Low Back Pain Handbook. A Guide For The Practicing Clinician by Andrew J. Cole, M.D., F.a.C.S.M. and Stanley A. Herring, M.D., F.a.C.S.M. (Eds.)

Publisher: HANLEY Et BELFUS, INC.
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Library of Congress Control Number 2002114022
THE LOW BACK PAIN HANDBOOK, 2nd edition ISBN 1-56053-493-1
© 2003 by Hanley & Belfus, Inc. All rights reserved. No part of this book may be repro-
duced, reused, republished, or transmitted in any form, or stored in a data base or retrieval
system, without written permission of the publisher.
Last digit is the print number: 9 8 7 6 5 4 3 2 1

Dedication
To Carolyn and Anne, with love; and to Anita Cerulli, who has in-
spired so many of her students with her love of science
A.l.e.
To the memory of Mary Ann and Earl Herring, my parents, whose

presence and teachings are forever with me; and to Betsy, Tracy,
and Nathan. for such remarkable unending love and support.
SAH.
I
Contributors
Thomas Agesen, M.D.

Clinical Instructor, Physical Medicine and Rehabilitation, Kessler Institute for
Rehabilitation; Staff Physiatrist, Kessler Institute for Rehabilitation, West Orange, New
Jersey
Joseph T. Alleva, M.D.

Director of Sports and Occupational Medicine, Division of Physical Medicine and
Rehabilitation, Evanston Hospital Corporation; Instructor, Physical Medicine and
Rehabilitation, Northwestern University Medical School, Chicago, Illinois
Paul A. Anderson, M.D.

Associate Professor of Orthopedic Surgery, Department of Orthopedic Surgery, University
of Wisconsin, Madison, Wisconsin
Steven J. Anderson, M.D.

Clinical Professor, Department of Pediatrics, University of Washington; Children's
Hospital and Regional Medical Center, Swedish Hospital and Medical Center, Seattle,
Washington
Ray M. Baker, M.D.

Clinical Instructor, Anesthesiology, University of Washington; Overlake Hospital Medical
Center, Evergreen Hospital, Bellevue, Washington
Nikolai Bogduk, M.D., Ph.D., D.Sc.

Professor of Pain Medicine, University of Newcastle; Staff Specialist, Royal Newcastle
Hospital, Newcastle, New South Wales, Australia
Richard Paul Bonfiglio, M.D.

Assistant Professor, Environmental and Occupational Health Graduate School of Public
Health; Medical Director, Health South Harmarville Rehabilitation Hospital, Pittsburgh,
Pennsylvania
Ronald Lee Bonfiglio, M.D.

Private Practice, Hurricane, West Virginia
Joanne Borg-Stein, M.D.

Assistant Professor, Tufts University School of Medicine; Lecturer, Department of Physical
Medicine and Rehabilitation, Harvard Medical School; Spaulding Rehabilitation Hospital,
Boston, Massachusetts
xl
xii ConlribulDrs
Cary C. Bucko, M.P.T.

Olympic Physical Therapy, Denton, Washington
Craig C. Callewart, M.D

Director, Spine Center, Orthopaedics, Baylor University Medical Center, Dallas, Texas
Andrew J. Cole, M.D., F.A.C.S.M.

Northwest Spine and Sports Physicians, Bellevue, Washington; Medical Director, The
Spine Center at Overlake Hospital and Medical Center, Bellevue, Washington; Clinical
Associate Professor, Department of Rehabilitation Medicine, University of Washington,
Seattle, Washington
Susan J. Dreyer, M.D.

Assistant Professor, Physical Medicine and Rehabilitation; Assistant Professor,
Orthopaedic Surgery, Emory University; Emory Healthcare, Atlanta, Georgia
Paul Dreyfuss, M.D.

Clinical Professor, Department of Rehabilitation Medicine, University of Texas Health
Science Center, San Antonio, Texas; Washington Interventional Spine Associates,
Bellevue, Washington
Avital Fast, M.D.

Professor and Chairman, Department of Rehabilitation Medicine, Albert Einstein College
of Medicine/Montefiore Medical Center, Bronx, New York
Robert J. Gatchel, Ph.D.

Professor of Psychiatry and the Elizabeth Penn Professor of Clinical Psychology,
University of Texas Southwestern Medical Center at Dallas, Dallas, Texas
Michael C. Geraci, Jr., M.D., P.T.

Fellowship Program Director and Medical Director, Buffalo Spine and Sports Medicine,
P.c., Buffalo, New York; Clinical Assistant Professor, Department of Physical Medicine
and Rehabilitation, State University of New York at Buffalo, Buffalo, New York; Michigan
State University College of Osteopathic Medicine, East Lansing, Michigan
Terrence P. Glennon, M.D.

Assistant Professor, Department of Physical Medicine and Rehabilitation, Northwestern
University, Chicago, Illinois
Kenneth B. Heithoff, M.D.

Medical Director and Chairman, Center for Diagnostic Imaging, Minneapolis, Minnesota
Stanley A. Herring, M.D., F.A.C.S.M.

Puget Sound Sports and Spine Physicians; Clinical Associate Professor, Department of
Rehabilitation Medicine, Department of Orthopaedics, University of Washington, Seattle,
Washington
Richard J. Herzog, M.D.

Professor of Radiology, Department of Radiology, Weil Medical College of Cornell University;
Chief, Division ofTeleradiology, Hospital for Special Surgery, New York, New York
ConlribulDrs xiii
Brenda Hight, J.D.

Fletcher and Springer, L.L.P., Dallas, Texas
Donald W. Hinnant, Ph.D.

Director, Pain Management Center, Candler Hospital, Savannah, Georgia
Gerald P. Keane, M.D.

Clinical Assistant Professor, Division of Sports Medicine, Physiatry Medical
Group/SOAR, Stanford University School of Medicine; Stanford Medical Center,
Palo Alto, California
Donald Liss, M.D.

Assistant Clinical Professor, Department of Rehabilitation Medicine, Columbia College of
Physicians Et Surgeons at Columbia Presbyterian Hospital Medical Center, New York,
New York
Howard Liss, M.D.

Assistant Clinical Professor, Department of Rehabilitation Medicine, Columbia College of
Physicians Et Surgeons at Columbia Presbyterian Hospital Medical Center, New York,
New York
Ian B. Maitin, M.D.

Assistant Professor, Department of Physical Medicine and Rehabilitation, Temple
University School of Medicine, Philadelphia; Attending Physiatrist and Director of
Inpatient Rehabilitation, Temple University Hospital, Philadelphia, Pennsylvania
Gerard A. Malanga, M.D.

Associate Professor, Physical Medicine and Rehabilitation, UMDNJ-NJ Medical School,
Newark, New Jersey; Director, Sports, Spine Orthopedic Rehabilitation, Kessler Institute
for Rehabilitation, West Orange, New Jersey
Carolyn A. Marquardt, M.D.

Assistant Clinical Professor, Department of Rehabilitation Medicine, University of
Washington; Northwest Spine and Sports Physicians, Seattle, Washington
Tom Mayer, M.D.

Clinical Professor, Department of Orthopedic Surgery, University of Texas Southwestern
Medical Center; Medical Director, PRIDE, Dallas, Texas
Daniel Mazanec, M.D.

Director, Center for the Spine, Cleveland Clinic Foundation, Cleveland, Ohio
Frederick B. McAdam, M.D.

Buffalo Spine and Sports Medicine, P.C, Buffalo, New York
Scott F. Nadler, D.O.

Associate Professor, Department of Physical Medicine and Rehabilitation, UMDNJ-NJ
Medical School, Newark, New Jersey; University Hospital, Kessler Institute for
Rehabilitation, West Orange, New Jersey
xiv ContribulDrs
Jeff Pavell, D.O.

Columbia Presbyterian Hospital Medical Center, New York, New York
John H. Peloza, M.D.

Clinical Assistant Professor, Department of Orthopedic Surgery, University of Texas
Southwestern Medical School, Dallas, Texas; Texas Back Institute, Plano, Texas
Douglas Phil\ips, J.D.

Attorney at Law, Bellevue, Washington
Peter Barth Polatin, M.D.

Associate Professor, Department of Psychiatry and Department of Anesthesia and Pain
Management, University of Texas Southwestern Medical School at Dallas; Attending
Physician, Parkland Hospital, Zale Lipsky Medical Center, Baylor University Medical
Center, Dallas, Texas
Joel M. Press, M.D.

Associate Professor, Physical Medicine and Rehabilitation, Northwestern University
Medical School; Medical Director, Center for Spine, Sports, and Occupational
Rehabilitation, Rehabilitation Institute of Chicago, Chicago, l1linois
Thomas J. Puschak, M.D.

Department of Orthopedic Surgery; University of Wisconsin; Madison, Wisconsin
Jerome Schofferman, M.D.

Director, Research and Education, San Francisco Spine Institute, Daly City, California
Richard Seroussi, M.D.

Clinical Assistant Professor, Rehabilitation Medicine, University of Washington, Seattle,
Washington
J. David Sinclair, M.D., F.R.C.P.(C.)

Independent Consultant for Chronic Pain, Puget Sound Sports and Spine Physicians,
Seattle, Washington; Physician Consultant, United Back Care, Redmond, Washington;
Swedish-Providence Medical Center, Seattle, Washington; Evergreen Medical Center,
Kirland, Washington
Charlotte H. Smith, M.D.

Physical Medicine and Rehabilitation, Medical Director for Rehabilitation Services, SETON
Healthcare Network, Austin, Texas
Mark J. Sontag, M.D.

Team Spinal and Pain Consultant for the San Jose Sharks, Oakland Raiders, San
Francisco Giants, and San Jose Sabercats; Founder of SPARCmed Medical Group, Portola
Valley, California
Christopher J. Standaert, M.D.

Clinical Assistant Professor, Department of Rehabilitation Medicine, University of
Washington; Puget Sound Sports and Spine Physicians, Seattle, Washington
Steven A. Stratton, P.T., Ph.D., A.T.C.

Associate Clinical Professor, Physical Medicine and Rehabilitation, University of Texas
Health Science Center at San Antonio, San Antonio, Texas
Contribulors xv
C. David Tollison, M.D.
Director, Center for Health and Occupational Services, Greenville Hospital System,
Greenville, South Carolina; Associate Clinical Professor, Medical College of Georgia,
Augusta, Georgia
John J. Triano, D.C., Ph.D.

Co-Director, Conservative Care, and Director, Chiropractic Division, Texas Back Institute,
Plano, Texas; Graduate Faculty, Biomedical Engineering Program, University of Texas at
Arlington, Arlington, Texas
Robert Gerard Viere, M.D.

Clinical Assistant Professor, Department of Orthopaedics, University of Texas
Southwestern Medical Center; Baylor University Medical Center, Scottish Rite Hospital for
Children, Dallas, Texas
Michael M. Weinik, D.O.

Assistant Professor, Department of Physical Medicine and Rehabilitation, Temple
University School of Medicine, Philadelphia; Assistant Chairman and Director of Trauma
and Musculoskeletal Rehabilitation, Temple University Hospital, Philadelphia,
Pennsylvania
Robert P. Wilder, M.D., F.A.S.C.M.

Georgia Spine Et Sports Physicians, P.c., Atlanta, Georgia
Robert E. Windsor, M.D.

Director, Sports Rehabilitation Services, Tom Landry Sports Medicine Et Research Center,
Baylor University Medical Center, Dallas, Texas
Keith Andrews Wohlberg, M.A.T.P., P.T.A.

Physical Therapy Assistant, Chronic Pain Program, SPARC Med, Menlo Park, California
Michael W. Wolff, M.D.

Medical Director, Southwest Spine and Sports; Scottsdale Healthcare (North), Scottsdale,
Arizona
Way Yin, M.D.

Assistant Clinical Professor, Department of Anesthesiology, University of Washington,
Seattle, Washington; Medical Director, Interventional Medical Associates of Bellingham,
PC, Bellingham, Washington
Irene An-Mel Young, M.D.

Clinical Assistant Professor, Department of Rehabilitation Medicine, University of
Washington, Seattle, Washington; Overlake Hospital, Bellevue, Washington
Jeffrey 1. Young, M.D., M.A., F.A.C.S.M.

Physical Medicine and Rehabilitation, Spine and Sports Medicine, Hospital for Special
Surgery, New York, New York
Muhammad B. Yunus, M.D., F.A.C.P., F.A.C.R.

Professor, Department of Medicine, Section of Rheumatology, University of Illinois
College of Medicine at Peoria, Peoria, Illinois
I
Preface to the First Edition
Every physician who treats musculoskeletal problems sees patients with low back pain
(LBP), which is second only to the common cold as a cause for primary care office visits.
Low back pain is extraordinarily common, with a lifetime prevalence of 60 to 90010 and
an annual incidence of 5010; the prevalence of sciatica ranges from 11 to 400/0. No popula-
tion appears immune. Up to 35010 of sedentary workers and 47010 of physical laborers re-
late a history of LBP. More than 15010 of claims for work-related injuries are related to the
lumbar spine, and more than one-third of the costs for work-injury claims are due to
lumbosacral spine problems. Ten percent of the claims account for 80010 of the costs of
work-related LBP.
Although physical fitness might maintain the health of the lumbar spine, sporting ac-
tivities can often result in LBP. Gymnastics, football, weight lifting, wrestling, dancing,
and rowing frequently produce low back pain and injury. Low back pain ranks second
among injuries to professional golfers, first among amateur golfers, and second among
basketball players. The literature also mentions baseball, jogging, and cycling as causes of
LBP. Swimming, often prescribed as therapy for LBP, has also been associated with lum-
bosacral injury and pain.
The natural history of LBP is reported to be self-limited and to have a favorable prog-
nosis. Nearly 20 years ago it was noted that 90010 of LBP episodes resolved without physi-
cian intervention. Similarly favorable data have been published about patients who seek
medical attention. Reports indicate that 40 to 50010 of patients improve within 1 week,
and 85 to 90010 of injured workers who seek treatment improve within 6 to 12 weeks.
Even with conservative care, 75010 of patients with sciatica recover within 6 months, and
surgery may not necessarily affect long-term prognosis. Those same studies, however,
also report a recurrence rate of 70 to 90010. Indeed, more recent studies following patients
for at least 6 months suggest that back pain typically is recurrent and more chronic than
is usually believed. At follow-up intervals of 1 and 2 years, 44010 of primary-care back
patients were in a chronic phase (90 or more days of back pain during the previous 6
months). Forty percent of patients with acute low back pain reported pain at the 6-month
follow-up, 20010 of whom reported moderate to severe pain. Thus, while there might be an
initial improvement in symptoms, frequent recurrences indicate thatjimction has not
been restored. In many cases, simply reassuring patients that back pain will "go away"
does not constitute an appropriate treatment plan. Clearly, for some patients LBP is not a
benign, self-limiting condition.
Low back pain can be medically and economically devastating. It is the number-one
cause of disability in patients younger than 45 years of age and the number-three cause
of disability in those older than age 45. At any given time, 9 million people in the United
States are disabled by LBP; 2.6 million are chronically disabled. Low back pain accounts
for 25010 of disabling work-related injuries. Between 1970 and 1981, a 14-fold increase in
the rate of disabling LBP far exceeded the rate of population growth. The rate of disabling
LBP continues to escalate. Direct medical costs to treat LBP amount to more than $25 bil-
lion a year; the total cost for managing LBP exceeds $50 billion annually. From 1956 to
xv"
xviii Preface10 "'e FirstEdition
1976, awards for LBP disability increased by nearly 27000/0. All costs related to LBP un-
doubtedly will continue to rise until more cost-effective quality care is instituted.
This problem, which supposedly has a favorable natural history although it can be re-
markably disabling, has challenged health-care providers. While a small percentage of
patients with LBP accounts for a disproportionate amount of medical and economic ex-
penses, the medical system often is unable to identify them early. Indeed, patients at high
risk for becoming disabled often receive more diagnostic tests and treatment (including
surgery) because they persist in making complaints.
The family practitioner, internist, or other nonsurgeon often is the first physician to ac-
cess the patient with LBP. These physicians may have little formal postgraduate training
in musculoskeletal medicine and pain management. Orthopedic surgeons and neurosur-
geons also routinely see and consult on patients with LBP. These physicians are particu-
larly knowledgeable about the surgical aspects of lumbosacral problems; however, asking
them to assess patients with pain syndromes, or to be primarily responsible for a disease
process that is 99% nonsurgical, may be a misappropriation of resources. Management of
LBP through alternative measures by nonphysicians often relies on a single belief system,
frequently without benefit of complete diagnostic evaluation. In this setting, pain behav-
ior is rarely understood and often unintentionally reinforced by the practitioner. Physical
medicine and rehabilitation physicians have been educated in musculoskeletal medicine
and pain management and can distinguish pain and disability.
Controlling the escalating emotional and medical costs associated with LBP requires
physicians to clearly differentiate between pain and disability so that rational, cost-
effective care is provided in a timely manner. An overwhelming number of LBP patients
are not pain patients but still need appropriate evaluation and treatment prescriptions,
which may limit the duration of pain and speed functional recovery.
A better understanding of the variety of spine-pain populations and of cost-effective
assessment and management is necessary for primary spine-care specialists. A working
knowledge of relevant anatomy, biomechanics, and epidemiology allows for an orga-
nized, functional approach. A directed history and musculoskeletal physical examination
coupled with the appropriate selection, interpretation, and use of imaging studies are es-
sential. Another important component of spine care is a detailed understanding of physi-
cal therapy treatment techniques. Choosing appropriate electrodiagnostic studies that will
affect care also may play an important role. Appropriate timing and selection of diagnos-
tic and therapeutic, fluoroscopically guided, contrast-enhanced spinal injection proce-
dures may be coupled with other treatment measures to improve symptom resolution and
promote functional recovery.
Understanding the roles of psychologists, psychiatrists, pain clinics, and functional
restoration programs is important for the cost-effective management of LBP.
Furthermore, use of orthopedic or neurosurgical consultants is more cost-effective when
the treating physicians understand the indications for and limitations of surgical inter-
vention. Too often treatment ideas are championed or dismissed on the basis of research
that is poorly designed or controlled. Physicians treating patients who have LBP must
thoroughly understand all these areas so that they can coordinate and integrate function-
ally based programs, because no single medication, modality, exercise regimen, or other
treatment technique may result in LBP recovery.
The current system of LBP management (medical, legal, and insurance) in the United
States has not effectively controlled costs or limited disability. To improve the medical
care of LBP, an integrated knowledge of radiologic imaging, oral medication prescription,
physical therapy, electrodiagnosls, selective injections, pain management, and surgical
indications is essential. Specific issues of injured workers and young back pain sufferers
Preface 10 theFirst Edition xix
must be addressed. Physicians who choose to see LBP patients must have these skills and
be able to coordinate treatment.
This book has been written with primary care clinicians as its focus. The outline format
allows busy clinicians to quickly obtain practical information that directly affects treat-
ment decisions. Therefore, the chapters summarize relevant clinical information and pur-
posely avoid exhaustive reviews. The authors have provided reading lists at the end of
their chapters for easy access to more detailed information. We hope that this book will
help busy clinicians provide high-quality, cost-effective treatment to all their patients
with LBP.

