate a parient indicates where the hands are placed but gives l i ttle or no indicarion of the feel of tissues being pal pared. Many individuals have a dom inant hand with which rhey prefer to palpate or motion test. This may or may not be the hand with which they write. Recognition of a dominant hand will allow the individual to develop a compensatory mechanism to obtain accurate information when using both hands. Exercise 2: The Dominant Hand
LEARNING PALPATORY TECHNIQUE
To accomplish rhis rask, ir is necessary to teach rhe fingers to feel, rhink, see, and know. One feels through rhe pal paring fingers on the parient; one sees rhe strucrures under the palpating fin gers through a visual image based on knowledge of anatomy; one thinks what is normal or abnormal; and one knows wirh a con fidence acqu i red by practice thar whar is felr is real and accurate. Through complex peripheral and central processing, the smal lest sensory perception can be amplified to rhe point of con scious recogni tion and analysis.
Purpose The purpose of this exercise is to derermine the dominant hand. It is believed that when a person does not consciously think about it, he or she will put his or her dominant hand on top when the hands are clasped.
Position This exercise can be done in a sranding or sitting position.
Procedure Exercise 1: Palpating Inanimate Objects
Goal To perceive slight tacrile differences of tissue rexture and motion. Exercises on inani mate objects serve to sharpen tacrile concen tration and attention. Concentration is essential. Close rhe eyes to eliminate extraneous stim uli. Pay attention to kinesthetic sen sations received rhrough rhe fingers.
Procedure I.
II.
III.
IV.
Put a m ixture of coins in a pocket or purse. By touch, distin guish between heads and tails , and between pennies, di mes, nickels, and quarters. I dentify date l ines on the coins. Locate a hai r that has been placed under a sheet of paper; attempt to estimate its length . Add sheers of paper until you can no longer palpate rhe hair. Palpate several types of h uman bones. I dentify the bones and their component parts, envisioning rhe tissue that normally surrounds them. Palpate a h uman bone and a solid plastic imitarion of rhe same bone. I dent i fy rhe characreristics of the h uman bone that distinguish it from rhe replica.
M irchell (2) calls palpation a two-way communication system in which the patient's rissues react to rhe presence of the palpa tor's hand. This is more l i kely to occur when palparion has been practiced over a period of time. Th ree steps define the process. The fi rst is detection, the sec ond is internal amplification or magnification, and the third is
Without consciously thinking about ir, clasp your hand together in front of you, with one hand on top of the other.
Results The hand that is on top will most likely be your dominant hand. It is also believed that palpatory results are more consistent if the examiner has the dominant eye over the area that is being palpated. For example, if one hand is stronger rhan the other, practice in applying equal pressure over equivalent structures can result in accurate i nterpretarion of such manual informarion. Interpretation of dominant and nondominant proprioceptive feedback from each hand is also a response that the individual can adjust. Exercise 3: The Dominant Eye
Purpose The purpose of this exercise is to determine the dominant eye. Some believe thar palpation and the i nterpretation of palpatory findings are more accurate if palpation is performed with the dominant eye over the area being palpated.
Position This exercise can be performed standing or sitting with a distant clock or visible object to look at.
38. PaLpatory SkiLLs and Exercises for Developing the Sense of Touch
5 59
Some physicians find that variations in skin temperature are best perceived by the dorsum of the hand, especially the dorsum of the m iddle phalanges of fi ngers two, th ree, and four; others use the palmar surface. Try both and see which is more effective for you. The coordi nated use of the palms and the fi ngers around an object is best suited for obtaining a stereognostic sense of co ntour (3) . Flexibil ity o f the j o i nts o f the elbows, wrists, hands, and fi n gers is i m portant. Relaxation is also impo rtant t o eliminate any muscle tension that would block perception. Strength of hands and fi ngers can be i ncreased by using a fi nger exerciser, squeezing a ball , or play i ng a m usical i nstrument that req ui res fi ngering. Because the hands are so i m portant to a physician, they should be carefully protected and cared for. They are sensitive diagnostic II1struments . Light touch is thought b y many persons experienced in pal pation to be the most useful and easy to use. Very l ight touch, or l ight touch, consists of lay i ng the hands passively on the skin or moving the hands l ightly over the skin . Such light touch can be used to determine skin tem perature, texture, moistness, oiliness, resistance, tone, and elastici ty. It may be possible to determ ine skin temperature sensation by passing the hand j ust above the skin. Fi rmer p ressure com m u n icates with the deeper cutaneous layers and fascial sheaths. It explores superficial muscles to de termi n e their tone and mob i l i ty. Firm pressure and com pression explore deeper m uscle, fascia, and bony relationships. Exercise 4: Layer Palpation
Goal The goal of this exercise is to palpate your own tissues and con cen t rate and perceive various layers and structures of the body by varying the pressure of palpation.
Position FIGURE 38.1. Right eye dominance. A: Both eyes open. B: Right eye closed; left eye open. C: Left eye closed; right eye open. (Modified from WA Kuchera. with permission.)
Procedure Look at the distant object with both eyes open ( Fig. 38. 1 ) . II. Extend you r domi nant hand and make a circle with your thumb and i ndex fi nger that encircles your view of the distan t object. III. Now, close one eye, then open it and close the other eye. I.
Result The eye that saw the object enci rcled with the fingers of your domi nant hand is generally your dominan t eye (2). Recognition of domi nance, if it exists, and development of a compensatory mechanism is the main issue here; in ti me, apparent palpatory ambidexterity may result. There are more touch (ki nesthetic) nerve endi ngs i n the pads of the fingers than elsewhere in the hand. It is generally agreed that the thumb and/or the fi rst twO fi nger pads, rather than the fi nger tips, are the most sensitive part of the hand to train and use for pal pation (Frymann V Syllabus for workshop on palpation, 1990) .
The position for this exercise is seated comfortably beside a table with your nondominant arm resting on the table.
Procedure Close you r eyes and relax. Concentrate your attention th rough the palpating fingers of your dominant hand. II. Lightly palpate the dorsum of the nondo m i nant hand using the fi ngers of your dominant hand. Scarcely touch ing the surface, feel the contour of the hand. I I I . Test palpation with the dorsal and pal mar aspects of the palpating fi ngers to determine which is most sensitive to tem pera tLI reo IV. Using very l ight touch, palpate and describe skin texture, moisture, and th ickness. v. Gently pinch the skin on the back of the hand. Elevate it and release it. How long did i t take for the skin to resume i ts normal configuration? V I. Evaluate skin drag on both the palm and dorsum of the hand. Skin d rag is the estimation of the amount of resistance experienced when the pads of the fi ngers are l ightly applied and moved (dragged) over the skin su rface. On which aspect of the hand do the palpating fingers move I.
560
VII. Osteopathic Considerations in Palpatory Diagnosis and ManipuLative Treatment
most eas i ly? Why? Describe any increase in skin drag that is due to excessive d ryness, sl ight perspiration, or edema. Describe any decrease in drag resu lting from excessive perspi ration, oil iness, or atrophy. V I I. Locate the veins and note the i r size and texture. Make a fist several ti mes to engorge the veins and then describe the differences observed. V I I I . Locate the radial artery and describe the differences berween it and a vein. I X . I ncrease the contact berween your palpating fingers and the skin of your hand sc that you create a shearing stress in the subcutaneous tissues. Shearing in this context refers to movement of tissues berween layers. Note that w i th this palpation one can shear only so far before the palpating fingers slide on the skin. Shear across the hand in various directions describing what you feel. Does the skin move equally and easily in all d i rections? x. Palpate the extensor tendon of the ring finger. Place rwo fin gers along the length of the tendon ; Aex the ring finger, and palpate the sense of the l inear movement along the tendon. X I . Palpate the tendon of the biceps at the elbow. How does i t feel? It should be ropelike, smooth, a n d firm. X I I . Place the thumb and index finger of the palpating hand on either side of the m id-phalangeal articulation of a finger on the opposite hand. Note the q uality and range of various elements du ring fle xion and extension. Now l ighten your touch while performing the same movements. Notice how little contact is needed to d istingu ish Aexion and extension. X I I I . Place your palpating fingers on the anterior surface of the proximal third of your other forearm. Using slightly more pressure than that used for skin, palpate the muscles used to Aex the fingers. Now maintain palpatory contact during Aexion of the m iddle finger. Describe the feel of these flexor m uscles and fascia d uring the maneuver. When you are examining a patient, tell the patient in gen eral terms about the procedure as it goes along. This is especially i m portant if signi ficant tenderness might be elicited during deep palpation. Take the necessary ti me, moving gently and deliber ately. I nitially it is common to apply too m uch pressure in an attempt to feel the tissue. Avoid poking, prodding, tickling, or stirring the tissue. These actions can cause reAex irri tation (3). Louisa Burns, a noted early osteopathic researcher, made the following suggestions to those beginning to develop palpatory skills : Palpate t h e objects with t h e lightest possible touch, scarcely touching the surface Be aware of surface elevations and temperature differences Using sl ightly more contact, palpate the surface Try to ascertain the q ualities or characteristics of the substance of the object Describe perceptions as accurately as possible Exerc ise 5: P alp ate Yo u r P a rtner's Fo rea rm
Goal The goal of this exercise is to determine the characteristics of different structu res in the forearm of another person.
Position You are seated comfortably, facing your partner, who is seated, facing you from across a narrow table.
Procedure Grasp your partner's left forearm with your nondominant hand. I I . Lightly place the palm and fingers of your dominant hand over the dorsal forearm of your partner, just distal to the elbow. Close your eyes, relax, and concentrate your attention through the palmar surface of your fingers. I I I . Without moving your hand, think skin. Try to perceive and describe skin temperature, texture, thickness, and moisture. IV. Next, compare the dorsal and palmar aspects of the fore arm, and describe the differences. Which aspect is smoother? Thicker? Warmer? Drier? v. Now, with a slightly firmer touch, concentrate on the second layer, the subcutaneous fascia. Gently move the skin of the forearm longitudinally and horizontally. How thick is it? How loose? Many of the tissue texture changes associated with somatic dysfunction are within this layer. V I . Gently and slowly increase the depth of touch until you feel the deep fascial layer that forms a sheath around the underly ing structures. Think deep fascia. Is it smooth? Continuous? Fi rm? V I I. While palpating the deep fascial layer; slowly move the hand horizontally across the forearm to identify areas of thick ening that form fascial compartments berween bundles of m uscles. Identifying enveloping layers of deep fascia is of ten helpful in separating one m uscle from another; use it to work with even deeper structu res. V I I I . Palpating through the deep fascia, concentrate on the under lying m uscle. Is it soft and compliant? How is i ts elasticity? Pay attention to individual muscle fibers and the directions in which they run. I X . Have your partner slowly open and close their hand as you note the quality and range of movement created by the con tracting and relaxing m uscle. Describe the d ifference. Pal pate the forearm m uscles as the hand is clenched. This sen sation s i mulates the feel of the most common tissue texture abnormality at the level of muscle or in areas of somatic dysfunction. x . Stil l palpating at the level of muscle, move your hand slowly down your partner's forearm until you feel the musculo tendinous j unction, an area or region where the muscle is vulnerable to inj ury. X I . Move past the musculotendinous junction toward the wrist. Note the transition from m uscle to musculotendinous j unc tion to the smooth, round, fi rm feel of tendons. X I I . Follow the tendons distally until you feel a structure that binds them at the wrist. This is the transverse carpal lig ament (Aexor retinaculum) and palmar carpal ligament (a th ickening of the deeper anterolateral fascia) . Note fiber di rection, t hickness, and firmness. How does it feel in compar ison with the tendon? Compare the palpatory sensation over this area with that over tendons that are more superficially located. I.
38. PaLpatory SkiLLs and Exercises for DeveLoping the Sense of Touch
X I I I.
XIV.
Now place your index fi nger over the proximal radiohumeral joint at the di mple of the elbow. Place your thumb opposite your i ndex finger, on the ventral side over the lateral side of the humeroulnar attachments. You should now be palpating the head of the radius. Describe the characteristics. Compare the feel of this living bone with a plastic model or with your memory of bone from a cadaver. Move your thumb and index fi nger proximally until you locate the joint space. Your fi nger and thumb fal l i n to it. You should not be able to feel the joint capsule. The joint capsule is not palpable because palpable joint capsules signal pathologic changes.
Palpatory skill involves more than a mechanism for fi nely tuned sensory perception. A more significant component is to be able to focus on the mass of i nformation bei ng petceived, paying close attention to those qualities associated with tissue texture abnormal ity, and bypassi ng many of the other palpatory clues not relevant at the time. These skills m ight be enhanced by trying to palpate a hair through several pages of a telephone d i rectory. Exercise 6: Palpat o ry Sensiti vity
Goal The goal of this exercise is to determine and i mprove your sensory awareness.
Position For this exercise, sit comfortably i n front of a table with a phone book and objects of various thicknesses, includi ng a human hair.
Procedure I.
II.
Starting with the thickest object, place them, one at a time, under a page i n the phone book and see i f you can palpate their edges and dimensions. Then add pages and palpate unt i l you can no longer determine the objects' di mensions. How many pages were between your fi ngers and each object before you could no longer palpate it? Can you palpate the human hai r through a si ngle page from the phone book?
Palpatory sensitivity involves a process of developing mental fi l ters. Consider an analogy i n music, where the orchestra con ductor focuses on the violins. The conductor is aware of the entire orchestra playing, bur is d iverting attention to a specific portion ofsound that he or she perceives. The brain can not process every thing at once. By concentrating only on the portion you want, i t becomes easy and fast t o detect areas of s ign ificant tissue texture abnormality. In a comparison of student musculoskeletal exami nations with experienced examiners, Kappler et al. (4) observed that the experienced examiners recorded fewer fi n d ings than stu dent examiners, but the experienced examiner's findings were more sign i ficant. This shows that experienced physicians apply a filtering process to their palpatory data, rejecting insignificant findings without being consciously aware that they are doing this. The student is overwhelmed with the mass of palpatory data and has not yet developed this filtering process to reduce the data to a manageable component.
561
MOTION PERCEP TION
I f any motion is present, describe the sensations transmi tted through the fi n gers. Also, est imate the weight of objects, the amount of pressure needed to move them, and the resistance or force exerted against your pressure. Perception of motion is an essential component of palpation. A major d i fference i n palpation of l iving tissue is this sensed motion. Motion of the body is described as passive, active, and inherent ( 5 ) . Passive motion is brought abour b y t h e physician; it i s move ment done to the subject. Active motion is performed by the sub ject; it is deliberate, conscious m uscular activity. I n herent motion is activity unconsciously generated w i th i n the body (Goodridge ]. M i ch igan State Universi ty Col lege of Osteopath ic Medicine. Biomechanics syllabus, ] 986), such as respiratory motion or peri stalsis. I nherent motiol� is postulated to occur in any of several ways: Biochem ically, at the cellular or subcellular level As parr of m u ltiple electrical patterns As a combination of a n u m ber o f circulatory and electrical patterns As some periodic pattern not yet u n derstood Experts agree that individuals can perceive tissue movement as m i n ute as 1 mm (6) . With practice and patience, i nherent motion may be palpated. By varying the palpation pressure, successive layers o f tissue can be palpated. In palpating superficial tissue, use the l ightest effective touch . To palpate successively deeper layers, apply o n ly as m uch addi tional pressure as necessary. As a general rule, th is means palpating to the depth of the tissue o r structure to be ex ami ned, that is, down to but not through the structure being exa m i ned. The use of various depths of touch differs from physi cian to physician, usually depending on the model of diagnosis and treatment chosen. Exerc ise 7 : Palpat ing Spina l Mot ion and Pa ra vertebra l Tiss ues
Goal The goals of this exercise are to learn how to palpate l iving tis sue in the classroom s ituation with an i nstructor available to demonstrate and i n terpret as needed and to be able to palpate the thoracic and lumbar spinal areas, testing for and finding any regions with relative resistance of the vertebrae and their spinous processes when passive Aexion is i n troduced.
Position Your partner sits on the table and you stand beh ind your partner.
Procedure I.
Using your fi nger pads, place the fi rst three fi ngers of your dominant hand between the spinous processes of Tl and T2, T2 and T3, and T3 and T4. Remember to use the pads of your fi n gers. Place your other hand on the top of your partner's head.
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VIII.
bral soft tissues. Then use deeper pressure, but less pressure than that req u i red to palpate bone. You may notice that in some areas, tissues compress more easily while in others, there is more resistance. Signi ficant resistance indicates an area of tissue texture abnormal i ty (TTA) ( I ) , which bears further i nvestigation. Lightly palpate the skin and subcutaneous tissue over the resistant si te. This helps you identify the outer limits of tissue texture i nvolved.
SOMATIC DYSFUNCTION PALPATION
FIGURE 38.2. Palpating upper thoracic flexion-extension.
Locate the spinous processes and int e rspi nous l igaments, noting how they feel . Compare differences between the feel of the bone and the feel of the ligament. I I I . Passively Rex the head and neck while sensing for increasing tension of the i nterspi nous l igaments. Note: One spi nous process may move more easily than another ( Fig. 38.2). IV. Usi ng the fi ngers o f both hands, palpate for temperature d i f ferences along the paravertebral thoracic and lumbar spine. Use either the palmar or dorsal surface of your fingers, de pending on which you find to be more sensitive. v. Using both hands simul taneously, stroke the back fro m C7 to L5. Which areas are warmer? Try to find a segment within the thoracic area that is ei ther warmer or cooler than another segment. Compare left with right sides, and superior with i n ferior. Stroking of t h is type is useful in identi fyi n g changes in contour, as well as identifying areas ofedema and i ncreased tissue tension. V I . Palpate for moisture d i fferences, noting stickiness, dryness, wetness, waxiness, and sl ipperiness. V I I . Proceed ing from T2 to L5, ligh tly compress the paraverteII.
The osteopathic physician uses all palpatory skills to diagnose somatic dysfunction. The defi n i tion of somatic dysfunction is i m paired or altered function of related com ponents of the somatic (body framework) system: skeletal, arthrodial, and myofascial structures, and related vascular, lymphatic, and neu ral elements ( I ). The osteopathic diagnostic criteria for somatic dysfunction are discerned through palpation and can be conven iently recal led through the m nemonic TART. These letters stand for: Tissue texture abnormali ties A: Asymmetry (static, motion, tonici ty, turgor, color, temperature) R: Restriction of motion T: Tenderness (in the area of the abnormal ity) T:
By grouping these palpatory fi ndings according to [he charac teristics of acute and ch ronic i n Rammation, somatic dysfu nction can be further classified, as shown in Table 38. 1 .
AC UTE SOMATIC DYSFUNCTION
Palpate with l ight to somewhat fi rmer touch. Several types of change may be present; biochemically mediated tissue texture changes often predomi nate. First, the skin over the somatic dys function may feel warmer. The skin and deeper tissues directly
TA BLE 38. 1 . CLASSIFICAT ION OF SOMATIC DYSFUNCTION Chronic
Acute H istory: recent; often an injury Pain: acute pain. severe. cutting. sharp Vascu lar: vessels i n j u red. release of endogenous peptides chemical vasod i lation. i nflammation Skin: warm. mo ist. red. infla med (via vasc u l a r and chemical changes) Sympathetics: systemica l ly i ncreased sympathetic activity but local effect overpowered by bradykinins so there is local vasod i l ation due to chemical effect Musculature: local i ncrease in m uscle tone. muscle contraction. spasm. i ncreased tone of the muscle spindle Mobil ity: range often normal. q u a l ity is s l u g g ish Tissues: boggy edema. acute congestion. flu ids from vessels and from chemical react ions i n tissues Adnexa: moist skin. no trophic changes Visceral: m i n imal somatovisceral effects =
(From Kuchera
WA.
Kuchera
M l. Osteopathic Principles in Practice.
History: long-sta nding Pain: d u l l . achy; paresthesias (craw l i ng. itching. burni ng, gnawing) Vacu lar: vesse ls constricted because of sympathetic tone S k i n : cool. pale (via chronic sympathetic vascu lar tone i ncrease) Sympathetics: has vasoconstriction due to hypersympathetic tone; reg ional sympathetic hyperactivity; systemic sympathetic tone may be reduced toward normal Musculature: decreased muscle tone. flaccid. mushy. l i m ited range of motion because of contracture Mobil ity: l i mited range. with normal qual ity i n the motion that remains Tissues: chronic congestion. doughy. stringy. fibrotic rOf f. thi kened, increased resistance. contracted. contractu res Adnexa: p i m p l es. scaly. d ry. fol l iculitis. pigmentation (trophic changes) Viscera l : somatovisceral effects are common
2 n d ed. C o l umbus.
OH
Greyden Press;
1 994:25.
with permission.)
38. PaLpatory SkiLLs and Exercises for DeveLoping the Sense of Touch
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over the area of somatic dysfu nction may be tender. The skin and subcutaneous tissues may also feel tense and less mobile. Super ficial muscle tension may be detected through a slight increase in palpatory pressure. F i nally, there may be ful lness caused by edema. Deep palpation, defined as pressure sufficient to contact the periaxial soft tissues o f the spinal column, can also identify several types of change. Pain or tenderness over acute areas of dysfunction is common. It is also common to find swelling in the deep peri articular tissues, giving the area a soggy, swollen texture. Muscles directly concerned w i th the affected vertebral segment demon strate a doughy tightness or hypertonicity. Finally, there are per ceptible changes in interosseous relations that are best evaluated by motion testing a vertebral unit. This reveals restricted motion in one d i rection and a preference or freedom of movement i n the other direction. FIGURE 38.3. Assessing cervical spine side-bending translation.
CHRONIC SOMATIC DYSFUNCTION
Procedure
Palpation with l ight to sl ightly more fi r m touch may elicit evi dellCe ofseveral types of chronic tissue changes. The skin may be somewhat immobile and tense in the presence of chronic fibrotic changes beneath the skin. These changes reduce the skin's elas ticity. Temperature changes in the skin may be present or absent. Usually the skin is cool to touch. The muscles have a hard, ropy, and non resil ient texture as a result of fibrotic changes. When the dysfunction is chronic, it may actually have lost i ts tone and not feel fibrotic. The amount of tenderness is less than that found in acute dysfunction, often described as a dull, u ncomfortable, or burning pai n . In the absence o f i rritation, infla mmation may subside and there may be little or no tenderness. Deeper palpation reveals additional changes. Most notably, there is a decreased range of motion berween the vertebral seg ments. As stated before, often there is little or no tenderness. I t i s helpful t o evaluate mobi l i ty changes and i nterosseous changes together, usi ng each to check the other. At this level, too, fibrotic changes replace edema. When a chronic somatic dysfunction has reached an advanced stage, fibrotic changes result i n dysfu nction of the surrounding fascias, musculature, and l igaments, some times to a point of producing contractures and joint ankylosis.
Cradle the patient's occiput in your palms. This position frees the fingers for check i ng cervical soft tissue and vertebral me chanics. 1 1 . Lightly palpate the posterior cervical skin. 1 f you identify an area of localized tissue tension, palpate for swelli ng, deep m uscle tension, and i n terosseous mob i l i ty. 111 . Straighten the cervical curve by passively flex ing the neck. Place the pads of the fi ngers of one hand berween the spi nous processes and check for separation o f the spinous processes. IV. Reverse the procedure w i th passive backward bend ing of the head and neck. What happens to the spi nous processes? v. Assess side-bending and translational movements ( 1 ) . With the pads of the fingers on either side of the articular col umn and d i rectly across fro m each other, assess side-bending by translating to the right, then left ( Fig. 38.3). V I . Using deep p ressure over the posterolateral margin of the ar ticular column, translate anteriorly (both righ t and left sides), checking for spontaneous vertebral rotation capability.
Exercise 8 : Pa l pation for Somati c Dysfun ction
Goal ( Review the types of tissue changes that are encountered i n pa tients with vertebral somatic dysfunction before undertaking the final exercises i n this section.) The goal of this exercise is to be able to palpate each area of the spine and detect tissue changes that may be perceived i n areas of somatic dysfunction. These ex ercises assume a classroom si tuation, i n which partners take turns acting as the patient.
I.
Th o ra ci c Region
Position Stand behind your seated patien t. The pads of the thumbs are most effective for palpation in this exercise.
Procedure I.
II.
III.
Cervi ca l Region
Position Stand or sit at [he head of the table behind you r supine patient.
IV.
Lightly stroke the skin over the thoracic area, noting any temperature difference. For this part of the exercise, you may find that the dorsal surfaces of the middle phalanges are more sensitive to temperature change (Fig. 38.4). With a slightly deeper touch , palpate the subcutaneous and myofascial structures, noting soft tissue changes, such as m us cle tension and swelling. Increase the depth of touch until you can feel the periarticular tissue changes; note the deeper tissue characteristics. Examine the facets and transverse processes, one side at a time and together, along with the spaces berween spi nous processes.
VIi. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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IV.
lational force to one transverse process, then test the other d i rection . Note differences in the mechanical response when the pa tient is seated and prone. Maxi mum spinal loads occur when seated; they are the least when supine.
Sa c roilia c Region
Position Stand to the side of your prone patient, at the level of the hi ps.
Procedure Palpate the entire gluteal area. The palm of the hand is useful for palpati ng gross m uscle changes. Ask the patient to extend the opposite h i p as you palpate the contraction of the gluteus max i m us m uscle. Compare the right and left sides. I I . Now assess the superficial tissues overlying and lateral to the superior and inferior poles of the sacroil iac joint , noting any tension in the gluteal m uscles. Ad j ust your depth of touch as needed to assess various tissue layers. The pads of the thu mbs are best used for this deep palpation, although other methods may be used (Fig. 38.6). I I I . Bilaterally check the posterior superior il iac spi nes fo r asym metry. Use the pads of each thumb, placed directly caudad to the posterior superior i l iac spi nes ( P S I S) and note their levels. The PSIS are called pure landmarks, because they can be affected o nly by the position of the innominates. The level of the PSIS is a clue to possible innominate rotation. Is one more cephalad or more caudad ( Fig. 38.7)? IV. Check depth of the sulcus berween the posterior surface of the P S I S of the ilium and the posterior surface of the sacrum. This sulcus depth is called a m i xed landmark, be cause its depth can be affected by the i n nom inate or the sacrum. v. To determine rotation of the sacrum, palpate deeply i n the sulci using the tips of the thumbs. [s the sacral base level, or is I.
FIGURE 38.4. Checking temperature using back of hand and fingers.
v. Check motion response d u ring passive Aexion, extension, ro tation, and side-bending of the thoracic area.
Lumba r Region
Position Stand hips.
ro
the side of your prone patient, at the level of the patient's
Procedure I.
II.
III.
Using light touch, palpate bilaterally for lumbar contour and any tissue texture abnormali ties. Systematically compress the tissues over the transverse processes until you feel bony resis tance. Test passive and active motion capabil ity o f ind ividual ver tebrae. I nd uce rotation by d i rect anterior pressu re over one transverse process while no pressure is on the contralateral side. Then test rotation to the opposite side ( Fig. 38 . 5 ) . I nduce side-bending to o n e side by applying lateral trans-
Test sulcus
Sulcus
depth here
Sacral base
Middle aXIs
.���..p-......- -
, I
r ILA
(anterior poste r i o r)
)
sacrotuberous l i ga m e n t FIGURE 38.5. Testi n g l u m ba r spine rotation.
FIGURE 38.6. Posterior pelvic landmarks. ( I l l ustration by WA Kuchera, with perm ission.)
38. Palpatory Skills and Exercises for Developing the Sense of Touch
565
These palpatory skills provide a method of obtaining practi cal experience in developing the art o f pal pation . There are many other exercises. In itially, palpation is practiced on a partner in the skills laboratory. During clin ical clerkships , one gains addi tional experience by exami n i n g attending physicians' patients. Ultimately, palpatory experience is gained from palpatory exam i nation o f the physician's own patients. The physician contin ues to learn and never stops gai ning experience. The preced ing section shows how to get started in the process of obtai n i ng palpatory data fro m the patient. Remember that developmen t of a h igh level of palpatory skill is an ongoing process, requ i ri ng patience and practice.
FIGURE 38.7. Checking level of the posterior superior i l iac spine (PSIS) with the patient prone.
one side more anterior or posterior than the other side? This is a pure land mark that i nd icates sacral base rotation. Check for rotation of the innominates by evaluating the anteroposterior levels of the psrs on both right and left. CONCLUSION
ACKNOWLEDGMENTS
Barbara Peterson collected the materials and Judith McPherson organized and assisted with the writing of this chapter.
REFERENCES I . The Glossary Review COlll m i rree of [he Educat ional Cou n c i l on OStCO pathic Principles. G lossary of Osteopathic Terminology. I n : D'Alonzo J r G E, ed. A OA Yearbook and Directory o/ Osteopathic Physicians. Chicago,
Position your dominant eye over the structure being palpated. Place thumbs or fi nger pads over the area to be palpated. To ensure greater accuracy, mentally transfer your thoughts to the i n terface of your hand with the patient's body. Realize that resil iency or resistance to motion can be sensed i n the i n i tial movement dur i n g motion testi ng. You can m iss these subtle fi nd ings and get hung up on gross motion restrictions, for exam ple, how far a vertebral joint or tissue moves rather than the q uality of the movement. Avoid these cOlll mon errors in palpation: Lack of concentration Too much pressure Excessive movement
I L: Amcrican Osteopathic Association; 2000. 2. M i tchell J r F. The t ra i n i n g and measurement of sensory l i teracy i n relation to osteopathic structural and pal patOry d i agnosis. J Am Osteopath Assoc. 1976;75 :881.
3. Kuchera WA, Kuchera ML. Pal pation of soft tissue. I n : Osteopathic Principles ill Practice, 2 n d ed. Col u mbus, O H : Greyden Press; 1 994: 1 12. 4 . Kappler RE, Larson N J , Kelso AF. A comparison of osteopath ic findi ngs on hospital ized patients obtained by trained student exami ners and expe rienced osteopath i c physicians. J Am Osteopath Assoc. 1 971 ;70( 10 ) : I 09 1 1 092. 5. Van Allen P, Sti nson J. The development of palpation. J Am Osteopath
Assoc. 1941 ;40(5): 207, 208. 6. Greenman PE. Principles o/Manua! Medicine, 2 n d ed. Bal t i more, M D: W i l l iams & W i l k i ns; 1996.
EXAMINATION AND DIAGNOSIS: AN INTRO DUCTION MICHAEL L. KUCHERA
THE OSTEOPATHIC EXAMINATION KEY CONCEPTS
An integrated osteopathic neuromusculoskeletal regional examination that links structure and function: Specifically identifies somatic dysfunction Provides somatic clues to internal or systemic disease • Expands the database for diagnosis and treatment •
•
Recognition of patterns of somatic dysfunction: Facilitates diagnosis of impending or underlying problems before there is subjective evidence of that primary diagnosis or disease process • Permits implementation of preventive education or action
•
Information from an integrated osteopathic examination used in a management program: Directs specific treatment of neuromusculoskeletal dysfunction, primary musculoskeletal overuse syndromes, trauma, strains, and sprains • Supports homeostatic mechanisms • Aids the patient's own body defenses in the fight against a systemic disorder
•
An osteopathic perspective provides unique insights into physical examination and the Formulation of a differential diagnosis. This orientation begins on the first day of anatomy class and continues throughout a liFetime of osteopathic practice. Osteopathy em phasizes the interrelationship between structure (anatomy) and Function (physiology), and this leads to physical examination skills that many consider to be second to none (1,2). Without specific knowledge of pertinent anatomy and physiology, the os teopathic approach could be very time-consuming. With focused knowledge, however, it is not only time efficient but also cost eFFective (3-5). A strong case can be made that the true diag nosis is reached more quickly, with Fewer unnecessary expensive tests and that disorders are identified at the earliest dysfunctional state, when prognosis is good and treatment costs are relatively minimal.
Emphasis on the neuromusculoskeletal system, supported by an in-depth knowledge of functional anatomy and physiology, pro vides osteopathic practitioners the opportunity to consider and incorporate additional viscerosomatic and somatovisceral reAex clues that are largely unavailable in many other health care sys tems. This is one reason that the complete history and physical of each patient admitted by an osteopathic physician to an Ameri can Osteopathic Association (AOA) accredited hospital is to in clude an osteopathic structural examination (6). A professional standardized osteopathic structural examination For hospitalized patients is discussed in Chapter 71. Integration of these physical findings is Further enhanced by the profession's emphasis on understanding body unity as com pletely as possible. A survey of patient stressors and the indi vidualized response to those stressors is necessary, along with information on the following: Symptoms and pain patterns Activities and ergonomics of daily living Past accidents, surgeries, and significant illness Medications, supplements, and toxins Nutritional, liFestyle, and environmental data These can all be translated or interpreted with an understand ing of their anatomic and/or physiologic impact on the patient's body unity, and provides insight inro the unique individual who is placing his or her trust in the physician's skill and judgment. A hands-on approach and willingness ro listen to the patient (oFten cited by patients as a characteristic of an osteopathic physician) initiate within the patient subtle therapeutic mechanisms, even as data are being gathered to make a diagnosis. Patients are highly satisfied with this type of attention, examination, and synthesis. An osteopathic physician examines the homeostatic reserve of each patient and seeks optimum function within each structure. "To find health is the object a/the physician; anyone canfind
disease"
(7). This portion of the examination is essential For determin ing prognosis and treatment design when host mechanisms are compromised. It is also helpful in the examination oF noncompro mised or compensated hosts, in designing preventive strategies, or in directing a patient toward optimum health levels. It is central in the sports medicine approach. In an osteopathic approach to examination and diagnosis, it is not enough to study the disease
39.
and its by-products; an ineimate and thorough knowledge of the individual is esseneial. Analyzing an individual's homeostatic reserve considers the impact on the whole body but screening may focus on historic, observational, or manual testing factors in a singular region. For example, in the respiratory-circulatory model (8), observation of passive respiration extending motion down to the pubic sym physis provides the osteopathic physician with a screening as sessment of the homeostatic capabilities of that patient to move venous and lymphatic Auids. The degree to which a patient is able to moune a fever in response to an infection provides informa tion abour that individual's immune status. A synopsis of general reactions to emotional or job-related stress provides insights into the reactivity of the sympathetic nervous system. Even postural alignmel1[ provides information on the compensatory capabilities of the neuromusculoskeletal system. Each speaks to homeostatic mechanisms inherent to maintaining the health of the patient. An osteopathic examination strives to provide all pertinent in formation needed for diagnosis. The osteopathic physician prac ticing osteopathic medicine must diagnose beyond the disease; osteopathic diagnosis strives to know all about the whole per son. A whole person approach is one that encompasses structure function interactions, self-healing mechanisms, and unique re sponses to stressors, all within the context of that individual patient's internal and external environments. The osteopathic examination is not just a standard history and physical exami nation with a palpatory diagnosis of somatic dysfunction added to It.
CHAPTER SCOPE AND DESIGN This chapter provides a framework for applying the basic skills discussed in the previous chapter and provides an introduction for the "Overview: Evaluation and Management" chapters that follow (Chapters 40 through 44). Other portions of this text will elaborate on the general perspectives that this chapter introduces. The regional chapters of this text (Chapters 45 through 53) emphasize functional anatomy and diagnostic tests that are cen tral to an osteopathic examination of each body region. Informa tion in these chapters is selected to examine representative struc tural and functional considerations that may produce symptoms or compromise homeostasis. The process of arriving at a differen tial diagnosis using the osteopathic approach is enhanced through more thorough discussions of a select number of common clinical conditions. (Also see Chapter 19, Clinical Problem-Solving.) This text does not attempt to replace standardized texts on physical examination or medical and surgical differential diagno sis, nor does it attempt to replace exhaustive anatomy, physiology, or physical examination texts. Instead, chapters are designed to augment and focus the osteopathic physician's synthesis of skills needed to perform an osteopathic medical examination. They are designed to raise awareness and recognition of functional dis turbances that inAuence a patient's progress (therefore requiring additional atteneion) and to make a presumptive diagnosis and transition from examination to treatment. The "Palpatory Diagnosis and Manipulative Treatment" chap ters of this text (Chapters 54 through 73) discuss specific options and outcomes of various treatment techniques or approaches.
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These chapters rely on applying "evaluation and management principles" to improve the function of the body and to manage somatic dysfunction identified in the overall examination and diagnosis. The importance of synthesizing individual tests and historic information into a working knowledge of a complete individual is the overall perspective that this chapter emphasizes. To recog nize individual (host) strengths and weaknesses in such fashion permits a patient-physician interaction that promotes health and reduces dysfunction and disease.
FUNCTIONAL ANATOMY A fundamental understanding of anatomy is the basis of the os teopathic examination. Knowledge of the body framework-of pertinent skeletal, arthrodial, and myofascial structures-is essen tial. Emphasis is placed on how these anatomic structures relate to their intended functions-alone and in interrelated units. Func tional relationships of somatic structures extend to anatomically and physiologically related neural, lymphatic, and other vascular elements. In an osteopathic examination, viscera are examined individ ually, in relationship to their respective organ system, and as they are structurally and functionally related to the body framework. A complete understanding of function and its interrelation ship with structure leads to the ability of the physician to recognize dysfunction, often before the dysfunction progresses to the classic signs, symptoms, and anatomic alterations that can be diagnosed as disease. The definition of somatic dysfunction (9) requires an assessment of the functional and physiologic interrelationships between certain anatomic structures, including: Skeletal tissues Arthrodial tissues Myofascial tissues Nerves (including the autonomic system) Arteries and veins Lymphatics It also warrants assessment of these factors of possible interre lationships between somatic and visceral structures. The physical examination for somatic dysfunction, rarely cov ered in other medical texts, is a central component (but not the only component) in the osteopathic medical examination. Therefore, the chapters in this and other sections of Foundations of Osteopathic Medicine therefore center on the anatomic and physiologic information that is provided by discovering somatic dysfunction. Most employ one or more representative clinical conditions to enhance understanding of the application of the osteopathic examination in arriving at a presumptive diagnosis and/or in initiating treatment.
ANATOMY AND SOMATIC DYSFUNCTION Structures Predisposing to Somatic Dysfunction Identification of structure predisposing to somatic dysfunction is important in differential diagnosis, in selecting diagnostic tests or
568
VII. Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment
therapeutic inrervenrions, and in focusing on educational strate gies for the patienr. Structure may be altered by a number of facrors. The patient may be born with a "congenital" abnormality in which a struc ture is absenr or does not function maximally. Structural change may also be "acquired" through acute traumatic disrortion and through degenerative or protective-adaptive change. Structural change that alters function may .occur grossly or may occur at organ, tissue, cellular, or even genetic levels. Many congenital abnormalities require functional compensa tion. An example is the presence of a wedge vertebra causing a group curve, roroscoliotic postural disorder, and muscle imbal ance; this same problem can create auronomic disturbance and compromise respirarory and circularory function. Several degen erative or traumatically acquired disorders, such as arthritis or destruction of joint supportive structures, alter joint function. Here too, compensation leads ro significanr secondary somatic dysfunction. ldenrification and understanding of the pathophys iology of structural abnormalities is especially important in the osteopathic medical examination. Such knowledge speeds diag nosis of secondary, compensarory somatic dysfunction patterns that can be addressed ro optimize health. Many congenital and acquired structural disorders will place a specific patienr at increased risk for injury. That patient's structure may not support certain functional challenges in everyday life or in response to certain forms of medical diagnosis or treatmenr. Examples include developmenr of chondromalacia patellae in patients with genu valgus who initiate running programs, and the increased risk of rib fracture in patienrs with osteoporosis if the selected choice of an activating force for an OMT technique is high velocity/low amplitude thrusr. The standard of care for addressing a patient's education ap proaches ro health promotion and risk facror reduction must be expanded to include avoidance of biomechanical risk facrors unique ro that individual and must include the recommendation of unique strategies that will functionally compensate for that patient's structural deficits. Patient education based on the os teopathic examination should include strategies designed ro seek health while protecting structure and maximizing efficient, pain free function within any nonreversible structural limitations.
SOMATIC DYSFUNCTION AND PHYSIOLOGY Somatic dysfunction is capable of modifying physiology (J 0,11). Finding tissue texture changes during an osteopathic physical ex amination is important because it reflects certain functional as pects of a patienr's autonomic nervous system and trophic mech anisms. Important physical findings include: Warmth or coolness of the skin Cutaneous humidity Lymphatic congestion Sympathetic hyperactivity Muscle reactivity Myofascial points and viscerosomatic reflex clues Systemic consequences
Findings discussed in many of the regional chapters include mention of myofascial trigger and tender points (also see Chap ters 63 through 67). If present, these can be palpated in each region and are often related ro the production of referred pain phenomena, as well as lymphatic congestion, neural entrapment, and/or auronomic sequelae (12). Differentiation of these points by palpation alone is difficult; presumptive diagnosis requires an integrated hisrory and physical examination. Regional somatic clues associated with sympathetic or parasympathetic hyperactivity are also often revealed in the os teopathic examination. For example, spinal somatic dysfunction that is segmentally related to an organ's autonomic innervation may occur as a consequence of visceral dysfunction (13-15). Conversely, there are a number of examples where the primary problem lies in the soma; through somatovisceral reflex mecha nisms, it produces a similar palparory finding (16). Identification of palparory viscerosomatic reflex findings can often be traced to systemic dysfunction (13) while palpatory somarovisceral reflex findings can often be traced ro postural dysfunction. Although spinal cord facilitation is one way of explaining how this cross talk berween the somatic and the visceral systems occurs (J 0), again, diagnosis depends on an integrated hisrory and physical examination. Lymphatic congestion is commonly associated with somatic dysfunction (8). It is important to examine local tissues, lym phatic drainage pathways, and locations of sites where early dysfunction of this mechanism can be palpated. The osteo pathic examination must evaluate regional anatomic structures and pathways that might especially impede lymph flow, as well assess homeostatic mechanisms, such as the efficacy of res piration, which is pertinent to the generalized movement of lymph.
SOMATIC DYSFUNCTION AND STRUCTURE Mismatch of functionaL demand and somatic infrastructure often resul ts in structuraL change. Wolff's law (17) observes that calcium is laid down along lines of stress, which results in internal bony remodeling, bony spurs (exosroses), joint immobility, and calcified ligaments. After regional trauma, osteoarthritic changes should be suspected and an appropriate examination performed. Muscle hypertrophy occurs in overworked muscles; disuse atrophy occurs in those inadequately worked. Chronic skin changes, including dryness, scaling, cracking, thickening, and pimples, are expected to occur when trophic substances, carried via vascular channels and/or by axoplasmic flow (10), do not provide adequate nutrition. In the presence of structural change, an osteopathic history and physical examination seeks ro evaluate the patient's somatic infrastructure, its ability ro function, and its response ro func tional demand. Analysis of the findings from this examination attempts ro differentiate berween: Structural and functional problems Congenital and acquired problems • Static, irreversible and dynamic, reversible problems •
•
39.
Often, this evaluation helps the osteopathic physician deter mine short-term and long-range prognoses. Patient education may be directed toward minimizing functional demands under lying unwanted structural change. Treatment goals might center ·on achieving maximum function within the patient's existing structure.
SOMATIC DYSFUNCTION AND OSTEOPATHIC MANIPULATIVE TREATMENT Knowledge of functional anatomy is not only central to the osteo pathic examination; optimization of functional anatomy is also a major osteopathic treatment goal. The accurare diagnosis of somatic dysfunction, using motion characteristics, is vital for designing apptopriate osteopathic ma nipulative treatment (OMT). The arthrodial component of so matic dysfunction often affects the minor motions of the joint. The minor motions then affect the major motions. Major and mi nor motions are discussed in greater detail in each of the regional chapters. Many·osteopathic manipulative techniques require that an ac tivating force be applied in the plane of the joint being treated for somatic dysfunction. Anatomic knowledge of joint facings and the alignment of the joint spaces is a prerequisite to maximiz ing treatment results. In addition, different types of joints have different palpatory characteristics and permit different motions. The regional chapters will discuss what classification of joints is involved and where this is important. For example, diagnostic and treatment approaches with OMT are very different for so matic dysfunction of a synchondrosis compared with diagnosis and treatment of a synovial joint.
PRINCIPLES OF SPINAL MOTION Spinal and vertebral mechanics can be described according to a number of conventions. The following discussion discusses two of these concepts and touches on a third. These include: Fryette concepts Neutral and nonneutral mechanics A right-handed orthogonal coordinate system The latter, representing an x, y, z orthogonal coordinate sys tem, where the z-axis is in the craniocaudad direction, is men tioned for the sake of completeness, as its concepts permit math ematical modeling of spinal movement. Regardless of the convention used, it is important to remem ber that the physician is describing well-documented arthrodial findings. These systems can be used for describing normal mo tion or motion found in joints with somatic dysfunction. Motion findings for joints with somatic dysfunction describe the motion preference remaining in those joints that have impaired or altered arthtodial motion. The descriptors of motion are standardized and specific to the tests used to evaluate the motion; the me chanics of motion and somatic dysfunction obey physical and physiologic laws.
Examination and Diagnosis: An Introduction
569
General Spinal Motions All spinal and vertebral movements are described in relation to motions of their anterior and superior surfaces. A single vertebra is called a vertebral segment (see Glossary: seg ment) (9). Two adjacent vertebrae and their associated arthrodial, l igamentous, muscular, vascular, neural, and lymphatic elements make up a vertebral unit (see Glossary: vertebral unit) (9). Vertebral units demonstrate simple or compound motions. Sim ple motions in the spine occur in a sagittal plane around a trans verse axis and are termed flexion (forward bending motion) or extension (backward bending motion). Compound motion de notes movements that are linked to one another. For example, spinal side-bending and rotation always occur together rather than separately, i.e., they are "coupled" (18). Coupled motions in the thoracic and lumbar spines are conventionally characterized as neutral ("type I") or nonneutral ("type I I") responses.
Origin of Coupled Motions: Type I, Type II, and Simple-Compound Concepts Fryette (19) was an early osteopathic physician who discussed two fundamental physiologic spinal motions that he labeled "simple" and "compound" movements. In his system, simple movements referred to "free and easy" forward and backward bending ac tivities with minimal facet and ligamentous/bony interferences (19). Compound movements, on the other hand, involve increas ingly complex combinations of coupled vertebral unit activities that link extension or flexion with both side-bending and rota tion (19). He labeled these combinations "flexion-side-bending rotation (FSR)" and "extension-rotation-side-bending (ERS)" (J 9). These coupled movements change in response to the posi tion and the degree of flexion or extension of the sagittal plane of the spine. Fryette noted that facet joints are "in control in any area ofthe spine"and they "govern rotation... and side-bending" (19). A variant of Fryette's convention is still widely referenced in osteopathic l iterature and elsewhere. This variant, the type I (neu tral) and type I I (nonneutral) labeling system, has considerable practical use. In type I motion of the thoracic and lumbar regions, side bending and rotation occur to opposite sides, usually in groups and often as part of spinal compensation. For example, type I neu tral somatic dysfunction involving three vertebral units might be designated as "TS-7 F SRRL somatic dysfunction." This record would convey to another osteopathic physician that three verte bral units-TS on T6, T6 on T7, and T7 on T8-a1low motion into flexion, right side-bending, and left rotation and have re strictive barriers preventing normal extension, left side-bending, and right rotation. Often, when recording type I mechanics, the sagittal plane designation is not included in the formula or it is substituted with the designator "N" to indicate that the sagittal plane was within the narrower range of Aexion or extension where free and easy type I mechanics are expected. In type I I motion of thoracic and lumbar spines, rotation and side-bending occur to the same side; usually in a single vertebral unit. Example: A diagnosis of "TS E RRSR somatic dysfunction"
570
ViI. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
denores that T5 on TG is exrended, rotated righr, and side-bent right with freedom of motion in that direction and restriction in attempting to Aex, rotate, and side-bend left. Through discussions coordinated by rhe Educational Council on Osreopathic Principles (ECOP), the nomenclature for de scribing spinal motion has evolved to where the profession uses the terms neutral (N) and nonneutral (NN) as adjectives to de scribe specific types of mechanics, positions, and tests. The "neu tral" and "non neutral" adjectives may also be employed to name and record the diagnosis of specific somaric dysfunctions derived from synthesizing the motion characteristics palpated using pas sive or active morion testing in neutral and/or nonneutral posi tions (Fig. 39.1). Example 1: A person's lumbar spine would have been moved into a "non neutral position" if that sagittal plane position would typically induce "nonneutral mechanics." • Example 2: Palpation of motion characteristics consistent with •
coupled motion in one neutral mechanical pattern that simul taneously resists motion in the diametrically opposed opposite neutral mechanical pattern is diagnosed as a "neutral somaric dysfunction." • Example 3: A specific "neutral somatic dysfunction" at the fifth thoracic vertebral unit could be recorded as "T5 N SRRl," if there was no preference ascertained for Aexion or extension at that vertebral unit; as "T5 F SRRL" if Aexion was also free and extension was resrricted. For those wishing more background, complicated combina tions of interacting neutral and non neutral mechanics are de scribed by Hoover in a 1950 paper (20). A third principle, described by Beckwith (21) and Hoover and Nelson (22) came later. It suggests that initiation of vertebral seg ment motion in any one plane modifies and reduces movement in all other planes. As mentioned previously, coupled motions change in response to the anteroposterior curves of the vertebrae.
Passive Testing for Motion
(N
SR RL)
L
Resistance
Physician presses alternately on
Physician translates alternately
left and right transverse processes
to the right and to the left
Active Testing
(F RR SR) R
L
becomes exaggerated
Patient moves into flexion
Patient moves into extension (less symmetrical)
(more symmetrical)
FIGURE 39.1.
Motion Testing.
Passive motion testing (top)
involves the physician pressing alternatively
over each transverse process and translating between spinal segments to assess the quality of the barrier at the end of motion. In the diagram, the left thumb meets sudden resistance in both side-bending and rotation while the end-feel for both is springy under motion initiated by the right thumb. The somatic dysfunction is a spinal segment that is side-bent right and rotated left
(bottom),
(NSRRLl.
In
active motion testing
the patient flexes and extends while the physician palpates the motion over the transverse
processes. In the diagram, both thumbs move forward equally with flexion. With extension, the right facet closes but the left does not. At the end of extension, the right transverse process is more posterior
(FRRSR). (From Kuchera ML. Spine: State of the Art Reviews.
that the left. Here, the dysfunction is flexed, rotated, and side-bent right Gravitational stress, musculoskeletal strain, and postural alignment.
1995;9(2):463-490,
with permission.)
39.
Furthermore, a common application of this principle is ob served in the setup of manipulative techniques. For example, side-bending and/or sagittal plane motion is often introduced to limit the amount of rotation needed to engage a barrier.
Active and Passive Motion Testing According to the Glossary of Osteopathic Terminology (9), "active motion" refers to patient-initiated voluntary motion. Conversely, "passive motion" is induced in a subject by the physician with the subject remaining passive or relaxed. These terms may also be applied to palpatory tests used to diagnose somatic dysfunction. Passive motion testing of a vertebral unit assesses the direction, quantity, and end-feel of each motion individually in each of the three cardinal planes of motion. It is usually assessed with that region of the patient's spine in an anatomically neutral position. Passive motion testing components may be used as a screening examination or to specifically identify and name somatic dys function. Active motion testing assesses the vertebral unit's combined motion by palpating over the transverse process area as the patient bends forward and backward outside the "easy and free" neu tral range. The changes in position of the palpated site, found at the extremes of flexion and extension and as the vertebral unit moves from the neuual position to these nonneutral sagittal plane positions, provide significant information (see Chapter 52, Fig. 52. 16). Active testing may be used to palpate normal spinal mechanics or to identify somatic dysfunction. Each motion testing system provides valuable information about different aspects of vertebral unit motion. Each can be used to identify impaired or altered function. Each provides sufficient information to "name" somatic dysfunction and to formulate a treatment plan to reestablish motion. Some practitioners incor porate only one system of palpation; others combine or integrate systems of diagnosis.
Neutral (Type I) Mechanics Neutral (type 1) mechanics typically occur in the thoracic and lumbar spine in the presence of free and easy articular and soft tissue motion (9,18). Side-bending movements are accompanied by vertebral segments rotating away from formed concavities and toward the convexities. Clinically, the transverse processes rotate posteriorly on the side of the formed convexity. For example, in the neutral position, right lumbar side-bending creates left rotation of one or more vertebral segments. A typical neutral, type I, response involves three or more segments.
Nonneutral (Type II) Mechanics Nonneurral (type I I) ERS/FRS segmental motions occur in the thoracic and lumbar regions when vertebral facets, soft tis sues, and costovertebral attachments are asymmetrically engaged during compound movements. This is especially likely to oc cur outside of the easy neutral range described previously (see Chapter 52, Fig. 52.16). The sooner facets and soft tissues asym metrically engage, the earlier the nonneutral, type II, responses
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571
TABLE 39.1. PHYSIOLOGIC SPINAL MOTIONS Segmental Region
Physiologic Motion(s)
(0-1 (occipitoatlantal joint)
For E; SxRy only; combinations
(1-2 (atlantoaxial joint)
Rx or Ry only
(2-7 (typical cervicals)
ForE; SxRx; combinations
T1-12 (typical thoracics)
ForE; type I (SxRy) or type II (RxSx);
L 1-5 (typical lumbars)
ForE; type I (SxRy) or type II (RxSx);
combinations combinations
begin. Under these conditions, the involved segments and unit (or units) rotate into the intended concavity.
Mechanics in Other Anatomic Regions The spinal mechanics outlined above for the thoracic and lumbar regions are normal physiologic motions for these regions. The specific motions that normally occur, however, depend on the anatomy of the structure being examined. Different normal physiologic mechanics are found for varying structures in different regions (e.g., cervical, sacral, rib, sternal, pelvic, and extremity regions). Tn the cervical region, for example, the anatomy of the most superior two vertebral segmems of the superior cervical division are very different from each other and from the other vertebral segments in the inferior cervical division (C2-7). This variation in structure results in three different sets of motion mechanics in this one region of the spine alone. Refer to specific regional chapters (Chapters 45 through 53) to understand the normal physiologic motions that exist in the various regions of the body from head to toe. See Table 39.1 for a summary of physiologic spinal motions.
Physiologic Mechanics and Somatic Dysfunction Somatic dysfunction demonstrates impaired or altered function of somatic structures, and altered motion characteristics are one objective finding in the osteopathic examination that defines it. It may be initiated by a variety of causes, and a number of postulated mechanisms have been advanced for its continued presence (16). Somatic dysfunction commonly occurs while engaged in common daily activities. Osteopathic examination reveals that a significant amount of somatic dysfunctions demonstrate the arrested physiologic motion specific to the region and activity involved. Motion findings in this type of somatic dysfunction typically reveal one combination of permitted physiologic motion with simultaneous restrictions in each of the opposing directions. The pattern of motion permitted is typically consis tent with the physiologic motion that was occurring at the time the dysfunction was initiated. Traumatic causes are another story, due to the uncontrolled forces that impacted the body region. Traumatically induced so matic dysfunction may or may not result in patterns associated with the patient's position or activity; it may not even follow the physiologic motion pattern of the region traumatized.
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
EXAMPLE OF SPINAL MECHANICS LEADING TO DYSFUNCTION Case: A woman bends forward and side-bends to the right to pick up a box. It is heavier than she expected, and when she stands up after completing her task, she experiences low back pain. It is made worse by side-bending to the left, and it is made better by bending forward or lying down. Pal pation of her lumbar region reveals asymmetrical warm and tender tissues at the level of the L3 vertebral unit. With passive motion testing, L3 prefers right rotation, and the end-feel in that direction has normal, physiologic characteristics. Rotation to the left, however, is restricted and the end-feel in that direction is abruptly fi rm. L3 prefers to side-bend to the right, and the end-feel is restricted when side-bending to the left. Gapping of the spinous processes between L3 and L4 is permitted, but induced extension is restricted. Active motion testing reveals that the asymmetry of the poste rior left L3 transverse process accentuates with backward bending but becomes more symmetric with forward bending. The specific motion diagnosis made when testing by either the passive or the active method is " L3 F SRRR somatic dysfunction," or al ternatively, " L3 FSR right somatic dysfunction." This could also be expressed in terms of the "restricted" characteristics of the joint and would be written as " L3 restricted E SL RR". The remainder of her history and physical examination are unremarkable relative to possible differenrial diagnoses; no re Aex abnormalities or other findings indicative of pathology were revealed by examination. The correlation between the type of physiologic motion occurring during activity and the somatic dysfunction characteristics found on examination, the timing of her symptoms, and the reactive characteristics of the tissues sug gest a correlation between the diagnosis and the condition. The presumptive cause of her chief complainr is diagnosed as l umbar somatic dysfunction. It is judged by standard criteria to be of moderate severity. (See Glossary of Osteopathic Terminology and Fig. 7 1 . l .) In the definition of somatic dysfunction, it is specifically stated that "somatic dysfunction is treatable by osteopathic manipula tive treatment (OMT)" (9). After O MT, re-examination of this patient demonstrated resolved tenderness, normal morion char acteristics, and reestablishment of symmetry. Her back pain was no longer presenr in the upright, weight-bearing position or with motion. The patienr was instructed in proper lifting techniques to prevent recurrence and advised to return if symptoms recurred. Case Summary: This simple case demonstrates a focused inregration of history and physical fi ndings, elimination (or prioritization) of differential diagnoses, and implemenration of treatmenr based on a presumptive diagnosis. Resolution of the problem helps support the initial correlation, and patienr educa tion to avoid the initiating biomechanical evenr completes this visit.
and assessment. Dysfunction of the soma and its related elements plays a significanr role in the production of a variety of patient complaints, signs, and/or symptoms, and is frequently accom panied by visceral dysfunction. For these reasons, a conscious search for somatic dysfunction through the use of pal pation and motion testing is an important part of a patient examination. Information obtained through a regional neuromusculoskeletal examination is inregrated with the history and all other findings related to the enrire individual. This approach by an osteopathic physician provides the data essenrial for making differential and working diagnoses and for developing a rational and total treatment program to promote the patienr's health and/or to support a patienr with disease or dysfunction. By studying anatomy and physiology from the philosophical vanrage point needed to formulate a "rational osteopathic treat ment," an osteopathic physician discovers a unique and valuable perspective of health and disease. By interpreting somatic clues through an understanding of physiology as they can relate to the underlying symptoms, the physician may surmise the dysfunc tion or pathophysiology that is most likely occurring in a given patient. This knowledge also offers di rection and information for the physical examination, the differential diagnosis, and pri oritization of tests to confirm the diagnosis. Rather than simply diagnosing and treating symptoms or symptom complexes, the osteopathic physician seeks to augment the health that is found within the individual ( 1 3).
REFERENCES I . Nort h u p G W. Osteopathic Medicine: An Arneriraf/ Reformation. Ch icago I L: American Osteopathic Association; 1 966. 2 . Koop CEo In describing osteopathic physicians remarked, " Knowledge able Americans who know somet h i n g about the h istory of medicine and their own desires, would l i ke a fam i ly doctor l i ke that described to them by their grandparents, b ut one who has assess to a CAT scanner and a M Rl . . . [their] emphasis o n rural health care, general practice, fam i l y medicine, SPOrtS medicine and geriatrics is q u i te i n concen w i t h t h e present needs o f thi s n a t i o n , n o t only i n practice but also i n phi loso phy." Verbatim from a n add ress to K i rksville Col lege of Osteopathic Medicine on the Cente n n i a l o f the Fou nding School of Osteopathy,
1 992. 3 . Rudduck GA. "Colorado Workers Compensation Closed Claim Study." Tilli nghast/Towers- Perri n; 1 99 1 . 4. M i ll i ma n & Roberrson , I nc. "Colorado Workers Compensation An nual Report." Til l inghast/Towers-Perrin; 1 996. 5 . Tillinghast/Towers-Perrin. " H awa i i Workers Compensation Closed Claim Study." 1 993. 6. AOA Buteau o f Healthcare Faci l i ties. Accreditation Requirements fo r
Healthcare Facilities, Appendix C. Ch icago I L: American Osteopathic
Association; 200 1 .
7 . Tru h l a r RE. Stlge Sayings 0/ A . 7: StilL. I nd i a napolis, I N : American Academy o f Osteopathy; 1 994. 8 . Zink G , Lawson WE. An osteopathic structural exam i nation and fu nc
tional i n terpretation of the soma. Osteopathic Ann. 1 979:7: I 2- 1 9 (433-
440). 9. The G lossary Subco m m i ttee o f the Educational Council on Osteopathic
CONCLUSION The close and cl inical relationship of structure and function of fers refreshing and distinctive insights into patient examination
Principles. Glossary of Ostcopat h ic Terminology. In: D'Alonzo GE, J r, ed. A OA Yearbook and Directory a/ Osteopathic Pbysicia/lS. Chicago I L:
American Osteopat h ic Association; 2000.
1 0 . Peterson B , ed. The Collected Papers 0/ frvin M. Korr. Newark, O H : American Academy o f Osteoparhy; 1 979.
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I I . Nort h u p C W. Os/eopatlJic Research: Growth and Development. Ch icago, 1 L: American Osteopat h ic Association; 1 987.
1 2 . Simons DG, Travell JG, S i mons LS. Myofoscial l'ain and Dysfimction:
The Trigger Point Mflllual, Vol u me I . Upper H alf of Body. 2 n d ed.
Baltimore, M D : Will iams & W ilkins; 1 999.
1 3 . Kuchera M L, Kuchera WA. Osteopathic Considerations in Systemic Dys
function, 2nd ed . Columbus, O H : G reyden Press; 1 994.
1 4 . Beal MC Viscerosomatic reAexes:
a
review.
J
A m Osteopath Assoc.
1 985;85 :786-80 I . 1 5 . Nicholas AS, DeBias DA, Ehrenfeuchter W, et a1. A somatic component to
myocardial i n farction. EM}. 1 9 85;29 1 : 1 3- 1 7 .
1 6. G i l l iar WG, Kuchera M L, G i u l ianetti DA. Neurologic basis of manual medicine. PI)ys Med Rehflbil Clin N Am. 1 996;7(4) :693-7 1 4.
1 7. Wolff J. Das Gl'setz der Transformation dey Knochen. Berl i n , Germany: H i rschwald; 1 892.
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1 8 . Greenman PE. Principles ofManual Medicine, 2nd ed. Balti more, M D: W i l liams & Wilki ns; 1 996: 6 1 -63.
19. Fryerte H H . Principles of Osteopathic Ti!Chnic.
I n d ianapolis,
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20. Hoover HY. Compl icated Lesions. In: American Academy of Osteopa
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2 1 . Beckwith CG. Vertebral Mechanics.
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DIAGNOSIS AND PLAN FOR MANUAL TREATMENT: A PRESCRIPTION ROBERT E. KAPPLER WILLIAM A. KUCHERA
DIAGNOSIS KEY CONCEPTS • Definition of somatic dysfunction, and possible
causes • Essential elements of diagnosing somatic dysfunction,
Somatic dysfunction is an impaired or altered Function of related components of the somatic (body framework) system, such as these elements:
including observation, screening tests, palpation, and
Skeletal
motion testing
Arthrodial
MyoFascial Vascular Lymphatic Neural
• Effects of somatic dysfunction on range of motion and
end-feel • Decisions physician must make after diagnosis of somatic
dysfunction • Answers to: When is it important to use manipulative
Four criteria are used for diagnosis of somatic dysFunction:
treatment? • Considerations when developing a treatment plan,
I.
including sequence in which somatic dysfunctions should
II.
be treated, dose and frequency of treatments, and choice of
III.
techniques
IV.
Tissue texture abnormalities (T) Asymmetry of bony landmarks (A) Restriction of motion (R) Tenderness or soreness to examiner pressure (T)
These Form the acronym TART. Following is a plan for conducting an osteopathic eval uation for diagnosis of somatic dysFunction. The physician first looks at the whole person; noting characteristics of gait and evi dence of asymmetries. Screening tests are performed. Abnormal findings on general impression tests, such as asymmerrical bony landmarks or regional motion, suggest regions that require Furrher palpatory evaluation for tissue texture changes and asymmetry of segmental motion characteristics. Palpation reveals localized areas that stand out From surround ing areas by exhibiting temperature differences, swelling, hyper esthesia, or firmness, which can be identified as tissue texture changes (TTC). Palpation of these areas is almost always tender. The segmental areas of TTC and tenderness are then tested For motion characteristics. Motion testing may be active or passive. The characteristics of motion of a joint and its tissues can be described in various ways (Fig. 40.1). It may involve rotation around one of three axes (vertical, transverse, anteroposterior) or translation in one of the three planes of the body, or it may be a shearing of myoFascial tissue layers. For the spine, Forward and backward bending indicares mo tion in the sagittal plane about a transverse axis. Pressure on the transverse process initiates rotation in a horizontal plane The
Many treatment procedures follow the principles of osteopathic philosophy. The use of manual intervention to remove impair ment of normal body function was emphasized by A. T. Still. This intervention, osteopathic manipulative treatment (OMT), requires a careFul evaluation and diagnosis of the patient before, during, and aFter treatment. The evaluation of the patient leads to a precise and individual plan for treatment. The plan is the guide For the patient's treatment developed from observations and findings about him or her at that mo ment. The plan is written in the record for later reference. A note is recorded stating whether the procedure was effective or ineffective. Osteopathic examination methods and procedures have been categorized. Dinnar (1,2) listed four categories: General impressions
Regional motion testing evaluation Local characteristics of motion Superficial and deep tissue
40. Diagnosis and Plan for Manual Treatment: A Prescription What is the quality of motion? What does the end range of motion feel like?
Concepts Regarding Joint Motion in a Single Plane AS
PS
PS
o
-
I
575
AB
_
Normal Range of Motion
No Somatic Dysfunction (SO)
Motion has direction, range, and quality. Visual observation measures the range of motion; palpation reveals the quality of motion. The quality of motion is described as: Smooth Ratcheting Restricted Exhibiting resistance to the motion introduced
I�
AS
PS
o
AS
PS
o
I
AS
PS
AS
-
II
II PS
PS
I
-
AS
11
o
PS
AS
AS
The presence of normal passive motion in one direction of one plane of motion and resistance in the other is presumptive evidence of somatic dysfunction. The range of motion with somatic dysfunction is decreased. This decrease of motion occurs within the normal range of mo tion for the joint. The quality of motion can be shown in a graph (Fig. 40.2). The joint will move farther in the direction in which the somatic dysfunction occurred; its movement is restricted in the opposite direction. There is a resrriction to motion in one direction, called a restrictive barrier. As the joint is moved in the direction of the restrictive barrier, the curved line of resistance rises at a much more rapid rate than the resistance encountered when moving toward the physiologic barrier in the opposite di rection. The restrictive barrier of the joint occurs before motion reaches the physiologic barrier on that side. Kappler (3) describes the resistance near the limits of motion as end-feel. The end-feel of motion in a direction toward the somatic dysfunction (restrictive barrier) is different from the end-feel away from the direction of the somatic dysfunction. The end-feel in a normal joint should be the same in either direction. End-feel characteristics may be used to differentiate which of the many manipulative procedures to use.
TREATMENT Approach
o
Somatic dysfunction is identified with the following diagnostic findings: Asymmetry of tissue texture Range of motion Perception of tenderness Characteristics of the end-feel
Indicates increasing tissue tension
The physician makes further decisions based on the answers to these questions: FIGURE 40.1. Normal motion in a single plane: three methods of il AB, anatomic barrier; PB, physiologic barrier; RB, restrictive
I.
lustration. barrier.
[I. HI.
about a vertical axis; side-to-side translation of the vertebral body produces side-bending. Regardless of how the segments of a region are tested, the questions that must be answered are: Does it move? Does it move appropriately? (Is it restricted in motion?)
Are the findings significant and related ro the patient's prob lem(s)? Should the findings be altered by manipulation? If so, which of the many techniques are indicated and likely to be effective for this patient?
Additional questions relate to the areas of restricted motion. Are they: I.
A primary somatic dysfunction related to the musculoskeletal system?
VI!. Osteopathic Considerations in Pafp atory Diagnosis and Manipulative Treatment
576
Concepts Regarding Joint Motion in a Single Plane PB
AB �I\
AB
, , ,
II
"
"
I I I I I I I
AB
The position of a body part, as determined by palpation and referenced to its adjacent defined structure (the upper segment is named in relation to the lower). The directions in which motion is more free and the directions in which motion is restricted (6).
I.
NormalMotion II.
,
1\
I
, , , , , ,
\
\
\
"
AS
PS
RS
AS
PS
RS
I
1\f+; /II
RS
PS
AS
00
PS
AS
I
f+l
Normal_ , Motion , , , , , ,
f+!
00
When the challenge is not overly severe, but the body is not responding adequately to the appropriate treatment regimen, or when appropriate (manipulative) treatment may aid the body's response or may accelerate the healing process. • When the body is critically ill, and life's continuance is in the balance, a more optimal musculoskeletal reaction to illness may be the factor that tips the balance of recovery in favor of the patient. • Zink and Lawson (7) answered, "The findings are significant to treat until a physiologic state existed that included eupnea in the supine position. The osteopathic physician focuses on the whole person. While the person's symptom may be localized, the major influence can be elsewhere." •
00
II PS
The goal of treatment is to enhance movement to resolve somatic dysfunction. Hoag (5) asked, " When is it important to use manipulative treatment?" He answered the question as follows:
/
-(SD)
AS
PB
00
-(SD) f+:
The positional and motion aspects of somatic dysfunction can be described using two parameters:
II
PS
AS
00 AS
Methods
The dose of treatment is limited by the patient's ability to respond to the treatment. The physician may want to do more and go faster; however, the patient's body must make the necessary changes toward health and recovery. II. The physician's ability to execute a technique effectively is a major factor in determining which techniques to use. There are many different rechnique approaches. The physician must choose from the various techniques that are effective in his or her hands. Ill. There must be an objective to be accomplished by the treat ment. Treatment should be outcome-oriented, meaning that the intended objective is accomplished. Do not allow OMT to become oriented only to the process, meaning that once you have given the OMT, the process is viewed as completed. Examples of objectives are: mobilize the sacrum, decrease rib tenderness, improve motion at T5, or relax cervical muscles. IV. The objective is the constant; the method is the variable. v. The technique chosen must be safe and potentially effective. Risk/benefit relationships must always be considered. VI. The physician must be able to execute the technique effec tively. The technique must be modified to meet the needs of the patient and the physician. I.
o
D-
Indicates Motion Loss
FIGURE 40.2. Somatic dysfunction in a single plane: three methods of illustrating the restrictive barrier (the restrainer). AB, anatomic barrier; PB, physiologic barrier; RB, restrictive barrier; SD, somatic dysfunction.
II.
Ill.
IV.
A somatosomatic reflex relared to some other musculoskeletal problem? A viscerosomatic reflex from a dysfunctional or diseased or gan? Clinical investigations (4) have found the presence of somatic components related to visceral disturbances. A mechanism protecting some damaged tissue or weakened structure? Treatment of the somatic dysfunction in this situ ation is not indicated at this time; strengthening of the weak ened area is indicated (5).
Sequence
There are different opinions regarding what should be treated first. Absolute rules for sequencing do not exist. Patient problems vary and may require deviation from the physician's usual ap proach. One school of thought suggests that the initial approach
40. Diagnosis and Plan for Manual Treatment: A Prescription is to balance the pelvis. Another opinion suggests that the sacrum should be treated first because the sacrum is the base of support. A sample sequence is as follows:
577
DOSE GUI DELINES
The sicker the patient, the less the dose. Caring, compassionate novices often err on the side of over dose. Ill. Allow time for the patient to respond to the treatment. IV. Do not waste the dose on insignificant areas. Concentrate on key areas needing treatment. v. Chronic disease requires chronic treatment. VI. Pediatric patients can be treated more frequently; geriatric patients need a longer interval to respond to the treatment. VII. Acute cases should have a shorter interval between treatments; as they respond, the interval is increased. I.
II.
For low back pain, especially with psoas involvement, treat the lumbar spine first. II. Treat the upper thoracic spine and ribs before treating the cervical spine. Ill. Treat the thoracic spine before treating specific rib dysfunc tions. IV. For very acute somatic dysfunctions, treat secondary or pe ripheral areas to allow access to the acute area. v. Cranial treatment can produce relaxation and allow OMT to work in other areas. VI. For extremity problems, treat the axial skeletal components first (spine, ribs, sacrum) . I.
These guidelines on sequencing are not absolute rules. Each physician, afrer gaining experience, develops his or her own approach.
Dose and Frequency
A quotation frequently repeated 111 osteopathic circles is at tributed to A. T. Still: Find it, fix it, and leave it alone. The statement addresses dosage, with the admonition to resist con tinuing treatment but give the patient time to respond. The abil ity of patients to respond is variable. Pediatric patients respond quickly, while geriatric patients respond more slowly. Patients who are very ill and debilitated respond slowly; they cannot re spond appropriately to a treatment dose that is appropriate for an ambulatory patient. Some forms of osteopathic manipula tive treatment, such as thoracic pump, may be performed several times a day. Soft tissue stretching may be performed frequently. Specific joint mobilization is an example of a treatment approach that requires a longer interval between treatments. The frequency of visits for ambulatory patients has several guidelines, as well as some confounding factors. The availability of time in the physician's appointment schedule is a practical factor in the scheduling of the next visit. The physician may work at more than one site and not be available at a particular location every day. Patient availability must be considered, as well as factors such as travel distance, work, and prior commitments. Apart from physician or patient availability, the acuteness of the patient's problem is a major consideration in the scheduling of the next visit. The ambulatory patient disabled with an acute low back problem would be reevaluated in 24 to 48 hours. A patient with chronic low back discomfort might be seen every 2 weeks. Consider response to treatment in a decision for timing the next visit. A favorable response suggests lengthening the interval. A poor response might suggest that the patient is not yet able to respond appropriately and should be seen again when the ability to respond improves. At times, the patient may exhibit more dysfunctions than can be appropriately handled in one visit. A plan of treatment involves immediate objectives along with longer-term objectives. Provide palliative treatment with the understanding that the real task is yet to be addressed.
Direct or Indirect Method
Two major factors determine choice of technique: The ability of the patient to respond to the treatment The ability of the physician to execute the technique We lack precise answers for when to choose one technique instead of another. There are only general guidelines. Sometimes certain techniques are inappropriate to achieve the intended ob jective. There are times when the risk/benefit relationship is such that certain techniques should be avoided. The use of forceful high-velocity technique in a patient with advanced osteoporosis might lead to pathologic fracture. This text contains chapters on a number of technique types and their use. The ability of the physician to execute the technique is prob ably the greatest factor in determining choice of technique. For many years, direct action thrust techniques were taught and were used very successfully by osteopathic physicians in the treatment of their patients. Those physicians did not face the challenge of trying to decide which type of technique to use. They knew thrust techniques and learned how to modify the techniques to make them work. Some osteopathic physicians tended to use one type of tech nique approach other than high-velocityllow-amplitude force (HVLA) direct action thrust. Some physicians used only mus cle energy. Others used only functional or indirect techniques. Many of these physicians were considered experts in their field. This illustrates the reality that there is more than one method to achieve the objective. Precise answers to choice of technique do not exist. Indirect technique is of no value to a physician who lacks skills in using indirect technique. HVLA is of no value to a physician who lacks skills to use that technique. The model for today's osteopathic physician is eclectic, with knowledge and skill in a broad spectrum of techniques. The more methods available, the greater the chance is of success in treating a wide range of patients and patient problems. Techniques are classified as direct and indirect. Direct tech nique means rhat the initial positioning of the patient's somatic dysfunction is in the direction of the restrictive barrier, and then a final activating force is applied. Indirect technique involves po sitioning away from the restrictive barrier. Indirect technique is usually comfortable for the patient be cause the physician is moving the tissues in a direction that is freer, in a direction the tissues want to go. Most of these procedures
578
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
involve holding in the proper position; release is by inherent forces rather than physician forces. Examples of the indirect method are the Sutherland ligamentous release technique (8), functional technique, and counterstrain technique. Direct technique usually involves a greater amount of force. Procedures of this rype are soft tissue, articulation, myofascial, muscle energy, and thrust techniques. Descriptions of these tech niques are found in other chapters in this text. A muscle energy procedure for the treatment of a patient with an acute, stiff neck is clinically effective, but the initial position ing is not toward or away from the restrictive barrier. The neck is positioned in a neutral, pain-free position and held while the physician instructs the patient to turn the neck in a direction in which it will not move. The muscles that are contracting are not the shortened, painful muscles, but the antagonist, non-painful group. After the patient completely relaxes this contraction, the physician rotates the neck a few degrees toward the new bar rier, being careful to avoid a painful position. This procedure is repeated several times and usually results in significant improve ment of the patient's condition. An osteopathic manipulative treatment has been described as a transaction between two unique persons (9). The amount of HVLA used for one patient may be inappropriate for another. The presence of osteoporosis suggests a lesser force. Thus, thrust or impulse must be titrated. How much force should be used in a HVLA thrust? Kimberly (10) states" ...enough to affect a phys iologic response (increased joint mobiliry, produce a vasomotor Rush, produce palpable circulatory changes in periarticular tis sues, and/or provide pain relief) but not enough to overwhelm the patient."
symptoms have been present for 5 days. She complains of nasal discharge and postnasal drip. She has had a mild fever. She has no known allergies, has otherwise been very healthy, and has had OMT in the past with no complications. There has been no change in bowel or bladder activiry.
0:
Objective
The patient's heart rate is 88 and regular, blood pressure is regular at 130/72, temperature is 99° F orally, and respirations are 16 and not labored but shallow. There is anterior and posterior tender lymphadenopathy, the pharynx is hyperemic, and the nasal pas sages are congested and contain thick creamy mucus. The umbo of the rympanic membranes is congested and hyperemic, but no Ruid is seen, and there is a normal cone of light. The chest is clear to auscultation over all lobes, and auscultation of the heart revealed no murmurs or adventitious sounds. There is decreased diaphragmatic breathing with best motion on the left side; C2-4 is RR SR, the thoracic inlet is side-bent and rotated left; T12 is N RL SR. The anterior superior iliac spines (ASIS) are inferior and the PSIS are superior on the left.
A: Assessment I. II.
Acute upper respiratory infection Somatic dysfunction of the cervical, cervicothoracic, thora columbar, and pelvic regions
P: Plan Cervical soft tissue Direct action side-bending thrust to C3 Ill. Indirect action myofascial unwinding to thoracic inlet IV. Effleurage of face and neck provided. Soft tissue to thora columbar region and direct action muscle energy to T12 SO. Diaphragm re-domed with indirect method. Classic lym phatic pump soft tissue given v. Counterstrain creatment of anterior innominate VI. Prescribe amoxicillin 250 mg, 30 tabs, 2 tabs four times a day I.
Plan of Intervention
A plan of intervention requires a specific diagnosis. Decisions must be made based on the answers to these questions: What doesn't move? What direction will it move? In which direction doesn't it move? The plan includes the decision to use a direct or indirect method of treatment to improve the movement. It considers in what direction the treatment can most effectively be applied. It includes choosing the best technique for the patient from the variery of therapeutic procedures available. The plan of treatment and the patient's response to the treat ment should be recorded in the chart's progress note. A review of the record at a follow-up visit can change the plan for the next visit. The record also is used for purposes of research, reimburse ment, or legal documentation. One example of the subjective, objective, assessment, plan note (SOAP) method of recording an osteopathic office call follows: SOAP
S: Subjective A 28-year-old woman complains of a cold with coughing, dif ficulry getting a deep breath, fatigue, and low back pain. The
11.
Manipulation was successful and the patient left the clinic improved with this note: Take all of the prescription and expect to be improved in 24 hours and know YOlt are better in 48 hours. if this is not the case, or you have any problem with medications, call me or corne to clinicfor recheck.
(Personal Signature, DO)
CONCLUSION
There are several parts to a treatment plan, including the se quence in which somatic dysfunctions should be created, the dose and frequency of treatments, and the choice of techniques. Such intervention requires a careful evaluation and diagnosis of the patient before, during, and after treatment. The evaluation of the patient leads to a precise and individual plan for his or her treatment.
40. Diagnosis and Plan for Manual Treatment: A Prescription RE FERENCES
579
6. The Glossary Review Committee of the Educational Council on Osteo pathic Principles. Glossary of Osteopathic Terminology. In: Allen TW,
1. Dinnar U. Classification of diagnostic tests used with osteopathic ma nipulation. jAm Osteopath Assoc. 1980;79:451-455. 2. Dinnar U. Description of fifty diagnostic tests used with osteopathic manipulation. j Am Osteopath Assoc. 1982;81:314-321. 3. Kappler RE. Direct action techniques. j Am Osteopath Assoc. 1981; 81 (4):239-243. 4. Beal
Me.
Viscerosomatic reAexes: a review. jAm Osteopath Assoc. 1985;
85:786-801. 5. Hoag
JM.
The musculoskeletal system: a major factor in main
taining homeostasis. book. 516.
Newark,
OH:
1977 American Academy of Osteopathy Year American Academy
of
Osteopathy;
1979:
ed. AOA Yearbook and Directory of Osteopathic Physicians. Chicago, IL: American Osteopathic Association; 1990:675. 7. ZinkJG, Lawson WE. An osteoparhic structural examination and func tional interpretation of the soma. Osteopath Ann. 1979;7:12. 8. Lippincott H. The osteopathic techniques of Wm. G. Sutherland, D.O. In: Northup TL, ed. AOA Yearbook. Indianapolis, IN: American Academy of Osteopathy; 1949: 124. 9. Korr 1M. Somatic dysfunction, osteopathic manipulative treatment and the nervous system: a few facts, some theories, many questions. j Am Osteopath Assoc. 1986;86:1 09-114. 10. Kimberly P. Forming a prescription for osteopathic manipulative treat ment. jAOA. 1980;79:512.
CONSIDERATIONS OF POSTURE AND GROUP CURVES MICHAEL L. KUCHERA ROBERT E. KAPPLER
KEY CONCEPTS II • • • • • • •
W hat constitutes optimal posture Faccors chat produce postural decompensation Mechanisms of compensation and spinal parcerning M echanics of group curves Physical findings that occur with group curves and cheir clinical significance Role of ceneral nervous system in maineaining posture Possible treatmencs for postural decompensation Direct osteopathic manipulation creatmenc techniques for group curves
" I f we regard posture as the resulc of the dynamic ineeraction of two groups of forces-the environmental force of graviry on one hand, and the strength of the individual on the other-then posture is but the formal expression of the balance of power existing at any time between these two groups of forces. Thus, any deterioration of posture indicates that the individual is losing ground in his comest with the environmental force of gravity" (1). Analysis of a patienc's posture provides an enormous amount of information about the body. The endurance of antigravity (postural) muscles, the capability of the musculoskeletal system to adjust homeostatically to physical srressors, the presence and type of group spinal curves, and the locations of postural spinal crossovers all offer insight into structure-function relationships on a physical level. Observation of posture may also offer the clin ician the first clues to the emotional, spiritual, and psychological elements of a patient's health. Treatment of posture has wide implications in the general health status of each patient. It especially involves reduction or elimination of a constant precipitating and perpetuating factor of group curves and recurrent somatic dysfunction. Postural treat ment can also play a significant role in the treatment of certain specific spinal conditions associated with postural decompen sation, such as scoliosis and spondylolisthesis. Finally, postural treatment can be effective in improving symptoms associated
with a tremendous J1Llmber of neuromusculoskeletal conditions, including myofascial pain syndromes, trigger points, segmental facilitation, and recurrent somatic dysfunction. According to Osteopathic Research: Growth and Development, "Biomechanics from the osteopathic perspective has evolved into a dual study of the adaptive responses of the body to gravitational force and the effects of alterations in joint mechanics that result from injury or impaired function" (2).
ASPECTS OF POSTURE Base of Support
Posture is the distribution of body mass in relation to gravity over a base of support. The base of support includes all structures from the feet co the base of the skull. The effect of the lower extremities, (3) pelvis, (4) and base of the skull (5) are especially important. Distribution of weight over the base of support depends on the following: Energy requirements for homeostasis I ntegrity of musculoligamentous structures • Compensation that structures at or below the base of the skull have on the visual andlor balance funcrions of the body •
•
Optimal Posture
Optimal posture is a balanced configuration of the body with respect to gravity. I t depends on normal arches of the feet, ver tical alignment of the ankles, and horizontal orientation (in the coronal plane) of the sacral base. The presence of an optimum posture suggests that there is a perfect distribution of the body mass around the center of gravity. The compressive force on spinal discs is balanced by ligamentous tension; there is minimal energy expenditure from postural muscles (6,7). Structural or functional stressors on the body, however, may prevent achievement of opti mum posture. In this case, homeostatic mechanisms provide for compensation in an effort to provide maximum postural function within the existing structure of the individual. Compensation is the counterbalancing of any defect of structure or function (8).
41. Considerations of Posture and Group Curves
Compensated Posture
A compensated posture is considered CO be the result of the pa tiem's homeostatic mechanisms working through the emire body unit co m aximize funnion. Poscural compensation in the mus culoskeletal system occurs in all three planes of body motion co keep the body balanced and the eyes level. The cemral nervous system (CNS) places a high prioriey on visual and vestibular (bal ance) functions. Spinal compensation involves CNS correlarion of proprioceptive information from tendons and muscles as well as vestibular informarion from rhe semicircular canals. The CNS also imegrates this proprioceptive information with information received from rhe eyes (9). Postural homeos(aric lessons are learned gradually by the CNS from visual and proprioceptive input as the individual grows and develops. The process has implications for rreatmem prococols that include postural reeducation; this should be progressive and consisrem if it is ro succeed. Stl'uccural compensation allows a person co function despite musculoskeletal imbalances. Because of an accumulated h isrory of genetic, rraumatic, and habicual pro cesses requiring com pensation, few patiems have ideal poscure. Poscure is both static (srructural) and dynamic (functional). It is stati� in its alignmem of body mass with respect co graviry. it is dynamic because this alignment constanriy adjusts co rhe individual's changing poscural demands. Over time, individual static postural alignmem conforms co inherem connective tissue srructure. It also responds co the cumu lative functional demand placed upon it by static and dynamic posrural conditions. Both static and dynamic poscures are in fluenced by and influence sofe tissue functions. Examination in cludes analysis of static postural alignmenr in the upright weight bearing position. It also includes osteopathic examination of the selecrive tensions of the soft tissues. Palpacory examination of dynamic posture and segmemal motion testing is vital ro under standing struccure-function inrerrelarionships. This combination of examinations provides clinical clues about the inherenr ca pability of the patienr's neuromusculoskeletal system ro balance and mainrain biomechanical alignmenr. Radiographic analysis of bony posrural relationships can furrher add co this understanding (see Chaprer 42).
Group Curves
A group curve is a spinal curve that involves several segmenrs. The motion pattern in these curves follows the first principle of physiologic motion of the spine. When the spine is in neutral position, that is, with an absence of marked flexion or extension, and side bending is inrroduced, the verrebrae rotate inro the pro duced convexiry (10). In these curves, rotation is co the opposite side of side bending. Compensarory changes of the spine are often named according co the group curve with the most prominenr posrural feacure (Fig. 41.1). Lateral group curves that exceed 5 degrees as measured by the Cobb method are called scoliosis. Group curves in rhe sagirral plane are called kyphotic or lordotic curves. Scoliotic curves are sometimes referred co as roroscoliotic curves because roration and side bending are inseparable. A curve may be called a kyphoro coscoliotic curve if all three planes are significanrly involved.
581
MECHANICS OF GROUP CURVES
Spinal joinrs are designed ro provide motion; spinal motion is necessary in most of our ordinary activiey. Most spinal motion involves a group of vertebral segments. This morion follows the first principle of physiologic motion of the spine and is necessary co allow for positional changes of rhe body. Every time a person bends co the side, a lareral curve is produced. This sometimes leads co restricrion of motion. Lateral curves become a problem when restriction occurs and the spine no longer straightens. Spinal curves may be produced by unilateral muscle conrrac tion. This muscle pull creates a concaviey, resulting in a curve. The verrebrae rotate into the convexiey. This eype of lateral curve disappears when the m uscle hyperconiciey is gone. Another eype of lateral curve involves long-term anacomic adaptation associated with positional change. Examples would include the spine that is initially in a curved position [0 com pensate for an anacomic short leg or certai n structural deform i ties, postural balance adaptation, or even long-term positional change (such as may be required for a certain occupation) that becomes a parrern. Over time, the tissues associated with this curve change. Tissues on the convex side become lengthened. Tissues on the concave side become shortened. Deformiey of a verrebral body with lateral wedging results in a spinal curve. Long-standing curves with anaromic adaptation resist change. Over time, the curved position becomes the neutral position.
DIAGNOSIS OF GROUP CURVES
A patient presenrs with humping of a paraverrebral region on the convex side of a coronal plane curve as a result of stretched muscles or deformation of ribs brought about by rotation of the verrebrae in the curve. Stretched muscles may be tender co palpation. Side bending is coward the concaviey, and rotation occurs inro the con vexity with m aximal rotation occurring at rhe apex of the curve. The physician should consider a diagnosis of kyphoscoliosis. Anreroposterior (AP) curves may be increased at the apex. AP curves flatten at rhe crossover. The crossover is a poinr where an S curve crosses the m idline co the other side. By international convenrion, scoliotic curves are named for their convex side. For example, rocoscoliosis right means a curve that is convex co the right by being side bent ro the lefr.
POSTURAL DECOMPENSATION
Gravitational force acts universally co affect upright poscure. De com pensation occurs when an individual's homeostatic mecha nisms are overwhelmed (11). Several conditions can overwhelm host facrors. Traumatic decompensation occurs when macrorrauma or re currem m icrorrauma disrupts ligamencous stabiliey of the spine. Fractures of the spine, pelvis, or lower extremiey may produce sacral base unleveling or the need for other compensarory changes above the area of the rrauma. Congenital or acquired struccural changes may create chronic poscural srrain and decompensation. Conversely, chronic postural
582
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Rib hump
Cervical hyperlordosis -:=�'--r-.,;<..j�
Right rotoscoliosis
Right Increased
short leg
thoracic
syndrome
kyphosis -------r- V"),. ...
Lumbar hyperlordosis ---+-C"n
,
\ J v------1r---+_ Grade I spondylo Iysthesis
A.
8.
FIGURE 41.1. A: Disorders in the coronal and horizontal plane: short leg syndrome and rotoscoliosis. B: Disorders in the sagittal plane: lumbar and cervical hyperlordosis, thoracic kyphosis, and LS-S1 isth mic spondylolisthesis. (From Kuchera WA, Kuchera Ml. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:47, with permission.)
stress can initiate structural change. This is a classic example of the reciprocity of structure-function interrelationships. Unlevel ing of the sacral base or a deformed vertebra due to fracture or congenital deformation leads to compensatory curvatures of the spine. Occasionally an unlevel sacral base is observed in an x-ray image with a straight spine above it. This requires mus cular effort, resulting in spinal musculoligamentous srrain that may manifest as back pain or even as headache. As the person grows older and the muscular compensation becomes inadequate, functional scoliosis manifests and structural scoliosis eventually develops (12). Likewise, isthmic L5-S1 spondylolisthesis is a bony structural change often initiated by stress occurring pre dominantly in the sagittal plane ( 1 3 ) . This leads to decompensa tion, spondylo(ysis, and finally spondylolisthesis. These acquired bony structural changes often necessitate functional demand on
musculoligamentous structures to resist postural stresses in the region. Personal conditions, inactivity, and aging potentially predis pose people to decompensation of the spine. Changes of body · habitus that accompany pregnancy, obesity, muscular weakness related to aging, and poor sitting or standing habits produce pos tural stress and can initiate decompensation. Work environments or recreational activities requiring strenuous posturing may also result in postural decompensation. Abnormal gait may initiate the need for compensation or pre cipitate decompensation. Examples include the gait produced from unilateral pes planus (Hat foot), wearing shoes with high or worn heels, and dysfunctional gait following ankle sprains or strains. These conditions affect the base of support and there fore stimulate compensatory changes in posture. If continued
41. Considerations of Posture and Group Curves
Segmental Facilitation at �-+-+--7' Crossovers ,----L-' and Apices
Gravity line I
Gravity line I
FIGURE 41.2. Gravitational strain pathophysiology. Crossover sites are found where the center of gravity line crosses bony posture. These sites have a high incidence of segmental facilitation. (From Kuchera WA, Kuchera ML. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:47, with permission.)
indefinitely, these changes could progress ro decompensation with rotation, scoliosis, lordosis, and/or kyphosis. Postural progression from a healthy state ro a dysfunctional state leads ro symproms and a structural pathologic state. The body first tries ro compensate for imbalance by altering motion characteristics and tissues in its spinal structure. The result is a functional scoliosis in the coronal plane. I f this remains roo long, it develops a fi xed componenr and becomes a structural scoliosis (12). Other symproms occur in a person with spinal decompensa tion. These usually originate at the areas of crossover where the spinal curve crosses from side ro side or anterior ro posterior across the weightbearing line (Fig. 4 J .2). These crossover points may be [he site of local subjective j oint and tissue symproms. They could also result in facilitated segments ( 1 4 , 1 5) and somarovisceral re Hexes, producing inappropriate increases in sympathetic activity and related organ dysfunction.
PATTERNING Spinal Patterning
The nature of postural compensation is ro react ro a disturbance of posture with change throughout the remaining somatic tis sues. These changes tend ro overcorrect slighdy for postural dis turbances. They alternate from one body region ro the next and tend ro occur in regions above and below the initial change. Most commonly these changes occur at the so-called transition zones, areas where anaromic structure changes create the potenrial for the greatest functional change (Fig. 4 J .3). Describing these regional changes in a patient can lead ro recognition of panerns (l 6-18). Pa[[erning provides a convenient way of summarizing common
583
prorotypes of compensation. Postural patterns or panerning refer ro classifiable combinations of regional compensarory change. Compensation involves all three cardinal planes because spinal motions are biomechanically linked (10). Scoliotic, rotational, lordotic, or kyphotic group curves can therefore develop as com pensation for postural stressors. The curve in a given plane often occurs in one direction in one region and in the opposite direc tion in the next spinal region so that the body can maintain some type of postural balance. Postural panerns can be classified by whether they can be re duced by specific functional maneuvers. If some spinal motion such as side bending can reduce a lateral curve, it is known as a functional or secondary scoliotic curve. I f it is unable ro be re duced, it is known as a structural, fi xed, or primary scoliosis. Func tional scoliosis is reversible. Structural scoliosis is fi xed. Because structure and function are interrelated, many scoliotic curves are a mixture of these two classifications. This phenomenon is also seen with postural patterns in the other planes. Clinical Significance of Group Curves
Lateral curves contribute ro postural imbalance by producing po sitional asymmetry that may lead ro back pain or predispose a patient ro recurrent somatic dysfunctions. They may involve a loss of energy because of the increased active muscle contraction ( 1 9) needed to counteract gravity or need ro ambulate. Not all anaromic asymmetries can be corrected. In searching for an an swer ro the significance of a lateral curve in a patient, consider both structure and function. Although the physician often tries ro improve the structure, reducing asymmetry does not necessarily improve the function of the patient. The obj ective of treatment is to maintain or improve function of the patient within their eXlstlI1g structure. Group curves (type J, neutral) typically involve multiple seg ments. Often the longer outer muscles are involved rather than the short, deep segmental muscles. Multiple segments lack seg mental specificity in terms of altered neural activity. By con trast, type I I nonneutral dysfunction typically involves single seg ments. Segmental dysfunction is more likely to be associated with changes in spinal cord function, which osteopathic physicians as sociate with somatic dysfunction. Osteopathic physicians differ regarding the significance of group curves. Some physicians focus on nonneutral type II sin gle segmental dysfunction, while others emphasize treating group curves as well. The approach should depend on the individual patient: what is the functional significance of a group curve for the patient? I f the group curve contributes to dysfunction of the patient, it should be treated. Clinical Significance of Fascial Patterns
Postural panerning influences and is influenced by the fascias and related structures. J. Gordon Zink described patterns (18) that are clinically relevant to the diagnosis and treatment of fascial compensation and decompensation. Based on the palpatory fas cial preference to motion (see Chapter 68), these fascial patterns may be classified as ideal, compensated, or uncompensated (Fig. 41.4). The postural influence on fascial patterning is important
584
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 41.3. Transition zones are anatomically defined and their function is affected by skeletal, arthro· dial, and myofascial anatomy. Transition zones occur at occipitocervical junction, cervicothoracicjunction, thoracolumbar junction, and lumbosacral junction. Between each transition zone lies a definable region of spine. (From Kuchera WA, Kuchera ML. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:47, with permission.)
41. Considerations of Posture and Group Curves
I
Compensated patterns
ItI
Uncompensated patterns
585
I
OA
I
CT
I
TL
I
----
Alternating
----�
----
Not
alternating
_ ____
FIGURE 41.4. Fascial patterns that alternate in direction from region to region are typically compensated
patterns. Those that do not are uncompensated and usually traumatically induced. OA, occipitoatlantal; CT, cervicothoracic; TL, thoracolumbar; LS, lumbosacral. (From Kuchera WA, Kuchera ML. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:47, with permission.)
for understanding the effect that postural management has in improving the respiratory-circulatory model (20). Conversely, fascial preference inAuences tissues and skeletal structures of each region producing the dynamic postural characteristics of that body region. Tensegriry is an additional model in which fascial patterning and musculoligamentous tensions take on primary im pOl·tance. Described by Buckminster Fuller in 1929, tensegrity modeling explains a number of low-energy integrated structure function arrangements. A number of clinical models cite tenseg rity principles (21,22,33) with respect to orthopedic medicine, osteopathic medicine, and postural balance.
Clinical Significance of Musculoligamentous Patterning
Musculoligamentous structure and function are also significantly inAuenced by, and responsible for, static and dynamic postural alignmenr. Gravitational stress placed on these structures to main tain a patient's posture is a constant and greatly underestimated stressor. In a patient with less than ideal postural alignment, grav itational stresses are amplified. When the viscoelastic deforma tion properties of muscle are unable to resist the stress imposed, predictable pathophysiologic changes occur (23). These changes are both functional and structural. The elastic component repre sents the transient functional change in connective tissue length occurring in response to stress. The viscous component, on the other hand, is responsible for the more permanent deformation of connective tissue that occurs with static postural change. Musculoligamentous structures are affected early in patients with gravitational strain and can be easily recognized. The symptoms arising from the resultant pathophysiologic condition have certain associated palpable characteristics, including the following: Muscle spasm in postural (antigravity) muscles Subtle weakness to muscle testing in postural antagonist (pha sic) muscles • Tenderness over ligamentous and osseotendonous attachments involved in postural stability
•
•
• •
M yofascial trigger points Edema or bogginess
Not missing such palpable changes or postural pattern clues is important. M yofascial strucrures undergo sustained changes in length; studies (24) suggest that deleterious change is most pronounced in shortened muscles. New collagen, with a half-life of 10 to 12 months, realigns the connective tissues in response to vectors of stress, perpetuating postural problems and maintaining the biomechanical amplification of gravitational stress. Postural patterns that are compensated can decompensate. The structure of the muscle and its function are related. Struc ture and function play a major role in the muscle patterns com monly seen in posture-initiated pain and dysfunction. Postu ral stress on muscles leads to chronic, recurrent trigger points (25), consistent myotomal and scleroromal pain patterns (26), and predictable functional changes. Postural muscles are struc turally adapted to resist fatigue and function in the presence of prolonged gravitational exposure. When their capacity to resist stress is overwhelmed, these postural muscles become irritable, tight, and shortened (27). M any muscles, antagonists to these postural muscles (27), react when stressed by becoming weak or pseudoparetic. Therefore, gravitational strain patterns reveal a dysfunctional pattern of tight and weak muscles in a postural pattern (Fig. 4l .5) (13,27). Patterned involvement of a number of the muscles s hown in Tables 4l .1 and 41.2 should alert the osteopathic physician ro this underlying cause. In these patients, treatment of the dysfunctional postural alignment yields more lasting results than treatment of the recurrent myofascial trigger points or muscle imbalances in isolation.
TREATMENT
Treating a patient with postural decompensation requires appro priate diagnosis of the functional capabilities of that individ ual's structure. The treatment goals may depend on how long the imbalance has been present and how much decompensation has already occurred. Structural treatment goals are directed at
586
VII. Osteopathic COrLSideratiorLS in Pafpatory Diagnosis and Manipulative Treatment
Weak,
Weak,
Pseudoparetic
Pseudoparetic
Tight, Spastic
Muscles
Muscles
Muscles
Quadratus lumborum Internal and external obliques Quadratus lumborum
Rectus
Psoas
abdominus
Gluteus medius
Iliolumbar ligaments Posterior Sacroiliac Ligaments Gluteus Medius Sacrotuberous Ligaments
Glutei
Tensor fasciae latae
Quadriceps
Piriformis
(except
Iliotibial tract
rectus femoris)
of fascia lata Hamstrings
Gastrocnemius and Soleus Gastrocnemius Tibialis
and soleus
anterior
Peroneus longus and brevis
FIGURE 41.5. Coronal and horizontal postural patterns usually alternate from side to side in adjacent regions with stressed muscle groups typically on the convex side of each postural curve. Sagittal plane postural patterns involve postural muscles and their antagonists as listed in Tables 41.1 and 4 1.2. (From Kuchera WA, Kuchera Ml. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:47, with permission.)
establishing the optimal function their existing structure is capa ble of achieving. Functional treatment goals promote free motion within an optimally balanced posture. Treatment of postural problems emphasizes compliance, espe cially in the initial phases of the reeducation program. Compli ance by the patient is essential and can be enhanced if the patient understands the rationale behind the treatment procedures and requirements. The choice of treatment modalities to achieve these goals also depends on the degree of decompensation present in the patient and an estimate of the patient's homeostatic reserves. The physi cian may choose a combination of the modalities discussed in the following sections of this chapter and discussed more fully in Chapter 43. Osteopathic Manipulative Treatment
M anipulation plays an intimate role in the formulation of any postural treatment protocol. M anipulation is defined as the use
of the hands in a patient management process using instructions and maneuvers to achieve maximum painless movement of the musculoskeletal (motor) system in postural balance. Osteopathic manipulative treatment (OMT) helps prepare muscles, j oints, ligaments, and other supportive soft tissue to bet ter accept positive postural change. Tension that is not addressed in these structures often prevents an optimal compensatory re sponse. Additionally, hypomobiliry often creates pain or ache in the sites seeking to compensate or change under the fotces of homeostasis. Manipulative Treatment of Group Curves
Several principles govern the management of group curves. First, the physician needs to identify and treat the cause of the curve. If a patient has an anatomic shorr leg with sacral base unleveling, the shorr leg is treated to level the sacral base and decrease the curve. As a patient adjusts to treatment for postural rebalancing, the spine must remain mobile to compensate for
41. Considerations of Posture and Group Curves
TABLE 41.1. SPASTIC MUSCLE SYMPTOMS Structure Iliopsoas muscle
Symptoms Inability to stand straight (psoas posturing);
587
stretching or mobilizing the concavity while strengthening the convex side. If a curve has been present for some time, treatment of the curve improves motion within the curve. However, the curve itself or some asymmetry within the spine may remain.
knees flexed; recurrent L 1-2 somatic dysfunction; pain referral to back and anterior groin; positive Thomas test Quadratus lumborum muscle
Low back pain referred to the groin and hip; exhalation 12th rib somatic dysfunction; diaphragm restriction
Hamstring muscles
Pain sitting or walking; pain disturbs sleep; pain referral to posterior thighs; straight leg raising limited mechanically
Piriformis muscle
Pain down posterior thigh; may entrap peroneal portion of sciatic nerve;
OSTEOPATHIC MANIPULATIVE TREATMENT DIRECT TECHNIQUES Epigastric Thrust
Findings A patient presents with group curve (type I, neutral) convex right, apex at T7. The curve is rotated right, side-bent left. There is restriction of right side bending and left rotation.
perpetuated by sacroiliac dysfunction; associated with pelvic floor dysfunction, dyspareunia, and prostatodynia Thigh adductor muscles (short) Gastrocnemi us-soleus complex
Pain referral to the inguinal ligament, inner thigh, and upper medial knee Nocturnal leg cramps; pain referral to upper posterior calf, instep, and heel
Procedure (Fig. 41.6) 1. Stand behind the seated patient.
2. Patient's hands are behind their neck. 3. Place a towel or small pillow over apex (T7 right side). 4. Place your arms under axilla and over patient's wrists. 5. Contact pillow (T7 right side) with your epigastrium.
the change; this is where osteopathic manipulation is useful. Long-term anatomic change, however, does not disappear with manipulation. Second, if focal muscle hypertonicity has produced a curve, the muscle hypertonicity that produces the curve must be found. When this is removed, the curve disappears. Causes of muscle hy pertonicity are varied. Segmental dysfunction may be the cause. The dysfunction may be the result of a viscerosomatic reflex. My ofascial triggers may be involved. Kimberly and Funk (28) looked for nonneutral dysfunction within a neutral curve. A nonneutral segment involves rotation into the concavity. This might be a segment that is out of step with the rest of the segments forming rhe group curve. The concavity of a curve is the tight or restricted side, while the convexity is the unstable side. Exercises or manipulation involve
6. Side bend right, translate T7 left to engage barrier.
TABLE 41.2. INHIBITED MUSCLE SYMPTOMS Symptoms
Structure Gluteus minimus muscle
Pain characteristic when arising from chair; pain referral to buttock, lateral and posterior thigh; "pseudosciatica"; antalgic gait; positive Trendelenburg test
Gluteus medius muscle
Pain aggravated by walking; pain referral to posterior iliac crest and sacroiliac joint; positive Trendelenburg test
Gluteus maximus muscle Vastus muscles
Restlessness; pain sitting or walking up hill; antalgic gait Buckling knee; weakness going up stairs; thigh and knee pain; chondromalacia patellae
Rectus abdominis
Increased lordosis; constipation
muscle Tibialis anterior muscle
Pain referred to great toe and anteromedial ankle; may drag foot or trip when tired
FIGURE 41.6. Epigastric thrust for group curve convex right. Treatment position reverses side bending.
588
VI!. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
FIGURE 41.8. Treatment with muscle energy with emphasis on side FIGURE 41.7. Patient astride table for treatment of group curve convex
bending.
left.
3. Place left hand over apex (T9 on right), adding forward or backward bending to localize to that level.
7. Final corrective force is a thrust with your epigastrium over the apex, combined with genrle upward traction force through the patient's axilla/arms.
4. Side bend right by depressing patient's right shoulder.
8. Recheck
6. Engage side-bending barrier. Hold.
Patient Astride Table
Findings The patient presents with group curve (type I, neutral) convex left, apex at L1. The curve is rotated left, side-bent right. There is resrriction of left side bending and right rotation.
5. Translate apex (T9) to the left. 7. Patient attempts to raise right shoulder for 3 to 5 seconds. 8. Wait, then engage new barrier. 9. Repeat several times. 10. Recheck.
OTHER TREATMENTS
Procedure (Fig. 41.7) 1. Stand behind the patient seated astride the end of the table. 2. Patient places hands behind the neck, interlacing fingers. 3. Place right arm in front of the patient's thorax and contact the patient's left arm. 4. Contact apex (Ll left side) with your hand, adding forward or backward bending to localize the sagittal plane barrier.
5. Side bend the patient to the left, to barrier. 6. Rotate the apex (Ll) right, engaging the barrier. 7. Apply a high velocity/low amplitude final force, increasing the rotation to the right. 8. Recheck. Muscle Energy
Findings The patient presents with group curve (type I , neutral) convex right, apex at T9. The curve is rotated right, side-bent left. There is rem'icrion of right side bending and left rotation.
Procedure (Fig. 41.8) 1. Stand behind the seated patient. 2. Drape right arm over patient's right shoulder.
Postural Education
Educating and modifYing a patient's perspective are often re quired in addition to the treatment of the myofascial system. Teenage girls, for example, may slump severely because. they are embarrassed about the development of their breasts. They may also not want to look taller than teenage boys who chronologi cally mature later. This personal attitude many teenage girls have toward their body must be changed by education about normal growth and development. Other patients need treatment of their primary psychologic depression that results in a secondary postu ral slump. Proper postural education for the work site and other activities of daily living is also beneficial. Postural Exercise
Exercise programs must be carefully prescribed. Exercise of a mus cle that is under continued stress only weakens and stresses asso ciated soft tissues further. Rest and reduction of postural stressors with adjunctive postural orthoses and/or manipulation may be required before prescribing a directed exercise ptogram. Pelvic coil exercises (29) are often beneficial for sagittal plane postural problems. In patients with coronal plane postural decompen sation, the Konstantin (30) exercise program has been statisti cally shown to improve postural alignment. Effective postural exercise protocols optimally include the goal of proprioceptive
41. Considerations of Posture and Group Curves
589
reeducation. Promotion of Aexibiliry for realignment and selec tive strengthening for stabiliry in hypomobile areas are goals for postural exercise.
and postural realignment to prevent return of musculoligamen tous strain, this protocol can be an effective conservative approach to hypermobiliry and ligamentous laxiry (33) .
Postural Bracing
Surgery in Postural Decompensation
Static structural bracing has both positive and negative aspects. Although such devices support the structure and initially reduce ligamenrous and muscular stress, the m uscles soon become de pendent on the support provided. The longer the brace is worn, the weaker the patient's own muscles become. It is therefore im perative that the physician links the patient's brace treatment with an ongoing exercise program. Static braces are better for provid ing rest in an acute condition than for treating a chronic one. I deally a physician should not introduce a static brace without having a plan to replace it (3 1 ) .
When an insurmountable problem is primarily structural, its treatment is primarily structural. I n unstable situations, or in situations that have not responded to conservative care, surgery m ay be performed. I n the case of severe scoliosis or highly sym p tomatic spondylolisthesis, this could consist of fusing vertebrae. Surgical implantation of orthopedic rods or other stabilizing ap paratuses may also be required. Surgical techniques have even been successfully used to lengthen anatomically short legs.
CONCLUSION Postural Orthotics
Functional orthotics serve to direct, guide, and/or reeducate the body, as opposed to directly taking over support. They are capable of inAuencing physiologic parameters and reducing asso ciated low back pain. With respect to postural realignment, this class of treatment modalities includes several specific orthotics (see Chapter 43). The Levitor® pelvic orthotic, which was biomechanically designed specifically to reduce graviry-induced musculoligamentous stress, has its greatest effect within the sagit tal plane. Foot orthotics incorporating heel lifts have their effect primarily within the coronal plane. Anterior sole lifts maxjmally affect the horizontal plane. All three of these examples, however, affect posture in all cardinal planes simultaneously (32), and each ultimately has systemic effects . Functional orthotics in conj unc tion with an osteopathic approach have been documented ( 13) to reduce or reverse lordosis, kyphosis, and scoliosis, decrease low back pain and other musculoskeletal symptoms, improve respiratory-circulatory functions, decrease energy demands, and decrease segmental facilitation. Flexible foot orthoses and the Levitor® pelvic orthotic do not replace normal muscular func tion. Therefore, their use does not weaken associated muscles. Electrical Stimulation and Posture
Electrical stim ulation of paras pinal muscles has been used in some centers. Electrodes are placed in the muscles on the side of the spinal convexiry. The electrodes are connected to a direct current from a control box. An electrical current causes contraction of the muscles on the side of the convexiry and is postulated to help reduce scol iotic curvatureo Research suggests, that used alone, this modaliry is not effective in reversing scoliotic curves but is recommended by some centers as part of a unified treatment regimen to assist in muscle strengthening or pain relief. Prolotherapy
Prolotherapy (sclerotherapy) is injection of a proliferant solution into a ligament (26). When postural strain biomechanically over whelms structural integriry, ligamentous laxiry can result. Injec tion of a proliferant solution into the ligament at its fibro-osseous insertion can increase stabiliry. Combined with exercise, OMT,
Postural diagnosis and treatment are perfectly consistent with the tenets of the osteopathic philosophy. Careful exploration of the homeostatic response of the body unit as reAected in the structure and function of that individual's posture permits specific treatment design for total patient management. Posture is not j ust a stack of spinal curves with muscu loligamentous connectors. Posture is inAuenced by the patient's emotional-spiritual-psychological self. It has been astutely ob served that posture, to a large degree, is also a somatic depiction of the inner em otions. In this fashion there is no doubt that posture can be considered a "somatization of the psyche" (34) . Postural realignment requires reintegration of peripheral and central fac tors that are physiologically, psychologically, and biomechanically linked. Several conservative modalities are available to the osteopathic physician to aid in the realignment process. These include OMT, functional orthotics and orthopedic braces, exercise prorocols, and patient education. There is an intimate relationship between OMT and postural balance. The osteopathic physician seeks to achieve maximum function of the neuromusculoskeletal system in postural balance and to prepare the patient's neuromuscu loskeletal system to respond to postural realignment. Postural treatment generally supports the patient's homeostasis. Postural gravitational stress s hould be considered a factor in the general health status of each and every patient. It should not be reserved only for consideration in cases of recurrent so matic dysfunction, myofascial trigger point syndromes, scoliosis, or spondylolisthesis. Rather, consider postural treatment strate gies (Chapter 43) whenever postural patterning of group spinal curves or recurrent skeletal, arthrodial, or myofascial dysfunction is diagnosed.
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RADIOGRAPHIC ASPECTS OF THE POSTURAL STUDY MICHAEL L. KUCHERA WILLIAM A. KUCHERA
KEY CONCEPTS • • • • • •
Use of postural study x-ray series Impo.rrance of standardization of postural x-ray series Equipment used in performing a postural study Essential views for complete postural x-ray series Methods for obtaining postural x-ray series and reasons for following standardized procedures Explanations of concepts related to radiographic image analysis: --Vertebral rotation and side bending -Cobb angles -Sacral base unleveling -Pelvic rotation -Angle of sacral base -L3 weightbearing line -Pelvic index -Lumbos�cral and lumbo-lumbar lordotic angles -Evidence-based reliability and validity
tion of postural studies. J. Stedman Denslow and his co-workers called for standardization in 1955 (3), although even roday, out side of the osteopathic profession, relatively few academic medical institutions have adopted that recommendation. Standard proto cols provide measurable, accurate, reproducible data ro correlate with the osteopathic palpatory structural examination. Standardized postural x-ray views documenr "repeatable find ings when the state of the patienr is unchanged and provide valid information concerning improvemenrs or regressions in skele cal structure which are associated with changes in the patient's condition." (3). Postural x-ray views taken according to a stan dardized protocol can be accurately and consistently measured for postural information by radiologists or attending nomadiologist physicians (4). Many radiologists are not trained to do postural studies specif ically for osteopathic analysis but will conduct them for referring physicians if given an appropriate protOcol. This chapter provides a method (5) for evaluating the pelvis and spine. This method has the following advantages: • • • • •
Osteopathic physicians have used radiographs for many years to better understand and study structure and function. The roenr gen ray was discovered in 1895; by 1898 the American School of Osteopathy in Kirksville, Missouri had acquired the second ma chine west of the Mississippi. In 1898, this equipmenr provided the earliest roentgenologic studies of circulation (1). Hoskins and Schwab introduced the standing postural x-ray series in 1921, opening the field for clinical interpretation and integration. Martin Beilke in 1936 acknowledged the value of the technique by observing: "The osteopathic profession can lay claim to these contributions as being strictly original and especially applicable ro our approach in finding etiological facrors in a given pathological process and in applying corrective measures" (2). For many years, lack of standardization for a postural x-ray procedure prevemed the profession from combining important multicenter data. It also prevented universal clinical interpreta-
Standardized Accurate Reproducible Practical Inexpensive
The measuremems obtained through the use of this protOcol can be imerpreted clinically in the context described in other chapters of this text, including postural diagnosis and treatment (see Chapters 41 and 43). MATERIALS
The following equipmem is needed to employ this standardized protOcol: I.
2. 3. 4. 5.
Vertical Bucky diaphragm Adjustable holder for plumbed wire Piano wire or metal core fishing line Plumb bob Level metal base plate or level floor
592
VII
Osteopathic Considerations in Palpatory Diagn osis and Manipulative Tr eatment
''' I :", '''
':'�'-'
,
INTERNAiiON Al
'"
I
I ,j I
FIGURE 42.2. Adjustable film cassette holder.
FIGURE 42.1. Vertical Bucky diaphragm and piano wire reference.
The vertical Bucky diaphragm is mounted on (he wall for best results (Fig. 42.1). The adjustable holder (Fig. 42.2) is designed to move the plumbed wire exactly over the desired point on the base plate. Piano wire, 0.020 inches in diameter, is ideal for this system. It is pliable and durable for adjusting to the desired shape, and it is readily identified on the exposed film because of its density. Alternatively, metallic core fishing line has been used and is reported to kink less over time. A plumb bob (Fig. 42.3) of any size or configuration is attached to the wire. These items are relatively inexpensive and available from hardware stores. A level, rectangular metal base plate (Fig. 42.4) is made from 1/4-inch gauge steel and measures 70 x 50 cm. It is leveled and cemented or fixed to the floor. This insures a level plane for the patient to stand on (unlevel floors may accentuate or hide an unlevel sacral base). The floor may be used instead of the metal plate if it is absolutely level in two planes. A modified
cross-hatched grid is permanently marked on the surface of the plate or on the floor to ensure accurate alignment of the patient's feet. The metallic wire is attached to the adjustable holder. If pos sible, it is passed behind the protective covering on the Bucky diaphragm (Fig. 42.1). The plumb bob is attached to the wire to establish a vertical reference line. It is adjusted to lie directly over two main cross-sectional base lines that are perpendicular to each other (Fig. 42.4). The posterior line (Fig . 42.4, 1) lies in a plane parallel to the film and the coronal plane of the body. The midheel line (Fig. 42.4, 2) and the plumbed wire lie in the sagittal plane of the body, perpendicular to the posterior line. This plane is equidistant from both heels when exposing the anteroposterior (AP) view. It is just anterior to the lateral malleolus for exposure of the lateral view. The reference line in the AP radiograph is also known as the midheel line. In the lateral radiograph, the reference line is referred to as the postural or weightbearing line (WBL).
PROCEDURE
In patients with suspected postural disorders, a palpatory ex amination and osteopathic manipulative treatment of somatic dysfunction followed by reevaluation ideally precedes referral for
42. Radiographic Aspects of the P ostural Study
593
FIGURE 42.3. Plumb bob and piano wire.
a posrural radiograph. The somatic dysfunctions most likely to create significant transient postural asymmetry are: • • • • •
Sacral shear (unilateral sacral Aexion) Innominate shear (upslipped innominate) Psoas muscle spasm Quadrarus lumborum spasm Innominate rotation
Prior to referral for a postural x-ray series and again imme diately prior to this procedure, it should be ascertained that the patient is not pregnant. The patient prepares for postural x-ray views by removing all clothing and putting on a gown. He or she stands on the ad justable metal base plate with the back facing, but not touching, the Bucky diaphragm (Fig. 42.5). Postural films of the pelvis or any section of the spine are then exposed at a consistent film-rube distance of 40 to 44 inches (72 inches is used by some centers). Information, including radiographic factors and the position of the feet, is recorded on a separate form that is filed with the patient's radiographic records so that positioning of the patient is consistent when a posrural x-ray is repeated at a furure date (see example in Table 42.1). Future examinations are then per formed using the same technical factors. This ensures a uniform, acceptable, and reproducible method. The metallic piano wire, located behind the patient but in front of the Bucky diaphragm and film, will be recorded in an undistorted fashion on the film. It becomes a relevant reference line for assessing deviation from ideal weightbearing in AP and
FIGURE 42.4. Rectangular metal base plate with reference lines. 1, pos 2, midheel line.
terior line;
lateral films. Radiographic measurements can then be obtained using this reproducible gravitational reference line. Anteroposterior Postural Radiographs
To obtain radiographic information relative to coronal or hori zontal plane posture, AP standing postural views are exposed. The patient is asked to stand on the level Aoor plate with the head facing forward, eyes looking straight ahead, arms relaxed to the sides, and knees extended in a locked but comfortable position (Fig. 42.5). The feet are positioned equidistant from and parallel to the midheel base line (Fig. 42.6), far enough apart so that they are directly under the femoral heads. This distance is recorded by noting the distance from the midheel line to the medial aspect of the heels, as indicated by the markings on the base plate. The heels are placed equidistant from the posterior line (Fig. 42.4, 1), with the patient standing as close to the film as possible, in a relaxed posture. This method ensures a reproducible, standard position for the feet (the base for support of posrure). The Bucky diaphragm is adjusted to the desired height so that the AP lumbopelvic film includes the femoral heads, the pubic symphysis, and most of the lumbar vertebrae. The lower part of the Bucky will be slightly lower than the femoral greater
594
VII.
Osteopathi c Considerations i n Palpatory Diagnosis and Manipulative Treatment TABLE 42.1. SAMPLE ANALYSIS REPORT ON WEIGHT BEARING POSTURAL X-RAY SERIES Subject Other Examiners:
Examiner
Date _____
_____ ______________
Height of Femur Heads: (Indicate side of shortness by R or L; measure in millimeters.) Height of Iliac Crests: (Repeat process used above.) Sacral Base: (Is it level or is it depressed? How many millimeters on R or L side? How does this finding relate to the plane of the femoral heads?) Lumbar Rotation: (Indicate R or L and which ones.) Lumbar Lateral Flexion: (Indicate side·bending, right or left, and vertebrae involved.) Pelvic Rotation: (R or L; measure millimeter difference.) Pelvic Tilt: (R or L) Lateral Disalignment of Trunk: (At LS; R or L) Lumbosacral Angle: (Degrees) Relation of L3 to the Sacral Base: (Where is the weight-bearing line in relation to the sacrum?) Lordosis: (Qualitative: Normal, decreased, or increased? Quantitative: Measurement of lumbosacral or lumbolumbar lordotic angle.) Pelvic Index:
FIGURE 42.5. Patient positioned for anteroposterior postural x·ray view.
X= y= PI = X/Y=
mm mm
Anomalies: (Bat-wing, sacralization, lumbarization, facet asymmetry, spina bifida, etc.) Summary:
rrochanrers in order ro include rhe enrire pelvis including rhe pubic symphysis. For a lumbopelvic x-ray exposure, rhe cenrral ray should be ar rhe level of rhe iliac cresr. When raking an AP posrural srudy of rhe rhoracic spine, rhe Bucky heighr is adjusred and rhe cenrral beam is aimed ar rhe xiphoid process, which corresponds ro approximarely rhe T9 level.
the AP view ro insure inclusion of lumbar vertebrae, lumbosacral junction, sacrum, and pubic bones.
Lateral Postural Radiograph
General Considerations
To obrain radiographic information relative ro sagittal plane pos ture, a lateral standing postural view is exposed. The lateral view is obtained by having the standing patient turn ro the lateral position so thar the ankle closesr ro the wire is in a position where it lies just anterior ro rhe ankle's lateral malleolus (Fig. 42.7). This positioning is very important, because the metallic wire will then identify the plane of the patient's lateral WBL. In a patient with an ideal posture, the lateral WBL (gravitational line) should pass through a point just anterior ro the lateral malleolus, and through the greater trochanter, the center of the L3 vertebral body, and the external audirory canal. (6) The other foot is positioned parallel ro the contralateral foot and the same distance apart as was determined when the AP x-ray view was exposed. The patient's arms are crossed in front of the body ro obtain an unobsrructed view of rhe spine. The knees are locked and the normal posture maintained as for rhe AP view (Fig. 42.8) . The Bucky diaphragm and the cenrral ray are adjusted as described in
The x-ray method described is amenable ro rapid adjustment and placement, making it useful in a busy department. It also positions the patient in a weightbearing posture that is repro ducible and records an independent vertical reference line on the film (see Fig . 42.11, RL) that can be used ro obtain accurate measurements. The reference line is unrelated ro the position of the cassette, yet it is perpendicular ro the line of the horizon. Measurements taken from rhe edge of the film may be inaccu rate because of the variable position of the film within the cas sette and therefore would produce misleading or nonreproducible results (7). AP and lateral postural films are typically performed with the patient's shoes off ro determine postural discrepancies . At times, films may also be obtained wirh the patient wearing their shoes, wirh a therapeutic lift in place, ro determine rhe amount of sacral base unleveling that still remains ro be corrected. Both views are exposed immediately after positioning the patient ro eliminare movement from fatigue.
(Comment concerning disalignment and related disturbances. This includes changes in the density of both osseous and soft tissues such as muscles and ligaments.)
42. R adiographic Aspects of the P os tural Study
595
-
FIGURE 42.8. Patient positioned for lateral postural x-ray view.
FIGURE 42.6. Midheel positioning.
Somerimes borh righr and lefr oblique x-ray views are necessary ro evaluare rhe neural arches, rhe inrerverrebral foramina, and a parienr wirh suspecred spondylolysis. Such oblique views may be obrained wirh rhe parienr sranding, alrhough rhis has nor proved helpful in evaluaring a parienr's posrure. The exposure of rhe parienr ro ionizing radiarion in rhis srudy is minimal. For example, rhis prorocol is calculared ro expose rhe parienr ro 0.12 rad for rhe AP posrural view bur could be
reduced even furrher wirh only 0 .011 rad ro rhe gonads, using a lead gonadal shield (7). RESULTS
Admirredly, clinical correlarion wirh radiographic findings of lumbosacral anomalies is not as straighrforward as many would like. Staric findings from posrural radiographs should be corre lated with various dynamic aspecrs of the clinical examination, including palpation. In this manner, relevanr structure-function and postural-biomechanical insights may be uncovered. In 1934 Ferguson noted, "Our spines were developed for the four-footed position and are not yet adapted ro the erect, so mechanical weak ness at the lumbosacral area is usual rather than exceptional. We must consider the lumbosacral area, not as normal or abnormal, bur as mechanically sound or mechanically unsound (8)." In j udging whether the lumbopelvic region is mechanically sound, a standard postural x-ray series may reveal a number of findings that may or may not be clinically relevanr, including: • • • • • • • •
FIGURE 42.7. Patient's feet positioned for lateral postural x-ray view.
•
Facet tropism Sacralizarion Lumbarization Scoliosis Spondylolisthesis Spondylosis Facet arthritis Small hemipelvis Fracture
596
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipula tive Treatment
A L5 essentially becomes
Mayor
S1 becomes
attached to
essentially
the sacrum,
a 6th lumbar
functionally
vertebra
becoming the sacral
maynot
base
articulate
S2 act like
with the
sacral base
sacrum
Coronal One side is
plane facet
o Sagittal -___-4I-3u plane
essentially
E
attached to
One side unattached
Incomplete fusion of
facet
L51aminae
"'" \,",--/
�'�1_E?' -:y
;'":>
2(!
_
Incomplete fusion of S1 laminae
3_- r'
� .-�p
FIGURE 42.9. Common lumbosacral anomalies: A: Batwing transverse processes of L5. B: Lumbarization of 51. C: Sacralization of L5. 0: Facet asymmetry (zygopophyseal tropism) of L4. E: Partial sacralization of L5 (Bertolotti) . F: Spina bifida occulta of both Ls and of 5.
Common lumbosacral anomalies appearing radiographically are depicted in Fig. 42.9. Several of these anomalies complicate selection of landmarks used in postural measurements or inter pretation of postural radiographic data. A few are recognized to cause low back pain or instability in a percentage of patients; oth ers are widely believed to be incidental insignificant anomalies. Some may be viewed as "risk factors;" others are potentially com plicating findings in those patients diagnosed to have regional instability. Interpreting Anteroposterior Thoracic and Lumbar Postural Radiographs
The standing AP film of the thoracic and lumbar regions contains both qualitative and quantitative information about posture in the coronal and horizontal planes. By noting the relative positions of the two pedicles and the spinous process, vertebral rotation can be qualitatively assessed (Fig. 42.10B). In the absence of vertebral rotation, the spinous process is located equidistant from each pedicle. With right verte bral rotation (named in relation to the direction of movement of a reference point on the anterior portion of rhe vertebral body),
the spinous process visualized on the x-ray film appears closer to the left pedicle. With left vertebral rotation, rhe spinous process appears closer to the right pedicle on the x-ray film. . Vertebral side bending is also easily observed on rhis radio graphic view and can be qualitatively reported. Quantitative mea surement of group curves is often more formally reported using scoliosis nomenclature. Scoliosis, by convention, is reported in reference to the convexity of the curve. A right scoliosis is side bent left (convex right). The Cobb method is commonly used to measure scoliotic curves (Fig. 42.lDA). Lines are constructed across the top of the superior vertebral segment and across the bot tom of the inferior vertebral segment of a spinal scoliotic curve. Perpendicular lines are then constructed from these lines. These perpendicular lines intersect to form an angle, the Cobb angle measurement. (Scoliosis, its diagnosis and treatment, is more fully discussed in Chapter 43.) Interpreting Anteroposterior Postural Radiographs of the Pelvis
The standing AP film of the pelvis contains coronal and hori zontal plane postural data. This film is especially important in
42. Radi ographi c Aspects of the P ostural Study A.
Curvature and Cobb measurements Left side
Highest vertebra
Right side
597
B. Right lumbar scoliosis. Note how the vertebral landmarks indicate the rotational component.
_
with superior
Left side
border inclined toward thoracic concavity
Left thoracic scoliosis
Transitional vertebra--Iowest Inferior border thoracIc cavity
__"r-
��:.:/ � Left pedicle overlaps edge �_/ .
vertebra with inclined toward
process
+ ___
�
�(--� � � "h
barely visi le
and highest
lumbar concavity
in normal position
Right thoracolumbar scoliosis
Lowest vertebra , with inferior border inclined toward lumbar
�!f-
Left pedicle posterior . SplnOUS process
' if---
SL Left side
Right rotation, R. pedicle
slightly toward midline
++ Right rotation, R. pedicle -closer to midline
Left pedicle
inclined toward
superior border
No rotation, pedicles
. Spinous
of vertebra
vertebra with
Right side
+++
.
.
.
Right rotation, R. pedicle
--in the midline
-
++++
Right rotation, R. pedicle
beyon d the ml'dl'Ine
RR
=
Right side
=
concave side
convex side
of the curvature
of the curvature
concavity
FIGURE 42.10. Measurement of curvature and rotation by Cobb method. (Illustration by W.A. Kuchera.)
evaluating the degree of sacra! base unleveling as well as deter mining structural leg lengrhs and pelvic rotation with the patient in a weightbearing position. Refer ro Fig. 42.11 when reading the following description of measuring postural radiographs. Lines are drawn from the most superior aspecr of the femoral heads (D), perpendicular to the reference line, and discrepan cies are measured in millimeters. Similar lines are drawn from the superior margins of the iliac crests (E), perpendicular to the reference line, to determine the relative iliac crest heights. A sacral base line (1) is constructed either from the juncrion oEche arricular pillars and the sacral ala (a-d), the sites where the sacral ala and the iliac crests cross each other on the x-ray film (b-Y), or, alternatively, along the line of eburnation across the top of the sacrum ( c-!, as shown in Fig. 42.11 B). The alternative selected should be the one that has the least ambiguity or in which the set of reference points are most easily and accurately identified (9,10). For clinically relevant reasons, this line is extended to the verrical lines extending from the femoral heads (3,4). The amount of sacral base unleveling is reporred as the measured height differential of the sacral base as extrapolated by the sacral base line intersecting the femoral head lines (points Cand C). The margin of error in measuring sacral base unleveling, using this radiographic protocol, has been reporred to be ±O.75 mm (7). Measurements using the different choices of landmarks for identifying the sacral base are reported to have a variability of up to 2 mm (4,7). The osteopathic physician is more interested in leveling the sacral base than making the leg lengths equal, that is, the sacral base unleveling is usually of more clinical significance than com parison of anatomic leg lengths. In the presence of sacral base un-
leveling, the direction of the lumbar side-bending component is also clinically relevant. Roughening of the iliac crest where the il iolumbar ligament attaches or calcification of the iliolumbar liga ment (11) should be noted, as these are markers for postural stress. Pelvic rotation is recognized qualitatively by observing asym metry of the obturator foramina. It can be quantified by measur ing the distance between the pubic symphysis and either the dark line representing the air in the gluteal crease or the median sacral crest (Fto G). (12) The pelvis is said to rotate in the direction in which the anterior portion of the pelvis (pubic symphysis) moves. In Fig. 42.11A rhe pelvis is rotated to the left. Interpreting Lateral Postural Radiographs of the Pelvis
The standing lateral film of the pelvis provides a means for deter mining a number of sagittal plane posrural measurements. These include the angle of the sacral base, the WBL from L3 relative to the sacral base, lumbar lordotic angles, and the pelvic index (PI) (Fig. 42.11C) (see Chapter 43). The angle of the sacral base, also known as the Ferguson angle, or the lumbosacral angle (LSA), is calculated by drawing a line (A) across the sacral base. Another line (B) is constructed to cross line A and to be perpendicular to the reference line (Fig. 42. 1 1 C, lines A and B). The ideal line of weightbearing, previously described as run ning j ust anterior to the lateral malleolus, is represented by the lucent line produced by the image of the metallic reference wire on the x-ray film. This reference line (RL) can also be used to evaluate the position of the center of gravity (normally located
VII
598
Os teopath ic Considerations in Palpatory Diagnos is and Man ipulative T reatmen t
Diagram A
Diagram C RL
4
3 7 L Right side
L
Spinous process
Diagram B
of L5
H
(8) -7"''---1--++1---+(A) S
(G)
'
"
X p F
c'
7
--
Extended
__
,
Extended
laterally
RL
�
-laterally /'"" Most radio-opaque line "_ __ ,I
£}
� i / \' 'I A ----- ---
C'"""-
FIGURE 42_11. Measurements for postural x-ray view. A: Anteroposterior postural measurements. B: Landmark options for measuring sacral base unleveling. C: Lateral postural measurements. (Figs. 42.11 A and C adapted from Kuchera WA, Kuchera ML. Osteopathic Principles in Practice, 2nd ed rev. Columbus, OH: Greyden Press; 1994:63. Fig. 42.11B adapted from Irvin RE. Suboptimal posture: the origin of the majority of idiopathic pain of the musculoskeletal system. In Vleeming A, Mooney V, Dorman T, et ai, eds. Movement, Stability and Low Back Pain: The Essential Role of the Pelvis. New York, NY: Churchill-Livingstone; 1997: 133-155.)
in the center of L3) relative to the lateral malleolus of the ankle, the sacral base, and the femoral heads. The measured L3 WEL is created by constructing a line parallel to the gravitational refer ence line through the center of the third lumbar vertebra (line E in Fig. 42.11 C). This L3 WEL should ideally fall through the anterior one-third of the sacral base. If this line falls posterior to the sacral base, the lumbar facets are subject to increased load. Especially in the case of long-standing, significant stress, the in volved facets on the radiograph will exhibit arthritic change, seen as eburnation (increased density) of these articulations. The PI is calculated from measurements obtained from the lat eral pos[Ural x-ray view (Fig. 42.11 C). The PI is a calculation of the ratio of measurements, in millimeters, of x/y (Fig. 42.11C, Let ters F, G, x, and y). P I quantitatively reflects the relative position of the innominates to the sacrum. Normal PI values are age-related (13) and are typically less than l.00. As the patient ages, this pos-
tural intrapelvic ratio approaches (or, in the same conditions, may exceed) the value of 1 .00. PI has been documented to be increased in some patient populations (Fig. 42.12), including those with chronic low back pain and those with L5- S1 isthmic spondylolis thesis (14). In this latter group, patients with an extremely high PI for their age should be examined for spondylolysis or spondy lolisthesis. Conversely, PI has been shown to decrease in patient populations with L4-5 degenerative spondylolisthesis (15). Lumbar lordosis can be qualitatively assessed as normal, in creased, or decreased. It can be quantified by measuring the an gle created by lines along the top of L2 and S1 (Fig. 42.13L umbosacraL Lordotic angLe), or the top of L2 and the bottom of L5 (Fig. 42.14-L umb o-L umbar L ordotic angLe) (16). These angles average 60 and 43 degrees, respectively (17). A synopsis of nor mative values for measurements reflecting postural relationships in the sagittal plane are found in Fig. 42.15.
42.
R adiographi c Aspects oft he Postural Study
599
1.00 ..... I
�
0.90
w I ...... I ..... 0
0.80
:t
0.70
......
Chronic Low Back pain� ............... "'''''''''' ......
......
......
.....
... ...
.... ...
x w 0 z u > ...J W a..
0.60 0.50
'-N o Low Back
.
Pain
-
FIGURE 42.14. Lumbo-Iumbar lordotic angle using L2 and the bottom 43 degrees). (Illustration by W.A. Kuchera.)
of LS (average
OAO 0.30
o
10
20
30.
40
INCREASING AGE (YEARS)
50
70
80
--------+
FIGURE 42.12. Pelvic index. (Illustration by W.A. Kuchera.)
EXERCISE IN MEASUREMENT OF POSTURAL RADIOGRAPHS
Two exercises follow. One is for measuremenr of the AP postural radiograph and the other is for measuremenr of the lateral postural radiograph (see Figs. 42.11A, B, C). These exercises provide step by-step practice in measuring postural x-ray films taken with the method described in this chapter. Exercise One: Anteroposterior Postural X-Ray View of Pelvis (Fig. 42.11A, B)
4.
5.
6.
Initial Markings and Measurements
Using a fine tip marker, make a dot at the most superior margin of each iliac crest (Eand E'). 2. Place a dot at the most superior margin of each femoral head (Dand [j). 3. Also make a dot at any one of these pairs of sites, whichever are the most easily and accurately idenrified (any one of these I.
7.
FIGURE 42.13. Lumbosacral lordotic angle using L2 and 51 (average 60 degrees). (Illustration by W.A. Kuchera.)
pairs determine a line parallel to the sacral base): a. Where (he superior articular processes of the sacrum inter sect (he sacral ala (a-d), or b. Where the sacral ala and the iliac crest intersect (b-b' ), or c. At the right and left margins of the line of eburnation (i.e., the "mos( prominenr radio-opaque line" ( c-c) running along the top of the S I segment (Fig. 42.11B). To measure femoral head height discrepancies ("short leg"): a. Draw lines I and 2 perpendicular to the reference line (RL). One line passes through Dand the other through [j. b. Measure the difference, in millimeters, berween the points where lines I and 2 inrersect the reference line (RL). To measure iliac crest height discrepancies: a. Draw lines 5 and 6 perpendicular to the reference line (RL). One passes through £ and the other passes through £'. b. Measure (he difference, in millimeters, berween (he points where lines 5 and 6 intersect the reference line (RL). To measure sacral base height discrepancies (the unlevel sacral base): a. Draw lines 3 and 4 parallel to the reference line (RL). One passes through D and the other passes through [j. These lines indicate the WBLs of each femoral head. b. Using your choice of a-d, b-b', or c-c in step 3 above, draw line 7 to pass through this selected pair. The sacral base line, 7, must be long enough to intersect at points Cand C on lines 4 and 3, respectively (constructed in step 6a above). c. Draw lines 8 and 9 perpendicular to the reference line (RL). One passes through Cand the other through C. d. Measure the difference, in millimeters, berween the points where lines 8 and 9 intersect the reference line (RL). To measure the amount of pelvic rotation present: a. Make a dot with a fine tipped marker on the middle of the pubic symphysis (E). b. Identify the gluteal crease (C) which appears as a dark line in the region of the lower pelvis, or identify and place a dot on the median sacral crest (G). c. Measure the difference, in millimeters, for one of the fol lowing: I. Distance berween the pubic symphyseal dot (F) and the gluteal crease (G), or II. Distance berween the pubic symphyseal dot, F, and point G on the median sacral crest.
600
VII.
Osteopathic Considerations in PaLpatory Diagnosis and Manipulati ve Treatment
, " tH
�L4L55152 Ferguson's Angle (Lumbosacral)
Mitchell's Angle
(LSA) ° ° (n = 30 - 40 )
Jungmann's Pelvic Index (PI) age dependent; see Fig.
Weight-Bearing Line (WBL) (n
L2 - L5
nO
=
( + ) -+-1ffi�"H;='---( -)
(MA) (norms not set) Sagittal Plane Postural Measurements
(n
L3
43.12)
=
over anterior' /3 of sacral base)
L2-S,
Lumbolumbar
Lumbosacral
Lordotic Angle (average n = 43 °)
Lordotic Angle (average n = 60°)
FIGURE 42.15. Sagittal plane standing postural radiographic measurements and their normal ranges.
Exercise Two: Lateral Postural X-Ray View of the Lumbopelvic Region (Fig. 42.11C) Initial Markings and Measurements
1. Identify the center of the L3 vertebral body. a. Place a dot with a fine tipped marker at each of the four corners of the L3 vertebral body. b. Construct diagonal lines from the dots on the corners of L3 so that they intersect at a midpoint. 2. Identify the superior surface of the L2 vertebral body. a. Put a dot at the anterior and posterior corners of the supe rior surface of the L2 vertebral body. b. Draw a line, L, that passes through these two dots on L2 and extends some distance posteriorly. 3. Identify the sacral base. a. Place a dot at the sacral promontory and another dot at the posterior-superior extent of the vertebral body of S1. 4. To assess the center-of-gravity L3 WBL: a. From the midpoint in the body of L3 (step 1 above), con struct line E parallel to the reference line (RL) of gravity. b. Line E, the L3 WBL, should ideally pass through the an terior third of the sacral base. 5. To measure the LSA (also known as the Ferguson angle, or sacral base angle): a. Draw line A that passes through two points marking the sacral base. b. Draw line B that crosses line A (point H) and is perpen dicular to the reference line (RL).
c. Measure the angle formed between lines A and B. This is the LSA, alternatively referred to in the literature as rhe Ferguson angle or sometimes as a sacral angle. 6. To measure lordosis (lumbosacral lordotic angle and lumbo lumbar lordotic angle; Fig. 42.13): a. If lines L and A intersect posterior to the lumbar spine (point /), measure the angle they form. This is the lum bosacral lordotic angle (Fig. 42.13). b. If lines L and A will run off before they intersect on the radiograph posterior to the lumbar spine, construct lines that are perpendicular to lines A and L so that these perpendicular lines cross (point Ja). Measure the angle superior or inferior to point 1a . Mathematically, this also measures the lumbosacral lordotic angle and should be identical to that measured by the method used in 6a above. c. The lumbo-lumbar lordotic angle (Fig. 42.14) is measured by drawing an alternative line (A) across the inferior margin of the body ofL5 rather than through the top of the body of S 1. Using the line, L and the "alternate line A," steps 6a or 6b can be employed to determine the lumbo-Iumbar angle.
7. To measure PI (Fig. 42.11C): a. Put a dot on the most anterosuperior point of the pubic symphysis (5). b. Draw a line (G) through point 5 that is perpendicular to the reference line (RL). c. Now construct a line Fthat passes caudally from the sacral
42. Radiographic Aspects ofthe Postural Study
promontory and is parallel to the reference line (RL) . This line must cross line G (point P). d. The distance, in millimeters, from the most anterosuperior point of the pubic symphysis (5) to this intersection point (P) is the measurement "x. " e. The distance, in millimeters, from the sacral promontory to this intersection point ( P) is the measurement "y." f. The PI is a calculated ratio determined by dividing mea surement x by measurement y. (PI xly ; see Fig. 42.12 for age-dependent values.) =
Clinical interpretation of all measurements obtained using the exercises outlined here are dependent upon observing standard osteopathic postural protocols before and during the radiographic studies described. THE EVIDENCE BASE Reproducibility and Validity
Lack of a standard osteopathic postural radiographic protocol renders many measurements meaningless for the purposes of pos tural diagnosis, patient follow-up, or research. In the context of standard protocols however, many postural measurements have been studied extensively for reproducibility, validity, and clinical relevance (21 ,29). Greenman notes the importance of first removing somatic dysfunction and normalizing lumbopelvic mechanics (9) before obtaining a postural x-ray series. Others point out that muscle imbalance involving the quadratus lumborum (7) or iliopsoas ( I4), for example, distorts postural interpretations. Interexam iner standard measurements of error are acceptably small and are remarkably consistent in multiple studies ( I 8-20) using the standard protocols. These might best be summarized as a mean error of less than 1 .0 mm and a maximum error of 2.0 mm for linear measures and 2 degrees for angular measures. These were also the conclusions obtained when manual and computer assisted measurements by different practitioners (radiologist, pri mary care physicians, and osteopathic medical students) (4) were compared. For decades, osteopathic literature has documented the natu ral history of postural changes and also the consistency of radio graphic postural findings (21,22). Repeat studies on leg length inequality of 1 08 subjects found 85% with less than a 1.5-mm difference in measurement and 10% with less than a 3-mm dif ference; in only 3 subjects did the repeat study differ as much as 5 mm (23). The incidence of low back pain symptomatology and coronal plane postural asymmetry is more completely discussed in Chap ter 43, however, prevalence data and radiographic measurements definitely correlate much better than either of the following clin ical estimates of postural asymmetry: Comparison of malleolar levels (24) Mechanical assessment of leg length with a tape measure (7,25) Postural radiographic measurements in the coronal plane have also been correlated with degenerative osteoarthritis of the hip, (23) lumbar osteophytes, (26,27) lumbar vertebral wedging, (26) and a variety of somatovisceral symptoms ( 1 0,28).
601
CONCLUSION
The postural x-ray protocol described in this chapter provides a simple and inexpensive way to obtain accurate, reproducible structural measurements for either research or clinical interpreta tion (Table 42.1). In those sites without a standardized protocol, the radiographic technical requirements are easily shared with and implemented by a consultant DO or MD radiologist. Application of a standardized protocol results in consistent AP standing (postural) views of the lumbopelvic and thoracic regions as well as lateral standing views of the lumbopelvic re gion. A reliable gravitational reference line is produced on each radiograph-essential for proper evaluation of the patient when various postural treatment strategies are being considered or ap plied (see Chapter 43). These protocols and measurement meth ods provide a means of comparing a patient's present posture with established standards of other patients of the same age. It also pro vides a means of gathering data from which, at some future date, a patient's weightbearing posture can be reliably and accurately calibrated and compared, determining if there has been contin ued decompensation with age or an improvement in posture, following some form of corrective treatment. Just as important, these static (structural) findings can be ef fectively correlated with dynamic (functional) physical findings for a more complete assessment and follow-up of patients with suspected postural problems.
REFERENCES 1 . Smith W. Skiagraphy a n d the circulation. j Osteopath. 1 899;3:3 56-378. 2. Beilke M . Roentgenological spinal analysis and the technic for taking standing x-ray plates. jA OA. 1 936;35:4 1 4-4 1 8.
3. Denslow ) S , Chace)A, Gutensohn OR, Kumm M G . Methods in taking and interpreting weight-bearing films. jA OA. 1 95 5 ; 54:663-670.
4. Kuchera ML, Bemben M G , Kuchera WA, Willman M K . Comparison of manual and computerized methods of assessing postural radiographs.
jA OA. 1 990;90(8) : 7 1 4-7 1 5 . 5. Willman M K . Radiographic technical aspects of the postural study. jA OA. 1 977;76:739-744. 6. The Glossary Review Com m irree of the Educational Council on Os teopathic Principles. G lossary of osteopathic terminology. In : D'Alonzo G E ) r, ed. A OA Yearbook and Directory o/Osteopathic Physicians. Chicago I L: American Osteopathic Association; 2000:860.
7. Travell JG, Simon DG. Myofoscial Pain and Dysfunction: The Trig ger Point Manual. Vol I I . Baltimore M D : Will iams & Wilkins; 1 992: 22-88. 8. Ferguson AB. The cli nical and recent roentgenographic interpretation of lu mbosacral anomalies. Radiology. 1 934;22:548-588.
9 . Greenman PE. Lift therapy: use and abuse. jAOA. 1 979;79:238-250. 1 0. Irvin RE. Suboptimal posture: the origin of the majority of idiopathic pain of the m usculoskeletal system. In VleemingA, Mooney V, Dorman T, et aI, eds. Movement, Stability and Low Back Pain: The Essential Role
o/the Pelvis. New York, NY: Churchill-Livingstone; 1 997: 1 33- 1 5 5 . 1 1 . Lapadula G , Covell i M , Numo R , Pipitone V. Iliolumbar ligament ossification as a radiologic feature of reactive arthritis. j Rheltmatol.
1 99 1 ; 1 8 : 1 760-1 762.
1 2. Denslow ) S , Chace )A. Mechanical stresses in the human lumbar spine and pelvis. Postural balance and imbalance. In: Peterson B, ed.
1 983 MO Yearbook. Newark, OH: American Academy of Osteopathy; 1 983:76-82. 1 3 . Kuchera ML. Aging, postural decompensation and low back pain . jA OA . 1 986;886( 1 0):74.
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
1 4 . Kuchera M L. Treatmell( of gravitational strain pathophysiology: I n Vleeming A , Mooney V, Dorman T, e t ai, eds. Movement, Stability and
Low Back Pain: The Essential Role o/the Pelvis. New York, NY: Churchi l l
over a 1 5 year period. jA OA 1 964;63:546-557.
23. Gofron
jP,
Trueman G E. Studies i n osteoanhritis of the h i ps, Pan I I .
Osteoanhritis o f the h i p and leg length disparity. Can Meel Assoc j.
Livingsrone; 1 997:477-499.
1 5 . Kuchera M L, M i ller K. Postural measurements in L4 degenerative spondylolisthesis. jA OA. 1 995;95 (8):496.
1 6. Fernand R, Fox DE. Evaluation of l u mbar lordosis: a prospective and
1 97 1 ; 1 04:79 1 -799. 24. Friberg 0 , Nurminen M , Korhonen K, et al. Accu racy and precision of clin ical estimating of leg length inequality and lumbar scoliosis and comparison of clinical and radiological measurements. International Dis
retrospective study. Spine. 1 98 5 ; 1 0(9):799-803.
1 7. Kuchera M L, Gi tl i n R, Frey- G itl i n K . Aging, lumbar lordosis and low
ability Study. 1 988; 1 0:49-53. 25. Beal Me. A review of the shon-Ieg problem. jAOA. 1 9 50;50: 1 09-
back pain. jA OA. 1 992;92(9): 1 1 82 .
1 8 . Friberg O. C l i n ical symproms and biomechanics of lumbar spine and h i p j o i nt in leg length inequality. Spine. 1 983;8:643-65 1 .
1 9. Friberg O . The statics of postural pelvic tilt scoliosis: a radiograph ic study on 288 consecutive ch ron ic LB patiell(s. Clin Biomech. 1 987;2 : 2 1 1 -2 1 9.
20. Henrad j -CI, Bismuth V, deMol moll( C, Gaux
22. H agen DP. A continuing roell(genograph i c study of rural school chi ldren
J-e.
Unequal length
of the lower l i mbs: measuremell( by a simple radiographic method: application ro epidemiological studies. Rev Rheum Mal Osteoartic.
1 974;4 1 :773-779. 2 1 . Peterson B , ed. Postural Balance and Imbalance (1 983 AAO Yearbook). Newark, O H : American Academy of Osteoparhy; 1 983.
121. 26. G iles LG F, Taylor j R. Lumbar spine Structural changes associated with leg length inequality. Spine. 1 98 1 ;6: 5 1 0-52 1 .
27. Morscher E. Etiology and pathophysiology of leg length discrepancies. Prog Orthop Surg. 1 977:9- 1 9. 28. Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dys fitnction, 2nd ed rev. Columbus, O H : Greyden Press; 1 994. 29. Mense S, Si mons D G . Muscle Pain: Understanding Its Nature, Diagno sis, and Treatment. P hi ladelp hi a, PA: Lippi ncott, W i l l iams & Wilkins; 200 1 .
POSTURAL CONSI DERATIONS IN CORONAL, HORIZONTAL, AND SAGITTAL PLANES MICHAEL L. KUCHERA
KEY CONCEPTS
General Principles • Anatomic landmarks associated with the ideal postural
weightbearing line
• Clinical presentation of spondylolisthesis and different
age-related manifestations
• Two basic rules of exercise and importance of patient
compliance
• Implications of faulty postural alignment
• General somatic patterns in primary postural
dysfunction
• Specific effects of gravity on postural muscles and
Be sure the foundation is LeveL and aLL wiLL be weLL. -A.T. Still
ligaments
• Clinical relevance of gravitational strain
pathophysiology
• Observation, palpation, and radiology in
GRAVITATIONAL STRAIN AND POSTURAL DECOMPENSATION
evaluating postural decompensation and instability
• Osteopathic manipulative treatment used in postural
problems
• Orthotics and types of devices in treating postural
insufficiencies
Coronal and Horizontal Plane Posture • Short leg syndrome as a misnomer
• Biomechanical changes contributing to short leg
syndrome • Biomechanical principles and osteopathic manipulative
treatment in treatment of short leg syndrome
• Treatment modalities for pelvic rotation
• Major classification criteria for scoliosis
• Treatment goals for scoliosis, and implications of each
treatment modality as it relates to the patient's lifestyle and activities
Sagittal Plane Posture • Modalities useful in treating hyperlordosis and
spondylolisthesis
• Classification and general structural condition of
spondylolisthesis
• Radiographic grading severity of spondylolisthesis
Gravity is one of the major disrupters of postural homeosta sis ( 1 ,2). Although it exerts a constant force on all structures, some individuals appear ro be less capable of resisting gravita tional stress than others. These individuals often have weakened support mechanisms, increased functional demand on postural structures, and/or biomechanical risk facrors that augment the gravitational stress challenging their homeostatic resources ( 1 -
5 ) . A postural treatment approach ro these patients is often effec tive in ameliorating their recurrent, predictable patterns of pain and dysfunction as well as relieving a wide range of secondary complaints (6) . A homeostatic response ro gravity begins as soon as the in dividual assumes an upright position (Fig. 43. 1 ) and continues throughout life. Two secondary lordotic curves normally develop in the cervical and lumbar regions ro counterbalance the primary thoracic curve present at birth. These three spinal curves rogether will resist gravity much better than one single sagittal plane curve. They allo w a person ro function in an upright position; how ever they also result in some uniquely human problems affecting both structure and function. These problems are characterized by coordinated compensation occurring in multiple regions and planes. The presence of a number of anaromic and/or congenital con ditions can create significant homeostatic stress on postural mech anisms or can aggravate existing postural decompensation. These
604
VfJ. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
A
B
c
D
E
FIGURE 43.2. Ideal postu ra l a lignment of body in relation to gravita tiona l line. A: Ext erna l audit ory meatus. B: Shoulders. C: Center of t he body of L3. D: T hrough t h e knee. E: Just anterior to t h e lat era l ma l leolus. 10Yrs. 8Yrs. 3 Yrs. 13 Mo. Day 1
5 Mo.
two equal parts. Ideally, there would be no rotati o n in the horizon tal plane of any body region and no coronal plane side-bending asymmetry. Ideal postural alignment i n the sagittal plane (Fig. 43.2) has a center of gravity or weightbearing l i ne that passes through the followi n g anatomic landmarks:
FIGURE 43.1. Changes in sagitta l plane spina l curves from day 1 through age 10 y ea rs. (From Kapandji IA. The Physiology of the Joints. Vol 3. N ew York, NY: C hurchi l l- Livingstone; 1974:17, with permission.)
•
include:
•
•
•
•
•
• • •
•
Anatomic short leg Scol iosis Small hemipelvis Spondylolisthesis Wedge vertebrae
D iagnosis of any one or a combination of these disrupts sym metry and requi res the body to compensate i n order to mainrain postural balance. Ideal postural alignment depends, in part, on balancing the cervical, lumbar, and thoracic curves against the effects o f gravity. Failure to do so i n the sagittal plane results i n lordosis or kyphosis and numetous symptoms associated with posrural decompensa tion . Lordosis has been i mplicated as a destabilizing factor in the development and p rogression o f scoliosis (7). Ideal standing postural alignment in the coronal plane will place the center of gravity line midway between the feet, extend superiorly up the midline of the spine, and divide the body i n to
•
•
Just anterior to the lateral malleolus Just behi n d the mid-knee Femoral head Anterior third of the sacral base (x-ray landmark) M iddle of the body of the L3 vertebra (x-ray landmark) H u meral head External auditory mearus
Failure of the body to align with respect to its center of gravity functionally stresses the soft tissues and joint facets. These struc tures are not designed for weightbearing. Strucrural change and pain i s the result of postural decompensation ( 1 ) . Postural Homeostasis and Strain
Each person with asymmetric postural stress will progressively compensate i n a different way depending, i n part, on his or her u n i que biomechanical risk factors. Nonetheless, certain guid i n g postural principles apply. Posrural changes will take place throughout the musculoskeletal system in an attempt to coor d inate visual, vestibular, and kinesthetic i n put and to distribute stress. Typically, the changes occur more predictably in the lum bopelvic region because of i ts proximity to the center of gravity.
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes C
GR
- Scoliotic Response
605
S - Scoliotic Response
Lumbar spines
Pubis
)\
--------+---11- Horizontal plane
GR
)(
Internal rotation
Internal
FIGURE 43.3.
Pelvic mec hanics. Intra pe lvic rotations occu r b iomec han icaliy a bout their axes of rotation in relation to g ravitati ona l line (GR). The sac rum rotates anteriorly b ecause weightbea ring fa l l s anterior to its 52 axis (F1). Innominates rotate posteriorly b ecause weightbearing is posterior to femora l axes (F2). (From Jungmann M. The Jungmann Concept and Technique of Antigravity Leverage. Rangely, M E: Institute for Gravitationa l Strain Pathology, Inc; 1982, w ith permission.)
Biomechanics
The biomechanical principles that govern gravity's effect on the lumbopelvic region are specific. In the sagittal plane, gravity encourages the sacral base to rotate anteriorly and encourages innominates to rotate posteriorly (Fig. 43. 3) (8,9). This occurs be cause the L3 weightbearing gravitational line falls anterior to the middle transverse sacral axis and behind the femoral axis. Home ostatic mechanisms to resist this counter-rotation are provided by muscular tone as well by as pelvic and l umbosacral ligaments (l0). The body's response to sacral base unleveling in the coro nal plane also follows homeostatic biomechanical principles. The lumbar spine side bends away from and rotates toward the low sacral base. The biomechanics of the typical spinopelvic response to sacral base unleveling is shown in Fig. 43.4. As a curve forms in one spinal region there is a change in the curvature of all other spinal regions. Early compensation is associated with the devel opment of a single, long scoliotic curve in the lumbar or l um bothoracic spine. In this C-shaped curve, the horizon tal cephalad planes are typically depressed on the side opposite the depressed pelvic horizon tal plane. Later, the compensatory mechanisms re distribute postural responsibilities resulting in the formation of several lateral curves. In an S-shaped scoliotic curve, the shoulders and the greater trochanteric planes are typically depressed on the same side as the depressed sacral base.
FIGURE
43.4. Ty pica l postu ra l com pensation for short leg syndrome.
Compensatory changes associated with leg length inequality can also be generalized. The pelvis as a unit typically side shifts and rotates toward the long leg side. The innominate may attempt to compensate for the "short leg" by rotating anteriorly on the short leg side. This fun ctionally lengthens that extremity. The innomi nate on the side of the apparent long leg may rotate posteriorly to functio n ally shorten that extremity. Often , on the long leg side, the foot assumes a pronated positio n , and the lower extremity internally rotates. The lumbosacral angle ( LSA) (see Chapter 42) increases 2 to 3 degrees. The increased LSA and pelvic rotation often mask the presence of an unlevel sacral base (11). The ver tebrae of the most caudal scoliotic curve usually side bend away from and rotate toward the side of the apparent short leg. Pelvic rotation in the horizontal plane occurs con comitantly with biomechanical stresses in the cotonal plane (such as the short leg syndrome) ( 1 2) . This can present a therapeutic challenge when prescribing foot orthotics in an attempt to treat leg length and/or to level the sacral base. Alternating directional patterns of the transitional regions of the body occur in compensation (61) to the rotation of one or more of these regions ( Fig. 43. 5 ) .
Somatic Structures Stressed: Muscl es
Gravity stresses a n umber of somatic structures involved in homeostasis. Each of these structures responds predictably when stressed. For example, postural muscles that are structurally adapted for prolonged stress typically respond by becoming tight
606
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
LClan ro consider a postural diagnosis and can often be traced biomechanically ro gravitational srress on these muscles. Somatic Structures Stressed : Ligaments
FIGURE 43.5. Com pensation in t h e horizonta l p lanes: A lt e rnating pat tern of rotation at t ransition z ones.
when oversrressed. Postural a ntago n ists (phasic muscles) typi cal ly become pseudo paretic and are somewhat weak when tested (Table 43. 1) (13 ) . Patients with postural stress will also o ften have trigger points in a n umber of the muscles listed i n Table 43.1. I n comb ination, the responses of the many i ndividual structures create a recognizable pattern of postural decompensation (1,14). Such patterns o f i nvolvement should alert the osteopathic clin-
Somatic Structures Stressed : Skel etal-Arthrodial
TABLE 43.1. POSTURAL ANTAG O N I STS
Postural Muscles Cervica l and u p pe r t horacic musc l es U pper t ra pezius musc l e Levator scapu lae musc le P ectora lis major (upper part) P ectora lis minor musc l e Cervica l erect or spinae musc les Scalenus musc les Lumbar and lum bope lvic musc l es Tensor fasciae latae musc le Hamstring musc l es H i p adductor musc l es ( short adductors) Gastrocnemius/soleus musc les Piriformis musc l e I liopsoas musc les
Gravity's effect on i ndividuals with postural imbalance or dimin ished homeostati c abilities ro resist gravity functionally srresses a n umber of stabil izing ligamen ts. These ligaments include the i l iolumbar, sacrotuberous, and long dorsal (posterior) sacroiliac l igaments. The i liolumbar l igaments (ILL) are critical structures for sta b i l izing the lumbar vertebrae on the sacral base (10). They are usually the fi rst structures ro be involved with postural decom pensation and are affected by both sacral and i nnominate rota tions (Fig. 43.6) . When stressed, the attachments of these l ig aments become bilaterally tender ro palpation. Uni lateral stress and tenderness are very common in coronal plane postural strain; bilateral tenderness is more common i n sagirral plane srrain con ditions. ILL calcificarion may be seen when there has been long standing postural srrain because calcium is laid down along l ines of stress (Wolff's law) (15 ) . Functional changes include tender ness,.edema, and pain referred ro the lower exrremity (Fig. 43.7); these findi ngs disappear with treatment. The sacrotuberous l igament (STL) and long dorsal sacroi liac (LDSI) ligament respectively resist anterior and posrerior rotarion of rhe sacrum (Fig. 43.8) (16). The LDSlligament con nects the sacrum and the posrerior superior iliac spine ( PSlS) whereas the main part of rhe STL con nects rhe sacrum and ischial tuberosity wirh fibers connecting ro the iliac bone as well. Posrural stress involves a more complex biomechanical in rerac tion than is depi cted i n Figs. 43.6 and 43.8. It involves i n teracrion between these l igaments , the sacroiliac joint, the thoracolumbar fascia, and a variety of muscles including rhe multifidi, biceps femoris, and glutei (16 ) . The pelvic girdle as a foundarion for function and support musr rherefore be i n rerprered in i rs rela tionship ro other areas of the spine and all four extremiries.
Phasic Muscles
Latissimus dorsi musc l e Mid/ lower t ra pezius musc les Rhom b oid musc les Anterior c e rvica l musc les
Quad ric eps muscles Dorsif lexor musc les A bd omina lis musc l es G luteus maxim us musc l e
Reprinted with permission from Kuchera M. Gravitational stress, muscu loligam e ntous stra i n and postura l alig nment. In: Dorma n T, ed. Spine: State of the Art Reviews on Prolotherapy. Philadelphia, PA: Han ley and Belfus; 1995:463-490.
Bone remodels over rime in response ro rhe stress placed upon ir (15). Over rime, rhe vertebrae of parienrs wirh exaggerated or lareral posrural curves will develop wedgi ng of rhe vertebral body and exosroses (spurs). Posrerior weightbearing mechanics trans fer weighr onro rhe spinal facers resulring in mod ified function, i ncreased calcium deposirion rhar may appear on radiographs, and pai n . Degenerative structural change i n joints is also common when there is accentuared functional demand and asymmetry. This af fects both spinal joi nts and orher weight bearing structures, such as rhe h ip joint. Degenerative arthritis of the hip j o i nt often devel ops on rhe long leg side, (17) and is accompanied by tenderness over that grearer trochanter. Long-term radiograph i c postural studies (see Chapre r 42) have shown chronic, progressive postural decl i n e. The resulrant pos tural pattern of spinal curvature continued ro evolve wirh age i n o ne-th i rd of the population srudied (18). The likelihood rhar several lareral curves will evolve is higher when the leg length .
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes
A
607
B FIGURE 43.6. A: Anterior rotation of sacrum bilaterally stresses fibers labeled 1. Posterior rotation of innominates bilater a l ly stress f i bers labeled 2. B: C a lc ification of i liolum b a r ligament is an exc e l l ent exam ple of structu ral c hange resulting f rom excessive functi ona l d em and. ( Radi ogr a p h fr om the Institute for Gravit ational St rain Pathol ogy, Inc., with permission.)
inequality is greater than 10 mm (19). The stereotypic posture of the geriatric patienr depicts a decrease in total height as their kyphotic and lordotic curves accenruate and the radiograph ic measuremenrs show a height diminution (an increased pelvic in dex ratio) within the pelvis (see Chapter 42) (2,20).
POSTURAL DIAGNOSIS
Accurate postural diagnosis requires an understanding of both static and dynamic componen ts of postu ral stress. Importan t pos tural information is gained from independenr and inreractive ex amination of each of these components. These components must then be interpreted with respect to their relative contributions to the stress upon the person as a whole fu nctional being. Correlation of static-dynamic information within the structural-functional continuum of a given postural diagnosis plays a significant role in postural treatment regimens and in ptoviding patient education concerning prognosis. Observation and palpation form the cornerstones of postural evaluatio n . Radiographic a n d computerized range-of-motion analyses pro vide additional or supportive information.
I n itial observation of asymmetry p rovides the in itial clue to variance from the " ideal ." Looking at the space around the body in addition to spinal alignment is also very insightful. Is the space berween one arm and the body greater on one side than the other? Look for the presence of group curves (Chapter 41) . Screen for rotoscol iosis by comparing symmetry in levelness of key paired landmarks with the patient in the static anatomic position and then when the patient bends forward (see the "Screen ing and Symptoms" section under " Scoliosis" later in this chapter). Palpation identifies key landmarks for structural symmetry and gathers information about the fu nctional characteristics of the body u n it. It is also the best tool for uncovering patterns of somatic dysfunctio n , pain and strain, or adaptations charac teristic of postural d isorders. Palpation of the postural response to certain movemen ts helps to differentiate the degree to wh ich a given postural curve is structural (fixed) or functional (Aexi ble) (i.e., does it stay the same or increase or does it reduce or disappear?). Radiographic analys is (see Chapter 42) is used to quantify static postural distortion from the ideal . It may also be used to objectively mon itor progress of a postural treatment regimen. Furthermore, it can indicate congen ital or acqu ired abnormalities
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
608
A.
FIGURE
43.7. I l iolumbar
ligament
pain
pattern
from
postural
imbalance.
that predispose the patient to postural decline or that will com promise the results of a treatment program. Observation and Palpation
Observation and palpation of the spine and pelvis are essential when evaluating the dynamic or functional component of pos ture. Observation and palpation of postural muscles, their antago n ists, and regi onal or group spi nal curves should be performed with the patient in an upright , weightbearing position . With the patient in this upright pos i ti on , they are asked to move into var ious positions to determine whether any observed thoracic or lumbar rotoscoliotic group curve asymmetry can be functionally reduced or elimi nated. The structural component in t hese planes is represented by the spinal asymmetry that is n ot modified by active or passive motion. With the patient supine, the physician determines whether the l umbar curve can relax and be flat against the table. I n functional lumbar lordosis, bendi n g the knees as shown (Fig. 43.9) should permit the lumbar region to flatten onto the table (or floor) . Inability to flatten this curve actively or passively represents a sagittal plane structural component. Be sure to palpate t he lumbar spine when evaluating this element, as hypertrophy of soft tissues in the adjacent flanks may mask the lordotic curve. Alternatively, or additionally, objective measurements can be ascertai ned using varying computerized measuring i nstruments. Some of these i nstruments can measure i ntersegmental as well as regional motions and are used to rei n force the palpatory
B. FIGURE 43.8. A: Sacrum rotating anteriorly winds u p sacrotuberous lig a m ent. B: Sacrum rotating posteriorly winds up the long dorsal sacroiliac ligament. (From Vleeming A, Snijders CJ, Stoeckart R, Mens JMA. T h e role of t h e sacroiliac joints i n coupling between spine, pelvis, legs and arms. In: Vleeming A, Mooney V, Dorman T, et a I . , eds. Movement, Sta bility and Low Back Pain: The Essential Role of the Pelvis. New York, NY: Churchil l-Livingston, 1997, with permission. ) .
A.
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I �. ";I ""
..
0.... ...
,. f,
.
I
'
I
I
-
.
FIGURE 43.9. Lumbar lordosis, with patient actively attem pting to flat ten spine to table. A: Structural component (no red uction of lordotic curve). B: Flattening indicative of functional lordotic curve. (From Si mon DG, Travell JG, Simons LS. Myofascial Pain and Dysfunction: The Trigger Point Manual. Vol I. Ba ltimore, MD: Williams & Wilkins; 1999, with permission.)
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes determination of areas requiring manipulative treatment (hy pomobile areas) and those that need strengthening exercise, prolotherapy, or extrinsic stabi lization (hypermobile areas). Coronal plane decompensation is suspected with certain con stellations of asymmetry, recurrent somatic dysfunction, and tis sue texture change. When this diagnosis is the result o f leg l ength inequality, the standing trochanteric plane, the plane of the PSIS, and the iliac crests are usually depressed on the side o f the de pressed sacral base. Usually the more horizonral cephalad p lanes (shoulders, occipital) are also depressed to compensate for the unlevelness of the sacral base (19) . The number of curvatures between the pelvis and the upper body will determine on which side the more horizontal cephalad planes are depressed i n relation ro the sacral base. The following horizontal planes ( Fig. 43.10) are assessed by standing behi nd the patienr and palpating these key anatomic landmarks:
609
•
PSIS Greater trochanrers • Knee creases •
These static landmarks are helpful in predicting underlying spinal response to coronal plane postural asymmetry. Sagittal plane decompensation is associated with alteration of the anreroposterio r regional curves of the body and specific palpable somatic patterns. In addition to myofascial and l iga mentous clues, anrerior sacral base and lumbar hyperlordosis, craniosacral extension mechanics often accompanies this condi tion. The extension phase of the craniosacral mechanism is o ften accompanied by fatigue, loss of energy, and/or psychological de pression. It is clinically i m portant to recognize that these patients may have problems i n many activities of daily living as well as poor compliance, even with an apparently appropriate postural treatment program.
•
Mastoid processes Acromioclavicular joints • Inferior scapula • Iliac crests •
Radiographic Findings
A B
c
FIGURE 43.10. Levelness of horizonta l p l a nes. A: Occipita l plane. B: Shoulder plane. C: Scapular p lane (inferior). D: I liac crest plane. E: Posterior superior iliac spine plane. F: Greater trochanteric plane.
As mentioned, posture and postural diagnoses involve the un derstandi ng o f both static (structural) and dynamic (functional) characteristics. X-ray i m ages primarily visualize the static or struc tural aspect of posture. They also aid in identifying congenital anomalies and other structural deficiencies that enable gravita tional and other functional strain to overcome the body's home ostatic mechanisms. Finally, postural radiographs may be used to quantify spinal decompensation i n the coronal and horizontal p lanes using the Cobb m ethod (Fig. 43.11) for rotoscoliosis and the M eyerding or Tai llard classification systems ( F ig. 43.12) for spondylolisthesis i n the saggital p lane. Abnormal static postural m easurements can be viewed as be i ng biomechanical (or functional) risk factors for a patient. Using a standard protocol (21) , radiographic measurements outside the normative range suggest a biomechanical disadvantage that in creases functional demand. As the number of biomechanical risk factors i ncreases, homeostatic maint enance of posture is more li kely to fail. These factors not only strain m usculoligamentous structures but also predispose the patient to the development of scoliosis, spondylolysis or spondylolisthesis (22) , or other postu ral diagnoses. A number of coronal plane radiographic studies (23) indicate that sacral base unlevel ing and leg l ength inequality are fairly com mon. About 5 0% of an unselected population had radiographic l eg length inequality o f more than 3/16 o f an inch. Approximately equal declination o f femoral head, sacral base (extrapolated later ally to the femoral head line), and iliac crest were often p resent. Other radiographic studies have also documented the distribu tion of lumbopelvic posi tional relationships with respect to pro vidi ng a foundation for the lower extremity. Yet other stud i es have monitored sco liotic patterns with regard to natural h i story or 111 response to treatment. Radiographic series are also extremely valuable in m ea suring sagittal plane posture. Key radiographic measurements (Fig. 4 3 . 13) used to evaluate a patient for postural management of sagi ttal plane problems are the weightbearing l i ne from L3 (n anterior one-third to one-half of the sacral base) and the modifi ed LSA o f Ferguson (n 30 to 40 degrees) . =
=
A.
B. Right lumbar scoliosis. Note how the
Curvature and Cobb measurements Left side
Highest vertebra
vertebral landmarks indicate the
Right side
rotational component.
� �
with superior
Right side
Left side
border Inclined toward thoracic concavity
No rotation, pedicles
. Spinous
Left thoracic scoliosis
Transitional vertebra--Iowest
in normal position
process
_.;�-
��:.'-Left pedicle �. overlaps edge �/-
.'_
Inferior border
Left pedicle
inclined toward
I Ole barely visible . Left pedlc
thoracic cavity and highest superior border
Right
Inclined toward
thoracolumbar scoliosis
Splnous process
+++
� SL
.
.
++++
Right rotation, R. pedicle
beyond the midline
RR
Lowest vertebra
Left side
with inferior
concave side
convex side
of the curvature
of the curvature
border inclined toward lumbar
.
Right rotation, R. pedicle
-�in the midline
�_
posterior �
vertebra with
lumbar concavity
� �
Right rotation, R. pedicle
slightly toward midline
++ Right rotation, R. pedicle .-closer to midline
�
�(" � �
of vertebra
vertebra with
+
=
Right side
=
concavity
FIGURE 43.11. Measurement of cu rvature and rotation using the Cobb method. In t h e Cobb method, identification of the top and bottom of each curve is most important.
o o
60% slip (Taillard)
cJ o
4/4slip
o o
CJ
FIGURE 43.12_ A: Classification of spondylolisthesis using the Meyerding system. B: Taillard method of classifying spondylolisthesis.
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes
SI
-
IFL � ��L4L55152 .� 0"
level line
30° -40°)
Ferguson's Angle (Lumbosacral)
Mitchell's Angle
=
Weight-Bearing Line
(MA) (norms not set)
(LSA) (n
611
(WBL) (n
=
over anterior 1/3 of sacral base)
Sagittal Plane Postural Measurements
L2 -L5 Jungmann's Pelvic Index (PI) (n
=
age dependent; see Fig. 43.12)
43°)
60°)
Lumbolumbar
Lumbosacral
Lordotic Angle
Lordotic Angle
( average n
=
(average n
=
FIGURE 43.13. Sagittal plane postural (standing) radiogra p h i c measurements and their normal ranges.
Another clinically relevant sagi ttal plane radiographic mea surement is the Jungmann pelvic i ndex (age-dependent norma tive values) . This pelvic index (PI) is the ratio of measurements representing the position of the sacrum relative to the i nnomi nates. The index appears to rise as gravity overcomes the i ndi vidual's homeostatic ability to resist it. The i ndex i s higher for patients with chronic low back pain (20) and for those with other elevated sagittal plane postural measurements (24) . It is also el evated for athletes with high functional demand in the sagittal
A
plane ( 5 ) . The h ighest PI measurements are seen in people with i sthmic (L5-SI) spondylolisthesis (64) . For this reason, if the PI is very high and spondylolisthesis is not visualized on routine lumbopelvic x-ray views, the clinician may eject to order oblique films of the l umbosacral area to detect a spondylolytic defect at the pars interarricularis (Fig. 43.14) . Lumbo-Iumbar or lumbosacral lordotic angles are objective measurements of lumbar lordosis (25). The observation of hy perlordosis i s significant i n the evaluation o f patients with sagittal
B
Spmous process of L5
D
c "Collar" (lysis of
Right superior
pars interarticularis)
articular process Lamina on right side Left
Right
inferior
transverse
articular
process
process
Lumbosacral disc
Spondylolisthesis of
L5 on S 1 makes the
A normal oblique X-ray Image
"scotty dog" appear to be
of the lumbosacral region
L5 on S 1 makes the
makes each lumbar posterior
"scotty dog" appear
arch look as If it were a "scotty dog"
decapitated. Note the for· ward slip of L5 on Stat the lumbosacral junction. This
to be wearing a
would be a grade I
collar.
Spondylolisthesi s.
"Scotty dog" Collar deformity
FIGURE 43.14. A: Norma l 45-degree oblique radiographic view best visua lizes pars intera rticularis. B: Spondylolysis. C: Spondylolisthesis. D: Lysis pars interarticularis appearance as a col l a r. (From Roy S, I rvin R. Sports Medicine: Prevention, Evaluation, Management, and Rehabilitation. Englewood Cli ffs, NJ: Prentice-Hall; 1983:280, with permission.)
61 2
VlI. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
plane postural problems. Some of these measurements may even tually prove to be relevant, whereas others may n ever add any clin ical relevance. Current research by the I nstitute for Gravitational Strain Pathophysiology at the Kirksvill e College of Osteopathic M edicine is delineating these and other postural m easurements that may add to the understanding of postural decompensation.
6. Recovery
1. Activity
POSTURAL TREATMENT: OVERVIEW
Regardless of the planes involved, the principles used to prescribe individualized treatment plans for patients with postural decom pensation do not vary significantly. Rational treatment depends on an accurate diagnosis, recognition that every postural curve has both a structural and a functional component, and the con sideration of the homeostatic, structure-function characteristics of the specific patient that is being treated. Identification of dys functional factors, such as muscle imbalance and j oint somatic dysfunction, focuses strategies for treatments designed to reduce postural stress and reverse the process of postural decompensa tion. Identification ofstructural involvement also provides insight into the patient's prognosis. [f compensatory mechanisms are overwhelm ed, treatment of postural decompensation should include some combination of the following: 1 . Sound biomechanical and ergonomic education. This includes emphasizing appropriate footwear including the reduction of high heels, promotion of functional arches, and correction of pronation. Other useful education includes proper l ifting technique and dietary counseling when necessary for appro priate weight distribution.
2. Functional orthotics such as a heel lift, a sole l ift, or a Levitor to biomechanical ly reverse the m echanics involved in decom pensation. 3 . Specific exercise designed fi rs t to rest and then to functionally enhance ineffective soft tissue structures.
4. Osteopathic manipulative treatment (OMT) addresses the so matic dysfunction that consistently and recurrently accompa nies postural problems and facilitates postural compensation that will be associated with treatment intervention. 5. I n j ection techniques using prol iferative m ed ication (prolother apy) for ligamentous laxity if other conservative modalities alone fail to restore stabil ity. Compliance is a must, especially in the initial phases of the program of reeducation or in the wearing of an orthotic. It can be enhanced if the patient understands the rationale behind the treatment procedures and requirements. The amount of com pliance that can be expected from a person can be estimated by evaluating body unity factors including vanity, dedication, self image, energy l evels, and a number of biopsychosocial factors. Exercise
Exercise is an often misunderstood and misused activity. Cl ini cally, the patient needs a precise and realistic prescription for the goal, the dose, the frequency, and the duration of physical activi ties. [n this manner, an exercise prescription can help the patient
3. Inactivity FIGURE 43.15. B ioenergetic model. (Modified from Jungmann M. The )ungmann Concept and Technique of Antigravity Leverage. Rangely, ME: Institute for Gravitational Strain Patho logy, I nc; 1982.)
achieve rest, flexibility, strength, and endurance, depending on the desired goal. Further tissue damage may also be prevented. Exercise prescriptions should always consider the present sta tus of the muscles and their ability to respond to a desired goal. I n general, a person with decompensated posture requires a period of rest before exercise and compensation are effective; overly stressed or strained muscles cann ot effectively be exercised until they have fi rst recovered (26) . Thus, rest, medication , indirect OMT, and certain physical modalities may be necessary before beginning an individually designed exercise program; the appropriate exercise prescription for a patient with postural decompensation may be to decrease activities of daily living. The bioenergetic cycle (Fig. 43. 1 5) espoused by Jungmann (27) describes the requirement of resting the body until it is phys iologically capable of resuming its postural fight against gravity. E nergy expenditure throughout each day is cyclic; sequencing is important for the efficacy of the process. Postural strain increases the load in the early stages of the cycle and delays or even sub verts later stages. When a person whose homeostatic reserves have been exceeded fi rst l ies down at night, it may take 30 minutes (or more) before the erector spinae and quadratus lumborum muscles relax and allow comfort in the supine position. These muscles, therefore, n eed to be mon itored . The reduction in ili olumbar ligament tenderness and edema are indicators of when active postural exercises may be introduced to achieve strength, stabil ity, and proprioceptive reeducation. The exercise prescription should promote healing of strained and injured tissues before striving to accomplish any other pos tural goal. Two basic rules of exercise are advocated for these patients (28): 1 . Avoid exercising to the point of fatigue.
2. Discontinue any exercise that causes pain until a reason for the pain is d iscovered .
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes
613
Ilium
Sacrum
"::iIfI
----
-t -f
---
-
....=. --- Horizontal plane
---
FIGURE 43.16. Pelvic lever action and Levitor®. (From Jungmann M. The Jungmann Concept and Tech nique of Antigravity Leverage. Rangely, ME: Institute for Gravitational Strain Pathology, Inc; 1982, with permission.)
Osteopathic Manipul ative Treatment
OMT should be selecred ro improve srrucrure-funcrion re larionships wirh a minimum of side effecrs for parienrs wirh posrure-induced parhophysiologic change. Indirecr merhod OMT is parricularly useful for rrearing somaric dysfuncrion in hypermobile areas. Ir should be recognized rhar hypermobile ar eas may represenr eirher primary rraumarized rissue or regions of secondary compensarion for orher regions of resrricred morion. Direcr merhods, physical modaliries, and srrerching exercises are parricularly useful in regions of hypomobiliry. The percussion hammer rechnique, as was raughr by Roberr Fulford, DO, is clinically helpful in rreatmenr of some chronic postural problems.