Acknowledgments
There are many people to whom we will always be grateful: our former chairman, John
Downey, M.D., D.Phil. (Oxon), F.R.C.P.(C) and Justus Lehman, M.D., for the education they
provided and the passion to search for scientific truth; Sandra Pinkerton, Ph.D., who taught
us an appreciation of the English language; Seneca Stemm, for reviewing the proofs; Josh
Gunkler, for making sure our correspondence was timely and secure; our physical therapy
team, Steve Stratton, Ph.D., P.T., Cary Bucko, P.T., AT.C., John Miller, P.T.,AT.C., Wolfgang
Brolley, P.T.,Joe Farrell, M.S., P.T., and Rick Eagleston, P.T.,AT.C., who taught us how back
pain really affects people and what can be done for it; Carl Sameulson, who leads with dig-
nity, honesty, and joy; T. Cara Nguyen-Trata, M.D., for rendering the superb line drawings
for chapters 13 and 14; and finally, Morris Mellion, M.D.
Andrew J. Cole, M.D., F.AC.S.M.

Stanley A Herring, M.D., F.A.C.S.M.
Preface 10 theFirst Edition xix
must be addressed. Physicians who choose to see LBP patients must have these skills and
be able to coordinate treatment.
This book has been written with primary care clinicians as its focus. The outline format
allows busy clinicians to quickly obtain practical information that directly affects treat-
ment decisions. Therefore, the chapters summarize relevant clinical information and pur-
posely avoid exhaustive reviews. The authors have provided reading lists at the end of
their chapters for easy access to more detailed information. We hope that this book will
help busy clinicians provide high-quality, cost-effective treatment to all their patients
with LBP.

Acknowledgments
There are many people to whom we will always be grateful: our former chairman, John
Downey, M.D., D.Phil. (Oxon), F.R.C.P.(C) and Justus Lehman, M.D., for the education they
provided and the passion to search for scientific truth; Sandra Pinkerton, Ph.D., who taught
us an appreciation of the English language; Seneca Stemm, for reviewing the proofs; Josh
Gunkler, for making sure our correspondence was timely and secure; our physical therapy
team, Steve Stratton, Ph.D., P.T., Cary Bucko, P.T., AT.C., John Miller, P.T.,AT.C., Wolfgang
Brolley, P.T.,Joe Farrell, M.S., P.T., and Rick Eagleston, P.T.,AT.C., who taught us how back
pain really affects people and what can be done for it; Carl Sameulson, who leads with dig-
nity, honesty, and joy; T. Cara Nguyen-Trata, M.D., for rendering the superb line drawings
for chapters 13 and 14; and finally, Morris Mellion, M.D.
Andrew J. Cole, M.D., F.AC.S.M.

Stanley A Herring, M.D., F.A.C.S.M.
I
Introduction to the Second Edition
We are flattered to bring to the reader the 2nd edition of the Low Back Pain Handbook:
A Guide for the Practicing Clinician. The prevalence and complexity of low back pain
prompted us to produce the first edition of this text in order to try to provide a prag-
matic, easily readable resource for the healthcare practitioner. This handbook was orga-
nized to be utilized as an on-the-spot guide for the busy practitioner and was supple-
mented with suggested readings at the end of each chapter.
This new edition remains designed for that busy clinician trying to distill low back
pain management down to the most treatment-effective and cost-effective interventions.
We have kept the overall structure intact. The three main sections of the text, Evaluation,
Treatment Options, and Special Populations and Problems, remain in place. We have re-
organized some material and added new topics.
The new additions to our book start with the very first chapter, now dedicated specifi-
cally to the epidemiology of low back pain. Three chapters later, new material addressing
the critical concepts of acute versus chronic pain and the mind/body continuum are pro-
vided in a chapter that focuses on low back pain from a biopsychosocial model. In the
Treatment Options section of the 2nd edition, we have dedicated a chapter to manipula-
tion, as practitioners are often asked about this form of treatment for low back pain.
There is a chapter on implantable technology focusing on neurostimulation and intrathe-
cal drug delivery systems, and a chapter on percutaneous intradiscal therapies. These
works help provide information to the healthcare provider regarding some of the more es-
oteric but frequently publicized issues involving low back pain management. Like many
musculoskeletal problems, low back pain management, particularly nonoperative man-
agement, is a challenging area for research. We have included a chapter on evidence-
based medicine to help the reader critically analyze available research knowledge about
low back pain. This chapter also discusses the limitations of available evidence-based
medicine in regard to the management of spinal problems, demonstrating that practition-
ers must combine the application of the best available research with their skill and expe-
rience to most effectively treat patients with lumbar spine problems.
We have added new authors and new material in the 2nd edition, and many of our pre-
vious authors have graciously agreed to update their chapters. All of our contributors are
recognized, seasoned experts in diagnosing and treating patients with low back pain. Their
very expertise makes these individuals very highly sought after clinicians and researchers.
We very much appreciate their efforts, finding time when there is none, to provide the
quality work incorporated in their writings. Finally, and most importantly, we are grateful
for the reader of this text who has placed value in what we have written and edited. We
hope that the use of the 2nd edition of the Low Back Pain Handbook continues to help
limit the suffering and maximize the level of function of the low back pain patient.

xxi
1
I
Epidemiology
Gerard A. Malanga, M.D., Scott F. Nadler, D.O.,
and Thomas Agesen, M.D.
Key Points
• Low back pain is the second leading cause for individuals to consult their physician.
• The causes of low back pain are multifactorial, including physical, environmental and
psychosocial factors.
• The single greatest risk factor for having a future episode of low back pain is a prior
history of either medically treated or untreated low back pain.
I. Economic Costs
A. United States
1. A 1991 study estimated the direct and indirect costs to be from a low of $50 bil-
lion to a high of $100 billion per annum. The same study estimated 75010 of total
cost attributed to only 5010 of individuals who become permanently disabled.
2. 1986 study of low back pain economics
a. Mean cost per case was $6807.
b. Median cost was $391.
c. Medical cost was 31.5010.
d. Indemnity costs were 67.2010.
e. Total compensable cost was $11.1 billion.
3. From 1988 to 1996, the average cost per claim decreased 41.4010 while the me-
dian cost increased 19.7010.
a. The average length of disability decreased from 156 days to 61 days, reduc-
tion of 60.9010.
4. In 1995, estimated costs of low back pain claims were $8.8 billion.
5. A 1992 review found the costliest 10010 of LBP claims account for 86010 of the
total claims cost.
6. 1998 study found that 20010 of claimants were disabled greater than 4 months
and accounted for 60010 of the health care costs.
a. Diagnostic procedures 2SOlo of total medical costs.
b. Surgical procedures 21010 of total medical costs.
c. Physical therapy 20010 of total medical costs.
d. Mental health care 0.4010 of total medical costs.
e. Chiropractic care 2.9010 of total medical costs.
II. Incidence of Low Back Pain

A. General population
1. Annual incidence of LBP in general population is SOlo.
2. 25010 of individuals who experience LBP episode will seek medical care.
2 Epidemiology
3. 50% of low back pain episodes resolve within 4 weeks.

4. 90% of low back pain episodes resolve within 3 months.
5. 75% of patients with pain radiating to legs are pain free within 6 months.
6. Up to 75% of patients who suffer one episode will have a recurrence of low
back pain.
7. In primary care 4 weeks after LBP onset, 47% were somewhat improved, 25%
were unchanged or worse, and only 28% pain free.
8. After initial LBP episode, only 20.9% are pain free 1 year later.
9. After initial LBP episode, 7.9% are in severe pain 1 year later.
B. Overall for injured workers, expect:
1. Missing 6 months of work have 50% chance of returning to work.
2. Missing 1 year of work have a 25% chance of returning to work.
3. Missing 2 years of work have close to zero chance of returning to work.
C. United States injured workers
1. In 1995, the rate of filing a claim was 1.8 per 100 workers.
2. From 1987 to 1995, there was a 34% decrease in the claims rate for low back
pain.
3. On average, only 7% of claims for LBP have a length of disability greater than
1 year.
a. The same 7% accounted for 75% of the cost and 84% of the total disability
days.
4. Farmers
a. 1992-1994, 31% had daily back pain for greater than 7 days' duration at
least once over 12-month period.
5. Annual incidence of LBP complaints is 18.5% in the general working popula-
tion.
6. Marine recruits.
a. During basic training, incidence of LBP was 11.4%.
III. Individual Characteristics Affecting Low Back Pain

A. Age
1. Greatest incidence in 30-50 year old individuals
2. Peak incidence is 40-45 years old for herniated discs.
3. Almost all who undergo surgery for disc herniations are between 35 and 45
years old.
B. Height
1. Men greater than 72 inches (6'0") tall have a relative risk of 2.3 to 3.7.
C. Weight
1. Obese individuals have greater incidence of sciatic type pain from disc hernia-
tions.
2. Obesity
a. The heaviest quantile has a low back pain prevalence 1.7 times the lightest
quantile.
D. Gender
1. Females have equal generalized low back pain complaints when compared with
males.
2. Males have more back pain radiating to the legs from disc herniations.
E. Tobacco
1. Cigarette smokers suffer a greater incidence of low back pain.
a. Smoking >20 cigarettes/day odds ratio (OR) of 1.5 (confidence interval
1.1-2.0) to have low back symptoms.
Epidemiology 3
b. One study over 12-year period, farmers who smoked had OR 9.6 (CI
1.7-53.0) to have sciatic pain compared with control who never smoked.
F. Fitness level
1. Cady found the least physically fit firefighters had a ninefold increase in low
back pain compared with the most physically fit group.
a. In Cady's study, whether poor physical fitness was the cause or effect of LBP
remains unanswered.
G. Trunk isometric strength in flexion, extension, and lateral bending
1. Low back pain sufferers have 60010 the absolute trunk strength of individuals
without back pain.
a. Whether back pain leads to weakness or weakness causes low back pain is
unknown.
H. Scoliosis
1. Greater than 80° increases chances of suffering from low back pain.
2. Study of idiopathic childhood scoliosis found no relationship between degree
and type of curve with low back pain.
I. Leg length inequality (LLI)
1. Study of military recruits with LLI of 0.5 to 1.5 em found no correlation to LBP
over 4-year follow-up.
2. Study of people of working age found LLI of up to 0.5 em not associated with
LBP.
3. LLI greater than 2.5 em may be associated with BP.
J. Spondylolisthesis
1. Soldiers complaining of low back pain had an incidence of spondylolisthesis of
5.3010 vs. 2.2010 in asymptomatic control group.
2. Spondylolisthesis greater than 10 mm on lateral film increases chances of suf-
fering from low back pain.
IV. Environmental Factors Affecting Low Back Pain

A. Occupational risks
1. Repetitive forward bending and twisting
a. Firefighters lifting> 18 lbs., opening structure to look for fire, and breaking any
window on the job had greatest risk of having 1 day off from work due to LBP.
2. Frequent lifting on the job.
a. Nurses moving patients in bed > 10 times per shift reported LBP more often.
3. Whole body vibrations (WBV) are energy delivered to the body.
a. A human's natural frequency is 4-6 Hz.
b. Helicopter pilots had increased LBP and increased sciatica compared with
non flying officers.
c. Employers who spent >50010 of working time in automobile had increased
herniated lumbar discs (relative risk 2.75).
V. Psychosocial Factors Affecting Low Back Pain

A. Job dissatisfaction
1. Papageorgiou found that dissatisfaction with work status doubled the risk of re-
porting new episode of LBP.
a. Individuals having inadequate income had threefold increase in LBP symp-
toms regardless of employment status.
B. Workplace environment
1. Hoogendoorn concluded that low social support from co-workers or supervisors
is a risk factor for reporting LBP.
4 Epidemiology
VI. Low Back Pain Incidence in Athletes

A. Gymnasts and rhythmic gymnasts
1. Over a lO-month period, 86% in the study reported LBP episode.
2. The most common overuse injury was LBP.
3. Spondylolysis reported in 2.3-11 % in various studies.
B. Football players
1. Up to 30% of players in any given season miss playing time secondary to
LBP.
2. In college players, 50% of interior linemen have history of LBP.
C. Golfers
1. Professional golfers 29% report a history of recurrent LBP.
2. 90% of tour players report history of previous back injuries.
3. One-year follow-up study found lifetime cumulative incidence of back pain
was 63%.
4. At baseline, 28% reported back pain in the past 1 month.
5. During follow-up, recurrent LBP incidence was 45%.
D. Retired wrestlers and weight lifters
1. Lifetime incidence for wrestlers was 59%.
2. Lifetime incidence for weight lifters was 23%.
3. Lifetime incidence of control group was 31%.
E. Equestrian riders
1. Incidence in female riders was 58%.
2. Incidence in male riders was 27%.
3. General purpose saddle users had greater incidence of 66%.
4. Western saddle users had incidence of 23%.
5. Shorter stirrup length associated with greater incidence of LBP.
6. Greater than 15 years of riding was associated with LBP.
F. Tennis players
1. Prevalence of 18.6% over the same week.
2. LBP with sciatica was 7.1% in tennis players and 4.3% of control group.
G. Other athletes
1. Cyclists.
a. Incidence reported from 30-70%.
2. Female basketball players.
a. Over a 6-year period, 11.7% of players reported LBP.
3. Cross-country skiers
a. 64% reported recurrent LBP.
4. Middle age runners
a. 9% report history of LBP.
5. Female field hockey players
a. Back pain reported in 59%, with the low back the most common site.
6. Male youth soccer players
a. Prevalence of back pain over I-year period was 14%.
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2
I
Anatomy and Biomechanics
N. Bogduk, M.D., Ph.D., F.A.F.R.M.
Key Points
• The posterior elements of the lumbar vertebrae sustain the forces that stabilize the
vertebral bodies.
• Compression loads are borne by the anulus fibrosus, which is braced internally by the
nucleus pulposus.
• The role of ligaments in the lumbar spine has been overemphasized with respect to
biomechanics and injury.
• Half the power of the lumbar back muscles stems from tiny muscles spread over the
back of the thorax.
• The discs and zygapophyseal joints are the leading contenders as sources of low back
pain.
• The lumbar spine is strong in flexion and resistant to injury.
• Flexion combined with rotation may result in various injuries.
• Compression injuries during lifting may result in painful, internal disc disruption.
I. Introduction
Physicians interested in back pain are not inclined to read essays on anatomy; they are
more interested in the bottom line-how do I treat? However, physicians need an under-
standing of anatomy to appreciate which elements of the lumbar spine can be injured
(and thus become painful) and to prescribe treatment on a rational basis. Modem research
has revealed the leading contenders for previously unexplained back pain.
II. Anatomy
A. Lumbar vertebrae
1. Each lumbar vertebra may be divided into three sets of functional elements]
(Fig. I):
a. Anterior element, consisting of the vertebral body
b. Middle elements, consisting of the pedicles
c. Posterior elements, consisting of the laminae, articular processes, spinous
process, transverse processes, mamillary processes, and accessory processes
2. Anterior elements or vertebral bodies are the quintessential components ofthe verte-
bral column, endowing it with bulk and height. They sustain the compression
loads applied to the vertebral column, including not only body weight but also
the compression loads imparted by contraction of the back muscles (a critical
point for appreciating lumbar biomechanics and injuries).
3. As a whole, the posterior elements regulate the passive and active forces applied
to the vertebral column and thereby control its movement.
a. The articular processes provide a locking mechanism that resists forward
sliding and twisting of the vertebral bodies.
9
10 Anatomy ana Biomechanics
FIGURE I. Thedivision of a lumbarverte-

bra into its three functional components.
(From Bogduk N, Twomey LT: Clinical
Anatomy of the lumbor Spine, 2nd ed.
Melbourne, Churchill livingstone, 1991,
with permission.)
b. The spinous processes, transverse processes, mamillary processes, and acces-

sory processes (Fig. 2) provide areas for muscle attachments and constitute
levers that enhance the action of the attached muscles.
c. The laminae transmit the forces from the spinous processes and inferior ar-
ticular processes to the pedicles; thus they are susceptible to injuries such as
pars interarticularis fractures.
4. The pedides, which are the only connection between the posterior and anterior el-
ements, transfer the controlling forces from the posterior to the anterior elements.
B. Joints
1. When any two consecutive lumbar vertebrae are articulated, they form a three-
joint complex called the motion segment (Fig. 3). The principal joint, which lies
between the vertebral bodies, is formed by the intervertebral disc. The other two
joints are formed by the articulation of the superior articular processes of one
vertebra with the inferior articular processes of the vertebra above. These joints
are officially known as the zygapophyseal joints. Other names used for the zyg-
apophyseal joints are apophyseal joints and facet joints.
a. Apophyseal is merely a contraction of zygapophyseal, which is the correct term.
b. Facet joint is an essentially ambiguous term that carries no formal endorse-
ment. Facets are not restricted to zygapophyseal articular processes; thus,
the term facet joint does not imply only zygapophyseal joints.
2. Intervertebral discs
a. Each intervertebral disc consists of three components (Fig. 4):
i. Central gelatinous nucleus pulposus
ii. Surrounding anulus fibrosus
iii. Pair of vertebral endplates that sandwich the nucleus
b. The nucleus pulposus consists of a matrix of proteoglycans that bind a consid-
erable amount of water.
c. The anulus fibrosus consists of concentric laminae of collagen fibers. In each
lamina the fibers are parallel and oriented 6So from the vertical, but the direc-
tion of inclination alternates in successive laminae. The inner fibers of the anu-
Ius fibrosus envelop the nucleus pulposus and are attached to the vertebral end-
Anatomyand Biomechanics 11
FIGURE 2. Theparts of a typical lumbar vertebra. VB = vertebral body, P = pedicle, TP = transverse process,
SP = spinous process, L= lamina, SAP = superior articularprocess, lAP = inferior articular process,saf =
superior articular facet, iaf = inferior articularfacet, MP = mamillary process, AP = accessory process, vf =
vertebral foramen, RA = ringapophysis, NA = neuralarch. (From Bogduk N, Twomey LT: Clinical Anatomy
of the Lumbar Spine, 2nd ed. Melbourne, Churchill Livingstone, 1991, with permission.)
plate. The outer fibers of the anulus fibrosus are attached to the margins of the
vertebral bodies and constitute the ligamentous portion of the anulus fibrosus.
d. The vertebral endplat85 are cartilaginous structures that cover the superior and
inferior surfaces of each vertebral body within the area encircled by the ring
apophysis. The two endplates of each disc cover the nucleus pulposus in its
entirety as well as the inner two-thirds of the anulus fibrosus. Via the inser-
tions of collagen fibers of the anulus fibrosus, the vertebral endplates be-
come strongly bound to the intervertebral disc. In contrast, the endplates are
only weakly attached to the vertebral bodies and may be wholly tom from
the vertebral bodies in certain forms of spinal trauma.
12 Anatomy and Biomechanics
FIGURE 3. The joints between two lumbarvertebrae. (From Bogduk N, Twomey LT: Clinicol Anotomy of the
Lumbar Spine, 2nd ed. Melbourne, Churchill Livingstone, 1991, with permission.)
e. The foremost function of the disc is to separate the vertebral bodies so that
movements may occur between the vertebral bodies. The discs must be suffi-
ciently compliant to allow movement but sufficiently strong to withstand
the transmission of compression loads between vertebral bodies.
f. The intervertebral disc is well designed to withstand compression. Compres-
sion between vertebral bodies is fundamentally resisted passively by the
sheer bulk of the anulus fibrosus. The role of the nucleus pulposus is to
brace the anulus internally and to prevent it from buckling inward. As long
as the anulus is thereby braced, it is able to withstand the compression load.
Any impairment of nuclear function, however, compromises the ability of
the anulus to withstand compression loads and causes it to fail by buckling.
FIGURE 4. Detailed structure of the vertebral endplate. Thecollagenfibers of the innertwo-thirds of the anu·
Ius Rbrosus sweep around into the vertebral endplate, forming itsRbrocartilaginous component. Theperiph-
eral fibers of the anulus are anchored into the bone of the ring apophysis. (From Bogduk N, Twomey LT:
Clinical Anatomy of the Lumbar Spine, 2nd ed. Melbourne, Churchill Livingstone, 1991, with permission.)
Analomy and Biomechanics 13
FIGURE 5. Twisting movements of the interbody [oint, The ~bers of

theonulus thatare orientated inthedirection ofthetwist havetheir
points ofaHachment seporatedand are therefore stretched. Fibers
in everysecond lamella of the anulus have their pointsof aHach-
mentapproximated and are relaxed (From Bogduk N, Twomey
IT: Clinical Anatomy of the lumbar Spine, 2nd ed. Melbourne,
Churchill livingstone, 1991, with permission.)
g. The obliquity of the collagen fibers of the anulus fibrosus enables them to
exert tension in both vertical and horizontal directions. The vertical tension
withstands separation (distraction) and bending movements of the vertebral
bodies, whereas the horizontal tension withstands twisting and sliding
movements of the vertebral bodies. For a particular movement, the degree of
participation of the collagen fibers depends on the orientation and direction
of the fibers with respect to the movement.
h. Because all fibers of the anulus fibrosus have a vertical component, the in-
tervertebral disc is well able to resist distraction of the vertebral bodies and
forward and backward bending. 10
i. When a vertebra twists, only the collagen fibers of the anulus fibrosus in-
clined in the direction of rotation resist the movement. The remaining 500/0
are effectively shortened and do not develop tension to withstand the move-
ment (Fig. 5). Because of its relative weakness in torsion, the intervertebral
disc requires protection from the posterior elements of the vertebra. 10 This
protection is afforded by the zygapophyseal joints.
3. Zygapophyseal joints
a. The zygapophyseal joints are typical synovial joints endowed with cartilage,
capsule, meniscoids, and synovial membrane. The articular facets exhibit
variations in both the shape of their articular surfaces and the general direc-
tion in which they face (Fig. 6). Such variations determine the extent to
which joints can prevent forward shear translation between vertebral bodies
and axial rotation of the interbody joint. These movements are resisted by
the impaction of the inferior articular process of the moving vertebra against
the opposing surface of the superior articular process of the vertebra below.
b. The only movement permitted by the lumbar zygapophyseal joints is a slid-
ing movement in a vertical direction, which is executed during flexion and
extension of the vertebral column.
c. Ligaments
1. The role of ligaments in the stability of the lumbar spine has been overempha-
sized. In effect no ligaments can stabilize the lumbar spine.
14 Analomy ana Biomechanics
FIGURE 6. The varieties of orientation and

curvature of the lumbarzygapophysealjoints.
A, Flat joints orientated close to 90" to the
sagittal plane. B, Flat joints orientatedat 60°
to the sagittal plane. C, Flat,'oints orientated
parallel (0°) to the sagittal pane. D, Slightly
curved joints with an average orientation close
to 90° to the sagittalplane. E, C-shaped joints
orientated at 45° to the sagittal plane. F, J-
shaped joints orientatedat 30° to the sagittal
plane. (From Bogduk N, Twomey LT: Clinical
Anatomy of the lumbar Spine, 2nd ed.
Melbourne, Churchill livingstone, 1991, with
permission.)
2. The Interspinous ligaments connect adjacent spinous processes (Fig. 7). However,
only the anterior two-thirds constitute a true ligament, for only this portion
connects adjacent bones. It resists separation of the spinous processes, but its
capacity to limit flexion of the intervertebral joint is weak. The dorsal third of
the interspinous ligament blends with the supraspinous ligament.
3. The supraspinous hgament is a midline structure that runs dorsal to the posterior
edges of the spinous processes to which it is attached (see Fig. 7). Rather than
forming a ligament, however, it consists largely of tendinous fibers derived
from the back muscles and does not exist below the level of L3.
4. The intertransverse hgaments are essentially membranes that extend between adja-
cent transverse processes. They constitute part of a fascial system that separates
the muscles of the ventral compartment from the muscles of the posterior com-
partment.
5. The diolumbar ligament is a substantial ligament that binds the transverse process
of L5 to the ilium; it is not developed, however, until the third decade. At ear-
lier ages it is muscular and represents the L5 component of iliocostalis lumbo-
rum; with age it undergoes fibrous metaplasia. The ligament resists forward
sliding, lateral bending, and axial rotation of the L5 vertebra on the sacrum.
6. The ligamentum flavum is a short but thick ligament that joins the laminae of con-
secutive vertebrae (see Fig. 7). It is unique because of its elastic nature.
Analomy and Biomechanics lS
FIGURE 7. A mediansagittal sectian aF the lumbar spine

showing its various ligaments. All = anteriorlongitudinal
ISL
ligament, Pll = posterior longitudinal ligament, SSl =
supraspinous ligament, ISl = intraspinous ligament, v =
ventral part, m = middle part, d = dorsal port, IF = lig- PLL SSL
amentum Ravum, viewed from within thevertebral canal
and in sagittalsection at the midline. (From Bogduk N, ALL
TwomeylT: Clinical Anatomy of the lumbar Spine,2nd
ed. Melbourne, Churchill livingstone, 1991, with per-
mission.)
Although it contributes some resistance to flexion of the lumbar spine, it does

not limit movement. Rather, its role is to maintain a constant but distensible
smooth surface along the roof the vertebral canal.
7. The posterior longitudinal bgament is thin in the lumbar spine and constitutes little
more than a carpet in the vertebral canal, separating the dural sac from the pos-
terior surfaces of the vertebral bodies (see Fig. 7). It has only a nominal role in
resisting separation of the posterior ends of the vertebral bodies during flexion.
8. The anterior longitudinal ligament of the lumbar region is an ambiguous structure
that consists largely of the tendons from the crus of the diaphragm. Because its
fibers are blended so closely with the anulus fibrosus of the intervertebral discs,
it is artificial to segregate them in either a biomechanical or pathologic sense.
D. Musdes
1. On anatomic and functional grounds, the paravertebral musculature of the lum-
bar spine may be divided into three groups":
a. Psoas major and psoas minor
b. Quadratus lumborum and intertransversarii laterales
c. Lumbar back muscles
2. The psoas major arises from the anterolateral aspect of the lumbar spine and inserts
into the lesser trochanter of the femur. It is a flexor of the hip. Its fibers run too
dose to the lumbar spine to exert significant bending moments on the lumbar
vertebrae. Therefore, it cannot flex the lumbar spine. However, upon contraction,
as in the exercise of sit-ups, the psoas exerts immense compression on the inter-
vertebral discs.'
3. The quadratus lumborum is a wide and somewhat rectangular muscle that consists
of a complex aggregation of various oblique and longitudinally running fibers
that connect the lumbar transverse processes, the ilium, and the 12th rib. Its
principal action is fixation of the 12th rib during respiration. It has a weak ac-
tion to flex the lumbar spine laterally.
16 Anatomy and 8iomechania
FIGURE 8. Thedisposition and span of theseg-

mental fascicles of the multifidus.
4. The intertransversarii laterales connect consecutive transverse processes but are

too small to exert significant forces on the lumbar spine. They are presumed to
serve as proprioceptors.
5. The lumbar back muscles lie behind and cover the posterior elements of the lumbar
vertebrae. Although multiple and seemingly complex, they are systematically
arranged.
a. Intertransversarii mediales
i. The intertransversarii mediales are small muscles that connect the acces-
sory process and mamillary process of one vertebra to the mamillary
process of the vertebra below.
ii. Because of their small size, it is questionable whether these muscles con-
tribute appreciable force in either lateral flexion or extension of the lumbar
spine. Instead, it is believed they serve as large proprioceptive transducers.
b. Interspinales
i. The lumbar interspinales are short muscles that connect the spinous
processes of adjacent lumbar vertebrae.
ii. Like the intertransversarii mediales, they probably seNe a proprioceptive
function.
c. Multifidus
i. The multifidus is a paramedian muscle with fascicles that stem from each of
the lumbar spinous processes and radiate to caudal insertions on the mam-
illary processes and the ilium and sacrum (Fig. 8). The multifidus is the only
muscle covering the back of the lumbar spine at the lumbosacral level.
ii. The fundamental action of the multifidus is to extend the lumbar spine
or control its flexion, but it also opposes the flexion effect of the abdom-
inal muscles when they contract to produce rotation of the lumbar spine.
d. Longissimus thoracis
i. The longissimus thoracis consists of intrinsic lumbar and thoracic fibers.
The lumbar fibers stem from the accessory processes and the adjacent
dorsal surface of the transverse processes of Ll-L5 vertebrae and are an-
chored to the ilium (Fig. 9). The thoracic fibers contribute to the erector
spinae aponeurosis (see page 10).
Anatomy and Biomechanics 17
FIGURE 9 (Right). The lumbar ~bers of the