Orthotics, Braces, and Other Adjunctive Treatment
Adjunctive rherapy is ofren necessary. Staric braces are ofren help ful by promoring rest and healing in a region of acure srrain. Chronic postural strain, however, is a situation in which the use of functional orrhotics or elimination of biomechanical risk fac rors is required ro supporr homeostasis. Irs chroniciry precludes replacing funcrion and mandates rhat functions be modified. Use of static bracing in chronic situations requires careful and conrin uous exercise as well as care designed ro prevenr muscle arrophy and rhe parient's dependence on the static brace . A funcrional orthosis, such as the Leviror®, is a more appro priate choice than a static brace for patients with chronic postural decompensation. This pelvic orrhosis has been used in the United States since 1939 and is a prescription, custom-fitted device. Ir weighs 6 ounces and is made of a high-test aluminum alloy thar
rransfers pressure ro cushioned pads, one over the superior por tion of the pubic symphysis and the other on the posterior parr of rhe sacral apex below rhe S2 middle rransverse axis. This or thosis was specifically designed ro resist the counter-rotation of rhe sacrum and innominates (Fig. 43.16) rhar occur under rhe influence of the strain of graviry. It aids bur does nor replace rhe funcrion of posrural muscles, thus avoiding rhe dependency side effects of sraric braci ng. A funcrional orthosis is added ro a parient's treatment regi men ro enhance homeosratic postural mechanisms and increase efficacy. A functional orthosis is indicated in those chronic or recurrent conditions resulting from, or aggravated by, postural srrain or decompensation. Its use can realistically be expected ro improve the body's abiliry ro resist strain and decompensation by altering biomechanical alignment or assisting soft tissue srruc rures. Concomitanr symptoms such as back pain, headache, fa rigue, muscle imbalance, and functional visceral complaints may be relieved in a program that incorporates a functional postural orthosis, OMT, and patient educarion. These symproms alone in rhe absence of the underlying postural cause are not a sufficient indicarion for the use of orthoses. Funcrional orrhotics may be especially indicated for parienrs who have had failed back surgery for chronic back pain or patienrs with chronic disc disease, spondylolisthesis, or who have had failed medical rrearment for low back arthritic conditions. All of these strucrural conditions make it more difficulr for the patient ro functionally resisr graviry. A functional orrhosis should nor ro be used alone. It re quires systemic OMT and carefully prescribed exercise to be maximally effective. Conversely, the effects of OMT and ex ercise for patienrs with chronic postural decompensation may
614
V/l. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
be greatly benefited by the addition of an orthotic device. Ad j unctive use of the Levitor®, for example, has been demonstrated to improve m easurable sagittal plane risk factors and to reduce posture-related low back pain (29,30). I n a 1 985 study involv ing 1 09 patients with recalcitrant chronic low back pain 30% of patients were found to improve with manipulation and postural exercise alone. W hen a functional orthosis (Levitor®) was added to this program, 76% improved. The likelihood of improved re sults is achieved by decreasing functional demand on postural structures, m odifying biomechanical risk factors, and allowing postural homeostatic m echanisms to operate under m ore optimal conditions. In summary, numerous m odalities are used to assist the body's postural response to gravity. An individually designed program includes a carefully selected combination of patient education, OMT, exercise, and functional orthotics. All of these are aimed at m odifying the structure-function relationship and enhancing the body's ability to self-heal. Postural balancing t herefore requires an understanding of the biomechanical nature and functional anatomy of each patient and a full understanding of osteopathic philosophy.
CORONAL AND HORIZ ONTAL POSTURAL CONDI TIONS
Scoliosis and rotoscoliosis are posrural diagnoses with origll1s dating back to ancient G reece. References to the existence of leg length inequality in 90% of the population have appeared in the m edical literature since the latter half of the 1 800s (31-33). John H ilton specifically m entioned lift therapy as a treatment for this problem in 1863: Thus 1 have seen many patients wearing spinal supports, in order (Q correct a lateral curvature when the deformity might have and has been subsequenrly, corrected by placing within the shoe or boot a piece of cork thick enough to compensate for the shortness of the less well developed limb (34) .
The osteopathic profession began studies on the diagnosis and treatment of coronal plane asymmetry in 1 92 1 , when H oskins and Schwab introduced the standing postural x-ray view (35 ,36). A compilation of many of the classic osteopathic articles dis cussing diagnosis, clinical impact, and treatment of this and other postural subj ects can be found in the 1983 Yearbook o/the Amer ican Academy o/Osteopathy, Postural Balance and Imbalance (23). SHORT LEG SYNDROME
Within the profession, the term "short leg syndrome" is recog nized as a m isnomer. This text, however, will continue to refer to short leg syndrome because of historical precedence. Regardless of the name, the actual cause of the condition may not be related to the actual length of the legs at all. It is called a syndrom e be cause it is associated with a variety of biomechanical findings and symptoms. An unlevel sacral base is the clinically relevant element in this so-called short leg syndrome. B ecause a short lower extremity
35
0. :::J
J�: _\I"
30
e (9 25 :; E If 20 #.
D
Low right femur group
•
Low left femur group Key:
Iliac crest Sacrum
15 10 5
FIGURE 43.17. Frequency d istribution of l u m bosacral relationships to unlevel femoral head heights. N = 738. (From Kirksville College of Os
teopathic Medicine, Kirksville, MO, with permission.)
usually resul ts in an unlevel sacral base, the spine com pensates by changing its spinal curvatures. Subsequentl y, the person often must stand and walk differently. If the sacral base is unlevel for any reason, the innominates often rotate to compensate. This creates the appearance of a functionally short lower extremity. In either case, the m ost common spinal response is development of a rotoscoliosis with side bending of the m ost caudal curve toward the side that is opposite the low sacral base, or short leg. Atypical patterns do occur, however, and provide clinically challenging cases (Fig.43. 1 7). Diagnosis
Compensatory m easures are sometimes so good that any single landmark m easurement may fail [0 provide a true and accurate diagnosis. N either alignment of spinous processes nor level of iliac crests is a good single indica[Or of sacral base unleveling or short leg syndrome. Anterior superior iliac spine (AS IS) or hip-to-ankle m easurem ents using a tape m easure are also inaccurate (37,38). Comparison of the levels of the medial malleoli in the supine position is similarly inaccurate or m isleading (39). The greater trochanters in the standing position are somewhat more helpful clinically but can be in error when unilateral coxa varus or coxa valgus is present (40). Therefore, it is difficult and not always accurate [0 make a diagnosis based on clinical findings alone. In one study of standing patients with known radiographic leg length inequality, the wrong extremity was identified as being short in 1 3% of the clinical observations; more than half of the 1 96 clinical estimates of leg length were incorrect by more than 3/16 of an inch (4 1 ). Recurrent somatic dysfunction of the pelvis, spine, cranium, or m yofascial structures may also be a clue that the sacral base is unlevel or that a short leg is present. Soft tissue involvement with respect to the compensation occurring in the short leg syn drome is particularly comm on and a cause of many patient com plaints. Tissues on the concavity shorten and demonstrate in creased electromyographic activity (42,43). Tissues on the convex
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes side l en gthen. Patients with coronal plane postural imbalance de velop tight abductors on one side and tight thigh adductors on the contralateral side. Associated horizontal plane imbalance of ten results in tight hamstrings on one side and tight rectus femoris on the other thigh. The iliolumbar ligament on the side of the convexity of the lumbopelvic curve is often the fi rst structure to react to added mess in the lumbosacral area. The iliolumbar ligament is pain sensitive. The point of maximal tenderness to p alpation is typ ically located over the attachments of the iliolumbar ligament at the iliac or L4 or L5 transverse processes. When stressed, it often refers pain around the ipsilateral side to the groin, and sometimes into the testicle or the labia and the upper medial thigh (Fig. 43.7) (44). The pain may be mistaken for arthri tis of the hip, greater trochanteric bur sitis, or even an inguinal hernia. The sacroiliac ligaments on the side of the con vexity may also become stressed and ten der to palpation and may refer pain down the lateral side of the leg. Unilateral sciatica an d hip pain, as well as pain over the greater trochanter however, are more often expressed on the long leg side. Numerous postural muscles are mained, and significant p hysiologic changes related to segmental facilitation have been documented. Subsequenrly, there may b e visceral dysfunction related t o in creased sympathetic hyperactiv ity coming from spinal crossover areas located between T1 and L2. Before definitive diagn osis of a patient's p osture, a thorough OMT should be directed ro all somatic dysfunction. It is ex tremely important n ot to overlook sacral or innominate shear somatic dysfun ction s. After OMT, the presence of a positive stan din g flexion test coexisting with a n egative seated flexion test should raise the suspicion that lower extremity influences, such as a shorr lower extremity, are affecting the function of the sacroiliac joint and the patient's posture (45). When the spine is as mobile as possible an d any n onphysi ologic (shear) somatic dysfunction s have been removed, it is a good idea ro obtain a standard standing p ostural x-ray series (see Chapter 42). After fi rst removing the patient's somatic dysfunc tion, this x-ray series primarily p ortrays structural data associated with the best homeostatic compensation possible by the patient at the time. These stan dardized stan din g p ostural x-ray images can then be used to measure coronal plane values accurately, in cludin g the following: •
Iliac crest heights Femoral head heights • Sacral base unleveling • Degree, location , and type of scoliotic compensatory curva tures •
When readin g the x-ray image (Fig. 43. 18) obtained by stan dard methods, remember that there is still potentially a 2-mm human error in measurement. This can occur even with flawless technique by the radiologic technician and p erfect patient co operation . There can also be up to a 25% bony magnification (distortion) (46,10 1) . Compensatory changes such a s inn ominate rotations, p elvic rotation, and changes in the LSA may alter the x"-ray appearance.
615
This can misrepresent the extent of the patient's actual prob lem. For these reasons, a leg len gth difference of less than 5 mm may n ot be treated unless the patient has other clin ically relevant complaints and risk factors. Conversely, the desire to attain "peak p hysical performance" may b e an indication for treating a patient in this case. Patterns of imbalance recorded along the spine may b e caused by as little as a 1/16 of an inch (1.5 mm) difference in leg length. Clinical symptoms can occur in these cases, in cludin g low back p ain ( 19,47). Lift T herapy
Typically, treatment of the short leg syn drome in volves lifting the heel of the leg on the side of the depressed sacral base. This is especially true if there is a compensatory curvature that side bends to the side opposite the short leg. In the less common situation where the curve has its con cavity toward the side of the short leg, it may be n ecessary to lift the side of the long leg. This fi rst effects a change in the lumbar scoliosis and also relieves some of the p elvic and lumbar strain (48) . The lift on the long leg side is later reduced to begin lifting the depressed side of the un level sacral base. Heel lift treatment within the osteopathic profession is always combined with OMT and is usually n ot attempted until after an appropriate trial of OMT. The rationale for both was clearly implied by H arrison Fryette: In rhe average case I do nor attempt a correction until l have mobilized the lumbar joints and established rotation in them; furthermore, if this region cannot be rotared tOward the midline, the lift will not do what it is intended of it, for the correcrion will nor rake place in rhe lumbar region-rhe spine higher up will compensate by increasing i rs curve and only more trouble will resulr (49).
OMT may alleviate a functional con dition that presents as an app arent short leg syn drome. In the situation in which lift therapy is indicated, OMT p repares the somatic tissues to accept the realignment n eeded in response to the newly established sacral base level. Whenever lift therapy is initiated, osteopathic physician s con sider the implications of postural realign ment and reeducation, which must take p lace throughout the entire body. For many rea sons, the initial amount of lift selected is rarely the full amount n eeded. In most cases, compensation and decompensation have occurred over a p eriod of time, leading to shortening and fibrosis of soft tissues, bony remodeling, an d regional somatic dysfun c tion. The easiest but least sensitive guideline used by clinician s is to select an initial lift that is on e-third to one-half of the measured sacral b ase differen ce. Attempts to formulate specific guidelin es ro better quantify the amount of lift are best appreciated by studying the writ ings of David H eilig (50) . H eilig foun d that one-third to one half the measured sacral base unleveling was too much initial lift in selected clinical situation s. He developed a formula ( 50) (Table 43.2) that con sidered the amount of lift to be direcrly p roportional to the measured sacral base unleveling an d in versely p roportional to host factors such as the age, duration of the con dition, and amount of compensation or adaptation acquired by the body.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
616
A
B FIGURE 43.18. X-ray i mage marked for coronal (A) a n d horizontal (B) plane measurements. Ideal values would be n o side-to-side u n leveling of any of these landmarks and no pelvic rotatio n .
H eilig o ffered examples o f patien ts who all had a 1/2-inch sacral base unleveling but who, based on the formula, would receive different initial lifts (Table 43.3). One of the safest protocols taught at m an y of the colleges of osteopathic medicine is less complicated than the H eilig formula yet sensitive to individual host factors. It employs conservative rules of thumb that can later be modified by the physician's clinical experience and judgment. This protocol is designed to avoid any un expected flare-ups of pain or somatic d ysfunction that can occur if lift therapy is introduced toO rapidly or if it exceeds the capability of the body to realign in respon se to the changes being made in the sacral base level.
The following are only guidelines for the application of con servative lift treatment and must be adapted to each patient ac cording to their individual evaluation and respon se ( 5 1) . •
I f lift therapy i s required and if the patient is con sidered to be a fragile patient (arthritic, osteoporotic, elderly, having signif icant acute pain , etc.) , begin with a 1/ 1 6-inch lift and lift no faster than 1/ 1 6 of an inch every 2 weeks. • If the spine is flexible and no more than m ild-to-moderate strain is noted in the myofascial system, begin with a lIs-inch TABLE 43.3. PATIENTS WITH SAME SACRAL BASE LEVEL ING BUT RECE I V I N G D I FFERENT L I FTS
TABLE 43.2. THE H E I LIG FORMULA
Case 1 : Following fracture, minimal d u ration, no compensatory changes
The Heilig form u l a suggests that the initial lift can be calcu lated
Case 2: Patient age 35, injured in early youth, minimal compensation
L
as follows:
<
[SBU]/[D + C]
L, lift required; SBU, sacral base un leveling; 0, duration; C, compensation. Duration al lotted as: (0 = 1 ), 0-10 years; ( 0 = 2), 1 0-30 years; (0 = 3), 30+ years. Compensation allotted as: (C = 0), none observed; (C = 1 ), rotation of lumbar vertebrae into convexity of compensatory side-bend ing; (C = 2), wedging of the vertebrae, altered size of facets, horizontal osseous developments from end plates, and/or spurring.
L L
=
=
Case
[SBUI/[D + CI [SBUI/[D + CI
3:
=
=
W'/[O + 1 ] W'/[2 + 1 1
=
=
W'
'/2"/3
=
development, rotation is marked L
=
W'
Patient age 75, injured in youth, spu rring, horizontal end plate
[SBU]/[D + C]
=
W'/[3 + 21
=
W'/5
=
'110"
Case 4: Patient age 26, polio affecting right leg in youth, minimal compensatory change L
=
[SBU]/[D + C]
=
W'/[2 + 0]
=
W'/2
=
W'
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes lift and lifr ar a rate no faster rhan 1/ 1 6 of an inch per week, or 1/8 of an inch every 2 weeks. • If there was a recenr sudden loss of leg length on one side, as might occur following fracture or a recenr hip prosthesis, and the patient had a level sacral base before the fracture or surgery, lift the full fractional amount that was lost.
617
A
Regardless of the method used to select the amount of the ini tial lift, certain other guidelines should be followed for optimum clinical results. •
Because of magn ification, measuremen r error, and compen satory changes, the final lift heighr in a chron ic short leg syn drome may only be one-half ro three-fourths of the shortness in that leg measured by the standard standing x-ray method. • When a proper lift has eventually been reached and rhere are no pelvic or lower exrremity somaric dysfunctions, the stand ing Aexion test should become negative. If a repeat x-ray image is desired, it should be taken using the same radiographic pro tocol and paramerers rhat were used in the inirial x-ray series, but wirh the shoes on and the lift in place. Guidelines used in lift treatment are n ot absolute rules. One aspect of the art of medicine is an appreciarion ofrhe concerns that patients have about cost, cosmeric appearance, and convenience. Ideally, the shoe is rebuilt with every increment of lift to prevent ' alteration offoot mechanics and inrroducrion of unwanred pelvic rotation. Few patients, however, would agree wirh this approach. The following guidelines emphasizing clinical tolerances can be pragmatically used in lift rreatment. If problems arise, reducin g the tolerances or insisting on the ideal may be necessary. •
The true height of a l ifr is measured from the bortom of the l ift to a point where the calcaneal bone strikes the lift; it is n or measured at the posterior edge of the lift. • Up to and including 1 /4-inch of replaceable lift can be used inside of the shoe before rhe shoe no longer firs well. • Up to and including a total of a liz-inch lifr can be placed between the heel of rhe patient's foot and the A oor before foot mechanics are sign ificantly disturbed. • As a heel is progressively lifted, rhere is an increased tendency toward pelvic roration, muscle imbalance, and alterarion of foot mechanics. Application of these principles to change rhe relarive leg lengrh by liz inch may result in: •
a 1/4-inch lift being placed in side the shoe and 1/4 inch added to the heel of that shoe • 1/2 inch added to the heel of one shoe • 1/4 inch added to one sole and 1/4 inch removed from the opposire sole (50-52). Many other combinations e xisr within these general guide lines, permitting the osreoparhic pracririoner the laritude to bal ance non physical factors (such as vanity and cost) wirh rhose relared to posture. Any increase in height beyond rhe liz-inch heel lift must be added to rhe heel and also to the anterior half-sole of the shoe (Fig. 43. 19) . This principle preserves rhe relarionship of the heel to rhe forefoor by main taining a certain n ormal angle.
D FIGURE 43.19. Principles of lift therapy. Heel lift measu rements made at midcalcaneal line. A: Foot in a typical shoe. B: Heel lift in place. Maxi
mum left in shoe is 1/, inch. C: If more lift is needed, add to outside heel. D: If more than 1/2 inch is required, or to create minimal disturbance of
foot mechanics, the entire sole can be lifte d .
Studies (4,47) indicare thar an 80% reduction in subjective pain and other posture-relared symptoms could be expected as a result of properly balancing rhe sacral base with lifr therapy to wirhin 1 mm of levelness. The physician must rry to balance rhe weight of both shoes, especially if large lifts are required. If a big lift is needed, cork material between the shoe and t he heel may be necessary to reduce the weighr being added to one side. In some cases, small lead weights may be added to the other shoe to maintain balance . OMT helps the patient's spine to compen sate better for the new posture that results from lift rherapy for a short leg. Compressive force makes bone grow faster. A lift under a grow ing child's short leg may be expected to stimulate faster growth in that leg. The physician must therefore closely monitor leg len gths when using lift rherapy for a child. The heighr of the lift musr be adj usred according to clinical responses and the resulrs observed on follow-up x-ray studies. In growing athletes, alternatin g lower exrremity growth paramerers have been reported ( 50). This has prompred rhe clinical recommendation to check the pelvic and extremity levels at regular intervals. Fryette even remarked: " I n the last 1 5 years I have added lifts to the short side in many cases under the age of fourteen and in every case that I have kept un der my observation for some rime I have been astonished to fin d that rhe legs grew to the same len gth" (53) .
VII. Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment
618
Anterior Lift T herapy : Pelvic Rotation
The clinical use of anterior sole lifts (in distinction from heel lifts) or the combin ation of an anterior lift in one shoe and/or a heel lift in the opposite shoe to affect posture in the horizontal plane has largely been explored by Ross Pope and J ames Carlson (54) . An increase in the sole height of a shoe encourages rotation of the pelvis toward that same side. A un ilateral heel lift rotates the pelvis to a lesser degree and rotates it away from the lifted side (5 1) . Because this method is new, few clinical trials have been performed. The predominance of clinical experience, how ever, suggests the fo llowing guidelines, which are adapted to each individual patient's evaluation an d response . Anterior lift therapy rotates t he pelvis toward the same side; heel lifts may rotate the pelvis away from t he lift side . Treatment of both planes simultaneously is often warranred, as side bend ing and rotation are biomechanically linked morions . A heel lift pushes that s ide of the pelvis anteriorly in the horizontal plane because the lift is behin d t he axis of motion (i.e., rotates the pelvis away from the side of the heel lift) . Anterior sole lifts are in front of the axis and so they rotate that side of the pelvis posteriorly in a horizontal plane (i.e., rotate the pelvis toward the side of the sole lift) (Fig. 43. 20 ) . I n the treatment o f pelvic roration assuming coexistent sacral base unleveling, follow these prin ciples:
For peLvic rotation Less than 5 mm: Usually it is not necessary to treat a pelvic rotation less than 5 mm. However, if the sacral base unleveling is treated with heel lifts, this should be done accordin g to the prin ciples outlined for coronal plane postural balancing . Recheck t o determine if a n y un wanted pelvic rotation occurs secondary to the heel lift t herapy. For peLvic rotation of 5 to 10 rnrn: For pelvic roration of 5 to 10 mm, both sacral base (coronal plane) and rotational (hori zontal plane) components are treated simultaneously. Begin with appropriate lIB-inch anterior and heel lifts, progressively increas ing in l Is-inch increments every 2 weeks . For peLvic rotation greater than 1 0 rnrn: Pelvic rotations more than 10 mm should fi rst be treated with an anterior (sole) lift of l/4 inch, and the postural stu dy then rechecked before attempting heel lifts . Thereafter, sacral base unleveling and pelvic rotation are treated simultaneously with 1/8-inch incremental changes in anterior (sole) and heel lifts every 2 weeks .
Lift Summary
Lift therapy is initiated to help the body return to better struc tural alignmen t and function . Properly managed, the patient's postural mechanisms are reeducated toward the ideal posture . Balancing mechanisms have been shown to become more pre cise as evidenced by graphic center-of-gravity plots before and after appropriate lift therapy. Paraspinal muscle tension and var ious spinal physiologic parameters become more symmetrically normalized, and patient symptoms rhroughout the body are dra matically reduced.
SCOLIOSIS (ROTOSCOLIOSIS)
With lifts in the heel or in the oppOSite half sole, the pelvis can be derotated.
R
� &
Ten in every 200 children ( 10:200) develop scoliosis by the age of 10 to 15 years; 1 in every 200 ( I :200) has clinical symptoms related to the curvatures . Boys and girls are equally affected, bur the curvatures in girls are 3 �o 5 times more likely to progress an d produce subjective symptoms . Curvatures are more likely to progress during times of rapid bone growth. Most cases (75% to 90%) of scoliosis in children are discovered between the ages of 1 0 and 15 because of widespread screen in g programs and because this is the time when rapid bone growth occurs . Diagnosis
The right half-sole rotates the pelvis to the right
Bottom of shoe
The left heel lift rotates the pelvis to the right
�
S coliosis primarily affects the coronal plane . I t is offi cially named according to the direction of the convexity of the curve. A curve that is side ben t to t he left is called a right scoliosis because the convexity of the curve is toward the right. Scoliosis may be classified by its reversibiliry, severi ty, cause, or location .
.
Bottom of shoe
FIGURE 43.20. Right anterior h a l f-sole l ift andlor left heel l ift rotating pelvis to the right.
Classification: Reversibility
S coliosis can be functional or srructural. A simple physical ex amination technique ro assess the proporrion of functional to structural scoliosis can be accomplished by standing behind a
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes , \
619
Idiopathic
This d iagnosis account s for 70% to 90% of scolioric curves. By definition, the term " idioparhic" implies rhat there is no known reason for this type of scoliosis to occur. Osteopathic physicians believe that som e of these may be explained as com pensatory curves occurring because of an un level sacral (47) or cranial base (56) . I n those cases where such a biomechanical basis exists for the development of scoliosis, a diagnosis of an idiopathic scoliosis is inappropriate. Other clinicians have implicated sagittal plane biomechanics in the genesis and progression of different types o f idiopathic scoliotic patterns (7) . B etter understanding of scoliosis may further reduce the number of cases classified as idiopathic . Congenital
Of con genital cases, 75% are progressive. This classification is the second most common type according to cause of scoliosis . Acquired
Acquired scoliosi s m ay result from the following conditions: •
• •
•
• •
O steomalacia Response to inAamm ation or irradiation Sciatic irritability Psoas syndrome H ealed leg fracture Following a hip prosthesis
Obviously, if a short leg syndrome is documented as the reason for the patient's scoliosis, this should be reclassified as an acquired scoliosis. FIGURE 43.21. Assessment of structu ra l or functional scoliosis.
patient (Fig. 43.21). The patient bends forward until maximal rib hump appears on horizon. With that much of the bod y for ward bending, the patient swings the upper body first left, then right, while the cli nician observes the functional ability of rib hump to reduce. The amount of rib hum p remain ing during this man euver indicates the associated structural scoliotic com ponent. Functional scoliotic curves go away with side bending, rotation, or forward bending. I f they remain in the body toO long, they may become structural (55). Structural scoliotic curves are fixed curves thar do not reduce with side bending, rotation, or lift therapy.
Classification: Loca tion
Various locations of scoliosis are given here according to decreas ing frequency (Fig. 43.23). Regions in volved in scoliosis may be balanced or un balanced. Un balanced curves are more likely to decompensate, while balanced curves are subjecr to d egeneration ar crossovers. Double Major Scoliosis
These are balanced curves but they are subject to degen eration at the crossover regions of the spin e (see G lossary at the end of the textbook). This is the most common scoliosis, with a thoracic and lumbar combi nation being the mosr frequent. Single Thoracic Scoliosis
Classifica tion: Severity
There are four degrees of severity. The normal case shows no sco liosis. A cur ve of 5 to l 5 degrees is classifi ed as m ild (Fig. 43.22). Moderate scoliosis curves measure 20 to 45 degrees . Severe scol iosis has a curve of more than 50 degrees. Severe scoliosis affecrs structure and systemic function. A thoracic curve of more than 50 degrees comprom ises respiratory function. A thoracic curve of more than 75 degrees com promises cardiovascular function.
Cosmetical ly, this curve is rather noticeable. It is usually side-bent right and rotated left, producing a left paraspinal rib hump. I f this type of curve should progress, it could com promise the function of the heart or lungs. I t is the second most common scoliosis. Single Lumbar Scoliosis
This curve is associated with arthritic chan ge. It is the third most common scoliosis. Junctional Thoracolumbar Scoliosis
Classifica tion: Cause
The fo llowing causes are lisred according to decreasing frequency.
This single curve scoliosis often results in structural (arthritic) change because it tends to be a longer curve that function ally overstresses the spine. I t is not a common scoliosis.
620
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
�B
C FIGURE 43.22. Curve patterns in idiopathic scoliosis. A: Mild ( 1 4 degrees and 1 5 degrees). B: Moderate (38 degrees). C: Severe (59 degrees and 85 degrees). Assessment of scoliotic severity defined by Cobb
angle measurements (see Fig. 43 . 1 1 ) for each portion of coronal plane curve. C lassification system q u oted a l lows a 5-degree gray zone between severity classes.
Junctional Cervicothoracic Scoliosis
This scoliosis is very uncommon . Symptoms and Screening
Children with scoliosis are usually asympcomatic, yet by checking them between the ages of 1 0 to 1 5 years when they are experi encing rapid bone growth, the scoliosis can be found. For this reason , school children should be routinely screened for scoliosis. An adolescent with scoliosis is also often asymptomati c and therefore would be overlooked un less a spinal screen in g exami nation was performed. The patient may have only noticed that cl othi ng does not fit properly. As the person gets older, several symptoms brin g the scoliotic patient to the physician . These include: •
• •
•
• •
Arthritic symptoms Backaches Chest pain s Neck aches H eadaches Symptoms of organ d ysfun ction
Physicians casually looking for scoliosis may miss a curve of up to 35 degrees. Careful screening with physical examination alone should pick up all types of scoliosis more than 1 0 degrees. In the stan ding position , the space aroun d the patient's body is analyzed, especially in the arm and waist area. Observe whether one hand hangs by the side and the other hand lays on or over the thigh. Look at the levelness of the occipital, shoulder, iliac crest, PSIS, and trochanteric planes (Fig. 43. 1 0) . Run your fi ngers alon g the spinous processes from cop to botcom. H ave the pa tien t forward bend and observe for an asymmetric "hump" alon g the horizon of vision . [ts presence would indi cate rocoscoliotic
deformiry with rotation co that side and side bending·of the spine to the side opposite the hump. I f spinal curvature is foun d, have the patient bend over to that area of the spin e and determin e if the asymmetry goes away with side bending coward the side of the rib hump (Fig. 43.2 1 ) . Check the patient for condition s that could give the appearan ce of a shorr leg, such as sacral shear somatic dysfun ction on that side . If you fi n d somatic dysfunction , it can be corrected with manipulation. Recheck following OMT for a lower extremity induced postural problems.
Radiographic Measurement
I f thete is continued recurrence of a scoliotic curve, provid e OMT until there is good mobilization of the spine and then obtain a standardized standing postural x-ray image (see Chapter 42). The x-ray image provides the quantitative data to determin e: •
Bony pathology Type and sevetity of spinal curvatures • Amount of sacral base unlevelin g • Femoral head and iliac crest levelness •
Scoliotic curvatures are measured from the radiographs by the Cobb method (Fig. 43 . 1 1 ) . The same vertebrae used to define the cop and the b otcom of the curve are used for future Cobb measurements co see if the curve is progressing. Scoliosis often increases rapidly during the growth spurt of adolescen ce. Take an x-ray image of the hands and epiphyses and obtain a bone age for those patients who have significant scoliotic progression. For females, the scoliosis is more likely co undergo a rapid pro gression . Significant progression of the curve is con sidered co be occurring if, on a second standardized postural x-ray taken within
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes
Right thoracic curve of 70°
Right thoraco lumbar curve of
70°
Left lumbar curve of
Double major curve of 70° (right thoracic, left lumbar)
70° (note pelvic obliquity)
FIGURE 43.23. C u rve patterns in id iopathic types o f scoliosis classified b y location.
621
622
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
5 months o f the first one, there is a 5-degree or greater increase in the curvature . The Cobb method is used to classifY scoliosis by severity (Fig . 43.22) . Treatment of Rotoscoliosis
Appropriate treatment protocols are based on classification of the scoliosis, taking into consideration factors affecting potential compliance. The treatment for scoliosis according to its severity follows these general guidelines (5 1) . For mild scoliosis, use: . OMT • Konstantin exercises • Functional orthotics • Patient and family education For moderate sco liosis, use: . OMT • Konstantin exercises • Patient and family education • Bracing • (Electrical stimulation-debatable efficacy) For severe scoliosis, consider surgery and adjunctive measures, including those listed for moderate scoliosis. Anyone with scoliosis of more than 15 to 20 degrees, with progression of curvature, or with intractable low back pain in spite of adequate conservative treatment measures, should be referred to a physician who specializes in the treatment of this condition. The goals of treatment are to obtain fl exibility and improved balance of the spine. D ecide what can be improved and then correct the primary cause or at least prevent the scoliosis from progressing. Postpone fusions as long as possible without en dangering function or the patient's life. Osteopathic manipu lation is a definite part of the management of a patient with scoliosis . The perso n with sco liosis must be able to compensate for the new posture that is introduced by the treatment meth ods used to prevent progression or reduce the severity of the curvatures . Osteopa thic Man ipula tive Treatm e n t
When structural scoliosis is present, the goal o f direct manipu lation is to optimize the function of the existing structure. It is not primarily intended to straighten the curvatures . Treatment should remove joint somatic dysfunction but should also include improvement of the general range of body motion through soft tissue, fascial releases, and indirect treatment s . Stretch the lum bosacral tissues and institute exercises to reduce the LSA and strengthen the psoas and abdominal muscles. After structural strains are allowed to heal, introduce Konstantin exercises . Orthopedic appliances, o rthotics, braces, and electrical stim ulation may also be used in the management program. These adjunctive modalities were conceived to support, align, or pre vent deformity and may stabilize function of a hypermobile part of the body. Braces are more effective if the scoliosis is moderate, if the spine is mobile, and if the spine still has not fully matured .
Braces
The Milwaukee brace (Fig. 43.24) was introduced in 1945 and has been the standard for scoliotic bracing for many years. It is individually fitted and easy to prescribe, but it is also hard to wear and is costly. It is worn 23 hours a day with only 1 hour allowed out of the brace for applying skin care. This brace is used in a growing patient with 20- to 40-degree curves. It works to conttol the scoliotic (lateral) curves until the spine matures, which is generally around age 2 1 . I t is necessary to exercise the muscles that are supported by static braces or appliances . Studies suggest that even for pati ents with a good reduction in the Cobb measurements, after a few years t heir curves return to approximately the extent present at the time that the brace was inttoduced. An alternative brace for some patients with scoliosis is the Boston brace (Fig . 43.25) . This brace is made of plastic and is designed to work on deformities such as lordosis and totation as well as scoliosis . The Boston brace can be used only if the apex of the curve is below Tl O. In these particular patients, it is helpful in addressing postural curves in all three cardinal planes. Electrical Stimula tion
Electrical stimulation was introduced in the 1970s . It was applied to the convexity of the curve and may be considered when the curve is in the thoracic regio n, it measures 10 to 40 degrees, and the spine is flex ible . This concept enjoyed some degree of popularity but is not often used today. Its efficacy is debatable. If electrical stimulation is applied to a patient's lumbar curve, it increases the lumbar lordosis . Surgery
Surgical fusion is performed only in I of every 1,000 cases of scoliosis . It is usually considered for patients with progressing scoliotic curves at 45 to 50 degrees to prevent the heart and lu ng complications that accompany curvatures over 50 degrees . The placement of stainless steel Harrington rods (Fig. 43.26) and spinal fusio n is an extensive surgery. The mechanical power of the body is dramatically demonstrated by the propensity of the rods to become stressed and break, requiring another extensive surgery to replace them.
SAGITTAL PLANE DISORDERS
Posture-related disorders in the sagittal plane include those de fined by their lordotic and kyphotic curves; those defined by their distinctive pattern of somatic dysfunctions including mus cle imbalance and trigger points; and those with related structural change such as isthmic L5-S 1 spo ndylolisthesis . As with any spec trum ranging from functional to structural disorders, there can be a great deal of overlap in diagnostic findings and treatment strate gies . Each relies upon the biomechanical principles discussed in the earlier sectio ns of this chapter. Often treatment focuses on modifYing the underlying functional disorders that aggravated or precipitated the eventual structural changes that define the structural, codable diagnosis .
43. Postural Considerati ons in Coronal, Horizon tal, and Sagittal P lanes
FIGURE 43.2 4. Milw auke e brac e.
FIGURE 43.25. Bost on brac e.
623
624
VI/' Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Incision through
Harrington
fascia and Skin
supraspinal
in cision
ligament
hook
Outrigger ---+
2
1
4
5
Ilial bone graft harvest
7
FIGURE 43.26. Surgica l fusion with H a rrington rod implantation. This extensive surgery is reserved for patients with c urves greater than 45 degrees. A major clinical goal is to stop structural progression of a curve before it seriously com promises cardiopul monary function .
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes
SPONDYLOLISTHESIS
The biomechanical principles of diagnosis and treatment of patients with sagittal plane postural problems can be directly applied to the management of patients with spondylolisthesis. The generic term spondylolisthesis is derived from Greek roots roughly meaning "vertebra sliding down a slippery path. " It de scribes the common fi nding of a group of spinal disorders i n which there is a forward d isplacement of one vertebra over an other, usually the fifth lumbar over the body of the fi rst sacral segment. Cl assification
With the advent of modern radiology, the srudy of spondylolis thesis began, including i ts true incidence, location, classification , and significance. The classification of spondylolisthesis subse quently evolved into the currently accepted causal categories delineated by Wiltse, Newman, and MacNab ( 57) shown in Table 43.4. Causes
Regardless of specific hereditary and developmental factors, spondylolisthesis refers to a group of disorders having a particu lar common mechanical consequence. Applying the mechanical perspective permits berter understanding of the general symptom complex. Applying mechanical treatment protocols provides the rational basis for osteopathic conservative management of pa tients diagn'osed as having spondylolisthesis. Hereditary Predisposition
Two observations argue against a person having a direct i nher itance of spondylolisthesis. First, although there is an increased incidence ofspondylolisthesis within fam i ly groups (58,59), a sig nificant number of these fam ily members exhibit differen t types of spondylolisthesis. Second, infants are rarely reported to have spondylolysis, or prespondylolisthesis. The incidence i ncreases after children assume an active upright position and continues up until age 20, when it matches the 5% i ncidence of the general population (60). The genetic link appears more likely to involve those factors that predispose the region to i nstabi lity. Posterior defects such as spina bi fida occulta and open sacrum are almost i nvariably in heri ted in dysplastic spondylolisthesis and i n a third of patients with the isthmic type (60). This lack of posterior support may concenrrate postural weightbearing forces in the area, resulting in forward subluxation of the enrire l5 unit in dysplastic spondy lolisthesis. 1 n this fash ion and under certain biomechanical stres sors, genetics could predispose a patienr to stress fracture of the pars i nrerarricularis and then sliding of the anrerior elements of l5 on S I in isthmic spondylolisthesis (59). Conversely, degenerative spondylolisthesis ( formally called pseudospondylolisthesis), occurs two to th ree ti mes more fre quently in African Americans, who are also known to have greater L5-S 1 stabi lity (62) . In general, patienrs with degener ative spondylolisthesis have a low PI for age (63) and higher incidences of sacralization of L5 and/or block-shaped L5 verte-
625
brae. They also have a much lower incidence of posterior defects (62) than seen in the general population. The increased stabil i ty at l5 encourages i nstability higher in the lumbar spine. Developmenta l Factors
Certain developmental factors have been statistically and/or log ically implicated in spondylolisthesis. Foremost among these fac tors are posrure and m icrotrauma (64-69). Posture is strongly implicated i n the development of spondy lol isthesis and spondylolysis (prespondylolisthesis) . Spondylo lysis does not develop prior to the assumption of the standing posture. I n one study of 1 2 5 i nstitutional ized patienrs who had never assumed a standing position, none demonstrated a pars defect (65). No other primate has fully adopted h uman up right posture, nor does any other primate develop a lytic type of spondylolisthesis. Postural decompensation as measured by the ]ungmann PI is substantially h igher i n patients with L5-S 1 spondylolisthesis (64) than in the general population. I ncreasing PI and i ncreasing lum bosacral i nstability may, in parr, address Wiltse's observation ( 57) that many patients develop lesions in the pars at approximately age 6 and then have no problems with it until their mid-30s. Hyperlordosis, i n parricular, has been the posrural fault most impl icated i n isthmic spondylolysis and spondylolisthesis (67,69,70) . Increased lordosis transfers weightbearing from the vertebral bodies onto the articular facets i n joint capsules (28). These strucrures are ill-designed to carry the body's weight con tin uously. An anterior weightbearing l i ne is also known to create sim ilar mechanics and should be looked for and evaluated. Certain activities such as gymnastics further increase backward bendi ng demands in the l umbar spi ne. Subsequently, many young gym nasts permanently adopt an exaggerated lordotic posture. Not surprisingly, many female gymnasts demonstrate spondylolysis, having an i ncidence four times that of the general female popu lation (7 1 ) . Other groups are specifically subject to i ncreased stress in the lumbopelvic area and each has been shown to have an increased incidence of spondylolysis. These included weight lifters, sol diers carrying backpacks, and college football l i nemen. Repeti tive lumbosacral motion is a common characteristic in all types of spondylolisthesis except that due to trauma. Therefore, frequent stress in posrurally or congenitally unstable areas is implicated, especially during the adolescent growth spurt, in the develop menr of fatigue fracture, the proposed basic lesion in isthmic spondylolisthesis ( 5 9 ) . Diagnosis
Of the estimated 5% of the population with spondylolisthesis, approximately half are asymptomatic (72) . Those who become symptomatic do so commonly after the age of20. Preventive care depends on early and accurate diagnosis. Diagnostic testing should i nclude the following: •
Radiography PI measurement • H istory • Physical exam i nation •
Vlf. Osteopathic Considerations in Palpator)l Diagnosis and Manipulative Treatment
626
TABLE 43.4. CLAS S I F I CATION OF SPONDYLOLISTHES I S
Diagnosis Type I
Type Dysplastic
Percent 21
Dysp l a stic spondylolisthesis
� �
Type I I A
Isthmic spondylol isthesis
�4 � 4
Isth m i c
51
Criteria Congenital deficiency of neural
Comments 2 g i rls: 1 boy is the ratio;
arch of L5 or upper sacrum.
a lmost exclusively L5;
Insuff iciency of superior sacra l
lumbosacral facets also
facets.
approach horizontal
Pars interarticularis defect
Su btype A
A. Lytic-fatig ue fracture of pars
Su btype B
B . Elongated but intact pars
Subtype C
C. Acutely fractured pars
Almost exclusively L5 A. Most common type below age 50 years B. Probably due to repeated microfractures
L5
hea ling e longated fashion as slippage occurs
S
C. H i story of severe trauma may heal with
Type liB
immobilization
L5
S
Type I I I
Degenerative
25
Degenerative spondylo l isthesis
Degenerative changes at apophyseal j oints d u e to long-standing intersegmental
l
instabil ity
4 female: 1 ma le; 3 black: 1 wh ite; 6-9 times more common a t L4; sacrali zation 4x general popu lation; not seen before age 40; rare between 40-50; slippage 30% maximum
Type I V
Tra umatic
Due to fractures in other areas of
Tra u m atic spondylolisthesis
Type V
Heals with i m mobilization
the bony hook than the pars
Pathologic
2
Generalized o r localized bone disease
Neoplasm. osteogenesis imperfecta, Paget's disease, arthrogryposis, iatrogenic postlu mbar fusi on; Kuskokwim disease
Reprinted with permission from Kuchera WQ, Kuchera ML. Osteopathic Principles in Practice. Colum bus, Ohio: Greyden Press; 1 994 .
•
•
Spinal pal pation Neurologic testing
Radiographic Analysis
Radiology has greatly enhanced our ability to diagnose spondy lolisthesis even in totally asymptomatic patients; it i s a modality that provides prognostic data (64,73). It must be realized that there are sign i ficant diFFerences between the measurements ob-
tained from weightbearing and non-weightbearing x-ray fi lms (73,74). From a pragmatic point of view, the standardized postu ral standing film series oFFers reproducible, Functional, postural data and is preferred. Radiographically, gross spondylolisthesis Cl i l be '<'en and quantified on a lateral x-ray view. However, 45-degree oblique films may be necessary to see a subtle or uni lateral spondylolysis ( Fig. 43. 1 4) . l n this view, the pars interarticularis in isthmic type 1 1 - 8 spondylolisthesis has been described as the Greyhound of
43. PosturaL Considerations in CoronaL, HorizontaL, and SagittaL PLanes Hensi nger because of the "long neck" rather than the "collar" on the "Scotry dog" (75). Meyerding (76) provided the s i mplest system of grading ( Fig. 43. 1 2) . Spondylolisthesis is assigned the classification of I, I I , I I I , or IV, respectively, for each one fourrh of rhe verrebral body that the upper venebra is displaced forward on the verrebra below. The more precise displacement measurement of Taillard (77) can detecr minor progression but i t is rarely needed clinically. The Meyerding system is more commonly used, more q uickly ap plied, and is clinically relevant. The fastest progression of isthmic spondylolisrhesis is seen be tween ages 9 and 1 5 . Rarely is there progression i n the Meyerding grading over the age of 20, especially in patients having a sclerotic buttress o n the anterior lip of the sacrum (65 ,78) . Other signs of instabiliry o r its effects i n the area can b e seen with radiographic analysis (9,20,24,70,79), including: • • •
•
•
•
•
Angle of slip Osteophytes Calcified ligaments (especially il iolumbar) 1 ncreased PI Anterior weightbearing mechanics I ncreased lordosis or LSA Disc narrowing
Whenever possible, radiographic ryping of the spondylolis thesis should be performed because it may affect treatment or prognoSIS. Clinical
The age of the symptomatic patient determines the clinical pre sentation . While spondylolisthesis is perhaps the most common cause of persistent low back pain and sciatica i n children and adolescents (80) , most children with spondylolisthesis in this age group do not have pain . These individuals are often identi fied when a school official or parent notes a change in gait or posture (80) . If any pain is expressed, it is usually described as a dull ache in the buttock or posterior thigh. Symptoms are rarely expressed below the knee (75 ) . Tight hamstrings (73,8 1 ) are found i n 8 0 % o f young peo ple with symptomatic spondylolysis or spondylolisthesis and to . a lesser extent in asymptomatic patients. This fi nding probably results from postural stress and an attempt to stabi lize the unsta ble lumbosacral j u nction (and is not from root impingement). l nabiliry to bend over to touch o ne's toes reveals this deficit. I t can also b e used t o uncover t h e nonfixed scoliosis ( 6 5 , 8 2 ) that exists in approximately 30% of these patients secondary to lum bar irritation and paraspinal spasm. Furthermore, as a result of having tight hamstrings, those patients having spondylolisthesis rated greater than grade I I have a pathognomonic stiff-legged, short stride, waddling gai t (8 1 ,83) in which the pelvis rotates with each step. Distortion of the pelvis and trunk appears in patients having a Meyerding grade II or I I I (8 1 ,83) . They have a flared ilia in the back and an abdomen that is thrust forward. These young peo ple have a shorr waist, a transverse abdominal crease at the level of the umbilicus, and Aattened heart-shaped buttocks. Only 2% of young people demonstrate any objective neurologic change
627
(28) requlflng extensive electromyographic or myelographic workup. One of the most consistent physical findings associated with patients younger than 30 years of age and with dysplastic or isth m ic spondylolisthesis is tight hamstrings that restrict forward flex ion of the trunk. I n contrast, the most constant physical finding i n patients older than 50 years of age with degenerative spondy lolisthesis is the ease with which they are able to touch their toes without bending their knees or obliterating their lumbar lordosis. The Aexibiliry of a patient with degenerative spondylolisthe sis is thought to result from laxiry o f the pelvicotrochanteric and hamstring muscle groups. The unstable spondylolisthetic joint at the L4-5 level predisposes the patient to manifest L5 root neuro logic symptoms. The patient is more l i kely to have somatovisceral complaints of a hypersympathetic nature i nclud ing constipation or i rregular menses (2). Symptoms o f pelvic congestion and vague complaints i n the lower extremiry are also common in adults with spondylolisthesis. These result from the hyperlordosis, viscerop tosis, and poor thoracic abdominal diaph ragmatic function that accompanies spondylolisthesis (2,6 1 ,84,8 5 ) . Adult patients are more likely t o complain of pai n . Their pain is usually aggravated by moderate activiry or prolonged stand ing and relieved by rest or l i m i ted activiry. Because of chronic overt instabiliry of the lumbosacral region, these patients have poorly responsive soft tissues (86) , somatic dysfunction, and multiple myofascial points that, when stressed, react out of proportion to the i ni tiating event and produce palpable spasm and low back pain. Pain can thus be caused by several structures in the area other than the spondylolisthetic segment. These structures are also subject to the instabiliry of the region and the mechanical disadvantage that is localized there. I t is, therefore, difficult to sort out when the pain is caused by spondylolisthesis, when it is the result of somatic dysfunction o f muscular, l igamentous, or joint structures, or when it is of discogenic origin . I n patients older than 2 0 years o f age with spondylolisthe sis of less than 33%, pain is probably caused by one of three mechanisms (65) : •
D isc degeneration at the level of the defect Root i m p ingement by fibrocartilaginous build-up • Referral from stressed posterior l igaments and soft tissues
•
In our clin ical experience, pain in these patients is most com monly referred from trigger points in the quadratus lumborum, glutei, and piriformis muscles, and from il iolumbar and poste rior sacroiliac ligaments. This best supports the third mechanism above. The cauda equina becomes physically involved in isthmic spondylolisthesis patients with more than a 50% slip (more than a grade I I ) (65 ) . In these patients, low back pain is attributed directly to the spondylolisthesis i tself. Because the dysplastic rype carries the posterior arch forward, no more than 25% slippage is necessary to manifest a cauda equina syndrome (59). Degen erative spondylolisthesis, by nature of i ts mechanism, does not progress beyond a 30% slip (59,65,70) . The i nstabiliry o f this joint (usually L4- 5 ) , coupled with physical continuiry with the posterior arch , usually results i n L5 root impingement. Myel ograms performed on these patients generally show hourglass
628
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
consrriction (70) at that level. Therefore, the differential and ac curate diagnosis of the primary cause of back pain in a patient with spondylolisthesis requires careful palpatory and neutologic phys ical exam i nation and diagnosis in addition to the radiographic and historical fi ndi ngs j ust oudined. Palpa tory
I ncreased i n rersegmental motion i n the lumbosacral region is usu ally a sign of instability and severe degeneration. This i ncreased motion is grossly apparenr even on x-ray films. H owever, palpa tory evidence (86) by those trained to palpate segmental motion is generally considered to have twice the diagnostic yield for i nstabil ity (28.6%) when compared to diagnosis by x-ray studies ( 1 5 % ) . Palpatory findi ngs i n patients with spondylolisthesis reveal an anreriorly located spinous process (Fig. 43.27) or drop-off sign. The anterior spinous process is associated with the vertebra that has slipped forward in dysplastic and degenerative spondylolis thesis. It is the adjacent vertebra, above the slipped segment, in isth mic spondylolisthesis. Sacral base motion is excessively lax when it is rocked ante riorly around the m iddle transverse axis; this may also result i n associated subjective buttock o r posterior thigh discomfort. I f testi ng sacral base motion causes neurologic symptoms, particu lar care should be taken in designing a treatment protocol that does not produce neurologic symptoms. Paraspinal tissues vary in palpatory qual ity depending on the degree of symptoms presen L Often they display m ultiple my ofascial tender points. Even in the asymptomatic state, they are slow to relax and are somewhat boggy (congested) to palpation. Muscle strength testing of the low back muscles demonstrates nearly full Aexibility but decreased srrength and endurance. The il iolumbar l igament should be palpated b ilaterally i n ev ery patienr with symptomatic spondylolisthesis. Attached to the transverse processes of L5, the anterior sacroi liac joint, and the i l iac crest, the il iolumbar ligament is anatomically positioned to resist any forward slip of L5 o n the sacrum ( 1 0) . Bi lateral palpatory tension and subjective tenderness are often noted over its attach menrs. The patient may experience lateral thigh and/or groin referral ( Fig. 43.7). Palpation of the iliolumbar l igament is a valuable and sensitive indicator of the success of conservative management programs designed to reduce mechanical srress i n patients w i t h symptomatic spondylol isthesis.
L5
slides forward
taking posterior
A
elements along
L5 B
slides forward
leaving posterior element behind
L4
slides forward
taking posterior element along
c
Neurologic
The physical examination of each patient should i nclude a neuro l ogic evaluation i ncluding deep tendon reAexes, muscle srrength testing, and straight leg raising. Electromyographic testing and/or myelography are indicated if radicular symptoms are present. I t is especially important t o assess the condition o f the L 4 disc (65) if surgical fusion is conremplated. Treatment
Conservative management is 8 5 % to 90% successful in degenera tive spondylolisthesis (65 ,70) . In the m i nority ofchildren who are symptomatic, only 50% are successfully m anaged with conserva tive care (65,75 ) . For immature patients with Meyerding grade
FIGURE 43.27. Location of anteriorly located spinous process (drop off sign) depends o n underlying mec h a nism of spondylol isthesis. A: In dysplastic spondylolisthesis, LS-S 1 horizontal facets a l low entire spi ne to glide forward creating drop-off between LS and 5 1 . B: In isthmic spondy lolisthesis, pars defect between L S a n d 51 a llows anterior e l ements of LS to slide forward a long with the rest of the spine. Posterior elements of LS rem a i n behind with the sacrum creating drop-off between L4 a n d LS. C: Degenerative spondylolisthesis at L4-S does not affect a n terior a n d posterior elements o f t h e vertebral unit a n d therefore t h e d rop-off sign is located between L4 a n d L S .
43. Postural Considerations in Coronal, Horizontal, and Sagittal Planes I I I or I V spondylolisthesis, those with progressive subluxation, or those with spondylolisthesis secondary to acute fractures, conser vative management is probably not indicated without extensive bracing or surgical fusion. The acute fracture group responds best to immediate i mmobil ization (65 ) . For those patients requiring surgery (or bracing) , conservative management should be added afterward because the conditions that led to the instabi lity preoperatively are still present postop eratively. In all cases, conservative management should attempt to maximize structure-function relationships. Pa tient Education
Education is a key element in conservative management (72,87,88) of the patient with either asymptomatic or symp tomatic spondylolisthesis. Goals center on decreasi ng stress i n the unstable lumbosacral region through application o f back me chanics, proper exercise and nutrition, and i mprovement of pos ture. Back schools, offering 36 hours of instructio n in teachi ng back mechanics and appropriate choices for optimum back care, are effective (87) . These approaches i m mensely i ncrease patient complian.ce. I n the absence of a back school, the individual prac titioner should use a minimum of one patient visit (more if nec essary) to explain lumbosacral mechanics. Patients are taught to lift properly and to avoid im proper lifting, especially over the head, as this increases lumbar lordosis. The osteopathic physician should advocate proper footwear; high heels in particular i ncrease l umbar lordosis (28). Patients should be advised on correct sleeping, si tti ng, and standing postures; they should also be counseled o n weight loss, if necessary. This minimal investment o f time reduces the fre quency of rei njur y or the failure of an otherwise well-conceived conservative program. Pregnancy significantly affects posture by shifting the weight bearing line anteriorly and accen tuating the l umbar lordotic curve. Unfortunately, this postural stress occurs at a time when the hormonal changes of pregnancy also reduce soft tissue sta bilization. Women with spondylolisthesis contemplating p reg nancy should prepare their posture and muscle tone i n advance, if possible. They should also strictly adhere to their obstettician's weight gain limits. Often the addition of a Levitor® is extremely beneficial, even if it is only for the duration of the pregnancy. For asymptomatic young people with less than a Meyerding grade I spondylolisthesis, avoid creating a back cripple with ex cessive restrictions. It is wise to direct these i ndividuals toward a vocation not requiring heavy lifting or strenuous activity (89) . I n asymptomatic young people with more than grade I spondylolis thesis, the same vocational goals are upheld but these individuals should also avoid con tact sports. I n form young patients and their parents of the concerns and uncertainties i nvolved; stress the need for close follow-up. Exercise
The response to exercise does not depend on the type of spondy lolisthesis ( I , I I , or I I I) (88). The goals ofexercise are to eventually stabilize the lumbosacral region and dimi nish the l u mbar lordo sis (84,8 8 ) . Weight loss for an overweight patient can also be facilitated by exercise.
629
Exercise should be of a Aexion-type only, rather than Aexion extension combination programs (82). Gramse has repo rted ex cellent results with the Aexion program ( 8 8 ) . The variables ex ami ned i ncluded relief of pain, need for back supports, return to work status, and recovery. Combination Aexion-extension exer cise significantly reduced the effectiveness in all of these variables. Pelvic narrow and coil exercise (90-92,98) with the knees benr i n the supine position i s extremely effective ( Fig. 43.9), although Aattening the back against the wall while standing or bringing the chest to the thigh while sitting i n a chair can also be beneficial. The patient m ust be able to demonstrate their ability to main tain a reduced lordosis before abdom inal strengthen i ng exer cises such as bent-knee sit-ups are considered. Good abdomi nal strength adjunctively supports weightbearing and unloads the spine. Gymnastics, diving, and contact sports are not encour aged. Swi m m ing, however, is considered an excellent activity to cultivate. Man ipula tion
Several authors report a benefit (2,6,9,2 8,93) from the manipula tive management of patients with spondylol isthesis. Man i pulative treatment of the patient with spondylolisthesis is extremely help ful in attempting to redress some of the postural decompensation that has occurred over time and to alleviate segmental limitation of motion known to upset the forces resisting spondylolisthesis (70) . The goals (2 ,6,9,93,94) are reduction of lumbar lordosis and somatic dysfunction. This transfers weightbearing from the pos terior elements and tissues back to the vertebral bodies. It specif ically relaxes strained, irritable lumbar paraspinal tissues, permit ring them to better resist stresses of the activities of daily livi ng. It also reduces the patient's somatic pain and somatovisceral symp tomatology. These goals seek gradual reestabl ishment of fascial and m uscular balance to promote maximal fu nctional weight bearing posture. The manipulative program is not j ust directed to the lordosis and specific somatic dysfunctions, but to all support structures as well. Because of the i nstability and i nj ury in the lumbosacral j unction, h igh-velocity techniques should be avoided in that area. In correcting lordosis and recurrent lumbopelvic clin ical con ditions, the first concern is often balancing the pelvis horizon tally ( 1 1 ,2 8 , 9 5 ) . An undiagnosed or uncorrected unilateral, sacral shear somatic dysfunction thwarts the most expert manipula tor in achieving this goal and renders fu nctional orthoses such as the Levitor ineffective. This and other non physiologic so matic dysfunctions can be treated promptly and effectively with OMT. An un level sacral base needs gradual heel lift orthotics before i nstability and recurrent somatic dysfunction can be effectively addressed. A m i nimal heel l i ft, when indicated, can reduce the LSA by 2 to 4 degrees ( 1 1 ) and may move an anterior weight bearing line as much as an inch posterior (96). Correction o f a short leg is also extremely helpful in reducing long-term strain on the i liolumbar ligament. It eliminates somato-somatic referral of groin pain from this structure as well as reduces low back pain and i nstability in the lumbosacral junction (94,97) . A heel lift may also be helpful to the one-third of spondylolisthetic young
630
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
people who have concomitant scoliotic change and the long-term somatovisceral changes resulting from it. Any i ntrapelvic somatic dysfunction should be removed; the sacroiliac articulations should be freely mobile. Tight hamstring muscles are gently stretched with isometric muscle energy tech nique. The use of a vapocoolant spray and stretch over the ham strings to achieve this goal is often helpful (see Chapter 66). Fascial unwindi ng of the lower extremities is well received by pa tients and elimi nates many of the vague congestive complaints i n this area (J . G . Zink, personal commun ication, 1 978). The thoracic spine and thoracolumbar j unction are addressed next. Schwab (93) reported i mprovement of compensatory lum bar lordotic stresses with mobil ization of i ncreased thoracic kyphosis. Fryette (28) emphasized that somatic dysfunction i n t h i s area must b e corrected before a n y effective changes could be maintai ned in the lower lumbosacral j unction. Additional con sideration of the diaph ragm and quadratus lumborum has proven particularly successful in hel p i ng to promote lymphatic drainage (6 1 ) . The quadratLls l umborum and the i liolumbar ligament are functionally and structurally related (97) and both should be treated. Lastly, the lower lumbar region should be approached in a general manner with soft tissue, coun terstrain, myofascial release, and fascial unwinding techniques. Address any specific somatic dysfunction with indirect techn ique. A clinically usefu l end point is achieved when the i n trinsic rhythm of the craniosacral mech anism is easily palpated between hands that are moni toring both the thoracolumbar j unction and sacrum. Orthotics, Braces, and Casts
Orthotics play a significant role in the conservative management of patiems with spondylolisthesis. The benefits of a heel l i ft or thotic in hel ping to lend stability to the lumbosacral regio n have al ready been discussed, and the heel lift orthotic is potentially a permanent part of the patient's treatmem program. A corsedike lumbosacral support, conversely, should only be considered for short-term stability (72,86). Grieve (86), however, writes that a support should never be suppl ied without a plan to eliminate i t. Most lumbosactal supports worn for prolonged periods weaken the patient's own supportive mechanisms (72) , thereby increasi ng long-range instability and promoting dependence on the support. For short-term management oflu mbar strain, however, these sup ports can be i nvaluable i n reducing pain and preparing the tissues for a subsequem exercise program . Types of i m mobilization, rangi ng from knee to nipple casting to ordinary body casts and corsets, have been stLldied for use by patients with spondylolisthesis resulting from an acute fracture (75 ) . The latter two types of i m mobilization suppress the ex tremes o f bending but do a poor job of d i m i n ishing l umbosacral motion with walking (78 ) . The Levito r® functional pelvic orthotic has proven extremely effective as an adjunct in the long-term managemem of symp tomatic isthmic spondylolisthesis (2,9,22). Exerting pressure be tween the pubic symphysis and the base of the sacrum, the Levito r® effectively (30) aids in decreasing postural decompensa tion as measured by PT, in reducing the LSA, and in transferring weightbearing o ff the posterior tissues and forward to the ver-
tebral bodies. By reducing the chronic strain on these tissues, symptomatic relief from low back pain is accomplished in days to weeks, and implementation of an exercise program can begin shortly thereafter. Medication
Ant i i nAammatory medication, analgesics, muscle relaxants, and bowel softeners all have a limited role in the symptomatic re l ief of various common symptoms experienced by patients with spondylolisthesis. Because spondylolisthesis is a chronic prob lem, narcotics have no place in symptom management of these patients. Vapocoolant spray-and-stretch tech nique (98) and trig ger point injection with local anesthetics (98) may be helpful in relieving the secondary myofascial points that occur (see Chapter 66) . I njections of proliferative agents are also useful for cases of ligamentous laxity uncorrected by conservative means (99). CONCLUSION
Patients' philosophies toward illness, their way of life, and the en vironment in which they function may affect their compliance, in tLlrn affecting the outcome of the treatmem program . Conser vative protocols, i ncluding individually adapted combinations of OMT, orthotics, exercise, patient education, and other modali ties, help the patient's spine compensate better for the new pos ture that results ftom treatment for functional disorders. These disorders range from short leg syndrome to hyperlordotic condi tions as well as structural component disorders such as scoliosis o r spondylolisthesis. Rational, conservative management of a patiem with ortho pedic and structLlral d isorders with postural componems presup ' poses early and accurate diagnosis and a thorough understand ing of the biomechanics i nvolved. While the cause is important for prognosis, treatment addressing the underlying i nstability, spinal mechanics, and patient homeostasis provides optimum benefit. Postural decom pensation in the sagittal plane ·is partic ularly prominent in patients with isth m ic spondylolisthesis and in the coronal and horizontal planes of patients with rotoscol iosis. These patients m ust be treated to maximize both patient homeostasis and body mechanics. Finally, physicians' changing perspectives on posture mech an isms as a dynamic process affecting i nt errelated structures throughout the body (9, I 00) have allowed postural treatment ap proaches to evolve and improve. As stated by H ippocrates nearly 2,500 years ago: "The regimen I adopt will be for the benefit of my patiems according to my abili ties and judgment." The guide lines in this chapter provide principles to enhance your abil i ty to design an individualized treatment regi men for patients with pos tLlral components. They will benefit from your continued study and total body application of postural homeostatic mechanisms and structLlre-fu nction i n terrelationships.
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•
MUSCULOSKELETAL EXAMINATION FOR SOMATIC DYSFUNCTION WILLIAM A. KUCHERA ROBERT E. KAPPLER
KEY CONCEPTS • •
• •
•
Elements, p rocedure, and interpretation of initial osteopathic musculoskeletal screening examination Additional, more focused, screening examination Musculoskeletal examination of hospitalized patients and outpatients. Examination of ambulatory patients Recording of examination fi n dings
•
Areas in which somatic structures are 111 need of help and support • Areas where manipulative treatment can help relieve a somatic component of disease • Areas in which manipulative treatment can improve the body's natural support and defense mechanisms Sometimes musculoskeletal examinations may be conducted for the purpose of collecting osteopathic research data to be an alyzed at a later date in accordance with the research protocol.
IDENTIFICATION OF SOMATIC DYSFUNCTION
INTRODUCTION
An osteopathic musculoskeletal examination is preceded by tak ing and recording the patient's history. Its significance includes: • • • • •
Indication of the patient's mental, physical, and physiologic concerns Directing the physician's physical examination by indicating the significance of certain body regions I ndicating regions of the body related to the patient's com plaints and/or concerns Uncovering significant history that the patient may not have thought was significant to his or her complaints Helping the physician decide on the method, type, activat ing force, duration, and frequency of mallipulative treatment when indicated.
Evaluation of the musculoskeletal portion of an osteopathic physical examination helps the physician in many ways. Clues obtained from a musculoskeletal examination relate to: • •
•
•
•
•
Information about the present efficiency of the musculoskeletal system Musculoskeletal indications to dysfunction of other systems The general health status of the patient Musculoskeletal problems Somatic response to systemic problems Information about the primary etiology of a dysfunction
An osteopathic examination is unique in that palpation, inte grated with motion testing, is the major component of the mus culoskeletal porrion of the physical examination. Discovery of musculoskeletal dysfunction often provides additional physical clues that direct, focus, and/or expand the physical examina tion. I nterpretation of the data gathered fro m a musculoskeletal dysfunction or diagnosis expands the logical conclusions that can be drawn from the physical examination. Several researchers have discussed aspects of the musculoskeletal examination ( 1 -8 ) . A physician uses trained, skilled hands as primary tools for this portion of the physical; they gather information necessary to evaluate and assess tissue texture change, qualiry or motion, and quantity of motion. Tenderness is a relatively objective response of the patien t elicited by the physician's palpation . Tenderness alone can not be an indication of somatic dysfunction. Osteopathic diagnostic criteria for identifying somatic dys function can be recalled with the mnemonic TART: T: Tissue texture abnormalities. This is a palpatory assess ment of quality of tissues, usually paraspinal. Tissue changes accompany somatic dysfunction. Skilled osteopathic physicians recognize immediately the palpatory quality of tissue texture abnormality. Tissue texture abnormality could be described as palpable evidence of disturbed physiology in the tissues. Tissue texture change is evaluated in layers, from superficial or skin to deep, such as deep muscle. Tissue texture changes are described as acute or chronic.
634
VJJ. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
A: Asymmetry of position of bony (or other) landmarks. Findi ngs are discovered by inspection. Though the key element i n determining the presence o r absence o f asymmetry is observation, or visual inspection, pal patory asymmetry is also evident. R: Restriction of motion. Active motion testing i nvolves in structing the patient to move, with the physician observing and recording range of motion. Passive motion testing involves the physician slowly in troducing motion (with the patient i nactive or passive) . The quanti ty of motion is assessed by taking the joint to the end point of motion in both directions, or in all directions i f multiple planes of motion are being assessed. Quality of motion is assessed by palpation, that is, the physician introduces motion and assesses compliance or resistance to the motion being intro duced. The motion quality of somatic dysfunction is asymmetric, with relative freedom in one direction and relative restriction in the other direction. Motion restriction occurs within the limits of normal physiologic motion o f a joint. T: Tenderness. Tenderness is said to be present when the phy sician appl ies a stimulus, usually palpatory pressure, and the pa tient reports discomfort, fli nches, has a facial change, or otherwise indicates discomfort. The test is objective in that the physician appl ies a measured force to the patient. Patient response i nvolves a degree of subjectivity, depending on the i ndividual's sensitivity or threshold for pai n . Tenderness differs from pain. Pain is a to tally subjective cerebral (cortical) perception of nociceptive i nput reported by the patient in the absence of palpatory stimulus.
A MUSCULOSKELETAL EXAMINATION
A musculoskeletal examination for somatic dysfunction is best performed in stages, progressing from overview or screen i ng ex ami nations to a more detailed segmental definition of TART at specific joints, facets, myofascial tissues, or vertebral units and their related vascular, lymphatic, and neural elements. This pro gressive approach, fro m a screening examination to a more de tailed exam ination, is applicable in most situations. The patient may be outpatient and ambulatory. They may be a hospitalized patient or a patient with a specific musculoskeletal problem who is referred to the physician who has a special proficiency in os teopathic mani pulative medicine. The following is an example of a multistep musculoskeletal exam i nation. For the purpose of simplicity, the components of this exam ination are identified as stage I (general or screen ing) or stage I I (more focused or segmental) tests. We realize that there are many tests that could be performed. Basic screening and seg mental examples are presented here. The physician does not do all of these tests. Those that best fit the i nvestigative needs as i ndi cated by the patient's history and the physician's knowledge and experience in working through a differential diagnosis are chosen. The medical student needs practice and should p reform a com plete regional physical examination on each patient. After this is completed the student usually looks at the results and then tries to make a working diagnosis. With this repetition during medical school and in the early practice years as a physician, the physician becomes able to perform any combination of these and other regional physical exami nations and tests with ease and efficiency. During the history and routine physical, an experienced physician mentally formulates the most likely regions and/or systems that
are directly or indirectly and/or anatomically or physiologically related to the patien t's complaints. The physical examination may focus more on some systems than others. This chapter presents a si mple musculoskeletal examination that can be performed by a medical student or a begin ning practitioner. A method of recordi ng results of this examination is also presented. Following these presentations, examples of applying a simple musculoskele tal screening examination for an ambulatory patient and a patient that is bedfast at home or in the hospital are presented. An osteopathic musculoskeletal examination is a prerequisite for manipulative treatment and determines where to treat and how to treat. Rarely, if ever, will a physician include all of these test procedures in a single examination. If a problem is suspected in a specific region, as many tests as indicated are performed to gather as much information as is needed with the patient in a specific position. The goal is to develop a time-efficient examination sequence and a method that will gather enough information from each patien t to allow the studen t or physician to make a working diagnosis. How much information? What tests? This is based upon the experience of the physician and his or her preference using treatment procedures. For efficiency, it is importan t that the examination sequence be organized and responsive to the patient's chief complaint re quires minimal changes of a patient's position and is responsive to the physician's preferred treatment procedures. The structural examination portion must identify obvious significant muscu loskeletal changes (false-negative resul ts must be minimized). Its database of findings must be sufficient to begin development of a treatment plan. Again, with experience, one better understands how the various findings are interrelated within the whole body. Some musculoskeletal examinations may not lead to an imme diate musculoskeletal treatment plan following the examination. A musculoskeletal screening examination, as is often performed on the hospital ized patient, may be used to identify potential problem areas that will be further evaluated and treated later, maybe in the physician's office after the patient has been released. An organized total body musculoskeletal screening examina tion includes i nspection, palpation, and motion testing to iden tify a problem or problems in one or more of the body's regions:
Somatic Dysfunction (SO) Severity of Regions Examined
Cranial Cervical Thoracic Costal Lumbar Abdomen Pelvis Appendages
Examined Regions
o No somatic dysfunction (SD) or background (BG) levels Obvious TART findi ngs (especia l ly restriction of motion and Tissue texture changes, with or without pat ient sym ptoms 2 More than BG levels and m, i nor TART findings present 3 A key lesion (inciting SD), symptomatic patient, and restriction of motion and tissue texture changes stand out.
The physician considers these questions and relationships while examin ing the patient: 1 . Is a problem (dysfunction) present? 2. Is there a problem with the base of support or is i t a weight bearing problem?
44.
3. Is the problem in one or more regions of the body, and if so, which ones? 4. Is there tissue texture abnormality (temperature, turgor, tension, or discomfort with compression)? 5. Is there asymmetry? 6. Is there a restriction of active, passive, or inherent motion? 7. Is there tenderness? 8. How do the findings correlate with known medical, personal, and social histories? 9. How do these areas correlate with the areas of sympathetic or parasym pathetic innervation to the viscera, that is, can they be attributed to or result from a visceral dysfunction or disease? 1 0. Are there other objective findings associated with the same segmental level?
II. How do the findings correlate with a com mon or known
pattern, such as the common compensatory pattern of the fasciae of the body? (9) 1 2. What are the identified problems and can they be listed clearly? The brief initial screening examination is a scan of all areas of the body, while focusing attention on the area involved in the patient's history of the chief complaint and/or the viscerosomatic region or regions related to it. Remember that the optimal func tions of the thoracic inlet, the abdominal diaphragm, the thoracic and upper lumbars, and the craniosacral mechanism , within the capacity of the patient to respond, are important to the health of every individual. Also remember that a "hyperactive sympathetic nervous system" is detrimental to the healing process and to the maintenance of health. Record the result of the examination on the patient's chart, documenting all areas that were examined and the basic elements of somatic dysfunction that were or were not diagnosed in a given region. It is very helpful to include a specific segmental diagnosis in the report to support the somatic dysfunction in the region, especially if osteopathic manipulative treatment (OMT) will be performed that day as part of the patient's treatment program. This last statement is meant to emphasize that a musculoskeletal segmental examination must be performed in the region or re gions to be treated before an O MT is performed. This is repeated previous to each OMT as it directs the goal, method, and acti vating force that is needed. It is then rechecked after treatment to assess the results.
AN OVERALL EXAMPLE OF A MUSCULOSKELETAL EXAMINATION (TABLE 44.1) Specific Tests for the Musculoskeletal Examination
The following are exam ples of some of the screening tests used in an organized, multistep musculoskeletal screening (scanning) examll1anon . General appearance: Look for asymmetry of the body; is the body type typical? Estimate the nutritional status; does the weight and height look proportional? Observe posteriorly, lat-
MuscuLoskeLetaL Examination for Somatic Dysfunction
635
erally, and anteriorly (Figs. 44. 1 through 44.3). Observe head carriage (rotation or side bending in relation to shoulders ) , shoulder a n d scapular levels, rib cage configuration , sternal de formities (pectus carinatum, pectus excavatum ) , clavicular de formities or elevation, supraclavicular fossae for ful lness and depth, carrying angle of elbows, linea alba hair patterns, or scars. Record the body type, muscle development, weight, and nutri tional status. Palpate for more segmentaL asymmetry of paraspinal muscles. Palpate relative thickness and tension of the Achilles tendons (unilateral full ness is indicative of congestion , ten sion is i ndicative o f increased weightbearing on that side); and relative tension o f the right and left muscle groups, such as the trapezius, erector spinae, gluteus maximus, hamstrings, and gastrocnemius. Palpate for hypertonicity (tight) or hypotonicity (loose) of left and right trapezius, erector spinae, iliolumbar ligament attachments, gluteus maximus, iliotibial bands, ham string, and gastrocnemius. Palpate arches of feet for height and tension. Note: Was there change in these results when the patient per formed active motion while in the sitting position? I f so, record these changes. Observe gait: Describe the gait in medical terms, if possible, or be brief but as descriptive as possible. Is weight transferred in a continuous manner from heel to toe for push off? Is there a limp? Is there toeing i n , toeing out, or excessive p ronation or supi nation? Is either leg internally or externally rotated? Is there symmetric motion through the pelvis and lumbar area, through the thoracic area, the shoulders? Is arm swing present and equal bilaterally? Observe symmetry of the body and the space around it (Figs. 44 . 1 through 44.3): This includes observation of the pa tient fro m the front, side, and back, describing the resting position of one upper extremity in relation to the other, and the anterior, posterior, lateral, and paraspinal symmetry of the body. It also includes any obvious rotational positions of one body region in relation to the next. The rotation of body regions is best ob served when the physician is looking down on the patient from a cephalad vantage point (Fig. 44.4). Spinal curvatures (Figs. 44. 1 through 44.3): Examine the patient, especially fro m the front and side. (Findings may include visual evidence of scoliosis, kyphosis, or lordosis. ) This part of the screen is done while observing the general appearance. Again observe symmetry and curvatures Posterior screen for evidence of lateral spinal curvatures (scoliosis). Sometimes this is expected by having the patient bend forward at the waist as the physician observes the horizon of the patient's back. A rib hump or paraspinal asymmetry i n thoracic or lumbar regions may indicate presence of rotoscoliosis (Fig. 44. 5 ) . Anterior screen of the body (see Fig. 44.3) . LateraL screen for anterior/posterior asymmetry and for in creased lordosis or kyphosis in cervical , thoracic, and lumbar areas ( Fig. 44.2 ) . Observe to determine if the weightbearing line passes through the external auditory meatus, acromioclavicular joint, greater trochanter, or lateral malleolus. The patient's knees should be partially flexed or hyperextended. Horizontal plane levelness: Posterior and anterior evalua tion s take place here.
TABLE 44.1. A PROGRESSIVE M USCULOSKE LETAL EXAMI N AT I O N : AN EXAMPLE Stage II: Examination of Regions Failing Stage I Screens
Stage I Examination (Screening) STAN DING
General appearance, body type, estimate nutritional status, weight and height Observe gait Observe symmetry of the body and space around it Spinal curvatures-AP and lateral (scoliosis, kyphosis, lordosis) Horizontal p l a ne levelness Standing flexion test Active screening motion tests (cervical), thoracic, upper extremities, and lumbar spinal regions H i p drop test Pelvic side-shift test
Record: appearance and body type; weigh the patient and check
his/her height. Record: the ga it
Consider postural decompensation, unleveled sacral base, congenital deformities Record: reg ion, extent, apex. Observe-with forward bending and Record-degree of functional or structura l scoliosis. Consider spinal curvatures, muscular imbalances Consider dysfunction in structure or muscles of lower extremity or of the sacro i l iac joint on the positive side Segmenta l ly test the reg ions involved Consider lumbar and thoracolumbar junction dysfunctions Consider postural problem
SEATED
Observe symmetry-d id it change? Observe curvatures-d i d they change?
Record
or
General appearance-describe spinal curvatures AP curves-identify range and apex Lateral curves-classify as m i l d, moderate, or Severe (see Chapter 43, "Osteopathic Considerations in Coronal, Horizontal, and Sagittal Pla nes") Seated: Thoracic i n l et-depth of infraclavicular space; i nhalation test the fi rst rib. Segmenta l ly test upper thoracic reg ion. Supine: coracocl avicular angle and spring upper rib reg ion. Supine: segmental cervical motion testing Segmentally test reg ions involved Segmenta lly test atypical and typical rib motion (Figs. 44.13 and 44. 1 8)
Six-quadrant rib cage screen (see F i g . 44. 1 6) Alternate stra ight leg ra ising test Trunk sidebending test (acromion drop test) Seated flexion test Palpation of thoracic and lumbar paraspinal reg ions for tissue texture changes and tenderness-fa i rly easy in this position
Consider lumbar and pelvic region dysfunctions Consider upper thoracic somatic dysfunction Consider sacro i l iac dysfunctions on the positive side Passive or active segmental motion tests for thoracic and lumbar spine (See Chapter 39, Fig.39. 1 , and Cha pters 48 and 50)
Pal pate for apparent elevated first rib (elevated rib or thoracic i n let dysfunction ?) Active motion testing of cervical spine (and upper extremities) Passive motion testing of upper and lower cervical divisions Pal pation for rib angle tenderness
SUPINE POSITION (properly position the patient)
Pal pate CRI and sphenobasi l a r symphyseal motion-added experience necessary
Supine: Basic Diagnostics: sphenobasilar motion pattern and
Observe symmetry of rib cage, pelvis, and lower extrem ities Abdom i n a l pal pation Anterior pelvic la ndmark levelness Pa l pate cervical region for tissue texture changes and tenderness (see also Chapter 46) Rib compression tests Pal pate thoracic and lumbar paraspi n a l regions for tissue texture changes and tenderness-more d ifficult in this position Passive flexion screen of lower extrem ities (see also Chapter 53) ASIS compression test (See Chapter 52, Fig. 52.8)
synchrony of the temporal bones. Complete Diagnosis: for somatic dysfunction of cranium-special tra i n i ng required Specific segmental tests for reg ion with asymmetry Correlate findi ngs with parasp inal thoracic and upper lumbar paraspinal tissue texture changes Correlate with posterior landmarks. Prone: segmental diag nosis of sacrum and innomi nates Supine: segmental cervical motion testing Seated o r Supine: segmenta l ly test atypical and typical rib motion
(Figs. 44.13 and 44. 1 8; see also Chapter 49) Segmental diag nosis of thoracic and lumbar reg ions-more d ifficult (see Chapters 48 and 50) Segmentally test the joints fa i l i ng the flexion screen (see Chapter 53) Record: segmental pelvic pal patory data for the side of the positive com pression test
PRONE POSITION
Posterior pelvic landmark levelness
Prone: complete segmental test ing of sacrum and i n nominates
Spinal compression test or spinal spring test (thoracic and lumbar spinal regions) Pal pate thoracic and lumbar paraspinal reg ions for tissue texture changes and tenderness-easiest in this position Test rotation of each lumbar verteb ra l unit
Prone: Seg menta l ly test for rotation; then test asymmetric regions for
i nclud ing motion testing
AP,
anteroposterior;
ASIS,
anterior posterior iliac spines;
(RI, cranial
sidebending preference Segmental d iagnosis of thoracic and lumbar regions (See Chapters 48 and 50) Prone: segmenta l l y test sidebend ing of lumbar spi ne, if R and S to same side, also test preference of F or E
rhythmic impulse
Note: Finding any abnormalities during stage I screen warrants a more detailed evaluation and segmental diagnosis of the region as suggested in stage II. Some o f t h e more detailed tests a r e explained. how those findings affect the total patient.
In
order t o make these findings clinically helpful i n t h e treatment of the patient, i t is necessary t o postulate on
44.
Musculoskeletal Examination for Somatic Dysfunction
FIGURE FIGURE 44. 1 .
Observe posterior body a l i gnment.
637
44.3. Observe anterior body a l i g n ment.
A
B
c
D
FIGURE 44.2. Observe lateral body for anteroposterior and weight bea ring a l i g nment.
FIGURE 44.4. Observe cephalad/caudad for horizontal plane body a l i g nment.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
638
Posterior Screen of Horizontal Planes (Fig. 44.6 or see Table 44.3) .
This screen determines the levelness of bilateral structures. Position: Patient standing and physician stands beh ind the patient Procedure: 1 . Assess masroid processes with the transverse plane ( Fig. 44.6A) 2. Assess acromion ( Fig. 44.6B)
processes
with
the
transverse
plane
3. Assess inferior angle of scapulae with transverse plane ( Fig. 44.6C)
Forward bend
4 . Assess iliac crests with the transverse plane (Fig. 44.6D) 5. Assess psrss with the transverse plane ( Fig. 44.6E) 6. Assess superior aspect of the greater trochanrers wi th the rrans verse plane (Fig. 46.6F) Interpretation: I fa plane or planes are nor level consider lower extremity abnormalities, an unlevel sacral base, spinal scoliosis, and/or congenital vertebral abnormal ities. \ \
, ,
Side-bending left A B
c
D F
Forward bending
Side-bending right FIGURE 44.5.
Standing forward bend ing test.
FIGURE 44.6. Posterior exa m i nation of bony landmarks (horizontal pla nes) of the body.
44. Musculoskeletal Examination for Somatic Dysfunction
639
if there is innominate or lumbosacral somatic dysfu nction. Early postural decompensation may be asymptomatic to the patient but can be indicated if these ligaments are tender to palpation. With a positive test, question the patient further about back fatigue or backache when they first lie down at night. Test for a shorr leg with an unlevel sacral base and for scoliosis.
--;---8 7+---C
Upper Extremity Screen for Joint Dysfunction: Extend A r ms over Head, Active (or Passive) (Fig. 44.8)
�---- D 44.7. Anterior examination of bony landmarks (horizontal pla nes) of the body.
FIGURE
Position: Patient is standing or seated and the physician stands in fron t or behind the patient. If the patient is supine, the physi cian stands beside the table or bed. Procedure: The patient actively and fully abducts both arms in the coronal plane over their head, fi rst with the backs of the hands together and then with the palms together. Interpretation: Negative test: With the head and neck in a neutral position , the medial surface of the u pper arms should touch the ears. The el bows should be straight, the arms touching the ears, the forearms pronated and the hands equally approximated with the backs of the hands together over the head. This is repeated with the patien t putting t h e palms together over his or h e r head. If a l l t h i s can be accomplished, the j oints of the shoulder, elbow, radioulnar, and wrist are probably normal.
Anterior Screen of Horizontal Planes {Fig. 44.7)
Position: Patient supIne and physician stands behind the patient Procedure:
I. H i p Rop test is done to align the patient on the table. 2. Assess iliac crests with transverse plane ( Fig. 44.7 A).
3. Assess anterior superior il iac spine (AS IS) levels with transverse plane ( Fig. 44.7B). 4. Assess pubic tubercles with transverse plane ( Fig. 44.7C). 5 . Assess medial (Fig. 44.7D) .
malleoli
levels
with
transverse
plane
Interpretation: If a plane or planes are not level consider lower extremity abnormalities, an unlevel sacral base, spi nal scoliosis, and/or congenital vertebral abnormalities.
Test for Clue to Early Postural Decompensation (Iliolumbar Ligament Palpation)
After screening for posterior superior iliac spine (PSIS) levels, move the palpating thumbs 1 i nch lateral and 1 inch cephalad from their posi tion on the PSISs. This will place them approxi mately over the il iac attachment of the i liolumbar ligaments to the ilium (see Chapter 50, Fig. 50.8). Press toward the iliac crests, test ing for tissue texture changes and tenderness of these attachments. Positive test: Ten derness of these attachments to the ilia. Interpretation: These are normally not tender but become tender if there is postural decompensation and may be tender
F I G U R E 44.8.
U p per extremity screen for joint dysfunction.
640
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Positive test: The patient is unable to bring the arms to the ears and/or the elbows and wrists are unable to be fully extended. The joints of the upper extremity need to be examined specif ically for motion restriction (see Chapter 47) . Dysfunction of the upper extremity can also occur because o f somatic dysfunc tion of the shoulder joints (including the acromioclavicular [AC], sternoclavicular [SC], clavicles, and scapulae) , the upper ribs, up per thoracic area, and the large m uscle groups providing shoulder movement. If the dorsal sur face o f the hands cannot be equally ap proximated, hypertrophied shoulder m uscles or myofascial trig ger points in muscles associated with the shoulder may be found. Truncal Forward Bending (Fig. 44.5)
Observe range of motion, group restrictions, accessory motions, and rib h ump (observe this and a s tanding flexion test at the same time) . Standing Flexion Test (Table 44.3)
The standing flexion test is a localization test to determine which s ide o f the pelvis and/or lower extremity has somatic dysfunction; it does not determine if it is related to the innominates or the lower extremi ty. Position: The patient stands erect with knees extended, feet at an acetabular distance apart, and the toes forward. The physician stands behind the patient. Procedure:
I. Physician places h is or her thumbs in contact with the PSISs at their inferior notch. The PSISs may be level or unlevel before the test begins. Note which is present. 2. Patient is asked to keep the legs straight and bend forward at the waist, placing the fingertips as close to the floor as is comfortable.
3. The physician's thumbs ride with the iliac spines as the patient flexes. Assess the position of the left and right PSISs relative to a transverse plane before and at the terminal position of forward bending from the waist. Interpretation: Positive test: l fmotion ofone thumb at the inferior notch of the PSIS continues to rise after termination of motion o f the other thumb, the standing flexion test is positive for that side. The asym metric superior motion that occurs near the end of forward bending is especially important. Note: A positive standing flexion test indicates that there is somatic dysfunction somewhere in the leg or the pelvis (usually the innominate) on the side of the positive test.
Standing Gross Spinal Flexion Test
The gross motion test screens the ability of the spine to forward bend. By measuring the distance of the fingers from the floor when the patient is fully forward bent, the amount o f spinal flexibility can be roughly calibrated. The standing flexion test and the gross spinal flexion test can be performed with the same procedure (Table 44.3).
FIGURE 44 . 9 .
Standing right side-bending test.
Active Screening for Gross Spinal Motions
This includes asking the patient to flex and extend the head and neck, forward bend ( Fig. 44.5) and backward bend the spine, side bend right and left ( Figs. 44.9 and 44. 1 0), and rotate the trunk (Table 44.3). Flexion (Forward Bending) See standing flexion tests described previously and Fig. 44. 5 . Flexion can b e measured i n several ways. Forward bending may be assessed by observation. The position of the patient's fingertips in relation to the floor can be measured and recorded as an objective test and used to determine the effect of certain types of treatment. An inclinometer can be placed over the l umbar spine, and' the number of degrees offorward bending recorded. A horizontal line can be drawn on the patient's skin at the sacral base and at Ll. The distance berween these lines is measured with a tape measure with the patient in the upright position and in a forward-bent position. Extension (Backward Bending) This is usually measured by inspection. A goniometer or incli nometer may be used for a more precise measurement. Side-Bending Test (Active) (Fig. 44.9) This is sometimes called lateral flexion. By slid ing the hand down the lateral aspect of the thigh toward the knee, observe for the presence of a smooth curve, abrupt changes in the curve, or the absence of thoracic and lumbar lateral curves while the patient side bends as far as possible to the left and the right. Thoracolumbar Rotation Test (Active) (See Table 44.3) Cervical Motion Test (Active) A variety of physician hand contacts can passively explore cer vical motion with the patient seated. The hand contact should
44. Musculoskeletal Examination for Somatic Dysfunction
641
5. Step 4 is repeated with the physician passively rotating the head i n the othet direction . Interpretation (Calculations): Normally, the superior cervi cal division supplies 45 degrees of rotation in each direction and the i n ferior cervical division supplies 4 5 more degrees o f rotation with a total of 90 degrees rotation of the head and neck ro the right and ro the left. Example for Calculating Superior and Inferior Cervical Division Dysfunction Findings: Restriction in right rotation of the neck. Gross right rotation is 65 degrees. Superior division right rotation is 30 de grees. Calculations (90 degrees is normal range of gross right and left rotation):
'\
J
l
(
A. 90 degrees Total normal right rotation -65 degrees Actual total right rotation =
=
25 degtees B. 4 5 degrees
FIGURE 44.10.
Trunk side-bending test (normal right acromion drop
test).
sense the beginning of restriction before the patient experiences discomfort. Note the sense of resistance, the range of movement in degrees, and the characteristic of the end-feel of motion. Position: Patient is seated and physician usually stands Ot sits behind the patient. Procedure: Patient is asked to Aex the head and neck, extend the head and neck, totate to each side (Table 44.3), and side bend to the left and right. Interpretation: Observe sensation of resistance to motion or unilateral restriction of motion, and record the fi ndings. Passive Screens for Motion
Passive Cervical Rotation to Quantitate Motion in the Superior and Inferior Cervical Divisions Position: Patient is seated and physician stands to the side andlor behind the patient. Procedure: 1 . Physician puts one hand on the patient's shoulder and the other on top of the patient's head. 2. The physician's hand, cOl1[acting the patient's head, passively rotates the head and neck to its barriers of right and left rotation and records the degrees of right and left rotation of the head and neck. 3. Physician then moves the hand from the patient's shoulder and uses the thumb and i ndex finger to palpate over the spinous process of the axis, C2. 4. Physician uses his or her other hand to rotate the head and neck to the poi nt where motion is fi rst fel t by the hand contacting the spinous process ofC2. The amount of rotation is recorded in degrees.
Total right rotation loss due to dysfonction of both the superior and inferior cervical divisions
=
Normal range of right rotation for superior cervical division Actual right rotation of superior cervical
=
-30 degrees
=
division 15 degrees C. 2 5 degrees
Right rotational loss due to dysfonction of superior cervical division
=
Total (calculated) right rotation loss due to su perior and inferior division dysfunction - 1 5 degrees Actual right rotational loss of superior cervical =
=
division 1 0 degrees
=
Right rotational loss due to dysfonction of inferior cervical division
Trunk Side-Bending Test (Acromion Drop Test) (Fig. 44.10) This tests upper thoracic side bending. Position: Patient is seated and the physician stands behind the patient. Procedure: 1 . Physician places one hand on the AC joint on the side to be tested. The physician then p laces the other forearm on the contralateral side of the patient's head with the hand on top of the patient's head to provide stability and prevent side bending o f the cervical spine. 2. The physician's hand, o n the AC j oint, produces caudad pres sure on the patient's shoulder until a restrictive barrier is reached. 3. Steps 1 and 2 are used to test the patient's opposite side.
Interpretation: Positive test: The AC horizontal plane depresses less than 20 degrees on the "positive" side and the barrier has a resistant end-feel. A positive test indicates that the upper thoracic spine has difficulty side bending toward and rotating away from the side of the test.
642
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment plane through the contact poinrs on the patienr's iliac crests. These findings are compared with those observed in step I.
Negative test: The AC horizonral plane depresses 20 to 25 degrees on both sides. Passive Motion Tests of Thoracolumbar Side Bending and Rotation Procedure (Table 44.3): An additional method For passive testing of any of the gross motions of the upper thoracic spine is to place one hand on the patienr's head and inrroduce Aexion down to the cervicothoracic junctio n . The other hand con racts the upper thoracic area and monitors further motion Aexion, side bending and rotation being inrroduced through the head and neck. The upper thoracics can be tested in neutral, flexed, or extended po sition by producing these motions beyond the cervicorhoracic Junction. Hip Drop Test (Fig. 44.11) The hip drop test is an active test. It screens for the ability of the lumbar and lumbothoracic region (especially the lumbosacral region) to side bend away From the side of the hip drop. Position: The patient is standing and the physician kneels or sits behind the patient. Procedure: 1 . The physician's fingers are placed on the superior and most lateral surFace of the patient's iliac crests, palms Facing down ward (parallel to the Aoor) , and a mental note is made of the observed horizontal plane passing through these rwo conract pOints. 2. The patient is instructed to bend one knee without lifting the heel From the Aoor and let the hip drop downward. The patienr m ust do this in a manner that does not rotate the pelvis in the transverse plane, nor translate the pelvis in a coronal plane. 3 . The physician again observes the level ness o f the horizonral
4. Steps 2 and 3 are repeated with the patienr's other lower extremlry. Interpretation: Negative test. Indicates normal side-bending abiliry of the lum bar and thoracolumbar regions of the spine to the con tralateral side of the hip drop test. Normal is a hip drop of 20 to 25 degrees and a smooth curve away from the side of the hip drop test (its convexiry is on the same side as the hip drop). Positive test: The plane of the iliac crests drops less than 20 degrees and/or the lumbar and thoracolumbar spine does not side bend with a smooth lateral curve, or is Aat, or is angled at one unit in its attempt to side bend away from the side being tested. The test is called positive on the side that was being tested . A positive hip drop test indicates that there is some somatic dysfunction or pathology in the lumbars or thoracolumbar junction that prevents the region of the spine from side bending normally to the side opposite the hip drop. Example of a Positive Hip Drop Test (Fig. 44 . 1 I): With weight being supported on the righ t leg, the left hip drops only 1 5 degrees and there will also be an angled curvature observed in the lumbar region . This indicates that lumbar and the tho racolumbar spine should be segmentally examined to determine the site of the side-bending dysfunction. Note: In all cases, as the hip drops the lumbar spine and tho racolumbar junction side bends away from the test side. Under normal conditions the side that drops the most has the greatest convexiry of lumbarlrhoracolumbar curve on the side of the test. The hip drop test can also be used to estimate the rype of scoliosis present in a patient. I F you observe a left scoliosis (thoracic region side bent to the righ t) in a patienr and the left hip drop test is neg ative, a C curve (side-benr right) is most likely present. IF the right hip drop test is negative in that person, an S-rype spinal curvature is most likely present. The area o FAattened or angled spinal curva ture seen in this patient is probably where the con tralateral curves meet and is often called a crossover poi n t. Somatic dysfunction at a crossover has expanded sign ificance because it is more likely to be associated with visceral dysFunction in organs receiving sym pathetic innervation from that level of the spinal cord. Pelvic Side-Shift Test (Passive) ( Fig. 44.12) With perfect posture, viewed From the back, the midline of the sacrum should be in the midheel line (the anreroposterior vertical gravitational line) and should not deviate to the right or leFt. This test determines whether the sacrum, as the cenrer of the pelvis, is in the midline. Position: The patienr is standing and the physician stands behind the patient. Procedure: 1.
The physician's left hand is placed on the lateral side of the left pelvis of the patient.
2 . The physician's right hand is placed on the patient's right shoulder to stabilize the thoracic spi nal segmenrs. FIGURE 44.11.
Positive left h i p d rop test.
3. The physician translates the patient's pelvis to the right side (while stabilizing the shoulder with his or her right hand) .
44. MuscuLoskeLetaL Examination for Somatic Dysfunction
643
4. The physician switches hand placements and translates the patient's pelvis to the left side. Interpretation: The physician is aware of amount of move ment, resistance to movement, and the end-feel at the barrier. Positive test: A positive test reveals freer translation to the side of side shift. This means that the sacrum (base of support) is positioned o n the side of the freer motion. If the deviation to one side is obvious with gross observation, pelvic shift is confirmed and rhis tesr need not be performed. Palpate for Elevated First Rib (Fig. 44.13A) (See also Chapter 49.) The most posterior part of the first rib in located in the fleshy part of the cervicothoracic junction just below and 1 /2-inch lateral to the end of the articular column of the cervical spine. Each is palpated with the i n dex and m iddle finger of each hand and the horizontal plane through these contact points is estimated. Position: Patient can be seated or supine. Seated examination seems to be easier to evaluate. Positive test: The rib head and posterior end of the first rib is elevated i n comparison with the oppos i te side. Note: This is only a presu mptive sign and musr be supported with first rib motion testing. This is because an apparent elevation of the first rib is present on rhe side opposite the side-bending FIGURE 44.12.
Right pelvic side-shift test.
A
FIGURE 44. 1 3 . A ,
B 1 , B2. Segmental d iagnosis of atypical ribs.
644
vrr
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
component of a thoracic inlet problem due to dysfunction of the cervicothoracic fascial diaphragm. The thoracic inlet dysfunction can be confirmed by estimation of the infraclavicular space and spring testing of the upper thoracic rib cage. If thoracic inlet dysfu nction is removed and the fi rst rib head is still elevated, a true elevated first rib somatic dysfunction is more l ikely to also be present. Palpate for Rib Angle Tenderness (Fig. 44. 1 4) This screens for dysfunction of ribs but does not indicate i f the dysfunction prefers i nhalation, exhalation, p u m p handle, o r bucket handle motion. That determination requires s tage I I seg mental evaluation for ribs (see Figs. 44. 1 BA and B ) . Position: Patient i s seated and physician stands behind and to the side opposite the side to be palpated. Procedure:
l. Patient's arm, on the side to be tested, crosses his or her chest
and the hand grasps the opposite shoulder. This glides the medial scapular border away from the spine and better exposes the rib angles of the upper ribs. This "glide" is i ncreased as the physician's anterior hand pulls the patient's shoulder or arm across the chest. 2. The physician places the index and m iddle fingerpads of his or her posterior hand over the rib angle of the second rib.
Costal Cage Motion-Four-Quadrant or Six-Quadrant Screen for the Ribs (Figs. 44. 1 5 and 44.16) Position: Patien t is supine and physician stands at the side of the table. Procedure for a Six-Quadrant Rib Screen: 1 . With hands flat, the physician places his or her fi ngers or hands up into the axilla to evaluate movement of ribs 1 and 2 during i nhalation and exhalation. 2. The hands rest o n the upper chest wall j ust lateral to the sternum with the fingertips on the clavicle and upper ribs and the thumbs on the sternum and touching each other. Duration of inhalation and exhalation pump handle motions of ribs 2 through 6 are evaluated. 3. The hands are placed over the lower rib cage with fingers pointing posteriorly and al igned with the patient's in tercostal spaces. The bucket handle motion of the ribs is evaluated in the lower rib cage (7- 1 0) as the patient breathes, first normally and then with exaggeration, if necessary. 4 . Some physicians will screen ribs 1 1 and 1 2 by applying pres sure posteriorly over those ribs, genrly springing them. Their hands then become passive as the patient breathes fully in and out and they evaluate pincer (caliper) motion of these two ribs with i n halation and exhalation.
4. The physician and patient reverse contact points and steps 2 and 3 are carried out on the opposi te rib angles.
Note: Six-quadrant screen versus the four-quadrant screen: In the six-quadrant screen the physician also places the fingers of each hand up i n to the patient's axillae to determ ine move ment of rib 2 and possibly rib l . Also note that neither the four-quadrant screen (Fig. 44. 1 5) nor the six-quadrant rib screen ( Fig. 44. 1 6) adequately check ribs 1 , 1 1 , or 1 2 ( Fig. 44. 1 3 A, BI and B2).
Interpretation: Increased palpable tissue texture change and tension is easily palpable and also often brings on a patient remark or expression of tenderness.
Alternate Straight-Leg Raising Test Though this is a test for sciatic nerve i rritation it is mentioned here because the patient does not normally associate this with sciatic
3 . The fingers of the posterior hand are moved caudad in a jerky nature to maintain equal palpatory pressure on the rib angles of the patient as the fingers glide along the different rib angles. This is con tinued down to the tenth rib angle.
Physician's one hand glides and rotates the scapula away from the
,t <-
rib angles
3 5
5 8 9 10 11 12 2
3
3
Physician's other hand palpates the rib angles
8
L 5 J
FIGURE 44. 14.
Palpation of rib angles.
L
5
J
44. Musculoskeletal Examination for Somatic Dysfunction
645
B v
2 4
FIGURE 44. 1 5.
Four-quadrant rib screen.
nerve testi'n g and the test may help to differentiate between a patient who truly has sciatic irritation and one that is malingeri ng. It merely i nvolves passive straightening (extension) of the knee of the sitting patient so that the h i p is fully flexed, the knee is extended, and the foot dorsiflexed. Interpretation: Positive test: The patient is unable to fully extend the knee with the hip flexed and there is pain along the distribution o f the SCIatic nerve. Seated Flexion Test (Table 44.3) This is an active test to localize which side of the pelvis most l i kely has the somatic dysfunction. Position: The patient sits with the knees approximately an acetabular distance apart. The physician stands behind the patient. Procedure:
I. The physician places his or her thumbs in contact with the psrss at their inferior notch. The PSISs may be level or unlevel before the test begins. Note which is present. 2. The patient is asked to bend forward at the waist, arms passing between the knees and the hands reaching for the floor. 3. The physician's thumbs ride with the iliac spines sensing any superior motion as the patient forward bends the trunk. The position of the left and right P S ISs are assessed relative to a transverse plane, both before and at the terminal position of forward-bending activi ty. Interpretation: Positive test: If motion of one thumb at the i n ferior notch of the PSIS continues to rise after termi nation of motion of the other thumb, the standing flexion test is positive for that side. The asymmetric superior motion that occurs near the end of forward bendi ng is especially important. S ince the patient is seated, the positive test indicates somatic dysfunction on the side
of the positive test, that is, in the sacrum or innominate (usually in the sacrum ) . Palpation for Tissue Texture Abnormality and Tenderness This stage I screen looks for areas of tissue texture changes and tenderness. I t is fairl y easy to do this in thoracic and lumbar regions of the spine, with the patient in the sitting position. These paraspinal regions and the ribs can be palpated for tissue texture abnormali ty and tenderness. The palpatory screen is performed using several fingers covering a broad expanse of the patient's back. Palpation of more local areas, in regions where there was a sense of tissue texture change or asymmetry, is performed with one or two fi ngers. With train ing, a physician can sense many tissue changes by palpation ( Fig. 44. 1 7) . The rib angles are most easily palpated with the patient in the seated position and the patient's arm , on the side of palpation, placed across h is or her chest and with the hand on the opposite shoulder ( Fig. 46. 1 4A) . Hip Flop Procedure Before beginning a screen or segmentally testing a supine patient the physician must settle the pelvis and spine in a relaxed resting position. Position: Patient is supine and the p hysician stands beside the patient. Procedure: 1 . The patient is i nstructed to flex the knees and hips, pick the buttocks up, and then relax all m uscles and let the pelvis drop to the table. 2. The physician passively brings both of the patient's lower ex tremities onto the table in full extension. Interpretation: This reduces asymmetry that is caused by poor i n itial alignment o n the table or asymmetry caused by m i no r muscle spasm.
646
VII Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
A v 2
:
� '
/
�
FIGURE 44.16.
'
Six-quadrant rib screen,
Optimal Patient Position for Segmental Musculoskeletal Examination of B ody
is possible but not evident, record the lower extremity findings on the side of the standing flexion test (Table 44,3) ,
Regions (Table 44.2)
Paraspinal palpation is an art perfected with time and practice, It is usually accomplished using the index and middle fingers of each hand to sense the superficial and then deep fasciae and muscular layers of the paraspinal regions. It can be performed in any position, Various characteristics are noted and expressed ( Fig, 44, 1 7) , Segmental Motion Testing
For spinal complaints and dysfunction , record findings on the side o f the positive seated flexion test. I f a lower extremity dysfunction
Passive Cervical Segmental Motion Testing See Chapter 46 for supine cervical segmental motion testing, For rotation and side bending, contact the articular column on both sides, Anterior pressure tests for rotation to the opposite side. Lateral translation tests for side bending to the side opposite the direction of translation, (For flexion and extension, monitor the spinous process-interspi nous area,) Passive Segmental Testing for Joints of the Upper Extremity This is discussed in Chapter 47,
44. Musculoskeletal Examination for Somatic Dysfunction
647
Warm, H ot E rythema, Erythematous
P i m p l e , B l e m i s h , Pust u l e hy
T h i c k ened R e s i l i e nt
" Soreness "
Res i l i ency
"Tenderness"
{
" Dull, Nagging" " Bu r n i ng " Paresthes i a
Congested
Spongy
Boggy Ede matous
Scaly I t chy
N o d u l e , N od u l a r
Fi brotic Contracture Resistant
Constncted
�x
� o
0
'\.
'\.
Tone, F i r m Res istant Stringy, Ropy Cont racte d , S p ast i c Cont ract i o n , Contract u re R e l axed F l a c ci d , Ato n i c
Const n ct l o n
Palpation o f tissue properties and abnormal ities. (Repri nted with permission from K uchera W, Kuchera M, Osteopathic Principles in Practice. 2nd ed rev. Greyden Press: Col u m bus, OH; 1 994:20.)
FIGURE 44.17.
Active Typical Rib Segmental Motion Testing (Figs. 44.18A and B) Position: Patient is seated or supine and physician srands behind or ar the side of the table. Procedure: 1 . T he physician uses rhe index and middle fi ngerpads of one hand to 5[I'addle the rib angle and the index and middle finger of the other hand to srraddle rhe same rib at irs midclavi cular line. The rhumbs can be placed o n rhe rib shaft ar rhe midaxillary line to evaluate bucker handle morion of rhe rib.
TABLE 44.2. BEST
POS ITION
FOR
A
PATIENT'S
INATION Region
Cervical Thoracic Ribs Lumbar Sacrum Pelvis Upper Extremities Lower extremities
Position
Supine Seated Seated Seated Prone Supine Seated
or prone or supine or prone
or supine
Seated or supine
EXAM
2 . T he patient is i nstructed with the mouth open,
to
take a deep brearh in and out,
Positive test: The rib will move freely throughout one of these phases bur nor move complerely thtoughout the other phase of rhe respiratory cycle. The rib somaric dysfu ncrion is named for the motion and axis in which i t moves. Example: Rib 5 , exhalation, pump handle rib (about a transverse axis ) . Active Atypical Rib Segmental Motion Testing First rib segmental resting (see Fig. 44. 1 3 A) Rib 1 1 or 1 2 segmental tesring (see Figs. 44. 1 3 B 1 and 82) Passive Lumbar Segmental Motion Testing This screen is done by paraspinal rh umb pressure over the trans verse processes, looking for rorarion preference. Position: Parient is p rone and the physician stands to the side of the patient. Procedure:
Assess rotation:
I. The physician places the pads of their rhumbs over the trans verse processes of a single vertebral segment wi th the rest of the hand wrapped around the lumbar paraspinal area. 2. The physician "grabs some torso" (i .e., hold the torso), and
648
VIf Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 44. 1 8 .
Segmental palpation of the typical ribs.
with both hands as a unit, rotates the vertebrae and soft tissue structures. * 3. The process is repeated in the opposite direction. Compare one side with the opposite side and segments above with seg ments below.
Assess side bending With the hands in the same position, the physician uses both hands as a unit to translate the vertebrae to the left and the right. t Compare one side with the opposite side and segments above with segments below.
Assess flexion or extension:
Apply direct pressure over a spinous process. t Repeat for the spinous ptocess o f each l u mbar vertebra and compare each seg ment with the segment above or below. Positive test: There is a p reference for rotation and side bend i ng. If a group curve is present, several units are involved with rotation and side bending to opposite sides. If nonneutral somatic dysfunction is present, rotation and side bending are to the same side and usually in a single vertebral unit. If the test reveals a
*
Rotation: A force d i rected anteriorly over a rransverse process rotates the
vertebra ro the opposite side. Anterior pressure over a right transverse process anempts to rotate the vertebra to the left and vice versa. t Side bending: Translating a vertebra
the vertebral u n it
to
to
the right induces side bending i n
the left a n d vice versa.
j Flexion and extension : An extended vertebral u n i t will move anteriorly
easily and will spring back slowly. A Hexed unit will resist anterior pressure.
nonneLltral somatic dysfunction, flexion or extension preference m ust also be determi ned. Passive Pelvic Segmental Motion Testing Position: Patient is usually in prone position but the condition o f the patient may require that he or she is supine, lateral recumbent, or seated. Physician stands at the head of the bed, to the side of the bed, or beh ind the patient. Procedure: 1 . The posterior and anterior landmark data collected from hor izontal plane determi nations is considered (i.e., levelness of the PS ISs and ASISs). 2 . The physician palpates sacral sulcus depths. Are they equal or is one deeper than the other? (See Chapter 52, Fig. 5 2 . 1 . ) 3. Physician palpates the inferior lateral angles for their ante rior/posterior and the inferior/superior positions. i s one more posterior and inferior than the other or is one more anre(ior and superior than the other? 4 . Palpate the sacrotuberous l igaments. ls one more tense than the other? 5. Palpate for levelness of the ischial tuberosities. Is one more i n ferior to the other? 6. Palpate for levelness of the iliac crests. (The patient in the supine position is preferred for this test.) Is one more superior to the 0 ther?
44.
7. The physician's thumbs place anterior pressure on the patient's con tralateral sacral base and inferolateral angle ( I LA) to test for ease or restriction in motion of the sacrum about its middle transverse axis. Some physicians will place fingers on the sacral base and then , using the palm of the other hand, attempt to produce motion about the sacral middle transverse and oblique axes. Interpretation: Diagnoses are made by comparing the data with standards established for the diagnosis of various sacral so matic dysfunctions. Passive Test for Lower Extremity Joints (Tables 44.3 and 44.4; see Chapters 50 and 5 3 ) SOMATIC DYSFUNCTION I N AMBULATORY OR BEDRIDDEN PATIENTS
OMT of somatic dysfunctions benefits the patient's general well being and the medical, preoperative, or surgical healing mecha nisms. Somatic dysfunctions found in a "heal thy person" should also be treated with manipulation to prevent future obvious dys function, to maintain health, and to increase the patient's level of health. The American Osteopathic Association (AOA) presently requires that three positions be used in the osteopathic muscu loskeletal examination if possible. Record the posi tions for the examination at the begin ning of the physical report. If the pa tient cannot achieve some position or some of the examinations were not completed, record the reasons in the progress notes or the physical exam ination. The patien t's history draws attention to areas of potential in volvement, including viscerosomatic relationships. An adequate examination should reveal significant positives and negatives im portant in arriving at an accurate working diagnosis. Although many of the tests presented here were screening exam inations, if any of them have a positive response and the physician believes them to be significant, segmental data m ust be obtained. The fi nal result is a recording of all areas examined and the somatic dys function that is related to the patient's complaints and problems. It is best to have a routine by which either the screens or segmental examinations are performed on a patient. These rou tines can be modified as the situation warrants, fitting them to the individual patient's needs, time available, and environmental constraints. The examples offered here have been helpful to the authors in screening office and hospital patients. It is not the only sequence. Developing a routine sequence makes it less likely that portions of the examination � ill be inadvertently omitted. A minimal screening examination is sufficient unless there is, Ot this screen indicates, reason for seeking additional data. The osteopathic musculoskeletal screening should not take more than a few minutes as it is usually integrated with other aspects of the history and physical examination. When doing the regional examinations for TART changes, remember that motion lim itation is more important than static asymmetry. The combination of motion asymmetry with any one additional TART criterion is sufficient to diagnose somatic dysfunction. Motion asymmetry may be noted passively (with physician-controlled motion) and/or actively (patient-controlled
MuscuLoskeletaL Examination for Somatic Dysfunction
649
motion ) . Passive motion testing may be more reliable for actual possible range of motion of a joint, since a patient may not achieve full active range of motion if fearful or if active motion is uncom fortable. H owever, active motion testing may be more indicative of the actual functional limitations of the patient because of its associated induced pain. The approach to the examination can be adapted according to whatever posi tional or motion limitations are imposed on the patient by his o r her condition o r treatment protocol . When the patient cannot stand or cannot sit, examination is obviously lim ited to that which is possible (i.e., in the prone, supine, or lateral recumbent positions) . When the history and physical examina tion are completed, the osteopathic physician arrives at one of four concl usions:
I. There is a significant somatic component related to the pa tient's condition. 2. There is no significant somatic component related to the pa tient's condition.
3 . There is a significant somatic component not related ro the patient's presenting problem that requires evaluation and con sideration in the treatment plan. 4. There is significant somatic dysfunction that is not directly re lated to the patient's present problem that should be addressed at a later time to result in an improved overall level of health. When a patient fai ls the screen in any given region, segmental tests of that region are i ndicated. Note: Motion disturbances in somatic dysfunction can be recorded in three ways ( 1 0) . Where is i t ? (position) What will it do? (direction of more free motion) What will it not do? (direction of restriction; this formula must be preceded by the word "restricted") The goal of recording the musculoskeletal screening examina tion for all inpatients and outpatients is to be able to answer the following questions: 1 . Are there significant somatic dysfunctions related to the pa tient's problems? 2. Can the regions involved for further study and for adminis tration of OMT be located to support the patient? 3. Could there be a viscerosomatic or somatovisceral connection? I f there is a significant somatic component, note a diagnosis of somatic dysfunction as one of the patient's problems and incorpo rate appropriate OMT in the treatment protocol. It is likely, for i nstance, that a patient entering the hospital for cholecystectomy will have a viscerosomatic reflex inducing somatic dysfu nction in the thoracic region, facilitating the visceral dysfunction. An effi cient screening should reveal that information , ifit is present. The diagnoses entered in the chart on this particular patient would include: 1 . Chronic cholecystitis with choleli thiasis 2. Thoracic somatic dysfunction secondary to number 1 Guidelines may be usefu l for organ izing knowledge into a practical and useful form. The following presents these guidel i nes
650
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
TABLE 44. 3 . SCREE N I NG MUSCULOSKELETAL EXAM I N AT I O N FOR THE A M B U LATORY PAT I E N T Tests
Body Pla nes
Arms
11
Neg.
Pos.
Estimate levelness of horizontal planes under the mastoid bones, shou lders, inferior scapular ang les, i l iac crests, posterior superior i l iac spines (PSIS), a nd the cephalad margins of the greater trochanters. Positive = un leveled horizontal planes. This ind icates postural change that could be related to com pensatory mechan isms, visceral dysfunction, and/or scoliosis.
Neg.
Pos.
The patient raises h is/her arms above the head; upper arms touch ears, back of hands are together. Repeat the test having patient put palms together over the head. Positive = unable to fully extend the extremity with upper arms alongside of the ears and hands together. Ind icates dysfunction i n any one or combination of the joints of the upper extremity and a lso i ncl udes the upper back and upper thoracic reg ion. I ndividual joints listed above are specifically exami ned accord i n g to the patient's history and concerns.
Neg.
Pos.
The patient squats down and returns to upright position. This tests h i ps, knees, ankles, and strength of the legs. Positive = i n a b i l ity to flex legs while weightbearing to a point where the thighs are at least level with the ground or patient is unable to return to the upright position without help. Individual joi nts listed above are specifica lly examined according t o the patient's history and
, ,
, , ,
, .
· · ·
Legs
t 2
Explanation
Test Results
concerns.
(continued)
TABU: 44.3.
(continued) Tests
Test Results
Standing Flexion Test
A
Seated Flexion Test
\\
Neg.
Pos.
The physician mon itors the inferior notches of the PSISs as the patient bends forward with arms hanging toward the floor. This loca l izes pelvic and/or leg somatic dysfunction to one side. (A rib hump can also be visual ized at this time if there is thoracic rotosco l i osis.) Positive = the PSISs rise asymmetrical ly. It is the PS I S that rises farthest and last w i t h forward bending: and/or there is a " r i b hump" visual ized. Because the patient is weightbearing this test i n d icates dysfunction in the leg and/or in the pelvis on the "positive" side. (A rib hump i n d icates rotoscoliosis with rotation toward the side of the h u m p and side bending away; often due to scoliosis resu lting from an un leveled sacral base.)
Neg.
Pos.
The physician mon itors the i nferior notches of both ' PSISs w h i l e the patient bends forwar d with arms hanging toward the floor. The test localizes somatic dysfunction to one side of the pelvis. (A rib hump can a l so be visual ized at this time if there is thoracic rotoscol iosis.) Positive = the PSISs rises asymmetrical ly. It is the PSIS that rises farthest and last with forward bending: and/or there is a " r i b h u m p " visual ized. Because the patient is not weightbearing the positive side i n d icates some problem with the i n nomi nate or sacral joints on the positive side. (A rib hump ind icates rotosco l i osis.)
Neg.
Pos.
Passive rotation of the tru n k is produced to the right and to the left. Normal = 90'" . Positive = rotation restricted in one d i rection. Ind icates restriction to rotation somewhere in the thoraco l u mbar spine. If there is a problem in rotation there is a problem in side bend i n g . If screen fails, follow w i t h segmental exa m i nation for somatic dysfunction and correlate findi ngs with neurologic exa m i nation.
Neg.
Pos.
The physician d epresses the shoulder on one side and then the other. This action tests side bend ing and rotation of the u p per thoracic spine. Normal = acromion drops 2 5 . Positive = acromion does not drop as far on one side as o n the other (i.e., drops less than 2 5°) . I n d icates restriction of the upper thoracic area to side bend toward the side of the positive test. With neutral dysfunctions those un its rotate to the opposite side of side bending. With non-neutral dysfunction the vertebral unit rotates to the same side as the side bend ing.
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(continued )
V[I. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
652 TABLE 44. 3 .
(continued) Tests
Cervical Rotation
Test Results
Neg.
Pos.
Passive rotation of the head and neck to the left and to the right. Positive = head a nd neck has less rotation to one side compared with that of the other side. Norma l is 90' i n each d i rection. Ind icates restriction to rotation somewhere i n the cervical spi ne. If rotational dysfunction is noted, there w i l l a lso be restricted side bending to the same side somewhere i n the inferior cervical d ivision (C2-7). Test segmental ly.
Neg.
Pos.
Steady d igital pressure over the collateral sympathetic ganglia of the abdomen-test for tenderness of the celiac, superior mesenteric, and inferior mesenteric ganglia. Positive = tissue texture change and/or pain to pal pation. Tenderness ind icates possible dysfunction of the organs i n nervated by the tender col lateral ganglion. Correlate tenderness of any of the ganglia with appropriate organ h istory, more specific physical findi ngs, and/or la boratory work.
Neg.
Pos.
Passively test rotation preference or restriction of fascias at specific total body reference zones (i.e., occipitoatlantal, cervicothoracic, thoracol u mbar, a nd lum bosacral regions). Positive = fascias to not alternate d i rection of their ease of motion from one region to the next. Fascial patterning is classified as compensated or uncom pensated. An uncompensated fascial pattern does not alternate motion preference from one region to the next. The uncompe nsated pattern ind icates the greatest hindrance to fluid movement in the body. The compensated fascial pattern alternates motion preference from one region to the next. Approximately 85% of these w i l l be left, right, left, rig ht, labeled from the head down. The compensated pattern poses less of an obstruction to fluid flow i n the body.
Collateral G a n g l io n Pal pation
Sup. mesenteric
Celiac ganglion
Inf. mesenteric
11 \(
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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
",
,
,
.... .. . - - - - .. .
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-
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: •
•
• • •
•
•
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FIGURE 44.19. A:
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
656
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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<'IPlfhlC Mrd.dne.
FIGURE 44.19.
(continued)
c
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
658
Outpatient Osteopathic Assessment and Plan Form
A
ICD Code
Dx No.
I
Somatic Dysfunction of R i bs
0
A l l nOl done
OMT
y
Regioll
Head and Neck
cc
Thora i
Face
N
0 0 0 0 0 0 0 0
'1' 1 -4 '1'59
T I O- 1 2 Ribs Lumbar
Pe lv is
Sacrum
0 0 0 0 0 0 0 0
0 0 0 0
Abdomcn/Olher Upper EXlremily Lower EXlremily
ART
IH.T
0 0 0 0
es
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
CR
0
0 0 0 0 0
0
0
I)IR
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
Meds:
Nulrilion: Soli
""'om '"
2
ovod / stnblo
ntSdlllonnJ WCNku
,
3
Level
.--->1 < 1 pI. I
I
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
W
0 0
0 0
0 0 0 0 0 0
0 0 0
0 0
U
0 0 0 0 0 0
0 0 0 0
0 0 0 0
0
only
2
II
above
I
Levol III
2 pI. 3
I
0
I
Level IV
3 pI. 0
I
I
L.v.1 1
Level V
> 4 pI. 0
(problems, risk and dota
•
---I
Level
I
1 I
----
ExnmlnnbOfl
Comp/oxllyl A6.Sossmonl Plan
II
III
II
III
II
IV
Minutes spent with lhe patient:
0
IV
III
0
10
0
1$
0
2.'
O M T pcrformed as Abovc:
0
0
'.
W
o
areas
Other Procedu res CPT Codes: Performed : I Wri tten Dx: ElM Code: I New I 0 0 I Write 992 Vlll'\" . . .
I
Sigl1:lturc o r transcriber:
J 02
hlOdcd hy (I Wl1U1 frlllll the fhm,:;1U u( RC\C!II"l;h, n,:",t:ncd \0 (CHIIJIII.llc
....
I I
0
0
0
l.vel n
Min.
I
0
I
Low
Mod.
Lev.I IV
I
0
t
I
0
I
rl
Now poHonlS
V
I
Rovlow
'000I'd$. Oi�, """ 11
VlsuahzruJQn Ol lf L el l Lov.1 1I
l.vel V
.... ..-- 1
High
0
I
V
0
1 -2 areas
0
I
03 I 04 1 05 I
EST . . .
$1 pI.
(ml(Wtos)
----0
0
I I
I
0
0
0
,
,
)
3-4
arcas
0
I
0
0 ,
0
I
0
•
0
0
0
5-6 areas
0
0
7
I
0
•
0
9
I
/ I I /2 I /3 J 14 I / 5 1
I•
3 pt.
0
30
20
10
L.v.I IV
I
iotal time
III
IS
10
I
IV
0
0
11
"
7-8
Consults . . .
Units:
areas
I I
0
0 I 0 j 41 I 42
I
0
0
.... I V
>4 I'll. 0 L
.
V
45
60
25
40
0 0 0 us a brlof doscrlptlon of topics discussed
Dictate totnl tlmo and counselingI coordinating limo.pl
0
2 pI.
Ltvol ill
II
2 2 I
0
0
.
I
Final level of service
0
on
I
an
ol lh. INlcoun'.t 'a coun,oUn I COOfdlnaUn Ih. 10v.I I, del.rmlned b
E$t."lbIlsnod pallOf't15 (minutes)
I
0
I
l.v.1 1It
Wh.n rna
V
Follow·up:
>W
I
030
Oon,in 1fJeXM'05 Of Hie from othefs
Optional Method-Codlnq by Time IV
"0"'''
OiSCtaJ ....,lh
of com laxity :;; avera e of Included aroas.
0 {} All thoso orens roqulrod. Avor8go of throo lovols of service. Final level 01 .orvlco
I
MOOIOne
Traditional Method-Codlnq by Components HISIOf'(
1
Lab
..
1 mQll;
Uldmum Point.
R,,,,,
manl'lgemo n l opllons)
1
Now--noworku
ulres
0 0
0 0 0 0 0 0
0 0 0 0 0
0 0 0 0
R
onl
D...
Mm.mnl _ Mm Low MOCIOtate Mod ",
2 mnx
1
E�ti'lblISho()-WOI'5011'
Ro
0 0 0 0
0 0
0 0 0 0 0
Risk; (prolflnllno problem!.), dlagnOIUc ptouduro(a) and
l
0 0 0 0
Worse Response
\'l'"
,"T
�'n
0
'Default to level 2-same criteria
Probloms
L ove l
0
Unchanged
Othcr
Complexity / Assessment / Plan (Scoring)
Now
Somatic Dysfunclion of Lowcr EXlremity
0 0
0 0 0 0
/ Olher
PT:
E xe rc i sc :
EatallhSNKl
0
0 0 0 0
0 0 0 0
0 0 0 0 0
of Abd
Somalic Dysfunction of
�Il':
0 0 0 0
0 0 0
0 0 0 0 0
0 0 0 0
(..AS
0 0 0 0
0 0 0 0
0
0 0 0 0
I�R
1�1l
11\'1..\
Uppe r EXlremilY
So malic Dysfunclion of Pelvis Somalic Dysfunclion
I mprovcd
Treatment Method
Fl'tt
0 0 0 0 0
0 0 0
0
Resolvcd
Somatic Dysfunction of Sacrum
739.9 739.6 739.7
Somalic Dysfunction o f Thoracic
FirSI visil
Written Diagnosis
739.4 739. 5
Somatic Dysfunclion of Neck
Physic i a n · s cl';! lumion of palienl prior 10 Ircal menl:
f
ICD Code
Somatic Dysfunction of Head and Face
Somalic Dysfunclion of Lumbar
B 5·02 1402
use on l y:
Ox No.
Writtcn Dial!l1osis
739.0 739. 1 739.2 739.8 739.3
version
For office
Datc
amc
.'alicnt's
wak SOAP Office of:
0
w
0
"
9· 1 0 areas
0
0
y
0
l'lt]'.
{}
0 0 0 43 II 44 JI 45
S i gll
Nlll c Form, RC'f."(1I1m'ICndcd h) AmerH.:,," A�'i(k:':!lllin (,( College, of (hlcup;JlhlC MCl.hclI\c.
10 2002 Ament:.1n
,Ih Olllp:ulcnl O:'\('(IP.llhK" SOAP
,\(.utem), uf O�ll!llpalh).
FIGURE 44.19.
(continued)
D
44. Musculoskeletal Examination for Somatic Dysfunction SAMPLE HISTORY AND OSTEOPATHIC MUSCULOSKELETAL EXAMINATION
A 38-year-old woman presents with low back pain of insidious onset and of 3 months duration. She is exami ned in standing, seated, prone, and supine positions. Review of systems is not relevant ( N R) . The back pain is worse at the left lum bosacral area. Neurologic exami nation is N R. The patien t failed screening examination for body planes, standing and seated Aexion tests, collateral gangl ia, and fascial planes. Standin:g: right iliac crest, trochanter, and PSIS planes -t . (+) right standing and seated Aexion tests. Right lumbar paravertebral hump, apex at L2. A n teroposterior curves appear normal. Supine: abdominal tenderness in subxiphoid and right epi gastric regions; celiac gangl ion tender; right ASIS L left ASI S -t . Cranial screen and cervical spine negative. Prone: Right PSIS, -t and left PSIS t; right sacral sulcus deep; tenderness TTA present. Right I LA posterior and -t . Is chial tuberosities are level. Right lumbar paravertebral muscle mass; tenderness and TTA right paravertebral l umbar muscula ture. Lumbars SLRR; TTA at right T6-9 region, T8 is ESRRR. Patient denies Food i n tolerances. Segmental Musculoskelet al Findings
T8 ESR RR , standing and seated FT + R, R P S I S -t , R ASIS t , R sulcus deep, R I LA post. and -t , ischial tuberosities are level; inlet Fascia RLS L ; T L Fascias RL. Wor king Diagnosis I.
Somatic dysfunction (SO) of pelvis: right sacral shear and posterior right innominate
2. S O of thoracic region: nonneutral T8 S O 3. Probable subacute dysfunction of gallbladder 4. Myofascial S O
659
has produced, and the American Academy of Osteopathy has recently adopted, standardized subjective, objective assessment plan (SOAP) note forms to simplify the physician's recording of "essential" history, exam ination, and treatment documentation concerning patients seen in the office (Fig. 44. 1 9A through D ) . Actual preliminary clinical trials using these forms have revealed improved completeness and recording accuracy. Up to a 33% in crease in collections has been reported. These and a SOAP Note Form Usage G uide, i nstructing the physician on how to use these forms, are available fro m the American Academy of Osteopathy, 3500 DePauw Blvd, Suite 1 080, I n dianapolis, I N 46268- 1 1 36; phone (3 1 7) 879- 1 88 1 ; www.academyoJosteopathy. org.
CONCLUSION
The osteopathic musculoskeletal evaluation provides informa tion about the m usculoskeletal system and musculoskeletal clues to dysfunction of other systems or of the general heal th status of the patient. I t is unique in that palpation integrated with motion testing is the major component o f that portion of the exami nation. Discovery o f m usculoskeletal dysfu nction often provides additional clues that direct, focus, or expand the exam ination; the musculoskeletal diagnosis also expands the logical conclusions that can be drawn from that examination.
REFERENCES I . D i n nar U. Classificarion of d i agnosric resrs used with osreoparhic ma ni pularion. jA OA. 1 980;79:4 5 1 -4 5 5 .
2 . D i nnar U, er a ! . Descriprion offifry d i agnosric rests used w i r h osreoparhic manipularion. jAOA. 1 982 ; 8 1 : 3 J 4-32 1 .
3. Johnsron WE. H i p s hi fr: resri ng a basic posrural dysfuncrion. jAOA.
1 964;63:923-930. Repr i nted i n Pererson B , ed. Postural Balance and
fmbalance. Newark, O H : American Academy ofOsreoparhy; 1 98 3 : I 091 1 2.
4. Kappler RE. Postural balance and morion parrerns. jA OA. 1 982;8 1 : 5 98606. Repri nred in Pererson B, ed. Postural Balance tlnd Imbalance.
Newark, O H : American Academy of Osreoparhy; 1 983:6 1 2.
Rx
1 . Lateral recumbent pull for shear 2. ME for posterior right innom inate 3 . Rib raising, mid thoracic 4. Paraspi nal soft tissue 5. Myofascial direct method treatment to dome diaphragm
5. M i rchell FL J r, Morall PT, Pruzzo NA. An Evaluation tlnd Treatment Manual of Osteopathic Muscle Energy Procedures. Published by the au
rhors, Valley Park, M O ; 1 979.
6. Surron SE. Postural i mbalance: exa m i narion and trearment urilizing Aex
ion resrs. jA OA. 1 97 8 ;7 7 :456-465 . Rep r i nted in Peterson B, ed. Postural
Balance tlnd fmbaltlnce. Newark, Ohio: American Academy of Osreopa
thy; 1 983 : I 02-1 0 8.
7. Sutron SE. A n osreoparh i c merhod of h isrory taking and physical exam inarion, parr 1 . jA OA. 1 978;77: 780-788.
6. ME to in let fasciae
8 . Sutton SE. All osteopathic merhod o f h isrory raking and physical exam
7. H igh velocity/low amplitude technique to thoracic SO (pillow localization)
9 . Zink J G , Lawson WA. An osteopath i c strucrural examination a n d func
9. Recheck in I week, (consider possible gallbladder dysfunction) 8 . Avoid concentrated fatty foods
Note: Although this example does not follow the proposed new recording forms, the Louisa Burns Research Com m i ttee
inarion, parr 1 1 . jA OA. 1 97 8 ; 77 : 845-8 5 8 .
rional i n terprerarion of rhe soma. Osteoptlth Ann. 1 979;7(5): 208-2 1 4.
1 0. Glossary Review Com m i ttee of rhe Educarional Council on Osteopathic Principles. Glossary of osteopathic terminology. In: Allen TW, ed. A OA Yearbook and Directory of Osteopathic Physicians. Ch icago, l L: American
Osreoparhic Associarion; 1 994.
I I . Kuchera M L, Kuchera WA. Osteoptlthic Considerations in Systemic Dys function, 2 nd ed rev. Columbus, O H : Greyden Press; 1 994.
Part B. Regional Examination and Treatment
HEAD: DIAGNOSIS AND TREATMENT ROBERT E. KAPPLER KENNETH A. RAMEY
SKELETAL STRUCTURES KEY CONCEPTS • • • • • •
• • • • • • • • • •
Cranial motion in terms of flexion and extension of certain bones and how to do a cranial motion assessment Origin and location o f trigger points in musculature o fhead and neck Role o f connective tissue in craniosacral motion and role of dural continuity in referred pain How somatic dysfunction can alter arterial supply, leading to symproms, and venous flow producing congestion Routes of lymphatic flow in head and neck and possible points of blockage Parasympathetic and sympathetic i nnervation of head and neck and consequences of parasympathetic hyperactivity or altering sympathetic input Function and location o f cranial nerves II through XII, including possible dysfunctions Effects of compressing fourth ventricle Understanding and treatment of sinus, eye, and ear disorders Goals and methods of osteopathic treatment of common cold Four major classifications of headaches Physiology of migraines, cluster headaches, and tension headaches, and osteopathic treatment of whole person Physiology and causes of traction and inflammatory headaches Presentation of trigeminal neuralgia Presentation o f Bell palsy Anatomy, motion, diagnosis, and muscle energy treatment o f temporomandibular joint dysfunction
The adult skull is composed of 29 bones (Figs. 4 5 . 1 through 4 5 .7 ) . These are summarized in Table 4 5 . 1 . From a cran iosacral perspective, they can be divided into m idline and paired bones. During craniosacral flexion, the midline bones (sphenoid, occiput, ethmoid, and vomer) move into flexion around their re spective transverse axes. The paired bones externally rotate dur ing craniosacral flexion. During craniosacral extension the reverse occurs ( 1 ).
MUSCLES The myofascial system is often involved i n head symptoms. Trav ell and Simons have described various myofascial trigger points (TPs) that may refer pain to and/or cause dysfunction of struc tures of the head (2) (Fig. 4 5 . 8 and Table 4 5 . 2 ) . Somatic dys function and TPs are closely related and potentiate one another. Emotional stress may be associated with clenching of the teeth and may produce TPs i n the masseter and pterygoid muscles. Frowning or squinting may set up TPs in the orbicularis oculi and occipitalis muscles. TPs i n the sternocleidomastoid muscle may refer pain to the eye and may be associated with balance abnormalities. Motor vehicle accidents, especially from the rear, may produce TPs in the sternocleidomastoid, splenius cervicis, and trapezius m uscles. TPs in the orbicularis oculi muscle may produce such ipsilateral visual disturbances as blurred vision, de creased l ight perception, tears, and conjunctival reddening. TPs in the occipitalis muscle may refer pain behind the eye and orbit. TPs in the trapezius muscle may refer pain to the orbit (2) .
CONNECTIVE TISSUE Sym ptoms involving the head, ears, eyes, nose, and throat ( H EENT) structutes are often seen and may be sources of signif icant fu nctional disability. Consideration of structural and func tional relationships allows the clinician to more accurately diag nose various conditions and im plement appropriate treatment.
The dura mater l ines the skull and produces folds, or intracranial membranes, that act as partitions between, and support for, the cerebral hemispheres and cerebellum (Figs. 45.9 and 4 5 . 1 0) ( 1 ) . These structures form the reciprocal tension membrane (RTM)
45. Head: Diagnosis and Treatment
Temporal lines
661
� ,..----.....;-...;;,sr--:-
Remains 01 metopic suture
,------.- Glabella Temporallossa--_
p:;.------..,.i-- Nasion r-----.;-..;..--iiiii""""- 1 nternasal suture Perpendicular �:ir......;�::::;..Iiit:;r':'-"jF�t---- of ethmoid plate
Zygomatic arch _
��--�r----���- Vomer �-- -Anterior nasal spine
;,:..;..---Intermaxillary suture
Angle of mandible -
-------...;;.-- Symphysis menti (line 01 union 01 mandibular , halves) .
Inferior border of mandible ---...
M,"'" " , .,, ' ,
A, Anterior view
/
Mental protuberance
FIGURE 45.1. Frontal view of sku l l . (From Agur A M R . Grant's Atlas of Anatomy, 9th ed. Ba ltimore, MD: W i l l iams & Wi l k ins; 1 99 1 :452. )
and are i ntegrally involved in craniosacral motion. The dura lin ing the skull extends through the cranial sutures and becomes contin uous with the periosteal covering of the skull. The fal x cere bell i extends i nferiorly from the straight sin us and fi rmly attaches to the foramen magnum. It attaches to the bodies of the second and third cervical vertebrae and extends downward as a tube that
ulti mately attaches to the second sacral segment (Fig. 4 5 . 1 1 ) . The dura becomes continuous with the extracranial fascia at var ious foramina in the base of the skull and contin ues outward as sheaths (perineurium) surrounding various cranial and spinal nerves. Extracranial and i n tracranial dural continuity explain why dysfunction in the periphery can be referred to the head ( 1 ) .
662
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Optic canal (foramen)
Supraorbital notch
o
'(\,
1:;
ex.
1
"LaCrimal foramen"
-'"""-----4-=:.;;:.!.- Trochlear notch (or spine)
Lesser and greater wings of spllenold bone
�----Lo::""' : :---r --....-+--_-�... --",;---..,n;
Anterior and posterior ethmoidal foramina
Superior and inferior orbital fissures -------..;; Crest of lacrimal bone (posterior lacrimal crest)
]
Infraorbital groove Suture cloSing canal Infraorbital foramen
::.. ..I..:t.���� .:::_ -= _________ _ "
Fossa for lacrimal sac
M
FIGURE 45.2. Orbita l view of sku l l . (From Agur A M R. Grant's Atlas of Anatomy, 9th ed. Balti more, MD: Wil l iams & Wilki ns; 1 99 1 :482.)
ARTERIAL SUPPLY The face and scalp are supplied by branches of the external carotid arrery (primarily the facial arrery) ( 3 ) . The i n ternal structures of the head are primarily supplied by the i nternal carotid and ver tebral arreries (Fig. 4 5 . 1 2) . The internal carotid arrery passes through the carotid canal in the petro us porrion of the tem poral bone. I t supplies the anterior portions of the cerebrum (3). Cranial dysfunction in the arriculations between the tem poral bones, occiput, and sphenoid can alter the normal func tion of these arreries ( 3 ) . This can produce symproms includ ing weakness and al tered sensation on the opposite side of the body. The vertebral arreries arise from the subclavian artery and ascend through the transverse foramen of C6-C3. At C2 they make several right angle turns before p iercing the dura to an gie anteriorly and enter the skull through the foramen magnum (3). The vertebral arteries supply the visual area of the cerebrum (occipital lobe) , brainstem, and cerebel l um. Dysfunctions affect ing th is arrery can be associated with visual abnormalities and dizziness (3).
VENOUS DRAINAGE Approximately 85% of the venous drainage from the head oc curs via the i nternal j ugular veins (Fig. 4 5 . 1 3) . These veins pass through the j ugular foramen which is formed by both the occiput and temporal bones and is located along the occipitomastoid
suture. A n occipitomastoid compression can compromise venous flow through the j ugular foramen, leading to congestion of the large valveless venous sinuses within the head. Sacral, upper tho racic, cervical, and associated regional connective tissue dysfunc tion can also contribute to congestion and impaired venous flow from the head (2).
LYM P H ATIC D RAINAGE A knowledge of lymphatic drainage patterns assists t h e physi cian in localizing pathologic conditions in the head (Fig. 45. 1 4) . Lymphatic vessels i n the forehead and anterior part of the face drain i n to the submandibular lymph nodes. Lymph vessels from the lateral face and eyelids drain i n feriorly toward the parotid lymph nodes and ultimately drain into the deep cervical lymph nodes (3) . The superficial lymph nodes of the head include the submandibular, occipital, retroauricular, and superficial parotid lymph nodes. Lymph from the occipital region of the scalp drains into the occipital lymph nodes. The temporoparietal region drains into the retroauricular lymph nodes. The frontoparietal region drains into the superficial parotid lymph nodes. Lymph from the su perficial lymph nodes eventually drains into the cervical lymph nodes. The deep cervical lymph nodes are located along the inter nal j ugular vei n . Lymph from the deep cervical structures passes through the j ugular trunk into the left (thoracic duct) and right lymphatic trunks (Fig. 4 5 . 1 5) (3) .
45. Head: Diagnosis and Treatment
663
Bregma
j Pterion
Lambda- \
I
Posterior pole--
J�1
'; r
i
>
, 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
Sternocleidomastoid (sternal)
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
Sternocleidomastoid (sternal)
Sternocleidomastoid (sternal)
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
Sternocleidomastoid (sternal)
Platysma
Temporalis (TP1) Splenius cericis
Orbicularis oculi Zygomaticus major
Temporal Headache
Masseter (superficial) Suboccipital group
Toothache
Sternocleidomastoid (clavicular)
Occipitalis
Sternocleidomastoid (sternal)
Orbicularis oculi
Temporalis (TPs1 ,2,3)
Semispinalis capitis
Trapezius (TP1)
Masseter (deep)
Frontalis Sygomaticus major Zygomaticus major Frontal Headache
Sternocleidomastoid (clavicular)
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
45. Head: Diagnosis and Treatment
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... . __ . �'
Right brachiocephalic vein ----->.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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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 -
Internal carotid artery
, ,
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:
Internal carotid artery
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
45. Head: Diagnosis and Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.)
678
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
45. Head: Diagnosis and Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
47. Upper Extremities
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.
47. Upper Extremities
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.)
47. Upper Extremities
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).
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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,
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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
anterior primary rami
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
anterior primary rami
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
Proximal/Medial Attachments
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,
Proximal/Medial Attachments
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
Proximal/Medial Attachments
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
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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.
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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.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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·
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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
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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
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
[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
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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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
N
731
0
u
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.
v
w J
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
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
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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
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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
VIi.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
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.
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
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
..
2t4
Ri9ht
'
hypochodriac region
"
'·0
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.
•
.' .
v •
'-,/
{� ./<.'
•
FIGURE 51.12. A: The nine-quadrant abdomen.
,,>,
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v
B: Approximate location of visceral organs.
2. From the periphery. This approach includes such tech niques as thoracic and pedal lymphatic pumps, diaphragmatic redoming, and thoracic inlet and pelvic diaphragm releases. These techniques are used to improve the ability to move Auids through out the abdominal region, thus improving the delivery of oxygen, nutrients, and arterial blood to affected areas, and facilitating ve nous and lymphatic drainage for the removal of the waste prod ucts of cellular metabolism. This approach also includes the use of diagnostic Chapman reAexes and their soft tissue treatment, such as treatment of Chapman points for the large bowel that are located on the lateral thigh areas. 3. Direct techniques to the abdomen. These techniques are applied through the abdominal wall directly to collateral ganglia or the organs to be treated. These techniques are described in the following section. It should be noted that, as in the approach to other structure function relationships, these approaches are often used in com bination with each other. Paraspinal Inhibition
Follow the steps below for ileus prevention and treatment of sympathicotonia. 1.
The patient is supine.
2. The physician is seated on either side of the patient. 3. The physician's hands are placed under the patient's thora columbar spine with the fingertips over the opposite side erector spinae tissues and the thenar and hypothenar emi nences over the ipsilateral erector spinae tissues.
51. The Abdominal Region
759
Bronchus, myocardium,
Palpatory findings:
(esophagus and thyroid) Upper lung
Chapman's left
I
Lower lung
right
(R) liver (L) stomach
2 3 4 5 6 7
;r
8
(R) gall bladder, liver
/
(L) stomach
9 10 11 12
0 [1
(�
Urethra
0 [)
Ureters
O<5[)
�
3
Iliotibi 1 band Colon
� {9 cr
broad ligament prostate
Chapman's reflexes you did NOT test: URI (But you can see this)
Gonads
Cerebellum
Upper limb
Tongue
FIGURE 51.13. Thirty-second screening examination for Chapman reflex points.
4. The physician's fingers are flexed toward the base of the palms and the erector spinae masses are thus gently squeezed, approximating them, and effectively moving the thoracolum bar spine inro extension. 5. The point of tissue tension balance or equalization is obtained by adjusting the pressure between the two hands to match the tension in the erector spinae tissues; the forearms can be moved closer to or farther away from the patient's body, if necessary, to equalize tissue tension.
6. Erector spinae tension is maintained until these muscles relax (usually 60 to 90 seconds). 7. The tension in the erector spinae tissues is reassessed. 8. Steps 2 through 5 are repeated until tissue tension is greatly reduced Ot eliminated. Collateral Ganglia Inhibition
Follow the steps below for treatment of sympathicotonia.
760
I.
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
The patiem is supine.
2. The physician stands on either side of the patiem, facing the patiem's abdomen. 3. The length of the examining fingers are standardized by bend ing the longer fingers. 4. The skin over the celiac (then superior, then inferior) ganglion is contacted with the fingerpads and assessed for tenderness and tension in the soft subcutaneous tissues.
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5. When an area of increased tissue tension is noted, the physi cian instructs the patiem to inhale partially and hold their breath as long as possible. 6. When the patient exhales, the physician gently increases the pressure on the tissues as they relax, until the next restrictive barrier is met. 7. Repeat steps 5 and 6 umil the tissue tension is greatly reduced or eliminated. Falciform Ligament (Linea Alba) Release
To relieve fascial tension on the liver and relieve general mental tension, follow these steps: 1. The patient is supine. 2. The physician stands at the left side of the patient. 3. The physician places the fingerpads of both hands on the midline of the patient's abdomen. The physician's right fifth fingerpad is just below the xiphisternal joim. 4. The fingerpads are aligned so they are even in comact with the skin, each fingerpad with the same pressure.
FIGURE 51.14. Direction of hand movement for treatment of abdom inal mesenteries.
5. The mesentery to be treated is moved gently until resistance to motion is felt. 6. The patient takes a partial breath in and holds it as long as possible.
5. The pressure of comact is gently increased, matching the ten sion of the soft tissues under the fingerpads along the linea alba or falciform ligament as the patient takes long, slow, deep breaths.
7. As the patiem exhales, the physician increases the pressure on the tissues umil the next restrictive barrier is met.
6. The pressure of contact is increased as the tissues permit and adjustments are made according to the patient's comfort level.
8. Steps 2 through 5 are repeated until the: colon feels compliam to mobility testing.
7. The technique is completed when there is no resistance felt in the soft tissues under the fingerpads. Mesenteric Releases
To relieve mesenteric tension and thereby improve lymphatic drainage from and innervation and circulation to and from the viscera, follow these steps: 1. The patient is supine. 2. The physician stands at the patient's right side. 3. The physician contacts the mesentery to be treated (ascend ing colon, descending colon, sigmoid colon, root of the mesentery) with the ulnar edges of their fingers (not the fingerpads). 4. The intestine is gently moved at right angles to the attach ment of its mesentery (ascending colon and descending colon are moved medially toward the umbilicus; the sigmoid colon and the root of the mesemery are moved in a diagonal line from the lower left abdominal quadrant toward the upper right abdominal quadrant (Fig. 51.14).
A variation on this technique is as follows: 9. The tissues are moved only a few centimeters until resistance is felt, then the colon is allowed to recede (recoil). 10. This process is repeated three to four times umil the colon feels compliant to mobility testing.
CONCLUSION
One should not forget that somatic dysfunction may be present with abdominal visceral conditions. Optimum treatment of these conditions should be based on osteopathic philosophy and prin ciples, and should include appropriate OMT. Using osteopathic manipulation as part of a complete treatmem approach to the patient with an abdominal visceral disorder serves several pur poses. It provides a more holistic, total body approach to the treatmem of a patiem's medical problems, it addresses imporram structure-function relationships, and it helps to optimize the pa tiem's self-healing and self-regulatory mechanisms.
51. The Abdominal Region REFERENCES
761
9. Pikalov AA, Kharin VV. Use of spinal manipulative therapy in the treat ment of duodenal ulcer: a pilot study. jMPT. 1994; 17:5.
1. Still AT. Autobiography ofA. T Still. Published by the author, Kirksville, MO; 1897. 2. Still AT. The Philosophy and Mechanical Principles ofOsteopathy. Kansas City, MO: Hudson-Kimberly Publishing Company; 1902. 3. Hazzard C.
The Practice and Applied Therapeutics of Osteopathy.
Kirksville, MO: The Journal Printing Company; 1901. 4. Conrad CF. A Manual of Osteopathy. 4th ed. New York, NY: The Uni versity Book Company; 1919.
5. McConnell CP. Ventral Technique. Indianapolis, IN: The American Academy of Osteopathy; Yearbook; 1951. 6. Owens C. An Endocrine Interpretation of Chapmans Reflexes. Carmel, CA: Reprinted by the American Academy of Osteopathy; 1932.
7. Hermann E. The DO. I 965(Oct):163-164. 8. Radjieski ]M, Lumley MA, Canteri MS. Effect of osteopathic manip ulative treatment on length of stay for pancreatitis: a randomized pilot study. jAOA. 1998;98:15.
10. Travell ]G, Simons OG. Myofascial Pain and Dysfunction: The Trigger
Point Manual. Baltimore: Williams & Wilkins; 1983.
11. Barral JP, Mercier P. Visceral Manipulation. Seattle, WA: Eastland Press; 1988. 12. Barral]P. Visceral Manipulation II. Seattle, WA: Eastland Press; 1989. 13. Finet G. Wiallame C. Treating Visceral Dysfunction. Portland, OR: Stillness Press; 2000. 14. Williams PL, Warwick R, eds. Gray's Anatomy. Philadelphia, PA: WB Saunders; 1980:1319. 15. Spraycar M, ed. Stedmans Medical Dictionary, 26th ed. Baltimore, MO: Williams & Wilkins, 1999:1.
16. Willms JL, Schneiderman H, Algranati PS. Physical Diagnosis. Balti more. MO: Williams & Wilkins; 1994:347. 17. OeGowin EL, OeGowin RL. Bedside Diagnostic Examination. New York, NY: Macmillan; 1969:452. 18. Sutherland WG. In: Wales AL, ed. Teachings in the Science ofOsteopathy. Forr Worrh, TX: The Sutherland Cranial Teaching Foundation; 1990.
PELVIS AND SACRUM KURT P. HEINKINCi ROBERT E. KAPPLER
KEY CONCEPTS
Functional anatomy of the pelvic girdle Motion and dysfunction of in nominates, pubes, and sacrum • Diagnosis and history of pelvic region • Motion testing of pelvic region, including special tests • Pelvic diagnoses and causes of sacroiliac dysfunction
• •
Accurate and efficient diagnosis of the pelvic girdle is of great im ponance to practitioners of manual medicine. The pelvis holds a central role in coupling the mechanical forces of the lower ex tremities with the axial skeleton above, as it is the foundation for body support and locomotion. Alterations and restrictions of motions in the pelvic girdle may have a profound effect on vertebral function, the thoracoabdominal diaphragm, and the urogen ital diaphragm. Alterations i n the biomechanical function of the pelvic girdle can also influence the craniosacral mecha nism and vice versa. The pelvis functions in reproduction and elimi nation of wastes and is the site of parasympathetic inner vation to the left colon and pelvic organs. Somatic dysfunction of the pelvic girdle may be causative, contributory, or d iagnos tic for a wide range of patient complaints. Such complaints may be somatic, visceral, or emotional in nature. The role of manual medicine in the management of the pelvic girdle is the restoration of functional symmetry between the arthrodial, neural, vascular, lymphatic, and connective tissue elements.
FUNCTIONAL ANATOMY Skeletal/Ligamentous Anatomy
The pelvis consists of three bones and three joints forming an open ring shape. The false pelvis is a part of the lower abdomen and is walled laterally by ilia. The true pelvis is located inferior and posterior to the abdomen. I t begins at the level of the sacral promontory, arcuate l ine, pectinate l i ne, and pubic bones, ending with the inferior fascia of the pelvic diaphragm. In the past the hip bones were referred to as the innomi nate bones because each was composed of three bones joined
together at the acetabular notch. Initially there is a single carti laginous model for the entire element, and the ischium, ilium, and pubis are the primary ossification centers before birth. Epi physeal centers form in the cartilaginous iliac crest, anterior su perior iliac spine, and ischial tuberosity (at puberty) and even tually fuse in the late teens or early 20s. The only remnants of the original cartilaginous model are the bilateral sacroiliac joints. The three joints of the pelvis include the symphysis pubis and the two sacroiliac joints . The sacrum is attached to the lumbar ver tebra by a lumbosacral disc, two lumbosacral synovial joints, and ligaments. Anomalous development commonly results in asym metric l umbosacral facets ( facet tropism) and, less commonly, incomplete separation and differentiation of the fi fth lumbar ver tebrae (sacralization) . When the transverse processes of the fifth lumbar vertebra are atypically large, a pseudoarthrosis may occur with the sacrum or ilia(um ) . When this occurs bilaterally, it is termed a bat-wing deformity. The acetabulum occupies the lateral aspect of the ilium and articulates with the head of the femur to create the hip joint. The two i nnominates are joined anteriorly by the symphysis pu bis and cephalically with the sacrum via' the bilateral sacroiliac j oints. The female pelvis is less robust than the male pelvis, with smaller weightbearing areas and less height. The female pelvis grows more rapidly in transverse dimensions during adolescence. This growth leads to a larger, more rounded pelvic inlet and out let, a larger i n frapubic angle, and a greater distance between the ischial tuberosities and the coccyx. Functionally, each innomi nate can be viewed as a lower extremity bone; and the sacrum, as a component part of the vertebral axis. The pubic symphysis is a fibrocartilaginous joint that has mo tion determined by its anatomic shape, l igaments, and muscular attachments. Muscular forces acting on each pubic ramus can cause rotation upon each other at the symphysis, about a trans verse axiS. The sacrum is shaped like an inverted triangle with the supe rior aspect being the base and the inferior aspect being the apex. The most anterior and superior portion of the first sacral vertebral body is called the sacral promontory. The anterior surface is con cave, and the posterior surface is convex with palpable spinous tubercles. The medial row of tubercles is formed by fusion of the sacral articular processes. The lateral row is formed by the fusion of sacral transverse processes and inferiorly ends in a curve of
52. Pelvis and Sacrum
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Lesser sciatic foramen and notch .l.--l---i--i'- Sacrotuberous ligament
FIGURE 52.1. Cross-section of pelvis. Differenti al static landmarks for deter m i n i ng sacral su lcus depth (A and B) versus sacral base anterior or posterior (a and b). ( I l l ustration by W.A. Kuchera.)
bones the bone called the inferolateral angle. The sacrum contains the sacral canal and four bilateral sacral foramina for the passage of the ventral and dorsal.rami of the first four sacral spinal nerves. The sacral hiatus is a defect near the apex, formed by a failure of laminal closure of the fifth sacral vertebra. I t is at this location that sacral epidural nerve blocks are performed. The coccyx attaches to the sacral apex via the sacrococcygeal joint. The ganglion im par (where the right and left sympathetic chains join) rests on the anterior surface of the coccyx. The sacroiliac joints have been described as L- or C-shaped and are conroured with a shorter upper arm and longer lower arm, with the junction occurring approximately at 52. The apex, or junction of the two arms of the sacroiliac joint, points anteri orly. The sacroil iac articulation is typically convex at the upper arm and concave at the l ower arm. The sacroiliac joints converge inferiorly and posteriorly. The lumbosacral facets are predomi nantly coronal with the surface of the inferior lumbar facet slant ing posteriorly. The sacral sulcus ( Fig. 5 2 . 1 ) is a palpable groove just medial to the posterior superior iliac spine. Much variation exists between anatomic description and an individual patient's anatomy. Weisl's work ( 1 ) demonstrates the varying contours of the articular surfaces of the sacrum and the ilia at their articulation with each other. The sacrum is suspended between the innominate bones by three true and three accessory ligaments. The true pelvic l ig aments include the anterior sacroiliac ligaments, interosseous sacroiliac ligaments, and posterior sacroi liac ligaments. The ac cessory pelvic ligaments include the sacrotuberous, sacrospinous, and iliolumbar ligaments. The iliolumbar l igaments attach from the anterior surface of the i liac crest and the anterior surface of the sacral base to the transverse processes of L4 and L5 (Fig. 52.2). The lower fibers blend i n with the anterior sacroi liac l ig ament, thus integrating sacroiliac mechanics with the lumbar spine. There are anterior and posterior portions to the sacroiliac ligaments. The anterior ligaments are flat bands, while the poste rior l igaments are thicker with multiple layers (2). The bilateral sacrotuberous l igaments run from the inferior medial border of the sacrum and insert on the ischial tuberosities and the pos terior margins of the sciatic notches. The bilateral sacrospinous
foramen
FIGURE 52.2. Pelvic l iga ments and foramen. (M odified from Kuchera WA, Kuchera M L. Osteopathic Principles in Practice, 2nd ed. rev. Colum bus, OH: G reyden Press; 1994.)
l igaments lie anterior to the sacrotuberous ligaments and attach to the ischial spines, dividing this space into a greater and a lesser sciatic foramen (Fig. 5 2 . 2 ) . The sacrospinous a n d sacrotuberous ligaments restrain the an terior movement of the sacrum within the pelvic bones. The an terior, posterior, and interosseous ligaments restrain the posterior, lateral, and axial rotation movements. No m uscles are specific for the movement of the sacroiliac joints. Motion at the sacroiliac joints results from actions of muscles that function to move the back or legs (3). In the weightbearing position, without strong pelvic liga ments, the sacral base tends to rock anteriorly. The downward effects of gravity, combined with environmental and genetic fac rors, can stress the tensile strength of these ligaments. These liga mentous stresses can create lumbosacral imbalance, chronic back pain, and joint degeneration. The iliolumbar ligament is prone ro irritation by l u mbosacral instability. When an iliolumbar liga ment becomes irritated, its attachments to the crest and transverse processes of L4-5 become tender to palpation. Pain may be re ferred to the groin via the ilioinguinal nerve, mimicking the pain felt in an inguinal hernia. Palpatory diagnosis should therefore always i nclude ligamentous attachments (Fig. 52.3) . Muscles and Connective Tissue
Muscles and connective tissue of the thoracoabdominal wall aid in coordinating movements and pressures between the thoracic cage and the pelvic girdle. Muscles acting on or through the pelvis can be classified as primary (intrinsic muscles of the pelvic diaphragm) and secondary (muscles considered to have partial attachment to the true pelvis) .
PRIMARY MUSCLES
Primary m uscles and connective tissue intrinsic to the pelvic gir dle include the pelvic and urogenital diaphragms. The pelvic
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
SECONDARY MUSCLES
Secondary muscles include: Rectus abdominis Transverse abdominis • I nternal and external oblique • Quadratus lumborum •
•
The external abdominal oblique muscle forms the inguinal ligament as it cou rses between the anterior superior iliac spine and the pubic tubercle. The lower extremity may influence the pelvic girdle through its m usculature and connective tissue. The anterior and medial compartments of the thigh may affect il iac and pubic motion and contain the following muscles: Quadriceps femoris Sartorius • Gracilis • Adductor group
•
•
The il iopsoas may also be considered with this group. The deep fascia of the thigh ( fascia lata) is continuous with the super ficial thoracolumbar fascia of the thorax and splits to form the compartments of the lower extremity. Dysfunction of muscles or fascia of the posterior compartment or gluteal region may affect function of the pelvic girdle. These muscles include:
FIGURE 52.3. Pain referral pattern from iliolumba r l igament. ( M odi· fied fro m G eor g e S. Hackett, M D.)
diaphragm consists of the levator ani and coccygeus muscles, which form a basin, supporting the pelvic viscera and closing the pelvic outlet. The urogenital d iaphragm spans the area between the ischiopubic rami and is formed by the deep transverse per ineal and sphincter ureth rae muscles and their fasciae. The pelvic diaphragm slants downward from the lateral wall to the midline perineal structures while the urogenital diaphragm is rather level. This creates a small potential fi ngerlike space (ischiorectal fossa) on either side superior to the urogenital diaphragm and inferior to the pelvic diaphragm, wh ich may provide an anterior avenue for the spread of perineal infections.
� � � �Hgv
• • • • • • •
Glutei maximus, medius, and minimus Piriformis Obturator externus Superior and inferior gemelli Biceps femoris Semimembranosus Semitendinosus
Collectively, the muscles of the gluteal region, the quadratus femoris and the i l iopsoas, comprise the rotator cuff of the hip ( Fig. 52.4).
Greater Trochanter--Lateral View
Gluteus medius
Gluteus
muscle Gluteus minimus muscle PIriformiS muscle
Ih
�S
Obturator mternus
Piriformis O
muscle
minimus Obturator internus
Inferior gemelli
With superior and
muscles
r-=7 'V- Obturator
muscle
externus muscle
muscle Gluteus
s
and superior and
Quadratus fem O
medius
inferior gemelli muscles
muscle -"':;""f!-v'-fO -- bturator externus muscle
Quadratus femoris
Iliopsoas
muscle
muscle
Acetabular--Lateral View
FIGURE 52.4. Rotator cuff muscles of right h i p . (M odified from Kuch era WA, Kuchera ML. Osteopathic Principles in Practice. 2nd ed. rev. Col u mbus, O H : G reyden Press; 1994.)
riS
52. Pelvis and Sacrum
The structure of the pelvic girdle and its function are inti mately i nterrelated. The true pelvis is situated like a cul-de-sac or diverticulum off from the false pelvis and is not in the main stream of lymphatic flow from the legs to the abdomen. The pelvic diaphragm does not rhythmically contract, but when re laxed, it works synchronously with the abdominal diaphragm. This synchronous movement with the abdominal diaphragm pre serves interstitial fluid homeostasis in the true pelvic region. A relaxed pelvic diaphragm is absolutely necessary for the efficient movement of lymphatic fluids away from the pelvis and perineal tissues. Somatic dysfunction of the symphysis pubis or disturbed il ioil ial mechanics (asymmetry of the relationship between the two innomi nates) can place asymmetric tensions on the pelvic and urogenital diaphragms. These tensions may result in ten sion myalgia of the pelvic floor, low back pain, dyspareunia, and painful defecation with associated constipation (4). Appropri ate pelvic musculoskeletal performance is essential for adequate bladder fu nctioning. Tension on the pubovesicular and pubopro static fascia from innomi nate dysfunction (especially pubic shears and compressions) may produce urinary tract symptoms such as burn i ng, frequency, ful lness, and a weak stream. Such tensions on the inguinal ligament from disturbed ilioiliac mechanics can affect the lateral femoral cutaneous nerve, resulting in anterior thigh pain. Dysfunction of any of the abdominal muscles or their fasciae may disturb respiratory excursion, compromising the imraab dominal pressure changes that promote lymphatic and venous return. The thoracolumbar and lumbosacral fasciae contribute to the origin of the i nternal abdominal oblique and the transverse abdom inis muscles. Fascial restrictions in these areas can restrict both thoracolumbar and sacral motion. The inner membranous layer of the superficial thoracol umbar fascia (Scarpa) attaches to the iliac crest and pubic symphysis. I t is continuous with the fascia of the thigh inferior to the inguinal l igament (fascia lata) , the posterior perineal membrane, and the tunica dartos scrota. Fascial restrictions along its course may affect the thigh, per ineum, or abdomen, as fluid collections can traverse along these planes. Dysfunction of the rectus femoris and the ipsilateral adductor group may cause an anterior rotation of the innominate and inferior shear at the pubes. Adductor dysfunction may be related to reflex changes at the ipsilateral iliolumbar ligament, while a pubic shear may affect the pelvic and urogenital diaphragms. Gait may be affected by lumbosacral somatic dysfunction, affecting the superior gluteal nerve ( L4-5, S 1 ) and the gluteus medius and minim us. Piriformis hypertonicity related to sacral somatic dysfunction may produce benign sciatica. Hamstring tension may cause a posterior rotation of the innominate and affect pelvic mechanics. Female patients under the influence of hormonal and structural changes during pregnancy, which shi fts the cemer of gravity, are prone to pelvic somatic dysfunction.
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arteries diverge and descend to the lumbosacral j u nction. Here they divide into the internal and external iliac arteries. The in ternal iliac arteries have two trunks that supply the pelvic viscera, perineum, and gluteal region. The proximal anterior trunk sup plies the urinary bladder, uterus, vagina, and rectum. Distally the artery branches into the internal pudendal artery, supplying the genitalia and perineum, and the inferior gluteal artery, supplying the gluteal region. The posterior trunk contains the iliolumbar, lateral sacral, and superior gluteal arteries collectively supplying the imrinsic muscles of the pelvis, the sacrum, and the superior gluteal region. Veins of the pelvic girdle form venous plexi encircling the pelvic organs and the sacrum and generally following the arte rial distribution. The rectal venous plexus communicates with the portal system via the superior rectal vein, which is valveless ( Fig. 5 2 . 5 ) . Lymphatic drainage from the pelvic girdle generally follows the corresponding arteries. Lymphatic flow from the lower ex tremities and pelvic viscera (apart from the gut) passes through the pelvic girdle, terminating ultimately in the lateral aortic groups.
Superior ---+ vena cava
1
Inferior
Sinusoids of l iver
---+--U���
Segmental vei ns (valvel ess)
Vertebral veins (valvel ess)
Portal ---l-i---,ivein Capill aries of the al i mentary canal
-++-t���'11
Vascular/Lymphatic Anatomy
Following the bifurcation of the abdominal aorta at the approx imate level of the umbil icus, the right and left common i liac
FIGURE 52.5. Va lveless vertebral venous plexus. ( I l l ustration by W.A. Kuchera; adapted from G . Zink.)
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Organs and tissues drained by these groups include: • • • • • • •
Testes Ovaries Fallopian tubes Uterus Kidneys Ureters Posterior abdominal, pelvic, and perineal walls
Lymph from the remaining viscera (bladder) and gluteal re gion passes in itially ro regional nodes along the .i n ternal iliac arteries. The external genitalia drain to the inguinal nodes and then deeper into the external i liac and the intermediary l umbar groups. Lymphatic drai nage of the rectum and anal canal is unique in that, above the pectinate line, lymph follows a deep course to the i nternal iliac nodes and preaortic nodes. Below the pecti nate li ne, the lymph drains superficially to the inguinal nodes. As lymph Aows through a number of intermediary groups i n t h e l umbar region, on up t o t h e cisterna chyli a n d thoracic duct, the diameter of the thoracic duct and lymphatic chan nels is under sympathetic con trol similar to blood vessels. Hy persympathetic activity can reduce lymphatic Aow capacity. Ac cumulation of pelvic lymph may occur in the p reaortic, lateral aortic, or retroaortic lymph node groups. Peripherally compro mised lymphatic drainage has been linked to the pathogenesis of atherosclerosis and to the development of hypertension (5). Correction of pelvic girdle dysfunction may allow improved Iym phaticovenous return, blood Aow, and gait for a patient whose ac tivities of daily living are already compromised by a cardiovascular condition. Nerves
The nervous system may i n Auence the pelvic girdle through one of fou r areas. These are the: Lumbar plexus Sacral plexus • Coccygeal plexus • Autonomic nerves of the pelvis • •
The l umbar plexus l ies between the anterior and posterior m asses of the psoas major, anterior to the transverse processes of the lumbar vertebrae. The plexus is formed by the contributions of the ventral rami from TI2 to L4 with only partial contributions fro m T 1 2. The lumbar plexus gives motor supply to muscles i n t h e abdomen and thigh, which a c t on t h e pelvic girdle. These muscles include the: • • • • • • • • •
Psoas major and minor Iliacus Pectineus Internal abdominal oblique Transverse abdom inis Quadriceps group Adductor group Sartorius Gracilis
The l umbar plexus also supplies sensation to the thigh, but tocks, lower abdomen, and pubic area. The sacrum contains sacral foramen for passage of the sacral nerve roots, which exit anteriorly and posteriorly. The lum bosacral trunk (ventral rami of L4 and L5), the fi rst three sacral ventral rami, and a portion of the fourth form the sacral plexus. The ventral rami divide into anterior and posterior branches. The anterior branch forms anterior nerves that innervate the Aexors and adductors; the posterior branch forms posterior nerves that innervate the extensors and abductors. The sacral plexus also has motor and sensory i nnervations in the pelvis and lower extremi ties and contains parasympathetic fibers (52, 53, 54) for innerva tion of the left colon and pelvic organs. The muscular branches include the: Sciatic Pudendal • Superior gluteal • Inferior gluteal • Smaller muscular branches • •
The cutaneous innervation is through the posterior femoral cutaneous nerve. The sciatic nerve is a m uscular branch of the sacral plexus composed of fibers from the ventral rami of L4-S3. Pathology at the L4-5 or L5-S I level is the usual cause of nerve root compres sion, as it is uncommon within the sacrum. The sciatic nerve is closely associated with the piriformis muscle. Eighty-five percent of the time the sciatic nerve passes through the greater sciatic notch j ust inferior to the piriformis; it passes through the muscle in less than 1 % of the population. Since injections are sometimes given in myofascial trigger points when the muscle is spastic, it is important to realize that more than 1 0% of the time the per oneal portion of the sciatic nerve passes through the muscle, and in 2% to 3% of instances it exits above the piriformis and passes posterior to the piriformis muscle (6) (Fig. 52.6). Piriformis hy pertonicity can cause sciatica. Evidence indicates that this may not be due to pressure but to a chem ical'reaction that i rritates peroneal fibers of the sciatic nerve. For this reason there is referred pain down the posterior thigh but not past the knee. The coccygeal plexus is located on the pelvic surface of the coccygeus muscle and formed by the coccygeal nerve with con tributions from 54 and 5 5 . This plexus gives rise to the anococ cygeal nerve that pierces the sacrotuberous ligament to supply the skin over the coccyx. The autonomic nerves of the pelvis include the sacral sympathetic trunks, the parasympathetic nerves of the pelvic splanchnics, and the inferior hypogastric plexus. The right and left sacral sympathetic trunks are extensions of the lumbar sympathetic chain ganglia and are locared on the ventral surface of the sacrum medial to the sacral foramina. They contain four or five ganglia and eventually fuse over the coccyx to form the single ganglion i mpar. The sacral sympathetic trunks have gray rami communicantes that follow the sacral and coccygeal nerves for in nervation of blood vessels and sweat glands in the body wall and extremities. Because the sacral and coccygeal nerves do not have white ram i, visceral afferent impulses returning from sites of sympathetic innervation by the sacrum and coccyx refer vis cerosomatic symptoms to the thoracolumbar region of the body.
52. Pelvis and Sacrum
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phatic return with firm continuous pressure over the sacral base treats primary dysmenorrhea.
MOTION AND DYSFUNCTION
2-3%
The pelvic girdle holds a central role in coupling the mechanical forces fro m the lower extremities to the axial skeleton. An analysis of the mechanics and motions occurring in the lumbar spine and pelvis during walking demonstrates physiologic motions occur ring around various axes of the pelvic girdle. Somatic dysfunction affecting any of these axes h inders gai t, requires compensatory changes, and increases energy expenditure. Somatic dysfunction of the pelvis occurs when there are motion preferences during activiry that become restricted when activiry is completed and the joint has returned to a resting position. Shears are somatic dysfunctions that do not fol low an axis. I ndividual axes of the pelvic bones are described in the fol low ing paragraphs, as well as the motion about or around those axes. This is fol l owed by a discussion of the integration of coupled movements during the motion cycle of walking. Innominates
FIGURE 52.6. Position of sciatic nerve in relationsh i p to the piriformis muscle. (Adapted from Beaton LE, Anson BJ. The sciatic nerve and the piriformis muscles: their interrelation as a possible cause of coccygody nia. J Bone Joint Surg (Br). 1938;20:686-688.)
Examples include anrerior lower thoracic or sacral exostoses and anterior disc protrusions or ruptures. Contractions of the uterus refer pain to the thoracolumbar region, as the visceral afferent nerves travel to this level from the uterine body. Sacral splanch nics come off the chain and conrribute to the formation of the inferior hypogastric plexus. The pelvic splanch nics arise directly off the ventral rami of52-4 and supply parasym pathetic innervation to the left colon and inferior hypogas tric plexus for pelvic viscera. Visceral afferent nerves fol lowing parasympathetic nerve pathways produce viscerosomatic symp toms in the sacrum . An example is sacral pain and pressure fro m uterine contractions. The inferior hypogastric plexus contains both sympathetic and parasympathetic fibers; it gives rise to smaller plexi to the rectum, bladder, prostate, uterus, and vagina. Somatic dysfunction of the lumbar spine may affect the lum bar plexus and produce symptoms in both the pelvis and lower extremiry. Dysfunction of the quadratus lumborum may p roduce symptoms simi lar to a groin pull or hernia, by i rritating the ilioin guinal and il iohypogastric nerves (Ll) as they pass j ust anterior to this muscle. Dysfunction of the piriformis, or sacrum, can affect the sciatic nerve and cause signs and symptoms of sciatica. Many visceral complaints are related to an imbalance in the autonomic control of the pelvic viscera. When irritable bowel syn drome is domi nated by parasympatheric hyperactiviry ( headache, nausea, diarrhea, and cramps), relaxation of rhe pelvic diaphragm through ischiorectal fossa techniques rel ieves the congestion and pain by inAuencing the pelvic parasympathetic (52, 53, 54). Nor malizing parasympathetic tone and encouraging venous and Iym-
The innominates rotate anteriorly and posteriorly about the in ferior transverse axis of the sacrum. The innominates may also be considered to rotate posturally around an axis passing through the greater uochanters of the fem u r. By virtue of their construc tion, a lower extremiry, including the attached innominates, is l i kely to shear superiorly or inferiorly rather than have true pelvic rotation around an anteroposterior axis. Reynolds (7) demonstrated that there were multiple varying instantaneous axes of rotation of the il i um about the sacrum when the thigh was used to introduce motion at the sacroiliac joint. Pubes
The pubic bones may rotate about a transverse axis. Pubic so matic dysfunctions may occur where i liac movement is maximal and pubic shear is min imal . They may also be sheared (subluxed) superiorly or inferiorly along with the rest of the respective in nomi nate. Anterior and posterior shears can also occur. These are rare and usually resul t fro m a significant traumatic event. Sacrum
Ordinarily, sacroi liac motion is a resul t of mechanical forces act ing on the sacrum . These forces can come from above, associated with changes of position or center of graviry within the torso, or from below, as i n walking. While muscles are attached to the sacru m , sacral motion is not caused by sacral Aexors, extensors, lateral Aexors, or rotators (3). Describing motion of the sacrum about certain axes is a model by which we explain how the sacrum seems to work as a result of the forces acting upon it. We are also able to gather palpatory information, use this model, and describe the motion present and motion restricted. This becomes objective evidence of sacroil iac motion disturbances. We can then design methods of manipulative treatment to remove the dysfunctions.
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VIJ Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
By palpating landmarks and motion testing after manipulation we are able to evaluate the effectiveness of treatment.
AXES OF MOTION
Mitchell (3) describes three transverse axes. The superior trans verse axis is at the level of the second sacral segment, posterior to the sacroiliac j oint, in the spinous process area. This is the respira tory axis where flexion and extension associated with respiration occur, as well as nutation and counternutation in craniosacral mechanics. The middle transverse axis is located at the anterior convexity of the upper and lower l imbs of the sacroiliac joint. Sacral postural flexion and extension occur abou t this axis. The inferior transverse axis is located at the posteroinferior part of the inferior limb of the sacroiliac joint and is the axis about which innominate (ilial) rotation occurs. There are two oblique axes of the sacrum, named according to the side of the body toward which the superior end of the oblique axis is located. Motion abou t an oblique axis may actually result through motions occurring about a vertical and transverse sacral axis (combination of rotation and side bending) . Sacral movement can occur around an individual axis or si multaneously around multiple axes. Cadaveric studies of sacral/pelvic motion document movement of the sacroiliac joint and movement of the ilia i n relation to the sacrum (8).
TYPES O F SACRAL MOTION
Considering these principles, fou r types of sacral motion can be described. These include: Postural Respiratory • Inherent • Dynamic
•
•
Postural Motion
In the standing or seated patient, postural motion of sacral flex ion or extension occurs abou t a middle transverse axis. Flexion and extension of the sacrum correspond to anatomic nomencla ture, with a reference poin t at the anterior portion of the sacral base. Flexion (forward bending) occurs when the sacral base is moving forward or anteriorly. Extension is backward bending of the sacral base. Terminology for sacral motion uses the same reference point as terminology for spinal motion, the most an terior superior part of the body (in the case of the sacrum, the sacral base) . Postural flexion/extension of the sacrum is some times referred to as sacral base anterior (for flexion) or posterior (for extension). This prevents confusion of understanding sacral motion that occurs during flexion and extension of the sphe nobasilar joint during craniosacral motion (see "Inherent Mo tion") . When a person is seated and the torso is forward bent, the sacral base moves anteriorly. When a person is standing and begins forward bending, the sacral base begins to move anteri orly, tightening the sacrotuberous ligaments. As forward bending
continues, the pelvis moves posteriorly in relation to the feet. This shift in the base of support causes the sacral base to move posteriorly.
Respiratory Motion
Respiratory motion also affects the sacrum, partially because the diaph ragm is attached to the top th ree lumbar vertebrae (Ll-2 on the left and Ll-3 on the right). Mitchell and Pruzzo (9) showed that the sacrum moves in response to respi ration along a transverse axis. As inhalation occurs, the l umbar lordotic curve decreases, and therefore the sacral base moves posteriorly. As we exhale, the lumbar lordosis increases and the base of the sacrum moves slightly forward.
Inherent Motion
Inherent motion of the sacrum is considered in Chapter 62. Older osteopathic l i terature regarding the craniosacral mecha nism reversed the terms flexion and extension in relating sacral inherent motion to palpated motion of the cranium about the sphenobasilar synchondrosis. However, when the sphenobasilar synchondrosis is in (craniosacral) flexion, the sacrum extends (by postural and respiratory terminology). Because of this confusion, the Educational Council on Osteopathic Principles has encour aged the use of the terms nutation and counternutation to de scribe sacral movement in the cranial cycle of flexion/extension. Nutation means nodding forward, referring to anterior motion at the sacral base. During the flexion phase of cran iosacral inherent motion, the sacrum counternutates. During the extension phase, the sacrum nutates.
Dynamic Motion
Dynamic motion of the sacrum and pelvis occurs during walk ing. As weightbearing shifts to one leg, unilateral l umbar side bending engages the ipsilateral oblique axis by shifting weight to that sacroiliac j oint. The sacrum now rotates forward on the opposite side, creating a deep sacral sulcus. With the next step, this process reverses as weightbearing changes to the other leg. The sacral base is constantly moving forward on one side, then the other, about oblique axes. As this occurs, the two innomi nates are rotating i n opposite directions to each other about the inferior transverse sacral axis. One side rotates anteriorly as the other side rotates posteriorly. With the next step, this process reverses as the anteriorly rotated hip bone moves into posterior rotation. Interacting with the bony and l igamentous structure during this motion are the viscera, the weight of the upper body, the muscles of locomotion and balance, and the pelvic diaphragm, all revolving around the constantly changing axes at the pelvis.
NORMAL MOTION OF WALK CYCLE
In the following passage from his paper, "Structural Pelvic Func tion" , Mitchell (3) described the interplay of locomotion and
52. Pelvis and Sacrum balance as being the walking cycle: The cycle of movemenr of the pelvis in walking will be described in sequence as though the patienr were starting to walk forward by moving the right foot oU[ first. To permit the body to move forward on the right, trLlnk rotation in the thoracic area occurs to the left accompanied by lateral Aexion to the left in the lumbar with movement of the lumbar vertebrae into the forming convexity to the right. There is a torsional locking at the lumbosacral junction as the body of the sacrum is moving to (he left, thus shifting the weight to the left foot to allow lifting of the right foot. The shifting vertical cenrer of gravity moves to the superior pole of the left sacroiliac, locking the mechanism inro mechanical position to establish movemenr of the sacrum on the left oblique axis. This sets the pattern so the sacrum can torsionally turn to the left, thereby the sacral base moves down on the right to conform to rhe lumbar C curve rhat is formed to the right. When rhe right foot moves forward there is a tensing of the quadri
769
fashion. This is often done in cases of trauma before the physician tests for passive motion, allowing the physician to see whether there is a significant problem prior to i nducing motion to poten tially damaged structures. A patient may have compensatory motion patterns that cover dysfunction but are revealed by careful inspection offocal areas in an overall pattern of satisfactory motion. Passive motion testing allows the physician to assess the qualiry and quantiry of motion. Motion may be limited by pain rather than by the tightness of m uscles. Left and right sides are compared for asymmetry, restriction in motion, and changes in tissue texture. Tenderness is assessed. The sacral and pelvic regions are examined as part of the screening examination. If the screen is positive, the regions are examined joint by joint, as well as by muscle groups. I f indicated, individual m uscles, fascial restrictions, and p ulses are assessed.
ceps group of muscles and accumulating tension at the inferior pole of the right sacroiliac at the junction of the left oblique axis and the inferior transverse axis, which eventually locks as the weight swings
Diagnosis by History and
forward allowing slight anterior movement of the innominate on the
Physical Examination
inferior transverse axis. The movement is increased by the backward thrust of the restraining ground, tension on the hamstrings begins; as the weight swings upward to the crest of the femoral support, there is a slight posterior movement of the right innominate on the infe rior transverse axis. The movement is also increased by the forward thrust of the propelling leg action. This iliac movement is also being inAuenced, directed and stabilized by the torsional movement on the transverse axis at the symphysis. From the standpoint of total pelvic movemenr one might consider the symphyseal axis as the postural axis of rotation for the entire pelvis. As the right heel strikes the ground and trunk torsion and accom modation begin to reverse themselves, and as the left foot passes the right foot and weight passes over the crest of the femoral support, and the accumulating force ftom above moves to the right, the sacrum changes its axis to the right oblique axis and the sacral base moves forward on the left and torsionally turns to the right. The cycle on the left is repeated identically to the right half move ments. The shifting vertical center of gravity moves to the superior pole of the left sacroiliac locking the mechanism into mechanical po sition to establish movemenr of the sacrum on the left oblique axis.
Somatic dysfunctions may accentuate and retain portions of the motion described above. These are called physiologic somatic dysfunctions, because the muscles, connective tissue, and joi nts remain in positions that are normally a parr of physiologic motion bur are dysfunctional when the body should have returned to a neutral position but did not do so. Nonphysiologic somatic dysfunction is generally induced by trauma. It is evidenced by the joint, muscle, and connective tissue elements being in positions and/or relationships that are not part of the physiologic range of motion and do not involve the physiologic axes of motion. Examples include sacral, innominate, and pubic shears.
HISTORY AND PHYSICAL EXAMINATION
Motion restriction is palpated as part of the osteopathic screen ing examination . Motion testing is active, passive, regional, and segmental. Active motion testing is part of the observation or inspection. The physician asks the patient to move i n a d irected
History
In the diagnosis of pelvic girdle dysfunction, the importance of taking a complete history and performing an in-depth physical examination cannot be overemphasized. The osteopathic exami nation is not a traditional history and physical with a palpatory examination added to it. An osteopathic examination strives to provide a time- and cost-effective diagnosis while encompassing the interrelationship between structure and function. I ntegration of the physical findings with the emotional, environmental, and genetic factors a llows the osteopathic physician to understand their i mpact on body u n iry. In this fashion an osteopathic physi cian examines the homeostatic reserve of each patient, an area crucial in determining prognosis, treatment design, and preven tion. To find health is the object of the physician, anyone can fi nd disease ( 1 0) . A history i s n o t j ust the complaint, the symptoms, a n d the history of the disease, but it is the history of the patient who has the disease. If the physician l istens carefully, the patient's history usually reveals the diagnosis ( 1 1 ) . I n patients with pelvic girdle complaints, physicians should always be aware of their expressions, remarks, and gestures. A diseased organ does not walk into the physician's office, but an anxious and fearful patient does, who may m isinterpret or be sensitive to the issues at hand. A physician should never aSSllme that a patient's low back or pelvic pain has a solely m uscular cause. The history should always clarify if a visceral or an emotional cause exists. Because the pelvic region includes the sexual organs, the pa tient's sexual history needs to be obtained when the patient presents with a complaint i n the pelvic region. Considerations of the chief complaint should i nclude several questions (12 ) . Tables 5 2 . 1 and 5 2 . 2 show the two mnemonics that are widely used. In addition, ask the fol lowing questions: Are there any associated symptoms? Is there a relationship to bodily functions and activities? • Have there been any changes in bowel or b ladder habits? • •
770
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
TA BLE 52 . 1 . PQRST
MNEMONIC
FOR
I N VESTIGATING
Position, Pa l l i ation Qual ity Radiation Severity Time
TABLE 5 2 . 2 . C O L D E R
MNEMONIC
FOR
I N VESTIGATING
PA I N
PA I N
Is it related to a particular position? Does anyth ing make it better or worse? What is it l i k e ? Sharp, stabbing, d u l l ache, burn ing, or e l ectric? Where is the pain? Does it go anywhere else? On a scale of 1-10, with 10 being worst, how bad is it? When d i d it start? How long does it last?