longissimus thoracis pars lumborum. Left,
the five fascicles of the intact muscle and
the formation of the lumbar intermuscular
aponeurosis by the lumbarfascicles of the
longissimus. Right, the lines indicate theat-
tachments and span of the fascicles. (From
Bogduk N, Twomey LT: Clinical Anatomy
of the Lumbar Spine, 2nd ed. Melbourne,
Churchill Livingstone, 1991, with permis-
sion.)
FIGURE 10 (L,'t). The lumbar fibers of the ilio-

costalis lumborum pars lumborum. Left, the four
lumbar fascicles of iliocostalis. Right, their span
and attachments are indicated by the lines. (From
Bogduk N, Twomey LT: Clinical Anatomyof the
Lumbar Spine, 2nd ed. Melbourne, Churchill
Livingstone, 1991, with permission.)
18 Analomy and Biomechanics
ii. By contracting unilaterally, the lumbar fibers of the longissimus thoracis

bring about lateral flexion of the vertebral column. By acting bilaterally,
they produce posterior sagittal rotation and posterior translation of the
lumbar vertebrae.
e. lIiocostahs lumborum
i. The iliocostalis lumborum also consists of intrinsic lumbar and thoracic
fibers. The lumbar fibers stem from the tips of the transverse processes of
Ll-L4 and are attached to the iliac crest (Fig. 10). The thoracic fibers of
the iliocostalis lumborum contribute to the erector spinae aponeurosis
(see page 10).
ii. The actions of the lumbar fibers of the iliocostalis are similar to those of
the lumbar fibers of the longissimus thoracis.
f. Erector spinae aponeurosis
i. The thoracic fibers of the longissimus thoracis and iliocostalis lumborum
are formed by tiny muscle bellies that stem from thoracic transverse
processes and ribs. These fibers send long caudal tendons to cover the
lumbar region. The side-to-side aggregation of these tendons forms what
has been known as the erector spinae aponeurosis, which is essentially a
wide tendinous sheath attached to the tips of the lumbar and sacral spin-
ous processes and to the sacrum and ilium (Fig. 11).
ii. By spanning the lumbar spine, the erector spinae aponeurosis can exert
tension across it, but the critical feature is that the energy for this ten-
sion is provided by muscle bellies distributed across the entire posterior
region of the thorax; these muscles do not lie in the lumbar region.
FIGURE 11. The erector spinae aponeurosis (ESA) is

formed by the caudal tendons of the thoracic fibers of
longissimus thoracis (IT) and iliocostalis lumborum
(ll). (From Bogduk N, Twomey IT: Clinical Anatomyof
the Lumbar Spine, 2nd ed. Melbourne, Churchill
livingstone, 1991, with permission.)
Analomy and Biomechanic5 19
g. Strength of the back musdes

i. Collectively, on maximal contraction the lumbar back muscles in an
average person can exert up to 4000 N in longitudinal tension and
200-250 Nm of extension moment.
ii. About 500/0 of the extension power of the lumbar spine is provided by the
thoracic fibers of the longissimus and iliocostalis muscles acting through
the erector spinae aponeurosis. Of the remainder, 500/0 is exerted by multifi-
dus and 500/0 by intrinsic lumbar fibers of the longissimus and iliocostalis."
iii. The principal role of the back muscles is to control sagittal rotation of
the vertebra, that is, forward bending. The back muscles have no power
for other movement. Their orientation is essentially vertical; they lack a
substantial horizontal component to achieve or withstand axial rotation
or to resist forward shear.v!'
E. Thoracolumbar fascia
1. The thoracolumbar fascia consists of three layers of fascia that envelop the
muscles of the lumbar spine, thereby separating them effectively into three
compartments (Fig. 12). The thin anterior layer is the fascia of the quadratus
lumborum. The middle layer, which lies behind the quadratus lumborum, is at-
tached to the tips of the lumbar transverse processes and directly continuous
with the intertransverse ligaments.
all
pit If
FIGURE 12. Innervation of the lumbar spine. A cross-sectional view incorporating the level of the vertebral
body(VB) and itsperiosteum (p) (right) and the intervertebral disc(IVD) (left). PM = psoas major,QL = quad-
ratus lumborum, IL = iliocostalis lumborum, LT = longissimus thoracis, M = multi~dus, aldf = anterior layer
of the thoracolumbar fascia, pldf = posterior layer of thoracolumbar fascia, esc = erector spinae aponeu-
rosis, ds = dural sac, zj = zygapophyseal joint, pll = posterior longitudinal ligament, all = anterior longi-
tudinalligament, vr = ventral ramus, Or = dorsal ramus, m = medial branch, i = intermediate branch, I =
lateral branch, svn = sinuvertebral nerve, grc = gray ramus communicans, st = sympothetic trunk. (From
Bogduk N, Twomey LT: Clinical Anatomy of the Lumbar Spine, 2nd ed. Melbourne, Churchill Livingstone,
1991, with permission.)
20 AlKllomy and BiamechaniC5
2. The posterior layer, which is formed by the aponeurosis of the latissimus dorsi,
arises from the tips of the lumbar spinous processes and wraps around the back
muscles to blend with the other layers of the thoracolumbar fascia along the
lateral border of the iliocostalis lumborum. The posterior layer may have a role
in assisting the back muscles during lifting, but its contribution has not been
reliably quantified and appears to be only minor.'
F. Innervation
1. The lumbar spine receives an extensive nerve supply (see Fig. 12).
2. Anteriorly, the ventral rami supply the psoas major, quadratus lumborum, and
intertransversarii laterales.
3. The vertebral bodies receive their nerve supply form the gray rami communi-
cantes and the ventral rami in the form of anterior longitudinal and posterior
longitudinal plexuses that accompany the respective Iongitudinal ligaments.v?
4. Components of the posterior longitudinal plexus are the sinuvertebral nerves,
which supply the posterior longitudinal ligament, the posterior aspect of the
discs, and the ventral aspect of the dura rnater.v?
5. The innervation of the intervertebral discs is derived from the rami communi-
cantes anterolaterally, the ventral rami posterolaterally, and the sinuvertebral
nerves posteriorly. In addition, the anterior and posterior longitudinal nerve
plexuses send fine penetrating branches into the discs. Histochemical studies
have shown that only the outer third of the anulus fibrosus contains nerve
fibers. Various types of nerve terminals, such as free nerve endings, have been
identified. As in other tissues of the body, the free nerve endings have been as-
cribed a nociceptive role, as confirmed by immunofluorescence techniques,
which demonstrated within the nerve endings the presence of neuropeptides
typically found in nociceptive axons.?
6. The structures posterior to the intervertebral foramen are supplied by branches
of the dorsal rami":
a. The lateral branches are distributed to the iliocostalis lumborum.
b. The intermediate branches supply the lumbar portion of the longissimus tho-
racis,
c. The medial branches innervate the multifidus, interspinous muscle and liga-
ment, and zygapophyseal joints (see Fig. 12).
7. Any structure that receives innervation is in principle a potential source of
pain, if it is affected or afflicted by an appropriate pain-producing pathology.
G. Blood supply
1. Arteries
a. The arterial blood supply of the lumbar spine at various vertebral levels is
derived from pairs of lumbar arteries, the upper four of which arise from the
descending aorta, whereas the fifth arises from the median sacral artery.
b. Each lumbar artery passes backward around its related vertebral body and
sends branches into the substance of the vertebral body. These branches sup-
ply the spongiosa of the body, whereas terminal branches form a capillary
plexus beneath the vertebral endplates.
c. On reaching the intervertebral foramen, each lumbar artery divides into sev-
eral external and internal branchesf
i. The external branches supply the paravertebral muscles, zygapophyseal
joints, and middle and other posterior elements of the vertebral body.
ii. Two internal branches (the anterior and posterior spinal canal arteries)
enter the intervertebral foramen and are distributed to the floor and roof
of the vertebral canal, respectively. A third internal branch becomes the
radicular artery, which supplies the spinal nerve and its roots.
d. The intervertebral disc has a minimal blood supply. Consequently, it relies

primarily on the diffusion of nutrients from two systems of blood vessels for
its nutrition-the small arteries found in the outer perimeter of the anulus fl-
brosus and the capillary plexuses beneath the vertebral endplates. Each sys-
tem contributes about half the nutritional requirement of the dtsc.'?
Diffusion is facilitated by the passage of fluids into the proteoglycan matrix
of the disc but at the same time is controlled by the electrostatic properties
of the proteogtycans, Diffusion is further enhanced by repeated compression
of the disc during activities of daily living, which essentially pumps fluid in
and out of the disc.
2. Veins
a. The lumbar spine is surrounded by several venous channels and plexuses.
b. Tributaries from the back muscles drain into the ascending lumbar veins,
which run longitudinally in front of the bases of the transverse processes.
c. From the ascending lumbar veins, the lumbar veins accompany the lumbar
arteries across the vertebral bodies to reach the inferior vena cava.
d. The anterior external venous plexus covers the front of the vertebral bodies.
e. The anterior internal venous plexus lines the floor of the vertebral canal and
the posterior internal venous plexus lines its roof. The anterior and posterior
plexuses drain the surrounding skeletal elements as well as the neural tissues
contained in the vertebral canal. At the intervertebral foramina they com-
municate with the ascending lumbar veins.
f. The venous drainage of the vertebral bodies starts as a subchondral postcap-
illary plexus beneath each vertebral endplate, From this plexus collecting
veins drain toward the center of the vertebral body. They communicate with
the anterior external venous plexus and lumbar veins but drain largely into
the basivertebral veins, which emerge from the posterior aspect of the verte-
bral body and join the anterior internal plexus.
III. Biomechanics
The cardinal movements of the lumbar spine are flexion, extension, compression, axial ro-
tation, and lateral flexion. Flexion and extension are clinically the most obvious; compres-
sion is the most overlooked and underrated movement yet clinically the most relevant.
A. Flexion and extension
1. Flexion and extension involve the combination of sagittal rotation and transla-
tion. During flexion of the lumbar spine, each vertebra rotates and translates
anteriorly; a reciprocal combination occurs in extension. The range of rotation
is about 6-10° per segment, and the range of translation is about 2 mm.
Anterior sagittal translation is resisted primarily by the zygapophyseal joints
and secondarily by the anulus fibrosus of the intervertebral disc. Anterior sagit-
tal rotation is resisted by the anulus fibrosus, the capsules of the zygapophyseal
joints, the ligaments of the intervertebral joints, and most importantly, by ac-
tive or passive tension of the back muscles supplemented by passive tension in
the thoracolumbar fascia.
2. Extension is limited primarily by bony impaction. Either the spinous processes
impact against each other or an inferior articular process impacts against the
lamina below. Only secondarily does tension in the anterior anulus fibrosus
contribute to resisting extension.
B. Compression
1. Compression is the neglected and underestimated movement of the lumbar
spine because it has such a minimal magnitude and it is not clinically visible.
Compression occurs under body weight, but body weight is not the major
source of compression loads on the lumbar spine. Up to 900/0 of the compres-

sion load exerted on the lumbar spine is produced by the lumbar back muscles.
When a person leans forward, a tendency to bend anteriorly is produced by the
weight of the trunk and whatever external load is carried. This forward bending
has to be balanced by the action of the back muscles acting posterior to the
vertebral column.
2. Quantitatively, the tendency to bend forward is determined by the flexion mo-
ment, which is the product of the sustained weight and the perpendicular dis-
tance of that weight from the lumbar spine. Forward bending moment has to be
balanced by an equal but opposite extension moment provided by the back
muscles. The back muscles, however, act very close to the lumbar spine and
therefore must exert large forces to achieve the appropriate moment.
a. In a stoop lift, for example, if Fw is the force of the weight of the trunk and
the weight to be lifted; Dw is the horizontal distance of the weight from the
lumbar spine; Fm is the force of the back muscles; and Dm is the lever arm
of the muscles:
r, X n, = Fw X n,
Fm = (Fw X Dw) / n,
b. With a trunk weight of 400 N and an external load of 250 N [i.e., 25 kg), if
both loads act at 40 em from the lumbar spine and the back muscles act at 5
em from the lumbar spine:
r, = (650 X 0.4) / 0.05
Fm = 5200 N
c. To lift 25 kg, 520 kg of back muscle force is required; as the back lifts, this
force is experienced as a compression force on the vertebral bodies and discs
(Fig. 13).
e. Axial rotation
1. Because there are no primary rotators of the lumbar spine, axial rotation is a
movement imposed secondarily on the lumbar vertebrae and their joints.
FIGURE 13. The geometry integral ta the calculation of Rex-

ion moments affecting the lumbar spine during a stoop lift.
2. Rotation is achieved by the oblique abdominal muscles acting on the thorax,
the movements of which impose a screwing effect on the lumbar spine from L1
to the sacrum.
3. This motion is resisted by impaction of the zygapophyseal joints and by tension
developed in the anulus fibrosus; resistance limits the range of rotation at each
lumbar segment to < 3°.
D. Lateral flexion
a. Little is known about lateral flexion of the lumbar spine, which involves a
complex and variable combination of lateral bending and rotatory movements
of the interbody joints and diverse movements of the zygapophyseal joints.
2. Because of this complexity, lateral flexion of the lumbar spine has not been
subjected to detailed biomechanical analysis.
IV. Mechanical Injuries