Was there any previous medical care for a similar condition? What was the treatment outcome? • Is the patient currently on any medications, including over the-counter medications? • Are there any allergies? •
•
Even when pain is the primary complaint and clinical suspi cion centers on m usculoskeletal causes, the physician remembers that pain is a liar and should address the contributory topics l isted in Table 52.3. Physical Examination
The physical examination of the pelvic girdle begins the moment the patient enters the room. Observe the patient's gait, structure, body habitus, and n utritional status. Ask permission to perform a genital or rectal examination. For female patients, a male physi cian may requ i re a female health care provider to be in the same room during the exami nation. Along with general observation, the osteopathic structural ex amination includes analysis of: Gait Structu ral asym metry • Curvature of the spine • Postural balance •
Condition, Character Onset Location Duration Exacerbation Remission
What does it feel l i ke (character or qual ity)? When did it start? What were the ci rcumstances? Where is it located? Does it radiate anywhere else? How long does it last? Does anyth ing make it worse? Does anyt h i n g make it better?
amination. A palpatory exami nation is essential; the two forms of examination, observation and palpation, focus on the fou r crite ria for identifYing somatic dysfunction. The mnemonic TART tenderness, asymmetry, range of motion differences, tissue tex ture changes-(Table 5 2 .4) helps to recall these. PALPATORY EXAMINATION
The palpatory examination begins with the structural examina tion as bony anatomic landmarks are found. In the pelvic region, these should include: • • • • • • • • •
Anterior superior iliac spines (ASISs) Pubic symphysis Posterior superior iliac spines (PS ISs) Sacral sulci Sacral base I nferior lateral angles of the sacrum Ischial tuberosities I liac crests G reater trochanters
Ligamentous structures to be pal pated include the iliolum bar, posterior sacroiliac, and sacrotuberous l igaments. Soft tissue palpation should include:
•
Rotator cuff muscles of the hip Thoracolumbar and lumbosacral fasciae • Lumbar paraspinal muscles
•
A screening structural examination is done to indicate whether a region has problems requiring a more in-depth or segmental ex-
•
TABLE 5 2 . 3 . C O N S I D E RATI O N S FOR COMPLAI NTS OF PA I N I n Male and Female Patients
I n the Female Patient
Employment risks Exercise risks/contact sports Hernia Past gen itou rinary surgeries Cancer of the genitourinary tract Chronic i l l ness Family history Psych iatric history Med ications, including contraceptive use Sexual activity h istory Sexual orientation Sexually transm itted diseases Cancer of the reproductive organs Infertility Significant and related medical history (e.g., d i a betes) U ri n a ry tract symptoms
Menstrual history Obstetric history Cleansing routines Douch ing h istory Abnormal vag i n a l bleed i ng Vag i n a l discharge Date of last pelvic exa m i nation Date of last Pap smear and results Past gyneco logic procedures or surgery
I n the Male Patient
( 1 6)
Difficulty m a i nt a i n i ng or achieving erection Difficulty with ejaculation Discharge or penile lesion Infertil ity Urinary symptomatology U rinary stream, good or poor E n l a rg ement of the inguinal area Testicu lar pain or mass Testicular self-exami nation practices
52. Pelvis and Sacrum
TABLE 52.4. TART CRITERIA FOR I DE N T I FY I N G SOM ATIC DYSFUNCTION
Tissue texture abnormalities Asymmetry
Restriction of motion Tenderness
How the tissue feels to the palpating hand Apparent re lationsh i p of landmarks and tissues How the tissue moves Pain el icited by palpation
Classify as acute or chronic
Made by observation, not palpation; is genera lly static positional asymmetry Arthrodial, m uscular, or fascial elements Genera l ized as in traumatic tissue damage, such as contusion, o r specific for ind ivid ual muscles or sclerotomal levels, as i n tender point diagnosis
Trochanreric bursa Piriformis and location of the sciatic nerve • Abdominal wall • Pelvic diaphragm •
•
Palpation of the lower extremiry may be indicated, if the ham stri ngs or il iopsoas are of unequal length when motion tested. In addition to general ized changes in the pelvic girdle tissues, the physician may detect small myofascial tender poinrs. Such areas may be characterized by a small, palpable, circumscribed thickening of tissue that is tender with moderate to deep pal pation. These tender poi nrs may be associated with autOnomic dysfunction or refer pain to a neurologic distribution. Muscles containing tender poinrs reveal pain with active or passive range of motion. There may be areas of patchy weakness in the range of motion of m uscles conraining painful tender poinrs. Joints conrrolled by muscles with tender poinrs may have a dimin ished range of motion. The pelvic girdle conrains many of these myofascial tender points because myofascial structures are con stantly working to mainrain postural balance. Numerous authors ( 1 3, 1 4) have indicated continuous postural strain as the cause of precipitating and/or perpetuating myofascial tender points. Osteopathic physicians may discover paraspinal tissue texture changes that have characteristic palpatOry qualities and conclude that these changes are due to visceral disturbances. These tis sue texture changes are caused more by changes of the spine, subcutaneous tissue, and superficial and deep fascia rather than pinpoinr tissues and muscle. The maximum i n tensiry is at the costOtransverse area in the thoracic spine and the region of the transverse processes i n the lumbar spine. The qualiry of motion is a reluctance to move rather than an absolute restriction with loss of range. The skin and subcutaneous tissue findings exceed the muscle-bone-joint fi ndings. In chronic viscerosomatic problems, they take on the characteristics of any chronic somatic dysfunc tion. Sometimes they present as an acute exacerbation ofa chronic problem with the superficial puffiness of acute change and the motion restriction of chronic somatic dysfunction. Skilled osteopathic physicians are able to palpate inherent mo tion of the human body. This motion has been described as a
771
cyclic, rhythmic wave of motion; Sutherland referred to it as the primary respiratOry mechanism ( 1 5) . This motion has been demonstrated in numerous studies, and there are various theo ries as to its origin. This motion continues even when the patienr holds their breath. Physicians trained in craniosacral diagnosis can palpate this motion i n the sacrum as the craniosacral mecha nism moves the sacrum between the two ilia. Cli ni cal significance of this motion is discussed in Chapter 64. The palpatOry examination should include an assessmenr of the patienr's cardiovascular status. Pulses should be palpated and auscultated for bruits bilaterally. An abdominal pulse should be identified, classified, and auscultated. Peripheral edema, sacral edema, and trophic changes in the skin should be evaluated. In addition to the auscultation over arteries in the periphery, auscultation of the heart, lungs, and abdomen should accompany any patienr evaluation. If atheromatous disease is suspected, aus cultation over the carotid and femoral arteries is imperative, and the diameter of the abdo minal aorta is evaluated carefully. For evaluation of the pelvic girdle, a complete examination of the abdomen is required. Following inspection, auscultation, and palpation, the physician can percuss the liver, spleen, and stom ach, and palpate for any pelvic masses. Diaphragmatic excursion can be percussed posteriorly to evaluate respiratory dysfunction. A rectal examination, a pelvic examination i n the female, and a prostate examination in the male should be a part of a complete examination of the pelvic/sacral region. Neurologic Examination of Pelvic Region
Muscle testing and sensation are the focus of the neurologic ex amination of the pelvis and hip (3). Muscle Testing
Muscles of the lower extremiry and buttocks require assessment when evaluating the pelvis and hip. Descriptions of the inner vation, functional anatomy, and dysfunction are discussed in Chapter 57. Primary i ntrinsic muscles of the pelvis, although not tested for strength, may be palpated for tension, tissue tex ture changes, and tender points. Lumbar and pelvic muscles that may have trigger points referring pain to the pelvis should also be investigated. Sensation Testing
The dermatomal distribution of sensory nerves to the pelvic girdle ranges from TI 0 to 5 5 , involving nerve roots from the thoracic, lumbar, and sacral regions ( Fig. 52.7). Dermatomes of the ante rior abdominal wall run in transverse and oblique bands. These dermatOmes begin at the umbilicus with the T I O strip followed inferiorly by the T I l strip. The T l 2 strip l ies j ust superior to the inguinal ligament, while L l l ies j ust inferior to it. I n ferior to the L l dermatOme lie the L2 and L3 strips covering the anterior thigh and ending at the patella. The buttOcks, posterior supe rior iliac spines, and i liac crest are supplied by the cluneal nerves ( 1 6) (posterior primary divisions of L l , L2, L3) . The posterior femoral cutaneous nerve (52) supplies sensation to a longitu dinal band traversing the posterior thigh. The lateral femoral
772
VJI. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
• • • • • • •
Sacral base Inferior lateral angle ( I LA) Sacrotuberous ligament Ischial tuberosity Iliac crest Piriformis muscle Iliolumbar l igament insertion on ilium
Motion Testing Sequence
An example of a motion testing sequence follows: Patient standing Trendelenburg test II iac crests • PSISs • Standing flexion test • Pelvic side-shi ft
• •
FIGURE 52.7. Anterior thoracic dermatomes. (Reprinted with permis sion from Kuchera WA, Kuchera ML. Osteopathic Principles in Practice, 2 n d ed. rev. Colum bus, O H : G reyden Press; 1994.)
cutaneous nerve (S3) supplies sensation ro the lateral thigh. The cutaneous in nervation of the perineum is arranged in concentric rings around the anus: the outermost (S2), m i ddle (S3, S4), and innermost ( S 5 ) .
Patient seated Seated flexion test Lateral translation sacroiliac motion test • Upper lumbar for flexed somatic dysfunction and psoas • •
Patient supine ASISs Pubes • Medial malleoli • Hamstri ngs • Sacrum (for cranial rhythmic impulse) •
MOTION TESTING O F THE PELVIC REGION
Multiple methods are available for motion testing, which is cus romarily done in an integrated fashion with examination of the anaromic landmarks. The i m mediate objective of manipulative treatment is ro improve motion. An i nitial diagnosis is made and treatment is begun; repeated i ntegral motion testing and treatment follow. Movement of tissues is contin uously assessed, determi n i ng freedom of, or resistance, ro motion testing.
•
Patient prone • • • • •
Anatomic Landmarks Used to Assess Pelvis
•
To assess static posi tional relationships and perform motion test i ng, the physician should be able ro correctly locate ( i n the fol lowing positions) several landmarks: Patient standing
•
Level of il iac crests • PSISs • Greater trochanters of the femurs •
Patient supine ASISs Pubic symphysis • Pubic tubercles • Medial malleol i • Sacrum • •
Patient prone • •
PSISs Sacral sulcus
• •
PSISs Sacral sulci Sacral base I LA Sacrotuberous l igaments Spring test Backward bending test Prone sacral motion tests Hamstring palpation for tension
Special Tests of Pelvis
Trendelenburg Test
This test determines the strength of the gluteus medius muscle. During gait, the gluteus medius acts as a stabilizer, preventing the unsupported hip from dropping during the swing phase. 1 . Stand behind the patient and observe the sacral di mples. With equal weight distribution over both legs, these dimples should be level. 2. Now have the patient stand on one leg. The opposing gluteus medius should contract, elevating the pelvis on rhe unsup ported side and i ndicating a negative test. If the muscle is weak, the pelvis on the unsupported side stays level or drops, indicating a positive rest.
52. Pelvis and Sacrum
Conditions that could cause a weakening or paralysis of the gluteus medius include: • • • • • • • •
Fractures of the greater trochanter Slipped capital femoral epiphysis Coxa vera Poliomyelitis Meni ngomyelocele Nerve root lesions Lumbar somatic dysfunction Disturbed ilioi liac mechanics
Iliac Crest Levelness
Place your index fingers over the iliac crests, and maintain a position so that your eyes are level with the crests. I nspect to see whether the crests are at equal heights. Posterior Superior Iliac Spine L e velness
Place your thumbs on the inferior slopes of the PSISs and note whether they are level. If one is more cephalad or caudad at the begi nning of the standing flexion test, be sure that you include the di fference in your end-point estimate before call ing the test posJ(Jve. Standing Flexion Test
The standing flexion test identifies the side of i liosacral dysfunc tion. It does not identify the specific type of dysfunction, only which side to treat. Mechanical forces from the lower extre m i ty may in fI uence th is test. A positive standing flexion test indicates three possibilities: 1 . l liosacral dysfunction 2. Contralateral tight hamstrings 3. Carryover from the seated flexion test False-positive and false-negative test results do exist. A false negative standing flexion test may be caused by ipsilateral ham string shortness, but since hamstring tension can cause a false negative result on the ipsilateral side, or a false-positive result on the contralateral side, testing for hamstring length identifies a hamstring cause for false-negative or false-positive standing flex ion tests. If there are unilaterally tight hamstrings, the dysfunc tional side should be treated so that both sides are equal, and the standing flexion test repeated. When the sacroiliac dysfunction is created, the standing flexion test may become negative. Some physicians believe that if a patient has unequal i liac crest heights, a false-negative test result may exist unless shimming is done to level the i liac crests prior to performing the test.
773
Procedure
1 . Place your thumbs on the inferior slopes of the PSISs, and your fi ngers on the superolateral surface of the i liac crests. Obtain fi rm pressure on the PSISs to follow bony landmark motion rather than skin motion. 2. Ask the patient to bend forward, touching the floor i f possible, but stopping short of pain . 3 . Let your thumbs follow the motion of the PSISs. A s the patient bends forward, allow the pelvis to come back toward you. If you do not, the patient will fal l forward. 4. Your eyes should be level with the PSISs at all times, so that as the patient bends forward, you rise from a kneeling position to one where you are standing over the PSISs . 5 . I f o n e P S I S moves more cephalad at t h e e n d range of motion, the test is positive on that side. ( Do not count the side that moves superior first as the positive side. Fascial drag can cause the positive side to end up inferior to the negative side at the completion of the test. I f both sides are equal, the test is usually i nterpreted as negative.) Seated Flexion Test (Seated Forward Bending Test)
A positive seated flexion test indicates sacroiliac dysfunction. In the seated posi tion, mechanics of the lower extremity are not influencing the pelvis. A positive test indicates the dysfunctional side but not the specific type of dysfunction. Patient Position
Seated, with both feet flat on the floor, or on the rung of a bench, shoulder width apart, and with the popliteal fossa against the edge of the table. Physician Position
Kneel i ng or standing behind the patient , with eyes level with the PSISs. Procedure
1 . Place your thumbs on the inferior slopes of the PSISs. 2 . Have the patient cross the arms in front of the chest. 3. Ask the patient to bend forward, as far as possible without palJ1 . 4. Note the movement of t h e P S I S . I fo n e side has moved cepha lad at the end point of forward bending, the seated flexion test is positive for that side. If the PSISs remain equal , the test is negative. Interpretation o f Standing/Seated Test Results
I f both tests are negative, there is no problem in the sacrum/pelvis. A true positive standing or seated test indicates a problem on that side. If positive, the tests should become negative after proper treatment.
Patient Position
Standing with shoes removed, heels on a line and feet under the hips. Physician Position
Kneeling or standing behind the patient, eyes level with the P S l Ss .
Supine
Align Pelvis on Table
This is sometimes called a h i p flop. The purpose of this maneuver is to reset the pelvis so that the least effect of postural muscles
774
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
is present. This should also be a comfortable position for the patienr.
1 . Place your cephalad hand on the patient's opposite ASIS. 2. Place your other hand under the ankle of the leg on your side of the table.
Procedure
1 . Ask your supine patient feet on the table. 2. Ask the patient the table.
Procedure
(0
(0
raise the knees while keeping the
raise the but(Ocks slightly, so they are off
3 . Now have the patient drop the but(Ocks lower the knees.
(0
the table and then
4 . Conti n ue your assessment with the following tests.
Medial Malleoli Levelness
The levelness of the medial malleoli used to be correlated with the findings of the standing structural examination, innominate rotations, and pelvic shears. Medial malleoli levelness is not very reliable for making a diagnosis of innominate dysfunction, as it may not fit the result expected. This is because the ankle, the knee, the hip, and all the fasciae and muscles between the malleoli and the pelvis can affect the levelness of the malleoli. However, when the planes between the malleoli are unlevel, the physician is alerted to leg, hip, and ankle stress; this increases general body stress. A patient with a short leg is similar to a building with the foundation slightly lower on one side. The body must adapt by seeking a new balance, and this produces tensions in all of the postural m uscles. A short leg also places additional stress on the joints of the longer lower extremiry. As the body seeks a new level of balance, there is generally a slight scoliotic curve in the lumbar region with the convexiry on the short leg side and side-bent (Oward the long leg side. This is usually then compensated for with additional curve(s) in the superior por tions of the spine. The cause of a shorr leg may be anatomic (e.g., the patient had a fractured tibia as a child and growth was sl ightly shortened) or functional (e.g., the patient has a pos teriorly rotated ilium, sacral rorsion, or l umbar curve, causing one leg apparently to be shortened by its displacement in three planes) . Procedure
1 . With the patient supine, place your thumbs on the inferior sur faces of the medial malleoli, with your fingers curved around the anterolateral aspect of the ankles. 2. Put slight traction, equal on both sides, on the legs. 3 . Note whether one malleolus is more cephalad than the other, and if so, record the difference in length of the short leg.
Hamstring Test
3. Slowly lift the leg until you feel slight motion at the opposite ASIS. This occurs after the hamstrings on your side are tight enough (0 begin rotating the whole pelvis, which is when you feel the motion in your monitoring hand. 4. Note the angle at which this occurs. 5. Perform the same test on the opposite leg (from the opposite side of the table). 6. Mentally compare the angles at which you felt motion at the ASIS. If the leg angles are equal and about 85 to 90 degrees, the test is considered negative. If you felt the motion sooner on one side, that side has restricted (tight) hamstrings. Note: The hamstrings can be palpated di rectly for tension with the patient in the prone position. This is a good screening test but does not directly measure hamstring shortness.
Anterior Superior Iliac Spine Levelness Procedure
1 . Place your th umbs on the inferior surface of the AS1 Ss. 2. Note whether one side is more inferior or superior. 3. Note whether one side or the other is more medial or lateral. Integrate this information with the rest of your diagnostics to make an iliosacral diagnosis. Note: The innominates may be motion tested at this time. Normally, motion is freer in the direction of positional change. With a left posterior innominate, a posterior and superior direc tion motion to the supine patient's left ASIS is freer. With a left anterior innominate, a posterior- and superior-directed motion to the supine patient's left ASIS is restricted.
Pubic Symphyseal Levelness Procedure
1 . Inform the patient that you will need to palpate the pubic symphysis and ask the patient's permission to do so. 2. Place the heel of your hand at about the level of the umbilicus. With slight pressure, slide it down the patien t's abdomen until you reach the p ubic symphysis. 3 . Place your thumbs or fingers at the superior aspect of the pubic symphysis and move them slightly medial, slightly lateral. 4 . Note whether one side is more caudad, the other more cepha lad. Note also any tenderness or tissue texture abnormali ties. Integrate this information with that from the rest of your diagnostic tests to make an iliosacral diagnosis.
Patient Position
Supi ne.
Sacrum: Indirect Diagnosis
Physician Position
This assessment is often made after gross level motion dysfunc tions have been treated with muscle energy, high velociry/low amplitude (HVLA), strain/counterstrain, or other techniques.
Standing at the side of the table, facing the patienr.
52. Pelvis and Sacrum
775
Patient Position
Physician Position
Supine.
Standing at the side of the table, dominant eye centered.
Physician Position
Procedure
Sirring at the side of the table facing the patient.
1 . Place your thumb pads on the inferolateral angles of the sacrum.
Procedure
2. By inspection, note which side appears (a) anterior/posterior and (b) superior/in ferior.
1 . Ask the patient to raise the opposite knee, with the foot on the table, and to roll the opposite hip toward you. 2. Starr with hand lateral to rhe raised hip and place it between the patient's sacrum and the table.
3. Mentally record which side is anterior/posterior and which is superior/inferior from your motion testing and continue the eXamll1atlon.
3. Have the patient roll the hip back to regain the supine position, and lower the knee. 4. Assess sacral motion for both respiratory effects and the cranial rhythmic impulse. Posterior Superior Iliac Spines Procedure
Notes:
The I LA may be equal anteriorly/posteriorly; equal superI orly/inferiorly. • One side may be anterior or posterior but level superi orly/inferiorly. • One side is anterior and superior; or one side is posterior and inferior. •
1 . Place your thumbs on the inferior surface of the PSIS. 2. Note whether one side is more inferior o r superior than the other.
Motion Test about Transverse Axis
3. Integrate this information with the results of the rest of your diagnostic tests to make an iliosacral diagnosis.
Prone.
Note: The innominates may be motion tested at this time. Normal ly, motion is freer in the direction of positional change.
Sacral Base Patient Position
Prone. Physician Position
Standing at the side of the table, dominant eye centered.
Patient Position
Physician Position
Standing at side of table at hip level with palpating hand over sacrum, fi ngers pointing cephalad. Procedure
Place your hand over the sacrum with your fi ngers pointi ng cepha lad. Alternatively apply pressure with the tips ofyour fi ngers, then with the heel of your hand in a gentle, slow, rocking motion. This introduces anatomic flexion and extension about a transverse axis. Assess the quality and quantity of motion and note which move ment is freer.
Procedure I.
Place your thumb pads about one-half inch above where you tested levelness of the PSISs and curl your thumbs from the iliac crest into the sacral sulcus at the base of the sacrum (Fig. 52. 1 ) .
Motion Test about Oblique Axis Patient Position
Prone.
2 . Evaluate depth of the sacral sulci as a n indication o fsacral base posi tion. Are both sides the same? Is the sacral sulcus depth normaP Is one side deep? Is one side shallow?
Physician Position
3. Push forward on one side of the sacral base, then the other. Note which side moves more easily. Motion should be freer on the deep side.
Procedure
4. Mentally record the position of the sacral base and contin ue the exam ination. Note: At this time, palpation of the sacral sulci for tissue texture abnormality is appropriate.
Sacral In ferola tera I Angles Patient Position
Prone.
Standing at the side of the patient at hip level.
Place the pads of the index and middle fingers of your monitoring hand so that one fi nger contacts the PSIS and the other finger rests in the sacral base. Place the heel of your active hand in contact with the i n ferior lateral angle on the contralateral side. With your active hand, apply downward (anterior) pressure on the I LA of the sacrum about an oblique axis. Note freedom or restriction of motion. With your mon itoring hand appreciate anterior or posterior motion of the sacral base. Assess both quali ty and quantity of movement as the forces are slowly i ntroduced. Evaluate motion o n both left and right oblique axes. If the sacral base has rotated forward and become restricted, posterior motion
776
VII. Osteopathic Considerations in Palpatory Diagnosis and ManipuLative Treatment
Prone.
anteriorly; the sacral base moves anteriorly (sacral flexion) on both sides, reducing asymmetry at the sacral base. The sacral sulci and I LAs are more equal in position if the lumbar spine is backward bent. If the sacral base is posrerior on one side with a shallow sulcus (as with backward torsions), and the lumbar spine is backward bent with the patient propped up on rheir elbows, the sacral base posterior side (shallow sulcus side) resisrs anterior movement of the sacral base. The orher side of the sacral base will move anteriorly. This i ncreases the asymmetry, making rhe sacral base, sacral sulci, and I LAs less equal in position.
Physician Position
Patient Position
Standing at the side of the patient at h i p level.
Prone.
of the sacral base at the sulcus is restricted. Palpatory examination rypically finds the restriction; however, somatic dysfunction I S named for the freedom of motion. Test for Posterior Sacrum
This tests for restriction of lower l imbs of L (C) . Patient Position
Procedure
Physician Position
Bilaterally contact the i n ferior portion of sacrum somewhere be tween the caudal border of the i n ferolateral angle and where you tested for levelness of the PSIS. Apply a cephalad, downward force. The inferior arms of the sacroi liac joints run anterior and superior, and their posterior borders are abour 1 inch inferior to the caudal border of the PSIS. If there is restriction of the lower limb of the sacroiliac j o ints, this downward, cephalic pressure meets with resistance.
Standing ar rhe side of rhe table, dominant eye centered.
Lumbosacral Spring Test
This test may determine if an i ncreased or decreased lumbar lor dosis is present, as well as whether or not the sacrum is tilted forward at the base. I f there is i ncreased lumbar lordosis and/or the sacral base i s forward, there i s increased mechanical stress at the lumbosacral joint and i n the articular structures of the lumbosacral region. This comes about because of changes i n the postural l i ne of the body. I f the sacral base is able to move ante riorly, there is good spring (a negative spring test) . If the sacral base is posterior, spring provides poor or nonexistent motion at the sacral base (a positive test) . Patient Position
Prone. Physician Position
Procedure
1 . Place your rhumbs in rhe sacral sulci or on the I LAs. 2 . Ask the patient to take a posi rion propped up on elbows, and rhen to relax rhe low back. 3 . Exami ne the sacral sulci and I LAs. Nore wirh each whether one side is deeper or shallower than rhe orher. Tesr with morion (anterior pressure) on one side, rhen on rhe orher, to see in which direction the sulcus or I LA moves mosr easily. 4. Mentally record whether rhe parient's condirion improved (position and motion were more symmetric and appropriate) or became worse i n this position. On a forward torsion, the asymmetry of the sacral base, sacral sulci, and l LAs decreases. On backward torsions, the asymmetry 1I1creases. A nterior Superior Iliac Spine Compression Test
This is a test for lateralizarion of somatic dysfuncrion of rhe sacrum, i nnominate, or pubic symphysis ( Fig. 52.8). It can be used to confirm the findings of rhe seated flexion test or to help localize to one side or anorher or both sid�s when the standing or seated flexion test results are equivocal.
Standing at the side of the table. Procedure 1.
Place the heel of one hand over the lumbosacral j unction, and the heel of the other hand on top of it.
2 . Apply a gentle but rapid downward pressure on the lum bosacral j unction, in a repeated fashion, twO or three times. 3 . If there is good springing motion, i t is a negative test. If there is poor spring or no spring, it is a positive spring test. Backward Bending Test
This test helps evaluate sacral somatic dysfunction at the upper arm of the sacroi liac joint. If the sacral base i s anterior on one side, it continues to move anteriorly with the patient propped up on the elbows. The opposite side of the sacral base also moves
FIGURE 52.S. Anterior superior i l i a c spine compression test. (Modified from Kuchera WA, Kuchera M L. Osteopathic Principles in Practice, 2nd ed. rev. Colum bus, O H : Greyden Press; 1 994.)
52. Pelvis and Sacrum Patient Position
Supine. Physician Position
Standing at side of the patient, facing the head. Procedure
Contact the ASISs; apply a posterior compression on one AS I S while stabilizing the other. Test both sides. A posterior compres sion normally produces a palpatory sense of give or res i lience as the i nnominate glides slightly posterior at the sacroiliac joint on that side. ·Somatic dysfunction of the pelvis on the side of com pression produces resistance to the test. This is i nterpreted as a positive ASIS compression test. Bilateral pelvic somatic dysfunction would produce s i milar findings on both sides and may be interpreted as negative. How ever, none of the normal resi liency would be found on either side. Fascial Restrictions of Pelvis
The physician should be able to determine the direction offreer or restricted motion of a fascial plane through palpatory assessment. The direction of the fascia, determined by this palpation, often is a vector in three planes. Fascial assessment is more than an active, doing process. The hands must l isten to the tissues and detect change. This is a sensorimotor skill, one in which the physician must "read" or "listen" to the tissues and respond to the palpatory messages received. A common fascial restriction of the pelvis exists berween the rwo innominates. Positional asymmetry and motion disturbance berween the rwo i nnominates may be related to fascia as well as to disturbance within the sacroiliac joints. Patient Position
Supine. Physician Position
Standing at the side of the table, facing the head, with the dom inant eye centered.
777
is the sacrum, and the other i s the ilium. A disturbance in one will always affect the other. I nnominate disturbances may sometimes be a primarily disturbed relationsh i p berween the rwo sides, mai n tained by m uscle and fascial alterations. With in the ten regions of somatic dysfunction (International Classification of Diseases, Ninth Revision) , i l iosacral diagnoses are listed as pelvic diagnoses. In the M i tchell m uscle energy model of diagnosis, rwo assump tions are made when determ ini ng an il iosacral diagnosis. The first is that the dysfunction i s due to neuromuscular imbalance, with the muscle(s) on one side being hypertonic and their opposites being hypotonic. The second is that the side of dysfunction is the side of the positive standing flexion test. lliosacral Somatic Dysfunctions
I l i osacral somatic dysfunctions i nclude: • • • • • •
I nnominate rotations, anterior and posterior Innominate subluxations (shears), superior and inferior Innominate flares (inflares and outflares) Pubic shears (subluxations) , superior and inferior Unequal hamstring length Unequal i liopsoas length
Anterior Innominate Rotation
This exists when the dysfunctional side has the following char actenstlcs: Entire innominate appears to be rotated in a direction anterior to the other hip bone • ASI S i s more i n ferior (caudad) • PSIS is more superior (cephalad) •
Subjective complaint s may include ipsilateral hamstring tight ness and s p asm and sciatica (secondary to piriformis dysfunction) . Palpatory findings may i nclude tissue texture changes at the i psi lateral f LA of the sacrum, as well as i l iolumbar ligament tender ness. Motion characteristics should indicate freedom of anterior rotation, about a low transverse axis, on supine motion testing, and resistance to posterior rotation.
Procedure l.
Place your hands on the ASISs and adjoining crests.
2. Apply downward pressure in a posterior superior direction alternatively to each side, monitoring for resistance or freedom of motion. Freer motion is i n the direction of positional change and is how somatic dysfunction is ordinarily named. This dysfunction can be treated using fascial release tech nique.
PELVIC DIAGNOSES
M i tchell divided pelvic and sacral diagnoses into i liosacral dys functions ( including innominate and pubic dysfunctions) and sacroiliac dysfunctions (sacral diagnoses) . The sacroi liac joint is composed of two bones with a j oint separating them. One bone
Posterior Innominate Rotation
This exists when the dysfunctional side has the following char acteristics: Entire innominate appears to be rotated in a direction posterior to the other hip bone • ASI S is more superior (cephalad) • PSIS is more inferior (caudad)
•
Subjective complaints may i nclude inguinal/groin pain (sec ondary to rectus femoris dysfunction) and/or medial knee pain (secondary to sartorius dysfunction). Palpatory findi ngs may in clude inguinal tenderness as well as tissue texture change at the ipsilateral sacral sulcus. Motion characteristics include freedom of posterior rotation about a low transverse axis on supine motion testing and resistance to anterior rotation.
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VIi. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Superior Innominate Shear (Subluxation)
This exists when the dysfunctional side has the fol lowing char acteristics: AS I S is more superior (cephalad) PS I S is more superior (cephalad) • Pubic ramus may be more superior (cephalad) •
•
Note: The reciprocal positio n ing of the AS I S and P S I S exists only if there is a pure superior shear without any rotation of the II1nomll1ate. The two innominates appear ro be sheared so that the one hip bone is subluxed superiorly ro the other. Subjective complaints may include pelvic pain. Palparory fi nd ings may i ncl ude tissue texture changes at the i psilateral sacroiliac j oint and ipsilateral pubes. Motion characteristics incl ude free dom of superior translatio n .
Inferior Innominate Shear (Subluxation)
This cond ition exists when the dysfunctional side has the follow i ng characteristics: AS I S is more i nferior (caudad) PS I S is more inferior (caudad) • Pubic ramus may be more inferior
• •
ro diagnose. However, there are times when the ASI Ss appear ro be equal, the PSISs appear ro be equal, and yet the pubes are definitely displaced so that one is detectably superior and the other inferior. Since the ASISs and PSISs are equal, it does not appear that the h i p bone is rotated or sheared. When the dysfunctional s i de is superior, it is said ro be a superior pubic shear; if the dysfunctional side is inferior, it is an inferior pubic shear. Anterior pubic shears are uncommon but possible and are usually associated with trauma. I n these cases, one side of the symphysis is anterior ro the other. Pubic Symphysis Compressions
Pubic symphysis compressions occur, evidenced by bilateral ten derness. Using the adducror muscles of the thigh in a muscle energy tech nique can reduce these compressions. The L5 anterior counterstrain poi nt is also located on the pubes. Treatment of this tender point with counterstrain tech n ique may be appropriate and necessary in treating pubic sym physis symproms because what appears ro be a pubic dysfunction may actually be reflexive evidence of L5 dysfunction. Unequal Hamstring Length
The two innomi nates appear ro be sheared so that the one hip bone is subl uxed inferiorly ro the other. This condition i s rare, and wal king tends ro reduce it. Subjective complaints may incl ude pelvic pain. Palparory fi nd i ngs may incl ude tissue texture changes at the i ps ilateral sacroi l i ac joint and ipsi lateral pubes. Motion characteristics i nclude free dom of inferior translation.
Unequal hamstring length can be considered either a pelvic or a lower extremity somatic dysfunction because the hamstri ngs are attached ro both the pelvis and the lower extremity. I f the hamstrings are of unequal length, standing flexion test results may be either falsely positive or negative. Therefore, it is i m perative ro treat the hamstri ngs and retest. I f the standing flexion test and pelvic landmark positions normal ize, the dysfunc tional hamstrings were the problem. Otherwise, treat as indicated by the second diagnosis.
Innominate Flares
Unequal Iliopsoas Length
This condition is a positional change of an innomi nate i n which the ASIS is medial or lateral ro i ts usual position. This may be thought of as rotation of an innom inate in relation ro a vertical axIS. Flares are determined by imagi n i ng a transverse line goi ng through the ASIS. Visually connect this l i ne between the AS I S . Then connect a l i ne from each AS I S ro the umbilicus, form i ng a triangle. Bisect this triangle by visually connecting a line from the umbil icus ro the pubic symphysis, dividing the triangle i nto two triangles. Examine the length of the b isected transverse line between the twO ASI Ss, and determine which ASI S is more medial or lareral. I f the ASI S is more lateral on the dysfunctional side, the patient has an innominate outflare. If the ASIS is more medial on the dysfunctional side, the patient has an innominate i nflare. Subjective complaints may i ncl ude pelvic or sacroi liac pai n . Palparory findings may indicate grearer laxity in the muscles o n the side that is more lateral a n d more tautness on the side that is more med ial.
Unequal psoas length may be suspected when pelvic side shift is present, when the upper lumbar lordotic curve is flattened, or when seated or prone eval uation suggests upper lumbar flexed somatic dysfunction. To test the ability of the psoas muscle ro lengthen, place the patient in a prone position. Stand at the side of the table. Grasp the thigh j ust above the knee and extend the hip until the ASI Ss begin ro rise off the table. Note the ease and degrees (quality and quantity) of h i p extension on both sides. Also, on the tighter side the leg appears heavier. Compare the twO sides.
Vertical Pubic Shears
Vertical pubic shears (subl uxations) may or may not actually exist. There may be evidence of a rotation or subluxation that is difficult
DIAGNOSIS OF SACROILIAC DYSFUNCTION
The most common and standard diagnoses of sacroil iac somatic dysfunction include (but are not limited ro) : Sacrum anterior Sacrum posterior • Forward rorsions (rotation of the sacrum on the same oblique axis): -Left rotation on left oblique axis -Right rotation on right oblique axis
•
•
52. Pelvis and Sacrum •
• • • •
Backward torsions (rotation of the sacrum on the opposite oblique axis): -Right rotation on left oblique axis -Left rotation on right oblique axis Bilateral sacral Aexion Bilateral sacral extension Uni lateral sacral Aexion (sacral shear) Unilateral sacral extension (sacral shear)
In the osteopathic profession, several models of sacroiliac dys function have been described. Two systems of nomenclature cur rently used to define sacropelvic mechanics are those described by Strachan (HVLA) and M i tchell (muscle energy). The HVLA system is described in Walton's text, Osteopathic Diagnosis and Technique, Sacroiliac Diagnosis ( 1 7) . Both models describe simi lar events, but from differing poin ts of reference. Both systems are based on physiologic motion of the sacrum, pelvis, and l umbar spine. However, the Strachan model does not describe or identifY what the Mitchell system refers to as backward sacral torsions, j ust as the M i tchell system has no equivalent for Strachan's posterior sacrum. Sacroiliac dysfunction is described in this chapter using the most consistent criteria of both systems. To i ntegrate the fol lowing information into the clinical arena, the physician must consider three questions: 1 . Is the sacrum in trouble? 2. Why is the sacrum restricted?
TABLE 52.5. EXA M I N ATION FOR SOMATIC D Y SF U NCTION O F SACRO I LIAC ARTICU LATION Position
Examination
1 . Position of body part 2. Direction of freer motion 3 . Direction of restriction Strachan's model describes sacral dysfunction i n relation ro the ilium rather than to L5. Historically, prior to M i tchell 's paper i n 1 95 8 on structural pelvic function ( 3 ) , sacroi liac problems were described as the sacrum in relation to the ilium, or the ilium in relation to the sacrum. Dysfunctions include anterior sacrum and posterior sacrum. Sacral movement is around a n oblique axis: motion may be restricted at either the upper or lower arm of the L- (C-) shaped sacroiliac joint. Note that the I LA is not the lower arm of the j oint, but a portion of the sacrum used for
Results
Step 1. Patient sta n d i n g
Eva luate anatomic landma rks, standing flexion test
A positive sta n d i n g flexion test means dysfunction i n the leg a n d/or pelvis on that side.
Step 2 . Patient seated
Perform seated flexion test
Will specifica lly determine whether there is a sacro i l iac dysfunction, and if so, which side (but not which arm) of the sacroi liac joint is dysfunctiona l .
Step 3. Patient supine
Positional assessment of ASISs, pubic tubercl es, and medial mal leoli
H e l ps determ ine the etiology of the problem and whether it is purely sacral or a " m ixed " problem, incorporating i l iac and pubic dysfunction.
Step 4. Patient prone
Pal pate for tissue texture changes, motion test i n g of the sacrum, motion testing of L5, ligamentous tension testing
H e l ps the physician d i scover which axis is involved, find what portion of the sacro i l iac joint is restricted, determine L5 motion and position, and evaluate pelvic l iga mentous tensions.
3. What are we going to do for the patient? The information in Table 5 2 . 5 can be used clinically i n a four-step process using four patient pos itions. This step-by-step approach can lead to the diagnosis of any somatic dysfunction of the sacroiliac articulation. Collectively, these four steps integrate information in a logical and time-efficient way of approaching sacroiliac problems. Diag nosing these syndromes is complex, because they may occur i n combination, jointly producing symptoms. For this reason, many experienced osteopathic physicians repetitively diagnose during treatment to evaluate the efficacy of their therapeutic decision. Positional terminology, such as Strachan's, was historically used in naming most somatic dysfunctions, although this did not imply that diagnosis was based o n positional observation alone. The glossary of osteopathic termi nology states that somatic dys function can be named in three ways:
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ASI Ss, anterior superior iliac spines.
palpation and positional reference. The sacrum is diagnosed as either anterior or posterior to the ipsilateral ilium. Anterior Sacrum
An anterior sacrum is a posirional rerm describing a somatic dysfunction in which the sacral base has rotated forward and side bent to the side opposire rhe rotarion. The upper limb of rhe sacroiliac joint has restricred motion, and the dysfunction is named for the side on which forward rotation occurs. An anterior sacrum is probably one type of M i tchell 's forward torsion. For example, anterior sacrum left describes a condition in which the sacrum is rotated right and side ben t to the left, the directions of ease of motion. (This could also be considered right rotation about a right oblique axis.) There is restriction of left rotation and right side bending. The sacral sulcus is deep on the left, with tenderness and tissue texture abnormality in the left sulcus. When downward pressure is applied over the right I LA, attempting ro rotate rhe sacrum about the right oblique axis, the left superior portion of the sacrum resists moving posteriorly, toward the iii LI m. Posterior Sacrum
A posterior sacrum is diagnosed when the sacrum has rotated backward and is side bent to the side opposite of rotation. It is
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Vii. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
named For the side of the backward or posterior rotation. This rotation side bending ro the opposite side could be considered [Omtion about an oblique axis. The posterior sacrum is on the side opposite the deep sulcus at the inFerior pole of the joim. The patiem experiences discomfon at the i n ferior arm of the sacroiliac joint and possibly sciatic pai n . There is a pelvic side shih ro the side of dysFunction, spi nal asymmetry, and postural imbalance. There is a positive seated flexion test on the side of dysfunction, as well as ipsi lateral piriformis tension, and the ipsilateral I LA is posterior and i n Ferior. There may be contralateral psoas tension, and there is generally a contralateral shon leg. For example, a posterior sacrum right has rotated right and side-bem leh, the directions of ease of motion; rotation leFt and side-bending right are restricted. A posterior sacrum involves restriction of motion at the lower limb of the sacroiliac articulation. Tissue texture ab normality and tenderness are located over the inferior ponion of the dysFunctional sacroiliac j oi nt; i n this example, the tenderness is on the right. The rotation, in this case, is in relation ro the right oblique axis. A posterior sacrum is probably a form of For ward rorsion in which the major joim motion restriction is on the side opposite the deep sulcus. A motion test for lower pole (lower limb of the L) restriction (e.g., posterior sacrum right) is ro contact the i nferior borders of the sacrum with both thumbs and apply a cephalad/amerior Force, attempting ro glide the sacrum i n the direction of the lower limb of the joint. Restriction is felt on the posterior sacral side. Although there are similarities be tween the posterior sacrum and the Forward rorsion, there is no true M i tchell equivalent ro Strachan's posterior sacrum. A poste rior sacrum should not be confused with a backward rorsion, a posterior sacral base, or an extension of the sacrum. The M i tchell system, based on the cycle of walking (as previ ously detailed), describes sacral motion relative ro L 5 . The sacrum can move forward or backward about left and right oblique axes depending on the individual's center of gravity and gait, can flex or extend around a transverse axis, or can shift in the L- (C-) shaped arriculation, causing a shear. M i tchell's dysfunctions in clude sacral rorsions, shears, flexion , and extension.
TABLE 5 2 . 6 . POSITION
FINDINGS
FOR
TWO
FORWARD
TORSIONS Left Rotation o n
R i g h t Rotation on
Sacral Rotation on
Left Oblique
Right Oblique
Same Oblique Axis
Axis
Axis
Sacral base anterior, deep sacral su lcus Posterior, inferior lateral angle Lumbar curve convex t o LS rotated to
Right
Left
Left
Right
Right Right
Left Left
posture, the sacrum is i n a flexed forward posItIon (45 ro 5 5 degrees from the venical, or 3 5 ro 45 degrees From the horizontal) . The Ferguson lumbosacral angle is measured from the horizontal. There are two forward rorsions: leh [Otation on a left oblique axis (left o n left), and right [Otation about the right oblique axis (right on right) . Positional findings with each of the two forward rorsions include those shown in Table 52.6. I n the normal motion cycle of walking, the sacrum rotates from side ro side. Dysfunction in the Form of a Forward rorsion occurs when the sacral base rotates Forward, becomes restricted, and does not rotate back as far as it should. The forward sacral torsion and anterior sacrum have several findi ngs in common. Subjective complaints include sacroiliac, inguinal, or g[Oin dis comFort and low back pain . Objective findi ngs i nclude Freedom of rotation amerioriy about an oblique axis, with sacral side bending and rotation in opposite directions. There is an increased lordotic curve. Spinal asymmetry and postural imbalance are noted: The sacrum has rotated in a direction opposite to the supported lum bars. There is an ipsilateral positive seated flexion -rest, deep sacral sulcus with tissue texture abnormali ty, possible psoas tension, and shon leg. Neutral mechanics apply to L5, with side bending and rotation to the opposite side. H owever, rotation of L5 is also i n a direction opposite to that of the sacrum. Backward Torsions
Sacral Torsions
Sacral rorsions reFer ro motion at the lumbosacral j u nction where the sacrum and L5 are rotating in opposite directions. Rotation of the sacrum is movement about an oblique axis or diagonal axis. Sacral torsion does not describe a relationship between the sacrum and the ilium. Forward Torsions
Forward rorsions occur when the lumbar spine is in neutral. I n this example, side bending o f the l umbar spine r o the left (during the motion cycle of walking) engages the leh oblique axis. The lumbar spine, in neutral, [Otates right with leFt side bending. Si nce the leFt oblique axis is engaged, the sacrum rotates left about the left oblique axis, producing a deep sacral sulcus on the right. Torsion impl ies that the sacrum has [Otated left, while the lumbar spine has rotated right. (Note that, with neutral lumbar mechanics, leFt side bending p[Oduces rotation right.) The term Forward rorsion is derived from the observation that, in the erect
Backward rorsions (non neutral) occur when the lumbar spine is in non neutral (flexion or, where the curve exceeds normal lor dosis, extension) and the sacral base rotates posteriorly about the opposite oblique axis. While they do not occur within the cycle of walking, they are associated with physiologic motion when a person forward bends and then side bends. Consider a patiem i n the standing position who bends forward. The sacrum actually extends or backward bends at this time. The l umbar spine is flexed to a point where any m ultiple plane motion results in nonneutral multiple plane motion. The patient reaches sideways ro pick up an object. The lumbar spine side bends to the right From the non neutral sagittal plane position. The right oblique axis is engaged as a result of the right side bending. L5 [Otates right according ro nonneutral l umbar mechanics. The sacral base moves posteri orly at the left base as the sacrum rotates to the left according to sacral non neutral mechanics. This example is called left on right (left rotation about the right oblique axis). There are two types of backward sacral torsions: right rotation on a left oblique axis (right on left) , and left rotation on a right oblique axis (leFt on
52. Pelvis and Sacrum TABLE 5 2 . 7 . POSITIONAL
FINDINGS
FOR
TWO
BACK
WARD TORSIONS Left Rotation on Sacral Rotation on
Right Rotation on
Right
Opposite Oblique Axis
Left Oblique Axis
Oblique Axis
Sacral base anterior, deep sacral su lcus Posterior, inferior lateral angle Lumbar curve convex to L5 rotated to
Left (tender right)
Right (tender l eft)
R i g ht
Left
R i ght Left
Left R i g ht
right). Positional findings with each of the two backward torsions include those shown in Table 52.7. A backward torsion is not the same as a posterior sacrum . A posterior sacrum i s a rype o f forward torsion i n which the inferior portion of rhe sacrum is posterior. In a backward torsion, the posterior portion is at the sacral base (rhe shallow sulcus) . Subjecrive complaints include low back pain or sacroiliac dis comfort that gets worse when bending forward or walking. Objec tive fi ndings include those l isted above, plus a decreased lordotic curve. Palpatory fi ndings include tissue texrure abnormali ry and a shallow sacral sulcus on rhe side of the dysfunction, wirh rissue rexrure abnormaliry at L5. Nonneutral mechanics apply to L5, wirh rotarion and side bending occurring to the same side and opposire the side of the sacrum's rotation. Bila teral Sacra l Flexion
If rhe sacrum is flexed forward, with the sacral base anterior, the lumbar lordosis appears to be increased, the seated flexion test is negative, the sacral sulci are bilarerally deep, and the I LAs are posterior. It is postulated thar rhis motion occurs about a middle rransverse axis of the sacrum. This is called a bilateral sacral flexion. When rhe lumbosacral spring resr is performed, rhere is good spring (a negarive resr) because the sacral base, al ready anterior, moves forward easily. If rhe backward bending rest is done, rhe sacral sulci is still deep (if nor deeper), and the ILAs are sri II posterior (or more posterior) because rhe base of rhe sacrum normally moves forward and rhe apex moves posteriorly during backward bending of the l umbar region. This is an extremely common dysfunction i n the posrpartum female because of birth mechanics (see Chapter 3 1 ) . Subjecrively, rhe patient complains of low back pai n thar becomes worse when bending backward. Objective findi ngs include: Increased lumbar curve Deep bilareral sacral sulci wi th tissue texrure changes • Bilateral I LAs posterior • Negative lumbar spring test • No change with the hyperextension resr • •
Motion characteristics include resistance to posrerior rotation of the base of the sacrum i f pressure is placed on rhe apex. Bilateral Sacral Extension
In some cases, the parienr does not have a positive seared flexion test, yet complains of low back pain, and the sacrum seems to be
781
ar rhe cenrer of the problem. At thar rime, rhe sacral sulci should be examined, rhe I LAs checked, rhe spring test and backward bending resr performed, and a careful analysis made of the rela tionship of the sacrum to rhe lumbar spine. The lordotic curve may be increased or decreased. Wirh posrural flexion at the lum bar spine (forward bending), the sacrum extends (the base moves posterior) , and there is a decrease in the l umbar lordotic curve. I f the lordotic curve seems t o b e decreased, i t may b e that there is a posterior sacral base. I n a bilateral extension, the sacrum is held in a backward benr position and does not easily bend forward. The lumbosacral spring test is rherefore positive, which means there is either poor spring or no spring. Sacral sulci and l LAs should appear symmetric in either prone or backward bending positions, and, i f there is any difference on the backward bending test, the sulci look more shallow, and the ILAs more anrerior. Subjectively, the parienr complains of low back pain or fatigue that becomes worse wirh forward bending. Objective findi ngs i nclude: • • • • • •
Decreased lumbar curve I LAs equal and perhaps anrerior Positive l u mbar spring rest lLAs stay equal during hyperextension rest (superior/inferior) Sacral sulci are bilaterally shallow, with tissue rexrure changes Sacrum resists posteroanrerior pressure at base, but yields to posteroan rerior pressure on apex
Sacral Shears
The sacrum can appear as ifit has slipped anreriorly or posteriorly around a rransverse axis that allows it to shift withi n the L- (C-) shaped sacroil iac joinL If it sl ips forward, ir produces a finding called a sacral shear or unilateral sacral flexions and exrensions. Unilateral Sacral Flexion
I f there is a positive seated flexion rest, with the base of rhe sacrum anrerior o n the dysfunctional side (sacral sulcus deep on that side) and the ipsilateral I LA is posterior, the patienr has a unilareral sacral flexion. The ipsilateral medial malleolus is more i nferior, and the transverse process ofL5 is more posrerior on the dysfunctional side. Both sides of the sacral base move anteriorly with exhalation bur do not move easily in a posrerior direction with in halation . The spring test should be negative, since the base of the sacrum moves anreriorly easily when it is flexed. The backward bending test should show improvement because, wh ile the one side is flexed forward, making rhe sacral sulcus deep, when the parienr bends backward the orher side of the sacral base should be pulled forward, increasing symmerry. Unilateral Sacral Extension
If rhere is a positive seated flexion test, wirh rhe base of the sacrum posterior o n the dysfunctional side (sacral sulcus shallow) , and the ipsilateral I LA is anterior, the patient has a unilateral sacral extension. To confi rm this, test the parient with the spring test and rhe backward bending tesL The spring test should be posi tive, since the base of the sacrum does nor move anteriorly easily when the sacrum is held in an extension position. On the backward bending test, the sulci and I LAs should look even less symmetric
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
because, while the one side is held backward, making the sacral sulcus shallow, when the patient bends backward, the other side of the sacral base should be pulled forward, making the results look worse.
CAUSES OF SACROILIAC DYS FUNCTION Psoas
Psoas muscle hyperactiviry compresses the l u mbosacral area. To test for psoas muscle tension with the patient prone, extend the thigh (hip) . Psoas problems also have a flexed upper lumbar so matic dysfunction with restriction of extension. Ordinarily, L 1 or L2 i s flexed, rotated, and side bent to the side of the shorter psoas. Short Leg Syndrome
The first symptoms of short leg syndrome are usually sacroiliac discomfort or pai n. Symptoms are worse with excessive walking or running. Examination of the sacrum usually reveals a deep sacral sulcus on the shorr leg side with significant tissue texture abnormaliry and tenderness. Postural Imbalance
these cases, treating the sacroiliac restriction i s not associated with the relief of pain. Simple Traumatic Sacral Somatic Dysfunction
These patients usually limp i n , leap out, and are forever grateful for the one-treatment cure. Reflex Causes
Reflex causes such as viscerosomatic reflexes from pelvis or unilat eral sympathetic nervous system dysfunction are causes of sacroil iac pain. Viscerosomatic reflexes are associated with tissue texture abnormaliry along the sacroiliac joint, which is puffy and warm. This is similar to acute tissue texture abnormal i ry found in the thoracic area from abdominal or thoracic visceral problems. Clinical Pearls on Low Back Pain
1 . L5 is a frequent site of pain and may be unstable as well as painful. Plan: M obilize adjacent segments that are restricted. Avoid excessive HVLA to unstable j oints. 2. Treat shorr hypertonic psoas. 3. Sacroiliac pain may be caused by L5 problems. I n these cases, mobilization of the sacroiliac j oi nt does not relieve the pain.
Spi nal asymmetry, lateral curves, and repetitive asymmerric ac tiviry can produce sacroiliac dysfunction.
4. l I iolumbar ligament i nsertion on the ilium may be very tender. Causes include ipsilateral lumborhoracic i rritabiliry, anterior rotarion of L 5 , and pelvic side shift to that side. This may be the first l igament to be strained with postural decompensarion.
Pelvic Side Shift
5. Nociceptive activity at the lumbosacral junction causes lum bothoracic irritabiliry with increased sympathetic tone.
When the sacral base is to one side of the midline (e.g., pelvic side-sh ift right), the com pensatory change is for body mass to be moved to the opposite side (e.g., pelvic side-shift right, lumbar curve convex left) . In this example, the sacrum has to side bend left to accommodate the l umbar curve. When the sacrum side bends left, it rotates right, producing sacroiliac dysfunction. This is the mechanism of sacroil iac dysfunction associated with a shorr leg problem. LS Problems
L5 problems such as spondylolysis, spondylolisthesis, and con genital anomalies predispose to sacroi liac dysfunction.
G.
Active exercises are essential to strengthen and stabil ize a back. O MT can create an environment that allows exercises to work and compensations to occur. The primary rule for exercise is ro Stop short of pai n.
CONCLUSION
Manual medicine can restore functional symmetry between the arthrodial, vascular, lymphatic, and connective tissue elements of the pelvic girdle. Ie can relieve a wide range of somatic, visceral, and emotional patient complaints and contribute to the health of vertebral function, the thoracoabdominal diaphragm, and the urogenital area.
Lumbar Somatic Dysfunction
Lumbar somatic dysfunction, particularly rype II flexed dysfunc tions, may contribute to sacroiliac dysfunction. Effective treat ment of the lumbar somatic dysfunction will often release the sacroiliac restriction. Disc
Disc problems at L4 or L5, in the early stages, radiate pain i nto the buttock region that is i nterpreted as sacroi l i ac pain. Often the sacrum is restricted from secondary muscle hyperroniciry. I n
RE FERENCES I . Weisl H . The articular surfaces of rhe sacroiliac joim and rheir relarion ship to [he movemenrs of rhe sacrum . Acta Anat. 1 954;22: I ; 1 4 . 2 . Greenman PE. Principles ofManual Medicine. Balri more, M D : Williams & Wilkins; 1 989:226-227. 3. M i rchell FL Srrucrural pelvic fu ncrion. In: American Academy of Osteopathy Yearbook. Indianapolis, I N : American Academy o f Os reopa rhy; 1 9 58:7 1-90. 4 . Thiele G H . Coccygodynia: cause and rrearmenr. Dis Colon Rectum.
1 963;6:422-436. 5. Korr 1 M . Susrained symparhicotonia as a factor i n disease. In: The
52. Pelvis and Sacrum Collected Papers of Irvin M. Korr. Newark, O H : American Academy of Osteopathy; 1 979:77-89.
1 2 . Seidel H M , Ball ) W. D ai ns ) E, Benedict G w. Mosby's Guide to Physical
Examination. Sr. Louis, M O : CV Mosby Co; 1 987.
6. Bcaron LE, Anson BJ. The sciatic nerve and the piriformis muscle: their
1 3. Travell
)G,
Si mons DC. Myofoscial Pairl and Dysfimction: The Trig
i merrelationship as a possible cause of coccygodynia. j Bone joint Surg
ger Point Marlua!' Vol
(Br). 1 938;20:686-688.
1 983.
7. Reynolds H M. Three dimensional ki nematics in the pelvic girdle. jA OA. 1 980;80: 277-280.
ratory mechanism. jAOA. 1 97 1 ;70: 1 1 09-1 1 1 2. 1 9 50.
Disrri buted,
J n dianapolis,
IN:
American
Academy of Osteopathy; p. 62. 1 1 . Kuchera WA, Kuchcra M L. Osteopathic Principles in Practice. 2nd ed. rev. Columbus, O H :
Grcyden
1 5 . Sutherland AS, Wales AL. Coffected Writings of Wiffiam Gamer Sltther
Press; 1 994.
Cranial Teach ing Foundation, 1 967. 1 6. Hoppenfeld S.
Doctor A. T Still in the Living. Privately published,
OH;
1 4 . Kuchera WA, Kuchera M L. The Kuchera Marilla!: Osteopathic Principles
land. D. o., D. Sc. (Hon.}. Produced under auspices of the Sutherland
jA OA. 1 938;43( 1 2} : 576-578. 9. M i tchell FL, Pruzzo NA. I n vestigation of vol u n tary and primary respi
Cleveland,
1 . Balti more, M D: Wi l l iams & W i l k i ns;
in Practice. Kirksville, M O : KCOM Press; 1 99 1 .
8 . Strachan WF, et al. A srudy of the mechanics of the sacroil iac joi nr.
1 0. Truhlar RE.
783
Physical Examination of the Spine and Extremities.
Norwalk, CT: Appleton & Lange; 1 976: 1 5 1 - 1 5 2, 1 64 . 1 7. Wal ro n
W) .
Osteopathic Diagnosis and Technique. Sacroilitle Diagnosis,
J St ed. Sr. Louis, M O : Matthews Book Co; 1 966: 1 87- 1 97 . Distributcd, Colorado Spri ngs, CO: American Academy of Osteopathy; reprinted. 1 970.
LOWER EXTREMITIES MICHAEL L. KUCHERA
Compartmenr syndromes Myofascial trigger poinrs • Patellar tracking problems
• KEY CONCEPTS • • • • • • • • •
•
Structure, functional anatomy, and somatic dysfunction of the lower extremities Differential palpatory end-feel c haracteristics associated with dysfunction, i nflammation, and trauma Recognition of each distinctive "capsular pattern" for h ip, knee, and ankle Classification of ligamentous sprains Structures and biomechanical factors i n fl uencing major and minor motions of lower extremity joint regions Meaning and biomechanical impact of coxa varus, genu valgus, and/or pes planus Motions of fibular head and how motions of ankle affect fibular head motion Most common ankle sprains, how they occur, and related somatic dysfunction Relationship of related neuromuscular, vascular, and lymphatic elements to lower extremity dysfunction and clinical symptOms Neuromuscular i mbalance i n the lower extremi ties and myofascial trigger points
•
Neuromusculoskeletal system evaluation of the lower extrem i ties typically includes a screening evaluation of the region dur ing walking, standing, and squatting as well as eval uation of a standing Aexion test; one-legged stOrk (also known as Gillet or modified Trendelenburg) test; and straight-leg raising test. These are integrated with standard screening functional tests for neural, lymphatic, and vascular disorders. A positive finding in any of these screen ing examinations, or an indication in the histOry of a need for closer scann ing of the region, requires palpation; assess menr of range of motion of each joint; and assessmen t of muscle strength, stability, and Aexibility. This chapter reviews the func tional anatOmy and basic examination of the lower extrem ities in three sections: l.
Skeletal, arthrodial, and ligamentous structure and function
2 . Neuromuscular structure and function
3. Vascular and lymphatic structure and function
SKELETAL, ARTHRODIAL, AND LIGAMENTOUS STRUCTURES AND F!,JNCTION
The lower extremities provide for support and locomotion with strong bones and powerful muscles. Functionally, the lower ex trem ities extend to the iliosacral joint (covered in Chapter 52); anatOmically, most texts begin at the hip. While many clinicians consider the pelvis to be the foundation on which the spine bal ances, the lower extremities form the final common platform for postural al ignmen t (I). Somatic dysfunction in the lower extrem ities has local, postural, and systemic i mplications. The lower extremities are often the site of referred pain from somatic structures in the lu mbar and pelvic regions and/or from certain abdominopelvic viscera. While these relationships are mentioned in this chapter, refer also to those chapters in this text associated with the primary problem. Examples of lower ex tremity clin ical considerations discussed in this chapter i nclude: • •
Ankle sprains Bursitis and arthritis
The bony skeleton of each lower limb ( Fig. 53. 1 ) includes the: • • • • • • •
I n nominate (pelvic bone) Femur Tibia Fibula 7 tarsal bones ( including the talus, calcaneus, navicular, cuboid, and 3 cunei forms) 5 metatarsal bones 14 phalanges Functionally, the joints of the lower extremities include:
H ip (femoroacetabular joint) Knee (femorotibial, proximal tibiofibular, and patellar joints) • D istal tibiofibular joint • Ankle (tibiotalar joint) • Subtalar (talocalcaneal joint) •
•
53. Lower r.xtremities
Femoroacetabular Joint
Knee Joints
Fibula---->..d
Fibula -----tL-----i1 Talus
Tibia Ankle joint Calcaneus Tarsals Metatarsals
Ankle and Foot Joints
Tarsal metatarsal
Distal interphalangeal Proximal interphalangeal Metatarsal-phalangeal
Intertarsal Navicular ---fTalonavicular
1 st metatarsal
Cuboid Cuboidocalcaneal
Talocalcaneal FIGURE 53.1. Bones and joints of the lower extremity.
785
Several i ntertarsal joints ( i ncluding the talonavicular, the cuboidocalcaneal, and two small talocalcaneal joints) collec tively called the Chopart joint • Numerous tarsometatarsal, metatarsophalangeal, and i nter phalangeal joi n ts in the foot
•
The bones making up these joints are covered In articular cartilage. The majority are synovial joints with a capsule and synovial membrane while the distal tibiofibular joint is a fibrous syndesmosis with an i nterosseous membrane. Each of these joi nts is stabilized by l igaments, which limit joint motions and are a part of the normal end-feel sensed when palpating joint motion . Joint capsules are subject t o pathologic a n d i nAam matory processes. Such processes result in "capsular patterns" of restricted motion in which all or most passive movements of the joi n t prove painful and limited. A capsular pattern due to inAammation or pathology is palpably differen t from the patterns of tenderness and restricted motion assessed in somatic dysfunction (2) (Table 53. 1). Palpation of the capsular pattern is also dramatically dif ferent from the laxity appreciated in l igamentous sprains. Thus palpation of the end-feel provides sign ificant information about the differential diagnosis of a painful or i m properly functioni ng jOIl1t. In the diagnosis of ligamentous sprains, the joint line and stabilizing l igaments should be palpated directly for tenderness followed by end-feel assessment for arthrodial motion or laxi ty. The greater the structural damage due to l igamentous spraining, the greater the laxity with resultant loss of normal end-feel and stability. Palpation of joint play end-feel is therefore useful in classification of traumatic and orthopedic conditions i ncluding sprall1s.
Ligamentous Sprain Classification
Ligamentous sprains are generally classified by degree. A first degree sprain assumes that the i ntegrity of the ligament is undis turbed, resulting in generally i ntact tensile strength. (Some label this degree of injury a "strain," while others reserve the term, strains, for muscle injuries.) A first-degree sprai n , while tender to specific palpation and painful when stressed, is generally stable to most orthopedic l igamentous tests. A first-degree sprain responds well to conservative osteopathic care and recovers with normal function and no l igamentous laxity. A third-degree sprain (also known as a grade ! I I sprain) in dicates complete disruption of the l igament with no remai ning tensile strength. Orthopedic testing i ndicates the sloppy end-feel of complete i nstability. Good splinting and early surgery may offer the best prognosis when dealing with third-degree ligamen tous sprains around the structurally unstable knee; with ligaments of the i nherently more stable ankle joint, surgery may be delayed or unnecessary to reestablish stability. Second-degree sprains make up the ligamentous injuries i n between these two diagnoses. Second-degree sprains may b e di vided into grade I (partial tearing with slight laxity) and grade 11 (more complete tearing and moderate laxity) sprains. Second degree sprains, even grade II, do not usually require surgical re pair if they are appropriately i mmobilized for a time appropriate to the amount of structural damage. Prolotherapy (3) and/or
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
786
TABLE 53.1. THE CAPSULAR PATTERNS Region Involving Capsular Pattern (Common Diagnoses)
Capsular Pattern of Motion Specific to Joint (Contrast with Somatic Dysfunction Patterning)
"Sign of the Buttoc k " Indicates major lesion such a s osteomyelitis, ischiorectal abscess, iliac neoplasm, etc.
Passive hip flexion more limited and more painful than straight leg raise
A prematurely empty end-feel on passive hip flexion accompanies the sign of the buttock
Hip Rheumatoid, traumatic, or spondylitic arthritis; osteoarthrosis
Marked limitation of internal rotation and flexion, some limitation of abduction, little or no limitation of adduction and external rotation
Hard end-feel palpated especially at the end of internal rotation (advanced cases: patient may walk with foot turned outward)
Knee Traumatic arthritis, rheumatoid arthritis, osteoarthritis, Baker cyst
Gross limitation of flexion, slight limitation of extension
In arthritis, the palpated end-feel on passive flexion is usually hard. Most common primary capsular conditions signaled by warmth, fluid, and synovial thickening
Ankle Osteoarthrosis, reactive arthritis
More limitation of plantar flexion than of dorisflexion
Capsular patterns unusual
Talocalcaneal Joint Osteoarthrosis, rheumatoid or subacute traumatic arthritis, Sudeck atrophy
Increasing limitation of varus until fixation in valgus position
Mid tarsal Joint Osteoarthrosis, monarticular or subacute rheumatoid arthritis
Limitation of adduction and internal rotation, other movements full
Peroneal spasm involved
Big Toe Rheumatoid arthritis, osteoarthrosis, gout
Gross limitation of extension, slight limitation of flexion
Advanced pattern demonstrates fixation in neutral position (hallux rigidus)
(From Cyriax permission.)
JH,
Cyriax
PJ. Cyriax's Illustrated Manual of Orthopaedic Medicine,
certain rehabilitative procedures may be employed to restore a component of the laxity and lost joint stability.
HIP
The hip, or coxa, is a term used loosely to i ndicate the artic ulation of the head of the femur with the acetabular socket of the innominate bone. ( Recognize that the term, hip, may also be commonly used to refer to any part of the region between the waist and the thigh.) Throughout this chapter the term, hip, will be i nterchangeable with the structural and functional elements associated wi th the femoroacetabular joint itself. The hip is a ball-and-socket synovial joint with a socket deeper than the glenoid fossa of the shoulder, reRecting the stability characteristic of the joint. In the newborn with a congenitally shallow acetabulu m, this lack of stability can be evaluated using the Ortolani test for dislocation ( Fig. 5 3 . 2) and the Barlow test for red uction (Fig. 53. 3 ) . Early discovery perm i ts satisfactory results with triple diapering or conservative brace management. Failure to perform a satisfactory exam ination risks a late diagnosis and the necessity for surgical correction.
FEMUR
The femur is the longest and heaviest bone in the body, at tai ning a length about one-fourth the height of an adult (4).
End-Feel and Other Comments
2nd ed. Oxford, England: Butterworth-Heinemann Ltd;
1 993:6-8,
with
This fact allows the forensic pathologist or archaeologist to es ti mate an individual's height from the femur alone. The angle formed by the i ntersection of the anatomic ;Lxis of the shaft of the femur and the longitudinal axis of the neck of the femur is called the angle of inclination. This angle normally measures 12 0 to 1 3 5 degrees. If the angle of inclination is larger than J 35 degrees, the condition is referred to as coxa valgus. If it measures less than 12 0 degrees, the cond ition is called coxa varus ( Fig. 53.4). The femoral shaft is twisted so that the condyles of the distal femur are in a transverse plane even though the femoral neck angles forward 12 to 1 5 degrees. Th is is called the angle of an teverslon .
Longitudinal Axis
The anatomic longitudinal axis runn ing down the shaft of the femur is not its functional axis. The functional longitudi nal axis of the femur runs from the femoral head distally to a poi nt midway between the condyles. With i nternal rotation at the hip on this functional axis, the femoral head glides posteriorly. With external rotation, the femoral head glides anteriorly. I nternal rotation with posterior glide and external rotation with anterior glide are minor motions of the femoroacetabular joint. Since arthritic change modifies gliding motions and occurs early in the m i nor motions of the joint, (5) screening for arthritic changes in the hip should combine the standard Patrick screening test ( Fig. 5 3 . 5 ) with evaluation for a hip capsular pattern. The acronym FABERE is often used to describe the order in which
53. Lower J:.)ctremities
787
Femoral head Acetabulum
FIGURE 53.2. Ortolani test. Ortolani test for hip dislocation can be used in the first few weeks of life. In a subluxated hip, this maneuver creates resistance felt at 45 to 60 degrees. A positive sign is a palpable click (not heard) when resistance is overcome and the femoral head reduces. (Top: From Kuchera ML, Kuchera WA. Osteopathic Principles in Practice, 2nd ed. rev. Columbus, OH: Greyden Press; 1994:636, illustration by W.A. Kuchera. Bottom: Modified from Burnside JW. Physical Diagnosis: An Introduction to Clinical Medicine, 1 6th ed. Baltimore, M D : Williams & Wilkins; 1 98 1 :246.)
FIGURE 53.3. Barlow test. Barlow test for hip reduction is a modifica tion of the Ortolani test used to identify an unstable hip in infants up to 6 months of age. To perform the Barlow test, the Ortolani test is first performed followed by a posterolateral pressure over the inner thigh. If the femoral head slips out over the posterior lip of the acetabulum and reduces spontaneously when the pressure is released, then the joint is not dislocated but is unstable. (Top: From Kuchera M L, Kuchera WA. Osteopathic Principles in Practice, 2nd ed. rev. Columbus, OH: Greyden Press; 1 994:636, illustration by W.A. Kuchera. Bottom: Modified from Burnside JW. Physical Diagnosis: An Introduction to Clinical Medicine, 1 6th ed. Baltimore, MD: Williams & Wilkins; 1 98 1:246.)
the " Patrick FABERE" test is performed:
Ligaments
Aexion Abduction External Rotation Extension Positive without a hip capsular pattern, the Patrick test is more likely to reRect pain from the sacroil iac joint or anterior sacroiliac ligament than hip pathology. Arth ritic change ptogresses from functional demand accen tLlated by biomechanical stress to pathophysiologic response to structural change. For example, the biomechanical stress placed on the hip joint by a short lower extrem ity results in a h igher i ncidence of greater trochanteric bursitis and of osteoarthri t is (6,7), both on the long leg side. Somatic dysfunction and arthritic pathology often coexist within this structLIre-function spectrum. Each should be addressed with appropriate therapeutic tools in tegrated into a regimen for total patient treatment (8) .
The iliofemoral ligament on the anterior aspect of the hip joint is the strongest ligament in the body. Because i t is shaped like the letter Y, it is also called the Y-ligament of B igelow. Th is ligament tenses with ful l hip extension. Ir helps to maintain posture in the mil itary at-ease position with minimal muscle activity. On the posterior side, the ischiofemoral ligament attaches to the isch ial portion of the acetabular rim and wraps over the posterior and superior part of the hip joint to attach just medially to the base of the greater trochanter of the femur. This important anatomic configuration tends to screw the femoral head i nto the acetabu lum with extension, thereby preventing hyperextension. Normal extension is l i m i ted to about 35 degrees (Fig. 53.6). Motion
The motions of the hip (femoroacetabular) joint that are grossly tested are:
VII. Osteopathic Considerations in PaLpatory Diagn.osis and ManipuLative Treatment
188
Angle of inclination 13So Normai
Greater trochanter
FIGURE 53.4. Angle of inclination in coxa varus (120 degrees) and coxa valgus ( 1 3 5 degrees). (Illustration by w.A. Kuchera.)
Flexion-extension • Abduction-adduction • External rotation-internal rotation •
M inor motions of the joint are glides that are assessed with end-feel palpation. For example: • •
Anterior glide occurring with external rotation Posterior glide occur ri ng with internal rotation
Flexion
A b du ctio n
External rotation
FIGURE 53.6. Top: Bones and ligaments of the right hip (anterior view). a: Iliofemoral ligament (Y-ligament of Bigelow). b: Pubofemoral liga ment. The iliofemoral ligament on the anterior aspect of the joint is the strongest ligament in the body. Bottom: Bones and ligaments of the right hip (posterior view). The ischiofemoral ligament on the poste rior side of the joint limits extension to 35 degrees. (Illustration by W.A. Kuchera.)
Gross hip ranges of motion and passive assessments of end feel are usually tested with the patient supine and the pelvis stabilized. Ranges of motion vary from individual to i ndivid ual and differ in different populations tested. ( For example, ex pect different averages for male high school football players than for teenage female gymnasts.) More important than the abso lute n umber of degrees measured is side-to-side symmetry and the quality of the barrier at the end of motion. This holds true for all lower extremity joi nts assessed as well. In the presence
Extens ion
FIGURE 53.5. Patrick FABERE test of the hip. (Illustration by W.A. Kuchera.)
53. Lower Extremities
of asymmetric motion, also differentiate hypomobility fro m hypermobility. The character and pattern of the end-feel of each hip mo tion may be springy (physiologic) or it may suggest a capsular, rraumaric, or dysfunctional pattern. Subrle differences in somaric dysfuncrion of myofascial rather rhan articular origin may also be appreciared by evaluari ng the end-feel of rhe hip joint. The muscles and soft tissues of the hip typically limit Aexion more than the ligaments. Straight leg raising at rhe hip around a transverse axis is limired by rhe hamstring m uscles to 85 to 90 degrees. If the knee is bent to remove the hamsrring inAu ence, rhe thigh can normally be Aexed up to 1 3 5 degrees ar rhe hip. If sign ificanr improvement in range-of-motion is nor seen after bending rhe rhigh, rhe si tuation is nor consisrent with a biome chanical cause. Thus when more pain and l i mirarion of morion (with an empty end-feel) occurs wirh bent-knee hip Aexion rhan with srraighr-Ieg raising, a serious condirion, such as sepric bur sitis, ischiorectal fossa abscess, osteomyelitis or neoplasm of the upper femur, or other significant parhology of the ilium, m ust be ruled our (9) (see Table 53. 1 .) . Extension with the subject prone and legs extended may mea sure as much as 35 degrees; bending the hip and knee of the opposite lower extremity relaxes some of the m uscular restricrion to hip extension and should increase this measurement. Around an anteroposterior (AP) axis through the femoral head rhe hip may abduct and adduct as m uch as 55 degrees and 3 5 degrees, respectively. To test adduction i n a supine patient with the knee locked, the leg must be lifted to cross anterior to the opposite leg. Around a functional longitudinal axis, hip external rotation may measure up to 55 degrees; i nrernal rotarion to 45 degrees. In summary, the major morions of rhe hip and the minor mo tion glides of anterior glide (with exrernal rotation) and posterior glide (with internal rotation) should be assessed and thei r pattern evaluated. A physiologic end-feel to one m o tion compared to a barrier in rhe opposite is consistenr wirh a dysfunctional pattern. A capsular partern of marked limitation to inrernal rotation, with l i m iration to Aexion and abduction as well, should raise suspicions of an i n Aammatory process. If findings do not follow functional biomechanical principles, rhey warranr further evaluation.
KNEE
While rhis section also covers the patellofemoral j o i nr, the true knee, genu, or femororibial joinr is a double condylar, complex synovial articulation formed by the femoral condyles and rhe tibial plareau (Fig. 53.7) . This j o i n t contains medial and lateral semilunar cartilages to provide some stabili ty, smoothness, and resil ience to pressure. The medial condyle of the knee is longer than the articular surface of the lareral condyle ( Fig. 53.8) . This structural con figuration affects joint function. With extension of the knee, the lateral condyle reaches its physiologic limir of motion while the medial condyle of the femur contin ues to track posreriorly on the tibial plareau. This results in posterolateral glide of the
789
\
----T-l��--
Femur Articular capsule Posterior
m:---f.JWr-_ cruciate
ligament Infrapatellar fold
��"""''"7::::
e.::""�-W7'tI- Alar folds --t-Itt+/--- Patella
*-I+-II'I-+\�,--
Gastrocnemius, medial head Posterior cruciate ligament Tibial collateral ligament Medial meniscus
Tendon of quadriceps femoris
P lantaris Gastrocnemius, lateral head
Fibular collateral ligament Lateral meniscus
Semimembranosus tendon
Popliteus tendon
Popliteus, medial fibers cut away
Posterior meniscofemoral ligament
FIGURE 53.7. Knee joint. Top: Anterior view. Bottom: posterior view.
tibia wirh ful l extension of the knee. Full extension locking re quires this minor rotational glide. The opposite (anteromedial glide) occurs with ful l Aexion of rhe knee. These m inor motions of the joinr should be checked for somatic dysfunction by adding an anteromedial glide while i nducing exrernal rotation of the tibial plateau and a posterolareral glide while inducing i nternal rotation of the tibial plateau (Fig. 5 3 . 9 ) .
790
V[f. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
-160-
Hypothetical position had slide not occured
�,---I' ' I I
(Seated)
I I I I I I I
\ \ \
,
,
(Standing)
FIGURE 53.8. Structure-function relationship of the medial condyle. In knee extension, the medial, but not the lateral, femoral condyle will continue to track posteriorly, resulting in internal rotation of the femur (if the tibia is stationary) or external rotation (Ext. rot.) of the tibia (if the femur is held stationary). The condylar glide occurring with external rotation of the tibia is called the anteromedial glide.
53. Lower Extremities
A
791
B
I
External rotation
Internal rotation with posterolateral glide
FIGURE 53.9. Physical examination o f anterome dial glide with external rotation (A) and pos terolateral glide with internal rotation (B) of the knee. (Illustration by W.A. Kuchera.)
The osteopathic palpatory exami nation of the knee incorpo rates standard knee testing positions and maneuvers while noting the presence and pattern of these fi nd ings: Gross range of motion Restricted gliding minor motions (end-feel) • Hypermobility and loss of stability (end-feel) •
•
The same testing maneuvers needed to diagnose somatic dys function offer orthopedic and rheumatologic i n formation about knee structure. In general during testing, if the end-feel of the test is too loose, there is an orthopedic diagnosis. If generally re stricted in both directions of a given paired motion (e.g. , Aexion extension), there is often a rheumatologic diagnosis. If a pattern of pai red motions are assessed to be physiologically free in one direction but ends too abruptly in the other, the diagnosis is joint somatic dysfunction. Thus, i n terpreting each test for the available dual structure-function i n formation provides rwice the diagnostic information in the same amount of time usually spent in examining the knee structure alone.
e
Midpoint of p at ll a
Q-Angle and the Patella
The angle formed by the intersection of the functional longitudi nal axis of the femur and the tibial longitudinal axis is referred to as the Q- (or Quadriceps-) angle. Normally the Q-angle measures 1 0 to 12 degrees (Fig. 53.1 0) . An angle of2 0 degrees or more is defin itely abnormal. As the Q-angle increases, the patient ap pears more knock-kl1eed, a condition referred to as genu valgus. A bowlegged appearance is known as genu varus. Biomechani cally, coxa varus increases the Q-angle, as does a pronated foot. Each enhances the possibility of genu valgus. The Q-angle has a major effect on the tracking of the patella, a sesamoid bone in the tendon of the quadriceps femoris muscle group. Patellofemoral joi nt dysfunction and structural change may each arise from abnormal tracking of, or pressure on, the patella. Accentuated Q-angles may be associated with symptoms of patellar pai n due to ligamentous stress at the knee or through
Genu V:lgus
! r- \ �:r��
� 0 20
10
0
0
/
0
FIGURE 53.10. Q-angle (quadriceps angle) normally measures 10 to
1 2 degrees. Key landmarks for establishing the Q-angle are the ante rior superior iliac spine, the patella, and the tibial tuberosity. Note the change in the Q-angle in genu valgus and varus.
792
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
secondary develop ment of muscle i mbalance and trigger poi nts. The patella may even sublux laterally with these biomechanical forces, especially with dysfunction or weakness of the vastus me dialis muscle. Locking of the patella strongly suggests myofascial trigger points in the vastus lateralis m uscle. Complete locking of the patella i mmobilizes the knee joint in slight Aexion, wh ile partial locking causes difficulty in straigh teni ng the knee after sitting in a chair. Prolonged patellofemoral dysfunction, due to these biome chanical factors, predisposes to structural change such as i rregu lar or accelerated wearing or roughening of the articular surface on the posterior surface of the patella (chondromalacia patellae) . This coexistence of structural and functional d isorders must be considered and appropriately diagnosed and treated to encourage optimum healing. Patellar structural problems also arise from:
A Medial collateral ligament stress --+
Valgus stress
Patellar dislocation Chronic or direct patellar trauma • Fracture of the lower extremity • •
Structural problems of the patella are evaluated, in part, by palpating over and around the patella. Look for subpatellar ten derness, crepitus, grinding, or clicking with compression agai nst the underlying fem ur (patellar gri nd test) when gliding the patella med ially and laterally as well as superiorly and i nferiorly. Ef fusion within the knee joint also strongly suggests structural change. As a consequence of secondary bony alignment and muscular imbalance, functional patellar tracking difficulties may also be the presen ting symptom of postural disorders (see Chapter 43) . Ligaments and Cartilage
Lateral and medial collateral ligaments, placed to limit lateral glide of the tibia with adduction and medial glide of the tibia with abduction, stabilize the true knee joint. The lateral (fibular) collateral ligament does not attach to the lateral semilunar carti lage (meniscus), while the medial (tibial) collateral l igament does attach to the medial semilunar cartilage (men iscus) ( Fig. 5 3. 1 1 ) .
B
Lateral collateral l igame nt stress
Varus stress
FIGURE 53.12. Tests for collateral ligament injury at the knee. Tibial abduction or genu valgus stress (A) tests for medial collateral ligament stability. Tibial adduction or genu varus stress (B) tests for lateral collat eral ligament stability. (Illustration by W.A. Kuchera.)
Lateral meniscus Lateral collateral ligament
Medial meniscus
Medial collateral ligament
FIGURE 53.11. Relationship of collateral ligaments to knee cartilage
(anterior view).
This anatomic arrangement makes the medial cartilage more susceptible to injury. It also predisposes to displacement, espe cially from a blow to the knee that comes through the knee from the lateral to the medial side, or to twisting injuries of the knee. Valgus stress testing of the knee at 30 degrees (Fig. 50. 12 A) induces abduction of the tibia with medial glide and provides information on stability of the medial collateral ligament. Varus stress testing at 30 degrees ( Fig. 5 3 . 128) induces adduction of the tibia with lateral glide and provides i nformation on stability of the lateral collateral ligament. A palpable click accompanied by pain while performing McMurray meniscal tests ( Fig. 53.13) strongly suggests a meniscal tear. I n addition to ligamentous evaluation, these positions permit assessment for medial and lateral glide somatic dysfunction.
53. Lower Extremities
c
793
The cruciate ligaments run between the tibia and fem ur and are named according to their tibial attachments. The posterior cruciate ligament attaches to the posterior part of the tibia and prevents excessive posterior glide o f the tibia. The anterior cruci ate ligament attaches to the anterior part of the tibia and prevents excessive anterior glide of the tibia at the knee joint. Stability o f the anterior cruciate ligament ( Fig. 53. 1 4A) is checked with an anterior drawer test (knee flexed toward 90 degrees) or, even more specifically, a Lachman test (knee flexed up to 30 degrees) . Stability of the posterior cruciate ligament is checked with a posterior drawer test (Fig. 5 3 . 1 4B) . These maneuvers also perm i t assessment of anterior and posterior glide end-feel for dysfunction. The combination o f torn anterior cruciate and medial col lateral ligaments along with a torn medial meniscus occurs predictably fro m certain traumas featuring valgus stress forces (such as a tackle to the outside of the knee with the knee ex tended fully and the foot fixed) . Because this injury causes signif icant knee instabili ty, historically many clinicians referred to this constellation as the "terrible triad," or "O'Oonaghue's triad." Motion
The major motions of the knee joint are flexion and extension. Because of the irregular shape of the joint surfaces, these two mo tions are combined with some minor involuntary glides, rolling, and rotational motions. Minor motions of the tibial plateau at the knee include: Anterior and posterior glides Medial and lateral glides • Internal rotation with posterolateral glide • External rotation with anteromedial glide • •
FIGURE 53.13. McMurray test for medial and lateral meniscal injury. The knee is fully flexed. One hand (1) palpates the knee at the me dial and lateral joint line. The other hand (2) holds the foot to control internal (a) and external (b) rotation of the foot and tibia. A test for lateral meniscus injury: The foot and tibia are internally rotated (a), the two hands (c) place the tibia into adduction (genu varus), and while holding this positioning, the leg is extended. A test for medial meniscus injury: The foot and tibia are externally rotated (b), the two hands (c) place the tibia into abduction (genu valgus), and while holding this positioning, the leg is extended. (Illustration by W.A. Kuchera.)
Complete extension o f the knee creates a bony lock. Testing of m inor motions of the joint and ligament assessment should therefore be performed with the knee in variable degrees of flex ion. Abduction and adduction of the tibia are passive motions of the knee that cannot be voluntarily created by the patient. A varus stress motion applied in an attempt to create adduction of the tibia produces a lateral glide (with slight internal rotation) . A valgus stress motion inducing abduction of the tibia produces a medial glide (with slight external rotation) of the tibia. Restric tion of glide in one direction suggests somatic dysfunction; laxity in one direction suggests ligamentous sprain or tear. The knee should move into full extension with locking, freely and without restriction. This is tested by grasping the foot o f t h e supine patient w i t h o n e hand a n d raising that lower extrem ity just off the table. The knee is flexed slightly with the other hand. The slightly flexed knee is then released, allowing it to extend. A normal knee drops freely into extension and bounces off the ligaments. Structural injuries, especially medial menis cal tears, may result in inability to extend ful ly, or guarding on extension. The hyperextended knee is referred to as genu recurvatum. A knee with gross l i mitation of flexion and slight limitation of extension is consistent with a capsular pattern of that joint. This palpatory finding, correlated with history and other physical findings, leads to an appropriate differential d iagnosis o f varying
V[J. Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment
794
types of arthritis and synovitis affecti ng the knee. The capsular pattern of the knee ( 1 0) differs significantly from a somatic dys function in which minor motions of the joint are restricted in one aspect of each paired motion and free i n the opposite direction.
Fibular Motion Anterior cruciate ---""'--717' ligament
/'
/'
/'
/'
/'
/'
A
Palpable laxity
Anterior drawer
The proximal tibiofibular joint is a separate synovial joint at the knee ( Fig. 53. 1 5) . While the angulation of the articulation actually permits the minor motions of anterolateral and postero medial glide of the fibular head, clinicians si mply report fibular head glide as anterior or posterior. The fibular head lies in the same horizontal plane as the tibial plateau. The distal tibiofibular articulation is a syndesmosis. This joint allows the fibula to move laterally from the tibia to accommodate the i ncreased width of the talus presented dur i ng dorsiflexion. Restricted dorsi flexion of the ankle warrants exami narion and treatment of this syndesmosis. When the fibular head glides anteriorly, reciprocal motion is i n itiated at the distal fibula (lateral malleolus) , which glides pos teriorly. Posterior fibular head motion is accompan ied by anterior motion at the distal fi bula. External rotation of the tibia and ankle carry the d istal fibula posteriorly and elevate and glide the prox imal fibular head anteriorly. The opposite occurs with internal rotati o n of the tibia and ankle (Fig. 53. 16) . With pronation of the foot, ligamentous attachments glide the d istal talofibular joint posteriorly with reciprocal gl ide of rhe head of the fibula anteriorly. The opposite occurs with supination.
20°-30°
Lachman position
Posterior drawer
B FIGURE 53.14. Structure-function tests of the anterior (A) and poste
rior (B) cruciate ligaments using the Lachman and drawer tests.
Fibular Head Dysfunction Fibular head dysfunction is checked by gliding the fibular head posteriorly (and slightly medial) and anteriorly (and slightly lat eral) . In grasping the fibular head, the physician must take care nor to cause undue pressure on the peroneal (fibular) nerve, which lies directly posterior to this structure. Posterior fibular head somatic dysfunction may itsel f cause symptoms related to entrapment neuropathy or compression of the common peroneal (common fibular) nerve. Fibular head dysfunction often occurs in recurrent ankle sprains and responds well to man ipulative procedures ( 11). In the more common ankle sprain in which the foot tends to supinate, the distal fibula is often found to be anterior and the fibular head is posterior. I n ankle sprains however, the physician must be sure to check both ends of the fibula, because with trauma and lig amentous sprain, the physiologic, reci procal motion described earlier may not occur. Palpation and man i pulative treatment of tibiofibular in terosseous membrane strain may also help in treating patients who have incurred an ankle sprain. This may be achieved with ligamentous balancing techn iques between fibula and tibia while palpating at both ends of the fibula. ANKLE
The ankle has both an upper and lower joint. Together, these j oi nts act as a functional unit ( 12 ). The upper joint is the tibiota lar (talocrural) joint and the lower is the subralar (talocalcaneal)
53. Lower Extremities
( Late ral)
I Or-) I�
Note angulation of the facet
795
Small superior ledge
( Medial) Fibular head
(Anterior)
Tibial tubercle Superior view
Lateral view
joinr. As the patient walks forward and bears weight on the foot, there is visible medial rotation of the tibia with i ncreasi ng dor siflexion at the ankle. The calculated ( 1 3) amollnt of medial rotation of the tibia ( 1 3, 1 4) however is greater than can be at tributed to movement only at the tibiotalar joint. The i ncreased medial rotation coincides with a relative calcaneal eversion about the subtalar axis. As the stance phase of the walking cycle contin ues to the toe-off i nterval, the tibia externally rotates with simul taneous calcaneal i nversion about the subtalar axis. H icks repons that without movement at the subtalar joi n t it would be difficult for a person to balance their body over one lower limb ( 1 5 ) .
Tibiotalar Joint
The tibiotalar (or talocrural joint) i nvolves the talus moving in the ankle mortise. Until the publication of Inman's studies (12, 1 3), the axis of the tibiotalar joint was thought, and described in anatomic textbooks, to be a horizontal axis that corresponded
R e c ip ro c al motions Al
B
A
FIGURE 53. 1 5 . Proximal tibiofibular joint. Note that the fibu lar head and the tibial tuberosity are on the same horizontal plane.
with the articular surfaces of the joi n t. Inman demonstrated that a single empirical ( functional) axis in 80% of his specimens was not horizontal. He described an oblique axis d irected laterally and downward (average 8 degrees) on a coronal plane and laterally and posteriorly (average 6 degrees) on a transverse plane. De spite this knowledge, the major motions of the tibiotalar joint are simply described as dors iflexion and plantar flexion. Mi nor motions occur with each, posterior glide with dorsiflexion and anterior glide with plantar flexion. These minor motions are important when setti ng up manipulative techniques of the fibula. Adduction, toeing-in, and some supination of the foot accom pany plantar flexion . This motion also carries the lateral malleolus anteriorly. Through reciprocal action of the fibula, the proximal fibular head also g lides posteriorly and i n feriorly. The talus glides anteriorly, placi ng the narrow ponion of the talus in the ankle mortise, a less stable position. S ince the tibiotalar axis passes distally to the tip of each malle olus, i ts position may be estimated by placi ng the fi ngertips at the most distal ends of the malleoli. At this pos ition the fingers are over the transverse axis of the tibiotalar j o i n t. Abduction, toei ng-out, and some pronation of the foot ac company dors i flexion. This type of motion also carries the lateral malleolus posteriorly, and through reciprocal action glides the fibular head anteriorly and superiorly. With dorsiflexion, the talus glides posteriorly. Because the talus is structurally wider anteri orly, it fits more securely with the posterior glide component in the ankle mortise (Fig. 5 3 . 1 7) . Dorsiflexion is therefore function ally a more stable posi ti o n because of i ts structure. This stability is the reason taping to treat or prevent ankle sprains usually empha sizes a dorsi flexed position. Ankle sprains, more l ikely to occur when the tibiotalar joi n t is plantar flexed, are d iscussed w i th foot position (supination and pronation) later in this chapter and were classi fied by severity earlier i n the chapter. Recurrent somatic dysfunction of the ankle at the tibiotalar joi n t is more commonly found to prefer plantar flexion with a resistant barrier at the end of dors i flexion. The tibiotalar capsular pattern however is restricted in both directions, but especially resists plantar flexion.
T i bial rot at i ons Reciprocal fibular motion
t i b i al a n d f i bul ar gl i d es
FIGURE 53. 1 6. External rotation of the tibia (e) moves the distal fibula posteriorly (B) and reciprocally is associated with the fibular head mov ing anteriorly (B1). The opposite is true (A, A 1 ) with internal rotation (O) of the lower leg. (Illustration by W.A. Kuchera.)
Subtalar Joint
The subtalar or talocalcaneal joint (Fig. 53. 1 8) has been called the mai n "shock-absorber" joi n t ( 16). It earned this designation
796
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Transverse axis
for rotation
Axis of Rotation
Talus Wider A nteriorly
A nterior G l i d e
Posterior g l i d e o f t h e T a l us
\.
Plantar Flex;on
FIGURE 53 . 1 7 . Ankle major and minor motions. Dorsiflexion with posterior glide is the most stable joint p os it ion because the wedge-shaped talus is engaged. {Illustration by W.A. Kuchera.}
because, in coordination w i th the i ntertarsal j o i n ts, i t determines the distribution o f forces upon the skeleton and soft tissues of the foot. The strong talocalcaneal l igament stabilizes i t. It i s a synovial j o i nt w i th a s ingle oblique axis that declines backward and laterally. The subtalar j o i nt acts like a mitered h i nge so that movement of the calcaneus ptoduces leg totation. Inversion of the calca-
I nterosseous t a localcaneal ligament ( i n s i nu s tarsi)
A FIGURE 53.18. Subtalar joint. Persons with flat feet have a more hor izontal axis and greater foot motion. Those with a more vertical axis have a more rigid, pes cavus foot. A: Posterolateral glide. B: Anterome dial glide. {Illustration by W.A. Kuchera.}
neus produces external rotation of the tibia, and the talus glides posterolaterally over the calcaneus. Eversion of the calcaneus pto duces medial rotation of the tibia and anteromedial glide of rhe talus on the calcaneus. Clinically, rhese mechanics seem to ex plain rhe palpable talocalcaneal motions: posterolateral glide of the talus when the ankle is supinated and the anteromedial glide ar the talocalcaneal j o i n t when the ankle is pronared. I nman ( 1 3) found the average i nclination of rhe subtalar axis from the horizontal plane on the sagittal plane to be 42 degrees (rang i ng from 2 0 to 68 degrees). I f rhe i ncli nation of the axis is 45 degrees, rotati o n of the tibia and calcaneus has a one-to-one relationship. The more horizontal the axis, rhe more rhe calcaneus rotates and the less the leg rotates. This calcaneal rotation is nor very obvious during walking because rhe metatarsals of the fore foot appear to remain stationary. I nman's studies concluded thar approximately half of the population has some l i near displace ment of the talus along the axis with movemenr in the subtalar joint. Pes Planus and Pes Cavus
Persons w i th pes planus (Hat foot) have rhe more horizontal sub talar axis and greater motion in their feet. This explains why rhey break down rheir shoes quickly and prefer to go barefoot. Persons
53. Lower Extremities
797
Plantar Flexion + Adduction
Adduction
=
Eversion
l-
(
Eversion
Supination
+ Dorsiflexion =
+ Abduction
Pronation
Abduction --
with pes cavus (high arch) have a more verrical subtalar axis angle and a more rigid foot.
FIGURE 53. 1 9. Inversion, eversion, supination, and prona tion of the left foot.
toe-off. Pronation during weightbearing stabilizes the ankle and creates eversion of the calcaneus with anterolateral glide of the talocalcaneal joint. Pronation unlocks the foot for surface adap tation and shock absorption during funning.
FOOT
The movement of the foot (or pes) is a composite movement of the talocalcaneal joint of the hind foot and movement of the forefoot about the talonavicular and calcaneocuboid joints. Inversion is that movement in which the heel (calcaneus) faces medially as the inside edge of the foot is lifted. Eversion occurs when the heel faces laterally as the outside edge of the foot is lifted. In the non weightbearing foot, inversion and eversion can be applied to the forefoot as it moves more medially or more laterally, respectively ( Fig. 53. 1 9). In the upper extremity, pronation and supination are move ments of the forearm and muscles of the forearm ptoduced by supinator and pronator muscles. Supination means that the palm is up, such as when holding the hand out waiting for someone to put something into it. In the foot, however, there are no mus cles anatomically labeled as pronators or supinators. An active attempt to supinate the foot results in a combination of adduc tion, plantar Aexion, and inversion of the foot. Likewise, an at tempt to pronate the foot results in abduction, dorsiAexion, and eversIon. Gray's Anatomy has described pronation and supination in the foot as movements of the forefoot not including movement of the calcaneus. This is not true with weightbearing and active motion. With weightbearing, supination of the foot is accom panied by eversion of the calcaneus and posterolateral glide of the talus with respect to the navicular at the talocalcaneal joint. While providing less stability at the ankle, supination locks the foot. This allows stabilization at heel strike and propulsion at
L ATERAL STABILIZING LIGAMENTS AND ANKLE S PR AINS
Ankle sprains are very common in a general practice. The supina tion position, which includes the less stable plantar Aexion posi tion, predisposes the ankle to such injuries. Approximately 80% of all sprains are of the supination type ( 1 7) . These supination sprains traumatize the lateral stabilizing ligaments of the ankle. Additionally, somatic dysfunction occurs during the mechanism of injury, which extends well beyond the local l igamentous stress ( Fig. 5 3 . 20) . In a supination sprain, eversion of the calcaneus and postero lateral glide at the talocalcaneal joint occurs. Abrupt stretch i ng of the lateral and anterior compartments often initiates peroneus (fibularis) or other �ofascial trigger points ( Fig. 53.21) ( 16 ) . The distal fibula may be drawn anteriorly with reciprocal poste rior glide of the fi b ular head. If the anterior talofibular ligament is torn, the distal fibula may move posteriorly with anterior glide of the fibular head. ( Because sprains are traumatically induced, somatic dysfunction may therefore not follow simple biomechan ical predictions.) Somatic dysfunction does not stop here. The tibia often exter nally rotates with an anteromedial glide of the tibial plateau. The femur internally rotates. Myofascial forces (postural forces) then continue upward into the pelvis and spine. Failure to diagnose and treat or rehabilitate beyond the ankle itself increases recur rence rates and prolongs the healing and rehabi l i tation process.
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
798
Classification by severity was discussed earlier in this chapter. A pure i nversion sprain can result in sprain of the calcane ofibular ligament alone. This occurs in basketball players dur i ng rebounding when they land directly on the lateral aspect of the foot (without any plantar Aexion ) . An understanding of the biomechanics of the foot and ankle explains why this is an un common ankle sprain.
Mechanism of supination ( inversion) strain o r sprain Posterior right innomi nate
Sacrum rotates right on a
MEDIAL STABILIZIN G LIGAMENTS
right oblique axis
The deltoid ligament (Fig. 5 3.23) stabilizing the medial side of the ankle is so strong that trauma stressing this structure is more l i kely to fracture a piece of medial malleolus than tear the ligament. Pronation sprains are uncommon. This is due both to the strength of the deltoid ligament and the stability imparted by gliding the wide portion of the talus i n to the tibiotalar joint during dorsiAexion.
Femur rotates internally
FUNCTIONAL ARCHES OF THE FOOT Anteromedial glide o f the tibia
The fWO main functional arches of the foot are the longitudinal arch (with medial and lateral components) and the transverse arch. They are maintained by:
External rotation of the right tibia
Interlocking articular facets of the bones I n terosseous ligaments • Special fascial sheathes • Plantar ligaments • Muscles and muscle tendons •
•
T
=
talus
Posterolateral g l i de of the talus
C
=
c u boid
N
Navicular
Plantar g l ide a n d plantar surface glides laterally
Plantar glide a n d plantar
A so-called "metatarsal arch" is not a functional arch. It refers to the heads of the five metatarsals. Restrictions or al tered rela tionships here are usually secondary to dysfunction of the other arches of the foot ( I 8) .
surface rotates medially
FIGURE 53.20. Somatic dysfunctions and structural stress occurring in the more common supination ankle sprain.
It also increases complaints in distant sites due to the patient's involuntary attempts to compensate for continued dysfunction. Three separate ligaments stabilize the lateral side of the ankle (Fig. 53.22). From anterior to posterior, these are the: Anterior talofibular l igament Calcaneofibular ligament • Posterior talofibular l igament •
•
Because the biomechanical stresses associated with a supina tion strain progress from anterior to posterior, ankle sprains are often named by type accordi ng to the extent of ligamentous i n volvement: Type 1 : Type 2: Type 3:
Involves anterior talofibular ligament only Involves the anterior talofibular and calcaneofibular ligaments Involves all three lateral supporting ligaments.
Longitudinal Arch
The longitudinal arch is divided i nto medial and lateral compo nents. The tibialis posterior muscle supports it. Its tendon at taches to the navicular, first cuneiform, and bases of the second, third, and fourth metatarsals. The bony lateral longitudinal arch is the calcaneus, the cuboid, and the fourth and fifth metatarsals. The bony medial longitudinal arch consists of the talus, nav icular, the three cuneiforms, and the first three metatarsals (Fig. 53 .24) .
Transverse Arch
The transverse arch is composed of the cuboid, the navicular, the three cuneiforms, and the proximal ends of the metatarsals. This arch is supported by the peroneus (fibularis) longus muscle inferiorly and by the tibialis anterior muscle, which attaches to the medial and undersurface of the fi rst cuneiform and proximal fi rst metatarsal (Fig. 5 3 . 2 5 ) .
53. Lower Extremities
799
FIGURE 53.21. Trigger points (TPs) and ligamentous strain are somatic sources of pain in the more common supination ankle sprain. Muscles placed on stress are (in order): peroneus, tibialis anterior, and extensor digitorum longus. Ligaments (lig.) stressed are (in order): anterior talofibular, calcaneofibular, and anterior tibiotalar. T, talus; N, navicular; C. cuboid.
PL ANTAR LIGAMENTS AND F ASCIAE
The plantar aponeurosis (Fig. 53.2 6) exrends from rhe calca neus to the phalanges and encompasses the sesamoid bones un der the great toe. Functional demand causes chronic stress on rhis structure. Irritation caused by either excessive pronation or a high-arched cavus foot may result in plantar fasciitis. With time, calcium is la id down along lines of stress, leading to formation of a calcaneal heel spur. COlTecrion of the underlying biomechanical dysfunction is the treatment of choice. Surgery is rarely necessary. The long plantar ligament runs from the calcaneus to the lateral three metatarsals. It forms a tunnel for the passage of the peroneus longus muscle as that tendon passes under the foot to the
first cuneiform and first metatarsal. The short plantar ligament is, by defin i tion, short. It lies medial to the lateral longitudinal arch and is attached berween the calcaneus and the proximal end of the cuboid. The spring ligament (calcaneonavicular) runs from the susten taculum tali of the calcaneus to the navicular. The spring ligament strengthens the medial longitudinal arch.
TR ANSVERSE TARS AL J OINT
The transverse tarsal joint contains the talonavicular and cal caneocuboid articulations, which are separate joints that act
800
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Anterior talofibular ligament
FIGURE 53.22. Ligamentous stability of the lateral ankle.
together as a functional unit. It has i ts greatest i n fl uence dur ing the stance phase o f the walking cycle because i t responds to eversion or i nversion of the heel. The talonavicular and cal caneocuboid j o ints plus the two small talocalcaneal j o i n ts are collectively called the Chopart joint. When amputating a foot, the surgeon follows the articulations of the Chopart j oi nt. Between the i n tertarsal j o ints and the subtalar joint is a groove called the s inus tarsi. Attached along this groove is the very strong i n terosseous talocalcaneal l igament that provides stability for the subtalar and i n tertarsal j o ints. With i n ternal rotation o f the leg and i nvers ion o f the heel, the l ines of the talonavicular and calcaneocuboid axes coin ci de. This produces enough freedom in the transverse tarsal joint so that the forefoot can evert or i nvert to accommodate for an uneven terrain. When the leg rotates externally and everts the heel on a weight bearing forefoot, the transverse tarsal j o i n t appears to become more rigid. This is because the two axes do not coincide. The forefoot can no longer accommodate for an uneven terrain i n this position. As the heel rises in plantar flexion, the transverse tarsal j o i n t must follow t h e movement about t h e subtalar axis a n d i nvert with the heel to assist the toe-off interval.
METATARS A L AND PHAL A GEAL FINDINGS
Hallux valgus and bunions have a significant hereditary com ponent. Hammer toes are acqui red. Each of these are structural changes with associated biomechanical effects and related somatic dysfunction. Hallus Valgus, Bunions, and Hammer Toes
TARS AL SOM ATIC DYSFUNCTION
Somatic dysfunction of the tarsal bones (cuboid, navicular, andlor cunei forms) is relatively common. In middle- and long-distance runners these bones may even sublux. Somatic dysfunction of the cuboid involves the edge nearest the middle of the foot. This edge glides toward the plantar sur-
T i bionavicular
face of the foot and rotates laterally around its AP axis. Somatic dysfunction of the navicular i nvolves the edge nearest the middle of the foot gli d i ng toward the plantar surface and rotating me dially around its AP axis ( Fig. 53.27) . Cuneiform somatic dys function is usually mani fested by the second cuneiform gliding directly plantarward. Somatic dysfunction of these tarsal bones can be diagnosed by the combination of tenderness and i ncreased tissue tension over the plantar surface of each of these bones. Osteopathic manipu lative treatment (OMT) is effective, although some patients find orthotics to modi fy predisposing biomechanical factors useful as well. There are five metatarsophalangeal j o ints. As the forefoot in verts with plantar flexion, the body weight is transferred to these articulations for push-off. Foot structure provides two functional axes for push-off: an oblique axis that passes through the heads of the second through fi fth metatarsals, and a transverse axis that passes through the heads of the fi rst and second metatarsals. Structurally, a Morton foot is characterized by a short first metatarsal that is not designed to accept the normal weightbear i n g function i nvolved i n the push-off portion of gait. Callus forms under the second and third metatarsal heads as they assume the weightbearing function. I ncreased functional de mand remodels bone. This results in thickeni ng of the second metatarsal; the thickening is evident on x-ray films. Treatment consists of orthotics to modify the structure-function relation ships (Fig. 53 .28) and OMT to permit realignment.
T i biocalcaneal
Hallux valgus is a structural deformity resulting from contracture of various periarticular structures of the first metatarsophalangeal joint. It is progressive. Bun ion protrusion is accentuated by varus deviation of the first metatarsal. Muscle imbalance aggravates symptoms, but surgical i ntervention of the structure may be required for symptomatic
Deltoid l igame nt :
Selective tension used
deep portion
to elicit pain originating
P osteri o r
ti bi o talar
FIGURE 53.23. Deltoid ligament.
in the deltoid l igament
53. Lower Extrem ities
801
Tendon of peroneus brevis Ten don of peroneus
lo ngus
2
FIGURE 53.24. Supports of the longitudinal arch of the foot. I, plantar aponeurosis, abductor dig iti minimi, and flexor digitorum brevis IV and V; 2, long plantar ligament; 3, short plantar liga ment; P, phalanges. (From Hamilton JJ, Ziemer LK. Functional anatomy of the human ankle and foot. In: AAOS Symposium on Foot and Ankle. St Louis, MO: CV Mosby; 1 983:1 3.)
3
relief. Counterstrain OMT to a tender point on the medial aspect of the great toe often provides symptomatic relief. Hammer toes are often functional and may be associated with myofascial trigger points in the dorsal i nterossei. Deformation may disappear after treatment of this somatic dysfunction ( 1 9) . Somatic Dysfunction
relax. The joint is then slowly returned to a neutral position and rechecked for motion.
NEUROMUSCULAR STRUCTURES AND F UNCTION Neurologic Examination
Somatic dysfunction of the tarsometatarsal, metatarsophalangeal, and interphalangeal joints involves their minor motions: Plantar or dorsal glide Internal or external rotation • Lateral or medial glide
•
•
It also involves compression or, less commonly, traction. Indirect stacking OMTs are especially helpful in jammed toes. A stacking technique is one where the physician moves a joint in the di rection of preference in all of i ts planes, s tacking one motion upon the other. Compression or traction is then applied to that combined position. The technique may require holding that position of ease for 90 seconds or until the joint tensions
T endon of
T endon of tibialis posterior
Tendon of
A tradi tional neurologi c examination to rule out associated neu rologic d isease or a structural problem affecting the nervous sys tem is a part of the lower extremity work-up. This should in clude Achilles and patellar deep tendon reflexes, assessment for ankle clonus, straight-leg raising assessment, and evaluation of lower extremi ty muscle tone, strength, flexibi l ity, and coordina tion. Evaluation of sensation may be indicated as wel l . Upper motor neuron d isorders are characterized b y hyper reflexia, often with pathologic reflexes such as ankle clonus or Babinski upgoing toe reflex. Lower extremity muscles may demonstrate spasticity or rigidity. Lower motor neuron disorders are generally characterized by hyporeflexia accompanying muscle weakness and/or flaccidity. Dermatomal patterns of pain and/or dysesthesia associated w i th radicular (nerve root) problems in the lower extremities follow general patterns as depicted in Fig. 53.29. (Depending on the location of the lower motor neuron problem, the pattern may be that of a plexopathy, a neuropathy, or a peripheral neuropathy instead of a radiculopathy.) In any case, review of the l umbar and pelvic regions is necessary to thoroughly understand neuromus cular problems affecting the lower extremities.
Radiculopathy Oblique head of adductor hallicis FIGURE 53.25. Supports of the transverse arch of the foot. Stippled tube represents tendon of tibialis posterior; black areas represent oblique head of adductor hallucis. (From Hamilton JJ, Ziemer LK. Func tional anatomy of the human ankle and foot. In: AAOS Symposium on Foot and Ankle. St Louis, MO: CV Mosby; 1 983: 1 3, with permission.)
Radiculopathy may have as i ts cause, for example, a herniated nucleus pulposus, osteoarthritic spur, advanced spondylolisthe sis, or mass lesion. Regardless of the cause, there are relatively predictable structural and functional effects to be evaluated in the lower extremities. History and physical findings w i ll uncover patterns of lower extremity sensory changes, pain, and reflex
802
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Spring l i gament (calcaneonavicu l ar)
Tunnel for tendon of peroneus longus muscle
Long plant a r ligament Plantar aponeurosis
FIGURE 53.26. Plantar ligaments supporting the arches of the foot.
Tendon of tibialis posterior Tendon of peroneus longus
Oblique head of adductor hallucis
Phalanges
cuneiform glide in somatic dysfunction
Talus
--fi'------ Talar articular
Direction of glide of the cuboid and navicular bones in somatic dysfunction
surface of the tibia
-J.,--.j'--- Calcaneus FIGURE 53.27. Navicular, cuboid, and cuneiform somatic dysfunction.
53. Lower Extremities
2nd Digit Longer
- - - -
I
/
I
I
/
/
"'
I riemove this
Part
803
\
\ \
2nd Metatarsal Thickens Sesamoid Bones Displaced Posteriorly
Reg ular
1 st Metetarsal Short
Shoe I nsert
Hypermobile Joint
Felt S upport
FIGURE 53.28. Orthotic used for Morton foot to modify structure-function relationships. Toe portion of the sole insert is removed so support is under only the first metatarsal head. Lateral side of the support must not extend under second metatarsal head. Insert should reach to the distal end of the first metatarsal.
changes as well as muscle weakness, atrophy, predisposition to trigger points, and imbalance. The diagnosis of lumbar or up per sacral radiculopathies by electromyography focuses on the discovery of fibrillation potentials i n patterns of lower extrem i ty muscles sharing a common involved nerve roor. L4 radiculopathy is suspected when there is reduction of the patellar deep tendon reflex, dysesthesia in the L4 distribution, and
patterns of weakness, cramping, and/or trigger points in those muscles i nnervated by the L4 nerve roOt, such as the quadriceps and tibialis anterior. Often this patient will complain of a knee that gives way or difficulty cli mbing stairs. L5 radiculopathy has no abnormal deep tendon reflex; it is suspected when there is dysesthesia in the L5 distribution and patterns of weakness, cramping, and/or trigger points in the glu teus medius and ankle dorsi flexors, such as tibiali s anterior, ex tensor hallucis, and extensor digitorum brevis. This patient may often complain of tripping over carpets or "small cracks in the sidewalk" because of a foot drop. S I radiculopathy is suspected with reduction of the Ach i lles deep tendon reflex, dysesthesia in the S 1 distribution, and pat terns of weakness, cramping, and/or trigger poin ts of i ntri nsic foot m uscles, the gastrocnemius-soleus complex, and the buttock/ gluteal m uscles. This is the most common radiculopathy, often resulting from a herniated disc between L5 and S 1 . Referred Pain
Pai n and dysesthesia are not l i m i ted to a nerve root or dermatomal pattern . Pain patterns referred from the facet joints of the lumbar spine overlap myofascial trigger point pain arising fro m the fol lowing muscles ( 1 9) : Multifidi Quadratus lumborum • Glutei • P ir i formis • Obturator i n ternus • •
FIGURE 53.29. Dermatomal or radicular (nerve root) patterns. (illus tration by W.A. Kuchera.)
804
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
Myotomal referral often results in a charley horse or a crampy sensation. A myotomal distribution is associated with the location of muscles that share the neural (root, plexus, or peripheral nerve) in nervation. Muscle i nnervations are reviewed in Tables 53.2 and 5 3 . 3 . Sclerotomal referral is a deep, achy sensation that is toothache like in quali ty. Sclerotomal (bony/ligamentous) distribution has also been mapped out (Fig. 53.30) but is often overlooked. Pa tients may dismiss it as lower extremity arthritic pai n . Notice that different aspects of the knee and the hip j o i nts share the L3 and L4 sclerotomes. Referred pain in general is reproducible. An understanding of the patterns associated with each referral improves patient diag nosis and treatment design. Failure to appreciate nondermatomal patterns may lead a practitioner to i ncorrectly consider a patient with legitimate symptoms a mali ngerer.
Referral from Lumbopelvic Structures
In addi tion to lumbar nerve roots and sclerotomes discussed ear lier, a number of other l u m bopelvic region myofascial, arthro dial, ligamentous, and visceral structures commonly refer pain to the inguinal area and/or hip. Somatic examples i nclude iliolum bar and posterior sacroiliac ligaments (20) , quadratus lumborum muscle (2 1 ) , and lumbar zygapophysial j o i n ts (22) . Referral from visceral structures in this region are also often seen, as i n a urinary tract stone passing down the ureter radiating into the ipsilateral flank and the in ner thigh regio n (23) .
Referral Originating in the
(Fig. 5 3.31) ( 2 5 ) . When stressed, the i liopsoas, piriformis, ham strings, gastrocnemius-soleus complex, adductor magnus, rectus femoris, and tensor fasciae latae all tend to tighten while the vasti (especially the vastus medialis), glutei, peroneus, and tibialis an terior all tend to be i nhibited and weak (26). An understanding o f the myotatic unit, muscle agonists and antagonists, and pat terns of use is necessary for efficient diagnostic and therapeutic approaches in the neuromuscular system.
MUSCLES OF THE HIP
Muscles of the hip are generally large and powerful. They can be grouped according to their functional role (Table 53.2). Dysfunc tion leads to a n umber of patient symptoms responding readily to a variety of OMTs, especially soft tissue, muscle energy, and counterstrain activating forces. Myofascial trigger points in these muscles respond to these techniques as well as adj unctive use of the following: Vapocoolant spray and stretch Injection of procaine • Dry needling •
•
O ften the joints straddled between muscle origin and insertion need treatment. Alternatively, viscerosomatic referral should be entertained as a primary source of secondary muscle dysfunction , particularly when the h istorical review of systems is suggestive of the possibility. Because crosstalk between the viscera and the soma tends to take place in the spinal cord, innervation of each muscle becomes clin ically relevant for more than j ust the recognition of nerve root pathophysiology.
Lower Extremities
Structures in the hip region often refer pain to the knee. For ex ample, an adolescent male with knee pain and no sign of knee dysfunction or structural abnormality should have a hip x-ray to rule out a slipped capital epiphysis or other hip j o i n t patho logic conditions. Lower extremity myofascial trigger points create predictable patterns of pain and dysfunction.
Lower Extremity Myofascial Trigger Points
Myofascial trigger points as described by Travell and Simons ( 1 9,24) also have predictable referral patterns not associated with dermatomes. See Fig. 66. 1 for a synopsis of representative trig ger poi n ts associated with the lower extremities. By defin ition, these points are a form of somatic dysfunction (see Chapter 66). They represent impaired or altered function of myofascial tis sues with effects also in related neural, vascular, and lymphatic elements. Asymmetric postural stress creates recurrent predictable pat terns of lower extrem i ty muscle somatic dysfunction. Neuro muscular imbalance and/or myofascial trigger points characterize this. In neuromuscular i mbalance, s tressed postural (antigrav ity) muscles exhibit i ncreased irritability (short and tight) , while their antagonists demonstrate in hibition (weak and atrophic)
NERVE SUP PLY IN THE BUTTOCK AND THIGH
In the buttock and/or thigh, nerve supply may be affected func tionally by the piriformis muscle. Biochemical irritation of the sciatic nerve is possible with irritation of the piriformis because of the close anatomic relationship between the two (Fig. 53.32). In approximately 1 0% of the U.S. population, the peroneal por tion of the sciatic nerve actually passes through the piriformis muscle; this occurs in one-th ird of patients of Asian descent. In the presence of this anatom ic variation, peroneal entrapment is likely. Because of this variant anatomy, therapeutic injections (especially those con taining a steroid) into the piriformis muscle should be approached with caution to avoid permanent nerve lI1Jury. The sciatic nerve divides into a posterior tibial and common peroneal (common fi bular) nerve in the thigh. The obturator and femoral nerves i n nervate the other thigh muscles. The gluteal nerves innervate the gluteal muscles.
MUSCLES OF THE THIGH AND LE G
Muscles of the thigh and leg include those affecting knee, ankle, and foot function (Table 53.3 and Fig. 53.33): Several thigh
53. Lower Extremities
805
TABLE 53.2. FUNCTI ONAL MUSCLE CHART FOR THE HIP Muscle Innervation Hip flexors Iliopsoas (L2-4)
Rectus femoris (L2-4; femoral n.)
Pectineus Also sartorius thigh adductors, t. fascia latae Hip extensors Gluteus maximum (LS-S2; superior gluteal)
Hamstrings (LS-S2; sciatic n.)
Adductor magnus (ischiocondylar portion : L4-S 1 sciatic n.) Hip abductors Gluteus medius (L4-S 1 ; interior gluteal)
Functional Anatomic Features
Dysfunction
Strongest flexor of thigh Postural significance: extension of spine while standing (lumbar lordosis); flexion of spine with bending Psoas attaches to T 1 2-LS vertebral bodies and associated intervertebral discs Psoas crosses lumbar intervertebral, lumbosacral, sacroiliac, and hip joints Crosses both hip and knee Primarily an extender of the knee; only causes hip flexion when knee extended Flexion and adduction of thigh at hip Designed for power not speed Contribute to hip flexion
Psoas posturing and psoas syndrome Activated by sit-ups or bending over a low table Aggravated by weightbearing; relief recumbent with knees bent Referral back and anterior groin Positive Thomas test = iliopsoas contracture Usually develops spasm when stressed Referral patellar and deep knee pain Usually develops spasm when stressed
Type I (slow twitch) muscle fibers suited for continuous use Location and size unique, providing anatomic basis for upright posture Most powerful extensor
Decreases hip flexion Restlessness, pain on sitting or walking uphill Antalgic gait Referral to buttock Usually becomes inhibited when stressed Decreased hip flexion with straight leg raising test
Restrains hip flexion produced by body weight during stance phase of walking; extension during walking
Only portion of adductor magnus assisting flexion and then only when the femur is flexed more than 70° Stabilizes pelvis during single limb stance (prevents nonstance in nominate from falling inferior-negative Trendelenburg test)
Gluteus minimus (L4-S 1 )
Stabilizes pelvis during single limb stance (prevents nonstance innominate from falling inferior-negative Trendelenburg test)
Piriformis (S 1 -2)
Acts as abductor when thigh flexed
Referral deep-seated groin ache
Pain sitting and walking; disturbs sleep Perpetuated by chair pressure under thighs Referral posterior thigh Usually develops spasm when stressed Referral to inner thigh Usually develops spasm when stressed
TPs aggravated by walking, slouching i n chair, o r lying on back Referral to posterior iliac crest, sacroiliac joint, sacrum, and minor to buttock Positive Trendelenburg test = weakness in hip abductors Usually becomes inhibited when stressed Travell calls TPs in this muscle "pseudosciatica" Characteristic pain arising from chair or walking; can be constant and excruciating M istaken for LS or S 1 radiculopathy (but may coexist) Antalgic gait Referral buttock, lateral and posterior thigh Positive Trendelenburg test = weakness in hip abductors Usually becomes inhibited when stressed May entrap peroneal portion of sciatic nerve or cause sciatica Perpetuated by sacroiliac somatic dysfunction or irritation (especially sacral shear) and sitting on billfold Associated with pelvic floor dysfunction, dyspareunia, prostatodynia Usually develops spasm when stressed (continued)
806
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
TABLE 53. 2 .
(continued)
Muscle Innervation
Functional Anatomic Featu res
Dysfunction
Also to lesser extent: sartorius, gluteus maximus, iliopsoas Hip adductors Adductor longus, brevis and magnus (L2-4; obturator n.) External rotators of the hip (LS-S2) Obturator internus (LS-S2)
Internal rotators of the hip Gluteus medius and minimus (L4-S 1 ) Also from: gemelli and quadratus femoris (L4-S 1 ). Less from piriformis
Early in swing phase, these muscles pull limb toward midline
Referral distal to inguinal ligament, inner thigh, and upper medial knee Usually develops spasm when stressed
When the thigh is extended, cause external rotation; when flexed, cause abduction
Responsible for pelvic floor symptoms (fullness in rectum) Referral to anococcygeal region (some to posterior thigh)
(See Hip Abductors above) Piriformis only involved with external rotation when the femor is extended
(See Hip Abductors above)
TPs, trigger points.
m uscles have already been described i n relation to their effect at the hip. These include the: Hamstri ngs Rectus femoris • Tensor fasciae latae
• •
The hamstrings and the short head of the biceps femoris are the chief flexors of the knee. The hamstri ngs, by definition m uscles that attach to the ischial tuberosity, attach to the leg below the knee and are supplied by the tibial division of the sciatic nerve (2 7). The head of the biceps femoris crosses the knee and is innervated by the peroneal portion of the sciatic nerve. Both heads o f the biceps femoris also cause external rota tion of the knee while the remaining hamstrings cause i nternal rotation.
NERVE S U P PLY IN THE THIGH, LE G, AND FOOT
Nerve supply in the thigh, leg, and foot is derived from the pos terior tibial and common peroneal (common fibular) nerves (Fig. 53.34). As noted, a vulnerable s i te for entrapment or trauma ex ists as the common peroneal nerve passes behind the fibular head. The tibial nerve supplies the posterior compartment of the leg and the muscles of the foot. The deep peroneal nerve supplies the anterior compartment of the leg with sensation to the webbing between the fi rst and second toes. The superficial peroneal nerve supplies the lateral compartment of the leg as well as the skin on the anterolateral side o f the leg and the dorsum o f the foot.
VASCULAR AND LYM PH ATIC STRUCTURES AND F UNCTION
Enhancing homeostasis associated with vascular and lymphatic elements is a sign ificant portion ofan i ntegrated osteopathic treat ment regimen in the lower extremities. By definition, removal of
somatic dysfunction is linked to its inAuence on related neural, vascular, and lymphatic elements (Fig. 5 3 . 3 5 ) . Treatment of somatic dysfunction i s postulated t o improve blood delivery by reducing hypersympathetic activity. This is i m portant for nutrition of the tissues in the lower extremities. It would also benefit delivering medications such as nonsteroidal antiinflam matory drugs to target tissues in the lower extremities where pharmacologic effectiveness is proportionate to tissue or synovial concentration of the drug. Cell bodies for the sympa thetic nerve supply of the lower extremities are found at the level of T l l -L2 . Opening fascial pathways and eliminating myofascial trigger points can improve venous and lymphatic drainage of the ex tremities. Drainage can be enhanced using a variety of lymphatic pump techniques. This is especially true of the pedal pump tech niques described in other chapters. Lym phaticovenous rerurn is also enhanced by improving the mechani cal lymphatic pumping produced by muscular contraction, and maximal pressure gradi ents between the thorax and abdomen produced by improving respiratory efficacy.
Hip
The inferior margin of the acetabulum is incomplete, forming an acetabular notch through which the hip joint receives its blood vessels (Fig. 5 3.36) . These vessels are easily disrupted by a femoral neck fracture, which creates the possibility of delayed healing or nonunion. The femoral artery is the major vessel supplying the lower extremities. Easily located in the femoral triangle, this artery is bounded by the sartorius and adductor muscles and the inguinal ligament. The m nemonic NAV EL provides a reminder of the order, from lateral to medial, of the structures in the femoral triangle: Nerve Artery
53. Lower Extremities
807
TABLE 53.3. FUNCTIONAL MUSCLE CHART FOR THE THIGH AND LEG Muscle In nervation Knee flexors Biceps femoris (L5-S2; sciatic n. long head tibial portion; short head = peroneal portion)
Semimembranosus and semitendinosus (L5-S2; sciatic n. tibial portion)
Also popliteus and gastrocnemius
Knee extensors Quadriceps ( L2-4; femoral n.)
Knee external rotator Biceps femoris Knee internal rotators Popliteus (L4-S 1 ; tibial n.)
Semimembranosus and semitendinosus Also sartorius (L2-3; femoral nerve) and gracilis (L2-3; obturator n.)
=
Functional Anatomic Featu res
Dysfunction
Long head crosses both hip and knee Short head crosses only knee Both heads plus semimembranosus establish a tripartite anchor on the fibular head Short head active in knee flexion for toe clearance during walking Active contraction also induces some external rotation of the knee Also hip extensors H amstrings are not consistently active for knee flexion during walking (passive knee motion when the hip is flexed is more common) Active contraction also induces some internal rotation of the knee
Pain referral is distalward from trigger points (TPs) in the posterior thigh to the back of the knee or to the region of the fibular head Often wakes patient at night
Pain referral proximally to lower buttock; aggravated by walking often causing limp TPs often misdiagnosed as "sciatica" or "osteoarthr itis of the knee" or "growing pains'" TPs remaining post-op often cause of "postlaminectomy syndrome" b Tightness in the hamstrings is associated with inhibition and laxity of the gluteal muscles
Contribute somewhat to knee flexion Popliteus initiates flexion from fully extended position before hamstrings act Rectus femoris crosses both hip and knee joints (proximal attachment to anterior posterior iliac spine [ASIS]); also a hip flexor Three vasti cross only knee joint All four tendons unite into patellar tendon with patel la anchored to tibial tuberosity by patellar ligament Q-angle is the quadriceps angle measured from ASIS to midpatella to tibial tuberosity (Fig. 53.5)
Thigh and knee pain and weakness of knee extension especially going up stairs Anterior knee pain is referred from vastus medialis and rectus femoris; may interrupt sleep Posterior knee pain and pain anywhere along the lateral thigh to the iliac crest are referred from vastus lateralis TPs in v. medialis cause "buckling knee" and may cause patient to fall TPs in v. lateralis may restrict motion of the patella; pain with walking TPs in v. intermedius have difficulty straightening knee after prolonged sitting Imbalance in quadriceps with one another or with the hamstrings predispose to chondromalacia patellae as does an increased Q-angle Direct trauma to the quadriceps should be observed for myositis ossificans Usually becomes inhibited when stressed
Also a knee flexor
See description with Knee Flexors above
Unlocks knee at the start of weight bearing by "externally rotating the thigh on the fixed tibia"; internally rotates tibia when thigh is fixed Prevents posterior glide of tibia relative to femur while crouching
Pain behind the knee when crouching, walking down stairs, or running downhill Aggravated by braking forward motions during twists (e.g., skiing), high heels by excessive foot pronation, d and by training on uneven ground Mimics symptoms of Baker cyst but no associated swelling in the region See description under Knee Flexors above Pain from the sartorius in the anterior thigh is superficial and described as tingling or sharp; may exhibit symptoms of meralgia paresthetica (entrapment of lateral femoral cutaneous nerve)" Pain from gracilis is a hot stinging, superficial pain in the medial thigh; it may be relieved by walking
Also knee flexors (primary) Sartorius is the longest muscle in the body crossing both hip and knee; it is a hip flexor and knee internal rotator Gracilis is the second longest muscle in the body crossing hip and knee
(continued)
TABLE 53.3.
(continued)
Muscle Innervation Ankle dorsiflexors Tibialis anterior (L4-S 1 ; deep peroneal n.)
Functional Anatomic Features
An anterior compartment muscle A dorsiflexor at the taloitibial joint Also supinates foot at the talocalcaneal and transverse tarsal joints
Extensor digitorium longus (L4-S 1 ; deep peroneal n.)
Also everts the foot balancing inversion of tibialis anterior Helps prevent posterior postural sway
Peroneus tertitus (L5-S 1; deep peroneal n.)
An anterior compartment muscle A dorsiflexor at the talotibial joint Also everts foot Tendon passes in front of lateral malleolus to insert on proximal 5th metatarsal
Ankle plantar flexors Gastrocnemius (L5-S2; posterior tibial n.)
Soleus (S 1 -2; tibial n.)
Peroneus longus and brevis (L4-S 1 ; superficial peroneal n.)
Gastrocnemius-soleus complex referred to as triceps surae; constitutes close functional unit; shares Achilles tendon attachment to calcaneus
Gastrocnemius-soleus complex constitutes close functional unit; shares Achilles attachment to calcaneus Soleus function during gait is to add to knee and ankle stability Acts as " second heart"g in moving venous and lymphatic fluid from lower extremity (e.g., fainting with military "attention" position) Also aids in inversion of foot and extension of knee Lateral compartment muscles Plantar flex and pronate foot p. longus attaches to fibular head and to upper 2/3 of lateral fibula, crosses behind the lateral malleolus over the cuboid, and divides to attach to the 1 st cuneiform and the base of the 1 st metatarsal p. brevis travels with p. longus but inserts on the lateral aspect of the 5th metatarsal
Dysfunction
Pain and tenderness referred into great toe and anteromedial ankle Weakness leads to varying degrees of foot drop; patients may complain of tripping over carpets, dragging foot, or "foot slap " Weakness in muscle may be caused by L5 radiculopathy, peroneal mononeuropathy, the habit of crossing the legs at the knee, or posterior fibular head somatic dysfunction Pain pattern over dorsum of foot and ankle Dysfunction often results in foot slap after heel strike TPs may entrap fibers of the deep peroneal nerve Muscle imbalance may lead to formation of hammer toes Pain referred along anterolateral ankle and sometimes to lateral heel; failure to identify and treat TPs post-ankle sprain can prolong rehabilitation process Weakness in ankle dorsiflexion predisposing to ankle instability and repeat sprains May be mistaken for ankle arthritis f Weakness in muscle may be caused by L5 radiculopathy, peroneal mononeuropathy, the habit of crossing the legs at the knee, posterior fibular head somatic dysfunction or prolonged immobilization (as in an ankle cast) Dysfunction often results in nocturnal leg cramps TP pain may be referred to upper posterior calf and/or to instep "Tennis leg" is a partial tearing of the gastrocnemius; symptoms include a sudden intense calf pain, as if kicked, followed by swelling and local tenderness; failure to recognize may lead to a posterior compartment syndrome Heel pain with TPs in this muscle and/or may refer proximally to sacroiliac joint or even temporomandibular joint May restrict dorsiflexion at ankle; pain severe walking up hill or stairs May be cause of growing pains in children Soleus TPs easily mistaken for Baker cyst, thrombophlebitis, and/or Achilles tendinitis
Pain and tenderness projected to lateral malleolus and some of lateral leg TPs initiated by inversion twisting of ankle or prolonged immobilization in ankle cast Predispose to weak ankles and recurrent sprains May have deep peroneal nerve entrapment with some foot drop p. longus and brevis aggravated by Morton foot structure Pain easily mistaken for arthritis in ankle h TPs in p. longus can entrap the common peroneal nerve and weaken both anterior and lateral compartment muscles; numbness often noted in web of great toe (continued)
53. L o wer Extremities
TABLE 53.3.
(continued)
Muscle Innervation Foot supinators Tibialis anterior (L5-S 1 ; deep peroneal n.)
Foot pronators Peroneal muscles (L5- 5 1 ; deep peroneal n.)
Functional Anatomic Featu res
Pain and tenderness referred into great toe and anteromedial ankle Weakness leads to varying degrees of foot drop; patients may complain of tripping over carpets, dragging foot, or " foot slap" Weakness in muscle may be caused by L5 radiculopathy, peroneal mononeuropathy, the habit of crossing the legs at the knee, or posterior fibular head somatic dysfunction
Lateral compartment muscles are p. longus and brevis; p. tertius is an anterior compartment muscle Pronate the foot (eversion and abduction) p. tertius also dorsiflexes at the talotibial joint; p. brevis and longus also plantar flex Tendon passes in front of lateral malleolus to insert on proximal 5th metatarsal
Pain referred along lateral ankle and foot; sometimes to lateral heel; failure to identify and treat TPs post-ankle sprain can prolong rehabilitation process Weakness in ankle dorsiflexion predisposing to ankle instability and repeat sprains May be mistaken for ankle arthritisi Weakness in muscle may be caused by L5 radiculopathy, peroneal mononeuropathy, the habit of crossing the legs at the knee, posterior fibular head somatic dysfunction, or prolonged immobilization (as in an ankle cast) TP pain referred to sole of foot; worse with walking TP perpetuation by Morton foot, running on uneven ground, or barefoot in the sand TP pain referred to plantar surface of great toe and first metatarsal head TP perpetuation by Morton foot, running on uneven ground, or barefoot in the sand Intolerably sore feet, limited walking range, limp
Flexor hallucis longus (L5-S2; tibial n.)
Also intrinsic foot muscles Foot and/or toe extensors Extensor digitorum longus (L4-S 1 ; deep peroneal n.) Extensor hallucis longus (L4-S 1 ; deep peroneal n.)
Dysfunction
An anterior compartment muscle Supinates foot at talocalcaneal and transverse tarsal joints Also dorsiflexes at the talotibial joint
Foot and/or toe flexors Flexor digitorum longus (L5-S 1 ; tibial n.)
(See above under Ankle Dorsiflexors) Dysfunction makes foot less adaptable to the ground while walking TP referred pain to dorsum of foot at the base of the great toe TPs may be perpetuated by L4-5 radiculopathy; often follow anterior compartment syndrome, prolonged jogging, or dorsiflexed ankle position during sleep Intolerably sore feet, limited walking range, limp
Also intrinsic foot muscles
'Travel l JG, S imons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol bTr avell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol
'Travell
809
JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol
dBrody D M . Running Inj ur ies. c/BA Clin Symp. 1 980;32(4): 1 5- 1 6. "Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol ' Travell JG, Simons DG . Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol
II. II. II.
Bal timo re, M D : Wil liams Baltimore, M D : Williams
Bal timore, MD: W i l liams
& Wilkins; 1 992:324. & Wilkins; 1 992:324. & Wilkins; 1 992:250.
II. Bal timore, M D : Wi l l iams & Wilkins; 1 992:229-232. II. Bal timore, MD: W i l liams & Wilkins; 1 992:377. 9Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol II. Bal timore, MD: Wil liams & Wilkins; 1 992:427. hReynolds MD, Myofascial trigger point syndromes in the pr a ctice of rhe umatology. Arch Phys Med Rehabil. 1 98 1 ;62: 1 1 1-1 14. i Tr avel l JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol II. Bal timore, MD: Williams & Wilkins; 1 992:377.
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
C5
82 -....<....l .-.:-
FIGURE 53.30. Sclerotomal pain patterns.
Vein Em pty space Lymphatics Evidence of terminal lymphatic drainage dysfunction for the lower extremities may be palpated j ust inferior to the inguinal ligament. Dysfunctional drai nage results in tissues that are tight, tender, and/or ticklish in this region.
brane thickens, and diffusion is i mpeded while oxygen demands in that joint i ncrease (2 8) . Lower Leg
The lower leg is divided into three compartments ( Fig. 53.37): Anterior osseofibrous compartment Lateral osseo fibrous compartment • Two posterior osseofibrous compartments-deep and super ficial •
•
Knee
The vascular supply is very poor to the meniscI Il1 the knees (especially the central section) and to synovial joint tissues i n general. T n large part, nutrition t o the joints depends o n good blood Aow to the region ( Fig. 5 3 . 3 5 ) and then diffusion i nto the synovial Auids. Metabolic waste products out of the arthrodial tissues l i kewise diffuse i n to the synovial Auid. I n term inen t non-weigh tbearing compression-decompression of the joints (joint pump) provides for Auid movement and may aid in the exchange of nutrients i n to and waste products our ohhe arthrodial structu res. In rheumatoid arthritis the synovial mem-
Clin ically, a compartment syndrome can arise from trauma or vigorous overuse, leading to a rise in intracompartmental pres sure. This in turn compromises the circulation within that com partment, i ncluding venous return. Recurrent mild compartment symptoms are managed with ice and OMT. Ice decreases pain and metabolic demand after activity. OMT also decreases pain and improves venous and lym phatic return. Management of co-existing trigger points is also helpful but not with i njections; they would increase pressure in an
53. Lower Extremities
TIght, Spastic Muscles
Erector spinae mass
Weak, Pseudoparetic Muscles
Quadratus lumborum Rectus .,.------+-ffi abdominis
Quadriceps (except._______ft-t rectus femoris) Peroneus
Piriformis
Quadratus lumborum
Internal and external obliques
Iliolumbar ligaments Posterior sacroiliac ligaments
Gluteus ____+--#JI,I;W medius
Gluteus medius
""-1,1------ Hamstrings
_ _ _ _
Tibialis _______-\-1 anterior
TIght, spastic muscles
Weak, Pseudoparetic Muscles
.\itr.a\\---- Psoas
Glutei -=:::::::=----\;:W�
81 1
Sacrotuberous ligament Tensor fasciae latae
Gastrocnemius
IfH------ and soleus
Iliotibial tract of fascia lata Adductors Gastrocnemius and soleus
FIGURE 53.31. Muscle imbalance caused by biomechanical stressors.
Piriformis' myofascial point (MFP)
I nferolateral angles of sacrum
�-I--- G reater trochanter
.,...-..... -
, , , , , , I
Sciatic nerve exits 1 " below MFP
OMT: Counterstrain position
Anatomic variations
Indirect OMT duplicates muscle action, thus external rotation and abduction
Majority
FIGURE 53.32. Piriformis structure-function relationsh ips.
1 0-1 2%
(up to 1 /3 of Asians)
<1%
VII Osteopathic Considerations in Palpatory Diagnosis and ManipuLative Treatment
812
Psoas min or Iliacus
Psoas mal o r
Anterior superior Iliac spine
I l ia c u s
Psoas ma l or
Tensor fasciae latae
Fascia lata
Tensor fasciae latae
Rectus femoris ( c u t)
Pu b i c tubercle
Gluteus minimus
Adductor longu: (cut)
Pectineus
Adductor brevIs
Sartorius
Adductors
(7)
(1)
Pectineus (cut)
Adductor longus
Rectus femoris (2)
Adductor longu! (cut)
GraciliS
GraCilis Vast u s I n te rm e d i u s I l iotibial tract Adductor m a g n us
Vastus lateralis (3)
--..;;o;;:,,;;,,�
Vastus me d ia li s
(6)
Vastus lateralis
Sartorius (cut)
--\ �::--;:::--Ti..---
(4)
Patellar ligaments
l''i-H'--T'---- Vastus
medialis
Rectus femoris (cut)
Palella
--,,?
Patellar l igament
(5)
��
_ _
_ _
Sartorius
--+-+-
.-:�:.:.;---
A FIGURE 53.33. Muscles of thigh (A) and leg (8). (From Moore KL. Clinica lly Oriented Anatomy, 3rd ed. Baltimore, MD: Williams & Wilkins; 1 992: 394, 395, 442, 453, with permission.)
M e di a l meniscus
Sartorius
53. Lower Extremities
Semitendinosus
.-r'--- Biceps lemolls
---J;H7":T-+
Semlmembranosus
813
l/i-.i'r.ii':--- Popliteal vein
--,rnni-ii-h
_'-:'--,---- IiIOllb,,' lracl GastrocnemiUS, laleral head Gastrocnemius. medial head Biceps femoriS tendon
Common hbular (peroneal) nerve
--firm _ilr-...,..-;"L...
-- Fibular collateral ligament
Medial Infenor genlcular vessels
--'cHi'ftr
uncovered by retracting fascia
Gastrocnemius
Af,"";i1Ti--- Sole us
_ _ Deep lasc,.
� _
Fibutans (peroneus) longus Gastrocnemius
--...,...,�m
-4i/--- I: xtensor dlgltorum longus SuperfiCIal Ilbular (peroneal) nerve
Ir
/I
---+.lH....
tj � li � II I t I j\ r "", iJ I,-- " .\t.., _ !'tb\[' \�I t I I
\
Flbulans (peroneus) brevIs ___
""*-;r,.
I,
- E xtensor halluclS l o n g u s
.
Flexor dlgltorum longus_ _ _ T,b,.11S pOSlellor _ r h a l l u c l s brevIs
.,
Fibularis (peroneus)
.. " "",",,, """,'
Tendo calcaneus or calcaneal tendon
��+-'>N------l' x ler1Sor dlQllorum brevIs 1101,..A;&J-----l' xle'nsor dlgllorum l o n g u s
\
FIGURE 53.338. (continued )
already tight compartment. Modification of the running surface or the running shoe may also be required to prevent recurrent compartment syndromes.
ANTERIOR COM PARTMENT
The anterior compartment is covered anteriorly by a relatively nonexpansile fascia. Structurally, this creates the potential for de velopment of an anterior compartment syndrome. Bleeding i n to this compartment from a fracture or other trauma creates in creased pressure in this enclosed space. For runners, sometimes muscle swell i ng impairs venous outAow, resulting in a rise in in tracompartmental pressure. If i n tracompartmental pressure be comes great enough, arterial circulation is reduced, and ischemia with potential necrosis of muscle in the compartment can occur. An acute compartment compression is a surgical emergency re quiring fasciotomy. Such a situation is more l i kely to occur in the anterior compartment than in other divisions of the leg. The
acute compartment compression may occur in run ners where symptoms of i ntense pain develop during the run but do not subside afterward. Palpation reveals the entire tibialis anterior m uscle to be hard and tender. Anterior compartment muscles may also exh ibit weakness upon testing. Peripheral pulses are usually present. De creased sensation is often present between the first and second toes as a result of entrapment of the deep peroneal nerve. While primarily a clinical diagnosis, intracompartmental pressure can be measured with a wick catheter ( 1 9) . Because of the location of the pain on the anterolateral side of the leg, recurrent anterior compartment syndrome is also called anterior shin spli nts.
L ATER AL COM PARTMENT
In the lateral compartment syndrome, pain is located diffusely along the lateral aspect of the lower leg. It recurs in runners with
VII. Osteopathic Considerations i n Palpatory Diagnosis and Manip ulative Treatment
814
excessive pronation of the foot or may result from rupture of the peroneus longus muscle.
Tensor fasciae latae Gluteus medius Gluteus minimus
4
5
POSTERIOR COM PARTMENT Gluteus maximus
The posterior compartment syndromes typically refer pain an teromedially. While some reserve the term shin splints only for periostitis along the line of attachment of a repeatedly overloaded muscle ( 1 9) , others include posterior compartment syndrome in the differential diagnosis along wi th stress fractures of the tibia and chronic periostitis (the soleus syndrome) . Posterior com partment syndromes are o ften b i lateral and difficult to manage conservatively.
2 -'--'--
3 ---t--_
}.. '� ( \1
Obt. int. Quad. fem.
Isch. tuber.
Tibial diViSion
Semitend.
Common peroneal division
Biceps (long) Semitend.
}
Bursae and Bursitis
Sciatic n.
Add. mag. Semimemb. I
Biceps (short)
\
�----------
Trochanteric Bursitis
Add. tuber.
Head of fibula
Gastrocnem.
Tibialis ant. FI. dig. long.
\\
Med. mall.
�-----------Abd. hallucis FI. dig. brevis FI. hall. brevis Lumbr. to 2nd digit
Fl. hall. long. - - - - - - - _ .
�
l � Peroneus brevis - --
Peroneus Tib. post. longus
A number of bursae are located aro_und the hip, knee, and ankle. They may swell as a response to direct trauma or stresses placed on the j oints of the lower extremities ( Fig. 53.38). Bursitis is inflammation of a bursa. There is palpable swelling that can be defined and that is sensitive to deep pressure. Pain alone in the region of the bursa often leads to misdiagnosis.
Ext. hall. longus
-
Ext. dig. longus -
All other muscles in the sole Ext. dig brevis
FIGURE 53.34. Nerve supply of the lower extremity arising from the sciatic nerve and its branches.
In the hip region, trochanteric bursitis is a common clinical diag nosis or, in many cases, a misdiagnosis. The subgluteus maximus (trochanteric) bursa lies at the root of the iliotibial tract. Here it separates the greater trochanter of the femur from the converging fibers of the gluteus maxim us and the tensor fasciae latae. The bursa also separates these fibers from the origin of the vastus later alis muscle. Trigger points in any of these muscles can refer pain to this site and are commonly m isdiagnosed as a trochanteric bursitis. This is also the case in quadratus lumborum trigger points (2 1 ) and in the ligamentous pain referral from iliolumbar l igament (20) . True inflammation al1d swelling of the trochanteric bursa (trochanteric bursitis) causes intense pain over the bursal loca tion with radiation into the lateral thigh. Palpation of the bursa j ust below the greater trochanter reveals the swell ing and heat. Pressure here increases the pain. Walking, hip abduction, and i nternally rotating the hip can aggravate the pain. I njection of the bursa with a local anesthetic with or without accompanying steroids quickly and significantly reduces pain. A higher incidence of trochanteric bursitis is found on the long leg side of individuals with unequal leg length (7).
Patellar Bursitis The knee is a common site for trauma to the bursa designed to protect the relatively exposed superficial structures from injury against those underlying them. A large prepatellar bursa separates the patella from the skin anterior to it. Inflam mation of this bursa from long-term kneeling or from other trauma results in a condition known as "housemaid's knee."
53. Lower Extremities
815
To Hypothalamus Substantia G elati nosa Somatic Dysfunction
Afferent Stimuli
Efferent Sympathetic
Vasospasm (and Shunting) --
Facilitated Segment T 2 - 8 U p per Extremities
Spasm
T 1 1 - L 2 Lower E xtremities
Reduced Blood Flow 1.
2.
� ..j,
Reduced D r a i n age
Nutrition
1.
02 Anoxia
2.
t t
FIGURE 53.35. I nfluence of somatic dysfunction on normal vascular and lymphatic elements of the lower extremity. (From Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dys function, 2nd ed. rev. Columbus, OH: Greyden Press; 1 994, with permission.)
F l u id s Proteins
Ant. sup. iliac spine
,
I l iac crest
Ext. lip of iliac crest
Posterior superior iliac spine
Anterior superior
Inguinal lig.
Head of femur
Pubic tubercle
Femoral a. -+---t1�-Tt-
Beginning of
,-+tfflt-- adductor canal Articular surface
fft""-- Adductor longus Sartorius-----t---;"7';'I:tt
Inferior
Ischium Ischial tuberosity
A
.,4'---- pubic
ram us
'ri---- Adductor tubercle
Obturator foramen Ischial ramus
B
FIGURE 53.36. Anatomy of the acetabular notch (A) and femoral triangle (B).
816
VfJ. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
-':-tL-t+-- Gluteus medius Trochanteric bursae under gluteus medius or gluteus maximus muscles
compartment syndrome ( lateral shin
Ischial bursa (over ischial tuberosity)
Achilles (calcaneal) tendon
FIGURE 53.37. Fascial compartments of the lower extremity.
The suprapatellar bursa con nects to the synovial cavity of the knee joint and can be used in physical diagnosis to determine i f knee trauma has caused significant swelling. The physician first milks any fluid in this bursa from medial to lateral. Then, by palpating anteromedially for a fluid wave i n i t i ated by a gentle squeeze from the anterolateral side of the suprapatellar tendon, i t is possible to detect 1 0 to 1 5 m L of effusion in the knee. This bulge test is used for small effusions (Fig. 53.39A) . If the effusion is so large that the tissues become turgid, a fluid pulse may not be able to create a bulge and the test may provide a false-negative result. Large effusions are more accurately diagnosed with a bal lottement test ( Fig. 53.39B) in which the kneecap is tapped gently (ballotted) . A palpable transm ission o f bony contact is palpated if the effusion is large enough to have distanced the patella from the bone beh ind it. The superficial and deep i n frapatellar bursae are less often involved in clinical problems. A Baker cyst arises fro m enlargement of either the sem imem branosus bursa or the bursa behind the medial head o f the gastroc nemius ( Fig. 5 3 .40) . The swollen cyst is often painful, especially with flexion of the knee. The swelling is more pro m inent i n the stand i ng position. Both of these bursae commonly communicate
Gluteus maxim us
Bursa of Achilles tendon
FIGURE 53.38. Bursae of the lower extremity.
with the synovial cavity of the knee. For this reason, knee trauma such as a meniscal tear, or disease such as rheumatoid arthritis, can i n itiate the cyst. Rupture of a Baker cySt may be m isdiagnosed as thrombophlebitis.
Bursa of the Achilles Tendon I n the ankle region, the superficial bursa of the Achilles tendon may be i rritated by poorly fi tting shoes and may swell . This results i n a tender "pump bump."
53. Lower Extremities
81 7
A
B
FIGURE 53.39. Tests for effusion in the knee. The bulge test (A) is useful for finding a minimal amount of effusion in the knee. The ballottement test (B) is positive if there is a large amount of effusion present. (Illustration by W.A. Kuchera.)
CONCLUSION
Baker's cyst
A thorough understanding of the functional anatomy of the lower extremi ties establishes a foundation for the osteopathic approach to the lower extremities and their effect on the body u n i t. Palpation assists in d ifferential d iagnosis of a wide range of structural and functional disorders in this region. The osteo pathic physician then seeks to balance and improve biomechani cal and homeostatic functions to inAuence a wide range of patient conditions. From a sports medicine practice to the care of patients with deep vei n thrombosis i n an i n ternal medicine practice, the os teopath ic approach to the lower extrem i ties offers an effective approach to diagnosis, prevention, and/or treatment.
REFERENCES I . I rvin RE. Suboptimal posture: the origi n of the majoriry of idio
FIGURE 53.40. Bursae of the knee and Baker cyst.
pathic pai n of the musculoskeletal system. I n : Vleeming A, Mooney V,
818
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Dorman T, Sni jders C, eds. Movement, Stability, and Low Back Pain: The
Essential Role oftbe Pelvis.
N ew York: Church i l l - Livi ngstone;
1 997: 1 33-
1 5 5.
rev. Columbus, OH: C reyden Press. 1 994. 1 7. Roy S, I rvi n R. Sports Medicine: Prevention, Evaillation, Management,
2 . Cyriax J H , Cyriax
PJ.
Cyriax5 Illustrated Manual of Ortbopaedic
Medicine, 2nd ed . Oxford, England: B utterworth- Heinemann Ltd;
and Rebabilitation. Englewood C l i ffs,
N] :
Prentice- H al l ; 1 98.3:380.
1 8 . Greenman PE. Principles ofManual Medicine, 2nd ed. Balti more, M D: W i lliams & W i l k i ns ; 1 996:4 1 1 -446.
1 993:6-8. 3 . Dorman T A. Refurbishing l igaments with prolotherapy. Spine: State o f t h e Art Reviews. 1 995; 9( 2) : 509-5 1 6. 4. Moore KL.
1 6. Kuchera WA, Kuchera M L. Osteopathic Principles in Practice, 2nd ed.
Clinically Oriented Anatomy, 2nd ed. Baltimore, M D:
Wi l l iams & Wilki ns; 1 98 5 :403. 5 . C h ristma nn OD. Biomechanical aspects of degenerative joint disease.
Clin Orthop. 1 969;64:77-8 5 . 6 . Cofton J P, Trueman C E o Studies in osteoarthritis of the h ip, Part 1 1 : osteoarthritis of t h e h i p and leg-length dispari ty. Can Med Assoc j. 1 97 1 ; I 04:79 1 -799. 7. Brody D M . R u n n i n g i n j u ries. ClBA Clin Symp. 1 980;32(4) : 2 5 . 8 . Kuchera WA, Kuchera M L. Osteopathic Principles i n Practice, 2 n d ed. rev. Columbus, OH: C reyden Press; 1 994. 9 . Cyriax J H , Cyriax PJ.
Cyriaxs Illustrated Manual of Ortbopaedic
Medicine, 2nd cd . Oxford, England: Butterwort h - Heinemann Ltd; 1 99 3 : 8 1 . 1 0. Ombregt L, tel' Veer HJ. Disorders of the inert struCtu res: capsular and
1 9. Travell JG, Simons DC. Myofoscial Pain and Dysfimction: The Ti'igger
Point Manual. The Lower Extremities. Vol I I . Baltimore, M D : Williams
& Wilki ns; 1 99 2 . 20. Hackett G S. Ligament and Tendon Relaxation Treated by Prolotherapy, 3rd ed. Spri ngfield, I L: Charles C Thomas; 1 95 8 . 2 1 . Travell J C , Simons D C . Myofoscial Pain alld Dysfill1ction: The Trigger
Point Manllal. Vol I I . The Lower Extremities. Balti more, M D: Will iams & Wilkins; 1 992:28-88. 22. Travell JC, Simons DC. Myofoscial Pain and Dysfill1ction: The Trigger Point Manllal. Vol I I . The Lower Extremities. Balti more, M D : Williams & Wilkins; 1 99 2 :23-27. 23. Walsh PC, ed. Campbells Urology, 7th ed . Philadelphia, PA: WB Saunders; 1 998:2698. 24. Ti"flvell and Simons' Myofoscial Pain and Dysjillictioll: The Ti'igger Point
Manual. Vol I . Upper H al f of Body. Baltimore, M D : Williams &
Wilki ns; 1 999.
non-capsular patterns. In: Ombregt L, Bisschop P, ter Veer H], Van de
25. Janda v. Muscle weakness and i n h ibition (pseudoparesis) i n back pain
Velde T, eds. A System ofOrtbopaedic Medicine. London, England: WB
syndromes. In: Grieve C P, ed. Modem Medicine Therapy of the Verte
Saunders; 1 99 5 :783-800. I I . Blood SD. Treatment of the sprained ankle. jA OA. 1 980;79:680-692. 1 2. I n man VT. joillts of the Ankle. Balti more, M D: Will iams & Wilkins; 1 976:42. 1 3. I n man VT, Mann RA. Biomechanics of the foot and ankle. I n : Du Vries'
Surgery ofthe Foot, 3rd ed . St. Louis, M O : 1 97 3 : 1 7. 1 4. Levens SA, et a ! . Ti'ansverse rotation of the segments of the lower ex tremity in locomotion. j Bone joint Surg. 1 948;30A:8 59-872. 1 5 . H icks J H. The mechanics of the foot, I: the joints. j Anat. 1 95 3;87: 345.357.
bral Column. Edi nb u rgh, Scotland: Churchill-Livi ngstone; 1 986: 1 97200. 26. Kuchera M L. Treatment of gravi tational strain pathology. In: Vleeming A, Mooney V, Dorman T, Sni j ders C, eds. Movement, Stability, and LolV
Back Pain: The Essential Role of the Pelvis.
New
York, NY: Churchill
Livi ngstone; 1 997:477-499. 27. Basmajian Jv. Grants Method of Anatomy, 9th ed. Balti more, M D : Will iams & Wilkins; 1 97 5 :327-328. 28. Kuchera ML, Kuchera WA . Osteopatbic Consideratiolls in Systemic Dys
function, 2nd ed . rev. Columbus. O H : C reydcn Press; 1 994: 1 59- 1 67 .
Part C: Palpatory Diagnosis and Manipulative Treatment
SOFT TISSUE TECHNIQUES WALTER C. EHRENFEUCH TER DAVID HEILIG ALEXANDER S. NICHOLAS
8. Improve local and systemic immune responsiveness KEY CONCEPTS • Soft tissue techniques and classification as direct or indirect
techniques • Goals attainable with soft tissue techniques • T hree basic mechanisms used in soft tissue techniques • Manner in which soft tissue techniques can be used alone
or in combination with other manipulative techniques • Objective, patient positioning, physician positioning, and
implementation of soft tissue techniques for following regIOns: -Cervical
9. Provide a general state of relaxation 10. Provide a general state of tonic stimulation
The choice of technique is based on the treatment goals. There are three basic mechanisms used in applying soft tissue technique to muscular structures and their associated fascial elements: l. Tractional technique, also called stretching, in which the ori
gin and insertion of the myofascial structures being treated are longitudinally separated.
2. Kneading, a rhythmic, lateral stretching of a myofascial struc
-T horacic
ture, in which origin and insertion are held stationary and the
-Lumbar
central portion of the structure is stretched like a bowstring.
-Sacrum -Upper extremity -Lower extremity
3. Inhibition, sustained deep pressure over a hypertonic myofas cial strucrure. Other mechanisms used on more superficial fascial structures include variants on techniques developed in the European mas sage movement:
Soft tissue techniques are defined as direct techniques that ad dress the muscular and fascial structures of the body and associ ated neural and vascular elements. Soft tissue techniques may be applied in a number of differenr ways to:
1. Relax hypertonic muscles
• Effleurage • Petrissage • Tapotemenr • Skin rolling
Soft tissue techniques may be used alone or in combination
2. Stretch passive fascial structures
with any other manipulative technique. Many of the positions
3. Enhance circulation to the local myofascial structures
used for soft tissue techniques readily lend themselves to conver
4. Improve local tissue nutrition, oxygenation, and removal of metabolic wastes
5. Improve abnormal somato-somatic and somatovisceral reflex activity
6. Identify areas of somatic dysfunction 7. Observe tissue response to the application of manipulative
technique
sion to other techniques such as the following: • Articulatory • Muscle energy • Counrerstrain • Functional • Cranial • High velocityllow amplitude
(HVLA) thrusting
820
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
CERVICAL TECHNIQUES Suboccipital Inhibition
Objective Decrease in suboccipital muscle tone. Position Supine (Fig. 54.1). Procedure I.
Sit at the head of the table.
2. Place the pads of your fingers just inferior to the superior nuchal line in the suboccipital tissues. 3. Lift the head so that the patient's weight is entirely supported on the pads of your fingers. The head is slightly above, but not resting on, your palms.
4. Maintain this position until you achieve the desired relaxation of the suboccipital soft tissues.
Note: This technique is similar in position to the method used by A.T. Still when he created a rope sling to relieve his own headaches.
FIGURE 54.2. Cervical rotation.
3. Rotate the patient's head away from you slowly until tissue tension restricts you from f�rther motion.
4. Genrly increase the tension by rotating into the restrictive bar rier, hold the tension for 12 seconds, and then slowly release it. 5. Repeat as many times as necessary to achieve the desired effect.
Note: This neck position allows for conversion to a muscle energy cervical range of motion technique or for an HVLA thrust for atlantoaxial segmental dysfunction.
Rotation
Objective Increase cervical rotation.
Traction
Objective Position Supine (Fig. 54.2).
Position
Procedure I.
Stretch paravertebral muscles.
Si t at the head of the table.
2. Use your hands to cradle the head, taking care not to occlude the ear canals.
Supine.
Procedure l.
Sit behind the patient at the head of the table.
2. Place one hand cradling the occiput between the thumb and index finger. Place your other hand across the patient's fore head. 3. Exert a gentle axial tractioo with your occipital hand.
4. Use your hand on the forehead to prevent forward tilt of the patient's head, also applying slight traction. 5. Apply the tractional force slowly; release it slowly. 6. Repeat as many times as necessary to achieve the desired effect.
Forward Bending
Objective FIGURE 54.1. Suboccipital inhibition.
Stretch posterior cervical soft tissues.
54. Soft Tissue Techniques
821
3. Grasp the forehead lightly with your cephalad hand. 4. With your caudad hand, draw the paravertebral muscles lat erally and anteriorly until you reach the initial restrictive barrier.
5. Increase the anterolateral traction slightly to take the tissues slightly beyond the barrier. 6. Repeat as many times as necessary to achieve the desired effect.
Note: By increasing the rotational force, this technique may be converted to a deep articulatory technique. By adding more of a milking motion, ir may be used to enhance lymphatic drainage in the cervical lymph node chains.
Longitudinal Traction
Objective Relax the cervical paravertebral muscles.
FIGURE 54.3. Cervical forward bending.
Position Supine (Fig. 54.4).
Position Supine (Fig. 54.3). Procedure
Procedure
1. Sit at the head of the table.
1. Si t or stand at the head of the table.
2. Bring the palmar surfaces of the fingers of both hands under the neck near the spinous processes.
2. Cross your forearms and place them behind the patient's head with your hands on the patient's shoulders.
3. Lift the cervical paravertebral musculature and draw it cepha lad.
3. Exert a slow, forward bending stretch until a restrictive barrier is engaged.
4. Slowly releasing the musculature, carry the hands caudally.
4. Gently, slowly increase the stretch; then release it just as slowly. 5. Repeat as many rimes as necessary to achieve rhe desired effect.
5. Repeat as many times as necessary to achieve the desired effect, shifting position along the length of the cervical spll1e.
Note: This position allows use of a range-of-motion muscle energy technique, and it may also be used to treat anterior coun terstrain tender points. Contralateral Traction
Objective Relax the cervical paravertebral muscles. Position Supine. Procedure
1. Srand at the side of the head of the table. 2. With your caudad hand, reach across the patient and under rhe opposite side of the neck to grasp the paravertebral muscles with the pads of your fingers.
FIGURE 54.4. Cervical contralateral traction.
822
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
THORACIC Prone Pressure
Objective Relax the thoracic paravertebral muscles. Position Prone (Figs. 54.5 and 54.6). Procedure 1. Stand at the side of the patient, whose head is turned away from the side ro be treated. 2. Place your thumb an'd thenar eminence of one hand on the far side of the thoracic spine berween the spinous and transverse processes. 3. Place your other hand reinforcing the first or working in tan dem with it along the spine. 4. Exert an anterolateral pressure on the soft tissues, directed away from the spine. 5. You may maintain the pressure as a sustained, inhibitory pres sure or use it in an intermittent kneading fashion.
FIGURE 54.6. Caudad hand reinforcing thumb pressure for thoracic thumb pressure.
Procedure 1.
Stand at the head of the table.
6. Repeat as many times as necessary at various levels to achieve the desired effect.
2. Place the thumbs of both hands just lateral to the spinous pro cesses, on the paravertebral muscles, with your fingers fanned out.
Note:Additional downward vertical pressure converts this into a deep articulatory technique.
3. Exert a caudad, anterior pressure, allowing muscle to relax and stretch, finishing with a lateral sweeping motion. 4. A kneading motion or inhibitory pressure may be used.
Prone Thumb Pressure
Objective
5. The technique is repeated at as many spinal levels as is desired, as many times as necessary to achieve the desired effect.
Decrease paravertebral muscle hypertonicity. Prone Pressure with Counterpressure
Position
Objective
Prone.
Relax deep intrinsic spinal muscles. Position Prone. Procedure 1.
Stand at the side of the table.
2. Have the patient turn his or her head toward you. 3. Place one hand on the far side of the spine, over the transverse processes, with your fingers pointing cephalad. 4. Place your other hand on the near side of the spine with your fingers pointing caudad.
FIGURE 54.5. Placement of thumb for thoracic thumb pressure.
5. Exert simultaneous longitudinal and anterior pressure with both hands, imparting a side-bending motion to the thoracic segments under the treating hands. The degree of vertical pressure exerted is varied according to the patient's condition and the degree of vertebral and costal articulation desired.
54. Soft Tissue Techniques 6. Use a repetitive kneading mQ[ion. 7.
Repeat as many times as necessary ro achieve the desired effecr.
823
Position Lateral recumbenr, rreatmenr side up.
Note: This technique can be used as a deep anicularory tech nique or can readily be convened ro a thrust technique direcred ar rhoracic segmenral dysfuncrion.
Procedure
Upper Thoracic: Lateral Recumbent
2. Reach borh hands under rhe patiem's arm, comacring the paravenebral muscles just lateral ro the spinous processes wirh the pads of your fingers.
Objective Relax upper rhoracic paraverrebral muscles. Position Lareral recumbenr (Fig. 54.7).
1. Srand at rhe side of rhe rable.
3. Pull rhe pads of your fingers roward rhe cenrer of rhe body, drawing the muscularure larerally like a bowstring. 4. Slowly release this lareral tracrion, and reposition your hands along rhe spine ro neat other levels as desired. 5. Repeat as many rimes as necessary ro achieve rhe desired effecr.
Procedure
Lateral Recumbent Thumb Pressure
1. Srand at rhe side of rhe table facing the patienL
Objective
2. Pass your caudad hand under the patiem's arm, grasping the upper side paravenebral muscles jusr lareral ro the spinous processes with the pads of your fingers. 3. Comacr the amerior ponion of rhe shoulder wirh your cepha lad hand ro provide an effecrive coumerforce. 4. Draw rhe paravenebral muscles larerally away from the spine unril resrricrion i s palpated.
Relax the thoracic paraverrebral muscles. Position Lareral recumbem, treatmem side down (Fig. 54.8).
5. Conrinue ro apply lareral rracrion unril rhe rissues relax, sofren, and lengthen. The lareral tracrion is then slowly released.
Procedure
6. Work your way up and down the spinal column from the cervicothoracic junction ro abour rhe midrhoracics.
2. Reach across the back of the patienr unril your thumbs are comacting the paraverrebral rissues jusr lateral ro the far side of rhe spinous processes.
7.
Repeat as many rimes as necessary ro achieve the desired effecL
Lower Thoracic: Lateral Recumbent
1.
Stand at the side of the table, facing the patienr.
3. Exerr pressure with your rhumbs roward rhe cenrer of the body and down roward rhe table.
Objective
4. You may use an inrermitrent kneading or susrained inhibirory pressure.
Relax rhe lower thoracic paraverrebral muscles.
5. Repeat as many rimes as necessary ro achieve rhe desired effecr.
54.8. Lateral technique.
FIGURE FIGURE 54.7. Lateral recumbent position for upper thoracic technique.
recumbent
thumb
pressure
for
thoracic
824
VII.
Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
Side Leverage
Objective Relax thoracic paravertebral muscles.
Position Lateral recumbent, treatmem side down (Fig. 54.9).
Procedure 1. Sit at the side of the table, facing the patient.
2. Position your caudad arm so that the patient's shoulder is in your axilla, with your thumb medial to the paravertebral muscles on the far side of the spine. 3. Lift the patient's head away from the table, introducing a cervical and upper thoracic side-bending force. 4. Simultaneously, your caudad thumb exerts a downward pres sure on the upper thoracic paravertebral musculature. This may be applied as a combination of intermittent traction and kneading or with a sustained inhibitory pressure. 5. Repeat as many times as necessary to achieve the desired effect.
Note: This technique can be converted to either a deep articu
FIGURE 54.10. Seated position using over/under method for thoracic
technique.
Position Seated (Fig. 54.10).
latory technique or an HVLA thrust with minimal repositioning of the physician's caudad hand.
Procedure
Seated, Over/Under
2. Reach under the patient's forearms and over his or her shoul ders.
Objective Relax upper thoracic paravertebral muscles.
1. Stand facing the patient. Have the patient cross his or her arms, hooking the patient's thumbs in the antecubital fossae.
3. Contact the paravertebral tissues over the upper thoracic trans verse processes with your fingerpads. 4. Lean back, drawing the patient toward you as you simultane ously exert an upward leverage on the forearms. 5. Exert a downward pressure into the soft tissues with the pads of your fingers; then draw them cephalad with a kneading motion. 6. Repeat as many times as necessary to achieve the desired effect.
Note: This technique may be converted to a deep articulatory technique by increasing the amount of inward pressure on the pads of the fingers, producing thoracic backward bending. Supine Extension
Objective Relax the thoracic paravertebral muscles. Position Supine (Fig. 54.11). Procedure FIGURE 54.9. Side l everage for thoracic technique.
1. Sit at the side of the table.
54. Soft Tissue Techniques
825
FIGURE 54.11. Thoracic extension in supine position.
2. Slide your hands under the patient until the pads of your fingers contact the paravertebral soft tissues on the near side. 3. By leaning down onto the elbows, you create a fulcrum, transmitting pressure upward into the paravertebral soft tissues.
FIGURE 54.12. Seated position for midthoracic extension.
4. Simultaneously draw your fingerpads toward you. 5. This may be performed in a kneading fashion or with deep inhibitory pressure.
LUMBAR
6. Repeat as many times as necessary to achieve the desired effect.
Supine Flexion
Note: This technique is commonly used in the postop erative setting to prevent and/or treat postoperative paralytic ileus. In this setting, the technique has been referred to as rib ratsll1g.
Objective Relax the lumbar paravenebral muscles.
Position Midthoracic Extension
Supine.
Objective Relax the midthoracic paravertebral muscles. Position
Procedure 1. Stand at the side of the table.
Seated (Fig. 54. 12).
2. Have the patient flex both hips, drawing the knees up toward the chest.
Procedure
3. Grasp the patient's knees, further flexing the hips until the pelvis begins to follow, exerting a rractional force on the lum bar paravertebral muscles.
1. Stand behind the patient, and have the patient clasp their hands behind the neck. 2. Grasp the patient's arms under rhe elbows. 3. Place your other hand so that it is straddling the spine, with fingers pointed cephalad. 4. Elevate the patient's elbows, applying tractional force as you simultaneously press forward with the hand straddling the spll1e. 5. Repeat as many rimes as necessary to achieve the desired effect.
Note: This rechnique may be convened to a deep articulatory rechnique by varying rhe amount of anterior pressure applied through your posterior hand.
4. Continue the tractional stretch in an intermittent or contin uous fashion. 5. Additional traction may be brought to bear on either side of the spine by adding side bending away from the side to be treated. 6. Repeat as many times as necessary to achieve rhe desired effect.
Supine Rotation with Counterleverage
Objective Relax lumbar paravertebral muscles.
826
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 54.13. Supine technique.
rotation with counterleverage for lumbar
FIGURE
54.14. Prone
pressure with counterleverage for lumbar
technique.
Position
Prone Scissors Technique
Supine (Fig. 54.13).
Objective
Procedure I.
Stand at the side of the table and have the patient flex the knees and hips.
2. Draw the patient's knees toward you with your caudad hand while the cephalad hand reaches under the lumbar region to grasp the paravertebral ti ssues with your fingerpads.
Relax lumbar paravertebral muscles. Position Prone (Fig. 54.15). Procedure
3. Pull your cephalad hand upward toward the ceiling.
1. Stand at the side of the table.
4. Produce a rotational counterforce by simultaneously pushing the knees away from you.
2. Grasp the patient's opposite leg just above the knee with your caudad hand, lifting the leg far enough to cross it behind the nearer leg. Your hand is now between the patient's knees.
5. Apply the technique in either a kneading manner or with deep i nhi bitory pressure. 6. Repeat as many ti mes as necessary to achieve the desired effect. Prone Pressure with Counterleverage
Objective Relax lumbar paravertebral muscles.
3. Contact the lumbar paravertebral muscles (on the far si de) with the heel of your cephalad hand. 4. Apply an anterior and lateral pressure with the cephalad hand, while simultaneously increasing the amount of scissoring with the legs. 5. Use an intermittent kneading moti on, or sustained inhibitory pressure.
Position Prone (Fig. 54.14). Procedure I.
Stand at the side of the table.
2. Contact the lumbar paravertebral musculature on the opposite side of the spine with the heel of your cephalad hand. 3. Grasp the anterior superior iliac spine with your caudad hand, pulling upward toward the ceiling. 4. Apply a simultaneous anterior and lateral force, stretching the lumbar paravertebral tissues like a bowstring. 5. Use either a kneading motion, or deep inhibitory pressure. 6. Repeat as many times as necessary to achieve the desired effect.
FIGURE 54.15. Prone scissors technique.
54. Soft Tissue Techniques
821
Procedure 1. Stand at the side of the table, near the patient's knees.
2. Place the thumbs of both hands on the paravertebral muscles overlying the transverse processes, with the fingers fanned out over the lateral abdominal muscles. 3. Apply bilateral pressure anteriorly and cephalad until the limits of tissue motion are reached. 4. Sweep your thumbs in a lateral direction. 5. Reposition your thumbs at a different lumbar segment. 6. Repeat steps 4 and 5 in a kneading fashion, as many times as necessary to achieve the desired effect. Supine
Objective FIGURE 54.16. Prone traction technique.
6. Repeat as many times as necessary to achieve the desired effect.
Relax lumbar paravertebral muscles. Position Supine. Procedure
Prone Traction
1. Sit at the side of the table.
Objective
2. Reach under the lumbar region with both hands, contact ing the ipsilateral paravertebral tissues overlying the transverse processes with the pads of your fingers.
Relax lumbar paravertebral muscles.
Position Prone (Fig. 54.16).
3. Lean down into the elbows, producing an upward leverage at the wrists and hands, simultaneously drawing your hands toward you. 4. Use either a kneading motion or sustained inhibitory pressure. 5. Repeat as many times as necessary to achieve the desired effect.
Procedure 1. Stand at the side of the table.
Lateral Recumbent
2. Place your cephalad hand over the base of the sacrum, with the fingers pointing toward the coccyx.
Objective
3. Place your other palm straddling the spinous processes of the lumbar vertebrae, with your fingers pointing cephalad. 4. Exert a separating tractional force in the directions in which the fingers point. 5. Use either intermittent traction or sustained inhibition. 6. The position of the caudad hand may be altered by placing it to one side of the spine, thus bringing more force to bear on the paravertebral soft tissues on that side. 7. Repeat as many times as necessary to achieve the desired effect.
Bilateral Thumb Pressure
Objective Relax lumbar paravertebral muscles.
Relax lumbar paravertebral muscles. Position Lateral recumbent, treatment side up (Fig. 54.17). Procedure 1. Stand at the side of the table.
2. Have the patient flex their hips and knees; place your thigh against the infrapatellar region. 3. Reach over the back and grasp the paravertebral muscles of the lumbar region, drawing them toward you and away from the spine simultaneously. 4. Your thighs against the patient's knees may simply be used for bracing or they may also be simultaneously flexed to provide a combined bowstring and longitudinal traction force on the paravertebral musculature.
Position
5. Use either a kneading motion or sustained inhibitory pressure.
Prone.
6. Repeat as many times as necessary to achieve the desired effect.
828
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment 2. Have the patient place their hand on the side to be treated behind the neck. The opposite hand grasps the elbow of the first hand. 3. Reach under the near axilla, grasping the far arm just proximal to the elbow. 4. Place the heel of your posterior hand over the paravertebral tissues on the far side of the spine. 5. Have the patient allow their weight to drop forward onto your arm. 6. Rotate the patient toward you with your anterior hand. 7. Your posterior hand provides a lateral force on the lumbar paravertebral muscles, away from the spine. 8. Repeat as many times as necessary to achieve the desired effec(.
Note: This technique may also be used for deep articulation. It is also readily converted to muscle energy and HVLA thrust techniques.
SACRUM FIGURE 54.17. Lateral recumbent position for l umbar technique.
Sacral Rock
Objective Seated
Relax the muscles at the lumbosacral junction.
Objective Relax lumbar paravertebral muscles.
Position Prone (Fig. 54.19).
Position Seated (Fig. 54.18).
Procedure 1.
Procedure l.
Stand behind the patient, opposite the treatment side.
Stand at the side of the patient's pelvis.
2. Place the heel of your cephalad hand on the sacral base, with your fingers pointing toward the coccyx. 3. Place your caudad hand on top of the first hand, with your fingers pointing in the opposite direction. 4. Exert a gentle pressure straight down toward the table.
FIGURE 54.18. Seated position for l umbar technique.
FIGURE 54.19. Prone position for sacral rock.
54. Soft Tissue Techniques
829
5. Alternate the direction of your pressure to synchronize it with and augment the natural motion accompanying respiration, rocking the sacrum into flexion and extension. 6. Repeat as many times as necessary to achieve the desired effect.
Note: This technique may be converted to a craniosacral tech nique by following the cranial rhythmic impulse rather than pul monary respiration. Sacral Inhibition
Objective Inhibit sacral motion, altering parasympathetic nervous system balance. Position Prone. FIGURE 54.20. Upper extremity pectoral traction.
Procedure 1. Stand at the side of the patient's pelvis. 2. Place the heel of your cephalad hand on the sacral base, with your fingers pointing toward the coccyx. 3. Place your caudad hand on top of your other hand, with fingers pointing in the opposite direction. 4. Direct deep pressure straight down toward the table. 5. Maintain this pressure (without rocking motion) for 30 sec onds to 2 minutes.
Note: This technique may be converted to a craniosacral tech
expansion of the rib cage is noted or until you achieve the desired effect.
Note: This technique is often applied following thoracic pump technique to relieve a patient's sense of chest compression. It may also be used as a lymphatic pump by increasing inhalation excur sion of the upper seven ribs, thus increasing inhalation negative pressure. Posterior Axillary Folds
Objective
nique by following the cranial rhythmic impulse to a still point. This is sometimes referred to as a sacral CV4.
Relax the posterior muscle attachments to the upper extremity.
UPPER EXT REMITY
Position
Pectoral Traction
Supine, treatment arm palm down on abdomen (Fig. 54.21).
Objective Relax the anterior muscular attachments of the upper extremity. Position Supine (Fig. 54.20). Procedure 1. Stand at the head of the table.
2. Hook the pads of your fingers into both anterior axillary folds. 3. Apply an anterior cephalad traction. 4. Have the patient inhale. 5. With inhalation, increase your cephalad and anterior traction, and maintain it as the patient exhales. 6. This cycle of inhalationltractionlresisted exhalation may be repeated until no further stretch of the pectoral muscles or
FIGURE 54.21. Upper extremity posterior axillary folds technique.
830
VII.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Procedure 1.
Sit at the side of the table, facing the patient's head.
2. Using the hand closest to the patient, grasp the posterior ax illary fold between your thumb and fingers. 3. Starring near the trunk, apply a milking motion, rolling along the fold toward the thorax. 4. Gradually, as the muscle softens, work your way away from the trunk, including more of the posterior axillary fold in the sequential rolling motion until the entire fold has been treated.
Note: A similar approach may be applied to the anterior axil lary fold. Interosseous Membrane of Forearm
Objective FIGURE 54.22. Upper extremity rhomboids technique.
Relax the interosseous membrane and soft tissues of the forearm. Position
5. Use either a kneading motion or sustained inhibitory pressure. 6. Repeat as many times as necessary to achieve the desired effect.
Seated. Procedure 1.
Stand facing your patient.
LOWER EXT REMITY Fascia Lata (Method 1 )
2. Grasp the hand of the arm to be treated, as if to shake hands.
Objective
3. Wrap your other hand over the top of the forearm.
Relax the fascia lata.
4. Slowly induce pronation through the patient's hand. 5. Use your other hand to apply a gentle, opposing wringing mo tion to the soft tissues of the forearm, stretching and relaxing the muscles. 6. Apply similar treatment in the opposite direction, inducing supination to stretch and relax the muscles. 7. Repeat as many times as necessary to achieve the desired effect. Rhomboids
Position Prone (Fig. 54.23). Procedure 1.
Stand at the side of the patient, opposite the side to be treated.
2. With your caudad hand, grasp the leg to be treated just above the knee.
Objective Relax the rhomboid muscles. Position Lateral recumbent, treatment side up (Fig. 54.22). Procedure 1.
Stand at the side of the table, facing the patient.
2. Grasp the shoulder with your cephalad hand to control tension in the rhomboid and trapezius musculature. 3. Grasp the rhomboid muscles with your caudad hand, just medial to the vertebral border of the scapula. 4. Gently pull up toward the scapula, drawing the scapula slightly away from the ribs.
FIGURE 54.23. Lower extremity fascia lata technique.
54. Soft Tissue Techniques
831
3. Anchor rhe pelvis against the rable wirh your cephalad hand. 4. Exrend rhe hip of rhe leg being rreated and adducr rhe hip across the midline unril rhe desired tension is developed in rhe lateral sofr rissues of the rhigh. 5. Apply eirher intermirrent or susrained tracrion as in a direcr myofascial release rechnique. 6. Repear as many rimes as necessary ro achieve rhe desired effect. Fascia Lata (Method 2)
Objective Relax rhe lareral sofr rissues of rhe rhigh.
Position Lareral recumbent, trearment side up (Fig. 54.24).
Procedure 1.
Si r on the side of the rable beh ind rhe parient's knees.
2. Place rhe rhigh ro be [I'eared jusr in fronr of the other leg with the foot on the table, so that there is a downward slope ro the thigh. 3. Apply pressure against the ilioribial band just caudad ro the greater trochanter, using the flats of the middle phalanges of your closed fist. 4. Maintaining this inward pressure, drag your fisr down the length of the iliotibial band ro the level of the knee. 5. Repeat as many times as necessary ro achieve the desired effect (i. e. , srretch in the lateral fascial structures of the thigh).
Fascia Lata (Method 3)
Objective
FIGURE 54.25. Lower extremity fascia lata technique.
Position Prone (Fig. 54.25). Procedure
1. Stand at the side of the table, opposite the thigh ro be treated. 2. Flex the patient's knee ro 90 degrees and grasp it with your caudad hand. 3. Use the pads of the fingers on your cephalad hand ro hook the iliotibial band and pull upward roward yourself. 4. Simultaneously carry the foot of the same leg away from the midline, increasing the tension on the iliotibial band. 5. Continue with a kneading motion. 6. Repeat as many times as necessary ro achieve the desired effect.
Relax and stretch the iliotibial band. Piriformis
Objective Relax the piriformis muscle. Position Prone (Fig. 54.26). Procedure 1.
FIGURE 54.24. Lower extremity fascia lata technique.
Stand at the side of the table, opposite the muscle dysfunction.
2. Beginning near the sacrum, apply double thumb pressure inro the piriformis muscle, rolling roward the trochanteric inser tion. (The piriformis muscle may be accessed on a line be ginning midway between the posterior superior iliac spine and the inferior lateral angle of the sacrum, extending ro the posterosuperior pole of the greater trochanter. )
832
VJ/.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment 2. Use the proximal phalanges of your closed fist to contact the sale of the patient's foot just posterior to the metatarsal heads. 3. While applying pressure toward the dorsum of the foot, drag your fist over the plantar fascia toward the heel. 4. Repeat as many times as necessary (toes to heel) to achieve the desired effect.
Arch Springing
Objective Relaxation of the muscles of the arch of the foot. FIGURE 54.26. Location of piriformis tender point.
3. Move sequentially along the muscle toward the trochanter, taking care not to exert too much pressure directly over the sciatic nerve. 4. For heavier patients, you may use your elbow rather than double thumb pressure. 5. Use either a kneading motion or sustained inhibitory pressure. 6. Repeat as many times as necessary to achieve the desired effect.
Position Supine (Fig. 54.28). Procedure I.
Sit at the foot of the table.
2. Grasp the foot with both hands, with your thumbs under the arch and fingers on the dorsum of the foot.
Relax and stretch the plantar fascia.