A. Flexion
1. Flexion movements of the lumbar spine are not hazardous if the movements re-
main strictly in the sagittal plane. The discs and zygapophyseal joints are well
designed to withstand this movement.
2. Biornechanical studies have failed to demonstrate injury to the intervertebral
discs simply with flexion.
3. Because the back muscles are the major contributors to controlling or resisting
flexion, in principle, they are foremost liable to injuries during flexion. Acute
muscle tears, therefore, may occur during forceful flexion or extension; other-
wise, however, the lumbar spine is intrinsically resistant to injury under these
circumstances.
B. Extension
Several types of injuries may befall the lumbar vertebrae during forceful extension
movements [e.g., in falls or sporting activities that involve backward arching
movements). During forceful extension, movement is initially arrested by im-
paction of the inferior articular process against the lamina. This impaction may
cause a chiselling effect on the lamina, resulting in a pars interarticularis fracture.
Otherwise, if the lamina resists the impaction, the continued extension force is
dissipated as posterior rotation of the contralateral zygapophyseal joint, which
may result in disruption of the joint capsule. J
C. Flexion and torsion
1. The lumbar spine is particularly vulnerable to injury during flexion movements
combined with torsion. The flexion movement prestresses the anulus fibrosus,
thereby reducing its capacity to withstand subsequent axial rotation. Mean-
while, because the zygapophyseal joints are subluxated, smaller portions of
their surfaces are in contact to resist rotation.
2. Initially, axial rotation occurs around an axis through the vertebral body, but
the contralateral zygapophyseal joint soon becomes compressed (Fig. 14).
Continued torsion results in rotation about an axis through the compressed
joint. The contralateral joint moves backward, and the intervertebral disc shears
sideways.
3. The resultant injuries are several. Subchondral fractures may occur on the com-
pression side as well as overt fractures of the articular processes and fractures
of the pars interarticularis. In the contralateral zygapophyseal joints, tears of
the capsule or fracture avulsions of the capsules may occur. In the interverte-
bral disc, the anulus fibrosus may be tom in a peripheral, circumferential man-
ner. Each of these injuries may be a source of pain.
tear
fracture,
avulsion, fracture
capsular tear
FIGURE 14. Rotation injuries of the lumbarspine. Axial rotation of a lumbarsegment is initially limited by im-
paction of a zygapophyseal joint, but further rotation may occurabout a new axis in the impacted joint; as
a result, the disc is exposed to a lateral shear force and the contralateral zygapophyseal joint swings back-
ward. The impacted zygapophyseal joint may suffer fractures of its articular processes or of the pars inter-
articularis. The contralateral joint may suffer fracture avulsions of tears of itscapsule. Theanulusfibrosus of
the intevertebral disc may suffer peripheral, circumferential tears. (From Bogduk N, Twomey LT: Clinical
Anatomy of the Lumbar Spine, 2nd ed. Melbourne, Churchill Livingstone, 1991, with permission.)
D. Compression
1. Compression injuries of the intervertebral disc may result from excessive axial
loading by gravity or muscle action. Gravitational injuries occur in instances
such as a fall onto the buttocks. Muscular injuries may result from severe exer-
tion while pulling or lifting.
2. The critical feature of a compression injury is fracture of the endplate (Fig. 15),
which in itself is of no immediate consequence; it does not hurt, and it may heal.
However, an endplate fracture may initiate the process known as internal disc dis-
ruption, by interfering with the homeostasis of the matrix of the nucleus pulpo-
sus, by an unbridled inflammatory repair response, or even by an elusive auto-
immune mechanism.? The matrix of the nucleus pulposus undergoes biochemical
and biophysical degradation. Internal disc disruption is not the same process as
age-related degeneration; it is a specific response to injury to the endplate. As
the biophysical properties of the nucleus deteriorates, its water-binding capac-
ity is decreased and its bracing effect on the anulus fibrosus is compromised.
As a result, the anulus fibrosus progressively fails in compression and the ver-
tebra subluxes (Fig. 16). This process is manifested as loss of disc height and
the condition ofisolated disc resorption. Alternatively, progressive deterioration of
the nucleus pulposus may extend into the anulus fibrosus, producing radial fis-
Anatomyand Biomechanics 2S
END' PLATE
FRACTURE
FIGURE 15. Compression injury of an interverte-

bral joint. Excessive compression forcemay result
in fracture of a vertebral endplate. The fracture
may heal and be of no consequence; on the other
hand, it may initiate a process of disc degrada-
tion that affects the nucleus pulposus near the
fracture site and gradually extends into the rest
I \
of the nucleus. (From Bogduk N, Twamey LT: Clin-
icalAnatomyofthe Lumbar Spine, 2nd ed. Mel-
bourne,Churchill Livingstone, 1991, with permis-
sion.)
sures without affecting disc height. In this condition disruption of the anulus fl-
brosus is the cardinal feature of internal disc disruption (see Fig. 16).
3. Disc resorption becomes painful by chemical and/or mechanical means. Inflam-
matory chemicals from the nucleus pulposus may stimulate the endings of the
nerve fibers in the outer anulus fibrosus. As fewer and fewer laminae remain
to sustain the normal everyday forces applied to the anulus fibrosus, the re-
maining intact fibers have to bear an increasingly greater load. The increasing
INTERNAl DISC DISRUPTION

FIGURE 16. Disc degradation and internal
disc disruption. Disc degradation spreads
to involve allof the nucleus pulposus. Ifthe
anulus fibrosus remains relatively intact,
the disc narrows because of the loss in
water-binding capacity of the nucleus, re-
sulting in isolated disc resorption. On the
other hand, disc degradation may spread
radiallyintothe anulusFibrosus, causing a
fissure. The external appearance of thedisc
remains normal; the pathologic process
remains wholly within the disc, and the
condition of the disc is describedas inter-
nal disc disruption. Ifthe remaining fibers
of the anulus fibrosus are breached, nu-
clear herniation may follow internal disc
disruption. (From Bogduk N, Twomey LT:
Clinical Anatomy of the Lumbar Spine,
2nd ed. Melbourne, Churchill Livingstone,
1991, with permission.)
HERNIATION
26 Anatomy and Biomechanics
stress on these fibers constitutes a mechanical basis of pain from the anulus
fibrosus.'
4. Recent biomechanical studies have shown that compression injuries do not
need to be acute or severe in order to produce internal disc disruption. Endplate
fractures can occur as a result of fatigue failure following repeated compression
loading. Such failure can occur under loads as small as 600/0 of the ultimate
compression strength of the endplate, and as rapidly as within 100 repetitions.
Such loads and repetitions are within the range experienced during moderately
heavy work.
References
I. Adams MA, McNally OS, Wagstaff J, Goodship AE: Abnormal stress concentrations in lumbar inter-
vertebral discs following damage to the vertebral bodies: A cause of disc failure? Eur Spine J
1:214-221, 1993.
2. Bogduk N: The lumbar disc and low back pain. Neurosurg Clin North Am 2:791-806, 1991.
3. Bogduk N, Twomey LT: Clinical Anatomy of the Lumbar Spine, 3rd ed. Melbourne, Churchill
Livingstone, 1997.
4. Bogduk N, Pearcy MJ, Hadfield G: The anatomy and biomechanics of the psoas major. Clin Biornech
7:109-119,1992.
5. Bogduk N, Macintosh JE, Pearcy MJ: A universal model of the lumbar back muscles in the upright
position. Spine 17:897-913, 1992.
6. Bogduk N, Tynan W, Wilson AS: The nerve supply to the human lumbar intervertebral discs. J Anat
132 :39-56, 198 I.
7. Bogduk N, Wilson AS, Tynan W: The human lumbar dorsal rami. J Anat 134:383-397, 1982.
8. Crock HV, Yoshizawa H: The blood supply of the lumbar vertebral column. Clin Orthop 115:6-21,
1973.
9. Groen GJ, Baljet B, Orukker J: Nerves and nerve plexuses of the human vertebral column. Am J Anat
188:282-296, 1990.
10. Hickey OS, Hukins OWL: Relation between the structure of the annulus fibrosus and the function and
failure of the intervertebral disc. Spine 5: 100-116, 1980.
I I. Macintosh JE, Pearcy MJ, Bogduk N: The axial torque of the lumbar back muscles: Torsion strength
of the back muscles. Aust NZ J Surg 63:205-121,1993.
12. Maroudas A: Nutrition and metabolism of the intervertebral disc. In Ghosh P (ed): The Biology of the
Intervertebral Disc, vol. II. Boca Raton, FL, CRC Press, 1988, pp 1-37.
3
I
Pathophysiology, Neurophysiology, and
Biochemistry of Lumbar Spine Pain:
The Degenerative Cascade Model
Key Points
• Spinal structures must be viewed as dynamic, not static, mechanisms.
• Back care and treatment must be viewed with an understanding of the mechanical and
physiologic forces at play.
• The relationship of pain to spinal structure and function remains highly controversial.
• Neurologic complaints do not always equate with neurologic dysfunction.
• Neurologic dysfunction does not always correlate with prior or active nerve
compression; inflammation alone may suffice.
• Injury or deterioration of spinal structures may lead to changes in other areas, which
at a later time may become a primary source of active problems.
• The spinal motion structures interact intimately; changes in one structure inevitably
affect other structures.
• The degenerative cascade model provides a functional model for the pathophysiology
and clinical course of patients with recurrent back pain.
I. Definitions
A. Sclerotomal pain Pain emanating from an area of bone or fascia supplied by a sin-
gle nerve root. Nerve distribution varies greatly among individuals.
B. Radicular pain Pain in the distribution of a single nerve root; does not produce
neurologic loss. Distribution varies greatly among individuals.
C. Radiculopathy Pain in the distribution of a single nerve root; produces neurologic
loss. Nerve distribution varies greatly among individuals.
D. Dermatomal pain Pain in the distribution of a single nerve root that innervates a
specific area of skin; may be associated with neurologic loss. Nerve distribution
varies greatly among individuals.
E. Myotomal pain Pain in the distribution of a group of muscles innervated by a sin-
gle nerve root; may be associated with neurologic loss.
F. Referred pain Pain felt at a site remote from the site of pathology; does not cause
neurologic loss; thought to be due to an error in perception by the brain. Referral
patterns characteristic of a particular structure vary greatly among individuals,
depending on the make-up of sclerotomes, dermatomes, and myotomes.
G. The above (A-F) may occur in isolation or combination.
27
28 Pathophysiology, Neurophysiology, and Biochemislry
II. Anatomy
A. Intervertebral disc
1. Old concept that disc is not innervated has been disproved.
2. Nerve endings have been found in multiple structures.
a. Posterior longitudinal ligament
b. At least outer portion of disc anulus (approximately 'h)
c. Vertebral body
d. Dural sac
e. Epidural venous and arterial structures
3. Innervation from combination of sinuvertebral and local ventral and gray rami
4. Because disc innervation goes to multiple levels, localization of structures for
pain referral is less clearly defined.
5. Disc comprised primarily of:
a. Collagen (types I and II)
b. Water
c. Proteoglycans
6. During degenerative process, type II collagen is replaced by type I, with in-
creased amounts of elastin.
7. Disc circulation is poor, primarily by diffusion through vertebral bony endplate;
healing and reparative processes are therefore tenuous.
8. Unclear whether changes in disc collagen and enzymatic activity are cause or
result of degenerative disc disease ("chicken or the egg")
9. Strong evidence now exists that discogenic inflammatory responses, which may
be enzyme (PLA 2)-mediated, may serve as source of discogenic pain (see
"Inflammation-role in pain," page 3 I).
B. Neurologic components
I. Nerve roots subject to mechanical compression by:
a. Disc
b. Venous dilatation
c. Bony encroachment
i. From facet hypertrophy
ii. From vertebral body osteophytes
d. Tumors
e. Thickening of ligamentous structures
2. Distal motor innervation and sensory (limb) distribution are generally consis-
tent but can vary (not everyone is "wired" the same).
3. Most muscles are innervated by 2-3 spinal roots.
4. Sensory patterns (dermatomes) are usually more discrete, although they vary
somewhat among individuals.
5. Nerve roots have some elastic properties but typically lack the protection of
peril epineurium, which is found in peripheral nerves.
6. Different roots exit at different angles (lower roots are more oblique and have a
longer path), potentially changing risk of mechanical stress (higher risk for
lower roots).
7. Arranged to exist as complex structure:
a. Structural stability varies from within thecal sac to lateral recess and foramen.
b. Load forces increase as nerve root travels from central to lateral orientation.
c. Suspended or supported-small local ligamentous (Hoffmann's) structures
C. Dorsal root ganglion (DRG)
I. Located in middle zone of intervertebral foramina
2. Contains multiple types of sensory cell bodies
Pathophysiology, Neurophysiology, and Biochemislry 29
3. Modulating center for peripheral to central transmission
4. Site of significant neuropeptide production
a. Substance P
b. Eukephalin
c. VIP
d. Multiple other neuropeptides present
5. DRG as source of primary pain
a. Local mechanical compression (disc, bony narrowing, stenosis)
b. Local alteration in neuropeptide balance
c. Chemical irritation or inflammatory reaction
d. Vascular phenomenon-nerve root compression alters local blood supply,
leading to distal vascular compromise to DRG and pain.
D. Facet (zygapophyseal) joint
1. Paired posterior spinal structures
2. Diarthrodial and weight bearing (approximately 20% of weight borne by spinal
segment); surface spatial alignment variable
3. Implicated in pain syndromes
4. Local injection of hypertonic solutions causes local and distal (leg, calf, foot) pain.
5. Clinical correlation with back pain syndromes (e.g., facet synovitis as a primary
cause of pain) remains controversial.
6. Contains numerous nerves mediating proprioception and nociception
7. Susceptible to same derangements as other diarthrodial joints
E. Ligamentous structures
1. Provide major component of spinal structural support-passive structures
2. Resist tensile but not compressive loading
3. Designed to facilitate motion but to prevent and protect against excessive sud-
den forces
4. Multiple, separate ligaments with apparent protective interaction
5. Prone to degenerative change over time
6. Relationship of ligamentous injury (sprain or strain) to painful spinal condi-
tions is not easily defined; disruption is likely to result in some segmental in-
stability, with pain due to loss of support.
F. Musculature
I. Also complex association of multiple layers and alignments (like ligaments)
2. Active components
3. Unsupported spine collapses under an axial load of approximately Sibs; thus
musculoligamentous structures provide crucial support.
4. Intrinsic spinal musculature is likely inadequate to maintain support alone.
5. Support comes from abdominal (rectus abdominis and oblique) musculature
through lumbodorsal fascia and iliopsoas musculature.
6. Different groups contract under variable anatomic spinal positions to increase
level of spinal stability (e.g., lateral bend causes increase in muscular activity
on opposite side).
III. Biochemistry
A. Complex relationship involving structural components of the spine-particularly the
intervertebral disc and DRG-appears to mediate many spinal pain disorders.
B. Intervertebral disc
I. Largely avascular
2. Nucleus is 85-90% hydrated in adolescence, about 60-70% hydrated by age 70
years.
a. Dry weight:
i. About 65010 proteoglycans
ii. About 25010 noncollagen proteins
iii. About 10- 15010 collagen (mainly type II)
3. Anulus
a. 700/0 hydrated
b. Dry weight
i. 20010 proteoglycans
ii. 50-60010 collagen (mainly type I)
iii. 10010 elastin
4. Proteoglycans
a. Responsible for imbibing water
b. Interact with collagen for disc integrity
5. Proteoglycan-collagen interaction
a. Responsible for maintaining disc integrity
b. Proteoglycans attach to collagen by "linked protein" structure.
c. If this relationship fails or if protein link changes, proteoglycans are lost.
i. Probable early step in biochemical degenerative disc cascade
ii. Reason for initial breakdown is still unknown; possibilities include:
(a) Genetic factors
(b) Mechanical forces
(c) Unknown biochemical triggers
6. Enzyme systems
a. Multiple types
i. Collagenase
ii. Elastase
iii. Lysosomal enzymes
iv. Phospholipase A z
v. Proteinases
b. Probably mediated by pH and other environmental factors
c. Alteration in enzyme activity and control probably releases a biochemical
cascade of deterioration that supplements mechanical forces (Fig. 1).
Mechanical and Disc Herniation

PLA Release
ChemicalFactors Anular Fislure 2
/
~ ActIvation
Perineural Wlammat'. ~ .
/ ~~ta~dW LeuIcotrienea
Pain
Weakness
----.... SeNaryLoss
FIGURE I. Mechanisms of nerve injury in lumbardiscdisease. (From Saal JS: Role of inAammation in lumbar
pain. Spine 20:1821-1827, 1995, with permission.)
Pathophysiology, Neurophysiology, and8iochemislry 31
C. Dorsal root ganglion