3. Move the middle of the foot toward supination, using your proximal hand, while simultaneously moving the fore foot toward pronation with your distal hand. (This wring ing motion tends to stretch the fasciae of the foot toward a position of reestablishing the longitudinal arch of the foot.)
Position
4. Repeat as a kneading rype of motion, as many times as neces sary to achieve the desired effect.
Plantar Fascia
Objective
Supine (Fig. 54.27).
Note: This could also be considered a deep articulatory tech nique for the arch.
Procedure 1.
Sit at the foot of the table.
FIGURE 54.27. Lower extremity plantar fascia technique.
FIGURE 54.28. Lower extremity arch springing technique.
54. Soft Tissue Techniques CONCLUSION
SUGGESTED READINGS
Soft tissue direct techniques address the muscular and fascial structures of the body and associated neural and vascular ele ments. They can relax and stretch structures and muscles, enhance circulation and nutrition, improve reflex activity and immune response, identifY areas of change or dysfunction, and provide a state of relaxation and ronic stimulation.
Nicholas NS.
833
Atlas ofOsteopathic Techniques. Philadelphia, PA: Philadelphia
College of Osteopathic Medicine; 1981. Rubinstein S, Eimerbrink JH, Heilig D, Prarr W.
Osteopathic Techniques.
Philadelphia, PA: Osteopathic Publications; 1949. Zink JG. Holistic approach ro homeostasis. In: Barnes MW, ed.
Academy of Osteopathy Yearbook. of Osteopathy; 1973.
American
Indianapolis, IN: American Academy
ARTICULATORY TECHNIQUES DAVID A. PATRIQUIN JOHN M. JONES, III
KEY CONCEPTS • • • • • • • •
Design of articulatory, or springing, technique Uses of and additions to articulatory activation Diagnostic findings suggesting use of articulating technique Special cases suitable for application of technique Contraindications General instructions of design of technique Rib raising and Spencer techniques Specific articulatory techniques by region, including cervical, cervicothoracic, thoracic, costal, lumbar, pelvic, and the extremities
Articulatory technique, also called springing technique, is a di rect technique. The physician genrly and repetitively forces the part of the body being treated against the restrictive barrier (gen erally maintained by tight muscles and connective tissues act ing as restrainers), with the intent of reducing the resistance or changing the position of that barrier and improving physiologic motion . This form of osteopathic treatment is also called low velociry/moderate- to high-amplitude, or long-lever, technique. Rib raising with the patient supine, or the Spencer series of tech niques for articulating all ranges of motion of the dysfunctional shoulder are examples of this rype of technique.
DESIGN AND USE OF ARTICULATING TECHNIQUE Articulating activation can help resolve a simple problem with a single restrictive barrier or a complex problem with multiple joint and tissue restrictive barriers. This rype of technique is par ticularly useful where the application of slow, genrle, controlled movements is a requirement. Postoperative patients and older patients suffering from arthritis or osteopenia find this rype of direct treatment more acceptable than more vigorous ones. Respiratory cooperation (inhalation to accentuate tissue ten sion or exhalation to relax tissue tension further) and active mus cle contraction or relaxation are frequently added. These addi-
tions enhance the effect ofpassive articulating motion by resisting it or permitting increased range of motion. The standard tech nique is modified to increase the range of motion while limiting the amount of discomfort induced by the procedure. As an example, a direct articulating treatment can be applied to a ver tebral unit restricted in right rotation. The physician makes repeated attempts to increase right rotation of the vertebra by slowly, gently encouraging the affected vertebra into right rota tion against the restrictive motion barrier. The physician increases the force or induces a wider range of motion on each cycle. Fi nally, once the barrier to motion is firmly engaged, the patient is instructed to take as deep a breath as comfortable. The pos itive increased intrinsic force generated by this action markedly augments the stretching, mobilizing forces applied by the physi cian. The added intrinsic force opposes those forces the physician has already induced. The combination of operaror and intrinsic forces results in more tension in soft tissues and produces greater stretching and lengthening in them than would result from physi cian force alone. The repetitive application of gentle force may be directed to the reduction of one barrier at a time, in successive steps, or the physician may engage two or more barriers with one move ment. The principles of technique design apply in the case of motion restriction in multiple planes, but the actual directions and forces used may be so complex as to defy accurate descrip tion in a text. There are many possible combinations of vectors of motion and sequences during one treatment when applying this rype of manipulation to multiple-plane restrictions. The simple, passive physician efforts strongly reinforce the addition ofintrin sic forces, such as respiratory cooperation or isometric muscle energy actiVIry.
COMMON QUESTIONS Diagnosis What diagnostic findings suggest the therapeutic use of artiCLI lating technique? The cardinal clinical indicator for applying an ar ticulating technique is limited or lost articular motion. The most common cause for this loss of articular motion is a dysfunc tion in the local (periarticular) supporting tissues or in the longer muscles or ligaments associated with the ar ticulation. There are also secondary indicators for the application of an ar ticulatory
55. Articulatory Techniques
835
technique. These include a need to increase the frequency or am plitude of motion in a body region. An example of this is the need to increase the frequency and amplitude of motion in the chest of a person with respiratory disease. Accomplish this by applying thoracic lymphatic pump treatment. Expect increased amplitude and efficiency of chest motion to follow this treatment.
gentle force against it to the limit of tissue motion or the patient's tolerance to pain or fatigue. Then return the articulation slowly toward the neutral portion of its motion. Repeat this process several times, each time gaining range and improved quality of motion. Cease repetition of motion when no fur ther response is achieved.
Special Cases
Enhancement
Are there special cases most suitable for the application of ar ticulating technique? Very young and very old patients respond well to this type of treatment. They also suffer less reaction in terms of discomfort and post-treatment stiffness than if a high velocityllow-amplirude technique is employed. Articulating tech nique permi ts accurate dosage offorce and duration of treatment. It also permits careful and accurate localization of forces. The amount and direction of force can be altered during the course of treatment because movements are slow, deliberate, repeated, and constantly monitored by palpation through the physician's hands. Because the treatment is applied slowly and patient response is sensed, adjustments can be made immediately.
Intrinsic forces, such as respiratory assistance or a muscle energy technique may be added once maximum range of motion has been achieved by positioning alone. Similar modifications can measurably increase motion range and quality.
Contraindications Are there contraindications to the use of articulating technique? There are general cautions that apply to the use of any manual procedure in the treatment of a patient (see Chapter 74, E fficacy and Complications). Because articulating technique consists of repetitive applications of force, it can be quickly modified be tween applications of force in response to the reaction of the patient. For example, in treating the upper cervical region, it is wise to avoid simultaneous hyperrotation and extension. Re peated application of force to the upper cervical area positioned in extension and hyperrotation may damage the vertebral arter ies. It is also not appropriate to use forceful, repetitive motion on an acutely inflamed joint, especially one where the cause of inflammation may be infection or reaction to a fracture. Instructions For Design
SAMPLE CLINICAL APPLICATION Rib Raising Diagnosis and Findings
A patient has viral pneumonia with a resistant or noncompliant chest wall in which the motion of all ribs is reduced in both inspi ration and expiration. There is paraspinal soft tissue tenderness to light pressure, with decreased rib motion and accompanying increased soft tissue tightness ( tension/tone) throughout the pos terior thorax, especially at the level of the upper five thoracic vertebrae and ribs. Patient Position
Supine, with the thorax and head slightly elevated as necessary for patient comfort. Procedure 1.
Stand at the head of the treating table facing the patient.
2. Reach under the patient's back, extending the forearms and hands palms upward, so that the finger tips can, on flexion, engage paired upper ribs near their angles on each side of the midline. This is a bilateral treatment technique.
What are the general instructions for the design of an articulating technique?
3. Gently pull cephalad. This attempts to mobilize the costo transverse and costovertebral articulations and stretch the intercostal and more superficial thoracic tissues.
Patient Position
4. Hold, then slowly release.
Use any comfortable position that permits the problem area to be passively moved completely through all ranges of motion.
5 . Rib raising (articulatory) technique is markedly augmented with patient inspiration after full cephalad tension is applied to the ribs.
Physician Position
Use a comfortable position that permits the application of passive motion through the complete range of motion of the affected articulation. Procedure
Move the affected joint to the limit of all ranges of motion. As the restrictive barrier is reached, slowly and firmly continue ro apply
6. When repetition of this treatment no longer produces in creased range of motion at this level, move your hands to the next inferior group of ribs and repeat the articulating treatment process. Treat groups of two to four ribs progres sively, from above downward, until all ribs on both sides are moving freely. 7. Then move to the side of the table, beside the patient's hips, and face the head of the table. S.
Extend your forearms and hands palms up, placing them under the upper thorax of the patient, with your finger tips
836
ViI. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
engaging the supetior surface of the upper ribs at their angles. (This is a unilateral rib arriculating procedure.) 9. Pull caudally, attempting to move the ribs inferiorly in rela tion to other thoracic structures. 10. Repeat the process until there is no increase in motion. Treat successive lower groups of ribs in the same fashion. 1 1 . Rib raising (articulatory) technique is markedly augmented in this phase of treatment by the addition ofa deep inhalation by the patient after full caudad tension is applied to the ribs.
Alternate Technique Patient Position
Supine. Procedure I.
Stand facing the foot of the treatment table at the level of the patient's shoulder on the side of the rib cage to be treated.
2. Hold the patient's forearm berween your arm and chest while grasping the patient's midarm with your hand. 3. Place your other arm obliquely downward under the patient's rib cage. Flex your fingers so that the fingertips engage the caudad edges of the angles of the upper ribs. 4. Pull cephalad on the rib angles with your fingers, reinforced by an augmenting pull on the patient's arm (generated by a cephalad sway of your entire upper body). 5. Hold the tension for approximately 3 to 5 seconds before releasing. After a few seconds of rest, repeat the process, hold 3 to 5 seconds, and release. 6. Repeat this cycle until increased motion results or patient fatigue or discomfort suggests termination of the treatment. 7. When repetition of this treatment no longer produces in creased range of motion at this level, move your hands to the next inferior group of ribs and repeat the articulating treat ment process. Treat groups of rwo to four ribs progressively, from above downward, until all ribs on both sides are moving freely.
This technique may be modified by adding the patient's inspi ration to produce more tension and therefore induce increased range of motion. Direct the patient to take a deep breath after you have generated maximum tension. Instruct the patient to ex hale and relax as the tensions diminish. Then release the passive external traction. Note that the above techniques may be modified by starting on the lower ribs and progressing cephalad, rather than starting on the upper ribs and progressing downward. In this case, trac tion is in the caudad direction. Exhalation might enhance this procedure.
ried out in sequence in this treatment. Separate ranges of motion are consecutively engaged, beginning with those least likely to be disturbed ( flexion/extension) and progressing to those most commonly restricted (internal/external rotation). It is easy to per form an articulatory technique to increase one or more ranges of shoulder joint motion, using the arm as a long lever against a shoulder girdle fixed to the patient's thorax by the other hand of the physician. Each step of the treatment may be enhanced by the addition of muscle energy activation and/or respiratory force after the barrier has been engaged. For example, once the lateral traction, stretching, and fluid pumping of the initiating stage of Spencer have been completed, carry the patient's arm, flexed at the elbow, slowly but firmly into extension against the resistance of a fixed scapula and clav icle. A fter release of the tension, repeat the process until no in crease in motion results from application of this phase of the treatment.
ARTICULATORY TECHNIQUES BY REGION Reminders 1. An articulatory technique may be used to increase motion generally in all joints in that region, or it may be used more specifically at a particular joint by repetitively engaging a spe cific motion restriction. Most of the force is applied at the end-range of motion. 2. Articulatory techniques use passive, smooth, rhythmic mo tions designed to stretch contracted muscles, ligaments, and capsules-and, to a lesser extent, move fluids. 3. Articulatory techniques decrease tissue tension, enhance lym phatic flow, and stimulate increased joint circulation. We do not know the effects in the associated autonomic and central nervous system components. 4. Articulatory techniques are especially useful in treating spinal transitional zones (e.g., cervicothoracic, thoracolumbar, and lumbosacral areas). 5 . Articulatory techniques may be used to pave the way for high velocity/low-amplitude ( HVLA) treatment. 6. Discomforr during treatment is usually expected. As a rule, pain is not acceptable, except, for example, during the treat ment of "frozen shoulder" using the Spencer techniques when discomfort is expected but limited to patient tolerance. 7. Although the treatment is directed to a restriction on one side, some physicians prefer to apply these treatments bilat erally, so as not to induce an imbalance in the tonicity of the musculature or cause nervous system dysfunction/imbalance.
Indications l.
Restriction of joint motion.
SHOULDER TREATMENT: SPENCER TECHNIQUE
2. Myofascial shortening (primary or secondary).
This is a classic clinical application of stepwise articulating tech nique. Seven different but related articulating procedures are car-
4. Preparation for HVLA-specific thrust.
3. Bilateral or unilateral somatic dysfunction in a region or at a segmental level.
55. Articulatory T echniques
Contraindications (Relative) 1. Advanced bone-wasting diseases.
837
6. Repeat slowly in a smooth, rhythmic fashion unril there is improved motion (or ro the rolerance of the pariem).
2. Fractures. 3. Acute local inAammarory condition.
Alternative Procedure
4. Acure localized infection.
1. Cross both forearms and place your hands on the patiem's shoulders ro support the head.
5. Neurologic signs elicited during prerest or rrearmenr means that you must srop treatmenr by this method and reevaluate the patienr.
2. Raise your arms ro flex the head and neck.
Extension CERVICAL TECHNIQUES
Diagnosis
Flexion
Decreased cervical extension.
Diagnosis
Reduced cervical Aexion.
Objective
Increase cervical extension. Objective
Increase cervical flexion.
Patient Position
Patient Position
Supine. Caution: Do not perform this technique on a patienr wirh neurologic signs on cervical extension or a parienr who reports symproms of verrebrobasilar insufficiency.
Supine.
Procedure
Procedure I.
1.
Sit above rhe head of the patienr (Fig. 55.1).
2. Place one hand on the parienr's shoulder. 3. Place the orher hand cradling rhe occipital region. 4. Lift the head unril full Aexion is obrained. 5. Hold in full Aexion for 3 ro 5 seconds or unril no fur ther response is palpated or observed; then rerurn roward neutral.
Sir above rhe head of rhe parienr (Fig. 55.2).
2. Place one hand under the patient's neck. 3. Use your rhumb and forefinger as a fulcrum by pressing them against rhe posterior aspects of a cervical verrebra. 4. Grasp the patient's chin with your other hand and lift it ro extend the neck. In patiems with temporomandibular joinr (TMJ) dysfunction, grasp rhe patienr's forehead instead. 5. Using smoorh, rhythmic morion, repeal' several times. 6. Shift your fulcrum ro another vertebra and repeal' unril you have treated all of rhe cervical vertebrae.
FIGURE 55.1. Cervical flexion technique.
FIGURE 55.2. Cervical extension technique.
838
VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Rotation Diagnosis
Decreased cervical rotation. Objective
Increase cervical rotation. Patient Position
Supine. Caution: Do not perform this technique on a patient who demonstrates neurologic s igns on cervical rotation or a patient who reports symptoms of vertebrobasilar insufficiency. Procedure
1. Sit above the head of the patient. 2. Grasp the patient's chin with your hand, with your forearm contacting the patient's zygoma. 3. Cup the patient's occiput w ith your other hand. 4. Rotate the head toward the side of decreased motion. 5. Hold, then return toward neutral. 6. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient).
FIGURE 55.3. Cervical regional side-bend i n g technique.
3. F irmly s ide bend the neck away from the restriction. You may reinforce this lateral movement by gently leaning against the head (with your abdomen). Do not use inferior vertical pressure on the vertex, especially if the patient has any signs of nerve root compression. 4. Hold, then return toward neutral. 5. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient).
Alternative Procedure
1 . You may rotate one direction, go through neutral, and rotate the other direction if you are treating a patient with bilat eral decrease due to myofascial shortening. (This may require change in hand position.) 2. You may also do this rotation procedure w ith the patient in flexion. 3. DO NOT DO I T IN EXTENSfON!
Regional Side-Bending Diagnosis
Decreased cervical side-bending (lateral flexion). Objective
Segmental Side-Bending Restriction Procedure
1. Place the medial aspect of your middle phalanx or the pad of your d istal phalanx against a specific joint level as a fulcrum. This should be done on the side opposite the restriction. 2. Grasp the posterior aspect of the head with the palm and fingers of your opposite hand. 3 . Use lateral translation to induce side-bending toward the re striction with your localized digit. At the same time, use lateral translation of the head in the opposite direction, achieving s ide-bending around the fulcrum. 4. Hold, then return toward neutral. 5. Repeat slowly in a smooth , rhythmic fashion until there is improved motion (or ro the rolerance of the patient).
Increase cervical side-bending. Patient Position
Supine. Procedure l.
CERVICOTHORACIC TECHNIQUE Flexion, Extension, Side-Bending Diagnosis
Decreased regional fl e xion, extension, side'-bending ion), or rotation.
Sit above the head of the patient (Fig. 55.3).
2. Place one hand on the shoulder opposite the side of restricted side-bending, using the other hand to cradle the occipital region.
Objective
Introduce motion where it has been inappropriately restricted.
55. Ar ticulatory Techniques
839
FIGURE 55.4. Cervicothoracic side-bending technique.
Patient Position
FIGURE 55.5. Thoracic flexion technique.
Lareral recumbenr (resrricred side up). Procedure
1. Srand in fronr of rhe patienr ( Fig. 55.4). 2. Support rhe parienr's head and neck wirh your hand and fore arm . The parienr's arm nearesr the table should be flexed ar rhe shoulder and elbow while the opposire arm is adducted on rhe lareral rhorax and hip area. 3. Grasp rhe spinous process of Tl with your caudal hand to stabilize ir againsr forces applied from above. 4. Use your other hand to extend, side-bend, or rorare rhe head and neck to the restricrion of morion ar rhe joinr level you are rrearing. 5. Hold, rhen rerurn toward neutral. 6. Repear slowly in a smoorh, rhythmic fashion until there is improved motion (or to the tolerance of the parient). 7.
Move sequentially to the next inferior joint and repeat the process.
THORACIC TECHNIQUES Flexion Diagnosis
Procedure
1. Srand behind the patient (Fig. 55.5). 2. Put your arm over the patient's shoulder across his or her chest and place your hand on rhe patient's opposite shoulder. The parient hooks his or her hands over your arm. 3. Stabilize the lower of the rwo ver tebrae being treared by grasp ing and fixing rhe spinous process with your fingers and rhumb. 4. Use your orher arm to flex rhe upper rhorax of the parienr to rhe level of your stabilizing hand, achieving maximal AexlOn stretch at the joint space above. 5. Hold, then rerurn toward neurral. 6. Repeat slowly in a smoorh, rhyrhmic fashion �lI1ril rhere is improved motion (or to the tolerance of the patJenr). 7.
Move your srabilizing hand to the next inferior vertebra and repear rhe process until you have treated all the involved segments.
Extension Diagnosis
Decreased thoracic extension.
Decreased flexion. Objective
Increase thoracic flexion.
Objective
Increase thoracic extension.
Patient Position
Patient Position
Seated.
Seared.
840
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Procedure I.
Stand behind the patient.
2. Put your arm over the patient's shoulder across his or her chest and place your hand on the patient's opposite shoulder. The patient hooks his or her hands over your arm. 3. Stabilize the lower of two vertebrae with the thenar eminence of your other hand or by grasping and fixating the spinous process with your fingers and thumb. You also use this hand as a fulcrum. 4. Introduce extension by anterior translation of your stabilizing hand as your other arm bends the upper thorax backward around the fulcrum, achieving maximal extension stretch at the joint space above. 5. Hold, then return toward neutral. 6. Repeat s lowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 7. Move your stabilizing hand to the next inferior vertebra and repeat the process until you have treated all the involved segments.
Note: This technique is contraindicated in a patient with facet arthritis, because increased pressure exerted on the facets by the use of extension can aggravate that problem.
FIGURE 55.6. Thoracic rotation techn ique.
Side-Bending Diagnosis
Decreased thoracic side-bending. Rotation Diagnosis
Decreased thoracic rotation.
Objective
Increase thoracic side-bending. Patient Position
Objective
Seated.
Increase thoracic rotation. Procedure Patient Position
Seated.
Procedure
1. Srand to the right, slightly behind the patient. Place your right arm across the front of (he patient's thorax, grasping the interior left shoulder (Fig. 55.6). 2. Place your thumb and fingers on both sides of the spinous processes to stabilize the vertebra below the restricted segment. 3. Use your hand on the shoulder to induce rotation to the right, to the point that you feel the rotation at the joint space above your stabilizing hand. 4. Hold, then return toward neutral. 5. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 6. Move your stabilizing fingers to the next inferior vertebra and repeat the process until you have treated all the segments desired.
1. Stand to the right, behind the patient, who is seated with arms folded across his or her chest. 2. Pass your right arm over the patient's right shoulder and across the chest. Pur your hand into the left axilla, palm against the thoracic wall. 3. Apply a stabilizing pressure with your index and long fingers and thumb on the sides of the spinous process at the vertebra below the segment you wish to treat. An alternative is to use the thenar eminence placed against the side of the spinous process as a fulcrum. 4. Introduce right side-bending by applying a downward pres sure through your axilla on the patient's right shoulder and an upward lift of the patient's left shoulder with your right hand. This forms a convexiry on the left, side-bending the spine to the right. You should feel maximal stretch at the joint space above your stabilizing hand (fulcrum). , 5. Hold, then return toward neutral. 6. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient) . 7. Move your stabilizing hand to the next inferior vertebra and
55. Articulatory T echniques
repeat the process until you have treated all the involved segmenrs.
COSTAL ARTICULATORY TECHNIQUES For a patienr who has difficulry breathing, whether because of chronic obstructive pulmonary disease or any other reason, you may need to adjust the timing of these techniques ro minimize interference with the already limited breathing cycle. It is generally best ro treat the ribs on both sides, even if restriction is most apparenr on one side. Reminder:
Anterior Approach Diagnosis
841
2. Stabilize the anrerior right ribs with your caudad (right) hand. Use the hypothenar eminence and little fi nger, the thumb and thenar eminence, or group the fi ngertips in a row along the superior border ro stabilize the lower of the two ribs being treated. 3. Use the patienr's right arm ro stretch soft tissues in the in tercostal space superior ro your stabilizing hand. Have the patienr breathe in deeply, synchronizing your stretch with full inspiration. 4. Hold, then return toward neurral. 5. Repeat slowly i n a smooth, rhythmic fashion u nril there is improved motion (or ro the rolerance of the patient). 6. Move your stabilizing hand ro the next superior costal bor der and repeat the process unril you have treated all the ribs desired.
Decreased costal motion during the breathing cycle. Posterior Approach Objective
Diagnosis
Enhance or optimize costal motion.
Decreased costal motion during the breathing cycle.
Patient Position
Objective
Supine.
Enhance or optimize costal respirarory motion .
Procedure
Patient Position
I.
Stand on the restricted (right, in this example) side of the supine patienr (Fig. 55.7). Grasp his or her right wrist with your cephalad (left) hand. Stretch the patienr's arm upward ro the poinr where it is ful ly extended at the elbow and flexed at the shoulder superior ro the head.
Prone. Procedure
1. The patienr lies prone with head facing ro the left (Fig. 55.8). Stand ro the left at the head of the table and use your right hand ro grasp the patienr's left arm just proximal ro the elbow, stretching the arm inro full abduction with a slight posterior angle and external rotation. 2. Stabilize the i n ferior of the two ribs being treated with your left thumb and thenar eminence at the superior border of the lower rib near the angle. 3. Achieve a stretch of the latissimus dorsi and the inrercostal muscles by using the arm as a long lever (with abduc tion/extension) at the same time that you stabilize the inferior rib. 4. Hold, then return roward neurral. 5. Repeat slowly in a smooth, rhythmic fashion unril there is improved motion (or ro the rolerance of the patienr). 6. Move your stabilizing hand ro the next superior rib and re peat the process unril you have treated all the restricted (or involved) ribs.
Lateral Recumbent Diagnosis FIGURE 55.7. Costal technique, anterior a pproach.
Decreased bucket-handle excursion during the breathing cycle.
842
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
3. Srabilize the inferior of the two ribs being treated in the mid axillary line with your right thumb and thenar eminence. 4. Achieve a stretch/separation of the soft tissues between the ribs by abducting the arm as a long lever at the same time that you stabilize the inferior rib. Synchronize this with the parient's full inspiration. 5. Hold, then return roward neutral. 6. Repeat slowly in a smooth , rhythmic fashion until rhere is improved motion (or ro rhe rolerance of the patient). 7. Move your stabilizing hand ro rhe next superior rib. Repeat the process until you have treared aJI involved ribs.
Posterior Rib Raising Diagnosis
Decreased cosral motion during rhe breathing cycle. Objective
Enhance or optimize costal respirarory morion. FIGURE 55.8. Costal technique, poste rior a pproa c h .
Patient Position Objective
Enhance or oprimize cosral respirarory morion.
Supine. Procedure I.
Patient Position
Lareral recumbenr (restricted side up; lefr in this example).
Procedure I.
Srand on the restricred side ofyour supine patient (Fig. 55. 1 0).
2. Place rhe parient's arm in full abducrion, holding rhe wrisr wirh rhe operaror's righr hand. 3. Place your caudal hand under rhe patient's thorax. Press the tips of your fingers firmly against the inferior surface of rhe
Srand in fronr of your right lateral recumbent patlenr ( Fig. 55.9). The patient's left elbow should be flexed.
2. Grasp the patient's left elbow with your left arm and place rhe shoulder in full abduction.
FIGURE 55.9. Costal technique, latera l recumbent.
FIGURE 55.10. Costal technique, posterior rib raising.
55. Articulatory Techniques
843
angles of the patient's ribs and at the same time, extend and abduct the patient's arm (long lever stretch). Synchronize this with the patient's full inspiration. You may need to bend your knees slightly to do this comfortably. 4. Hold, then retmn toward neutral. 5. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 6. Move your (fulcrum) hand to the inferior border of the angle of the next inferior rib and repeat the process until you have treated all the involved ribs.
LUMBAR ARTICULATORY TECHNIQUES Flexion (Seated) Diagnosis
Decreased lumbar flexion. FIGURE 55.12. Lumba r flexion technique, posterior view.
Objective
Increase lumbar flexion.
chest with your hand on the opposite shoulder. The patient hooks his or her hands over your arm.
Seated.
3. With the thenar eminence of your other hand, stabilize one vertebra in the lumbar spine. With your forearm against the patient's sternum, direct the force of flexion straight through the patient toward your stabilizing hand, gapping the joint above it.
Procedure
4. Hold, then return toward neutral.
1. Stand behind and to the side of your patient, who is seated on or straddling the table (Figs. 5 5 .1 1 and 5 5 . 12 ) .
5. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the rolerance of the patient).
2 . Put one arm over his o r her near shoulder and across his o r her
6. Move your stabilizing hand to the next inferior vertebra and repeat the process until you have treated all the involved segments.
Patient Position
Flexion (Lateral Recumbent) Diagnosis
Decreased lumbar flexion. Objective
Increase lumbar flexion. Patient Position
Lateral recumbent. Procedure
1. Stand in front of the patient. 2. Face the patient and flex his or her knees and rest them together against your anteromedial thigh or inguinal area.
FIGURE 55.11. Lumbar flexion technique, anterior view.
3. Bend forward at the waist and flex your own knees. Gently flex your patient's lumbar spine by swinging your pelvis with the patient's knees toward the head of the table area.
844
VlI. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
4. Use your caudal hand to pull the inferior lumbar vertebra in a caudal direction as you induce flexion to the joint space above it. Your cephalad hand should stabilize the superior lumbar vertebra. 5. Hold, then return toward neutral. 6. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 7.
Move your stabilizing hand to the next superior vertebra and repear the process until you have treated all the involved seg ments.
Flexion (Supine) Diagnosis
Decreased lumbar flexion.
Objective
Increase lumbar flexion.
FIGURE 55.13. Lumbar extension technique, seated.
Patient Position
Procedure
Supine.
1. Stand behind and to the right side of your patient, who is straddling the table (Fig. 5 5 . 13 ) . Have the patient cross arms in front, with each hand grasping the opposite shoulder. As the patient leans slightly forward, place your righr arm under his or her arms with your hand under the opposite axilla.
Procedure
1 . Stand to the side of your supine patient and flex his or her hips and knees. Resting your pectoral area on the knees, place your hands below the patient's lumbar region, one on each side of the spine. 2. Press toward the table through the patient's knees and thighs, in a superior anteroposterior fashion, to spring the lumbar joint space in flexion. Use your hands to pull caudally, stretch ing the joint space above. 3. Hold, then return toward neutral. 4. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 5 . Move your stabilizing hand to the next superior vertebra and repeat the process until you have treated all the involved segments.
Extension (Seated) Diagnosis
Decreased lumbar extension.
2. Place your left thenar eminence against the spinous process of a lumbar segment as a fulcrum around which you extend the lumbar spine. 3. Use your right hand or arm to lift the patient's elbows, intro ducing thoracolumbar extension to the joint space/segment above your fulcrum. Accentuate this extension with your left thenar eminence, applying an anterior translatory force at the segment level. 4. Hold, then return toward neutral. 5. Repeat slowly in a smooth, rhythmic fashion until there is imptoved motion (or to the tolerance of the patient). 6. Move your stabilizing hand to the next inferior vertebra and repeat the process until you have treated all the involved segments.
Extension (Lateral Recumbent) Diagnosis
Decreased lumbar extension.
Objective
Objective
Increase lumbar extension.
Increase lumbar extension.
Patient Position
Patient Position
Seated.
Lateral recumbent.
55. Articulatory Techniques
845
FIGURE 55.14. Lumbar extension technique, lateral recumbent.
Procedure I.
Stand in front of and facing the patient in the right lateral recumbent position (Fig. 5 5 . 14). Flex the patient's knees and hips to 90 degrees, resting the knees against your anteromedial thigh or inguinal area.
2. Place your hands posterior to (WO adjacent lumbar vertebral segments so that your fingertips meet at rhe joinr space. 3. Bend forward at the waist and flex your own knees. By induc ing posterior and caudad motion through the patienr's knees, extend your patient's lumbar spine. Localize motion to the joinr space at which your fingers meet. Pull the inferior lum bar vertebra in an inferoanterior direction as your cephalad hand pulls the superior vertebra in a superoanterior direction. 4. Hold, then return toward neutral. 5. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 6. Move your stabilizing hand to the next superior vertebra and repeat the process until you have treated all the involved segments.
shoulder, and your right hand grasps his or her opposite shoul der or axilla. 2. Place your left hand (thenar eminence, or the pads of several fingers) on the right side of a vertebra in the patienr's lumbar spine, just lateral to the spinous process. 3. Use your left hand as a fulcrum to induce left lateral transla tory force as you create right side-bending by depressing the patienr's right shoulder. Repeat in a rhythmic manner to all segmenrs, side-bending more for the lower lumbar segments. 4. Inrroduce right side-bending by applying a downward pres sure through your right axilla on the patienr's shoulder and an upward lift of the patienr's left shoulder with your right hand. This forms a convexity on the left, side-bending the spine to the right. You should feel maximal stretch at the joint space above your stabilizing (fulcrum) hand. 5 . Hold, then rerurn toward neutral. 6. Repeat slowly in a smooth, rhythmic fashion unril there is improved motion (or to rhe tolerance of the patienr).
Side-Bending (Seated) Diagnosis
Decreased lumbar side-bending (lateral flexion, right example)
FIGURE 55.15. Lumbar side-bending technique, seated.
1I1
this
Objective
Increase lumbar side-bending (lateral flexion).
7. Move your stabilizing hand to the next inferior vertebra and repeat the process unril you have treated all the involved segmenrs.
Side-Bending (Lateral Recumbent) Diagnosis
Decreased left lumbar side-bending (lateral flexion). Patient Position
Seated.
Objective
Increase left lumbar side-bending (lateral flexion). Procedure l.
Stand behind and to the right side of your seated patient (Fig. 5 5 . 15). Your right axilla overlies the patienr's right
Patient Position
Right lateral recumbent (right side down).
846
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 55.16. Lumbar side-bending technique, lateral recumbent.
FIGURE 55.17. Lumbar rotation technique, seated.
Procedure
1. Stand at the side of the table, in front of and facing the patient ( Fig. 5 5. 16). 2. Flex his or her knees and hips to approximately 90 degrees. 3. Place your left hand so that your fingers are palpating the spinous processes of the lumbar spine. 4. Place your right hand and forearm under the patient's ankles and lift them toward the ceiling until your left hand palpates that you have introduced left side-bending in the lumbar re gion at the desired level. 5 . Hold this stretch, then return toward neutral. 6. Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patient). 7. If you are performing this as a regional motion, complete the treatment by treating the other side in the same manner. S.
If you are attempting to induce more specific articulatory treat ment to a particular segmental level , your left hand placement is such that your thumb and fingers hold the spinous process of a particular vertebra, stabilizing it as you induce side-bending to the joint below via the long lever moved by your right hand. When you have achieved the desired effect at a particular level, move to the next superior level to be treated.
Procedure
1. Stand behind and to the right of the patient, who is straddling or sitting on the table ( Fig. 55. 17 ) . Your right axilla overlies the patient's right shoulder and your right hand grasps the opposite shoulder or axilla. The patient hooks his or her hands over your arm. 2. Regional : Place your left hand just to the right of the spinous processes and encourage right rot;ltion by applying a left lateral force to the spinous processes. 3. Segmental: If you want to be more specific in your treatment, stabilize a particular spinous process with your thumb and fingers, and resist the rotation you induce with the other hand or arm, confining the stretching, rotational forces to the joint above the segment you are stabilizing. 4. Induce right rotation to the lumbar spine by rotating the patient's thorax to the right with your right arm and hand. 5. Hold, then return toward neutral. 6. Repeat slowly in a smooth , rhythmic fashion until there is improved motion (or to rhe tolerance of the patient). 7. Move your stabilizing hand to the next inferior lumbar region or segment and repeat the process until you have treated the lumbar region or the specific involved segments.
Rotation (Seated) Diagnosis
Decreased right lumbar roration.
Note: For decreased left lumbar rotation, make the appropriate adjustments to treat the other side.
Objective
Increase right lumbar rotation.
PELVIC ARTICULATORY TECHNIQUES Rotation to Innominate
Patient Position
Diagnosis
Seated.
Posteriorly rotated innominate.
55. Articulatory T echniques
847
Note: This technique can easily be adapted to the lateral re CLlmbem position, with the physician standing behind or in from of the patiem and treating the upper hemipelvis. Rotation to Innominate Diagnosis
An teriorly rotated innominate. Objective
Normalize innominate position and motion. FIGURE 55.18. Pelvis technique, anterior rotation of innominate.
Objective
Normal ize innominate position and motion.
Patient Position
Supine. Procedure I.
Patient Position
Supine, with the leg of the posterioriy rotated innominate hang ing over the side of the table, inducing hip extension. Procedure
Stand on the dysfunctional side of the patient (Fig. 5 5 . 18).
1.
2. Place your cephalad hand behind the posterior superior iliac spine (PS IS), cupping it. 3 . Place your caudad hand on the amerior surface of the distal thigh to induce further hip extension. 4. Induce further hip extension by pressing down on the dis taJ rhigh while simulraneously pushing the PSIS amerioriy, inducing anterior rotation to the innominate. 5. Hold, then return toward neutral. G.
Repeat slowly in a smooth, rhythm ic fashion until there is improved motion (or to the tolerance of the patient).
FIGURE 55.19. Pelvis technique, posterior rotation of innominate.
Stand ar the side of your patien t's ameriorly rotated in nominate (dysfunctional side), facing the patiem's head (Fig. 5 5 . 19 ) .
2. Flex the patient's knee and hip, grasping the knee between your caudal arm and pectoral area. 3. Place your cephalad hand on the anterosuperior iliac spine (ASIS). 4. Use your caudad hand to grasp the ischial tuberosity. 5. Apply a posterior rotational torque with both hands by ex erting downward pressure on rhe ASIS while pulling upward on the ischial tuberosity. You may slightly adduct the thigh to gap the sacroiliac (51) joint. G.
Hold, then return toward neutral.
7.
Repeat slowly in a smooth, rhythmic fashion until there is improved motion (or to the tolerance of the patienr).
Note: This technique can easily be adapted to the lateral re cumbem position, with the physician standing behind the patiem and treating the upper hemipelvis.
FIGURE 55.20. Pelvis technique, i n nominate outflare.
V!I. Osteopathic Considerations in Palpatory Diagnosis and ManipuLative Treatment
848
with caution and gentleness on patients who have tissue contrac tures. Remember to inform your patients that some discomfort during treatment is normal. With that knowledge, they can give you the feedback you need to adjust the force applied in these techn iq ues. An example of extremity treatment using articulatOry tech nique is the treatment of the shoulder with techniques described and improved by Spencer ( 1 -3). They are useful in diagnosing and treating m usculoskeletal dysfunction of the shoulder, and are o utlined here as they are presently being taught in most osteo pathic colleges. Spencer's original techniques have undergone some modifi cation with use. An important modification is the addition of muscle e nergy and the use of compression or traction.
FIGURE 55.21. Pelvis technique, innominate inflare.
Sacroiliac Joint Gapping Diagnosis
In nominate outAare or inAare. Objective
Normalize in nominate position and motion. Patient Position
Supine. Procedure
1 . Stand at the patient's dysfunctional side (Figs. 5 5 . 20 and 5 5 .2 1 ) . 2. Grasp the patient's Aexed knee with your caudal hand. 3. Grasp the patient's A S I S (inAare) or P S I S (outAare) with your cephalad hand. 4. I n Aare: Pull the AS IS laterally and tOward the table as you abduct the hip by pulling laterally on the knee. 5. OutAare: Pull laterally on the PSIS as you adduct the hip by pushing medially on the knee. G.
Hold, then return tOward neutral.
7. Repeat slowly in a smooth, rhythmic fashion u ntil there is improved motion (or to the tOlerance of the patient).
ARTICULATORY TECHNIQUES IN THE EXTREMITIES The same principles that apply to the spinal segments can be used to treat the extremities. In the extremities, the techniques are particularly useful when a degree of restriction or fibrosis has developed in the surrounding soft tissues during a period of in activity after injury. This problem often follows a healed capsular tear or immobilization in a cast. These tech niques should be used
Stage 1 : Stretching Tissues and Pumping Fluids with the Arm Extended Note: This technique is performed as Stage 1 and stretch tissues" (see Fig. 5 5 .28, pg. 85).
to
"pump Auids
1 . Position the patient's arm on your shoulder, elbow ex tended (an alternate patient positioning and hold is shown in Fig. 5 5.7). 2 . Grasp the patient's proximal humeral area as close to the h umeral head as possible with both hands. 3. Pull the patient's humerus tOward you (traction) , ge ntly and slowly, holding tension on the periarticular tissues. Do not press on the medial neurovascular bundle with your thumbs. Release traction force slowly. 4. Compress the articular area (shoulder) by guiding the humerus tOward the glenoid fossa with both hands. Release compres sion. The traction and compression can be done rhythmically or in a random on-and-off man ner. 5 . Repeat steps three and four in sequence until motions are freer. G.
Move the patient's shoulder in translatOry directions ante rior/posterior, mediaillateral, and cephalad/caudal to the lim its of motion. Hold, release forces, and repeat until motions are freer.
Stage 2 : Glenohumeral Extension/Flexion with the Elbow Flexed Patient Position
Lateral recumbent (affected shoulder up) . 1 . Neutral position of the patient's arm with the elbow Aexed (operatOr to side of table facing the patient). Grasp the patient's elbow using the caudal hand. The cephalic hand compresses the scapula and clavicle (shoulder girdle) against the thorax (a critical component) (Fig. 5 5.22). 2 . Move the patient's arm (elbow Aexed) intO extension in the horizontal plane while holding the shoulder girdle firmly against the superior thorax. Move slowly against the resistive barrier and repeat until no further range of motion (ROM) is achieved.
55. ArticuLatory Techniques
849
2. Move the patient's arm into flexion (elbow extended) in the horizontal plane while holding the shoulder girdle firmly against the superior thorax. Move slowly against the resistive barrier and repeat until no further ROM is achieved. 3. Muscle energy activation: Engage the barrier and instr uct the patient to "pull your elbow toward your feet." Resist isometri call y until effective contraction is localized at the shoulder. At that point, ask the patient to relax. the muscular contraction and simultaneously "take up the slack motion," then slowly release the isometric resistance. 4. Take the arm from its new position of resistance to flexion and repeat steps three and four until no further ROM is achieved.
Spencer recommended this procedure be repeated-in exten sion with the elbow flexed.
FIGURE 55.22. Extension with elbow flexed.
3. Muscle energy activation: Engage the barrier and insrruct the patient to "push your elbow toward the physician" (flexion). Resist isometrically until effective contraction is localized at the shoulder. At that point, ask the patient to relax the m uscu lar contraction and sim ultaneously "take up the slack motion," then slowly release the isometric resistance. 4. Take the elbow from its new position of resistance to extension and repeat step three until no further ROM is achieved.
Spencer recommended this technique be repeated in flexion with the elbow flexed. Stage 3: Glenohumeral Flexion/Extension with the Elbow Extended
Stage 4: Circumduction and Slight Compression with the Elbow Fl exed/Extended I.
With the elbow flexed, the patient's arm is abducted to 90 degrees. Grasp the patient's elbow with caudal hand. The cephalic hand compresses the scapula and clavicle (shoulder girdle) against the thorax (Fig. 5 5 .24).
2. Move the patient's arm through full clockwise circumduc tion with slight compression on the glenohumeral joint. Move slowly and firmly and repeat several times to gain ROM. This step evaluates circumduction ROM with the elbow flexed and also assesses the comfort of moving the articular surface of the h umeral head over the articular surface of the glenoid fossa. 3. Move the patient's arm through full counterclockwise circum duction. Move slowly and firmly, repeating several times to gain ROM. 4. A m uscle energy activation does not apply in this step.
1. Neutral position of the patient's arm with elbow flexed. Grasp the patient's forearm using the cephalic hand. The caudal hand compresses the scapula and clavicle against the thorax. (Fig. 5 5 .23).
FIGURE 55.23. Fl exion with elbow extended.
FIGURE 55.24. Circumd uction with sl ight compression and elbow flexed.
850
VII. Osteopathic Considerations in PaLpatory Diagnosis and ManipuLative Treatment
FIGURE 55.25. Circumduction with traction with the el bow extended.
FIGURE 55.26. Abduction a n d internal rotat i o n with the a r m be h i n d the back.
Stage 4 (Continued): Circumduction and Traction with the Elbow Extended I.
With the elbow extended, the patient's arm is abducted to 90 degrees. Grasp the patient's forearm with the caudal hand. The cephalic hand compresses the scapula and clavicle (shoul der girdle) against the thorax (Fig. 5 5 .25).
external rotation) and repeat steps three and four until no further ROM is achieved.
Stage 6: Abduction with Internal Rotation with the Arm Behind the Back With the arm abducted and the elbow Aexed, position the patient's hand behind the back (to the extent permitted by the patient's comfort with this positioning), observing if the dorsal surface of the hand can be placed against the dorsal surFace of the ipsilateral Aank area (Fig. 5 5 . 26 ) .
2. Move the patient's arm through full clockwise circumduction with slight traction. Move slowly and repeat several times to gain ROM. This step evaluates circumduction ROM with the arm extended and also assesses the comfort of applying tension to the capsule of the glenohumeral joint.
I.
3. Move the patient's arm through full counterclockwise circum duction with traction. Move slowly and repeat several times to gain ROM.
2. Grasp the patient's elbow (or place your index and middle fingers around the elbow) and slowly move the elbow ventrally (toward you). Repeat to gain abduction and especially internal rotation.
4. A muscle energy activation does not usually apply in this step.
Stage 5 : Adduction and External Rotation with the Elbow Flexed I.
Neutral position of the patient's arm with the elbow Aexed. With the caudal hand, grasp the patient's elbow. The cephalic hand compresses the scapula and clavicle (shoulder girdle) against the patient's thorax. The patient's hand (oF the arm be ing treated) is resting palm down on the wrist of your cephalic hand to stabilize the patient's arm.
2. With your caudal hand, move the patient's elbow in an arc toward his or her face and toward the Aoor; this produces adduction and external rotation at the shoulder. 3. Muscle energy activation : At the resistive barrier (barrier en gagement), instruct the patient to, "pull your elbow toward your waist." Resist isometrically until effective contraction is localized at the shoulder. At that point, ask the patient to relax the muscular contraction, "take up the slack," then release the isometric resistance. 4. Move the elbow
to
its new resistive barrier (to abduction and
3. Muscle energy activation : Position the patient at the resistive barrier, then instruct the patient to "pull your elbow away From me." Resist isometrically until eFFective contraction is localized at the shoulder. At that point, ask the patient to relax the muscular contraction, "take up the slack," slowly release the isometric resistance. 4. Move the elbow to its new position of resistance to abduction and internal rotation and repeat steps three and four until no Further ROM is achieved.
Stage 7: Stretching Tissues and Pumping Fluids with the Arm Extended This stage is a repeat of Stage 1 (Fig. 5 5. 27) .
COMMENTS ON SPENCER SHOULDER TECHNIQUES Spencer used his shoulder treatment program to increase pain Free range of motion by pumping Auids and stretching tissues
55. ArticuLatory T echniques
851
clinical prognosis of a patient undergoing treatment for shoulder dysfunction. CONCLUSION Articulatory technique consists ofmovements against a diagnosed barrier to (limitation of) motion in an articular structure. These movements are: Controlled Slow Repetitive Passive
FIGURE 55.27. Stretch i n g tissues a n d p u m p i ng f l u ids with the arm extended; stretching tissues a n d p u m p i n g f l u ids with t h e extremity extended and the e l bow flexed.
around the shoulder. Spencer would treat the patient with the elbow flexed and then repeat the stage with the arm extended. He stated that in this way the lever arm was short for initial testing and treatment and was then increased by arm extension, stretching the shoulder and elbow flexors in the extended state. The modified Spencer motion techniques add compression and traction to steps three and four. They also add muscle energy to the applicable steps to enhance treatment possibilities. Experienced physicians report that the Spencer techniques do not seem to have rapid results in patients with metabolic or other debilitating disease, such as poorly controlled diabetes. Treatment of the shoulder using the seven motions of Spencer (2,3) in their original form or in their modified form provides objective diagnostic tests and articulatory treatment for soft tissue restrictions and gives objective evidence supporting the
Pressure against the resistant barrier is held long enough in each cycle to allow a stretching of the tissues controlling and limiting the motion of the joint. These techniques are designed to deal with one or several ranges of motion, as indicated by the diagnosis and the nature of the articulation being treated. Passive force against the barrier may be augmented by incorporating· patient generated (intrinsic) force, such as that found in the final stage of muscle energy tech nique or in respiratory cooperation. Articulatory technique may be the principal component of a treatment program. It is also used to prepare an articular area for other forms of manipulative treatment. It may be preferred to high-velocity treatment in infants, postoperative patients, com promised or debilitated patients, and older patients. Articulating technique is often applied to support general body functions, such as respiratory efficiency. REFERENCES I . Spencer H. Shoulder rechnique. J Am Osteopath Assoc. 1 9 1 6; 1 5 : 2 1 8-220. 2. Spencer H. Treannenr of bursiris and rendoniris. J Am Osteopath Assoc. 1 926;25:528-529. 3 . Paniquin DA. The evolurion of osreopathic manipulative technique: the Spencer technique. J Am Osteopath Assoc. 1 992;92: 1 1 34- 1 1 46.
THRUST (HI(iH-VELOCITYfLOW-AMPLITUDE) TECHNIQUES ROBERT E. KAPPLER JOHN M. JONES, III
HISTORIC PERSPECTIVE KEY CONCEPTS • • • • • • • • • • • •
Definition and development of thrust technique Indications and uses for thrust technique Quantity and quality of motion loss with somatic dysfunction End-feel at restrictive barrier and barrier engagement Accumulation of force and corrective force velocity and amplitude Patient relaxation Exaggeration technique Mechanism of thrust technique action Effect of technique on unstable, hypermobile joints Dose, precautions, and contraindications for thrust technique Guidelines for safety and benefits of technique HVLA treatment technique examples by regions and diagnosis
Thrust tech nique is defined as a type of direct technique that uses high-velocity/low-amplitude forces ( 1 ). "Thrust techniques" are a collection of direct method manipulative treatments that use h igh-velocity/low-amplitude (HVLA) activation to move a joint that is exh ibiting somatic dysfunction through i ts restrictive bar rier so that when the joint resets itself, appropriate physiologic motion is restored . The term direct refers specifically to position ing the restricted joint(s) toward the restrictive barrier. Simply stated, you move the restricted joint in the direction it won't move. After precise positioning against the restrictive barrier, the final force is a short (low-amplitude) , quick (h igh-velocity) thrust. Greenman (2) described the force as impulse. Ordinarily, a click or pop is heard at the time the force is applied. There is an imme diate increase in the range of motion and the freedom of motion.
Thrust technique has been the major type of technique taught in colleges of osteopathic medicine and has been practiced by osteopathic physicians for years. In the 1970s, the osteopathic medical school curricula began to include other types of tech niques. Until recently, however, osteopathic manipulation and high-velocity technique were essentially synonymous. Graduates are now exposed to a complete spectrum of direct and indirect techniques; therefore, osteopathic mani pulation is no longer syn onymous with thrust technique. A. T. Still used very little thrust tech nique. Instead, he used what we now describe as myofascial release and indirect tech niques (see Chapters 58, 60, and 70) . It is interesting to specu late why osteopathic manipulative techniques taught in the col leges evolved into the exclusive domain of thrust techniques and remained that way for so many years. Faculty may have been responsible for the change. Students, in the early days, assisted in the teaching of techniques. These students may have played a major role in moving the curriculum to thrust techniques. Thrust techniques can be taught by precisely describing the nature of the restriction and providing techniques for treating the dysfunction. These techniques can be practiced. In contrast, fascial release and indirect techniques require skill in assessing motion patterns in the tissues. The technique is difficult to describe because the physician is responding to tactile and proprioceptive input from his or her hands. Faculty find release techniques difficult to teach, and students may perceive them as abstractions. Thrust tech niques are easier to teach and to learn. However, al though thrust techniques can be described in a precise manner, the motor co ordination necessary to use these techniques effectively requi res extensive practice and experience.
MOTION LOSS AND SOMATIC DYSFUNCTION
Somatic dysfunction is impaired or al tered function of related components of the somatic system (1):
853
56. Thrust (High- Velocity/Low-A mplitude) Techniques
Skeletal Arthrodial structures Myofascial structures Related vascular lymphatic and neural elements Diagnostic tests for somatic dysfunction include TART: T: Tissue texture change (feel) A: Asymmetry or positional change (look) R: Restriction of motion (move) T: Tenderness
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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
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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
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Motion loss in somatic dysfunction Range between physiologic and anatomic barriers
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56.1. Somatic dysfunction:
quality and
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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
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= Anatomical barrier =Physiological barrier R =Restrictive barrier (Xl Is start point of manipulation 0= Usual" neutral" for this joint
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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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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. =
=
56. Thrust (High- Velocity/Low-Amplitude) Techniques
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
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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 .
56. Thrust (High- Velocity/Low-Amplitude) Techniques
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
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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
56. Thrust (High- Velocity/Low-Amplitude) Techniques
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
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
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.
56. Thrust (High- Velocity/Low-A mplitude) Techniques
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
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
56. Thrust (High- Velocity/Low-A mplitude) Techniques
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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).
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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.
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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).
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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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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).
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VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.
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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.
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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
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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.
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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)
Type of Muscle Energy Joint mobilization using muscle force.
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.
Type of Muscle Energy Joint mobilization using muscle force.
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
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
59. Balanced Ligamentous Tension Techniques
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
59. Balanced Ligamentous Tension Techniques
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
59. Balanced Ligamentous Tension Techniques
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
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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.
59. Balanced Ligamentous Tension Techniques
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
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Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.
60.
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
Neuromusculoskeletal and Myofascial Release
933
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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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
Neuromusculoskeletal and MyoJascial Release
935
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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VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.
60.
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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.
938
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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VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.
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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
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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.
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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.
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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.
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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.
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
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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.
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
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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.
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VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
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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.
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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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Neuromusculoskeletal and Myofoscial Release
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.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Neuromusculoskeletal and Myofoscial Release
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.
961
962
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.
Neuromusculoskeletal and Myofoscial Release
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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 • • • • • •
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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.
Functional Technique: An Indirect Method
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.
Functional Technique: An Indirect Method
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
Functional Technique: An Indirect Method
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.
VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
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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
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Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
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.)
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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
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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<-""=:--��-+--
Firm dural attachments Second sacral
Osteopathy in the Cranial Field
991
own sensorium. It is essential to be relaxed, physically, mentally, and emotionally. Your attitude should be similar to one who is trying to hear a m inor sound-complete attention is given to listening. Keep the hand contact l ight. Pressure by the hands will sup p ress the inherent motion and/or distract the sensors (proprio ceptors) i n the hands. If excessive hand pressure is continued, the patient may get a headache. If you have difficulty perceiving the motion in one patient, try other patients. The cyclic characteristics of the motion and its amplitude (strength or power) usually vary fro m one i ndividual to another. The biphasic cycle of motion of the PRM most often en countered occurs 1 0 to 14 times per m i nute. When observing the rate, allow one full minute and count the number of cycles (one flexion phase plus one extension phase equals one complete cycle). Evaluating the amplitude of the PRM in patients who have clinical problems requires experience, but has been found to be statistically possible (59) and may reveal the most useful clinical data about the patient. After palpating five or ten indi viduals, one can determine that the strength or vitality of the rhythm is stronger in one or two individuals, fair or medium in some, and weak or poor in others. With experience in palpation and clinical knowledge of the patient's history and symptoms, the rate and amplitude become an additional diagnostic indi cation of their state of health and is helpful in determining a p rognosIs. The rate and quality of the PRM may be increased slightly: Following vigorous physical exercise With systemic fevers • Following effective OMT of the craniosacral mechanism •
H/---- Filum terminale
•
The rate and quality of the PRM may be decreased with: FIGURE 62.2. Craniosacral mechanism with arrows i n d i cating d i rection of motion d u ring flexion phase of physiologic motion. (From Magoun H I . Osteopathy in the Cranial Field, 2nd ed. K i rksvi l l e, MO: Journal Print ing Company; 1966, with permiss i o n . )
• • • • •
that sense the subtle cranial motion are proprioceptors located in tendons and around j oints. The numerous tactile sensors i n the fingerpads are n o t a s receptive t o this motion. Even though a gentle and light contact is essential, it is not a fingertip contact.) 4. Allow your mind to become quiet and direct your attention to the space between your hands, allowing what is sensed by your proprioceptors to be perceived by your brain . (Continue to stay relaxed; do not try to feel something. I f the patient's head has fairly normal motion, you may feel a slow, rhythmic swelling or widening followed by a receding or narrowing. This constitutes one cycle of inherent motion. This cycle is usually steadily repeated. The motion is so m ild and subtle that it may actually feel as i f the head is breathing.) Subtle motion is easier for some physicians to palpate than for others. Some find this difficult to sense because they try too hard. Their intensity is so set, their effort so strong, that they block their
•
Stress (mental, emotional, physical) Chronic fatigue Chronic infections Mental depression and other psychiatric conditions (60) Chronic poisoning Other debilitating conditions
The cyclic, biphasic motion onglI1atlng within the PRM, is most evident to palpation in the head region but is palpa ble in every part of the body. The i m pulse moves longitudi nally through the body and extremities, with m idline structures moving through flexion/extension and paired structures mov i ng through external/internal rotation. Its presence or absence and its deviation fro m normal direction are useful diagnostic SIgns. The body is subject to stresses and strains from before birth until death. Pressures and forces affect the developing fetus, the neonate during birth, and the individual through childhood, ado lescence, and adulthood. These forces cause minor to major dis tortions of the cranium that result in strains of the sphenobasilar synchondrosis (SBS). With induced strain, the efficiency of the PRM is compromised. The compromise may be minor to major i n its effect on the health of the individual.
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Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
STRAINS
Several types strains of the S BS are known. Torsion occurs around an anteroposterior (AP) axis of the skull that extends from nasion through the symphysis to opisthion (Fig. 62.3A). The sphenoid and related structures of the anterior cranium rotate in one direction about this axis; the occiput and related structures of the posterior cranium rotate i n the opposite direction, producing a twist o r torsion at the SBS. This strain is
Axis of
A
named for the side of the high wing of the sphenoid, right torsion ( RT) or left torsion (LT). Side bendi ng/rotation (SBR) at the SBS occurs around an AP axis and around two parallel vertical axes, one through the body of the sphenoid and one through the foramen magnum, perpendicular to the physiologic transverse axes and the AP axis (Fig. 62.3B ) . This is a compound movement similar to physi ologic motion in the spine when rotation and side bending are concomitant movements. Because the sphenobasilar symphysis is slightly convex upward, as the two bones side bend away from
A
rotation
Vertical strain
�)
Torsion
l
l
" '�j/'i; �
. �.
Axis of rotation
B
B Side-bending/rotation
FIGURE 62.3. Schematic patterns of sphenobasilar junction. In torsion and side bending/rotation, sphenoid and occiput rotate i n opposite di rections about axes indicated. A: Torsion with great wing high on the right. Occiput is lower on the side of high great wing. B: Side bend ing/rotation with convexity to the left. Both great wings of sphenoid and occiput are lower on the side of convexity. (From Sutherland WG, Wales AL. Teachings in the Science of Osteopathy. Portland, OR: Rudra Press; 1990, with permission.)
Lateral strain
FIGURE 62.4. Schematic patterns of sphenobasi lar junction. In vertical and lateral strain patterns, sphenoid and occiput rotate in the same direction around para l le l axes. A: Superior vertical strain. As a result of rotation of the bones, the base of the sphenoid is relatively elevated with the base of the occiput relatively depressed. B: Right latera'i stra in. As a result of rotation of the bones, the base of the sphenoid is relatively displaced to the right with the base of the occiput relatively displaced to the left. (From Sutherland WG, Wales AL. Teachings in the Science of Osteopathy. Portland, OR: Rudra Press; 1990, with permission.)
62.
each other (around the (wo parallel axes), both bones rotate in feriorly on the convex side (around the AP axis) and superiorly on the concave side. This strain pattern is named for the side of the convexiry, SBR right (SBRR) or SBR left (SB Rd . These four strain patterns ( RT, LT, S BRR, SBRd are common and are considered physiologic if their presence does not i nterfere with the flexion-extension motion of the mechanism. Extreme or exaggerated flexion with decreased extension of the SBS is considered a strain pattern. Conversely, marked or ex aggerated extension with decreased flexion is considered a strain pattern. Normally, the PRM moves through the flexion and ex tension phases equally and fully. Vertical and lateral strains or displacement occur at the SBS and can be superimposed on the above strains. Vertical strain at the SBS is present when movement occurs i n the same direction for the sphenoid and the occiput, around the (wo transverse axes as in flexion-extension (Fig. 62.4A). This creates a superior or inferior strain at the SBS and disrupts normal flexion-extension. Verrical strain is named for the relative position of the basisphe noid, superior or inferior. Lateral strain at SBS occurs when both bones rotate in the same direction, clockwise or counterclockwise, around (wo parallel ver tical axes (fig. 62.4B). Basisphenoid and basiocciput veer in op posite directions, producing a shearing rype of resultant motion. When this strain occurs in utero or during the birth process, i t results i n a parallelogram-shaped head i n the infant. Lateral strain is named for the direction the basisphenoid shifts, right or left. SBS compression is a strain in which the sphenoid and occiput have been forced together so that physiologic flexion-extension is impaired. Compression varies from mild to moderate to severe and occurs from a force to the back of the head, to the front of the head, or from a circumferential compression (as during birth) that exceeds the resiliency of the tissues. Strains of the SBS involve the entire cranial and facial strucrure and influence the position and motion of the sacrum by way of the RTM . The midline bones and paired bones accommodate to the strain or strains in the base of the skull. Trauma to the head, face, spine, sacrum, pelvis, or lower extremities is a common strain-producing factor. Pelvic function is affected by a strain i n the base o f the skull. Such strain i s also accommodative t o a strain in the pelvis. The body, including the head, truly functions as a uni t.
PRINCIPLES OF DIAGNOSIS
Trauma Obtain the following information about trauma: 1 . Age at which the trauma occurred; this incl udes birth trauma. 2. Type of force as well as amount, veloci ry, direction, and the area of i mpact; vehicular accidents, blows to the face or head, and falls on the tailbone or buttocks are common. 3. Dental history including extractions, orthodontia, malocclu sion, bruxism, and temporomandibular joint problems. 4. Fractures, concussions, inertial injuries, coma. 5. Habitual head pressures, such as sleeping positions, thumb sucking, ear phones, orthodontic head gear, new dentures, etc. 6. Extremes of temperature: chilling of the face or head may precede Bell palsy; heatstroke or sunstroke may be related to headache. 7. Surgical procedures i nvolving the head such as the mouth gag, the bite block, the bronchoscope or gastroscope, or the anes thetic mask held over the nose-mouth for prolonged periods with a tight headband to keep it in place. 8. Changes in appearance or personaliry following severe trauma. Adult patients tend to recall only injuries of the recent past. They believe that injuries from infa ncy, childhood, or adoles cence are of no importance and tend to forget past trauma. They may need leading questions to elicit this information. Some pa tients have amnesia related to trauma to the head and cannot relate accurate information. A family member may be able to give additional history.
History of Delivery and Newborn Period If the patient is an infanr or child, a more detailed history from the parent(s) is essential. Questions concerning the health of the mother during pregnancy, the number and character of pregnan cies, the details of the delivery, the appearance and action of the newborn, and the development of the infant should be asked. Signs and symptoms compatible with severe forces of labor and delivery are an indication for considering OMT in the care of these patienrs. These signs and symptoms include: • • • • •
Patient History
Taking the patient's history includes asking leading and pertinent questions to encourage the patient to recall relevant past events and to describe the complaint in some detail. In addition to the usual questions pertaining to herediry, childhood diseases, adult diseases, and surgeries, (wo other areas for questioning are pertinent to dysfunction of the craniosacral mechanism: trauma
993
history and information about the delivery and newborn recovery period.
•
The diagnosis of a pathologic condition or malfunction of the PRM is based on the history, observation, and palpation. Palpa tion by a well-trained and sensitive operator is the most reliable source of information.
Osteopathy in the Cranial Field
• • • • • • • •
Distortion of the cranium Excessive molding Ridging or overriding along any suture Diffi. c ulry in suckling or swallowing Vomiting Respiratory distress Bradycardia Tachycardia Abnormal crying Strabismus Nystagmus Spasticiry or flaccidiry of the limbs Opisthotonos Drowsiness
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VII
Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Cyanosis Convulsions • Fever • Tremors • •
Abnormal habits such as lying with the head turned ro one side only, head banging, or constanr rubbing of the back of the head against the sheet are indicative of strains of the cranium.
Diagnosis by Observation
Look for symmetry or disrortion of the osseous structure be neath the soft tissues. Observe the face and head: the shape and conrours of the head and face show hereditary influences as well as the combined effect of the forces of labor on the bones. At birth the sphenoid, temporals, and occiput are made up of several osseous parts with cartilage between parts and between bones ro allow for compression and molding of the head during bi rth. Strains within a bone may occur and are called inrraosseous strains. The Aexion type of skull is round in shape with a wide trans verse and a shortened AP diameter, with the temporals in relative external rotation (Aared laterally). In this type ofskull, the fronrals are wide and sloping upward, the cheek bones are wide, and an open mouth view of the maxillary region of the hard palate re veals it ro be wide and with a low arch ro the vault. All paired structures are in a position of relative external rotation. The extension type of skull is long and narrow with temporals in relative inrernal rotation, fronrals narrow with the brow ap pearing more vertical, orbits and face narrow, and maxillae (hard palate) narrow with a high arched vault. All paired structures are in a position of relative inrernal rotation. Note the positioning of the bones. The position of the sphe noid bone inAuences the position of the peripheral bones of the anrerior cranium, which includes the fronrals and all bones of the face except the mandible. The position of the occiput in A uences the position of the bones of the posterior cranium (the parietals and temporals) and i n turn influences the position of the mandible. With rorsion and side bending/rotation of the SBS, the facial structures tend ro appear asymmetric as they assume a position of relative external rotation on the side of the high wing and a position of relative i n rernal rotation on the side of the low wing. I f the sphenoid is rotated on an AP axis, the eyes and orbits will appear unlevel. Compare the relative positions of the cheekbones and the maxillae. Note the relative positioning of landmarks. It is sometimes difficult ro determine if the occiput has rotated on the A P axis because it is hidden by hair. As the occiput tilts on this axis, i t carries the temporals with i t . The temporal on the low side o f the occiput i s positioned roward relative external rotation, and the temporal on the high side of the occiput is positioned roward relative inrernal rotation. Therefore, the relative position of the ears gives an indication of the tilt of the occiput. Compare right and left ear lobes ro see i f they are level; note flari ng of the ears. A temporal positioned roward external rotation tends ro be more Aared; a temporal positioned roward i n ternal rotation tends ro be more Aat. By combining the findings of the anrerior and posterior
cran ium, the observer is able ro arrive at a tenrative or working diagnosis of rorsion or side bendinglrotation of the SBS. Viewing the midline of the face, noting the nose, mouth, and cenrer of the chin, provides additional information. Nasal devia tion may indicate the relative position of the maxillae and sphe noid or may indicate past trauma or fracture. The ch in (mandible) tends ro deviate ro the side of the externally rotated temporal bone. Heredity also inAuences facial characteristics and is a sig nificant consideration for establishing a prognosis. Strains of the cranial base occur during birth or from trauma. If trauma is induced inro a prior strain pattern, the findings of observation are not reliable for diagnosis. Diagnosis by Palpation
To become expert at the art of palpation for diagnosis and treat ment requires repeated experience, patience, and perseverance. These guidelines help improve palparory skill: l . Use a light hand conract. I fyour conract is stronger than the force of the inherenr motion, you inrerfere with the mechanism you ate attempting ro diagnose or treat. Do not interject yourself inro the patienr's P RM . 2. Have a clear visualization of the structure(s) beneath your hands. This requires a detailed study of the anaromy and phys iologic motion of each of the bones of the body, including the cranium and face. The design of the articulations between bones and their mechanical and physiologic relationship is a complex study, but it is essential ro providing accurate diagnosis and suc cessful treatment. (Space constrainrs do not permit such detailed study in this chapter.) 3. Understand that the job of the physician is ro assist the patienr ro obtain or mainrain optimal health. The physician does not do the healing; healing comes from within the patienr. With knowledge and experience, one learns ro tune in ro and be guided by the PRM of the patien t ro facili tate this healing process, assist ing the patienr's own inherent healing capacity ro release biome chanical impedimenrs. The auromatic processes that promote healing are much more intelligenr and efficienr in the manage menr of the health of the individual than any external force or person can be.
CLINICAL PROBLEMS REQUIRING OSTEOPATHIC MANIPULATIVE TREATMENT Neonatal
OMT of infanrs and children can be a rewarding experience for the patient and the docror. Children respond ro treatment faster than adults. Compromised function of the PRM is a cumulative process beginning in utero or during birth, combined with the various traumatic incidents of growing up, as well as one or more trau matic events sustained as an adult. The physician must keep this in mind when taking the hisrory. Consideration of the trauma of the birth process deserves fur ther explanation. The base of the skull is formed in cartilage and the vault is formed in membrane. At birth, the sphenoid is in three parts, the temporal is in three parts, and the occiput is in four
62.
Lesser wing Greater wing
Pterygoid plates
FIGURE 62.5. Sphenoid at b i rth in three parts. Cartilage i ntervenes be· tween body·l esser wing u n it and greater wi ng-pterygoid u n its. (From Sutherland WG, Wales Al. Teachings in the Science of Osteopathy. Portland, OR: Rudra Press; 1990, with permission.)
pans, with canilage intervening between the osseous elements (6 1 ). The frontal and mandible are in two pans and each maxilla is in two parts. This is nature's way of protecting the CNS and providing for compressibility of the head as it passes through the birrh canal. The bones of the vault are osseous plates that over lap at the edges. The canilaginous base tends to compress, bend, twist, or buckle depending on the amount and direction of com pression and rotational forces of labor and binh. These various pans are vulnerable ro misalignment; the brain , cranial nerves, and intracranial membranes are subject ro possible inj ury or mal function. One or more of the strain patterns of the SBS generally has its beginning during the binh process (Figs. 62. 5 and 62.6). The infant's first breath and subsequent crying with deep breathing, kicking, squirming, and suckling assist with decom-
Squama: ...---- Interparietal Supraoccipital
Cartilage
Condylar part
1llii!iiiJ----
Occipital condyle
Basilar p rocess Two condylar parrs along the lateral sides o f foramen magnum • Squama extending from the posterior border of the foranlen magnum to the lambdoid suture • •
The medulla oblongata rests on the basilar part, and the spinal cord extends through the space within the four parts. Cranial nerves IX, X, and XI and the j ugular veins pass through the j ugular foramina at the anterolateral border of each condylar part. Cranial nerve XII passes through the anterior condylar canals located within the condylar parts near the j unction between the condylar parts and basilar part. Compression with rotation of the posterior cranium during birrh with distortion, displacement, and j amming ofthese four osseous plates and intervening cartilage is easily visualized (Fig. 62.6) . The symptoms manifested in the newborn or young infant that indicate the presence of abnormal mechanical stress in this area include:
• • • • • • •
41.------ Basilar process
• •
FIGURE 62.6. Occiput at b i rth in four pa rts with i n a carti l a g i nous ma trix. Articu lar condyles receive contributions from both condylar and basilar pa rts of the occiput. (From Sutherland WG, Wales Al. Teach ings in the Science of Osteopathy. Portland, OR: Rudra Press; 1990, with permission.)
995
pression of the crani um , face, and pelvis (6 1 ) . Decades of clinical experience have shown that if the activities of the neonate are not strong enough to open up the entire PRM to i ts optimal function, these neonates benefit fro m the assistance of an osteo pathic physician trained in the cranial concept and in treatment procedures. Examination and treatment are best given during the first few days oflife, at which time a great deal is accomplished by releasing the compressive forces of b i rth. If no treatment is pro vided, as time passes and growth p rogresses, the strains become more established. In time, the formative parts of the various bones of the base change from canilage to osseous tissue. If overlapping of the osseous plates of the vault is allowed to remain, the plates grow together, forming a synostosis. Osteopathi c physicians uti lizing OCF have found that when synostosis pervades the vault, the osseous case cannot grow and expand at the same rate as the brain inside, and the brain function of that individual appears to be compromised. Expert treatment given early in the life of an in dividual can be one of the most imporrant therapeutic measures in preventive medicine. Treatment given later is beneficial, but more can be accomplished in less time and with less effort and expense i f treatment is given soon after the stresses and strains occur. An example of disturbance of function directly related to the compressive forces of birth concerns the posterior part of the cranial base. The four parts of the developing occiput are the:
• Kerckring's center
Osteopathy in the CraniaL FieLd
Respiratory distress Excessive crying Inability to suckle or weak suckling Vom i ting Bradycardia Tachycardia Tremors Spasticity or flaccidity of the limbs Cyanosis Torticollis
This abnormal mechanical stress on the brainstem, cranial nerves, and venous drainage is treated by gentle application of mild, sustained spreading of the formative parts of the base of the skull by a physician trained to apply OMT in this manner.
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Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
The relative position and motion of the temporal bones affect drai nage from the middle ear through the pharyngotympanic tube; their somatic dysfunction is clinically capable of resulting in tinnitus, dizzi ness, and decreased auditory acuity. Treatment is ai med at releasing membranous strains of the cranial base, temporal bones, and upper cervical spine to help reestablish equal and synchronous motion to the temporals as well as the entire PRM. Consider these factors: 1 . Without normal motion present, stasis of fluids and lack of oxygen provide an ideal medium for m icroorganisms. 2 . When the inherent motion throughout the cranium and face is optimal, the movement of fluids and mucus is enhanced (a provision of nature for emptying the ethmoid, sphenoid, and maxillary sinuses). 3. The autonomic nerve supply to the nasal mucosa by way of the sphenopalatine ganglion is vulnerable to impinging adnexa. 4 . Middle ear infections, sinusitis, pharyngitis, and other acute inflammatory processes are often associated with altered cra nial Functions (62). Vascular Supply
Consider the vascular supply to the brain. The internal carotid arteries enter the petrous portions of the temporal bones, extend Forward and medial ly within those bones, exit from the tips of the petro us, and turn superiorly along the sides of the basisphenoid to enter the cranial cavity. Disturbance in physiologic motion, in which the petro us portion of the temporal articulates with the basiocciput and the basisphenoid, compromises the optimal func tion of these arteries through related dural tension. The vascular i nterchange between the choroid plexus and the CSF (occurring within the ventricles of the brain) is affected by the widening and narrowing of the ventricles, which occurs with each biphasic motion of the PRM. The venous drainage from the brain is by way of the vari ous in tracranial veins emptying i nto the venous sinuses, which are channels between layers of dura mater. The great cerebral vein enters the straight sinus, which joins the transverse sinus to become the sigmoid sinus. That sinus becomes the j ugu lar vein, which passes through the j ugular foramen to exit the skull. The j ugular foramen is an aperture between the occiput and temporal bones. N inety-five percent of the venous blood from the brain exits the skull through these two apertures ( 1 2) . This area i s extremely vulnerable to trauma to the back o r side of the head. I m paired venous drainage leads to venous stasis. The movement of venous blood along the various venous si nuses directly depends on the biphasic motion of the RTM and the bones to which it attaches (62). Consider venous stasis as a causative factor for headache, decreased cerebral function, and depression. The pituitary body is located in the sella turcica o n the superior surface of the sphenoid bone j ust anterior to the SBS. This neu roendocrine gland, an extension of the brain, secretes a number of hormones that afFect all the glands of the endocrine system. A red upl ication of dura, the diaphragma sella, encircles the stalk of the pitu i tary like a collar. The hormones secreted by the pituitary pass into the vascular plexus surrounding it. Pituitary Function is
compromised iF the inherent motility of the CNS or the move ment of blood through the cranial vascular system is impaired (5). The dura mater lines the skull and spinal canal, and extensions of it continue beyond the various apertures as the sheaths of the cranial and spinal nerves. Entrapment neuropathy describes the localized inj ury or irritation to nervous tissue from the mechanical effect of impinging adnexa. There are multiple examples (62-64) of entrapment of cranial and spi nal nerves and their branches throughout the body, all of which are amenable to osteopathic treatment by releasing membranous and/or ligamentous articular strains. The interstitial fluids of the entire body are constantly influ enced by the biphasic cycle of the PRM. This movement o F fluids is slow, steady, and efficient even at the cellular level with the ex change of metabolites across the cell membrane. In that sense, the CNS functions as a pump. Sutherland compared this fluid motion in the body to the tide of the ocean ( 1 2) . I t is a major Factor in the repair of damaged tissue From contusions, sprains, strains, and inflammatory processes ( 1 2). Knowledge of the PRM and its effects on the health of the total being broadens our un derstanding of the self-healing and self-regulatory mechanisms taught by Dr. Still. Trauma
Trauma is by far the major cause of disruption and malFunction of the PRM. The force of trauma is extreme in vehicular acci dents. The force from a Fall is transmitted From the Feet or ischial tuberosities upward through the body into the base of the skull. The vector of force established through the body or head is pal pable (65 ,66) and is an important diagnostic sign. The direction of motion of the CSF and CNS is disrupted, and the function of the PRM is mildly to severely impaired, depending on the severity of the trauma and the response of the patient. Trauma to the PRM can occur from mild, sustained force such as wearing a spring type of headset or from orthodontic appliances on the teeth (67); wearing a tight hat or swim cap will augment or create or alter existing patterns. Trauma occurs in various degrees and i n innumerable forms. The PRM functions as a unit; trauma to one area aFFects the entire RTM. The PRM does its best to continue to function, but the quality of that function decreases with the passage of time and additional trauma. The rate and amplitude of the PRM is a most valuable diagnostic and prognostic indicator of the severity of the compromise and response to treatment (68). A slow rate and a low amplitude are dependable indicators of a long-standing and/or overwhelming problem during which the patient's vitality has been depleted, indicating more treatmen t over a longer period of time will be required (68). The reciprocal is also true. In the course of treatment, improvement is associated with a rate and amplitude increase toward a more normal pattern. Dentistry
OCF is especially pertinent to the practice of complete d� ntistry (69). Improperly directed forces of extraction, fillings, swing of crowns, and improperly fitted dentures alter the occlusion of maxillary and mandibular teeth and disturb the PRM (70).
62.
Osteopathy in the Cranial Field
Resultant symptoms i nclude: Headaches Vertigo with its attendant gastroi ntestinal symptoms • Cervical syndromes • Temporomandibular joint dysfunction syndrome •
•
Clin ical en igmas of the head and neck (such as arypical facial pain) require evaluation of dental problems and the effects of dental procedures and orthotics on the P RM (7 1 ). Satisfactory therapeutic response depends on evaluation and treatment by both the dentist and the osteopathic physician.
PRINCIPLES OF TREATMENT
The aim of treatment, as with any osteopathic procedure, is to normalize structure and function. The optimal function of the PRM affects not only the CNS bur also every cell and tissue i n the body. Regardless of which method or procedure a physician elects to use, this constant cyclic motion is at work behind the scenes every mi nute of every hour of every day of every year of an individual's life. Goals of Treatment
The goals of treatment include: • •
• • • • •
Normalizing nerve function, including all cranial and spinal nerves as well as the autonomic nervous system Counteracting stress-producing factors by normalizing func tion of the cerebrum, thalamus, hypothalamus, and pituitary body Eliminating circulatory stasis by normalizing arterial, venous, and lymphatic channels Normalizing CSF Auctuation Releasing membranous tension Correcting or resolving cranial articular strains Modifying gross structural patterns
Some hindrances to treatment are myofascial strains from be low the cranium or the sacrum, local or general infections, n u tritional deficiencies, and organic poisons ( 1 2). Removal of non structural hi ndrances must be addressed as well as OMT in the management of the patient's health problems. To use the power or potency of the inherent activiry of the PRM within the pa tient to assist with the release of strains (somatic dysfunctions), it is necessary to understand balanced ligamentous tension and balanced membranous tension. Balanced ligamentous tension is used in treating any articulation supported and protected by l ig aments. Balanced membranous tension refers to the dura mater (RTM) and is used to treat the articulations of the cranium, face, and sacrum. The point of balanced membranous tension is defined as that point in the range of motion of an articulation where the mem branes are poised between the normal tension present throughout the free range of motion and the increased tension preceding the strain or fixation that occurs as a joint is carried beyond its nor mal physiologic range ( 1 2) . Thus, it is the most neutral position possible under the inAuence of all the factors responsible for the
�O 0-+ A
997
cJ
�O o o+-0
c ...
FIGURE 62.7. Methods for arriving at the point of bala nced membra nous tension. A: I n d i rect action (exaggeration). B: Di rect action. C: Dis engagement. D: Opposite physiologic motion. (From Magoun HI. Os teopathy in the Cranial Field, 2 n d ed. K i rksv i l le, MO: Journal Pri nting Compa ny; 1 966, with permission.)
existing pattern, all attendant tensions having been reduced to the absolute minimum. This point is unique for each strain that occurs. I t is the point at which the inherent force can move through the i nvolved tis sues at its maximum efficiency. The operator seeks to position the bones making up the articulation at the point of balanced mem branous tension by keen, sensitive, knowledgeable palpation. Dr. Sutherland expressed this as palpating with seeing, feeli ng, thinking, knowing fingers. Figure 62.7 illustrates arriving at the point of balanced mem branous tension by positioni ng the components. The squares indicate two bones making up an articulation, and the arrows represent the directions the operator employs for positioning ( 1 2) . Figure 62.7A illustrates indirect action or exaggeration. This procedure is commonly employed from the age of 5 through adulthood. It is not used in acute trauma to the head when ex aggeration of misalignment may produce or increase intracranial hemorrhage. To employ this method, increase the abnormal re lationshi p at the joint by moving the articulation slightly in the direction toward which it was lesioned. Figure 62.7B illustrates direct action. This treatment method is employed when exaggeration is not desirable, as i n acure trauma and in young children i n whom the sutural pattern has nor yet developed. This treatment is also used when there are overriding sutures. The components are gently guided back toward their normal position. Figure 62.7C illustrates disengagement. This treatment method is used when force or excessive membranous tension im pacts the osseous components. Disengagement technique merely separates the opposing surfaces within the anatomic and physio logic li mits of permitted motion. Figure 62.70 illustrates opposite physiologic motion. This method is seldom used, but when needed i t is employed to re lease a strain when a traumatic force has severely violated the physiologic pattern. One component is inAuenced by direct ac tion; the other is inAuenced by indi rect action. The physician selects the method of choice according to the patient's age and history, as well as by palpatory diagnosis. Respiratory cooperation may be used to enhance the effort of i nherent motion. The patient is asked to hold their breath in full inhalation or exhalation after the physician has positioned the articulation at balanced ligamentous or membranous tension. Holding the breath at ful l inhalation is more commonly used, but i f the articulation is held toward extension or internal rotation, holding the breath at ful l exhalation is more effective.
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VI!.
Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
Example One An example of treatment fol lows.
Diagnosis Somatic dysfunction of the midcervical spine (C4 E RR SR).
Treatment Treatment is indirect method, using balanced ligamentous ten sion, exaggeration, and inherent force.
Procedure 1 . Position the patient supine. 2 . Sit at the head of the table. 3. Place the fingerpads of the two index fingers at the lateral border of the articular pillars of C5. The long (third) fingerpads are at the articular pillars of C4. This gives you optimum contact for precise positioni ng of the two bones and for maximum sensing of the soft tissues over the articulation. 4. Slowly and gently position the two segments so that C4 is side bent right, rotated right, and slightly extended to the point of balanced l igamentous tension. Note that the tension on the involved muscles and ligaments eases, softens, and cannot be perceived as tension. The joint is nor in physiologic neutral, but is in neutral for this ligamentous strain in all three planes. 5. Maintain this position and allow the inherent force to work. Keep your sensing apparatus alert so that it perceives the slow cycl ic movement of the P RM. This movement feels l ike a longitudinal ebb and Aow or a subtle pumping effect up and down the spi ne. 6. Continue to maintain the positioning and to observe this cycl ic motion; the inherent force is working through the tissues that are maintaining the somatic dysfunction. As they accom plish their task for this articulation at this time, the amplitude of the inherent rhythm lessens and the pumping decreases, and the tissues beneath your palpating fingers seem to soften o r melt. 7. At this time, cease to hold the articulation in the treatment position. Gently recheck the motion of the articulation to ascer tain the therapeutic response. Physiologic motion is restored to varying degrees. A strain of the cranial base can be treated using the inherent forces and positioning for balanced membranous tension of the reciprocal tension membranes. This technique is applicable for an uncompl icated strain of the SBS. If a strain of the cranial base is compl icated by additional traumatic strains such as a frontosphe noidal or occipitomastoid strain, the technique as described will probably not be successful. The complicating strains from in duced trauma are treated before treating the sphenobasilar strain.
Example Two Diagnosis Somatic dysfunction of the sphenobasilar symphysis is side bend ing/rotation right (SBS is S BRR). The sphenoid and occiput have rotated on an AP axis so that the right side of the cranium is relatively inferior (caudad) and the left side is relatively superior (cephalad). Concomitant with that position, the greater sphenoid wing and the lateral angle of
FIGURE 62.S. "Vault h o l d " for contact of the cra n i u m (From Hruby R. Craniosacral Osteopathic Technique: A Manual, 2nd ed. Okemos, MI: The I nstitute for Osteopathic Studi es; 1996:33. with permission.)
the occiput on the right side are slightly spread and the greater sphenoid wing and the lateral angle of the left occiput are slightly approximated.
Treatment Treatment is indirect method, balanced membranous tension, with exaggeration and inherent forces to balance the RTM.
Procedure 1 . Position the patient supine. 2 . Sit at the head of the table. 3. Place your hands on the lateral sides of the patient's head with the index fingers contacting the greater wings of the sphe noid and the little fingers contacting the lateral angles of the occiput (vault contact) (Fig. 62. 8 ) . 4 . Gently palpate the rhyth mic activity of the patient's PRM and RTM. 5. The right hand slowly moves slightly caudad with index and fifth fingers spreading slightly while the left hand moves slightly cephalad and fingers approximate slightly. This position ing is slight and must be accurate, being guided by the ease of tension in the membranes within the cranium. With (he ease of membranous tension, the inherent forces begin to manifest with i ncreased vigor. The amplitude of the primary respiratory mechanism (PRM) automatically increases. 6. Maintain the positioning and carefully and continuously observe the increased activity of the inherent forces at work within the patient's mechanism. As the inherent forces work .through the membranous strain, they gradually cease the increased activity and become quiet. This cessation of the inherent rhythm is called a still point (6 1 ). 7. After the still point occurs, cease to maintain the position ing of the bones and membranes and continue to observe the Auctuant activity by light palpation. The quiet period passes, the rhythmic fluctuation resumes, increasing slowly and steadily in amplitude until it has returned to a more normal Aexion extension of the SBS. 8 . Gently remove your hands. 9. There is no substitute for thorough training and practice
62.
A
B FIGURE 62.9. Compression of forth ventricle (CV4). A: H a n d position for CV4 tec h n ique. B: CV4 tech n ique. (From H ruby R. Craniosacral Os teopathic Technique: A Manual, 2nd ed. Okemos, M I : The Institute for Osteopathic Studies; 1996, with permission.)
in the developmenr of skill in OMT based on the principles of OCF/CO. Well-known and typically utilized treatmenr proce dures based on the principles of OCF/CO are the compression of the forth venrricle (CV4) and the V-spread procedures. The CV4 (Fig. 62.9 A and B) is typically used to stimulate the body's inherent therapeutic capacity to deal with whatever dys function is present. By inducing extension (or i nternal rotation) of the PRM the inherent capacity for self-regulation and healing is facilitated by a stimulation of CSF flow. The technique is as follows: 1 . Operator at head of table. 2. Patient supine. 3. Place one hand in the palm of the other so that the thenar eminences lie uppermost and parallel to each other. Then slip them under the head, permitting the lateral angles of the occiput medial to the occipitomastoid suture to rest on them. The thenar emi nences provide a cushion for the occiput that should be com fortable for the patienr and operator. The fingers are free and not pressing on the neck. The weight of the head rests o n the thenar eminences and thereby gently compresses the lateral angles.
Osteopathy in the Cranial Field
999
FIGURE 62.10. V-spread of occipitomastoid suture. (From H r u by R. Craniosacral Technique: A Manual, 2nd ed. Okemos, M I : The I nstitute for Osteopathic Studies; 1996, with permission.)
4. Become aware of the cyclic motion of the occiput. Follow it toward extension (i.e., as the hands rock gently toward the op erator). Discourage flexion (hands moving away) . The amplitude of the motion will get progressively smaller until the still poinr is reached. This may pass so swiftly it may not be detected, but it is followed by a sense of softening and warmth in the occiput and a gentle rocking motion of flexion/extension. At the same time thoracic respiration should become primarily diaphragmatic and approximate the same cycle as the PRM. 5 . Observe the cranial activity to be sure that it remains quiet and then very gently remove your hands and put the patient's head on the table. Figure 62.9 demonstrates the CV4 via the occiput, it is possible to accomplish a CV4 via the temporals, parietals, and sacrum. The V-spread (Fig. 62. 1 0) is a very simple, safe technique for releasing any peripheral suture such as fron tonasal, nasomaxillary, or occipitomastoid. The technique is as follows: l . Place the index and middle fingers of the ipsilateral hand on either side of the suture. For a linear suture like the occipito mastoid, use the palmar surface of the length of two fingers. For a small suture like the frontonasal, use the fingertips. 2. Place the palm of the other hand on the patient's head at the other end of the longest diameter of the head from the suture (e.g., for the left occipitomastoid [Fig. 62. 1 0] ) , place the hand on the right frontal only. You will soon perceive a gentle impulse coming into the palm of this hand. Now cluster the fi ngers at the site of that impulse. You have thereby localized the optimum place from which to direct a palpatory sensation of a "fluid wave" to the restricted suture. As long as the suture is restricted, the fluid sensation will "bounce" back, but as soon as it releases, you will feel a gentle, easy motion between your hands.
Treatment procedures of the cranium should be used only by physicians experienced with palpation of the subtle activity of the PRM. Guidance by a physician experienced with the function of the PRM and the i n herent forces is essential to learning this techniq ue.
1 000
VII.
Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
CONCLUSION
22. Abd-EI-Basset EM, Federoff S. Contractile units in stress fibers of fetal
Much research remains to demonstrate the exact mechanisms involved In craniosacral dysfunction and recovery. However, more than 50 years of clinical experience has indicated that the use of OCF/CO has given relief to many patients i n whom no other treatment was effective.
23. Dani Jw, Chernjavsky A, Smith SJ. Neuronal activiry triggers calcium
human astroglia in tissue culture. j Chern Neuroanat. 1 994;7: 1 1 3- 1 22. waves in hippocampal astrocyte networks. Neuron. 1 992;8:429-440. 24. DuBolay G H , O'Connell J, Currie J, et al. Furrher investigations on
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62. Magoun H I . Enrrapmenr neuropathy in rhe Cralllll1l1. jAOA. 1 968;67:643-652. 63. Magoun H I . Enrrapmenr neuropathy of the central nervous system, part [ 1 . jAOA. 1 968;67:779-787. 64. Magoun H I . Enrrapmenr neuropathy of the cenrral nervous system, parr lll. jA OA. 1 968;67:889-899. 65. Magoun H I . Whiplash injury: a greater lesion complex. jAOA. 1 964;63: 5 24-535. 66. Harakal ] H . An osteopathically integrated approach ro the whiplash complex. jAOA. 1 975;74:94 1 -9 5 5 . 67. Lay E M . In: Gelb H , e d . CLinicaL Management ofHead. Neck and TMj Pain and Dysfonction. Philadelphia, PA: WE Saunders; 1 977; 1 7. 68. Becker RE. Lecture: Sutherland CraniaL Teaching Foundation Basic Course. Colorado Springs, CO; 1 98 5 . 6 9 . Magoun H I . Dental equilibration and osteopathy. jA OA. 1 975;74:98 1 99 1 . 70. Magoun H I . Osteopathic approach ro denral enigmas. jAOA. 1 962; 62: 1 1 0- 1 1 8. 7 1 . Magoun H I . The denral search for a common denominaror in cranio cervical pain and dysfunction. jAOA. 1 97;78 : 1 -6.
STRAIN AND COUNTERSTRAIN TECHNIQUES JOHN C. GLOVER PAUL R. RENNIE
KEY CONCEPTS • • • • • •
History Theoretical physiologic basis Treatment Instructions to patients Clinical pearls Specific treatments by body region
HISTORY Counterstrain began as an unexpected discovery in 1955. A young, athletic-looking man visited Lawrence H. Jones, DO, FAAO (1) because he had developed a condition 2 months prior that left him unable to stand erect. The injury was nor caused by trauma, but it gradually worsened over the 2 months. Since the onset, the man had received treatment by rwo chiropractors with no substantial improvement. Jones treated the man several times over the course of 6 weeks with no better results. At one visit, the man reported difficulty sleeping due to pain . Jones worked with the patient to find a comfortable position for the man to sleep in. After finding the position , Jones left the young man in the position and went to treat another patient. When Jones returned 20 minutes later, he assisted the young man to a standing position and to their mutual surprise, the patient stood erect and pain free for the first time in 4 months. Jones was impressed by the results and decided to investigate these findings. Jones experimented by treating patients with positions of comfort. He had frequent success, but wanred to shorten the waiting time of the treatmenr position. He observed that paravertebral areas that were tender to palpation prior to positioning were pain free after placing the patient in a position of comfort for a period of rime. Dr. Jones then began positioning only the affected region of the body, and this reduced the time in the treatment position. Ninety seconds in the position of comfort proved to be the optimal time required to benefit the patient. Shorter periods of rime
did not always produce lasting relief, and longer periods did not necessarily yield greater benefit. He also began mapping the discrete areas of tenderness and correlating them to specific somatic dysfunction identified by the methods he learned in osteopathic medical school. However, Jones found that he could only find the discrete paravertebral areas of tenderness in half of the patients. More answers came when Jones saw a patient with a groin injury. Although the examination revealed no inguinal hernia, there was a discrete area of tenderness. Jones placed the man in a position of comfort and palpated the tender area. To their surprise, it was no longer render. Jones slowly returned the patient to a neutral position and palpated the area of complaint again. He found no evidence of tenderness. Jones discovered that there were anterior, as well as posterior, render points. Jones began to search for render points in the anreriorrissues (2). This observation is consistent with the osteopathic principle of the body as a unit. The emphasis on spinal function and posterior diagnostic evaluation had eclipsed this connection . Other treatment approaches to the musculoskeletal system have identified discrete areas of tense, tender tissue. Travel! (3) developed an approach and used the term trigger point to describe tense areas. Jones ( 1,4) initially used the same term, bur later referred to these areas as tender points. Jones described over 200 specific tender points, and new tender points continue to be found. Through correspondence, Travell and Jones identified similarities and differences berween their diagnostic and treatment approaches. Initially, Jones referred to his new treatment approach as spontaneous release by positioning(5), but found this term to be cumbersome. Jones decided to use a shorter term, counterstrain, describing what Jones believed happened when his technique was used to treat somatic dysfunction. The initial injury produces a sudden "panic" lengthening of the antagonistic muscle to the originally strained and painful agonist muscle. Jones treats the render point associated with the antagonistic muscle by shortening this muscle, which also places the originally strained and painful muscle back into a stretched position-the position of the original strain. Dr. Jones made rwo important discoveries that contributed to manual medicine:
63. Strain and Counterstrain Techniques 1. Placing the body into a position of maximum comfort can treat somatic dysfunction. 2. Th.e anterior aspect of the patient must be evaluated, as well as the posterior, to effectively diagnose and treat somatic dysfunction.
THEORETICAL PHYSIOLOGIC BASIS OF COUNTERSTRAIN Physicians have demonstrated the clinical benefits of counterstrain for almost 50 years (6-14,19,22). However, research to confirm the physiologic basis of manual techniques has been limited. Therefore, we must draw on physiologic studies to shed light on how counterstrain works. Because tender points are found in myofascial tissue, undersranding muscle physiology provides some answers. This includes the palpatory changes in the myofascial tissue, as well as hypertonic muscles associated with somatic dysfunction. The neural system is another key component in the development and maintenance of somatic dysfunction . A third element important to understanding counterstrain is the role of the circulatory system. At the rime Jones was formulating his ideas about counterstrain, Korr (15) published an article on proprioceptors and somatic dysfunction. The article helped explain the role of the proprioceptors in muscle tone and the response to injury. Another important part of the model is the gamma system and irs role in muscle tone. Van Buskirk (16) described the important role of nociception in somatic dysfunction . The role of the circulatory system has not been adequately explained. One of the most important characteristics of the counterstrain model is the relationship between tender points and somatic dysfunction. The location of a specific tender point is constant from one patient to another. This suggests a strong anatomic basis for their location . Different myofascial structures, including tendons, ligaments, and muscle bellies have all been found to contain tender points. Myotomal, dermatomal, and sclerotomal relationships have been proposed to explain the relationship between a specific anatomic segment and the related tender points ( 17, 18,20). Another interesting anatomic correlation is the close location of tender points in areas where motor points are found. A motor point is the site where the motor nerve pierces the investing fascia and enters the muscle it innervates. Mapping the pathways of afferent nerves and the central system is important to understanding the role of the afferent nervous system. The bulk of afferent input comes from the soma (as opposed to the viscera). This difference is so great that nociceptive messages from the viscera are typically interpreted as being of somal origin. This unequal distribution can also be seen with the illustration of the homunculus in the cerebral cortex. The homunculus illustrates the proportional area in the cortex devoted to sensing and interpreting afferent input from different locations in the periphery. The neuronal "crosstalk'' in the central nervous system between sensory and motor nerves is the source of the various reflexes between the viscera and the soma. It also provides an explanation for why counterstrain treatment can have an effect on visceral function and circulatory flow.
1003
Normal function of the gamma efferent system is responsible for the change in muscle tone with changing demand. Jones proposed that the gamma system is responsible for the development of an inappropriate proprioceptive reflex associated with somatic dysfunction. A rapid shortening, then lengthening of the myofascial tissue sets up the inappropriate reflex. An event occurs that produces rapid lengthening of a muscle. Afferent feedback indicates possible myofascial damage from a strain. The body tries to prevent the myofascial damage by rapidly contracting the myofascial tissue that may be strained. This produces a rapid lengthening in the antagonist muscle. It is proposed that the rapid shortening, then lengthening of the antagonist produces the inappropriate reflex, and this is manifest as a tender point. The theory is that the nociceptive feedback from the antagonist is interpreted as a muscle strain (although a strain has not occurred). The end result is hypertonic myofascial tissue and restricted motion . A guarding reflex by the patient, without actual mechanical trauma, can also produce the inappropriate reflex. Although this model does explain the development of some tender points, it does not explain all of them. Trauma produces change in myofascial tissues at microscopic and biochemical levels (21). The force of the trauma causes damage to myofibrils and their microcirculation. Myofibril damage interferes with the actin-myosin bridges and changes the chemistry around them. Nociceptive information is carried to the central nervous system to alert the body to the tissue damage. The tissue disruption and subsequent chemical changes cause the tissue to become more sensitive to touch and may be part of the reason for the formation of a tender point. The damage to the microcirculation changes intramuscular pressure and muscle function. A small increase in intramuscular pressure can produce muscle fatigue due to decreased cellular metabolism (21). This change in metabolism changes the chemical matrix around the myofibrils and can produce nociceptive activity, resulting in tenderness (21). A tender point is sensitive to palpation and therefore must be related to nociceptive activity. The position of comfort used to treat a somatic dysfunction with countersrrain is a very specific, three-dimensional position in space. When the optimal position of comfort is established, the tenderness of the tender point disappears or becomes insignificant. This seems to indicate a neural relationship between the tender point and the somatic dysfunction. Neural messages are rapidly transmitted and used by the body when quick responses are needed. If counterstrain treats the neural component of somatic dysfunction, why did Jones determine 90 seconds as the optimal rime to maintain the position of comfort? Palpation of changes at the tender point and in the surrounding tissue suggests that in addition to the neural component, the position of comfort also produces changes in the myofascial tissue and small circulatory vessels. A clue for the treatment time comes from the palpation of a pulsation, the therapeutic pulse, at a render point location. The frequency of the pulsation is the same as the cardiac cycle and would therefore indicate a circulatory relationship. Another important fact is that the pulsation is not present before positioning, develops only when the patient is moved close to the position of comfort, and disappears after myofascial tissue relaxation. This process takes approximately 90 seconds to occur. The pulsation phenomenon does not occur with every tender point bur when it
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
is palpated, it does correlate with markedly improved treatment response.
TREATMENT Counterstrain is a very gentle technique that is well tolerated by most patients. The patient is not subjected to any external force other than gentle positioning. In addition, patients do not generate force From their own muscle contraction to produce effective treatment. It is an indirect technique, with positioning away from restrictive barriers; therefore, it is tolerated in both acute and chronic problems. Counterstrain is based on identifying render points associated with a somatic dysfunction and positioning the patient to eliminate the tenderness of the point. Counterstrain is easy to understand and apply, but mastery requires rime to learn the location of render points; skill in fine-tuning the treatment position for maximum results; and clinical experience to understand the correlations between symptoms, structural findings, and associated render points. The basic steps for treating with counterstrain are: 1. Find a significant render point. 2. Position the patient for maximum comfort. 3. Maintain rhe position For 90 seconds. 4. Slowly rewrn rhe patient to a neutral position. 5. Recheck the tender point.
Find a Significant Tender Point Tender points are rypically located in tendinous attachments or on rhe belly of a muscle. Additional render points are found in other myofascial tissues (often ligaments) associated with the joint dysfunction. Tender points are rypically discrete, small, tense, and edematous. The areas are about the size of a fingertip, and they are exquisitely render. A significant render point is at least Four rimes more render than the adjacent tissue. Tissue changes of the render points may range from several inches to virtually nonexistent. The tissue of the render point is found to be tenser than the surrounding tissue. Ir is essential to identify the most significant render point associated with the somatic dysfunction rather than just finding a point rhar is render. Due to rhe exquisite tenderness of significant render points, a patient will rypically wince, guard, or push your hand away when you press the render point. Patients are often surprised with the amount of tenderness, especially when they were unaware of rhe existence of the tender point. In rare cases, a patient does not perceive tenderness when a tender point is pressed. These patients are referred to as stoics and can be treated with counterstrain by monitoring tissue changes that occur durmg treatment. Palpate for a tender point with the pad of your finger or rhumb. The pads of the fingers are profoundly more sensitive to tactile input and are better at identifying the location of tender points. Avoid using the fingertips, especially if you have long fingernails. Fingertips are less sensitive and can elicit iatrogenic tenderness. Palpation should be firm bur gentle. The pressure used to elicit a tender point is rypically a Few ounces and nor strong enough
to elicit tenderness in normal tissue. Jones recommended using the amount of force needed to blanch the nail bed of the palpating finger. The vector of pressure is also important. Typically, the tissue of the render point is pressed onto more rigid tissue like bone or cartilage. Do not forger to check for other pathology that might produce tenderness that is not related to neuromusculoskeletal tender points, such as infection, inflammation, or viscerosomatic referred pain. · Verify rhe presence of a render point by asking the patient if the area is tender while the potential tender point is pressed. The tenderness of a tender point is an objective sign elicited by physically palpating the dysfunctional area. In contrast, pain is a subjective symptom that the patient may experience without undergoing palpation. Again, Jones found that often pain and weakness are found in areas away from where tender points may be found . One method to determine where tender points may be found is to perform an osteopathic structural examination, noting any alteration of movement, asymmetry of paired landmarks, or tissue texwre changes. Palpating these areas for tender points is how Jones originally found many of the tender points he described. Evaluate the patient for variations from ideal posture and palpate those areas for tender points. For example, a patient presenting with flattening of the normal thoracic kyphotic curve is likely to have one or more posterior thoracic tender points associated with the extension in this region. Tender point locations can also be suggested based on clinical history and presenting complaints. The most likely places for significant tender points can be deduced from knowing the position in which the original injury occurred. Many myofascial pain patterns have been described by Travell (3) and may provide additional correlation. A significant tender point results in the patient attempting to obtain a comfortable poswre to alleviate the functional distress. This is an unconscious attempt by the patient to shorten and relieve tense myofascial tissues. Patients tend to bend around tender points. That is, tender points tend to be at the apex or focal point of the concaviry of the postural adaptation. If the patient is forward bent, tender points tend to be anterior. If a patient is backward bent, tender points tend to be posterior. Jones found that a patient who presents side-bent to the right usually has tender points on the left side of the spine. Conversely, a patient who is side-bent to the left usually has tender points on the right Uones LH. Personal communication, 1993). Tender points are frequently found in areas other than the area of pain or discomfort. The primary or key strain may induce a secondary or compensatory strain elsewhere, which may be more symptomatic. Treatment of the primary dysfunction often alleviates symptoms reported elsewhere. For example, when the psoas muscle chronically stays in spasm, patients seldom complain of abdominal or anterolateral hip pain. Instead, they complain of pain in the lumbosacral or sacroiliac regions, due to the strain and compensation of those regions by the psoas spasm. Tender points are frequently 180 degrees around the body from the sire of the presenting pain. For example, in a patient with pain between the shoulder blades, the tender point is often on the sternum. Ir is also possible to have both anterior and posterior or right and left tender points associated with the same anatomic segmental level. This is because tender points are mediated through the nervous system and can result in multiple points for a single somatic
63. Strain and Counterstrain Techniques dysfunction. If there are multiple tender points in a given area, ask the patient which is the tenderest. Treat the most severe tender po_int first. Associated but less significant tender points often disappear after successful treatment of the tenderest point. If the tender point results from a viscerosomatic reflex, tenderness returns within minutes or hours. When this happens, a thorough review of the patient's medical history and more careful physical examination is needed. Be sure all of the possible causes of the original tenderness have been considered. For more information about viscerosomatic reflexes, refer to the discussion of viscerosomatic reflexes in the basic science section of this book, or read Beal's imide (18). This information is also important when treating patients in the hospital. Refer to the article by Schwartz (19) on the treatment of hospital patients with counterstrain.
Position the Patient for Maximum Comfort One of the advantages of counterstrain is that treatment is always in a position of comfort. The position of comfort correlates with the same position in which the patient suffered the original injury. If an adequate history is elicited, the position in which to treat the patient can frequently be deduced and used for treatment. For example, if the patient was injured attempting to lift an object while bending forward at the waist and side bending to the right, then the treatment position would be with the patient forwardbent and side-bent to the right. By placing the patient in a position of comforr, discomfort is avoided and further injury is unlikely to occur. Counterstrain can be used for patients with a wide variety of medical conditions, unless gently moving the patient into the specific treatment position is contraindicated. A word of caution: Medical judgment must always be used to determine the appropriateness of any treatment. Counterstrain may be contraindicated for some patients with metastatic carcinoma, uncontrolled infection, and some other conditions. Every patient needs to be evaluated on an individual basis. The only absolute requirement is that the patient must be relaxed while the physician places the dysfunctional area of the body into the treatment position. The optimal position of comforr is a very specific position in space. The position is similar for the same tender point in different patients, but the exact position is unique for each patient. To find the optimal position, the physician uses a combination of palpation and feedback from the patient. To test the tender point, press this area and immediately release the pressure, but maintain light contact with the myofascial tissue. Then ask the patient for the level of tenderness. Maintaining continuous light contact with the tender point during treatment is important for maximum effectiveness. To facilitate the communication between physician and patient, it is imporrant to establish a means of monitoring the level of tenderness of the tender point. Physicians typically use a tenderness scale to enhance verbal feedback with the patient. Several scales have been used effectively. The one most commonly used is a 0-to-1 0 scale, with 10 being equal to the level of tenderness prior to positioning for treatment and 0 representing the absence of tenderness. The scale allows the patient to communicate changes in tenderness and is correlated with palpatory changes. The same amount of pressure should be used each time the physician at-
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tempts to elicit tenderness of the point. It should be emphasized to the patient that this is not acupressure or a form of massage. Firm pressure is applied only when trying to determine the level tenderness. At other times, only light contact is maintained. This feedback provides a means for monitoring the effectiveness of positioning and treatment for both patient and physician. The first step in positioning is to approximate the position expected. The expectation may be from previous clinical experience, patient history, or from looking at an illustration of the positioning in a counterstrain book. The purpose of the positioning is to reduce the tension on the dysfunctional myofascial structures. Slowly move the patient toward the described or expected position of comfort while monitoring the tender point for relaxation of the tissue. When relaxation of the tender point is palpated, stop moving the patient. Press the tender point and ask for the level of tenderness. If the level of tenderness is greater than 3 on the 10-point scale, continue to move the patient in the same direction. Then, as further relaxation is palpated, stop movement and test again. Repeat this process until the tenderness level is three or less. If the number increases, return in the direction just traveled and retest. It may be necessary to change direction or add other directions to find the correct position. As you get close to the optimal position, fine tuning the position with small motions is required. A small change in position at this point in the treatment markedly reduces tenderness. For example, several inches of movement close to the neutral position may reduce the tenderness by one on the scale. Whereas, it m4y take only one-quarter inch of movement close to the optimal position to reduce the tenderness the same amount. Slow, small movements, constant light contact of the tender point for monitoring, and retesting the tender point for reduction of tenderness with each new position all allow the practitioner to find the precise position of optimal comfort. If the optimal position is overshot, the level of tenderness will increase. Fine-tune the position until the tenderness has been reduced by at least 70% (3 on the scale), preferably 100%. The position of comfort must be at least 70% improved over the initial tenderness, or the technique is ineffective. Jones recommended a reduction of two-thirds, and other practitioners have suggested three-fourrhs. An efforr should be made to maximally reduce the tenderness. The extra time spent trying to eliminate the tenderness will significantly increase the effectiveness of the treatment. A common mistake is to use constant firm pressure on the tender point throughout the treatment sequence. Instead, constant light contact should be maintained. Once the optimal treatment position has been determined, be sure to maintain only light contact with the myofascial tissue of the tender point. There are three important reasons for maintaining contact: 1. Tissue changes that occur in the tender point can be monitored more easily and can aid in determining the end point of treatment.
2. The tender point can continue to be fine-tuned while maintaining the optimal position of comfort, because the position may change slightly during treatment. 3. Both the patient and the practitioner can be confident of the location of the tender point.
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The third reason may seem unimportant, bur when contact with the render point is lost, the patient may question whether the same point is being pressed. Also, the practitioner may have difficulty reestablishing contact with the point with enough confidence to allow an accurate recheck. At times, a pulsation in the render point may be palpated. T his is referred to as the therapeutic pulse. Although irs intensity may vary, it is often close to the intensity of the radial pulse. In fact, palpating the patient's radial artery with the other hand typically shows it to be synchronous with rhe therapeutic pulse. For th is reason, it is postulated that the position of release results in a sympathetic vasodilation of the small arterioles in the myofascial tissue. At rimes, the therapeutic pulse can be palpated while attempting to find the optimal position of comfort, enabling the practitioner to establish rhe position more accurately. At other times, the therapeutic pulse will not be palpated until the treatment position has been maintained for 90 seconds. In either case, the appearance of the therapeutic pulse can be used to enhance the treatment. As a rule, the closer render points are to the midline, the more fl exed o r extended is the patient's presenting posture, and more flexion or extension is required for the treatment position. With tender points more lateral to the midline, more side bending and rotatio n are usually required for treatment. Side-bending and/or rotatio n of the body away from the tender point are the most common positions needed for effective treatment.
Maintain the Position for 90 Seconds Once the position of comfort has been established, hold it fo r 90 seconds. It is important to remember that the patient must remain relaxed without contracting the affected myofascial tissue. The 90 seconds does not begin until the patient is completely relaxed. It may be necessary to remind the patient to stay relaxed several times during the 90 seconds, because often the patient contracts muscles un co nsciously. Patients who are not comfortable will not be able to relax for the entire 90 seco nds. Also, if the practitioner is not comfortable, it is difficult to hold the patient in the treatment position for 90 seconds. You may need to experiment to find the best way to remain comfortable during treatment. Each patient and clinical setting offers different challenges. It may be necessary to invent a new treatment position to enable both the patient and yourself to remain comfortable. This is especially true with pregnant patients, patients with some degree of paralysis, and hospitalized patients. Feel for tissue changes in the tender point and surrounding tissue . As time in the treatment position increases, the tissue relaxes and can feel like melting butter. The myofascial tissue around the tender point may begin to move in a seemingly random pattern. T his sensation is due to the relaxation of myofascial tissue in different planes. Once the tissue changes that signal the end of treat ment can be palpated with confidence, watching a clock is no lo nger needed. The ab ili ty to palpate myofascial release patterns enhances counterstrain treatment and can also be used to improve palpatory ski lls needed for myofascial release techniques. As discussed earlier, you may also feel the therapeutic pulse. Once the random motion has stopped or the therapeutic pulse disappears, it is time to move the patient back to the starting position.
Slowly Return the Patient to Neutral After maintaining the position of comfort for 90 seconds, it is time to slowly return the patient to neutral. The first few degrees of motion during return are the most critical. Before starting to move, ask the patient to remain passive and not assist you by actively moving. Patients may unconsciously try to help. A common error when learning counterstrain is to move the patient too quickly. Watch the patient for signs of flinching or other guarding gestures. Palpating for muscle contraction could also provide a sign. An apparent decrease in the patient's weight as yo u support them in the treatment position is another indication that the patient is contracting muscles. If the patient starts to help or move, stop the return and remind the patient not to help. When the patient has relaxed, start moving again, more slowly.
Recheck the Tender Point Once the patient has been returned to a relaxed position, recheck the tender point for tenderness. To consider the treatment successful, no more than 30% of the original tenderness should remain. Ideally, all of the tenderness will have resolved. If more than 30% of the tenderness remains, several possible reasons may exist. The patient may not have been optimally positioned or may have moved during the 90-second holding time. Repeat the positioning, with particular attention to obtaining and maintaining the optimal position with the patient completely relaxed. Another cause for failure may be that another tender point is the primary problem and, therefore, the most significant point was not treated. Evaluate the area aro und the tender point to see if another, more significant tender point is present. Consider the possibility that the primary tender point is distant from the area evaluated or on the opposite side of the body from the reported problem. More than one treatment may be necessary to completely resolve a tender point. Also, failure to completely resolve the tenderness does not necessarily indicate 2n ineffective treatment. Although treatment rime may not always be exactly 90 seconds, it is important to maintain the treatment position for 90 seconds when learning counterstrain. Recheck the original structural findings to evaluate the effectiveness of the treatment. You are treating a somatic dysfunction, not a tender point, so rechecking cannot be overstated. Motion restrictions should disappear and tissue texture changes shou ld start to return to normal after effective treatment. With ch ro nic somatic dysfunction, the tissue changes may be slower to return to normal.
INSTRUCTIONS TO PATIENTS It is most prudent to start instructions before the patient gets off the treatment table. Patients are curious to see if the treatment eliminated the presenting complaint. Warn the patient not to test previously restricted motions and to avoid extremes of motion for several days. This is especially true if the movement approximates the original position of injury, because it m ay reproduce' the inappropriate reflex just treated. Active movement that reproduces the position of injury is different from the careful positioning performed by the physician while the patient is passive.
63. Strain and Counterstrain Techniques The patient should stay well-hydrated for several days after treatment. This helps with the elimination of increased metabolic waste products that may be released into circulation after ~elaxarion of the tense myofascial tissue. Water is recommended over other fluids, which may contain sugar and other dissolved chemicals. Although counterstrain techniques are well tolerated, a treatment reaction may occur. Approximately 30o/o of patients experience a generalized soreness or a Au-like reaction 1 to 48 hours after treatment. This usually is experienced by the patient on the morning after treatment and may last 1 to 5 days, although 1 day is most typical. The reaction usually happens only after the first treatment bur may occur for several treatments. The cause of the reaction is unclear, bur may be related to the washout of metabolic waste products from the dysfunctional myofascial tissue. There also is a correlation with treating dysfunctions where the therapeutic pulse is palpated during treatment. In any case, the patient should be alerted to the possibility of a treatment reaction. Prescribing an analges ic for one or two days may help reduce rhe reaction. This possibility of a treatment reaction also provides a reason for caution in using counterstrain to treat some severely ill patients. Patients want to know how often they need to be treated and how long it wi ll rake to resolve the complaint. As with all forms of manipulative treatment, there is no single, definitive answer. One treatment may eliminate some somatic dysfunction, although other dysfunction requires treatment over a more extended period of rime. On average, the patient is asked to return 3 to 7 days after the initial treatment. As the somatic dysfunction resolves, the rime between treatments is increased. The end point of treatment depends on the cause of the problem, rhe underlying tissue damage, preexisting medical problems, the response of the patient, cooperation by the patient to avoid painful positions, and the skill of the physician.
CLINICAL PEARLS • Examine the patient thoroughly. • A single somatic dysfunction may have more than one associated render point. • Test for tenderness with the same amount of pressure each rime. • Use less pressure to monitor a render poim than to test ir. • Your palpatory abilities are more reliable than a patient's tenderness report. • Anterior points typically require flexion, although posterior points typicall y require extension. • Midline points typically require pure flexion (if anterior) or pure extension (if posterior), whereas the more lateral a point is from midline, the more rotation and/or side-bending is required . • Treat the most significant render point first. • If several tender poin rs of equal tenderness occur in a row, treat the middle one first. • Spend a little extra rime to fine rune and completely eliminate the tenderness of a tender point. • The optimal position of comfort is obtained when the render point is no longer render.
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• Monitor myofascial changes and adjust the treatment position for maximum results. • Maintain light contact with the render point throughout the treatment. • For maximum results, the patient must be completely relaxed (passive) during treatment. • Recheck the tenderness of a point several rimes while in the treatment posmon.
SPECIFIC TREATMENTS BY BODY REGION
General Comments The after illustrations are intended as an imroduction to counterstrain technique. Because this presentation is aimed at the introductory level, primary focus has been placed on the review of vertebral and pelvic dysfunction with limited coverage to the extremities. More in-depth counrerstrain reference texts are availab le for complete coverage of the techniques (1,4,17,20). The treatment positions presented may be modified as appropriate for the comfort of rhe physician and the patient. Therefore, knowledge of the three-dimensional position that is typically used to treat a tender point site could be used to treat the patient, for example, while seated, supine, or side-lying. As long as the treatment can be successfully performed, modifications may be helpful adaptations to these techniques. The following figures are presented by permission of Rennie PR, G lover JC, Carvalho C, Key LS. Counterstrain and Exercise: An Integrated Approach. Williamston, MI: RennieMatrix; 2001.
Cervical Spine The cervical spine has several maverick tender points (points where the position of comfort is different from what might be expected). Anterior tender points are typically located on the most lateral aspect of the lateral masses or slightly anterior on the lateral masses. Posterior render points are found on the occiput or associated with the tip of the spinous processes or lateral to the spmous processes.
Anterior First Cervical (AC1) (Fig. 63. 1) Tender Point Locations Found on the posterior surface of the ascending ramus of the mandible approximately a finger width above the angle of the jaw. Treatment Position Rotate the head approximately 90 degrees away. Slight side bending away may further reduce the sensitivity by applying a slight caudal force on the contralateral parietal aspect of the cranium. Do not apply extension and do not maintain this position if discomfort increases.
Anterior Second to Sixth Cervical (AC2-6) (Fig. 63.2) Tender Point Locations Found at the anterior surface of the transverse processes of the named vertebrae. The sternocleidomastoid muscle crisscrosses over this line of tender points.
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FIGURE 63.1. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Treatment Position Flexion of the head and upper neck (by approximately 45 degrees) to the segment involved. Side bend and rotate the head and upper neck away from the tender point side.
FIGURE 63.3. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Treatment Position Marked flexion of the head and neck by lifting from the middle of the neck. Rotate the head away and side bend the neck toward (away for AC8) from the tender point side.
Posterior Second Cervical (PC2) (Fig. 63.4) Anterior Seventh to Eighth Cervical (ACl-8) (Fig. 63.3) Tender Point Locations AC7: 2 to 3 em lateral from the medial portion of rhe clavicle at the origin of the clavicular division of the sternocleidomastoid muscle. AC8: at the medial end of the clavicle at the sternal notch and involves the sternal division of the sternocleidomastoid muscle.
FIGURE 63.2. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Tender Point Locations Within the semispinalis capitis in association with the greater occipital nerve (which pierces this muscle near the render point site). Another render point can be found at the superior lateral surface of the C2 spinous process. Treatment Position Mild extension of the head at the occiput with simultaneous mild caudal push on the vertex of the head to create slack in the occipital muscles.
FIGURE 63.4. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
63. Strain and Counterstrain Techniques
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FIGURE 63.5. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Posterior Fourth to Eighth Cervical (PC4-8) (Fig. 63.5) Tender Point Locations The C4 tender point is at the inferior portion of the C3 spinous process (named for the spinal nerve associated with this level). The remaining inferior tender points at each cervical segment follow this nomenclature. Treatment Position Extension of the segment involved with side bending and rotation to the opposite side.
Thoracic Spine Anterior thoracic spine tender points are located in two major areas. The first group of tender points, ATl-6, are located midline on the sternum. They can be located by palpating for tense, tender tissue overlying the sternum. The second group is located in the abdominal wall. Most are located in the rectus abdominis muscle and can be found an inch or two lateral to midline on the right or left. Posterior thoracic tender points are found on two parts of each vertebra. One location is associated with the spinous process, typically on either side. The second location is on either transverse process. The treatments described here are given for different spinal levels, but are not hard and fast requirements. Extension, sidebending, and rotation to any level can be introduced either from above or below the segment. The physician's choice is based on the flexibility of the patient, patient comfort, and the relative size of the patient and physician.
FIGURE 63.6. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Treatment Position Flexion of the involved vertebrae by placing a vector force from the top of the shoulders to enhance the flexion. The arms are internally rotated.
Anterior Seventh to Ninth Thoracic (ATl-9) (Fig. 63.7) Tender Point Locations AT7: under the costochondral margin, lateral, and inferior to the xiphoid process. ATS: approximately 3 em below the xiphoid process. AT9: 1 to 2 em above the umbilicus, 2 to 3 em lateral to the midline.
Anterior First to Sixth Thoracic (AT1-6) (Fig. 63.6) Tender Point Locations AT 1: apex of the sternal notch. AT2: middle of the manubrium. AT3 to AT6: on the sternum at the same numbered costal level.
FIGURE 63.7. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
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FIGURE 63.9. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001, with permission .
FIGURE 63.8. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission .
Treatment Position Flexion of the involved vertebrae by placing a vector force from the top of rh e shoulders ro enhance the flexion. Flexion is also enhanced at the hips, more as the lower thoracic levels are involved. Add side bending toward and rotation away from the render side.
Anterior Tenth to Twelfth Thoracic (A T1 0-12) (Fig. 63.8) Tender Point Locations AT IO: 1 ro 2 em below the umbilicus, 2 to 3 em lateral to the midline. AT II: 5 to 6 em below the umbili cus, 2 to 3 em lateral to the midline. AT 12: inner surface of th e iliac crest at the midaxillary line. Treatment Position Hips are placed in marked fl exion while rhe legs are pulled to the same sid e to create slight side-bending toward the render side. Rotation is typicall y minimal , ro llin g the pelvis toward the render side.
Posterior Tenth to Twelfth Thoracic (PT1 0-12) (Fig. 63. 11) Tender Point Location On the inferolareral side of the deviated spi nous process. This signifies vertebral rotation of rhis segment to rhe opposite direction . Treatment Position Ex tend the trunk on the ipsilateral side of the deviated spinous process by lifting the pelvis in a posterior direction. T his creates extension with the needed rotation of the lower vertebrae toward the render point side.
Lateral Posterior First to Twelfth Thoracic (LPT1-12) (r=ig. 63.12) Tender Point Location T hese points are found more alo ng the transverse process. Treatment Position Side-bending is the main actio n away from the tender sire. Rotate the head toward the tender side. Side bend the trunk away from the te nder side by pullin g rhe ipsilate ral shoulder in an abducted direction without placing pressure or inducing pain in the axill a.
Posterior First to Ninth Thoracic (PT1-9) (Figs. 63.9 and 63.10) Tender Point Location On th e infero lareral side of the deviated spinous process of the named vertebra. T his signifies vertebral rotation of this segment to rhe opposite direction. Treatment Position PTI-4: exte nd the involved vertebral level, avo iding extension of the occipitoarl antal region . Side bend and rotate the involved segment away from the render side. PT5-9: ask rhe patient to turn their head opposite to th e render side. Side bend the trun k away from the deviated side of the spinous process by pulling the opposite shoulder in a caudal and posterior direction. T his creates extension with rotation and side-bending away from rh e deviated side.
FIGURE 63.10. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston , Ml : Ren nieMatrix; 2001, with permission.
63. Strain and Counterstrain Techniques
FIGURE 63.11. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
This creates extension with rotation toward and side-bending away from the render side.
Ribs
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FIGURE 63.13. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001, with permission.
they do occur. The posterior tender points are located on rhe angle of the ribs.
Anterior (Depressed) Second Rib (AR1-6) (Figs. 63. 13 and 63. 14)
Jones used the terms depressed and elevated to refer to the render points associated with rib somatic dysfunction. This was done to emphasize what needed to be done with the patient to find a position of maximum comfort. The convention in current use is to name the render points for their location on the body. In the examples used here, both conventions have been combined. Anterior tender points correspond to depressed ribs, although posterior render points correspond to elevated ribs. The anterior rib render points start just below the medial end of the clavicle where the first rib attaches to the sternum, and move laterally in an arc to the anterior axillary line. Most of the anterior rib render points are on the ribs along the anterior axillary line. It is nor common to find render points below the sixth rib, but
Tender Point Location ARl: on the first rib where it articulates with the manubrium . AR2: on the second rib in the midclavicular line. AR3-6: on the numbered rib in the anterior axillary line.
FIGURE 63.12. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission .
FIGURE 63.14. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Treatment Position ARl-2: neck flexion, rotation toward, side bending toward. AR3-6: flexion of the thoracic cage, head, and neck with elevation of the shoulder and translation away from (side bend toward) the tender point. Rotate toward tender point. Side-bending can be increased with patients legs placed the table opposite the elevated shoulder. The elevated shoulder is usually supported on the physician's thigh.
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FIGURE 63.15. From Rennie PR, Glover JC, Carvalho C, et a!. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Posterior (Elevated) Second to Sixth Ribs (PR2-6) (Fig. 63. 15) Tender Points On rhe posterior aspect of ribs 2 through 6 at the rib angles. Treatment Position Flexion of the thoracic cage, head, and neck with elevation of rhe shoulder and translation roward (side-bent away from) the render point. Rotate away from render poinr. Side-bending can be increased by placing the patient's legs on rhe side of rhe table opposite rhe elevated shoulder. The elevated shoulder is usually supported on rhe physician's thigh.
Lumbar Sp ine Anrerior lumbar spine render points are mostly located around rhe rim of the pelvis anreriorly. They can be found in association with the anrerior superior iliac spine (ASIS), anterior inferior iliac spine (AIIS), and anrerior surface of the pubic rami. Posterior lumbar render points are found mostly in the same places as in the thoracic spine, although the render points found on the rips of the transverse processes need ro be approached by pressing anteromedially at about a 45 degree angle. The naming convention used for describing spinal dysfunction in the osteopathic profession is to describe the dysfunctional segment relative ro the segment below ir. If motion is introduced from below the dysfunctional segment, the vertebral segment below it moves first, producing a position relative to rhe dysfunctional segment that can seem confusing. As an example, if the vertebra below the dysfunctional segment is rotated to rhe right, then the relative position of the dysfunctional segment to the vertebra below is described as rotated lefr. This is importanr to understand when reading the treatment descriptions for this section.
FIGURE 63.1 6 . From Rennie PR, Glover JC, Carvalho C, et a!. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
AL2: medial side of the AilS, press laterally (Fig. 63.17). AL3: lateral side of the AilS, press medially (Fig. 63.17). AL4: inferior side of the AilS, press cephalad (Fig. 63.17). AL5: anterior surface of the pubic rami about 1 em lateral to the symphysis, inferior ro the pubic tubercle, press posteriorly (Fig. 63.18). Treatment Position ALI: marked flexion of the hips ro the level of the L I vertebrae. The feet are pulled toward rhe render point side ro side bend rhe lumbar spine. The knees are pulled slightly toward the render side ro induce lumbar rotation of the Ll segment away from the tender point side. AL2-4: Stand on the opposite side as the tender point. Moderate flexion of the hips and lumbar spine ro the level of the named vertebrae. Rotate knees away from tender side, with rhe amount varying at different levels. Side bend by moving feet away from the render point side.
Anterior First to Fifth Lumbar (AL 1-5) (Fig. 63. 16) Tender Point Location All: medial side of the ASIS, press laterally (Fig. 63.16).
FIGURE 63.17. From Rennie PR, Glover JC, Carvalho C, et a!. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
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FIGURE 63.19. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001, with permission .
Iliacus (Fig. 63.20) Tender Point Location Half way between the midlin e and the ASIS about 7cm deep in the abdomen toward the iliacus. FIGURE 63.18. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
AL5: Marked flexion of the hips up to the level ofL5 . Pulling the knees toward the tender side and the feet toward the opposite side produces the side-bending away and torso rotation away from the tender side.
Posterior First to Fifth Lumbar (PL 7-5) (Fig. 63. 19) Tender Point Location On the inferolateral side of the deviated spinous process. This signifies vertebral rotation of this segment to the opposite direction.
Treatment Position Marked flexion of the hips bilaterally to shorten the iliacus muscles. Both hips are laterally rotated with the knees abducted from the center of the body.
Lower Pole Fifth Lumbar (LPL-5) (Fig. 63.21) Tender Point Location Found 2 em below the PSIS of the ilium , pressing cephalad. Treatment Position Flexion of the ipsilateral hip to approximately 90 degrees to enhance posterior rotation of the innominate. Sli ght medial rotation and adduction of the hip is also added. Treatment can be performed in the prone or supine positions.
Treatment Position Extend the trunk on the ipsilateral side of the deviated spinous process by lifting the pelvis in a posterior direction . This creates extension with the needed rotation of the lower vertebrae toward the tender point side.
Pelvis There are several anterior tender points and several posterior tender points that are important for diagnosis and treatment of pelvic somatic dysfunction. The anterior points typically require fl exion. Rotation of varying amounts is also needed and, to a lesser degree, side-bending. Posteriorly, tender points are associated with sacral problems and muscles of the pelvis. Extension is the predominant motion associated with the posterior tender points, although several points require some degree of flexion.
FIGURE 63.20. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001 , with permission .
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Vll Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 63.21. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Piriformis (Fig. 63.22) Tender Point Location In the middle of the piriformis muscle, half way between the greater trochanter and where it attaches to the lateral side of the sacrum. Treatment Position Marked flexion of the ipsilateral hip to about 135 degrees and marked abduction. Lateral rotation of the hip may also be required, particularly if tenderness is found more lateral on the piriformis muscle.
FIGURE 63.23. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
ommended that a text devoted to counterstrain (1 ,4, 17,20) is consulted for more extensive discussion of the tender points associated with this body region.
Supraspinatus (Fig. 63.23) Tender Point Location In the middle of the supraspinatus muscle, superior to the spine of the scapula. Treatment Position Flexion and abduction to 45 degrees and external rotation of the humerus.
Upper Extremity The after three tender point locations and treatments demonstrate the counterstrain approach to the upper extremity. Because there are many tender points in the upper extremity, it is rec-
FIGURE 63.22. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001, with permission.
Subscapularis (Fig. 63.24) Tender Point Location On the anterior and lateral surface of the scapula.
FIGURE 63.24. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston , Ml: RennieMatrix; 2001, with permission .
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FIGURE 63.25. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Treatment Position Extens ion, internal rotation, and slight abduction of the humerus.
Biceps (Fig. 63.25) Tender Point Location On the tendon of the long head of the biceps in the bicipital groove.
FIGURE 63.27. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml : RennieMatrix; 2001, with permission .
Treatment Position Flexion of the elbow to shorten the biceps followed by adduction and internal rotation of the upper arm.
that a text devoted to counterstrain (1,4,17,20) is consulted for more extensive discussion of the tender points associated with this body region.
Lower Extremity
Rectus Femoris (Fig. 63.26)
The afte r two render point locations and treatments demonstrate the counterstra in ap proach to the lower extremity. Because there are many render points in the lower extremity, it is recommended
Tender Point Location Tenderness can be found at the musculotendinous region at the distal end, above the patella, and at the patellar ligament. Treatment Position Mild hyperextension of the knee and slight internal rotation of the hip.
Gastrocnemius (Fig. 63.27) Tender Point Location With!n the two bellies of the gastrocnemius at the lower popliteal margm. Treatment Position Marked plantar flexion of the ankle.
ACKNOWLEDGMENTS FIGURE 63.26. From Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, Ml: RennieMatrix; 2001, with permission.
Appreciation to Charlene James, DO, PhD and Gabriele Rennie for their editorial review of this chapter and to C laudio Carvalho, DO, for his help in modeling the treatment positions.
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REFERENCES I . Jones LH. Strain and Counterstrain. Newark, OH: American Academy of Osteopathy; 198 1. 2. Jones LH. Missed anterior spinal lesions. A preliminary report. The DO.
1966;6:75-79. 3. Travel! JG, Simons DG. Myofoscial Pain and Dysfunction: The Trigger Point Manual, vol. I. Baltimore, MD: Williams & Wi lkins; 1999. 4. Jones LH, Kusunose R, Goering E. jones Strain-Counterstrain. Boise, ID: Jones Strain-Counrersrrain; 1995. 5. Jones LH. Spontaneous release by positioning. The DO. 1964;4:109-
116. 6. Brandt J r B, Jones LH. Some methods of applying counterstrain. jAm
Osteopath Assoc. 1976;75 (9) :786-789 . 7. jones LH. Foot trauma without hand trauma. jAm Osteopath Assoc.
1973;72(1):87-95. 8. Ram irez MA, Haman J, Worth L. Low back pain: diagnosis by six newly discovered sacral tender points and treatment with counterstrain . jAm
Ostepath Assoc. 1989;89(7):905-906, 911-913. 9 . Anonymous . Reader's thoughts on treating low back pain with counrersrra in technique. jAm Osteopath Assoc. 1989;89(11):1379, 1384, 1387 passim. 10. Jacobson EC, Lockwood MD, Haefner Jr VC, et al. Shoulder pain and repetit ion strain injury to the supraspinatus muscle: etio logy and manipulative treatment. jAm Osteopath Assoc. 1989;89(8): 1037-1040,
1043- 1045. II . Cislo S, Ramirez MA, Schwartz HR. Low back pain: treatment of
forward and backward sacral torsions using counterstrain technique.
jAm Osteopath Assoc. 1991 ;91 (3):255-256, 259. 12. Bailey M , Dick L. Nociceptive considerations in treating with counrersrrain. jAm Osteopath Assoc. 1992;92(3):334, 337-341. 13. Radjieski JM, Lum ley MA, Cantieri MS. Effect of osteopathic manipulative treatment of length of stay for pancreatitis: a randomized pilot study. jAm Osteopath Assoc. 1998;98(5):264-272. 14. Luckenbill-Edds L, Bechill GB. Nerve compression syndromes as mod els for research on osteopathic manipulative treatment. JAm Osteopath
Assoc. 1995;95(5):319-326. 15. Korr IM. Proprioceptors and somatic dysfunction. jAm Osteopath Assoc. 1974;74:638-650. 16. Van Buskirk RL. Nociceptive reAexes and the somatic dysfunction: a model. jAm Osteopath Assoc. 1990;90(9):792-794, 797-809. 17. Yates HA, G lover )C. Couruerstrain: A Handbook of Osteopathic Technique. Tulsa, OK: Y Knot Publishers; 1994. 18. Beal MC. Viscerosomatic reAexes: a review. j Am Osteopath Assoc. 1985;85(12):786-801. 19. Schwartz HR. The use of counterstrain in an acutely ill in-hospital population. jAm Osteopath Assoc. 1986;86(7):433-442. 20. Rennie PR, Glover JC, Carvalho C, et al. Counterstrain and Exercise: An Integrated Approach. Williamston, MI: RennieMarrix, 2001. 21. MenseS. Pathophysiologic basis of muscle pain syndromes: an update. Phys Med Rehabil Clin N Am. 1997 8(1):23-53. 22. Woolbright JL. An alternative method of reaching strain/countersrrain.
jAm Osteopath Assoc. 1991;91(4):370, 373-376.
FACILITATED POSITIONAL RELEASE STANLEY SCHIOWITZ EILEEN L. DIGIOVANNA DENNIS J. DOWLING
THEORY OF EFFECTIVENESS
KEY CONCEPTS • Technique of facilitated positional release • Possible mechanisms for effectiveness of facilitated positional release • Benefits of using facilitated positional release • History of facilitated positional release • Diagnosis of any form used with this technique • Two levels of facilitated positional release and treatment programs appropriate to each level • Specific treatments for these tissue texture changes and intervertebral motion restrictions • Cervical soft tissue • Cervical segmental somatic dysfunction • Thoracic, seated • T horacic, prone • First rib • Lumbar soft tissue • Lumbar extension somatic dysfunction • Lumbar fl exion somatic dysfunction • Sacroiliac discogenic pain syndrome • Gluteal and hip soft tissue
Facilitated positional release (FPR) is an indirect positional method of treatment of either abnormal muscle tension or somatic dysfunction. The physician initially places the region or somatic dysfunction into a position between flexion and extension to approach the neutral position defined by Fryette (1). An activating force is then applied to facilitate immediate release of tissue tens ion, joint motion restriction, or both. The goal of treatment is to decrease the tissue hypertonicity that maintains somatic dysfunction, and the technique can be modified to influence deep muscles involved in joint mobility. The modality is easily applied, nontraumatic, effective, and efficient. When properly performed, patients report immediate relief of point tenderness and restoration of function . If complete normalization is not achieved, the treatment can be repeated or other methods of treatment can be applied immediately.
A neurophysiologic explanation that may explain the effectiveness of this method of treatment was first suggested by Korr (2), who wrote that the immobility of a lesioned segment was initiated or maintained by an increased gain in gamma motor neuron activity of that segment. Subsequently, Bai ley (3) proposed that an inappropriately high gain-set of the muscle spindle results in changes characteristic of somatic dysfunction. When using FPR, the region of somatic dysfunction is first placed into its neutral position to unload the joints' articulating surfaces, which allows the area of dysfunction to respond easily and rapidly to the applied motion and force. In the case of the spine, the articular facets are placed into an idling position between the flexed and extended extremes. This most often involves flattening of the spinal region. A facilitating force (compression and/or torsion) is applied and maintained, followed by decreasing the length of the involved muscle and/or further positioning of the somatic dysfunction into all three planes of relative freedom. The whole application of the positioning into neutral, engaging all directions of relative freedom, and then return to the original position takes only a few seconds. The dysfunction is then reassessed. This method may result in an immediate effect on the muscle spindle-gamma loop, which then allows the extrafusal muscle fibers to lengthen to their normal relaxed state. In discussing the feedback mechanism of the muscle spindle stretch reflex, Carew (4) stated that shortening the muscle more than intended caused a decrease in spindle output and lowered the afferent excitatory input to the spinal cord through the Ia nerve fibers. This results in a decrease in gamma motor gain to the spindle and, by reflex action, decreases tension of the extrafusal muscle fibers . As a result, hypertonicity of the muscle mass is reduced. Joint motion asymmetry decreases after treatment with FPR if its mobility was impaired by muscle hypertonicity. If the asymmetry of joint motion is caused by other factors, such as meniscus or synovial impingement or degenerative arthritis, mobility is not restored; the joint remains restricted. This may account for the need to repeat the application or use other modalities of osteopathic manipulation to complete treatment of the dysfunction.
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HISTORY FPR wa developed by Stanley Schiowitz, DO. Because of his busy practice and limitation on providing time-intensive treatmems, he sought treatment methods for providing fast and effective re lief for patients that were soundly based on anaromic and phys iologic principles . Other practitioners had already used some of the components employed in FPR, wh ich probably date back to the time of Andrew Taylor Still. In 1977, he was able to further develop and systematize the principles of this form of treatment. Over time, faculty members in many colleges of osteopathic medicine have added FPR to the curriculum.
DIAGNOSIS Many publications have described diagnostic methods. Methods may consist of: Skin rolling described by Mennell (5) Testing for thoracic/lumbar rotoscoliosis in rhe method of Mitchell and colleagues (6) Palpatory motion resting as described by Johnston (7) Other direct or indirect tissue or motion testing procedures described in the literature Diagnosis of somatic dysfunction is described in other chapters in this text. The use of FPR treatment procedures does not require special d iagnostic tests unique to FPR. However, diagnosis is a prerequis ite to treatment.
TREATMENT
Intervertebral Motion Restriction Treatment The same procedures used for tissue changes are used to address intervertebral motion restrictions, with the additional requirement that the physician place the vertebra into a position th at allows freedom of motion in all planes. In the following exam ple, with a restriction at C3 ESRI~, the fourth cervical vertebra moves more easily into extension, right rotation, and right sidebending. 1. The cervical lordosis is flattened. 2. Place the third cervical vertebra inro a position of extension, right lateral flexion, and right rotation with respect to the fourth cervical vertebra. 3. Apply a facilitating force: compression, torsion, or a combination. 4. Hold the position for 3 to 5 seconds; release should be palpable. 5. Reevaluate the patient.
SUMMARY FPR is easily applied, nontraumatic, effective, and efficient. When it is properly performed, rhe patient reporrs immediate relief of poinr tenderness and restoration of function. If com plete normalization is not achieved, it can be repeated or other methods of trearmenr can be applied immediately.
FACILITATED POSITIONAL RELEASE TECHNIQUES Cervical
FPR treatments are classified into rwo categories: a) one directed at normalization of palpable abnormal tissue texture, and b) rhe other modified to influence deep muscle involved in joint mobility. Sometimes iris difficult to make a clear diagnostic distinction as to which one of these is primarily involved in the somatic dysfunction. If in doubt, rhe palpable tissue changes should be treated first. If motion restriction persists after this treatment, the technique can be adapted to treat the deep muscle component involved in rhe specific joint motion restriction.
Tissue Texture Change Treatment 1. The anteroposterior spinal curve of rhe area to be treated is flattened. Th is position places that region of rhe spine into its position of ease of motion, which shortens and softens rhe associated muscle. 2. A facilitating force is applied. This may be compression, torsion, or a combination of the rwo. 3. The physician places the patient's involved myofascial structures into a shortened, relaxed position. This softens the tissues and reduces srrerch receptor activity. 4. The position is held for 3 to 5 seconds and then released. 5. The patienr's condition is reevaluated.
So ft Tissue Treatm ent Findings Posterior cervical muscle hypertonicity (soft tissue texture abnormalities). Patient Position Supine on the table; rhe parienr's head is beyond the end of the table, resting on a pillow on the physician's lap (Fig. 64.1 ). Procedure I. Sit at the head of the table. 2. Cup the patient's neck in the palm of your hand with the pad of rhe index or other finger acting as both monitoring finger and fulcrum on the con rralareral tense tissue to be treated. Your thumb rests on the other side of rhe neck. 3. Use your non-monitoring hand on rhe top of the patienr's head to straighten the cervical lordosis by slightly forward bending the neck. 4. Use rhe same hand to apply a compressive facilitating force to the neck through the patient's head until felt ar the monitoring finger. 5. Maintain the compressive force and introduce extension of the neck to rhe level of the monitoring finger. (If the tissues being
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FIGURE 64.2. Typical cervical C3 ESLRL technique. FIGURE 64.1. Cervical soft tissue technique .
treated are anterior rather than posterior, introduce flexion rather than extension .) This should cause a palpable softening of the tissue being treated. 6. Add side-bending and rotation (usually toward the side of the tense tissues) to the point that the tissues continue to soften. 7. Hold in this position for 3 to 5 seconds and then return the neck slowly to a neutral position. 8. Reevaluate the tissue being treated. Note: If tissue changes are found anteriorly, forward bending is usually required. Some muscles have a contralateral side-bending, a rotary component, or both. Those muscles must be placed in their individual shortened positions determined by palpation and tissue response. Careful localization of the component motions of forward/backward bending, side-bending/rotation, and compression to the area of tissue texture change will result in faster and more efficient results. Cervical Segmental Somatic Dysfunction Findings C3 ESLRL.
6. Side bend C3 to the left by adding a translatory force th rough your monitoring finger, pulling C3 to the right. 7. Add a slight left ro tation of the head and neck through the level of C3 . This places C3 in all three planes of freedom of motion. 8. Hold this position for 3 to 5 seconds then slowly return the neck to neutral. 9. Reevaluate C3 motion. Note: If the diagnosis is flexion rather than extension (C3 FSLRL), step four is replaced by adding flexion through the level of C3 rather than adding extension. Similarly, if the diagnosis is one of right side-bending and right rotation, the appropriate adjustments should be made. When applying this procedure to dysfunction of the suboccipital area or to the occipito-atlantal articulation, localize the flexion-extension using a slight nodding motion to the skull (not total flexion-extension of the cervical spine) . Also, the occipitoatlantal (0-A) joint side bends in one direction and rotates in the opposite direction. The appropriate motions should be added to the positioning to place the 0-A joint into its relative freedoms.
Thoracic Patient Position Supine, with the patient's head beyond the end of the table resting on a pillow on the physician's lap (Fig. 64.2) . Procedure 1. Sit at the head of the table.
2. Cup the patient's neck in the palm of your right hand with the pad of the index or other finger on the left articular pillar ofC3. 3. Use your left hand on the top of the patient's head to straighten the cervical lordosis by forward bending the neck to the monitoring finger on C3. 4. Add a compressive force through your left hand, directed through the head to the neck. The force should be sufficient enough to be felt with the monitoring finger. It should not exceed this. 5. Extend the neck through the level of C3 while maintaining the compression.
Thoracic Spine, Seated Findings T6 FSLRL. Patient Position Seated on the edge of the table (Fig. 64.3). Procedure 1. Stand behind and to the left of the patient. 2. Ask the patient to sit up as straight as possible and push his or her chest forward . This will straighten the thoracic kyphosis. 3. Monitor the transverse process ofT6 with your right index or other finger. 4. Place your left axilla over the patient's left shoulder as close to the cervicothoracic junction as possible, with your forearm in front of the patient and your left hand in the patient's right axilla or grasping the patient's right shoulder.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 64.4. Thoracic spine T7 ESLRL technique, prone.
FIGURE 64.3. Thoracic spine T6 FSLRL technique, seated.
5. Add a compressive force through your left axilla downward (toward the table), causing left side-bending down through the level of the monitoring finger at T6. 6. Add flexion to the level of T6 by pulling forward on the patient's shoulders while maintaining the side-bending. 7. Rotate the thoracic spine to the left down through the level ofT6 by pulling the patient's right shou lder forward. 8. Hold this position for 3 to 5 seconds and then slowly return the patient to a neutral position.
Procedure 1. Stand at the right side of the patient. 2. Palpate the T7 posterior transverse process (right) with the fingers of yo ur right hand. 3. With your other hand, grasp the patient's left shoulder. The patient's entire shoulder should be held with your fingers on the upper and outer surfaces. 4. Pull the patient's left shoulder medially toward the spine (this flattens the spine in the anteroposterior plane) then toward the patient's feet (this compressive force creates left side-bending). 5. Extend the spine through the level ofT7 by mainraining traction on the shoulder as you step further down the table until motion can be palpated at the level of your monitoring fingers. 6. Stand up straighter, pulling the pati ent's shoulder posteriorly and creating left rotation down through the level ofT7. 7. Hold this position for 3 to 5 seconds then slowly return to the neutral position. 8. Reevaluate T7 motion. Note: If the diagnosis is flexion rather than extension (T8 ESRRR), FPR is more easily accomplished with the patient in the seated position.
9. Reevaluate. Note: If the diagnosis is extension rather than flexion (T6 ESLRL), replace step 6 by creating extension through the level of T6, pulling back on the shoulders. Similarly, if the diagnosis is side-bending and rotation is to the right, make appropriate adjustmenrs. If the somatic dysfunction is neutral, do not induce flexion or extension and adjust so that side-bending and rotation are achieved in the appropriate directions.
Thoracic Spine, Prone Findings T7 ESLRL . Patient Position Prone, with pillows beneath the abdomen and head. The patient's arms are at his or her side (Fig. 64.4).
First Rib Soft Tissue Treatment Findings First rib elevated on left. Patient Position Supine (Fig. 64.5). Procedure 1. Stand to the left of the patienr facing the head of the table. 2. Place the monitoring finger of your left hand over the posterior portion of the left first rib. The finger should conract the tensest tissue overlying the superior posterior part of the rib. 3. With your right hand, grasp the patient's left elbow, flex the upper arm to approximately 90 degrees, and abduct the upper arm to the position in which the tissues soften maximally.
64. Facilitated Positional Release
FIGURE 64.5. Treatment for first rib. A: First rib elevated on left. B: Internal rotation and flexion introduced. C: Adduction and circumduction added .
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 64.6. Lumbar soft tissue technique. FIGURE 64.7. Lumbar extended L3 ESLRL technique.
4. Create a compressive force through the left elbow downward, directed toward the monitoring finger. 5. Press the volar surface of your left forearm against the dorsal surface of your patient's left forearm. This will act as a fulcrum for the additional movements. Increase the amount of shoulder flexion. This also causes an internal rotation of the humerus. 6. Hold this position for 3 to 5 seconds. 7. Maintain the compressive force and internal rotation, adduct the upper arm across the patient's chest, swing it down through a curving motion, and finally into a neutral position. 8. Reevaluate the motion of the first rib.
9. Lift it slightly toward you so that the dorsal surface of your left hand is against the back of the right thigh. This creates a slight increase in adduction of the left leg. 10. Stand upright with your arm straight, using postural rather than arm muscles to pull the left leg further toward the dysfunctional side. Adduct it and induce external rotation. At the same time, extend the lumbar region and induce a relative rotation of the upper trunk toward the right. 11. Hold this position for 3 to 5 seconds then slowly return the patient to the initial position. 12. Reevaluate the soft tissue.
Lumbar
Extension Somatic Dysfunction
Soft Tissue Treatment
Findings L3 ESLRL·
Findings Hypertonic right paravertebral lumbar muscles. Patient Position Prone, close to the right edge of the table, with a sufficient number of pillows beneath the abdomen to cause flattening of the lumbar lordosis (Fig. 64 .6). Procedure 1. Stand at the right side of the table facing the patient.
2. Monitor the tissue tension with a finger of the right hand. 3. Place your left knee on the table next to the patient's pelvis. This acts as a fulcrum to position the patient's legs. 4. With your left hand, grasp the patient's left knee. 5. Pull the patient's legs toward you to induce right lumbar side-bending until yo u feel motion and/or softening at your monitoring finger. 6. Remove your knee from the table. 7. Cross the patient's legs by placing the left ankle over the right. 8. With your left hand, reach around the left thigh from the lateral surface and place your fingers between the patient's thighs so that yo ur palm is on the anterior and medial left thigh.
Patient Position Prone, close to the left edge of the table with a sufficient number of pillows beneath the abdomen to cause flattening of the lumbar lordosis (Fig. 64.7). Procedure 1. Stand at the left side facing the head of the table.
2. Monitor the posterior transverse process (left) with a finger of the right hand. 3. Place a small pillow between the patient's left thigh and the table. This will provide a fulcrum for the treatment while protecting the thigh from the pressure of the table's ·edge. 4. Use your left hand to abduct the right leg, creating left lumbar side-bending, and stand between the table and the patiem's abducted leg. 5. Grasp the patient's left lower leg or ankle and internally rotate the leg until you feel motion at the monitoring finger (this creates relative rotation of the trunk to the left). 6. Move the patient's abducted leg toward the floor (hip flexion) umil you palpate motion at the monitoring finger. With the thigh pillow acting as a fulcrum, lift the pelvis from the table and introduce lumbar extension.
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FIGURE 64.8. Lumbar flexed L4 FSLRL technique.
7. Hold this position until there is a sudden release of the somatic dysfunction (usually in about 3 to 5 seconds), then slowly return the patient to a neutral position. 8. Reevaluate L3 motion. FIGURE 64.9. Discogenic pain syndrome treatment .
Flexion Somatic Dysfunction Findings L4 FSLRL. Patient Position Prone, close to the left edge of the table with a sufficient number of pillows beneath the abdomen to cause flattening of the lumbar lordosis (Fig. 64.8). Procedure 1. Siron a rolling stool (thighs parallel to the table) on rheleftside of table at the level of the patient's pelvis, facing the patient's head. 2. Monitor the posterior transverse process (left) with a finger of your right hand. 3. Flex the patient's left leg at the knee and hip, with the lower leg coming to rest between your knees to create a relative amount of flexion of rhe spine to the point where you feel motion at your monitoring finger. 4. Use your left hand to grasp the patient's left knee, and adduct it toward and under the edge of the table until you feel motion at the monitoring finger. Hold and support the knee during the rest of the technique. Rotate your body clockwise (This induces left rotation, because internal rotation of the leg causes pelvic rotation to the contralateral side, and relative lumbar rotation toward the posterior transverse process.) Some compression may be added through the patient's knee. 5. Hold this position until there is a sudden release of the somatic
dysfunction (usually in about 3 to 5 seconds) then slowly return the patient to a neutral position. 6. Reevaluate L4 motion .
Discogenic Pain Syndrome Treatment Findings Left lumbar disc pathology with left radiculoparhy. Patient Position Prone, close to the left edge of the table with a sufficient number of pillows beneath the abdomen to cause flattening of the lumbar lordosis (Fig. 64.9). Procedure 1. Sir on a rolling stool at the left side of table (thighs parallel to the table) at the level of the patient's pelvis, facing the patient's head. 2. Use a finger of your right hand to monitor the area of documented or suspected disc pathology. 3. With your left hand, flex the patient's left hip and knee. 4. Place the upper leg across your anterior thighs, moving to create abduction and external rotation . 5. Localize motion to the involved segment by moving the patient's leg in a cephalad direction. It is easiest to do this by rolling the stool closer to the head of the table. 6. Raise your left knee by lifting your heel off the floor. Push the lateral part of your knee into the popliteal fossa of the patient's knee. Create a traction force that can be modified (as you further raise and move your knee lateral ly) until you
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Vll Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment 6. Ask the patient to take a deep breath and hold it for 3 to 5 seconds. 7. As the patient exhales, return the leg to a neutral position and release your pressure from the ILA. 8. Reevaluate motion of the SI joint.
Gluteal and Hip Soft Tissue Treatment Findings Right hip muscles or gluteal musculature hypertonicity. Patien t Position Prone, close to the edge of the table with a sufficient number of pillows under the abdomen to flatten the lumbar lordosis. FIGURE 64.10. M ot ion restr ictio n treatment for the sacroiliac jo int.
palpate motion at your monitoring finger. Your knee is now at the medial surface of the popliteal fossa. The lateral surface of your knee acts as a fulcrum for the rest of the technique. 7. Use your left hand to push the patient's left lower leg toward the floor until you palpate motion at your monitoring finger. Note a slight amount of initial tension at the monitored location. 8. Maintain this position until a release is noted, generally in 3 to 5 seconds, and then slowly return the patient to a neutral position . The patient generally experiences some relief of his or her radicular symptoms with this treatment. 9. Reevaluate the lumbar region.
Sacroiliac Joint Motion Restriction Treatment Findings Left sacroiliac motion restriction. Patient Position Prone, with a sufficient number of pillows under the abdomen to flatten the lumbosacral junction (Fig. 64.10). Procedure 1. Stand on the left side of the table facing the head of the table. 2. Place a small pillow between the patient's left thigh and the table. This will provide a fulcrum for the treatment while protecting the thigh from the table's edge. 3. Monitor the left sacroiliac (SI) joint with a finger of your right hand and place your right hypothenar eminence on the left inferior lateral angle (ILA) of the sacrum. 4. Use your left hand to abduct the left leg until the thigh is over the edge of the table. 5. Use your left hand to press the left leg down toward the floor. Simultaneo usly press your hypothenar eminence down on the ILA to bend the base of the sacrum backward on the left. Apply an upward (cephalad) force to slide the sacral portion of the SI joint along the ileal portion.
Procedure 1. Sit on a rolling stool at the right side of table (thighs parallel to the table) at the level of the patient's pelvis, facing the patient's head. 2. With a finger of your left hand, monitor the soft tissue to be treated. 3. Use your right hand to slightly abduct the patient's right leg and flex the hip and knee until you feel motion at your monitoring finger. The patient's lower leg will come between your knees, and the ankle will rest on your lap. Insert a small pillow between the patient's inner thigh and the table edge for comfort and to provide a fulcrum. 4. Push the patient's flexed knee into adduction beneath the table until you palpate motion at the monitored location. 5. Induce internal rotation of the thigh with your hand on the knee. This can be further accentuated by swiveling your own body and right shoulder forward, causing adduction and internal rotation of the lower leg. 6. Place your right palm and fingers so that they encompass the patient's knee. 7. Direct a compressive force upward along the long axis of the femur toward the hip and gluteal region. 8. Maintain this position until a release is noted, generally in 3 to 5 seconds, then slowly return the patient to a neutral position. 9. Reevaluate the soft tissue.
CONCLUSION Although axial procedures have primarily been described here, it is possible to use FPR for other regions of articular and soft tissue dysfunction. Rather than describe these in detail , it is left to the reader to apply these principles to rhe individual region.
REFERENCES 1. Fryene HH. Principles of Osteopathic Technic. Carmel, CA: Academy of Applied Osteopathy; 1980:19.
64. Facilitated Positional Release 2. Korr IM. Proprioceptors and so matic dysfun ction . JAm Osteopath Assoc. 1975;75 :638-65 0. 3. Bai ley HW. So me problems in makin g osteopathic spin al manipulative thcrapy appropriate and specific. jAm Osteopath Assoc. 1976; 75:486--499. 4. Ca rew TJ . T he control of refl ex actio n. In: Kandel ER, Schwartz JH , eds. Principles ofNeuraL Science, 2 nd ed. New York, NY: Elsevier Science; 1985:464.
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5. Men nell J M. Back Pain: Diagnosis and Treatment Using ManipuLative Techniques. Boston , MA: Little, Brown and Co mpany; 1960:75. 6. Mitchell Jr FL, Moran PS, Pruzzo NA. An EvaLuation and Treatment ManuaL of Osteopathic MuscLe Energy Procedures. Valley Park, MO : Mitchell , Moran & Pruzzo Assoc; 1979:229-253. 7. Johnsto n WL. Segmental definiti o n, Parr 1: A focal point for diagnosis of so matic dysfunction. JAm Osteopath Assoc. 1988;88:99- 105.
PROGRESSIVE INHIBITION OF NEUROMUSCULAR STRUCTURES TECHNIQUE DENNIS J. DOWLING
KEY CONCEPTS • Technique of progressive inhibition of neuromuscular structures • History of development of progressive inhibition of neuromuscular structures • Review of other modalities of point diagnosis and/or treatment • Diagnostic considerations • Method of applying the progressive inhibition of neuromuscular structures technique • Proposed mechanisms of action • Possible side effects and contraindicarions • Considerations for inclusion in treatment
More than 20 years ago, I had several years in which I suffered from headaches. Most of the treatments offered had a limited impact or undesirable side effects. Other, apparendy related symptoms accompanied the cephalgia, including a boring pain of rhe righr eye, increased lacrimation, right-sided facial pain, nasal congestion, and scalp sensitivity. Suboccipital pain occurred, which appeared to be related ro the periorbital pain, although no direct connection was apparent. Precipitating events leading ro the symproms included excessive reading, eyestrain due ro exposure to bright sunlight, and dehydration. There were no sensory deficits. Some symproms occurred independently and were usually worsened by stress. With little knowledge of anatomy at the time, early attempts at self-treatment involved the application of manual pressure to various locations of the head. Pressing painful sires appeared to bring about temporary relief when any were pressed singly. However, the pain recurred almost immediately after release of the pressure. Sometimes other adjacent regions of the scalp developed pain during or after release of pressure. Eventually, some patterns seemed to develop as secondary and even subsequent points appeared. The most successful approach, more so than addressing any individual or pair of points, was the treatment of a sequence of points.
As an osteopathic student and physician, I began to integrate knowledge of osteopathic manipulative medicine theory along with my personal clinica.l observations. The method of self-treatment was used with patients and taught to other students of osteopathy. Gradually, the rationale, as well as further expansion of use of this inhibitory technique beyond treatment of headaches, became clearer (1). Some similarities and differences were noted in relationship to other manipulative methods of point or applied pressure techniques.
INHIBITION Progressive inhibition of neuromuscular structures (PINS) is most closely related to the osteopathic modality of inhibition. The Glossary of Osteopathic Terminology defines inhibition as " ... a term that describes steady pressure to sofr tissues to effect relaxation and normalize reflex activity" (2). The "steady pressure to soft tissues" is perhaps one of the oldest methods of manual treatment, regardless of the name applied. C lassically, inhibition is a constant mild-to-moderate amount of force exerted by the fingers, elbow, knee, or foot on regions of hypertonic muscle. Although the patient's presenting complaint may be of pain or decreased function, the objective of the treatment is to decrease the tonicity of the muscles. Any symptom the patient has is assumed to be directly related to this increased dysfunctional muscular tone (3). The larger, more superficial muscles are the most easily identified, whether they are in the normal-relaxed or hypertonic stares. Regional muscles can be selected and treated individually or in pairs. Positioning the patient either supine or prone may facilitate the process, because these positions do not usually require the use of some muscles for positional support of the trunk and neck. A muscle, such as the trapezius, can be easily located in the cervical, shoulder, and upper thoracic regions. Some portion of the muscle can be grasped, pressed, or pinched. A hypertonic muscle is commonly found to be firmer than the same muscle on rhe opposite side and perhaps more firm than its antagonist. An increase in d1e firmness and perhaps greater sensitivi ty are noted as the pressure is introduced. As long as the pressure remains constant, the structures should relax. Attempts should be made to
65. Progressive Inhibition of Neuromuscular Structures Technique avoid altering the position or amount of pressure, because these wi ll more likely be stimulatory. The relationship berween musculoskeletal structures and the underlying visceral organs is also of consideration. These organs receive innervations from the same spinal cord segments that serve the skin, bones, joints, ligaments, and muscles. The sympathetic chain lies just anterior to the rib heads, and dysfunction of the vertebral or rib joints may result in increased stimulation to related structures, visceral and musculoskeletal (4). Acute response to increased sympathetic activity is the same as to any new injury: redness (rubor) , pain (dolor), swelling (tumor), heat (calor), and decreased function (funcio laesa) (5). More superficial structures, such as the skin and subcutaneous tissue, may have a "doughy" consistency, and the pai n noted by the patient would be typically sharp and throbbing. With continued hyperactivity in the absence of adeq uate treatment and/or recovery, the signs and symptoms demonstrated are altered. T he muscles may feel fibrotic ("ropy") . T he skin is thinner, paler, and cooler. Pain responses can range from relative insensitivity ("anesthetic") to altered sensitivity ("paresthesia") to hypersensitivity. The pressure provided by the application of modalities (s uch as inhibition) may result in a transitory increase in the palpatory findings or symptoms. Almost ir.evitably, subsequent reduction of some or all of these components can be readily app reciated. When the visceral organs are the primary dysfunction, the persistence or recurrence of a musculoskeletal somatic dysfunction may indicate the underlying problem. When a musculoskeletal injury is the etiology, any other reflexive activity or manipulative treatment may result in a more persistent reduction or elimination of all pathologic components. Inhibitory techniques have a different visceral focus in the suboccipital and sacral regions. Rather than reacting to external danger as the sympathetic system does, the parasympathetic system modifies the body's own reconstructive processes . Increased parasympathetic activity influences such elements as increased gastrointestinal motility, decreased sphincter closure, reduction of heart rate, co nstriction of pupils, and sleepiness. Somatic dysfunction of the upper cervical, occipital, and sacral regions may reflect or result in inappropriate parasympathetic activity. Inhibitory treatment results in reduction of increased regional musculoskeletal tone and congestion , and theoretically downregulates the more internal mechanisms. A thorough understanding of the structure and function of the factors related to somatic dysfunction should guide accurate treatment. Inhibitory and PINS treatments may be moved about several locations with the intent of reducing all relevant related dysfunction. When Andrew Taylor Still (6) was a yo ung man suffering from chro nic headaches, he treated himself with a rope-swing by lowering the rope to a few inches above the ground. A blanket was slung across it. He positioned himself on the ground with the contraption supporti ng his neck at the base of the skull , and subsequently fell asleep. He awakened refreshed and pain free. Whether intentionally or inadvertenrly, the method he employed appears to represent inhibition as much as positional intervention. Despite his usual tendency to avo id specific types of treatment in his writings, Dr. Still included some descriptions of both inhibition and stim ulation methods (7). Some of Sti ll's early students likewise described inhibitory techniques, as well as th e rationale for their use. In A Manual of
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Osteopathy, Goetz (8) described and ill ustrated inhibition for various conditions, both somatic and visceral . The accompanying photographs in this small handbook clearly demonstrate and detail inhibitory treatment of several regions . Of special note are the orbital and suboccipital regions of the head. A few minutes of pressure applied individually to each of these points is recommended. A more extensive description appears in Tasker's The Principles of Osteopathy (9). Tasker describes reasoning as to the effectiveness of inhibitory techniques, especially because inhibition is a natural phenomenon. Bodily functions, such as defecation and urination could not come under conscious and unconscious co ntrol without the adapted or learned ability to perform inhibition. In discussing the effectiveness of externally applied inhibitory pressure directed toward decreasing hyperactivity (as is applied by an osteopathic physician), he states that it is not the surface pressure that is effective but the initiation or alteration of the reflex arc that subsequently occurs. Observation reveals that the initial response to the placing of a pressure is, in effect, a form of stimulation, because it impacts the soft tissue. However, the inhibitory process of applied steady pressure sets in motion aremoval of the lesion and brings about some alterations both deep to and distant from the location of the applied pressure. In citing the Hilton law "that the skin , muscles, and synovial membran e of a joint, or the skin, muscles of the abdomen, and contents covered by peritoneum are innervated from the same segment of the cord," Tasker states that the "overstimulation" caused by inhibition results in diminution or elimination of the overreactivity.
OSTEOPATHIC POINT AND/OR PRESSURE TECHNIQUES Many types of passive direct and indirect systems of osteopathic treatment of somatic dysfu nction exist. Some standard points and diagnoses are used as fulcrums and/or monitoring locations in practically all of these modalities. Monitoring by constant palpation at the points is one of the best means fo r an osteopathic physician to experience feedback and monitor the success of the treatment when performing Jones strain-counterstrain treatment (10-12). T he patient can likewise appreciate the alteration . The muscle spindle sensory organ is embedded into the larger extrafusal muscle. The sensory ends of nerve fibers to these smal l muscles are stimulated by stretch of any kind, whether it is static or dynamic. The result is a single spinal segment increase in alpha motoneuron activity, which results in contraction of the whole muscle. It is quite successful as a means of preventing overstretching, and should decrease as soon as th e danger retreats . Sometimes the reflex pers ists longer than is appropriate. The signals from the spindle continue to fire as if the tissue were being too rapidly overstretched, although the overall length may be fairly short. The sensitivity of a tender point reflects increased activity. The external pressure at the tender point elicits the complaint while the positioning during strain-counterstrain technique shortens the whole muscle. This allows the spindle reflex mechanism to be reset, and the sensitivity disappears. Facilitated positional release (FPR) (13) is similar in many respects to strain-counterstrain. It differs in its use of an activating force (usually compression or torsion) after initial ly positioning
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
the region in neutral. Strain-counterstrain is a form of positional release, whereas FPR uses an additional facilitating force. Both strain-counterstrain and FPR theoretically use the same neurophysiologic mechanism, the muscle spindle. Van Buskirk (14) has recently contributed what he describes as the Still technique. It shares many similar applications to strain-counterstrain and FPR. Van Buskirk based his recovery of components of the technique on the writings of Hazzard (15), as well as Still himself The techniques use palpatory diagnosis of dysfunction followed by therapeutic motion into the freedoms. Finally, the osteopathic physician introduces movement past the neutral point into the barrier directions. This low-velocity, relatively low-amplitude articulatory movement toward the barriers follows the positional treatment into the freedoms. Functional technique (16) uses diagnostic points to define the somatic dysfunction that exists at that level relative to its two adjoining vertebrae: the one above and the one below. Detection of somatic dysfunction is typically made by percussion and more specific testing to scan and screen the regions . Wallace developed torque unwinding (17), and has taught it on a limited basis. She uses a theoretical construct whereby the body is imagined as a collection of adjacent or overlapping cubes. Injuries direct forces into a whole "cube." When the patient is twisted, the initial vector force may be straight. Because of bodily composition, motion, or twists, the resultant pathway becomes arced or more twisted as the person straightens. Memory of the force in the form of adaptation adversely affects the tissues, especially the fascia. Torque unwinding treatment involves the introduction of direct and rhythmic balancing pressures directed centrally from two opposing imaginary cube faces. The intent is for the therapeutic forces to negate the residual traumatic ones. Other variations of myofascial or fascial release techniques (18,19) that use point contacts as references , contact points, and/or diagnostic reflections occur in the osteopathic literature. Trigger band technique, described by Typaldos (20), is a method of changing the pathologic cross-linkages offascial bands. Either instruments or fingers are used to exert significant deep pressure along certain connective tissue path~ays . Chaitow (21,22) describes neuromuscular technique consisting mostly of point localization. Reflected dysfunction is treated by pressure followed by deep stroking and/or rolling of the tissue. Chapman point treatment (23) reflects a neurologic/ endocrine/lymphatic alteration reflected to specific points on the surface. Although they may not be tender or sensitive to pressure, the location of a Chapman point should raise suspicion of a possibly latent visceral correlate. Some of the specific mapped points are similar in location and correlation to those of acupuncture. The treatment consists of the application of circular pressures applied rhythmically by the pad of the physician's finger(s) to the nodular findings .
provides the treatment by pressing the patient's soft tissue. The overall intent is to bring about a persistent alteration. Each builds on a foundation of a system of diagnosis and/or treatment points. Cyriax, a medical orthopedist, practiced joint mobilization and massage. He used a pinching technique on several locations. Trigger point therapy, developed by Travel!, maps out the relationship between a remote referral region and a damaged myofascial nexus. The methods of treating these findings can include manual pressure, dry needling, or a combination of anesthetic and/or steroid agents injected into the trigger point. A vapocoolanr spray is directed from the trigger point toward the referral zone in another form of the treatment. If used, the pressure applied to the selected points must be deeply administered . An apparent variant of the trigger point concept, Prudden myotherapy, consists of primary points, as well as satellite points. Both of these points are treated for short intervals several times per day over several sessions (31 ,32). Stretching may also be incorporated in either Prudden myotherapy or trigger point therapy. Acupressure uses similar surface points that represent reflections of energy or chi forces within the body. Traditional oriental concept meridians align the specific point locations. Although several points may be treated within a session, the practitioner generally treats one or two points at any given time. The technique generally involves the application of pressure, as well as circular motions. Rolf (33) developed the eponymous system called Rolfing. Sometimes called "Dr. Elbow" because of her use of it to appl y pressure, she proposed using deeply applied forces on regions of the body as a tool to reestablish symmetry and normal function. The actual amount offorce applied in this modality exceeds that commonly employed in osteopathic inhibition. There is a great deal of emphasis placed on approximating ideal symmetry and alignment. Followers of Rolf made some alterations to the technique and integrated them into other modalities involving movement patterns (Hellerwork, Aston-Patterning). Shiatsu, one of the oldest forms of manual therapy, also usually involves relatively heavier pressures applied for short intervals. Improvements are reflected by the resultant reduction of the tissue tension. Although brief, the amount of force can be quite intense (especially in the hands of a traditional practitioner). Specific treatment patterns are used for certain conditions Reflexology relates energetic or visceral components to resonant areas located on the hands, feet, and ear. In theory, as with acupuncture, the name of the organ has more to do with the functional contribution to the integrity or energy component of the organ than the actual physical structure of the viscera.
NON-OSTEOPATHIC POINT AND/OR PRESSURE SYSTEMS
The PINS method requires the localization of points and the application of pressure in a logical fashion to treat persistent or resistant dysfunction. The PINS system of treatment allows for versatility that is based on the osteopathic physician's capability to use anatomic and clinical knowledge to determine involved structures and sequence of treatment. The osteopathic physician must have a thorough knowledge of the typical and variant courses
Cyriax method (24), trigger point therapy (25,26), acupressure (27,28) , reflexology, Rolfing, and shiatsu (29,30) bear some similarities to typical inhibition techniques, as well as to some other manual medicine systems of treatment. In each, the practitioner
PROGRESSIVE INHIBITION OF NEUROMUSCULAR STRUCTURES METHOD
65. Progressive Inhibition of Neuromuscular Structures Technique of nerves, fascial bands, and muscles, and this knowledge must be augmented by clinical decision-making skills for efficacy and accuracy. T his may involve the treatment of contiguous muscles, dealing with the overlapping zones where more than one nerve, muscle, or fascial tissue may be contributing to the persistence of somati c dysfunction, as well as the development of a sequence of PINS treatment. It is not as simple as locating a sensitive point. Any patient can do that. An example would be the assumption that shoulder pain originates in the glenohumeral joint. If the treatment is successful in increasing mobility and decreasing discomfort, further investigation is halted. However, when that is unsuccessful, more of the same treatment is not the answer. This may prove frustrating to both the patient and the doctor. If the restrictions of motion of the shoulder involve the combination of flexion, abd uction, and external rotation, as well as reduction of scapu lothoracic motion, then this indicates something outside of one of the shoulder joints. The latissimus dorsi, which attaches in the bicipital groove of the humerus, pulls the arm into extension , internal rotation, and adduction, the motions directly opposite the restrictions. Treatment may have to go beyond this focus by including the upper ribs, pectoralis muscles, lower cervical spine, clavicle, thoracic spine, lumbar spine, pelvis, and lower extremity in the process. Fascial planes, and therefore fascial stresses, must also be considered. With PINS, patients can offer feedback. They participate in the treatment by describing the amount of pain or other sensitivity at the palpated areas . As the treatment proceeds, the osteopathic physician takes note of the changes that occur, as well as the comparison of patient's subjective experience. The PINS method does not have to be the only treatment modality employed. It can be used before or after other methods of treatment (manipulative or otherwise).
Procedure The development of an appropriate and specific diagnostic and treatment protocol using PINS requires: 1. In most cases, the patient should be supine or prone to allow postural muscles to be in a fairly relaxed state. 2. Stand or sit near the region to be treated. The fingers of both hands should be able to contact the patient comfortably and accurately. 3. Examine the patient. Determine any relationship berween the patient's symptoms, somatic dysfunction, and the soft tissue findings. 4. Determine the components of the somatic dysfunction. The mnemonic "S.T.A.R." (34) can be used to track the different aspects: • Inquire about (S) sensitivity changes. These are the patient's subjective responses to palpation, and can include tenderness, numbness, radiation, warmth, irritation, throbbing, and so on. • Locate (T) tissue texture changes. They can be chronic (prolonged blanching of the skin, ropy or fibrous texture of the muscles and fasciae, coolness, dryness, vascular changes) or acute (increased redness, swelling and edema, moist, and/or increa ed temperature). Palpation may initially worsen this component.
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• (A) asymmetry can be noted by visual inspection or by palpatory examination. The so-called nondysfunctional side is used as the standard of expected form. Theoretically, an imaginary lin e down the middle of the body should reveal symmetry of one side to the other in a nondysfunctional condition. • Perhaps the most important determinant of somatic dysfunction is (R) restriction of motion. Restriction can be measure by quantity (degrees of motion) or quality (i.e., stiffness, tremors, cogwheel rigidity, extraneous movement, etc.). 5. The site of subjective complaints of pain can be deceptive and may not help in the actual localization of the true problem , but it is fairly reliable as an indicator that a problem exists. Tight muscles on one side may be relatively pain free while the contralateral stretched muscles may be more "attention-seeki ng." Symptoms may distract treatment from the more needy locations. Pain or any other symptom indicates a problem, but may or may not correlate with the dysfunction. 6. Locate a "primary sensitive" point by examination of the tissue in the region of the patient's complaint. If a significant point is not found, then use your knowledge of anatomic relationships to widen the search to adjacent areas. 7. Use knowledge of anatomic structures to locate another point. This may be designated as the "end point" for treatment purposes. It is located either distally or proximally to the primary point in a structure that links the two points. A thorough working knowledge and understanding of muscle origins/insertions, nerve pathways, and ligamentous attachments is a good beginning in determining this pair of points. If the primary point is at a muscular origin, the end point may be at the insertion, or vice versa. Sometimes one or the other point is located in the belly of the muscle. In that case, exploration of both ends of the attachments to bone may reveal the location of an end point. Ligaments, which are generally shorter and more fibrous, have points that are probably also fairly close to one another. Keep in mind that fascia encompasses all structures, and the path between one point and another may seem to cross other strucrures. The more specialized the fascia, the more palpable and tendinous it is. Tracing superficial and deep pathways of nerves is useful when determining paths that apparen rly do nor correlate with the other structures. Primary and end points may be found where a nerve passes our of a foramen, between or through muscles, or around bony protrusions. If more than one nerve innervates a region, the primary point can sometimes be found at the beginning of one nerve and the end point or the beginning of the other. In the case of nerve distriburion of an extremity, one point will typically be found closer to the body while the other will be closer to the end of the extremity. There are no exhaustive maps of points and sensitive point locations, and there is no substirution for an excellent working knowledge of anatomy. The designated primary point will most likely be nearer to the symptoms. The end point may also elicit the presenting symptoms, but usually to a lesser extent. As part of the reason for the maintenance of the dysfunction, all intervening points between the primary and the end points must be addressed. In any case, the first steps are to make a determination of the two ends of the pattern. A patient's complaints of apparently unrelated regions of the body being related may give a clue as to the location of some components.
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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TABLE 65.1. EXAMPLES OF PRIMARY POINTS AND END POINTS Primary Point
End Point
Connection
Surpaorbital notch
Sub-occipital region
Superior medial scapular border Greater trochanter of femur Sternum at 2nd rib Gluteal region
Base of occiput Fibular head Coracoid process Greater trochanter Popliteal region Pubic ramus Wrist
Frontalis and occipitalis muscles Trigeminal and greater occipital nerves Levator scapula Iliotibial band Pectoral is minor Piriformis muscle Sciatic nerve Rectus abdominus Median nerve
Xiphoid process Antecubital region
Figure No! 1A 1B
2 3 4 5 6
7 8
•see Appendix II (pp. 1258-1261) for figs.
Assuming rhat their knowledge of anatomy is small, it is left to you to draw conclusions necessary to begin treatment. These are indications that there is a problem. 8. For the purpose of proceeding in a logical fashion, the point that is more sensitive is designated as "primary." Put this in more easily understood language by referring to it as the "first point" with the patient. Both you and the patient can consider the other point, which is found on the other extreme, as the "end point." See Table 65.1 for a few examples of some primary and end points. 9. Determine a muscular, fascial, and/or neurologic pathway between the primary point and the end point. The line may be curved rather than straight. The direction of treatment may be from distal to proximal, or vice versa. 10. Understand the connection between the two points using knowledge of anatomy, especially: Nerve innervation: • Direct connections (e.g., the connection of a point near the antecubital region of the elbow at the elbow to a point along the middle of the forearm near the wrist- median nerve). • Consider overlap or "watershed regions" of innervation (e.g., the ophthalmic division of the trigeminal nerve travels from the supraorbital notch over the frontal region to the top of the head. The greater occipital nerve exits the suboccipital region in the occipital sulcus and travels over the occiput to the top of the head. They overlap in the scalp near the vertex). Muscle origins and insertions: • Typical (e.g., a sensitive point may be found at the medial aspect of the clavicle and another found at the mastoid process representing involvement of the sternocleidomastoid muscle). • Overlap (e.g., the location of a sensitive point on the superior anterior chest may involve the intercostal muscles, pectoralis major, and/or pectoralis minor) . • Contiguity (e.g., the tensor fascia latae and iliotibial band actually form a continuity for two possible tender points located at the greater trochanter and the fibular head, respectively. If a terminal point was actually found near the lateral malleolus instead of the fibular head, then there might be a tensor fascia latae, iliotibial band, peroneal muscle connection) . Fascia: • Specialized (e.g., interosseous ligaments are actually specialized fasciae connecting the radius and ulna in the arm and the fibula
and tibia in the leg. Consider their involvement if a pattern appears to overlie their locations). • Septums (e.g., although it is mostly muscular, the diaphragm has fascial components, including the central tendon and crus of the diaphragm. It supports and separates. Points found around the lower costal cartilage, the twelfth rib, and T10-12 and may represent diaphragmatic involvement). • Overlaps (e.g., the common thoracolumbar fascia acts an attachment for muscles, such as the latissimus dorsi, and overlaps muscles, such as the quadratus lumborum, iliocostalis, and other erector spinae muscles. Points may be found anywhere within the region and may extend to the lateral edge of the 12th rib [quadratus lumborum], or even to the bicipital groove of the humerus [latissimus dorsi]). Ligamentous attachments: • Typical (e.g., the attachments of either end of the collateral ligaments in the elbow and knee can be considered). • Relationships to muscles (e.g., specific points can be fo und on the superior or lateral C7 spinous process, and the base of the occiput may represent spinalis muscles or the nuchal ligament). • Relationships to nerves (e.g., the flexor retinaculum and palmar aponeurosis of the hand are related to the median nerve in the forearm. These structures, in turn, are related to attachments with at least four [pisiform, hamate, scaphoid, and trapezi um] carpal bones by means of the flexor retinaculum). Bones (the bones and their components should also be considered connective tissue): • Construction of joints (e.g., joint capsules represent connections between two or more bones. At the elbow and the knee, the capsules are stronger and reinforced on their medial and lateral surfaces by collateral ligaments. The anterior and posterior surfaces are relatively weaker and may tighten or loosen in one extreme of motion or the other. Points may occur in the middle of the capsule and at the bony attachments). • Lever action (e.g., muscle, tendons, and ligaments attach to bony prominences. Because of the forces placed on them, they enlarge into tubercles, trochanters, and other processes. Points located at tendinous insertions may also theoretically represent a contribution from the bony attachments). 11. Press both the primary point and the end point simultaneously using the pad region of a fi nger on each hand (Fig. 9,
65. Progressive Inhibition ofNeuromuscular Structures Technique Appendix II). (Again, for the sake of simplicity, identify the primary point as the "first point" for the patient.) The pressure exerted is a few ounces. It should be enough to elicit the patient's symptoms, and should be and of equal amount on both points. The patient may initially experience a mild to moderate increase in sensitivity. Also note the soft tissue response to the pressure: • Acute dysfunction may be more sensmve than chronic. A muscle that has been hypertonic will usually be more sensitive to pressure than the same muscle on the contralateral side. • Chronic hypertonic muscles will usually be larger than those on the contralateral side: -Larger muscles do not necessarily indicate dysfunction. Asymmetric use (where there is preference with one side being used more) will result in the dominant side becoming typically larger. An enlarged muscle does not indicate dysfunction. - Whether dysfunctional or nor, frequently used muscles or ones in chronic dysfunction may not be quite so sensitive to pressure. This may due to the chronicity of usage. • Both sides can be dysfunctional. One side may be more symptomatic than the other. Treat the more dysfunctional tissue first; re-examine, and then the lesser-involved side can also be treated. • A firmer muscle is probably in greater dysfunction. 12. Exert the same amount of pressure on both the primary and end points. • Patients may assume that a more sensitive location is being pressed harder. They should be reassured that the reason for the asymmetry is the greater dysfunction or hyperactivity of the involved tissue. • Patients may indicate to the practitioner that they can tolerate greater pressure. This does not accelerate the treatment. It is not necessary to increase, and may even be counterproductive. • Pain or tenderness may not be the only sensations experienced from the applied pressure. The patient may report other sensations that occur alone or in combination with pain. 13. Maintain constant pressure on the end point throughout the treatment. Initiate pressure on the point with greater sensitivity (primary point). Ask the patient to report what they are feeling. When inhibition is used properly, any increase in sensitivity at a point will most probably be transient. Also, a typical, rapid decrease in sensitivity occurs as the tissue accommodates the irritation of the inhibition. Ultimately, it may totally disappear. The duration can vary from several seconds to minutes. 14. Maintain contact with the primary point for 20 to 30 seconds before seeking any subsequent points. • One finger remains on the primary point. Use another finger of the same hand to locate a "secondary point." If the middle finger is on the primary point, then use the index finger to palpate the secondary point (Fig. 10, Appendix II). • Search for a secondary point approximately 2 to 3 em away from the primary point. An imaginary line connecting the primary and end points gives the approximate direction. This will
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typically follow the predicted course of an anatomic structure (innervating nerve, along the direction of the muscle fibers, or following fascial planes). • Identify the secondary point as "the second point" for the panent. 15. Exert equal pressure onto both the primary and secondary points while maintaining the constant pressure on the end point. 16. Ask the patient to determine which of the two points (primary vs. secondary or "first versus second") is more sensitive. • To make it simpler for the patient, use a phrase such as, "I am pressing on two points that are close together. Please tell me which of the two, the 'first' or the 'second,' is more sensitive?" • If the second point is more sensitive or equally as sensitive as the first: • Relieve the pressure from the first (primary) point and then remove it entirely. • Maintain constant pressure on the new, second (secondary) sensitive point for an additional 20 to 30 seconds . • It is not necessary to wait for the sensitivity at any point to be completely gone before moving on to the next point. It is more important that each subsequent point is more sensitive than the prior one. • Both increased tension and sensitivity can be found in the new secondary point. With practice, the "secondary" points can be located by palpatory sense of tension alone. A return to a lower level of sensitivity and response baseline usually occurs after a few seconds. The amount of time depends on the soft tissue response. Certain points may require further inhibition before progress can be made. After doing so, a new secondary point may be located where previously there was less sensitivity. If the original or a subsequent "first point" persists as the more sensitive of the two points: • Maintain pressure at the location of the primary point for an additional 20 to 30 seconds; and/or • Move the finger that was locating the secondary poi nt more laterally or medially from the connecting line. A located new secondary point should have at least the same sensitivity, if not more, as the primary point. (The anatomic structure, whether muscle, nerve, or fascia, that is being inhibited rnay have slight variations in the specific course in this individual.) • Once a secondary point that is equal ly or more sens itive is located, relieve pressure from the primary point and maintain on the new secondary point as described above. • The secondary point then becomes the new "first" po int in the continuing sequence of treatment toward the end point. 17. Inhibit the end point with constant pressure with a finger of the other hand throughout. The patient wi ll often forget that this point is being treated. As the anchor for the dysfunctional tissue, continuous treatment is necessary. It may lose sensitivity during the course of treatment. 18. Repeat the process unti l an ultimate "second" point is located 2 em from the end point. 19. Once the two final points have been treated with inhib ition, determine the amount of dysfunction that persists, especial ly
1032
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
at the end point location . It may have become significantly reduced or may completely disappear. 20. Another modality of treatment can be used if the dysfunction (including the end point) remains persistent. The end point and overall dysfunction may now be easier to treat than they were previously. Facilitated positional release, straincounterstrain, muscle energy, balanced ligamentous tension techniques, or some other modality may be used. The use of highvelocity/low-amplitude (HVLA) techniques that were difficult to perform before may now be easier. G uidelines for determining the choice include: • The persistence of the dysfunction or related components after treatment. • The ability of the practitioner to perform other modalities of treatment. • T he need or capability of the patient to tolerate additional treatment. 2 1. The concl usion of manipulative treatment for the session should be based on the findings for the individual. It should not be based solely on the patient's subjective complaints. Overtreatment can cause as many problems as undertreatment. 22. Patients may limit types of treatment based on prior experience or misconceptions. They may have had a reaction to previous treatments or they may have had no previous difficulties but have developed a dislike for a particular modality (i.e., "popping" seco ndary to HVLA). Attempting to coerce a patient to allow certain forms of treatment would be counterproductive to the therapeutic relationship. In many locales, it could also be considered illegal (i.e., battery). 23. The somatic dysfunction is always reassessed. 24. Despite a relatively comfortable treatment, a posttreatment reaction may occur. Inform the patient that some treatment reactions can include transient soreness, aches, and fatigue. In patients prone to bruising, when certain other predisposing factors exist (e.g., medication) , or if excessive pressure has been used, ecchymoses can occur. Generally, all such side effects resolve in 24 to 48 hours.