1. Contains probably hundreds of various neurotransmitters and chemicals
2. Mechanically sensitive to compression
3. When altered either biochemically or mechanically, DRG increases firing, caus-
ing an alteration in local neural pathways and increased potential for pain per-
ception.
4. Local mechanical pressure on DRG-herniated disc, bony osteophytes, foraminal
narrowing, or degenerative biochemical agents-alters pain pathways.
5. As the anatomic, biochemical pathway deteriorates from normal, neural sensi-
tivity increases.
IV. Neurophysiology
A. Referred pain
1. Seemingly designed only to confuse everyone involved
2. Why does brain "misidentify" site of pain?
a. Classic example: primary complaint of arm or jaw pain during myocardial
infarct
b. Several theories proposed
i. May be due to antidromic stimulation from somatic visceral afferents,
which causes distant nociceptor response at secondary pain site
ii. May be due to visceral afferent supply entering spinal cord and brain
(spinothalamic tracts) at same point as painful spinal structure, leading
to CNS "misunderstanding" of actual nociceptive source
B. Sympathetic pain
1. Frequently invoked as source for chronic pain syndromes
2. Designated by multiple terms
a. Complex regional pain syndrome
b. Reflex sympathetic dystrophy (RSD)
c. Causalgia
d. Sympathetically mediated pain
e. Sudeck's dystrophy
f. Shoulder-hand syndrome
3. Recent research suggests that phenomenon may not involve simply activation
of sympathetic pathways.
a. Many of the classic signs and symptoms of RSD cannot be reproduced in all
patients.
b. Sympathetic blockade does not always stop RSD pain.
c. Many long term sympatholytic methods are unsuccessful in providing pain
relief.
d. Diseases of sympathetic nerves are, for the most part, nonpainful.
e. Recent research has focused on visceral afferents as a source of such symp-
toms.
i. Sensory nerves may travel along with autonomic fibers as pain media-
tors.
ii. Visceral afferents have been shown to mediate visceral pain patterns.
iii. Cell bodies lie in DRG.
iv. Interaction with other nerve pathways is likely cause of pain.
e. Central response due to peripheral nerve injury and immune system activation
V. Inflammation-Role in Pain
A. Important in understanding mechanism of pain production in discogenic, neuro-
genic, and facet spinal pain
B. Awareness that chemical factors are required for production of pain changes prior percep-
tion of mechanical compression and structural dysfunction as sufficient causes.
1. Lesion size, therefore, need not always correlate directly with extent of pain in
discogenic pain production.
2. Patients with significant findings and complaints of lumbar radiculopathy may
be found on scans or surgery to have minimal neural compression because
symptoms are of an inflammatory etiology (see Fig. 1).
3. Patients frequently improve well in advance of anticipated or documented mor-
phologic disc change because of improvement in chemical factors.
C. Significant evidence indicates that inflammatory processes are major contributors tospinal
pain disorders.
1. Humoral mechanisms (IgG, IgM, interleukin, nitric oxide)
2. Cellular mechanisms (fibroblasts, macrophages]
D. Pain due to release of various inflammatory mediators.
1. Leukotrienes
2. Prostaglandins
3. Platelet-activating factors
4. Bradykinins
5. Cytokines
E. High concentrations of phospholipase A2 are found in herniated discs.
1. Acts as rate-limiting enzyme for release of arachidonic acid from cell mem-
branes
2. Leads to initiation of multiple portions of inflammatory cascade
3. Phospholipase A2 has been demonstrated to be inflammatory in animal models.
4. Identification and pursuit of blocking and mediating agents may allow therapeu-
tic biochemical interventions to replace structural approaches for pain treatment
(Fig. 2).
Memlmme phospholipids
~
Phospholipase ~ ....- - - - - InrL'?
ArachidOnic acid
(~le)
Platelet Activating
Factor
(Cyclo-oxygenase)
prostaglins 5 HPtE
Leukotneri: A 4
B4
C4
D,
FIGURE 2. Phospholipase A2 liberates arachidonic acid at site of inAammation. (From Saal JS: Role of in-
flammation in lumbarpain. Spine 20:1821-1827, 1995, with permission.)
Pathophysiology, Neurophysiology, and Biochemislry 33
Facet Joints Stage Disc
Synovial reaction Outer

annulus
I tears
Meniscal tear Dysfunction
I
End-plate
Cartilage destruction separation
Nuclear
HNP peripheralization
I
Capsular laxity } Disc~tiOn
Instability
Subluxation
{ Loss of disc
height
Enlargement} Osteophytes
of facet Fixed Deformity
(Stenosis) { form
& osteophytes
FIGURE 3. Degenerative cascade: overview. (From Selby0, Saal JS:Degenerative Series. Camp International,
with permission.)
VI. Degenerative Cascade Model (Fig. J)

A. Attempts to define and outline biochemical, physiologic, and anatomic forces
leading to spinal pain
1. Based on concept ofmotion segment consisting of:
a. Adjacent vertebrae
b. Intervening disc
c. Central spinal canal containing thecal sac and nerve roots
d. Paired facet joints and capsules
e. Ligamentum flavum
f. Lateral nerve canal leading to foraminal exit zone for nerves
2. Spinal motion segment
a. Static stability is based on multiple support mechanisms.
b. Dynamic as well as muscular and ligamentous supports allow mobility
within physiologic ranges.
c. As structural supports change, disc-facet "tri-joint" complex begins to un-
dergo repetitive microtrauma.
d. Restraining forces fail, and further degenerative changes result.
B. Based on work of Kirkaldy-Willis
C. Helps to predict anatomic, biochemical, and clinical changes over time
34 PathophY5iology, NeurophY5iology, andBiochemi5try
D. Injury and cumulative trauma: lead to changes in integrity of:

1. Intervertebral disc
2. Facet joints
3. Ligamentous components
4. Vertebral body endplates
E. Recent research has focused on increased understanding of both biochemical and
anatomic processes involved.
F. Stage I: dysfunction: (Fig. 4) Trauma and cumulative stress lead to changes in:
I. Facets
a. Joint (facet) synovitis
b. Subluxation
c. Cartilage degeneration
2. Discs
a. Anular tears, release of inflammatory chemicals
b. Local ischemia
c. Sustained segmental muscle hypertonicity
d. Ligamentous strain
G. Stage II: instabdity (Fig. 5)
I. Facets
a. Increasing cartilaginous deterioration
b. Capsular laxity
c. Increased rotational movement in physiologic range
FIGURE 4. Degenerative cascade:

dysfunction phase. (From Selby 0,
Saal JS: Degenerative Series. Camp
International, with permission.)
Pathophysiology, Neurophysiology, and Biochemistry 3S
2. Discs
a. Increasing frequency of tears with coalescence
b. Nuclear and anular disruption
c. Increased translational forces
d. Anular laxity
3. Changes in disc and facet increase ligamentous stress and dysfunction.
H. Stage III: stabihzation (Fig. 6)
I. Facets
a. Loss of joint surface-cartilage
b. Intra- and extraarticular fibrosis
c. Hypertrophy and spurring
d. Joint space narrowing
e. Osteophyte formation according to Wolffs law
2. Discs
a. Nuclear deterioration
b. Changes in collagen types
c. Endplate irregularities
d. Osteophytes and spurring
e. Disc resorption and fibrosis
f. Progressive loss of disc space height
g. Central and/or lateral canal stenosis
h. Ligamentum flavum hypertrophy and calcification
i. Nerve root scarring

instability phase. (From Selby D,
Saal JS: Degenerative Series. Camp
International, with permission.)
36 Polhophysiology, Neurophysiology, and Biochemislry

stabilization phose. (From Selby 0,
Saal JS: Degenerative Cascade
Series. Camp International, with
permission.)
3. Leads to loss of mobility at segment and restabilization at level of deterioration

from original normal function
4. Clinical improvement depends on extent and pattern of changes. The process
resembles a race between (1) injury and pain and (2) eventual internal system
stability.
5. Explains in large part relative peaks of spinal syndromes, especially root com-
pression
a. Dlscogentc-Iate 30s to late 40s (dysfunction phase)
b. Stenotic (bony and ligamentous hypertrophy, space narrowing)-50s/60s (sta-
bilization phase)
VII. Degenerative Cascade As a Clinical Model

A. Early changes due to trauma, vibration forces, and overuse begin to occur in the
functional spinal motion segment.
1. Normal dynamic support forces are altered, and degenerative cascade is initiated.
2. Alteration takes place early in vascular, nutritional, and biochemical relationships,
leading to a lower tolerance for further insult and therefore a cascade effect.
B. Discal pressure and position
1. Intradiscal pressure varies substantially with spinal position.
2. As discs load, pressures shift within the disc substance.
PalhophY5iology, Neurophysiology, ami8iochemi51ry 37
3. Healthy disc
a. Loading in compression causes an increase in pressure away from nucleus to
outer anulus.
b. Outer layers act with increased tensile stress and greater endplate load in center.
4. Degenerative disc
a. Less nuclear material, with shift of load to anulusb. Endplates under in-
creased load on periphery
c. Leads to more compressive axial stress
5. Changes in load characteristics lead to self-fulfilling prophecy as degenerative
process becomes self-accelerating.
6. Clinical manifestations are based on mechanical load factors.
a. Patient treatment can flow, in part, directly from this concept in terms of
exercise, education, and body mechanics.
b. Patient can be trained to shift body mechanics to decrease loading of painful
structures.
C. Clinical manifestations
1. Anular disc tears
a. Limited to low back pain; often diagnosed as muscular sprain or strain
b. Self-limited, with minimal leg involvement
c. Brought on and worsened by flexion or torsional motions, sitting, and bend-
ing
d. Typically improves with minimal intervention
2. Repetitive anular tears
a. Underlying alteration in local collagen-proteoglycan relationships, incom-
plete healing after original insult, scar formation
b. May begin to coalesce from circumferential to radial tears
c. Precursor to herniated nucleus pulposus-Ioss of nuclear material (see Fig. 4)
3. Facet synovitis
a. Disc space narrowing leads to increased facet joint loading, capsular defor-
mation, and synovial changes.
b. Early facet changes lead to local mechanical pain, which typically worsens
with extension and/or rotational motions.
c. Further deterioration leads to arthropathy, increased instability, and more
frequent and disabling spinal pain.
4. Facet hypertrophy
a. Occurs with further facet deterioration
b. Leads to bony narrowing of lateral recess and foramen
c. Bony narrowing leads to compression of exiting nerve roots and spinal
stenosis.
d. Evidenced by increasing leg pain and worsened by spinal extension, such as
prolonged standing (see Fig. 5)
D. Degenerative cascade asclinical predictor
1. One of the primary errors in prevention of back pain syndromes is failure to
recognize early back problems as a warning sign of the cascade potential.
2. Early education and emphasis on lifestyle changes, exercise, and awareness of
body mechanics may alter the long-term consequences.
a. Patients who have repetitive back injuries over time may be going through
this scenario, even though at first the injuries resolve.
b. This model predicts back injuries or episodes of increasing severity and du-
ration, with progressively shorter periods between events, as the degenera-
tive cascade progresses.
VIII. Conclusion: Lumbar Pain

A. Complex interaction of both structural and biochemical factors
B. Best fits model of degenerative cascade of both major factors. Posttraumatic (e.g.,
fracture) or medical (e.g., tumor, infection) disorders are exceptions.
C. Explains why structural improvements alone do not always result in clinical im-
provement
D. Explains high percentage of abnormal discs on scans in asymptomatic individuals
E. Traditional treatment has focused particularly on structural approaches; future
gains are more likely to result from biochemical/genetic methods of treatment.
F. Many of the changes identified with pain occur during aging. Pain may result
from the premature occurrence of such changes. Discogenic pain is much less
common in older population, even with widespread degenerative discs.
G. The degenerative cascade model, when viewed from an anatomic, biochemical,
and physiologic perspective, is currently the most comprehensive model of back
pain.
References
I. Franson RC, Saal JS, SaaIJA: Human disc PlA 2 is inflammatory. Spine 17(Suppl 6):S 129-S 132, 1992.
2. Harrington JF, Messier AA, Beretier 0, et al: Herniated lumbar disc material as a source of free gluta-
mate available to affect pain signals through the dorsal root ganglion. Spine 25:929-936, 2000
3. Hasegawa T, An H, Inufusa A, Mikawa Y. Watanabe R: The effect of age on inflammatory responses
and nerve root injuries after lumbar disc herniation: An experimental study in a canine model. Spine
25:937-940,2000
4. Hashizume H, Deleo JA, Colburn RW, Weinstein IN: Spinal glial activation and cytokine expression
after lumbar root injury in the rat, Spine 25: 1206-1210, 2000
5. Kirkaldy-Wallis WH: Three phases of the spectrum of degenerative disease. In Kirkaldy-Willis WH,
Burton CV (eds): Managing low Back Pain, 3rd ed. New York, Churchill Livingstone, 1992, pp
105-119.
6. lee H, Weinstein IN, Meller ST, et al: The role of steroids and their effects on phospholipase A2: An
animal model of radiculopathy. Spine 23: 1191-1196, 1998
7. Miyamoto H, Saura R, Harada T, et al: The role of cydooxygenase-2 and inflammatory cytokines in
pain induction of herniated lumbar intervertebral disc. Kobe J Med Sci 46[ I): 13-28, 2000
8. Nachemson A: The lumbar spine: An orthopedic approach. Spine 1:59-71, 1976.
9. Nordstrom 0, Santavirta S, Seitsala S, et al: Symptomatic lumbar spondylolysis: Neuroimrnunologic
studies, Spine 19:2752-2758, 1994
10. Saal JS: The role of inflammation in lumbar pain. Phys Med Rehabil State Art Rev 2:191-199,1990.
11. Saal JS, et al: High levels of inflammatory phospholipase A2 activity in lumbar disc herniations.
Spine 15:674-678, 1990.
12. Saal JS: The role of inflammation in lumbar pain. Spine 20:1821-1827, 1995.
13. Schott GO: Visceral afferents: Their contribution to "sympathetic dependent" pain. Brain
117:397-413, 1994.
14. Selby 0: The structural degenerative cascade. In Schofferman J (ed): Spine Care: Diagnosis and
Conservative Treatment. St. louis, Mosby, 1995, pp 9-16.
15. Wall PO, Melzack R (eds]: Textbook of Pain, 2nd ed. Edinburgh, Churchill Livingstone, 1989.
16. White AA, Panjabi MM: Clinical Biomechanics of the Spine. Philadelphia, 1.B. Lippincott, 1990.
4
I
ATheoretical Overview of the Diagnosis
and Management of Low Back Pain:
Acute vs. Chronic Pain and the
Mind/Body Continuum
Mark J. Sontag, M.D.
Key Points
• Low back pain is an interplay between real or perceived nociceptive tissue injury,
which is dampened or amplified at the brain and spinal cord level. The brain interprets
the pain, which then controls behavior. A patient's genetic history, birth history, child-
hood environment, and psychological makeup are equal1y as important as "the pain
generator" in assessment and treatment of low back pain.
• Pain = tissue injury (sensory) + suffering (emotional experience).
• Perceived potential tissue damage (i.e., myofascial back pain indicates I am dying of
cancer) can be more disabling than actual tissue damage (i.e., extruded lumbar disc in
a professional athlete).
• The individual's neural processing of a nociceptive painful input, is equal1y important
as the extent of the input.
• Physical activity contributes to the acute onset of pain, while psychosocial factors
propagate pain and disability.
• Acute and chronic pain syndromes are two distinct entities that require uniquely
different management approaches (see Table 1).
• Acute and chronic low back pain is under-treated,
• Neuropathic pain is often under-appreciated and under-treated.
• Old medical model of pain: Degree of injury or disease correlates with degree of pain,
function, and disability; inadequately describes what clinicians observe.
• The new biopsychosocial model of pain: The dynamic interaction of biologic, genetic,
sensory, cognitive, emotional, behavioral, economic, and environmental factors con-
tribute to pain, function, and disability. This accurately describes what clinicians observe.
• The assessment and management of real or perceived pain are over-emphasized, while
the assessment and management of the individual's psychological, social status, and
resulting disability, are under-emphasized.
I. Definitions.
A. Acute low back pain Pain lasting less than 3 months related to an injury or disease
process.
B. Subacute low back pain Pain lasting from 3-6 months following an injury or disease
process.
39
40 Acule V5. Chronic Pain andtheMind/Body Canlinuum
c. Chronic pain Pain lasting longer than 6 months following an injury or disease
process.
D. Acute pain syndrome Pain and resulting disability from an injury that resolves in 3
months.
E. Chronic pain syndrome Pain and resulting disability that persists longer than 6
months. This syndrome is characterized by:
I. Anger
2. Anxiety
4. Depression
5. Disrupted:
a. Sleep
b. Interpersonal relationships
c. Employment
d. Hobbies
e. Self-esteem
f. Goals
F. Cognitive restructuring Altering patients' thoughts and beliefs related to their pain
and suffering.
G. Chronic pain may be as "a disease of the nervous system mis-processing informa-
tion" (Allan Basbaun).
H. Behavior (what others see) plus emotions (what you feel) equals biological response
(hormonal response to emotions and behavior).
II. Introduction.
A. Low back pain lifetime prevalence of 60-90%.
B. Annual incidence is 5%.
C. Although up to 90% of injured workers improve within 3 months, up to 90% of
them suffer from recurring pain.
D. 40% of patients with low back pain report pain at 6-month follow-up.
E. 10% of work injury claims account for 80% of the cost, with 50% of these indi-
viduals having no objective physical findings.
F. Nine million Americans are disabled by low back pain.
G. 67% of chronic low back pain sufferers have experienced major depression prior
to their low back injury; 36% had a history of substance abuse before the injury
occurred.
H. 5% of the population is depressed currently, 19 million Americans (J% of the pop-
ulation) suffer from chronic depression, yet only 6% of these individuals seek and
receive adequate treatment.
I. The degree of depression correlates to the frequency, severity, and number of pain
complaints.
J. Patients frequently manifest psychological problems via physical complains, unbe-
knownst to clinicians.
K. Waddell's sign (non-physiological complaints or physical findings) indicates a
psychological component to the patient's pain complaints.
L. Comprehensive patient interviews inquiring about current and past experiences
are essential and include:
1. The mechanism of injury, severity/ frequency of pain, aggravating/relieving
factors of pain, and current psychosocial state.
2. Family history of pain, sleep disorders, substance abuse, depression and/or
anxiety, birth history, and history of physical, sexual, or emotional abuse as
a child.
AculeV5. Chronic Pain and Ihe MincJ/BoJy Canlinuum 41
3. These will assist the clinician in allocating resources directed at the physical
(nociceptive) vs. psychological (emotional) source of pain.
M. Physical (nociceptive) pain and psychological (emotional) pain are equally disrup-
tive to the human condition and require uniquely different approaches in low
back management.
III. The Old Medical Model of Pain Has been Discredited