Possible Mechanism of Action One important component that distinguishes an inhibitory contact from a stimulatory one is the use of a low level, but constant amount of pressure applied to dysfunctional tissue. Although the initial effect may be irritating, a contact of rhis type may initiate accommodation or habituation over rime. At first, the patient may be acutely sensitive with complaints of increased pain, sensitivity, pressure, or some other sensation. These reactions decrease and may disappear altogether as rhe system adapts (35). Part of this reduction in awareness may be from the screening mechanisms provided by the reticular formation. The body accommodates to other stimuli, such as body contact with eyeglasses, tight belts, stiff clothing, uncomfortable shoes, as well as constant background auditory and visual stimuli. This sensory filtering process may also involve the spinal cord acting as a mediator or "brake" when sensory overload (36) occurs. Some stimuli remain relatively subliminal if not of sufficient quality, duration, or quantity.
Effects may include pressure or contact as a counterirritant. Instead of actually inhibiting, they act as stimulation to the neighboring tissue, thus reducing the sensitivity of the original render point. Scratching in the region of an itch would be one such example. Rapid conducting, large-nerve afferent fibers may gate transmission in the dorsal horn of the spinal cord with collateral fibers in the substantia gelatinosa or adjacent inrerneurons inhibiting the transmission of pain to the central nervous system via the spinothalamic tract (37). Relative ischemia has also been proposed as a theory. Muscle maintained in prolonged contraction produces metabolites and waste products from rhe local tissue damage (38). Impaired circulation also occurs concomitantly with hyperemia and congestion. Some of the substances have vasoactive effects, which theoretically may have the purpose of reacting to tissue injury. Trophic and fibrotic changes may occur if the injury persists. Normally, the overlying skin shows a brief blanching followed by redness, which also fades when normal , but may persist when the tissue is damaged for a prolonged time. It appears that rhe use of therapeutic pressure may add to rhe ischemia. Initially, this does not make intuitive sense when considering the amount of nutrient deprivation. However, the increased ischemia may reduce the capacity of the nociceptive receptors to process information. Hyperemia may also occur once this pressure is removed, resulting in rhe flushing of rhe waste products from rhe location . A muscle in dysfunction may appear to be in irs neutral position, but may still be hypertonic. Further stretch from the relatively shortened length increases activity of the muscle spindle mechanisms, and will result in a reflexive and prolonged contraction. This is a means of protection (39-42). If stretching is used, slow stretching is the type. Pressure applied during inhibition introduces a gentle stretch while allowing the re-setting of the stretch receptors (43). Only a small amount of the tissue may be challenged without upsetting the whole structure. Once the small, localized component is overwhelmed, any affected adjacent area can subsequently be inhibited with similar results. Inhibition in general and PINS in particular may be very effective methods to deal with a series of irritated pieces. The osteopathic physician may treat the entire dysfunction by progressively treating all of the involved elements. The Golgi tendon organ is a sensory mechanism that becomes relatively stretched during muscular contraction (where the overalllength of the muscle does not change). When a critical amount of tension occurs, increased Golgi tendon organ activity brings about reflex relaxation of the muscle as a whole. An inhibitory interneuron between the afferent nerve ending in the spinal cord and the alpha motoneuron bring about sudden, almost complete muscular relaxation. The pressure from the osteop~thic physician's fingers may create an initial stretch that results in further contraction. This is then followed by resultant relaxation (44).
Contraindications and Side Effects There appear to be few conrraindications and side effects with the use of PINS. Pressure should not be exerted onto lo-calized inflammation, abscess, or infection, as the integrity of the skin or walled infection may be compromised.
65. Progressive Inhibition of Neuromuscular Structures Technique
CONCLUSION PINS represents a unique variant of the more traditional approach to using inhibition, as well as a means of discovering the ways in which dysfunction occurs and is maintained. It can be used solely or in combination with other methods of osteopathic manipulation. The effect of other treatment modalities can be enhanced by the use of PINS. Using PINS does require an investment of time. When it appears that other typical interventions are of limited success with recalcitranr dysfunction, alternative means must be used. However, when this occurs, the time necessary to perform PINS would be worth the effort.
REFERENCES 1. Dowling D]. Progressive inhibition of neuromuscular structures (PINS) technique. jAm Osteopath Assoc. 2000; 100(5),285-286,289-298. 2. Glossary of Osteopathic Terminology. AOA Yearbook and Directory of Osteopathic Physicians, 1998. 3. Dowling DJ, Scariati PD. Neurophysiology relevam to osteopathic principl es and practice. In: DiGiovanna EL, Schiowitz S, eds. An Osteopathic Approach to Diagnosis and Treatment, 2nd ed. Philadelphia, PA: Lippincocr-Raven Publish ers; 1997:33. 4. Ehrenfeuchter WC. Soft tissue techniques. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:78 1-794. 5. Robbins SL, Corran RS , Kumar V. Pathologic Basis of Disease, 3rd ed. Philadelphia, PA: WB Saunders; 1984:40. 6. Still AT. Autobiography ofA. T Still, rev. ed. Kirksville, MO: Published by the author; 1908:32. 7. Still AT. The Philosophy and Mechanical Principles of Osteopathy. Kansas City, MO: Hudson-Kimberly Publishing Co; 1902:101. 8. Goetz EW A Manual of Osteopathy, 2nd ed. Cincinnati, OH: 1905. 9. Tasker DD. Principles of Osteopathy, 4th ed. Los Angeles, CA: Bireley & Elson Printing Co; 1916:354-370. 10. Jones LH. Strain and Counterstrain. Newark, OH: American Academy of Osteopathy; 1981. 1 1. Jones LH , Kusenose R, Goering E. jones Strain-Counterstrain. Boise, ID: Jones Srrain-Countersrrain; 1995. 12. Glover JC, Yates HA. Strain and countersrrain techniques. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:809-8 18. 13. Schiowitz S. Facilirated positional release. In: DiGiovanna EL, Schiowitz S, eds. An Osteopathic Approach to Diagnosis and Treatment, 2nd ed. Philadelphia, PA: Lippincorr-Raven Publishers; 1997:91. 14. Van Buskirk VL. A manipu lative technique of Andrew Taylor Still as reponed by Charles Hazzard, DO, in 1905. jAm Osteopath Assoc. 1996;96(1 0):597-602. 15. Hazzard C. The Practice and Applied Therapeutics of Osteopathy. 1905. 16. Johnston WL. Functional technique: An indirect method. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:795-808. 17. Dowling D). Myofascial release techniques. In: DiGiovanna EL, Schiowirz S, eds. An Osteopathic Approach to Diagnosis and Treatment, 2nd ed. Philadelphia, PA: Lippincorr-Raven Publishers; 1997:381-383. 18. Chila AG. Fascial-ligamentous release: An indirect approach. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:819-830.
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19. Ward RC. Integrated neuromusculoskeletal release and myofascial release: An introduction to diagnosis and treatment. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:846--849. 20. Typaldos S. Introducing the fascial distortion model. Am Acad Osteopath J 1994;4(2). 21. Chairow L. Neuro-muscular Technique. Wellingborough, Northamronshire, England: Thorsons Publishers Ltd; 1980. 22. Chairow L. Modern Neuromuscular Techniques. New York, NY: Churchill Livingstone; 1996. 23. Owens C. An Endocrine Interpretation of Chapman's Reflexes, 2nd ed. Chartanooga, TN: Chartanooga Priming and Engraving Co; 1937. 24. Cyriax ]. Text-book of Orthopaedic Medicine Volume [[: Treatment by Manipulation and Massage, 6th ed. New York, NY: Harper & Row; 1959. 25 . Travell JG, Simons DG. Myofascial Pain and DysfUnction: The Trigger Point Manual: The Upper Extremities, vol I. Baltimore, MD: Williams & Wilkins; 1983. 26. Chaidow L. Osteopathic Self-Treatment. Wellingborough, England: Thorsons Publishing Group; 1990:105- 119. 27. Kenyon ]. Acupressure Techniques: A Self Help Guide. Rochester, VT: Healing Arts Press; 1988. 28. Cerney JV. Acupuncture Without Needles. West Nyack, NY: Parker Publishing Company, Inc; 1974. 29. Shultz W Shiatsu: japanese Finger Pressure Therapy. New York, NY: Bell Publishing Company; 1976. 30. Wei! A. Spontaneous Healing. New York, NY: Ballanrine Books; 1995. 31. The Burton Goldberg Group. Alternative Medicine: The Definitive Guide. Puyallup, WA: Furure Medicin e Publishing, Inc; 1994:106- 108. 32. Prudden B. Pain Erasure: The Bonnie Prudden Wtly. New York, NY: Ballantine Books; 1980. 33. The Burton Goldberg Group. Alternative Medicine: The Definitive Guide. Puyallup, WA: Future Medicine Publishing, Inc; 1994:102- 103. 34. Dowling D). S.T.A.R.: a more viable alternative descriptor system of somatic dysfunction Am Acad Osteopath j. 1998;8(2):34--37. 35. Bailey HW. Some problems in making osteopath ic spinal manipulative rherapy appropriate and specific. jAm Osteopath Assoc. 1976;75:486499 . 36. Parrerson MM. A model mechanism for spinal segmenral faci li tation. JAm Osteopath Assoc. 1976;76:62-72 . 37. Ganong WF. Review of Medical Physiology. Upper Saddle River, NJ: Prentice Hall; 1995:130-131. 38. Stoddard A. Manual of Osteopathic Practice. London, UK: Hutchinson Medical Publications; 1969:238. 39 . Buzzell KA. The poremial disruptive influence of somatic inpu t. The Physiological Basis ofOsteopathic Medicine. The Postgraduate Institute of Osreoparhic Medicine and Surgery. New York, NY: Insight Publishing Company; 1967:39-51. 40. Ganong WF. Review of Medical Physiology. Upper Saddle River, NJ: Prentice Hall; 1995 :113- 117. 41. Becker RF. The gamma system and its relation to the development and maintenance of muscle tone. 1976 Year Book ofthe American Academy of Osteopathy. Colorado Springs, CO: American Academy of Osteopathy; 1976:26-40. 42. Korr IM. Proprioceprors and somatic dysfunction. 1976 Year Book of the American Academy of Osteopathy. Colorado Springs, CO: An1erican Academy of Osreopathy; 1976:41-50. 43. Korr IM. Proprioceprors and somatic dysfunction. jAm Osteopath Assoc. 1974;74:638-650. Reprinred in The Collected Papers of Irvin M. Korr. Colorado Springs, CO: An1erican Academy of Osteopathy; 1979 :200207. 44. Ganong WF. Review of Medical Physiology. Upper Saddle River, NJ: Prenrice Hall; 1995:117- 118.
MVOFASCIAL TRIGGER POINTS AS SOMATIC DYSFUNCTION MICHAEL L. KUCHERA JOHN M. McPARTLAND
KEY CONCEPTS • Similarities and differences between var1ous myofascial points • Definitions of active and latent Travel! trigger points • Postulated physiologic mechanisms of referred pain • Trigger points as somatic dysfunction • Effect on somatic function , venous-lymphatic drainage, and autonomic function • Relationship to somatovisceral and viscerosomatic reflexes • Commonalities in palparory diagnosis, signs and symptoms • Osteopathic clinical approach to trigger points • Incidence in heal thy populations and those seeking medical care • Addressing contributing and perpetuating facrors • Techniques for treatment, including osteopathic manipulative treatment, soft tissue techniques, spray and stretch, deep massage, injection, and others
ings. Often they are associated with local or referred auronomic disturbances (2,3) . They may exhibit localized tenderness alone, or they may also have a referred pain pattern ro a reference zone that may or may not have an obvious neurologic distribution. Although many of these myofascial points have overlapping characteristics, they also have unique facrors (2) related ro the perspective and philosophy of the physician mapping rhem. Over rime, many clinicians have correlated tender points, reflex points, and trigger points with visceral pathology. In 1893, both Head (4) and Mackenzie (5) associated dermal and myofascial tender points with internal pathology. In the 1920s, Chapman found useful clinical correlations between palpable tender points and visceral complaints (6); his system of viscerosomatic reflexes is discussed further in Chapter 67. Beginning in the 1940s, an internal medicine physician, Janet Travell, spent over 50 years researching and documenting the myofascial genesis of pain parterns and their role in clinical diagnosis and treatment (2,7,8).
Myofascial Trigger Points in Osteopathic Practice
Throughout the hisro ry of medicine, render points in myofascial tissues have been observed and mapped. They figure prominen tl y, for example, in several ancient eastern patient care systems, including acupuncture. Increasingly, various western physicians have correlated palpable myofascial points with patient hisrories and their accompanying symproms. Today, many myofascial point systems are found in the modern physician's differential diagnosis and treatment armamentarium.
MYOFASCIAL POINT SYSTEMS Myofascial points have certain common clinical characteristics ( I); by meeting tenderness/asymmetry/range of motion/tissue texture changes (TART) diagnostic criteria, all are definable forms of somatic dysfunction. All are subjectively render with moderate ro deep palpation, and all are characterized and recognized as palpably small, circumscribed, hypersensitive myofascial thicken-
Travel! an d Simons (2,8) developed the most widely recogn ized myofascial point system used in diagnosis and treatmem. These physicians devoted their careers to the understanding of myofascial pain and dysfunction , and the clinical application of the trigger point system for their treatment. Travell's prominence in using this system in the care of President John F. Kennedy, and the excellent two-volume text, Trave/1 & Simom' Myofascial Pain and Dysfunction: The Trigger Point Manual (2,8) brought worldwide recognition ro this form ofsomatic dysfunction , which might otherwise have been overlooked. Diagrammatic summaries of trigger point maps affecting different regions are shown in Figure 66.1. When a patient complains of pain in a particular region, consider examin ing these points. A myofascial trigger point (TP) is a specific form of impaired or altered myofascial function with distinctive clinical and pathophysiologic characteristics; these characteristics are extremely well documented in the literature (1). A TP is defined as "a hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. The spot is painful on compression and can give rise to characteristic referred pain , referred
66. Myofascial Trigger Points as Somatic Dysfunction
a
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b
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FIGURE 66.1. Regional depiction of Travel I myofascial trigger points; referred pain patterns (black stippled area) and location of trigger points (arrows). A: Masticatory and two neck muscles, (B) several head and neck muscles, (C) neck muscles (scaleni) that refer pain in the upper extremity and for many shoulder girdle muscles, (D) arm and several forearm muscles, (E) forearm and intrinsic hand muscles, (F) shoulder girdle, chest, and iliocostalis paraspinal muscle, (G) superficial paraspinal, several deep paraspinal, quadratus lumborum back muscles, and two abdominal wall muscles, (H) pelvic girdle muscles and three parts (vastus medialis, rectus femoris, and ·vastus intermedius) of the quadriceps femoris muscle, (I) vastus lateral is of quadriceps femoris, several muscles of leg, and selected intrinsic foot muscles. (From Wall PD, Melzack R, eds. Textbook of Pain, 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 1989:368-385, with permission.)
SUBSCAPULARIS
1035
1036
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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FIGURE 66.1. (continued )
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66. Myofascial Trigger Points as Somatic Dysfunction
1037
VASTUS LATERA LIS
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FIGURE 66. 1. (continued )
tenderness, motor dysfunction, and autonomic phenomena" (2). In short, a TP is a specific form of somatic dysfunction . The term TP is reserved for a point that has the potential to refer ("trigger") pain in a certain predictable distribution. TPs are classified as "active" or "latent" depending on their ability to refer pain into the characteristic distribution empirically mapped for each point. Active points refer pain at rest, with muscular activity, or with palpation. Latent points produce pain only when probed with more steady pressure. Unless a skilled palpatory examination is conducted, latent points are often overlooked, and the true cause of dysfunction may be misdiagnosed. In several ways, this system is distinct from that described by Jones (see Chapter 63), in which locally tender myofascial points do not typically refer pain beyond the location being compressed. In general, however, Simons (9) describes a significant overlap in location between TPs and several systems of tender points. Chaitow (1 O) believes their distinction is arbitrary. He notes that tender points can develop referral capabilities by the simple introduction of a chill or strain to the affected muscle. Similarly, Bennett (11) suggests that tender points become trigger points as a result of enhanced patient pain perception. Comparing yet another system, Melzack (12) reported a 71 o/o correspondence between published locations ofTPs and classic acupuncture points used in the relief of pain. Myofascial TPs are only one manifestation of somatic dysfunction, but they provide significant osteopathic insights. This type of somatic dysfunction has far-reaching implications in the
differential diagnosis and treatment of: Pain syndromes and disability Repetitive strain injuries and overuse syndrome Reduced muscle functions Fibrositis, fibromyalgia, myofasciitis, and chronic fatigue syndrome Disrupted visceral homeostasis Diagnosing, interpreting, and treating myofascial points as a form of somatic dysfunction provides a better understanding of the osteopathic perspective. It expands our interpretation of structure-function relationships and offers possible mechanisms for treatment of other somatic tissues. It also enhances our clinical diagnostic and treatment skills. In return , osteopathic medicine continues to contribute greatly to the documentation , interpretation, and treatment of myofascial tender points and trigger points.
Incidence There are more than 200 pairs of muscles in the human body, with myofascial structures constituting approximately half of the body's mass. Not surprisingly then, these soft tissues are a common source of patient complaints. Different centers have reported the incidence of various primary myofascial syndromes: for example, the documented prevalence in a general internal ~edicine outpatient practice was 30% (13) compared with 55% of296 patients admitted for chronic head and neck pain (14) and
1038
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
85% of283 consecutive admissions for chronic pain (15) . Often misdiagnosed, a specific myofascial syndrome, fibromyalgia, has a reported incidence of 2% in the general population and 6% to 10% in general inrernal medicine clinics (16,17) . Inrerestingly, in one study, about 72% of patients with fibromyalgia syndrome also had active TPs, and 20% of those with active TPs also had fibromyalgia (18). The specific documented incidence oflatent TPs also varies. It has been reported (19) as 54% and 45%, respectively, in asymptomatic 19-year-old female and male Air Force recruits. Of 61 consecutive patienrs presenting to an internal medicine practice, 10% with general medical symptoms and 31% with the chief complaint of pain had TPs as the primary cause (20). Trigger poinrs are most likely to develop in the upper trapezius muscle (19). Overall, however, trigger points in the quadratus !umbo rum muscle are reported to be the most common, and most commonly overlooked, cause of myogenic low back pain (21) . TPs are both more likely to occur and, once present, are more likely to remain in patients with perpetuating factors. Postural and other mechanical disorders, including articular somatic dysfunction (I ,2,8,22,23), are reported to be some of the most pervasive perpetuating factors. An osteopathic structural analysis is therefore warranted in any patient with myofascial TPs. Other conrributing factors include: Hypothyroidism, hypoglycemia, and various metabolic/ endocrine dysfunction (11) Nutritional deficiencies (2) Chronic infections (2) Allergic rhinitis (2) Psychological stressors (2,24) Systemic perpetuating factors may include any structural or functional disorder that compromises homeostasis of the local energy supply to the involved muscle(s) .
Referred Pain Mechanisms and Causation Regardless of the exact mechanism or mechanisms proposed, afferenr information to the central nervous system from peripheral somatic and visceral structures figures prominenrly in the proposed origin of all myofascial points. In the Travell system, overuse of somatic structures, especially chilled muscle, is often implicated (2). Although primary visceral dysfunction related to facilitated segmenrs is more frequenrly associated with Chapman reflex points (25), Travell and Simons also note the association of segmenrally related visceral dysfunction in TP initiation and/or perpetuation (I ,2) . Proponenrs of Chapman poinrs (26), Jones poinrs (27), and Travel! TPs (2) all recognize the importance of segmenrally related somatic dysfunction in the interpretation and treatment of each myofascial poinr system. Unless physicians recognize and understand the basis for referral phenomena, appropriate diagnosis and treatment may result from mislocalization or misinterpretations of the true origins of the pain. Several mechanisms are postulated to play a role in TP referral phenomena: 1. Convergence-projection 2. Convergence-facilitation
3. Activity of the sympathetic nervous system 4. Convergence or image projection at the supraspinal level 5. Peripheral axon branching from certain dorsal root ganglion cells to two different muscles Most of the central mechanisms applied to understanding TPs suggest that pain referral may result from nociceptive information being misdirected in the spinal cord to reach somatotopically inappropriate dorsal horn neurons. T he first and fifth mechanisms relate to the structure of the nervous system, although the others relate to functional factors. (Further discussion of referred pain may be found in Chapter 15.)
Central Nervous Syst em The central inregration of afferent data with generalized, predictable modification of efferent responses is a neurologic model used to explain causation and maintenance of somatic dysfunction (including TPs), referred pain, and several reflexes between the soma, the viscera, and the sympathetic systems ( 1,28,29). This view is consistent with Korr's observations (30) that the spine can be viewed as an "organizer" of disease and dysfunctional processes, and may harbor a segmentally related "neurologic lens" for a wide variety of stressors (Fig. 66.2).
Peripheral Local Conditions Local conditions resulting from or accompanying the development of myofascial points have also been studied ( 1,3 1). These conditions suggest that palpatory tenderness and TPs are increased by endogenous tissue sensitizing and pain-producing substances (bradykinins, serotonin, histamine, substance P, prostaglandin E2, etc.) (1,31). Branching axon subpopulations, as well as local microtrauma and/or macrorrauma are also implicated in the wider release of these substances. Somatic dysfunction alters the local biochemical milieu and impairs or alters neural, vascular, and lymphatic mechanisms, preventing removal of these sensitizing and/or pain-producing substances (3,32). Physiologically, there appears to be local metabolic crisis in the presence of impaired circulation, a factor that leads to tissue texture abnormalities that aid in fi nding the myofascial point by palpation. Palpatory findings in the area of a TP include an alteration of cutaneous temperature and humidity. There is a small nodular or spindle-shaped thickening of the tissues, representing the myofascial point itself. The point is extremely tender to the patient and usually invokes a generalized "jump sign" or some other patent response of discomfort. In the case of myofascial trigger points, there is a "local twitch" of the taut muscle band containing the point when the muscle is palpated perpendicular to its long axis. There may be localized goose flesh or trophic changes at the site. A summary of these palpatory findings is proposed in Figure 66.3.
Biomechanical Conditions The activation of a TP is usually associated with some degree of mechanical abuse of the muscle. This may be associated with:
66 Myofascial Trigger Points as Somatic Dysfunction
1039
Area of Facilitation
Direct Stimuli
Indirect Stimuli Acute overload Overwork fatigue Chilling Gross trauma Gravitational stress (postural strain) Host factor predisposition nutrition endocrine biomechanical
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Descending colon Uterus Prostate Rectum ,)
Spinal cord segments FIGURE 66.2. The spinal cord as a neurologic lens for a variety of stressors to initiate somatic and/or visceral symptoms.
Muscle overload (acute, sustained, and/or repetitive) Myofascial postural stress Leaving a muscle in a prolonged shortened position (especially if the muscle is then contracted while in the shortened position) Muscle chilling Furthermore, dysfunction in a given muscle places additional biomechanical demand on other muscles in the functional myotatic unit. (A "myotatic unit" is made up of muscles sharing the same functional responsibilities.) Functional overuse may result in associated TPs in a given myotatic unit. "Satellite trigger points," on the other hand, may develop in muscles covered by the referred pain pattern of another myofascial TP. An understanding of the structure-function relationships and physiologic mechanisms involved in instigation and perpetuation ofTPs leads to a more accurate diagnosis of the patient. Successful treatment of that patient depends on removing the primary myofascial TP, its associated and satellite TPs, related articular dysfunction, and any underlying or perpetuating factors. Failure to address all of these elements usually results in the full return of rhe dysfunctional myofascial situation.
DIAGNOSIS Diagnosis of myofascial TPs depends on distinctive palpatory findings (local spot, palpable band, and rwirch response); muscle testing (strength and range-of-motion); distribution of the pain pattern; and the patient's history. TPs are locally very tender. They are palpated as small nodular or spindle-shaped thickenings within a taut band of tissue. Each suspicious muscle is examined. A muscle contains a myofascial TP when fingertip pressure across the long axis of the muscle produces a generalized "jump sign" by the patient and a "local rwitch" of the taut band. The rwo findings are not synonymous. (The jump sign is a general patient pain response characterized by wincing or a voluntary withdrawal response; the local rwitch is a transient contraction of the taut band of fibers housing the TP.) The local rwirch response is clinically significant because it is usually absent in the fibromyalgia syndrome bur present in myofascial pain syndromes due to TPs (19). Precise localization of the TP is required for accurate diagnosis, as well as in accomplishing many of the specific treatments. Depending on the muscle examined, use either Aat palpation or
1040
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
\
Local twitch of band
A
8
\
Pincer grip
FIGURE 66.3. Palpation for myofascial trigger points. A: Draw f ingertips across large, flat muscles, (B) use pincer grip for muscles like trapezius or those in axillary folds. (From Travel! JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:60, 61, 398, with permission.)
palpation with a pincer type grip (Fig. 66.3). In large, Aar muscles like the quadratus lumborum, fingertips can be drawn across the muscle perpendicular ro its fibers. Some muscles, like the trapezius or those in the axillary folds, are better palpated with a pincer grip. The most appropriate palpation for a TP is that which permits pressure to be applied perpendicular ro the long axis of the muscle suspected of harboring the point. Joints controlled by muscles with myofascial TPs may show resrricted ranges of motion in the direction of stretch, and the muscles are painful with either active or passive stretching. Patchy weakness during muscle testing may result from a conscious or unconscious desire ro avoid pain. If present, attention to the precise pain patterns is extremely important in the diagnosis, because the empirically mapped patterns for each given muscle are fairly consistent among patients (Fig. 66.1). Histories of activities leading ro the onset of pajn and dysfunction or detailed descriptions of the muscular activities no longer comfortable for the patient are often sufficient to identify specific muscles that need to be examined for TPs. Interrater reliability tests demonstrate the need for all examiners to be trained and experienced to perform reproducible examinations (2). Experienced examiners who were pretrained to conduct and interpret find ings similarly were able to generate good to excellent kappa values (33). Although no one diagnostic examination is considered a satisfactory criterion for diagnosing a TP, the combination of local spot tenderness and the finding of a palpable, taut band are essential elements in defining an active or latent TP. Current recommended diagnostic criteria are summarized in Table 66.1.
Laboratory, imaging, and neuroelectrodiagnostic tests are not diagnostic for primary myofascial TPs or for most other forms of somatic dysfunction. They may prove useful, however, in identifying factors that perpetuate trigger points or in ruling out a variety of clinical conditions from which secondary myofascial TPs may arise. For example, in the presence of nerve compression sufficient to create peripheral electromyograp;1ic changes, an increased number of active TPs will be found in the affected m us des (34).
TREATMENT Myofascial TPs have been treated in several ways, ranging from needles to manual techniques to medication. Treatment is directed toward inactivation of the trigger points in the involved muscles and toward identification and resolution of contributing and perpetuating factors. Lasting success depends on: Correction of associated somatic dysfunction Patient education to prevent recurrences Appropriate self-stretch exercise programs Correction of underlying perpetuating and facilitating factors Specific treatment of myofascial TPs can be accomplished with (2): In hi bi tion soft tissue technique Vapocoolant spray or other intermittent cooling with stretch Deep massage
66. Myofascial Trigger Points as Somatic Dysfunction TABLE 66.1. CRITERIA AND COMPARATIVE RELIABILITY FOR TRIGGER POINT DIAGNOSIS A. Recommended criteria for identifying a latent trigger point or an active trigger point Essential criteria 1. Taut band palpable (if muscle accessible). 2. Exquisite spot tenderness of a nodule in a taut band. 3. Patient's recognition of current pain complaint by pressure on the tender nodule (identifies an active trigger point). 4. Painful limit to full stretch range of motion. Confirmatory observations 1. Visual or tactile identification of local twitch response. 2. Imaging of a local twitch response induced by needle penetration of tender nodule. 3. Pain or altered sensation (in the distribution expected from a trigger point in that muscle) on compression of tender nodule . 4. Electromyographic demonstration of spontaneous electrical activity characteristic of active loci in the tender nodule of a taut band. B. Comparative reliability of diagnostic examinations for trigger points, estimate of the relative difficulty performing the examinations, and estimated relative diagnostic value of each examination by itself, regardless of other findings
Presence of
No. of studies
Mean kappa
Spot tenderness Pain recognition Palpable band Referred pain Twitch response
3 3 3 4 3
0.70 0.59 0.54 0.47 0.23
Difficulty
+ ++ +++ + ++ + +++
Diagnostic value alone
+a
+++ ++a
+ + +++
a The combined presence of these two will likely have a high diagnostic
value for sufficiently skilled examiners. From Simons DG, Travel I JG, Simons LS. Travel/ and Simons Myofascial Pain and Dysfunction: The Trigger Point Manual, vol. I. Upper Half of Body, 2nd ed. Baltimore, MD: Williams and Wilkins, 1999, with permission.
Injection Jones counterstrain Isometric muscle energy techniques Myofascial release Other osteopathic manipulative treatment (8,35) Other adjunct neuromusculoskeletal therapies may be added as needed. Successful TP treatment addresses the central nervous system's response to nociceptive information or modifies peripheral input. These techniques may be ineffective if the patient is unable to relax and involuntary tensing takes place. If the operator releases the pressure too soon or too quickly, or if perpetuating factors are not addressed, reoccurrence or incomplete resolution of the TPs may result. Neuroplastic structural and functional changes in the central nervous system arise from prolonged nociceptive input, and may not be reversible with rime alone (36,37). Thus, much suffering from chronic pain is preventable if nociception is controlled promptly and effectively (1). The earlier the treatment of somatic dysfunction (myofascial and articular), the less likely the patient is ro develop central processing dysfunctional patterns, and the more likely it is to have a favorable outcome. Outcomes and number of treatments required were directly related, for example, to
1041
the time between injury and onset of treatment in patients with pectoralis minor TPs from whiplash injuries (38). In this study, the longer it took to start treatment, the more treatments that were required and the less likely that complete symptom relief could be achieved.
Cooling with Stretching Intermittent cooling with a vapocoolant spray followed by myofascial stretch (spray with stretch) is reported to be the "single most effective noninvasive method" to inactivate acute TPs (2) . Stroking with plastic-covered ice followed by passive stretching is also effective, however. These techniques are believed to act through Wall and Melzack's (1) gate theory (Fig. 66.4). The cooling activates Kraus receptors, which report centrally through fast fibers. The afferent volley of neural impulses conveyed through these fast fibers reflexively block the TP nociceptive impulses conveyed by slow fibers at the substantia gelatinosa. Blocking this neurologic reflex allows the operator to restore the muscle containing the TP to its normal resting length with full range of motion without producing pain or reflex muscle contraction. The common adage is "spray is the distraction, stretch is the action" (2). Vapocoolant spray is best applied to the skin at an angle of 30 degrees at a rate of approximately 4 inches per second. Adjusting the distance for different coolant products permits the physician to stimulate cold receptors in the skin without chilling the underlying muscle. For example, apply Fluori-Methane from a distance of 18 inches, but the "colder" ethyl ch loride spray (or Gebaur Pharmaceutical's vapocoolant spray) at a distance of 12 inches. Apply cooling in unidirectional parallel sweeps over the entire length of the muscle in the direction of irs fibers, passing over the TP. Gently stretch the muscle by "raking up the slack" rather than forcibly stretching it. Subsequent passes of the spray should include simi lar application contin uing over the TP's reference zone. Again, follow this by a gentle stretch of the muscle. Care should be taken to activate the cold receptors of the skin while carefully avoiding chilling the muscle. Chilling of the underlying muscle will often activate a TP and prevent the effective muscle stretch needed to elimin ate that TP. After intermittent cooling with stretch, warm the area with moist heat and take the muscle through irs full active range of motion.
Injection Injection is sometimes necessary to inactivate a TP (2). Although dry needling of the TP has been reported to be successful by some operators, most inject procaine. Some mix the procaine with a steroid preparation. Aspirate before injecting. The needle should be placed directly into the TP (Fig. 66.5) for rhe greatest effect. This will often be intensely uncomfortable and reduplicate the patient's pain pattern, so warn the patient of this. Successful penetration of the TP will create a local twitch response that correlates highly with a successful injection. Injection of a TP may fail if: Primary or secondary trigger points are missed by the needle The injected solution causes irritation of the tissues
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Vapocoolant
2 oistracting stimuli
1
Pain
3 Noxious stimuli
Inhibition at (gate)
Skin---+
' ' Dysfunctional muscle
'...
·
... _ _ _
~
_ __ - - - - - - Spasm blocked
;
,;-:,_, ;
~
;~
Segmentally related spinal level
Therapeutic stretch allowed after blocking "gate" FIGURE 66.4 . Spray-with-stretch technique. Cooling (1} must occur at rate that significantly activates Kraus (cold) receptors in skin but avoids chilling underlying muscle. Cold is conveyed centrally by fast afferents (2} that block noxious afferent information (3} from dysfunctional muscle at the substantia gelatinosa (4} or gate. (From Travel! JG, Simons DG . Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:72, with permission.)
Local bleeding acts as an irritant to reinitiate a trigger point Perpetuating Factors are not addressed If injection of a TP with a radicular or peripheral nerve distribution is attempted, omit steroids to avoid accidental injection into the nerve itself.
OSTEOPATHIC APPROACH Somatic dysfunct ion is present when there is "impaired or altered Function of the somatic system and its related neural, lymp hatic, and circulatory elements" (39). Travell and Simons' description of myofascial (TP) dysfunction also includes: Neural entrapment Arterial entrap ment Venous entrapment Lymphatic entrapment Autonomic sequelae Viscerosomatic-somarov isceral reflex phenomena resulting from myofascial dysfunction With such inherent overlap, TPs can easily be integrated into th e diagnostic and treatment considerations of an osteopathic physi cian as a subse~ of somatic dysfunction. Professional collaboration has ensured that this insight is growing exponentially. As recently as 1991 , Simons reported that the interface between (myofascial pain syndromes) and somatic dysfunction was one of the "greatest voids" in our knowledge (28). However, the Following year, Basmajian () remarked that seco nd major text on myofascial pain and dysfunction opened up "new ground in sen-
sitizi ng clinicians to the important in terfaces between myofascial pain syndromes and articular (somatic) dysfunction. " Since that time, extensive interactions have taken place with practitioners of manual medicine worldwide, embracing the contributions of Simons and Travel!. The new, second edition of
Travel! & Simons' Myofascial Pain and Dysfunction: The Trigger PointManual(2), includes chapters with extensive correlation between articular somatic dysfunction and TPs, especially in chapters detailing the posterior cervical and suboccip ital muscles. It also extensively discusses the use of several manual medicine techniques to effectively treat TPs . Lewitt (40), a neurologist in the Czech Republic, has also described the close relationship between articul ar so matic dysfunction and myofascial trigger points. The in creased tension of the TP and facilitation of motor activity can maintain articular stress while abnormal sensory inpu t from articular dysfunction can reflexively activate TP dysfunction. For this reason, he emphasizes the importance of treating both the muscular and articular components of somatic dysfunction when both are present (40).
Trigger Points Affecting Regional Somatic Functions TPs typically result in weakness and/or dysfunction of the muscle harboring them (2). Overuse in the myotatic uni t because of this primary myofascial point may cause secondary associated myofascial points, resulting in Further weakness and reduced function. If the point is latent (2), it may be clinically silent unless it is palpated directly or the muscle harbori'ng it is functionally stressed. If the point is active (2), it weakens and prevents full lengthening of the muscle. It may produce referred
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66. Myofascial Trigger Points as Somatic Dysfunction TABLE 66 .2 . LIMI TATION S MOTION (ROM) M otion restrict ed•
OF
SHOULDER
RA NGE
OF
Myofascial point found
Flexion Abduction
Triceps Subscapularis Infraspinatus Supraspinatus Teres major (levator scapulae)
Internal rotation
Teres minor Infraspinatus
Extern a I rotation
Subscapularis Pectoralis minor
•stage of Spencer that is restricted. Note: The majority of muscles are rotator cuff muscles.
FIGURE 66.5. Triceps TP3 and injection-precipitated pain pattern. (From Travel I JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:83, 473, with permission.)
pain and/or autonomic phenomena in a predictable trigger or reference zone. These zones are characteristic for each muscle and have been empirically mapped and documented (Fig. 66.1) (2,8,19,31). Altered somatic function that has been noted includes (2, 19): Disturbed proprioceptor and motor coordination (2) Temporomandibular joint dysfunction (2) Depressed deep tendon reflexes (19) Muscular stiffness and weakness (2) Diminished ranges of motion (2) The patient often complains of these symptoms, as well as dysesthesia, paresthesia, and pain. The pain is described as steady, deep, and achy in nature. Symptoms are often aggravated by: Use of the muscle Chilling Psychogenic stress Viral infection Prolonged shortening of the muscle Pressure over the trigger point
Chronic pain may lead to secondary depression, sleep disturbance, and chronic pain behavior (2). Diminished range of motion caused by myofascial TPs should be differentiated from structural limitations of the joints, such as occur in osteoarthritis, and functional arthrodial limitations, such as occur in other forms of somatic dysfunction. In particular, Travel! myofascial points should be distinguished from fibromyalgia syndrome (2, 11) and other rheumatologic disorders (41). Appropriate recognition and treatment of TPs have provided dramatic restoration of function in numerous patients previously misdiagnosed with these other conditions. Similarly, as a component element of somatic dysfunction, myofascial TPs must sometimes be specifically addressed to allow complete resolution of the joint dysfunction (2,40). Clinically, this is often the case in recurrent exhalation somatic dysfunction of rib 12 related to quadratus lumborum TPs. The presence of trigger points must be considered when the usual treatment for shoulder dysfunction fails to respond fully to manipulative techniques, such as the seven stages of Spencer (see Chapter 47). Table 66.2 delineates the trigger points associated with Spencer technique. Many clinical diagnoses have associated myofascial trigger points in which the dysfunctional trigger zone overlaps with the structural symptoms profile. Although a cause-and-effect relationship has not been demonstrated, treatment of those myofascial elements contributes significantly to patient management and symptom reduction. This point is very well illustrated by two common clinical diagnoses: lateral epicondylitis and carpal tunnel syndrome. In lateral epicondylitis, or tennis elbow syndrome, TPs in the supinator, wrist, and finger extensor muscles, anconeus, and triceps are all capable of referring symptoms to the lateral epicondyle (2). Conversely, all become significantly stressed with the altered biomechanics adopted in a true inflammatory process of the lateral epicondyle. In carpal tunnel syndrome (CTS), TPs are found in the pronator teres, and wrist, finger, and thumb flexors (42). Here also, triggered referral zones from the myofascial points overlap with the wrist pain, finger and thumb paresthesias, grip weakness, and referred forearm pain perception common to patients with CTS. Forearm muscles also become significantly stressed with the altered extremity mechanics adopted by patients with CTS.
1044
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
A
~ ~
FIGURE 66.6. (A) Spray and stretch of the SWEAT muscles most commonly found in tennis elbow syndrome, (B) spray and stretch in carpal tunnel syndrome. (From Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:471,492,504,517,544, with permission.)
Failure to address TPs results in failure to help a significant number of these patients. For example, in CTS, osteopathic treatment protocols that specifically address treatment of these myofascial structures in addition to traditional conservative care have been more effective than wrist splints and medication alone (43). T he stretch component addressing each of these conditions is pictured in Figure 66.6. Note in Figure 66.6A that the same general
position is modified to localize the supinator, wrist, and finger extensors, in turn, with a separate position for the anconeus and triceps. In Figure 66.6B , general positioning with slight localization modifications during the stretch component effectively, and in a time-efficient manner, addresses the ventral forearm muscles most commonly involved in patients with CTS or its symptoms.
66. Myofascial Trigger Points as Somatic DysfUnction
SEMISPINALIS CERVICIS
1045
MULTIFIDI
LEVATOR SCAPULAE
SCALENI
CARDIAC ARRHYTHMIA
A
P E CTORALIS
MAJOR VASTUS MEDIALIS
FIGURE 66.7 . Trigger points common ly precipitated by poor posture. Referred pain patterns (black stippled area), location of trigger points (arrows) . (From Wall PD, Melzack R, eds. Textbook of Pain, 2nd ed . Edinburgh, Scotland : Churchill Livingstone; 1989:371, 372, 376, 377, with permission .)
Trigger Points and Posture TPs may result from and/or contribute to postural disorders (1,22,23,44). Patterns of recurrent TPs in va rious combinations should alert the clinician to an underl ying postural disorder. Likewise, all patients with postural disorders should be evaluated for patterns ofTPs to add ress in th e postural treatm ent regimen . Patients with postural deco mpensatio n have a higher propen sity to develop patterns of recurrent somatic dysfun ction, TPs, facili tated segments, and related visceral dysfun ction (4 5). (See C hapter 43 and Figure 66.7, depicting muscles most commonly contributing to postural patterns.) Fo r this reason , numerous cl inicians ( I ,2,44,46,5 1,52) cite postural disorders as one of the primary precipitating and/or perpetuating factors of myofascial T Ps, even staring that "postural training should be one of the first parts, if nor the fi rst part, of the treatment program" (8). T he so-called "sho rt leg synd ro me" (see C hapter 43) has been impli cated in causing multiple T Ps, including those in the paras pin al (19), sternocleidomas toid (19), and quadratus lumborum (8) muscles. Quadratus lumborum T Ps have already been implicated as an extremely co mmo n primary cause of myogenic low back pai n (2 1). Conversely, T Ps in this muscle are capable of producing a false sho rt leg syndro me caused by muscular ar-
tachments to the iliac crest (8) . T his situatio n is likely to res ult in compensatory postural charges, recurrent so matic dysfun ctio n, and T Ps in local and distant areas. lr also may lead to lift therapy being incorrectly or inappropriately instituted .
Impairment of Venous and Lymphatic Drainage Optim al venous and lymphatic drainage depends o n uno bstructed myofascial pathways th ro ugh which these circulatory vessels pass, and on respiratory-circulato ry mechanisms effi cientl y creating pressure differenti als. Z ink (47,48) stated th e relevance of this perspective to the osteopathic clini cian. Travel! and Simo ns have also documented the effect of certain myofascial poi nts in creating lymphatic dysfunction and have reported improvement of congestive sequelae by removin g this type of so matic dysfunction. T he osteopathic professio n and Travell (2) emphasize the importance of proper and effective respiratio n and attentio n to the somatic factors involved. The scalene muscles are often referred to as the entrappers (19) because of their clinical tendency to entrap structures passing thro ugh the superior thoracic aperture (tho racic inlet). T he
1046
VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment Infraclavicular space
Thoracic inlet
Anterior scalene muscle dysfunction and TPs
Left rib head/neck area 1st rib
Reflex supression of lymph peristalsis Axillary artery Triggered pain pattern
Axillary vein Median nerve Radial nerve
8
Ulnar nerve
A
Pectoralis minor
~ Puffy fingers and dorsum of hand
FIGURE 66.8. A: Entrapment of vascular and lymphatic structures in the thoracic inlet, (B) anterior scalene muscle referred pain and lymphatidvenous congestion in affected extremity. (From Travel I JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:345, 356, with permission; A: top illustration by W. A. Kuchera.)
subclavian lymphatic trunk and the subclavian vein are particularly susceptible to muscular compression caused by TPs in the anterior scalene muscles (Fig. 66.8). This compression is further aggravated by elevation of the first rib, which may result from a variety of dysfunctional phenomena, including TPs in the anterior or middle scalene muscles. Somatic dysfunction of the first rib and other parts of the functional superior thoracic inlet should also be treated because of their effect on this region (2). Scalene TP activity has been implicated in reflex suppression oflymphatic duct peristaltic contractions in the affected extremity (19) . Palpation of the posterior and anterior axillary folds for evidence of myofascial dysfunction is clinically important in assessing the degree of lymphatic dysfunction affecting the upper extrem ities and/or breasts. The posterior axillary fold is the
location of palpable myofascial points in the subscapularis, teres major, and latissimus dorsi muscles. It is also the site of terminal lymphatic drainage dysfunction for the upper extremities (Fig. 66.9). Zink (49) discusses diagnosis and treatment of this region to relieve lymphatic congestion in the upper extremity. Those findings closely parallel the palpatory and clinical findings described independently by Travel! and Simons, using myofascial points located in the posterior axillary fold (2). Figure 66.9B shows that points higher in the posterior axillary fold correlate predominantly with shoulder referral, although lower points refer distally. Zink and Travel! () both report that treatment of myofascial dysfunction in this area results in reduction of swelling, joint dysfunction, and dysesthesia (Fig. 66.1 O). Likewise, appropriate treatment of anterior axillary fold dysfunction results in
66. Myofascial Trigger Points as Somatic Dysfunction
1047
A
B FIGURE 66.9. A: Zink's posterior axillary fold technique, (B) location and overlapping patterns of Travell and Simons' trigger points located in the posterior axillary fold . (1), subsca pularis; (2), teres major; (3), latissimus dorsi; (4), serratus anterior. Overlapping patterns between (1) and (2) and between (3) and (4) are shown in b lack. (Grom Travel I JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Will iams & W ilkins; 1983:398, w ith perm ission.)
reduction of breast tenderness and congestive changes attrib uted to entrapment of breast lymphatics traveling around and through the pectoralis muscle toward the subclavicular lymph nodes ( 19).
Autonomic Effects of Travell Myofascial Points
Patient perception sites
FIGURE 66.10. Compression of the posterior axillary fold at the palpatory site of each thickened tender point. (From Travel I JG, Simons DG . Myofascial Pain and Dysfunction: Th e Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:418, with permission.)
C linically, autonomic effects of myofascial dysfunction are common (2, 11 ). Travell's term "referred auto nomic phenomena" (2) refers to the vasoconstriction (blanching), cold ness, sweating, pilomotor response, ptosis, and/o r hypersecretion that is caused by activity of a trigger point in a region separate from the trigger point. T he phenomena usually appear in the same area as the pain referral for that TP (19). Travel! and Simons (19) and Korr (30) have postulated an organizing role for the spinal cord by relating somatic and visce ral input to palpatory and sympto matic fi ndings in both systems (Fig. 66.11 ). Afferent input to the spinal cord may faci litate the segment at the spinal level it enters. Efferent consequences include sympathetic changes to somatic and visceral tissues at the same spinal level, and palpable somatic dysfunction, including tissue texture changes. A series of refl exes and referred symptoms resu lt.
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Vll Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Association with Viscerosomatic and Somatovisceral Reflexes Acute overload Overwork fatigue Chilling Gross trama Gravitational stress (Postural strain) Host factor Predisposition Nutritional Endocrine Biomechanical
When considering the interaction between somatic and visceral systems, recognizing somatovisceral and viscerosomatic reflexes is important for arriving at a differential diagnosis. The twovolume TraveL! & Simons' Myofoscial Pain and Dysfunction: The Trigger Point Manual (2,8) adds extensively to the literature documenting these reflexes. TPs in the pectoralis major muscle provide an example of each phenomenon. They illustrate the clinical concern that should be raised by the discovery of this important somatic clue. Pectoralis TPs may result in cardiac rhythm dysfunction, a demonstrable somatovisceral reflex. Supraventricular tachyarrhythmias have been documented to arise from TPs located in the right pectoralis major muscle (at the level of the fifth intercostal space), midway between the sternal margin and the nipple line (Fig. 66.12) (2). (Pectoralis trigger points are also common in patients with a slumped posture and rounded shoulders.) Treatment of the somatovisceral reflex involves both removing the trigger point and correcting the underlying postural problem if present. Correction of this somatic dysfun ction results in immediate return of normal cardiac function (19).
Somatovisceral Reflex Right pectoralis major trigger point Palpable tissue texture changes T(1 ),2,3,4,(5)
Palpable Chapman's reflex left 2nd intercostal space
Palpable myofascial point in pectoralis major
FIGURE 66.11. The spinal cord as an organizer of disease processes.
Trigger zones for each muscle (Fig. 66.1) have been mapped by Travell and Simons. Viscerosomatic reflexes have been documented by C hapm an (see Chapter 67). The autonomic effects produced in both somatic and visceral systems should be recognized in the patient and elicited in the history. Furthermore, the associated tissue texture changes should be actively sought througho ut the physical examination to enhance the differential diagnosis process. C linical sym ptoms attributed to the autonomic sequelae of myofascial dysfunction include (1 ,2,8, 19): • Diarrhea and dysme norrhea due to autonomic control changes in the activity of smooth muscle • Diminished gastri c motility and aggravation of duodenal ulcer activity • Vasoconstriction with headache • Dermatographism • Proprioceptive disturbances and dizziness • Excessive secretio n from the maxillary sinus • Localized sweati ng • Cardiac arrhythmias • Gooseflesh • Ptosis, excessive lacrimatio n, conjunctival reddening
Viscerosomatic Reflex
FIGURE 66.12 . Pectoralis trigger points and associated reflexes. SA, sinoatrial node of the heart.
66. Myofascial Trigger Points as Somatic Dysfunction Pectoralis TPs occur as a viscerosomatic reflex in the majority of patients with cardiac disease (2) . They arise as a consequence of coronary artery insufficiency. This example of a viscerosomatic reflex has a significant prevalence as demonstrated by one study of 72 patients. Chest muscle TPs were reported in 61% of patients with cardiac disease (2). Treatment of these TPs is an important factor in reducing reflex coronary artery spasm (19), but reduction of chest pain in this particular situation may inadvertently present an associated clinical dilemma. Symptomatic relief provided by treatment of somatic findings does not eliminate the need clinically to assess and treat a specific underlying primary visceral cause. In the case of somatic findings resulting from viscerosomatic reflexes, healing of the primary visceral component does not mean that the secondary somatic dysfunction will spontaneously resolve. Pectoralis TPs originating in this manner have been shown to be self-perpetuating and a source of referred chest/arm pain even after recovery from or successful treatment for the initial visceral event (19). Precipitated by cold or overuse of the pectoralis muscles, these somatically referred symptoms may unfortunately promote unnecessary emotional distress and disability in a cardiac patient until identified and removed. Similar myofascial points occur in patients with a variety of visceral disorders, including duodenal ulcer (19) (Fig. 66.13) and post-cholecystectomy syndrome (50).
1049
External oblique on the left Typical Pain Pattern: Cholelithiasis with Colic
CONCLUSION An analysis of the system of myofascial pain and dysfunction pioneered by Travell and Simons provides additional insight into the system conceived a century earlier by Andrew Taylor Still. Both systems reinforce the clinical use of careful musculoskeletal palpation when looking for clues to a differential diagnosis. Each views the body as an interconnected unit with all parts and systems working together. Each expresses a common goal: the identification and treatment of somatic elements to reestablish normal functional characteristics that promote beneficial changes in body homeostasis. TPs can be viewed as a particular subset of somatic dysfunction. They represent impaired or altered function of the myofascial system and its related neural, lymphatic, and circulatory elements. Several TPs have been linked to viscerosomatic and somatovisceral reflexes; others are known to entrap circulatory and/or neural structures. Many have autonomic sequelae, and most involve pain and/or musculoskeletal dysfunction. All require careful and skilled palpation for diagnosis and an understanding of the underlying anatomy and physiology for successful treatment. As a form of somatic dysfunction, TPs respond to a balanced osteopathic approach integrating postural, psycho/emotional, and nutritional factors with manual techniques and modalities to reestablish the homeostatic relationship between the musculoskeletal system and the central nervous system. The general clinical impact resulting from "somatic dysfunction" is consistent with that potential seen for "myofascial points." Each may: Contribute to a wide range of clinical conditions Impair homeostatic mechanisms
External oblique on the right
Causes diarrhea FIGURE 66.13. Myofascial trigger points associated with viscerosomatic reflexes. (See also Fig . 66.12.) (From Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Williams & Wilkins; 1983:662, with permission.)
Evoke depression and sleep disturbances Cause pain, weakness, dysesthesia, and restricted range of motion Recognition of somatic dysfunction as an aid in the differential diagnosis and treatment of patients with both musculoskeletal and visceral disturbances has greatly enhanced the understanding of students of myofascial trigger points. Recognition ofTPs and the significant research and clinical contributions by those studying that phenomenon has also greatly enriched the understanding
1050
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
of students of osteopathic m edicine. In the end, all of our patients benefit.
REFERENCES I. MenseS , Sim o ns DC . Muscle Pain: Understanding its Nature, Diagnosis, and Treatment. Phil adelphi a, PA: Lipp incon Wi lliams &Wilkins; 2001. 2. Sim ons DG , Travel! JG, Simons LS . Travell and Simons' Myofascia! Pain and Dysfimction: The Trigger Point Manual. Volume 1: Upper HalfofBody, 2nd ed. Ba lt im ore MD : W illiams & W ilkins; 1999. 3. Hu bba rd DR, BerkoffGM. Myofascial trigger po in ts show spo ntaneous need le EMG activity. Spine. 1993;18( 13):1803- 1807. 4. Head H . O n d isturbance of sensation with especial refe rence to the pain of viscera l d isease. Brain.l 893; 16: 1- 133 . 5. Mackenzie] . Some po in ts bearing on the associatio n of senso ry disorders and viscera l d isease. Brain. 1893; 16:32 1-354. 6. Owe ns C. An Endocrine Interpretation of Chapman's Reflexes, 2 nd eel. C hatta nooga, TN : C hattan ooga Printin g & Engraving Co; 1937. 7. Travel! J, Rinzler SH . T he myofascial genes is of pain . Postgrad Med. 1952; II :425-434. 8. Travel! JG, Sim o ns DG. Myofoscial Pain and DysfUnction: The Trigger Point Manual. Volume fl. The Lower Extremities. Ba lti more, MD: W illi ams & W il kins; 1992:547. 9. Sim o ns DG. M uscle pain sy nd ro mes.} Man Med. 199 1;6:3-23 . 10. C haitow L. Soft Tissue Manipulation. Ellington, G reat Brita in : Thorsto n Publishin g; 1987. 11 . Be nn ett RM. Myofascial pa in synd ro me and the fi bro myalgia syndrome: a comparative ana lysis. j Man Med. 1991 ;6:34-45. 12. Melzack R, Still well OM, Fox EJ . Trigger points and acupu ncmre points fo r pa in: Co rrelations and imp lications. Pain. 1977;3 :3-23. 13. Skootsky SA, Jaeger B, Oye RK. Prevalence of myofascial pai n in general imerna l med icine practice. West} Med. 1989; 15 1: 157- 160. 14. Fricto n J R, Kroeni ng R, Haley D, et al . Myofascial pain syndrome of the head and neck: A review of cl inical characteristics of 164 patients. Oral Surg Ora!Med Oral Patho! Oral Radio! Endod. 1985;6:615623 . 15. Fishba in DA, Goldberg M, Meahger BR, eta!. Male and fema le chron ic pa in patients categorized by DSM- lll psychiatric d iagnostic criteria. Pain. 1986;26: 18 1- 197 . 16. Wolfe F, Ross K, Anderson J, et al. T he prevalence and characteristics of fibromya lgia in the general population. Arthritis Rheum. 1995;38 : 19- 28. 17. Ca mpbell SM, C lark S, T in dall EA, et a!. C linical characteristics of fibros it is. I. A "blinded" controlled sm dyofsym ptoms and tender po ints. Arthritis Rheum. 1983;26:8 17-824. 18 . Ge rwin RD . A study of96 subjects exa mined both for fibromya lgia and myofasc ial pai n. J Muscu!oske Pain. 1995;3(Su ppl 1): 121 (abst). 19. Travel! JG, Sim ons DC. Myofoscial Pain and DysfUnction: The Trigger Point Manual. Volume I. The Upper Extremities. Baltimore, MD: Wi lliams & Wi lki ns; 1983. 20. Skootsky SA, Jaeger B, Oye RK. Prevalence of myofascial pain in general imernal medi cine practice. West} Med. 1989; 151 :1 57-160. 2 1. Sim ons DG, Travel ! JG. Low back pain, Pan 2: torso muscles. Post Grad Med. 1983;73(2):8 1- 92. 22. Kuchera ML. G rav itational stress, m uscu loli gam emo us strain and posmral ali gn me nt. Spine State Art Rev. 1995;9(2) :463-490. 23. Kuchera ML. Grav itationa l stra in pathop hys io logy, Pam I and II . In: Yleeming A, eel . Low Back Pain: The Integrated Function of the Lumbar Spine and Sacroiliac joints. Proceedi ngs of the 2nd In terdisciplinary Wo rl d Congress, Novem ber 1995. 24. McN ul ty W H , Gev irtz RN, Hu bbard DR, et a!. Need le electromyograp hic evaluation of trigger point respo nse to a psycho logical suessor. Psychophysiology. 1994;3 1:3 13-3 16. 25. Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dysfimction , 2 nd eel. rev. Co lu mb us, OH : Greyden Press; 1994:200- 201.
26. Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic DysfUnction, 2nd eel. rev. Columbus, OH : Greyden Press; 1994: 79-84. 27. Jones LH. Missed anterior spinal lesions. A preliminary reporr. The DO. 1964;4: I 09-116. 28 . Simons DG. Muscle pain syndromes. j Man Med. 1991;6:3-23 . 29. vanBuskirk RL. Nociceptive reflexes and th e somatic dysfunction: a model. jAm Osteopath Assoc. 1990;90(9):792-809. 30. Korr IM . The spinal cord as organizer of disease processes. In: Peterson B, ed. The Collected Papers of Irvin M Korr. Newark, OH: American Academy of Osteopathy; 1979:207-221 . 3 1. Simons DG . Myofoscial Pain Syndrome Due to Trigger Points. (Internationa l Rehabi litation Medicine Association Monograph Series Number 1). C leveland, OH: Rademaker Printing; 1987. 32. Gi ll iar WG, Kuch era ML, Giu lianeni DA. Neurologic basis of manual med icine. Phys Med Rehabil Clin N Am. 1996;7(4):693-714. 33 . Gerwin RD , Shannon S, Hong C-Z, et al. lnterrater reliability in myofascial trigger po int examination. Pain. 1997;69:65-73. 34. Wu C-M, Chen H-H , Ho ng C-Z. Inactivation of myofascial trigger points associated w ith lumbar radiculopathy: surgery versus phys ical therapy. Arch Phys Med Rehab if. 1997;78: I 040- 1041. 35. Greenman PE. Principles ofManual Medicine. Baltimore, MD: Williams & Wi lkins; 1989:106-122. 36. Yaksh TL, Abram SE. Focus article: preemptive ana lgesia: a popular misnomer, but a cl inically relevant truth) Am Pain Soc}. 1993;2: 116121. 37. Panerson MM, Steinmetz JE. Long-lasting alterations of spinal refl exes: a basis for somatic dysfunction. Man Med. 1986;2:38-42. 38. Hong C-Z, Simons DG . Response to treatm ent for pecto ralis minor myofascial pa in syndrome after whiplash . j Musculoske Pain. 1993; 1 (1):89131. 39. T he G lossary Rev iew Comminee of the Educational Council on Osteopathic Principles. ln : All en TW, ed. Glossary of Osteopathic Terminology. AOA Yearbook and Directory of Osteopathic Physician s. C hicago, IL: American Osteopathic Association; 1991 :678- 690. 40. Lewit K. Manipulative Therapy in Rehabilitation ofthe Locomotor System, 2nd ed. Oxford, UK: Butterworth-Heinemann ; 1991 . 41. Wolfe F, Smythe HA, Yunus MB , eta!. Ameri ca n College of Rheumato logy 1990 criteria for the classificat ion of fibromyalgia: Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33: 160- 172. 42. Melchio r DE, eta!. A study of the components of soma tic dysfunction in relatio nsh ip to the carpal tunnel syndrome. Residency paper accepted by the Osteopath ic Manipu lative Med icine Department, Kirksville College of Med icine, Kirksvi lle MO, 1990. 43. Snair B, Kuchera ML. Osteopath ic manipu lation for patients with co nfirmed mi ld, modest, and moderate carpa l tunnel syndrom e.} Am Osteopath Assoc. 1994;94(8):673 . 44. Janda V Muscles, central nervous motor regu lat ion, and back problems. In: Korr lM, ed. The Neurobio!ogic Mechanisms in Manipulative The1'11py. New York, NY: Plenum Pub lishing; 1978 :27-41. 45 . Ko rr IM, Wright HM, Chace JA. Cutaneous patterns of sym pathetic activity in clinical abnormalities ofthe muscu loskeletal system (1964). In: Peterson B, eel. The Collected Papers of f. M. Korr. Newark, OH: America n Academy of Osteopathy; 1979:66-72. 46. Jungmann M. Backaches, Postural Decline, Aging and Gravity Strain. Lewiston, ME: Penmor Lithographers; 1988. 47. Z ink JG. Respiratory and circu latory care: the conceptual mod el. Osteopath Ann. 1977;5(3): 108- 112. 48. Z inkJG, Lawson WB. An osteopathicsuuctural exam ination and functional interpretation of the soma. Osteopath Ann. 1979;7(12):433-440. 49 . Zink JG, Ferchik WD, Lawson WB . The posterior axillary folds: a gateway for osteopathic treatment of the upper extremities. Osteopath Ann. 1981;9(3):8 1-88 . 50. Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic DysfUnction, 2 nd eel. rev. Columbus, OH: Greyden Press; 1994:87. 51. Irwin R. Red uction of lumbar scoliosis by use of heel li ft to level the sacral base. jAm Osteopath Assoc. 1991 ;91 (I ):34, 37-44. 52. Hench PK. Myofascial pain syndromes in clini cal in sights into nwsculoske letal problems. Myology. 1980;5( 1):5.
CHAPMAN REFLEXES DAVID A . PATRIQUIN
PALPATORY CHARACTERISTICS
KEY CONCEPTS • General uses of anterior and posterior Chapman reflex points, and the relationship between them • Distinguishing characteristic of Chapman reflexes • Importance of treating the whole person when using this reflex technique • Importance of resolving pelvic dysfunction before treating Chapman reflexes • Locations and uses of Chapman reflexes • How to treat Chapman reflexes
Most physicians and basic scientists have never heard of Chapman reflexes, yet these particular viscerosomatic reflexes are an osteopathic entity dating from the 1920s. They are described as a viscerosomatic reflex mechanism that has diagnostic and therapeutic importance. Chapman described the reflex as a gangliform contraction that blocks lymphatic drainage, causing inflammation in tissues distal to the blockage. Current thinking links this involvement of the lymphatic system with concurrent sympathetic nervous system dysfunction . Regardless of the mechanism, both somatic and visceral tissues suffer from the presence of this reflex. Chapman did not write about his reflex system, but his brother-in-law, Charles Owens, and Chapman's wife, Ada Hinckley Chapman, published the only reference text on this subject. Their book (1) discusses using the anterior and posterior points for diagnosis and treatment and for evaluation of the outcome of treatment. Today, physicians tend to use these reflexes as a diagnostic indicator of which organ is most likely to be dysfunctional. In current clinical practice, Chapman reflex points are used more for diagnosis than for treatment. Treatment of the somatic representations of visceral dysfunction is a part of a complete osteopathic health management plan. Many posterior Chapman reflexes are located in the paraspinal areas near the transverse processes. Those reflexes may be treated incidentally as "standard" soft tissue treatment is applied to the area. Chapman reflexes may thus be treated by design or inadvertently. Treatment of these somatic points still remains an additional procedure for enlisting the patient's body in its own recovery from dysfunction.
On palpation, Chapman reflexes are located deep to the skin and subcutaneous areolar tissue, most often lying on the deep fascia or periosteum. For the most part, they are found paired on both the dorsal and ventral surfaces of the body. For example, an anterior point found next to the sternum at the fifth intercostal space has a corresponding posterior point between the transverse processes of T5 and T6, adjacent to the costotransverse junction. Both reflex points represent the same viscus (Fig. 67.1). A Chapman reflex point is fixed in its anatomic location. It may have a characteristic palpatory quality that makes its identification positive. When an anterior Chapman point is gently compressed, the patient's response is one of greater pain than expected. Attempts to microscopically describe the reflex change have failed; biopsy attempts have provided no information concerning the tissue or pathology of the reflex change. Still, Chapman reflexes have good interexaminer reliability and correlate well with final hospital diagnoses (2) .
Distinguishing Characteristics What are the distinguishing characteristics of a Chapman reflex? They are nodules that are: Small Smooth Firm Discretely palpable or grouped in irregular patches Approximately 2 to 3 mm in diameter when found alone Sometimes they are described as feeling like small pearls of tapioca lying, partially fixed, on the deep aponeurosis or fascia. The masses are dense but not hard. One gets the impression of a circumscribed area of firm edema. They move slightly bur are otherwise firmly moored in place and cannot be displaced. Occasionally, they are confluent and then thought to represent longstanding visceral reflexes of greater magnitude, or chronicity, than those palpable as a single, discrete mass. Once a Chapman reflex point is identified and isolated by the examiner's fingertip, gentle but firm pressure usually causes a deep, disagreeable pain response in the patient. The pain is
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
1/ 2 FIGURE 67 .1. Often, anterior Chapman reflex points have co rresponding posterior po ints. (From Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed . rev. Columbus, OH: Greyden Press; 1994, with permission.)
characteristically: Pinpoint Located under the finger Nonradiating Sharp Exquisitely distressing Patients invariably wince or complain while stating that they did not know they had such a sore spot. Equivalent deep pressure on any adjacent normal tissue will produce only vague, mild, local distress.
the efficacy of the reflex system after Chapman's death, by using it in his practice. Osteopathic physicians who use Chapman reflexes select from the many reflex points they have frequently found to be helpful to them in their practice. They refer to Chapman charts if they wish to search for a less common point. For example, one pathologist palpated the tip of the right 12th rib to identifY the typical appendix reflex. Some physicians learn the location of the Chapman reflex for the appendix during their internship. The presence of this particular reflex point for the appendix helps to direct the differential diagnosis of lower right quadrant abdominal pain in children or in women of childbearing age toward acute appendicitis more than toward acute mesenteric lymphadenitis, acute right salpingitis, ruptured right ectopic pregnancy, or chronic appendicitis. This sort of focal push-button diagnosis has great appeal to any physician faced with the dilemma of undiagnosed abdominal pain. This noninvasive examination is performed quickly and without altering the position of the patient. The whole-person approach is critical in the application of Chapman's system just as it is the basic principle of all osteopathic treatment. Chapman's description of the pelvic-thyroid-adrenal syndrome (PTAS) confirmed his dedication to the concept of the interconnectedness and interrelatedness of all pans of the body. It also suggests a connectedness via the autonomic nervous system. He insisted that treatment of reflex points should not begin until the pelvis is made to function properly. This requires an accurate diagnosis of pelvic function or dysfunction with proper and successful pelvic treatment before these local reflexes are dealt with. Chapman emphasized the important relatedness of the endocrine components, the thyroid and adrenals, by including them in his acronym for treatment of neuroendocrine dysfunction. A physician using Chapman reflex treatments finds that a much enhanced response follows a complete Chapman reflex treatment, especially when all pelvic dysfunction is successfully resolved as the initiating step of the treatment protocol (see C hapter 52, Pelvis and Sacrum).
CURRENT CLINICAL USE Locating Reflexes How are these reflexes found? Owens' personal commentary on Chapman's work suggests that the novice practitioner should refer to the book early and often. When a differential diagnostic dilemma exists, look in the book for the location of reflexes related to the items on the differential diagnostic list. Then find the reflex locations identified on the chart as relating to the organs to be considered. The subsequent identification of a reflex can help to call into question or reduce the number of diagnostic items on the list.
HISTORY AND PHILOSOPHY This systematized method of diagnosis and treatment is an empirical system developed from the observations recorded by Chapman, an osteopathic physician who practiced in Chattanooga, Tennessee. Ada Hinckley Chapman, Charles Owens, and W. F. Link collected his notes, arranged them, and, in 1932, published the only reference text material on the subject (1) . Owens notes in a later edition of the book that he only became convinced of
Today, Chapman reflexes are more likely to be used as an integral part of an osteopathic physical examination than as a specific therapeutic intervention. They are more likely to contribute to the differential diagnosis and implicate dysfunction of an organ system rather than be the basis of a specific pathophysiologic diagnosis. They are more likely to be used selectively than as a complete systematized diagnostic process.
Specific Reflexes to Seek and Treat What specific reflexes might be sought and treated frequently or advantageously in practice? The reflex for appendicitis can be valuable in the differential diagnosis of lower abdominal pain. We need all the help we can find when we are faced with the lower right quadrant dilemma. The presence of Chapman reflex for appendicular involvement can help in differential diagnosis of this vexing complaint. The presence of colon reflexes aids in the clinical identification of chronic constipation or irritable bowel syndrome (IBS). Such reflexes are easily identified by palpatory examination along the
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67. Chapman Reflexes
Colon "flipped" anatomically on this axis
U)-------- lliocecal
~A
area
lU
(
\-------w
~} ;:~:oid
mOJ-
~~~~ending
~~~~ndijn 0
Hepatic · flexure
Splenic flexure Left 3/5ths of transverse colon
Right 2/sths -{ of transverse colon
The palpatory finding of tissue texture changes consistent with Chapman reflexes alerts the practitioner to screen the lower gastrointestinal system even more carefully. It also leads to seeking and correlating more thorough history, abdominal and rectal examination findings, and other musculoskeletal reflex clues with the Chapman findings. Because of the proximity of this reflex to those associated with the prostate or broad ligament, clinicians should carefully screen these viscera as well. Other reflex points that are clinically useful in a general practice include those in the upper respiratory system (sinus, pharynx, middle ear), the upper gastrointestinal system (stomach, gallbladder), and the genitourinary system (kidney, gonads, prostate/broad ligament) . Figures 67.3 and 67.4 show anterior and posterior Chapman points, as summarized from C hapman's book by the College of Osteopathic Medicine (3).
Chapman's reflex areas for the colon
FIGURE 67.2. Anterior Chapman reflexes for the colon . Sinuses
anterior aspect of the iliotibial fascial tract from the trochanter to within 1 inch of the patella on one or both legs. Those reflexes lie just superficial to the deep fascia and are slightly adherent to it. The reflex gangliform masses may be single, multiple, or in chronic or severe cases, coalescent mats or even "strings of pearls. " Owens suggests that the anatomic location of the Chapman reflexes on the iliotibial tracts correlates with specific portions of the colon (Fig. 67.2): Starting with the trochanter on the right side, a gangliform contraction in the tissues of the upper fifth shows inflammation within the mucous membrane of the cecum or a spastic state of the circular fibers of the cecum. The next succeeding three-fifths show a similar state of the ascending colon. The last fifth has the same indication as the first two-fifths of the transverse colon. Starting on the left thigh just above the knee, the first fifth corresponds to the last three-fifths of the transverse colon, indicating the same condition explained regarding the right side. The middle three-fifths show a similar state of the descending colon. T he last fifth corresponds with the sigmoid. More especially, the extreme upper end of the trochanter on the left side effects the junction of the sigmoid with the rectum, which will often cause a stricture to form, almost closing the lumen of the bowel (1). The reflexes for the colon are distributed along the lateral thigh, lateral to the shaft of the femurs. It is as if the upper portions of the large bowel were removed from the abdomen and rotated ventrally around a transverse axis through the cecum and low sigmoid regions so that the transverse colon lies on the ventral surfaces of the two legs extended side by side. The ascending colon then lies over the proximal and midportion of the right femur. The hepatic flexure and right half of the transverse colon lie over the distal right femur. The left half of the transverse colon and the splenic flexure both lie in relation to the distal left femur. The descending colon lies along the midshaft of the left femur, and the sigmoid and rectum are represented on the proximal left femur in order (Fig. 67.2).
Neck
Middle ear Nasal sinuses Pharynx Tonsils Tongue ._,__.,.._.-- Esophagus, bronchus thyroid, myocardium Upper lung Lower lung Stomach (acidity) liver @ Stomach (pertstalsis) liver, gall bladder @ Spleen([;), pancreas @
©
©
Ovanes, urethra Uterus Rectum
Colon
All are bilateral except where indicated as@ for right and ([;) tor left
FIGURE 67.3. Chapman reflexes: anterior points. (From Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed . rev. Columbus, OH: Greyden Press; 1994, with permission.)
1054
VII Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment Retina, conjunctiva ----......_
Cerebellum Middle ear Pharynx, tongue, -------\~~~~-----Nasal sinuses
-=-=-=--:::;;;=r.Jft~l:(f:3~~~.,.._-
larynx, sinuses, arms Cerebrum NeckEsophagus, bronchus, thyroid - - - - - - ......._ Arms Upper lung, myocardium - - - - ---:-..~~~2,Jt.r<:!:J~r':=~-=7'",-- (also pectoralis minor) Upper lung ' Lower lung Stomach (acidity), ---------,~~"'i""4l liver@ Stomach (peristalsis),© liver, gall bladder@ _ __./
(D
Spleen
CD , pancreas @
Neurasthenia (also pectoralis minor)
Pylorus @
Small intenstines --"""""'::..__-~\ ....,-=~"'-7~.+-7----- Ovaries Adrenals
Intestines (peristalsis) Appendix@
Kidneys - - - - - - : :i¥1,.,;( Abdomen , bladder - - - Urethra--~
Uterus - - - --.tu Vagina, prostate, uterus , -~>-;'----;--;:..;----=- Sciatic nerve (posterior) broad ligament - - - , o• Rectum, groin glands _ _ _ _ . , (~ Fallopian tubes, ) seminal vesicles _ _..c..__ _--::---7-"""""'""'.,----...,e Hemorrhoidal plexus
Clitoris, vagina - - - - - - . -•
All are bilateral except where indicated as @ for right and ©for left
FIGURE 67.4. Chapman reflexes: posterior points. (From Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic Dysfunction, 2nd ed. rev. Columbus, OH : Greyden Press; 1994, with permission.)
67. Chapman Reflexes Use of Chapman Reflexes How do we use C hapman reflexes? In some clinical situations, the differential diagnosis hinges on whether the cause is visceral dysfunction or primary musculoskeletal dysfunction . Palpating for Chapman refl exes provides clinical evidence of the presence or absence of visceral disease. It suggests the possible cause of abdominal pain to the physician. The clinical ability to better differentiate a pathologic condition in the urinary bladder from that in the uterus or prostate can be critical. Chapma n reflex di agnosis is highly efficient in these days of expensive diagnostic, medi cal, and surgical care. Imagine how useful it is to have evidence that a patient's abdominal pain more likely arises from the colon than from the ovary. C hapman reflexes can also be clinically manipulated to specifically reduce adverse sympathetic influence on a particular organ or visceral system. Improved function of the disturbed organ often follows treatment of its corresponding Chapman point. For example, patients with frequent bowel movements from the effects of irritable bowel syndrom e report that they have more normal bowel movements for days to months after soft tissue treatment over the iliotibial bands and/or the lumbosacral paraspinal tissues and associated Chapman reflexes. Research into the efficacy of Chapman reflex treatment has been limited. One stud y of hypertensive patients, in whom posterior points to the adrenals were treated, reported a blood pressure drop of 15 mm Hg systolic and 8 mm Hg diastolic pressure, and decreased serum aldosterone levels 36 hours after Chapman treatment (4).
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itself is described as a neurol ymphatic gangliform structure. The few histopathologic studies of biopsies of C hapman reflexes have identified nothing. Although irs cellular structure has yet to be described, the anatomic location of a C hapman reflex is predictable and consistent. T his suggests that the sympathetic nervous system may play an important role in the generation and maintenance of the reflexes. It further suggests that treatment of the reflexes m ay alter sympathetic influences on any related viscus. Other important reflex sites include the iliotibial tracts overlying the femora and in several locations related to the pubic symphysis. A C hapman reflex treatment includes general and specific components. The general component deals with manage ment of postural factors, as well as the care of short-term and long-term pelvic dysfunction. Specific treatment consists of deep rotary finger pressure applied to one or a series of C hapman refl exes. The combination of general and specific treatm ent supports and assists the self-regulating and self-healing capabilities of the patient.
REFERENCES I. Owens C. An Endocrine Interpretation ofChapman's Reflexes. Carmel, CA. Reprinted by the American Academy of Osteopathy; 1932. 2. Byrnes TR, Kuchera ML, G uffey JM , et a!. Correlatio n of palparory findings with visceral d iagnoses. JAm Osteopath Assoc. 1992;92(9): J 177. 3. Kuchera ML, Kuchera WA. Osteopathic Considerations in Systemic DysfUnction, 2nd ed. rev. Co lumbus, OH: Greyden Press; 1994:65, 90-92, 119, 124,200-201 ,23 1,233. 4. Mannino JR. The applicatio n of neurologic reflexes ro the treatment of hypertension . JAm Osteopath Assoc. 1979;79(10):607-608.
Treatment How does one treat Chapm an reflexes? Treat these reflex points with firm pressure on the volar-distal finger pad of one finger. Assum ing that the pelvis has been normalized first, apply somewhat heavy and even uncomfortable pressure to the gangliform mass. Slowly move the rip of the finger in a circular fashion and attempt to work (flatten) the mass as if to mobilize a localized fluid accumu lation. Continue the moving pressure for 10 to 30 seconds. Cease treatment when the mass disappears or the patient or physician can no lo nger tolerate the procedure.
CONCLUSION C hapma n reflexes have particular value in the differential diagnosis of visceral disease and should be integrated with historic and other physical examination findings. Most of these reflexes are fo und loosely attached to the deep fascia near the costotransverse structures posteriorly and in the intercostal spaces near the stern um anterio rl y. T hese anatomic sires are typically viscerasomatic representations in o r on somatic structures. The reflex
ADDITIONAL READING Brown EA. C linica l aspects of the C hapman's reflexes. In: Northup TL, ed . Academy ofApplied Osteopathy Yearbooks, 1949. Ann Arbor, Ml: Edwa rds Brothers, Inc; 1949:2 I 2-2 I 4. (Brown discusses the possible physio logic basis of the refl exes with more attention paid ro patterns of reflexes and their possib le mechanism of action.) Pauiqu in DA. Viscerosomatic reflexes. In: Patterson MM, Howe! JN, eds. The Central Connection: Somatovisceral Viscerosomatic Interactions. 1989 International Symposium. Athens OH: University C lass ics, Ltd; 1992:418. (Patriquin introdu ces Chap man reflexes as a model of osteopathic diagnosis and treatment of visceral dysfunction . He suggests that the so matic changes termed C hapman reflexes, whi ch clinicians find by palpati o n, represent specifi c visceral dysfunction and that the sympathetic nervous system is most likely the co nnectin g lin k.) Soden C H . Lecture notes on C hapm an reflexes. In: No rthup TL, ed. Academy ofApplied Osteopathy Yearbooks, 1949. Ann Arbor, Ml: Edwards Brothers, Inc; 1949:20 1-2 11. (Soden reviews C hapma n's work from a theoretical and practical perspective. Several pages conta in labeled di agrams much li ke those found in Owens' book.) Young MD . Osteopathy unlimited. In : Northup TL, ed. Academy of Applied Osteopathy Yearbooks, 1947. Ann Arbor, Ml : Edwards Brothers, Inc; 1947:34-35. (Yo ung presents C hap man reflexes integrated in to osteopathic practice.)
LYMPHATIC SYSTEM: LYMPHATIC MANIPULATIVE TECHNIQUES ELAINE WALLACE JOHN M. MCPARTLAND JOHN M. JONES, Ill WILLIAM A. KUCHERA BOYD R. BUSER
KEY CONCEPTS • • • •
Anatomy of the lymphatic system Physiology and pathophysiology of the lymphatic system Theories of treatment Diagnostic techniques and treatment approaches to lymph-related problems • Techniques to remove impediments to lymphatic drainage
Wt> strike at the source oflife and death when we go to the lymphatics. -A. T STILL (1)
The lymphatic system is known as the second circulatory system of the body and as the great integrator for all body fluids. If this system were to stop functioning, the patient would be dead within 24 hours as a result of massive edema and the effects from retention of toxic metabolic wastes. The lymphatic system is a passive system whose functioning can be greatly influenced and altered by extrinsic forces. Of all the systems of the body, osteopathic manipulative treatment (OMT) can exert perhaps its greatest influence on lymphatic function. This chapter reviews the anatomy, physiology, pathophysiology, and theories of treatment of the lymphatic system. Diagnostic techniques, as well as treatment approaches and techniques are presented. When Harvey solved the circulation ofthe blood, he only reached the banks ofthe rivers oflife. -A. T. STILL (1) In the field of lymphatics, osteopathic physicians have made brilliant advances that parallel the osteopathic advances in the cranial field. William Harvey's student, Olaf Rudbeck, a Professo r of Medicine and Botany at Uppsala University, first described the lymphatic system in 1653. More than 200 years later, Andrew Taylor Still became the first medical researcher to emphasize treatment of the lymphatic system for maintaining health and treating disease. The next major contribution to
thought was made by Frederic P. Millard, who was a student of Dr. Still alongside William Sutherland. Beginning in 1904, Millard researched the structure and function of the lymphatic system. In 1922, he published Applied Anatomy ofthe Lymphatics (2), with contributions from 15 authors constituting a veritable "Who's Who" of early 20th century osteopathy, including Evelyn R. Bush, Edwin Martin Downing, George M. Laughlin, and T.J. Ruddy. They add res sed controversial issues, such as the effects of vaccines and surgery (tonsillectomy!) on the lymphatic system. Millard's brilliant anatomic illustrations grace many pages of the text; the beauty and precision of these illustrations has never been surpassed. The editor of Millard's text, A. G . Walmsley, practiced in Bethlehem, Pennsylvania. Another osteopath from Bethlehem, C. Earl Miller, first described the lymphatic pump technique in 1926 (3). Three years later, in nearby Philadelphia, William Galbreath developed the well-known Galbreath technique, a method for mobilizing lymphatic fluid in the mandibular region , and for draining accumulated fluid from the middle ear (4). Frank C hapman, another student of Still, elucidated a series of neurolymphatic reflexes, which became popularized as "Chapman reflexes" in the 1930s. His work is highlighted in the Foundations chapter authored by David Patriquin. J. Gordon Zink, a self-professed "lymphomaniac," contributed a myofascial app roach to treatment of the lymphatic system. His work is described later in this chapter.
EMBRYOLOGIC DEVELOPMENT The lymphatic system and the immune system both begin developing at approximately 20 weeks of fetal age. The lymphatic system is immature at the time of birth and continues to undergo changes until approximately puberty. In infancy, lymphoid tissue is plentiful and actually increases in amount until approximately 6-9 years of age. At that time, a regression in the system begins, and by the age of 15 or 16, stable adult levels of lymphoid tissue rem am.
68. Lymphatic System COMPONENTS The .lymphatic system comprises approximately 3% of the total body weight (5). It can be divided into three distinct components: Organized lymph tissues Collecting ducts Lymph fluid
Organized Lymph Tissues Organized lymph tissues consist of the spleen, the thym us, the tonsils, the vermiform appendix, the visceral lymphoid tissues located in the gastrointestinal (GI) and pulmonary systems, and the liver. These are structures of lymphoid material that are not located along the course of the lymph ducts and that do not directly function in the filtration of lymp h. Each organ serves a specialized and ancillary function in the immune system. T he spleen is the largest single mass of lymphoid tissue in the body. Located deep to ribs 9, 10, and 11 on the left side of the thorax, the superior surface of the spleen abu ts the abdominal surface of the diaphragm, and its inferior surface extends to the area just cephalad to the left costal margin. In the normal physiologic state, the spleen is approximately 12 em long and 7 em wide and is generall y nonpalpable. T he spleen serves important ancillary services for the lymphatic system by destroying deformed or dam aged red blood cells and synthesizing immunoglobulins. The spleen is also a clearance site for particulate antigens and microorganisms, especially poorly organized bacteria. The liver also clears bacteria; this is one reason why the liver is sometimes considered an organ of the lymphatic system. T he thymus is located in the superior mediastinum, anterior to the great vessels of the heart and extending upward into the neck. In infancy, the thymus is a relatively large structure that continues to develop, reaching its greatest size at the age of2 years. The thymus provides immunologically potent cells that appear to be essential to the development of mature immune functions . It is the preprocessing site for the T lymphocyte immune cells. After puberty, the thymus undergoes involution, and by adulthood, most of the gland has been replaced by fatty tissue. It is presently believed that the minimal tissue that does remain serves little or no function in the adult. The tonsils are a ring oflymphoid tissue lying at the posterior oropharynx. The palatine tonsils line the lateral aspects of the pharynx at the base of the to ngue and are continuous with the lingual tonsils, which cover the posterior one-third of the tongue. The pharyngeal tonsils, known as the ade noids, lie in the mucosa at the nasopharyngeal border of the tonsillar ring. T he tonsils, like the thymus, provide cells that appear to influence and build immunity early in life but appear to be nonessential contributors to adult immunologic function. The vermiform appendix is a long, tapered structure, 2 to 20 em in length at the medial surface of the cecum . Although the exact function of the appendix is unknown, it is richly imbued with lymphoid tissue and presumably offers support to the immune system. However, like the thymus and the tonsils, we know that this support is nonessential to the adult patient.
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Visceral lymphoid tissue is also located in the respiratory and GI systems. The lymphoid tissue of the respiratory system aids filtration of toxins from the lungs. The lymphoid tissues located in the mucosa of the small intestine are the most highly organized of all visceral tissues . In the small intestines, both Peyer patches and lacteals can be identified. Peyer patches are nonencapsulated areas of lymphoid tissue that are most highly concentrated in the distal ileum. Lacteals are small lymphatic capillaries located centrally in each small intestinal villus. These capillaries converge to form a lymphatic capillary plexus in the submucosal layer. Both Peyer patches and the lacteals are the structures by which fats in the digestive system enter the circulatory system. These tissues drain into the superior and inferior mesenteric lymphatic trunks and ultimately into the thoracic duct. Autonomic regulation of Peyer patches and the lacteals are controlled by the enteric nervo us system (ENS) . The ENS contains an enormous number of neurons (2 x 10 8 ), nearly equaling the number of neurons in the central nervous system (6). Many neurotransmitters associated with the brain also function in the ENS, including acetylcholine, dopamine, glycine, norepinephrine, serotonin, endogenous opioids, and endogenous cannabinoids. The discovery of these neurotransmitters and their receptors in the gut offers new insights concern ing psychosomatic diseases of the GI system, such as irritable bowel disorder. The proximity and interaction between Peyer patches and ENS tissues (such as Auerbach and Meissner plexi) suggest the potential benefit of lymphatic treatment for functional bowel disorders. Lymph nodes are perhaps the most highly organized of all lymphoid tissues. Lymph nodes differ from other organ ized lymphoid tissues in that they are dispersed along the course of the lymph vessels and are involved primarily in the filtration of lymph. The nodes can be divided into two categories: the superficial nodes, located in the subcutaneous connective tissues accompanying the superficial veins; and the deep nodes, which lie beneath the fascia and muscle layers and are adjacent to the deep veins. A normal, yo ung adult body contains some 400 to 450 lymph nodes (7) . Aggregates of lymphocytes intermeshed with lymphatic sinuses are supported in a framework of reticular tissue and encased in a connective tissue capsule. These structures vary in size from a few millimeters to a few inches in diameter. They serve a dual function of filtration and synthesis (production). Afferent lymph vessels deliver lymph to the node wherein reticuloendothelial cells phagocytize bacteria, particulate matter, and fragments of cells. In the germinal centers of the nodes, lymphocytes are manufactured and enter into the lymph as it passes through the node. The superficial lymph nodes receive lymph from the ski n, as well as from the deeper tissues of the upper extremities, lower extremities, head, and neck. Superficial nodes drain into three main groups of nodes located in the cervical, axillary, and inguinal regions. The cervical nodes receive lymph from the head and areas superior to the clavicle and send it on to the jugular nodes. Lymph from the superficial areas between the clavicle and the umbilicus drain into the axillary nodes that drain into the deeper subclavian nodes; superficial areas caudal to the umbilicus drain into the inguinal nodes and eventually into the right and left lumbar nodes in the deep tissues. Deep nodes drain into a system of collecting channels.
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VII. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment
Lymph Channels The second component of the lymphatic system is the lymph channels. These channels perfuse all tissues of the body with the exception of the central nervous system (brain and spinal co.rd), the epidermis (including the hair and the nails), the endomys~um of muscles and cartilage, the bone marrow, and selected pornons of the peripheral nerves. Although these tissues are devoid of lymph channels, they are perfused by minute interstitial conduits or by direct diffusion. The anatomic arrangement of the lymph channels mirrors that of the lymph nodes in that there are both superficial and deep vessels. The superficial lymph vessels follow the course of the superficial veins and the superficial nodes. The deep lymphatic vessels, as in the case of the deep nodes, follow the course of the deep veins and drain the deep structures of the thorax, the abdomen, the pelvis, and the perineum. Deep lymph channels lie aro und all major organs of the body. The structure of the lymphatic system differs significantly from all other fluid flow systems in the body. It begins in the tissues as lymphatic capillaries or blind endothelial tubes composed of a single layer of leaky squamous epithelium (Fig .. 68.1). These thinly walled capillaries are supported by anchonng filaments that are attached to the endothelial cells and extend into the surrounding interstitium. These filaments bind the endothelial tubes to the proteinaceous fibers in the interstitial matrix. They also function to open spaces between the endothelial cells as fluid accumulates, and prevent collapse of the thinly walled lymph capillaries. At the level of the arterial capillaries, filtration of intravascular fluid occurs, allowing for the passage of fluid, proteins, and particles from the vascular system directly into the interstitium . This fluid then diffuses along the connective tissue fibers and the anchoring filaments in the interstitium, where it actively mixes with extracellular fluids. More fluid gets into the interstitial spaces than is removed by the capillaries, even when all is normal. Because the simple squamous epithelium of the lymphatic capillaries contains no basement membrane, it possesses a greater permeability than do the blood capillaries. This promotes ready passage of
Anchoring fi lament
Endothelial cell
FIGURE 68.1 . The beginnings of the lymphatic system. (Illustrat ion by W. A . Kuchera.)
the excess transudate from the interstitium back into the closed circuit of the lymphatic system. Peripheral lymphatic capillaries join to form capillary plexus that, in turn, form larger trunks. In the superior portion of the body, the chest wall and the pleural spaces are drained ~y the intercostal trunks. The mediastinal trunks drain the thoraCic VIScera. The internal jugular trunk drains the left side of the head and neck, and the subclavian trunk drains the left arm and shoulder. The pelvis is drained by the internal iliac trunk, and the lower extremities are drained by the external iliac trunk. The lumbar trunk drains the lumbar area; the small intesti ne trunk drains the small intestine, the lacteals, and Peyer patches. The colon and the mesentery are drained by the superior and inferior mesenteric trunks. The gastric trunk receives drainage from the liver, spleen, stomach, and pancreas. All of these trunks eventuall y drain into two main trunks that empty into the venous system in the cervicothoracic area, either the right lymphatic duct (RLD) or the thoracic duct, also called the left lymphatic duct (LLD). The trunks of the abdomen, pelvis, and lower limbs drain into the cisterna chyli, a saccular dilation of the thoracic duct that lies on the anterior right side of the Ll and L2 vertebral bodies at the level of the renal vessels. The cisterna chyli lies beh ind the right crus of the diaphragm next to the abdominal aorta and represents the distal portion of the thoracic duct. In some cases, the lumbar trunks unite above the level of the L2 vertebra, forming a plexus of vessels that drain directly into the thoracic duct, in which case the cisterna chyli is absent. All of the aforementioned trunks (from the left side of the head and neck, the left arm and thorax, left and right portions of the lower body, and the thoracic viscera) drain into the LLD . Only the right side of the head, the right side of the neck, the right arm, and the right chest (inclusive of the heart and portions of the lungs) drain into a separate main duct, the RLD. Sodeman and Sodeman (8) state that sometimes the posterior portion of the left upper lobe of the lung drains into the thoracic duct. The thoracic duct is the largest lymph vessel in the body, typically measuring 36 to 45 em in total length . The thoracic duct lies directly against the vertebral column as it courses cephalically. It passes through the aortic hiatus of the diaphragm and traverses the posterior mediastinum between the aorta and the azygos vem, passing in front of the phrenic nerve and behind the vagus nerve. At the level of the sternal angle (T4), it inclines to the left of midline and enters the superior aperture of the thorax behind the aortic arch and to the left of the esophagus. At this juncture, it passes laterally across the carotid sheath and then a~ches caudally and anteriorly to the subclavian artery. The thoraCic duct terminates at its junction with the venous system. It empties into the venous circulation in the region of the junction between the left subclavian and left brachiocephalic vein . The RLD is formed by a merger in the right jugular trunk, the right subclavian trunk, and the right transverse cervi~al trunks. This short duct courses the medial border of the antenor scalene muscle and terminates in the jugulosubclavian junction in the anterior neck. A distinct RLD, approximately 1 em in le~gth, is present in only 20% of patients (8). Usually, the three main contributing trunks of the duct empty separately via two or three separate openmgs.
68. Lymphatic System
The terminal points of both main trunks are protected by valves that prevent the back flow of blood into the lymphatic systc::m. These are one-way valves under sympathetic autonomic control. In addition, the lymph vessels possess a series of one-way valves situated in the vessels every few millimeters that prevent regression of lymph as it returns to the central lymphatic collection sites. All lymph moves unidirectionally. Each segment between valves acts independently, filling and emptying on fluid demand. The larger lymph vessels contain smooth muscle, which is also innervated by the sympathetic nervous system. The extent of sympathetic innervation suggests that response to stress may hinder optimal decongestion of tissues via the lymphatic system.
Lymph Lymph is the final component of the lymphatic system. Lymph is the substance that leaks out of the arterial capillaries, into the interstitium, and into the single-cell lymphatic vessels. Lymph is usually clear in color and contains proteins (2 to 6 gmo/o) (9) and salts. After a meal, the lymph in the thoracic duct becomes richly laden with emulsified water-soluble fats, and its color may actually change to yellow. The primary cells of lymph are lymphocytes. Lymphocytes have been found in quantities of2,000 to 20,000/mm in the thoracic duct (10). Lymph also contains clotting factors; it clots on standing. Finally, large particles, such as bacteria and smaller viruses, are found in the peripheral lymph before filtration through a lymph node or one of the organized lymphoid tissues. These larger particles are brought into close contact with lymphatic cells that have immune functions.
PHYSIOLOGY Let the lymphatics always receive and discharge naturally, if so we have no substance detained Long enough to produce fermentation, fever, sickness, and death. -A. T. STILL (1)
Function The lymphatic system has four basic functions: Maintaining fluid balance in the body Purification and cleansing of tissues Defense Nutrition
Fluid Balance One of the most important functions performed by the lymphatic system is that of fluid balance. At least 50% of all plasma proteins that diffuse out of the vascular system within a 24-hour period return to the body by way of the lymphatic system (5). On a daily basis, approximately 30 liters of fluid filters out of the capillaries and into the interstitial spaces (10). Of this 30 liters, approximately 90% (27 liters) drains back into the blood capillaries, but the remaining 10% (3liters) drains into the lymphatic channels. In addition to absorption of this 3-liter volume, the system has a capacity to absorb a limited amount of excess fluid from the cavities of the pleura, the peritoneum, the pericardium, and the
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joints. Although 1Oo/o is a proportionately small amount of fluid that is returned to the circulation by way of the lymphatics, this lymph flow is vital because proteins and other substances of high molecular weights that are unable to pass easily into the pores of the vascular capillaries because of their large size are able to enter the lymphatic capillaries with relative ease. In the case of significant fluid overload, it is the lymphatic system that provides the homeostatic reserve to resist or forestall damage (10).
Purification and Cleansing The lymphatic system serves important functions in cleansing the body, both within the structure of the lymphatic conduits and without. Because lymph forms as a filtrate from the arterial capillaries into the extracellular spaces, lymph actually bathes all of the organs of the body. Before passing into the capillaries of the lymphatic system, it cleanses the extracellular spaces of particulate matter, exudates, and bacteria. Once inside the lymphatic system, it readily delivers all of these substances to the lymph nodes, which act as purifYing filters for removal of this waste matter from the circulation.
Defense Intimately associated with the cleansing and purification functions of lymph are the defensive properties of the lymphatic system. Because of the pervasive quantities and locations of lymphoid tissues in the body, lymph comes in fairly immediate contact with any toxins, bacteria, and viruses entering the system. The lymphatic system provides the first line of defense against this invasion. Acquired immunity does not develop until the body has first exposure to these invading antigens. All of these substances contain proteins, polysaccharides, or lipoprotein complexes, and these are the essential substrates by which the body is able to develop acquired (adaptive) immunity. The lymphatic system's importance is underlined by the fact that any individual who genetically lacks lymphoid tissue or who has had chemical or radiation obliteration of the body's lymphoid tissue cannot defend against antigenic invasion and will die. The lymphatic defense system is broken down into two separate divisions, both embryologically derived from lymphocytic stem cells in the bone marrow. The T-lymphatic division contains those sensitized lymphocytes that have been processed through the thymus gland and function to provide cellular immunity. The majority of this preprocessing occurs before birth of the infant, and the remainder shortly thereafter. Cellular immunity, also known as lymphocytic immunity, is the capability of the sensitized lymphocyte to attach to a foreign substance and to destroy it. The B-lymphocytic division is named for the bursa of Fabricius, a structure not found in mammals but found in birds, where B lymphocytes were first identified. These B lymphocytes are believed to be processed in the liver or the spleen in humans (although the exact location is unknown) and give rise to humoral immunity. Humoral immunity is the capability of the body to produce globulin molecules known as antibodies, which possess the specific capability of attacking the invading antigens. The lymphatic system is not only responsible for the production and maintenance of these two essential defensive armies;
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VII Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
the free flow of lymph is also vital for direct contact of the invading agents with the defense factors. Whenever injury occurs, the subsequent inflammation brings increased vascular perfusion, increased capillary filtration, and increased lymph production to the area. This is the body's obvious mechanism for increasing contact between antigens and antibodies, as well as phagocytes. The greater the lymphatic flow through the body, the greater the contact of body defenses with all toxins, particulate matter, and other foreign substances.
Nutrition As stated earlier, 50% or more of all plasma proteins are carried by the lymphatic system back to the vascular system after their efflux from the arterial capillaries into the extracellular spaces. Many of these proteins are capable of binding nutrients that the cells need. Long-chain fats, chylomicrons, and cholesterol are absorbed in large quantities from the lacteals in the villi of the small intestine. After a large and fatty meal, the thoracic duct may contain up to 2% fat. With fat absorption, the lymph of the gastrointestinal tract changes from its normal clear appearance to a yellow or milky color. This particular kind of lymph is called chyle.
Mechanisms of Flow Several factors determine the rate oflymph flow in the body. Interstitial fluid pressure is one important factor. Normally, interstitial fluid pressure is maintained at -6.3 mm Hg. Any increase in this pressure increases the absorption oflymph into lymph capillaries. An increase from -6.3 mm Hg to 0 mm Hg increases lymphatic flow approximately 20 times its normal rate of 120 ml!hr (10). At 0 mm Hg, a ceiling of efficiency is reached. Above that level, interstitial fluid pressure becomes greater than the pressure inside of the lymph channels, causing them to collapse and obstructing the pathways; drainage ceases. Several elements increase intersti rial pressure: In creased arterial capillary pressure (such as m systemic hypertension) Decreased plasma colloid osmotic pressure (as in cirrhosis of the liver, in which there is a decrease of plasma protein synthesis) Increased interstitial fluid protein (as in plasma hypoalbuminemia associated with starvation) Increased capillary permeability (associated with toxins such as rattlesnake poisoning) A second factor affecting lymph flow is the lymphatic pump. As stated earlier, each section between the valves of the lymph channels functions as an independent unit. This provides the lymphatic vessels with an intrinsic, active pumping mechanism . When lymph enters a segment of the lymph vessel, distension of that individual section occurs. In the larger vessels, this distension causes contraction of the smooth muscle within the walls of the lymph channel and effectively pumps the lymph to the next independent segment, where the dilation and pumping process is repeated. A similar process occurs in the lymph capillaries. Although there is no smooth muscle in the lymph capillary, the endothelial cells contain contractile fibers (myoendothelial fibers) that respond to fluid distension in the same way. This lymphatic
pumping at the capillary level also creates a slight degree ofsuction as the capillary passes from relaxed to distended to relaxed states, and it is this suction that helps pull fluids from the interstitium. In the extremities, the rhythmic motility oflymphatic vessels has an intrinsic rate of6 to 8 seconds per cycle (11). This duration equals a frequency of7.5 to 10 cycles per minute, similar to that of the cranial rhythmic impulse (CRI). Indeed, the CRI may be a palpable harmonic wave ("summation signal" in the language of chaos theory) that integrates the lymphatic rhythm with other biologic oscillations, such as heart rate, respiration rate, TraubeHering modulation, and oscillating fluctuations in cerebral blood volume (12). The pacemaker responsible for the rhythmic contractility oflymphatic vessels has not been identified. Pacemaker activity in the gut, which drives peristalsis and secondarily propels lymphatic fluid, appears to be stimulated by the interstitial cells of Cajal (13). A hypoplasia of these pacemaker cells leads to intestinal dysmorility ( 14) . Pacemaker cells are influenced by autonomic nerve function, which suggests that OMT directed at dysfunctional autonomic tone will provide therapeutic effects (12). Finally, in the same way that lymph flow is pumped by intrinsic mechanisms, extrinsic pressures on the lymph channel also promote passive filling of lymp hatic segments with subsequent pumping effect. Direct external pressure on a lymph channel increases the flow of lymph . Internally, wherever pressure is exerted over the lymph vessel, flow increases. Wherever arteries with their rhythmic contractions cross lymph channels, flow increases. The diaphragm is considered by many to be an extremely important extrinsic pump for the lymphatic system. Movements of the diaphragmatic crura exert a pumping influence on the cisterna chyli. All movemems of internal organs, such as respiration and abdominal peristalsis, as well as movements of the extremities, exert an effective external pump. Not only does the diaphragm directly massage the lymphatics, but respiration produces pressure gradiems between the chest and the abdomen . These pressure gradients, along with the one-way valves, help ro pull lymph toward the venous circulation. If a person breathes 12 breaths per minute, this produces 17,280 pressure changes per day. Therefore, rate and depth of breathing can increase or decrease lymphatic flow. The overall effect of the extrinsic pump is best underlined by the fact that vigorous exercise, with its movemem of extremities, organs, and the diaphragm, may increase lymph flow 15 to 20 times the normal resting flow amount. Other functional diaphragms, such as the pelvic diaphragm, normally work in synchrony with the abdo minal diaphragm. When this happens, there is optimal movement of interstitial fluids from the pelvis and optimal pressure gradients from abdominal diaphragmatic contractions. The pelvic organs predominantly rest on the soft tissues of the perineal floor, in comrast to the abdominal contents that rest against the large iliac fossae. The soft tissues that form the urogenital diaphragm, pelvic diaphragm, and other perineal ligaments and tissues close the pelvic outlet. They form a solid, yet elastic floor that also allows for periodic opening to occur for excretion and, in females, for childbirth. · The abdominal viscera constitute a dynamic column that rests on the iliac fossa and the edge of the ischiopubic rami. In spite
68. Lymphatic System of these supports, some pressure is still exerted on the pelvic inlet from above. The pelvic organs themselves add their weight and, along with the effects of gravity, add to the load that must be supported by rhe perineal floor. To completely fulfill irs function, the pelvi c floor needs to provide elasticity in addition to irs supportive function. If the floor were rigid , thoracic inhalation would compress the pelvic organs from above. Compensation by the pelvic floor must dissipate or alleviate the permanent, cyclic respiratory pressure and also the transient o r temporary increased press ures produced by coughing, sneezing, hiccups, pregnancy, and so o n. This synchronized contraction of the abdominal diaphragm and descent of the relaxed pelvic diaphragm, as well as the reciprocal motions with exhalation, produce a mechanical pump for the lymphatic vessels and ve no us sinuses in the pelvis and aro und the rectum and penneum. Within the perineal floor are openings for the urogenital traer and rectLtm. T hese orifices are anato mic weak points, and because of th e number and size in women, the female perineum is much more fragi le than the male perineum. Structurally, these orifices provide a weakness that may allow hern iation or ptosis in the ad ult. Because of these weak areas where the urinary and vaginal tracts exit, the body has developed a second layer of reinforcement distal to the shelf of the levator ani muscles. T his is called the urogenital diaphragm. The pelvic diaphragm needs to act as a support and yet remain elastic. Distension of the pelvic diaphragm must be in phase with the continual movements of the thoracic diaphragm and also with the transient changes in intrapelvic pressure. This helps assure that the pelvic organs escape undue pressure and that there is a free flow of fluids within the vascular and lymphatic channels of the pelvic region.
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Conditions of starvation and cirrhosis of the liver, as well as other stares of abnormal protein metabolism, affect interstitial fluid gradients by altering rhe osmotic effect of plasma protei n levels . Decreased osmotic pressure gradi ents across rhe capillary, which occur with decreased plas ma protein level or the accumulation of osmotically active substances in rhe interstitium, promote increased accumulation of fluid in the extracellular spaces with al l the ramifications that go along with the edematous state. Inadequate drainage also results in the development of edema because of the relative imbalance created in pressure gradients, even in the face of normal capillary filtration . Posttraum atic or postsurgical scarring may cause mechanical obstructions ro absorptive flow and mechanical blockages, such as those produced by filariasis or intraluminal carci noma, creating absorptive insuffi ciency that will eventually lead to edema. The results of edema are pervasive and profound to all surrounding tissues. Edema causes compression not only on the lymphatic channels but also on the nearby vascular and neurologic structures, thus potentially diminishing their function. Edema is associated with increased tissue congestion . Stasis of in terstitial fluids promotes changes in the pH of tissues and organs, which further compromises fun ction. T his promotes inflammation that, in turn, produces greater edema and co ntinuation of the cycle. It also is associated with infiltration of fibroblas ts, which can lead to fibrosis and contracture of tissues. Edema also affects the delivery of nutrients to the affected sires and is associated with even greater changes in tissue fun ction and healing abili ties. Finally, edema affects bioavailability of drugs and hormon es, hampering nor only medical manage ment of th e primary fluid build-up but also, because of tissue co ngestion , decreasi ng the efficacy of any pharmacologic treatment.
PRINCIPLES OF TREATMENT PATHOPHYSIOLOGY T he consequence of a poorly functioning lymphatic system is congestion or frank edema from the build-up of interstitial fluids . Edema is rhe result of too much fluid getting into the interstitium or roo li ttle fluid getting out. Its presence sign ifies that the body's compensatory mechanisms have already failed. Conditions th at overload the interstitium produce congestion and edema by overriding the absorptive capabi lities of the lymphatic system. Excess ive interstitial fluid produces excessive interstitial pressure, which, in turn, is associa ted with collapse of the lymph capillaries, resulting in further interstitial congestion and edema. Edema has a second deleterious effect of dilating the lymphatic capillaries. With dilation, the endothelial cells separate and the flap valves of the capillaries become nonfunctional. This is associated with a shutdown of the intrinsic lymphatic pumping of the capillaries. Conditions of high veno us pressure are associated with increased capillary fi ltration rates and have an increased tendency ro produce edema. These conditions include congestive heart failure, incompetent heart valves, venous obstruction, and the effects of gravity. Arteriolar dilation and venous constriction are also associated with increased capillary permeability, as are the effects of substances such as cyrokines and histami nes.
Goals T he goal for treatment of the lymphati c system is to have a balan ced, well-functioning system in which no edema occurs. T he fact that the lymphatic system is a passive system underlines the importance of motion and adequate drainage of lymph . OMT has long provided an extra measure of movement that promotes proper fluid dynamics . Manipulation is associated with: Increased resorption of fluids Increased circulation and respiration Decreased proteins in the interstitium Facilitation from a more beneficial pH balance
Fascial Pa t tern Diagnosis (Zink) Although there was previous ralk abo ut the fasciae of the body havi ng rotatory preferences, Z ink ( 15) was the first to provide a written, understandable, and clinically useful explanation for treatment, with a method of diagnosing and manipulative methods of creating the fascial patterns of the body. Fasciae form rhe pathways for lymphatic vessels, as well as for arteries, veins, and nerves. Torsion of these pathways can hinder the flow of lymph through the lymphatic vessels. Zink identified four areas of the
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
body as cross-over sites where fascial tension could occur (15): Occipito-atlanral (0-A) Cervicorhoracic (CT) Thoracolumbar (TL) Lumbosacral (LS) He rested the fascial preference for rotation and side-bending of those regions of the body. Zink had observed rhar almost all people who rhoughr rhey were well and healthy had alternating patterns of rotatory preference ar rhe key sites. When testing rotation from rhe 0-A ro the LS regions, he found rhar approximately 80% of rhese people had rhe body pattern of LIR/LIR, and the orher 20% had R/LIR/L, so he named rhe former pattern rhe common compensatory pattern (CCP). Zink reasoned rhar, ideally, rhere should be equal motion to rhe right or to rhe lefr in all of these reference zones, bur apparently the stress of gravity and living produced rhe alternative patterns. People in the hospital tend to have patterns rhar do not alternate; rhis is also true for people who are easily stressed, who ger sick easily, and who have low levels of wellness. When reference zones do nor indicate equal or alternating patterns of rotational preference among rhe four regions of rhe body, Zink called these uncompensated fascial patterns, and they need OMT. The goal of treatment for these people is to return their fascial patterns to ideal so that their bodies can establish more efficient fascial patterns, usually of the compensated form. Because fascia attaches to bone, direct (thrust or muscle energy) or indirect methods of OMT can be performed to normalize the fascial preferences. Zink's diagnostics and treatment for the fascial regions of the body improved the pathway for lymph flow.
Types of Treatment Lymphatic treatments are essentially divided into two broad categories: those techniques that remove restrictive impediments to lymphatic flow, and those that promote and augment the flow of lymph. A thorough treatment regime usually includes techniques from both categories, in that sequence. A sequence for a basic lymphatic treatment program includes: 1. Rib raise and/or use paraspinal inhibition (Tl-L2). This is designed to reduce hypersympathetic activity to the lymphatic vessels in the area of concern and around the major lymphatic duct that anatomically drains that area or region. Mobilizing the ribs also enhances respiration. 2. Diagnose and treat any thoracic inlet somatic dysfunction. The thoracic inlet is the common obstruction to lymphatic flow from anywhere in the body. 3. Dome (relax) the abdominal diaphragm. This improves the ability of this major fibromuscular diaphragm to produce effective pressure gradients between the thoracic and abdominal cavities. 4. Apply some additional form oflymphatic pump and/or techniques to further promote lymphatic flow. This may be optional in a basic plan bur would further enhance lymphatic flow. More than one type of treatment affects the lymphatic system. For instance, use of high-velocity/ low-amplitude treatment
alters muscle tone and neural reflexes rhar affect structures such as the diaphragm, adding to the efficiency of rhe system. Muscle energy, deep articulatory, or otl1er di rect techniques do rhe same rhing. An example of a deep articulatory technique is rib raising in a repetitive fashion, freeing rhe ribs and diaphragm to have a more relaxed, efficient performance and normalizing sympathetic autonomic activity from the thoracolumbar sympathetic chain ganglia. Conversely, myofascial release techniques are particularly effective in eliminating inappropriate tension in tissues surrounding lymphatic channels rhar rend to be constrictive in nature. Cranial techniques are thought to have a balancing effect on the sympathetic/parasympathetic nervous system, leading to deeper diaphragmatic breathing, as well as promoting appropriate cranial venous fluid rerum.
Treatment Plan (One Example) Treatment of the lymphatic system should begin with rhe removal of all restrictions resulting from tissue hypertonicity that may be affecting lymph flow. Release of rhe central lymphatic system should be accomplished first, followed by release of the periphery. This decreases the likelihood of exceeding the system's innate 7 mm Hg maximum increase in capability of handling increased flow. Treatment begins by releasing rhe central lymphatic system: rhe area of the thoracic inlet, then rhe abdominorhoracic diaphragm, and rhe pelvic diaphragm. Release of rhe peripheral lymphatic systems should include drainage techniques of rhe head and neck, as well as the extremities (in each case beginning centrally and progressing peripherally). Lymphatic treatment should be accompanied by a release of all respiratory restrictions (rib or clavicular somatic dysfunctions), as well as restrictions of rhe muscles, joints, and abdomen. Rib raising and treatment of any spinal somatic dysfunction are also prudent to optimize autonomic activity. Attention should also be given to dysfunction of the cranium (including the temporals, rhe occiput, and the sphenoid) to promote optimal functioning of the cranial nerves, particularly the vagus nerve (cran ial nerve X).
Contraindications of Lymphatic Treatments Contraindications of individual treatments are included along with the following individual techniques. Relative contraindicarions for lymphatic treatment techniques include osseous fracture, bacterial infections wirh a rem perature over 102° F (38.8° C, in which case antibiotic control should first be implemented to reduce rhe chance of seeding and encouraging a generalized body infection) and certain stages of carcinoma.
LYMPHATIC MANIPULATIVE TECHNIQUES Even under normal conditions, more blood gets to the tissues than can be removed by the venous system. This amount is even greater when there is dysfunction or inflammation. An important principle in rhe efficient care of patients with dysfunction or disease is to be sure that rhe lymphatic drainage is as efficient as possible. This can be performed by djagnosing impediments to flow and then designing osteopathic manipulative techniques
68. Lymphatic System to remove those impediments, improve the pumps, and di rectly promote decongestion of an organ or region of the body. T he lymphatic system has no intrinsic pum p an d m ust rely heavily on the production of efficient p ressure gradients between th e thoracic and abdominal regions, produced by th e efficient actio n of a well-domed abdom inal diap h ragm . Recent studies reveal that there are sympathetic fibers in nervating muscle fi bers in the large r lymphatic vessels, implying that sympathicotonia m ay reduce the amount of lymph th at the lymp hatic vessels can carry.
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TABLE 68 .1. THORACIC INLET DIAGNOSIS: STATIC AND MOTION TEST FINDINGS Inlet fa scia rotated and side-bent left
First rib Infraclavicular space Coracoclavi cular ang le Spring upper ribs
Left rib ~ /rig ht rib t Left deep Left posterior Left spring/right res ist
Inlet fascia rotated and side-bent right
Left rib t /right rib ,!Right deep Right posterior Rig ht spring/left resist
TECHNIQUES TO REMOVE IMPED IME NTS Tho racic In let: Two -Step with Muscle En ergy Activation
Open Thoracic Inlet Fascia Anatomical ly, the thoracic inlet (Fig. 68.2) is th e first ribs, th e fi rst thoracic vertebra, and th e manubri um. C linically, the thoracic inlet is the first two ribs, the first fo ur thoracic ven ebrae, and the manubrium of the sternu m. Fascia from the scalenus and the longus coli muscles joins together to produce a fun cti onal fascial diaphragm for the superior thoracic inlet. Lym phatic fluid returning from any site o utside the thorax m ust pass th ro ugh this diaphragm. The thoracic fascial inlet is a common d iaphragm for both th e right and the left lymphatic ducts. The LLD (thoracic duct) passes through this diaphragm twice. The tissues of the tho racic inlet are frequently subjected to the stresses associated w ith carriage of the head on the shoulders, as well as the muscul ar pull of the shoulders themselves. Some phys icians evaluate the th oracic inlet fasciae by examining first rib motion d uring respiration and then determining the direction of fascial ease or restr iction to the application of traction in all directions at the cervicotho racic junction. This is an organized method of determining preference of the tissues at the cervicothoracic junction: 1. The patient may be supine or seated, and th e physician may approach the patient from either the anterior or the posterio r position. 2. Place the fingertips at the superior aspect of the sh oulders in the region of the first rib (Tab le 68. 1). The fasc iae at the inlet tend to pull the cervicothoracic regio n into side-bending and rotation to the same side. Opening the thoracic in let relieves obstruction to lymphatic fl ow at this level.
/
Patient Position Supine. Physician Position Sitting or standin g at the head of the table (to treat side- bendin g restriction). Procedure 1. Side bend th e neck to the side of restri cted side- bendin g, usin g IP joints of the index fin g.;:r of o ne hand as a fulcrum at th e cervicoth oracic junction on that side (Fig. 68.3). 2. Rotate th e p atient's h ead to th e opposite side to lock out the cervical spine above th e cervicothoracic jun cti o n. 3. Ask the patient to attempt side- bendin g the head to the side opp osite the fulcrum h and as yo u isom etri cally res ist th e effo rt. 4. Ask the patient to completely relax and repeat step 3 three or four tim es. 5. Place the h ead and neck back to neutral position ; now, ro tate th e h ead to the restri cti ve barri er of ro tation (wi thou t sidebending) using yo ur hand on the side of th e h ead and th e fin gers of the IP joints of the index fin ger of that hand at th e cervi cothoracic jun ction (the fulcrum) (Fig. 68.4) . 6. Ask th e patient to attempt to ro tate th e h ead and neck toward your fulcrum hand as yo u isometrically res ist the effo rt. 7 . Ask the patient to completely relax, and repeat Step 6 three o r four times. 8. Rech eck the fascial p reference at the tho racic in let.
Infrac lavicu lar space ' \
Le f t
Right Ri g ht co racoclav icu la r . ( . a ng le
FIGURE 68.2. Thoracic inlet: st atic landmarks. (I ll ustration
Left rib head / neck area: First rib
Right rib head/neck a rea: First rib
by
w. A.
Kuchera .)
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 68.3. Thoracic inlet: side-bending.
FIGURE 68.5. Thoracic inlet: direct myofascia l release.
Thoracic Inlet: Direct Myofascial Release Patient Position Supi ne with arm abducted 90 degrees from the body. Physician Position Seated at the side of the patient. Procedure 1. Use your knee to support the patient's elbow and cephalad hand to support the patient's wrist. 2. W ith caudal fingers placed on the superior aspect of the supraclavicular fossa, apply downward pressure to the patient's wrist (Fig. 68.5). The caudal fingers apply gentle anterior pressure agai nst the clavicle. 3. Move the patient's wrist superior. The caudal hand follows the rotatio n of the clavicle posteriorly until tension develops. Hold this until some relaxation is noted. 4. Repeat this two o r three times. Note: T his technique can be uncomfortable to those who need it the most. Please be aware of your whole patient and not just the clavicle.
Normalize Sympathetic Activity Treatmen t by rib raising reduces constriction oflarger lymphatic vessels. Rib raising that raises the rib heads also stimulates rhe
thoracic sympathetic chain ganglia. T his initially stimulates regional sympathetic efferent acriviry to organs related to rhar spinal level of sympathetic innervation. But in the long run, rib raising results in a prolonged reduction in sympathetic outAow from rhe area treated. By freeing rib motion, rhe excursion of rhe rib cage during respiration is also freed. By freeing the rib heads, the excursio n of the chest during breathing is increased, and lymphatic Aow is improved.
Rib Raising Seated Patient Position Seared on table. Physician Position Standing at the side of rhe table, fac ing the patient. Procedure 1. Ask the patient to cross his or her arms and grasp rhe deltoid muscles. 2. Ask the patient ro lean toward yo u resting his or her crossed arms on your chest. (A variation: patient's arms raised overhead and draped on your shoulders instead of crossed.) 3. Grasp rhe posterior, inferior rib angles bilaterally in rhe area you are treating (Fig. 68.6). (Begin cephalad, move caudad, return ro cephalad.) 4 . Apply a lateral traction bilaterally ar rhe rib angle while pulling the patient toward you. 5. Have rhe patient breathe deeply to aid rhe mobilization of rhe entire rib cage.
Rib Raising Supine Patient Position Supine.
FIGURE 68.4. Thoracic inlet: rotation .
Physician Position Standing or seared ar rhe patient's side.
68. Lymphatic System
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taken to treat both sides of the rib cage with equal traction, and motions of the operators must be synchronous.
Improve Extrinsic Lymphatic Pump Osteopathic manipulative techniques affect diaphragms so that they can more efficiently create alternating pressure gradients. This can usually be done most time-efficiently if the abdominal diaphragm's m uscular attachments are first treated for maximal structure-function; cervical somatic dysfunction should also be treated because this is the region associated with the diaphragm's innervation. The tho racoabdominal diaphragm is a strong muscular structure innervated by the phrenic nerve (C3-5). Tension in this structure produces substantial alterations in lymphatic Aow. The body is constructed in such a fashion that lymph flow predominately runs in a longitudinal plane. At several significant regions, however, horizontal tissues transect this pattern. Should these horizontal tissues be placed on tension for any reason, lymph flow could be significantly impeded. Osteopathic physicians have long considered that there are four of these regions: FIGURE 68.6. Ri b rais ing: seat ed.
Procedure 1. Place your hands (palms) under the patient's thorax, contacting the rib angles with the pads of your fingers (Fig. 68.7).
2. Flex your fingers to achieve contact with the rib angle and the patient's posterior thorax. 3. Apply traction on the rib angle. 4. While maintaining traction, bend your knees and lower your trunk to raise the ribs by moving your hands upward. This is a fulcrum/lever action. Do not bend your wrists. (Particularly if the patient is in a hospital bed, it is easier to move your hands upward if you reciprocally push your forearms down.) 5. Move your hands to subsequent rib angles until all ribs are treated. 6. Treat the opposite side of the rib cage in the same manner. Note: If you have an assistant, a two-person technique can be used treating both sides of the rib cage at once. Care must be
Abdominal diaph ragm: located between the abdomen and the chest cavity, it is m uscular and tendinous in nature, forming a continuous sheer interrupted only by the aorta, esophagus, inferior vena cava, and accompanying blood vessels, lymphatics, and nerves. Thoracic inlet or oudet: these are located in the cervicorhoracic regwn. Tentorium cerebelli: this diaphragm affects venous return from the brain because the brain has no lymphatic system and relies on the veins to perform both functions. Pelvic diaphragm: this is a group of muscles and fascia rhar span the perineum and form a lower border to the abdominal cavity. Some writers describe a fifth diaphragm, the paired arches of the fee t; a collapse of the pedal arches can profoundly affect the pelvic diaphragm.
Dome Abdominal Diaphragm Doming the diaphragm is a term used to refer to relaxing the resting state of the abdominal diaphragm (or the pelvic diaphragm). If the diaph ragm can be completely relaxed and well-domed, its contraction and relaxation produce greater pressure gradients between the thoracic and abdominal cavities, along with the oneway valves, and promotes better lymphatic drainage back into veno us circulation. The pressure gradients act as an extrinsic pump for the lymphatic system. The doming techniques may also directly engage the inferior surface of the diaphragm and augment irs excursion during expiration.
Thoracoabdominal Diaphragm Diagnosis of Fascial Restriction at the Thoracoabdom inal Diaphragm
FIGURE 68.7. Rib ra isi ng : supine.
Procedure 1. Place the palmar surfaces of your hands on the right and left side of the lower rib cage of the patient, with the fingers pointing toward the table (Fig. 68.8).
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V!!. Osteopathic Considerations in PaLpatory Diagnosis and Manipulative Treatment 3. Maintain the rotation bur adjust tension through yo ur hands ro produce a vertical shearing force on rh e thoracoabdominal rube, and ask the patient ro repeat the big breath in and our through the mo urh. 4. Adjust the tensions through your bands until there is equal excursion produced by the right and the lefr side of the thoracoabdominal diaphragm. 5. Hold those vecrors while the patienr breathes deeply two or three times. 6. Return the patient ro neutral and retest rotational preference of the tissues of rhe thoracoabdo minal region.
Thoracic Diaphragmatic Fascial Release: Myofascial FIGURE 68.8. Diagnosis of thoracoabdominal restriction .
2. Rorare rhe tissues of rbe rhoracoabdominal cylinder ro rhe righ r and then ro the lefr abo ut a vertical axis, ro rest rhe ease of or restriction ro rorarory motion. 3. T his region can rhen also be tested for side-bending preference by inducing translation of rhe region in each direction . Treatment examples for thoracic diaphragm dysfunction point our a problem: fasc iae at the thoracoabdominal diaphragm prefer ro rotate ro rhe left side.
Thoracic Diaphragmatic Fascial Release: Direct Method Patient Position Supine o n rhe table.
Physician Position Standing beside rhe table.
Procedure I. Rotate rhe tissues of the thoracoabdominal region (tube) in rhe directio n of their restriction; rotate ro the restrictive barrier (Fig. 68.9). 2. Hold there and ask the patient ro rake a deep breath in and our through rhe mouth. No rice rhe side of greatest movement and rhe side of least movemen r.
Patient Position Seared , erect and not slumped; rhe patient may relax but not collapse.
Physician Position Stand ing behind the patient.
Procedure 1. Pass your hands around the thoracic cage (under the patient's
arms) and gently but firmly introduce your fingers underneath the costal margin. 2. Test for mo tio n by passively rotati ng rhe thorax ro the left and ro the right. Determine (in one cycle of motion resting) in which direction there is greater freedom/ease of motion. 3. Treatment phase: with the fi ngers on the diaphragm (i.e., underneath the costal margin), carry the thorax in the direction roward wh ich it moves more free ly. Hold it in that position. Follow it as it goes through its fascial release (un winds) and con tin ue until it fi nally settles down into a free, gen tle, rhythmic, vertical motion. 4. Retest the range of motion and evaluate treatment effectiveness.
Dome Abdominal Diaphragm: Direct Mechanical Patient Position Supine.
Physician Position Standing ar the patient's side.
Procedure 1. Place fingers o n the outer aspect of the inferior border of rhe ribs with thumbs pointed toward each other medially and positioned directly caudad ro the xiphoid process of the sternum. 2. On the first respiration, gently press downward with thumbs toward the table as the patient exhales; fo llow the diaphragm monon. 3 . Hold this end position (barrier); the patien t inhales again. (Note: The thumbs will sense resistan ce ro respiration.) 4 . On the second exh alation, press in further downward roward the table, following the diaphragm. FIGURE 68.9. Direct fascial release of thoracic diaphragm.
5. Repeat step three.
68. Lymphatic System 6. On the third exhalation, press the thumbs cephalad following the superior course of the diaphragm.
Dome Pelvic Diaphragm The pelvic diaphragm is a muscular sling located on the bony floor of the true pelvis that provides support for the pelvic organs. It is composed of two main muscles, the coccygeus muscle and the levator ani muscle. The coccygeus muscle attaches to the ischial spine and then to the sacrum and coccyx. The levator ani muscle is subdivided into two main parts according to its attachments to the innominate bone. The various muscles are as follows: Iliococcygeus muscle: attaches to the iliac bone and the tendinous arch of the obturator intern us to the coccyx and the anococcygealligament Pubococcygeus muscle: attaches to the pubic bone and then to the coccyx and the midline structures of the perineum; it can be divided into three attachments according to attachments to the midline structures Pubococcygeus proper muscle: pubic bone to the coccyx and anococcygealligament Puborec:alis muscle: pubic bone to rectum forming a muscular sling behind the rectum near the anorectal junction Pubovaginalis or puboprostatic muscle: pubic bone to one of these structures in the midline
Diagnosis of Pelvic Diaphragm Somatic Dysfunction Procedure 1. To approach the pelvic diaphragm, position the patient supine and sit on the side of the pelvis to be treated. Face toward the patient's head. 2. Flex the patient's knee and hip on this side. Identify the ischial tuberosity with your outside hand. Introduce the fingers of the other hand medial to the ischial tuberosity, letting the pads of the fingers keep contact with the medial surface of the ischium. Your fingers are now pressing into the ischiorectal fossa, the inclined roof of which is the pelvic diaphragm (Fig. 68.10). (See also Chapter 57).
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3. As the patient inhales, the pelvic diaphragm should press down on your fingertips. With exhalation, the pelvic diaphragm should move cephalically. 4. If the pelvic diaphragm is unable to descend, it is in an exhalation somatic dysfunction and is restricted in its inhalation phase. If it does not ascend well, it is in an inhalation somatic dysfunction and is restricted in its exhalation phase.
Dome Exhalation Pelvic Diaphragm: Indirect Method Diagnosis The pelvic diaphragm is in a cephalad position and does not descend during inhalation. Patient Position Supine, with knee and hip flexed on the side to be treated. Physician Position Sitting by the table on the side of the pelvis to be treated. Procedure 1. With the hand closest to the patient, introduce the fingers as described above into the ischiorectal fossa. Place the other hand just below the costal margin on the same side to monitor movement of the thoracic diaphragm. 2. Ask the patient to take a deep inhalation, then exhale to the limit and hold the exhalation until forced to breathe. Repeat this procedure two or three rimes. 3. Recheck pelvic diaphragmatic tension. 4. Repeat treatment until both the thoracic and pelvic diaphragm come into phase with good amplitude (i.e., descend and ascend together).
Dome Inhalation Pelvic Diaphragm: Indirect Method Diagnosis The pelvic diaphragm is in an inferior position and does not ascend in exhalation. Patient Position Supine, with knee and hip flexed on the side to be treated. Physician Position Sitting by the table on the side of the pelvis to be treated. Procedure 1. Instruct the patient to hold his or her breath to the limit in inhalation. The pelvic diaphragm begins to ascend a moment before forced exhalation occurs. 2. The procedure may need to be repeated two or three times.
Dome Inhalation Pelvic Diaphragm: Direct Method
FIGURE 68.10. Dome pelvic diaphragm.
Diagnosis The pelvic diaphragm has descended and is restricted in moving superiorly into an inhalation position.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Patient Position Supine, with knee and hip flexed on the side to be treated. Physician Position Sitting by the table on the side of the pelvis to be treated. Procedure I . Use the same hand placements as above. 2. Ask the patient to inhale, then exhale. With exhalation, encourage the d iaphragm to move superiorly into its exhalation phase by providing fingertip pressure in a cephalic direction. 3. Maintain this position. Ask the patient to inhale. Be sure to hold ground, not allowing the pelvic diaphragm to descend. 4. As the patient exhales a second time, follow the diaphragm cephalically even more. 5. Repeat the treatment until both the thoracic and pelvic diaphragm come into phase with good amplitude (i.e., descend and ascend together). FIGURE 68.11. Pectoral traction.
TECHNIQUES TO PROMOTE LYMPHATIC FLOW
Pump Techniques Lymphatic pump techniques are techniques designed to augment the pressure gradients that develop between the thoracic and abdominal regions during normal respiratio n. Some techniques are rhythmic; some are continuo us. Some of the techniques influence the negative intrathoracic pressure of the thorax and some affect the abdominal pressure gradient.
Pectoral Traction Pectoral traction influences lymph flow by means of influencing the pectoralis minor muscle. By exerting a cephalic traction on the pectoralis minor, the range of motion of the first six ribs is augmented during inhalation, thereby increasing the negative pressure in the thorax, as well as the volume of the chest. It is estimated that a 1-cm increase in the diameter of the chest increases the inrake of air by 200 to 400 cc (16) . T his is an efficacious technique that can be used with relative ease for patients with brittle bones, patients in the intensive care unit where multiple rubes and monitoring dev ices may be in place, and postsurgical patients.
3 . While maintaining traction, have the patient breathe deeply. The combinatio n of traction and respiratory motion releases the upper thoracic muscle tension.
Thoracic Pump T horacic pump techniques, like pectoral traction, affect the intrathoracic pressure gradients by augmenting the thoracic range of motion and also by increasing expiratory efficacy. These techniques are indicated as initial treatments for clearing the thoracic duct region and are also especially effective for patients with chronic obstructive pulmonary disease (COPD), upper and lower respiratory infections, mastitis, or swollen upper extremities, and for postsurgical reduction of respiratory volume. Preliminary studies and a long history of clinical efficacy suggest that lymphatic pump techniques enhance immune function (17). Contraindications to these (and rib raising) techniques include: 1. Thoracic cage bony derangements: fractures, dislocations, and osteoporosis (relative contraindication). 2. Malignancy of the lymphatic system . 3. Use caution in patients with a decreased cough reflex.
Patient Position Supine.
Repetitive (Classic) Thoracic Pump
Physician Position Stand ing at the head of the patient.
Patient Position Supine. Caution: be sure that the patient does not have any food, gum, or foreign body (loose dentures, etc.) in the mouth.
Procedure I. Gently grasp the inferior border of the pectoralis muscles of each anterior axilla in a meat hook fashion, taking care not to gouge with the fingertips (Fig. 68.1 1). 2. With your arms fully extended, apply a bilateral cephalad traction. (Lean back, using your body to produce the traction.)
Physician Position Standing at the head of the table. Procedure 1. Place your hands o n the patient's thoracic wall with the thenar eminence of each hand over the pectoralis muscles, just distal
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Abdominal and Pedal Pumps The abdominal and pedal pumps work by intermittently pushing the abdominal contents up against the diaphragm, therefore indirectly affecting intrathoracic/abdominal pressure gradients. These techniques also indirectly massage the thoracic duct at its origin in the cisterna chyli.
Indications 1. Congestive heart fai lure (CHF) 2. Infective processes (in these patients, it may increase immune competence) 3. Upper respiratory tract infection, asthma, and COPD 4. Restricted mobiliry of the lumbar spine and thoracic cage FIGURE 68.12.
Thoracic pump.
to the respective clavicle; fingers are spread and angled toward the sides of the patient's body. The heels of the hands are on ribs 2 through 4 (Fig. 68.12). (With females it is important not to apply heavy pressure to the breast, but gentle pressure can assist in lymphatic drainage of congested breasts.) 2. A rhythmic pumping action is induced by alternating pressure and release through the physician's hands at a rate of approximately 110 to 120 times/minute. The motion is generated through a slight extension/flexion of the elbows, with forearm, wrist, and hand acting as a fixed lever. 3. The rate of pumping action should be in sync with the natural response of the patient's body tissues; during this rhythmic treatment, the patient continues to breathe as usual.
Thoracic Pump Variation of Activation Patient Position Supine. Be sure that the patient does not have any food, gum, or foreign body (loose dentures, etc.) in the mouth. Physician Position Standing at the head of the table. Procedure 1. Position hands the same as in the first step of the classic pump technique. 2. Have the patient breathe in deeply with the mouth open. As the patient exhales, and with your elbows straight, follow the exhalation motion downward and maintain the end point. This applies a compressive force. With each subsequent breath, follow the exhalation motion downward, increasing the intrathoracic pressure with each exhalation. 3. One-third of the way through the fourth or fifth inhalation, as the patient's inhalation is creating a negative intrathoracic pressure within the thoracic caviry, briskly remove your hands. This will suddenly release the pressure from the chest, and you will hear suction or vacuum release as air rushes into the lungs. 4. The rate of pumping action should be in sync with the natural response of the patient's body tissues.
5. Hiatal hernia 6. Upper and lower GI dysfunction • Contraindications 1. Thoracic cage mechanical derangements : fracture, dislocation 2. Traumatic disruption ofliver, spleen, or adjacent organs 3. Recent surgery to gallbladder or other adjacent organs 4. A full stomach (postprandial)
Abdominal Pump Patient Position Supine. Physician Position Standing or kneeling at patient's side (on table). Procedure 1. Place your palms on the patient's abdomen with your fin gers pointing to the patient's head, thumbs side by side (Fig. 68.13). (For small patients, or for greater control, you may place your hands on top of one another.) 2. Keep your arms extended and elbows locked. 3. Pump in a rhythmic manner. (The pumping motion is simi lar to the pedal or thoracic pump.) The rate shou ld be 20 to 30 times/minute.
Pedal Pump (Dalrymple Pump) Patient Position Supine (or prone). Physician Position Standing at the patient's feet. Procedure 1. Grasp the patient's feet and dorsiflex (Fig. 68 .1 4). 2. Introduce a force that hyperdorsiflexes the feet. Co ntinue the force along the longitudinal axis of the body. The force should send a wave of motion cephalad, which is followed by a
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 68.15. Pedal pump: plantarflexion.
FIGURE 68.13. Abdominal pump.
rebound wave moving caudally. (Note: Use the umbilicus, an osseous landmark, or a dermal lesion to appreciate the wave motion.) 3. As the rebound wave returns to the feet, reapply the dorsiflexion force, thereby creating an oscillatory pump. 4. The above technique may also be combined with the application of force through the plantar flexed feet (Fig. 68.15), thereby stretching the anterior body wall fascial structures.
infection . The proximity of these organs to the diaphragm and their pressure-sensitive nature suggest that this attribute may be important in the homeostatic functional mechanisms associated with these structures. Although other lymphatic pump techniques and diaphragm techniques indirectly or secondarily enhance pressure gradients affecting the liver and spleen, these pumps have long been available in the osteopathic arman1entarium and are specifically designed for the liver and spleen.
Indications 1. Passive congestion of liver or spleen 2. Congestive heart failure (especially right-sided failure)
Liver and Spleen Pump Techniques
3. Consider in patients with infective processes (may increase immune competence)
Both the liver and spleen are pressure-sensitive organs in the sense that they respond quickly to intermittently changing pressure gradients. The liver has a rich bed of lymphatic vessels, and irs decongestion is postulated to aid in detoxification and in relief of visceral congestion (17). The spleen stores red and white blood cells and screens the blood of damaged cells; the spleen pump is most commonly used for patients with systemic infections and for selected anemic patients with low resistance to
4. Consider in patients with parenchymal disease of liver or spleen (may affect disease process by modulating blood and lymph fluid dynamics)
Contraindications 1. Thoracic cage mechanical derangements: fracwre, dislocation 2. Lymphatic system malignancy 3. Traumatic disruption of liver, spleen, or adjacent o rgans 4. Acute hepatitis 5. Friable hepatomegaly, as in infectious mononucleosis
Lymphatic Drainage of the Liver ("Liver Quiver")
FIGURE 68.14. Pedal pump: dorsiflexion.
Stand on the right side of the supine patient, beside the lower thorax facing the head (Fig. 68.16). Pass the left hand underneath the lower ribs and the right hand on the abdomin~l wall immediately below the costal margin . Request the patient to take a deep breath and identifY the inferior border of the liver with the tips of the fingers of the right hand. As the exhalation occurs, the fingers penetrate over the liver and underneath the thoracic cage. Again, a deep breath; this time, as the breath goes out, use a vibratory motion of the right hand on the liver. This may be
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Direct Pressure Techniques to Move Lymph Direct pressure techniques exert their influence by extrinsically increasing pressure on the lymphatic vessels. This extrinsic pressure facilitates movements of lymph inro segmemal regions of the lymphatic channel that, in turn, dilate the lymph vessel and invoke the intrinsic pressure of the lymphatic conduit via contraction of the smooth muscle within the lymph channel and the myoendothelial fibers within the lymph capillaries. This is especially effective for locally decongesting tissues. Effleurage is defined in the Glossary of Osteopathic Terminology as "light or deep stroking of the skin roward the heart from any place in the body to force fluids through lymphatic vessels." Petrissage is defined as "deep kneading or squeezing action ro express swelling." FIGURE 68.16. Liver drainage.
done three or four times; each time penerrate a little deeper imo the area underneath the costal margin in relation ro the liver.
Head Effleurage Mandibular Technique (Galbraith Technique) (4) Patient Position Supine (Fig. 68.18).
Liver/Spleen Pump An alternative technique for the liver pump is performed with the patient lying on the left side with the hips and knees flexed ro stabilize the body (Fig. 68.17). Sit on the table behind the thorax, facing the patiem's feet. Ask the patient ro place his or her right hand on the back of your right shoulder. Place both your hands on the lower thoracic cage, the left hand anteriorly, the right posteriorly, and the thumbs meeting in the axillary line. As you lean slightly backward, open up the rib cage while increasing abduction on the arm, and ask the patient ro take a deep breath. As the patient exhales, lean on the thoracic cage with a vibrarory motion ro apply the pumping action ro the liver. A similar technique can be used for the splenic area with the patient lying on the right side while you sit behind the patient on the left side of the table.
FIGURE 68.17. Liver drainage: alternative method.
Physician Position Standing beside the patient. Procedure 1. Rotate the patient's head to face you.
2. With your right hand, place your fingers at the temporomandibular joint and your thenar eminence along the ramus of the mandible as shown in Figure 68.18. 3. Apply a repetitive, downward traction on the mandible. Anterior and medial motion should be done slowly.
Submandibular Technique Patient Position Seated.
FIGURE 68.18. Mandibular technique: supine.
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VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
FIGURE 68.20. Cervical stroking. FIGURE 68.19. Mandibular drainage: seated.
Physician Position Standing. Procedure l. Starr at the angle of the jaw (Fig. 68.19). 2. Use the palmar aspect of the fingertips and walk your fingers medially on the inferior mandibular line until you reach the chin. 3. The fingertips make contact with the submandibular nodes using a gentle vertical karate-chop motion.
Preauricular and Postauricular Node Patient Position Seared. Physician Position Standing behind patient (may be performed in front of patient). Procedure 1. The preauricular and posrauricular nodes are situated in front of and behind the ear. 2. Spreads your fingers and contact the lateral side of the head so that the index fingers contact the posrauricular node and the third fingers contact the preauricular node. 3. Apply a rotary motion both in clockwise and counterclockwise directions over the ear.
Cervical Soft Tissue
Contraindications 1. Structural derangement, bony abnormalities, or fractures in rhe area to be treated
2. Cervical ribs 3. Malignancy
Cervical Stroking Cervical stroking is a method of stretching rhe muscle groups surrounding the cervical vertebrae.
Patient Position Supine. Physician Position Standing or seared at the head of the table. Procedure 1. Place your hands along the paravertebral muscles (Fig. 68 .20). 2. Slowly stroke these muscles in a cephalic direction, not letting the muscles slip, bur giving the muscles a good stretch.
Anterior Cervical Traction Patient Position Supine. Physician Position Standing or seared at rhe head of the patient.
Indications 1. As an initial central lymphatic treatment to be followed by peripheral lymphatic treatments
2. As an integrated treatment for an upper respiratory traer infection 3. Swollen upper extremities 4. Mastitis 5. Infections of the HEENT system
Procedure 1. Locate the anterior and posterior border of the inferior portion of the sternocleidomastoid (SCM) muscle. Place your rhumb along the anterior margin, and second through fifth digits along the posterior margin (Fig. 68.21). 2. Beginning in the lower portion of the SCM and anter.ior cervical fascia, gently lift anteriorly and laterally until you note relaxation.
68. Lymphatic System
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FIGURE 68.22. Suprahyoid and infra hyoid node technique. FIGURE 68.21. Anterior cervical traction.
Thoracic Soft Tissue 3. Move superiorly to the middle portion, and repeat again on the superior portion . This procedure may be repeated up to three times.
See Chapter 55, Articulatory Techniques, on rib raising.
Abdominal Suprahyoid and lnfrahyoid Node Technique Patient Position Prone (must allow the hyoid to fall forward off the nodes, which are located superior and inferior to the hyoid bone). Physician Position Standing. Procedure l. Place your fingers on the lateral aspect of the hyoid bone (Fig. 68.22). 2. Gently move the hyoid bone from side to side four or five times. 3. If notable restriction continues, gently position the hyoid by translating it to the soft tissue barrier and ask the patient to swallow as you maintain the resistance.
Manipulative techniques can be used in the abdominopelvic region to reduce congestion and improve circulation to the abdominal and/or pelvic viscera. Mesenteric lift techniques involve careful hand positioning to apply direct pressures in directions that take stress off of the mesenteries and/or ligaments supporting that organ. Barra! (18) describes release techniques for each abdominopelvic organ; his work is highlighted in the Foundations chapter authored by Ken Lossing. Visceroptosis, most commonly resulting from upright postural problems, is a major cause of congestion in the abdominopelvic organs. Treatment improves organ function and can decrease many functional visceral symptoms, including bloating, constipation, and pelvic or abdominal pain. Application of this principle can be seen with the following mesenteric lift techniques (17). The small intestines have an
Anterior Tracheal Technique Patient Position Seated or supine. Physician Position Standing in front of the patient. Procedure 1. Place your fingers along the lateral borders of the trachea. Move the trachea from side to side (Fig. 68.23). 2. Move lymph in the cervical region in a downward fashion toward the thorax.
FIGURE 68.23. Anterior tracheal technique .
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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Liver mesenta ry
1
Proximal end of stoma ch
_ _ _--..L
Mesentary of spleen
Umbilicus
"IJ;.?;:=:::=~'kJhi-L M esentary o f ascending colon - - --1--+-
(one inc h over, on e inc h up from unbilicus}
(this mesentary is o nly 6 inc hes long}
Proxima I duodenum
JJ+-1-+- +-- Pro ximal
M esentary of small intest ines
jejunum Dece nding )
co lon
Sigmoid colon FIGURE 68.24. Mesenteric atta chments. (Illustration byW. A. Kuchera.)
A
interesting anato mic relatio nshi p to its mesentery (Fig. 68 .24). T he small intestin es hang fro m a 6-in ch mesenteri c attachment located under a line fro m a po int approxim ately 1 inch to the left and 1 inch above the umbili cus to the lower right quadrant of the abdo men just anterio r to the right sacro iliac joint and the cecum .
Mesenteric Lift: Small Intestines Patient Position Supin e. Physician Position At the patient's right side. Procedure I . To relax the abdo men, bend th e patient's kn ees with his o r her Feet pl aced o n the table o r bed. 2. Ge ntl y apply yo ur fin ge rs From the middle interphalangeal joints to the fin ge r pads in to the left lower quadrant of th e abdo men. 3. Ge ntl y scoop the abdo minal wall and underlying loops of small intestin e towa rd th eir mesenteric attachment (Fig. 68.25). Do not Fo rce tissues o r cause pain. 4 . It is often helpful to ge ntly turn the tissues in slight clockwise o r counterclockwise directio ns fo r maximal tiss ue freedo m. 5. H o ld the tissues until a sense of relaxation is palpated, or hold fo r approxim ately 90 seconds to all ow rim e fo r visceral tissues to decongest.
FIGURE 68.25. A: Direction for tissue treatment of intestinal mesen teries . (Illustration by W. A. Kuchera .) B: Mesenteric lift: small intestine.
Procedure 1. To relax the abdomen, bend the patient's ri ght kn ee with that foot placed on the tabl e or bed. 2. Gently apply the heel of yo ur right hand to the inferior portion of the ri ght lower quadrant of the abdo men. 3 . Ge ntl y lift the cecum superi orl y away fro m any pelvic entrapment by pushing towa rd the hepatic fl exure of the colon (Fig. 68 .26). 4. Hold the tissues until a sense of relaxa tio n is palpated, o r hold fo r approximately 90 seconds to allow time for visceral tissues to decongest.
Petrissage with Cough Activation: Abdominal Scars Mesenteric Lift: Cecum Patient Position Supin e. Physician Position At the pati ent's ri ght side.
T hroughout the body, petrissage and deep fri ctio n soft tissue techniques can also be used to break down co nnecti ve tissue impediments to lymph ati c drainage and free move ment berween adjacent fasc iae (Fig. 68.27). In the case of an abdom inal scar where superficial tissue restricts complete motion between the region of the scar and deeper fascial laye rs, th e fasc iae associated
68. Lymphatic System
FIGURE 68.26. Mesenteric lift: cecum.
with the scar can be treated with gentle petrissage and a cough activation to improve mobility in the region and to subsequently improve lymphatic Row. This technique should be used only in well-healed scars where restriction of motion between fascial layers is noted. This can be evaluated by gently attempting to move the scar in various directions on the abdomen and either sensing restriction or observing fascial dimpling/retraction adjacent to the scar at the end of motion testing.
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FIGURE 68.28. Abdominal scar: treatment.
4. Ask the patient to cough deeply enough to feel the deeper fascia of the abdominal wall pull into the scar that you are holding, but not so deep that you cause discomfort. 5. Recheck and repeat in any other direction where restriction is palpated. 6. This technique can be taught to the patient to perform at home.
Extremities Patient Position Supine. Physician Position At the patient's side. Procedure 1. Gently grasp the abdominal scar between the thumb(s) and fingers. Include some of the nearby adjacent superficial tissue. 2. Lift the scar and superficial tissues perpendicularly away from the abdomen to tissue tension (Fig. 68.28). 3. Now take the scar and superficial tissues in the direction of restricted motion to tissue tension.
Indications 1. Edema 2. Infection 3. Lymphatic stripping (especially postmastectomy)
Contraindications 1. Fracture 2. Friable skin or stasis ulcers (for example, from diabetes) 3. Malignancy
Posterior Axillary Fold Technique This technique is related to ipsilateral upper extremity congestion.
Diagnosis Thick, tender, and congested right axillary fold. Patient Position Supine. Physician Position Seated at the right side of the patient facing the patient's head.
FIGURE 68.27. Abdominal scar: identification.
Procedure 1. Place the extended fingers of your right hand high up under the posterior surface of the posterior axillary fold with the index finger next to the patient's chest cage. Place your right
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 68.29. Posterior axillary fold technique.
thumb over the axillary fold high in the axillary cavity and also next to the patient's chest wall (Fig. 68 .29). 2. Bring the thumb and fingers toward each other along their longitudinal surfaces chest wall, creating tension between the extended thumb and fingers. The fingers of your right hand can be strengthened by the fingers of your left hand. 3. Hold the compression until the tissues relax. 4. Move the grip inferiorly to a new area and repeat the inhibition if signs of congestion are found. Continue caudally until the border of the latissimus muscle disappears over the back as it progresses medially toward the spine.
FIGURE 68.30. Effleurage and petrissage: upper extremity.
Effleurage and Petrissage: Lower Extremity Diagnosis Signs and symptoms of a congested right lower extremity. Patient Position Supine; the right knee is flexed to a right angle; the lower leg is horizontal, parallel with the table; the thigh is flexed at a right angle with the body. Physician Position Seated on the table facing the patient's head.
Effleurage and Petrissage: Upper Extremity Diagnosis Signs and symptoms of a congested right upper extremity. Patient Position Supine. Physician Position Seated at the right side of the patient facing the patient's head. Procedure 1. Tuck the patient's right hand into your right axilla and hold it there. 2. Grasp the upper arm close to the shoulder, and with a hand on either side of the limb, apply a wringing motion, moving from proximal to distal (Fig. 68.30). 3. When the second step is completed, start closer to the elbow with the wringing motion, and again move distally. 4 . Continue this process of lymphatic movement an additional three or four times or until adequate drainage has been achieved in the arm. 5. When step four is completed, go to the forearm, placing your thumbs on the ventral surface between the flexor and extensor muscle masses and the rest of your digits around the other side. Squeeze the muscle masses simultaneously, and then relax. 6. Repeat this process again, moving from proximal to digital.
Procedure l. Balance the patient's right leg on your shoulder. 2. Place the palmar surface of both hands on opposing sides of the proximal end of the thigh, and perform a rotatory wringingout type of movement in a clockwise direction. 3. As tissue change takes place, move distally down the thigh toward the knee, one hand's width at a time. 4. Repeat the sequence of motions, going back again to the inguinal area and progressively moving toward the knee. 5. When the tissues have softened and there is less congestion in the thigh, move below the knee. 6. Place the hand on either side of the lower leg; with the thumbs, press deeply between and into the calf muscles, squeezing out the muscles, progressing down from the knee toward the ankle. 7. During each squeezing motion, rock your body forward and backward using your body weight to flex and extend the knee and hip in a rhythmic fashion.
Effleurage: Arms and Legs Effleurage is the stroking of appendages from distal to proximal. This faci litates the flow oflymph to the axilla and the thorax from the upper limb and facilitates the flow oflymph to the abdomen from the lower limb.
68. Lymphatic System
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FIGURE 68.32. Petrissage: lower extremity.
REFERENCES FIGURE 68.31. Effleurage: lower extremity.
Patient Position Supine. Physician Position At the patient's side. Procedure With effleurage, you stroke the appendages from distal to proximal (Fig. 68.31) using a milking motion. Petrissage: Arms and Legs
Petrissage is a method of draining lymph from the extremities into the thoracic duct.
Patient Position Supine. Physician Position At the patient's side. Procedure Knead the extremity, starting distally (Fig. 68.32) and proceeding toward the trunk.
CONCLUSION Because lymphatic function can be critically influenced and altered by exrrinsic forces, osteopathic diagnosis, and manipulative rreatment, use of the techniques outlined in this chapter can greatly influence lymphatic function.
I . Still AT. Philosophy of Osteopathy. Kirksville, MO: A. T. Still; 1809: I 08. 2. Millard FP. Applied Anatomy of the Lymphatics. Kirksville, MO: Th e Journal Printing Company; 1922. 3. Miller CE. The lymphatic pump, its appl ication to acute infections. JAm Osteopath Assoc. 1926;25:443-445. 4. Pratt-Harrington D. Galbreath technique: a manipulative treatment for otitis media revisited. JAm Osteopath Assoc. 2000; 100:635- 639. 5. Gangong WF. Review of Medical Physiology, 14th ed. Los Altos, C A: Lange Medical Physiology; 1989. 6. Mein EA, Richards DG, McMillin DL, et al. Physiologic regulation through manual therapy. Phys Med Rehabil: State of the Art Rev. 2000; 14(1):27-42. 7. Williams PL, Warwick R, Dyson M, et al. Gray's Anatomy, 37 th ed. Edinburgh, Scotland: Churchill Livingstone; 1989:841. 8. Sodeman Jr WA, Sodeman TM . Protective mechanism of the lungs; pulmonary disease; pleural disease. Pathologic Physiology: Mechanism of Disease, 6th ed. Philadelphia, PA: WB Saunders; 1979. 9. Guyton A. Textbook ofMedical Physiology. Philadelphia, PA: WB Saunders; 1976. I 0. Woodburne R. Essentials of Human Anatomy, 8th ed. New York, NY: Oxford University Press; 1988. 11. Olszewski WL, Engeset A. Intrinsic contractility of leg lymphatics in man: preliminary communication. Lymphology. 1979; 12:81 - 84 . 12. McPartland JM, Mein EA. Entrainm ent and the cranial rhythmic impulse. Altern Ther Health Med. 1997;3:40-44. 13. Huizinga JD, Thuneberg L, Kluppel M , et al. WIkit gene required for interstitial cells of Cajal and for intestinal pacemaker activity. Nature. 1995;373:347-349. 14. Masumoto K, Su ita S, Nada 0, eta!. Abnormalities of enteric neurons, intestinal pacemaker cells, and smooth muscle in human intestinal atresia. J Pediatr Surg. 1999;34: 1463- 1468. 15. Zink G, Lawson WB . An osteopathic structural examination and functional interpretation of the soma. Osteopath Ann. 1979;7: 12- 19, 433440. 16. Kuchera ML, Kuchera WA. Considerations in Systemic Dysfimction. Columbus, OH: Greyden Press; 1994:43 . 17. Measel) r JW. The effect of the lymphatic pump on the immune respon se: preliminary studies on the antibody response to pneumonococcal polysaccharide assayed by bacterial agglutination and passive hemagglutination. JAm Osteopath Assoc. 1982;82(1 ):22, 28- 31, 59- 62, 89, 219. 18. Barra! J P, Mercier P. Visceral Manipulation. Seattle, WA: Eastland Press; 1988.
VISCERAL MANIPULATION KENNETH LOSSING
THEORY
KEY CONCEPTS • • • • •
History of visceral technique Theory of visceral technique Mobility, motility Visceral diagnosis Treatment of thorax, abdomen, and pelvis
A visceral dysfunction is impaired or altered function of related components of the visceral system, including the ligaments, fascia, lymph atic and vascular channels, neural connections, and the skeletal system. Visceral dysfunctions may be associated with local symptoms (e.g., gastroesophageal reflux disease or stress inco ntinence), distant symptoms (shoulder pain from gallbladder disease), or with presympromaric strain patterns.
HISTORY Osteopathic manipulation of the viscera began with Dr. A.T. Still. H e described treating many different digestive, respiratory, and urogenital complaints (1). For Dr. Still, almost all medical conditions had an osteopathic treatment, in some cases curative, in some cases supportive. Dr. Still left few descriptions of techniques of any kind, but some of his early students, Carl McConnell (2) and E. Barber (3) did. Gaddis (4), Teal (5), Smith (6), Woodhall (7), Hover (8-10), Young (11,12), Hazzard (13), Riggs (14), Murray (15), Goetz (16), and Sutherland (17) later added to this literature. Hoover called it ventral technique, and addressed only the abdomen. Sutherland had techniques for both the pelvis and rhe abdomen. Woodhall's applications were gynecologic. As the case with all clinical sciences, with time and clinical experience the knowledge base increases. The current knowledge base has expanded to include all the organs of thorax, abdomen, and pelvis. Most medical conditions and musculoskeletal pains are found to have a component that is addressable with osteopathic techniques. Other current authors and ed ucators in visceral technique are Bensky (18), Barral (1924), Lossing (25), Finer and Willame (26), Davidson (27), and Blackman (28).
Visceral manipulation applies osteopathic theory and principles to the viscera, in addition to the musculoskeletal and the cran ial systems. In all cases, the theory and principles remain the same; only the area of anatomy changes. The implication , of course, is that by also addressing the viscera, the osteopathic physician is able to address a larger range of medical problems. While structural problems (like tumors) are relatively easy to document on standard medical rests, functional problems (like sustained abnormal mechanical tension) are less easy to document, bur are palpable. Sustained abnormal mechanical tension in the tissues adversely affects the exchange of fluids and nutrition, overstimulates the nervous system leading to facilitation, decreases the exchange of pressures, and taxes the homeostatic mechanisms of the body. Conversely, treating the sustained abnormal mechanical tension improves neurologic exchange, improves homeostatic mechanisms, and improves exchange of fluids, nutrition, and pressures. In the case of viscera, the main tissue addressed is the attachments (ligaments, peritoneum, pleura, and mediasrin urn) . For many years osteopathic literature has expres~ed the principle that one part of the body may affect another part, and indeed the whole body. Our neurologic model describes somarosomatic reflexes, somarovisceral reflexes, viscerosomatic reflexes, and viscerovisceral reflexes (29). Traditional osteopathic thought has always contained the idea that the intelligent physician should try to find the most primary problem, address that, and allow the body to do the rest of the job. This being the case, when the viscera are the primary problem, they should be addressed first. Visceral diagnosis follows Dr. Still's adage that "life is motion." With each inhalation the rib cage raises, while the respiratory diaphragm, thoracic inlet, pelvic floor, and all of the viscera descend. As measured by magnetic resonance imaging (MRI) scan, the respiratory diaphragm and inferior pericardium descend by 1.5 em with a normal volume inhalation (in approximate-vital-capacity breathing, diaphragmatic excursion increases to over 4 em), with the inferior pericardium swinging toward the middle line (30). The superior pericardium moves much less, giving an axis of rotation near the attachment of the aorta to the heart. Obviously, this area needs to be stable. Along with rhe mechanical displacement of these structures there is a corresponding change in the exchange of fluids . With
69. Visceral Manipulation inhalation, the flow of blood in the superior vena cava increases and the flow of blood in the portal vein decreases. Respiration-induced motions of the abdominal visceral are well documented (32-34). During respiration the diaphragm and abdomin al organs move cephalocaudal (more so laterally than near the midline), and anterior/posterior, as measured by MRI (31). An osteopathic perspective is that abnormal mechanical tension in these structures decreases their respiratory motion and adversely affects their function. Preliminary work has been done measuring the respiratory movements of the abdominal organs in symptom-free and symptom-present states, showing normal and abnormal axis of motion (26). The viscera are found to move, and have potential restrictions, in the same three planes of motion described for all joints and sutures.
VISCERAL DIAGNOSIS Palpatory diagnosis shou ld be performed both globally (to find the total body pattern), and locally. Appropriate medical tests should be ordered when indicated. Each organ can be evaluated for motion, like all cranial and musculoskeletal structures, with: 1. Inhalation and exhalation (described as mobiliry by Sutherland). 2. Motion testing the attachments (see Chapter 39) 3. Sympathetic and parasympathetic connections (viscerosomatic and somatovisceral reflexes; see Chapter 6) 4. Exchange of fluids (lymphatic; see Chapter 68) 5. Inherent motion (described as motiliry by Sutherland) 6. Temperature changes 7. Associated musculoskeletal structures (rib cage, attachments through the posterior peritoneum to the anterior longitudinal ligament and spine, etc.) 8. Associated cranial structures (e.g., the esophagus attaches to the temporals, occiput, and sphenoid by the pharyngeal constrictor muscles; see Chapter 62) 9. Chapman reflexes (see Chapter 67)
As with all osteopathic diagnosis, the general area of the body in trouble needs to be found. One diagnostic technique (general listening) uses a fascial continuiry model (see Chapter 60). Bones, muscles, blood vessels, and viscera are seen as tissues stuffed in a three-dimensional covering, the fascia. The fascia is tighter in an area of abnormal mechanical tension, and pulls into that location. With the patienr's body in the standing anatomical position, the physician's hand is placed on the top of the head to feel which direction the fascia pulls. In general, an anterior pull can be from a visceral restriction, anterior rib, or sternal problem. A posterior pull indicates a spinal or dural problem. A lateral pull indicates a problem in the extremities, or the paired bilateral viscera. Once the general area has been determined, specific localization of the restriction can be found using palpation of tissue pull in the local area (local listening). At that poinr, a thorough knowledge of anatomy becomes paramount. In the case of suspected visceral restrictions, the specific organ is palpated and evaluated
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for motion during respiration, it is named for the direction in which it moves the easiest. Next, motion testing is performed to evaluate the distensibiliry of all the attachments. Inherent motion (similar, but distinctly different from the cranial rhythmic impulse) is evaluated by palpating the viscera with a hand on its longitudinal axis. The active phase (inspir) is away from the middle line, the passive phase (expir) is toward the middle line. Palpation of the specific spinal segments of sympathetic innervation will reveal any tissue texture changes (29). Areas of parasympathetic innervation, and other mechanically associated structures are also examined for tissue texture changes. A simple test is then performed to find which of the structures is most primary by palpating two related structures and gently pressing on one to inhibit it, and see if the other responds immediately with decreased fascial tension. If this occurs, the structure is selected as the one to treat. This test is used to determine whether the problem is viscerosomatic, somatovisceral , or viscerovisceral.
TREATMENT For a visceral problem resulting from a somatovisceral reflex, the somatic structure responsible is treated. If a visceral or somatic problem is caused from a viscerosomatic reflex, the viscera are treated. In the case of viscerovisceral reflex causing a visceral problem, both involved viscera are treated. Once the area of the most primary problem is found, it may be addressed by a wide variery of principles and techniques, including short lever arm (direct contact), long lever arm (using a body part as a lever) , indirect (in the direction of ease), and direct techniques (in the direction of tension), and various activating forces like respiratory assistance. The goal of treatment is achieving a state of balanced ligamentous tension, normal movement with respiration, balanced inherent motion, and normalization of the nervous system, along with fluid, nutrition, and pressure exchange.
ABDOMEN The Lower Esophagus, Stomach, and Duodenum The lower esophagus, stomach, and duodenum should be checked in cases of gastroesophageal reflux disease, gastritis, duodenitis, ulcers, hiatal hernia, and gastric ptosis.
Stoma ch Dia gnosis (Fig . 69.1) Step 1. The patient is supine. The physician stands to the right side. Step 2. Place your right hand over the stomach, and point your thumb to the pylorus. Step 3. Palpate through the skin and abdominal wall to the abdominal contents. Step 4. Check the fascial pull, is it toward the gastroesophageal junction, gastrophrenic ligament, gastrosplen ic ligament, the left kidney, splenic flexure, greater omentum , or lesser omentum?
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 69.1.
Step 5. Have the patient take a deep breath. Does the stomach descend with inhalation and ascend with exhalation? Step 6. Palpate motility. Inspir is counterclockwise, superior, and posterior. Expir is clockwise, inferior, and anterior.
Sutherland Technique for Stomach (Fig. 69.2) The 12th rib attaches through the lateral arcuate ligament to the diaphragm, and provides access to the area of the diaphragm around the esophagus. Test Right hand on 12th rib, left under the right. Right hand monitors only, left hand provides the traction. Engage rib and traction laterally, feeling for tension.
FIGURE 69.3.
Still Stomach Technique (Fig. 69.3) This technique addresses the upper stomach and lower esophagus. Test Step 1. The patient is in a right lateral recumbent position. The physician stands behind.
Step 2. Use both hands on the stomach, your fingers are flat. Pull the stomach inferior and lateral to the left. Appreciate any tension. Treatment Maintain the tension on the stomach and slightly lean backward, until the tension releases and you are able to feel up through the esophagus.
Duodenal Diagnosis (Fig. 69.4) Treatment Maintain traction until the rib releases and you can feel the area of the diaphragm.
Step 1. The patient is supine. The physician stands on the right with the right hand over the transverse section of the duodenum.
FIGURE 69.2.
FIGURE 69.4.
69. Visceral Manipulation
FIGURE 69 .5.
Step 2. Palpate through the skin and abdominal wall until you reach che tissues in the abdomen. Seep 3. C heck the direction of fascial pull, and think of what attachments might be in that direction. Seep 4. Check movements with respiration (should descend wich inhalation, asce nd with exhalation). Step 5. Palpate motility. In inspir, the duodenum opens, and in exp ir it closes.
Duodenal Manipulation (Fig. 69.5) Step 1. T he patient is in the lefc lateral recumbent position. The physician stands behind the patient. Step 2. Palpate with the fingers to the lefc of the ascending portion of the duodenum and the attachment of the muscle ofTreitz. Step 3. Draw both hands toward the patient's right side, and spread your han ds inferiorly and superiorly. To treat the descending and transverse portions, the patient lies on the right, your hands are lateral and draw medially and superior/inferior.
FIGURE 69.6.
Root of Mesentery Manipulation (Fig. 69. 7) Step 1. The patient is supine, knees bent. The physician stands to the right, near the lower thorax, with the fingers below che root, the thumbs above. Step 2. Gently palpate deeper, until you feel the tension of che root. Step 3. Motion test the superior part inferiorly, and che inferior part superiorly. Step 4. Treat by taking the tissue to tension , chen relax and see what speed the tissues come back. Use that speed to rhythmically engage and disengage the tension. When it releases, there will be no more tension.
Small Intestine Motility (Fig. 69.8) Step 1. The patient is supine. The physician stands to che right. The right is hand over the patient's right side of the small intestine, the left hand is over the left small intestine. In inspir,
THE SMALL INTESTINE The jejunoileum should be evaluated in cases of intestinal ptosis, stress urinary incontinence, abnormal stool production, diverticulosis, ulcerative colitis, Crohn disease, asthma, and allergies.
Root of Mesentery Diagnosis (Fig. 69.6) Seep 1. T he patient is supine. The physician stands to the right, the base of the right hand is placed over the area of the root of che mesentery. Step 2. Palpate through the abdominal wall to the abdominal contents. Step 3. Pal pace the direction offascial pull. If chere is no abnormal tension, you will not feel any fascial pull. If there is a fascial pull, is it in the direction of the ileocecal valve, duodenaljejunal junction, inferior, or superior?
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FIGURE 69.7.
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VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Step 2. Palpate to the abdominal contents. Step 3. Test by palpating fascial pull. Step 4. Test motion superior, inferior, medial, and lateral. Step 5. Palpate motility. lnspir is a counterclockwise inferior movement. Expir is clockwise and superior.
Treatment Step 1. Take to the direct barrier, relax, and let the tissues come back, noting their speed. Step 2. Assume that rhythm, taking the tissues to the barrier and coming back until there is no tension left. Step 3. Treat the motility by gently encouraging the motion that is better.
FIGURE 69.8.
Transverse Colon and Flexures (Fig. 69.10)
Test the small intestine rotates counterclockwise, in expir the small intestine rotates clockwise. Step 2. Diagnose the movement. Step 3. Slightly encourage the better motion until it is even.
THE COLON The colon should be evaluated in cases of constipation, diarrhea, intestinal prolapse and ptosis, diverticulosis, history of appendectomy, irritable bowel, ulcerative colitis, Crohn disease, hemorrhoids, or anorectal pain.
Cecum and Ascending Colon (Fig. 69.9)
Step 1. The patient is sitting. The physician stands behind, with the fingers placed on the area of the hepatic flexure. Step 2. Draw the ascending colon superior, and spread your fingers medially and laterally. Step 3. Repeat on the left side for the splenic flexure. Step 4. Then, with one hand on each, lift the fl exures and the transverse colon superiorly.
Root of Sigmoid (Fig. 69.11) The root of the sigmoid is a thickening of the peritoneum, extending from the sigmoid to the area of the bifurcation of the iliac vessels. The mechanical tension extends further to the area of the duodenal-jejunal junction.
Test Test
Step l.The patient is supine with their knees bent. The physician stands to the right, with the right hand over the area of the cecUJn.
Step 1. The patient is supine. Place your fingers above, and thumbs below this line.
FIGURE 69 .9.
FIGURE 69.10.
69. Visceral Manipulation
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FIGURE 69.13.
FIGURE 69.11.
Treatment Step 2. Move the mesocolon superior-lateral and inferior-medial, checking for tension.
Treatment
Step 1. Take the tissues first in the direction they will go (the direction oflistening), sl ightly exaggerating the direction until you perceive a release. Step 2. Then take the tissues in the djrection they will not go. Mainrllin the barrier and use respiratory assistance.
Engage the tension, and let the tissue come back, noting the speed the tissue responds. Conrinue this rhythm until the tissue releases, and there is no more tension.
Colon Motility (Fig. 69. 13)
Sigmoid Colon (Fig. 69.12}
Step 1. The patienr is supine. The physician stands on the right, with the right hand on the descending colon and the left hand on the ascending colon. In inspir, the colon will rotate counterclockwise, in expir it wi ll rotate clockwise. Step 2. Encourage the better motion unril it is symmetric.
Test Step 1. The patient is supine. The physician stands on the right, your right hand over the area of the sigmoid. Step 2. Palpate the direction of fascial pull. Step 3. Test motion superior-medially and inferior-laterally.
LIVER The liver should be evaluated in cases of chronic hepatitis, right shoulder pllin, depression, chron ic excessive alcohol inrake, cholelithiasis, hormonal imbalances, and cirrhosis.
"Frozen" Liver (Fig. 69.14}
Test Step 1. The patient is supine. The physician stands on the right. Use both hands and engage the liver through the ribs. Step 2. Translate the liver to the left, noting if there is any resistance to movement.
Treatment Step 1. Take the liver to tension, taking up the slack through a few exhalations.
FIGURE 69.12.
Step 2. At the beginning of an inhalation , quickly release your hands. Repeat up to three times as needed. This wiU free up the bare area of the liver from the diaphragm, which may
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 69.14.
be stuck due to metabolic problems, inflammation, or old infections.
Liver and Gallbladder Diagnosis (Fig. 69. 15) Step I . T he patient is supine. The physician stands on the right and places the right hand slightly to the right of midline. Step 2. Compress through the abdominal wall until you feel the abdominal contents. Step 3. Check the direction of fascial pull. Does the tissue pull in the direction of the liver, gallbladder, duodenum , pancreas, right kidney, or the colon ? Step 4. Test the structure yo u believe to be dysfunctional with fascial pull and motion resting.
Liver, Sagittal Plane {Fig. 69.16) Test Step 1. T he patient is in the left lateral recumbent position . The physician stands behind and near the pelvis.
FIGURE 69.16.
Step 2. The right hand engages the liver anteriorly, the left hand is over the lower ribs. Compress the hands slightly to feel the liver. Step 3. Move the anterior liver inferior and the posterior liver superior, then reverse, noting restrictions in either direction.
Treatment Take the liver to tension and rake up the slack during the phase of respiration where there is some. Maintain the tension through a few phases of respiration, until it releases.
Liver, Transverse Plane {Fig. 69.17) Test Step 1. The patient is in a left lateral recumbent position. The physician stands behind the area of the liver. Both hands are used. Step 2. Bring the area of the liver anterior and toward the midline, then posterior and laterally, noting any restriction to movement.
Treatment Take the liver to tension, see which phase of respiration gives a little slack, and rake out the slack. Repeat this procedure until there is no more resistance.
Liver, Frontal Plane {Fig. 69.18) Test
FIGURE 69.15.
Step 1. The patient is in the left lateral recumbent position. T he physician stands behind rhe thoracic area. Both hands are used on the lateral area of the liver. Step 2. Bring the lateral portion of the liver inferior and medially, then laterally and superior, noting any direction of resistance.
69. Visceral Manipulation
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FIGURE 69.17. FIGURE 69.19.
Treatment Take the liver to tension, noting the phase of respiration where chere is some slack. Take up the slack. Repeat this until there is no more resistance.
Liver Lift (Fig. 69.19)
Test Step 1. The patient is seated. The physician stands behind. The inferior border of the liver is palpated with both hands. Step 2. Lift the liver, noting any resistance to distension, then let the liver drop, noting the speed and how well it drops. Lifting the liver tests the inferior attachments, dropping the liver tests the superior attachments. Step 3. Test the right side (for colon, kidney, and right triangular ligament). Step 4. Test the middle (for duodenum , lesser omentum, coronary ligament).
Step 5. Test the left side (stomach, descending colon, left triangular ligament).
Treatment Take the area and direction of the greatest resistance to tension. Take up the slack with the phase of respiration where it is available and maintain it through a few phases of respiration until there is no more resistance. If the tension is in the superior attachments, lift the liver and let it drop a few times until it drops easier.
GALLBLADDER The gallbladder should be evaluated in cases of cholestasis, cholecystitis, left-sided neck pain, chronic sinusitis, and postcholecystectomy chronic abdominal pain.
Gallbladder (Fig. 69.20) First treat the sphincter of Oddi, described later.
Test Step 1. The patient is sitting. The physician stands behind. Bring the fingers under the liver to the area of the fundus of the gallbladder. The right fingers are placed to the right of the gallbladder, the left fingers to the left. Step 2. Test the distensibility of the tissues medially and laterally, noting resistance.
Treatment
FIGURE 69.18.
Step 1. Take the tissue to the direction of ease until it softens. Step 2. Then take the tissues in the direction of tension, until it softens. Step 3. Press on the fundus, making a sweeping motion in the direction of the cystic duct and common bile duct until yo u meet resistance. Repeat up to ten sweeping motions until the gallbladder feels empty.
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VI!. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 69 .22. FIGURE 69 .20 .
Common Bile Duct (Fig. 69.21)
Test Step 1. The patient is sitting. The physician stands behind. Step 2. Use your left thumb to fix the sphincter of Oddi posteriorly and inferiorly. Step 3. Have the patient place their hands behind their neck, elbows together. Step 4. Use your right hand under the elbows to extend the body, and rotate to the right to tension. Repeat the movements until the resistance is no longer palpable.
Sphincter of Oddi (Fig. 69.22)
Test Step 1. The patient is supine. The physician stands on the righ
side, with the right thenar emmence over the area of the sphincter. Step 2. Press posteriorly until you feel a small rotational movement. Step 3. Motion test this area medially, laterally, superior, and inferiorly. Note distance of distensibility and end-feel.
Treatm ent Step 1. Take the tissue to the indirect barrier first, until yo u feel it release. Step 2. Take the tissues to the direct barrier, and hold until it releases. Step 3. When all barriers are gone, encourage the direction of the better rotation, until it normalizes . All other sphincterlike areas are treated in a similar fashion, including the gastroesophageal junction, pylorus, duodenal-jejunal junction, and the ileocecal valve.
KIDNEYS The kidneys are evaluated in cases of renal ptosis, low back pain, recurrent pyelonephritis, renal lithiasis, sciatica, and inguinal pam.
Kidney (Fig. 69.23)
Test
FIGURE 69 .21.
Step 1. The patient is supine. The physician stands on the side of the kidney that is going to be tested. Description here is for the right kidney. Step 2. With the left hand, find the space between the 12th rib and the crest of the ilium. The right hand is over the area of the kidney. Press posteriorly until you think you feel the kidney. Step 3. Lift the posterior hand anteriorly, until you can feel the anterior portion of the kidney with your anterior hand. Step 4. Palpate fascial pull.
69. VisceraL Manipulation
FIGURE 69.25.
FIGURE 69.23 .
Step 5. Motion test the kidney superior, inferior, medially, and laterally, noting any resistance to movement.
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Step 2. Lift the kidney superior while palpating above the bladder, if the ureter is tight you will feel a small pull on the bladder.
Treatment Treatment Step 1. Take the kidney in the direction it moves easiest, until you feel it release. Step 2. Then, take the kidney in the direction it does not move as easy. Take up the slack in the phase of respiration where it is available, until it releases.
Ureter {Fig . 69.24) The ureter should be evaluated in any case where there is a history of renalli thiasis.
Test Step 1. The patient is supine. The physician stands on the side of the dysfunction.
Place your finger on this area (bladder-ureter connection) and lift the kidney while maintaining tension on the area of the bladder.
SPLEEN The spleen should be evaluated in any case of impaired immunity, chronic fatigue, human immunodeficiency virus (HIV), or chronic infections. Since the spleen is not normally palpable, the attachments are evaluated by assessing the area of rhe spleen in relation to the diaphragm, pancreas, left kidney, splenic flexure of the colon, and the stomach. If the spleen is palpable, it needs to be worked up medically before any treatment is attempted (Fig. 69.25).
Test Step 1. The patient is supine. The physician stands on rhe opposite side. The right hand is behind the lower rib cage, the left hand is in the left upper quadrant of the abdomen. Compress the hands together. Step 2. Bring the area inferior, then superior, noting any resistance to distension. Step 3. Palpate fascial pull.
Treatment Take the tissue to tension and hold. During the phase of respiration that you can get some slack, take it, until you feel the tissues release.
PANCREAS
FIGURE 69 .24.
The pancreas is evaluated, very gently, in cases of chronic pancreatitis (Fig. 69.26).
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 69.27.
FIGURE 69.26.
Cervical-Pleural Ligaments (Fig. 69.28}
Test
Test
Step 1. The patient is supine. The physician stands on the right. The palm of the right hand is over the descending duodenum, fingers pointed toward the spleen. The left hand is posterior to the spine in the same area. Step 2. Compress through the abdominal wall contents.
to
the abdominal
Step 1. The patient is supine. The physician sirs near the patient's head. Step 2. Place a thumb on each dome, have the patient rake a deep inhalation. Both domes should descend, if they do not, there is a restriction .
Step 3. Palpate fascial pull. Step 4. T hen, compress a little more and rake the area inferiorly and superiorly, noting distance and end-feel of distensibility.
Treatment In the same position, rake tissue to indirect barrier until it releases using respiratory assistance.
THORAX
Treatment Step 1. On the side of the restriction (described here for the left), place your left thumb on the dome, and side bend the patient's neck to the left. Step 2. Have the patient inhale, and follow the dome inferiorly. Do not allow it to return on exhalation. Repeat until the area softens. Step 3. Then, maintaining the dome inferiorly, side bend the patient's neck to the right, stretching the fibers of the cervicalpleuralligament. '
The thorax should be evaluated in any respiratory problems (asthma, pneumonia, pleurisy, chronic bronchitis), heart problems, chronic postural problems, thoracic pain, and when the upper abdominal viscera will not descend with inhalation. Once the side of the dysfunction has been determined, more specific testing can be done to localize the structure in dysfunction.
Thoracic Diagnosis (Fig. 69.27}
Test Step 1. The patient is supine. The physician stands on the right side near the abdomen. Step 2. Place your right hand in the middle of the thorax. Step 3. Palpate the direction of the fascial pull. Is the pull toward the right or the left, toward the mediastinum, lungs, or pericardium? Step 4. Do further rests on the structures in question.
FIGURE 69.28.
69. Visceral Manipulation
FIGURE 69.29.
Parietal Pleura {Fig . 69.29)
Treatment Step 1. The patient is supine. The physician stands near the shoulder ofside of the restriction. With your right hand contact the upper cervical spine and lower cranium. Step 2. Place your left hand on the anterior-lateral lower rib cage. Step 3. Take the cervical spine in rotation and side bending to the opposite side to tension. This hand then remains stationary. Step 4. The left hand follows the ribs inferiorly with an exhalation, and maintains them inferiorly as the patient continues to breathe. Can you affo rd in treating diseases of the lungs to give your verdict and prescribe drugs or manipulations as a doctor of medicine, an osteopath, or masseur, without first carefully examining the pleura in all divisions and knowing that their blood and nerve supply are -A. T. Still (1) perfectly norm al?
Lung Fissures {Fig. 69.30)
FIGURE 69.30.
the same way, but with the patient in the left lateral recumbent position. Hand placement is on the same ribs for the obliq ue fissure, and the fingers move up to over and under the fo urth ribs anteriorly for the horizontal fissure.