A. The severity of the injury or disease determines the amount of pain, which influ-
ences behavior and function.
1. There is not a direct correlation between spinal pathology, pain, and function.
a. 34010 of asymptomatic people have abnormal computed tomography (CT)
scans; 20-25010 have abnormal magnetic resonance imaging (MRI) scans.
b. Often clinical recovery does not correlate with the change of clinical pathol-
ogy (i.e., extruded disc compressing spinal nerve roots becomes pain-free,
while normal discs on discogram and MRl scan hurt indefinitely).
2. Elite athletes present with significant pathology, minor pain, and extraordinary
function.
3. Chronic pain patients often present with insignificant pathology, severe pain,
and poor function.
B. 1980 accepted paradigm: Individual is born with a finite number of central ner-
vous system cells that do not replicate and can perform only one predetermined
specific function.
IV. The New Biopsychosocial Model of Pain (Fig. I)

A. Biopsychosocial paradigm integrates the nociceptive pain generator with genetic and
environmental factors that affect the transmission of pain through the spinal cord
to the brain, which interprets the pain.
1. Genetic factors that predispose to developing chronic pain syndrome.
a. Personal or family history of addiction.
b. Personal or family history of depression or anxiety.
2. Environmental factors that predispose to chronic pain syndrome.
a. Premature birth: Premature infants who survive months in pediatric ICUs
0% .-------------------"'"""""
~
~c:
0..-
altll
ua..
'u~
~~
~.~
O.c
rJla..
c~
al
(J)
100% x
t-....:...:.. ----l
0% 100%
Emotional/Psychological
(Suffering) Pain
x = Elite athlete (physical> suffering)

o =Chronic pain patient (suffering> physical)
42 Acute vs. Chronic Pain and the Mind/Bady Continuum
have three times the number of pain conducting fibers in the spinal cord
compared with full-term infants.
b. Poor child-mother bonding.
c. Sexual, physical, or emotional abuse as a child.
d. Adult child of an alcoholic.
3. Genetic factors that predispose to high pain tolerance.
a. No personal or family history of addiction.
b. Personal and/or family history of emotional and psychological well-being.
4. Environmental factors that predispose to a high pain tolerance.
a. Early exposure to pain in athletic settings in which children expect some
pain and receive psychological rewards for performing with pain.
b. Young athletes condition their spinal cords and brains to dampen nocicep-
tive pain input. The meaning of pain experienced during an athletic event is
dearly different from the pain experienced from an intoxicated parent who
beats the child for no reason.
B. New millennium theory The central nervous system does produce neuronal cells, and
each cell is "plastic" in that its particular function is determined by its environ-
ment. DNA is not a fixed blueprint, but rather a data processor that interprets and
responds to its environment.
V. Acute YS. Chronic Pain Syndrome (Table 1)

A. Acute pain syndrome Adaptive protective feedback mechanism that decreases the
probability of further injury.
1. Acute pain syndrome: Predictable, self-limited phenomenon.
2. Generally, the pain decreases as the soft tissue injury heals, correlating with
improved function and diminishing disability.
B. Chronic pain syndrome Maladaptive mechanism that increases disability despite the
fact that there is no ongoing tissue damage.
1. An unpredictable progressive phenomenon that can lead to death via suicide or
accidental overdose.
2. The pain increases out of proportion to the actual tissue damage with reduced
function and increasing disability.
Table 1. Pain Syndromes

Acute Chronic
Duration Less than 3 months Forever
Course Self-limited Progressive
Value Adaptive Maladaptive
Area of pain Specific Nonspecific
Intensity Rapid reduction of pain Gradual increase in pain
Disability Predictable and self-limited Unpredictable and infinite
Nature of pain Isolated Diffuse
Objective findings Numerous(swelling, reduced ROM and Few
strength, deformity)
Objective signs Elevated heart rate, sweating, fluctuation None
in blood pressure
Diagnostic studies Positive Negative or equivocal
Emotional status Fearful Angry
Cognitive Shock Anxious/depressed
Behavioral Protective of injury lsolation
Treatment lee, rest Heat, movement
Acule V5. Chronic Pain antllheMintl/Batly Conlinuum 43
VI. Delta Sleep Role in Low Back Pain, Fibromyalgia, Addidion, and Mental Illness
A. Delta sleep replenishes the body's serotonin, norepinephrine, endorphins, and
enkephalins.
C. A common link between chronic low back pain, fibromyalgia, addiction, and
mental illness is they all involve problems with delta sleep.
D. Inadequate delta sleep reduces the individual's ability to self-modulate pain im-
pulses being processed by the spinal cord and brain.
1. Fibromyalgia patients have disruption of delta sleep, reduced blood flow in the
pain processing centers of the brain, and elevated levels of substance P.
2. Individuals with low levels of serotonin, the neurotransmitter that contributes
to well-being and happiness, are more likely to seek these neurochemicals arti-
ficially through drugs and alcohol, predisposing them to addiction.
3. One hallmark of depression is early morning awakening. One hallmark of anx-
iety is an inability to fall asleep. Both of these conditions have delta sleep dis-
orders, which compromise replenishment of serotonin and norepinephrine.
VII. Neurobiology of Pain and Depression.

A. Depression and substance abuse are risk factors for developing chronic pain syn-
drome.
B. The severity of depression correlates with the intensity, frequency, and number
of pain complaints.
C. Low levels of serotonin and norepinephrine contribute to increased pain transmis-
sion through the spinal cord, subcortex, and brain. Adrenergic descending spinal
cord tracks serve as on/off switch at the dorsal root ganglion and spinal cord.
D. Mu narcotic receptor are inactivated by alpha-2 adrenergic antagonists and acti-
vated by alpha-2 adrenergic agonists.
VIII. New Millenium Theory: Unanticipated Physical Pain and Emotional Pain in Childhood Hard
Wires an Individual's Neuro-processing of Pain As an Adult.
A. Premature infants who survive to adulthood have a higher incidence of chronic
pain syndrome.
B. Women who have been exposed to physical, sexual, or emotional abuse in
childhood show exaggerated physiological responses to stressful events as
adults (Fig. 2).
1. Women exposed to mild stress, with a history of depression and child abuse,
showed levels of ACTH (a pituitary stress hormone) six times higher than
women without depression or abuse.
10 10
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-g,?;-
::;, til;;:
:~ coO
.- til
tIlCll
al
c.:c
a>
al
5 5 "0_
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0 low pSYCh ·~c
'0 oSOCia//). alal
0 l:!x
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44 Acule vs. Chronic Pain ancllhe Mind/Body Continuum
2. Women with a history of abuse without depression also showed hypersensitiv-

ity to stress, to a lesser degree.
C. Dr. Rachel Yehuda has documented similar abnormal stress responses in combat
veterans, rape victims, survivors of the Holocaust, and others who have endured
traumatic experiences.
D. Dr. Carragee's elegant article about discograms demonstrates the strong role psy-
chological factors play in the perception of pain.
E. Physical, emotional, and/or psychological stress during early childhood develop-
ment preloads the neurobiological matrix to increase the transmission and inter-
pretation of pain as an adult.
IX. How Depression and Anxiety (DSM-IV, Axis IFactors) Influences Pain Perception.
A. Psychic, emotional, or physical trauma alters the brain's neurophysiology.
B. Each additional trauma leaves a deeper permanent imprint on the central nervous
system, establishing a memory of the event that can be unmasked more readily in
the future by a less serious insult.
C. This process is called kindling, which can lead to permanent brain dysfunction af-
ter as few as three traumatic events in a lifetime.
D. Just as concussions are graded based on the frequency and degree of brain injury,
so too are psychic, emotional, and physical injuries graded based on the fre-
quency, nature, and severity of the life experience.
E. Depressed patients have recurring negative and hopeless thoughts often not accu-
rately reflecting reality. The anxious patient has recurrent thoughts of self-doubt
not accurately reflecting reality. The chronic pain patient has recurrent thoughts
of pain that no longer adequately reflect the reality of tissue injuries that have of-
ten actually healed.
X. How Personality Type (DSM-IV, Axis II Factors) Influences Pain Perception.

A. The personality of an injured person can enhance or complicate the treatment of
and recovery from pain.
B. The following three personality clusters have emotional suppression, which is as-
sociated with autonomic, autoimmune, and neuromuscular regulation problems:
1. Schizoid and dependent individuals
a. Inhibit and suppress negative emotions.
b. Interpersonally passive and show relatively low drive toward their own in-
terests and preferences.
c. Excessive/compulsive styles.
2. Paranoid, borderline, avoidant, and passive/aggressive personality styles.
a. Overreact to actual or vague perceptions of threat in their environment.
b. They respond to common somatic symptoms with exaggerated emotional
and physical reports of discomfort.
c. Exhibit high levels of emotional and functional impairment with chronic
pain.
d. Often present with mood, adjustment, anxiety, or symptoms of pathology
when confronted with the stress of chronic pain.
3. Histrionic and narcissistic personalities.
a. Dramatic, demanding, and self-centered.
b. They use pain as a means of manipulating and gaining control of others.
4. These three personality clusters are commonly diagnosed in patients with som-
atization disorders and chronic pain syndrome. 50-720/0 of these patients are
also diagnosed with one or more DSM-IV Axis I disorders.
Acute V$. Chronic Pain and "'e Mind/Body Canlinuum 45
5. Treatment utilizing cognitive restructuring.

a. Injured individuals' thoughts, beliefs, world views, religion, social interpreta-
tion, and values determine the meaning of their pain and how they react to
pain and/or injury.
b. Altering their opinions about the meaning of their pain can change patients'
pain, poor motivation, negative attitudes, distressful emotions, or self-
defeating thoughts.
6. A cognitive/behavioral psychotherapist can teach patients to alter negative
thoughts that impact the rate of healing, the amount of muscle tension, pain,
and the immune system's ability to function better.
XI. Acute Low Back Pain Management.

A. Thorough history of present injury, past medical history, family history, and
psychosocial history.
B. Thorough physical exam including observation for Waddell's sign.
C. Formulate a clinical diagnosis based on the pathophysiologic, neurophysiologic,
and biochemical factors.
D. Rational utilization of diagnostic studies to confirm clinical diagnosis.
1. Imaging studies.
2. Labs.
3. Electrodiagnostic studies.
4. Psychometric testing.
E. Appropriate medications.
F. Diagnosis-driven physical therapy.
G. Injections for diagnostic and therapeutic purposes.
H. Appropriate bracing techniques.
I. Psychological evaluations and treatment.
J. Surgical considerations.
K. Functional assessment and restoration programs.
L. Establishment of realistic goals.
XII. Chronic Back Pain Syndrome Management.

A. Review Section XI.
B. Careful personal and family history for substance abuse, sleep disorder, mental ill-
ness (depression/anxiety), personality disorders, premature birth, and childhood
physical, sexual, or emotional abuse.
C. Documentation of Waddell's sign suggesting psychological contribution to
pain.
D. Establish a definitive structural and psychological diagnosis. Think about misdiag-
noses, missed pathology, other medical explanations for pain, malignancy in the
elderly population, and conversion and somatization disorders in individuals with
psychological disorders or a family history of such.
E. Rational polypharmacy.
I. Utilize long-acting opiates rather than short-acting opiates, to provide 24/7
pain coverage, reduce the peak and trough delivery that contributes to addic-
tion and pseudoaddiction.
2. Second generation anticonvulsants for neuropathic pain relief (gabapentin).
3. Cox-II nonsteroidal agents for safe pain relief.
4. Alpha-II agonists to inhibit pain transmission at the spinal cord level and en-
hance the potency of the opiates.
5. Low dose tricyclic antidepressants for sedation and neuropathic pain relief.
46 Acule vs. Chronic Pain ancllhe Mincl/Bacly Canlinuum
6. Serotonin reuptake inhibitors (SSRIs) for treatment of premorbid and reactive

depression/anxiety.
7. Start with one medication and slowly increase until adequate pain relief is ob-
tained, or side effects occur. Continue the medication at a tolerable dose and
then add a second medication and slowly titrate up. The utilization of multiple
medications in appropriate doses can interrupt the inappropriate maladaptive
memory of pain in the peripheral and central nervous system.
F. Functional restoration program.
1. The goal of treatment is not pain relief but improved function.
2. Restore spinal and extremity range of motion.
3. Strengthen supporting joint musculature.
4. Initiate diagnosis-specific daily aerobic exercise [i.e., walking or swimming for
discogenic pain, cycling for stenotic pain).
G. Initiate stress reduction, psychotherapy, and cognitive restructuring with appropri-
ate caregivers familiar with chronic pain patients and psychopathology.
H. Establish functional goals that are not dependent on pain relief (i.e., reestablish
employment, interpersonal relationships, societal roles, etc.).
I. Empower low back pain sufferers that they are responsible for their recovery.
J. Educate chronic pain sufferers that there is not a cure for their condition; how-
ever, they can learn the skills to cope with their condition such that they can re-
sume a meaningful and enjoyable life.
XIII. Exacerbations of Chronic Pain.