·sronchi {Fig. 69.31)
Test Step 1. The patient is supine. The physician stands near the head. Palpate the upper trachea. Step 2. Traction the trachea superiorly, then to the left and the right. If there is more resistance tractioning to the right, it means the left bronchus is under more tension, and vice versa.
Treatment Step 1. While tractioning on the trachea, palpate the fasc ial pull over the area of the mainstem bronchus until you feel where it p ulls in. Check both sides.
Test Step 1. The patient is in the right lateral recumbent position. The physician stands behind the thorax. The left hand is over the fifth rib posteriorly and the seventh rib anteriorly. The right hand is over the fourth rib posteriorly and the sixth rib anteriorly. Step 2. Palpate through the ribs to the thoracic contents. Step 3. With an inhalation, follow the lung movement inferiorly. Maintain the tissue inferiorly during an exhalation phase. Translate the upper lobe relative to the lower lobe horizontally, noting direction of ease. Maintain inferiorly until it releases.
Treatm en t Remain in this position, and when at maximal tensio n, have the patient continue to breathe, taking out the slack with each exhalation, until you feel a release. The right fissures are treated in
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FIGURE 69.31 .
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VII. Osteopathic Considerations in Palpatory D iagnosis and Manip ulative Treatment
FIGURE 69 .33.
FIGURE 69.32.
Srep 2. Then, place one hand over each bronchus, and compress posteriorly ro "catch" rhe bronchus. Step 3. Tractio n rhe bronchus inferior and lateral, raking up rhe slack with respiratio n until yo u feel a release. Retest the disrensibiliry of both bronchi .
Mediastinum, Supine {Fig. 69.32) Treatment Step l. T he parienr is supine. Th e ph ysician stands on rhe side of rhe tensio n in rhe medias tinum (description here is for rhe ri ght side) . Step 2. T he left hand engages the sternum medially. Th e ri ght hand engages rhe fourth rib nea r the arricul arion with rhe sternum, and brings it laterall y. Srep 3. Take up rhe slack during rhe phase of respiration rhar the tensio n decreases . At maximum tension , quickly release your hands.
PELVIS
Bladder The bladder should be evaluated in cases of stress in continence, recurrent cys titis, bladder prolapse, and cystalgia. Stru ctures tested are the pubovesicular ligamenrs, median um bili ca l ligament, medial umbi lical liga ments, disrensibiliry of rh e obturaror membrane, obturator internus muscle, and the hips. Of course rh e pubis, pelvic fl oor muscles, sacrwn, and coccyx should also be evaluated. T he urethra, puboves icular liga ments, tr igone muscle, and the walls of rhe bladder itself may be evaluated wirh an internal examination and rreared . Intern al rreatmenr ca n be more effective than external treatment, due to better palpation and treatment access.
Bladder Diagnosis (Fig. 69.34) Step 1. T he patient is supin e. T he physician stands o n the ri ght, with the right hand just superio r ro the pubis. Step 2. Palpate the fascia for a directio n of pull . If th ere is a
Mediastinum, Seated {Fig. 69.33) Treatment Step 1. T he pati ent is seared. T he phys ician stands in fronr of rh e pari enr. The parienr fo lds their arms over each other and rests them o n the physician's chesr. Srep 2. Reach behind rhe parienr and engage rhe 12th rib bilaterall y. With an exhalation , bring the 12th rib laterall y and toward you . Step 3. Repeat unri l the 12th rib is free, then move your hand ro the 11th rib and repear. Srep 4 . Move up rhe spine unril it feels free. This will increase the distance between the superior mediastinum and its inferior attachm ents. FIGURE 69.34.
69. Visceral Manipulation
FIGURE 69.35.
problem, rhe bladder will pull just behind the pubis, in the area of rhe pubovesicular ligaments, or sometimes laterally toward the hip. Step 3. Do more specific tests in suspected dysfunctional areas.
Pubovesicular Ligaments {Fig. 69.35)
Test Step 1. T he patient is supine with knees bent. The physician stands on rhe side to be rested. Step 2. Palpate the top of the bladder, and gently press it inferiorly. Step 3. Check the opposite side and compare the distensibility.
Treatment Take the side that moves inferior better and slightly exaggerate it until it releases and comes back, then treat the other side.
Obturator Foramen {Fig. 69.36) With bladder dysfunction the obturator foramen is found to be tense, and does not distend properly.
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FIGURE 69.36.
Treatment Carry the membrane superior with exhalation, and maintain it there with inhalation. Hold until it releases. Recheck by comparing it with the other side.
CERVIX, UTERUS, FALLOPIAN TUBES, AND OVARIES This area should be evaluated in cases of prolapse, dysmenorrhea, pelvic pain, low back pain, sciatica, menopause, dyspareunia, infertility, and cervical stenosis. External examinatio n can point to the location of the largest tension, but internal examination is required to get more specific information. This area is quite amenable to osteopathic treatment, and the results are often dramatic. The easiest cases may be treated externally. Internal treatment has been found to be more precise, faster, and result in a larger percentage of improvement. Still (1), Woodhall (7), and Barra! (21) have described the internal techniques. The external examination is performed by placing your hand in the position used for diagnosing the bladder, but slightly higher. Fascial pull is also palpated over the area of the ovanes.
Cervix {Fig. 69.37)
Test Step 1. T he patient is supine with knees bent. Stand on the side to be tested. Step 2. Place your thumb posterior to the origin of the adductor longus muscle, and palpate into the obturator foramen. Step 3. Have rhe patient inhale. The membrane should descend, and with exhalation it should ascend, unless there is a problem. Step 4. Check the distensi bility of the membrane, it should move easily. W hen yo u press on it the bladder it should move to the opposite side, if not, it is restricted.
Test Step 1. The patient is supine, knees bent. The physician stands on one side, with the foot on the table. T he thigh is under the patient's calves. Step 2. Use your thumb to press posteriorly just above the pubis, until you feel the uterus, press it toward the opposite side, noting distance traveled and resistance at the end of the movement. Step 3. Then move to the opposite side and test and compare it.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 69 .39.
FIGURE 69.37 .
Treatment
Knee/Elbow Posit ion {Fig . 69.39)
Maintaining the same position, take the uterus to the indirect side first. When that releases, go to the opposite side and treat the direct barrier. T he legs are used as lever arms both to maximize yo ur palpation, and during treatment.
GENERAL TREATMENT POSITIONS
T his is a position preferred by Sti ll and McConnell (1 ,2). It also can be done with a small stool under the patient's chest. Still and McConnell used this position to "lift" the cecum, sigmoid, pelvic organs, stomach, liver, duodenum, small intestine, kidneys, and ureters. The position uses the effect of graviry to pull the viscera anteriorly, thus taking them to tension. Both hands can also be used to pull the peritoneum an teriorly, and stretch ing it.
General Lower Abdominal/Pelvic Lift {Fig . 69.38) This is one of the positions preferred by Still (1), McConnell (2), and Sutherland (17). T he patient is supine, with rhe hips and knee bent. T he fingers are flat, with area to be treated engaged. Gentl y lift rhe area superiorly until yo u hit a barrier, then let the tissue respond. Sutherland used one hand to engage the tissue, with the other hand over the first to do the lifting (1 7) . This technique can be used for pelvic organs, colon, ureters, and kidneys.
FIGURE 69.38.
REFERENCES I. Sri II AT. Research and Practice of Osteopathy. 1911. 2. McDonnell CP. Selected Writings ofCarl Philip McConnell, D.O. Squ irrel's Tai l Press, 1994. 3. Barber E. Osteopathy Complete, 1898. 4. Gaddis CJ. Bedside technique. JAOA. 1922(Jul);2l :69 J. 5. Teal CC. Palpation of rhe co lon wirh special reference ro the cecum. ]AOA. 1922(Apr);21:492. 6. Smith RK. Mechanical principl es of the human body. }AOA. 1912(Dec);12:210. 7. Woodhall P. Intrapelvic Technique, 1907. 8. H oover HY. A consideration of an osteopathic lesion of rhe whole liver and irs effects on hepatic dysfu nction. In: MO Yearbook. American Academy of Osreoparhy, 1948. 9. Hoover HY. Liver and gall bladder technique. In : MO Yearbook. American Academy of Osteopathy: 1947. 10. H oover HY. Technique for removing still lesion usually found in gal l bladder disease. In: MO Yearbook. American Academy of Osteopathy: 1950. 11. Young MD. Head's law and irs relation to the treatment of th e viscera. Osteopathic Profession. 1946(Aug). 12. Young MD. Illustration of visceral technique. In: MO Yearbook. American Academy of Osteopathy: I 948. 13. H azzard C. The Practice and Applied Therapeutics of Osteopathy. 1905. 14. Riggs W. A Manual of Osteopathic Manipulations and Treatment, I 90 I. 15. Murray C. Practice of Osteopathy: Its Practical Application to the Various Diseases of the Human Body, 6rh ed. 1925. 16. Goetz E. A Manual ofOsteopathy. 2nd ed . 1909. 17. Sutherland WG . Teachings in the Science of Osteopathy. Pordarrd, OR: Rudra Press; 1990. 18. Bensky D. Asthma. treated by visceral manipulation. MO}. 1995 (Sp ring).
69. Visceral Manipulation 19. Barra! J, Mercier P. Viscera Manipulation. Vista, CA: Eastland Press; 1988. 20. Barra I J. Visceral Manipulation fl. Vista, CA: Eastland Press; 1989. 21. Barra I J. Urogenital Manipulation. Vista , CA: Eastland Press; 1993. 22. Barra! J. The Thorax. Vista, CA: Eastland Press; 199 1. 23. Barra! J. Manual Thermal Diagnosis. Vista, CA: Eastland Press; 1996. 24. Barra I J P, Cro ibi er A. Trauma an Osteopathic Approach. Vista, CA: Eastland Press; 1999. 25. Lossing KJ. An Osteopathic Approach to Gastroesophageal Reflux Disease [res idency thesis]. Ohio Universiry, Athens, OH, 1997. 26. Finet G, C Willame C. Treating Visceral DysfUnction. Portland, OR: Sti llness Press; 2000. 27. Davidson SM Vitalize the viscera. Semi nar, Phoenix, AZ, January 12, 1992 . . 28. Blackman E. Posterior midline. Port Richmond , CA, Feb. 23-25, 200 I.
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29 . The Central Connection: Somatoviscerai/Viscerosomatic Interaction . Paper presented at the Amer ican Association of Osteopathy 1989 Imernational Symposium.
30. Fredrickson J. Simultaneous temporal resolution of cardiac and respiratory motion in MRl imaging. Radiology. 1995; 195:169- 175. 31. Gierada D. Diaphragmatic motion: fast grad ient-recall ed-echo MRJ imaging in healthy subjects. Radiology. 1995; 194:879-884. 32. Moerland M. The influence of respiration induced motion of the kidneys on the accuracy of radiotherapy treatmenr planning, a magnetic resonance imaging study. Radiother Oncol. 1994;30(2): 150-
154. 33. Dav ies S. Ultrasound quanritation of respiratory o rgan motion in th e upper abdomen . Br j Radio!. 1994;67(803):1096-1102. 34. Korin H. Respiratory kinematics of the upper abdom inal organs: a quantitative srudy. Magn Reson Med 1992;23( 1): 172-178.
TREATMENT OF SOMATIC DYSFUNCTION WITH AN OSTEOPATHIC MANIPULATIVE METHOD OF DR. ANDREW TAYLOR STILL RICHARD L. VAN BUSKIRK
Knowledge of any of the manipulative methods used by Dr. A.T. Still was severely limited for almost a century. The osteopathic profession was started to develop a cadre of practitioners who would apply Dr. Still's concepts about health and healing and utilize musculoskeletal manipulation to the benefit of patients. In spite of Dr. Still's reported mastery of musculoskeletal manipulation with attendant improvement of health, by the latter half of the 20th century no one could point to any manipulative m ethod and say with any certainty that this was the method used by Andrew Taylor Still. In fact Dr. Still seems to have intentionally prevented the preservation of his methods in favor of the preservation and advancement of rhe more general concepts underlying osteoparhy (1). The Still technique was redeveloped following the discovery of several quotes describing how Dr. Still performed manipulative treatment. These quotes were found in a text by Charles Hazzard DO (2), a student and colleague of Dr. Still at the American College of Osteopathy in Kirksville, Missouri. The initial discussion of this rediscovered merhod was an article tided "A Manipulative Technique ofAndrew Taylor Still" published in the journal of the American Osteopathic Association (3). The current description has evolved significantly from the original (4) : 1. Determine where the dysfunctional joint or tissue moves most easily. This is opposite the direction in which it is restricted. 2. Move the joint and/or tissues in the direction of its ease of motion until the tissue relaxes palpably. It is often useful to slightly exaggerate the position of ease, which further relaxes the dysfunctional tissue. 3. Introduce a vector of force of about 5 pounds (2 kg) into the affected tissue using the operating hand. 4. Using the force vector as a lever and maintaining compression, carry the tissue in the opposite direction toward and through the initial restriction. There will be a palpable and perhaps audible release as one passes through rhe former restriction. 5. The force vector and its compression is now removed and the tissue passively returned to neutral. 6. The procedure is retested and repeated if necessary.
One of the critical aspects and absolute requirement for the ability to use the Still technique is diagnostic specificity of musculoskeletal evaluation. If the diagnosis is not accurate this musculoskeletal manipulative technique is less likely to be successful, although it is rare that it will worsen a patient's condition. This chapter presents examples of the Still technique applied to portions of the spine and limbs. No attempt is made to be comprehensive. Many of the diagnostic techniques discussed are shortcuts based on the author's clinical experience. Classic diagnostic procedures can also be used (5-7) (see Chapters 42, 47, 49-56) .
CERVICAL SPINE (C2-C7) Normal and abnormal segmental motion of the cervical spine below d1e arlanto-axis interface generally involves coupling of side bending and rotation toward the same side. This is thought to result from the existence of four facet-type joints between cervical vertebrae rather than two as seen in the spine below the neck. Two synovial intervertebral facet joints are situated on the posterior-lateral articular columns of the vertebra and the two additional joints (joints of Luschka) are located on the anteriorlateral aspect of rhe vertebral bodies.
Diagnosis A typical cervical somatic dysfunction is found by palpating a usually tender prominence of the posterolateral margin of the articular column on one or both sides. The patient may not note pain at that site prior to being examined. The somatic dysfunction is specifically diagnosed by examining for ease/restriction in flexion, extension, side bending, and rotation. If a segment exhibits a multiple plane, extended somatic dysfunction, the articular pillar on the side toward which it is rotated will be prominent in neutral and flexion and much less prominent in extension. Palpably the vertebra will not move into A.exion as easily as it does into extension. The articular pillar on the opposite side of the same vertebra will not change with flexion or extei1sion. A classic test for cervical segment side bending is lateral translation. This involves pressing the articular pillars of the affected
70. Treatment of Somatic Dysfunction vertebra toward one side and then the other. The side toward which it rranslates most easily is opposite the side toward which it is side benr. For instance, translation easily to the left means side hending to the right is permitted. The superior segment of the functional unit tilts to the right, the side on which the pressure is exerted. A cervical segmenr that translates easily toward the left and not as well toward the right is side benr right. Because of the obligatory coupling of side bending and rotation toward the same side in the typical cervical vertebral spine, the vertebral unit will also be rotated toward the right. To test for cervical rotation the head and neck are held in neurral. The fingertips are maintained on the posterior margins of the segmenr's articular pillars. The head and cervical spine down to the vertebral unit are rotated to the right and left. The direction in which the segmenr moves most easily is opposite to the position of rotational restriction. This somatic dysfunction will be named for the position in which the segmenr moves most easily. This is generally the position in which it is found. In this case it will be extended, rotated, and side benr right (ERRSR). This naming co nvention designates the position of ease as well as delineating the side on which the ease is found as a subscript. An alternate diagnostic method is based on the author's experience. It also begins with assessment of prominence, tenderness, and bagginess on the posterior surface of the articular pillars. A unilateral finding corresponds to the side toward which the dysfunctional segmenr side bends and rotates most easily. A unilateral finding of prominence, tenderness, and bagginess over the posterior surface of an articular pillar allows one to reduce motion resting to determination of the effect of flexion and extension. One must be careful to distinguish these findings from any tenderness found lateral to rhe articular pillars or from the deeper exquisite tenderness over the rransverse processes that are found on rhe lateral side of the vertebra about a centimeter anrerior to the articular pillar. It is not recommended that the physician who is first mastering cervical segmental diagnosis use this shortcut until comfortable with the traditional diagnostic methods of testing for motion in all three planes and is satisfied that the author's observations are correct.
Cervical Treatment, Supine
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FIGURE 70.1. Initial position for treating typi ca l extended right rotated and side bent cervica l dysfunction.
4 . Physician's right hand appli es compression through the patient's head and neck down to the dysfunctional unit. 5. While maintaining the compression, the physician rotates the patienr's head and neck toward the left and carries the head and neck from extension into flexion in a si ngle smooth arc to and through the area of the restrictive barrier (Fig. 70.2). Release will be felt sometime between neutral and full left rotation. 6. Compression is released and the neck is returned to neutral. 7. The procedure is retested and repeated if necessary.
Note: Palpable and/or audible release may or may nor be experienced. In some cases a rraction force, rather than compression, might work better as a lever. This can be introduced by placing the operating hand under the basiocciput on the side of the dysfunction and applying traction along with rotation and anterior/posterior movement.
OCCIPITAL-ATLAS An occipital-atlas (0-A) somatic dysfunction is demonstrated by boggy, tense, and render tissue at the basiocciput at the origin of
Diagnosis: ERRSR Position The patienr is supine. The physician sits or stands at the head of the table. Procedure I. Physician's left hand (sensing hand) is placed behind the neck with the pad of the index finger on the articular pillar of the affected cervical vertebra. The remainder of the sensing hand supports the head and neck. 2. Physician's right hand (operating hand) is placed on the top of the patient's head. 3. Physician extends and side bends the head and neck to the dysfunctional cervical unit and then markedly rotates the head and neck to the right to the point where the tissues palpably relax (Fig. 70 .1 ).
FIGURE 70.2. Final position, typical extended right rotated and side bent cervical dysfunction.
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 70.3. Initial position, right extended occiputal-atlas dysfunction .
rectus capitus, the lateral margin of semispinalis capitus, and the medial margin of splenius capitus. T his is roughly at the site of the recurrent occipital nerve foramen. Restriction will be noted in either Aexion or extension of the 0-A and the overlying tissues will be most relaxed in the opposite direction. For example, if the right 0-A is extended and restricted in Aexion (OAER), the tissue will relax with extension of the basiocciput and become more prominent, tight, boggy, and tender with flexion.
Diagnosis: 0-A ER Position The patient is supine. The physician sits or stands at the head of the table. Procedure 1. Physician's left hand (sensing hand) is placed under the patient's occiput with the index finger on the affected tender joint and the thumb on the opposite splenius capitus muscle. 2. The physician's right (operating) hand is placed on the dorsum of the head. 3. Physician slightly side bends the patient's head to the right (side of the restricted joint) and extends the patient's head on the atlas.
FIGURE 70.4. Initial position, right rotated atlas-axis dysfunction.
side toward which it is rotated (the sulcus will be more shallow). Tenderness and tissue bogginess will be noted on the same side. Rotational motion testing will demonstrate easy motion toward the prominent side and restriction toward the opposite side. The somatic dysfunction will be named for the side toward which ir rotates most freely. Thus, if the transverse process is tender and boggy on the right, the axis is rotated right (A-ARR).
Diagnosis: A-A RR Position The patient is supine. T he physician sits or stands at the head of the table. Procedure 1. Physician's right (sensing) hand is placed under the patient's occiput with the pad of the index finger on rhe right atlas transverse process. The other finge rs of the sensing hand are beh ind the neck and the palm supports the occiput. 2. Physician's left (operating) hand is placed on the dorsum of the head. 3. Physician rotates the patient's head toward the right to the ease of the tissues. 4. Physician introduces compression through the head to the right A-A joint (Fig. 70.4) . 5. T he patient's head is rotated to the left toward and through the former restriction.
4. The physician's right hand (operating hand) introduces compression through the dorsum of the head to the right 0-A joint (Fig. 70.3) . 5. While maintaining compression the physician moves the patient's head into flexion with some right rotation. Movement should be done at a moderate pace. 6. When release is palpated, release compression and return the patient's head to neutral.
6. Compression is removed once release is felt and the head is returned to neutral.
7. The procedure is retested and repeated if necessary.
SUPERIOR {ELEVATED) FIRST RIB
ATLAS-AXI S The primary movement of the atlas on the axis is rotation. T he transverse process of the axis is identified between the angle of the jaw and the mastoid process. If the atlas exhibits somatic dysfunction , its transverse process will be more prominent on the
7. Retest.
No universal convention for naming first rib (Rl ) dysfunctions has been accepted. The terminology used here names a dysfunction by the ease of movement of the posterior portion most proximal to the spine (e.g., the Rl head). For a superior or elevated Rl the head is tender and presents superior and posterior relative to that of rhe opposite side. The anterior end of the R 1 will be inferior relative to the opposite side and is also generally render
70. Treatment of Somatic Dysfunction
FIGURE 70.5. Initial position, right superior first rib dysfunction.
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FIGURE 70.6. Intermediate position, right superior first rib dysfunction .
ro palpation. Testing the rib for respirarory motions the rib will move easily during inh alation and be restricted during exhalation.
Diagnosis: R1 lnferiorR
Diagnosis: R1 SuperiorR
Position The patient is supine. The physician stands near the patient's waist on the same side as the affected rib.
Position The patient is supine. The physician stands near the patient's right hip facing the patient's head. Procedure 1. The physician has the patient flex their right arm at the elbow. The patient's right palm is face down on the left shoulder.
2. The pad of the of the physician's right index finger is placed on the patient's Rl head . 3. The palm of the physician's operating hand is placed on the olecranon of the patient's right elbow. 4. T he patient's right elbow is moved medially until it lines up with the head of the R 1. The patient's wrist will now be in contact with the physician's sensing arm. 5. The physician introduces compression with the operating hand in a vecror roward the head of the affected Rl (Fig. 70.5). 6. The physician brings the patient's elbow superior along a li ne between the anterior and posterior attachments of the Rl whi le maintaining compression (Fig. 70.6). 7. T he physician now carries the patient's elbow in a backward arc until the patient's arm is passing their ear. Thereafter the motion arcs lateral roward the shoulder.
Procedure 1. The patient's right elbow is flexed with the palm down on the patient's chest.
2. T he pad of the physician's right index finger is placed on the rib head. 3. T he patient's right elbow is brought inro a lateral abducted position. The physician's left hand positions the patient's flexed elbow to maximally relax the right Rl head. 4. With the patient's wrist contacting the underside of the physician's sensing arm the physician's left hand (operating hand) introduces compression through the elbow toward the head of the Rl (Fig. 70.8). 5. The patient's right arm is now swung through an arc superiorly and laterally whi le maintaining compressio n toward the rib head (Fig. 70.9) .
8. Typically release is felt shortly after the arc starts away from the neck (Fig. 70.7). 9. Compression is reduced. 10. The procedure is retested and repeated if necessary.
INFERIOR (DEPRESSED) FIRST RIB In an inferior or depressed Rl dysfunction the rib head is inferior and tender relative ro the opposite side. The anterio r end of the rib will be relatively superior and also tender. The rib will move appropriately during exhalation and not during inhalation.
FIGURE 70.7. Final position, right superior first rib dysfunct ion.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 70.8. Initial position, right inferior first ri b dysf unction.
FIGURE 70.10. Final position, right inferior f irst ri b dysfunction.
6. The parienc's right elbow is carried anterior-medial. Irs final position is below the anterior end of rhe Rl (Fig. 70.1 0).
dysfunctions. The physician stands behind the seated parienr and runs their fingertips lightly along two lines parallel to and about 2.5 em lateral to rhe spinous processes. This positions rhe sensing fingers over the transverse processes and facet joints. Typically one finds a fullness, bagginess, and/or tissue ropiness over the transverse process of a vertebra wirh somatic dysfunction. If the segment shows type II mechanics the tissue texture changes will be found over the transverse process on rhe side toward which the segment is side bent and rotated. One can simply proceed to test whether the transverse process on rhat side becomes more or less prominent when the parienr flexes or extends the spine. However, iris my experience rhat testing is easier and more accurate when the physician induces flexion and extension. If the transverse process and irs overlying tissue become more prominent in extension and indistinguishable from irs neighbors in flexion, then it is flexed. Ifir does not improve in either flexion or extension, then it is probably a neutral or type 1 segmental somatic dysfunction and side bending and rotation will need to be assessed independently.
7. As rhe parienr's elbow reaches irs apex above rhe patient's ear, release will be felr. Compression is rhen released. 8. The physician's sensing finger is removed from the rib head and the sensing hand catches the patient's wrisr. 9. The patient's arm is returned to its resting position next to the rhorax. 10. The procedure is retested and repeated if necessary.
THORACIC SPINE The standard thoracic diagnostic method has the physician standing behind rhe patient. The physician has the patienr flex. The physician checks each segmenr for motion asymmetry in side bending and rotation. The patient is then eval uated in the same manner using extension (5-7) (see Chapters 47 and 51). An experienced osteopathic physician may use an alternative simple and rapid method for assessing segmental thoracic somatic
Upper Thoracic Vertebra Type II Dysfunction Note: This version is similar to rhar described by Dr. Srill (4). lr can be useful down to abour T8 on mosr patienrs.
Position The patient sirs. The physician srands in front of the pa ~ienr. Procedure 1. Physician's arms are placed over rhe parienr's shoulders. 2. Physician's left index finger (sensing hand) is on rhe right transverse process of the patient's third thoracic verteb ra. 3. Physician's arms on rhe parienr's shoulders flex and righr side bend the patient's thorax unril d1e tissues under rhe sensing finger are palpably reduced or softened and rhe transverse process is no longer prominent (Fig. 70.11). Physician's arms introduce about 5 pounds (2 kg) pressure in a vector d1rough the affected segmen r. FIGURE 70.9 . Intermediate position, right inferior first rib dysfunction.
4 . Physician rotates rhe parienr's shoulders and spine to the left,
70. Treatment of Somatic Dysfunction
1099
FIGURE 70.13. Initial position, thoracic vertebra, flexed, side bent, and rotated right. FIGURE 70.11. Initial position, upper thoracic vertebra, flexed, side bent, and rotated right.
Thoracic Vertebrae Type II Dysfunction This technique is usable for all thoracic vertebrae below T 1 or
reducing flexion until it becomes extension. As the segment is carried into left rotation with mild extension, release of the segmental restriction may be felt (Fig. 70.12). 5. Compression is released and the patient is passively returned to neutral.
Tz.
Position The patient is seated with the physician standing behind.
6. The procedure is retested and repeated as necessary.
Comment: It is quite easy to couple this treatment technique with diagnosis as was generally done by Dr. Still (1). The only reason I do not typically simultaneously diagnose and treat is that I prefer to write all my diagnoses down before treating so as not to confuse my memory. If one can dictate at the time of treatment or has a very good short-term memory, one could probably diagnose and treat at the same time, as did Dr. Still.
Procedure 1. The pad of the physician's right index finger (sensing hand) is placed over the prominent transverse process of the affected segment.
2. The patient's right hand is placed on their left shou lder. 3. The physician's operating arm (left) is passed over the patient's left shoulder around the patient's superior chest wall and the hand is placed on the patient's right shoulder. This gives the physician adequate leverage to introduce flexion or extension, compression, and rotation. 4. The patient's thorax and spine are flexed and rotated right producing palpable relaxation over the affected segment. 5. The physician introduces compression through the patient's shoulders (Fig. 70.13) vectored toward the affected segment. 6. The physician's operating arm simultaneously reduces the patient's spinal flexion, moves into extension, and rotates the spine through neutral into the previously restricted range of left rotation. 7. Once release is noted compression is removed and the patient passively returned to neutral. 8. The procedure is retested and repeated as necessary.
RIBS {BELOW RIB 1)
FIGURE 70.12. Final position, upper thoracic vertebra, flexed, side bent, and rotated right.
Rib motion is typically described based on the dominant axis of motion (pump handle versus bucket handle) and/or whether a rib or ribs move more easily in inhalation or exhalation (5- 7)
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VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment TABLE 70.1. SINGLE RIB DIAGNOSIS Diagnosis Rib angle Costochondral junction Compression Movement permitted Movement restricted
"Posterior Rib"
"Anterior Rib"
Posterior and tender Posterior and tender Anterior direction restricted Posterior direction permitted Exha lation Inhalation
(see Chapter 52). AJrhough both concep ts make sense when examining group restrictions, it has been the author's experience that single rib restrictions are more common and more likely to be symptomatic. To simplifY diagnosis I have developed a new terminology for ingle rib dysfunctions (Table 70. 1). Most single rib dysfunctions can be described in terms of a single plane of motion: anterior-posterior. lf the rib crosses under rhe scapula the patient often reports "something painful" berween the chest wall and scapula. Tissue bagginess is present over the rib angle in both types of rib somatic dysfunction and may make palpation of an "anterior" rib angle more difficult. Note that a posterior rib appears to correspond ro what is traditionally termed an exhalation rib and an anterior rib appears ro correspond to what is traditionally termed an inhalation rib. However, diagnosis as a "posterior" or "anterior" rib is eas ier, quicker, and respo nds well with the treatment methods of the Still technique described in the next paragraph.
Solitary Posterior Upper Thoracic Rib Diagnosis: Rib3PL Position The patient is seared on a table or stool. The physician stands behind the patient roward the side of the affected rib. Procedure 1. Physician places the pad of the right rhumb as a sensor on rhe angle of the patient's left third rib. The palm and fingers of that hand stabilize the patient's upper back.
Anterior and tender Anterior and tender Posterior direction restricted Anterior direction permitted Inhalation Exhalation
Note: To treat ribs 4 through 6, the initial positioning is similar, buc with the elbow at the level of the affected rib's angle, the arc of articu lation is progressively more lateral with each lower rib. At rimes the best arc ro treat below rib 5 may require the arm being used ro end above the level of the opposite shoulder to obtain a full release.
Solitary Posterior Rib Diagnosis: Rib3PL Position The physician stands in front of the seated patient. Treatment I. Physicia n places forearms over the patient's shoulders. A finger of rh e physician's right hand (se nsing hand) is on the angle of the rib.
2. Physician side bends the patient's spine left and rotates the patient's left thorax posterior until the tissues around the rib angle rel ax (Fig. 70. 17). 3. Physician develops compression of 5 pounds or less vectored through the physician's forearms to the rib head. 4. Maintaining compression, the physician side bends the pari em toward the right side and simultaneously rotates the patient's thorax ro the ri gh r. 5. Com pression is released and the patienr returned
to
neurral.
6. The rib is reresred.
2. Phy ician ho lds the patiem's left elbow with the left hand (o perating hand ). Depending on the relative size of the physician and the patient, the physician may encircle the patient's arm somewhat more proximally to the elbow. 3. Patient's left arm is brought posterior (extended at the shoulder). The patient's elbow will be at abo ur the level of the angle of the affected rib. 4. Physician in rroduces compression through the elbow vectored toward the dysfunctional rib's head (Fig. 70 .1 4). 5. Patient's left shoulder is articu lated in a smooth arc through abduction with partial flexio n (ro about 110 degrees) (Fig. 70.15) and then into adductio n. The final position of the patient's arm is in the area of the patient's right abdomen (Fig. 70.16) . 6. Axial compression is released. The patient's arm is returned ro a neutral position along the left chest wall. 7. Rib motion and position are reassessed.
FIGURE 70.14. Initial position, upper rib posterior leh.
70. Treatment of Somatic DysfUnction
1101
FIGURE 70.15. Intermediate position, upper rib posterior left.
Anterior Rib The treatment of an anterior rib from in front of the patient starts with the patient's shoulder and thorax anterior on the side of the somatic dysfunction. The treatmenr of single rib dysfunctions from in front of the patient coordinates well with the thoracic spinal segment techniques ap proached from in front. The alternative is to treat from behind.
Diagnosis: Rib3AL Position The patient is seared on a table or stool. The physician stands behind the patient toward the patient's left side.
FIGURE 70.17. Initial position, upper rib posterior left, treated from in front.
arm is adducted in the same plane as the affected cosrochondral junction to produce palpable easing in the tissues over the rib angle (Fig. 70.18). 3. Physician articulates the patienr's arm through partial Aexion (to 140 degrees) and abduction (Fig. 70.19) . Now it is carried inro extension in a smooth arc while maintaining compression through the arm toward the rib head (Fig. 70.20) .
Procedure I. Physician places thumb of the right hand on the affected rib angle with palm and fingers of the hand stabilizing the patient's upper back.
4. Physician releases compression and returns the arm to a neutral posmon .
2. Physician's left hand encircles patient's left elbow. The patient's
5. The rib is reassessed.
FIGURE 70.16. Final position, upper rib posterior left.
FIGURE 70.18. Initial position, upper rib anterior left.
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\!fl. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment will be prominent and boggy, representing the side toward which ir is rotated and side bent. Often there will be tenderness in the same area. The spinous process will be slightly displaced toward the opposite side due to vertebral rotation. To determine whether the segment is flexed or extended the physician passively induces flexion and extension, monitoring the prominent transverse process for palpable relaxation. Thus if the left transverse process of L3 is prominent and if it becomes indistinguishable from its neighbors during induced flexion, the segment is flexed, side bent and rotated to the left.
Flexed Lumbar Segment D iagnosis: L3FSLRL Position The patient is supine. The physician stands at the patient's left side. FIGURE 70.19. Intermediate position, upper rib anterior left.
Note: For ribs 4 through 6 the arc is lowered so rhat correction of a fifth rib w[ll involve an arc that is at the level of the patient's shoulder.
LUMBAR SPINE Treating the lumbar spine, pelvis (innom[nates), and sacrum using the Still technique requires a specific order to treatment. Diagnosis can be performed for all three areas prior to treatment. However treatmem must begin with the lumbar spine and pelvis with the sacrum being treated last. Doing so vasdy simplifies diagnosis and treatmem of the sacrum. U ually, there are five lumbar vertebrae. No ribs are attached to these venebrae. Generally the lumbar spine exhibits a mild lordotic curve. Normally there is no scoliotic curve. Like the thoracic spine most clinically significant somatic dysfunctions involve type II mechanics (e.g., flexed or extended, and side bent and rotated toward the same side). Palpably the tissues over one of the transverse processes of a type 11 segmental somatic dysfunction
FIGURE 70.20. Final position, upper rib anterior left.
Procedure I . Physician inserts left hand under the patient's lumbar area and a sensing finger is placed on the left transverse process of L3.
2. Physician flexes the patienr's left leg at the hip and knee until the sensing finger palpates relaxation. Now the physician's left hand is moved to the patiem's left (flexed) knee and the physician's right hand is placed on the patient's left ankle. The patient's left knee is then adducted and the ankle is swung laterally, internally rotating the patient's thigh. This effectively side bends the patient's hip toward the affected side and induces flexion of L3 on L4 (Fig. 70.21). 3. Physician introduces compression vectored coward L3. 4. Physician moves the patient's knee laterally into abduction, slightly rotating the patient's pelvis posterior coward the table on the side of the dysfunction (Fig. 70.22). 5. Physician extends the patiem's leg (Fig. 70.23). 6. Physician releases compression and returns the patient's leg co a neutral position. 7. Retest.
FIGURE 70 .21 . Initial position, lumbar vertebra flexed, side bent, and rotated left.
70. Treatment of Somatic Dysfunction
FIGURE 70.22. Intermediate position, lumbar vertebra flexed, side bent, and rotated left.
FIGURE 70.24. Initial position, lumbar vertebra extended, side bent, and rotated left.
ILIUM OR INNOMINATE
Extended Lumbar Segment Diagnosis: L3ESLRL Position The patient is supine. The physician stands at the patient's side. Procedure I. Physician inserts sensing hand under the patient's lumbar spine with a sensing finger placed on the dysfunctional segment's left transverse process. 2. The patient's knee and hip on the side of the dysfunction are flexed. The physician's operating hand is on the flexed knee. The flexed knee is abducted until the affected segment palpably relaxes. 3. Physician introduces compression vectored from the patient's left knee to th e affeC[ed segment (Fig. 70.24). 4. Physician adducts patient's left knee across the midline. 5. Physician extends the patient's knee and compression released.
1103
IS
6. Retest.
FIGURE 70.23. Final position, lumbar vertebra flexed, side bent, and rotated left.
The relationship between the ilium or innominate and the sacrum is traditionally termed iliosacral. The emphasis is on the orientation of the ilia. Diagnosis of iliosacral (IS) somatic dysfunctions is based on combinations of three basic rests and reflects the relative positions and movements of the two hemipelvic bones (in nominates). Two main types of innominate somatic dysfunction are known. Functionally, the ilium or innominate exhibits a camlike rotation with irs primary fulcrum of rotation at the hip joint. Because the hip joint is inferior and anterior to the largest portion of the ilium, as the hip flexes the iliac crest swings posterior, and as the hip extends, the iliac crest rotates anterior. Rotation of the innominate occurs primarily at its joint with the sacrum and normally is restrained anreriorly by the limited elasticity of the pubic symphysis synostosis and posteriorly by the ligaments of the sacroiliac joint. Most iliosacral rotational dysfunction seems to develop in the complex joint between the ilium and sacrum. A vertical shear is the other potential source of somatic dysfunction in iliosacral mechanics. The iliosacral joint has a normal, although minimal, amount of vertical glide. Within irs normal short vertical motion range the iliosacral complex appears behave as a shock absorber. Pushed to its limits by excessive or prolonged unilateral force from below and in line with rhe body's axis, the ilium can shear in a cephalad direction, producing the somatic dysfunction termed an upslipped innominate. Pelvic landmarks and their related tests used in the diagnosis of iliosacral dysfunction are: 1. Posterior superior iliac spine (PSIS): Levelness of the PSISs is easily assessed with the patient seated and the physician behind the patient. Although classically it is stated that PSIS position is assessed with the patienr prone, standing, or seated, there is little to be gained from testing in multiple positions. The seated rest starts with the physician placing the fingers of both hands on the patient's ili ac crests. The physician's thumbs slide down the patient's lumbar paravertebral spine about 3 em lateral to the midline where the superior surfaces of the bony prominences of the PSISs are encountered. One should then follow the PSISs caudad until their inferior margins are discovered. The physician then determines whether one of the thumbs is superior to the other.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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TABLE 70.2. TESTS FUNCTION
TO
Diagnosis
Anterior right rotation Anterior left rotation Posterior right rotation Posterior left rotation Upslipped right innominate Upslipped left innominate
DIAGNOSE
ILIOSACRAL
DYS-
PSIS
AS IS
Pelvic Translation
" Right " Left " Left " Right " Right · Left
· Left " Right " Right " Left " Right " Left
+ Right + Left + Right + Left + Right + Left
PSIS, posterior superior iliac spine; ASIS, anterior su perior iliac spine.
2. Anterior superior iliac spine (ASIS): Levelness of the ASISs can be performed seated (in mosr cases), standing, or supine. Si nce most of the IS treatments using the Sti ll technique are performed with the patient supine, rhe author has routinely performed this test with the patient supine. T he physician stands ar the patient's side, below the level of the patient's hips. The physician uses their thumbs to locate the inferior edge of the ASIS bilaterally, then judges which, if either, is superior. 3. Pelvic rocking or ASIS compression test: T here are two versions of this very common test. Both work equally well. Both are performed with the patient supine. In the first versio n the physician places rhe palms of rhe hands on the ASIS bilaterally and alternates pressure on each. The side toward which there is less easy movement is positive. The other test involves placing the fingertips of both hands on rhe lateral surface of both ASIS. Alternating gen tle pressure toward rhe midline will result in small lateral translation of the hips. The side toward which motion is restricted is positive. Table 70 .2 shows three tests used in the diagnosis of iliosacral dysfunction. T here is no single test or even a pa.ir of tests that predict the nature of the iliosacral somatic dysfunction. If there is a question about which innominate is dysfunctional, the author has found that there will be tender points just medial to the ASIS on the side of a dysfun ctional innominate. The use of tender points for diagnosing somatic dysfunction is nor generally a form al part of the diagnostic criteria for ei rher muscle energy or high velocity/low amplitude (HVLA) techniques. However, when there is a high correlation between particular tender points and functional problems the tender point can be used to help settle a d iagnosis that is in doubt.
FIGURE 70.25. Initial position, anterior right iliosacral dysfunction.
4. Physician introduces compression through the knee to the lower pole of the sacroiliac joint. 5. Physician moves the patient's knee in an arc through full hip flexion and into flexion wi th adductio n (Fig. 70.26) . 6. Physician carries rhe patient's hip into extension. 7. Physician releases compression at about 30 degrees of hip extension and rhen completes extension of the patient's leg. 8. Retest.
Posterior Left lliosacral Dysfunction (Left Posterior Innominate) Position T he patient is supine. The physician stands at the patient's left side. Procedure l. The physician's right hand is placed under the patient's pelvis so rhar a sensing finger can be placed o n the cephalad porrion of the sacroiliac join t. 2. The patient's left knee and hip are flexed to more than
Anterior Right lliosacral Dysfunction (Right Anterior Innominate) Posicion The patient is supine. T he physician stands on the patient's right side. Procedure 1. Physician's left hand is placed under the patient's pelvis so that a sensing finger can be placed on the lower pole of the sacroiliac joint. 2. Physician's right hand grasps the patient's right knee and partially flexes the patient's leg at the hip to 45 ro 60 degrees. 3. Physician slightly abducts or adducts the patient's right knee until the tissues of the sacroiliac joint relax (Fig. 70.25).
FIGURE 70.26. Intermediate position, anterior right iliosacral dysfunction.
70. Treatment of Somatic Dysfunction
FIGURE 70.27. Initial position posterior left iliosacral dysfunction.
90 degrees and adducted across the midline. Physician's left hand (operating hand) is on the patient's knee. 3. Physician introduces compression in a vector through the upper pole of the sacroiliac joint (Fig. 70 .27). 4. Physician abducts the patient's left hip while maintaining compression . 5. As the patient's knee reaches its most lateral point in the arc (as determined by tissue compliance), compression on the patient's knee is transferred from the physician's hand to the physician's abdomen and the operating hand slips down to capture the patient's left ankle (Fig. 70.28). 6. Maintaining compression through the patient's knee, the physician extends the leg. 7. Compression is discontinued after release is palpated or after the hip is extended approximately 30 degrees. The leg is then passively extended. 8. Retest.
Upslipped Innominate To date no single treatment using the Still technique has been found that resolves all of this dysfunction. Perhaps this is because the innominate shear is not physiologic, making it more of a joint strain than a simple somatic dysfunction. For the most part the Still technique is deployed within physiologic ranges, although the author has used the Still methods to help reduce and properly mobilize ankle sprains to good effect. Whatever the case, an upslipped innominate functionally acts as iflimitations at several joints or tissues are defining this dysfunction. The author has provisionally identified three separate restrictions involving
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FIGURE 70.28. Intermediate position, posterior left iliosacral dysfunction.
three embryonic remnants of the sacral transverse processes seen within the sacroiliac joint. Although this identification may be useful, it should not be thought of as any more than a focusing tool and should not be taken as an established fact.
Diagnosis: Innominate UR (Step 1) Position The patient is supine on the table. The physician stands at the patient's feet. Procedure 1. Physician grasps the patient's right ankle with both hands. The ankle and leg are gently externally rotated. 2. Axial compression is introduced toward the right sacroiliac joint (Fig. 70.29). 3. Physician internally rotates the patient's leg. 4. Compression is changed to gentle traction. 5. The leg is released and returned to rest. 6. If the ASIS is assessed at this point it will be found to be level with the opposite side, bur motion testing still demonstrates persistence of somatic dysfunction.
Step 2 Use the Still treatment technique for a posterior rotated innominate.
Step 3 Use the Still treatment for an anterior rotated innominate.
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VIJ. Osteopathic Considerations in Palpato ry D iagnosis and M anip ulative Treatment
FIGURE 70.29. Initial position, right upslipped innominate dysfun cti on.
PUBIC RAMUS T he prin cipal som ati c dysfun cti o n of th e pubic ramus is th at o ne side will be eith er superi or o r in fe ri or rel ati ve to the other. It is co mmo n for the pubi c ra mus dysfun ctio n to foLlow th e inn o min ate dysfun cti o n. T hus a superi or pubic ramus may be seen on th e sa me side as a posterio r inno minate, o r mo re commonly an upslipped inno minate. It is also co mmo n to see an inferior pubic ramus o n the same side as an anteri o r inn o minate. However, this relati o nship is not obligato ry. Pres um ably any un coupling o f pubi c ramus dysfun ction fro m inn omin ate dysfun ction reAects th e relati ve Aexibili ty of li ving bo ne. T he relati ve displ ace ment and imm obilizati on o f one side of the pubi c ramus pl aces considerable strain on th e pubic synostos is. It is typi cal ly acco m pani ed by tender po ints at th e superi or margin of th e pubic ramus and /o r at th e lateral margins of th e pubi c bo nes at th e in serti o n of th e inguinal ligaments. To eva luate fo r a poss ible pubic ramus dysfun ction th e patient is supin e. T he ph ys ician startS with the fin ge rtips about 2 inches (5 em) below th e umbilicus and abo ut ~ inch (1 em) out from th e midlin e bilaterall y. Usin g th e pads o f th e fin ge rtips, the physician sweeps downward until th e bo ny promin ence of th e pubic ramus is palpated . Recogni ze which side is superi o r. N ote as well th e sid e of tendern ess. T he tend er sid e ge nerall y indi cates th e side of dysfun cti o n. So metimes th e pubic ramus is just compressed or stretched , in which case both sides wo uld be tender. In every case th e manipul ati ve technique wo uld be app rox imately th e same. It sho uld be no ted that treatment of inno minate dysfun ctions often redu ces pubi c ramus dysfun cti o ns, so the innominates sh o uld be treated fi rst.
FIGURE 70.30 . Initial position, pubic ramus dysfunct ion.
2. Phys ician places o ne hand o n each of the pat ien t's knees (Fig. 70.30). 3. Ph ysician introduces co m p ress io n from the patient's k nees toward the pubi c ramus. 4 . Phys ician simultaneo usly brings t he pat ient's knees late rall y maintaining compress ion (Fig. 70.3 1). 5. Release may be felt thro ugh the legs as the knees pass 60 degrees.
Pubic Ramus Dysfunction Position T he pati ent is supine. The ph ys ician stands at the pati ent's feet. Procedure I . Phys ician bilaterall y Aexes th e pati ent's hips and kn ees so that th e patient's feet are o n th e table abo ut 12 inch es (30 em) from th e ischial tuberos ities. T he patient's kn ees are togeth er and verti cal relati ve to th e table.
FIGURE 70.31 . Intermediate position , pubic ramus dysfu nction.
70. Treatment of Somatic Dysfunction
FI GURE 70 .32. Final position, pubic ramus dysfunction.
6. Physician removes the hands from the patient's knees and captures both ankles. 7. Keeping the patient's legs at 60 degrees, the physician draws the patient's feet toward the foot of the table until the knees and hips are again extended (Fig. 70.32). 8. Retest.
SACRUM Sacroiliac motions are classically described as rotatory along two angled planes, and flexion and extension about a transverse axis. The two most common systems for describing, diagnosis, and treating sacral somatic dysfunctions are those from the Chicago school that focused on HVLA methods (7) (see also Chapters 47, 55, and 59), and those developed by Mitchell for the muscle energy methods (5 ,6) (see also Chapter 60). During the author's process of redeveloping applications of the Still technique, a great deal of similarity was found between the diagnostic and treatment positions in both HVLA and muscle energy treatment systems. Examples include sacral torsions, unilateral sacral flexions (shears), and the anterior and posterior sacral dysfunctions. For instance, the HVLA treatment for a unilateral flexed left sacrum is virtually identical to that for a left on left dysfunction. Nonetheless, early attempts were made to develop Still applications for each of the sacral dysfunctions described in the Mitchell model. Initially, no particular treatment order was imposed. However, over time, and without consciously deciding on an order of treatment, the author found himself treating the lumbar spine first because the patient was still seated after treating the thoracic spine. Further, when treating innominate and sacral dysfunctions with the patient supine, more often than not the author tended ro treat the innominate dysfunctions first. Surprisingly, it was found that prior treatment of the innominate and lumbar dysfunctions seemed to limit the number and type of sacroiliac dysfunctions that remained untreated. In the
1107
years since work began with the Sti ll technique, no bilateral sacral flexions or extensions have been found after treatment of lumbar and iliosacral dysfunctions. Likewise, the backward sacral torsions seemed to resolve after treatment of any concomitant anterior or posterior innominate dysfunction. One obvious reason for the paucity of sacral findings after treatment oflumbar and iliac dysfunctions must be the interdependence of lumbar, sacral, and iliac mechanics. Logically one would expect the sharing of joints, tendons, and muscles to create an interdependence of function. By treating those structures that are engaged with the sacrum, a number of dysfunctions that were due to the relation between the sacrum and irs neighbors should be, and in fact are, released. In view of the complexity of sacral diagnosis and mechanics in other systems of analysis, the limitation of sacral findings following treatment of lumbar and innominate dysfunctions has been an unexpected and pleasant side effect. After treatment of lumbar and innominate somatic dysfunctions only two types of sacral dysfunctions seem to remain. For a number of years, while developing the Still technique, rhe author tended to identify these two classes of sacral dysfunctions with the names used in the Mitchell model for sacral torsions. This terminology was used even though the method of analysis was severely truncated and the dysfunctions identified did not necessarily meet the criteria of Mitchell's diagnostics. Finally, it became apparent that the terminology was not reflecting either the diagnostic criteria used or the limited number of techn iques necessary for successful resolution of sacral dysfunctions following the proposed order of treatment and use of the Still techniques. Both of the residual sacral dysfunctions observed after successful treatment of lumbar and innominate dysfunctions behave as if the sacrum was fixated at two poles, one superior and one inferior. The two superior poles are inferior to L5 lateral on the sacral base and just medial to the PSISs. Functionally, a restriction of a superior pole seems to correspond to tension in the tendinous insertions of the erector spinae on the superior portion of the sacrum. The two inferior poles are near the origi ns of the sacrotuberous ligaments on the lower part of the sacrum. Restriction in one of them appears to correspond to tension in the sacrotuberous ligament. Although these residual restrictions are the hallmarks of the only sacral dysfunctions seen after treatment and resolution oflumbar and innominate dysfunctions, the restrictions are identifiable even before treatment. T his emphas is on fixation at two sacral poles is different from the models used by both the Chicago and Michigan schools that emphasize single pole dysfunctions. It does nor negate the findings of either. It does suggest that any abnormalities of sacral mechanics in isolation from lumbar and thoracic mechanics may be somewhat different than has been previously described . When the sacrotuberous ligament on one side is fixed or tight and the superior pole on the opposite side is fixed, the sacrum acts as though it can only rotate on the diagonal axis. hs ease of rotation at the sacral base would be in an anterior or posterior direction toward or away from the restricted sacral pole. Th is type of sacral dysfunction is now being termed a diagonal sacral dysfunction. In other cases the sacrum is found to have restrictions at the upper and lower poles on the same side. T hese are now being termed unilateral sacral dysfunctions. It is important to understand that the generation of these new terms is not a gratui tous exercise.
1108
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
After successfu l treatmenc of any lumbar and innominate somatic dysfunctions, all residual sacral dysfunctions seem to fit in one of these two restriction patterns and are treatable with one of two Still techniques. The implication of these findings is that there are two distinct residual restriction patterns in the sacrum following successful treatment of any lumbar and innominate dysfunctions. These residual sacral dysfunctions are quite different from those described by either the Chicago or Mitchell models of sacral dysfunction. Therefore, it would not be appropriate to extend either terminology to these "new" versions of sacral dysfunction. Sacroiliac somatic dysfunctions can be diagnosed fairly quickly using seated tests. Although it is common to perform many of the tests for sacral dysfunction in a prone position, the author has found that patients with lumbosacral pain have a problem tolerating transfers from one position to another. In particular they have a problem transferring from seated to supine or prone positions and back again. The less position changes required of these patients, the more they appreciate it. The following sacral tests are abbreviated significantly from those used by the Chicago schooJ and the Mitchell model: 1. The seated flexion test: This test differs in significant detai.ls from the classic seated flexion test (5-7) (see Chapter 47). This modified seated flexion test starts with the patient seated. Weightbearing on the ischial tuberosities should be equal. The tips of the physician's sensing fingers are placed firmly on the sacrum just medial to the PSIS at the level of the sacral base (sacral sulcus). The patient is instructed to bend forward. As the patient flexes the physician notes which side of the sacrum glides superior. The side that moves is noted and is the positive side. 2. Position of the inferior lateral angle (ILA): This is checked at the sacrotuberous ligament. This is said to be positive if one ILA is posterior and does not move anterior, if the sacrotuberous ligament is tight on that side, or if the ILA is more inferior on one side. The positive side is that of restriction. The sacroiliac diagnoses are named for the pattern offree poles (which is the same as the pattern of restricted poles) and the free direction of rotation of the sacral base (Table 70.3).
FIGURE 70.33. Initial position, diagonal right sacroiliac dysfunction.
2. The physician's hand closest to the patient's feet picks both feet up and increases the hip flexion to abo ut 90 degrees. 3. The physician's hand closest to the patient's head is placed on the patient's knees and is used to side bend the legs and knees to the left. This provides some anterior rotation to the right innominate that may be slightly lifted off the table. The physician now rotates the patient's feet and lower legs outward away from the midline (Fig. 70.33). 4. The physician introduces compression through the patient's knees vectored toward the sacrum. 5. The physician swings the patient's feet toward the right (away from the midline) at a moderate pace and simultaneously carries the knees across the midline toward the right (Fig. 70.34). When the patient's lower legs are about 30 to 45 degrees off the midline, the legs are carried into extension (Fig. 70.35).
Diagonal Right Sacroiliac Dysfunction Position The patient is supine on a table. The physician stands to the side of the patient. Procedure 1. Both of the patient's legs are flexed at the hips and knees. TABLE 70.3. SACROILIAC DIAGNOSES NAMED FOR THE PATTERN OF FREE POLES AND THE FREE DIRECTION OF ROTATION OF THE SACRAL BASE Diagnosis
Seated Flexion
Diagonal right Diagonal left Unilateral right Unilateral left
+Right + Left +Right + Left
Inferior Lateral Angle
+ Left (posterior, tight, long) + Right + Right +Left
FIGURE 70.34. Intermediate position, diagonal right sacroiliac dysfunction.
70. Treatment of Somatic Dysfunction
FIGURE 70.35 . Final position, diagonal right sacroiliac dysfunction.
6. The physician brings the patient's legs back to neutral (full extension). Since this is an unmonitored technique it is very possible that no release will be felt. 7. Retest.
Unilateral Left Sacroiliac Dysfunction Position The patient is supine. The physician stands at the patient's left side. Procedure 1. Physician's left hand monitors the patient's left sacroiliac joint for relaxation while the physician's right hand flexes the patient's right leg at the knee and hip. The patient's right hip is also abducted unril the sacroiliac joint relaxation is palpated (Fig. 70.36).
2. Physician moves the right hand to the patient's righr knee and the left hand to the patient's right ankle. 3. Physician carries the patient's right ankle laterally (away from the patient's body), internally rotating the hip. This relaxes the lower pole of the sacrum.
FIGURE 70.36. Initial position, unilateral left sacroiliac dysfunction.
1109
FIGURE 70.37. Intermediate position, unilateral left sacroiliac dysfunction.
4. Physician introduces compression through the patient's right knee vectored toward the patient's sacrum. 5. Maintaining compression, the patient's right knee is carried toward the midline (adducred), bringing the right pelvis slightly off the table. At the same rime the right ankle is brought toward the patient's left side, crossing the midline (Fig. 70.37). 6. The right ankle is drawn down toward the foot of the table until the right leg is fully extended (Fig. 70.38). Release will occur during extension of the patient's leg. 7. Retest.
HIP MUSCLES Five hip muscles are mentioned in Table 70.4. The sciatic nerve generally passes out of the pelvis just under the piriformis muscle. Occasionally the sciatic nerve exits the greater sciatic foramen over the superior margin of the piriformis. The sciatic nerve may also split so that part of it passes through the belly of the piriformis.
FIGURE 70.38. Final position, unilateral left sacroiliac dysfunction .
1110
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
TABLE 70.4. PELVIC MUSCLES Muscle
Origin
Psoas
Transverse processes of L1-4 (LS)
Gluteus maxi m us
Cou rse
Insertion
Over superior pubic ramus and anterior to the hip joint
Action
Lesser tuberosity of the femur
Hip flexion
Just above and lateral to posterior superior i Iiac spine (PSIS) down to sciatic foramen
Greater trochanter of the femur and the iliotibial band
Extends hip when flexed; externally rotates hip. Aids in extending knee .
Gluteus medius
Beneath iliac crest to the PSIS
Greater trochanter of the femur
Stabilizes hip during swing phase of opposite hip during walking . Contributes to hip adduction .
Gluteus minimus
Ala of the ilium beneath gluteus medius and lateral to gluteus maxim us
Greater trochanter of the femur
Stabilizes hip during swing phase of opposite hip. Contributes to hip adduction.
Piriformis
Anterior lateral sacrum
Posterior medial aspect of femur's greater trochanter
External rotator of the hip. Beyond 20° of hip adduction acts as a hip flexor.
Passes through the greater sciatic foramen
The diagnosis of a somatic dysfun ction among rhese hip muscles is li rrle different from that of any other somatic dysfunction. Typically t here will be a decrease in appropriate range of motion. Gait will often be so mewhat abnormal. The muscle belly and tendons may be quite render ro palpation. When somatic dysfunction is found in these muscles each will demonstrate signifi cant tender points at its origin and insertion, although these are hard to demonstrate in the case of the piriformis. However, a somatic dysfunction of the piriformis will demonstrate tender points in the muscle as it exits the sciatic notch. This may reAecr either tenderness in the muscle itself du e to spasms or in the origin of rhe neighboring and synergistic ge melli muscles. ln the case of restriction and inAammation of the psoas, termed psoasiris or psoas syndrome, the patient sta nds slightly Aexed at the waist and slightly side bent toward rhe side of the dysfunction. Leg extension is markedly restri cted and the foot will rend to be everted. Simil arly, hip Aexio n and intern al rotation will be restricted if rhe glute us maxim us is dysfunctional. Leg adduction may be somewhat decreased if either rhe gluteus m edius or gluteus minim us are restri cted. Leg internal rotation will be restricted if the piriformis group is dysfunctional. If the patient complains of pain in the area of the upper glureals, asking the patient to stand on the affected leg wi ll worsen spasms if the gluteus medius and minimus are involved. It is quire common that somatic dysfun ctions of the piriform is or o ne o r mo re of the glu teal muscles will produce numbness, tingling, paresthesia, and perh aps even a burning pain than runs down the back of a patient's leg. As long as there is no evidence that a spinal co mpression of the sciati c nerve is responsible, this fu nctio nal sciatica can be relieved, sometimes instantly, by treating those gluteal muscles that are exhibiting signs of somatic dysfun ction . (A comp lete treatment for this condition will also includ e any sacral and innominate dysfunctions.) Recalling irs course through rhe sciatic notch alo ng with the sciatic nerve, it is easy to see how piriform is spasms and restrictions could produce the sy mptoms of sciatica. Additionally, because it overlies
the sciatic nerve as it travels distal to piriformis, spasm in rhe gluteus maximus can provo ke sciatic-type symproms. T he gluteus minim us, when it is in spasm o r chronic activation, can also contribute to functional sciati ca because it li es just superior to the piriformis.
Right Psoas Dysfunction Position The patient is in a lateral recumbent position with the right side up with the right hip and knee fully Aexed. T he phys ician stands behind the patient. Procedure 1. A finger of the phys ician's left hand (se nsing hand) is on the patient's right L2 transverse process. T he remainder of the hand stabilizes the lower lumbar spin e and upper pelvis. The physician's right hand is placed o n the patient's Aexed ri ght kn ee. 2. The phys ician introd uces comp ression through the patient's kn ee vectored toward the right lumbar paravertebral gutter (Fig. 70.39). 3. Maintaining compression, the physician abducts the patient's kn ee and draws it inferio rly, carrying the hip through neutral and into extension (Fig. 7 0.40). During treatment no attempt is made by the phys ician or the patient to extend the knee, although commonly, some extension of the knee seems to develop naturally. 4. As the patient's hip is extended compression is released and the leg is return ed to neutral. 5. Retest.
Right Gluteus Maximus Dysfunction Position The patient is supine on the table. T he phys icia n sta nds on the ri ght side of rhe patient.
70. Treatment of Somatic Dysfunction
1111
FIGURE 70.39. Initial position, rig ht psoas dysfunction.
FIGURE 70.41. Initial position right, gluteus maximus dysfunction.
Procedure 1. Physician's left hand is placed under the patient's pelvis with a sensi ng finger on the tender points in the origin of the gluteus maxim us. The physician's right hand is placed on the patient's right knee.
Procedure 1. Physician's left hand is placed under the patient's pelvis with a sensing finger on a tender spot in the origin of the muscle.
2. Physician flexes the patient's right knee and hip and abdu cts the patient's thigh until relaxation is palpated at the origin of gluteus maximus (Fig. 70.4 1). 3. Physician introduces compression through the knee vectored toward the origin of gluteus maxim us. 4. Maintaining compression , the physician add uces the patient's thigh in a smooth arc, bringing it across the midline to the point where the ri ght hip is off the table (Fig. 70.42). 5. Physician carries the patient's knee into extension. Release occurs at about 30 degrees of hip flexion (Fig. 70.43). 6. The patient's leg is returned to neutral (full extension) and the patient is retested.
Right Gluteus Medius and Minimus Dysfunctions Position The patient is supine on a table. The phys ician stands by the right side for a right dysfunction.
FIGURE 70.40. Inte rm ediate position, right psoas dysfunction.
2. Physician draws the patient's right leg and knee into about 100 to 120 degrees flexion for gluteus medius. G luteus minimus requires somewhat less hip flexion, often on ly about 70 degrees. Both may require slight adduction . 3. Physician's right hand wraps around the patient's right ankle and externally rotates the patient's hip. The physician's left axi lla gently captures on the patient's right knee and supplies compression toward the sensing finger and the muscle origin (Fig. 70.44). 4. Physician draws the patient's ankle toward the patient's right side, internall y rotating th e hip. Once the patient's hip is internally ro tated, the physician maintains compression through the knee while abducting the knee (Fig. 70.45). 5. The physician draws the patient's ankle toward the foot of the table. Release of the somatic dysfunction and co mpression occurs when the patient's knee clears the physician's ax ill a (Fig. 70.46). 6. Retest.
FIGURE 70.42 . Intermediate position, right gluteus maximus dysfunction.
1112
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 70.43. Final position. right gluteus maximus dysf unct ion.
Note: If the physician is not so tall as to easily capture the patient's knee with the axilla, this technique can be performed as an unmonitored technique using one hand on the patient's knee and the other on the patient's ankle.
FIGURE 70.45. Intermediate position, right gluteus medius dysf unction.
patient's knee across the midline into adduction. The patient's right foot should pass over the patient's left thigh before rhe right knee does (Fig. 70.48). 5. Now the physician draws the patient's right foot back across the patient's left thigh, internally rotating the thigh (Fig.
Right Piriformis Dysfunctions Position The patient is supine. The physici an stands at right side of the patient. Procedure 1. Physi cian's left hand is placed under the patient's pelvis and the sensing finger is placed on the piriformis tender point in the area of the sciatic foramen.
70.49). 6. Thereafter the physician draws the patient's knee and hip into extens ion and re leases compression through rhe knee (Fig. 70.50). 7. Retest.
THE HAND
Right In-Rotated Scaphoid
2. Physician flexes and fully abducts the patient's right knee. Once the muscles are relaxed the sensing hand is withdrawn and transferred to the patient's right knee. The physician's right hand is placed on the patient's right ankle.
Position The patient is usually seared with the right hand palm up in the physician's right hand.
3. Physician develops and maintains a vector of compression through the patient's right knee toward rhe sciatic foramen (Fig. 70.47). 4. Leading with the patient's right foot the physician carries the
Procedure 1. Physician's fingers from rhe right hand are curled around rhe thenar eminence and one is placed over the scaphoid bone.
FIGURE 70.44. Initial position, right gluteus medius dysfunction.
FIGURE 70.46. Final position, right gluteus medius dysfunction .
70. Treatment of Somatic Dysfunction
FIGURE 70.47. Initial position, right piriformis dysfunction.
1113
FIGURE 70.50. Final position, right piriformis dysfunction.
2. Physician grasps the patient's thumb with the left hand. The patient's thumb is adducted until the scaphoid is palpably relaxed. 3. Physician introduces compression vectored through the patient's thumb toward the scaphoid (Fig. 70.51). 4. Physician rotates the patient's thumb outward into abduction with extension (Fig. 70.52). 5. Retest.
THE KNEE
FIGURE 70.48. Intermediate position, right piriformis dysfunction.
FIGURE 70.49. Late intermediate position, right piriformis dysfunction.
Many different possible dysfunctions around the knee are potentially treatable with the Still technique. For purposes of demonstration we will limit ourselves to that involving the fibular head. Typically the fibular head has a limited range involving, at most, a couple of millimeters of anterior and posterior gliding motion. However, if the fibular head is limited from its normal range it can result in a marked pain in the lateral side of the knee, a pain that is poorly localized by the patient. Palpation of the knee demonstrates marked tenderness of the fibular head. The foot is used as a lever to assess restriction and freedom of the fibular
FIGURE 70.51. Initial position, right in-rotated scaphoid .
1114
VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
FIGURE 70.52. Final position, right in-rotated scaphoid.
FIGURE 70.54. Final position, anterior fibular head dysfunction.
Anterior Fibular Head Dysfunction head. If the fibular head is assessed with the knee flexed, we find that foot dorsiflexion with a little external rotation produces anterior excursion of the fibular head. Likewise foot plantar-flexion coupled with internal rotation produces posterior excursion of the fibular head. Failure to move adequately in either direction is demonstration of dysfunction. When the author began to assess fibular head dysfunction with the patient supine and the knee extended he found, much to his surprise, that fibular mechanics reversed. That is, with the knee extended, the fibular head moved posterior with foot dorsiflexion and anterior with foot plantar-flexion. Further analysis suggests that the most likely explanation for this discrepancy has to do with the effect of tension in the iliotibial band. Whatever the cause, the author has typically treated fibular head dysfunctions with the patient in the supine position and, thus, the unusual mechanics influence how it is treated.
Position The patient is supine with the physician at the foot of the table. Procedure 1. Physician monitors the fibular head with one hand. The other hand grasps the patient's foot, plantar flexes it, and adds some internal rotation and supination on the tibial axis.
2. Physician introduces compression from the hand on the patient's foot with a vector through the fibular head (Fig. 70.53). 3. Physician maintains the compression while the patient's foot is passively moved through its range of motion into dorsiflexion, external rotation, and some pronation (Fig. 70.54). The fibular head may be felt to release. 4. Physician discontinues compression and returns the foot to neutral. 5. Retest. Note: If the fibular head dysfunction is to be treated with the patient's knee flexed, the opposite foot motions would be used.
REFERENCES I. Still AT. Osteopathy, Research and Practice. Published by the author,
FIGURE 70.5 3. Initial position, anterior fibular head dysfunction .
Kirksville, MO; 1910. Reprinred by Eastland Press, Seattle, WA; 1992. 2. Hazzard C. The Practice and Applied Therapeutics of Osteopathy, 3rd rev. ed. Kirksville, MO: Journal Printing Co; 1905. 3. Van Buskirk RL. A manipulative technique of Andrew Taylor Sri!!. )AOA. 1996;96:597-602. 4. Van Buskirk RL. The Still Technique Manual. Indianapolis, IN: American Academy of Osteopathy; 2000. 5. Greenman PE. Principles ofManual Medicine, 2nd ed. Baltimore, MD : Will iams & Wilkins; 1996. 6. Mitchell FL Jr, Moran PS, Pruzzo NA. An Evaluation and Treatment Manual of Osteopathic Muscle Energy Procedures. Valley Park, MO: Mitchell , Moran and Pruzzo, Associates; 1979. 7. Walton WJ . Textbook of Osteopathic Diagnosis and Technique Procedures. Newark, OH: The American Academy of Osteopathy; 1972.
TREATMENT OF THE ACUTELY ILL HOSPITALIZED PATIENT HUGH ETT L INGER
THE STRUCTURAL EXAMINATION
KEY CONCEPTS An osteopathic structural examination: • Providjng clues to the medical/surgical diagnosis of a hospitalized patient • Directed toward the underlying pathophysiology of the disease process An individualized osteopathic manipulative treatment plan: • At each visit • For each acutely ill hospitalized patient • Specifically directed toward dysfunction, discovered during a musculoskeletal structural examination • Appropriate for the patient's condition and directed toward improving physiologic function • For support and assistance to the pacient recovering from an illness or other acute stress
The science of osteo pathy is applicable to the full spectrum of medical and surgical problems. Osteopathic evaluation and treatment, integrated into the care of the acutely ill hospital patient, is based on an understanding of the mechanical and functional aspects of the body's viscera and systems, including the respiratory, circulatory, the immune, and auto nomic nervous systems. T his chapter specifi cally presents a template for an osteopathic structural evaluatio n that investigates body physiology related to a patient's disease processes, not just the mechanics of the neuromusculoskeletal system, and as such, beco mes an invaluable part of the physical exami nation . It presents the general principles upon which the treatment plan is based and suggests manipulative treatment techniques that apply these principles. T he resulting treatment plan is a natural exte nsion of the structural examination. T he osteopathic treatment that is administered supports the patient and assists in thei r recovery from illness or other acute stress. A unique and individualized treatment plan must be designed for each acutely ill hospitalized patient at each visit.
Accurate diagnosis is the key to appropriate treatment of any patient with any disease process. For this reason, a basic structural examination should be perform ed on all hospital patients. The structural examination offers the osteopathic physician additional clues that assist in the overall assessment of a patient's condition and the development of an appropriate treatment plan. T he hospital structural examin ation is a va riation of the general structural exam ination described in C hapter 44. The American Osteopathic Association (AOA) h as designed a standardized hospital structural examination form for use in all osteopathic services (Fig. 7 1.1 ). T his examination consi sts of required and optional parts. T he required section , which includes stati c symm etry, both anteroposterior (AP) and lateral, and regional screen for tissue tension , fulfills the requirements of a basic musculoskeletal examination . This pan of the examination is described in C hapter 44. Adaptatio ns must be made for the co ndition of the patient; so me patients are unable to sir, stand, or walk. Although listed as optional , this author strongly reco mmends that the focused examination described herein be carried out in the acutely ill patient, as it will provide clues to the diagnosis and overal l condition of the patient. It assesses the function of th e patient's major organ systems. Also, if an osteopathic manipulative treatment is to be performed on a hospitalized patient, a focused musculoskeletal examination is required. Notes regarding the focused examination ca n be recorded in the "optional" region of the standardized form, for later dictation with the physical exam ination o r the progress notes. T he as pects of this focused srructural examin ation will be described in detail in this chapter.
Assessing for Segmental Facilitation ReAex somatic dysfunctio n provides important clues to th e presence of acute and/or chronic disease. T he information gathered is com bin ed with the rest of the physical examination to reach a wo rking differential djagnosis. In o rder to most accurately interpret structural findings as they relate ro the systemic diseases they reAecr, reAex somatic dysfunctio n must be differentiated from postural, traumatic, and other purely somatic causes of so matic
1116
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Osteopathic Musculoskeletal Examination of the Hospitalized Patient Examiner: -'(::...P"_ ·nt!:...__ _ _ _ _ _ _ _ _ _ _ _ _ _-1
Optional Worksheet
Chief Complaint: _..:..R..:..:e:..: ~q1.:u::.:i::_re::cd=-------------l
Ant./Post. Spinal Curves I Cervical Lordosis Thoracic Kyphosis Lumbar Lordosis
N D
<&
0 0 0 0 0 0
Standing Prone/supine lat. recumbant
D severe
~
__j
L
examine
/
0
1 - - -- - 1 Aueument Toolo:
0 T "' Tenderness 0 A - Asymmetry
r
CIJ
0~§
0 D 0
0
Unable to
~
---0 < C1-2 ~= .---hr0 C3-7 ~~
Scoliosis (Lateral Spinal Curves) Sitting
0\
Anterior
-
right
~_n_~rf]P
0 0 0
0None 0Functional
0Mild
left
For Coding Purposes Only
I= increased N =normal D =decreased
0Moderate
Posterior
<&
--
-'-
r"'"-c
P-"'-
:~,~~ ~~
_____./'
0 12-L2 _____:::,_
~ ~:::
r--~0-R-·-~-~~:_·__.-o-S~I--~--,\:.._ r ~~ 0 ~\' 0 T ""
0:Jauave
...,
Sl
11Ssue Texture Change
II
Severity Key:
0 · NoSO or bac kground (BGJ levels
( i
:::o
@ ""'
)/
f Region Evaluated Head Neck Thoracic T1-4 TS-9 T10-L2 Lumbar Pelvis I Sacrum Pelvis /In nominate . R Extrem1ty (lower) L Extremity (lower) R L Ribs Other /Abdomen
Mmor T AAT more than BG levels
-:-symptoms
I'
q
Signature of the examiner:
C1)
(2) ' TART obvious fA ~ T esp )
Severity
0 1 2 3
0000 0000 0000 0000 0000 DD0 D 0000 0000 0000 0000 0000 0000 0000 000D
Symptomatic. A and T very easily found, ·key les 1on•
Abbreviation Key: OA = Occipitoatlantal joint TMJ =Temporomandibular joint Sympathetic ganglia: TMP =Temporal bone C = celiac ganglion SBS = Sphenobasilar symphysis S = superior mesenteric Ganglion · I = Inferior mesenteric ganglion
Specifics of Major Somatic Dysfunctions
Major Correlations With:
0 0 0 0 0 0 0
Neurologic
0 0 0
Viscerosomatic
0
Pulmonary
Primary Ms-skeletal Activities of daily living Other
0
Gastrointestinal
0 0
Genitourinary
Traumatic Orthopedic
Rheumatological EENT Cardiovascular
Congenital
Other: _ _ _ _ _ _ _ _ _ _ _ _-f
- - - - - - - - - - -- - - - - - - - - - - - - - - - D a t e of Examination: - - - - - - - - - - - - f
Signature of the examiner(s) :
Date of ExaminaUon:
05A2X.PCX MLK I WAK VERSION 8:041499
O"klal fonn of the American Osteopathic Msoclatlon and the Educational COuncil on Osteopathic Principles - f9!il8
FIGURE 71.1. The American Osteopathic Association standardized hospital structural examination form.
7 1. Treatment of the Acutely ILL Hospitalized Patient dysfunction. There are unique qualities ofviscerosomaric reflexes, which are related to the known pathophysiology of the reflex and rhe unique tissue changes they create. A viscerosomaric reflex is produced by the stimulation of nociceptors (pain carrying sensory fibers) within the diseased viscera or irs fascia. Nociceptors are particularly sensitive to inflammation, and their exaggerated response to inflammatory processes may explain the distinct and identifiable tissue changes they produce. For this reason, reflexes are most apparent in diseases associated with acute inflammation, particularly those with a presenting complaint of pain, and may nor be evident in a patient with a malignant nm1or if rhe tumor is not causi ng irritation or inflammation. The nociceptive input travels to interneurons in the dorsal horn of the spinal cord, where it converges with nociceptive inputs from all somatic tissues. These interneurons stimulate both sympathetic efferent fibers and a-motor neurons. Stimulation of sympathetic o utflow nerves produces changes in blood supply and swear gland activity at the body surface, in addition to visceral motor changes. l.M. Korr measured rhe cutaneous changes produced by segmental facilitation via alterations in skin resistance (swear) and temperature (blood flow) (1). T hese changes are palpable as increased temperature and sweat (moisrure and/or skin drag) in the paraspinal tissues, and are excellent and reliable indicators of segmental facilitatio n at that level of the spinal cord. In a srudy of the palpatory findings in acute myocardial infarction, Nicholas and colleagues found increased temperature as rhe second most common tissue finding (2). Yiscerosomaric reflexes initially produce vague, midline, gnawing deep pain (Fig. 71.2). As they progress they involve neuromuscular changes in rhe segmentally related tissues; this reflex effect on muscle tone is important, as it identifies their spinal segmental level and distinguishes them at a paraspinallevel (Fig. 7 1.3).ln his work with Korr, Denslow describes "doughy, boggy" paraspinal myofascial tissues ar rhe levels of facilitation (3). Parriquin describes a "fusiform soft tissue change in rhe paraspinal muscles" occurring over several segments which "rails out on the
Somesthetic Cortex
1
Thalamus
V iscera FIGURE 71 .2. Visceral pain pathway-vague and periumbilical. Palpable tissue texture change is found in the abdomen over the prevertebral (collateral) sympathetic ganglion associated with that organ.
1117
FIGURE 71 .3 . Viscerosensory pain pathway. This reflex produces the typical segmental viscerosomatic reflex. Palpable tissue texture changes are found over the somatic paravertebral t issues innervated by somatic nerves from the same cord level that suppl ies sympathetic innervation to the affected organ.
ends" (4) . He continues to say, "the multifidus and rotatores are the best place in rhe spinal region to pal pare for changes of viscerasomatic origin" (4). Beal, in his studies of cardiac and pulmonary patients, found a supine compression rest to be rhe most accurate indicator of reflex dysfunction (5,6). Beal's description of the response to the compression rest is ar rhe level of joint motion, but is considered secondary to deep muscle splinting. Nicholas and associates, in a study of acute myocardial infarction, most often found "firmness" and warmth (2). Osseous/articular motion changes also occur, bur these findings are most likely secondary to the altered muscle tone produced by the acute viscerosomaric reflex processes. William Johnston, DO, describes a "linkage" of thoracic vertebral and rib motion that he considers indicative of a viscerosomatic reflex (7). Once again, this articular motion finding is considered to be secondary to an altered neuromuscular response to a motion challenge. The movement restriction, found at a joint involved in this reflex process, is soft, with a springy feel, which, when palpated, suggests the viscerosomatic reflex. T hese regions also show unusual resistance to manipulative treatment, especially high velocity/low ampli tude, when directed toward primary joint somatic dysfunction. Somatic dysfunction that rapidly recurs after "successful" manipulative treatment also suggests viscerosomaric origin or accentuation. When visceral inflammation involves the parietal peritoneum, the patient's discomfort becomes localized over the viscera involved (Fig. 7 1.4). Acute segmental facilitation creates a variety of palpable tissue changes that may be used to identifY the presence of an underlying disease process. The most superficial clues, temperature and skin drag or moisture, are among the most useful, and are easy to idenrifY in the seated position . Palpation of the typical boggy, fusiform muscular changes can be performed with the patient either seated or supine. As with articular motion restrictions, viscerosomatic dysfunction is idenrified by motion restriction without a firm, stiff end-point but with a characteristic end-feel. It is likely that the differences between findings expressed by different examiners result from different diagnostic approaches. T he skills required to consistently identifY reflexes develop with time and experience. For the practitioner learning to recognize the unique tissue changes of viscerosomatic reflexes, it is
1118
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment TABLE 71.1. SEGMENTAL FACILITATION Type
FIGURE 71.4. Peritoneal cutaneous reflex of Morley. The pain is localized over the viscera due to involvement of the parietal peritoneum directly over the organ. Palpable tissue texture change and acute pain is found directly over the organ and segmentally at the innervation level of the peritoneum or pleura.
helpful to evalu ate reflex patterns in patients with clearly identified, acute disease processes. In this way the physician develops the ski lls required to recognize reflexes and to sense their unique qualities. If a reflex persists, as occurs in a patient with a chronic disease, the tissues, including the joints, become stiff and the qualities palpated become different. Beal states, "The chronic phase of reflex activity is . .. characterized by trophic changes in the skin, increased thickening of the skin and subcutaneous tissues and localized muscle contraction. The muscles are hard and tense and may be hypersensitive to palpation" (8). The chronic muscle spasm ultimately stiffens the joints, giving the articular motion restriction a more firm, definite end-feel that is much closer to a typical postural or somatic problem. When someone with a chronic problem has an acute attack, a warm, moist, boggy tissue reaction will be superimposed on the deeper hard, stiff tissues, leading to a separate tissue diagnosis that may be called an acute on chronic problem. The tissues tell the story. This finding may be helpful in understanding the history of a current problem where the patient may be unaware of previous episodes of the problem (Tab le 71.1).
Interpretation of Findings T here is a tremendous amount and variety of information available to the osteopathic physician provided through the evaluation for the presence of segmental reflexes. Although practice will obviously improve the accuracy of the examination, 10 years of experience doing structural examinations in the acute care setting has demonstrated to this author that the great majority of cases present with significant, obvious reflex patterns which are easily recognized. 1. The presence or absence ofan acute process (perhaps the most fundamental difference). Although this information alone should not determine workup and treatment, it can be a factor in how aggressively a patient should be worked up, especially with a
Characteristics
Acute
Increased temperature (a local chemical physiologic reaction), increased moisture and/or skin drag. Prolonged red reflex. Boggy, fusiform muscular changes. Articular motion restrictions without a firm, stiff end point.
Chronic
Thickened skin and subcutaneous tissues. Rapid fading red reflex. Localized muscle contraction (increased muscular tone). Muscles are hard, tense, and hypersensitive to palpation. Stiff joints with articular motion restrictions that are firm with more definite end-feel.
Acute on chronic
Warm, moist, and boggy superimposed on deeper hard, stiff tissues.
Nociceptive input from somatic tissue converges in the dorsal horn --> lnterneurons stimulate sympathetic efferents and a-motor neurons -> Palpable somatic changes are produced.
somewhat vague complaint. The presence of an acute reflex indicates an underlying acute process. For example, a right lower quadrant abdominal pain, appendicitis, a ruptured ovarian cyst, or Crohn disease will all produce an acute reflex pattern . Simple cramping or mild gastroenteritis will not. 2. Identification ofvisceral disease in the presence ofan acute reflex finding. There are some diseases that may be differentiated by localization of reflexes and some that may not. For example, the heart is innervated by levels Tl-5, whereas the stomach is innervated by levels T5-9. Although there is anatomic variation within these levels, it is usually clear if substernal pain has its origin in the heart or the stomach. On the other hand, the gallbladder and the duodenum are both innervated via the right side of the celiac ganglion, and cholecystitis and duodenal ulcer would produce a simi lar, if not identical reflex pattern. Although many sources identify unique sympathetic innervation levels for each viscus, clinically there are four important groupings which are easy to remember and practical for use (Fig. 71.5). All structures above the diaphragm are innervated (approximately) by the Tl-5 levels. This includes the heart, lungs (often extended to T6 or T7 in the literature), esophagus, and viscera of the head and neck. A vast majority of cardiac problems occur on the left side (left ventricle), and these problems would produce a left-sided somatic reflex. Spinal roots T5-9 (approximately) transmit and receive via the pathway of the greater splanchnic nerve primary sympathetic fiber synapse in the celiac ganglion. The liver, gallbladder, duodenum, and pancreas (head) are innervated from the right side at these levels. The stomach, spleen, and pancreas (tail) are innervated from the left. The inferior border of the scapula can help a physician identify this general spinal region in the seated patient. Spinal roots Tl0-12 (approximate) transmit and receive via the lesser splanchnic nerve pathway and primary sympathetic fibers synapse in the superior mesenteric ganglion . It should be remembered that these spinal levels include the innervation of kidneys and upper part of the ureters, testes, ovaries, and upper part of the fallopian tubes, as well as the entire small
71. Treatment of the Acutely 1ll HospitaLized Patient Parasympathetic innervations
Central nervous system levels
1119
Sympathetic innervations
FIGURE 71.5. Sympathetic and parasympathetic innervations.
bowel, ascending colon, and rransverse colon ro abour the splenic flexure (including the appendix) . Right-sided organs, including the appendix, cecum , and ascending colon have a right-sided innervation. The T I 0-11 spi nal region is contacted by placing one hand on the spin al region just posterior ro the xiphoid process and extending caudad. Spinal roots T12-L2 innervate the lower abdom inal and pelvic viscera. Fibers travel in the pathway of least splanchn ic nerve and primary sympathetic fibers synapse in the inferior mesenteric ganglion . This level also innervates the lower part of the fa llopia n tubes and the lower part of each ureter, as well as the uterus (prostate in males) and bladder. The colon here has a left-s ided innervation so irritations would produce left-sided paraspinal somatic reflexes. T he 12th rib is useful in differentiating the middle from lower abdominal levels. The Tl2-L2 region can also be approximated by putting one hand over the spinal region at the level posterior ro the umbilicus and extending it cephalad. It is suspected by this author that variations recorded between organs within the same general level may have more to do with individual variation of the populations investigated than with consistent differences in actual innervation. Regardless, this author does not believe it is clinically possible to differentiate between different viscera within a give n level if their innervation comes from the same side. Furthermore, gro uping the viscera by general level is easy ro remember and is clinically useful. In this scheme, it is impossible to distinguish appendicitis from a
right-sided ovarian cyst, but appendicitis can be differentiated from cholecystitis or a left-sided ovarian cyst with a midline pain presentation. Early visceral pain is referred to the midline of the abdomen, often around the umbilicus. ft is a good idea to have some way of recalling the basic autonomic innervation to the viscera of the body (Fig. 7 1.5). 3. Assessing degree ofdisease by degree of reflex facilitation. This is an intriguing thought, but an ill-advised one. Different individuals have different reactivity within their nociceptive nervous systems, and will therefore present with varying degrees of reflex facilitation with the same degree of inflammatory process and/or disease. One particular example from clinical practice would be the patient with diabetic neuropathy, which affects small caliber peripheral nerves. These patients often have blunted reflexes that are more difficult to identify and interpret. Once a baseline level of dysfunction is established, and compared ro other clinical indicators of disease severity, it may be possible to follow the progress of the disease by changes in the intensity of the reflex, although this has not been studied. However, it is not uncommon to find a reflex has changed or disappeared, indicating a change in the patient's clinical status before other indicators have changed. 4. Differentiating acute versus chronic processes. This can be important in several ways. First, it may allow the identification of a long-standing process in the face of an acute presentation (i.e., the "acute on chronic" tissue changes). Surprisingly, patients do not always recall past episodes of a problem. The examiner can
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VII. Osteopathic Considerations in Pa!patory Diagnosis and Manipulative Treatment
also identify if a known chronic problem is, in fact, the cause of a present complaint. A chronic reflex pattern, without an acute overlay in that region makes it is unlikely that the chronic organ or system is the source of the acute disease process. This might be useful in the evaluation of chest pain in a patient with a history of ischemia or myocardial infarction, who will undoubtedly demonstrate chronic findings with or without an acute process superimposed.
The Thorax Breathing is one of the most fundamental processes in human physiology. Respiration is responsible not only for the movement of air, but is also directly involved with venous and lymphatic circulation. A focused evaluation and treatment of the thorax is indicated in all respiratory diseases, such as asthma and pneumonia. Thoracic function also has an impact in less obvious situations, such as the postoperative abdominal surgery patient, whose most likely complication will be pulmonary, or the lower extremity cellulitis patient, whose body depends on diaphragmatic respiration for proper drainage of the infection . There are few, if any, acutely ill patients who do not warrant a focused examination of their respiratory mechanism. The structural examination of the thorax can reveal a great deal about the underlying condition of the respiratory system. Breathing may be divided into an inhalation and exhalation phase. Restricted motion in one phase may suggest one pathology over another. Pneumonia will reduce the excursion of the thorax toward inhal ation locally, over the area of consolidation, whereas asthma and other obstructive diseases will reduce the excursion of the thorax toward exhalation. T his finding may help differentiate the patient with a primary asthmatic attack from one whose asthmatic attack was triggered by pneumonia. The difference between restricted inhalation and exhalation may also help differentiate chronic obstructive pulmonary disease (COPD) from congestive heart failure (CHF), which often coexist in the same patient, and may present sim il arly with shortness of breath and crackles in the lung bases . If the present exacerbation is due primarily to C HF, there will be res triction of the lower thorax to inhalation, and the exhalation phase will be relatively effortless. If the present exacerbation is C OPD, the patient will have dramatic limitation to exhalation and the exhalation phase will be active (the patient will work to get the air out). This effort by the patient is easily observed by placing the fingerpads or palm in contact with the patient's skin, just below the costal margin. Structural examination of the thorax should be performed along with auscultation and percussion in the physical examination of the cardiac and respiratory systems. The structural examination includes evaluation of the entire spine, the pelvis, and sacrum, which move, in addition to the ribs, during respiration and contribute to the overall shape change of the thoracic cavity (9,10). The excursion of the thorax produces the volume and subsequent pressure changes that produce the movement of air and fluids. Compliance of the thorax is a separate, important functional parameter of respiration related to the structural evaluation of respiration , as it more accurately reflects the work of breathing, es pecially in obstructive and restrictive pulmonary disease. The
clinical difference between excursion and compliance may be understood by comparing the difference between an otherwise healthy patient with COPD, who wi ll have a limi ted but adequate excursion of a very stiff, noncompliant thorax, to a patient with no preexisting pulmonary disease going into acute respiratory failure due to exhaustion of the respiratory musculature. The latter patient will have a very limited excursion of their thorax, but may have a compliant spine and rib cage. Comparing excursion (by monitoring movement duri ng respiration) to compliance (by motion testing the spine and rib cage) wi ll yield a much more complete picture of the respiratory system than reviewing either of these factors alone. The length and tone of the respiratory musculature, including the diaphragm, will complete the structural examinatio n of the respiratory system. Evaluate the muscles, both during contraction (inhalation) and at rest (end exhalation). Ev idence of respiratory muscle fatigue and failure should be obtained during this part of the examination. Intercostal retractions may be observed during the evaluation of rib excursion. Paradoxic motion of the lower ribs (inward movement during inhalation), an indicato r of a flattened, tense diaphragm , may be observed during evaluation of the excursion of the lower rib cage. Paradoxic movement of the abdomen (inward movement of the abdomen during inhalation), a sign of impending respiratory failure, may be observed with a hand below the costal margin. A less obvious sign of diaphragm fatigue may be noted with the same contact, as the effort or force of contraction during inhalation will be reduced as the diaphragm fatigues .
Focused Structural Examination of the Thorax This is also discussed in C hapter 49, Ribs and Sternum.
Upper Thorax 1. Sternum. Evaluate movement of the stern um, both inhalation and exhalation. 2. Clavicle. Evaluate a sense of posterior/superior movement of the clavicle with inhalation, and an anterior/inferior movement during exhalation. Also evaluate in ferior movement at the sternoclavicular (SC) joint during upward shrug of the shoulders and its relati ve superior movement during return to resting state. Evaluate rotation on its long axis during forward flexion of the shoulder. Palpate for a normal slight movement of the acromioclavicul ar (AC) joint during add uction of the arm across the chest. Test for hinge motion of the sternomanubri al joint during inhalation and exhalation. 3. First rib. Evaluate when examin ing the clavicle. 4. Ribs 2 through 6. Evaluate pump handle motion of the upper ribs with hands lateral to the sternum; evaluate m iddle ribs with thumbs approaching the xiphoid and fingerpads over the midaxillary line; evaluate bucket handle motion with hands below the breasts (see Chapter 49, Fig. 49.8). 5. Musculature. Evaluate the tension of the scalene, sternocleidomastoid, and trapezius muscles when evaluating the clavicle and first rib. Evaluated the intercostals when evaluating rib motion. Evaluate the paravertebral musculature, particularly those with rib attachments.
7 1. Treatment of the Acutely Ill Hospitalized Patient
Lower Thorax and Diaphragm 1. Ribs 6 through 10. Evaluate bucket handle motion at the mid
The Abdomen Evaluation of the container should accompany rhe classic palpatory evaluation of the abdomen. The shape of a container will affect the function of its contents. The abdomen has a roof, a floor, and anterior and posterior walls. • The diaphragm is the roof of the abdomen; the liver, spleen, and supporting mesenteries are suspended from it. • The pelvic diaphragm is the floor. It, along with the shelf created as the posterior abdominal wall crosses the pelvic brim at the level of the pectinate line, and supports the abdominal and pelvic viscera from below. • The iliopsoas and quadratus lumborum make up the posterior abdominal wall. The insertion of iliopsoas on the lesser trochanter of rhe femur involves the hip in abdominal and pelvic function. • The abdominal wall is its anterior boundary.
1121
Skeletal Considerations The sacrum, pelvis, hip joint, lumbar spine, and lower six ribs and thoracic verrebrae form the structural and functional framework to which the soft tissue container of the abdomen is attached and supported. All should be evaluated for motion restriction and/or altered position. The diaphragm should be evaluated with emphasis on irs lower attachments to the 12th rib and lumbar spine. When the diaphragm becomes tense it flattens and carries the 12th ribs inferiorly at their tips. The lumbar spine will become flattened and resist anterior pressure in the supine patient. The same relative positions will be adopted when the diaphragm has a fascial "drag" placed on it, although the resistance encountered will be of a lesser degree and different quality. Rarely will the diaphragm be displaced superiorly from a dysfunction. The movement of the pelvic diaphragm may be inferred by the magnitude and intensity of the consequent nuration/counternutation movement of the sacrum occurring during respiration (see Fig 71.13). Although this movement may be more obvious with the patient prone, supine evaluation is often necessary in the acutely ill , hospitalized patient. A two-handed contact from the side of the patient, one hand contacting the sacral base and the other on the sacral apex may be used for this evaluation. More direct evaluation of the tension and movement of the pelvic diaphragm may be performed with a contact in the ischiorectal fossae. These are found just medial and slightly posterior to the tip of the ischial tuberosities (Fig. 71.6). The pelvic diaphragm will move inferiorly with inhalation and superiorly with exhalation. The quadratus lumborum may be palpated anterior and lateral to the erector spinae mass in the lumbar spine. Irs edge is usually discernible beginning just below the rip of the 12th rib. The psoas major is a deeper, more medial flank muscle that is more difficult to palpate directly. The increased amount of muscle tone observed and the combination of upper lumbar somatic dysfunction and external hip rotation on the same side may infer tension. The tendon of the iliopsoas is directly palpable just below the inguinal ligament in the floor of the femoral triangle. The iliopsoas tendon is usually tense, full , and tender when the muscle is in spasm. One can often sense the tension in the entire iliopsoas with one hand contacting the tendon in the femoral triangle and the other und er the upper lumbar attachments. Only the iliopsoas travels anteroinferolaterally here. Jones has also described anterior abdominal tender points related to spasm of the iliopsoas muscle (see C hapter 73, Counterstrain).
Palpation Palpation is an essential parr of any abdominal examination. However, extra care must be taken to avoid exacerbation of the patient's pain, as the resultant guarding by the patient will interfere with the examiner's ability to gather reliable information.
Light Palpation It is useful to begin the abdominal examination with light palpation and in a region of the abdomen distant to the patient's chief complaint of pain or discomfort. This will help secure the
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Vll Osteopathic Considerations in Pa!patory Diagnosis and Manipulative Treatment
A.
B.
Abdominal pressure from inhalation as abdominal diaphragm contracts
Sacrotuberous ligament (STL)
canal or (pudendal canal) Obturator intern us muscle
tuberosity External anal sphincter
C
tuberosity
Ischiorectal fossa
The ischiorectal fossae
D
Ischiorectal fossa treatment areas for a left lateral recumbent patient
FIGURE 71.6. The ischiorectal fossa and pelvic diaphragm. A. The broken line depicts the pelvic diaphragm during inhalation. B. The ischiorectal fossa as it would appear in a lateral recumbent patient.
patient's comfort and cooperation, and can yield information not obtainable with deep palpation. 1. Involuntary guarding by the patient. Involuntary guarding, present without any actual or perceived stimulation of the discomfort, should be distinguished from voluntary guarding due to actual or perceived exacerbation of pain induced by the examin ation . This determ ination is an essential part of the abdominal examination, and is most accurately evaluated with light palpation , as many healthy individuals will guard with deep palpation. 2. Ptosis. Dr. Still often taughtthatthereisasagoftheabdominal contents into the pelvis resulting in physiologic consequences. He wrote, "The caecum and the transverse and sigmoid flexure are often forced from their normal positions and piled into the pelvis, dragging the uterus and small intestine down with the caecum and obstructing all possible chance for the fluids of the small intestine to pass through the ileocecal valve and reach the colon" (11). Sag of the abdominal contents and the mesenteries that support them may be evaluated by comparing the resistance to normal limits and with the right and left sides, produced by a gentle lift just superior to each inguinal ligament. This quick test should be part of the light palpatory exam ination . 3. Congestion. A sense of fullness and or congestion will often be evident over areas of ac ute inflammation, such as cholecystitis or diverticulitis. It may be accompanied by a palpable sense of warmth. This somewhat subtle finding will be much more difficult to identi fy during deep palpation. T here may also be a subcutaneous puffiness palpable over the epigastric region of the abdomen, a terminal drainage site related to the abdomen. 4. Tenderness. Tenderness is a subjective symptom but can usually be identified accurately during light palpation. Identifying the tender area early in the examination and leaving that area for evaluation near the end of the exam ination will help maximize
patient cooperation for the bulk of the early abdominal examination. The area of the patient's tenderness can be evaluated in depth at the end of the abdominal examination.
Deep Palpation Deep palpation must be carefully performed. Slow, deliberate movements will minimize discomfort and voluntary guarding. Never palpate with your fingertips. Use the fingerpads. Palpation with one hand over the other may be more comfortable to the patient and enhance palpatory sensing. The fingerpads of a relaxed hand rest on the patient and receive information while the other hand, resting on top, exerts gentle, steady pressure to reach the desired depth . The abdomen is classically divided into four quadrants for palpation (see Chapter 51, Fig. 5l.l1). The epigastrium and suprapubic areas may be considered separately. The examiner should always keep a clear mental picture of all significant anatomic structures in the area being palpated (see Fig. 51.12). Although many viscera are not palpable in normal conditions, in pathologic situations they may become discernible and offer clues to an accurate working diagnosis. Several examples, that this author has been found to be useful in practice, are presented, but the possibilities of abdominal palpation are far greater than just these examples. 1. The tip of the gallbladder capsule is often palpable in cases of acute cholecystitis, with associated fu llness, congestion, and often warmth overlying it. When present, these signs are more accurate than the Murphy sign of right upper quadrant tenderness. 2. The stomach is palpable slightly left and inferior to the xiphoid. Sometimes the physician will note that the sto~ach resists gentle downward distraction produced with one hand, while the other hand contacts the xiphoid to stabilize the
7 1. Treatment of the Acutely ILL Hospitalized Patient diaphragm. This resistance is consistently present in patients with hiatal hernia and reflux disease. Full ness, congestion, and wa.rmth are often present in the left upper quadrant in acute gasmns. 3. The motion of the liver with breathing and the tension within the ligaments anchoring the liver to rhe diaphragm should be evaluated, along with rhe size and contour of the liver. The movement of the diaphragm is essential for efficient portal ci rculation (12).
The Fluid (Lymph) Mechanism The evaluation of the body's circulatory system is an integral parr of any physical examination. The evaluation of the status of the lym phatic circulation is indicated in any inflammatory process, as the lymphatic system is responsible for the drainage of inflammatory exudates, and is integral in the progression and resolution of an inflammatory process. Millard was the first osteopathic physician to discuss the evaluation of the lymphatic system in the physical examination. He said, "For every congested tissue there is a corresponding lymph disturbance. Wherever pus is present there is er. largement in the nearest nodes . The lymph stream ebbs and flows acco rding to the amount of blockage and nodular involvemenr at certain points" (13). Dr. Millard considered it possible to differentiate disease processes by the location, degree, and quality of lymph node enlargement. He also described a principle that is important in rhe treatment oflymph congestion: "The lymph stream is readily checked in many ways . The lymph vessels are pliable and readily compressed" (13).ln the evaluation of lymphatic function, one must investigate tissue tension along rhe course oflymphaticdrainage, with an emphasis on the regions where lymp h vessels are most vulnerable to altered tissue tension. J. Gordon Zi nk, a student of Dr. Millard, continued to develop methods for the evaluation of lymph function and dysfunction. He cal led attention to the congestion produced in the regions of lymph nodes when there was dysfunction of the lymph system, with or without frank edema, and the supraclavicular congestion found with dysfunction of rhe thoracic duct and "terminal lymph drainage from rhe head and neck. " He also described a specific rest he used in the evaluation of rhe lymphatic system, "There is a simple bur very practical test to confirm better circulation, because of restored diaphragmatic respiration, when the patient is supine. The hands of the physician are placed high on the patient's abdomen, just below the costal arch. Firm pressure is used downward toward the table and cephalad, as if to ' raise' or ' redome' the diaphragm. The patient should experience a sensation of'warmth' or 'heat' in the lumbar and sacral area" (10). WG. Sutherland introduced rhe concept of fluid fluctuation in his description of the primary respiratory mechanism (14). The movement of interstitial flu ids is important in the process of cellular respiration (the cellular exchange of gases), as well as rhe exchange of nutrients and was te products . Motion of the interstitial fluids occurs in response to intrinsic, rhythmic motions of the body, including pulse, respiration, and the primary respiratory mechanism. Interstitial fluid fluctuation may be evaluated passively, by rhe presence or absence of these inherent forces in the region of the body being evaluated. They can also be actively eva!-
1123
uared by assessing the response of the tissue and irs fl uid matrix to local or general lymph pump techniques aimed at fluctuating the interstitial fluid. The evaluation of the static and dynamic findings of the lymphatic circulation is important in the overall physical evaluation of the circulatory system (Table 71.2).
APPROACHING THE ACUTELY ILL HOSPITALIZED PATIENT Osteopathic treatment in the hospital setting is most effective when it addresses underlying physiologic mechanisms of the disease and supporrs the physiologic response of the host who has the disease. Although the manipulative treatment is ultimately based on the findings of the structural examination, these findings should be interpreted with regard to the body's response to rhe disease process and directed toward supporting the body's physiologic processes. This section will present a variety of conceprual models from which treatment plans should evolve. Techniques will be described to provide examples of how some of rhe underlying principles may be achieved, but should not be construed as the best or only way to treat an area or problem. One cannot overemphasize the importance of des igning treatments to the individual . There is, therefore, no such thing as a technique for asthma, congestive heart failure, or any disease, nor is there a manipulative technique for reducing segmental fac il itation, improving respiratory/circulatory function, or any other physiologic process. A variety of techniques can be employed for any of these treatment goals. Any technique is approp riate if it addresses the underlying physiology and mechanics, is appropriate for the present condition of the patient, and brings about the changes a physician expects to see from application of an efficient treatment to accomplish a specific physiologic goal.
Inflammation Inflammation is the generalized response to injury and disease. It is the hallmark of most acute illnesses. Inflammation involves the vascular system, the immune system, the nervo us system, and the connective tissues. It is essential to the initial respo nse of the body to the disease process, as well as the healing process. The lymphatic system is an integral part of the progression and ultimate resolution of inflammation. Besides draini ng areas of infection and injury, lymphatic drainage carries antigen to the nodes, where immune stimulation rakes place and T and B cells are produced. Nodal efferents provide migration routes for these cells to enter the primary circulatory system . The lymphatics are the only vascular system permeable to large particles, fats, and protein . In normal function, the lymphatics remove the proteins, which leak into the interstiti um from the capillaries, maintaining a de licate osmotic balance, and keeping the interstitial environment pristine. During any inflammatory process, increased capillary permeabi lity allows a tremendous efflux of protein into the interstitial spaces, producing an exudative swelling. This exudate can only be drained through the lymphatics. In addition, there is evidence that lymphatic drainage is necessary for the removal and deactivation of the chemical and immune mediators, which control inflammatory processes, making the lymphatics central in the progression and resolution of the
1124
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
TABLE 71 .2 . CLI N ICAL PEARLS Fi ndings
Patient
Compare:
1. Paradoxic movement of lower ribs 2. Paradoxic movement of abdomen
Compare:
1. Sign of impending respiratory fai lure 2. Sign of a flattened, tense abdominal diaphragm
Compliance of the rib cage Compare :
1. Poor excursion 2. Poor compliance
Sign: abdominal diaphragmatic fatigue Compare: Compare:
1. Inward movement of these ribs during inhalation; indicates flattened tense diaphragm 2. Inward movement of abdomen during inhalation; indicates impending respiratory failure 1. Paradoxic movement of abdomen during breathing 2. Paradoxic movement lower ribs The ease with which the rib cage will move 1. Evaluated by movement of the rib cage during breathing (i.e., poor observed motion) 2. Evaluated by motion testing of rib cage and sternum (i.e., poor motion tests) Force of diaphragmatic contraction is reduced during inhalation
1. Paradoxic movement lower ribs 2. Paradoxic movement of abdomen
1. Dramatic limitation of exha lation; patients uses active effort to exhale 2. Restricted lower rib cage during inha lation; re latively free exhalation
1. Congestive heart failure patient
1. Poor excursion; poor compliance 2. Limited excursion but often spine and rib cage compliant
2. Chronic obstructive pulmonary disease patient in relatively good health A manipulative technique is appropriate when:
1. It addresses the underlying physiology and mechanics 2. It is appropriate for the present condition of the patient 3. It brings about changes expected when applying efficient treatment to accomplish a specific physiologic goal
The work of breathing
A quantitative measure of the energy required by the body to overcome the resistance of the lung parenchyma and chest wall and accomplish inhalation and exhalation
35% to 60% of thoracic duct lymphatic flow is due to:
The response and effects of respiratory movements
process itself (15-18). Diseases including pancreatitis, asthma, rheumatoid arthritis, and even myocardial infarction will depend on lymphatic drainage for resolution. The large efflux of protein and water from the capillary bed leaves a very high concentration of erythrocytes, which pack into the small venules producing local venous stasis (17) . This makes the lymphatic system the only source of fluid drainage from an inflamed tissue. The tissue becomes saturated when the small hydrostatic gradient that produces capillary filtration is met by the increased interstitial pressure that the swelling tissue produces . At this point, the rate of blood supply will equal the rate oflymphatic drainage. Inflammation and healing are aspects of one continuous process, guided by the same group of cells. Cellular activity will shift from proinflammatory to healing as rhe proportion of relative controlling mediators shift their activity. Although this progression is related to the production of mediators, one must consider the role of the efficient breakdown and removal of these mediators in the progression and resolution of any inflammatory process. Prolonged inflammation leads to poor healing, smoldering infections, chronic inflammatory processes, and eventually tissue destruction. There is evidence that lymphatic drainage is involved in the removal and breakdown ofhistamine, bradykinin, prostaglandins, and leukorrienes (including cyrokines). Other mediators or the fate of other mediators simply have not been studied. As proinflammatory mediators are removed, those that stimulate fibroblasts and macrophages will predominate, and rhe heal-
ing process will ensue. Residual (interstitial plasma) protein from rhe inflammatory exudate will also stimulate fibroblasts to produce collagen. As with the inflammatory phase, rapid and efficient removal of these elements is essential to a physiologic healing process. A prolonged healing phase will lead to excess collagen production, fibrous adhesions, and eventually to tissue fibrosis. The lymphatic system is responsible for the removal of most, if not all, of the inflammatory exudate. It has been shown that lymphatic drainage is involved with controlling the rare of collagen production, both during the healing process and in the pathogenesis of diseases that result in tissue fibrosis . Diseases such as cirrhosis of the liver, interstitial lung diseases, and atherosclerosis have been linked to impaired lymphatic function (19). The lymphatic system is vulnerable to somatic dysfunction and irs dysfunction is responsive to osteopathic manipulative treatment. The function of the lymphatic system should be evaluated and treated as part of the osteopathic treatment of any patient with an inflammatory process.
Segmental Facilitation The treatment of acute segmental facilitation is fundamental and a broadly applicable model for the treatment of virtually any acutely ill patient. Reflex facilitation occurs in response to a vast majority of disease processes, and can alter and/or exaggerate the body's response to the disease, interfering with rhe recovery process. Facili ration is produced by nociceptor input, so that diseases presenting with pain are the most likely to produce significant
71. Treatment of the Acutely Ill Hospitalized Patient reflex patterns. Van Buskirk notes that the spinal cord may be activated ar a lower level of firing than is necessary to activate the corte~ and produce pain perception, so the perception of pain is not necessarily required for a reflex to be present (20) . Inflammation has been shown to greatly increase the firing of nociceptors. Therefore, those diseases that involve inflammation and/or a very tense patient are also likely to produce reflex facilitation, with or without the perception of pain (21). The effects of segmental facilitation will vary depending of the spinal cord levels involved and/or the organ systems involved in the disease process. The heart is extremely responsive to its innervation. Reflexes in the region of the sympathetic innervation of the heart have been shown to occur in ischemic heart disease and acute myocardial infarction (2,6). Increases in sympathetic outflow will increase heart rate and contractility, while simultaneously constricting rhe coronary vessels, reducing blood flow to the heart. This can produce an increased discrepancy between oxygen demand and supply available to a patient with coronary artery disease or to rhe ischemic portion of rhe heart after acute myocardial infarction. Segmental facilitation may also increase the arrhythmogeniciry of the heart, a potemially devastating occurrence following a myocardial infarction. Talman writes, "Parasympathetic influence tends to stabilize and adrenergic stimulation rends to increase the ventricle's propensity to develop arrhythmias. Asymmetrical sympathetic activity, particularly that which favors the left-sided sympathetic pathways to the heart, is especially arrhythmogenic" (22). The left-sided , upper thoracic segmental facilitation noted in response to acute myocardial infarction will produce an increase adrenergic influence to the heart that favors left-sided innervation. Finally, Korr noted other, less obvious effects of increased sympathetic activity to the heart, including a prolonged healing rime and reduced production of collateral circulation (23). Borh are important in the recovery period following a myocardial infarction. The heart also has a parasympathetic innervation via the vagus nerve. The vagus nerve will reduce heart rare and contractility, and carries information via the baroreceptors concerning blood pressure. Beal reports a less common cervical finding associated with cardiac disease that may reflect a reflex carried by the afferent fibers of the vagus nerve (6). It has been found that firing vagal afferent fibers stimulates the Cl and C2 segments of the spinal cord (24). Kuchera and Kuchera suggest that vagal sensory innervation of the heart is concentrated in the posterior and inferior walls, which explains the greater number of bradyarrhythmias from those infarctions (25). Although this idea has had little study, Rosero and colleagues did find a reduced correlation of upper thoracic somatic dysfunction wirh posterior/inferior wall myocardial infarction (26). His study did nor look at the presence of cervical findings in these patiems. The presence of upper cervical and cranial (especially occipitomastoid) somatic dysfunction should be treated in patients with cardiac disease, especially in the presence of a bradyarrhythmia (right vagus) or atrial ventricular block (left vagus). Reducing segmemal facilitation in patiems wirh acute cardiac disease is central ro rhe osteopathic treatment of their cardiac processes. However, extreme care must be taken in the rreannem of acute cardiac patients, as the heart is extremely sensitive to changes in autonomic firing, which may occur during the treatment if appropriate caution is not exercised. Techniques
1125
rhat have been found safe and effective are described in the treatment portion of this chapter. The response of the lungs to the autonomic nervous sysrem is important in a variety of disease processes. Vagal activity is related to the bronchospasm and mucous production in the pathophysiology of asthma. As stated previously, the vagus reflexes with the spinal cord at the C2 level. C2 somatic dysfunction has been consistently noted in diagnostic srudies of pulmonary disease (8). Ipsilateral cranial base dysfunction, in particular that of the occipitomastoid articulation, usually is associated with vagal type reflexes. The sensory ganglion of the vagus nerve lies within the jugular foramen, adjacem to the occipitomastoid suture. Though the cervical findings are reported less often rhan the upper thoracic findings, this may be because the vagus and other parasympathetic nerves will not vasodilate or stimulate swear glands, producing the associated temperature and skin moisture changes that are among the most common recognizable signs of acute segmental facilitation. It is therefore possible that segments facilitated in areas of parasympathetic innervation are underrecognized. Upper cervical findings in pulmonary disease, especially asthma, may be the most significant structural findings , due to the pathologic effects of segmental facilitation of the vagus nerve in this disease. Wilson also noted that, in asthmatic patients, he consistently found right paraspinal changes at T4-5 and somatic dysfunction of the right fourth or fifth rib (27). He reports significant improvement in acute asthmatic attacks following manipulative treatment of these dysfunctions. Asthma, an inflammatory disease, usually produces a more significant reflex at these levels than COPD. Recognizing the role of the vagus nerve in producing bronchospasm and secretions, reflex facilitation of the vagus from somatic dysfunction at C2, the occipitomastoid suture, and/or the cranial base will exaggerate the degree ofbronchospasm and secretions. Reducing the segmental facilitation may raise the threshold necessary for production of an asthma attack, reduce the need for medication, especially bronchodilators that are prone to overuse, and help reduce the severity of an acute attack. Vagal reflex somatic dysfunction should be identified and treated in patients with pulmonary diseases. A different type of reflex is present in pneumonia. Pneumonia is accompanied by a local reduction in rib excursion. This dysfunction pattern is described in standard physical diagnosis texts, as well as osteopathic literature (25,28). This phenomenon cannot be a typical viscerosomatic reflex, since the dysfunction levels in lower lobe pneumonia are outside the levels of the sympathetic innervation of the lung. It is more likely they are produced through the parietal pleura, which carries a local, intercostal innervation. These reflex changes are likely involved in the pleuritic chest pain (Fig. 71.4) which often accompanies pneumonia, and are very useful in locating and making the diagnosis of pulmonary consolidation. Treatment of these reflex changes is important in the overall treatment plan of patients with pneumonia. Upper thoracic findings associated with pulmonary disease (Tl-5, and occasionally T6) are commonly found in patients wirh acute and chronic bronchitis. This is consistent with the notion that the sensory innervation of the large airways travels mostly via the sympathetic nerves, while the sensory innervation of the small airways (asthma, lobar pneumonia) travels predominantly via the vagus. While sympathetic outflow may not be as
1126
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
detrimental to pulmonary function as vagal, the associated thoracic segmental spinal facilitation and somatic efferent outflow results in restriction of the upper ribs, reducing the ability of the patient with bronchitis to expectorate secretions. Somatic dysfunctions in these patients should be treated with osteopathic manipulation. The gastrointestinal (GI) system has an extensive autonomic innervation, which is involved in a variety of disease processes. The vast majority of nociceptors from the GI tract travel with rhe sympathetic nervous system, producing reflex somatic dysfunction at approximate spinal levels from T5-L2. Cervical findings are absent in diagnostic studies involving GI diseases (8). Increased sympathetic outflow can have a multitude of detrimental effects on patients with GI diseases. The sympathetic nervous system reduces blood flow to the entire GI tract, making recovery from virtually any problem more difficult. The other major effect of the sympathetic nervous system is to reduce GI motility. This effect may be most noticeable in postoperative ileus, a common complication of abdominal surgery. The skin carries the highest concentration of nociceptors of any tissue in the body. Therefore, the patient, whose dermatomes are affected by a midline incision from the xiphoid to pubes, will have the possibility of having nociceptive reflexes to the entire T5-L2 spinal region. This is also the segmental sire for sympathetic innervation of the entire GI tract. The bilateral segmental facilitation produced by a surgical abdominal incision, particularly a large midline incision, can significantly delay the body's ability to return to normal GI motility following abdominal surgery. Osteopathic treatment ro reduce segmental facilitation is indicated following abdominal surgery, and in any case of paralytic ileus. Normalization of the sympathetic nervous system by ileus prevention manipulative treatment given before abdominal surgery has been shown ro reduce the incidence of paralytic ileus. Alteration in GI motility is also a major parr of the pathophysiology of irritable bowel syndrome. Osteopathic treatment to reduce reflex facilitation is indicated in these patients as well. The sympathetic nervous system also affects the sphincters of the abdominal viscera. This can have an adverse effect in a number of situations. Cholecystitis accompanied by a stone lodged in the common bile duct will produce a reflex in the T6-9 region on the right. This is the origin of the innervation of the ampulla of Yarer, whose tone will be increased by the segmental facilitation resulting from this pathophysiology. This, in turn, makes the passage of the stone more difficult. A similar situation may exist with an irritation of the ureter from a ureteral calculus, affecting motility of the ureters, or from the viscerovisceral reflex facilitation from gastritis or a peptic ulcer, affecting rhe pyloric sphincter, delaying the emptying of the stomach. Sympathetic outflow will reduce the secretions throughout the GI tract. Of clinical significance is the reflex viscerovisceral facilitation that occurs in patients with either gastritis or a gastric ulcer. This results in reduction of secretions of stomach glands that would normally contribute to a protective bicarbonate barrier to stomach acid and therefore promotes an environment for increased mucosal damage. Finally, in experimental trials, pancreatitis has been found to become much more severe in the face of increased sympathetic outflow (25). Pancreatitis commonly
produces a significant, bilateral reflex that results in increased sympathetic output to the pancreas. The discussion of reflex facilitation would not be complete without a mention of the pelvic innervation. It is of note that there is no mention of sacral or pelvic findings in the literature in response to diseases of the lower GI or pelvic viscera (8) . Similar ro the discussion of vagal reflexes at C2, if reflex facilitation occurred via the pelvic nerves, it would not present with sweat gland or cutaneous vascular changes. In the pelvis, there is also the absence of deep, intersegmental musculature and, therefore, somatic muscular findings, the other most common finding associated with acute segmental facilitation, is not evident. If reflex facilitation did occur in the pelvis, it might present with a completely different set of palpatory findings than those occurring elsewhere in the body. Animal studies have demonstrated increases in Gl motility with stimulation of the skin of the lower abdomen and pelvis. The sacrum should be included in the evaluation and treatment plan of any viscera that have a pelvic innervation. The sacrum will be presented in this chapter when considering treatment of segmental facilitation. Often, the consequences of facilitation create physiologic imbalance that interferes with the body's response to a challenge. Segmental facilitation is a consequence of many acute diseases, especially those producing pain and/or inflammation. One osteopathic treatment goal is to remove somatic dysfunctions of related segments to reduce their somatic contribution to the facilitated spinal cord segments. Another goal might be to improve the general function of the nervous system.
Neuroendocrine Immune Considerations The hypothalamus, and the neuroendocrine immune system that it controls, is at the center of the body's response to the almost unlimited variety of challenges from the body's external and internal environments. It is central to the maintenance of homeostasis in the face of these challenges, and deeply involved in the body's response to virtually all acute illnesses. The hypothalamus exerts immense influence on the central functioning of the autonomic nervous system, the pituitary gland, and through it, by way of rhe autonomic nervous system and adrenal glands, the entire endocrine system and the immune system. The physiology of the hypothalamic-pituitary axis is also vulnerable to the neurophysiologic effects brought about by the mechanical dysfunctions resulting from somatic dysfunction. Information about the local functioning within the body is monitored by the hypothalamus in several ways. The ability of the hypothalamus to respond to internal and external changes will depend on the accuracy of its inputs. The hypothalamus receives a large input from the nociceptive system, via the spinohypothalamic tract (29). Spinal cord facilitation will exaggerate this source of input, affecting the degree and quality of the response. The hypothalamus also receives input about levels of inflammation and immune activity in the body from circulating leukotrienes, delivered to the systemic circulation by the lymphatics (18). Levels of circulating leukotrienes are monitored by circumventricular organs in the third and fourth ventricles (30). This system will operate at maximum effectiveness when circulation and fluctuation of cerebrospinal fluid is undisturbed. Reduced rate and
71. Treatment of the Acutely !LL Hospitalized Patient amplitude of the primary respirarory mechanism will reduce the fluctuation of the cerebrospinal fluid. The pituitary gland sits within the sella turcica of the sphenoid. the hypothalamus is just above, in close relation to the body of the sphenoid and sphenobasilar junction. The pituitary gland has a portal circulation, similar to the portal circulation of the liver. The liver is situated against the undersurface of the diaphragm and is anchored to it, and the respiratory movement of the diaphragm provides the motive power for its circulation. The pituitary gland has a similar anatomic relation to the diaphragma sella. The diaphragma sella continues into the sella turcica. Ir completely surrounds the pituitary gland and blends with its capsule (31). The diaphragma sella is a continuation of the anterior reaches of the tentorium cerebelli. The movement of the sphenoid and the tentorium cerebelli would, therefore, alternately change the shape of the gland with the phases of the primary respiratory mechanism, pumping the fluid within it. It has been suggested thar the portal circulation of the pituitary is bi-directional; the backward movement from the pituitary gland ro the hypothalamus is theorized to be important to the feedback regulation of the hypothalamic pituitary axis (31). This is also a possible mechanism for the central distribution of corricorropinreleasing factor (CRF), which has far reaching effects in the central nervous system. The alternating movement of the primary respiratOry mechanism would explain the ability of this circulation to move in alternating directions. W.G. Sutherland described the importance of the motion of the sphenoid to the functioning of the pituitary gland (32) It is important to consider treatment of somatic dysfunctions of the cranium, including the sphenobasilar area, in the management of the acutely ill hospitalized patient.
Approach to Thorax Sutherland writes, "The diaphragm is the 'piston' to the big 'combustion cylinder' of the body. Its crura are the 'legs' that lead down from the piston to the 'crankshaft' in the lumbar vertebrae. Its ligamenta arcuarta are the 'piston rings.' The lungs might represent the 'combustion chamber' to the cylinder while the nasal region the 'carbureror,' while the 'ignition' and 'self starter' might be found somewhere in the 'cranial bowl'." (32) The thorax contains the heart, lungs, and mediastinum and its contents. These structures are related anatomically by their fascial attachments. The fibrous pericardium blends inferiorly into the central tendon of the diaphragm, this relation is important ro diaphragmatic function. The fibrous pericardium attaches to the sternum via the sternopericardial ligaments, and is continuous superiorly with the mediastinal fascia, which blends with the anterior cervical fascia at the inner aspect of the clavicles and manubrium. The anterior cervical fascia, including the pretracheal fascia, has attachment to the hyoid bone and mandible before finally hanging from the cran ial base. This continuity must be considered in any approach to manipulative treatment of the thorax, neck, or cranium . Breathing is largely a mechanical process by which intrathoracic pressure changes are created via the action of skeletal musculature on the spine and bony thorax. It also produces pressure gradients berween rhe thoracic and abdominal cavities. This process is critical ro the movement of both air and fluids throughout
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rhe body. A detailed look at rhe mechanics involved will offer insight as ro how osteopathic treatment may improve the efficiency and effectiveness of breathing in the acutely ill patient, an important consideration whether or nor the patient is suffering directly from a respiratory problem. The physical action of producing a negative intrathoracic pressure requires a definable amount of energy, referred to as the work of breathing. Although difficult to quantify, increased work of breathing is clinically relevant, since many pulmonary problems dramatically alter the work of breathing. Restrictive lung diseases, by their very nature, increase the work of breathing. West considers increases in work of breathing an important factor in the pathophysiology of COPD (33). In the pathophysiology of asthma, patients progress to respiratory stage three and ultimately to respiratory failure due to an inability to maintain a state of hyperventilation caused by fatigue and the eventual exhaustion of the respiratory musculature. This failure is directly related to increased work of breathing in the patient with acute asthma. The work of breathing is a quantitative measure of the energy required by rhe body ro overcome the resistance of the lung parenchyma and chest wall and accomplish inhalation and exhalation. Compliance is the ease with which those tiss ues are stretched (moved). Lung compliance is clearly reduced in all of the above diseases, contributing to the overall increased work of brearhing. Restrictive diseases directly alter lung elasticity. Obstructive diseases reduce compliance through increased airway resistance and a variety of other factors. Somatic dysfunction, by its definition, will reduce the compl iance of the bony thorax in patients with pulmonary diseases and increase the work of breathing. Somatic dysfunction of the thoracic spine and ribs has been noted by a number of sources (5). The general shape changes of the thorax in COPD (barrel chest) can produce dramatic changes in chest wall compliance which are obvious on osteopathic structural examination and, in addition to the specific dysfunctions noted in association with pulmonary disease, actually stand out. General techniques will be described to address general compliance issues, as well as more specific techniques for individual somatic dysfunctions. Osteopathic treatment to improve the compliance of the tho rax will not necessarily directly alter the parenchymal pathology, especially those with chronic lung disease. However it will improve issues such as exercise tolerance, giving the patient the abi lity to function with their disease. West notes the effect of the work of breathing on exercise tolerance of rhe chronic lung patient (34) . In addition to general changes in compliance of rhe bony thorax, specific somatic dysfunctions may have an effect on the function of the respiratory mechanism that goes beyond the smal l changes in compliance they invariably produce. The movement of a typical rib during breathing operates in conjunction with the orientation of its costotransverse and costovertebral joints (Fig. 71.7). Rotation of the thoracic vertebrae with somatic dysfunction will not only create resistance ro movement, but will change the orientation of the costotransverse and costovertebral articulations, produce thoracic fascial torsions, and further impair the ability of the muscles to move the rib during inhalation. With rotation of thoracic vertebral units involved in somatic dysfunction, a rib with a predominantly bucket handle movement might become oriented to move more in a pump handle movement.
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
1128
Spinous process
Transverse process ---~-
Costotransverse
Pump handle motion
(Fig. 71.8). Lumbar somatic dysfunction, particularly in the upper lumbar spine, will alter the length and orientation of the crura and may, thereby, impair their function in connection with the contraction of the diaphragm. Cathie describes movement of the entire spine with respiration (9). During inhalation all spinal curves straighten, including rotation of the sacrum with the base moving posteriorly. The reverse movement occurs with exhalation. Somatic dysfunction anywhere in the body may adversely affect breathing. Increases in work ofbreathing contribute to respiratory muscle fatigue. Respiratory muscle fatigue has been generally implicated in the pathophysiology of respiratory failure. In particular, obstructive diseases produce respiratory muscle fatigue because of the effects of hyperinflation (35). Muscular fatigue has been long understood as the immediate factor leading to the demise of the patient with acute asthma. Their muscles of inspiration exhaust and the patient can no longer hyperventilate to maintain adequate air exchange. Respiratory muscle fatigue is also important in COPD, and has led to the identification of chronic respiratory muscle fatigue in the pathophysiology oflung disease (36) . Respiratory muscle fatigue has also been implicated in diverse problems such as pulmonary edema, lung shock, and difficulties weaning patients off ventilators (36,37). Increasing the compliance of the thorax will reduce the load on the respiratory muscles and may reduce the likelihood of fatigue in both acute and chronic conditions. Osteopathic treatment may also be used to improve the function and efficiency of the respiratory musculature. Respiratory muscles, like all skeletal musculature, operate on the principle of their length-tension relationship. In this relationship, muscles will develop a far stronger contraction at a longer resting tone. Consider the typical physical changes associated with exacerbations of obstructive lung disease, such as a flattened
motion
FIGURE 71.7. The orientation of the costotransverse and costovertebral articulations helps determine the direction of movement of a rib with respiration.
diaphragm visualized on radiograph or the hypertonicity of accessory muscles, such as sternocleidomastoid. These are indications of shortened musculature that will have a reduced contractile force in the face of an increased workload. In the case of chronic obstructive lung disease, the barrel type changes in the thorax will actually prevent inspiratory muscles from returning to full resting length during exhalation. Likewise, increased tone in the inspiratory musculature may prevent the thorax from fUlly assuming the position of exhalation, contributing to the overall shape change of the thorax. In addition to altering the length-tension curve, increasing the resting tone of the respiratory musculature will alter its blood supply and oxygen supply/demand ratio. Muscles get most of their blood supply during their resting or diastolic phase. The increased tone during contraction increases the pressure within the muscle, and shunts blood away via nonnutritive arterioles. This has been demonstrated in the diaphragm (36). It has also been shown that increased demand in an otherwise normal diaphragm will produce oxygen demand that is in excess of its supply (36). Increasing the resting tone of a muscle will increase its pressure and reduce the incoming blood supply, while simultaneously increasing its oxygen demand, further stressing the oxygen supply/demand ratio. Muscles forced to function anaerobically are as much as 15 times less efficient than those utilizing aerobic metabolism (38). Fatigued diaphragms have been found to have high levels of lactic acid, indicating anaerobic metabolism (36). Increased resting tone of the inspiratory musculature should be identified during the osteopathic structural examination. Osteopathic treatment directed toward increasing the length and decreasing the resting tone of inspiratory musculature is indicated in the treatment of acute and chron ic lung disease. The diaphragm in particular is prone to increases in tone and
71. Treatment of the Acutely ILL Hospitalized Patient
A.
Normal ribs 2-4
Mostly pump nana1e monon
B. Normal ribs 8-10
C. T6 with somatic dysfunction T6 =ERR S;:< Exaggerated
More bucket handle motion Also causes fascial torsions
FIGURE 71.8. Vertebral rotation will change the orientation of the rib and the movement of that rib produced with respiration.
associated flattening in acute and chronic obstructive disease. The flattening of the diaphragm may become severe enough to reverse the movement of the lower ribs during inspiration, called paradoxic rib motion. This will reduce the transverse diameter of the chest, and greatly reduce the efficiency of the entire respiratory mechanism. In osteopathic literature, restoration of the length and vertical orientation of the diaphragm is called doming of the diaphragm. Doming of a Battened diaphragmatic muscle will increase the pressure gradients that it is able to produce between the thoracic and abdominal regions and can help reverse paradoxic rib motion and improve the function of the diaphragm as well as the respiratory mechanism as a whole (Fig. 71.9). Addressing the mechanics of breathing, including the work of breathing, the comp lian ce of the thorax and spine, both specifically and generally, and the function and efficiency of the respiratory musculature will have far-reaching applications in the treatment of acute and chronic respiratory diseases. The physiologic impact of respiration is not limited to the exchange of air. The negative pressures produced by thoracic excursion are important to the function of the circulatory system as well.
1129
The role of respiratory movements on inferior vena caval and portal circulations has been extensively studied. Breathing has a tremendous influence on both the inferior vena cava and portal return (12). During inspiration, rhe negative intrathoracic pressure produced dramatically increases the flow in the inferior vena cava while, simultaneously, the compression of the liver by the descent of the diaphragm virtually eliminates hepatic Bow. During this rime, there is blood Bow into the liver, so its pressure increases. During exhalation, the vena cava loses irs pressure gradient and flow decreases substantiall y. This is balanced by the large portal flow from the pressurized portal veins of the liver, as the diaphragm lifts off. Return to the heart remains somewhat balanced. However, the composition of the blood differs greatly between these two phases of the respiratory cycle. The effect of respiration on central venous flow is greatest in supine, nonactive patients, who lose the effects of the peripheral pumps created by muscle contraction. Zink noted this when he presented his model of respiratory/circulatory function (1 0). This encompasses the vast majoriry of acutely ill hospital patients, who are bedridden most, if not all, of the time during their convalescence. Patients with congestive heart failure demonstrate a clinical application of this concept. These patients develop fluid congestion in their liver and lower extremities. They consistently have substantial restriction of their diaphragmatic excursion , as can be determined by structural examination . Treatment of the diaphragm improves the overall circulatory function and venous back pressure is reduced, decreasing afrerload on the heart (Fig 71. 10). The action of the diaphragm and thorax also has a major influence on the function of the lymphatic system. This is the second aspect to the "respiratory/circulatory" model. Zink's original model described the role of respiration, with its action on central venous flow and pressure, as they influence the emprying of the thoracic duct into the junction of rhe internal jugular and brachiocephalic veins. This idea has since been confirmed with studies measuring thoracic duct flow in relation to respiratory excursion. A variery of studies have measured the role of respiration in the movement of thoracic duct lymph , estimates from these studies show 35% to 60% of the total thoracic duct drainage is in response to movements occurring during respiration (39- 41 ). The excursion of the thorax has also been shown to be involved in the formation of lym ph in a variery of areas, including the lungs and abdome n. Lymph formation is a critical step in the overall mechanics of the lymphatic circu lation. A smal l but significant uphill hydrostatic gradient exists that must be overcome in order for fluid to move from the interstitium into the initial, blind lymphatic vessel (39). The excursion of the thorax has been shown to be the primary force moving fluid from the pulmonary interstitium to the initial pulmonary lymphatics. The expansion of the pulmonary interstitial tissue, to which the initial lymphatics are tethered by anchoring filaments, increases the volume of the initial lymp hatic vessel and produces a temporary pressure gradient for filling the initial lymph vessels. Exhalation then closes the vessel and moves the lymph forward, past the first valve and into the contractile part of the vessel. The respiratory cycle then produces a pump that initiates the process of lymph formation . All initial lymphatics have anchoring filaments, and will therefore respond to respiratory movements to the degree that they occur
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VII Osteopathic Considerations in Pa!patory Diagnosis and Manipulative Treatment
Well-domed diphragm with good contraction and good compliance of rib cage during inhalation
Flattened, spastic diaphragm, poor compliance and inward paradoxical movement of rib cage with inhalation
With contractionof well-domed diaphragm
With contraction of flattened diaphragm
With added compliance of thoracic cage
Inward movement of thoracic cage
FIGURE 71.9. The mechanical effects of contraction of the diaphragm. A: Normal excursion of a com-
pliant thoracic rib cage with contraction of a well-domed diaphragm. B: Reduced excursion of thoracic cage and even the possibility of paradoxic motion of the lower rib cage with contraction of a flattened abdominal diaphragm.
in the area. T he initial lymphatics in the abdomen and pelvis, in particular, respond significantly to respiratory excursions. The clinical sign ificance of this mechanism is considerable. Lobar pneumonia is an example of an intrapulmo nary inflammatory process that will greatly increase the demand on the local lymphatic ci rculatio n. T he local excursion of the thorax, however, is consistently and significantly reduced in the local region of the consolidation. T his discrepancy w ill reduce the drainage
of the exudate produced by the local inflammation, reduce the delivery of antigen to lymph nodes, and ultimately reduce the delivery of immunity and antibiotics to the area as interstitial pressure rises and shunts blood away from the area. Restoring local excursion of the thorax will improve the body's ability to move lymph in this situatio n; specific lymph pump techniques are also indicated. Asthma is an example of a more generalized inflammatory process of the pulmonary tissues. This disease produces
Excursion of a domed diaphragm
+
+
FIGURE 71 .10. The excursion of the diaphragm has a
powerful influence on venous and lymphatic return. This effect is reduced when the resting diaphragm is flattened.
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7 1. Treatment of the Acutely IlL Hospitalized Patient a significant, overall restriction of the thorax to the exhalation phase of respiration, reducing both local drainage of lymph from the small airways and central lymph drainage through the thoracic duct. This physiologic model should also be considered in patienrs who have had a thoracotomy and/or sternotomy. These procedures produce intrathoracic inAammation that simultaneously and dramatically reduces the patient's ability to produce excursion of the thorax in the postoperative period. The work of breathing, with its mechanical considerations associated with respiration, and irs respiratory/circulatory function, with its role in the body's response and recovery from disease (especially inAammatory processes), must be considered in the osteopathic evaluation and treatment of any disease of the thorax. The work of breathing directs one to consider the compliance of the thorax, most easily evaluated by motion testing of the spine and ribs. Respiratory/circulatory function depends on the excursion of the thorax, evaluated by passively observing the patient's respiratory excursion. Although there is an undeniable relationship berween compliance and excursion, separate evaluation and consideration of these will lead to a more accurate understanding of the patient and a more appropriate and effective treatment plan. For example, a relatively strong and healthy COPD patient may have a relatively good excursion, but a much reduced thoracic compliance, best seen by motion testing of the ribs and thorax. Alternately, a patient just out of surgery will have a greatly reduced excursion, but the compliance may be relatively good. These rwo simations will lead to very different treatment programs. The ability to address compliance and excursion of the thorax is an important reason for including osteopathic manip-
ulative treatment in the management program of patients with a wide variety of diseases.
Approach to Abdomen/Pelvis The abdomen and pelvis form a single space, even though anatomists separate this space into rwo divisions. The abdomen, viewed as a single space, functionally contains, supports, and inAuences the function of the GI and the genitourinary viscera (see Chapter 51, Abdominal Region, Fig. 51.1 ). The lower ribs and their thoracic vertebral attachments, lumbar spin e, sacrum, and pelvic bones form the osseous components of this container. The diaphragm, anterior and posterior abdominal walls, and pelvic diaphragm are the myofascial components. The abdominal diaphragm is as integrated to the function of the abdomen as it is the thorax. The diaphragm forms the roof of the abdomen, and suspends the liver, stomach and spleen, and colon via direct ligamentous attachments (Fig. 7 1.11). Flattening of the diaphragm, which may result from increases in its resting ton e, airway obstruction, or sag from fascial strain and drag, will allow sag of these viscera as well as those suspended beneath them. The posterior attachments of the diaphragm , which lie with in th e abdomen, are mechanically important. They provide the stable fulcrum necessary for effective contraction. The crura blend with the anterior longitudinal ligament of the upper lumbar spine, usually L1-3. Posterolaterally, the lumbocostal arches extend across th e posterior abdominal wall to the tips of the 12th ribs on either side. The medial lumbocostal arch is a thickening of the psoas major fascia (Fig. 71.12) . Its medial aspect blends with the crus of the
Coronary ligament Falciform ligament Liver
Esophagus
Recess of of lesser omentum
Parietal peritoneum
Liver
Duodenum
Small intestine
!H~-f-#f---
Reflection of posterior lamina of coronary ligament
Decending colon Hepatoduodenal or hepatogastric ligament (lesser omentum)
17-----h~+--
Sigmoid colon
fLC~--7"''-----\-
Rectum
B
A FIGURE 71.11. A: The attachments of the liver to the diaphragm. These are firm and allow the diaphragm to strongly influence portal circulation. B: The attachments of the abdominal mesenteries. These provide support for the abdominal viscera as wel l as providing the pathways for their neurovascular supply.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment Opening for: T8
Vena cava
T10
Esophagus
T12
Aorta
Gap for psoas muscle
ligament
Sympathetic paravertebral chain ganglia
Gap for quadratus M.
Right alnd left crura of the abdominal diaphragm
FIGURE 71.12. The abdominal surface of the diaphragm. The crura and lumbocostal arches blend, forming a continuous series of arches which anchors the diaphragm posteriorly to the 12th ribs and lumbar spine.
diaphragm. lt then crosses over the psoas muscle and is laterally attached to the front of the transverse process of the first lumbar vertebra near its tip. Here it blends with the lateral lumbocostal arch . The lateral lumbocostal arch is a thickening of the quadratus lumborum fascia. Medially ir is attached to anterior surface of the rip the transverse process of the first lumbar vertebra. It then crosses over the quadratus lumborum muscle and is attached laterally to the lower border of the 12th rib. Together, the lumbocostal arches and the right and left crus of the diaphragm, attaching to the lumbar spine, form a continuous series of five arches which integrates the function of the diaphragm and posterior abdominal wall. Mechanical support for the contraction of the diaphragm comes from the crural anchors to the lumbar spine and from the depression and stabilization of the 12th rib through the contraction of the quadratus and tension in the lumbocostal arches. The continuity of the posterior abdominal wall to the pelvic brim and to the lesser trochanter of the hip allows these more remote, but important, mechanical anchors to also be included as supports for diaphragmatic contraction. Evaluation and treatment of somatic dysfunctions of the crura and lumbocostal arches via the 12th ribs and lumbar spine will have a major impact on the excursion and physiologic function of the diaphragm. The diaphragm has openings for the passage of numerous structures between the thorax and abdomen (Fig. 71.12; and also Chapters 50 and 51). The esophagus passes through a loop in the righ r crus that acts as the most substantial functional portion of the gastroesophageal sphincter. Dysfunction of the crus is often present in patients with gastroesophageal reflux and hiatal hernia. Osteopathic manipulative treatment directed toward altering tension of the crus may be helpful in the management of
patients with these problems. The aorta and the cisterna chyle, or beginning of the thoracic duct, pass between the right and left crus. The potential effect of the phasic contraction of the crura on the normal central lymph flow, through the thoracic duct as part of an overall effect of respiration, must be considered. Conversely, the potential for obstruction of central lymph flow with increased tension in the crura must be considered as well. The sympathetic chain with its paraspinal ganglia ?ass through the medial lumbocostal arch. Several authors have implicated that altered tension of the fascia surrounding the chain ganglia has an effect on the function of the sympathetic chain ganglia (4,25,32). The passage beneath the lumbocostal arch is a small, tight space vulnerable to altered tension of the psoas and/or diaphragm. The inferior vena cava passes through the tendinous portion of the diaphragm near irs apex. Unequal tension in the diaphragm, either side to side or front to back can draw the central tendon off center and alter the size, shape, and position of this opening, interfering with passage of blood through rhe diaphragm. As stated by Dr. Still, "He cannot expect blood to quietly pass through rhe diaphragm if impeded by muscular constriction around rhe aorta, vena cava, or thoracic duct. The diaphragm can and is often pulled down on both rhe vena cava and thoracic duct, obstructing blood and chyle (lymph) from returning to [the] heart" (42). In this regard, one must consider rhe potential deleterious effects of altered tension in the diaphragm on venous and lymphatic circulation as an additional consideration , using treatment according to rhe respiratory circulatory model. The diaphragm, on avariety of levels, is intimately involved in the function of the GI system , the circulatory system, and the nervous system.
7 1. Treatmen t of the AcuteLy Ill H ospitalized Patient
A.
B.
1133
c.
(Paradoxical .., motion)
t~
l
¢:::1 I Good 11 abdominal muscle tone )
c::::;>,<= I '/'
I
~~
~
:,
Poor abdomina \ muscle tone or ~ surgical abdomen """'hI I
i
'
v'
FIGURE 71.13. A & B: Relative movements and function ofthe abdominal diaphragm, pelvic diaphragm, abdominal wall, spine and sacrum occurring during respiration . C: The effect of a significant abdominal surgical incision or presence of poor abdominal tone on the physiologic movements occurring during breathing .
T he iliacus, psoas, and quadratus lumbo rum constitute th e posterior abdo min al wall. T he role of the posterio r abdominal wall in the mechanical functio n of the di aphragm has been discussed, parricularl y the lumbocostal arches . T he posterior abdom inal wall is also involved in suppo rt of the abdominal viscera. T he psoas fasc ia blends with the fasc ia of the kidney and is the primary suppo rt fo r this o rgan. T he iliopsoas fo rms a shelf as it crosses th e pelvic brim and this helps to support the cecum and sigmo id colon. Increased tensio n in this region will reduce the overal l suppo rt of the colon , and may predispose to sag of the viscera and the mesenteries. T he posterior abdo minal wall is also the site fo r most of the posteri o r mesenteric root attachmencs (see abdominal mesenceries shown in Fig. 7 1.11), and this further increases irs importance as support of the abdominal viscera. T he ureter travels along the medial as pect of the psoas in the abdo men. It is not surprising that psoas spas m is a common fi nding in neph ro lithiasis and pyelo nephritis. T he deep abdominal lymph nodes also travel in relation to the ilio psoas as they ascend fro m th e inguinal area ro the di aphragm. T he tendo n of il iopsoas also forms the fl oor of the femo ral triangle where the inguinal lymph vessels and the femoral veins cross into the pelvis and abdomen. T he pelvic diaphragm form s the fl oo r of the abdominopelvic cavity. Irs muscLtlar attachmencs include the pubic symph ysis, the ischial tuberosities, and the coccyx and sacral apex. In addition to supporting the pelvic viscera, including the prostate in the male, the pelvic diaphragm form s the external anal sphin cter and has an opening for the passage of the urethra and, in the female, the vagina. Sensory nerves in the pelvic di aphragm are part of the
reflex control mechanism for urin atio n. In addi tio n to its ro les in the fun ctio n of the bladder and rectum, the pelvic di aphragm has a role in res piration. T he pelvic diaph rag m descends with the abdominal diaphragm during inhalatio n, creating space fo r the descending abdominal viscera (Fig 73. 13). C linicall y, there is tension palpable with its descent. T he pelvic diaphragm may act in conjunction with the anterio r abdominal wall , length ening under tensio n ro control the descent of the d iaphragm and stabi lize abdominal pressure. T he abdominal diaphragm will lose the important fulcrum created by the resistance of the viscera if abdo minal pressure is reduced by poor tone of the abdom in al wall o r dysfun ction of the pelvic diaphragm . If abdo minal pressure is allowed to rise, the increased resistance reduces the effec tiveness of the di aphragm and reduces inferio r ve na caval fl ow. One of the problems occurring after abdo minal surge ry is the redu ced ability of the abdominal wall to participate in this process. T he rol e of the pelvic diaph ragm beco mes heightened in the postsurgical patient, and freedom of the sacrum and pelvic di aph ragm are essential in rhis situation. T he integrated fun cti on of the diaph rag m, pelvic diaph ragm, and abdomen, occurring as the patient breathes, plays a signi ficant role in the prognosis of the postsurgical patient. T he most common co mplication from abdo minal surge ry is atelectasis and pneumo nia. The patient is predisposed ro these complicatio ns by the shallow, costal breathing that is so co mmo n in postoperati ve cases. Although usually considered to be one of the effects fro m pain, it has been shown that intrao perati ve epidura l injectio n, completely blocking posroperati ve pain does nothing to alte r the limited and dysfun ctional diaph ragmatic breathin g patte rn
1134
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
(43). Other explanations for the pattern of altered postsurgery diaphragmatic breathing include the effects of the somatovisceral reflex produced by the incision and the altered abdominal wall fun ction. A midline abdominal incision extending from the xiphoid to the pubes will produce bilateral reflex facilitation from the TS-7 region (including ribs) all the way to the L2-3 area. This includes the entire attachment of the diaphragm, including the crura, and disproportionately increases the lower thorax: workload and limits its excursion. The coordinated action of the abdominal wall and diaphragm is impaired. The abdominal incision alters the tone and reactivity of the abdominal wall, impairing its ability to help control inhalation. Osteopathic treatment of the lower thorax: and lumbar spine will improve compliance of these tissues, thereby reducing the resistance against which the diaphragm must push. lt will simultaneously reduce sympathetic outflow to the entire G [ tract and thereby reduce the chance of postoperative ileus, another common postoperative complication. Treatment of the sacrum and pelvis with a focus on maximizing the excursion of the pelvic diaphragm will help compensate for the reduced ability of the abdominal wall ro participate in the coordinated conrrol of inhalation. Respiration also plays a role in the abdominal lymph circulation. The role ofbreathing in the central movement oflymph h as already been discussed . Respiration also exerts a powerful influence on the formation of lymph in the abdomen (44); only peristalsis is more influenrial (45). The postsurgical abdomen, particularly when peritonitis is presenr, responds with a tremendous inAammaro ry process. At the same time, the two most powerful factors in the abdomen related to the accumulation of lymph and the red uction of lymphatic flow are impaired breathing and the absence of peristalsis. Osteopathic treatment ro promote lymph formation and flow is important ro the immediate healing process. The inability ro clear in8ammarory exudate increases the potenrial to produce the most common long-term complication of abdominal surgery, adhesions. Most diseases of the abdomen are inflammatory, and will respond to osteopathic treatmenr to promote rh e formation and propulsion of lymph. Lymph flow may be obstructed at the crura of the diaphragm, and this region must be evaluated and treated if indicated. Lymph vessels exit the peritoneal cavity via the mesenreric roots, and drag on these mesenteri es will increase the tension at the root, which may also obstruct the flow oflymph. M esenreric drag is a common finding in postsurgical and medical problems of the abdomen and pelvis, and may be treated carefully with mesenreri c lifts, ro promote the flow of lymph .
TREATMENT APPROACHES
General Considerations First the patienr is evaluated and the structural findings are inrerpreted in relation ro the above principles and an understanding of the parienr's disease process. Then a trearmenr plan is developed ro address the dysfun ctions in such a way as to improve the fun ction of the patient's underlying physiology. Often, a single area will need treatment based on several different models. In mo t, if not all cases, there will be multiple physiologic issues that can be addressed simultaneously through a treatment process. For example, an area of the thoracic spine and ribs may be
facilitated in a patient who has a dysfunctional breathing pattern and central lymph congestion. In such a case, the ribs need only be treated once to accomplish all th ree treatment goals, as the choice of technique is one that is consistent with accomplishing all three goals. Furthermore, the techniques described in each of the treatment areas that follow, may or may not be the proper choice for any particular patient, even if they have the same diagnosis. The choice of technique is based on th e effect desired and the condition of the patienr. Sometimes it is the combination of techniques in a particular sequence that best achieves the desired physiologic effects. It is importanr ro keep the treatment within the capabilities of the patient. It is often difficult, if not impossible ro know what those capabilities are before initiati ng th e treatment. lt is also difficult ro know in advance which techniques will be effective and well tolerated. Therefore, in the acutely ill patient, it is often best ro apply a focused manipulative treatment, in a minimal effective rime fram e and then recheck later to see how the patient responds. At that rime the type and dosage of treatment for that patient can be better formulated. A most effective way ro consistently provide a safe and effective treatment is to monitor the effect of a chosen technique on the patient while it is being performed, sensing how the tissues are reacting to the technique, and modifying the technique, as indicated, as it is being applied. A common mistake of the inexperienced practitioner is ro place all of their attention on the procedural aspects they are performing, and not sense the dynamic nature of the patient's tissue changes, occurring during the treatment process. By placing attention on the patient and their tissues as the treatment is performed, several things become possible. The technique and the forces involved may be continuously adjusted to the response of the tissue, maki ng the treatment more effective. This is particularly useful in deciding between a direct and indirect meth od of treatment in a particular area. T h e initial impression m ay be ro perform a direct method treatment, but, as the tissue barriers are engaged, the response of the tissue may suggest that an indirect approach should be performed instead. If the initial impression suggests an indirect approach, but as the tissue is positioned into its point of freedom there is no palparory sense that the tissues are responding ro the treatment method, the operator may need ro use a direct approach, or at least recheck the diagnosis and/or the original positioning of the patient. The choice between direct and indirect approaches is an important one; indirect approaches are, by their nature, gender than direct approaches. Since the activating force for the treatment comes from within the patient, it is virtually impossible to give a treatment in excess of the tolerance of the tissue, or the patient as a whole. However, since they require internal fo rces to generate the therapeutic response, sometimes the sickest patients are unable to generate enough force ro accomplish the desired effect from an indirect method and a direct method technique will be the more appropriate and effective one to use. If the findings on structural examination do not ini tially suggest a physiologic treatment plan, treatment ro arbitrarily reduce somatic dysfunction should not be initiated. It is far wiser to repeat the examination over the co urse of the illness, obtai ning· added clues as ro the relation between the osteopathic findings and the pathophysiology of the disease process. It stands to reason that those somatic dysfunctions involved in th e disease will change
71. Treatment of the A cutely Ill Hospitalized Patien t as the disease progresses, either improving or gening worse wirh rh e patient's condition. Once a ben er understanding of rhe rela ri o n ~ hip between rh e somatic dysfu ncti on and disease process is achieved , a ph ys iologic treatment plan to assist that patient's recovery from th eir disease wi ll be apparent, and may be in itiated.
Segmental Facilitation A visceroso maric reflex is produced when nociceptor in put from infl amed viscera reaches a level great enough to produce facilitatio n o f th e interneurons of rhe spinal cord on which they conve rge. Spread of th e impulses within the facil irared cord segment to invo lve th e so matic neuron s and rh e res ulring muscle spasm produces a palpable, segmental som ati c dysfunction , which , in rurn , stimulates so matic nociceprors. This somatic nociceptive input conve rges on th e same spinal cord segment and involves rh e inrern euro ns o f rh e original viscera l input, creating a positi ve fee dbac k loo p which furth er increases the reflex outp u t to segmentall y related viscera and som a. T he goal of osteopathic treatment is to re move rh e added so mari e in pur, reduce rhe overall fi rin g of rhe segmental inrern eurons, and remove rh e potentially devas tating, sel f-perpetu atin g effects of a positive feedback loo p. T here is no definiti ve technique for reducin g segmental facili tatio n; any procedure that no rm al izes th e somatic tiss ues and reduces the nociceptive input wi ll wo rk. Treatment is based on the cond itio n and res po nsive ness of the patient. However, several guidelines should be followed when designin g a treatment program to redu ce segmental facilitati o n. The remainder of rhis chapte r presents th ese guidelines and presents manipulative treatment techniques rh ar have been found usefu l in treating p atients w ith acure segmental fac ilitati on.
Nociception Visceroso mari c and som arovisceral refl exes are initi ated through pain-carry ing fi bers. Rapid m ovements ar rh e ve rtebral unit, and of co urse pa inful maneuve rs, have been shown to create a sympath eti c moto r o utburst fro m rh e related and also distant fa cilitated spinal cord segments. Pain experi enced at th e segment wi ll ereare further facilitati o n. Vigorous o r painful procedures should be avo ided wh en treating to reduce segm ental facilitation , especially in acute siruari o ns.
Order of Treatm ent Ne uro ns in fac ilitated segments have a low thres ho ld and ofren fi re off, even to signals pass ing through rh e spinal co rd from orher regio ns. Treatment o f rh e fac ilitated areas first wi ll help prevent rhese segments fro m excessively firin g impulses to rheir related viscera in res po nse to treatment given in another region . Extremely reactive segments may acrual ly require several treatments befo re o th er body areas can be effectively treated , although this is unusual. Ge ntle, deliberate procedures used throughout the entire trea tment will minimize this effect.
Frequen cy o f Trea t men t Facilitated segments are often rhe res ul r o f acure visceral processes. T he und erl ying disease will reproduce fa cil itation ar the segments, often qui te rapidly. Frequ ent treatm ent, even more than once
1135
daily, is indicated. As rhe process improves, treatment frequ ency m ay be decreased.
Articular Tissues Although th e mosr obvious signs o f acute segmental fac ilitatio n are found in the soft tissues, rem ember rhar treatment is directed to those tissues sending som ati c nociceptive informati o n back into the spinal cord. Muscle has a low concentrati on o f nociceprors, whereas a jo int capsule has th e seco nd highest, nexr to th e skin . Treatment directed toward articul ar tiss ues m ay have a greater effect on the segm ental fac ilitation than soft tiss ue tech niques, such as m yofascial releases o r counterstrain . T he techniques presented will all be directed toward th e tension in arti cular segm ents.
Skeletal/Fascial Relations Traditional focus has been on th e areas immedi ately surro undin g the sympath eti c chain gangli a as th ese have an in creased clinical importance in th e treatment o f segmen tal facilitatio n. Patriquin sugges ts an effect of res pirato ry mo ti o n o n rhe fun cti onin g o f the chain ganglia (4) . Ku chera and Kuchera discuss rh e fascial rel ati on of rh e ga nglia with th e rib head (25) . Johnston also focuses on rhe costove rtebral juncti on in his discussion of rh e di ag nos is of viscerosom atic reflexes (7) . Suth erl and di scusses rh e relati o nship between anterior vertebral ligam ento us and fasc ial te nsio n and autonomic funnion (32). Alth ough rh e kn own ph ys io logy of reflex phenomena fo cus o n rhe nocicepto r input as th e ca use of segmental facilitation , and bo rh som ati c and v isce ral moto r (via rhe ch ain ganglia) as the effects, o ne cann ot deny rhe im proved clini cal response when th e ap pli ca ti o n of manipul ative treatment is directed more specifi cally to th e so mati c dysfun cti o ns and paraspinal fascial and ligamento us tiss ues in rhe anaro mi locati o n of the ch ain ga nglia related to th e pari en t's visceral dysfun ction . T he sacral plexus lies anteri o r to rhe sacrum. T he lumbar chain ga nglia lie anterior to th e bodies of th e lumbar ve rtebrae, medi al to the edge of psoas. T he th o racic chain gangli a lie anterior to th e heads of th e ribs. T he cervical gangli a lie anteri o r to the cervical transverse processes.
SPECIFIC MANIPULATIVE TREATMENT TECHNIQUES All o f th e techniques described h ere are direct meth od ; rh ey engage a restri ctive barrier and invo lve rh e applica ti o n o f an acti va ting force. T hey are es peciall y applicable in rh e h os pital pati ent, and may be used to produce a wide vari ety o f phys iol ogic effects. Force should always be introduced gradually, with attenti o n to th e patient and to the patient's res ponse, and m aintained at the level rhat marches or balances rhe resistance o r tensio n felt in th e tiss ues . Ind irect method techniques may also be used in rh e treatment of acute segmental facilitati o n , and should be co nsidered especi all y in patients whose tiss ues are sensiti ve o r reacti ve to rh e app licati on of outside forces. Indi rec t technique, on the o th er hand, will nor always work, because th e acutely ill pati ent may nor be abl e to generate th e inherent forces necessary to affect a good res ponse to th e treatment process.
1136
VII. Osteopathic Considerations in Pafpatory Diagnosis and Manipulative Treatment
Paravertebral Ganglia Techniques Direct Rib Release Position 1. The patient is supine. The operator is seared at the side of the patient. 2. One hand of the physician identifies a single rib to be treated. The other hand extends under the patient to the spinous process and identifies the cwo segments with which a typical rib articulates. This is most easily done by gently springing the rib medially while monitoring at the spinous process. 3. Co ntact the cwo vertebrae at the spinous processes and simultaneously carry the rib and cwo vertebrae laterally. This will disengage the costovertebral articulation.
3. The physician slides that hand under the patient's upper lumbar spine, fitting the lumbar spinous processes in the depression becween the disral phalanges and the base of the hand. 4. The physician applies a gentle superior lift with the cephalad hand, the knuckles and base of the hand maintaining even pressure on the respective transverse processes. 5. With the caudad hand on th e patient's elbows, the physician uses downward pressure into the bed (or treatment table) to closely control the lift of the fingers, balancing the lift to the resistance felt in the tissues. 6. This positioning is held until release is felt.
Sacral Plexus Techniques First Rib/Stellate Ganglion Technique
Sacroiliac Decompression Position
The stellate ganglia sit just anterior to the heads of the first ribs.
1. The patient is supine. The operator is seated at the side of the patient.
Position
2. The physician contacts the medial aspect of the posterior superior iliac spine and associated medial ilium with the fingerpads of one or both hands.
l. The patient is supine. The operator is seared or standing ar the head of the bed.
2. The physician contacts the posterior aspects of the first ribs at th e angle with the thumbs of each hand.
3. The physician leans back, with the arms as straight as possible to create the traction with their shoulders and trunk, rather than with the forearms.
3. The physician simultaneously app li es gentle lateral traction to both ribs, gradually increasing until the traction force is equal to the resistance found in rhe tissues .
4. The physician's traction equally marches the resistance that is palpated. 5. The physician holds until yielding or release is felt.
4. Traction is held at this level until release is felt.
6. This process is repeated on the other side.
Suboccipital Decompression
Sacral Technique Position
The superior cervical ganglion and vagus nerve are related to the occipital-adanral and suboccipital tissues.
Position 1. The patient is supine. The operator seated at the head of the bed. 2. The physician places the fingerpads in the patient's suboccipital sulcus (groove) on both sides. 3. The physician carries their elbows medially, placing lateral traction on the suboccipital tissues. 4. The physician simultaneously places gentle traction on the occiput. The force of the physician's traction matches the resistance of the tissues. 5. This position is held until release of both sides is felt.
Lumbar Ganglia Technique Position 1. The patient is supine wirh their arms crossed over the chest. The operator is seared at the side of the patient. 2. The physician makes a fist with rhe fingers of the cephalad hand, leav ing the thumb extended.
1. The patient is sup ine with the arms crossed over rhe chest. The operator is seated at the side of the patient. 2. The physician contacts the sacrum in the midline, with the caudad hand on the inferior lateral angle near the sacral apex and rhe cephalad hand on the sacral base above the level of 52. Alternately, the physician may use only one hand and spread rhe fingers so that some rest above and the others rest below the 52 sacral vertebra. 3. The physician's fingers, contacting the patient's sacrum, are gently lifted anteriorly. The physician's arms are resting on the bed or table top and the degree of li ft is controlled by applying downward pressure on the elbows and upward pressure with the fingers . 4. This position of lift is held until a yielding or release is felt.
Collateral (Prevertebral) Ganglia Inhibition Techniques Abdominal Ganglia Inhibition The celiac and the superior mesenteric and inferior mesenteric ganglia may be treated by the same method, altering the hand position on the abdomen for the different ganglia. The celiac
7 1. Treatment of the Acutely Ill Hospitalized Patient area is below th e xiphoid, the inferior mesenteric just above the umbilicus, and the superior m ese nte ri c h alfway between.*
Position 1. T he patient is supin e. T he operator stands at th e side of th e patient. 2. T he physician's fingerpads of one or both hands are lined up alo ng the patient's midabdominal line, co ntacting the skin over the coLlateral ga nglion that is to be inhibited .* 3. The physician applies a ge ntle, downward press ure until th e resistance of the underlying tiss ues is Felt and its resistance is marched.
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Translation of the Spine Since the heads of ribs two through ten articul ate with a verteb ral unit, rather than a single vertebral segment, the motion of the thoracic spine is inrimatel y involved with rib motion and th o racic co mpliance.
Position 1. The pat ient is seated . The operator stands at th e left side of the patient. 2 . T he patient's left hand is placed o n the right sho uld er.
4. This pressure is held until a softenin g or release is felt.
3. T he phys ician places their left hand over th e patient's hand and right shoulder whi le allowing th e left axilla to rest lightl y on the pati ent's left shoulder for pati ent co ntrol.
Cervical Ganglia Inhibition
4. The physician's right palm is placed over the patient's left parave rtebral tissues near th e Tl 0-12 region.
Although the cervical ganglia are situ ated more like the collateral (paravertebral) ga nglia, the cervi cal gangl ia Function more like prevertebral ganglia, havin g their spinal origin in the thoracic spi nal co rd.
Position l. The par:ent is supin e. The operator is seated at the head of the bed or table. 2. The physician's fingerpads co ntact the articular pillars of the patient's cervical sp ine on both sides. 3. T he physician ge ntly lifts th e finger contacts in a n anterior and superi o r direction until articular (not soft tissue) resistance is perceived and matches the degree of lift. 4. This amo unt oflift is held until rel ease is sensed.
5. The physician simultaneously lea ns on the patie nt's left sho ulder and places a right lateral translatory force on the sp ine via the left axillary and right hand co ntacts. 6. T he phys ician moves the hand contact and the a pex of the translation superiorl y and the right late ral translatory force to th e spine is repeated until the entire hemitho rax is mobilized. A focused effo rt may be placed o n the region with the greatest res tri ction . 7 . The physician then moves to the patient's ri ght side, pos itions o f th e patient's arms a nd the physician's ar ms a nd hands are reversed and the other side of the thorax is treated with translation to the left.
Note: This mobili zatio n by spinal translation ca n also be carried into th e lumbar region of the body.
Thoracic Region Techniques The treatments described here are designed to increase thoracic compliance and excursion . C ho ice of method in clinical situations will depend primarily o n the conditio n and tolerance of the patient. O ne will be co nfronted with patients limited to th e supine position, such as the posto perative thoracotomy patient, and those limited to sitting, such as the patient with COPD. Adaptabi li ty in app lying treatment techniques is a key to giving an effective treat ment. Appropriate ca uti o n must always be exercised when wo rking with acutely ill pati ents. Autonomic and lymphatic consideratio ns sho uld also be applied to the thorax. T hey are described elsewhere in the chapter.
Seated Techniques
Rotation and Rib Raising Position 1. The patient is seared. The operator sta nds at the left sid e of the patient. 2. The pat ient's left hand is placed on th e right shoulder. 3. The physician places their left ha nd over th e patient's hand and right shoulder while allowing th eir left axill a to rest lightly on th e patient's left sho uld er fo r co ntrol of the patient. 4. T he ph ys ician's ri gh t palm is placed over the patient's lower right rib cage with the thena r eminence in the area of the tenth rib angle. 5. T he ph ys ician simultaneously produces a ri gh t an tero lateral translatory force as the patient's body is rotated to the left.
In acute respiratory illness, the pati ent is sometimes unable to lie down for treatment. Seated techniques are particularly useful in these situatio ns. All procedures described m ay be done very gently or more forcefully depending o n the particulars of the case. Care must always be exercised when using force in an acutely ill hospitalized patient.
6. The right hand co ntact with the patient's ri ght rib a ngles is moved superiorly and the right antero lateral translatory force and left rotation of the spine is repeated until the entire hemithorax is mobilized. A focused effort may be placed o n the region with the g reatest restriction.
*Th is technique shou ld nor be anempred in the posto perative patient with a midline abdomin al incision.
7. T he physician th en m oves to the patient's ri ght side, positio ns of th e patient's arms and the physician's ar ms and hands are reversed and the left side of the thorax is treated in a simi lar mann er.
1138
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Position
Note: The entire hand and palm shou ld be in contact with rhe rib cage to broaden surface area of contact.
I . The patient is seated with ar ms crossed in fronr of the chest. T he operator stands fac ing th e patient.
Pump Handle Ribs
Rib Raising
2. The patient's arms are supported on the physician's chest and rhe physician's hands reach around the patient ro contact the patient's rib angles on both sides. 3. The physician leans so that ge nrle extension of the patient's thoracic spi ne occurs and simu ltaneous ly carries the contact with the patient's ribs, anteriorly and superiorly. 4. Th e physician's hand contacts with the patient's rib angles superiorly and/or inferiorly and the procedure is repeated until all of the patient's ribs have been raised. A focused effort may be placed on any region rhar that exh ibits the greatest restriction.
Supine Techniques Mobilizing the Ribs This is rib raising coordinated with parienr respiration. If the patient cannot lie comp letely flat, these procedures may be performed by elevating rhe head of the bed or emergency room stretcher to a more comfortable angle. These techniques are useful in the acute asthmatic patient, who reacts with further increased difficulty in breathing, even when very light pressure is app lied to the rib cage. These techniques may be adapted to borh pump and bucket handle motion. It is best to begin in the area of greatesr rib restriction and conrinue up and/or down the enrire thorax un ti l all ribs are treated. By coord inating the procedure to the patient's respiratory rhythm, you can avo id any challenge to rhe parienr's breathing. Used in this way, any of these treatment techniques wi ll immediately lessen the patient's work of breathing, and can be used even in patients with the most acute respiratory problems.
Direct Method Bucket Handle Ribs This technique is most usefu l for lower rib restrictions .
Position 1. The patient is supin e. The operato r is at the side of the table, fac ing the patient. 2. The physician's fingerpads of the cephalad hand contacts rib angles posteriorly and the fi ngerpads of the caudad hand contact costochondral junction on the same side. The thumbs make a broad contact with rib shafts across midaxillary line. 3. The physician monitors rhe patient's breathing with li ght finger contact unril rhe patient's breathing rhythm is familiar. 4. Then , as the patient begins to inhale, the physician's hands turn in the same direction, moving both thumbs cephalad , exaggerating the inhalation motion of the bucker handl e-type ribs. 5. As the patient begins to exhale, rhe physician's hands also turn in the opposite direction to exaggerate the exhalatio n motion of these ribs.
Position 1. The patient is supine. T he operato r is seared at side of the table, facing the patient. 2. T he physician's fingerpads of the cephalad hand contacts a pump handle rib posteriorly at its rib angle. 3. T he phys ician's caudad hand contacts the san1e rib anteriorly with its fingerpads across the rib's costochondral junction. The palm of this hand is lifted to avoid the breast of a fema le patient. 4. The physician monitors rhe parienr's breathing with light finger contact until the rhythm of the parienr's breathing is familiar. 5. As the patient begins inhalation, the physician's caudal fingerpad contacts move superiorly while the fingerpad contacts of the cephalad hand simul taneo usly move inferiorly to exaggerate rhe inhalation motion of the pump handle rib. 6. As the patient begins exhalation, there is reversal of rhe physician's hand movements to exaggerate the exhalation motion of the pump handle rib.
Indirect Method Treatment Rib Raising T his method is described here for a single rib dysfunction , although it may be app lied to a group of ribs.
Position 1. T he patient is supine. The operator is at rhe side of the bed or table, facing rhe patient. 2. T he fingerpads of the index and/o r middle fingers of rhe physician's cephal ad hand conracr rhe restricted rib posteriorly across irs angle. 3. The physician's index and/or middle fingers of the caudad hand contact the same rib anteriorly across rhe parienr's costochondral junction. 4. The physician's rhumb pads sho uld co ntact the shaft of that rib at irs midaxillary line for added conrrol. 5. T he patient's inh alation and exhalation is monitored as the physician gen rl y encou rages the rib to move in the direction of its freedom. This is carried to the point of ligame ntous balance (poinr of greatest ease) and held there. 6 . Adjustments in cephal ad/ca ud ad, ante ri or/posteri or, and traction/compression may need to be ca rri ed our by passive motion resting and added to bring about the best balanced positioning of the rib. 7. Respiratory cooperation may be added by asking the patient to hold the ir breath in rhe direction associated with the greatest freedom. · 8. T he positioning is held in ligamentous balance until release is fe lt.
71. Treatment of the Acutely Ill Hospitalized Patient
9. The rib motion is reevaluated during active inhalation and exhalation.
Sternal Mobilization The mediastinal fascia is continuous with the fibrous pericardium ofthe heart and central tendon ofthe diaphragm. The fibrous pericardium ofthe heart is attached to the sternum via the superior and inferior sternopericardialligaments. A sternal release may be used to mobi lize this important fascial mechanism.
Position 1. The patient is supine. The operator is seated at the head of the table. 2. The physician's caudad hand contacts the sternum and manubrium and the palm of their cephalad hand is placed posteriorly across the patient's spinous processes, approximately in the Tl-6 region. 3. The physician's sternal contact moves the patient's sternum through its six motions-superior, inferior, lateral to the right, lateral to the left, clockwise rotation, and counterclockwise ro~ation-determining its directions of restriction in motion. 4. The hand of the physician's spinal contact will always be moved in the direction that is opposite to the sternal restrictions. 5. As the patient continues to breathe normally, each sternal preference is held at its motion barrier until release occurs. Rather than doing each motion separately, the sternal restrictions can be taken to their restrictive barrier and each "stacked upon the other" and the composite held until release occurs. Note: This can also be performed as an indirect method technique. To do this, the sternal motions are stacked, or each is separately carried to the point ofligamentous balance and held at that balance while intrinsic forces release the dysfunction. Respiratory force can be added to hasten release by having the patient hold their breath in the phase that produces the most ligamentous relaxation.
Abdominal Treatment Techniques The abdomen fo llows the principle that the shape of a container will affect the function of its contents. The abdomen has a roof, a floor, and anterior and posterior walls. The diaphragm is the roof of the abdomen; the liver, spleen, and supporting mesenteries are suspended from it. The pelvic diaphragm is the floor. It supports the abdominal and pelvic viscera, along with the shelf created as the posterior abdom inal wall crosses the pelvic brim. The iliopsoas and quadratus lumborum make up the posterior abdominal wall. The insertion of iliopsoas on the lesser trochanter of the femur involves the hip in abdomi nal and pelvic function. The aforementioned structures are usual ly treated before directly treating viscera. The autonom ic relationships and lymphatic drainage of the abdomen and pelvis should also be considered.
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Direct Hip Release Position 1. T he patient is supine. The operator is at the side of the table on the side of the leg to be treated. 2. T he physician's cephalad hand contacts the patient's hip behind the greater trochanter for monitoring. 3. The physician's caudad hand holds the leg so it can be maneuvered. 4. The physician's caudad hand induces abduction/adduction and internal/external rotation to find the point of balanced tension of the hip joint. 5. While monitoring with the cephalad hand, the physician's caudad hand places the patient's ankle into the axilla to control the patient's leg position. The caudad hand then moves up to or above the knee to create a fulcrum. 6. T he distal part of the patient's extremity is taken medially to create lateral traction at the femoral head and held in that position. 7. When lateral release is felt, the physician applies inferior traction on the patient's leg and holds that until another release is felt.
Pelvic Diaphragm Release Position (Fig. 71.6) 1. The patient is in the lateral recumbent position with the legs and knees flexed. The operator stands behind patient. This may also be done with the patient in the supine position with the operator standing by the patient on the side that is to be treated. The operator should explain the procedure to the patient and that a contact will be made near an intimate area before proceeding.
2. The extended fingers of the physician's caudad hand contact the ischial tuberosity of the patient on the side up off the table. The fingers are then moved at a point that is just medial and slightly caudad to the tuberosity; the fingerpads may stay in contact with the medial aspect of the tuberosity. 3. The physician's fingertips and rigid fingers are then gently but firmly advanced, medial to the sacrotuberous ligaments, into the ischiorectal fossa until the resistance of the pelvic diaphragm (on that side) is initially palpated. 4. At that point the excursion of the pelvic diaphragm is monitored during the patient's respiratory efforts. 5. Then the fingers are held at the point of tissue tension (not lifted to produce more tension). They simply resist the downward movement of the pelvic diaphragm that occurs as the patient inhales slowly and deeply. 6. The physician's fingers follow the pelvic diaphragmatic tension cephalad as the patient exhales slowly and completely. 7. Steps 5 and 6 are repeated until the maximal amount of d iaphragmatic lift (muscular tension release) has occurred. 8. The patient is turned to the opposite lateral recumbent position. With the physician behind the patient, the other half of the pelvic diaphragm is released in a similar manner.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
Posterior Abdominal Diaphragmatic Releases Releasing the Lumbar Spine/Crura Position 1. The patient is supine and the operator is at the side of the table facing the patient. 2. The physician evaluates T12 to L3 for somatic dysfunction or increased paraspinal tissue tension. 3. The physician then contacts the spinous processes on either side of the vertebral unit that has somatic dysfunction. 4. The vertebral unit is moved in directions that exaggerate its freedom of motion-flexion/extension, rotation, and right or left side bending. 5. These directions of freedom may be individually held at their point ofligamentous balance or each direction of motion preference might be stacked, one-upon-the other, and released. 6. Release occurs as the tissues are held at their point ofligamentous balance. 7. Respiratory effort of the patient may be added to hasten the release. This is performed by asking the patient to hold their breath in the respiratory cycle that is sensed to be accompanied by the greatest relaxation of the tissues. Releasing the 12th Ribs/Arcuate Ligaments Position 1. The patient is supine. The operator is at the side of the patient to be treated. 2. The physician contacts the patient's 12th rib near mid-shaft. Note: Doubling the finger contact may provide better control. Remember, the 12th rib does not have a rib angle. 3. The physician applies traction to the 12th rib in a direction between horizontal and the direction of the long axis of the 12th rib; settle on the composite direction that maximizes the perception of "tension in the lumbocostal arches," matching the traction force with resistance found in the tissues. 4. The rib is held in this position of traction until release is felt. This may occur as a change in the long axis of the rib rather than just a simple decompression. 5. The physician walks to the other side of the patient and the technique is repeated for the other 12th rib. Anterolateral Abdominal Diaphragm Releases Position 1. The patient is seated. The operator stands behind patient. 2. The physician reaches around the patient and contacts the soft tissues just below the costal margin (chondral masses) with the fingerpads of both hands. 3. The patient is asked to slouch as the physician supports the patient's back with their chest. This allows the physician's fingers to advance medially and superiorly arou nd the costal margm. 4. The excursion of the abdominal diaphragm during respiration is monitored. 5. The physician's finger placements gently resist the downward motion of the diaphragm as the patient inhales and follows
the diaphragm superiorly as the patient exhales. Note: Do not
push upward against the diaphragm. 6. Step 5 is repeated, as the patient continues to rake slow, deep breaths, until a release is felt. 7. The fingers of the physician's hands are then moved medially or laterally until the entire anterolateral surface of the diaphragm has been treated.
Abdominal Lifts Abdominal lifts provide a safe, simple means of addressing ptosis and congestion of the abdominal viscera and irs mesenteries. More specific treatment techniques for the viscera should not be attempted until palpatory skill and anatomic familiarity of the abdomen has been studied and achieved.
Position 1. The patient is supine with the knees bent to 90 degrees and the feet are flat on the table. The physician stands at the side of the patient that is to be treated. 2. The physician contacts the lower left quadrant of the abdomen just superior to the inguinal ligament and gently inserts the fingerpads into the patient's abdomen. 3. The physician then gently lifts the patient's abdominal contents obliquely toward the right upper quadrant until slight tension is palpable. 4. The tissues are then held in this position until a release is felt and the contents can be moved slightly further toward the patient's right upper quadrant. Note: The physician should be attentive so that the lift occurs to the internal organs and that they are not just lifting the anterior abdominal wall. 5. Steps 3 and 4 are repeated until the patient's maximal release has been accomplished. 6. Fort he right lower quadrant, repeat steps 1-5, lifting vertically towards the right upper quadrant.
Note: A minor vibration may be transmitted to the abdomen by the physician's finger contacts and be substituted for the lift. Also, respiratory force may accentuate and hasten the release of a lift. Respiratory force is instituted by asking the patient to take a partial breath in and hold it until they have to breathe. Just as the patient has to rake the breath, the physician will notice a release of the tissues.
Lymph Mobilization Stimulating the Movement of Lymph Osteopathic treatment to enhance lymph flow is described elsewhere in this text. In this chapter, the concept of interstitial fluid fluctuation was introduced in relation to lymph formation and flow. Techniques to stimulate the formation of lymph using this principle were taught by Anne Wales, DO, and will be presented here as an addition to those presented in Chapter 70. The respiratory mechanism, as well as any areas of restriction along the course of drainage should be treated before stimulating the formation and movement of lymph. · Osteopathic treatment designed to stimulate formation and movement of lymph is based on an understanding of the
71. Treatment of the Acutely !LL Hospitaliz ed Patient
1141
physiology and mechanics of lymph formation and propulsion. A limitin g factor in lymphatic drainage is the movement of fluid from the interstitium into the initial lymphatic vessels. T his is the fo~mat i on of lymp h. T here are no inherent hydrostatic or osmotic gradients to drive this process. Fluid fluctuation and rhythmic movement in the immed iate environment of the initial lymphatic vessels forms lymp h. T hese actions form the physiologic basis for most of the following lymphatic techniques. Successful treatment depends upon creating a rhythmic fluctuation of extracellular fluid. Th is movement of fluid can be palpated and monitored from the hand contact on the patient, and must be differentiated from the tissue movements monitored during treatment on the musculoskeletal tissues. The movement of the body's fluids in response to the treatment is the key. Propulsion of lymph is dependent on several factors. Stretch receptors located in rhe distal end oflymphatic vessels, responsive to the format ion of lymph , begins the peristaltic contraction of smooth muscle in the wall of the lymph vessels. The thin and pliable lymphatic vessels are also responsive to external pressures, such as skeletal muscle contraction in muscle adjacent to the vessel. The relative importa nce of these factors differs in different areas.
vibration to stimulate the movement of abdominal and thoracic lymph. The effect of the vibration is to produce a wave li ke that produced by a pebble landing in the center of a pond. The transmitred vibration to the abdomen will also act to lift the mesenteries in a very gentle manner. This can be useful in acute situations, such as rhe immediate postoperative period . These specific techniques were demonstrated by Dr. Wales and are based on this concept.
Lateral Fluctuation at the Knee
5. A palpatory sense of decongestion or lift of the mesenteries indicates successful treatment.
Position 1. The patient is supine. The physician sta nds at the side of the patient to be treated. 2. The physician flexes the patient's knee to 90 degrees and the hip to 4 5 degrees; the patient's foot is res ring Aat on the table. 3. The physician's caudad hand gently holds rhe dorsum of the patient's foot and ankle. 4. The physician's cephalad hand rests on top of the patient's knee. 5. The physician gently moves the patient's leg medially and laterally at the knee to find the position of greatest ease. 6. At that point of ligamentous balance, a small medial, lateral excursion is initiated and maintained.
Lateral Fluctuation at the Forearm Position 1. The patient is seared. The physician sirs facing the patient. 2. The physician grasps the hand of the patient on the affected side as if to make a handshake. 3. The physician's other hand supports the patient's elbow, keeping it at 90 degrees. 4. The patient's forearm is supinated and pronated to find the point of greatest ease. 5. From this point of ligamentous balance, a gentle, rhythmic pronation/supination excursion is initiated to fluctuate fluid
Abdominal Lymph Stimulation The abdominal lymphatics reside in the mesenteries of the abdomen. Dr. W.G. Sutherland described the use of a transmitted
Position J. The patient is supine with knees bent to relax rhe abdominal wall. The physician stands at the right side of the patient. 2. Physician contacts the patient's left lower abdomen just superior to rhe inguinal ligament, placing one hand over the other. 3. The tissues are gently lifted superomed ially until the first sense of resistance is palpable. 4. A transmitted vibration is directed toward the cisterna chyle- a point that would be approximately posterior to halfway between the xiphoid process and the umbil icus, sli ghtly to the right of center. This point will be approximately perpendicular to the suspension of the mesentery of the descending colon.
6. The physician walks to the left side of the patient and contacts the right lower abdomen in the same manner and steps 3 through 5 are repeated for the right side of the patient.
Thoracic Duct Technique Dr. Sutherland likened the thoracic duct to a siphon , indicating a functional significance to the turn located at its superior end, that allows it to drain downward into the superior aspect of the subclavian vein. The thoracic duct may be stimulated with a transmitted vibration at its proximal and distal ends.
Position l. The patient is supine and the physician stands at the right side of the patient. 2. The physician contacts the patient's abdomen just below the costal margin and to the right of center, in the area overlying the cisterna chyle. Use the contact of one-hand-over-theother- hand. 3. The physician induces a transmitted vibration directed toward the cisterna chyle. 4. Then the physician contacts the left ax ill a at the second or third intercostal space, near the midclavicular lin e, using the one-hand-over-the-other-hand contact. 5. The physician transmits a vibration of tissues directed posteriorly and slightly laterally. 6. A perceived change in the quality of the deep tissues or a sense of decongestion may become apparent as the treatment proceeds.
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
CONCLUSION The osteopathic treatmem of the acurely ill hospitalized patiem is designed ro supporr and enhance the underlying physiology of a patient as they recover from an illness or other severe stress. Care must be taken ro insure that the treatment is appropriate and within the physical capabilities of the patient ro respond appropriately. Specialist level intervention may be indicated in unusual and challenging cases, but many cases can be treated effectively by osteopathic physicians, residents, and students if the principles described in this chapter are followed. The structural exam ination findings , along with knowledge of the pathophysiology of the disease process and individual patient's condition, are combined to form a unique treatment plan for each patient, at each visit.
ACKNOWLEDGMENT Special thanks ro the guidance, hard work, valuable suggestions, and drawings from William Kuchera, DO, FAAO. This chapter is better because of his efforts.
REFERENCES I . Korr IM , et al. Effects of experimental myofascial insults on cutaneous patterns of sympathetic activity in man. J Transmission. 1962;23(22):330-355 . 2. Nicholas A, et al. A somatic co mpon ent of acute spontaneous myocardial infarction. JAOA. I 983;83(68). 3. Denslow JS, Korr l , er al . Quantitative studies of chronic facilitation in human motoneuron pools. Am} Physiol. 1947; 150:229-238. 4. Parriquin DA. Viscerosomaric reflexes. In: Patterson MM, Howell JN, eds. The Central Connection: Somatovisceral and Viscerosomatic Interaction. Athens, OH: University C lassics, Lrd; I 992. 5. Beal MC, MorlockjS. Somatic dysfunction associated with pu lm onary disease. JAOA. I 984;82: I 79-183 . 6. Beal MC. Palpatory resting for soma ti c dysfunction in patients with cardi ovascul ar disease. JAOA. 1983;82:822-83 1. 7. Johnston WL. Segmental definition: Ill. Definitive basis for distinguishing somatic findings of visceral reflex origin . JAOA . I 988;88:347-353. 8. Beal MC. Viscerosomaric reflexes: a review. JAOA. 85(12):53-68. 9. Cathie A. Physiological motions of the spine as related to respiratory activity. In: AAO Yearbook. American Academy of Osteopathy; 1974:5960. I 0. Zink JG. Applications of the osteopathic holistic approach ro homeostasis. In: AOA Yearbook. American Academy of Osteopathy; 1973:37-47. I 1. Sri II AT. The Philosophy and Mechanical Principles of Osteopathy. Kansas C ity, MO: Hudson -Kimberly Publishing Co; 1902:155. I 2. Rabinovici N , er al. The Relationship between respiration, pressure and flow distribution in the vena cava and portal and hepatic veins. Surg Gynecol Obstet. 1980; 15 I :753-763. 13. Millard FP. Applied Anatomy of the Lymphatics. Kirksville, MO: The Journal Printing Co; 1922:26. 14. Suth erland WG. Teaching in the Science of Osteopathy. Portland, OR: Rudra Press; I 990. 15 . Hurley JV. Inflammation. In: Staub NC, Taylor AE, eds. Edema. New York, NY: Raven Press; 1984:463-488. I 6. Atkinson TP Histamine and serotOn in. In: Gall in Jl , er al, eds. Inflammation: Basic Principles and Clinical Correlates. New York, NY: Raven Press; I 992: I 96. 17. Movat HZ. The !riflammatory Reaction. New York, NY: Elsevier; I 985. I 8. Olszewski WL, et al. Lymph drainage from foot joints in rheumatoid
arthritis provides insight inro local cyrokine and chemokine production and transport ro lymph nodes. Arthritis Rheum. 2001;44(3):541-549. I 9. Witte CL, Witte MH. Lymphatics in the pathophysiology of edema. In Johnston MG, ed. Experimental Biology ofthe Lymphatic Circulation. New York, NY: Elsevier; 1985:167- 188. 20. Van Buskirk R. Nociceptive reflexes and so matic dysfunction: a model ]AOA. 1990;90(9):792-809. 21. Schmidt RF. Neurophysiologic mechanisms of arthritic pain . In: Patterson MM, Howell JN, eds. The Central Connection: Somatovisceral and Viscerosomatic Interaction. Athens, OH: University Classics, Ltd; 1992. 22. Talman WT. The cenrral nervous system and card iovascu lar control in health and disease. In: Low PA, ed. Clinical Autonomic Disorders. Boston, MA: Little, Brown and Company; 1993. 23. Korr IM. Susta ined sympathicotonia as a factor in disease. In: The Neurobiologic Mechanisms in Manipulative Therapy. New York, NY: Plenum Publishing Co; 1978:229-268. 24. Fu QG, et al. Vagal afferent fibers excite upper cervical neuro ns and inhibit activity oflumbar spinal cord neurons in the rat. Pain. 1992;5 I ( 1): 91-100. 25. Kuchera M , Kuchera W. Osteopathic Considerations in Systemic Dysfunction, rev. 2nd ed. Columbus, OH: Greyden Press; I 994. 26. Rosero HO, et al. Correlation of palpatory observations with the anaromical locus of acute myoca rdial infarction. JAOA. I 987;87: 118129. 27. Wi lson P. The osteopathic treatment of asthma. JAOA. 1946;45(1 1):491-492. 28. Degowin, Degowin. Bedside Diagnostic Exam, 5th ed . New York, NY: Macmillan; 1987. 29. Geisler GJ. Studies of spinal cord neurons that project directly ro the hypothalamus. In: Willard FH, Patterson MM, eds. Nociception and the Neuroendocrine Immune Connection. Athens, OH: University C lassics, Ltd; 1994. 30. Dinarello CA. Role of in rerleukin-1 and rumor necros is factor in systemic responses ro infection and inflammation. In: Gallin J!, eta!: Inflammation: Basic Principles and Clinical Correlates, 2nd ed. New York, NY: Raven Press; 1992. 31 . Williams PL, ed. Gray's Anatomy, 38th ed. London, England: Churchill Livingstone; 1995: 1883. 32 . Sutherland WG . ContributionsofThought, 2nd ed. Portland, OR: Rudra Press; 1998:339. 33. West JB. Pulmonary Pathophysiology: The Essentials, 4th ed. Baltimore, MD: Will iams & Wilkins; 1992:74. 34. West JB. Respiratory Physiology: The Essentials, 5[h ed . Baltimore, MD: Williams & Wilkins; 1995. 35 . Roussos C, Macklem PT. Insp iratory muscle fatigue. In: Handbook of Physiology, Section III, The Respiratory System, Vol III. The Mechanics of Breathing, Part II. Bethesda, MD: American Physiological Society; 1986:521. 36. Grassino A, et al . Respiratory muscl e fatigue and ventilatory failure. Ann Rev Mecl. 1984;35:625-647. 37. Cohen C, et al. Clinical manifestations of insp iratory muscle fatigue. Am} Med. 1982;73:308-3 16. 38. West JB, ed. Best and Taylor's Physiologic Basis ofMedical Practice, 12th ed. Baltimore. MD: W illiams & W il kins; 1991:95- 96. 39. Aukland K, Reed RK. Interstitial mechanisms in the contro l of extracellular fluid volume. Physiol Rev. 1993;73 : 1. 40. Browse NL, et al. Pressure waves and gradients in the cani ne thoracic duct.] Physiol. 1971;237:401 -4 13. 41. Dumont AE. The flow capacity of the thoracic duct-venous junctio n. Am} Med Sci. 1975;269(3):292-301. 42 . Still AT. Philosophy of Osteopathy. Published by the author; Kirksville, MO: 1899:36. 43. Simonneau G, er al. Diaphragm dysfunction induced by upper abdominal surgery. Am Rev Respir Dis. 1983;128:899-903 . 44. Drake RE, Gabel ]C. Diaphragmatic lymph vessel dra inage of the peritoneal cavity. Blood Purif. 1992; 10: I 32- I 35. 45. Schmid-Schonbein GW. Microlymphatics and lymph flow. Physiol Rev. 1990;70(4):987- 1026. 46. Sutherland WG . Contributions of Thought, 2nd edition. Portland, OR: Rudra Press, 1998:34- 35.
EFFICACY AND COMPLICATIONS MICHAEL L. KUCHERA EILEEN L. DIGIOVANNA PHILIP E. GREENMAN
KEY CONCEPTS • Current state of research on efficacy of osteopathic manipulation, and problems in current studies • Difficulties of research trials studying effectiveness of osteopathic manipulation on low back pain, and success rates • Effectiveness of manipulation for patients with systemic disease • Osteopathic practice guidelines and difficulties for osteopathic physicians trying to follow existing written guidelines • Difference berween symptom exacerbation and true complication • Incidence of complications, difference between physician-related and patient-related complications, and best ways to avoid complications • Cervical spine manipulation as source of most serious manipulation complications • Difficulty in listing absolute contraindications to osteopathic manipulation • Complications most likely to result from high velocity/low amplitude manipulation • Discomfort or complications associated with muscle energy, counterstrain, and craniosacral treatments
Manipulation has enjoyed wide usage for many centuries of medical practice in most cultures. In most cases, it has been applied empirically, based on clinical observations. As with many forms of medical treatment, ongoing clinical successes have contributed to irs continuous and expanding use. Osteopathic manipulation uses palpatory diagnosis and manual treatment methods as integrated components of a patient encounter. This modality is an important element of an osteopathic approach to total patient care. Osteopathic manipulation is prescribed not on ly as care for a variety of musculoskeletal and system ic pathophysiologic problems but also as part of general health maintenance and enhancement strategies. It is directed toward optimizing structure-function relationships and assist-
ing the patient's homeostatic mechanisms. Its processes help to strengthen physician- patient relationships, allowing better diagnostic insights and treatment for all as pects of human problems. Osteopathic manipulative techniques are among the safest medical treatments a physician can provide. Whenever manipulative treatment is carried our, however, certain risks are present, along with potential side effects ranging from mi ld to severe, including death, when particularly aggressive maneuvers are used. Such risks also occur with pharmaceutical, surgical, and a va riety of other mechanical treatments. Even though osteopathic manipulation has a very low risk-tobenefit ratio, it is necessary that the operator be aware of inh erent risks and avo id untoward occurrences while weighing anticipated benefits against the risk of treating or not treating.
EFFICACY OF MANIPULATION Despite years of successful use of osteopathic and other forms of manipulation, components of the orthodox medical co mmunity continued to be critical of irs use, often referring to irs practitioners as cultists. The reasons are both cultural and scientific. The latter problem arises because of a lack of adequate scientific methods to explore not only clinical efficacy bur also basic mechanisms. Researchers with a directed osteopathic focus, such as Louisa Burns, DO; Irvin M. Korr, PhD;]. Stedman Denslow, DO; and Wilbur V Cole, DO, have been few. C linically, when osteopathic models were originally proposed, double-blind research methods were yet to emerge. When they were developed, they were more readily applied to pharmacologi c and surgical practices. More ambiguously defined clinical processes, such as osteopathic manipulation, remain difficult to evaluate. Progress is occurring, however. In 1975, the first of several international seminars brought together a gro up of international basic scientists and clinicians to examine the scientific basis for the use of manipulation (1 ). T he National Institute of Communicative Diseases and Stroke held this co nference in Bethesda, M aryland. Attendees were drawn from the osteopathic, allopathic, and chiropracti c professions. The goal was to define the current state of research and identifY areas for future study; several areas of agreement were reached.
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VI! Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
In 1977, a second imernational conference was held at Michigan State University (MSU). The conference focused on neurobiologic mechanisms thought to underlie the effects of manipulative treatment (2). Again, basic scientists and clinicians from the osteopathic, allopathic, and chiropractic professions discussed areas of mutual interest and concern, particularly in areas of neuroscience. Impulse and nonimpulse-based neural control mechanisms were discussed in a context that uses manipulative treatments for a wide range of conditions. In 1980, another international conference was held at MSU. This conference dealt with various models and mechanisms for the use of manipulation (3). Conferees examined the effects of a variety of manipulative models considered to be beyond neurally mediated factors. These included: Respiratory-circulatory models Biomechanical models of postural and structural techniques Inherent force concepts arising from the craniosacral treatment system In 1983, a fourth imernational conference, again at MSU, examined an increasing number of outcome-based clinical trials, particularly in relation to low back pain (4). Attendees also looked at issues necessary for development of future clinical trials. Many discussants were invited from the available clinical trials, along with a number of others with expertise in areas such as epidemiology. Their role was to discuss specific research methodologies, particularly in relation to the following: The specific diagnosis (i.e., the entity treated by the man ipularion) Inclusion and exclusion criteria Type of manipulation performed Outcome measures to identify efficacy, including statistical methods and data interpretation From the outset, it was clear that a variety of manipulative methods are used; procedures are seldom idemical. In many procedures, definition of the specific problem to be manipulated was limited and unclear. Most patients were treated for generic low back pain with or without radiation to the lower extremity. Despire the lack of specificity in these areas (such as lack of diagnostic and treatment specificity, small sample sizes, and differences in follow-up and outcome measures), the conference concluded that the trials demonstrated efficacy for the use of manipulative procedures when dealing with acute and acute recurrent mechanical low back pain. None of the trials dealt with chronic low back pain. By the end of the conference, generic issues surrounding the design and implementation of clinical trials were idemified. They continue ro be germane. In 1989 and 1992, the American Academy of Osteopathy organized and presented two international symposia to discuss the scientific underpinnings of osteopathic principles and the role that osteopathic treatment of somatic dysfunction plays in applying the osteopathic philosophy to patient care. The Academy asked a leading group of international basic scientists and clinical researchers to explore relevant research and to draw clinical corollaries. The 1989 conference, entitled The Cemral Connection: Somatovisceral!Viscerosomatic Interaction (5), focused on
structure-function relationships. Leading scientists from around the world examined central and peripheral reflex mechanisms, including the perpetuation of altered reflex patterns in the somatic and visceral systems. They also discussed effects of manipulative treatment, exploring its relevance to the practice of osteopathic medicine. The 1992 conference was entitled Nociceprion and the Neuroendocrine-Immune Connection (6). It was inspired by the osteopathic concept of body unity. Again the Academy brought in several of the world's leading authorities in the areas of nociception, immune function, spinal cord activity, and neuroendocrine function to provide a basis for understanding more of the far-reaching effects of adverse nociceptive and psychological inputs on total body function. The conference provided a forum to rationally discuss with osteopathic scientists and clinicians the mechanisms that might underlie osteopathic diagnosis and treatment designed to restore optimal health and function. The roles of somatic dysfunction and other somatic stressors were examined in relation to both psychological and immune functioning. Each of the aforementioned conferences published irs proceedings. Other Academy symposia are planned. In 1996, the Josiah Macy, Jr. Foundation hosted a second national meeting ofleaders of the U.S. osteopathic and allopathic medical professions to facilitate cominuing discussion between the two professions and to explore collaborative approaches to contemporary challenges confronting both professions. One of the papers commissioned by the conference, written by Kent Kwoh, MD, and emitled "Development of research protocols to study the efficacy of osteopathic manipulative treatment," made several recommendations for joim studies (7). In particular, it recommended analysis of three general outcomes: Symptom relief Improvement in health status Resolution of somatic dysfunction Each was then tailored specifically for the condition being studied. This conference paper went on to define a protocol for studying acute neck pain in posttraumatic, whiplash-type injuries. In 2001, the Kirksville College of Osteopathic Medicine in Kirksville, Missouri, coordinated and presented another international congress (8). It did so with sponsorship by both North American component societies of the International Federation of Manual/Musculoskeletal Medicine (FIMM), namely, the American Academy of Osteopathy and the American Association of Orthopedic Medicine. This was the first of the triennial FIMM Educational and Scientific Congresses to be held in North America, and it was notable for arranging critical and collaborative meetings between members of the FIMM Scientific Committee and U.S. osteopathic researchers. Both osteopathic and allopathic researchers reported on the state-of-the-art of evidencebased manual medicine internationally and outlined possible directions for conducting research ranging from analysis ofinterexaminer reliability to outcomes studies. The researchers also Identified possible solutions for confounding issues ranging from the adoption of descriptive, uniform nomenclature for the description of rests and palpatory findings to the use of various sham
72. Efficacy and Complications manipulation procedures and the need for standardized protocol training prior to conducting studies in this field .
Low Back Pain Manipulation of all types is widely used to treat musculoskeletal pain and dysfunction. It is considered beneficial by millions of patients receiving care from a wide variety of practitioners, including: Osteopathic physicians Allopathic physicians Chiropractors Physical therapists Laypersons Textbooks from the professional groups discuss indications and contraindications for manipulation, without clear scientific evidence that the recommendations are appropriate and useful. Empirical recommendations dominate. Considering the empirical effectiveness of manipulation in a wide range of neuromusculoskeletal disorders, it is surprising that most current studies focus nearly excl usively on low back pain. Relatively few studies have examined the benefits of cervical manipulation (9-12) or other musculoskeletal complaints. Over 70 serious studies concerning manual approaches to low back pain with and without radiation to the lower extremities have been published in the past 50 years (1 3, 14). Some recent studies have dealt with chronic back pain (15) in addition to acute, acute recurrent, and subacute populations. In the vast majority of these studies, design, methodologic, and descriptive difficulties coupled with type I or type II errors hinder effective interpretation of the literature (16). Furthermore, it is not always possible to identify the training of the individual(s) who performed the manipulations. In most cases in which training could be identified, the work was performed by chiropractors and physical therapists. Two studies describe manipulation performed by osteopathic practitioners trained in the British system (17, 18). In 1984, Stiles reported a 24% reduction in the length of hospital stay for patients admitted for low back pain when an osteopathic manipulative medicine consultation and treatment program was added to the patient's traditional medical care (19). In 1995 , a subacute low back pain project was completed by the Rush-Anchor health maintenance organization (HMO) network. It was a double-blind, matched, random sample patient study begun in 1992, co mparing osteopathic care (which included manipulation) with so-called standard care. Sponsored by the Bureau of Research of the American Osteopathic Association (AOA), the study was directed by Gunnar B. Andersson, MD, PhD, an internationally renowned orthopedic surgeon and researcher. Approximately 300 patients who met inclusion criteria were randomly assigned to either a standard care group, staffed by MDs, or an osteopathic care group, staffed by DO manipulation special ists from the Midwestern University, Chicago College of Osteopathic Medicine. T he study proposed to assess any differences in osteopathic care, including manipulative treatment and standard care. Results of the study were published in the New England journal ofMedicine (20). These indicated that osteopathic manipulation was equal to standard care in effective-
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ness bur achieved results with less medication, and fewer physical therapy treatments were used. Despite the many variations in trial design, implementation, and evaluation, all published studies suggest that manipulation is useful for syndromes of acute low back pain (3). This is demonstrated by reports of: Pain reduction Earlier return to work Generally shortened disability and impairment Other studies have looked at manipulation in subacute or chronic back pain populations, alone or in combination with other treatment modalities. Some studies have compared outcomes for manual approaches delivered by different practitioners. For example, Blomberg and colleagues (8,21). report significant benefit for treating both acute and subacute low back pain with spinal manipulation alone as well as with spinal manipulation in conjunction with steroid injections compared to current standard care without manipulation. After 4 months, experimental subjects in this controlled, multicenter trial had a less restricted range of motion in extension and in side bending, less local pain with those movements, less pain radiating to the lower extremities, and less positive straight-leg raising tests. They also had more positive quality of life reports, less drug consumption, less sick leave, and lower disability ratings reported by blinded orthopedic surgeons. Koes and colleagues (22) conducted a one-year follow-up of a randomized clinical trial for 256 subjects with persistent nonspecific back and neck complaints. They documented larger improvements in both the main complaint and in physical functioning for those in the manipulative therapy group than in those managed by general practitioners using medication, postural advice, exercise, and rest. Improvement in the main complaint was also greater after 12 months' follow-up in those subjects receiving manipulative therapy than in those receiving physiotherapy. Examples of studies of manual treatments of low back pain subjects in which higher percentages of patient satisfaction is a measured clinical outcome for manual approaches (23,24) are quite common when this question is a part of the study design . Analysis of clinical trial reports reveals that manipulative methods most used were: Soft tissue kneading Mobilization without impulse (articulatory procedures) Mobilization with impulse (high velocity/low amplitude [HVLA] thrust procedures) HVLA thrusting maneuvers were most common, with rotary thrusting to the lumbar area with the patient in a lateral recumbent position. A few studies identify muscle energy procedures (25). Few published studies describe use of the following procedures: Indirect Functional Counters train Myofascial/fascial release Craniosacral
VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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With the exception of the AOA/Rush-Anchor HMO protocol, other large-scale prospective research protocols have not accurately integrated the total patient approach characteristic of osteopathically oriented manipulative interventions. Conversely, the Tillinghast statewide studies of Workmen's Compensation outcomes (26) report the costs associated with total patient approach as delivered by practitioners including osteopathic physicians, allopathic physicians, allopathic surgeons, physical therapists, and chiropractors. However, these do not delineate the extent to which each group may have incorporated a manipulative or mobilization technique. In these latter studies, the osteopathic management of cases in each region studied was reported to be more cost-effective than that delivered by any other group.
Systemic Disease Controlled trials for manipulation in conditions other than low back and cervical pain are few. Most studies represent pilot observations by experienced osteopathic clinicians. Fitzgerald and Stiles (19) reports reduction in hospital length of stay when osteopathic manipulative care was used for patients with the following: 14% 1Oo/o 7% 12%
Asthma: Pneumonia: Cholecystectomy: Hysterectomy:
Fitzgerald and Stiles also reports a reduction in shock, dysrhythmias, and mortality when osteopathically oriented manipulative care was integrated into the care of a group of patients with myocardial infarction (Fig. 72.1). More recently, Cantieri (27) reports on a survey of the use ofOMT in 18 osteopathic hospitals. In those diagnosis related groups with documentation of more than 10 patients receiving OMT, a decreased length of stay of one day or more was noted in a number of systemic conditions including: Noncancerous pancreatic disorders Psychosis Upper gastrointestinal procedures Intestinal obstructions Transient ischemic attacks Cardiovascular disorders in acute myocardial infarction patients discharged alive
Complex cardiovascular catheterization
disorders
undergoing
cardiac
There are a greater number of studies in the osteopathic literature documenting the incidence of somatic dysfunction findings in certain systemic diseases. Kelso (28) reports on a double-blind clinical study of osteopathic findings in hospital patients. Student examiners were compared with experienced osteopathic clinicians. In 5,174 separate examinations, somatic findings were significantly more frequent in acute visceral disease than in controls. Nicholas (29) reports a pilot study that examined 286 hospitalized patients with 73 different diseases. Again, a variety of identifiable somatic patterns were found with different disease entities. The study focused on somatically identified cervical and thoracic spine pattern differences associated with respiratory, gastrointestinal, and genitourinary diseases. Other osteopathically based observational studies assessed somatic correlations with gastrointestinal diseases. Their findings closely mirror pain pattern discoveries recorded by surgeons at the Mayo Clinic (30). Several well-controlled studies have identified common somatic dysfunction patterns in patients with coronary artery disease and myocardial infarction (31 ,32). Somatic findings are primarily located in the left upper thoracic area (Fig. 72.2). Evidence of upper cervical (C2) dysfunction was also found in patients with
Right Thoracic Spine
Left Thoracic Spine
100 92 90 80 'iii ....c Cl)
...
70
ca
fl.. 0
lii E
J:l
60 53 50
: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
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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).
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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.
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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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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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) .
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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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
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(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
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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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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VII. Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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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VII Osteopathic Considerations in Palpatory Diagnosis and Manipulative Treatment
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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.
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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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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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VIII. Basic and Clinical Research for Osteopathic Theory and Practice
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)
74. Foundations for Osteopathic Medical Research
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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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
74. Foundations for Osteopathic Medical Research
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;
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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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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
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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
1196
VIII. Basic and Clinical Research for Osteopathic Theory and Practice
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
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I Study popul ati on I
~dom~nI Ex posed to intervention I Not exposed to interventio n or
l
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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.
1198
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
1200
VIII Basic and CLinicaL Research for Osteopathic Theory and Practice
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FIGURE 76.5. Comparison of reported pain or discomfort before and after receiving osteopathic manipulative treatment. A greater score indicates more pain or discomfort. The error bars represent one standard deviation.
FIGURE 76.6 . Comparison of reported mobility before and after receiving osteopathic manipulative treatment. A greater score indicates less mobility. The error bars represent one standard deviation.
a randomized clinical trial including double blinding and light touch sham treatments but failed to demonstrate any significant benefits associated with OMT in rehabilitation patien ts after knee or hip arthroplasty (36). More recently, the clinical outcomes and satisfaction of patients atte nding a university-based specialty OMT clinic during 1998 were reported (37). Patients described OMT as being highly efficacious and reported significant reductions in pain and improvements in mobility associated with their OMT regimen (Figs. 76.5 and 76.6). A unique finding of this study is that women experie nced significantly greater reductions in pain or discomfort than men. Patient satisfaction was generally high across all measured dimensions, with the sole exception of finances . More specifi cally, patients reported significam dissatisfaction with insurance coverage for OMT services. Another study conducted within the same OMT clinic during 1997 examined quality of life, functional status, and patient satisfaction (38). This OMT clinic populatio n was highly selected, often referred to the clinic after treatment failed elsewhere. Not surprisingly, clinic patients reported significantly poorer physical and mental functioning than patients in the general population on each of the eight SF-36 scales: physical functioning, role limitations because of physical problems, bodily pain, general health, vitality, social functioning, role limitations because of emotional prob lems, and mental health (Fig. 76.7). Perhaps the most interesting finding of the study was that patients referred to this OMT specialty clinic frequently reported poorer quality of life than national referents with hypertension , congestive heart failure, diabetes mellitus (type 2), recent myocardial infarction, or clinical depression. T his highlights the difficulties that osteopathic physicians often face in treating patients with chronic musculoskeletal conditions. Despite such challenges, clinic
patients reported a high level of satisfaction with their health care. The SF-36 health status survey was also used to ascertain the health of 2,700 patients attending six family medicine training clinics at a college of osteopathic medicine from 1996 through 1998 (39). As in the previously described study, clinic patients reported significantly poorer health status then the general population on all eight SF-36 scales. This has been att'ributed to the case mix of clinic patients, including a relatively high proportion of indigent and uninsured patients. C linic patients were given the option of completing the SF-36 survey in their preferred language, either English or Spanish, and the results were then compared. English-language respondents reported significantly better health in the SF-36 scales measuring general health, social functioning, role limitations because of emotional problems, and mental health. Interestingly, however, Spanishlanguage respondents reported significantly greater vital icy. Overall, patients reported high levels of satisfaction with their health care.
CONCLUSION Osteopathic outcomes research is a fledgling enterprise. The basic tools afforded by biostatistics and epidemiology, as presented herein, are readily available to investigato rs seeking to add to our body of knowledge. The need to demonstrate the benefits of osteopathic medicine, as well as its distinctiveness, has never been greater. The future of osteopathic medicine may well hinge on its ability to satisfy this need by identifyi ng, ·nurturing, and supporting a new breed of vibrant osteopathic Clinical researchers.
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83.3
81.3
74 .7
~
45 .1
62.4
43 .8 ;-
75 .2
72 .0
60 .9
SF-36 Health Scale FIGURE 76.7. Mean standard ized scores according to SF-36 health scale for osteopathic manipulative medicine patients and the general United States popu lation . Higher scores represent better health on each sca le. Each of the eight comparisons is significant at the p less than 0.001 level. SF-36 denotes the Medical Outcomes Study Short Form-36.
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VIII. Basic and Clinical Research for Osteopathic Theory and Practice
REFERENCES I . North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of ca rotid endarterectomy in symptomatic pariems with high-grade stenosis. N Eng/] Med. 1991 ;325:445-453. 2 . Executive Co mmirtee for the Asymptomatic Carotid Atherosclerosis Smdy. Endarterectomy for asymptomatic carotid artery stenosis. ]AMA. 1995;273 : 142 1- 1428 . 3. Cebu l R, Snow R, Pine R, er al. Indi catio ns, outcomes, and provider volumes for carotid endarterecto my. ]AMA. 1998;279: 1282- 1287. 4 . Donabedian A. The role of omcomes in quality assessmenr and assurance. Qual Rev Bull. 1992;18:356-360. 5. Licciardone JC. The evo lving role of outcomes measuremenr and manageme nt in healrh ca re.] Am Osteopath Assoc. 1997;97:290-292. 6. Ware JE, Snow KK, Kosinski M, er al. SF-36 Health Survey: Manual and fnte1pretation Guide. Boston, MA: New England Medical Cemer; 1993. 7. Duncan PW, Wallace D, Lai SM, er al. The stroke impact scale version 2.0. Evaluation of rel iability, validity, and sensitivity to change. Stroke. 1999;3 0:21 3 1-2 140. 8. Roland M, Morris R. A study of the namral hisrory of back pain: Part I. Development of a reliabl e and sensitive measure of disability in low-back pain. Spine. 1983;8: 141- 144. 9 . Roland M, Fairbank). The Roland-Morris disability questionnaire and rhe Oswesrry disability questionnaire. Spine. 2000;25:3115-3124. I 0 . Srrarford PW, Binkley J, Solomon P, er al. Assessing change over rime in pati ents with low back pain. Phys T/;er. 1994;74:528-533. 11. Bellamy N. WOMAC Osteoarthritis Index. User's Guide III, 1998. 12. Ware Jr JE, Snyder MK, Wright WR, er al. Defining and measuring patient sa tisfaction with medical care. Evaluation and Program Planning. 1983;6:247-263. 13. Press, Ga ney Associates, Inc. Effective cusromer services practices. Healthcare Executive. 2001;16:64-65. 14. Go ldstei n M. A chall enge to the profession: initiate evidence-based osteopathic medicine now [ed irorial]. JAm Osteopath Assoc. 1997;97:448, 451. 15. Committee on Quality of Health Care in America, lnsrirure of Medicine.
Crossing the Quality Chasm: A New Health System for the 21st Century 16. 17. 18 .
19. 20. 21. 22.
Washington , DC: National Academy of Sciences; 2001. Last JM. A Dictionary of Epidemiology, 2nd ed. New York, NY: Oxford University Press; 1988. Benson K, H artz AJ. A com parison of observational smdies and randomized, co ntrolled trials. N Eng/] Med. 2000;342: 1878- 1886. Concaro J, Shah N, Horwitz RI. Rando mi zed , co ntroll ed trials, observatio nal studies, and rhe hiera rchy of research designs. N Eng!] Med. 2000;342: 1887- 1892. MacMahon B, Yen S, Trichopoulos D, er al. Coffee and cancer of the pancreas. N Eng/] Med. 1981;304:630- 633. Hsieh C, MacMal1on B, Yen S, et al. Coffee and pancreatic cancer (Chapter 2) [lener]. N Eng/} Med. 1986;315:587-588 . Hoehl er FK, Tobis JS, Buerger AA. Spinal manipulation for low back pain. ]AMA. 1981 ;245: 1835- 1838. Panerson MM. Osteopathic research: rhe future. In: Ward RC, ed.
23.
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27. 28. 29.
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32 .
33.
34.
35.
36.
37.
38.
39.
Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins; 1997:1115-1 124. Andersson GB, Lucenre T, Davis AM, er al. A compa riso n of osteopathic spinal manipulation with standard care for pati ents with low back pain. N Eng/] Med. 1999;341:1426-143 1. Licciardone J, Sroll S, Fulda K, et al. A randomized , controlled trial of osteopathic manipulative treatment in patienrs with chroni c low back pain. Unpublished manuscript, 2001. Bigos S, Bowyer 0, Braen G, er al. Acute Low Back Problems in Adults. Clinical Practice Guideline No. 14. Rockville, MD: Agency for Health Care Policy and Research , Pub! ic H ealth Service, U. S. Department of Health and Human Services; 1994. Hadler NM, Curtis P, Gillings DB , etai.A benefirofspinalmanipularion as adjunctive therapy for acute low-back pain: a st ratifi ed conrrol led trial. Spine. 1987;12:703-706. McDonald RS, Bell CM. An open controlled assessme nt of osteopathic manipulation in nonspecific low-back pain. Spine. 1990; 15:364-370. Shekelle PG, Adams AH , Chassin MR, et al. Spinal manipulation for low-back pain. Ann Intern Med. 1992; 117:590-598. Anderson R, Meeker WC, Wirick BE, et al. A meta-analysis of clinical trials of spinal manipulation. J Manipulative Physiol Ther. 1992; 15:18 1194. Shekelle PG, Ortiz E, Rhodes S, er al. Validity of the Agency for H ealrllcare Research and Quality clinical practice gu idelin es: how quickly do guidelines becom e outdated? }AMA. 2001 ;286: 1461-1467. Gamber RG, Shores JH , Russo DP, er al. Osteopathic manipulation in conjunction with medication reli eves pain associated with fibromyalgia syndrome: results of a randomized clinical pilot project. } Am Osteopath Assoc. 2002 (in press). Knebl J, Shores J, Gamber R, er al. Improving functional abi lity in the elderly by osteopathic manipulative treatment: a randomized , conrrol led trial. JAm Osteopath Assoc. 2002 (in press). Radjieski JM, Lumley MA, Canrieri MS. Effect of osteopathic manipulative treatment on length of stay for pancreatitis: a randomized pilot srudy. JAm Osteopath Assoc. 1998;98:264-272. Noll DR, Shores JH, Gamber RG , er al. Benefits of osteopathic manipulative treatment for hosp italized elderly patients with pn eumonia.} Am Osteopath Assoc. 2000; 100:776-782. Jarski RW, Loniewski EG, Williams J, er al. T he effect iveness of osteopathic manipulative treatment as co mplementary therapy following surgery: a prospective, march-controlled outcome study. Altern Ther Health Med. 2000;6: 77-81. Licciardone JC, Sroll ST, H erron KM, er al. A random ized controlled trial of osteopathic manipulative treatment following knee or hip arthroplasty. JAm Osteopath Assoc. 2002 (in review). Licciardone JC, Gamber R, Ca rdarelli K. Patient sat isfaction and clini cal outcomes associated with osteopathic man ipulative treatment.} Am Osteopath Assoc. 2002; 102:13-20. LicciardoneJC, Gamber R, Russo D. Quality of life in referred patients presenting ro a specialty clinic for osteopathic manipulative treatm ent. ]Am OsteopathAssoc. 2002;102:151-155. Licciardone JC, Brittain P, Coleridge S. Health status and satisfaction of patients attending osteopathic medical training clinics. JAm Osteopath Assoc. 2002 (in press).
BIOBEHAVIORAL INTERACTIONS WITH DISEASE AND HEALTH BRIAN H. FORESMAN GILBERT E. D'ALONZO, JR. JOHN A . JEROME
KEY CONCEPTS • Biobehavioral mechanisms alter health and disease through three basic pathways: physiologic responses that lead to disease, behaviors that increase or decrease health risk, and behaviors that alter surveillance activities or adherence with medical interventions. • The major behavioral factors that have been studied and shown to have dear associations with health and disease include: diet, exercise, sleep, cigarette smoking, tobacco use, alcohol use, and prevention of excessive sun exposure. • Placebos are also a biobehavioral mechanism that must be addressed in most forms of research. Results are affected by race, direct suggestion, patient belief in the treatment, trust in the physician, genetic variation, environmental effects, and nonspecific cause-effect relationships with placebos. • Sleep and somatovisceral responses constitute major biobehavioral mechanisms that are common to all individuals, a rich area for research, and that suggest a strong role for biobehavioral approaches. • As with other types of research, the biobehavioral research process begins with the acquisition of information and the development of a hypothesis about the mechanisms involved with the processes under consideration. Selection of the study design, subjects, methods to be used constitute the major components of the process and lead to a systematic analysis of the data. • Biobehavioral measures and techniques may provide a more effective research paradigm and may render valuable insight into the impact of osteopathic principles and practice. Major topics in this area will likely focus on: behaviors leading to the development of somatic dysfunction, behaviors resulting from somatic dysfunction, quality of life (QOL), effects of pain, and relationships between locomotor function, somatic dysfunction, and subsequent behaviors.
Biobehavioral research involves the investigation of behaviors on the maintenance of health and the development of disease. The onset of disease is a complex phenomenon that incorporates the tissue pathology (musculoskeletal abnormalities), psychosocial and behavioral response to that physical insult, and the environmental factors that maintain or reinforce that disability (even after the initial cause has been resolved). A large portion of the variance in an individual response to any disease outcome is accounted for by the manner of behavior and emotional response to the stress of the illness (1). In fact, the majority of today's health woes-obesity, cancer, and anxiety disorders to heart disease, hypertension, and adult-onset diabetes- are actually relatively new "diseases of civilization" brought on by our behavioral choices and mind-body interactions. Although the concepts that the mind influences disease processes have long been a parr of osteopathic medicine, research involving mechanisms of disease modification through a mind-body interaction have only recently become a parr of mainstream medicine. Our current understanding ofbiobehavioral ·interactions suggests that these processes are a complex interplay between genetic, physiologic, environmental, and behavioral factors that influence health and disease (2). Behavioral mechanisms can alter rhe nervous system, endocrine system, and the immune system, directly and indirectly, thereby influencing such medical illnesses as cancer and cardiovascular disease. Diet, exercise, drugs, alcohol, and tobacco use, along with a variety of other behaviors, modifY disease progression and/or disease risk. Finally, behaviors directly related to seeking or avoiding medical care can have important consequences on prevention, early detection, and adherence with medical regimens. Thus, the implication is that biobehavioral factors may significantly affect health care and health maintenance through a variety of direct and indirect mechanisms (2), and these effects should be addressed in osteopathic research and clinical practice (3-5).
BIOBEHAVIORAL MECHANISMS IN HEALTH Behavioral components of the mind-body interaction manifest in cognitive processes, emotions, and/or physical behaviors. The
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TABLE 77 .1. ABBREVIATED CESSES
LIST
OF
COGNITIVE
PRO-
Language acquisition Reading Emotional appraisal Memory Attention Menta I models or representations Learning and cognition Problem solving Ascribing meaning, abstraction Actio n
study of cognitive processes (Table 77.1) primarily focuses on understanding the acquisition, retention, and processing ofinformation. However, under most circumstances, thoughts, emotions, and cognitive processes must transmit information , be translated into motor actio ns, o r have identifiable physiologic responses before a behavior can be identified. It is for these reasons that many consider mental phenomena to be a special form of physical phenomena (i .e., bio behavioral) and therefore inseparable from physiologic processes. Biobehavioral factors exert their influence through three defined pathways (2,6) and at least one alternate pathway. In the first of these pathways, emotional reactions or behaviors are associated with or occur in parallel with physiologic alterations that contribute directly or indirectly to the pathophysiology of rhe disease (Fig. 77.1). An example is the stress response rhar is associated with in creases in blood pressure and heart rate as part of global sympathetic aro usal. Sympathetic alterations can, in turn , contribute di reedy to the development of cardiac disease and sudden death. Excess ive stress, whether induced by external events or extreme exercise, can alter neural and hormonal responses, leading to enhanced vulnerab ility to infection and inappropriate res ponse to disease (i.e., viral infections, wound healing, and cancer). T he second pathway for biobehavioral interactions involves behaviors associated with increasing or minimizing health risk (Fig. 77. 1). T hese particular behaviors are referred to as healthenh ancin g or health-impairing behaviors. Examples of healthenhancing behaviors include diet and exercise (due to their ability to minimize rhe development cardiovascular disease and cancer).
Pathway "A"
Path way "B"
Tobacco use and alcohol abuse are examples of health-impairing behaviors typically associated with adverse effects that frequently lead to emphysema, lung cancer, and cardiovascul ar disease. Other examples include drug use and high-risk sexual activity. Each of these activities conveys a risk o r benefit to an alteration of the underlying physiology and/or exposure. The third and final pathway (Fig. 77. 1) in volves behaviors that occur in response to the possibility that a disease may be, or is, present. For individuals without disease, the behavio rs that lead to early detection include ongoing surveill ance (i.e., retained breast examinations, sigmoidoscopy, etc.), recognition of symptoms, and the decision to seek medical care or follow-up care. Once a disease or a symptom is identified and a medical regimen is prescribed, adherence with the medical regimen (o r lack thereof) is a behavior that can affect the outcome of the disease process . In addition, the sudden discontinuation of medications or their erratic administration may not only hinder the effectiveness of medical regimens; such behaviors may create secondary adverse consequences. Prior investigations have nor routinely included somatic or motor dysfunction as attributable to a biobehavioral pathway; however, there are many situations under which this theoretic framework would be applicable and might offer distinct advantages in understanding the relevant pathophysiologic relationships. The consideration of such pathways is in keep ing with known responses of the somatic musculature and would represent a modification of pathway"/\' (Fig. 77.1) . In this instance, we would substitute musculoskeletal impairment for altered disease risk, and the pathway becomes more consistent with the concepts of viscerosomatic pathways. T his theoretic framework is also consistent with the biologic and behavioral responses of individuals with acute and chronic pai n (see Chapter 11).
Disease Development (Pathway " A" ) The major biobehavioral influences on disease development that have been studied involve the effects of stress on health or illness (Chapter 15) . Because of the scope of the data involving stress, physiologic response, and behavioral issues, our intent is to discuss the major mechanisms wherein stress responses affect select diseases.
Pathway "C"
Behavioral
FIGURE 77.1. Common biobehaviora l pathways in health and disease.
77. Biobehavioral Interactions with Disease and Health From an evolu tio nary standpoint, most neural events can be considered to develop and have been selected by evolutionary process associated with species survival (2). In this viewpoint, stress ~es po nses and other emotio nal patterns are hardwired into the central nervous system (CN S) and modified by learnin g and experience. T hus, co ntent and enviro nmental conditions give rise to particul ar res ponses th at can modi fy th e emo tional or cognitive respo nse. Essential ly, our bodies "lea rn" about the external correlates of internal res ponses much like a baby learns that food and eating extinguish the uncomfo rtable res po nse later learned as hunge r. T his process of" learnin g" can be significantl y affected by the intensity and chro nicity of the stress res po nse under which the learnin g occur red. Less intense and intermittent stressors allow more complex and appropriate coping stra tegies to be learned ; whereas mo re severe and prolo nged stressors may cause a co nditio ned biobehav io ral response that is less adaptable. In this sense, lea rning may be either adaptive or maladaptive and may affect predispos ition to disease.
CARDIOVASCULAR DISEASE Previous research has shown that stress, whether physical or emotional, pe rceived or real, often results in characteristic physiologic and behavior res ponses (Table 77.2) . T he phys iologic and behavioral correlates may trigge r acute, disease- related events and alter the pathophysiology of the diso rders (7). Acute cardiovascular events, such as ischemic episodes, heart attacks, arterial occl usion, and arrhythmias, have been shown to occur with anxiety, bereavement, and anger (3,8,9) . Si milar effects are also seen with strong positive emotions associated with desirable events (e.g., weddings). Several mechanisms have been proposed to account fo r these res ponses, including alteratio n of sympatheti cparasympathetic balance, acti vation of platelets, alterations of intravascular fl ow dy namics, and changes of endothelial fun ction (10, 11 ). Wi thin these hardwired responses, heightened maladaptive processes may lead to secondary physiologic res ponses that m ay have addi tional adverse consequences. For example, when assessing cardiovascular res ponses, physiologic reactivity is measured by the magnitude and the duration of the particular response. Studies have shown that increased cardi ac reactivity may be a di rect index of the underlying predisposi tion toward develop ing
cardi ovascular disorders o r may refl ect the activ ity of med iato rs of cardi ovascular risk (12). In several studies, exaggerated blood pressure res po nses identi fied individuals at risk fo r developing hypertension and atheroscleros is ( 13-15). Similarl y, other behaviors may have adverse affects o n serum li pid co mpositi o n, silent ischemia ox idative dam age (9, 16) (s uch as that seen with smo kin g), personality styles (e.g., type A), and al tered co ping mechanisms (1 7) . T hrough the use of bi obehavio ral approaches, cardiovascular researcher are now beginning to enhance our un derstanding of the complex relationships between the mind and the body in the development and progressio n of ca rdiovascul ar disease (6,9) .
IMMUNE FUNCTION AND INFECTIOUS DISORDERS Immunologic activity has also been shown to be alte red by behavio ral res ponses; however, the impact o n disease developm ent is less clear. So me of the di fficul ty in making assess ments rega rdin g immune fun ction in volves the va riabili ty of the stresso rs and th e dy nami c nature of the immune system (see C hap ter 10). For instance, natural killer cells have a different respo nse to acute and chronic stress exposures (18), an d these respo nses are also subject to circadian vari atio ns. C hanges in latent viral activity, lymphocyte proliferatio n, and natural kill er cell activity have all been demonstrated in respo nse to stress (I 9- 2 1). T hese changes in immun e fun ctio n and cell numbers may also occur with physical stress, such as severe exercise (22) . Several immuno logic respo nses may also promote fac il itatin g res po nses. T he activati on of inflammatory mediators, such as in te rleuki n-6 and proin fla mm atory cytokines, may alter neural processes to enhance as pects of the C N S stress respo nse (23). However, the ro le rhat stressinduced changes in immune functio n have on the develo pm ent of subsequent disease has been debated and remai ns un clear. Behavio rs can have a mo re d irect effect o n the development of disease by altering bodily functions and behavio rs associated with disease risk (24). Perhaps the most class ic example involves h um an immunodeficiency virus (HIV) di sease. T he transmissio n of HIV typically occurs d uring sexual acti vity, intrave nous dru g use, or th ro ugh other forms of direct con tact with bod ily fluid s. An attenuation of these behaviors o r the additio n of pro tective measures can result in substanti al decreases in the risk of acq uiring
TABLE 77.2. SUMMARY OF MAJOR RESPONSES TO STRESS Behavioral Response Moderate/ Short Duration
Increased attention Increased alertness Enhanced memory and problem-so lving skills
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Severe/Long Duration
Physiologic Response
Di min ished attention An xiety Irritability Reduced retent ion and reca ll Dimi nished problem solving Insomnia
Increased heart rate Increased sympathetic activity (both neura l and humoral) Increased blood pressure Increased catabolism Altered immune function (dependent on the duration and intensity of the stressor)
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VI!!. Basic and Clinical Research for Osteopathic Theory and Practice
HIV Conversely, increases in risky behaviors or the occurrence of impu lse behaviors, as can occur with individuals with certain types of mental health problems (25) or during drug and alcohol use (26,27), can change routine behaviors of the individual and increase the risk of acquiring HIY. In this setting, stress or drug use may initiate impulsive behaviors or may inhibit intentions to avoid the risky behaviors (28) leading to impaired judgment, a lack of attention to derails, or in some instances, disregarding the potential consequences of their actions (29). Evidence for a direct effect of behaviors on immune status leading to outcomes in HIV is limited (30). In a recent study of 100 HIV-positive individuals, somatic findings were associated with progression disease; however, there was no evidence to suggest that these effects were mediated by the immune system. Cole and colleagues (31) suggested that some specific behaviors may affect the progression of disease development when present. In their srudy, the investigators identified that concealment of sexual identity was positively related to cancer morbidity and the incidence of pneumonia. However, there was no clear link with alterations in immune function, which might be related to the behaviors themselves.
SLEEP AND CIRCADIAN BIOLOGY Sleep and sleep wake activities also constitute a major biobehavioral mechanism. Sleep deprivation and sleep fragmentation result in excessive daytime sleepiness, chronic fatigue, and other symptoms. Many of the symptoms are indistinguishable from depression, and they may have some of the same adverse consequences on medical adherence as depression does (32). More recently, studies have suggested that alterations of sleep wake schedu le may contribute to the development of disease. In one recent study, Bursztyn and colleagues (33) assessed daytime napping in an older patient cohort (n = 455). The findings suggested that an afternoon nap appeared to be an independent predictor of mortality with a risk odds ratio of 2.1. In a separate srudy using self-administered questionnaires on health status and lifestyle (34), the investigators identified that significantly longer and shorter sleep times, compared with 7 to 8 hours, were associated with increases in total mortality in men. In addition, female users of sleeping pills and those with self-reported poor sleep quality also shared an increased risk of mortality independent of sleep duration. Similar findings have been noted by others (35), and were noted to be unaffected by later arousal times. However, a recent review of the literature on shift work, an extreme form of late risers, suggested there is an overall increase in cardiovascular risk of 40%. These data suggest that disrupted sleep or significantly altered sleep schedules may have adverse effects on medical outcomes through biobehavioral mechanisms.
PAIN SYNDROMES Specific diseases need not be the only focus of biobehavioral investigations. Major symptoms, and specifically chronic pain, may benefit from a biobehavioral approach to investigations (36-38). In a review from an NIH-sponsored workshop, the current status and major directions for biobehavioral pain research were our-
lined. Pain was identified as a subjective experience that could only be quantified through behavior (39), and there were many behavioral responses to chronic pain that impacted treatment and recovery. Consistent with the NIH initiative, investigators demonstrated that biobehavioral models offer significant insight into the mechanisms active in chronic pain (40,41). Several studies suggest that dysfunctional information processing occurs, accentuating the perception of pain and reinforcing the concept that learning plays a significant role in pain syndromes (40,42). Such mechanisms may also be actively involved in the disability associated with several disorders (e.g., low back pain, osteoarthritis, cardiac pain) (5,43), and may have a significant role in our understanding of the neurophysiology of somatic dysfunction (44).
Disease Risk (Pathway " B" ) Several behaviors exert their primary effect by modifying disease risk or factors associated with disease risk. The major behavioral factors within this category that are also supported by substantial data include: diet, exercise, sleep, cigarette smoking, tobacco use, alcohol use, and the prevention of excessive sun exposure. In general, modifications of diet, exercise, sleep, and relaxation constitute factors associated with a protective influence over physiologic sources of risks. They also function in an indirect manner by minimizing the effects of stress and enhancing coping mechanisms. Smoking, excessive alcohol consumption, and drug abuse typically fall into the category of health-impairing behaviors that directly influence disease processes and have secondary effects on mood and other behaviors. Physical behaviors (e.g., exercise, aerobics, and other types of physical exertion) often exert a protective influence and therefore fall in the category of health-enhancing behaviors. The consequences of these physical behaviors may directly or indirectly affect pain syndromes, medical interventions, and the natural history of disease. For example, an individual attempting to undergo a weight control regimen without substantiallifestyle changes that include increases in activity r.Jay experience difficulty in achieving and maintaining weight loss (45,46). In general, the preponderance of data demonstrating association between diet and disease outcomes is found in the cardiovascular literature. Weight gain, obesity, excessive salt consumption, and fat or cholesterol intake are major contributors in the development of coronary artery disease, hypertension, and stroke. Interventions directed at weight loss and weight maintenance have engendered some success when the interventions were maintained (47) and when the interventions target specific ethnic or socioeconomic groups (48). These interventions recognize that adherence and cultural affects were an important part of an effective regimen. The role of dietary influence on cancer risk is more speculative than the data regarding cardiovascular disease. For example, there appears to be an association between far/fiber content in the diet and the mammography profile associated with breast cancer (49) or recurrence of breast cancer among women with estrogen receptor-positive tumors (50). Whether patients can effectively alter their fat intake and weight has also been studied by investigators. Several studies have shown that diet can be effectively modified (51), secondarily leading to an increase in consumption of healthier food (52). These programs appear to be more effective when there is evidence to support the dietary changes and the
77. Biobehavioral Interactions with Disease and Health
1207
individuals are aware of the evidence (53). However, the effect of dietary imerventions on cancer-relevam ourcomes has been questioned by so me and may require furrher swdy, especially in parier1rs with established malignancies. Exercise appears ro exerr beneficial effects by reducing srress an d increasi ng calo ri c consumption. The increasing caloric consumption is imporranr in designing effective weight managemenr programs. T here are data ro sugges t that routine exercise programs reduce the relative ri sk of developing ca ncer (54) through either a reduction in sedemary activities or weight loss (5 5). Exercise also appears ro be an effective copi ng srraregy for srress (22). These effects may be related ro alterations in mood and a reduction in perceived srress that occurs with routine exercise (56). The latter of these effects may relate more specificall y roan attenuation of physiologic reactivity. Unfortunately, for many individuals, increasing stress red uces the amount of phys ical activity underraken (57). Reduction of stress and an improvemem in the physiologic adaptabil ity have also been cited as possible mechanisms by wh ich exercise cou ld exert its effect in cancer. Our knowledge of the effects of tobacco use dates back ro the early 1960s. Since that rime, extensive data have demon snared rhe adverse health co nsequences of cigarette smoking and tobacco use. T he hab itual use of robacco relates ro physiologic respo nses ro nicotine (e.g., sense of well-being, arousal, and appetite suppression) and the avoidance of or the relief from withdrawal (58) . Smoking co ntributes ro the develop mem of atherosclerosis, coronary artery disease, hypertensio n, stroke, emphysema, bronchitis, and several malignancies through recognized physiologic mechanisms (59). Even secondhand smoke may carry some of the hab ituating and cardiovascular res ponses related to nicotine exposure (60). ln this regard, prevention may be a more effective strategy for limiting cigarette smoking and its adverse health consequences (61). However, in indi viduals who smoke, stress appears ro be a significant comriburor ro the amount and frequency of robacco use (57), as well as ro relapse after smoking cessatio n. Th us, the co mbination of stress and robacco use is a self-reinforcing behavioral patte rn that is complicated by nicotine add ictio n. Behavioral srrategies des igned to alter tobacco use m ust address these interactive behaviors robe effective (62). The biobehavioral co mpon ents of successful addi ction management are fo und in Table 77 .3. Understa nding rhe issues relevant to the heal th consequences of su n exposure is illustrative of the complexity of some biobehavioral interactio ns. U ltraviolet (UV) radiation in sunlight has been lin ked ro the development of basal-cell cancers, squamous-cell cancers, and melano mas (63-65). For basal-cell and squamouscell cancers, the risk parallels cumulative lifetime UV exposure.
Routine use of avoidance measures or sunscreen ca n substantially decrease the risk of skin cancer. Unfortunately, despite increased awareness and knowledge of skin cancer, there has been little change in individual behav ior. One reason is the belief th at sun tanning makes an individual look healthier and that expos ure ro the sun is healthy (66). This persistence o f beliefs and behaviors underlies several medical disorders and high-risk behav iors.
TABLE 77 .3 . BIOBEHAVIORAL COMPONENTS OF ADDICTION-MANAGEMENT MODELS
PLACEBO AS A BIOBEHAVIORAL MECHANISM
1. 2. 3. 4. 5. 6. 7. 8.
A public declaration. Attend to withdrawal syndrome. Aerobic exercise. Attacking learned behaviors. A supportive group. Diary of progress. Track economic rewards . Tra ck interpersonal rewards .
Disease-Related Biobehavioral Activities (Pathway "C") The final general mechanism relating behav ior with disease involves behaviors that occur when illness is presem, suspected , or where th ere is risk of illness. Many facro rs influence individual behaviors u nder these conditions. When illnesses are suspected or where there is the potemial for illness, the perceptio n of illness (e.g., fear), and the potential impact (e.g., need for chemoth erapy) may significantly alter the response of the individual. Socioeconomic facrors, issues involved with physician suppo rt or co nfidence, the perception of risk, and emotional reaction of th e individual al l significantly affect surveillance efforrs (67,68). H eal th beliefs, perceptions of risk, and generali zed anxiety regarding disease or illness greatly co ntribute to avo idance on the part of the patient (67,69). Consistent with these concep ts, Lerman and associates (69) reported heightened anxiety about developi ng breast cancer in association with intrusive thoughts and demonstrated some relationship with adh erence (70). Similar findin gs were noted in women undergo ing genetic counselin g for breast cancer (71). However, the distress associated with disease ri sk does not have a consistent effect on surveillance ac tivities (72). These findin gs have also been noted in screening for HIV. Studi es have linked the associated anxiety with und ergo ing screening and failure to follow-up for test results. In ge neral, srress, emotional res ponses, and past behav io r are often the best predicrors (73) of adh erence. A variety of behav iors related to the presence of illness may arise. Two major behavioral mechanisms affect outcomes in indi viduals with existing d isease. The first of these mechanisms relates ro adherence. Medical regimens are rarely effective when patients are no nadh erent. However, nonadh erence may arise from many sources, including inadequate understanding (74), forgetfulness, confusion, health beliefs, personal (na·ive) theories of illn ess, and cost (75). There are few reliable predictors of adh erence; however, high-quality communication, patient supervisio n, social su pporr, and the recognition and management of underl yi ng impai rm ents, es pecially depression (32), all contribute to improving ad herence (32,75) .
Improvem ent of a condition durin g clinical trials or treatment ca n be attriburable to one of three causes: natural hisrory, specifi c effects of the imervention , and nonspecific effects ofintervention. The latter of the three causes is typically termed a "placebo effect" (76). If this effect were robe rep resented in graphic form with the spectrum of intervention along the horizo ntal axis and clinical improvement along the vertical axis, the pl acebo effect would be represe nted by gradual improvement in the clinical co nditio n.
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The perceived drug effect would be represented by a more significant clinical improvement over the same course of treatment. The difference between the placebo and perceived drug effect would then be considered the active drug effect (77). Because of the possibility that new interventions could show improvement simply due to a placebo effect, this has typically been cited as a major reason for including a placebo control in most studies. Factors that have been shown to affect the placebo response include race, direct suggestion, belief in the treatment, trust in the physician, genetic variation, environmental effects, and nonspecific cause-effect relationships with placebos. Environmental variations include personal interactions (e.g., the doctor-patient interaction), perceptions based on relevant previous experiences, and the influence of the setting (78). Each of these must be considered when planning research, especially in light of the potential for interactions between the researcher, an examiner, or an intervention. The importance of such effects has recently been reviewed with regard to cardiovascular disease (77) and pain treatment (76). The major mechanisms that have been proposed to explain the placebo effect include decreased anxiety, altered expectations, learning or classical conditioning, and endogenous opium release (76-78). In each of these mechanisms, there appears to be interaction between the behavioral aspects of the individual and the placebo, resulting in a biologic improvement. However, in a recent review of over 130 clinical trials, Hrobjartsson and Gotzsche (79) concluded that there is little evidence to support the contention that placebos have powerful clinical effects. In their review, the authors concluded that placebos had no significant effects in most studies with objective or binary outcomes. However, placebo effects were noted in trials involving continuous subjective outcomes and those trials involving the treatment of pain. In addition, there was a greater likelihood of identifying a placebo effect when the experimental and control group sizes were relatively small. Placebos can generally be categorized into pharmacologic, physical, or psychological (79). For the purpose of investigating manipulative interventions, an appropriate placebo control is both essential and difficult to achieve. For individuals who previously have undergone manipulative interventions, there is an element of learning on the part of the subject that may allow them to differentiate a placebo from an active intervention. Even when naive individuals can be used, the physical component of touching a patient or subject has an active component known as an active placebo that creates difficulty in designing clinical trials. In some instances, as has occurred with studies investigating antidepressant therapy (80), this placebo effect has some measurable physiologic effect that must be considered in the interpretation and the research paradigm.
OVERVIEW OF THE BIOBEHAVIORAL RESEARCH PROCESS The biobehavioral research process can be broken down into arbitrary steps beginning with the development of a research question and ending with a written report of the research findings (Table 77.2) (81). The choices involved in the process are not unique to biobehavioral research but have some methodologi-
cal considerations that should be understood by all researchers. Decisions made about the methodologies employed and measurements obtained will significantly affect the value and validity of any research (82). Overall, the primary goal of the medical researcher and clinician is to provide greater understanding of the relationship between biologic processes and behavior and to communicate those results effectively to both the professional and lay readership. Osteopathic medicine is being challenged to provide evidence of efficacy for osteopathic manipulative treatment. The outcomes important to third parry payers, clinical professionals, and patients all involve biobehavioral aspects that should be incorporated into research design. Further, solid experimental research will need to prove that osteopathic treatment is less costly than other alternatives, or that it is an effective alternative with measurable outcome improvement. In this setting, using biobehavioral measures and techniques may provide a more effective research paradigm and may render valuable insight into the impact of osteopathic principles and practice.
Basic Research Paradigms The essence of a descriptive research design is to identify the characteristics of a system or an intervention applied, in this context, to a patient or subject. Often, comparisons include intensity, magnitude, frequency, or duration of a characteristic (e.g., symptom or clinical finding) across different phases of the treatment or across time. Such research paradigms do not routinely give mechanistic insight. Hypothesis-driven research proposes that a certain intervention or perturbation will yield a specific result on the basis of prior knowledge of the system, disease, or condition being studied. The research hypothesis is based on an understanding of an active mechanism or mechanisms and is designed to assess how a particular intervention exerts a specific effect. For example, aresearcher might propose using a drug that affects a specific enzyme known to be the cause of a particular disease using an outcome measure pertinent to that disease. In this setting, the goal is to see whether there are differences in the groups that can be accounted for by the treatment delivered. In any research, the selection of subjects and other factors may affect the outcome or validity of the study. Some research designs use random selection of subjects while others may use a highly selected population or matched samples to minimize the variance and increase the likelihood of finding a significant effect. Other factors that need to be considered include the effect of preexisting conditions (covariants), the blinding of researcher and/or subjects, effect size, the power of the study (i.e., a deteimination of the number of subjects needed to have a valid study), and the utility of the outcome measures. Nonetheless, hypothesis-driven research is critical in developing new knowledge about cause and effect, and it is the backbone of good osteopathic medicine.
Starting the Research Process Before a hypothesis may be developed, the researcher must review or be knowkdgeable about the current body of scientific knowledge related to the research question . Occasionally, a paucity of
77. Biobehavioral Interactions with Disease and Health
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TABLE 77 .4. STEPS IN RESEARCH DESIGN AND IMPLEMENTATION Process Steps
Considerations
Develop the hypothesis and the components of the hypothesis
Is there sufficient published or preliminary data to develop a hypothesis? Is the hypothesis consistent with the available data? Is the hypothesis testable? Has the hypothesis been tested before? Would testing the hypothesis add to the current body of scientific knowledge? Refine the hypothesis.
Determine the methods necessary for testing the hypothesis
Determine the biologic and behavioral effects pertinent to the hypothesis. Determine the most optimal method for measuring the processes. Under some circumstances, this may require that methods be developed and validated before performing the research. Determine the conditions for the assessment.
Determine the research design that can be empl oyed
Determining the necessary comparisons. Assess the need for blinding and placebos. Determine the subject-selection process. Perform a power analysis.
Perform the project and analyze the results
Identify unforeseen problems with the methods or study design. Modify the processes to improve the study.
Evaluate the hypothesis in light of the results and th e limitations of the study.
What were the major findings of the study? How do the data support or refute the hypothesis? Are these data consistent with prior investigations?
Identify the major findings of the research that verify previous findings and those that add new information.
What are the implications of the study and how generalizable are the results? What were the limitations of the study and how do they affect the conclusions?
Communi cate the results .
Determine the most appropriate venue for presentation of the study. Identify areas for future investigation.
From Delahanty DL, Dougall AL, Schmitz L, et al. Time course of natural killer cell activity and lymphocyte proliferation in response t o two acute stressors in healthy men. Health Psycho/. 1996;15:48-55, with permission.
data exists sufficient so that a mechanistic hypothesis cannot be developed. In that circumstance, the initial research may be descriptive rather than mechanistic, but should be directed toward developi ng a sufficient body of kn owledge to advance to mechanistic inves tigations (Table 77.4). T he resea rch process begins with a question in the form of hypothesis abo ut the mechanism of an effect (83). In general, the hypotheses should center around testing mechanisms as opposed to descri ptive research or, "what happens if . .. ," as discussed above. T his simple understanding of the difference berween these rwo approaches is difficult for many individuals. In descriptive research (Fig. 77.2), a system is studied under a given test condition to determine the effect or the impact. This style of research is most appro pria te for simations where basic background informatio n or assess ments are needed before a more precise experimental model of mechanisms can be undertaken . Hypothesis-driven research will typically formulate a research question that may have rwo or mo re potential o utcomes (Fig. 77.2), depending on the mechanism that is active and the design that is being employed for the research. T he researcher then chooses conditions and measurements that allow the clearest delineation berween the potential outco mes.
Depending on the type of biobehavioral research employed, major interactions berween biology and behavior must be addressed. In simplest form, these interactions may be summarized as behavior affecting the physiologic response, a physiologic response affecting a behavior, or behaviors arising in relation to a disease process. The relationship that is hypothesized constitutes a possible cause and effect relationship and how to measure the constructs around variables and which the research plan will be initiated. To observe the cause and effect relationship, the exact behavioral and physiologic variables that are involved need to be specified. In addition, the conditions under which these measured variables interact must also be specified in significant detail. T he research model selected must include controls for the confounding effects found in the interaction berween the variables being smdied and the behavioral/biologic measurements. Essentially, specifying the specific conditions, behaviors, and biologic processes that are involved is necessary to limit outside interactions or variance within the measurements, determine cause and effect, and not jeopardize the validity of the study. There are six factors that may jeopardize validity, confound the results, and decrease the validity of any conclusions.
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V!I!. Basic and CLinicaL Research for Osteopathic Theory and Practice Maturation Internal cognitive/emotional processes operating during the experiment, including learning, getting ti red, unintended reinforcement or pun ish ment for certain behaviors, and so on, affect future scores.
Instrumentation A
Any change in the measuring instruments or in an observer's use of the instruments o r scoring methods produces changes in rhe obtained measurement over time and confounds results.
Measurement Variance
B
Basic research paradigms. A: Descriptive research. Descriptive research typically involves identifying the frequency of occurrence and/or characteristics of a system, condition, or population under specified conditions across time. B: Hypot hesis-driven resea rch. Hypothesis-driven research uses known data about a system, condition, or population to generate a mechanistic model of interaction. Using this model, predictions about the behavior of the system or causal relationships between variables are generated. Testing conditions and measurements are then selected to determine the predictive validity of the model. FIGURE 77.2 .
Selection into Groups G roups form ed for experimental reasons, w ith a specific illness, seeking medical care, and willing to participate in a hypothesisdriven design where they may receive a sham o r no treatment do not represent the universe of patients with that particular illness. We know, for example, that chronic pain patients who are enrolled in multidisciplinary pain clinics are a very unique group of self-selected patients with whom results do not generalize to the overall chronic pain population (42).
Intent to Treat There is a natural loss of subjects during a study from the beginning to the end. The drop-out rates are critical, but of particular importance is the question of, "who were the people who dropped out and why?" For example, they m ay have dropped o ut because the treatment was actually detrimental; if those scores were included, it wou ld have substantially altered the conclusion. Scores no t collected often cause a "type II" or false positive statistical conclusio n.
Multiple Treatment Interference T he effects of prior treatments are usually n ot erasable when multiple treatments are applied to the same person. Such is the case with manipulative treatment.
This is the most common factor invalidating research results. Most patients are treated and selected into the treatment gro ups by extreme scores to begi n with. For example, they may have high pain scores, severe impairment in range of motion, or activities of daily living, mood, on so forth . Because they were selected on an extrem e of a bell-shaped curve, they wi ll show su bsequent test scores that are improved simply as a function of movi ng from the tail of the curve toward the mean average, which is a statistical artifact in measuring. In other words, if you take the wo rst of the worst and measure them at that point and do anything to them and remeasure in the future, some wi ll have better scores on retesting and w ill have m oved toward the average by chance. For these reaso ns, th e exact specifica tions for the behavio rs to be studied and the methods for the measurement of intensity, frequency, and duration of symptoms are especially important in biobehavioral research. These characteristics of each behavioral measurement are important variables that must be quantified for the study design. U nder some circums tances, the characteristics may either be dependent o r independent variables, as determ ined by the specific interactio n that is being identified in the design of the study and how the variable is quantified and measured .
Quantitative Measurement Measurement of behavior req uires that we employ a quantification system to reliably describe and identify characteristics of beh avior in the context being studied. The spectru m of potential behaviors that may be studied in biobehavioral research is exceptionally broad and ranges fro m physical behaviors that may be directly quantified to particular thoughts, or thought patterns that must be ind irectly inferred. The assess ment of behavioral constructs may be further complicated by languages,. dialects, cultures, age, socioeconomic status, gender, race, and other situation al considerations. Experience or fam iliarity with many interventions or measurements may alter the conditions for a resea rch project, such as complicating or invalidating the results. For exam ple, a subject's fami liarity with osteopathic interventions may invalidate a research design using a placebo control because the patient is able to identify therapeutic intervention and is nor blinded to the study design. The basic clara resulting from m easurement are a seri~s of numbers. These numbers represent the measurements of some characteristic, and the m easurements obtained from one or more groups of individuals. We can seldom make much sense our of
77. Biobehavioral Interactions with Disease and Health these numbers if we leave them in their raw form. For that reason , we use statistical procedures to answer questions we have raised abou.t the basic data. We want to put some lcind of order into our numbers. We can graph the numbers, look at percentiles, rank order numbers, and see how group patterns are made clearer by sorting this raw data into frequency distributions and loolcing at the mean average. The arithmetic mean is simply the result of adding up all of the measures and dividing by the number of measures. We can look at the mode, which is defined as the score that occurs most frequently, and the median, which is a label for the point at which 50% of scores fall below and 50% of the scores fall above·. We can look at how individuals and groups vary and deviate from the mean score for each raw score obtained. This is called the variance. You find the variance by subtracting the mean average from each raw score, squaring that number, then dividing by the total number of scores. Find the square root of the variance, and you have the standard deviation. It is from the mean and standard deviation that all forther statistical techniques evolve. The simple goal of statistical techniques is to answer the question of whether the changes in scores obtained would have occurred by chance. In these statistical procedures, we set our confidence intervals at usually five times our of a 100 (i.e., 0.05 level). This means that we would be satisfied that the scores obtained would have happened by chance only five rimes out of a 100. This is a basis for common rests, such as the ttesr for two groups and analysis of variance (AN OVA) for more than two experimental groups. These two rests are commonly used statistical methods in biobehavioral research. Researcher's interest may also rest in the aggregate set of measures rather than on any one single measure considered apart from the others. The logic, algebra, distribution theory, numerical analysis, and computer programs for these types of analyses are all described elegantly and available at most computer and research facilities.
Measurements Measurements of behavior may be either quantitative or qualitative. Quantitative measurements typically convert the behavior to a categorical or numeric scale. The major benefit of using numeric measurements is that they are more amenable to statistical analysis. Categorical scales may be used to place subjects or behaviors into particular categories on the basis of specific characteristics. Under some circumstances, categorical scales may be based on qualitative or subjective assessments. Thus, the investigators shouJd consider that qualitative tools requiring subjective interpretation may be affected by examiner bias, and need to be applied in a uniform fashion to obtain reliable numeric results. Qualitative measurements are typically based on the assessment of particular characteristics that allow them to be placed in discrete categories or transformed into a numeric scale. Quantitative measurements should not be assumed to be better than qualitative assessments. The caveat that is best followed is to choose the most appropriate measurement tool for the physiologic and behavioral components given the study participants and situation under investigation. Frequently, the researcher may benefit from the work of other investigators and use known, standardized tools that have established validity and reliability. Some standardized tools may be used to obtain self-reporting of the data. In many instances, these tools can be easily administered, completed, and
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scored in a standardized fashion. There are many standardized measurement instruments available, but they should be carefully selected to address the specific needs of the research.
Design A wide variety of designs may be employed in the study biobehavioral research. One of the more common study designs involves comparisons among groups. In this setting, there may be two or more or groups wherein the comparison occurs. The specific design chosen will affect the number of independent variables that may be considered and the precision and power of the statistical analysis. Knowledge about the variance of the independent measurements that are being made allows the investigator to determine the number of subjects that will be needed within each group. The process of determining the number of subjects necessary for a particular design is referred to as power analysis. Another fundamental type of study design involves the assessment of effects across time or a comparison over time. This type of design paradigm is typically used to assess cumulative effects or gradually developing changes in the system. Designation of members within a group must also be considered by the researcher. Determining whether the population should be limited to a particular gender, race, or age may significantly affect the study design and measurements that may be employed. In some instances, variation in underlying physiology, such as with sleep wake cycles and circadian biology, may affect the rime of the day, the rime of the month, and the rime of the year the study or component of the study may be performed. These possible confounding variables can be controlled by the design of the study and by the predetermined statistical analysis.
Statistical Analysis AJthough the statistical analysis is performed after the actual study has been completed (or at least partially completed), the statistics to be employed must be determined before the study is implemented. In some instances, significant differences found among groups require additional separation to determine which group is different. This procedure is referred to as a post hoc analysis, bur should only be employed if the main effect model was significant. The goal of the post hoc analysis is to detail what specific factors account for the overall differences found. Occasionally, researchers employ a technique of identifying subgroups with significant differences when the main effect model failed to show significance. This process is generally discouraged unless the subgroup analyses were planned as part of the original research proposal and appropriate accommodations for the small group size were undertaken. Once the statistics are completed, a judgment is made about whether the research results confirm the initial hypothesis. Generally the results of the research study, if well designed, should be fairly clear. The statistical analyses should show whether an effect was significant or not. If the analyses confirmed the initial hypothesis, then the investigator should undergo rhe process of analyzing the results in light of other investigations. Comparing differences in techniques, the selected populations, and limitations in methodology are all valuable exercises in analy-Ling the results of the study. The investigator should then assess the
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implications or generalizability of the research findings. Elements of the study or the theoretical framework on which the study is based that were unclear or undefined can then be identified for future investigation. Once all these elements have been completed, the study and analyses should be communicated to the appropriate scientific audience. Under most circumstances, this occurs in the form of a publication in a scientific journal.
OPPORTUNITIES FOR OSTEOPATHIC RESEARCHERS Biobehavioral investigations present the osteopathic researcher a somewhat novel and rich environment for the development of investigations. Despite the variety of investigations that could be undertaken, a review of the literature demonstrates paucity of studies addressing biobehavioral mechanisms or effects in osteopathic principles and practice. Major topics in this area will likely focu s on: behaviors leading to the development of somatic dysfunction, behaviors resulting from somatic dysfunction, QOL effects of pain, and relationships between locomotor function, somatic dysfunction, and subsequent behavior (84). Manipulative intervention (85), alone or in combination, may have as much affect on subsequent behaviors as other types of medical intervention, and should not be ignored when considering a biobehavioral paradigm. For instance, the improvement in locomotor function or a decrement in pain resulting from manipulative intervention could result in substantial behavioral adjustments or improvements in QOL that may not be immediately apparent. In this regard, considering a biobehavioral approach would enhance the ability to detect improvements related to the manipulative intervention and may give additional insights into the effects of osteopathic principles and practice. The biobehavioral approach will require research designs directed more toward behavioral outcomes rather than physiologic measurements or end point assessments, as is commonly done. In this regard, all major types ofbiobehavioral designs should be considered (Fig. 77. 1) , including those associated with chronic illness, not commonly the focus of osteopathic research. Avoidance or development of emotional issues (e.g., depression), QOL, and changes in behavioral responses to chronic illness in relationship to osteopathic principles and practice represent investigations potentially adhering to the third pathway (Fig. 77.1) described above. This type of investigation may be less concerned with the direct effects of the disease process and more directly interested in the secondary effects on the behavior of patients (when adherence with medical regimens and tolerance of side effects are improved). Quantifying these relationships or the effect on QOL becomes the major issue in developing the research design, and might even include developing a specific osteopathic QOL instrument. Other types of investigations could focus on the interrelationship between somatic dysfunction or manipulative interventions and cognitive performance, health status, or other neurobehavioral manifestations. From these investigations, one could inquire about biophysiologic relationships, whether somatic dysfunction could serve additional diagnostic roles yet to be determined, or answers to questions not previously envisioned.
SUMMARY Biobehavioral interactions are a complex interplay between genetic, physiologic, environmental, and behavioral factors that have been shown to influence health and disease through many different pathways. Three major pathways for the effects of behavior to manifest on health and disease have been studied and verified. Some types of disorders manifest th ese interactions more directly than others; but in each case, we find that behavior alters the physiologic "landscape," and physiologic alterations result in significant behavioral accommodations that affect health and disease outcomes. Thus, physiologic phenomena are inseparab le from their behavioral counterparts and must be cons idered as part of the process wherein disease develops. For the osteopathic researcher, biobehavioral interactions and research may play a significant role in advancing our understanding of our patients, improving treatment regimens, and advancing the understanding of osteopathic principles in medicine.
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77. Biobehavioral Interactions with Disease and Health 18. Delahanry DL, Dougall AL, Schm itz JB, er al. Time co urse of natural killer cell activiry and lymphocyte proliferation in response ro two acure srressors in healthy men. Health Psycho!. 1996; 15:48-55 . 19. An'dersen BL, Fa rrar WB, Gold en-Kreu tz D, er al. Stress and immune responses after surgical treatment for regio nal breast cancer [comments] . J Nat! Cancer lnst. 1998;90:30-36. 20. Benschop RJ, Geenen R, Mills PJ, era!. Card iovascu lar and immune responses ro acute psychological stress in young and old women: A metaanalysis. Psychosom Med. 1998;60:290-296. 21. Pariante CM, Carpiniello B, Orru MG, ET AL. C hronic caregiv ing stress alters peripheral blood immune parameters: The role of age and severiry of srress. Psychother Psychosom. 1997;66:199-207 . 22. Perna FM, Schneiderman N , LaPerriere A. Psychological stress, exercise and immunity. lntj Sports Med. 1997;18(Supp l. l):S78- S83. 23. Goujon E, Laye S, Pamer P, er al. Regulation of cyrokine gene expression in rhe centra l nervous system by glucocorricoids: Mechanisms and functional consequences. Psychoneuroendocrinology. 1997;22(Supp l. I):S75S80. 24. Catalan], Beevor A, Cassidy L, er al. Women and HIV infection: Investigation of irs psychosocial consequences.jPsychosom Res. 1996;41 :39--47. 25. Cohen J I. Stress and mental health: A biobehavioral perspective. Issues Mental Health Nurs. 2000;21: 185-202. 26. Booth RE, Kwiatkowski CF, Chirvvood DO. Sex-related HIV risk behaviors: Differential risks among injection drug users, crack smokers, and injection drug users who smoke crack. DrugAlcohol Depend. 2000;58:219226. 27. Denison ME, Paredes A, Booth J B. Alcohol and coca in e interactions and aggress ive behaviors. Recent DevAlcohol. 1997;13:283-303. 28 . Fishbein M. Changing behavior ro prevent STDs/AIDS. lnt J Gynaecol Obstet. 1998;63(Suppl. I ):S 175-S 181. 29. Dingle GA, Oei TP. Is alcohol a cofacror of HIV and AIDS? Evidence from immunological and behavioral studies. Psycho! Bull. 1997; 122: 56-71. 30. Evans DL, Leserman J, Perkins DO, et al. Severe life stress as a predicror of early disease progression in HIV infection. Am J Psychiatry. 1997; 154:63 0-634. 3 1. Cole SW, Kemeny ME, Taylor SE, et al. Elevated physical health risk among gay men who conceal their homosexual identiry. Health Psycho!. 1996; 15:243-25 1. 32. Ciechanowski PS, Karon WJ , Russo JE. Depression and diabetes: Impact of depressive symproms on adherence, function, and costs. Arch Intern Med. 2000;160:3278-3285. 33. Burszryn M , Ginsberg G, Hammerman-Rozenberg R, et al. The siesta in the elderly: Risk facror for morraliry? [comments] Arch Intern Med. 1999;159: 1582-1586. 34. Kojima M , Wakai K, Kawamura T, er al. Sleep patterns and rota! mortaliry: A 12-year follow-up study in Japan. J Epidemiol. 2000; I 0:87-93. 35. Gale C, Marryn C. Larks and owls and health, wealth, and wisdom . BMJ 1998;317:1675- 1677. 36. Keefe FJ, Jacobs M, Underwood-Gordon L. Biobehavioral pain research: A multi-institute assessment of cross-cutting iss ues and research needs . Clinj Pain. 1997;13:91-103. 37. Morley S, Ecclesron C, Williams A. Systematic review and meta-analysis of randomized controll ed trials of cognitive behavioral therapy for chronic pain in adults, excl uding headache. Pain. 1999;80: 1-13. 38. Turk D. Handbook of Pain Assessment. New York: The Guilford Press; 2001. 39. Fordyce WE. Behavioral Methods for Chronic Pain and Illness. Sr. Louis, MO: Mosby; 1976. 40. Gerber WD, Schoenen J. Biobehavioral correlates in migraine: The role of hypersensitiviry and information-processing dysfunction. Cephalalgia. 1998; 18(Supp l. 21): 5-ll. 41. NaliboffBD, MunakataJ, Chang L, et al. Toward a biobehavioral model of visceral hypersensiriviry in irritable bowel syndrome. J Psychosom Res. 1998;45:485-492. 42. Jerome J. Transmission or transformation? Information processing theory of chron ic human pain. Am Pain Soc f. 1993;2: 160-171. 43 . Feuerstein M, Beattie P. Biobehavioral facrors affectin g pain and disability in low back pain: Mechanisms and assessment. Phys Ther. 1995;75:267-280.
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44. Foresman BH. Master's thesis/Ph.D. diss. Universiry of North Texas, Fort Worth, 200 l. 45. Katahn M, McMinn MR. Obesiry. A biobehavioral point of view. Ann NY Acad Sci. 1990;602:189-204. 46. Owens JF, Matthews KA, Wing RR, er al. Physical activi ry and cardiovascular risk: A cross-sectional study of middle-aged premenopausal women. PrevMed. 1990;19:147-157. 47. Metz JA, Kris-Etherton PM, Morris CD, er al. Dietary compli ance and cardiovascul ar risk reduction with a prepared meal plan compared with a self-selected diet [comments]. Amj Clin Nutr. 1997;66:373-385. 48. Fitzgibbon ML, Srolley MR, Avellone ME, er al. Involving parents in ca ncer risk reduction: A program for Hispanic American families. Health Psycho!. 1996;15:41 3-422. 49. No rdevang E, Azavedo E, Svane G, et al. Dietary habits and mammographic patterns in patients with breast cancer. Breast Cancer Res Treat. 1993;26:207-215. 50. Holm LE, Nordevang E, Hjalmar ML, et al. Ti·eatment failure and dietary habits in women with breast cancer. J Nat! Cancer lnst. 1993;85: 32-36. 51. Heber D, Ashley JM, McCarthy WJ, et al. Assessment of adherence ro a low-fat diet for breast cancer prevention. Prev Med. 1992;21 :2 18-227. 52. Arwood JR, Aickin M, Giordano L, et al. Th e effectiveness of ad herence intervention in a co lon cancer prevention field trial. Prev Med. 1992;21 :637- 653. 53. Patterson RE, Krista! AR, White E. Do beliefs, knowledge, and perceived norms about diet and cancer predict dietary change' Am J Public Health. 1996;86: 1394- 1400. 54. Drake DA. A longitudin al srudy of physical act iviry and breast ca ncer prediction. Cancer Nurs. 2001;24:371-377. 55. Shephard RJ. Exercise and cancer: linkages with obesiry' Crit Rev Food Sci Nutr. 1996;36:321-339. 56. Anshel M. Copin g sryles among adolesce nt competitive ath letes. j Soc Psycho!. 1996;136:311-323. 57. Step roe A, Wardle J, Pollard TM, eta!. Stress, social support and healthrelated behavior: A study of smoking, alcohol consumption and physical exercise. J Psychosom Res. 1996;41 :171-180. 58. Kassel JD. Smoking and attention: A review and reformulation of the stimulus-fi lter hypothesis. Clin Psycho! Rev. 1997; 17:45 1--478. 59. Gird ler SS, Jamner LD, Jarvik M, et a!. Smokin g status and ni cotin e administration differentially modify hemodynam ic srress reactiviry in men and women. Psychosom Med. 1997;59:294-306. 60. HausbergM, MarkAL, Winniford MD , eta!. Sympathetic and vascu lar effects of short-term passive smoke exposure in healthy nonsmokers. Circulation. 1997;96:282-287. 61. Eckhardt L, Woodruff SI, Elder JP. Related effectiveness of continued, lapsed, and delayed smoking prevention intervention in senio r high school srudents. Am j Health Promot. 1997; II :418--421. 62. Brandon TH. Behavioral robacco cessatio n treatments: Yesterday's news or tomorrow's headlines? J Clin Oncol. 2001; 19:64S-68S . 63. Katsambas A, Nicolaidou E. Cutaneous malignant melanoma and sun exposure. Recent developments in epidem iology. Arch Derrnatol. 1996; 132:444-450. 64. Marks R. An overview of skin cancers.lncidence and causatio n. Cancer. 1995;75 :607-6 12. 65 . Strom SS, Yamamura Y. Epidemiology of nonmelanoma ski n cancer. Clin Plast Surg. 1997;24:627-636. 66. BaumA, Cohen L. Successful behavioral interventions to prevent cance r: The example of skin cancer. Annu Rev Public Health. 1998; 19:3 19-333. 67. Aiken LS, West SG, Woodward CK, et al. Health beliefs and compliance with mammography-screening recommendations in asy mptomatic women. Health Psycho!. 1994;13: 122-129. 68 . Call e EE, Flanders WD, Thun MJ, et al. Demographic predictors of mammography and pap smear screening in U.S. women. Am J Public Health. 1993;83 :53-60. 69. Lerman C, Daly M, Sands C, eta!. Mammography ad herence and psychological distress among women at risk for breast cancer. j Nat! Cancer lnst. 1993;85:1074- 1080. 70. Lerman C, Schwartz M. Adherence and psychological adjustment among women at high risk for breast cancer. Breast Cancer Res Treat. 1993;28: 145-155.
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7 1. Lloyd S, Warson M, Waites B, era!. Familial breast cancer: A controlled study of risk perception, psychological morbidity and health beliefs in women attending for generic counseli ng. Br j Cancer. 1996;74:482-487. 72. Epstein SA, Lin TH, Audrain J , er al. Excessive breast self-examination among first-degree relatives of newly d iagnosed breast cancer patients. High-Risk Breast Cancer Consortium. Psychosomatics. 1997;38:253-
261. 73. Ickovics JR, Morri ll AC, Beren SE, er al. Limited effects ofHIV counseling and resting for women. A prospective study of behavioral and psychological consequences. }AMA. 1994;272:443-448. 74. Hussey LC, G illil and K. Comp liance, low literacy, and locus of control.
Nurs Clin North Am. 1989;24:605-611. 75 . Camero n C. Patient compliance: Recognition of factors involved and suggestions for promoting comp lian ce with therapeutic regimens. j Adv Nurs. 1996;24:244-250. 76. Turner ]A, Deyo RA, Loeser JO , eta!. The importance of placebo effects in pain rrearmenr and research [commen ts] . }AMA. 19994;271 : 1609161 4. 77. Bienenfeld L, Frishman W, G lasser SP. The placebo effect in cardiovascular disease. Am Heart}. 1996;132: 1207-122 1.
78 . Weiner M, Weiner Gj . The kinetics and dynamics of responses ro placebo. Clin Pharmacal Ther. 1996;60:247-254. 79. Hrobjarrsson A, Gotzsche PC. Is rhe placebo powerless? An analysis of clinical trials comparing placebo with no treatment [comments] [errarum appears in N Eng! J Med 2001;345(4):304] . N Eng! j Med.
2001 ;344: 1594-1602. 80. Salamone JD. A critique of recent stud ies on placebo effects of antidepressants: Importance of research on active placebos. Psychopharmacology (Berl}. 2000;152: 1-6. 81 . Cherulnick PD . Methods for Behavioral Research: A Systematic Approach. Thousand Oaks, CA: Sage Publications; 200 l. 82. Corcoran K, Fischer J. Measure for Clinical Practice. New York, NY: The Free Press; 2000. 83. Jerome]. Theory leads: Statistics follow. Am Pain Soc}. 1995;4:27 4-276. 84. Hallas B, Lehman S, Bosak A, et al. Establishment of behavioral parameters for rhe evaluation of osteopathic treatment principl es in a rat model of arthritis [commenrs]. jAm Osteopath Assoc. 1997;97:207-
214. 85. Northup GW Time ro reemphasize OMT as stress reliever. jAm Osteopath Assoc. 1990;90:681.
CLINICAL RESEARCH AND CLINICAL TRIALS B ERNARD R . RUBIN
PHASES OF CLINICAL RESEARCH
KEY CONCEPTS • Elements of research protocols are used to reinforce medical theory and support clinical practice • Food and Drug Administration good clinical practices guide research practices • The role of the investigator in clinical trials
Evidence-based medicine is the philosophic approach to the practice of medicine where results from clinical research studies allow for improved medical care. The results from good clinical trials with solid statistical results help physicians make sound clinical decisions. Results may lead physicians ro misleading conclusions if the quality of the research study and the statistical analysis are faulty. The role of clinical research is to discover truth. Clinical research differs from basic research in several ways. Clinical research can be done in a physician's office, in a hospital, or in a laboratory (l). C linical research is particularly important osteopathic medicine (2). In a discipline with only partially understood pathogenesis, it often appears that therapies are empirical. So, although many interventions are reported by observation, final judgment on their usefulness requires controlled clinical trials. Becau e it is possible that subjects may be selected who do not represent the population at large, subgroups may be selected and grouped to attempt to represent the population and reduce representation bias. Scientific method requires that the results of the clinical research trial be reproducible. T herefore, the objectives in a clinical trial are to determine if a new therapy is as good as or better than a standard therapy and (especially for pharmaceuticals) to determine if there is increased toxicity compared with other forms of treatment. T he model of clinical research used in clinical drug trials serves as prototype for clinical research in general. With regard to the specific clinical issues in osteopathic medicine, the specifics of clinical pharmaceutical research, such as the different phases of clinical trials, may not be relevant, but the rigorous manner and attention to detail in this type of research can serve as a benchmark to guide future researchers.
Many clinical research questions currently involve testing of novel therapeutic pharmaceutical agents and devices. The amount of money spent by industry on clinical research is enormous and approaches the amount spent by the National Institutes of Health. The remainder of this chapter focuses on clinical research using a model that is used by the United States Food and D ru g Administration (FDA). Good clinical practice is a term used by the pharmaceutical industry to encompass the federa l regulations and industry-accepted standards that govern clin ical trials conducted to support applications for FDA approval of new dr ugs and biologics (3). Good clinical practice ensu res that the righ ts, safety, and welfare of trial subjects are protected and also establishes the credibility and integrity of the trial data. Lastly, good clinical practices assure that a standard for the overall ethical and scientific quality of the erial has been maintained . C linical research is divided into several different types of studies based on the level at which the intervention or therapy is in the overall process of FDA approval (4).
Phase I Clinical Trials Phase I clinical trials are conducted to determ ine the safety of an investigational agent. In addition, pharmacologic data may be collected to determine the absorption, distribution, metabolism, and excretion of the compound. Generally, the dose used in p hase I trials is determined in preclinical animal trials . Most phase l trials are designed to begin dosing at a subtherapeutic level to avo id unexpected, catastrophic adverse events. These are usuall y what would be called "first-time-man studies." Data collected coul d be indicative of the effectiveness of the investigational agent. In phase I trials, usually all the subjects receive the experimental compound in either single or multiple doses. These are relatively small trials and last a very short time- perhaps several days or at most several weeks. The number of subjects enrolled is us ual ly less than I 00 . Often, the subjects involved in phase I clini cal trials are normal volunteers who have no confounding disea es or take no concurrent medications. The exception wou ld be in the case of testing therapy for a life-threatening or fatal illness. In this instance, the subjects, even in a phase I trial, m ight be patients who have failed all other available treatment.
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Phase II Clinical Trials Phase II trials are primarily conducted to demonstrate therapeutic efficacy in a particular disease. These trials are randomized and rightly co ntrolled. These studies use relatively small numbers (60 to 200) of carefully selected patients. If it were feasible, this phase of trials would use the placebo comparison or an active control with known efficacy, or both. Subjects might receive either a single or multiple doses, and these trials are usually done simultaneously at several different centers. These studies usually last longer than phase I studies. Although they are usually completed within a few months, they could potentially last several years. The patients involved in phase II trials usually have the disease that is being studied. They have no other serious medical problems such that the investigator would expect that the subject would do well if their primary disease were being treated adequately.
Phase liB Clinical Trials Phase liB trials, which may overlap with the preceding discussion of phase IIA trials, are conducted to gain specific efficacy and safety information in preparation for a new drug application to the FDA. These are often called pivotal trials. The FDA usually requires two "adequate and well-controlled" pivotal trials be performed. Phase II trials are also done to determine the appropriate dose to be used for the larger, phase III trials to follow. Pivotal trials may last for several months or several years. Again, subjects are usually well except for the disease being studied.
Phase lilA Clinical Trials Phase IliA clinical trials are designed to gain safety and efficacy information in a large number of patients. Some variables that may be studied include extended dosing, dose-ranging, and patient populations that are more representative of the population at large. Phase IliA trials are very rightly controlled and are conducted with the experimental agent versus placebo or an active control, or both . Different study designs might be employed during this process. Once again, these data are often supportive of an app lication for a new drug or device to be approved by the USFDA. T he duration of participation (or an individual patient varies. These phase IliA studies often are a longer duration and can last from 1 to 4 years. Phase IliA subjects are patients who have the disease being studied and are selected from a larger population of patients. Several hundred subjects are required in phase IliA studies to demonstrate efficacy and to adequately assess safety.
Phase 1118 Clinical Trials The purpose of phase IIIB trials is to gain experience with the experimental agent in a large number of subjects who represent a population that uses the treatment once it is approved. Therefore, these trials are less tightly controlled. All subjects may be receiving experimental drugs, entry criteria may be somewhat more relaxed,
and larger numbers of patients are enrolled. These trials may also be designed to specifically address special patient groups, such as geriatrics or pediatrics. Phase IIIB studies last 1 to 4 years and are used to gain additional safety and long-term efficacy data about the investigational agent. Phase IIIB trial subjects come from a larger heterogeneous population. The subject population may focus on specific concurrent illness to further delineate the drug's safety. This is especially true in specialized populations, such as geriatrics or pediatrics.
Phase IV Clinical Trials Phase IV trials are done for a variety of reasons. They may be done to place the drug in the commercial marker, to make marketing claims, to perform pharmacoeconomic or quality of life studies on the treatment, or to provide additional surveillance for unexpected or rare adverse events. The formulations or new indications for a drug that has already been approved by the USFDA must begin with phase I (new formulation) or phase II (clinical trial designs). The length of phase IV trials is determined by the purpose of the study and may be indefinite, such as would be the case in a continual postmarkering surveillance program. Subjects in phase IV clinical trials are drawn from the general population and have the disease being tested. Further conditions are defined by the nature of the specific protocol.
ELEMENTS OF CLINICAL RESEARCH Research Questions, Research Designs, Sample Size, and Data Analysis Clinical research requires that the investigator has a question to ask, a design for the study, an idea of who should be studied, and the knowledge of basic statistics to calculate the validity of theresults. The protocol is fundamental to any clinical trial, and is the basic question of the study. Generally, the protocol in -:ludes the purpose of the study. This is a clear statement of the hypothesis to be rested by the clinical trial. Specifically, what questions are going to be answered by this protocol about the investigational agent? The background and rationale of rhe protocol is what establishes the significance of the proposed study. The background section of the protocol should discuss the known information about the class of drugs or devices being studied. Also, this is the part of the research proposal that summarizes known information about the investigational agent-specifically referring to which side effects are known to date. This discussion should therefore lead to the rationale for studying this specific drug, at this dosage, in the disease to be studied, and with the current protocol. There are various types of study designs that can be used, but these studies primarily use the manipulation of a variable, such as a new pharmaceutical agent, followed by measurement of the effects of the new drug. The subjects are very important to define in any clinical study. In this section, the population to be studied would be defined. Sample size is critical to predetermine whether or not statistical significance will be attained if the study is completed successfully. A very large sample size often means that only s'l ight changes in the outcome variable are needed to achieve statistical significance.
78. Clinical Research and Clinical Trials One of the most important parts of any clinical protocol is the inclusion/exclusion criterion. This is the portion of the protocol that ~!early states the criteria for which subjects will be enrolled in the trial. When evaluating a clinical trial, an investigator should pay strict attention to the inclusion/exclusion criteria, because this section alone will probably define how difficult or easy it will be to find subjects to enroll. Very strict entrance criteria may make it very hard to locate enough subjects to adequately fill the study. The treatment plan is the roadmap used in the course of the study. The treatment course is outlined in detail. This would include not only the drugs to be used but also the dosages. Additional details of the treatment plan might describe the study of the medication, including not just its primary effect on disease but also any pharmacologic dosage modification recommendations, concomitant medication instructions, and dispensing instructions. The study procedures are critical in any protocol. This section includes information concerning the study design, treatment schedule, laboratory and diagnostic tests to be performed, and the time between patient visits. Any information concerning adverse events reporting, dose modification guidelines, and how subjects who drop from the study should be handled would also be included in this portion of the protocol. Often, the information in this section is put into a table and graphically displayed as a schedule of events. Additional administrative sections may be included in this section, but the major research focus has been covered as indicated. Response evaluation criteria are particularly important, because this is the place in a protocol where the criteria for patient response to the test agent is defined a priori. Therefore, this is where the hypothesis is placed to outline the criteria, which includes objective responses that are anticipated, the end point variables, and other evaluation criteria.
Informed Consent Another important part of any clinical trial is informed consent. The informed consent document is written in legible language, usually at a high school educational level. Informed consent means that the study protocol, including any potential adverse reactions, are fully explained to the patient or to the patients' guardian or caregiver before the subject is entered into the study. This permission is given in writing and is witnessed. Copies of this document are given to the subject and retained by the investigator. The institutional review board (IRB) is an organization that oversees and protects the safety of subjects enrolled in clinical research (5), and all research conducted on human subjects must be approved by an IRB. It monitors the progress of the study. Should any new facts occur that could potentially alter a subject's willingness to participate in the study, the IRB insures that the subjects are informed of the new events. It is imperative that the principal investigator communicate all protocol changes and any serious adverse events to the IRB. Any change in protocol necessitates a change in informed consent, and the subject must sign a new document. The randomized clinical trial that has been described is the method of choice for determining safety and efficacy under controlled conditions. Clinical trials are usually randomized, double-
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blinded, and controlled. Individuals that may or not respond to the therapy are randomly allocated to either the control or experimental group to guards against any treatment bias. This allows one to conclude that any outcome is probably related to the therapy being studied rather than inherent differences between the groups. Randomization begins with the appropriate selection of the cohort. As stated earlier, inclusion/exclusion criteria are a critically important portion of the protocol. The inclusion criteria establish the subjects who can specifically be enrolled in the clinical trial. The exclusion criteria eliminate any potential subjects who possess extraneous features that might affect the outcome or results. For a study to be random, it is not within the control of the investigator as to which subjects are allocated to which groups. Secondly, the process must be tamper-proof. Once the plan for randomization is established, it is irreversible and cannot be manipulated. The randomization process eliminates the patients' ability to influence a choice of assignment and the physicians' influence on choice of assignment (6) . The manner of administration of the agents to be tested is the same for all groups. Therefore, in a pharmaceutical study, this procedure prevents the research subjects, their physicians, and anyone else involved in the research study from knowing whether different drugs were placebo or administered. The outcome variables are measured and are the same for all subjects. The importance of blinding cannot be overemphasized. Outcome variables must be measured without knowledge of which group the subject has been assigned to. Double blinding eliminates subject and investigator bias, and is used when the assessment of an outcome requires judgment by the observer. A triple-blind design requires that the subjects, the person who is administering the intervention , and the person measuring the outcome are all unaware of the group assignment and the type of intervention being administered. In a triple-blind study, the measurements are protected against the investigators, his assistants, or the subjects influencing the outcome and therefore creating unreliable results (1).
Data Analysis As stated previously, plans for data analysis should be decided at the outset of the study (not after data have been collected) (7). The research question in the outcome variables is the basis for the determination of the type of statistical analysis to be used. Hypotheses must be tested. Therefore, if the hypothesis is too broad, it rarely provides reliable or reproducible data. In general, the research question asked is refined into a null hypothesis . Statistical analysis reduces the chance of making insupportable statements (8). Statistics test the null hypothesis, which states that there is no real difference between an observed sample value and the absolute value for the population that the sample represents. Statistically, tests evaluate if, at an acceptable probability level, the hypothesis is not true and should therefore be rejected. The null hypothesis may be tested using a variety of methods. There are type I and type II errors. Type I errors involve concluding the null hypothesis is true when it is false. Type II errors conclude that the null hypothesis is false when it is true. The levels of confidence are chosen arbitrarily by the investigator. A confidence level of 0.05 typically means that there is a 5% chance of concluding
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that the null hypothesis is false when it is true. If there is a difference seen in outcome variables at a p value "significance" of0.05, then there is a 5% likelihood that the results occurred by chance alone.
This chapter has briefly reviewed the structure and fun ction of clinical research and the responsibilities of the principal investigator.
REFERENCES CONCLUSION The goals of clinical research in both clinical pharmaceutical studies and clinical studies in general are to seek truthful answers to questions using the most appropriate and acceptable research methods available. Osteopathic physicians who use basic principals of clinical research, whether in testing pharmacologic agents or the validity of osteopathic manipulative therapy, will produce reliable data and results if appropriate experimental design and research guidelines are followed . The precision that is used in clinical pharmaceutical studies by osteopathic physicians must be emulated in all clinical research studies. These policies and procedures will then yield reliab le data that will stand the rest of repeated research trials to validate the outcomes.
1. Sheldon S. C linical Resea rch and C lini cal Tri als. ln : Wa rd RC, ed. Foundations fo r Osteopathic M edicine. Bosro n, MA: Willi ams & W ilkins; 1997:1091 - 1094. 2. Rogers FJ , Dyer MJ . Adopting resea rch. J Am Osteopath Assoc. 2000; I 00( 4):234-237. 3 . Kessl er DA. Th e regul ati o n of in ves tigati onal drugs . N Engl J Med. 1989;320(5):281 - 288. 4 . Kingham R. Hisrory of FDA regulatio n of clini cal research. Drug Information). 1988;22(2):1 5 1- 15 5. 5. Goebel P. Th e role of the instiwtional review board . Drug Information). 1988;22 (2):161 - 164. 6 . Trochim WMK. The Research Methods Knowledge Base. C incinnati , O H: Atomic Dog Publishing; 2001. 7. Dawson B, Trapp RG . Basic and Clinical Biostatistics. N ew Yo rk, N Y: Lang Medical Books/ McG raw-Hill; 200 I . 8. Shorr S. Statistics for Health Proftssionals. Phil adelphi a, PA: WB Saunders; 1990.
OSTEOPATHIC RESEARCH: CHALLENGES OF THE FUTURE MICHAEL M. PATTERSON
KEY CONCEPTS • The profession is starring from a srrong and growing research base • The strengths of research resources of the profession • The directions of research efforts of the profession • Important considerations for identifying and structuring future research • Important research questions for the future • Rewards of a successful research program
In his 1962 Andrew Taylor memorial lecture, George Northup (1) stared, "we are on the precipice of either our greatest success or ultimate defeat. T his success or failure depends not on the policy of organized medicine, but on the decisions and integrity of organized osteopathy." T hese words were spoken at a dark hour in the history of the osteopathic profession. There was a real question about the continued survival of the profession as an organization. One of the profession's six schools had been lost, and about 10% of its members had been granted an MD degree. Indeed, the decisions and integrity of the leaders, as well as the rank-and-file members, would decide its fate. Over the next few years, the decisions of the profession's leaders led to a revival and rebuilding of both the physical plant and the organization of osteopathic medicine. The profession's members responded to the challenges and supported a renaissance of unprecedented proportions. Between 1969 and 1996, 13 new schools were fo unded, about half university based. Today, the profession is growing at an unprecedented rate and enjoys support from the government and private sectors. However, today the osteopathic profession faces a future still filled with unknown and unpredictable forces that will shape and challenge it in many ways. It is increasingly challenged to show that the claims it makes for its unique philosophy and practice are beneficial to the patients it serves. Government and thirdparty insurance carriers mandate that the outcomes of health care be used as evidence of the quality of service. The existence of osteopathy as a unique and separate profession rests on its ability
to continually demonstrate that its practices are efficacious and its theories are sound. Meeting this challenge is not a simple task or one to be taken for granted. To achieve this goal, all components of the profession are required to take an active role. These institutions include: Educational institutions Hospitals Affiliated societies Individual physicians in practice However, the greatest challenge now facing the profession is that of building its research base to support and expanding its claims of efficacious and unique practices. Without demonstrable substantiation of its claims to a unique role in health care, the osteopathic profession risks its existence. It is not that data do not exist to show that the osteopathic profession has made unique contributions to health care and that its philosophy is sound. The research from the Kirksville group in the 1940s and 1950s, data from the Chicago College and other osteopathic schools, and papers published in the journal of the American Osteopathic Association QAOA) over the years show that the osteopathic contribution to health care is substantial. However, further substantiating the unique contributions and emerging quality of osteopathic care req uires new and innovative ways to measure health and clinical outcomes, as well as the development of new and innovative research techniq ues. The art of clinical research is a relatively new endeavor, and its practices are just now developing to the point of being able to show the unique features of osteopathic medicine. This chapter summarizes the present state of research in the profession , the opportunities and challenges ahead, and the areas critical to understanding the unique role of osteopathic medicine in human health and disease.
OSTEOPATHIC RESEARCH 2002 At the beginning of 2002, the research plant and efforts of osteopathic medicine have never been stronger. With the founding of the first osteopathic research center at the North Texas State Health Science Center College of Osteopathic Medicine (COM) in October 2001, the profession entered the fo u rth period of its
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research life (see Chapter 74 for a summary of these research periods). Since 1970, the profession's research had been expanding as new schools, many university based, began to mature and begin research programs. Recent developments in the building of research programs have been evident throughout the profession. Research programs at the Texas COM had been strongly fostered for many years, all owing that school the infrastructure to support a research center. The Michigan State University COM, using funds from a $9 million endowment, has recently announced the hiring of an internationally recognized scientist to head its interdisciplinary, multidepartmenral, neuromusculoskeletal research department. The founding school at Kirksville pledged several hundred thousand dollars in internal funding for expansion of its already successful research programs, with the funds to go preferentiall y to research directed to the elucidation of osteopathic principles and practice. The New Jersey COM announced the formation of a research institute to be heavily endowed. The New York and Chicago COMs have provided funds for internal seeding of research that have resulted in garnering of external federal and foundation support. West Virginia, Kansas City, Maine, and other COMs have endeavored to enhance research efforts . Newer schools, such as the Nova Southeastern University COM, have made strong commitments to fostering research programs. Indeed, at the Osteopathic Collaborative Clinical Trials Initiative Conference in October 2001 , almost all of the COMs reported research initiatives under way. While the academic research base of the profession has been growing and maturing, other efforts were being made to foster research among osteopathic physicians. Some of the specialty colleges have had some form of research requirement in their programs for several years. This requirement has fostered an understanding of the research process in students that was not given during undergraduate training. More recently, some of the new Osteopathic Postgraduate Training Insti tures (0 PTis) have instituted research training in their programs. Although only beginning, these efforts to train more practitioners in the art and process of research are another way to increase not only the development of research programs but also an appreciation of its importance. Other organizations of the profession have begun to take a more active role in research development and support. The AOA has, since 1951, had the Bureau of Research to promote and support research development. This group has taken an increasingly active role not only in granting resea rch funds, bur also in developing new programs. Ir now supports rhe training of osteopathic srudems in DO/PhD programs. Such combined degree programs are also available ar several of rhe university-based CO Ms. The bureau has also sponsored rhe development of an osteopathic bibliographic database as a joint venture between the Texas and Kirksville COMs. This database, when operational in later 2002, will provide much more ready access ro rhe profession's literaturea vital resource for research endeavors. Since 1989, the American Academy of Osteopathy (AAO) has supported two international research symposia whose proceedings have been widely used in furthering an understanding of osteopathic manipulative practice and irs underlying mechanisms (2,3) . The AO/\s Louisa Burns research committee has become increasingly active in developing research protocols and initiatives, such as the online SOAP note project and SOAP note forms rhar allow collection of large din-
ical databases in the near future. The American Association of Colleges of Osteopathic Medicine (AACOM) has led rhe organization and funding efforts for three national meetings to discuss research development, out of which came the osteopathic research center. Leaders within the organizations of the profession, especially the AACOM and the AOA, have increased their contacts with governmental funding agencies in efforts to secure federal funds and recognition for the profession's research efforts. These and other accomplishmenrs have taken place over the last several years and poinr to an unprecedenred effort to organize and support a profession-wide research effort. Although these efforts have been remarkable in a profession devoted to training practitioners since irs founding, they are only the beginning. Thus, the founding of a center for osteopathic research whose mission is to conduct research on the efficacy and mechanism of osteopathic manipulative rreatmenr indicates a maturing of rhe profession's research efforts and abilities as rhe fourth period of osteopathic research begins. However, it is only rhe beginning of the maturation process. What are rhe challenges now facing further development of quality research efforts?
INSTITUTIONAL CHALLENG ES FOR RESEARCH DEVELOPMENT Academic Challenges: The Schools Clearly, the teaching institutions of the profession have made great strides in the last 20 years in developing nationally competitive research efforts. As pointed our in the first chapter in this section, the profession's schools were not in a position to take advantage of the immense expansion of biomedical research infrastructure during the 1950s and 1960s. In fact, it was nor unril the 1980s that a few of the COMs were able to develop sufficiently strong research initiatives that they could attract significant federal funding. In 1974, the first NIH grant in many years was awarded to a researcher in an osteopathic instiwtion. Since then, large federal and private grants have been awarded to several of the CO Ms. The challenge for all the academic institutions now lies in harnessing the expertise of researchers now in place or being brought into the institutions, wirh the need to show the efficacy and mechanisms of manipulative treatment. The institutions rhar have done this most effectively have made several commitments: Stated commitment to an osteopathic research environment Internal funding for startup research Committed rime for research Support personnel Encouragement to rake research risks Recognize that research is longitudinal, not cross-sectional In any endeavor, experience has shown that one of the best ways to get started on a process of change is to publicly commit to the process. This provides an impetus for planning and goal setting against which the outcomes can be measured. A public announcement shows rhe commitment and produces expectations that are harder to shirk than if the commitment is private.· Although the announcement of intent is laudable, providing the means to begin the task is necessary. The days of having a
79. Osteopathic Research: Challenges of the Future good idea and simply going w the NIH or National Science Foundation and asking w be funded are largely gone. Public and private funding sources require demonstrated research capability (pilot 'data) before funding a projecr. Therefore, the commitment must be backed up with a dollar support w seed research efforts. The college administration must be willing w provide dollars to insure that researchers are able w do the necessary work on which to base their grant proposals. Often, such seed periods, especially in newer areas ofi nqui ry, take several years before external funding is successfully garnered. As important as funds are for the beginning researcher, it is often the lack of committed time that impedes a fledgling research program. If a researcher has sufficient funds to do a project, but the blocks of time are not available, the project will fail or the researcher will lose interesr. Unlike such things as committee meetings, patient care, and even teaching, the research endeavor requires large blocks of time on a regular basis. First, the researcher must be allowed time w look into the background of the project, to reflect on the availab le information, and to synthesize its meaning. This literature review and synthesis means a substantial intellectual effort that cannot be done in five-minute periods between patients or classes. The investigator must be allowed the free and unencumbered time to become an expert in the field-not only his or her field of training, such as internal medicine or osteopathic principles and practice, but in research design and practice. The administration can relieve the prospective researcher of some committee duties, give lighter teaching or patient care loads, and not expect the faculty member committed to research to attend all administration functions. Of course, the quid pro quo will be research productivity. There must be support personnel for research efforts. A faculty member pursuing a fledgling research effort must expect w initially do much of the footwork in getting a program under way. However, support is needed in terms of technical help, secretarial backup, and patient scheduling. As a research effort develops, support must be provided for grant writing and grant budget administration , as well as for keeping up on the latest federal, state, and local regulations. It is not logical or financially responsible to expect researchers to spend much of their productive time typing letters or purchase orders, rather than reading the latest literature or doing the actual study. The level of support personnel will be rewarded in exponential gains in research productivity. The institution must also make it clear that it understands that not all research efforts are successful. Research studies by their very nature are unknowns. The researcher, especially the beginner, will have studies that do not show significant results. The institution must show that its support is not only for successful studies, but also for the effort. Without this understanding, the researcher will not be free to undertake anything but the most mundane and predictable efforts. The institution, by showing that it rewards not only research efforts, but also risk taking in research, will foster a higher level of research endeavor. This can be shown by providing raises commensurate with cutting-edge research projects, granting advancement to those willing w take risks, and publicly acknowledging such activities. For any research endeavor w be anything but an isolated event, w become a program of research, not an isolated study, the researcher must become committed w continuing over an extended
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time. No one research study will tell a swry about an area. Several studies will begin w weave a tapestry that will answer meaningful questions. Research programs evolve with time and continued effort, not isolated, brief efforts. The instiwtional commitment wits researchers and research programs must be long term. Only then will a research effort make a meaningful contribution w showing the basis and efficacy of osteopathic medicine. The academic institutions of the osteopathic profession are beginning w build the bases for the long-term commitments necessary for meaningful research programs. Some have advanced further than others, as evidenced by the founding of the center for osteopathic research at the Texas school. Others are only starting the task and need the encouragement and support of the rest of the profession as they proceed.
Academic Challenges: The Faculty In Chapter 21 on Foundations of Osteopathic Research, we made the observation that the definition of osteopathic research must come from the investigawr and cannot be determined a priori. This means that the researcher, basic scientist, or clinician, must become sufficiently familiar with the background and clinical experience of osteopathic medicine that he or she can link the ideas and results of their research w the needs and experiences of the profession. Although data from studies not constructed or performed w test the tenets and clinical observations of the osteopathic profession can be used for that purpose, it is far more efficient and less risky of incorrect interpretation w perform studies stemming directly from questions generated by osteopathic theory and experience. Basic scientists, both from the biomedical tradition and from the social sciences, have been incorporated into the osteopathic profession in increasing numbers, especially since 1970. Earlier, it had been the usual custom in osteopathic teaching institutions w use DOs w teach most of the basic science subjects, as well as the clinical areas. With the explosive growth in numbers of schools in the 1970s and heightened expectations for subject experts in the basic sciences, faculty trained in non-osteopathic settings were increasingly hired. Many of these professors had research backgrounds, as well as backgrounds in their disciplines. These faculty face difficult challenges in doing research meaningful w the osteopathic profession. Although it is often argued that any research is valuable, the profession's research resources seem best spent on research projects that can be expected w provide information useful in giving answers w the theoretical and clinical underpinnings of osteopathic medicine. Some of the challenges faced by basic science researchers include: Lack of knowledge of the hiswry, theory, and basis of osteopathic medicine Difficult or impossible access w the literature of the osteopathic profession Lack of access w the clinical experience of osteopathic medicine Difficulty in understanding the practice or jargon of osteopathic clinicians Insecurity of switching from an established research program w an unfamiliar one
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VJJ/. Basic and Clinical Research for Osteopathic Theory and Practice
Unwillingness to make the effort to explore an unfamiliar and seemingly o ur-of-the-mainstream topic T hese challenges are severe bur surmoumable. The osteopathic profession is moving to provide the materials needed to acquaint irs basic sciemisrs with its background, theoretical basis, and research data. The Texas bibliographic project is soon to be ava ilable and should provide greater access to the literature of the profession. The AAO, as memioned earlier, has provided irs literature bibliography on CD-ROM. Such sources as this book and others now appeari ng provide the willing basic scientist with useful information. The ready access to the profession's older research literature is poor. Ways must be found to make those sources more available, not on ly to basic scientists, but to clinician researchers and students as well. Many of the works of Burns and other early anatomists and physiologists investigating basic mechanisms of manipulation are available in only a few college libraries. This is a continuing challenge to the profession. A basic scientist coming into an osteopathic school to teach is faced with the task of teaching in a profession about which he or she usually knows nothing. In this case, the only option is to teach a topic in the same way it was taught elsewhere. The osteopathic profession thinks of itself as a unique entity, implying that the reaching of its students should be somehow different from the experience of other medical students. How can that occur if the basic scientist does not know the basis of the profession? One way is to integrate osteopathic physicians into the teaching of the sciences. Of course, another is to inform the basic scientists of the profession. C linicians and others knowledgeable of the profession can provide seminars and workshops on osteopathic medicine for their colleagues. Basic scientists can be encouraged to sit in on the osteopathic courses. Clinicians can take basic scientists as shadowers in their practices and discuss the unique aspects of osteopathic medicine with them. Administrators can provide expectations and rewards for basic scientists who show a willingness to avail themselves of opportunities to become knowledgeable about the profession. In general, the profession has not held sufficiently high expectations for its basic scientists nor has it provided good opportunities for them to become familiar with the theory and practice of osteopathic medicine. A basic scientist coming into the profession with a budding or established research program faces real obstacles in retooling or realigning that program to the needs of osteopathic medicine. Funding may not be as readily available. The switch or realignment may rake several years to accomplish. The comfort of a known research enterprise is lost. The schools can help this transition by providing funding for the transition, understanding that productivity may decrease for a time, and finding clinicians to supply information and experience to the investigator. In addition, the expectation should be clear that such a transition will be rewarded in tangible ways. Korr (4-11) has published several articles on the challenges posed by osteopathic theory and practice that can be given to entering faculty. Although the school and profession can do much to help an investigator realign their research and intellectual efforts toward the questions of osteopathic medicine, there is also an onus
on those coming into the profession to make an effort to gain this understanding. Honest intellectual effort would seem to demand of a person coming into a profession that knowledge of that profession be acquired. The investigator should have some intellectual curiosity and desire to find out about what it is he or she is getting into. Thus, an investigator may be expected to make efforts to seek out opportunities to become familiar with the backgrounds, theoretical underpinnings, and research basis of the profession. Too often , this does not happen, but should be encouraged. Osteopathic clinicians can be very helpful in this by offering manipulative treatment to their basic science colleagues. Osteopathic students can challenge their basic science professors to investigate the profession. In this way, a healthier interaction can be accomplished. But what about osteopathic clinician researchers within the profession? They also need help in meeting the challenges of research. They often are not schooled in research methods and skills. They are pressured for rime and are expected to provide patient care to generate income, nor research studies. These individuals also need ro be given the rime, resources, and encouragement to pursue the difficult and often discouraging field of research. They need to have the backing of their administrators for time and resources to acquire research skills and protected time for intellectual pursuits. They need to become aware of the long-term nature of a research endeavor. They need collaborations with their basic science colleagues in designing and carrying out osteopathically oriented studies. In short, they have the same needs as do the basic scientists. The DO making a transition to research is venturing into unknown and uncertain territory, just as is the basic scientist trained in other institutions. Support and understanding are needed for both groups.
Academic Challenges: The Students In planning for the long-term health of osteopathically oriented research, rhe role of the students must be considered. At present, in most osteopathic schools, little attention is given to providing the students with a background in prior research of the profession, let alone in the basics of research design and process relevant to the profession. One of the best ways to increase research power in the profession is to orient its students early in their training to the basic properties and needs for research. Only a small percentage will become researchers, bur only a few are needed to make a large difference. If only one student per class aspireJ to become a full-rime researcher in the profession and were provided sufficient support to pursue that goal, the profession would soon have an abundance of trained and functioning researchers in irs institutions. The schools can implement lectures on research background, methodology, and process for all students. For those showing more interest, mentors can be provided to work with the more motivated students to provide initial training, research opportunities, and support. These students can be integrated into ongoing investigations of osteopathic manipulation and technique. There have been some efforts ro provide a model research curriculum to all the schools, and this should be encouraged. Too often , the schools are attracting students with research interests, 011ly ro destroy that interest by failing to provide opportunities and training.
79. Osteopathic Research: Challenges of the Future In addition, opportunities can be made available for graduate training for students interested in well-recognized laboratories outside the profession. However, it is imperative that such opportL;nities incorporate aspects of research particularly pertinent to the profession, lest the student be discouraged from building the knowledge bridges to the important issues of the profession. The profession is beginning to rake steps to add a research basis to the curriculum. In late 2001, a workshop was held at the Osteopathic C linical Trials Initiative Conference (OCCTIC) meetings for the purposed of ourlining a research curriculum for the years of osteopathic medical training. The results of this meeting have been endorsed by the Educational Council on Osteopathic Principles (ECOP) and made available to the schools. Should the schools adopt these guidelines for research training, a real step forward in producing research-oriented students wiLl have been taken. The recommended research curriculum consists of the following: By the end of osteopathic medical school years one and two, the student should have the following capabilities: l. History of osteopathic research 2. Knowledge of research vocabulary 3. Ability to do a literature search 4. Knowledge of basic statistics 5. Understanding of research problems that are uniquely osteopathic (OMT) 6. Awareness of support resources available consistent with level of competency expected By the end of osteopathic medical school years three and four, the student should have the following capabilities: 1. Ability to review and summarize journal articles 2. Ability to formulate a research question/hypothesis 3. Awareness of support resources available consistent with level of competency expected By the end of postgraduate years one through three, the student should have the following capabilities: 1. Understand the process of design and implementation of a research project 2. Ability ro critique journal articles 3. Ability to write a manuscript suitable for publication or a grant application 4. Awareness of support resources available consistent with level of competency expected.
Organizational Challenges: Other Osteopathic Institutions As the profession moves into the fourth research period, it is increasingly evident that the challenges of providing a research basis for osteopathic theory and practice cannot be mer by the COMs alone. The establishment of the new center for osteopathic research was not an isolated effort of one or more schools. It was an effort spanning several years and with its roots in the early days of rhe profession with the A. T. Still Research Institute. Several institutions of the profession came together to promote and fund the center's formation, including the AOA, AAO, AACOM, the American College of Osteopathic Family
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Physicians, and the American Osteopathic Healthcare Association. These and other organizations within the profession have realized the necessity of promoting a research culture in the p rofession. These institutions, the profession's leaders, and the rank and file of the profession must continue to support (in concept and financially) the development of researchers who understand the osteopathic profession and can apply their skills and intellectual abil ities ro answering the vital questions posed by this unique philosophy and practice. Without continued support and encouragement from al l, a research-friendly atmosphere will not flourish.
Collaborative Challenges: Building Research Networks As the research efforts of the profession mature, clin ical trials of the effects and efficacy of osteopathic techn iques, osteopathic manipulative treatment, and osteopathic care will move from the pilot study format to fu ll -blown clinical trials. These trials will be expensive and time consuming. A fu ll clinica l trial often requires hundreds of subjects (see Chapter 74) and many practitioners. The osteopathic profession is, despite its rapid growth, still a small profession. The conduct of full trials wi ll require collaboration between multiple sites and practitioners. The basis for planning such studies has yet to be advanced in the profession. The center for osteopathic research, with its mandate to conduct studies on osteopath ic man ipu lative themes, is an appropriate venue fo r such planning. However, there exist other avenues that can begin the process in preparation for these trials. One such avenue lies in the OPTI networks. These confederations ofhospiral training sites affiliated w ith osteopathic colleges provide ready-made resources for pilot studies of collaborative trials. Some OPTis already have provision for research efforts and research training. The OPTI networks can be valuable resting grounds for collaborative efforrs in the next few years. In addition, encouraging practitioners in their office practices to join research networks would lead to more viable cl inical trials. Recent developments in clinical research stimulated by the acquired immunodeficiency syndrome (AIDS) epidemic are also useful models for the osteopathic profession to fo llow. In the past, there has been lirrle clinical research performed outside major research centers. In response to increasing pressure fo r clinica l data on the AIDS epidemic, there has been an increasing use of smaller neighborhood clinics and solo practitioners to collect data on the disease (M. Goldstein, personal communication, 1992). It is becoming evident that there is an important ro le for the practicing physician in collecting data for clinical stud ies. Studies using this important resource for data co llection must be designed to take advantage of the practice of med icine in the office setting so as not to disrupt the dai ly flow of the practice. Howeve r, it is here that the real practice of osteopathic medicine takes p lace. It is here that there is the best chance to ask such questio ns as: What is the incidence of somatic dysfunction? What is its natural course? What is the effectiveness of manipulative treatment on it? The questions of real life in osteopathic medici ne can be approached at the office level. Such research must be encou raged.
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VIII. Basic and Clinical Research for Osteopathic Theory and Practice
That such research can be accomplished is seen in the recent report from the office ofFrymann (12) on the effects of osteopathic care on neurologic development in children. Other office-based studies that include many practitioners would provide many important data on the basis for and efficacy of osteopathic care.
Collaborative Challenges: Isolation The osteopathic profession began in the United States but quickly spread to other countries. Early in the 1900s, osteopathy was established in the United Kingdom; in 191 6, an osteopathic school was established there. Currently, there are osteopathic movements in many countries of the world, some nascent, as in Russia, and some well developed, as in the United Kingdom. Although the practitioners of most of these schools are licensed to practice manipulation only, they are valuable resources for research collaboration. In addition, many countries have active allopathic groups who have traditions of manual medicine, and some have become well trained in osteopathic techniques and theory, as is the case in Germany. The International Federation of Manual Medicine, or FIMM, has an active research component. Canadian students of osteopathy, in fact, must complete an extensive research thesis, practically comparable to a U.S. doctoral thesis before becoming certified as diplomats in osteopathy. T he U.S. osteopathic movement has an opportunity to greatly enhance its research efforts by encouraging interactions with these movements. In fact, it may be that, taken together, these organized osteopathic schools outside the U.S. have more potential for research on efficacy and outcomes tl1an does the U.S. profession. Clearly, there are aspects of osteopathic care that can only be studied in the U.S., because only here at present are osteopathic doctors fully licensed physicians; however, technique, reliability, and treatment studies can be collaboratively studied with many other sections of the world osteopathic community. These types of collaboration should not be wasted by isolationism.
CHALLENGES OF RESEARCH DESIGN As pointed out in Chapter 74, the design ofosteopathic clinical research faces unique challenges. T he design of clinical research is actually in its infancy, begi nning only about 50 to 60 years ago. Clinical research grew up around the testing of drug efficacy, and the gold standard design for such studies is the randomized, placebo-controlled, double-blind (RPCDB) study. T he challenges facing the osteopathic and manipulative medicine communities are rwo: Is the RPCDB methodology appropriate for studies of osteopathic manipulative treatment? What research designs are appropriate for studies of osteopathic manipulative treatment? These questions cannot be answered in a vacuum. The design of any study should flow from an understanding of the research question and the available research techniques. Parts of this challenge have been examined in the Foundations for Osteopathic Research, Chapter 74, but other aspects will be discussed here.
Shams and Placebos One of the most interesting issues faci ng the design of research in osteopathic manipulative treatment or techniques is whether to use placebo or sham controls and, if so, what to use. The use of placebos is well known and documented in clinical research literature (as is the use of sham controls), but these are being called into question (13,14). The placebo treatment was initially developed for research on the effectiveness of drugs, and entails the delivery of a substance that is, from the standpoint of the patient and physician , indistinguishable from the drug being tested. Such a placebo is often in the form of a capsule that is the same color, size, and weight as the capsule containing the drug, but the placebo contains only inert substances. The patient is given either the drug-containing capsule or the inert-substance capsule, not knowing which is being given. The sham is a procedure given to the patient that has been shown or is thought to have no affect on the symptoms being treated. With both placebos and shams, the intent is to keep the patient from knowing whether he or she is receiving an active or inactive drug or procedure. This should keep the expectations of both the experimental and control groups equal and thus allow the effect of the active ingredient or procedure to be seen, independent of patienr expectations. In the case of drug tests or for testing specific manipulative techniques, placebo and sham controls are entirely appropriate. T he intenr of such studies is to ascertai n the effect of the active ingredient alone. They look at the effect of either a certain molecule (or, more precisely, many millions of molecules) on the natural course of something like a bacterial invasion of the body, or of a particular procedure (such as a lateral recumbent roll) on the course of a particular symptom (15). The patient's expectations and conscious processes are not at issue. The use of placebo or sham procedures as control groups against which the drug or procedure groups can be compared gives the researcher a measure of the effectiveness of the drug or technique alone. Thus, in the design of manipulative technique research, it seems entirely appropriate to use sham treatment control groups. Here, the rationale is to test the effectiveness of a certain specific technique that is administered in the same way to each patient for presumably the same symptom or symptoms. The treating physician has no leeway in how the maneuver is accomplished, and the patients are screened closely so that the symptoms are much the same from patient to patient. However, at the heart of osteopathic philosophy is the premise that treatment should be aimed at normalization of function by removing the barriers to the body's ability to optimize irs function . Once these barriers are removed, the body can regain irs optimal function and return to or maintain health. To think that this is purely a physiologic fu nction and has nothing to do with conscious processes or the mind (i.e., the patient's expectations, desires, beliefs, and will) is to return to a belief in mind/body dualism holding that the mind has nothing to do with physiologic function, and vice versa. It is to deny the most vital part of the whole equation of health and disease: the patients themselves. In addition, the treating physiCian is a part of the equation. Both the skill and the manner of the treating physician affect the results of the treatment, because
79. Osteopathic Research: ChalLenges of the Future both the patienr's tactile and mental perceptions of the physician influence how rhe parienr responds to th e treatm ent. In osteopathi c rrearmenr, rhe rrearmenr is an interaction between patient and physician, each responding to rhe other throughout the treatment. T he osteopathi c physician relies on the very effect that is labeled placebo or expectation in drug testing to help with the alteration he or she is attempting to produce-that of normalized function. T he patie nt's expectation is an important and vital facto r in OMT; it must not be cast off as some spurious side effect. Ir is also a real and unusuall y safe therapeutic tool. There are few deleterious side effects to pos itive expectations. In addition, the use of a sham trearmenr gro up in which the patient is exposed to a treatment that is considered ineffective presents another real problem for the evalu ation of OMT (again, as contrasted ro the evaluation of a particular technique). It is assumed that in rhe sham control group, the treatment of a body area distant from a particular somatic dysfunction does not influence the resolution of a diagnosed dysfunction being treated in rhe experimental gro up. Many available data show that the simple act of touching and moving an individual produces real changes in funct ion and response. T he act of manipulative treatment involves touching and moving the patient as an integral parr of rhe process. To compare a manipulation gro up with some sham group rhar has also received rouch and movement may well lead ro an underestimation of the effects of manipulative treatment, unless it can be shown that the sham treatment had no effect on rbe total mind and body function of the patient. Thus, initial attempts ro evaluate the true effectiveness of manipulative treatment (as opposed to techniques) on either the progression of symptoms o r on total body function requires rhe use of a control gro up that either receives some standard medical therapy not requiring manipulation o r rbe use of a totally untreated contro l group that wo uld simply undergo rhe natural course of the malfunction being studied. T his could be done by simply requiring co ntro l subjects ro come to the physician's office for diagnostic measurements. To try to facto r our the mental process involved in manipulative treatment is to deny much of the actua l treatment. It is akin to stud ying the effectiveness of a drug by giving on ly a partial dose. To study the effects of osteopathic manipulation, one must study osteopathic man ipulation as it is give n, as an interaction between physician and patient, with all componenrs intact and function ing. To factor our any particular co mponem , such as rhe so-called hands-on effect, and call it an artifact is ro underestimate the effect of manipulative treatment and deny rhar rhe natural power of cognitive and recuperative processes is a factor in the effects of OMT. Once rhe overall effects of manipulative treatment have been establ ished, studies can be designed to tease apart the various components of the treatment, including rhe effects of touching the patient, and so forth. However, to try to do such studies in the absence of demonstrated effects is both inefficient and impractical. The study of OMT must flow from rhe philosophy of osteopathy and nor from some other philosophic orientation. The investigator designing studies of OMT must determine what is really being asked of the study so rhar the appropriate contrast control can be used. Usi ng the incorrect co ntrol may result in underestimation of the effect of manipulative treatment,
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although rhe san1e control may be rhe app ro priate one for evaluation of a manipulative technique. T h e decision rests on whether the total response of rhe individual to the interaction between patient and physician is being eval uated or whether manipul ative techn ique is being studied as a procedure. T he challenge here is to actively defend rhe use of appropriate designs for osteopathic manipulative research, and nor ro be forced inro inappropri ate designs by preconceived ·notions of how research is dorre.
PRIORITY CHALLENGES: WHAT RESEARCH IS MOST IMPORTANT? Iris tempting ro say rhar all research that can be done is important and no area should be singled o ut above others. H owever, some suggestions can be made as to areas that may be most valuable in determining the usefulness and value of osteopathi c theory and practice.
Basic Research Research on the mechanisms underl ying osteopathic practice begins with either rhe theoretical underpinnings of the profess ion , or clinical observations of practitio ners. As an exampl e, Korr (16) fo llowed both theory and clinical observation when beginning his line of research on transsynapric delivery of proteins from nerve to muscl e tissue. The nurturing of tissues by their nerve suppl y had long been a theme in osteopathic medicine, but almost ignored in other Western traditions. Clini cal observations showed that muscles deprived of nerve supply would degenerate, bur those only deprived of nerve activity would o nly atrophy. Certainly, Korr's resea rch program was clearly driven by osteopathic clinical and theoretical considerations. Clearly, some of the viral areas in rhe traditio ns and clinical experiences of the profession can lead ro distinctive basic research programs. Examples of such areas includ e: • The imeracrions between somati c and visceral structures are a viral issue that is receiving attention in laboraro ries now, bur is very under-researched. • How does rhe mechanoreceptor input from muscle affect sympathetic outflow? • How does sympathetic activity affect so matic structure and function ? • How can virus and bacterial activity be influenced by sympathetic activity? • What is the structure and function of the fasciae of the body? • How do strains in the somati c structures affect visceral function over rime? Certainly one of the most basic questions in the area of osteopath ic basic research is the prevalence and in cidence of the entity known as somatic dysfun ction . T his is perhaps one of the most pressing and most difficult questio ns that rema in un answered in rhe profession . Ir actually crosses the bounds of bas ic and clinical areas. The list of questions ge nerated by osteopathic theory and clinical experience is almost endless. However, to rap these areas, the researcher must be able to see how they apply to th e osteopathi c expenence.
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VIII. Basic and Clinical Research for Osteopathic Theory and Practice
Clinical Research As long as rhe lisr of questions in the basic sciences is flowing from rhe osteopathic theory and practice, iris perhaps longer in the clinical arena. Various lists of rhe mosr important areas of clinical research have been generated, bur consensus has nor been reached. Areas rhar seem ro be especially critical, although nor prioritized, are included here.
Teaching Techniques in Osteopathic Manipulation T he area of research on educational techniques, although nor clinical, wou ld provide important information on how ro pass on rhe techniques and skills of osteopathic medicine. Research in ro how ro besr reach palpation, recognition of rissues texture alrerarions, and so forth, is badly needed.
Inter- and lntraexaminer Reliability Studies One of the basic unknowns in osteopathic medicine (and manual medicine in general) is how ro assess and improve rhe reliability berween rhe examination skills of practitioners, and indeed, how reliable the same individual is when examining rhe same patient rwice. There are studies available on the reliability berween examiners of rhe same patient (17), bur rhe studies vary widely in qua li ty and findings. In addition ro being an important question in terms of how much value can be placed on palparory findings, studies on the factors influencing the reliability within and berween palparors would help inform the reaching of these skills. This is an area that probably shou ld be a priority in the profession and on which several projects are being mounted.
Outcomes and Cost Effectiveness of Osteopathic Manipulative Treatment Although seemingly obvious, simple outcome studies thar look at what happens ro patients, without the use of controls, is needed. One such study is under way at present in Maine (the Maine Osteopathic Outcomes Study, or MOOS), and more may be planned. However, with the amounr of data collected by state, federal, and private entities, the numbers of epidemiologically related studies that are now possible are immense. Models for these types of studies must be generated more frequenr ly in the profession.
Comparisons of Osteopathic Treatment Techniques with Other Forms of Manual Medicine Many other forms of manual medicine exist. How do treatmenr techniques generated by the osteopathic profession compare with rhese? Is a manipulative treatment driven by osteopathic theory more effective rhan thar given by other practitioners of manual medicine? Such questions are not only fasc inating, bur also viral ro understanding rhe value of osteopathic medicine.
Comparing Different Modalities of Osteopathic Treatment with Each Other There are several major treatment modalities used in the profession. How do they compare in outcomes when used on a common disease process? Is a high-velocity/low-amplirude thrust better than a muscle treatment for a sore neck? Comparing one modality with anorher would produce interesting insiglm into the potenrial mechanisms of the different modalities, as well as rheir efficacy in various conditions.
What Are the Effects of Manipulation on a Somatic Dysfunction? Just as rhe questions of prevalence and incidence of somatic dysfunction are basic ro the profession, so are the questions surrounding the actual influence of a manipulative treatment on a well-delineated somatic dysfunction. How do such parameters as chronicity and cause affect the outcome? Although it is assumed that an osteopathic treatment corrects somatic dysfunction , how long does the effect last in chronic cases, and how susceptible is rhe dysfunction ro reoccurrence?
What Is the Effect of Manipulation on Diagnosed Disease Entities? This question has been debated for years and is, in fact, a basic question for payment for services. Actually, the list of conditions to target for such research has received much attention. At a recent meetmg, several conditions were targeted for special consideration: Chronic low back pain Headache (type unspecified) Asthma Otitis media These conditions have a history of study in and outside the profession, and may be more amenable to tight research designs than many other conditions . There is a wide range of studies either under way or in planning stages at osteopathic schools and other institutions. All should be encouraged, as each will add to the body of design knowledge about how to do research in osteopathic manipulative treatment. It is likely that a few conditions will have to be selected for fullscale studies due to cosr and manpower limitations. Pilot studies will pave the way for selecting rhose conditions most likely to provide meaningful information on the large-scale effects of osteopathic treatment.
CHALLENGES OF THE BIGGER PICTURE: OSTEOPATHIC PHILOSOPHY AND LARGER RESEARCH QUESTIONS Although these specific areas of research are importanr, the role of rhe osteopathic philosophy in shap ing even larger questions, and directions of osteopathic research must be mentioned.
79. Osteopathic Research: Challenges of the Future Basic to the philosophy and theory of osteopathy is the idea that the body is an integrated functional unit. This unit includes the physical, cognitive, and spiritual aspects of the individual. Indeed, there is a growing body of evidence suggesting positive effects of spiritual interventions, such as prayer, in the healing process (18-21). How these elements interact within the total individual and with the external environment determine the long-term health status of the person. From the beginning of osteopathic medicine, osteopathic practitioners have held that there was an entity that would adversely affect a person's health status. This entity, which could be palpated and specifically treated with manipulation, was first known as the osteopathic lesion and then, more recently, as somatic dysfunction. In the 1940s and 1950s, Denslow, Korr (22), and their colleagues postulated that a major component of the osteopathic lesion was the facilitated segment. The facilitated segment concept arose from the data gathered by these researchers, which showed that, in most individuals, there was no uniform excitability throughout rhe spinal cord. The areas of hyperexcitability were shown to react more strongly to afferent input, exposing innervated structures, both visceral and somatic, to increased activation . This break in body unity was postulated to lead to early breakdown and malfunction over time-in short, to disease. Clinical disease was, then, a consequence of earlier body dysfunction. Indeed, this was a data-based theory that truly embodied one of Still's basic insights; that clinical disease was a manifestation of body malfunction rather than a primary event.
DETERIORATION OF NORMAL FUNCTION AS A CENTRAL CONCEPT That clinical disease is a result of earlier deterioration of normal function is central to osteopathic philosophy. It is perhaps best manifest in the treatment of somatic dysfunction, an entity not recognized by most medical practitioners as a clinical entity at all. Why treat it? Because it is the beginning of disease, the start of body breakdown. To treat the root of disease would seem to be more cost-effective than waiting until the final breakdown of clinical disease has occurred before beginning treatment.
OTHER ROLES FOR SOMATIC DYSFUNCTION Given this view, osteopathic research should be aimed at elucidating the relationships between disturbances of body function and health status: How does the presence of somatic dysfunction predict the health status of the individual? What is the incidence of serious somatic dysfunction and its natural history? What environmental and lifestyle attributes seem to contribute to the incidence of somatic dysfunction? How does lifestyle contribute to the incidence of somatic dysfunction in old age? Flowing from these questions are even larger questions that should be at the forefront of osteopathic thinking:
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What is the contribution of early lifestyle or evems that happen to the person and the health status of the individual in old age? What regime of manipulative treatment in early life will contribute most to deterring the deterioration of health usually associated with old age? More simply, why are some very old people vital and healthy and others completely overtaken by deterioration and disease? What role does long-lasting somatic dysfunction play in the presence or absence of vitality in old age? These questions are complex and not easily answered. The critical point is that at least some research of the profession should take as irs starting point body unity and the concept that the start of disease is the deterioration of that functional unity, not a bacterial or viral invasion.
INTEGRATION AND SELF-REGULATION IN HEALTH These questions suggest several important areas of research for the osteopathic profession. In the basic sciences, increasing attention must be paid to understanding the integration of body systems and what can cause the fine-tuned integration of body function to deteriorate. The capacity of the body to self-regulate (homeostasis) and the limits of that capacity in both the short-term and long-term must be better understood. Research aimed at elucidating the fine control and adaptation of body function would be especially useful. Integration of basic science data with data from studies of cognitive function gives a greater understanding of the role of the physician in the health maintenance process. A greater understanding of the effects of afferent input and cognitive function on the immune system, and how manipulative treatment can affect this system, would be useful.
HEALTH BENEFITS OF MANIPULATIVE TREATMENT Within the clinical research areas, there must be studies of the efficacy of manipulative techniques and manipulative treatment. Measurements of the effects of manipulation on specific disease entities, such as those listed above, need to be carried out to demonstrate that manipulation can be used effectively in treating specific disease processes. To rely on such demonstration studies to show the most significant benefits of manipulation would, however, be unwise. The most beneficial and lasting effects of manipulation and, indeed, of osteopathic care should be searched for in the effects on total functional capacity of individuals and in their long-term health status. The current health care system is preoccupied with the treatment of disease, especially in the chronic degeneration of old age. It is by no means clear that the chronic diseases commonly associated with old age are inevitable. What are the enabling or protective roles of early and continued normal body function in the aging process? Osteopathy is ideally suited by its philosophy and clinical experience to look at the effects of early disruptions of body unity on the deterioration of old age. This is a golden opportunity for osteopathic research.
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VIII. Basic and Clinical Research for Osteopathic Theory and Practice
TOTAL NATURE OF SOMATIC DYSFUNCTION C linical research should continue to look at the effects of manipulation on specific disease processes. Such studies can be effectiveness studies, such as rhe use of manipulative rrearmenr in low back and chronic pain syndromes. These studies could have fairly quick and valuable outcomes for rhe profession. Other less specific srudies, such as rhe effects of manipulation on sympathetic tone, vasomotor reactivity, and muscle spasticity, contribute to an understanding of the more general effects of manipulation on body fun ction. Swdies of the effects of somatic dysfunction and irs etiology, prevalence, and contributions to the long-term health of the individual form a solid base for a greater understanding of the fundamenral dynamics of health and disease. Investigations of the effects of manipulation on somatic dysfunction and of osteopathic care on old age health status are probably the most important area of study to which the profession can aspire.
CONCLUSION Northup (I ) wisely no red that the future of rhe profession rested in the decisions and integrity of organized osteopathy. Organized osteopathy now must rise to the challenge of mounring and susrai ning a research enterprise that will rest the central tenets and beliefs of the profession . These studies must be done on the playing fields of the profession , nor on those of other professions. The studies must resr the profession's questions and assumptions and be interpreted by those knowledgeable in the theories and practices of osteopathic medicine, nor by others. The risk of allowing others to do the srudies or inrerpret rhe results from other points of view is simply unacceptable. The furure of the profession now rests as much on irs research endeavors as on its teaching and clinical endeavors. T he three legs of the profession's stool are equal, and all are vital. By closely following the basic philosophy of osteopathy and the insights from irs years of clinical experience, the research efforts of the profession can truly add to the most beneficial aspects of health care to which osteopathy is fundamentally d edicated: the mainrenance of health and optimal function of rhe total person throughout life.
REFERENCES I. Norrhup GW. An advenrure in excellence. J Am Osteopath Assoc. 200 I; I 0 I ( 12) :726-730.
2. Patterson MM, H owell J N, eds. The Central Connection: Somatovisceral Viscerosomatic Interaction. Indianapolis, J N: American Academy of Osteopathy; 1992. 3. Willard F, Patterson MM , eds. Nociception and the Neuroendocrine-
Immune Connection. Proceedings of the 1992 American Academy of Osteopathy International Symposium. India napo lis, IN: American Academy of Osteopathy; 1994. 4. Korr !M. Biological basis for the osteopathic concept. l.n: 1960 and 1963 Academy Yearbooks. Indianapolis, IN: American Academy of Osteopathy; 1960:129 and 1963:11 4, respectively. 5. Korr IM. Some thoughts o n an osteopathic curriculum. JAm Osteopath Assoc. 1975;74(8):685-688. 6. Korr IM. Biologic process in the context of human uniqueness and diversiry. Osteopath Ann. 1978;6(1 ): I 0- 13. 7 . Korr lM. Osteopathic principles for basic scien tists. JAm Osteopath Assoc. 1987;87(7):5 13-5 15. 8. Korr IM. Medical education: The resistance to change. Advances. 1987;4(2):5-1 0. 9. Korr IM. Osteopathic principles: A way oflife. 711e DO. 1987;May:2527. 10. Korr IM. An explication of osteopath ic principles. In: Ward RC, ed. Foundations for Osteopathic Medicine. Baltimo re, MD: Williams & Wi lkins; 1997:7-12. II . Korr IM. Pathways to excellence in clinical research. In: Beal MC, ed. 1994 Yearbook, Louisa Burns, DO Memorial. Indianapolis, IN: American Academy of Osteopathy; 1994:60. 12. Fryman n VM, Carney RE, Springall P. Effect of osteopathic medical management on neurologic development in child ren. JAm Osteopath Assoc. 1992;92(6):729-744. 13 . Kienle GS, Kiene H. Placebo effect and placebo concept: A critical methodological and conceptual analysis of reporrs on the magnitude of the placebo effect. Altern Ther Health Med. 1996;2(6):3954 . 14. Kiene H. A critique of the double-blind clinical trial. A Item Ther Health Med. 1996;2(1):74-80. 15. Hoehler F, Tobis J , Buerger A. Spinal manipulation for low back pain. }AMA. 1981;245( 18):1835-1838. 16. Korr !M, W ilkinson PN, Charnock FW. Axonal delivery of neuroplasmic components to muscle cel ls. Science. 1967; 155(760):342345. 17. Beal MC, Patriquin DA. lnrerexaminer agreemenr on palpatory diagnosis and patienr self-assessment of disabili ry: A pilot swdy. JAm Osteopath Assoc. 1995;95(2):97-100, I 03-106. 18. Abbot NC, H arkness EF, Stevinson C, et al. Spiritual healing as atherapy fo r chronic pain: A randomized, clinical trial. Pain. 200 I ;91:7989. 19. Dossey L. T he rerum of prayer. A Item Ther Health Med. 1997;3 (6): I 017 . 20. Harris WS, Gowda M, Kolb JW, et al. A randomized, controlled trial of the effects of remore, intercessory prayer on o utcomes in patients adm itted to the coronary care un ir. Arch Intern Med. 1999; 159(0cr 25): 2273-2278. 21. Thomson KS. The revival of experiments o n prayer. Am Scientist. 1996;84:532-534. 22. Korr IM. The emerging concept of the osteopathic lesion.} Am Osteopath Assoc. 1948;47: 1- 8.
GLOSSARY OF OSTEOPATHIC TERMINOLOGY
Prepared by the Glossary Review Committee sponsored by the Educational Council on Osteopathic Principles (ECOP) of the American Association of ColLeges of Osteopathic Medicine (AACOM). -Revised April 2002 The Glossary of Osteopathic Terminology is revised twice each year by the Educational Council on Osteopathic Principles (ECOP), Chairman, John C. Glover, DO. Forward any comments or suggestions to rhe Chairman of the G lossary Review Committee, William Thomas Crow, DO, Philadelphia College of Osteopathic Medicine, 4190 City Line Avenue, Philadelphia, PA 1913-1693. The Glossary first appeared in the journal of the American Osteopathic Association (No. 80, pages 552-567) in April 1981. The 1995 version of the Glossary of Osteopathic Terminology was also published in the first edition of this textbook. The most current and revised version is printed annually in the American Osteopathic Association Yearbook and Directory of
Osteopathic Physicians. The February 2002 glossary review was performed by James Binkerd, DO; Jane Carreiro, DO; William Thomas Crow, DO; Robert Clark, DO; William H. Devine, DO; Dennis Dowling, DO, FAAO; John C. Glover, DO; Donald V. Hampton, DO; Robert Kappler, DO, FAAO; Michael Lockwood, DO; David Macon, DO; William Morris, DO; James Rechrien, DO; Mark Sandhouse, DO; Karen Steele, DO, FAAO; Edward G. Stiles, DO, FAAO; and Scott T. Stoll, DO, PhD. The purpose of this osteopathic glossary is to present important and often used words, terms, and phrases of rhe osteopathic profession. It is not meant to replace a dictionary. The glossary offers the consensus of a large segment of the osteopathic profession and is to serve to standardize terminology. The ECOP Glossary Review Committee specifically seeks to include those definitions that are uniquely osteopathic in their origin or common usage, distinctive in the osteopathic usage of a common word, and/or important in describing osteopathic principles and philosophy and osteopathic manipulative treatment. We also expect this glossary to be useful to the student of osteopathic medicine and to be helpful to authors and other professionals in understanding and making proper use of osteopathic vocabulary. Dictionary definitions are included from:
Dorland's Medical Dictionary, 29th ed. Philadelphia, PA: WB Saunders; 2000.
Gray's Anatomy Stedman's Medical Dictionary, 27th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000.
A abbreviations (for types of osteopathic manipulative techniques):
ART: articulatory treatment BLT: balanced ligamentous tension trearment/ligamen to us articular strain treatment CR: osteopathy in the cranial field CS: counterstrain treatment D: direct treatment DIR: direct treatment FPR: facilitated positional release treatment HVLA: high velocity/low amplitude treatment !: indirect treatment IND: indirect treatment INR: integrated neuromusculoskeletal release treatment LAS: ligamentous articular strain treatment/balanced ligamentous tension treatment ME: muscle energy treatment MFR: myofascial release technique NMM-OMM: neuromusculoskeleral medicine OCF osteopathy in the cranial field/cranial treatment OMT: osteopathic manipulative treatment PINS: progressive inhibition of neuromuscular structures ST: soft tissue treatment VIS: visceral manipulative treatment acceleration: Rare of increase in velocity. See also deceleration. accessory JOint motions: See secondary joint motion. accessory movements: Movements used to potentiate, accentuate, or compensate for an impairment in a physiologic motion (e.g., the movements needed to move a paralyzed limb). accommodation: A self-reversing and nonpersistent adapranon. active motion: See motion, active. acute somatic dysfunction: See somatic dysfUnction, acute. allopathy: 1. A therapeutic system in which a disease is treated by producing a second condition that is incompatible with or antagonistic to the first. (Stedman's) 2. A term used to refer those holding a Doctor of Medicine (MD) degree, a nonosreoparhic medical degree. anatomic barrier: See barrier (motion barrier). angle: Ferguson a., see angle, Lumbosacral. lumbolumbar lordotic a., an objective quantification of lumbar lordosis typically determined by measuring the angle between the superior surface of the second lumbar
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Glossary
FIGURE 1. Lumbolumbar lordotic angle (L2-5) . FIGURE 3. Lumbosa cra l lordotic angle.
vertebra and the inferior surface of the fifth lumbar vertebra; best measured from a standing lateral x- ray film (Fig. 1). lumbosacral a., represents the angle of the lumbosacral junction as measured by the inclinatio n of the superior surface of the first sacral vertebra to the horizontal (this is actllally a sacral angle); usually measured from standing lateral x- ray films; also known as the Ferguson angle (Fig. 2). lumbosacral lordotic a., an objective quantification oflumbar lo rdosis typically determined by measuring the angle between the superior surface of the second lumbar vertebra and the superior surface of the first sacral segment; best measured from a standing lateral x-ray film (Fig. 3) . anterior component: A positional descriptor used to identify the side of reference when rotatio n of a vertebra has occurred; in a condition of right rotation, the left side is the anterior component; usually refers to the less prominent transverse process; see also posterior component. anterior compression test: See ASIS (anterior superior iliac spine) compression test. anterior iliac rotation: See ilium, somatic dysfunction of anterior (forward) innominate (iliac) rotation. ART: See TART.
articular pillar: 1. Refers to the columnar arrangement of the articular portions of the cervical vertebrae. 2. Those parts of the lateral arches of the cervical vertebrae that contain a superior and inferior ar ticu lar facet. articulation: 1. The place of union or junction between two or more bones of the skeleton . 2. The active or passive progress of moving a joint through its permitted anatomic range of motion. See also osteopathic manipulative treatment, articulatory treatment (ART) system. articulatory pop: Sound made when cavitation occurs in a joint. See also cavitation. articulatory technique: See also technique; osteopathic manipulative treatment, articulatory treatment (ART) system. asymmetry: Absence of symmetry of position or motion; dissimilarity in corresponding parts or organs on opposite sides of the body that are normally alike; of particular use when describin g position or motion alteration resulting from somatic dysfunction. axis: 1. An imaginary line about which motion occurs. 2. The seco nd cervical vertebra. 3. One component of an axis system. axis of rib motion: An imaginary line through the costotransverse and the costovertebral articulations of the rib. anteroposterior rib axis, see bucket handle rib motion. See also Figs. 4 and 5. transverse rib axis, see pump handle rib motion. See also Figs. 6 and 7. ASIS (anterior superior iliac spine) compression test: Test for determining the side of pelvic somatic dysfunction. axis of sacral motion: See sacral motion axis. axoplasmic flow: See axop!asmic transport. axoplasmic transport: The amegrade movement of substances from the nerve cell along the axon towa rd the terminals, and the retrograde movement from the terminals toward the nerve
cell.
B
FIGURE 2. Lumbosacral angle (51-horizon) (Ferguson angle).
backward bending: Opposite of forwa rd bendjng. See- extenswn. backward bending test: 1. A rest that discriminates between
GLossary
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"Transverse Axes"
FIGURE 7. Pump handle rib motion.
B FIGURE 4. The functional anterior-posterior rib axis.
Anterooosterior Axes
FIGURE 5. Bucket handle rib motion.
--- .... - .-............. ~
,
FIGURE 6 . The functional transverse rib axis.
forward and backward sacral torsion/rotation. 2. A rest that discriminates between unilateral sacral flexion and unilateral sacral extension. balanced ligamentous tension technique: See osteopathic ma-
nipulative treatment, ligamentous articuLar strain. barrier (motion barrier): The limit to motion; in defining barriers, the palpatory end-feel characteristics are usefu l (Fig. 8) . anatomic b., the limit of motion imposed by anatomic structure; the limit of passive motion. elastic b., the range between the physiologic and anatomic barrier of motion in which passive ligamentous stretching occurs before tissue disruption. pathologic b., permanent restriction of joint motion associated with pathologic change of tissues (e.g., contracture, osreophytes). physiologic b., the li mit of active motion. restrictive b., a functional limit withi n rhe anatomic range of motion, which abnormally diminishes the normal physiologic range. batwing deformity: See transitionaL vertebrae, sacraLization. bind: Relative palpable resistance to motion of an articulation or tissue. Synonym : resistance; antonyms: ease, compliance, resilience. biomechanics: Mechanical principles applied to the rudy of b iologic functions; the application of mechanical laws to living structures; the study and knowledge of biologic function fro m an application of mechanical principles. body unity: One of rhe basic tenets of the osteopathic philosophy; the human being is a dynamic u nit of function ; see also osteopathic phiLosophy. bogginess: A tissue texture abnormaliry characterized principally by a palpable sense of sponginess in the tiss ue, interpreted as resulting from congestion due to increased flu id con rent. bucket handle rib motion: Movement of rhe ribs during respiration such that, with inhalation, the lateral aspect of the rib moves cephalad, resulting in an increase of transverse diameter of the thorax. T his type of rib motion is predominantly found in lower ribs (Figs. 4-6), increasing from the upper to th e lower ribs. See also axis of rib motion; pump handLe rib motion.
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Glossary Concepts Regarding Joint Motion in a Single Plane
PB
AB
' NormalMotion
AB
PB
RB
00
I 1 1
PB
AB
PB
AB
Normall Motion
II PB
AB
00
AB
AB
~
0 RB, restrictive barrier
~ Indicates Motion Loss FIGURE 8. Somatic dysfunction in a single plane: three methods illustrating the "restri ctive barrier" (the restrainer) : AB, anatomic barrier; PB, physiologic barrier; RB, restricted barrier; SO, somatic dysfunction.
c caliper rib motion: Rib morion of ribs 11 and 12 characterized by si ngle joint motion; analogous to internal and external rotatio n. caudad: Toward the tai l or inferiorly. caught in inhalation: See inhalation rib. caught in exhalation: See exhalation rib. cavitation: The formation of small vapor and gas bubbles or within fluid through local reduction in pressure. This produces an audible "pop." cephalad: Toward the head. cephalad pubic dysfunction: See pubic bone, somatic dysfUnctions of
cerebrospinal fluid, fluctuation of: A description of the hypothesized action of cerebrospinal fluid with regard to the craniosacral mechanism. Chapman reflex: A system of reflex points originally used by Frank Chapman, DO, and described by Charles Owens, DO. These reflexes present as predictable anterior and posterior fascial tissue texture abnormalities assumed to be reflections of visceral dysfunction or pathology (viscerosomatic reflexes). A given reflex is consisten tly associated with the same viscus; Chapman reflexes are manifested by palpatory findings of plaquelike changes or stringiness of the involved tissues. chronic somatic dysfunction: See somatic dysfUnction, chronic. circumduction: The active or passive circular movement of a limb; the rotary movement by which a structure or part is made to describe a cone, the apex of the cone being a fixed point (e.g., the circular movement of a ball-and-socket joint). combined technique: See osteopathic manipulative treatment, combined method. common compensatory pattern: See fascia/patterns, common compensatory pattern. compensatory fascial patterns: See fascial patterns, common compensatory pattern. compliance: The ease with which a tissue may be deformed. compression: 1. Somatic dysfunction in which two structures are held forced together. 2. A force that approximates rwo structures. conditioned reflex: See reflex, conditioned r. contraction: Shortening and/or development of tension in muscle. concentric c., contraction of muscle resulting in approximation of attachments. eccentric c., lengthening of muscle during contraction due to an external force. isolytic c., 1. Contraction of a muscle against resistance while forcing the muscle to lengthen. 2. Operator force greater than patient force. isometric c., 1. Change in the tension of a muscle without approximation of muscle origin and insertion. 2. Operator force equal to patient force. isotonic c., 1. Approximation of the muscle origin and insertion without change in its tension. 2. Operator force less than patient force. contracture: A condition of fixed high resistance to passive stretch of a muscle, resulting from fibrosis of the tissues supporting the muscles or the joints, or from disorders of the muscle fibers. Dupuytren c., shortening, thickening, and fibrosis of the palmar fascia, producing a flexion deformity of a finger (Dorland's). contractured muscle: In contrast to contracted muscle; contracted muscle is regarded as the physiologic function of neuromuscular excitation-response, whereas contractured muscle is due to histologic change substituting noncontractile tissue for muscle tissue, which prevents the muscle from reaching normal relaxed length. core link: T he connection of the spin al dura mater from the occiput at the foramen magnum to the sacrum . It coordinates the synchronous motion of these rwo structures. coronal plane: See plane, coronal.
Glossary
costal dysfunction: See rib dysfUnction. counternutation: Posterior movement of the sacral base around a transverse axis in relatio n to the ilia. See also nutation. counterstrain technique: See osteopathic manipulative treatment, counterstrain. cranial rhythmic impulse: A palpable, rhythmi c fluctuation believed to be synchro nous with the primary respiratory mechanism. (Term coined by Drs. John and Rachel Woods.) cranial technique: See also primary respiratory mechanism; osteopathic manipulative treatment, osteopathy in the cranialfield. craniosacral mechanism: A term used to refer to the anatomic connection between the occiput and the sacrum by the spinal dura mater, as used by William G . Sutherland, DO; it was not used by Dr. Sutherland in any oth er sense. C-SPOMM: Certification , Special Proficiency in Osteopathic Manipulative Medicine. Granted by the American Osteopathic Association through the American Osteopathic Board oF Special Proficiency in Osteopathic Manipulative Medicine from 1989 thro ugh 1999. CV-4: See osteopathic manipulative treatment, CV-4.
D deceleration: A rate of decrease in velocity. See also acceleration. decompensation: A dysfunctional, persistent pattern , in some cases reversib le, resulting when homeostatic mechanisms are partially or totally overwhelmed. depressed rib: See exhalation rib. dermatome: 1. Dermatomal area; the area of skin supplied by cutaneous branches from a single spinal nerve; neighboring dermatomes may overlap {Figs . 9A and 9B). 2. Cutis plate; the dorsolateral part of an embryonic somite. diagnostic palpation: See palpatory diagnosis. diagonal axis: See sacral motion, oblique axis (diagonal). direct method {technique): See osteopathic manipulative treatment, direct method. DO: 1. Doctor of Osteopathy (accredited by the American Osteopathic Association). 2. Doctor of Osteopathic Medicine {accredited by rhe American Osteopathic Association). 3. Dip lomate in Osteopathy (first degree granted by American School of Osteopathy). 4. Degree granted by so me schools of osteopathy outside the United States. drag: ee skin drag.
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elasticity: Ability of a strai ned body or tissue to recover its shape after deformation. See also plasticity; viscosity. elevated rib: See inhalation rib. end-feel: Perceived quality of motion as an anatomic or physiologic restrictive barrier is approached. enthesitis: 1. Traumatic disease occurring at the insertion of muscles where recurring concentration of muscle stress provokes inflammation with a strong tendency toward fibrosis and calcification (Stedman's); inflamm ation of the muscu lar or tendinous attachment to bone (Dorland's). ERS: A descriptor of spin al somatic dysfunction used to denote a combination extended {E), rotated {R), and sid e-bent (S) ve rtebral position. ERS left, somatic dysfunction in which the verteb ral unit is extended, rotated, and side-bent left; usuall y preceded by a designation of the vertebral unit{s) invo lved (e.g., T5 ERS left or equivalent T5 ERLSL). ERS right, somatic dysfun ction in which the vertebral unit is extended, rotated, an d side-bent right; usually preceded by a designation of the vertebral unit(s) involved (e.g., C3-5 ERS right or equivalent C3-5 ERRSR). exaggeration technique: See osteopathic manipulative treatment, exaggeration technique. exhalation rib: I. Somatic dysfunction usually characterized by a rib being held in a position of exhalation such th at motion toward exhalatio n is more free and motion toward inhalatio n is restricted. Synonyms: inhalation restriction of rib (s), exhalation strain, depressed rib. 2. An anterior rib tender point in strain/ coun terstrai n. extension: l. Accepted universal te rm for backward motion in a sagittal plane of the spine about a transverse axis; in a vertebral unit when the superior pa rt moves backward (Fig. 10). 2. In extremities, it is the straighten in g of a curve o r angle (b iomechanics) . 3. Separation of the ends of a curve in a spinal region. See extension, regional. craniosacral e., motion occurring during the cranial rhythmic impulse, the sphenobasi lar symphysis descends and sacral base moves anteriorly {Fig. 11). regional e., historically, the straightenin g in the sagittal plane of a spinal region; also ca lled the Fryette regional extension . See extension {Fig. l 0). sacral e., posterior movement of the base of the sacrum in relati on to the ilia {Fig. 12); see also flexion, sacral. extrinsic corrective forces: Treatment forces, the sources of which are external to the patient; they may include operato r effort, effect of gravi ty, mechanical tables, etc.; see also intrinsic corrective forces.
E ease: Relative palpable freedom of motion of an articulation or tissue. Synonyms: compliance, resilience. Antonyms: bind, resistance. easy normal: See neutral (definition 2) . -ed: A suffix describing status, position, o r condition {e.g., extended, flexed, rotated, restricted). effleurage: Stroki ng movement in massage used to move lymphatic fluids (Dorland's). elastic deformation: Any recoverable deformation. See also plastic deformation.
F facet asymmetry: Vertebral structure in whi ch the orientation of th e Facets is not anatomically bilaterally compa rable. See facet symmetry and tropism, facet. facet symmetry: Describes the structure of a vertebra in wh ich the facets are anatomically bilaterally comparable. See facet asymmetry and symmetry. facilitated positional release: See osteopathic manipulative treatment, facilitated positional release.
Glossary
1234
T
-s-
T
-s- CI
s
,.,,, ..,.., .._
- -L-
Key to ID
Key tolD of cervicals, thoracics, lumbar and sacral nerves
of ceiVicals, tboracics, lumbar and sacral nerves
B
A FIGURE 9. A: Dermatomal map (anterior). B: Dermatomal map (posterior). (Modified from Agur AMR . Grant's Atlas of Anatomy, 9th ed. Baltimore, MD: Williams & Wilkin s; 1991 :37.)
facilitated segment: See foci!itation. facilitation: 1. The maintenance of a pool of neurons (e.g., premoror neurons, moroneurons, or preganglionic sympathetic neurons in one or more segments of the spinal cord) in a state of partial or subthreshold excitation; in this state, less afferent stimulation is required ro trigger the discharge of impulses. 2. A theory regarding the neurophys iologic mechanisms underlying th e neuronal activity associated with somatic dysfunction. 3. Facilitation may be due ro sustained increase in affe rent input, aberrant patterns of afferent input, or changes within th e affected neurons themse lves or th eir chemical en-
vironment. Once establ ished, faci litation can be sustained by normal central nervous system (CNS) activity. fascial patterns: Systems for classifYing and recording the prefelTed directions offascial motion throughout the body. Major systems of fascial patterns include the observations of J. Go rdon Zink, DO , FAAO, and W. Neidner, DO. common compensatory pattern (CCP), th e specific finding of alternating fascial motion (Fig. 13A) preference at transitional regions of the body described by Zi nk. · uncommon compensatory pattern, the finding of a!ternating fascial motion preference in the direction opposite that
Glossary
1235
FIGURE 10. Extension. FIGURE 12. Sacra l extension.
of rhe commo n compensatory pattern described by Zink (Fig. 13B). uncompensated fascial pattern, the finding of fascial preferences that do nor demo nstrate alternating patterns of fi ndings at transitio nal regio ns. Because they occur following stress or trauma, they rend to be symptomatic. fascial release technique: See osteopathic manipulative treat-
ment, fascial release treatment. FAAO: Fellow ofAmerican Academy of O steopathy. An earned fellowship awarded by the An1erican Academy of O steopathy. Ferguson angle: See angle, lumbosacral.
FIGURE 11. Craniosacral extension.
flexion: 1. Accepted universal term fo r forward motion 1n a sagittal plane o f the spine about a transverse axis (Fig. 14); in a vertebral unit when the superio r part moves forwa rd; see forward bending. 2. In the extremities, an approximation of a curve or angle (biomechanics). 3. Approximation of the ends of a curve in a spinal regio n; see flexio n, regional. craniosacral f., motion occurring d uring rhe cranial rhythmic impulse, when the sphenobasilar symphysis ascends and the sacral base moves posteriorly (Fig. 15). regional f., historically, the approximation of the ends of a curve in the sagittal plane of the spine; also called the Fryette regio nal Aexio n; see flexion (Fig. 14). sacral f. , anterior movem ent of sacral base in relation to the ilia. See also extension, sacral (Fig. 16) . flexion tests: Tests for iliosacral or sacroiliac somatic dysfunction . seated, a screening rest which determines the side of sacroiliac somatic dysfunctio n (m otio n of the sacrum o n the ilium). standing, a screening test which determines the side of iliosacral somatic dysfunction (motio n of ilium on the sacrum). forward bending: Reciprocal of backward bending. See flexion. FRS: A descriptor of spinal som atic dysfun ctio n used to denote a comb ination Aexed (F), rotated (R), and side-bent (S) vertebral position. FRS left, somatic dysfunctio n in which a vertebral un it is Aexed, rotated, and side-bent left; usually preceded by a designation of the vertebral uni t(s) involved (e.g. , T5 FRS left or equivalent T5 FRLSL) . FRS right, somatic dysfunction in which a vertebral uni t is flexed , rotated , and side-bent righ t; usually preceded by
1236
GLossary
Right
Left Right
Left
....... QA OA
I
I
CT
TL
TL
I
I
LS
..... LS
t
A
a designation of the vertebral uni t(s) involved (e.g., C3-5 FRS right or equivalent C3-5 FRRSR). Fryette principles: See physioLogic motion ofthe spine. FSR: A descri ptor of spinal somatic dysfunction used to denote a combination Aexed (F), side-bent (S), and rotated (R) vertebral position . Typicall y, the involved vertebral unit(s) are specifi ed first and often a subscript is used to designate left (L) or right (R) in the formu la. (e.g., T5-6 FSRRL is interpreted to mean that T5 on T6 and T6 on T7 are Aexed, side-bent right, and rotated left). functional technique: See osteopathic manipuLative treatment,
functionaL method.
FIGURE 14. Flexion.
t,
FIGURE 13. A: Common compensatory fascial pattern (Zink). B: Uncommon co mpensatory fascial pattern (Zink).
G Galbreath treatment:
See osteopathic manipuLative treatment,
mandibuLar drainage. gravitational line: Viewing the patient from the side, an imaginary line in a coronal plane which, in the theoretical ideal posture, starts slightly anterior to the lateral malleolus, passes across the lateral condyle of the knee, the greater trochanter, through rhe lateral head of the humerus at the tip of the shoulder to the external auditory meatus; if this were a plane through the body, it wou ld intersect the middl e of the third lumbar vertebra and the anterior one-third of the sacrum; it is used to evaluate the anteroposterior curves of the spine (Fig. 17). See also mid-maLLeoLar Line.
FIGURE 15. Craniosacral flexion.
Glossary
(Cranioucral: aacral nutation)
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External audItory canal
Lateral head or the humerus.
Third lumbar vertebra Anterior third or the sacrum Greater trochanter
FIGURE 16. Sacral flexion .
Lateral condyle orthe knee
guiding: Gentle movement by the operator following the path of least resistance in rhe movement of a body part within irs normal range. Lateral malleolus
H habituation: Decreased response ro repeated stimulation; hypothetically, a short-term (minutes or hours) decremenral central nervous system (CNS) process; it interacts with the incremental CNS process of sensitization and yields a final behavioral outcome. health: Adaptive and optimal anainmenr of physical, mental, emotional, spiritual, and environmental well-being. hip bone: The os coxae; a large, irregular-shaped bone which consists of three parts: ilium, ischium, and pubis, which m eet at the acetabulum , the cup-shaped cavity for the head of the femur at the hip (femoroacetabular) joint; the pelvis is made up of the right and left hip bones, the sacrum, and coccyx. Also called the innominate bone or pelvic bone; see innominate, somatic dysfunctions of homeostasis: l. Maintenance of static or constant conditions in the internal environment. 2. The level of well-being of an individual maintained by internal physiologic harmony; it is the result of a relatively stable state or equilibrium among the interdependent body functions. homeostatic mechanism: A system of control activated by negative feedback (Dorland's) . hypertonicity: A condition of excessive tone of the skeletal muscles; increased resistance of muscle to passive stretching.
Gravitational Line FIGURE 17. Gravitational line.
ilia: See inferior lateral angle (!LA) ofthe sacrum. ilia! compression test: See ASIS compression test. ilia! rocking test: See ASIS compression test. iliosacral motion: Motion of the ilia on an inferior transverse axis through the sacrum, as occurs in walking; considered to be primarily infl uenced by the anachments and movements of the pelvis, hips, and lower extremities. ilium, somatic dysfunction of: See innominate, somatic dysfunctions of inferior ilium: See innominate, somatic dysfunctions of inferior lateral angle (ILA) of the sacrum: The point o n the lateral surface of the sacrum where it curves medially to the body of rhe fifth sacral vertebrae (Gray's) (Fig. 25) . inferior pubis: See pubic bone, somatic dysfimctions of inhalation rib: A somatic dysfunction usually characterized by a rib being held in a position of inhalation such that motion toward inhalation is more free and motion toward exhalatio n
1238
GLossary
is restricted. Synonyms: inhaled rib, anterior rib, inhalation strain, elevated rib, exhalation restriction. inhibition reflex: 1. In osteopathic usage, a term that describes the application of steady pressure to soft tissues to effect relaxation and normalize reflex activity. 2. Effect on antagonist muscles due to reciprocal innervation when the agonist is stimulated. See also Law, Sherrington; osteopathic and manipuLative treatment, inhibitory pressure technique. innominate bone: See hip bone. innominate, somatic dysfunctions of: anterior i. rotation, a somatic dysfunction in which the anterior superior iliac spine (ASIS) is anterior and inferior to the contralateral landmark and the innominate (os coxae) moves more freely in an anterior and inferior direction and is restricted from movement in a posterior and superior direction . The rotation occurs around the inferior transverse axis of the sacrum. inferior i. shear, a somatic dysfunction in which the anterior superior iliac spine (AS IS) and posterior superior iliac spine (PSIS) are inferior to the contralateral landmarks, and the innominate (os coxae) moves more freely in an inferior direction and is restricted from movement in a superior direction. inflared i., a somatic dysfunction of the innominate (os coxae) resulting in medial positioning of the anterior superior iliac spine (ASIS). The innominate moves more freely in a medial direction and is restricted from movement in a lateral direction. outflared i., a somatic dysfunction of the innominate (os coxae) resulting in lateral positioning of the anterior superior iliac spine (ASIS). The innominate moves more freely in a lateral direction and is restricted from movement in a medial direction. posterior i. rotation, a somatic dysfunction in which the anterior superior iliac spine (ASIS) is posterior and superior to the contralateral landmarks. The innominate (os coxae) moves more freely in a posterior and superior direction and is restricted from movement in an anterior and inferior direction. The rotation occurs around the inferior transverse axis of the sacrum. superior i. shear, a somatic dysfunction in which the anterior superior iliac spine (ASIS) and posterior superior iliac spines (PSIS) are superior to the contralateral landmarks. The innominate (os coxae) moves more freely in a superior direction and is restricted from movement in an inferior direction. intersegmental motion: Designates relative motion taking place berween rwo adj acent vertebral segments or within a vertebral unit; described as the upper vertebral segment moving on the lower. intrinsic corrective forces: Voluntary or involuntary forces from within the patient that assist in the manipulative treatment process. See also extrinsic corrective forces. -ion: A suffix describing a process or movement (e.g., extension, flexion, rotation, restriction) . isokinetic exercise: Exercise using a constant speed of movement of the body part. isolytic contraction: See contraction, isolytic c.
isometric contraction: See contraction, isometric c. isotonic contraction: See contraction, isotonic c.
J junctional region:
See transitionaL region.
K key lesion: the somatic dysfunction that maintains a total dysfunction pattern, including other secondary dysfunctions. kinesthesia: The sense by which muscular motion, weight, position, etc. are perceived. kinesthetic: Pertaining to kinesthesia. kinetics: The body of knowledge that deals with the effects of forces that produce or modifY body motion. klapping: Striking the skin with cupped palms to produce vibrations with the intention ofloosening material in the lumen of hollow tubes or sacs within the body, particularly the lungs. kneading: A soft tissue technique which utilizes an intermittent force applied perpendicular to the long axis of the muscle. kyphoscoliosis: A spinal curve pattern combining kyphosis and scoliosis; see also kyphosis; scoLiosis. kyphosis: 1. The exaggerated (pathologic) anteroposterior curve of the thoracic spine with concavity anteriorly. 2. Abnormally increased convexity in the curvature of the thoracic spine as viewed from the side (DorLand's). kyphotic: Pertaining to or characterized by kyphosis.
L lateral flexed: A term used to describe a position of a vertebral body; defined as the movement of a point on the anterosuperior aspect of the vertebral body about an anteroposterior axis in a coronal plane. lateral flexion: Also called lateroflexion; see side bending. lateral masses (of the atlas): The most bulky and solid parrs of the atlas; they support the weight of the head. law: Fryette I., of motion; see physioLogic motion ofthe spine. Head 1., when a painful stimulus is applied to a body part of low sensitivity (e.g. , viscus) that is in close central connection with a point of higher sensitivity (e.g., soma), the pain is felt at the point of higher sensitivity rather than at the point where the stimulus was applied. Sherrington 1., 1. Every posterior spinal nerve root supplies a specific region of the skin, although fibers from adjacent spinal segments may invade such a region. 2. When a muscle receives a nerve impulse to contract, its antagonist receives, simultaneously, an impulse to relax. (These are only rwo of Sherrington's contributions to neurophysiology; they are the ones most rei evant to osteopathic principles.) Wolff I., every change in form and function of a bone, or in its function alone, is followed by certain definite clianges in its internal architecture, and secondary alterations in its external conformations (Stedman's, 25th ed.) (e.g., bone is laid down along lines of stress).
Glossary lesion (osteopathic): See osteopathic Lesion. lesioned components: See osteopathic Lesion; somatic dysfUnc-
tion. ligamentous: I. articular strain, any somatic dysfunction resulting in abnormal ligamentous tension or strain ; see strain; Ligamen-
tous strain; osteopathic manipulative treatment, Ligamentous articular strain. I. articular strain technique, see osteopathic manipulative treatment, Ligamentous articular strain. I. strain, motion and/or positional asymmetry associated with elastic deformation of connective tissue (fascia, ligament, membrane). See strain; Ligamentous articular strain. line of gravity: See gravitational Line. localization: 1. In manipulative technique, the precise positioning of the patient and vector app li cation of forces required to produce a desired result. 2. The reference of a sense impression to a particular locali ry in the body. lordosis: 1. The anterior convexiry in the curvature of the lum bar and cervical spine as viewed from the side; the term is used to refer to abnormall y increased curvature (hollow back, saddle back, sway back) and to the normal curvature (normallorr:losis) (Dorland's). See also kyphosis; scoliosis. 2. Hollow back or sadd le back; an abnormal extension deformiry; anteroposte ri o r curvature of the sp ine, generally lumbar with the convexiry looking anter io rly (Stedman's). lordotic: Pertaining to or characterized by lordosis. lumbarization: See transitional segment. lumbolumbar lordotic angle: See angle, !umbo lumbar Lordotic. lumbosacral angle: See angle, Lumbosacral. lumbosacral lordotic angle: See angle, Lumbosacral Lordotic. lumbosacral spring test: See spring test. lymph pumps: See osteopathic manipulative treatment, Lymphatic pump. See also pedal pump or thoracic pump.
M mandibular drainage: Soft tissue manipulative technique using passively induced jaw motion to effect increased drainage of middle ear st ru ctures via the eustachian tube and lymphatics. manipulation: T herapeutic application of manual force. See also technique. manual medicine: Defined by the International Federation of Manual/Manipulative Medicine (FIMM). massage: Therapeutic friction, stroking, and knead ing of the body. See also osteopathic manipulative treatment, soft tissue
technique. mechanoreceptor: A receptor excited by mechanical pressures or distortions, such as those responding to touch and muscular contractio ns (Dorland's). membranous articular strain: Any cranial so m atic dysfu nction resulting in ab normal dural membra ne tensio ns. membranous balance: The ideal physiologic state of ha rm onious equilibrium in the tensio n of th e dura mater of the brain and spi nal cord. middle transverse axis: See sacral, s. motion axis, middle trans-
verse axis (postural).
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mid-heel line: A vert ical line used as a reference in standing anteroposterior radiographs and postural evaluation, passing equidistant between the heels. mid-malleolar line: A vertical line passing through the latera l malleolus, used as a point of reference in stand ing lateral radiographs and postural evaluation. motion: 1. A chan ge of position (rotation, and/or translation) with respect to a fixed system . 2. An act or process of a body changing position in terms of direction , co urse, and velociry. active m., movement produced volunta ril y by the patient. inherent m., spontan eous motion of every cell , organ, system, and their component units within the body. m. barrier, see barrier (motion barrie1). passive m., motion induced by the physician whi le the patient remains passive or rel axed. physiologic m., changes in position of body structu res within the normal range. See also physiologic motion ofthe
spine. translatory m.,
motion of a body parr along an ax is. See
translation. muscle energy technique:
See osteopathic manipulative treat-
ment, muscle energy. See osteopathic manipulative treatment, myofasciaf release. myofascial technique: See osteopathic manipulative treatment, myofascia! technique. myofascial trigger point: See trigger point.
myofascial release technique:
myotome: 1. All muscles derived from one somite and inne rvated by one segmental spinal nerve. 2. That part of the somite that develops into skeletal muscle (Stedman's) .
N Neidner, W: See fascial patterns. neurotrophicity: See neurotrophy. neurotrophy: T he nutrition and maintenance of tissues as regul ated by direct innervation. neutral: l. T he range of sagittal plane spi nal positioning in w hi ch the first principle of physiologic motion of the spine app lies (Fig. 18). See physiologic motion of the spine. 2. T he point of balance of an articul ar surface from w hi ch all the motions physiologic to that articulation may rake place. NMM-OMM: Osteopathic neuromusculoskeletal medicine, certification granred by the American Osteopathic Association through the American Osteopathic Board of Neuro muscul oskeletal Medicine. First gra nted in 1999. nociceptor: A peripheral nerve organ or mechanism for the ap preciation and transmission of painful or injurious stimuli
(Stedman's). nonneutral: T he range of sagittal plane spinal positioning in which th e second principle of physiologic motion of the spine applies. See physiologic motion ofthe spine. normalization: T he therapeutic use of anatom ic and physio logic mechanisms to faci litate the body's response towa rd ho meos tas is and improved health. NSR: A descriptor of spinal somatic dysfunction used to denote a combination neutral (N), side-benr (S), and rotated (R)
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Glossary
FIGURE 18. Neutral sp inal position .
verteb ral position; similar descriptors may involve flexed (F) and extended (E) position. nutation: Nodding forward; anterior movement of the sacral base aro und a transverse axis in relation to the ilia (Fig. 11).
0 oblique axes of the sacrum: See sacra!, s. motion axis, oblique (diagonal). OMM: See osteopathic manipulative medicine. OMT: See osteopathic manipulative treatment. ONM: See NMM-OMM. OP&P: Osteopathic principles and practice. -os1s: word element [Greek], disease; morbid state; abnormal mcrease. osteopath: a perso n who has ach ieved the nationally recognized academic and professional standards within their country to independently practice diagnosis and treatment based upon the principles of osteopathic philosophy. Individual countries establish the national academic and professional standards for osteopaths practicing within their co untries (International usage). 2. Co nsidered by the American Osteopathic Associatio n to be an archaic term when applied to graduates of U.S . schools. osteopathic lesion (osteopathic lesion complex): Term origin ally used to identify what is currently defined as somatic dysfunction. See somatic dysfunction. osteopathic manipulative medicine (OMM): T he application of osteopathic philosophy, structural diagnosis, and use of OMT in the diagnosis and management of the patient. osteopathic manipulative treatment (OMT): T he therapeutic appli cation of man ually guided forces by an osteopathic
physician to improve physiologic function and/or support homeostasis that have been altered by somatic dysfunction . OMT employs a variety of techniques including: active method, technique in which the person voluntaril y performs a physician-directed motion. articulatory treatment (ART) system, a low velocity/ moderate-to-high amplitude technique where a joint is carried through its full motion with the therapeutic goal of increased freedom range of movement. T he activating force is either a springing motion or repetitive concentric movement of the joint through the restrictive barrier. balanced ligamentous tension (BLT /LAS), see ligamentous articular strain. combined method, 1. Treatment strategy where the initial movements are indirect; as the technique is completed the movements change to direct forces. 2. A manipulative sequence involving two or more osteopathic manipulative treatment systems (e.g., Spencer technique combined with muscle energy techniq ue). 3. A concept described by Paul Kimberly, DO . compression of the fourth ventricle (CV-4), acranial technique in which the lateral angles of the occipital squam a are manually approximated, slightly exaggerating the posterior convexity of the occiput and taking th e cranium in to sustained extension. counterstrain (CS), a system of diag nosis and treatment that considers the dysfunction to be a continuing, inappropriate strain reflex, which is inhibited by applying a position of mild strain in the directio n exactly opposite to that of the reflex; this is acco mplish ed by specific directed positioning about the point of te nderness w achieve the desired therapeutic response. 2. Developed by Lawrence Jones, DO. Australian and French use: Jones technique (correction spontaneous by position), spontaneous release by position or strain/counterstrain. cranial treatment (CR), see primary respiratory mechanism; osteopathy in the cranialfie!d. CV-4, Abbreviation for compression of the fourth ventricle. See osteopathic manipulative treatment, compression of the fourth ventricle. Dalrymple treatment, see pedal pump. direct method (D/DIR), any osteopathic treatment strategy by which the restrictive barrier is engaged and a final activating force is applied to co rrect somatic dysfunction. exaggeration method, any osteopathic treatment strategy by which the dysfunctional component is carried away from the restrictive barrier and beyond the range of voluntary motion to a point of palpably increased tension. exaggeration technique, an indirect procedure that in volves carrying the dysfunctional part away from the restrictive barrier, then applying a high velocity/low amplitude force in the same direction. facilitated positional release (FPR), a system of indirect myofascial release treatment developed by Stanley Schiowitz, DO. The component region of the body is placed into a neutral position, diminishing tissue and·joint tension in all planes and an activati ng force (compression or torsion) is added.
Glossary
fascial release treatment, see myofascial release technique. fascial unwinding, a manual technique involving constant feedback to the physician who is passively moving a por. tio n of the patient's body in response to the sensation of movement. Its forces are localized using the sensations of ease and bind over wider regions. functional method, an indirect approach which involves findin g the dynamic balance point and one of the following: applying an indirect guiding force; holding the pos ition, o r adding compression to exaggerate the positio n and allow for spo ntaneous readjustment. The physician guides the manipulative procedure while the dysfunctional area is being palpated in order to obtain a continuous feedback of the physiologic response to induced motion; th e phys ician guides the dysfunctional part so as to create a decreasin g sense of tissue resistance (increased compliance). Galbreath treatment, see osteopathic manipulative treatment, mandibular drainage. hepatic pump, rhythmi c compression applied over the liver for purposes of increasing blood flow through the liver and enhancing bile and lymphatic drainage from the liver. indirect method (1/IND), a manipulative technique where the restrictive barrier is disengaged; the dysfunctional body part is moved away from the restrictive barrier until tissue tension is equal in one or all planes and directions. inhibitory pressure technique, the application of steady pressure to soft tissues to reduce refl ex activity and produce relaxatio n. integrated neuromusculoskeletal release (INR), a treatment system in which combined procedures are designed to stretch and reflexly release patterned soft tissue and jointrelated restrictions. Both direct and indirect methods are used interactively. ligamentous articular strain (LAS/BLT), a set of myofascial release techniques described by Howard Lippincott, DO, and Rebecca Lippin cott, DO. liver pump, see hepatic pump. lymphatic pump, a te rm coined by C. Earl Miller, DO, to describe the impact of intrathoracic pressure changes o n lymphati c fl ow; thi s was the name originally given to the tho racic pump technique before the more extensive physiologic effects of the technique were recognized. mandibular drainage, soft tissue manipulative technique using passively induced jaw motion to effect increased d ra inage of middl e ear structures via the eustachian tube and lymphatics . mesenteric release (mesenteric lift), technique in which tensio n is taken off the attachment of the root of the mesentery to the posterior body wall. Simultaneously the abdominal co ntents are compressed to enhance venous and lymphatic drainage from the bowel. muscle energy, l. A system of diagnosis and treatment in whi ch the patient voluntarily moves the body as specifically directed by th e physician; this directed patient action is fro m a precisely controlled position , against a defined resistance by the physician. 2. Refers to a concept first used by
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Fred L. Mitchell , Sr., DO, originally called muscle energy treatment. myofascial release (MFR), system of diagnosis and treatment first described by Andrew Taylor Still and his early students, which engages continual palpatory feedback to achieve release of myofascial tissues. direct MFR, a restrictive barrier is engaged for the myofascial tissues; the tissue is loaded with a constant force until tissue release occurs. indirect MFR, dysfunctional tissues are guided along the path ofleast resistance until free movement is achieved. myofascial technique, any technique directed at the muscles and fascia. See also myofascial release; soft tissue treatment. myotension, a system of diagnosis and treatment that uses muscular contractions and relaxations under resistance of the osteopathic practitioner to relax, strengthen, or stretch muscles or mobilize joints. osteopathy in the cranial field (OCF): 1. System of diagnosis and treatment by an osteopathic practitioner using the primary respiratory mechanism and balanced membranous tension. See also primary respiratory mechanism. 2. Refers to the system of diagnosis and treatment first described by William G. Sutherland, DO. 3. Tide of reference work by Harold Magoun, Sr. , DO. passive method, based on techniques in which the patient refrains from voluntary muscle contraction. pedal pump, a venous and lymphatic drainage technique applied through the lower extremities; also called the pedal fascial pump or pedal pump; also known as Dalrymple treatment. percussion vibrator technique, 1. A manipulative technique involving the specific application of mechanical vibratory force to treat somatic dysfunction. 2. An osteopathic manipulative technique developed by Robert Fulford, DO. positional treatment, a direct segmental technique in which a combination ofleverage, patient ventilatory movements, and a fulcrum are used to achieve mobilization of the dysfunctional segment; may be combined with spri nging or thrust technique. progressive inhibition of neuromuscular structures (PINS), a system of diagnosis and treatment in which the osteopath locates two related points and sequentially applies inhibitory pressure along a series of related points between the two points. 2. Developed by Dennis Dowling, DO. range of motion technique, active or passive movement of a body part to its physiologic or anatom ic limit in any or all planes of motion. soft tissue (ST), a system of diagnosis and treatment directed toward tissues other than skeletal or arthrodial elements. soft tissue technique, a direct technique which usual ly involves lateral stretching, linear stretching, deep pressure, traction, and/or separation of muscle origin and insertion while monitoring tissue response and motion changes by palpation; also called myofascial technique.
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Glossary
Spencer technique, a series of direct manipulative procedures to prevent or decrease soft tissue restrictions about the shou lder. See also osteopathic manipulative treatment OMT, articulatory treatment (ART). splenic pump technique, rhythmic compression applied over the spleen for the purpose of enhancing the patient's immune response. See also osteopathic manipulative treatment OMT, lymphatic pump. springing technique, a low velocity/moderate amplitude technique where the restrictive barrier is engaged repeatedly to produce an increased freedom of motion. StiU technique, 1. Characterized as a specific nonrepetitive articu larory method that is indirect then direct. A system of diagnosis and treatment attributed to A.T. Still. 2. A term co in ed by Richard Van Buskirk, DO, PhD . thoracic pump, a technique developed by C. Earl Miller, DO, which consists of intermittent compression of the thoracic cage. thrust treatment (HVLA), a direct technique which uses high velocity/low amplitude forces; also called mobilization with impulse treatment. toggle technique, short lever technique using compression and shearing forces. traction treatment, a procedure of high or low amplitude in which the parts are stretched or sepa rated along a longitudinal axis with continuous or intermittent force. v-spread, technique using forces transmitted across the diameter of the skull to accomplish sutural gapping. ventral techniques, see osteopathic manipulative treatment, visceral manipulation. visceral manipulation (VIS), a system of diagnosis and treatment directed to the viscera to improve physiologic function; typically the viscera are moved toward their fascial attachments to a point of fascial balance; also called ventral techniques. osteopathic medicine: A complete system of medical care with a philosophy that combines the needs of the patient with the current practice of medicine, surgery, and obstetrics, that emphasizes the interrelationship between structure and function and that has an appreciation of the body's ability to heal itself. osteopathic philosophy: A concept of health care supported by expanding scientific knowledge that embraces the concept of the unity of the living organism's structure (anatomy) and function (physiology). Osteopathic philosophy emphasizes the following principles: (a) The human being is a dynamic unit of function . (b) The body possesses self-regularory mechanisms that are self-healing in nature. (c) Structure and function are interrelated at all levels. (d) Rational treatment is based on these principles. osteopathic physician: a person with full, unlimited medical practice rights who has achieved the nationally recognized academic and professional standards within their country to practice diagnosis and treatment based upon the principles of osteopathic philosophy. Individual countries establish the national academic and professional standards for osteopathic physicians practicing within their countries. osteopathic postural examination: The part of the osteopathic musculoskeletal examination that focuses on the static
and dynamic responses of the body ro gravity while in the erect position. osteopathic structural examination: The examination of a patient by an osteopathic physician with emphasis on the neutomusculoskeletal system including palparory diagnosis for somatic dysfunction and viscerosomatic change, in the context of total patient care. The examination is concerned with range of motion of all parts of the body, performed with the patient in multiple positions to provide static and dynamic eval uation. osteopathy (osteopathic medicine): A system of medical care with a philosophy that combines the needs of the patient with current practi ce of medicine, surgery, and obstetrics, and emphasizes the interrelationships between structure and function, and an appreciation of the body's ability to heal itself. See osteopathic philosophy.
p palpation: The app lication of the fingers to the surface of the ski n or other tissues, using varying amounts of pressure, to selectively determine the condition of the parts beneath. palpatory diagnosis: A term used by osteopathic physicians to denote the process of palpating the patient to evaluate the neuromusculoskeletal and visceral systems. palpatory skills: , Sensory ski lls used in performing palparory diagnosis and osteopathic manipul ative treatment. passive motion: See motion, passive m. patient cooperation: Voluntary movement by the patient (on instruction from the operator) to assist in the palparory diagnosis and treatment process. pedal pump: See osteopathic manipulative treatment, pedal pump. pelvic bone: See hip bone. pelvic declination (pelvic unleveling): Pelvic rotat;on about an anteroposterior axis. pelvic index: An objective radiographic measurement representing the relative positions of the sacrum and inn ominates; normal values are age related and increase in subjects with sagittal plane postural decompensation. pelvic rotation: Movement of the entire pelvis in a relarively horizontal plane about a vertical (longitudinal) axis. pelvic side-shift: Deviation of the pelvis ro the right or left of the central vertical axis as translation along rhe horizontal (z) axis, usually observed in the standing position. pelvic tilt: Pelvic rotarian abour a rransverse (horizontal) axis (forward or backward rilr) or abour an anteroposrerior axis (right or left side tilr). percussion vibrator technique: See osteopathic manipulative treatment, percussion vibrator technique. petrissage: Deep kneading or squeezing action ro express swelling. physiologic barrier: See barrier (motion barrier), physiologic b. physiologic motion: See motion, physiologic. physiologic motion of the spine: Principles I and II of rhoracic and lumbar sp inal motion described by Harrison H. Fryerre, DO, C.R. Nelson, DO (1948); see rotation; r. ofvertebra. The
Glossary
FIGURE 19. Physiologic motion ofthe spine (type 1). Sid e-bending and rotation from neutral.
three major principles of physiologic motion are: I: When the thoracic and lumbar spine is in a neutral position (Fig. 18) (easy normal), the coupled motions of side-bending and rotation for a group of vertebrae are such that side-bending and rotation occur in opposite directions (with rotation occurring toward the convexity) (Fig. 19); see somatic dysfimction, type I. II: When the thoracic and lumbar spine is sufficiently forward or backward bent (nonneutral), the coupled motions of side-bending and rotation in a single vertebral unit occur in the same direction (Fig. 20). See somatic dysfunction, type II. III: Initiating motion of a vertebral segment in any plane of motion will modify the movement of that segment in other planes of motion.
plagiocephaly: An asymmetric condition of the head. plane: A Aat surface determined by the position of three points in space; any of a number of imaginary surfaces passing through the body and dividing it into segments (Fig. 21). coronal p., frontal plane. frontal p., a plane passing longitudinally through the body from one side to the other, and dividing the body into anterior and posterior portions. sagittal p., a plane passing longitudinally through the body from front to back and dividing it into right and left portions; the median or midsagittal plane divides the body into approximately equal right and left portions.
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FIGURE 20. Physiologic motion of the spine (type II). Forward-bending and side-bending from a nonneutral position.
transverse p., a plane passing horizontally through the body perpendicular to the sagittal and frontal planes, dividing the body into upper and lower portions. plastic deformation: A nonrecoverable deformation. See also elastic deformation. plasticity: Ability to retain a shape attain ed by deformation . See also elasticity; viscosity. posterior component: A positional descriptor used to identify the side of reference when rotation of a vertebral segment has occurred; in a condition of right rotation, the right side is the posterior component; usually refers to a prominent transverse process; see also anterior component. postural balance: A condition of optimal distribution of body mass in relation to gravity. postural decompensation: Distribution of body mass away from ideal when postural homeostatic mechanisms are overwhelmed; occurs in all cardinal planes bur is classified by rhe major plane(s) affected (Fig. 21). coronal plane p. d., scoliotic changes. horizontal plane p. d., rotational changes. sagittal plane p. d., kyphotic and/or lordotic changes. postural imbalance: A condition in which ideal body mass distribution is not achieved. posture: Position of the body; the distribution of body mass in relation to gravity. primary machinery of life: The neuromusculoskeletal system; a term used by l.M. Korr, Ph.D., to denote rhat body parts acr together to transmit and modify force and motion through which man acts out his life. This integration is achieved via the central nervous system acting in response
1244
Glossary
Planes of the body FIGURE 21. Pl anes of the body.
to continued sensory input from the internal and external environment. primary respiratory mechanism: A model proposed by William G. Sutherland, DO, to describe the interdependent functions amo ng five body components as follows: a: T he inherent motility of the brain and spinal cord. b: Fluctuatio n of the cerebrosp inal fluid. c: Mobili ty of the inrracranial and intraspinal membranes. d: Articular mobility of rhe cranial bones. e: The involuntary mobility of the sacrum between the ilia (pelvic bones). See also osteopathic manipulative treatment,
osteopathy in the cranial field. primary, refers to the internal tissue respiratory process. respiratory, refers to the process of internal respiration (i.e., the exchange of respiratory gases between tissue cells and their internal environment, consisting of the fluids bathing rhe cells). mechanism, refers to the interdependent movement of tissue and fluid with a specific purpose. prime mover: A muscle prim arily responsible for causing a specific joint action. progressive inhibition of neuromuscular structures (PINS): See osteopathic manipulation, progressive inhibition of neuromuscular structures. prolotherapy: See sclerotherapy. pronation: In relation to the anatomic position, as applied to the hand, rotat ion of the forearm in such a way that the palmar surface turns backward (internal rotat ion) in relationship to the anatomic position. Appli ed to the foot, a combination of eversion and abduction movements taking place in the tarsal
and metatarsal joints, resulting in lowering of the medial margin of the foot. See also supination. prone: Lying face downward (Dorland's). proprioception: The sensing of motion and position of the body. proprioceptor: Sensory terminals fo und in muscles, tendons, and joint capsules which give information co ncernin g movements and position of rhe body (Dorland's). psoas syndrome: A painful low back condition characterized by hypertonicity of psoas musculature. The syndrome consists of a constellation of typ ical related signs and sym ptoms: typical associated somatic dysfunctions, as a long resrrictor muscle, psoas hypertonicity is often associated with flexed dysfunctions of the upper lum bars, extended dysfunction of L5, and variable sacral and innominate dysfunctio ns. Tender points typical ly are Found in the ipsi lateral iliacus and contralateral piriformis muscles. typical gait, Trendelenburg gait. typical pain pattern, low back pain often accompanied by pain o n the lateral aspect of the lower extrem ity extending no lower than the knee. typical posture, flexion at the hip and side-bending of the lumbar spine to the side of the most hypertoni c psoas muscle. pubic bone, somatic dysfunctions of: anterior pubic shear, a somatic dysfunction in which one p ubic bone is displaced anteriorly with relation to its normal mate. inferior pubic shear, a somatic dysfunction in which one pubic bone is displaced inferiorly with relation to irs normal mate. posterior pubic shear, a somatic dysfunction in which one pubic bone is displaced posteriorly with relation to its normal mate. pubic abduction, see pubic gapping. pubic adduction, see pubic compression. pubic compression (p. adduction), a somatic dysfunction in which the pubic bones are forced toward each other at the pubic symphys is. This dysfun ction is characterized by tenderness to palpation over rhe pubi c symphysis, lack of apparent asymmetry, but associated with restricted motion of the pelvic ring. pubic gapping (p. abduction), a so matic dysfun cti on in which the pubic bones are pulled away from each other at the pubic symphysis . T his dysfun ction is often seen in women following childbirth . superior pubic shear, a somatic dysfunction in which one pubic bone is displaced superiorly with relation ro irs normal mate. pubic symphysis: Somatic dysfunctions of. See pubic bone, so-
matic dysfunctions of pump handle rib motion: Movement of the ribs durin g respiration such that with inhalation the anterior aspect of the rib moves cephalad and causes an increase in the anteroposteri or diameter of the tho rax. This type of rib motion is found predominantly in the upper ribs (Fig. 7), decreasing from "the upper to the lower ribs. See axis of rib motion; bucket handle rib motion.
Glossary
R recip.rocal inhibition: The inhibition of antagonist muscles when the agonist is stimulated. See also law, Sherrington. reciprocal tension membrane: The intracranial and spinal dural membrane including the falx cerebri, falx cerebelli, tentorium, and spinal dura. reflex: An involuntary nervous system response to a sensory input. The sum total of any particular involuntary activity. See also Chapman reflex. cervicolumba.r r., automatic contraction of the lumbar parave·rrebral muscles in response to contraction of postural muscles in the neck. conditioned r., one that does nor occur naturally in the organism or system bur that is developed by regular association of some physiologic function with an unrelated outside event; soon the physiologic function starts whenever the outside event occurs. See also focilitation; somatic dysfUnction. oculocephalogyric r., (oculogyric reflex, cephalogyric reflex), automatic movement of the head which leads or accompanies movement of the eyes. red r., 1. The erythematous biochemical reaction (reactive hyperemia) of the skin in an area that has been stimulated mechanically by friction; the reflex is greater in degree and duration in an area of acute somatic dysfunction as compared to an area of chronic somatic dysfunction. It is a reflection of the segmentally related sympathicotonia commonly observed in the paraspinal area. 2. A red glow reflected from the fundus of rhe eye when a light is cast upon the retina. soma to-somatic r., localized somatic srimul i producing parterns of reflex response in segmentally related somatic structures. somatovisceral r., localized somatic stimulation producing patterns of reflex response in segmentally re lated visceral structures. viscerosomatic r., localized visceral stimuli producing patterns of reflex response in segmentally related somatic structures . viscero-visceral r., localized visceral stimuli producing patterns of reflex response in segmentally related visceral structures. regenerative injection therapy (RIT): See sclerotherapy. region: An anatomic division of the body defined by either natural , functional, or arbitrary boundaries. 2. Body areas as defined in the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) using the codes 739.0 to 739.9. See also transitional region. resilience: Property of returning to the former shape or size after mechanical distortion. See also elasticity; plasticity. respiratory axis of the sacrum: See sacral motion, superior transverse axis (respiratory). respiratory cooperation: A physician-directed inhalation and/or exhalation by the patient to assist the manipulative treatment process. restnctton: A resistance or impediment to movement; for joint restriction. See barrier (motion barrier).
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Anatomical vertical axis (y)
FIGURE 22. Rotation of the vertebra (thoracic).
retrolisthesis: Posterior displacement of one vertebra relative to the one immediately below. rib dysfunction (rib lesion): A somatic dysfunction in which movement or position of one or several ribs is altered or disrupted; for example, an elevated rib is one held in a position of inhalation such that motion toward inhalation is freer, and motion toward exhalation is restricted. A depressed rib is one held in a position of exhalation such that motion toward exhalation is freer, and there is a restriction in inhalation. See also inhalation rib; exhalation rib. rib motion: See axis of rib motion; bucket handle rib motion; pump handle rib motion; caliper rib motion. ropiness: A tissue texture abnormality characterized by a cordlike feeling. See also tissue texture abnormality. rotation: Motion about an axis. r. dysfunction of the sacrum, see sacrum, somatic dysfUnctions of r. of sacrum, movement of the sacrum about a vertical (y) axis (usually in relation to the innominate bones). r. of vertebra, movement about the anatomic vertical axis (y axis) of a vertebra; named by the motion of a midpoint on the anterior superior surface of rhe vertebral body (Fig. 22). rule of threes: A method to locate rhe approximate position of the transverse process (TP) of a thoracic segment by using the location of the spinous process (SP) of that same vertebra. The relationship is as follows:
Tl ro T3:
T4 to T6: T7 to T9: TIO:
Tll: Tl2:
TP is at the same level as tip of the SP TP is one half vertebral level above the tip of the SP TP is one full vertebral level above the tip of the SP TP is one full vertebral level above the tip of the SP TP is one half vertebral level above the tip of the SP TP is at the same level as the tip of the SP
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Glossary
s Sacral: s. base, 1. In osteopathic palpation, the uppermost posterior portion of the sacrum. 2. The most cephalad portion of the first sacral segment (Gray's Anatomy). s. base declination (unleveling}, with the patient in a standing or seated position, any deviation of the sacral base from the horizontal in a coronal plane; generally, the rotation of the sacrum about an anterior-posterior axis. s. base unleveling, see s. base declination sacralization, see transitional vertebrae. s. motion axis, motion of the sacrum about any of its hypothetical axes (Fig. 23). anterior-posterior (x} axis, axis formed at the line of imersection of a sagittal and transverse plane (Fig. 23). inferior transverse axis (innominate}, the hypothetical functional axis of ilia! motion proposed by Fred Mitchell, Sr, DO, that passes from side to side on a line through the inferior auricular surface of the sacrum and ili a, and represents the axis for movement of the ilia on the sacrum (Fig. 24). longitudinal axis, the hypothetical axis formed at the line of imersection of the midsagittal plane and a coronal plane, see sacral, s. motion axis, vertical axis (y) axis . (longitudinal) (Fig. 23). middle transverse axis (postural}, the hypothetical functional axis of sacral nutation/counternutation in the standing position proposed by Fred Mitchell, Sr, DO, passing horizontally through the anterior aspect of the sacrum at the level of the second sacral segment (Fig. 24). . . oblique axis (diagonal}, a hypothetical functional axis proposed by Fred Mitchell, Sr, DO, that is from the superior area of a sacroi liac articulation to the contrala~eral inferior sacroiliac articulation; it is designated as nght or left relevant to its superior point of origin (Fig. 23). postural axis, see sacral, s. motion axis, middle transverse axis (postural) (Fig. 24). respiratory axis, see sacrum, s. motion axis, superior transverse axis (respiratory) (Fig. 24). superior transverse axis (respiratory}, the hypothetical transverse axis about which the sacrum moves dunng the respiratory cycle proposed by Fred Mitchell, Sr, DO;
Superior transverse axis (respiratory axis) Middle transverse axis (postural axis)
Inferior transverse axil (hip bone axis)
FIGURE 24. Sacral transverse axis.
it passes from side to side through the articular processes posterior to the poim of attachment of the dura at the level of the second sacral segment; involuntary sacral motion occurring as a part of the craniosacral mechanism is believed to occur about this axis (Fig. 24} . transverse (z) axes, axes formed by intersection of the coronal and transverse planes about which nutation/counternutation occurs (Fig. 24). vertical (y) axis (longitudinal), the axis formed by the intersection of the sagittal and coronal planes (Fig. 23). s. somatic dysfunction, see sacrum, somatic dysfunctions of s. sulcus, a depression just medial to the posterior spine iliac spine (PSIS) as a result of the spatial relationship of the PSIS to the dorsal aspect of the sacnun (Fig. 25). s. torsion, 1. A physiologic function occurring in the sacrum during ambulation and forward bending. 2. A sacral somatic dysfunction around an oblique axis in which a torque occurs between the sacrum and innominates. The L5 vertebra rotates in the opposite direction of the sacrum. 3. If the L5 does not rotate opposite to the sacrum, L5 is
Test sulcus depth here
Sulcus
Middleaxts ~~~--~~- -
' I
Left ll.A - 4 - (anterior posterior) Sacrotuberous ligament Axe• of sacral motion
FIGURE 23. Axes of sacral motion.
rlLA I
Right !LA (superior/inferior)
FIGURE 25. Sacral sulcus, anatomic base, clinical base, and inferior lat· era I angles (JLA) of the sacrum.
Glossary
termed maladapted. 4. Other terms for this maladaption include: rotations about an oblique axis; anterior or pos. terior sacrum, and a torsion with a noncompensated L5 (Archaic use). See also sacrum, somatic dysfunctions of sacrum, somatic dysfunctions of, any of a group of somatic dysfunctions involving the sacrum. These may be the result of restriction of normal physiologic motion or trauma to the sacrum. See also TART anterior sacrum, a positional term based on the Ch icago model referring to sacral somatic dysfunction in which the sacral base has rotated anterior and sidebent to the side opposite the rotation. The upper limb of the sacroiliac joint has restricted motion and is named for the side on which forward rotation has occurred. Tissue texture changes are found at the deep sulcus. anterior translated sacrum, a sacral somatic dysfunction in which the entire sacrum has moved anteriorly (forward) between the ilia; anterior motion is freer, and there is a restriction to posterior motion (Fig. 26). backward torsions, l . A backward sacral torsion is a physiologic rotation of the sacrum around an oblique axis such that the side of the sacral base contralateral to the named axis rotates posteriorly. L5 rotates in the direction opposite to the rotation of the sacral base. 2. Referred to as non neutral sacral somatic dysfunctions (Archaic use). Fred Mitchell, Sr, DO , described the backward torsion as being nonphysiologic in terms of the walking cycle. bilateral sacral extension (sacral base posterior), 1. A sacral somatic dysfunction that involves rotation of the sacrum about a middle transverse axis such that the sacral base has moved posteriorly relative to the pelvic bones; backward movement of the sacral base is freer, forward movement is restricted , and both sulci are shallow. 2. The reverse of bilateral sacral flexion (Fig. II) . bilateral sacral flexion (sacral base anterior), 1. A sacral somatic dysfunction that involves rotation of the sacrum about a middle transverse axis such that the sacral base has moved anteriorly between the pelvic bones; forward movement of the sacral base is freer, backward movement
FIGURE 26. Anterior translated sacrum.
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is restricted, and both sacral sulci are deep. 2. The reverse of bilateral sacral extension (Fig. 15) . forward torsions, I. A group of somatic dysfunctions described by Fred Mitchell, Sr, DO, based on the motion cycle of walking. Forward torsion is a physiologic rotation of the sacrum aro und an oblique ax is such that the side of the sacral base contralateral to the named axis glides anteriorly and produces a deep sulcus. L5 rotates in the direction opposite to the rotation of the sacral base. 2. Referred to as neutral sacral somatic dysfunctions (Archaic use). left on left (forward) sacral torsion, refers to left rotation torsion aro und a left oblique axis. See sacrum, somatic dysfunctions of sacral torsions. left on right (backward) sacral torsion, refers to left rotation around a right oblique ax is. See sacrum, somatic dysfunctions of sacral torsions. posterior sacrum, a positional term based on the C hicago model referrin g to a sacral somatic dysfunction in which the sacral base has rotated posterior and sidebent to the side opposite to the rotation. T he dysfunction is named for the side on which the posterior rotation occurs. The tissue texture changes are found at the lower pole on the side of rotation . posterior translated sacrum, a sacral somatic dysfunction in which the entire sacrum has moved posteriorl y (backward) between the ili a; posterior motio n is freer, and there is a restriction to anterior motion (Fig. 27). right on left (backward) torsion, Refers to ri ght rotation about a left oblique axis. See sacrum, somatic dysfunctions of sacral torsions. right on right (forward) torsion, Refers to right rotation about a right oblique axis . See sacrum, somatic dysfunctions of sacral torsions. rotated dysfunction of the sacrum, a sacral so matic dysfunction in which the sacrum has rotated about an axis approximating the longitudinal (y) axis; motion is freer in the direction that rotation has occurred , and is restricted in the opposite direction. sacral shear, a complex nonphysiologic translational
FIGURE 27. Posterior translated sacrum.
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Glossary unilateral sacral flexion, is a sacral so matic dysfunction described as an inferior shear of one side of the sacrum resulting in a deep sacral sulcus and ipsilateral inferior-posterior inferolareral angle of the sacrum. See sacrum, sacral shear. scan: An intermediate derailed examination of specific body regions which have been identified by findings emergin g from the initial examination. scaphocephaly: Also cal led scapho id head or hatchet head , it is a transverse compression of the cranium with a resultant midsagittal ridge. sclerotherapy: 1. Treatment involving injection of a proliferant solution at the osseous-ligamentous junction. 2. Treatment involving inj ection of irritating substances into weakened connective tissue areas such as fasciae, varicose veins, hemo rrhoids, esophageal varices, or weakened ligamenrs. The intended body's response to the irriranr is fibrous proliferation with shortening/strengthening of the tissues inj ected. sclerotome: l. Sclerotomal area; the pattern (Fig. 28) of innervation of structures derived from embryonal mesenchyme (joint capsule, ligament, and bone) . 2. The area of bone
motion of the sacrum in its relationship to the innominates. (Sometimes described as a side-bending in one direction and rotation in the opposite direction. Alternatively described as a unilateral movement along the arc of the L-shaped curve of the sacroiliac joint.) See also sacrum,
unilateral sacral flexion; sacrum, unilateral sacral extension. sacral torsions, a group of physiologic motions and somatic dysfunctions of the sacrum around an oblique axis, in which a torque occurs between the sacrum and innominates. T he L5 vertebra usually rotates in the direction opposite the sacrum. (If the L5 does not compensate, it is maladap ted. Other terms for this maladaption include: rotations abo ut an oblique axis; anterior or posterior sacrum, and a torsion with a noncompe nsared L5.) See sacrum, somatic dysfunctions of unilateral sacral extension, is a sacral somatic dysfunction described as a superior shear of one side of the sacrum resulting in a shallow (full ) sacral sulcus and ipsilateral superi or-anterior inferolareral angle of the sacrum. See sacrum, sacral shear.
Key to ID of cervicals, thoracics, lumbar and sacral nerves
9 12
II
6 9 12
Sl
S2
FIGURE 28. Anterior and posterior sclerotomal innervations.
Glossary
innervated by a si ngle spinal segment. 3. The group of mesenchymal cells emerging from the ventromedial part of a m.esodermal somite and migrating toward the notochord . Scleroromal cells From adjacent somites become merged in imersomatically located masses that are the primordia of the centra of the vertebrae. (sclerotomal) pain, deep, dull achy pain associated with tissues derived from a common sclerorome (Fig. 28). screen: The scan focuses o n segmental areas for further definition or diagnosis. scoliosis: 1. Pathologic or functional lateral curvature of the spine. 2. An app reciable lateral deviation in the normally straight verTical line of the spine (Dorland's) (Fig. 29). screen: T he initial general somatic examination to determine signs of somatic dysfunction in various regions of the body. See also scan. secondary joint motion: Involuntary or passive motion of a joint. Also called accessory joint motion. segment: A portion of a larger body or structure set off by natural or arbitrarily established boundaries, often equated with spinal segment. l. To describe a single vertebra, such as avertebral segment. 2. A portion of the spinal cord corresponding to the oites of origin of rootlets of individual spinal nerves. segmental diagnosis: The final stage of the spinal somatic examination in which the narure of the somaric problem is detailed at a segmental level. See also scan; screen. segmental motion: Movemem within a vertebral unit described by displacement of a point at the anterior-superior aspect of the superior vertebral body. sensttu.ation: Hypothetically, a short-lived (m inutes or hours) increase in central nervous system (CNS) response to repeated sensory stimulation that generally follows habituation (q.v.). shear: An action or force causi ng or tending to cause two contiguous parts of an articulation to slide relative to each other
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FIGURE 30. Side bent.
in a direction parallel to their plane of contact (e.g., pubic shear (q.v.}; sacral shear, innominate shear). Sherrington law: See law, Sherrington. side bending: Movement in a coronal (fro ntal) plane about an amerior-posterior (x) axis. Also called lateral flexio n, lateroflexion, or flexion right (or left) . side bent: The position of any one o r several vertebral bodies after side bending has occurred (Fig. 30). skin drag: Sense of resistance to ligh t traction appl ied to the skin; related to the degree of moisture and degree of sympathetic nervous system activity. soft tissue technique: See osteopathic manipulative treatment, soft tissue technique. somatic dysfunction: Impaired or al tered function of related components of the somatic (body fra mework) system: skeletal, arthrodial, and myofascial structures, and related vascular, lymphatic, and neural elemems. Somatic dysfunction is treatable using osteopathic manipulative treatment. The positional and motion aspects of somatic dysfu nction are best described using at least one of three parameters: (a) the position of a body part as determined by palpation and referenced to irs adjacent defined structure; (b) the directions in which motion is freer; and (c) the directions in which motion is restricted. See also STAR, TART acute s. d., immediate or short-term impairment or altered function of related componems of the somatic (body framework) sysrem; characterized in early stages by vasodilation , edema, tenderness, pain, and tissue contractio n; diagnosed by history and palpatory assessment of tenderness, asymmetry of motion and relati ve position, restriction of motion, and tissue texture change (TART). See also TART chronic s. d., impairment or altered function of rela ted components of the somatic (body framework) system, characterized by tenderness, itchi ng, fibrosi s, paresthesias, tissue contraction; identified by TART (q.v.). See also
TART
FIGURE 29.
Scoliosis.
primary s. d., 1. The somatic dysfunction that maintains a total pattern of dysfunction . See also key lesion. 2. T he initial or first somatic dysfunction to appear temporally. secondary s. d., somatic dysfunction (q. v.) arising either from mechanical or neurophysio logic response subsequent to or as a consequence of other etiologies. type I s. d., 1. A group curve of thoracic and/or lumbar vertebrae in which the freedoms of motion are in neutral with side bending and rotation in opposite directions with maximum rotation at the apex (rotation occurs toward the convexity of the curve) based upon the principles
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Glossary
Transverse axes
FIGURE 31 . Extension (sphenobasilar synchondrosis).
ofFryerre (American usage). 2. Second degree dysfunction based upon the laws of Loverr (French usage). typ e II s. d., thoracic or lumbar somatic dysfunction of a single verrebral unit in which the verrebra is significamly flexed or extended with side-bending and rotation in the same direction (rotation occurs inro the concaviry of the curve) based upon the principles of Fryette (American usage). 2. First-degree dysfunction based upon the laws of Loverr (French usage). somatogen ic: That which is produced by activiry, reaction, and change originating in the musculoskeletal system. somato-somatic reflex: See reflex, somato-somatic reflex. somatovisceral reflex: See reflex, somatovisceral reflex. spasm: (compare with hyperroniciry) a sudden, violem, involuntary comraction of a muscle or group of muscles, arrended by pain and interference with function, producing involumary movemem and disrorrion (Dorland's). Spencer technique: See osteopathic manipulative treatment, Spencer technique. sphenobasilar synchon drosis (symphysis), somatic dysfunctions of: any of a group of somatic dysfunctions involving primarily the interrelationship berween the basilar porrion of the sphenoid (basisphenoid) and the basilar porrion of the occiput (basiocciput). The abbreviation, SBS, is often used in reponing the following somatic dysfunctions: SBS compression, somatic dysfunction in which the basisphenoid and basiocciput are held forced rogether significandy limiting SBS motion. SBS extension, sphenoid and occipur have rotated in opposite directions around parallel transverse axes; the basiocciput and basisphenoid are both inferior in SBS extension with a decrease in the dorsal convexiry berween these rwo bones (Fig. 31). SBS flexion, sphenoid and occiput have rotated in opposite directions around parallel rransverse axes; the basiocciput and basisphenoid are both superior in SBS extension with
FIGURE 32. Flexion (sphenobasilar synchondrosis).
an increase in the dorsal convexiry berween these rwo bones (Fig. 32). lateral strain, sphenoid and occiput have "orated in the same direction around parallel vertical axes; lateral strains of the SBS are named for the position of the basisphenoid, right or lefr (Fig. 33). side-bending/rotation, sphenoid and occiput have rotated in opposite directions around parallel venical axes and rotate in the same direction around an anteroposterior axis; SBS side-bending/rotations are named for the convexiry, right or left (Fig. 34). torsion, sphenoid and occiput have rotated in opposite directions around an ameroposterior axis; SBS rorsions are named for the high greater wing of the sphenoid, right or left (Fig. 35). vertical strain, sphenoid and occiput have rotated in the same direction around parallel transverse axes; vertical strains of the SBS are named for the position of the basisphenoid, superior or inferior (Fig. 36). spondylo-: Combining form denoting relationship w a vertebra, or to the spinal column (Dorland's). spondylitis: Inflammation of verrebrae (Dorland's). spondylolisthesis: Anterior displacement of one verrebra relative ro one immediately below (usually L5 over the body of the sacrum or L4 over L5).
Glossary
1251
Vertical VA
FIGURE 36. Superior vertical strain (sphenobasilar synchondrosis) .
FIGURE 33. Right lateral strain (sphenobasilar synchondrosis).
FIGURE 34. Left side-bending/rotation (sphenobasilar synchondrosis).
FIGURE 35. Right torsion (sphenobasilar synchondrosis).
spondylolysis: Dissolution of a vertebra, aplasia of the vertebral arch, and separation at the pars interarricularis; platyspondylia; prespondylolisthesis. spondylosis: 1. Ankylosis of adjacent vertebral bodies. 2. Degeneration of the intervertebral disc. sprain: Stretching injuries of ligamentous tissue (compare with strain). First degree: microtrauma; second degree: partial tear; third degree: complete disruption. springing technique: See osteopathic manipulative treatment, springing technique. sphinx test: See backward bending test. spring test: 1. A test used to differentiate between backward or forward sacral torsions/rotations. 2. A test used to differentiate bilateral sacral extension and bilateral sacral flexion . 3. A test used to differentiate unilateral sacral extension and unilateral sacral flexion. STAR: A mnemonic for four diagnostic criteria of somatic dysfunction; sensitivity changes, tissue texture abnormality, asymmetry, and alteration of the quality and quantity of range of motion. static contraction: See contraction, isometric c. Still, MD, DO: Andrew Taylor. Founder of osteopathy; 18281917; first announced the tenets of osteopathy on June 22, 187 4, established the American School of Osteopathy in 1892 at Kirksville, MO. still point: A term used by William G. Sutherland, DO, to identifY and describe the brief cessation of rhythm attributed to the fluctuation of cerebrospinal fluid (a component of the primary respiratory mechanism which is observed by palpation during osteopathic manipulative treatment when a point of balanced membranous tension (or balanced ligamentous tension) is achieved. strain: 1. Stretching injuries of muscle tissue. 2. Distortion with deformation of tissue. See also ligamentous, l. strain. stretching: Separation of the origin and insertion of a muscle and/or attachments of fascia and ligaments. stringiness: A palpable tissue texture abnormality characterized by fine or stringlike myofascial structures. structural examination: See osteopathic structural examination. subluxation: 1. A partial or incomplete dislocation. 2. A term describing an abnormal anatomic position of a joint that exceeds the normal physiologic limit but does not exceed the joint's anatomic limit.
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Glossary
FIGURE 37. Symphyseal shear.
superior (upslipped) innominate: See innominate, somatic dysfunctions of, superior innominate shear. superior pubic shear: See pubic bone, somatic dysfunctions of superior transverse axis: See sacral, s. motion axis, superior transverse axis (respiratory); and transverse (z) axes. supination: 1. Beginning in anatomic position, applied to the hand, the act of turning the palm forward (anteriorly) or upward, performed by lateral external rotation of the forearm. 2. applied to the foot, it generally applies to movements (adduction and inversion) resulting in raising of the medial margin of the foot, hence of the longitudinal arch; a compound motion of plantar flexion, adduction and inversion; see also pronation. supine: Lyi ng with the face upward (Dorland's). Sutherland fulcrum: A shifting suspension fulcrum of therecip rocal tens io n membrane located along the straight sinus at the junction of the falx cerebri and tentorium cerebelli. symmetry: The similar arrangement in form and relationships of parts around a common axis, or on each side of a plane of the body (Dorland's). symphyseal shear: The result of an action or force causing or tending to cause the two parts of the symphysis to slide relative to each other in a direction parallel to their plane of contact; it is usually found in an inferior/superior direction but is occas io nally found to be in an anterior/posterior direction (Fig. 37).
T tapotement: Striking the belly of a muscle with the hypothenar edge of the open hand in rap id succession in an attempt to increase its to ne and arterial perfusion. TART: A mnemonic for four diagnostic criteria of somatic dysfunction; t issue texture abnormality, asymmetry, restriction of motion, and tenderness, any one of which must be present for the diagnosis. technic: See technique. technique: Methods, procedures, and details of a mechanical process or surgical operation . [. .. method, treatment, maneuver. .. ] (Dorland's); see also osteopathic manipulative treatment. tenderness: 1. D iscomfort or pain elicited by the physician th rough palpation. 2. A state of unusual sensitivity to touch or pressure (Dorland's). tender points: 1. System of points originally described by
Lawrence Jones, DO, FAAO, in strain/counterstrain diagnosis and treatment; see osteopathic manipulative treatment, counterstrain. 2. Small, hypersensitive points in the myofascial tissues of the body used as diagnostic criteria and treatment monitors. terminal barrier: See barrier (motion), physiologic b. thoracic aperture (superior): See thoracic inlet. thoracic inlet: 1. The functional thoracic inlet consists of T1-4 vertebrae, ribs 1 and 2 plus their costicartilages, and the manubrium of the sternum; see fascia! patterns. 2. The anatomic thoracic inlet consists of T1 vertebra, the first ribs and their costal cartilages, and the superior end of the manubrium (Moore). thoracic pump: See osteopathic manipulative treatment, thoracic pump. thrust: See osteopathic manipulative treatment, thrust treatment (HVLA). tissue texture abnormality (TTA): A palpable change in tissues from skin to periarticular structures that represents any combination of the following signs: vasodilation, edema, flaccidity, hypertonicity, contracture, fibrosis; and the following symptoms: itching, pain , tenderness, paresthesias; types ofTTAs include: bagginess (q.v.), thickening, stringiness (q.v.), ropiness (q.v.), firmness (hardening), increased/decreased temperature, and increased/ decreased moisture. tonus: The slight continuous contraction of muscle which, in skeletal muscles, aids in the maintenance of posture and in the return of blood to the heart (Dorland's). myogenic t., 1. Tonic contraction of muscle dependent on some property of the muscle itself or of its intrinsic nerve cells. 2. Contraction of a muscle caused by intrinsic properties of the muscle or by its intrinsic innervation (Stedman's) . torsion: 1. A motion or state where one end of a part is twisted about a longitudinal axis while the opposite end is held fast or turned in the opposite direction. 2. An unphysiologic motion pattern about an anteroposterior axis of the sphenobasilar symphysis/synchondrosis. 3. See also sacrum, somatic dysfunctions of, sacral torsions. traction: A linear force acting to draw structures apart. transitional region: Areas of the axial skeleton where structure changes significantly lead to funct ional change; transitional areas commonly include the following: occipitocervical (OA) region, typically the OA-atlantoaxial-C2 region is described. cervicothoracic (CT) region, typically C7-Tl. lumbosacral (LS) region, typically L5-S 1. thoracolumbar (TL) region, typical ly TlO-Ll. transitional vertebrae: A congenital anomaly of a vertebra in which it develops characteristic(s) of the adjoining structure or region. lumbarization, a transitional segment in which the first sacral segment becomes like an additional lumbar vertebra articulating with the second sacral segment. sacralization. 1. Incomplete separation and differentiation of the fifth lumbar vertebra (L5) such that it takes on characteristics of a sacral vertebra. 2. When transverse processes of the fifth lumbar (L5) are atypically large, causing pseudoarthrosis with the sacrum and/or ilia(um); referred to as batwing deformity, if bilateral.
Glossary
translation: Motion along an axis. translatory motion: See motion, translatory m. transverse axis of sacrum: See sacral, s, motion axis, transverse (z) axes (Fig. 24). Travell trigger point: See trigger point (myofascial trigger point). treatment, osteopathic manipulative techniques: See osteopathic manipulative treatment. trigger point (myofascial trigger point): A small hypersensitive site that, when stimulated, consistently produces a reflex mechanism that gives rise to referred pain and/or other manifestations in a consistent reference zone which is consistent from person to person. These points were most extensively and systematically documented by Janet Travel!, MD, and David Simons, MD. trophic: Pertaining to nutrition , especially in the cellular environment (e.g., trophic function-a nutritional function) . trophicity: 1. A nutritional function or relation. 2. The natural tendency to replenish the body stores that have been depleted. trophotropic: Concerned with or pertaining to the natural tendency for maintenance and/or restoration of nutritional stores. -tropic: A word termination denoting turning toward, changing, or tendency to change. tropism, facet: Unequal size and/ or facing of the zygapophyseal joints of a vertebra; see also facet asymmetry. type I somatic dysfunction: See somatic dysfUnction, type!. type II somatic dysfunction: See somatic dysfUnction, type fl.
u uncommon compensatory pattern: See fascial patterns. uncompensated fascial pattern: See fascial patterns.
FIGURE 38. Vertebral unit.
ventral technique: See osteopathic manipulative treatment, visceral manipulation. vertebral unit: Two adjacent vertebrae with their associated intervertebral disc, arthrodial, ligamentous, muscular, vascular, lymphatic, and neural elements (Fig. 38). visceral dysfunction: Impaired or altered mobility or motility of the visceral system and related fascial, neurologi c, vascular, skeletal, and lymphatic elements. visceral manipulation: See osteopathic manipulative treatment, visceral manipulation. viscerosomatic reflex: See reflex, viscerosomatic r. viscosity: 1. A measurement of the rate of deformation of any material under load. 2. The capability possessed by a solid of yielding continually under stress; see also elasticity; plasticity.
w
v velocity:
1253
The instantaneous rate of motion in a given direction.
weightbearing line ofL3:
See gravitational line (Fig. 17).
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CRANIAL NERVES: ACTIONS AND USUAL SOMATIC DYSFUNCTIONS ACTIVATING SYMPTOMATOLOGY
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CN
Name
Action
Symptoms
Activation and 50
II
Olfactory Optic
Sensory: Sense of smell Sensory: Sight
A ltered or imagined odors Visual disturbances
Ill
Oculomotor
Motor: upper eyelid, all extraocular muscles except sup. oblique and lateral rectus; and supplies parasympathetic fibers to pupil and ciliary muscles
Ipsilateral eye turns up and outward, double vision, ptosis of lid and poor accommodation
IV
Trochlear
Motor to superior rectus muscle
Diplopia esp. when looking down
v
Trigeminal Ophthalmic V1
Sensory to scalp, forehead, eyeball, ethmoid sinus, nasal cavity, conjunctiva Sensory to dura, maxillary sinus, nose, nasal septum, premolar and molar teeth, lower and upper eyelids Sensory teeth, mandibular gingiva, temporal skin, part of auricle, lower face, floor of oral cavity, part of tongue Motor to muscles of mastication Lateral rectus muscle of eye
Pain in any of these
(see 1-3 of CN Ill Activation and SD)
Maxillary pain, tearing, paresthes ias upper lip, nose, and eyelid; headache, tic douloureux Pain in any of these sites
SD of sphenoid, TMJ, poor fitted dentures
Eye turned inward
SD sphenoid or temporal with tension on petrosphenoidalligament; congestion of venous sinuses of cranium Congestion of venous sinuses of the cranium SD sphenoid, occiput (condylar compression), temporals (occipital mastoid compression), upper cervical and cervical facial SD Loss of taste Congestion of venous sinuses of the cranium SD Sphenoid, occiput and/or temporal
Maxillary V2
Mandibular V3
VI
Abducens
VII
Facial
Motor: muscles of expression, scalp, ear, buccinator, platysma, stapes, stylohyoid, post. Belly of digastric Sensory: taste buds ant. 1/3 of tongue, soft palate
Bell's palsy; loss of taste, dysphagia, salivation
VIII
Auditory (Vestibulocochlear)
1. Auditory-hearing 2. Cochlear-equilibrium Sensory: pharynx, tonsils, posterior part of pharynx Parasympathetic: to parotid
Hearing loss Loss of equilibrium poor feeding, swallowing, excessive gag reflex in newborns; problem swallowing, speech difficulty, neuralgia Reflex cough, posterior occipital headache, bradycardia, feeding problem in infants, t gag reflex, NN, shallow problem, respiration Gl upsets, NN, cough, irritable infant
IX
Glossopharyngeal
X
Vagus
XI
Accessory
XII
Hypoglossal
Sensory to posterior cranial fossa, pharynx, soft palate, carotic, sinuses, larynx Motor: heart, lungs, thyroid, Gl tract up to left colon, liver, gallbladder, pancreas, spleen, kidneys, upper ureter, gonads Motor: SCM, trapezius, pharynx and palate Motor: tongue
Difficult to rotate head to healthy side Torticollis (SCM}, Shoulder drop Sucking disorder in newborn, dysphagia, dysarthria, swallow problem
V1, ophthalmic branch; V2, maxillary branch; V3, mandibular branch; Gl, gastrointestinal; CN, cranial nerve; TMJ, tempore mandibular joint.
SD of frontoethmoidal suture SD of sphenoid or membranous tension of spheno-occ ipital suture 1. Tension of petrospheno idallig. (anterior aspect of tentorium cerebelli) 2. SD of temporal or sphenoid 3. Congestion of venous sinuses of the cranium This is a long nerve, therefore, easily torn with head injury Congestion of venous sinuses of the cranium
SD of sphenoid, TMJ, poor fitted dentures
Condylar compression
SD of occipitomastoid suture and condylar compression,
SD of jugular foramen-see CN IX and CN X Condylar compression
0 0 0 0 0
f--..
0
)
0 0 0 0 0 0 0 0
A
B FIGURE Appendix 11.1. Primary point: supraorbital notch; endpoint: suboccipital region; connection : frontalis-occipitalis muscles (A), trigeminal-greater occipital nerves (B) .
Appendix II
FIGURE Appendix 11.2. Primary point: superior medical scapular border; endpoint: base of occiput; connection : levator scapula .
1259
FIGURE Appendix 11.4. Primary point: sternum at second rib; endpoint: coracoid process; connection: pectoralis minor.
(
FIGURE Appendix 11.3. Primary point: greater trochanter of femur; endpoint: fibular head; connection iliotibial band .
FIGURE Appendix 11.5. Primary point: gluteal region; endpoint: greater trochanter; connection : piriformis muscl e.
1260
Appendix if
'
•
0 0 0 0 0 0
0 0
0 0 0
0 0 FIGURE Appendix 11 .6 . Primary point: gluteal region; endpoint: popliteal region; connection: sciatic nerve.
FIGURE Appendix 11.7 . Primary point: xiphoid process; endpoint: public ramus; connection: rectus abdominus.
FIGURE Appendix 11.8. Primary point: antecubital region; endpoint: wrist; connection: median nerve.
Appendix II
FIGURE Appendix 11.9. Press both the primary point and the end point simultaneously using the pad region of a finger on each hand.
1261
FIGURE Appendix 11.10. One finger remains on the primary point. Use another finger of the same hand to locate a "secondary point." If the middle finger is on the primary point, then use the ind ex finger to palpate the secondary point.
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SUBJECT INDEX
No te: Page numbers in italics are figures; page numbers followed by t indicate tables. Abdo minal pai n emerge ncy medi cin e, 395-397 su rgery, 400-405 Abdom in al regio n, 75 1-76 1 acutely ill patien t, 11 2 1- 11 23, 11 3 1- 11 34, 1122,
1131-1133 OMT, 11 39- 11 40 defin itio n, 752, 752 d iagnos is, 755-757 fu nctio nal anato my, 752-754 ligame nts , muscles, and fasc ia, 752-753, 752 r nerves, 753, 755 reflex of Mo rley, 753, 756 skeleton, 752 vasculature and lymph ati cs, 752,
754-755 visceral pain, 753, 755 viscerosomaric pain, 753, 755 h istor ical perspective, 75 1 key concepts, 75 1 lymphatic fl ow, 1069- 1070, 1073- 1075, 1070 osteopathic mani pulation. See Visce ra.! ma nipulation. topographi c anato my, 754, 756-758 treatment, 757-758 osteopathic, 758-760 co ll ateral gangli a inhibi tio n, 759-760 fa lcifo rm liga ment release, 760 mesenteric releases, 760, 760 pa rasp in al inhibition, 758-759 Abdo minopelvic regio n, auto nomic innervatio n, 104- 11 6, 106 gastro in testin al traer, 105-111 , 107-110, 11 1r heparobi liary tree and pancreas, Ill kid ney and urin ary traer, 111- 11 4, 112, 114 reprod ucti ve traer, 11 4- 11 6, 115 Abd ucens nerve, 67 1-672 Abel, John J., 189 Academi c institutions, 1220- 1224 Aca nthosis nigricans, in ca ncer, 466 Accessory nerve, 674 Acetabulum angul ar structu re, 80, 80 hi p dysplasia, 480-48 1 N-Aceryl aspartate, in pain transmi ss io n, 2 16 Acetylcho lin e, in ce rebral vascul ature, 99
Achilles tendo n, 8 16 Acquired immun odefi ciency syndrome (AIDS) hospital trea tm ent, 428 osteopathi c research, 1223 Acro mio n, 54 1, 690 Activiti es of daily living (ADL) geriatri c, 33 1-33 2 pelvic floor dys fun ction, 416-4 17 phys iologic mechani cs, 57 1 Acupressure, I 028 Acupun cture, 474 Adaptati on, and nociception, 13 8- 139 Adeno myosis, 4 15 Ad enosin e rriphosphare (ATP), in muscl e contraction , 7 5 Adrenal gland See also H ypoth alamic-pituitary-adrenal axis. horm one processin g, 182 Adrenoceprors, in peripheral vasculature, 98 Ad renoco rti cotropin (ACTH), and brainsrem arou sal system, 148- 149, 149 Adson res t, 701 Adult attention deficit di sorder, 252 Affecti ve disorders, 11 92 African sleepin g sickn ess, 169 Age factors See also G eri atri cs . bon e properties, 70 cartilage wear, 7 1 liga ments and tend ons, 73 pelvic floor dys fun ction , 4 17 Agency for H ealrh care Research and Quality, 1199 Airflow res istance, 502 Airway disease in children, 3 19t osteo pathic manipul ative th erapy, 5 13 Alcohol use, 201 - 202 biobehavioral fa ctors, 1206- 1207 and feral growth, 227 hos pital trea tm ent, 428 and stress, 239-240, 24 0r Al endron are, 493 All en tes t, 702 All ergic rhinitis, 376 Allodynia, primary afferent nocice prors, 140 Allosrasis, 150- 153 markers, 15 1r Altern ati ve medi cin e, in cancer, 474
Al zheim er's di sease and agin g, 334 diagnos is, 25 1 Ambularo ry pati ents, so matic dysfun cti on, 652-654,650-652 r heal th fo rms, 655-658 Am eri ca n Academy of Os teo path y, i m ern ario nal co nferences, 11 44 Am erica n Association fo r the Adva nce men t of Osteopath y, 25 Ameri ca n Coll ege of Osteo pathi c Surgeo ns (ACOS), 400 Am erican Medi cal Associatio n (AMA), and osteo path y, 22 Ameri can O steo pathi c Associati o n (AOA) education al standards, 22 fell owship progra ms, 420-42 1 hospital exa min atio n fo rm , 111 5, 11 16 orga nizatio n, 25-26 so mati c dys fun cti o n resea rch, 11 88 Ameri can Os teo pathi c Boa rd of Emergency M edi cin e, 383 Am eri ca n Schoo l of Os teo path y (ASO) es tablishm ent of, 2 1-22 neu ro phys iology, 12 1 orthopedi cs, 478 vaccin ati o ns, 7 Amin o acids, endocrin e, 182, 184- 185 Amph etamin es, 549 An abolic steroids, 548 An algesia adjuva nts, 22 1-222 opi oids addi cti o n, 22 1 side effects, 22 1 tol erance, 22 1 pati ent-co ntroll ed , 220 placebos, 22 1 transdermal parch, 220 An atomy abd omen , 752-754 ligaments, m uscles, and fasc ia, 752-753, 752t, 753 nerves, 753, 755 skeletal, 752 vascul ature and lymph ati cs, 753, 755 abdo min al pain , 400-401 auronomic nervous sys tem . See Auton omi c nervo us syste m. brainsrem reti cular fo rm ati on, 146 central nervo us system, 435-436
1264
Subject Index
Anatomy-continued ce rvi cal spine, 684-685 key concepts, 37, 44 limb anatomy, 58, 58 cartilage and bone, 47, 48 co nnective tiss ue, 46--47, 46 injury effects, 49 microsco pic, 46--49 skeletal muscle, 49, 49 mu sculoskel etal fun ction , 49-55 fascia and neurovascular bundle, 52-54,53-54 joint play, 51-52 muscle action, 54-55, 55 muscle- tendon complex, 52, 52 synovial and nonsynovial joints, 49-51,
50-5 1 myofascial conti nui ty, 58-60, 59-61 neuromuscular system embryology, 44--46, 45, 46 segmental organ iza tion , 55-56, 55-57 pelvis and sacrum , 762-767, 763 femal e, 409--412, 41~II muscles and co nnective tiss ue, 763-765 primary, 763-764 seco ndary, 764-765, 764 nerves, 767-777, 767 skeletal/ligaments , 762-763 vascular/ lymphatic, 765-766, 765 PI.NS method, 1030- 103 1 rib cage, 7 18-720 co nnective tiss ue and fascia , 720 lymphati cs, 720 muscles, 7 19-720,719 skeleto n, 7 18-7 19, 719 rul es of movement, 37-43 co nn ectedness wirh orher sires, 4 1--42 difference, 43 drainage, 40 fu nctional anatomy, 38-39 pa in , 41 proximity, 37-38 suppl y, 39--40 so mati c dysfun ction , 567-568, 1153-115 7 fac ili tation, 11 53- 11 54,1154 mechanoreceptors, 1154- 1155, 11 54r myofascia, 1156- 1157 spinal co rd and noci ception, 11 55- 1156 thorax, 705-7 12, 706 co nn ective tissue and fascia, 7 10-7 11 lymphati c system, 7 10, 711 muscles, 706-71 0, 707-7 10r neural connections, 7 11 -7 12, 712 upper ex tremities, 690-694, 69 1-693r,
693 An cient writings, 8 Aneurysms, 681, 744 Angina pecto ri s, 355, 355 Angioplasry, coro nary, 356-357 Angiotensin , 98 Angles of lordos is, 1230 Angu lar structu re of hip, 80, 80 Animal resea rch, I 17 1
Ankle anatomy, 794-797 pes planus and pes cavus, 796-797 subtalar joint, 795-796, 797 ribioralar joint, 795, 796 INR and MFR techniques, 96 1-962,961 inversion sprain, 543-544, 543 muscle energy techniques, 905-906, 905 Ankylosing spondylitis, 529 back pain , 491 in pregnancy, 452 Antecubital regi o n, primary and endpo ints,
1260 Antibiotics, 175 Antibodies, and infections, 173 Antihistamines, for allergic rhiniti s, 376 Anxiecy diagnosi s, 248-249 management, 237-239, 238t Aortic plexus, I 04, 105 Ap ley scratch resr, 702 Apnea in children, 323 Aponeurosis definition , 908 plantar, 799 thoracolumbar, 733, 734 Appendix, vermiform See also Lymphatic system. abdominal pain, 402 Chapman reflexes, I 052 functional techn ique, 982-983, 982 Apprehension rest, 702 Arches offoor, 798, 801 Arteriovenous malformations, 681 Arteritis, temporal , 681 Arthritis See also Rh eumawlogy. rheumatoid, HVLA complications, 11 49 Arrhrogryposis, 312 Arthroscopy, for knee osreoarrhriris, 485 Articular processes acutely ill patient, 11 35 superior and interior, 729-730 Articulatory techniques, 834-851 cervical extension, 837, 837 flexion , 837, 837 regional sid e-bending, 838, 838 rotation , 838 segmental side-bending, 838 ce rvicorhoracic fl ex ion , ex tension, sid e-bending, 838-839, 839 common questions, 834-835 costal. See also rib cage anterior, 84 I , 841 lateral recumbent, 84 1-842, 842 posterior, 841, 842 posterior rib raising, 842-843, 842 design and use of, 834 extremities, 848-851, 848-851 key concepts, 834 lumbar extension, 844-845, 844, 845 fle~on ,843-844,
843
rorarion , 846, 846 side-bending, 845-846, 845, 846
pelvic rotation to innominate, 846-847, 847 sacroi liac joint gappi ng, 848, 847-848 regional treatment, 836-837 co ntrai ndi cations, 837 indi ca tions, 836 sam ple clinical app li cation , 835-836 shoulder treatment, Spencer technique, 836,851 th o racic ex tensio n, 839-840 fl ex io n, 839, 839 rotation, 840, 840 side-be ndin g, 840-841 Ashmore, Edythe, 969-971 Asthma acutely ill patient, 11 30- 11 31 in ch ildren, 3 17-320 osteopathic manipulative therapy, 5 12-5 13 somatic dysfunction research, 11 92 thoracic reflexes, I 125 Asylums, mental, 247 Asympto matic Carotid Atherosclerosis Stud y, 1194 Atelectasis, 405--406, 5 13-5 14 efficacy ofOMT, 11 47 Arlantal-axial joint balanced ligamento us tension, 930, 930 muscle energy techniques, 889-890, 890 Atlas-axis, osteopathic manipulation, I 096,
1096 ATP synthesis and function, 158- 159 Atrioventricular (AV) node innervation, I 0 I Auditory nerve, 672-673 Auerbach's plexus, 103-1 04 Aura, migraine, 439, 679 Auscultation, lumbar, 740 Automobile accidents, 202, 660 cranial dysfunction, 996 Autonomic nervous system, 33, 39, 90- 119 abdo minal pain, 400--40 1 brainstem retic ul ar formation, 146 catecholamine release, 148 divi sions of, 93-97, 94 parasympathetic ANS, 96-97, 96 primary affe rent fibers, 97 sy mpath etic ANS, 94-96, 95, 96 emerge ncy medicine, 386, 387 head and neck, 372-373, 374, 373 key co ncepts, 90 myofascial tri gge r points, 1047-1048,
1048 o rga nizatio n, 91, 91 refl ex arcs autonomic, 92-93, 92-93 so matic, 91-92, 92 regio nal distribution, 97-1 16 abdomi nopel vic region, 104-116, 105 celiac gangli a, 106, 107-110 gas trointestinal traer, 105- 111, 107 hepatobiliary tree and pancreas, I I I kidney, 111 - 11 2, 112 reproductive tract, 11 4- 11 6, 1 I 5 penis and clitoris, I 16 testis and ovary, I 14- 1 I 5
Subject Index uterus, uterine rube, cervix, and vagina, 115- 11 6 ureter, 112-1 13 urinary bladder, 113-1 14, 114 head and neck, 99-1 00 tho rax, 100- 104, 100- 102 aortic plexus, 104 cardiovascular plexus, I 01 - 102 esophageal plexus, I 03-104 respiratory plexus, I 03 thoracic duct innervation, I 04 trunk and limbs, 97-99 sweat glands and co nnective tissue, 98-99 vasculature, peripheral, 97-98 terminology, 90 Axon reflex, 164 Axoplasmic Aow, 133-134 B lymphocytes, I 059 Babinski sign, 443 Back pain See aLso Low back pain; Lumbar region. in cancer, 465-466, 469 efficacy ofOMT, 1145-1146 injured mhletes, 539-544, 539 iliopsoas spasm, 539-540, 540 sacroiliac/sacral torsion dysfunction,
540,540 in pregnancy, 459 somatic dysfunction research, 11 88 Balanced ligamentous tension (BLT) techn iques, 9 16-930 articular mechanisms, 9 16-917 diagnosis, 9 17-9 19 treatment principles, 918-9 19, 919 key concept , 916 reciprocal tension, 9 17 specific regions atlanral-axial joint, 930, 930 cervical spine, 927-930, 929-930 clavicle, 926, 928 hip capsule, 921-924, 922-923 humerus/glenohumeral joint, 926-927,
928 in nominates, 920-92 1, 921 pelvis, 9 19- 920, 920 ribs, 924-926, 925 sacroiliac joint, 927, 929 scapulothoracic joint, 926, 927 thorax, 924, 924 Bankart lesion, 495, 541 Barlow test, 786 Baroreceptors, 128-129 Barriers HVLA treatment, 855 joint motion, 1232 Barr-Lieou syndrome, 667 Batson plexus, 469, 473 Bayes theorem, 278 Bedridden patients, somatic dysfunction , 649- 659,653-654t Behavior modification, pain management, 223-224 Bell's palsy, 68 1-682 Bending, in biomechanics, 66
Bias, clinical research, 1183, 11 97 Bickerstaff syndrome, 439 Bile ducts, osteopathic manipulation, I 086,
1086 Biobehavioral research, 1203-121 4 ca rdiovascular disease, 1205, 1205t disease development pathways, 1204-1205, 1204 in health, 1203-1205 cognitive processes, 1204t immune function and infections, 1205-1206 key concepts, 1203 opportunities, 12 12 pain syndro mes, 1206- 1207, 1207t placebos, 1207- 1208 research process, 1208-1212 basic research , 1208 design and implementation, 1209t group formation, 121 0 instrumentation, 1210 intent to treat, 1210 maturation, 1210 measurement variance, 12 10 multiple treatments, 12 10 hypothesis, 1209, 12 /0 quantitative measurement, 1210- 1211 statistics, 1211-1212 sleep and ci rcadian biology, 1206 Biofeedback pain management, 223 stress management, 242 Biologic response modifiers, in cancer, 472-473 Biomaterials, in knee osteoarthritis, 484 Biomechanics, 63-89 articular cartilage, 70-7 1, 70 behavior of materials, 66-68 elastic modulus, 66-67, 67 fa tigue, 68 isotropic or anisotropic, 66 strain vectors, 66, 66 viscoelasticity, 67-68, 67 bone,68-70, 68-69 cervical spine, 685 elbow, 8 1- 82, 81 entrapment neuropathies, 446 hip, 80-81, 80 injured athletes, 538-539 key concepts, 63 knee, 78-80, 78 ligaments and tendons, 71-73, 72 locomotion, 86-87, 87 motion and forces in three-dimensional space, 64-66, 64-66 musculoskeletal models, 75-78, 76-77 myofascial trigger points, I 038-1039 postural decompensatio n, 605, 605-606 in pregnancy, 456 rib cage, 720-72 1, 721 shoulder, 82- 83, 82 skeletal muscle, 73-75, 73-74 spi ne, 83- 86, 83-85 Bipolar disorders, 248 Birth canal, 458, 458
1265
Bisphophonates, 493 Bladder, osteopathic manipulation, 1090-1091, 1090 Blinding, in research, 11 80, 11 84, 121 7 Blood doping, 549 Blood Aow in cancers, 469 general mechanisms, 159- 160, 160 HVLA complications, 11 49 local control of, 160- 16 1 myocardial, 161-163, 162 in pregnancy, 452, 453 pulmo nary, 503 in skin, 163-164, 163 Blood pressure, and baroreceptors, 128-129 Blood vessels abdominal, 753, 754-755 brain, 996 cervical spine, 685 female pelvis, 41 1-4 12 ofhead and neck, 99, 662, 669 hip, 806,810,815 hip fractures, 482-483, 483 innervation, 97-98 knee, 8 10 lower leg, 810,813, 816 lumbar, 735, 736 pelvis and sacrum, 765-766, 765 thoracic, 706 upper extremity, 69 1-692 Blood-brain barrier, 192 Bo mbesin, and lung ca ncer, 464 Bonding, infants, 228 Bone abdominal , 752 bio mechanics, 68-70, 68 fractures, 69-70, 69 remodeling, 70 cervical spine, 684 cra nial, articular mobility of, 987, 989-990 lower extremity, 784-785, 785 metastatic disease, 465-466, 468-469 microscopic anato my, 47, 48-49 pelvis and sacrum, 762-763 PINS method, 1030 in postural decom pensation, 606-607 rib cage, 7 18-719, 719 of skull, 660, 661-666, 666t Braces in knee osteoarthritis, 485 postural, 589 for scoliosis, 622 for spondylolithesis, 630 Brachial plexus, 694 Bradykinins, in somatic dysfunction, I 154 Brain autono mi c innervation , 99-100 motility of, 986-988 tumors, 681 Brain natriuretic peptide (BNP), 360,361 Brainstem arousal system, 145- 147 ascending pathways, 145-146 and neuroendocri ne im mu ne network, 147- 152
1266
Subject Index
Brainstem , aro usal system-continued cy tokin es, 149 hormon al release, 147- 149, 149 reticul ar formation, 146 and baroreceprors, 128- 129 Breast ca ncer, bi obehavioral factors, 1207 Breathing, work of. See Res piration . Brief psychotic di so rder, 249 Bronchi , osteo pathic manipul ation , I 089- I 090, I 089 Bronchiolitis in children, 3 I 7-3 I 8 osteopathi c manipul ati ve th era py, 513 Bronchitis osteopathic manipul ative th erapy, 512 thoracic reAexes, 1 I 25 Bucheim, Rud olph , I 89 Bunions, 800-801 Burns, Loui sa, I 2 1, I I 56, I I 67 Bursitis, 8 14-8 16, 8 16 subacromi al, 54 I Cachectin , in ca nce r, 469-470 Caffei ne performance enh ancement, 549 so matic dys fun ction resea rch, 1191 - 1192, I I 98 Calcitonin gene- rel ated peptide (CG RP) in ca rdi ovascul ar inn ervation , 102 in cerebral vasculature, 99 in resp irato ry pl ex us, I 03 in so mati c dysfun ction , 1154, I I 55 Calcium , and ATP sy nth es is, 158- 159 Calcium pyrophosph ate depos ition di sease, 529 Capsulitis, adh es ive, 703 Carbon dioxide, pulm o nary, 504 Ca rdi ology, 345-369 angin a pectoris, 355, 355 co ro nary artery di sease, 350-355 cases, 357-358 diagnosis, 35 1-353, 352t pathophysiology and natural hi sto ry,
350,350 therapy, 353-355, 354t vascul ar biology, 35 0-35 I hea rt failure, 358-363 diagnosis, 360-36 1 exercise, 36 1 mu scle hypo th es is, 36 1-362, 362 osteopathy, 362-363 treatment, 36 1 key co nce pts, 34 5 myoca rdi al infarctio n, 355-357, 356 os teo pathi c overvi ew, 345-349, 346, 348, 348t, 349t un stabl e angina, 355, 355t Card iop ulm o nary system , emergency med icin e, 394-395 Ca rdi ovascular di sease all ostas is, 15 1- 152 biobehav ioral mechanisms, 1205, 1205t endocrine function, I 84 so matic dysfunction research, I 191 Ca rdi ovascular pl ex us, I 01 - 102 Ca rpal tunnel syndrom e, 445-446 myofascial trigger points, I 043
physiatry, 523 in pregnancy, 454 treatm ent, 702-703 Cartilage articular, 70-7 1, 70 in kn ee osteoarthritis, 484 lower extremity, 792-793 microsco pic anatomy, 47, 48-49 Casts, for spondylolithesis, 630 Catecholamines brainstem arousal system , 148 ho rmon e process ing, 182, 184 Catheterization, cardiac, so matic dysfunction research , 1191 Cauda equina syndrome, 744 Cement line of bone, 68 Center of rotation, 78 Central nervous system allostasis, 152 an atomy, 435-436 autonomic components, 9 I in cancer, 467-468 myo fascial trigger points, I 038 Cephalgia, in emergency medi cin e, 389-39 1 Cerebellar degeneration, and lung cancer, 464,467 Cerebrospinal Auid , 674-675 motility of, 987, 988 Cervical region articulatory techniques extension , 837, 837 Aex ion, 837, 837 rotation , 838 side-bending region al, 838, 838 segmental, 838 facilitated positional release (FPR), 1018- 101 9, 1019 fasc ial-ligamentous rel ease, 913,913 functional technique, 976-977, 978 HVLA treatment, 857-859 atlanto-axial joint, 857-858 occipito-a rlantal joint, 857, 857 rotational focus, 858-859, 859 side-bending focu s, 858, 858 lymphatic Aow, 1072-1073, 1072-1073 muscle energy techniques, 887-888, 888 so ft tiss ue techniques forward bending, 820-821, 821 rotation, 820, 820 suboccipital inhibition , 820, 820 traction , 820 contralateral, 821 longitudinal, 821 , 821 Cervical spine, 86, 684-689 anatomy blood supply, 685 ligam ents, 684 lymphatic system, 685 muscles, 684 neural , 685 skeletal , 684 balanced ligamentous tension , 927-930,
929-930 biomechanics, 685 clinical information , 688-689
key co ncepts, 684 moti o n testing, 686-688, 687 osteopathic manipul ation , 689, 1094- 1095, 1095 strain and counterstrai n technique, 1007- 1009, 1008-/009 Cervical spra in /strain , physiatry, 524 Cervico th o racic region, articulatory techniques, 838-839, 839 Cervix autonomi c innervation, 11 6 osteo pathic manipulatio n, 109 1- I 092,
1092 C hapman reAexes, 105 1- 10 55 clinical use, 1052-10 55 specifi c reAexes, I 052- 1053 ,
1053-1054 trea tm ent, 1055 emergency medi cin e, 386, 396 hi sto ry and philosoph y, I 052 key co ncepts, I 0 5 1 palpatio n, I 05 1- 1052, 1052 pelvic pain, 4 12 point and pressure techniqu es, 1028 in pregnancy, 454 upper ex tremity, 704 C hemoreceprors, 139- 140, 505 C hemoth erapy, I 74- 175, 175 C hest pain ca rdi ovascular disease, 352 emerge ncy med icin e, 392-394 C hildren, hospital treatment, 428-429 Chol ecystitis abdomin al pain, 403 segme ntal fac ilitation, I 126 C hol estero l, hormone processing, 182 C hopart joi nr, 800 C hroni c obstructive pulm onary disease (CO PD) efficacy ofO MT, I 147 osteopathic manipul ative therapy, 512-5 13 C ircadian rhythms, 1206 C ircul ato ry syste m See also Respirat ion and circu lation. co nn ecto rs, 4 1-42 in pregnancy, 452 C itric acid cycle, 158 C ivil War medicine, 20 C laudica tio n, 49 1 C lav icle acutely ill patient, 11 20 balanced li ga mentous tension, 926, 928 muscl e energy techniqu es, 906-907, 906 myofascial rel ease techniqu e, 88 C lini cal problem so lvin g, 257-279 abdominal pain , 258-259 Bayes theorem, 278 cavea ts, 259-264 decision analysis, 263-264 diagnosti c problems, 264-265 hypothetico-deducrive method, 260-26 1 problem -o ri ented perspective, 26 f--263 co ronary artery disease , 277-279 data gatherin g, 258
Subject index examples, 257, 265-270, 272-276 key concepts, 257 milnipulative treatment, 271 musculoskeletal system, 269 pain, 270-271 patient as whole, 271 patterns, 258, 259 Clinical trials. See Research, osteopathic. C litoris, autonomic innervation , 116 Cocaine addiction, 250-251, 250-251 t Cognitive function geriatric, 332 in he~lrh , 1204t pain transmi ssion , 219 Cole, Wilbur V. 121 Colic, 322 Co llagen in articular cartilage, 70-7 1 in connective tissue, 46-47, 47 of fa cia, 52 in ligaments and tendons, 7 1-72 Colon C hapman reflexes, 1052-1053 osteopathic manipulation, 108 2- 1083 cecum and ascending colon, 1082,
1082 root of sigmoid, I 082- 1083, 1083 sigmoid," I 083, 1083 transverse colon and flexures, 1082,
1082 Common cold, 677-678 Compartment syndrome, 813-8 14 bursae and bursitis, 814-816, 816 Complementary medicine, in cancer, 474 Compliance biobehavioral factors, 1207 pulmonary, 502 Com plications of OMT, 1147- 1150 incidence, 1147- 11 49, 1148t Compression in biomechanics, 65-66 bone fracture, 69 cervical spine, 688 spinal, 742 spi nal disorders, 442-443 vertebral body fractures, 727-728 Computed tomography (CT) , 38 Computer resources graphics, I 182 literature search, 11 75- ll 77, 11 76- 1 177t st~tistical analysis, I 181 Concussions, sports medicine, 543-548 Conferences, international, efficacy and complications of OMT, 1143- 1145 Confidentiali ty, 11 70 Confusion, geriatric, 333-334, 333t Connective tissue See als.o Ligaments; Tendons. as co nn ectors, 4 2 continui ty. See Fascial-ligamentous release and myofascial release (indirect approach). of head, 660-66 1, 668 innervation of, 98-99 mi croscop ic anatomy, 46-47, 46-47
pelvis and sacrum, 763-765 rib cage, 720 in somatic dysfunction, 1156-1158 thoracic, 710-7 11 Constipation Chapman reflexes, I 052 in children, 321 Coronary artery bypass graft (CABG) surgery, 356-357 Coro nary artery disease cases, 357-358 diagnosis, 35 1-353, 352t efficacy ofOMT, 11 47 pathophysiology and natural history, 350,
350 statistics, 277-279 therapy, 353-355, 354t vascular biology, 350-35 1 Corticosteroids, for arthritis, 531 Corticotropin-releas ing hormo ne, 186 and brainstem arousal system, 148- 149, 149 Cost effectiveness studies, 1226 Costal region art iculatory techniques anterior, 841, 841 lateral recumbent, 841-842, 842 posterior, 841, 842 posterior rib raising, 842-843, 842 functional technique, 977-980, 979 INR and MFR techniques, 958-96 1 muscle energy techniques, 890-894 ribs , 890-894, 890-894 Counseling, pain management, 223 Counrerstrain. See Strain and counterstrain technique. Cran ial nerves, 667-674 abducens (VI), 6 7 1-672 accessory (Xl) , 670 auditory (V11!), 672-673 facial (VII), 672 glossopharyngeal (IX), 673 hypoglossal (Xli), 674 oculomotor (Ill ), 669-670 olfactory(!), 667-668 opt ic (II), 668-669 parasympathetic, 99 and somatic dysfunction, 1255- 1256t trigeminal (V), 670-671 troch lear (IV), 670 vagus (X), 673-674 Cran ial region , 985-1001 clinical problems, 994-997 dentistry, 996-997 neonatal , 994-996, 995 trauma, 996 vascular supply, 996 diagnosis, 993-994 observation, 994 palpation, 994 patient history, 993 fascial-ligamentous release, 914, 914 history of OMT, 19-29, 985-986 INR and MFR techniques, 952- 96 1 key concepts, 985 mechanics of physiologic motion, 990-991, 991
1267
primary respiratory mechanism (PRM), 986-987 bone mobility, 987, 989-990, 989 brain and sp in al cord motility, 986-987,988 cerebrosp in al fluid, 987, 988 membrane mobility, 987, 988-989 research results, 988-990 sacral mobility, 987, 990 strai ns, 992-993, 992 treatment, 997-999, 997-999 Craniocervical spine, INR and MFR techniques, 952-955,
955-958 Craniosacral region, comp li cations of OMT, 1150 Cranium development, 309-31 0 myofascial co ntinui ty, 60 C reatin e, performance enhancement, 548 Creep in biomechanics, 68 li gaments and tendons, 72 Crossed extensor reflex , 883 Croup,3 16-317 Curriculum , osteopathic schoo ls, 22-23 Cushing syndrome, and lun g cancer, 464, 468 Cyriax, James, 477, 1028 Cyrokines biobehavioral mechanisms, 1205 and brainstem arousal system, 149 Data analysis, 121 7- 1218 Databases, computer, 11 76 Delirium diagnosis, 25 1-252 geriatric, 333, 333t Dementia and cancer, 464, 467 geriatr ic, 332, 332r, 333r Demographics eme rgency medicine, 384-386, 385t geriatr ic, 327 Denslow, J.S. neurophysiology, 121 , 129 research in OMT, 1167- 1168 Dentistry, cranial dysfun ction , 996-997 Depression and arthritis, 527 diagnosis , 248 ger iatric, 332, 332t management, 235-237, 236t de Quervain tenosynoviti s, in pregnancy, 459 Dermatomal bands, 56, 56 Derma tomes, 1234 lumbar, 734-735 thoracic, 772 Descartes, pain theory, 212-213,213 Design of research between-subject, 11 79- J 180 blinding, 1180, 1184 independent and d ependent variabl es, 11 79 random assignment, 11 79- 11 80 biobehavioral mechanisms, 1211
1268
Subject Index
Design of resea rch-continued ca. e studi es prospecti ve, 11 78 retrospective, I 178 clinical reseasch co ntrol groups, 11 84-1185 dependent variables, I 185-1 186 drop-o uts , 1185 inclusion/exclusion criteria, 1 185 pi lot vs. full studies, 1185 pi rfalls, I 186 popu lation selection, 1184 stud y size and power, I 185 ex perim ental, 11 79 hypothesis, 11 77- 11 78 lirerature sea rch, 11 75- 11 77, 11 76- 11 77 t observation, I 175 outcomes research, I 196- 1 I 98, I 198t, 1196-1197 sta ti sti cs, I 18 1- 1182 within -subject and crossover, 1180- 1181 data co ll ection and ana lys is, 1180- 1181 Development hip dysp lasia, 479-482, 480-481 hormonal co ntrol , 187 lym phatic system , I 056 musculoskeletal sys tem , 308-314, 309t Diabetes, and arthritis , 527 Diaphragm, abdom in al acutely ill patient, I 118- 1 12 1, I 129, 11 3 1-1132,1130,1133 OMl~ 11 39- 1140 anatom y, 7 19-720,724, 719 functional testing, 740-74 1 inn ervation , 7 12 INR and MFR release, 949-951, 952-955 and lymphati c system, I 060- 1061 , 1065- 1067, 1066 re-doming, 74 1 respirato ry function, 50 I, 720 Diarrhea, in children, 32 1 Diathermy, 5 17 Diet and asthma, 320 bi obehavio ral factors, 1206- 1207 Dirty half-dozen, 746, 746 Disabi li ty-Adjusted Life Yea rs, 197 Disc, intervertebral , 83-84 anato my, 729 sacroiliac dysfun ction , 782 Diverticu litis, abdominal pain , 404 Doctor-patient relationship, 240-206, 205t psychiatric, 247 Down syndrome, HVLA compli cations, 1149 Downing, C. Harri so n, 970 Drainage system s, 40 Drop arm rest, 70 I DSM-IV (D iagnostic and Statistical Manual of M ental Diso rders, Fourth Ed) alcohol abuse, 20 I class ification , 248 depress ion , 235
Duodenum, osteopathic manipulation , 1080-1081, /080-108/ Dura mater, cranial, 5 I, 60 Dynorphin , in nociceprion, 132 Dys menorrh ea, 413, 413r Ear, nose, and throat disease, 370-382 ears, 376-378, 377, 377t anatomy, 677, 677-678 otitis media, 378-379 emergency medicine, 390-392 head and neck autonomic nervous supply, 372-373,
373 lymphatic system , 371-372, 372 myofascia, 371,371 key concepts, 370 musculoskeletal system, 380-381, 381 rhinitis , all ergic, 376 sinuses, nose and paranasal, 373-375, 374, 374t sin usitis, 375-376, 376 throat/ pharynx, 379, 379 tonsilliris/ pharyngitis, 379-380, 380 Eaton-Lambert syndrome, 468 Eclecticism, disease treatment, 21 Edema and lymph Aow, I 06 1 in pregnancy, 452, 455 so matic dysfunction , 137, 140 Edinger-Westphal nucl eus, 99 Educatio n, medical AMA standards, 22 osteopathic colleges, 24 Educational Counci l on Osteopathic Principles, 1223 Educational Counci l on Osteopathic Principles (ECOP) , 10- 11 curriculum , 23 Efficacy and co mplications, I 143-11 52 complications and co ntraindi carions, 11 47-1150 choice of technique, 1149 counterstrain, I 150 cran iosacral, 1150 HVLA, 1149 incidence, 1147-1149, 1148t muscle energy, 11 49 prevention of, I I 50 guidel in es, 1150- 1151 international conferences, I 143- I 144 key concepts, 1143 low back pain, 1145-1146 systemic disease, 11 46-1 14 7, 11 46 Effleurage cancer patients, 473, 474 lymphatic Aow, I 071 - 1072, I 071 extremities, I 076- 1077, 1076 Egyptians, physi cal medicin e, 517 Elastic modulus, 66-67, 67 of ligaments and tendons, 72 Elbow anatomy, 696-699, 697 biomechanics, 81-82, 81 force movements, 75-76, 76 fractures in chi ldren, 312
HVLA treatment, 874-875, 875 !NR and MFR techniques, 964-966, 964-966 so ma ri c dysfunction , 699 Electrical stimulation and posture, 589 for scoli os is, 622 Embryology, neuromusculoskeletal system, 44-46, 45-46 Emergency medicin e, 383-398 abdominal/pelvic pain , 395-397 autonomi c nervous sys tem, 387 cardiopulmo nary system, 394-395 chest pain , 392-394 head and neck, 389-392 cephalgia, 389, 390, 39 1 eye and ea r pain, 389-392 neck pain, 390-392 nosebleeds/upper res piratory infectio n, 390,392 hi story of developm ent, 383-384 key concepts, 383 lymphatic sys tem , 387 osteopathic philosophy, 384-387, 385t, 387t screening exa min ation , 387-389 visceroso maric activity, 387 Emotion al stimuli , brainstem arousal system, 147 Emphysema, 502 Endarterecto my, carotid, I 194, I 198 Endocri ne system, 34 , I 79- 188 cardiovascular syste m, 184 key concepts, 179 nervou s system, 184-185 regulation of, 185- 188, 186 processes regul ated by hormones, 187-188 structure and function, 179- 184, 180- 181t cellular processing, 181 - 182 hydrophilic hormon es, 183 lipophilic hormones, 183- 184 mechanism of action, 183 transport and metabolism , 182-183 terms and definition s, 179 Endom etriosis, 4 14 Endomysium , 73 Endoplasmic reti culum , horm one process ing, 18 1- 182 Endorhelin , in periph eral vascul arure, 98 Endpoints. See Point and press ure techniques. Energy metabolism, 187- 188 Entrapment neuropathi es, 444-447, 445t Environment, and asthma, 320 Ep id emiology coro nary artery disease, 350 definition , I I 95 in emergency medi cin e, 389-390 heart fai lure, 358 mental di so rd ers, 24 5 osteopathic research, 11 73 Esophagus autonomic inn erva tion , I 03- 104 osteopathic manipulation, I 079- 1081
Subject Index
Erhical facto rs, I 170, I 197 Eustachian rube, 677 Evolution, biobehavioral mechanisms, 1205 Exercise, 199-200 and asth ma, 320 biobehavioral facrors, 1206-1207 C hinese rai chi , 483 coronary artery disease, 354 heart failure, 36 1, 362 postural, 588-589 decompensation, 6 12, 6 12 in pregnancy, 454 prescription for, 284-287, 284-285 spinal dysfunction , 286-287 spondylolirhesis, 629 Extension, 1235 Exrracellular matrix of bone, 68 ligamems and tendons, 7 1-72 Extremities See aLso Lower ex trem ities. articulatory techniques stage 1: stretching tissues, pumping Auid, arm extended, 848 stage 2: gleno humeral extension/flexion with flexed elbow, 848-849,
849 stage 3: glenohumeral flex ion/extension with extended elbow, 849,
849 stage 4: circumduction and co mpression with elbow Aexed/exrended, 849-850,
lymphatic drainage, 692-693, 693 muscles, 691, 692r skeletal and arthrod ial, 690-691, 691r symparhetics, 694 diagnosis, 694-696, 694r, 695r motion testing, 695-696 motor strength, 695, 695r elbow and forearm , 696-699, 697-699 key concepts, 690 tennis elbow, 702 rests Adson rest, 70 I Allen rest, 702 Apley scratch rest, 702 apprehension, 702 bicipital tendonitis, 702 drop arm, 701 Phalen, 702 Tine! sign, 702 Yergason, 70 I treatment, 702-704 adhesive capsuliris, 703 carpal runnel syndrome, 702-703 C hapman points, 704 myofascial triggers, 703 reflex sympathetic dystrophy, 703 thoracic ouder syndrome, 704 wrist and hand, 699-70 I , 700 Eyes anaromy, 675- 677, 676 ciliary ganglio n, 99 emergency medicine, 390-392
849-850 stage 5: abduction and external rotation with flexed elbow, 850, 850 stage 6: adduction with internal rotation with arm behind back, 850-851, 850 stage 7: stretching tissues, pumping Au ids with arm extended ,
851,851 development, 3 I 1-3 13 HVLA rrearmenr lower, 875-879 fibular head, 875-876, 876 Hiss plamar whip, 878-879, 879 malleolus, 877, 877 raloribial joint, 878, 878 talus in plantar flexion, 878, 878 upper, 874-875 abducted elbow, 874-875, 875 posterior radial head , 874, 874 wrist, 875, 875 lymph Row, 1060, 1075- 1077, 1076 muscle energy techniques, 900- 907 ankle, 905-906, 905 clavicle, 906-907, 906
hip,901-904,901-904 knee, 904-905, 904-905 snain and counrersrrain technique, 1014- 1015, 1014- 1015 upper, 690-704 anatomy, 690-694 blood supply, 691, 692 brachial plexus, 694
FABERE acronym , 786-787 Face, myofascial contin uity, 60, 61 Facial nerve, 672 Facilitated positional release (FPR), 101 7-1025, 1027 cervical region , 1018- 101 9, 1019 diagnosis and treatment, 1018 effectiveness, I 0 17 gluteal and hip regions, 1024 history, I 018 key concepts, 10 I 7 lumbar region , 1022-1024, 1022-1023 sacroiliac joint, I 024, 1024 tho racic region, 1019- 1022, 1020 ribs, 1020-1 022, 1021 Facilitation emergency medicine, 386 segmental, 436-437 acutely ill patient, 111 5-11 20, 11 24-1126, 1135,
1117-1119 so matic dysfun ction, 11 53- 11 54 spinal, 137 See aLso Spinal cord facilitation. primary afferent nociceprors, 139, 139 Falciform ligamem (linea alba) release, 760 Falling, and aging, 335, 335r Fallopian tubes autonomic innervation, 11 6 osteopath ic manipulatio n, 109 1- 1092 Family practice, 289-297 com muni ty outreach, 296
1269
disease man agement, 294 osteopathi c diagnos is and rrearmenr, 290-293 person as whole, 293-294 pharmacotherapeu tics, 294 prevemive health, 295 psychosocial facro rs, 295-296 Fascia abdominal, 752-753 acutely ill pariem, 1 135 anatomy, 52-54, 52-54 continui ty, 58-60, 59-61 defi ni tion, 908 head and neck, 37 1,371 innervation of, 98- 99 ligamentous laxity, 496-497 lumbar region, 732-733 PI NS method, I 030 rib cage, 720 thoracic, 7 10-71 I Fascial-ligamentous release (indirect approach), 908-915 conn ective tissue cominui ty, 908- 909 key concepts, 908 models, 909 philosophy, 908 supine treatmem, 9 10-9 14 cranium, 914, 914 diagnosis, 91 0 lower body, 910-9 12,911-912 observation and palpation, 910 upper body, 9 12-9 14, 9 12-9 14 rreannem issues, 909-9 10 Fatigue and arduiris, 527 in biomechanics, 68 bone fracture, 69 in ligaments and tendo ns, 72 and muscle comracrion, 7 5 Federal governmem, commissio ns for DOs, 26-27 Feedback, PINS method, I 029 Femoral head. See H ip. Femur anatomy, 786-789, 788 ligaments, 787, 788 lo ngirud inal axis, 786-787, 788 motion, 787- 789 hip dysplasia, 480-48 1 primary and endpoints, 1259 Fever, and inflammatio n, 17 1-172 Fibers, primary afferent, 97, 98 Fibrocarti lage, 47, 48 Fibro ids, uterine, 415 Fibromyalgia, 530 o utcomes research, I 199 Fibrosis, lung, 502 Finger injuries in child ren, 312 Flare, 164 Flexion, 1236-1237 standing and seared , 773- 774 Flexner Report, 22 Fluid balance, lymphatic system, 1059 Food and Drug Admi nistration (FDA), clinical research, 12 15 Food Pyramid , 198, 199
1270
Subject Index
Foot anaro my, 797-80 I, 797 arches, 798, 801 liga ments, 798, 800 plan tar li gamencs and fasc ia, 799, 802 sprains, 797-798, 798-799 transverse tarsal joint, 799-800 fascial-li gam ento us release, 9 12, 912 injuries in child re n, 3 12-3 13 IN R and MFR techniques, 961-962, 961 metata rsal and phalangeal fin d ings, 800-801 hallus valgus, bunions, and hammer roes, 800-80 I so mati c dysfun cti o n, 80 l neuro muscul ar stru ctu res, 801 , 803 radicul opathy, 801 -804 referred pain , 803-804, 805-806r tarsal so matic dys fun cti o n, 800, 802-803 Foorwa re, spo ndylolithesis, 629 Fo ramen, intervertebral, 73 1, 73 1 Fo rce definit io n. 64 in knee, 78-79 three-dim ensio nal, 64, 64 Fo rea rm anatomy, 696, 698 lN R and MFR techniqu es, 964-966,
964-966 lymph ati c flu ctuati o n, 11 4 1 so mati c dys fun cti o n, 699 Foreign bodi es emergency med icine, 390, 39 1 in kn ee os teoa rthriti s, 484 Fo urth vemricl e, 674-675, 674-675 Fracture bo ne, stress vecto rs, 69-70 hip, ge ri atric, 482-483, 483 spin al di so rd ers, 442 ve rtebral, 493 Fra min gham study, I 198 Frankenhu ser plexus, 11 5- 11 6 Fun ctio nal spinal unit, 488, 489 Fun cti o nal technique, 969-984, 1028 appendi cul ar regio ns, 982-983, 982 ce rvical regio n, 976-977, 978 cos tal regio n, 977-980, 979 hi sro ri cal perspecti ves, 969-973, 971-972 indirect meth od, 973-975. 973-974 co nce pt, 974-975 guidel ines, 974 inno min ate, 98 1-982, 982 key co ncepts, 969 tho racic, lu mbar, and sacral regio ns, 975-976, 976-978 th o racic cage, 980-98 1, 981 Fundin g fo r resea rch, 1220- 122 1 Gait ankl e rehabilitati o n, 543 bio mechani cs, 86-87, 87 in knee osteoa rthritis, 484 in pregnancy, 4 56 spinal diso rders, 443 Galbrea th mandibular drainage, 378, 380,
380
Galen, 4 Gallbladder, 1085-1086, 1086 Ganglia anatomy of, 9 1-93 in esophageal plexus, I 03- 104 in gastroinces rinal tract, 105-106 celiac, 106, 107 mesenteri c, 107, 109, 110 of head and neck, 99-100 of parasympatheti c auto no mi c nervous system, 96-97, 96 paravertebral, acutely ill pariem , 11 36-11 37 sympatheti c nervo us system, 95, 95 Gas exchange, pulmonary, 503, 504 Gastritis, segmental facilitati o n, 11 26 Gas troesophagea l reflux di sease, in children, 32 1 Gastrointestin al system See also Lymph atic system. acutely ill pati ent, 11 26 anaro mi c ba rri er, 17 1 autonomi c innervatio n, 105- 111 , li l t,
107-110 celiac gangli a, l 06, I 07 mese nteri c gangli a, 107- 111 , 110 C hapman refl exes, 1053 effi cacy of OMT, 11 46- 11 47, 11 46 pedi atri c, 320-32 1 somati c dys fun ctio n resea rch, 11 92 Gene express io n, in nociceptio n, 132 Generi cs, molecular, and ca rdiology, 348 Genito urinary system, C hapm an refl exes, 1053 Geriatri cs, 327-337 clinical co nce rns, 333-336 co nfusion, 333-334, 333t falling, 335, 335 t hip fractures, 482-483, 483 iatrogenes is, 335-336 urin ary inco ntin ence, 334-335 fun ctio nal assessm ent, 33 1-332 histori cal aspects, 327 key co ncepts, 327 medical assess menc, 330-33 1, 33 1t physiology, 329-330, 328-329 r psychological assess ment, 332, 332t social aspects, 333 th eo ries of agin g, 327 Germ theory of disease, 167-168 G lenohum oral joint, fasc ial-li gamencous release, 9 13 G lossary of os teopathi c terminology, 1229- 1253 G losso phary ngeal nerve, 672 G lucocortico ids, and brainstem arousal sys tem, 148- 149, 149 G luteal region osteopathic manipul ati o n, 1110- 111 2,
1111- 1112 primary and endpoints, 1259-1260 G lycolyti c fib ers, in muscle co ntractio n, 75 G lycosaminoglycans (GAGs), in so mati c dysfun ctio n, 11 54, 11 56-11 57 Go lgi apparatus, horm o ne processin g, 18 1- 182
Go lgi tend o n orga n, 1032 Gout, 529 G rav itati o nal lin e, 1237 G ravity, and postural deco mpensation, 603-607. 604 biomechani cs, 605, 605-606 ho meos tasis, 604 li gam ems, 606, 607-608 muscle stress, 605-606, 606r skeletal stress, 606-607 Ground reacti on force, gait in hi p, 80-8 1, 80 in kn ee, 79 G round substance, 47 G roup curves See also Pos ture. manipul ative trea tm ent, 586-587,
587-588 mechani cs and diagnosis, 58 1 signifi ca nce, 583 G rowth , ho rm onal co ntrol, 187 G uid el ines hum an subject research, I 17 1 OMT, 11 50- 11 5 1 osteopathic principles, 11 -12, 15-16, I 1t Gyneco logy, 409-4 19 key concepts, 409 pelvic pai n anaro my, 409-4 12, 4 10-4 1 It,
410-4 11 di ffe remi al diagnosis, 4 13-4 17 dys meno rrh ea, 4 13, 4 13r endo metriosis, 4 14 ova ri an pai n, 4 14-4 15 pelvic floo r dysfun ction, 416-4 17 pelvic inflan1matory disease, 4 15-4 16 premenstrual sy nd rome, 4 13-414, 4 13 t uterine pai n, 4 15 patient evaluation, 4 12, 44 1'2t H abi tuati on, 130 H ahn emann , Samu el, 2 1 H allus valgus, 800-801 Hamm er roes, 800-80 I H amstrin gs, 774 kn ee mu scle fo rces, 78-79 H and anato my, 698, 699-700 fasc ial-li gamentous release, 9 13-9 14, 914 osteo pathi c manipulatio n, 111 2-1113,
111 4 so mati c dysfu nctio n, 700-70 I washing of, 175- 176 H aversian canal of bo ne, 68 Head and neck auto no mi c inn ervatio n of, 99- 100 auto no mi c nervous supply, 372-373, 373 di agnosis and trea tment, 660-683 anato my blood vessels, 662, 669 co nn ecti ve tiss ue, 660-66 1, 668 crani al nerves, 667-674, 673 ear, 677, 677-678 eye, 675-677, 676
Subject Index fourth ventricle, 674-675, 674-675 innervation , 663-667 , 672 lympharic sysrem, 662-663, 670 muscles, 660, 667 sinuses, 67 5 skeleral, 660, 666r, 66/-666 rhroar, 677 common cold, 677-678 headache, 678-683 cranial marion assessment, 683, 683 key co ncepts, 660 emergency medicine, 389-392 cephalgia, 389-39 1 eyes and ears, 389-391 neck pain, 390-392 nosebleeds/upper respiratory infection , 390 , 392 injuries in children, 323 lymphatic system, 37 1-372, 372 myofascia, 37 1, 371 primary and endpoints, 1258 Headaches, 437-442, 678- 68.1 cia sificarion , 427r clusrer, 439-44 1, 680 migraine, 438-439, 679-680, 440r sports r:oedicine, 543-548 tension-type, 441 , 680 traction and inAammarory, 680- 681 aneurysms, 681 arteriovenous malformations, 68 1 brain rumors, 68 1 cerebrovascular disease, 680-681 hydrocephalus, 681 large lobar hemorrhages, 681 temporal arteritis, 681 transient ischemic arracks, 681 rrearment, 44 1-442 Health promotio n and maintenance, 197-207 docror-patient relationship, 204-206, 205t family and work, 2023 key co nceprs, 197 nutrition, 198, 198t, 199 obesity, 200 personal safery. 202 physical activity, 199- 200 sexuali ty, 20 2-203 srress, 203-204 substan ce abuse alcohol, 20 1- 202 illegal drugs, 202 robacco, 200-201 suppo rt systems, 204 Heart acutely ill patient, 11 25 blood Row, 16 1- 163, 162 mnervanon See also Cardiovascular plexus. parasympathetic, 126-127, 127 sympathetic, 125- 126, 125-127 Heart fai lure causes, 349t diagnosis, 360-361 emergency medicine, 394 exercise, 36 I , 362
muscle hypothesis, 36 1-362, 362 osteopathy, 362-363 pathophysiology and natural h isrory, 358-360 treatment, 36 I Heartburn , I 04 Heilig formula, 616t Hemorrhage, large lobar, 681 Hemorrhoids, in pregnancy, 452, 455 Heparobiliary tree, autonomic innervation, Ill Herbal producrs, 474 Herniation, lumbar spine, 486, 489, 492 Hibernation, 162 High velocity low amplitude (HVl.A) techniques, 473 See also Thrust (high velocity/low amplitude) techniques. back pain, I 145 co mpli cations, 1148, I 149 somatic dysfunction, 11 59 Hill-Sachs deformity, 542 Hip anaromy, 786, 787 muscles, 804 balanced ligamentous tension , 921-924,
921-923 biomechanics, 80-8 1, 80 d evelopmental dysplasia, 479-482,
480-48 1 faci li tated positional release (FPR), 1024 muscle energy techniques, 90 1-904,
901-904 osteopathic mani pulation, I I 09-1 I 12, Ill Or, ll 11- 1113 fractures, geriatric, 482-483, 483 Hip drop test, 74 1 Hippocrates, 4, 6, 8 physical medicine, 5 17 Hiss plantar wh ip, 878-879, 879 Hoffman (H ) reAex, 1159 Home safety, 202, 203r Homeopathy, 21 Homeostasis allostasis, 150, 153 emergency medicine, 386 endocrine function , 18- 185 postural decompensation, 604 Hormones See also Endocrine system. and brainstem arousal system, 147- 149 in cancer, 467 in pregnancy, 4 53 Horner syndrome, 664 Hospice care, 472 Hospitalization acmely ill parienr, I I 15-1 142 key concepts, I I I 5 structural examination, 1115, 11/6 abdomen, 1121- 1123, 1122 lymphati c system , 11 23, 11 24 r segmental facilitation, 1115- 1120,
l117- l119 thorax, 1120- 1121 rreatmenr, 11 34-11 35
1271
abdo men/pelvis, 1131-11 34,
113 1- 1133 inAammarion, 11 23-1124 neuroendocrine immune system, 11 26- 1127 segmental fac ilitation, 11 24-1 126 specific tech niques, 1135-1141 abdomen, I 139-1140 lymph mobilization, 11 40- 11 41 paravertebral ganglia, 1136-1137 thoracic region, 1137- 11 39 thorax, 1127-11 3 1, 1 128-ll30 in elderly, 335-336 and osteopath ic manipulative therapy, 512-513 outcomes research , 1199 parient treatment, 426-429 Hospitals, osteopathic, 27 Hot packs, 222 Hulett, C.M.T., 8 Hulert, G . D., 9 Human Genom ic Project, 348 Human growth hormone, perfo rmance enha ncement, 548 Human immunodefi cien cy virus (H IV) infection, 166 biobehavioralmechan isms, 1205- 1206 Humerus/glenohumeral joint, balanced ligamentous tension, 926-927 , 928 Hyaline carti lage anarom y, 47 in synovial joints, 70 of synovial joi nts, 49 H yaluronic acid, in articular carti lage, 70-7 1 H ydrocephalus, 68 1 Hygiene, 175- 176 H yperactivity, in h ildren, 323-325 Hyperalgesia, prima ry afferent nociceptors, 140 H ypercalcemia, in ca ncers, 464, 465, 468 H yperca pnia, pulmonary, 504 H yperemia, 160- 16 1 H ypermobil ity, 747 Hypertension efficacy of OMT, I 147 headaches, 680-681 and heart fail ure, 359- 361 pharmacology, 192- 193 pulmonary, 503-504 H yperviscosiry syndrome, in multiple myeloma, 465 Hypoglossal nerve, 674 H ypotension, in pregnancy, 455 H ypothalam ic-pitui tary-adrenal axis, 186 and glucocorticoid release, 148- 149, 149 H ypothalamus, in acutely ill parient, 1126- 11 27 H ypothesis resting, I 195- 1 196, 1195 biobehavioral resea rch, 1208-1 209 Hysteresis, 11 58, 1158 latrogenesis, and aging, 335-336 ICE (ice, co mpression, a.nd elevation), 494 ID ET (Intra Discal Elecrro rhermal T herapy), 492
1272
Subject Index
Ileus, 406--407 acutely ill patient, 11 26 efficacy of OMT, 11 47 Iliac crest, 773 Iliac spin e, motion restin g, 774-775, 776,
776 Ili olumbar ligam ent sy ndrom e, 746-74 7 Iliopsoas spasm, 549- 540, 540 llium HVLA trea tm ent, 872- 874, 872-874 os teo pathic manipulati on, II 03- 1 I 0 5, IJ04r, 1104- 1105 Image ana lysis, 37-38 Im mune system ac utel y ill pati ent, 11 26- 11 27 allosrasis, 152 biobehav io ral mechanisms, 1205- 1206 ca ncer patients, 472- 473 and infect ions, 172-173 lymphati c system, 1059-1060 Immun oglobulin A, in multipl e myeloma, 465 Impin gement syndromes, 54 1-542, 542 In clusion /exclusion criteri a, 11 85, 12 17 In continence, pelvic floor dysfun ction , 4 16--4 17 Indi viduali zati o n, pain manage ment, 220 Inert ia, 64 In fants See also Pedi atri cs. birth hi sto ry, 307-3 10 crani al dysfun ction, 993- 994, 994-996 developmental dys pl as ia of hip, 479-482,
480-481 hosp ital treatm ent, 428-429 respirato ry distress syndrom e, 5 13 resp irato ry dysfuncti o n, 3 14-3 15 Infectio us diseases, 165- 178 antimi crobi al therapy, 174- 175, 175 back pain , 49 1 biobehav io ral mechan isms, 1205- 1206 ge rm theo ry, 167- 168 global signifi cance, 165- 167 hygiene, 175- 176 immuni ty, 170- 173 , 17 1 infl ammati on, 17 1- 172 key co ncepts, 165 knee osteoa rthritis, 485 nutriti o n, 173- 174 pelvic pain , 4 16 respiratory, 5 11-5 12 smallpox, 176 vacc in es, 176- 177 virul ence and pathogeni city, 168- 170,
168-1 70 Inflam mation acutely ill patient, 11 23- 11 24 biobehav ioral mechani sms, 1205 in fect ions, 17 1- 172 noc icepri o n, 130 soma ri c dysfunction, 137 Influenza o utbreaks, 16 5, 11 74 l nfo rm ed co nse nt, 11 70 , 12 17 In nervation acutely ill patient, 1125- 11 26
au ton omic. See Auto nomic nervo us system. of cervical spi ne, 685 female pelvis, 4 10--4 11 of head parasympathetic, 663, 672 sympathet ic, 663-667, 672 pulmonary structu res, 506 in so matic dysfunction , 11 55-1 156 thoracic, 706,7 11-7 12, 712 upper extrem ity, 694 Inn ominate dysfun ction See also Pelvis and sacrum. balanced li ga mentous tensio n, 920-921,
921 functional tech nique, 981-982, 982 muscle energy techniques, 894-897,
in musculoskeleral biomechanics, 75-76, 76 patell ofe moral, 541 in pregnancy, 45 1 replacement, for knee osteoa rthritis, 485 rib cage, 7 18 of shou ld er, 82, 82 in somatic dysfu nction , 11 56- 11 58 thoracic, 705-706 upper extremi ty, 690 Jones, Lawrence H , 97 1, 1002
journaL ofthe American Osteopathic Association OAOA) , 11 75, 11 82 furure resea rch, 12 19 soma ric dysfunction research, I 189 Jun gman n pelvic index, 6 11
895-897 osteopathic manipulation , 1 I 03- 1 105, II 04r, 1104- 1106 Inso mni a managem ent, 242-243, 242t Institutional Revi ew Board , 11 70- 117 1, 1217 I nsrru menrarion biobehavioral resea rch, 121 0 so matic dysfunction resea rch, I 190 Intensive care unit, 428 Interl eukin -6, biobehavioral mechanisms, 1205 Intermuscul ar septa, 53 Internal med icin e, 298-304 key concepts, 298 osteopathic, 298-299 patient man agement, 299-302 pneumonia, 303, 303 r visceral and syste mic diso rders, 302-303 In ternatio nal Federation of Manual/Musculoskel etal Medicine (F IMM), 11 44, 1224 Ionic binding, in arti cular cartil age, 70-7 1 Iro n deficie ncy, 174 Irritable bowel syndrome, C hapma n reflexes, 1052 Irritation , PINS method, I 032 Irvin e study, 11 73-11 7 4 Ischemic heart disease. See H eart fa ilure. Isolation patients, 428 Jenner, 7 Joint reaction force, 76 hip, 81 in knee, 79 shou lder, 83 Joints See also specifi c jo ints. anato my joint play, 5 1-52 synovial and nonsy novial , 49-51 ,
50- 51 anhle, 795-796, 796 in cance r, 466 dys fun ction, upper extrem ity screen, 639-640, 639 lower extremi ty, 784-785 movement types, 77-78, 77
Kege l exe rcises, 4 17 Kennedy, John F. , 1034 Kidneys auto nomic innervation, 111 - 11 2, 112 osteopathi c manipulation , 1086--1087.
1087 Kinematic analysis, soma tic dysfunction resea rch, I I 90 Knee anato my, 789-794, 789-791 li gaments and cartilage, 792-793,
792-794 Q-a ngle and patell a. 79 1-792, 79 1 athl ete injuri es, 54 1, 541 bi o mechani cs, 78-80, 78 inrraa rri cul ar movements, 79 joint structure, 79 movement efficiency, 79-80 muscle forces , 78-79 range of motion , 78 react io n st ress forces , 79 injuries in children, 312-313 lymph aric flu ctuati o n, I 14 1 motion, 793-794, 795 muscle energy techniques, 904-905.
904-905 os teoa rthritis, 483-485, 484 osteopathic manipulation, 1113-1114,
11 14 Knee jerk refl ex, 122 Knee joint, 50 Koch's postulates, 167- 168 Korr, Irvin M. , 8-9 osteopathi c principles, 12-17 neurophysiology, 12 1, 129 resea rch in OMT, 11 68 Kyphoplasty, 493 Kyphosis , in pregnancy, 45 1 Labor and delivery, 457-459, 457-458 Lamina, lu mbar region , 730, 730 Langley, J .N., 189 Lasegue sign, 443 Learning disorders, 323-325 Leg. See Lower extrem iti es. Legg-Calve-Perthes disease, 312 Leiomyomas, urerine, 4 15 Length, and muscle cont raction, 74
Subject Index
Leptomeningeal carcinomatosis, 466 Levator ani studies syndrome, 4 17 Lhermitre sign, 443 Licen~ure, 24-25 Life expectancy. 165, 197 Life phases and health, 227-232 adolescence, 229-230 adu lthood, 230 ages one to five, 228-229 developmem, 227 elderly, 230-23 I infancy. 228 prenatal period, 227 school-age child, 229 Lifting, lumbar spine, 86 Ligamems See also Balanced ligamentous tension (BLT) techn iques. abdominal, 752-753, 792-793 biomechanics, 71-73, 72 of cervical spine, 684 laxiry, 496-498 lower extremity, 784-785 lumbar region, 73 1-732, 73 1-732r pelvis and sacrum, 762-763 PINS m ~rhod , I 030 in postural decompensation, 606,
607-608 of shoulder, 495 of synovial joims, 50 Lightening, in pregnancy, 452 Limbs anatomy, 58, 58 embryology, 46, 46 Lippincorr, Howard A., 970-97 1 Literature sources, 1175-1 177, 1222, 1176- 1177r glossary, 1229 Littlejohn, J. Marrin, 8- 9 Liver See also Lymphatic system. fascial-ligamentous release, 91 I lymphatic pumps, 1070-107 1, 1071 osteopathic manipulation, 1083-1085,
1084-1085 Load bearing in biomechanics, 66 bone fracture, 69 muscle moments, 76 in knee, 79 and muscle contraction, 74 by spine, 85-86, 85 Locomotion biomechanics, 86-87, 87 Locus coeruleus, and brainsrem arousal system, 148-149, 149 Lordosis angles, 1230 in pregnancy, 4 5 I radiography, 6 1 I Lordotic curve, normal, 727 Low back pain orthopedics, 485-494 causes, 486t differential diagnosis, 490-49 1, 492 history and physical exam ination, 486-488
management, 49 1-494, 493 pathophysiology, 488-490, 489-490 physiatry, 522-523 in pregnancy, 450-452, 456 Lower extremities, 784-8 18 See also Extremities. anatomy, 784-785, 785 ankle, 794-797, 796 fascial-ligamentous release, 9 11 -9 12,
912 femur, 786-789, 788 foot, 797- 80 1, 797-803 hip, 786, 787 INR and M FR techniques, 958-961 key concepts, 784 knee, 789-794, 789- 79 Q angle and patella, 79 1-792, 791 ligamentous sprains, 785-786 muscles, 804-806, 805-806r, 807-809r nerves, 804, 806, 81 1, 814 neuromuscular structure and function, 801, 803 rad iculoparhy, 80 1-804 referred pain, 803-804, 805-806t soft tissue techniques arch springing, 832, 832 fascia lata, 830-831, 830-831 piriformis, 831-832, 832 plantar fascia, 832, 832 vascular and lymphatic systems, 806-813,
815 Lubricin, 7 1 Lumbar region, 727-750 anatomy, 727-737 anterior element, 727-728 intervertebral disc, 729 vertebral body, 727- 728, 728 foram en, intervertebral, 73 1, 731 ligaments, 73 1-732, 73 1r muscles and fascia, 732-733, 732-732r posterior elements, 729-73 1 articular processes, 729-730 lamina, 730, 730 pedicles, 729, 729 spinal canal, 730-73 1 spinous processes, 730 transverse processes, 729 spinal cord and lumbar nerves, 733-735 dermatomes, myotomes, and sclerotomes, 734- 735, 736 lumbar plexus, 734, 736r spinal cord, 733-734, 735 vasculature and lymphatics, 735-737,
736-737 articulatory techniques extension, 844-845, 844 flexion, 843-844, 843 rotation, 846, 846 side-bend ing, 845-846, 845, 846 examination, 739-743, 739 auscultation, 740 palpation and motion resting, 740,
740-741 specific rests, 740-743 diaph ragm, 740-74 1
1273
hip drop rest, 741, 742 lumbar rotation, 742-743 paraspinal pal pation, 743 psoas rest variation, 7 43 spi nal com pressio n, 742 spinal spring rest, 742 render poi nts and trigger points, 743 T homas rest, 743, 743 thoracolumbar rotation, 741-742 exercise prescri ption, 286-287 facili tated positional release (FPR), 1022-1024, 1022-1023 fascial-ligamentous release, 9 10-9 11, 911 fun ctional tech nique, 975-976, 976-978 IN R and M FR techniques, 936-951,
937-955 key concepts, 727 motion, 737- 739 normal motion, 737-738, 737 somatic dysfunction, 738-739 vertebral unit, 737 muscle energy techniques, 885-886, 885 osteopathic manipulation, 1102-1103,
1103 soft tissue techniques bilateral rhumb pressure, 827 lateral recum bent, 827, 828 prone pressure with counterleverage, 826, 826 prone scissors technique, 826- 827, 826 prone traction, 827, 827 seared, 828, 828 supine, 827 supine fixation, 825 wirh counrerleverage, 825-826 strain and countersrrain technique, 1012-10 13, 1012-1013 treatment, 743-750 abdominal aneurysm, 794 cauda equina syndrome, 744 dirry half-dozen, 746, 746 hypermobiliry, 747 iliolumbar ligament syndrome, 746-747, 747 meralgia paresthericaa, 747 psoas syndrome, 747-748, 748 radiculopathy, 748-750, 749 Lumbar spine, 86 Lumbosacral arch, acutely ill patient, I 132 Lumbosacral pain, exercise prescription, 286-287 Lungs See also Pulmonology; Respiration. acutely ill patient, 11 25- 11 26 carcinoma, 464-465 osteopathic manipulation, 1089, 1089 Lymph. See Lymphatic system. Lymphatic pumps cancer patients, 473, 474 thoracic drainage, 507-508 Lymphatic system, 1056- 1077 abdominal, 753, 754-755 acutely ill patient, 11 23- 11 24, 11 29, 11 24r OMT, 1140-11 4 1
1274
Subject Index
Lymphati c system-continued anatomy, I 057-1059 channels, 1058- 1059, 1058 lymph, 1059 organized tissues, 1057 cervi cal spine, 685 emerge ncy trea tment, 386, 387 embryologic development, 1056 head and neck, 37 1-372, 374,, 662-663 ,
372, 670-671 key co ncepts, 1056 lumbar, 736-737, 137 manipul ati ve techniques, 1062-1077 flow improvement, 1068- 1077 abdominal and pedal pumps, 1069-1070, 1070 abdominal techniques, 1073- 1075,
1074-1075 cervi cal soft tissue, 1072- 1073,
1073-1074 direct press ure, 107 1- 1072,
1071- 1072 extremiti es, 1075-1077, 1076-1077 liver and splee n pumps, 1070-107 1,
1070-1071 pump techniques, 1068- 1069,
1068- 1069 thoracic soft tissue, 1073 impedim ent removal , 1063- 1068 di aphragm, 1065- 1067, 1066-1067 extrinsic pump, 1065 open thoracic inlet fascia, 1063- 1064, 1063-1064 sympathetic activity, 1064-- 1065,
1065 myofascial rri gger points, 1045,
1045-1047 pathophysiology, 1061 pelvis and sacrum, 765-766 ph ys iology, 1059-1061 fluid balance, I 059- 1060 mechanisms of flow, 1060- 1061 protocol for osteo pathi c exa mination, 426 rib cage, 720 thoracic, 7 10, 711 trea un enr, 1061-1062 upper extremity, 692-693 Magneti c heal ing, 2 1 Magneti c reso nan ce imaging (MRJ), 38 Major histoco mpatibility co mplex (MHC) , and infecti ons, 172-173 Malaria, 166, 168 Mandibular nerve, 670-671 Mathemati cal models, load resista nce, 76 Max illary nerve, 670 McCo nn ell , Carl P., 970 Mechanoreceptors, 1154-1155, 1154t In kidn ey, I 12 Medial mall eo li levelness, 774 Med iastinum , 1090, 1090 Medications adverse reacti ons, in agin g, 335-336 for arthritis, 53 1 for asthma, 320 in osteopathy, 7
for spondyloli thesis, 630 MEDLINE, 11 7 5 Meissner co rpuscles, 138 Meissner's ganglia, I 03 Membranes, intracranial and intraspinal, 987-989 Menopause, 41 7 Menstruation , pelvic pain, 4 13 Meralgia paresthetica, 747 Merkel discs, 138 Mesenteric release, 760, 760 Mesemeries lumbar, 733, 734 lymphatic flow, 1074, 1075 Meta-analysis resea rch , 11 72 Methotrexate, for rheumatoid arthritis, 53 1 N-Methyi-D-aspartate (NM DA) in nociception, 132 pain transmission , 216 in somatic dysfunction, 1155 Michigan State University, internation al co nferences, I 144 Microbial diseases. See Infecti ous di seases. Microbiology, 34 Migraine, 438-439, 679-680, 440 t sports medicine, 543-548 Models, th eo retical , 1172 Moment arm , 65 Mood diso rders, 209-21 0 Morning sickness, 454 Motion cervical spine, 686-688, 689 in cranial region. See Cranial region. injured athletes, 538 ofknee, 793-794, 795 lumbar, 737-739, 737 palpatory skills, 561-562 pelvis and sacrum, 767-768 axis of motion, 768 walk cycle, 768-769 segmental tesring, 646-649 cervical , 646 lumbar, 647-648 patient position , 647t pelvic, 648-649 rib, 647 thoracic, 7 16-717 should er, 695-696 spinal seg ments, 83, 83 thoraci c, 7 15-7 16 three-dim ensional, 64, 64 upper ex tremity, 695-696 vertebral and costal cage, 712-7 13 Moror neurons definition , 73 in heart innervation, 126 StrUC[llre, 122-123 Muscle energy techniques, 881- 907 complications, 1149 conrraindications, 884 diagnosis, 882 efficien cy factors, 884 history, 881 -882 key concepts, 881 physiologic principles crossed ex tenso r reflex, 883
joint mobili zation, 882-883 oculocephalogyric refl ex, 883 post-isomet ri c relaxation, 882 reciprocal inhibition , 883 res pi rarory ass istance, 883 sequenti al steps, 883-884 so matic dysfun ction, 11 59 techni cal principles, 88 1 techniques costal somatic dysfu nction , 890-894,
890-894 ext remiti es, 900-907, 901-906 innominate dys fun ction, 894-897,
895-896 sacrum , 897-900, 897-900 spinal segmental somatic dysfun ction, 885-890, 885-890 Muscle hypothesis, 36 1-362, 362 Muscles See also specific muscles. abdominal , 752-753 acutely ill patient, I 120- 11 2 1, 11 33- 11 34 in cancer, 466 of ce rvi cal spi ne, 684 contraction, 54-55 biomechanics, 73-75, 74 hip, 80-81, 80 in knee, 79 of head, 660, 667 hip, 804, 805-806t lumbar region, 732-733, 732 t, 733 r myofascial contin ui ty, 53, 58-60 pelvis and sacrum , 763-765 PINS method, I 030 in posrural decompensation , 605-606, 606t rib cage, 7 19-720, 7 19 of shoulder, 495 thigh and leg, 804--806, 807-809t thoracic, 706-7 10, 707-7 1Or upper extrem ity, 691 of urinary bladder, I 13-1 14 Muscle-tend on co mplex, 52, 52 Musculoskel etal syste m biomechanics, 75-78 cente r of rotation, 78 force moments, 75-76, 76 joint structure, 77 joint surfaces, 77-78, 71 load resistance, 76 mechani cal adva ntage, 77 range of motion, 77 segment movem ent, 75 tendon actions, 76, 76 in cancer, 465-467 back pain , 465-466 joints, 466 muscl e and ski n, 466-467 occult sy mptoms, 467 core of diagnosis and treatm ent, 14-- 16, 11 development, 308-3 14, 309t costal cage, 31 0 cranium, 309-3 10 lower extremity, 3 12-313
Subject Index uppe r extremi ty, 3 11 -3 12 vertebral spine, 3 10-3 1 1 ear, nose, and rhroat, 380-38 1 embryo logy, 44-46, 45--46 in emergency medicine, 388 functions, 49-55 fascia and neurovascular bundle,
52-54,52-54 joint play, 51-52 muscle action, 54-55, 55 muscle-tendon co mpl ex, 52, 52 synovial and nonsynovial joints, 49-5 1,
50-51 geriatri c, 329-330 limb anato my, 58, 58 microscopic anaro my, 46-49 cartilage and bone, 47, 48-49 co nnective tissue, 46-47, 46, 47 injury effects, 49 skeletal muscle, 49, 49 myofascial co ntinui ty, 58-60, 59-61 in pregnancy, 450-452 protocol fo r osteopathi c examinati on, 422-426, 424-427 somatic dysfunction, 633-659 in an:bulato ry or bedridden patients, 649-659 ambu lato ry, 650-652 t bedridden patient, 654 outpatient or hospitalized, 652-654, 653-654t key co ncepts, 633 outpatient fo rms, 655-658 specific tests, 635, 636t, 637 anterio r scree n of horizo ntal planes, 639, 639 joint dysfunction, 639-640, 639 patient position, 646-649, 647t, 650-652t posterior screen of horizo ntal planes, 638, 638 sta nd ing spinal fl exion, 640, 640-641 acti ve scree ning, 640-64 1,
640-641 passive screeni ng, 64 1-646,
642-647 TART mnemonic, 633-634 and vascular systems, segmental organization, 55-56, 55-57 Muscul otendoinous uni t, 74 Myasthenia gravis, 468 Mye loma, mul tiple, 465 back pain, 49 1 Myocardial in farctio n, 355, 356 efficacy ofOMT, 11 46- 11 47, 11 46 emergency medicine, 386 soma ti c dysfun ctio n research, 11 9 1 Myofascia See also Fascia. in somatic dysfunction, 11 56- 11 58 trigge r points. See Trigger points, myofascial. Myoto mes, lumbar, 734-735 Naffziger sign, 443 National institute of Agi ng, 327
National lnstiture of Co mmuni ca ti ve Diseases and Stroke, 11 43 Na tionallnstitu tes of Health , 11 68 Nat ional Library of Medi cine, 11 75 Nausea, in pregnan cy, 454 Neck auto nomic innervation of, 99-100 exercise prescription , 286-287 Neidner technique, 324t Nerve blocks, 222-223 ethyl chloride, 223 hot packs, 222 ice, 223 transcutaneous nerve stimulation, 222 vibration, 223 Nerve growth facto r (NGF.), 133 Nerves See also Au ro nomi c nervous system; central nervous system ; peripheral nervous sys tem. abdomin al, 753, 755 in children, 32 1-325, 323 t apnea, 323 closed head inju ry, 323 colic, 322 lea rning di so rders/ hyperacti vity, 323-325 crani al. See C ranial nerves. endocrin e fu ncti on, 184- 185 lower extremities, 804, 806, 811, 814 origin of, 39 pelvis and sacrum , 766-767, 767 spinal co rd and lumbar, 733-735, 735-736 Neural gia, cranial, 68 1-683 Bell palsy, 68 1-682 temporomandibul ar joint dysfun cti on, 682-683, 682 trigeminal neuralgia, 68 1 Neuroendocrin e-immune network, and brainstem arousal system, 147-152 Neurologic defi cits, sportS medi cine, 543-548 Neurology, 435-449 anato my, 435-436 chro ni c pain syndrome, 447 entrapment neuropathi es, 444-447, 445 t carpal tunn el syndrom e, 445-446 thoracic outl et syndrome, 446-447 headaches, 437-442,437 r cl uster, 430-44 1 mi grain e, 438-439, 440t tension-type, 44 1 treatm ent, 44 1-442 key co ncepts, 435 osteopathi c lesion, 436-437 spinal disorders, 442-444 Neuro musculoskel etal medi cine, 420-434 AIDS, 428 case study, 43 1-433 children, 428-429 dru g and alcohol detoxificati on, 428 hospital chart, 429, 430 hospital-based , 421 hospitalization, 426-429 trea tm ent prorocol , 428
1275
intensive care unit, 428 isolation patients, 428 key co nce pts, 420 O MM specialty, 42 1, 422t, 423 r osteopathi c co nsultation, 429-43 1 patient examination, 422-426 hisrory taking, 422 phys ical exa mination, 422-426,
424--427 postoperative or trauma patients, 429 psychiatric patients, 429 rehabilitarion , 428 Neuromusculoskeletal sys tem inhibition of. See Progress ive inhibi tion of neuromuscul ar stru ctures (PlNS) . lower extremity, 801 , 802 and myofascia, integrated rel ease, 93 1- 968 clinical assessment, 935 definiri on, 93 1- 932 exe rcise role, 936 key co ncepts, 93 1 mechani cs and forces, 932-934 asymm etry se nsing, 933-934 force effects, 932-933, 933 palpation to develop haptic skills, 933 posttrea tment disco mfort, 936 specific areas carpal and palmar runnel , 966-967,
966-967 crani ocervi cal spine, 952-955,
955-958 foot and ankle, 96 1- 962, 961 fo rea rm , elbow, and wrist, 964-966,
964-966 lower limb, 95 6-96 1, 958-961 lumbosacral spine and pelvis, 936-95 1' 937-955 upper limb and should er, 962-964,
962-963 three-dimensional patterns, 935 treatm ent goals, 935-936 treatment ski lls, 934-935 pain at loose sites, 934-935 ri ght-loose co ncept, 934 Neuropath ic pain , 2 15-2 16 Neuropeptide Y in ce rebral vasculature, 99 in ureter, 11 2 Ne uropeptides See also specifi c neuropeprides. in so matic dys fun ction, 11 56 Neurophysiology, 33, 120- 136 heart innervati on parasympath etic, 126- 127, 127 sympatheti c, 125-126, 125-126 integrati ve fun cti on, 129-130 key concepts, 120 nociceptive stimuli, 130- 133 nonimpulse-based integration , 133- 134 in osteopathy, 12 1 reflexes, 12 1- 123 excitability, 130 interactions, 123-125, 124-125
1276
Subject Index
Neurop hysiology, reflexes-continued so maro-so matic, 123 stru cture, 122-123, 122 viscero-visceral , 123 so mati c afferents and baroreceptor co ntrol, 128-129, 128, 129 viscera l fun ction co ntrol, 127-128, 127,
128 Neurotransmitters, lymp hatic system, 1057 Neurovascu lar accidents, HVLA co mpl.i cations, 11 49 Neurovascu lar bundle, 52-54, 52-54 Newron, definicion, 65 Nirric ox ide in myocardi al blood flow, 162-163 in peripheral vasculature, 98 Nociception, 137-156 abdominal pain , 400---401 acutely ill patient, 1 135 headaches, 441 neuroendocrine immune network, 147- 152, 150 al lostasis, 150- 153 all ostaric load, 151 - 153, 15 1t arousal system, 147-149, 149 cytok.in e network, 149 pain man agement, 216 pulmonary, 505 in respi rarory plexus, 103 and so mati c dysfunction, 137-140, 1154,
138, 1154 fib er systems, 138-139 pathophysiology, 137-138 periph eral sensitization, 139-140, 139 spinal faci litatio n, 140-1 45 brainstem arousal system, 145- 147 ascending pathways, 145- 146 reticular formation , 146 central se nsiti zation, 144 dorsal horn , 140-144, 141- 144 PANS model, 145 spinal cord outp ut, 145, 1155- 1156 Nodes, lymph atic, I 057 Nonsteroidal antiinfl ammatory drugs (NSAIDS) for arthritis, 53 1 orthopedic co nd.itions, 496 North American Sympromatic Carotid Endarterecromy Trial (NAS CET), 1194 Nose. See Ea r, nose, and th roar disease. Nosebleeds, 390-392 Nu ll hypothesis, 1195, 1217 Nurses' Health study, 356 Nutrition ca ncer pati ents, 472 geriatric, 330 health promotion, 198, 198t, 199 and infections, 173-174 lymphatic system, 1060 performan ce enhancement, 549 Obesiry, 200 Obstetrics, 450---461 bod y fluid s and circulation , 452, 453
first trimester, 453---454, 454 hormon al cha nges, 453 key concepts, 450 labor and delivery, 45 7---4 59, 457-458 postpartum, 459 second trimester, 454, 455-457 somatic dysfunction, 450---453, 451 low back pain , 450-452 third trimester, 455---457 Obturator foram en, I 091 , I 091 Occipital-arias, 1095-1096, 1096 Occipito-adamal joinr, muscl e energy techniques, 888-889,
888-889 Oculocephalogyric refl ex, 883 Oculomotor nerve, 669-670 O lfacrory nerve, 667-668 Oncology, 462---476 biologic response modifiers, 4 72---4 73 central nervous system, 467-468 cerebral malignancy, 467 indirect paraneoplasric, 467---468 complemenrary and alternative medicine, 474 ethics of presentation to pati ent, 470-47 1 key concepts, 462 lung carcinoma, 464---465 musculoskeletal system, 465-467 in ad ults, 467 back pa.in, 465-466 in children, 467 joints, 466 muscle and sk.in, 466-467 osteopathic manipulative th erapy, 473-474 contraindicatio ns, 473 , 473t indications, 474, 474r peripheral nervous system, 468-469 neuropathies, 469 peripheral manifes tations, 468 spinal cord compression, 468-469 plasma cell neoplasm, 465 renal cell cance r, 464 supportive care, 47 1-472 touchin g as commu nication, 463 viscerosomatic response, 469-470 rumor necrosis factor, 469-470 whole patienr, 463 Onuf's nucleus, 11 6 Ophthalmic nerve, 670 Opioids. See Analgesia. Optic nerve, 668-669 Orthopedics, 477-499 developmental dysplasia of hip, 479-482,
480-481 hip fracture, geri atric, 482-483, 483 key co ncepts, 477 ligamentous lax ity, 496-498 low back pain, 485-494, 486t differenrial di agnosis, 490-49 1, 492 history and physical examination, 486---488, 487 management, 491-494 pathophysiology, 488-490, 489 osteoarthritis of knee, 483-485, 484 patient examination , 479
principle of, 478 should er instability, 494---496, 495 Orthotics postural, 589,6 13-6 14, 613 for spondylolithesis, 630 Ortolani sign, 479, 786 Osmotic pressure, and lymph flow, 1060- 106 1 Osteoarthritis, 529-530 knee, 483-485, 484 Osteons of bone, 68-69, 68 Osteopathic manipul ative therapy (OMT) See also specific techniques. of abdomen, 758-760 collateral ga ngli a inhibition, 759-760 falciform li gament (linea alba) rel ease, 760 mesenreri c rel ease, 760, 760 paraspinal inhibition , 758-759 atelectasis, 405-406 1n cancer co ntraindi cations, 473, 473t indications, 474, 474t complica tions, 1 147- 11 50 co ronary artery disease, 357 ea r, nose, and throat disease, 37 1, 380-38 1, 381 efficacy, 11 43-1 147 in emergency med icine, 393-397 gro up curves , 586-587, 587-588 headaches, 439, 44 1-442 ileus, 407 ligam entous laxity, 496-498 lung disease, 508-5 14 neuromuscul oskeletal medicine. See Neuromusculoskeletal medicine. otitis medi a, 378-379 in physiatry, 5 19-520 postural hom eostasis, 6 13 in pregnancy, 459 rehabi li tation , 545 fo r rh eumaroid arthritis, 532 for scoli osis, 622 sinusitis, 375 so matic dysfunction, 569 spinal di so rders, 442-444 spo ndylolithesis, 629 Osteopathy ca rdiology, 345-349 definiti on of, 9- 10 diagnosis and rrearmenr, 574--579 dose guidelin es, 577-578 key co ncepts, 574 SOAP method , 578 so mati c dysfun ction, 574--577 TA RT acron ym, 574 Educational Co uncil , 10- 11 emergency medicine. See Emergency medi cine. examination and di agnosis, 566-573 key co ncepts, 566 so matic dysfun ction , 567-568 anaromy, 567-568 O MT, 569
Subject Index
physiologic mechani cs, 57 1 structure, 568- 569 spinal motion, 569-572, 570 active and passive tesring, 57 1 germ theo ry of disease, 167 history of, 19- 29 education and growth, 21 - 24 conAict with AMA, 22 curriculum, 22-23 research, 23-24 schools, 2 1- 22 federal government recognition, 26-27 hospitals, 27 key concepts, 19 organizations, 25-26 specialties, 26-27 stare licensure, 24-25 internal medicine, 298-304 organization, 25-26 pain management, 223-224 pediatrics. See Pediatrics. and pharmacology, I 90-193 philosophy of, 4-6, 32, 5r allosraric response, 153-154 h isroric developmenr, 8-1 I , 19-29 holistic aspects, 6 parienr care, 6-8 medications and vaccinations, 7 practice guidelines, 11-12, I It primary care. See Family practice. principles, 12- 17 musculoskeletal sysrem, 14- 16 person as a whole, 13-14 personal health care systems, I 5 psychiatry. See Psychiatry, osreoparhic. Osreoromy, for knee osteoarthritis, 485 Oriris media, 3 15- 3 16, 378-379 emergency medici ne, 389- 390 Outcomes research , 1194-1202 cosr effectiveness, 1226 hypothesis resting, 1195-1196, 1 195 osteopathic medicine, 1194-1195, 11 98-1200, 1200-1201 osteopathic research, 11 73 study design, I 196- 1 198, ll98t,
1196-1197 Ovary auronomic innervation, 114-115 cysrs, 4 14-4 I 5 osteopathic manipulation, 1091 - 1092 Oxidative fibers, in muscle conrractio n, 75 O xidative phosphorylation, 158- 159 Oxygen, pulmonary, 504 Pacinian corpuscles, 138 Pain abdom inal, 753, 755 acurely ill parienr, I 118-11 19 biobehavioral factors, 1206-1207 in cancer, 471 chron ic, 447 physical med icine, 52 1 definition, 2 14-215 discogenic, I 023- 1024, 1023 and embryologic developmenr, 401 growrh, in children, 313
h isrory of theories, 212-2 14, 2 13 information Aow, 21 7-2 19 cognitive/emotional appraisals, 219 perception of pain, 217,219,218 key concepts, 212 in kidney, 112 management, 219-220, 220r analgesics, 220-222 addiction, 221 adj uvanrs, 22 1-222 placebos, 22 1 side effects, 221 tolerance, 221 coping strategies, 224 individualization, 220 medications, 220 nerve blocks, 222-223 osteopathic, 223-224 behavior modification, 223-224 biofeedback, 223 cardiovascular fi mess, 223 counseling, 223 gait training, 223 proprioceptive neuromuscular facilitation, 223 stretching and strengthening, 223 support groups, 224 neuropathic, 215-216 nociception, 130, 216 pelvic. See Gynecology. psychology of, 214 referred, 386 lower extremities, 803-804, 805-806t myofascial trigger poinrs, I 038-1039 thoracic, 712 reAex interactions, I 23-124 rule of, 41 spinal, exercise prescription, 286- 287 spinothalamic pathways, 216- 21 7 Palpation See aLso Touch. abdomen, 757 acutely ill patienr, 1117-1123 cervical spine, 686 Chapman reA exes, I 05 1-1 052, I 052 cranial dysfunction, 994 injured athletes, 537-538 lumbar, 740 paraspinal, 743 pelvic and sacrum , 770-771 postural diagnosis, 608-609, 608 primary and endpoinrs, 1261 skills and exercises, 557-565 dominanr eye, 558-559, 559 dominanr hand, 558 forearm, 560- 561 with hands and fingers, 558 inanimate objects, 558 key concepts, 55 7 layer palpation, 559-560 motion perception, 561-562 sensitivi ty, 561 so matic dysfunction, 562- 565, 562t cervical region, 563, 563 lumbar region, 564, 564 research, I I 9 I
1277
sacroiliac region, 564-565, 564-565 thoracic region, 563-564, 564 spondylolithesis, 628, 628 thoracic region, 7 15 upper extremity, 694 Pancoast syndrome, 464 Pancreas autonomic innervation, Ill osteopathic manipulation, I 087-1088, 1088 Pancreatitis, segmenral facil itation, 1126 Parasympathetic nervous system, 96-97, 96 abdominal pain, 40 I head, 663, 672 heart innervation, 126-127, 127 protocol for osteopathic examination, 426 Parathyroid hormone-related peptide, in renal cell cancer, 464, 468 Pasteur, 6 Parch, transdermal, 220 Parella. See Knee. Patellofemoral joint. See Knee. Patient education ear, nose, and rhroar disease, 37 1 spondylolithesis, 629 Patienr satisfactio n back pain OMT, 11 45 osteopathic health delivery, 1194 outcomes research, 1200 See aLso Orrhoped ics Patterning fascial, 583-585 musculoligamentous, 585, 587r, 586 spinal, 583, 584 Pavlik harness, 480, 480 Pedal lymphatic pumps, 1069-1070, 1070 Pediatrics, 305-326 gastrointestinal system, 320-321 constipation, 32 1 diarrhea, 321 gastroesophageal reAux disease, 321 history and examination, 307-308 key concepts, 305 musculoskeletal development, 308-314, 309t costal cage, 31 0 cranium, 309- 3 10 juvenile rheumatoid arth ritis, 313- 31 4 lower extremity, 3 12- 3 13 upper extrem ity, 3 11 -312 vertebral spine, 3 10-31 1 neurologic dysfunction, 32 1-325, 323t apnea, 323 closed head injury, 323 colic, 322 learning disorders/hyperacriviry, 323- 325 Neidner technique, 324t respirarory dysfunction, 314-320 asthma, 318-320, 319r bronchiolitis, 317-3 18 croup, 3 16-3 17 newborn , 31 4-3 15 oriris media, 31 5- 3 16 pharyngitis, 316 Pedicles, 729, 729 Pelvic Aoor dysfunction, 4 16-4 17
1278
Subject Index
Pelvic inflammatory disease, 4 15--4 16 Pelvis See also Gy necology. acurely ill patient, 11 26, 11 3 1- 11 34,
1133 anatomic landmarks, 772 arti culatory techniques rotation to innominate, 846-847, 847 sacroi liac joim gapping, 848, 848 balanced liga mentous tension , 919-920,
920 emergency medicine, 395-397 fascial-ligamemous rel ease, 910, 911 HVLA trea tm ent, 871-874 extremities lower, 875-879, 876-879 upper, 874-875, 874-875 ilium , 872-874, 812-874 sacrum , 87 1- 872, 871-872 INR and MFR techniques, 936-95 1,
937-955 lymph atic system, 1067- 1068, 1067 osteopa thic manipulation. See Visceral manipLdation. in pregnancy, 45 1 and sacrum , 762-783 anato my, 762-767 muscles and connective tissue, 763-765 primary, 763-764 secondary, 764-765, 764 nerves, 766-767, 767 skeletal/ligaments, 762-763, 763 vascwar/lymphatic, 765-766,
765 history and ph ys ical examinatio n, 769-772, 770t neurology, 77 1-772 palpation , 770-77 1 key concepts, 762 motion and dysfunction , 767-768 axes of motion , 768 norm al walk cycle, 768-769 sacral motion, 768 motion res ting, 772-777 anato mi c landm arks , 772 special tes ts backward bending, 776 fascial restriction , 777 hamstring, 774 iliac crest, 773 iliac spine, 774, 775 comp ression, 776-777, 776 medial malleoli, 774 oblique axis, 775-776 pubic symphysis, 774 sacral base, 77 5 sacral inferolateral angles, 775 sacrum, 774-775 posterior, 776 seated flexion , 773-774 spring, lumbosacral, 776 standing fl exio n, 773-774 transverse axis, 775 Trendelenburg rest, 772-773
pelvic diagnoses iliosacral somatic dysfun ction, 777-778 sacroi liac dysfun ction , 778-782, 779t an rerior sacrum , 779 causes of, 782 posterior sacrum, 779-782 torsion , 780-78 1, 780r strain and co unterstrain techniqu e, 101 3- 101 4, 1013-101 4 Penis, autonomic innervation, 11 6 Peptides, endocrine, 181-182, 184 Percuraneo us reflex of Morley, 40 l Performance enhancement, 548-549 Perimysium , 73 Periodontal disease, 166 Peripheral nervous system autonomic components, 91 in ca ncer, 468--469 myofascial trigger points, I 038 primary afferent nociceptors (PANs), 138- 139 Person as whole, C hapman reflexes, I 052 Personality disorders, 252-253 Personalized treatment, 7-8, 13- 14 Pes planus, 796 Petrissage, lymphatic flow, I 074- 1075, I 075 extremiti es, 1076-1077, 1076-1 077 Phalen res t, 702 Pharmacology, 34 , 189- 193 history of, 189-190 hypertension, 192-193 key co ncepts, 189 osteopathic principles, 190- 192 Pharyngitis, 3 16, 379-380 Phosphocreatine, as ATP source, 158 Phys iatry. See Physical medi cine and rehabilitation. Physical medicin e and rehabilitation, 5 16-525 ca rpal tunnel syndrom e, 523 cervical sprai n/strain , 524 history of, 517-518 key concepts, 516 low back pain , 522-523 manipulation , 519-520 resea rch , 520-522 patient eval uation, 518-519 return to work issues, 522 sports medicine, 524-525 training, 516 Physical training, of li gaments and tendons, 72 Piriformis muscle osteopathic manipulation , 1112, 1113 primary and endpoints, 1259 strain and countersrrain, I 01 4, I 01 4 Pituitary gland, segmental fac ilitation , I 127 Pituitary hormones. See H ypothalamicpituitary-adrenal axis. Placebos biobehavioral factors, 1207-1208 osteopathi c research , 1224-1225 pain management, 221
Plagiocephaly, 309 Planes of body, 1244 Plasma cell neoplasm , 465 Plasticity, in biomechanics, 67 Pneum onia emerge ncy medi cine, 394 osteopathic manipul ative th erapy, 303, 511-512, 303t thoracic reflexes, 1125 Point and pressure techniques See also Progressive inhibition of neuromuscul ar structu res (PI NS). antecubital region, 1260 femur and gluteal region, 1259-1260 head, 1258 palpati on, 1261 shoulder and sternum , 1259 xiphoid process, 1260 Position of patient, visceral manipul ation, 1092, 1092 Posture coro nal, horizo ntal, and sagirtal planes, 603-632 diagnosis, 607-612 observati on and palpation, 608-609,
608-609 radiography, 609-612, 610-611 grav itational strain, 603- 607, 604 biomechanics, 605, 605 homeos tasis, 604 ligament stress, 606, 607-608 muscle stress, 605-606, 606 r skeletal -arthrodial st ress, 606-607 key co ncepts, 603 sagittal plane di so rd ers, 622 scoli osis, 618-622 diagnosis, 6 18-620, 619-620 radi ograp hy, 620-622 sy mptoms and scree nin g, 620 treatment, 622, 621 braces, 622, 623 electri cal stimulation, 622 OMT, 622 surgery, 622, 624 short leg syndrome, 614-6 18, 614 di agnosis, 6 14-6 15, 616 lift th erapy, 6 15-6 18,617, 616t pel vic rotation, 6 18, 618 spo ndylolisthesis, 625-630 causes, 625 classification, 625 , 626t di agnosis, 6255-628, 628 treatment, 628-630 treatment, 6 12-6 14 exercise, 612, 612 OMT, 613 orthotics, braces, 6 13-614, 613 group curves, 58 1 mechanics and diagnosis, 581 key co ncepts, 580 myofascial trigger points, 1045, 1045 patternin g, 583-585 fascial, 583-585 muscul oligamentous, 585, 586, 587r spinal, 583, 584
Subject Index posture bracing, 589 ~o mpe n sated , 58 1 decompensatio n, 581 - 583 educatio n and exercise, 588-589 optimal, 580 o rthotics, 589 radiography, 59 1-602 equipment, 59 1-592, 592-593 key concepts, 59 1 measuremcnr exercises, 599-60 I procedure, 592-595, 594, 594t anreroposterio r postural , 593-594,
595 general consideratio ns, 594-595 lateral postural, 594, 595 results, 595-598, 596 anrero posterio r pelvis, 596-597 antero posterio r tho racic, 596 lateral postural of pelvis, 597-598,
599-600 lumbar postural, 596, 597 treatment, 585-588, 587-588 electrical stimulatio n, 589 prolotherapy, 589 surgery, 589 Pregnancy See aLso O bstetrics. spondyloli thesis, 629 uterine innervation, 11 6 Premenstrual syndrome, 4 13-41 3, 4 13t Pressure, 64 Primary afferent nociceptors (PANs), 138- 139 peripheral sensitizatio n o f, 139- 140, 139 Primary care See aLso Fa mily practice. osteopathic, 26-27 Primary po ints. See Po int and pressure techniques. Primary respiratory mechanism . See C ranial regio n. Probabili ty, I 195 Procaine, myofascial trigger points, 104 1- 1042 Progressive inhibi tio n of neuromuscular structures (PI NS), 1026- 1033 co ntraindicatio ns and side effects, I 032 inhibitio n, I 026- 1027 key concepts, I 026 . mechanism of actio n, I 032 point and pressure techniques, 1027- 1028 procedure, I 029- 1032, I 030t Prolotherapy, 497-498 postural, 589 Pro prioception, large fiber system, 138 Prostacyclin, in peripheral vasculature, 98 Prostaglandins, in somatic dysfunction , 11 54 Proteins, endocrine, 18 1- 182 Proteoglycans in articular ca rtilage, 70-7 1 in ligaments and tendo ns, 72 Psoas muscle, 743, Ill 0, 1111 sacroiliac dysfun ction, 782
Psoas syndrome, 747-748, 748 Psychiatry, osteopathic, 245-254 adult arrenrio n defici t disorder, 252 Alzheimer's disease, 251 asylums, 247 bipolar disorders, 248 brief psychotic disorder, 249 cocaine addiction, 250-251 , 250t delirium, 251-252 depression and anxiety disorders, 248-249 doctor/ patient relationships, 247 epidemiology, 245-246 hospital treatment, 4 29 key concepts, 24 5 mental health and ill ness, 246-247 no menclature, 247 personality disorders, 252- 253 schizophrenia, 249 somatoform disorders, 249 substance abuse, 250 Psychon eurobio logy, 472 Psycho neuroimmunology, 208-2 11 key concepts, 208 mood disorders, 209-210 research, 208-209 stress effects, 2 10 treatment recommendations, 210 Psychosocial facto rs in family practice, 295-296 Psychotic disorders, somatic dysfun ctio n research , 1192 Pubic ramus, 1106-1 107, 1107-1108 Pubic symphysis IN R and MFR release, 945-946,
945-946 motion testing, 774 muscle energy tech niques, 896-897, 896 Pubovesicular liga men ts, 1091, 1091 Pulmo nology, 500-5 15 See aLso Lymphatic system. acutely ill patient, I 127 - ll3 I efficacy of OMT, I 147 key concepts, 500 lung disease chronic obstructi ve pulmonary d isease, 5 12-5 13 infections, 5 11-5 12 postoperative complicati ons, 5 13-5 14 prevention and treatment, 511 respiratory distress syndrome, 5 13 osteopathic approach, 506- 509, 506 manipulative treatment, 508-509 thoracic lymphatic drainage, 507-508 viscerosomatic refl ex, 507, 508 pulmonary fun ctio n, 509-5 10 respiratory function , 501 -506 gas exchange, 504 pulmonary circulation, 503- 504, 504 ventilation, 501-503, 502 venrilarory control, 505-506 so matic dysfunctio n research, I 191 tho racic pump, 5 10- 511 Pulses, upper extremi ty, 694 Pumps, lymphatic, 1065, 1068-1077 abdominal and pedal, 1069- 1070, 1070 liver and spleen, 1070- 107 1, 1071
1279
pectoral tracti on, I 068, 1068 tho racic, I 068- 1069, 1069 Q -angle, 79 1-792, 791 Quadriceps tendon, knee muscle fo rces, 78-79 Quali ty of li fe, ou tcomes research , 1200 Questionnaires osteopath ic health delivery, 11 94 sleep behavior, 1206 Radiculopathy lower extremi ty, 801 - 804 lumbar region, 748-750, 749 spinal, 442-443 Radiography postural. See Posture. posrural diagnosis, 607-608, 609-612,
610-611 spo ndylolithesis, 6 1 I , 6 26- 628 Rando mization in research, 11 96- 1 197, 1208, 12 17, 1224 Range of marion See aLso Balanced ligamenro us tension (BLT) techn iques. arthritis, 528 elbow, 8 1, 81 hip, 80 knee, 78 lower extremity, 788, 79 1 muscle movement, 77 myofascial trigger po ints, I 043 sho ulder, 82 somatic dysfunction, 575 spine, 84, 85, 84 Rapid eye motion (REM), and cl uster headache,439 Receptors in pharmacology, 192 pulmo nary, 505 Reciprocal inh ibi tion, 883, 9 17 Recruitment, 73 Reflex o f Mo rl ey, 753, 756 Refl ex sympathetic dystrophy, 703 Refl exes See aLso specific refl exes. acutely ill patient, I 125- 11 26 arcs autono mic, 92- 93, 92, 93 somatic, 91-92, 92 excitability, 130 facilitation, 130 fatigue, 130 interactio ns of, 123-125, 124, 125 in pregnancy, 453-454 sensitization, 130- 132 in somatic dysfu nction, 11 56 so maro-somaric, 123 structu re, 122-1 23, 122 upper extremity, 694-695 viscerosomatic and somatovisceral, 406 viscera-visceral, 123 Refl exology, I 028 Rehabilitatio n See aLso Physical medicine and rehabilitatio n.
1280
Subject i ndex
Rehabili tati o n- continued cance r patients, 472 hospital trea tm ent, 428 o utco mes resea rch, 11 99-1200 spo rts medi cine, 544- 546 co mpensatio n, 545 fun cti onal approach , 544-545 muscle fun ctio n, 545 O MT, 545 pronati o n and supin at io n, 545 Reiter syndrome, 529 Relaxatio n in bio mechani cs, 68 liga ments and tend ons, 72 Relaxin , in pregnancy, 453 Reli abili ty studi es, 1226 Remodel in g of bo ne, 70 in ligaments and tendo ns, 72 Renal cel l cancer, 464 somati c dysfun cti on resea rch, I J 9 1 Reproducti ve trac t auro nomi c inn erva ti on, 11 4- 11 6, 115 penis and cl iro ri s, 11 6 res ris and ovary, 1 14- 11 5 uterus, uterin e rube, cervix, and vagi na, 11 5- 11 6 hormo nal co nt ro l, 187 Research, osteopathi c biobehavioral mechanisms, 1208- 12 12 bas ic resea rch, 1208 design and implementatio n, 1208- 12 10, 1209t gro up selecti on, 12 10 instrum entatio n, 12 10 inrent to trea t, 12 10 maturati o n, 12 10 measurements, 12 10- 12 11 multipl e treatments, 12 10 stat isti cs, 12 11- 12 12 cl inical trials, 12 15- 12 18 data analys is, 12 17- 12 18 info rm ed co nsent, 12 17 key co ncepts, 12 15 ph ases of tri als, 12 15- 12 16 questi ons, designs, sample size, and data analysis, 12 16- 12 17 fo und ati o ns for, 11 67- 11 87 case studies, I 178 cl inical research, 11 82- 11 84 blinding, 11 84 control gro ups, 1184-11 85 dependent va riables, 11 85- 1 J 96 drop-outs, 11 85 gold stand ard , 11 83 incl usio n/excl usio n cri teri a, 11 85, 12 17 pil ot vs. full studi es, 11 85 pitfalls, 11 86 populati on selection , 11 84 srudy size and power, 11 85 val idi ty and bias, 11 83- 11 84 defini tio ns, 1 169 design betwee n-subject, 1 179- 11 80 experimental, 11 79 hypothes is, 1 177 - I 178
li terature search, 11 75-11 77, 1176--1 177t observation , 11 75, 1 198 within -subject and crossover, 11 80- 11 8 1 development 1874-1939, 1167 1940- 1969, I 167-1168 1970-2000, I 168 200 1 onward , 1168- 1169 erh icaJ co nsiderations, 1170 institutional review board autho ri ty, 1170- 11 7 1 anim al protectio n, 11 7 1 app li cations for research, 11 7 1 Irvine study, 11 73- 11 74 key concepts, I 167 manipul at ive techniqu es, 1173 professio nal knowledge, 1 169- 1 170 statistics, 11 8 1- 11 82 treatm ent stud ies, 1174- 1175 types, 11 7 1- 11 73 basic science, 117 1- 11 72 ep idemi ology and outcomes stud ies, 1173 integrative model building, 11 72 qualitative studies, 1 172-11 73 synthesis and meta-an alysis, 1172 writing and pub li cation , 1182 future challenges, 12 19- 1228 academ ic institutions fac ul ty, 122 1- 1222 schools, 1220- 1221 students , 1222- 1223 benefits ofOMT, 1227 des ign of study, shams and placebos, 1224-1225 key co ncepts, 1219 philosop hy, 1226- 1227 at present, 121 9- 1220 priorities, 1225- 1226 research networks, 1223-1224 other countries, 1224 self- regul ation in health, 1227 somatic dysfu nction, 1227, 1228 outcomes research, 11 94-1 202 design of study, 1196-1 198, 1198t,
1196--1197 hypothesis resting, 1195- 1196, 1195 osteopath ic medicine, 1194- 11 95,
11 98-1200, 1200-1201 somati c dysfunction, 1 J 88- 1193 cli nical correlations, 1190- 1192 histo ry, 11 88- 1 189 instrum entation, 1190 interexaminer agreement, 1189- 11 90 key co ncepts, 1188 Respiration and circu lation, 33-34, 157-164 See aLso Ear, nose, and throat disease; PLJmonology. acutely ill patient, 1120, 11 27- 11 3 1,
1130 autonomi c innervation, 103 blood Aow general mechanisms, 159- 160, 160 local control of, 160- I 6 1
myocardi al, 16 1- 163, 162 skin , 163- 164, 163 C hapman reAexes, I 053 in children, 314-32 1 airway o bstructio n, 3 19 t asthm a, 3 18-320 bronchi olitis, 3 17-3 18 croup, 3 16-3 17 newbo rn dysfun cti o n, 3 14-3 15 otiti s m edi a, 3 15-3 16 pha ryngitis, 3 16 in emergency medi cine, 390-392 key co ncepts, 157- 158 muscle energy assistan ce, 883 in pregnancy, 453 rib cage dysfun cti on, 723-724 primary respiratory mechanism. See C rani al regio n. regul ation of, 158- 159 Respirarory d istress sy ndrome, 5 13 Revascul ariza ri o n, 357 Rexed layers, 124, 124 Rh eum atoid arthriti s, 528-529 juveni le, 3 13-3 14, 529 in pregnancy, 452 Rh eumatol ogy, 526-533 dege nerati ve arthriti s, 529-530 di ffe rential diagnosis, 528 d isease- modify ing th erapy, 53 1 inA ammatory arthritides, 528-529 crystal-induced arthriti s, 529 rh eumatoid arthri tis, 528-529 juvenil e, 529 spo ndya rrh ro path ies, 5 29 key concepts, 526 management, 530-53 1 nonpharmacologic, 530-53 1 medi cati ons, 53 1 no narricular rh eum atism, 530 osteo pathi c manipulati ve treatme nt, 532 pati ent evaluati o n, 526-527 hi sto ry rakin g, 527 ph ysical examinati o n, 527-528 palpati o n, 527-528 range of moti on, 528 swellin g, 528 surge ry, 53 1 Rhinitis, alJ ergic, 376 Rib cage, 7 18-726 anatomy and phys iology, 7 18-720 co nnecti ve ti ssue and fasc ia, 720 lymphati cs, 720 muscles, 7 19- 720, 719 neural conn ecti o ns, 720 skeleto n, 7 18-7 19, 7 19 hi sto ry and ph ys ical exa min atio n, 72 1-726 di aphragm, 724 sternum , 724-726, 724-725 stru ctural dysfunctio n, 722-724 key concepts, 7 18 mechani cs, 720-72 1, 721-722 Ribs acutely ill pa ti ent, 11 20 O M -1~ 11 38- 11 39
Subject Index arricularory techniques, 835-836, 842- 843, 842 bal~nced ligamenrous tension, 924- 926,
925-926 development, 31 0 Facilitated positional release (FPR), 1020- 1022, 1021 Fascial-ligamentous release, 912, 912 HVLA treatmenr, 864-868, 864-868 and lymphatic system, 1064, 1065 osteopathic manipulation, I 097-1098, 1099- 1102, 1098,
1100-1102 strai n and cou nrerstrain technique, 1011 - 1012, 10JI- IOI2 Risk Facrors biobehavioral tacrors, 1205- 1207 coronary atherosclerosis, 348t heart Failure, 36 1 Rogers, Fe Iix, 190 Rolfing, I 028 Romans, physical medicine, 5 17 Romberg sign, 443 Rotation il iosacral, 777-778 lumbar, 742-743 thoracolumbar, 741 - 742 Rotator cuff INR and MFR release, 962-964,
962- 963 tendonitis, 54 1- 542 Rotoscoliosis. See Scoliosis. Ruffini endings, 138 Rush, Benjamin, 21 Rusk, Howard, 5 18 Sacroil iac dysfunction , 540, 778- 782, 779t,
540 anterior, 779 balanced ligamentous tension, 927, 929 causes oF, 782 disc, 782 L5 problems, 782 lumbar somatic dysfunction, 782 pelvic side shift, 782 postural imbalance, 782 psoas, 782 reflexes, 782 short leg synd rome, 782 trauma, 782 Facilitated positional release (FPR), I 024,
1024 INR and MFR release, 947- 949, 948- 951 posterior, 779-782 bilateral sacral flexion, 78 1 shears, 781 - 782 rorsions, 780-78 1, 780t, 78 1t Sacrotuberous ligament, INR and MFR release, 943-944, 943-945 Sacrum See aLso Pelvis and sacrum. tascial-ligamemous release, 910, 91 I Functional technique, 975- 976, 976-978 HVLA treatment, 87 1-82, 87 1- 872 mobility oF, 987, 990 motion, 1246
muscle energy techniques, 897-900,
897-900 osteopathic manipulation, 1107-1109, 1108t, IJ08-Il09 soft tissue techniques sacral inhibition, 829 sacral rock, 828-829, 828 somatic dysfunction, 1247 Sample size, 1216- 121 7 Scapulothoracic joint, balanced ligamenrous tension, 926, 927 Schizophrenia, 249 Schmeideberg, Oswald, 189 Sclerotomes, 1248 lumbar, 734-735, 736 Scolio is, 3 11 , 1249 diagnosis, 618-620, 619, 621 in pregnancy, 452 radiography, 620-622 symproms and screening, 620 treatment braces, 622, 623 electrical stimulation, 622 OMT, 622 surgery, 622, 624 Screening examination, emergency medicine, 387-389 Second messengers, 183 Segmental Facilitation. See Facili tation; functional technique. Segmenral organization muscle movement, 77 neuro musculoskeletal and vascular systems, 55-56, 55-57 SelF-regulation in health, 1227 Semmelweis, Ignaz, 175 Sensitization primary afferent nociceptors, 139-140 reflex, 130- 132 Sexual activity biobehavioral mechanisms, 1204, 1205 health promotion, 202-203 Sexually transmitted diseases, 166, 202-203 Sham treatment, 1224-1225 Shear iliosacral , 778 sacral , 781-782 symphyseal, 1252 Shear stress, 65 bone fracture, 69 Sherrington, Charles, 12 1-122, 129 Shiatsu, I 028 Short leg syndrome, 311, 614 diagnosis, 614-615 lift therapy, 615- 618, 616t, 617 pel vic rotation , 618, 618 myofascial trigger points, 1045, 1045 acroiliac dysfunction, 782 Shoulder biomechanics, 82-83, 82 birth injuries, 3 11 -3 12 IN R and MFR release, 962-964,962-963 instability, 494-496, 495 outcomes research, 1199 primary and endpoints, 1259 Spencer tech nique, 836, 851
1281
Side bending, 1249 Signal transduction , 183 Sinoatrial (SA) node, 10 1 Sinuses, nose and paranasal, 373-375, 675, 374, 374t Sinusitis, 375-376, 376 Skeletal muscle biomechanics, 73-75, 73 microscopic anaromy, 49, 49 Skeleron See aLso Bones. acutely ill patient, 11 2 1, 1127- 11 28,
ll22 Skiagraphy, 121, 1167 Skin anatomic barrier, 170-17 1 blood flow, 163-164, !63 in cancer, 466 Skull surures, 50 Sleep, biobehavioralmechanisms, 1206 Small bowel obstruction, 403-404 Smal l intestine manipulation, I 081-1082,
1081- 1082 Smallpox, 176 SOAP method, 578 Social Factors, geriatric, 333 Soft tissue techniques, 8 19-833 cervical tech niques, 820-821, 820-821 key concepts, 819 lower extrem ity, 830-833, 830-832 lum bar, 825-828, 826-828 sacrum , 828-829, 828 somatic dysfunction, 11 58, 1158 and spinal movement, 83 thoracic, 822-825, 822-825 upper extremity, 829- 830, 829-830 Somatic dysfunctio n, 1153-11 61 acutely ill patienr, 11 27 anaromy and physiology, 11 53-1157 faci litation, 1153- 11 54, 1154 mechanoreceprors, 11 54-1 155, 1154t myofascia, 1156-1157 spinal cord and nociceprion, 1155-11 56 brainstem arousal system, 147, 153 concept oF, 137 cranial nerves, 1255- 1256t efficacy otOMT, 1146-1147, l146 exercise prescription, 286-287 iliosacral, 777-778 in infants, 307-308 key concepts, 11 53 lower extremity, 800, 80 I lumbar, 738-739, 743 OMT effects, 1157- 11 59, JJ 57 articulatory techniques, 11 58 HVLA, 1159 muscle energy, 1 159 soft tissue and myofascia, 1 158, 1158 strain-counrersrrain, 11 58-1159 and lung disease, 507, 508 musculoskeletal examination. See Muscu loskeletal system . osteopathic manipu lation, 1094-1 114 atlas-axis, I 096, 1096 cervical spine, 1094-I 095, 1095
1282
Subject Index
Somatic dysfunction , osteopathic manipulation-continued hand, 111 2- 111 3, 111 4 hip muscles, 1109-1112, II lO t,
1111-1113 ilium o r inn om in ate, II 03- 1 I 05 , 1104t, JJ04-JJ06 knee, 111 3- 111 4, 1114 lumbar spine, 1102- 1103,1102-1103 occipital-atl as, I 095-1 096, I 096 pubic ramus , 1106-1107,1106-1107 ribs, 1096-1097, 1099-1102, 1097- 109~
1100-1102
sacrum, 1107-1109, 11 08r,
1108-1109 thoracic spine, 1098-1099, 1099 palparory ski lls, 562-565, 563-565, 562r pathophysiology, 137-138, 140, 138 pre- and postOperative, 406-407 in pregnancy, 450-453, 451 primary afferem nociceprors, 139, 139 research studies, 11 88- 11 93 cl ini cal correlations, 11 90-1192 hisro ry, I 188- 1189 instrumentation, 11 90 interexam iner agreement, I 189-1 190 spinal disorders, 442-444 spinal fac il itation, 137 Somaroform disorders, 249 Somatosymparheric reAexes, 127 Somatovisceral reAexes myofascial trigger points, 1048- 1049 ,
1048 sinusitis, 375 Spencer, Herbert, 8 Sphenobasilar synchondrosis, 991,
1250-1251 Sphincters ofOddi, 1086, 1086 upper eso phageal, 103 Spinal caJ1al , 730-73 1 Spin al cord co mpress ion, in cancer, 468-469 facilitation, 137, 140- 145 brainsrem arousal system, 145-147 ascending pathways, 145-146 reti cular formation , 146 ce ntral sensitization, 144 PANs in dorsal horn, 140-144,
141-1 44 spi nal cord output, 145 innervation, 733-734, 734 motility of, 986-988 Rexed layers, 124, 124 Spinal nerves, segmental organization, 55-56 Spin e biomechanics, 83-86 atl as and axis, 86 cervical spine, 86 imerverrebral discs, 83-84 loadi ng, 85-86, 85 lumbar spine, 86 motion segment, 83, 83 range of motion, 84, 85, 84 soft tissues, 83
translation and rotation, 86 vertebrae movemems, 84-85, 85 development, 31 0-3 1 I dysfunction , 442-444 exercise prescription , 286-287 mO[!On
exam in atio n and diagnosis, 569-572,
570 active and passive resting, 571 hip Aop resr, 645 seared Aexion rest, 64 5 standing Aexio n rests active screening, 640-641, 640-641 passive screening, 641-646 ce rvical rotatio n, 64 1 costal cage motion, 644, 645-646 hip drop rest, 642, 642 pelvic side-shi ft, 642-643, 643 rib angle tenderness, 644, 644 rib elevation , 643, 643 straight-leg raising, 644-64 5 thoracolumbar side bending, 642 trunk side-bending (acromion drop test) , 641 muscle energy techniques, 885-890 atlanto-axial dysfunction , 889-890,
890 cervical, 887-888, 888 lumbar dysfunction, 885-886, 885 occipiro-a tl antal joint, 888-889,
888-889 thoracic dysfun ction, 886-887,
886-887 neutral position, 1240 physiologic motion, 1243 Spinothalamic pathways, pain management, 216-217 Spleen See also Lymphatic system. lymphatic pumps, 1070-1071, 1071 osteopathic manipulation , 1087, 1087 Spondyarthroparhies, 529 Spondylolisthesis causes, 625 classificatio n, 625, 626t diagnosis, 625-628 neurologic, 628 palpatory, 628 , 628 racLography, 626-628 treatment, 628-630 exercise, 629 manipulat io n, 629-630 medication, 630 orthotics, braces, and casts, 630 patient education, 629 Spondylolys is, 490 Sporrs drinks, 549 Spons medicin e, 477, 534-550 in children, 312-313 concussions, headaches, and neurologic deficits, 546-548, 547t history of, 535 injured athlete, 536-544 ankle sprain, 543-544, 543 back pain and spondylolysis, 539-544,
539
iliopsoas spasm, 539-540, 540 sacroiliac/sacral torsion dysfunction,
540 ,540 funct ional biomechanical exam in ation, 538-539 hi sto ry, 536-537 knee pain , 54 1, 54! motion resting, 538 palparory examination , 537-538 ph ys i al exa mination, 537 rotator cuff rendon/impingemem syndrome, 541-542, 542 somatic dysfunction, 539 standing screening exam ination, 537 key co ncep ts, 534 performance enhancement, 548-549 physical medi cine, 52 1, 524-525 practitioners, 535 pre-pa rticipation physical, 535-536 rehabilitation, 544-546 co mpensations , 545 functional app roach , 544-545 mu scle fu nction, 545 osteopathic manipulative therapy, 545 pronation and sup in ation , 545 rewrn-to-play, 548 sideline and eve nt med ical managemem, 549 so mati c co mpon ent, 542, 543 trainin g, 535 Spra ins of ankle, 543-544, 543 li gamentous, 785-786 of should er, 494 Sprays, vapocoo lant, I 041 Spring rest lumbosacral , 776 spin al, 742 Spurling sign , 443 Statisti cs coronary artery disease, 277- 279 in research, 11 81-1182, 12 10- 121 1, 12 17- 12 18 Srernclavicu lar joim, 50 Sternum acutely ill pat ient , 11 20, 11 39 anatomy, 7 18-7 19 co mpress ion , 724-726, 724-725 primary and endpoims, 1259 Steroids, endocrine, 182, 184 Stiffness biomechanical, 67 li game ms and tendons, 72 Sri II, Andrew Tay lor, 3- 12 abdominal OMT, 751 biography, 19-2 1 education, 2 1-24 integration of body units, 120 mental disorders, 24 5-246 osteopathic ph ilosophy, 4-6 hi sto ric developmem, 8-1 I pariem ca re, 6-8 practice gu idelines, 11 - 12, lit research in OMl~ 1167 surgical train ing, 399-400
Subject Index Sromach, os teopathic manipulation, 1079-1080, /080 Strains in oiomechanics, 66, 66 and co unrersrrain techniques, 1002- 1016 compli ca ti ons, 11 50 history, 1002- 1003 insrrucrions ro patient, 1006- 1007 key co ncepts, I 002 physiology, 1003-1 004 somaric dysfunction, 11 58- 11 59 rrearment, I 004-1006 ceryical spine, 1007- 1009,
1008-1009 lowerexrremiry, 101 5, 1015 lumbar spine, 101 2-101 3,
1012-1013 patient position, I 005-1006 pelvis, 101 3- 101 4, 1013-1014 ribs, !OJ 1- 1012, 1011-1012 render point, I 004-1 00 5 thoracic spine, J009-10 II ,
1009- 1011 upper exrrem iry, 101 4- 101 5,
1014-1015 cran ial. 992-993, 992 Srre s alcohol use, 239-240, 240 r anxiety, 237-239, 238r biobehavioral mechanisms, 1204-1205 biomechanics, 65-66 and bone fracture, 69-70, 69 depression, 235-237, 236r health promotion, 203-204 injuries in child ren, 3 13 key concepts, 233 in knee, 79 in ligaments and tendons, 72 management, 240-243 biofeedback, 242 cognitive functio n, 24 1-242 desensirizarion, 24 1 inso mnia, 242-243, 242r lea rning and relaxatio n, 24 1 risk pe rception, 24 1 social and spiritual support, 240 psychoneuroimmunology, 210 theories, 234-235 Srrerch recepto rs, pulm onary, 505 Srrerching and cooli ng, myofascia1 trigger points, I 041, 1042 Subluxation, iliosacra1 , 778 Substance ab use alcohol, 201-202 biobehavioral mechanisms, 1204, 1206 diagnosis , 250 hospital treatment, 428 illegal drugs, 202 performa nce enh ance ment, 548-549 robacco, 200-20 I Substance P in card iovascular innervation, I 02 in cerebral vasculatu re, 99 in nociceprion, 13 1 pain transmissio n, 216 in peripheral vascul ature, 98
in respirarory plexus, I 03 in somatic dysfunction, 1155 Summation, 73 Sun exposure, 1206- 1207 Su ppo rt gro ups pain management, 224 stress managem ent, 240 Support personnel, for resea rch , 122 1 Surgery, 399-408 abdominal pain , 400-405 key concepts, 399 orrhopedi c. See Orrhopedics. postoperative co mplicati ons, 405-406, 405t atelectasis, 405-406 pre- and posto perative somaric dysfun cti on, 406-407 ileus, 406-407 pulmonary complications, 513-5 J4 for scoli osis, 622 visceroso mari c and so matov isceral reflexes, 406 Surveillance, biobehavioral mechanisms, 1204, 1207 Sutherland, William G., 985-986, 985 Swear gland innervation, 98-99 Syden ham, medical practices, 4 Sympathetic nervous sys tem, 94-96, 95-96 abdominal pain, 40 1 head, 663-667, 672 hearr innervation , 125- 126, 125-127 protocol for osreoparhic exa minarion , 425-426 rhoracic, 7 12 Symphys is pubis, 459 Sy ndrome of inappropriate anridiureri c hormo ne (SIAD H ), and lung cancer, 464, 468 Synovial joints anawmy, 49-5 1, 50-51 hyaline cartil age, 70 Systemic disease, effi cacy of OMT, 11 46- 11 47,// 46 T lym phocyres, I 059 TART (tenderness, asy mm etry, resrricrion of meri on, tissue texture changes), 574, 633-634, 972 abdominal, 753 myofascial trigger poi nrs, I 034 somatic dysfunction, 11 53 Temperature and muscl e co nrracrio n, 74-75 soma tic dysfunction, 11 53 Temporal bone dysfun cti on , newborn, 3 14-3 15 Temporomandibular joinr, 50, 682-683,
682 Tender poinrs. See Srrain and co un rerstrain technique. Tendon rap reflex, 122- 123 Tendonitis, bicipital, 702 Tendonosis, 496 Tendons anatomy, 52, 52 biomechanics, 7 1-73, 72
1283
defi niti o n, 908 knee muscle forces, 78-79 transfer of muscle mo ments, 76, 76 Tennis elbow, 702 myofascial trigger poi nrs, 1043 Tensegriry, 497 Tension in bio mechanics, 65-66 ligam ents and tendons, 7 1-72 Terminology functional techniqu e, 969-970 glossary, 1229- 1253 Testis, autonomi c innerva ti on, 11 4- J 15 Tetanus toxin transport by nerve termin als, 133 Tetany, 73 Theater cocktail sy ndrom e, 747 Theatre sign, 54 1 Thomas res r, 743, 743 Thoracic duct innervation , J 04 lymphati c sysrem, 1058, I 141 Thoracic lymph a ri c pump, 5 10-5 11 arelecrasis, 406 Thoracic curler syndrom e, 446-447 rrearmenr, 704 Thoracolumbar region HVLA rrea rm enr, 868-87 1, 871-870 IN R and MFR rel ease, 936-938, 937 Thorax acutely ill parienr, 11 20- 11 21, 11 27-11 3 1, 1128-113 0 OMT, 11 37-11 39 anatom y and phys iology, 705-7 12 co nn ective ti ss ue and fascia, 7 10-7 11 di visio ns, 705-706, 706 lymph ati c system, 7 10, 7ll muscles, 706-7 10, 707-7 10r neural co nnections, 7 11 -7 12, 712 variat io ns and dysfunction, 7 12-7 13 clinical characteristi cs, 7 13 spinal me rion , 7 13 vertebral and costal cage meri o n, 7 12-7 13 arri cul arory techniques ex tension, 839-840 fl ex ion, 839, 839 rorarion, 840, 840 side-bending, 840-841 auronomi c innervation , 100- 104,
100- 102 ao rti c plexus, 104 cardiovascul ar plexus, I 0 1- 102 eso phageal plexus, 103-104 res pi rarory plexus, 103 thoracic du cr innervation , 104 balanced li gamenrous tension, 924,
924 diagnosis, 7 16-7 17 facilitated positional release (FPR), 101 9- 1022, 1020 fascial-ligamentous release, 912-913,
9 12-913 functional techniqu e, 975- 976, 976-978 hisro ry and physical examin ation , 7 13-7 15 palpation , 715
1284
Subject Index
T horax-continued HVLA treatment, 859-864 multiple planes, 860-864, 860-864 single plane, 859-860, 859 key co ncepts, 705 lym phatic system, 1063-1064, 1063 motion tes ting, 7 15-7 16 muscle energy techniques, 886-887, 886-887 osteo pathic manipul atio n, 1088- 1090, 1088-1090 osteo pathic manipulation, 1098-1 099, 1099 soft tissue techniques lateral recumbent, 823, 823 mid thoracic extension, 825, 825 prone pressure, 822, 822 prone pressure with counterpressure, 822-823 prone thumb press ure, 822 seated, over/under, 824, 824 side leve rage, 824, 824 supine extension, 824-825, 825 strain and co unterstrain technique, 1009-1011, 1009- 1011 T hroat, 677 See aLso Ear, nose, and throat disease. Thrust (high velocity/low amplitude) techniques, 852-880 classification and mechanisms, 854-855, 854 clinical appl ication, 855-857 barrier engagement, 855 dose of thrust technique, 856 end -feel at restrictive barrier, 855 fin al corrective force velocity and ampliwde, 856 force accumulation at restri ction, 855 gu idelines for safety, 857 indications, 855 preca utions and contraindications, 856 technique improvements, 856 histori c perspective, 852 key co ncepts, 852 motion loss and so matic dysfunction , 852-854, 853 quality of motion , 853-854 regional treatment, 857-879 cervi cals, 857-859, 857-859 extremities lower, 875-879, 876-879 upper, 874-875, 874-875 pelvis, 871-874, 871-874 ribs, 864-868, 864-868 thoracic, 859-864, 85.9-864 thoracolumbar region, 868-871, 868-870 unstabl e hypermobil e joint, 854 Thymus. See Lymp hatic system . Thyroid gland, 182 T ibiofemoral joint. See Kn ee. Time commitments for research, 1221 Tinel sign, 702 Tinnitus, 389-390 Tissue texture changes, 574 acutely ill patient, 111 7
C hapman reflexes, 1053 facilitated positional release (FPR), 1018 lumbar, 743 Tobacco, 200-201 biobehavioral mechanisms, 1204 and feral growth, 227 and lung cancer, 464-465 and sinusitis, 376 Tolerance, pain management, 221 Tonsillitis, 379-380 Tonsils. See Lymphatic system. Torque, 65 Torsions bone fracture, 69 pelvic and sacral, 780-78 1, 780r, 78 1t stress, 65 Torticollis, 3 10, 688 Touch arthritis, 527-528 discriminative, 138, 140 Trachea, lymphatic flow, 1073, 1073 Transcutaneous nerve stimulation (TNS), 222 Transient ischemic attacks, 681 Transport of hormones, 182- 181 3 Transverse processes, 729 Trauma crani al, 993, 996 emergency medicine, 389-390 hospital treatment, 429 sacroiliac dysfunction, 782 spinal disorders, 442-444 render points, 1003 Travell, Janet, 1034, 1045- 1048 Trendelenburg rest, 772-773 Trigeminal nerve, 670-671 Trigger points, 1028 In emergency medicine, 388 lower extremity, 804 myofascial, 703, 1034- 1050 diagnosis, 1039-1040, 1041r incidence, 1037- 1038 key concepts, 1034 point system s, 1034- 1039, 1035- 1037 referred pain , 1038-1039, 1039 treatment, 1040- 1042 cooling with stretching, 1041 , 1042 injection, 1041- 1042, 1043 osteopathic, 1042-1049 posture, 1045, 1045 regional trigger points, 1042- 1044, 1043r, 1044 Travell points, 1047- 1048, 1048 venous and lymphatic drainage, 1045- 1047, 1046-1047 viscerosomaric and somatovisceral reflexes, 1048- 1049, 1048-1049 strain and counterstrain technique, 1002 Trochlear nerve, 670 Tuberculosis, 165- 166 Tumor necrosis factor in cancer, 469-470 Twitch, 73
Typhoid Mary, 168 Tyrosine hydroxylase, in ureter, 11 2 Ulcers, segmental facilitation, 11 26 Ulnomeniscotriquerral joim, 50 Upper extremi ty See aLso Extremiti es. fascial-ligamentous release, 9 13-9 14, 913 soft tissue techniques inrerosseo us membrane of forearm , 830 pecto ral traction, 829, 829 posterior axillary folds, 829-830, 829 rhomboids, 830, 830 Ureter autonomi c innervation, 11 2-1 13 osteo pathic manipulation, I 087, 1087 segmental facilitation , 11 26 Ur inary bladder auron omi c innervation, 11 3- 11 4, 114 inconti nence, and aging, 334-335 Urerus auton omi c innervation, 11 5-11 6 osteopathic manipul ation , I 091 - 1092 pelvic pain, 4 15 Vaccinations, 176- 177 in osteopathy, 7 Vagina, auto nomi c innervation, 11 6 Vagus nerve acurely ill patient, I 125 anatomy, 97, 99, 673-674 cardiovascular innervation, I 02 in esophageal plexus, 103- 104 in heart innervat ion, 126- 127 Validity in clinical research, 1183 Varicosities, in pregnancy, 452 Vasoactive intestinal polypeptide in cerebral vasculawre, 99 in respiratory plexus, 103 Vasodilators, 163-164 Vectors, force and motion, 64-66 Ventilation, 501- 503, 502 co ntrol of, 505-5 06 Vertebrae rotation, 1245 in spinal movement, 84-85, 85 thoracic, 706 Vertebral body anatomy, 727-728 Vertebral unit, 737, 1253 Vertigo, 389-390 Virulence, and pathogen icity, 168-170 Viscera dysfunction brainsrem arousal system, 147 emergency medi cine, 387, 388 protocol for os teopathi c exam ination, 426 innervation of, 127-128, 127-128 manipulation, 1078- 1093 abdomen, 1079- 1088 cervix, urerus, fallopian tubes, ovaries, 1091- 1092, 1092 colon , 1082- 1083, 1082-1083 esophagus, sto mach, and duodenuln, 1079- 1081 ' 1080 gallbladder, I 085- 1086, 1086
Subject Index kidneys, 1086-1087, I087 liver, 1083-1085, I084-I085 pancreas, I 087-1088, I088 small imestine, 1081- 1082,
I081- 1082 spleen, 1087, 1087 ureter, I 087, 1087 diagnosis, 1079 history, I 078 key concepts, 1078 pelvis, 1090-1091 bladder, 1090-1091, I 090 obturator foramen, 1091, 1091 pubovesicular ligaments, 1091 , I09I theory, 1078-1 079 thorax, 1088-1090, J088-I090 treatment, 1079 treatment positions, I 092, 1092 Viscerosomatic reflex acutely ill patient, 111 7, Ill7 lumbar region, 744 and lung disease, 507, 508
1285
myofascial trigger points, 1048-1049, I 048 in pregnancy, 453--454 Viscoelasticity of articular cartilage, 70-71 in biomechanics, 67-68, 67 in ligaments and tendons, 72 and muscle contraction, 75 Vision, geriatric, 329, 330 Vitamin A deficiency, 173 Vitamin E deficiency, 174
Whooping cough, OMT, 512 Wind-up phenomenon , 128- 129, 130, 128 Wolff's law, 70, 568, 712 Workmen's compensation, 1146 Wrist anatomy, 697, 699-700 fascial-ligamentous release, 913-914,914 fractures in chi ldren, 312 HVLA treatment, 875, 875 INR and MFR techniques, 964-966,
Walk cycle, 768-769 Walking, knee movements, 79 Wallace, Alfred Russel, 8 "Warming up", and muscle contraction, 75 Water cure, 21 Wear damage, articular cartilage, 71 Wheal, 164 Whiplash injury, 496, 524, 688 Whole patient with cancer, 463, 470-471 family practice, 293-294
somatic dysfunction, 700 Wristberg's ganglion, I 0 I Writing and publication of research,
964-966
1182 Xiphoid process, primary and endpoints,
I260 Yergason test, 701 Zinc deficiency, 174