A. Chronic pain syndrome patients often present with acute exacerbation of their
pain with no clear precipitating trauma or re-injury, and no change in their ob-
jective exam or imaging studies.
B. These acute flares of their chronic pain often correlate with an emotional or psy-
chological trigger, which often has its connection to the original source of the
pain. The original emotional psychic wound that contributed to the formation of
the memory of the pain and suffering in the central nervous system has been re-
activated, similar to the neurobiological concept of the flashback, posttraumatic
stress disorder, or trigger for an addict.
C. A physical cause of the chronic pain exacerbation then requires appropriate
medical, physical therapy, or injection care.
D. A negative thought, emotion, or psychological experience may trigger an acute
exacerbation of chronic pain. Appropriate neuropsychiatric medications in con-
junction with psychotherapy may then be indicated.
XIV. Summary.
A. An individual's experience and self-report of pain should be treated as real.
B. When a low back pain patient's recovery deviates from an expected recovery
path, think about psychosocial risk factors.
C. An individual's experience of pain is greatly influenced by genetic and environ-
mental factors that have no relationship to the tissue injury.
D. Acute and chronic back pain are completely different entities, and both are
under-treated.
E. Inadequately treated acute back pain can progress to chronic pain syndrome.
F. People with psychological problems not only cope poorly with pain, but also
their biological processing of pain intensifies the pain experience.
G. Clinicians often overemphasize trying to relieve chronic pain, which is often
permanently ingrained in the nervous system, at the expense of addressing the
patient's actual disability.
Acule V5. Chronic Pain and Ihe Mind/8oJy Continuum 47
REFERENCES
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Evaluation and Treatment of Chronic Pain, Third Edition. Williams l't Wilkins, Philadelphia, pp
83-290, 1999.
2. Beattie P, Meters S, Stratford P, et al. Associations between patient report of symptoms and anatomic
impairment visible on lumbar magnetic resonance imaging. Spine 25(7):819-828, 2000.
3. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic resonance scans of the lumbar spine in
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4. Boos N, Lander PH. Clinical efficacy of imaging: Modalities in the diagnosis of low back pain disor-
ders. Eur Spine J 5:2-22, 1996.
5. Boos N, Rieder R., Schade V, et al. 1995 Volvo award in clinical sciences: The diagnostic accuracy of
magnetic resonance imaging, work perception, and psychosocial factors in identifying symptomatic
disc herniations. Spine 20: 2613-2625, 1995.
6. Dersch T, Gatchel RJ, Polatin P. Chronic spinal disorder and psychopathology: Research findings and
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Vulnerability to Chronic Pain. RC Grzesiak, DC Ciccone (eds). Springer, New York, 1994.
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10. Feinberg S, Blackmon P. Cognitive restructuring-a treatment for chronic pain. CWCE 18(2):19-21,
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quence of chronic pain? A review. Clin J Pain 13:116-137, 1997.
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and physical functioning. Clin J Pain 12:118-125, 1996.
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spin in people without back pain. N Engl J Med 331 :69-73, 1994.
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17. Lewis T, Amini F, Lannon R. A General Theory of Love. New York, Vantage Books-Random House,
2000, pp 74, 86.
18. Linton, S. A review of psychological risk factors in back and neck pain. Spine 25(9): 1148-1156, 2000.
19. Linton S, Anderson T. Can chronic disability be prevented? Spine 25(21):2825-2831, 2000.
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2001, pp 262-286.
5
I
History and Past Medical History
Howard liss, M.D., and Donald Liss, M.D., and Jeff Pavell, D.O.
Key Points
• A specific symptom history is crucial to properly evaluate a patient with complaints of
low back pain because it allows a more specific diagnosis.
• The low back pain history should include age, gender, family and social history as well
as occupational history and a discussion of the patient's other medical problems.
• A thorough history help determine if causes of low back pain with high morbidity may
be present including cauda equina syndrome, tumors, infections, and aortic aneurysms.
• Urinary retention is the most common compliant in acute cauda equina syndrome, a
surgical emergency.
• Constitutional symptoms, nocturnal or rest, pain and pain unrelated to position are
"red flags" and should raise suspicion of infection, tumor, or pain referred from
gastrointestinal, urological, or reproductive systems.
• The quality and quantity of low back pain can be determined using a pain question-
naire, pain diagram, or pain scale.
• Pain worsened by sitting, lifting, twisting and bending, or with Valsalva maneuver
may suggest discogenic pain.
• Lateral disc herniations often present acutely in older people, primarily with lower
extremity pain and without a classic discogenic history.
• Suspect central lumbar stenosis and psuedoclaudication when leg and back pain
increase with walking variable distances and are relieved by sitting or forward flexion,
not just standing; in patients with vascular claudication, leg symptoms occur when
walking fixed distances and are relieved by standing.
I. General Considerations
A. The history isthe most powerful diagnostic tool.
B. A specific diagnosis leads to better management.
1. Avoid generalized diagnoses such as "lumbar sprain" or "lumbar disc disease,"
for which treatment approach is unclear.
2. A specific diagnosis results in a more accurate prognosis.
C. A working diagnosis directs patient care.
1. In most patients, diagnosis is not certain. However aspects of presentation sug-
gest a specific diagnosis.
2. Reevaluation helps confirm a diagnosis by providing additional information:
a. History
b. Physical examination findings
c. Response to specific treatments
D. The history helps to determine the patient's current emotional state and the effect of
pain on the patient's life.
49
so History and Past Medical History
E. It is a challenge to remain alert for unusual and serious causes of back pain. The over-
whelming majority of patients get better within 3 months, regardless of treatment
or lack thereof.
F. Three essential tools: an astute ear, a discerning eye, and an open mind.
II. Components of the Patient History

A. Demographic fadors
1. Age
a. Younger-disco genic pain
b. Older-osseous, stenosis, lateral disc herniation
2. Marital status-see social history (page 55)
3. Race, nationality
a. Caucasian, Northern Europe-increased incidence of osteoporosis
b. Caucasian-ankylosing spondylitis
4. Gender
a. Male-discogenic, ankylosing spondylitis, Reiter's syndrome
b. Female-osteoporosis, fibromyalgia
5. Handedness-influence on repetitive stress in sports, work
6. Occupation
a. Specific physical duties-increased incidence of back injuries with lifting,
twisting, vibration.
b. Emotional work-related stress-if significant, monitor closely for nonorganic
component to pain.
c. Job satisfaction-high correlation with time off work
d. Feasibility of working part time or light duty. Every effort should be made to
get patients back to work, in some capacity, as early as possible.
e. Time until retirement and since beginning current job
f. Last date that patient worked-the longer the interval off work, the less likeli-
hood of return to work
7. Recreational activities-sports, exercise, hobbies
a. Time spent per week
b. Recent changes in duration, intensity, frequency, surface
c. Specific style, position, strokes
B. History of present illness
1. Onset of pain
a. When did episode begin?
b. How did pain begin?
i. Spontaneously
(a) Sudden onset
(b) Gradual onset
ii. Traumatically
(a) Motor vehicle, work-related, nonlegal setting
(b) Mechanism-flexion, extension, twist, lift, fall, sneeze, cough, strain,
other
c. Motor vehicle accidents
i. Types of cars involved
ii. Direction of impact
iii. Extent of vehicle damage-however, significant injury can occur with
minor damage to vehicle.
iv. Seat belt used? Lap belt vs. shoulder harness-flexion injuries with lap
belts, torsional injuries with harness
HislDry and Past Medical HislDry 51
v. Loss of consciousness
vi. Did head hit windshield, or did chest hit steering wheel?
vii. Specific location of immediate pain, if any
viii. Visit to emergency department? Diagnostic and therapeutic measures
performed
d. Work-related injuries
i. Details of specific injury
ii. Litigation pending
iii. Compensation for time off work
e. Sports-related injuries
i. Sports involving torsion (e.g., golf, racquet sports, baseball)-higher
incidence of discogenic pain
ii. Sports involving hyperextension (e.g., gymnastics, dance, crew)-greater
loading of posterior elements
iii. Details of specific injury
2. Quantity, quality and location of pain
a. Quantity or intensity of pain can be measured by use of a visual analog scale.
i. Usually a 10 em line in which one end represents no pain while the
other end represents intense pain
ii. Scale is marked at each visit to signify current pain intensity.
iii. Can also mark least and greatest pain intensity since last visit
iv. More sensitive in quantifying pain than verbal descriptor and can be
used to assess response to specific treatment
b. A body pain diagram can be employed to mark the location of pain
i. Ask patient about area of most intense pain; is leg greater than back? Is
the pain unilateral or bilateral?
ii. Is there accompanying numbness, changes of sensation, or radiation of
pain?
c. Description of pain and its qualities; usually in patient's own words, or a
questionnaire can be employed to help patient describe pain.
i. McGill Pain Questionnaire separates words that describe pain into three
groups; sensory quahty of pain-spatial, temporal, thermal and pressure; af-
fective quality of pain-fear, tension, frustration; and subjective quahtyof
pain-overall intensity of pain.
ii. The number of words chosen overall is quantified and a rank value is
given to the words in each of the three groups.
iii. A pain rating index is then determined and can be redetermined at each
visit.
iv. A body pain diagram is also included in this questionnaire to show loca-
tion of pain as well.
3. Relationship of pain to dally routine
a. What positions increase the pain?
i. Prone-facet pain, lateral HNP, systemic process
ii. Sitting-anular tear, paramedian HNP
iii. Standing-central stenosis, facet syndrome, lateral HNP
b. Is there pain on arising from a seat? A positive answer is typical of disco-
genic pain.
c. How does walking affect the pain?
i. How far can the patient walk? Is the distance variable (lumbar stenosis)
or constant (vascular claudication)?
ii. Is there more pain with uphill or downhill walking?
52 Hi5tory andPa5t Meclical Hi5tory
(a) Patients with stenosis and facet pain have less pain while walking
uphill because the lumbar spine is flexed, which increases foraminal
and central canal space.
(b) Discogenic symptoms decrease while walking downhill because the
lumbar spine is extended and discs are unloaded.
iii. Is it more comfortable to walk holding a wagon or carriage or in a flexed
posture? A positive answer is typical of stenosis.
d. How is the pain affected by time of day?
i. Is the patient awakened from sleep? Consider a systemic process if so.
ii. Is there morning stiffness? Of what duration? Discogenic patients are
stiff for 20-30 minutes, whereas rheumatic patients may be stiff for 2
hours.
iii. Does the pain increase or decrease as the day progresses? The response
helps guide treatment.
e. Is pain intensified by coughing, sneezing, laughing, or Valsalva maneuver?
In which location?
i. Suggests disc disease or, rarely, an intraspinal tumor.
ii. Reproduction of distal pain strongly supports discogenic pain.
f. What activities is patient unable to perform?
g. Do any positions or maneuvers relieve the pain or other symptoms?
4. Associated neurologic symptoms
a. Location of anesthesia, hypoesthesia, hyperesthesia, paresthesias
i. Regional
ii. Dermatomal
iii. Sclerotomal
iv. Nonphysiologic
b. Does the patient note weakness?
i. Differentiate inability to perform a task due to pain from actual weak-
ness.
ii. Has the patient noted a dragging foot, buckling knee, difficulty with stairs
or curbs? Suggestive of myotomal, plexus, cord, nonphysiologic process.
c. Has the patient noted bladder, bowel, or sexual dysfunction? If so, consider
cauda equina syndrome.
d. Does the patient have associated upper extremity, CNS, or brainstem symp-
toms?
5. Diagnostic studies
a. The patient should be requested to bring in all images and reports.
b. Patient should report the results of unavailable studies.
6. Response toprior treatments-ask for specifics (answer helps guide treatment)
a. Bedrest-limited benefit in stenosis
b. Medications
i. Benefits
ii. Side effects
c. Modalities
i. Superficial heating and cooling
ii. Electrical stimulation
iii. Ultrasound
iv. Transcutaneous electrical nerve stimulation (TENS)
d. Manual or mechanical therapy
i. Centralization techniques-passive and active extension, shift correction.
Positive response suggests discogenic pain.
His/ory and PastMeJical Hislory 53
ii. Traction
iii. Stretching
iv. Mobilization
(al Relief with specific facet mobilization suggests facet disease.
(b) Mobilization may also treat other causes of pain, i.e., segmental dys-
function.
v. Manipulation may treat facet pain and other sources of lumbar spine
pain.
vi. Rapid response to facet manipulation suggests a facet syndrome.
e. Exercise
i. Flexibility
ii. Strengthening and stabilization
iii. Aerobic conditioning
f. Education in proper body mechanics
g. Corset or bracing
h. Biofeedback
i. Soft tissue injections
i. Trigger points
ii. Tendon
iii. Ligament
j. Spinal injections
i. Anesthetic phase relief or steroid phase relief
ii. Fluoroscopy and/or contrast used?
k. Percutaneous rhizolysis
I. Acupuncture
m. Surgery
i. Specific procedure and date performed
ii. Immediate change in symptoms/signs
iii. Long-term change in symptoms/signs
iv. Complications
C. Past histary
1. Prior and current medical conditions
a.
Diabetes
b.
Hypertension
c.
Cardiac disease
d.
Cancer
e.
Infections
f.
Rheumatologic diseases
g.
Gastrointestinal disorders (tolerance for NSAIDs)
2. Present medications and drug allergies
3. Operations, injuries and previous hospitahzations, with names, addresses, phone num-
bers of all practitioners involved in patient's care
4. Review ofsystems, asked selectively
a. Constitutional symptoms
i. Weight loss iv. Chills
ii. Loss of appetite v. Fatigue
iii. Fever or night sweats vi. Night pain
b. Integument-rheumatologic disorders
c. Lymph nodes
i. Malignancy
ii. Infection
S4 Hislory and PastMedical Hislory
d. Hematopoietic system
i. Anemia
ii. Bleeding
e. Endocrine system-symptoms suggestive of
i. Diabetes
ii. Thyroid dysfunction
f. Eyes
i. Visual loss
ii. Inflammation
g. Mouth
i. Pain
ii. Ulcerations
h. Bones, joints, muscles
i. Pathologic fractures
ii. Peripheral or cervicothoracic joint symptoms
iii. Muscle pain or weakness
i. Breasts
i. Pain
ii. Lumps
iii. Discharge
j. Respiratory system
i. Pain
ii. Shortness of breath
iii. Cough
k. Cardiovascular system
i. Chest pain v. Intermittent claudication
ii. Palpitations vi. Distal skin lesions
iii. Orthopnea vii. Edema
iv. Dyspnea on exertion
I. Gastrointestinal system
i. Dysphagia v. Jaundice
ii. Nausea vi. Change in bowel habits
iii. Vomiting vii. Bowel incontinence
iv. Hematemesis
m. Genitourinary system
i. Urologic
(a) Nocturia (e) Urinary frequency
(b) Dysuria (0 Retention
(c) Hematuria (g) Incontinence
(d) Pyuria
ii. Gynecologic
(a) Number of full-term pregnancies
(b) Last menstrual period (currently pregnant?)
(c) Are menses regular or irregular?
(d) Date and results of last pelvic exam and Papanicolaou smear
(e) Back or lower extremity pain associated with menses
n. Nervous system
i. Cranial nerves iv. Convulsions
ii. Movement disorders v. Mental status
iii. Coordination
D. family hislory
I. Familial conditions
Hisloty and Past Medical Hisloty ss
2. Family members with chronic pain syndromes/spine pain
3. Family members on disability
E. Social history
1. Open-ended: "Tell me about your family."
2. Marital status-impact of condition on relationship and vice versa
3. Children-impact of condition on relationship and vice versa
4. Substance abuse history
a. Alcohol intake
b. Smoking history
c. Illicit drug usage
5. Social and economic status
a. Extent of education
b. Special financial problems
III. History of Specific Conditions

A. Discogenic pain
1. Silent
a. Most patients over age 30 have pathologic evidence of disc degeneration,
according to autopsy studies.
b. At least 300/0 of asymptomatic individuals have abnormal imaging studies.
c. Treat the patient-not the imaging study.
2. Features common to most symptomatic presentations of lumbar disc disease
a. Risk factors
i. Height
ii. Prolonged sitting
iii. Twisting and rotation
iv. Occupations involving vibration (e.g., truck drivers, heavy machinery
operators)
v. Chronic cough
b. Onset
i. Usually spontaneous
ii. Discrete causative event in 10-200/0 of cases
(a) Prolonged driving
(b) Lifting
(c) Coughing
(d) Sneezing
(e) Flexion, flexion/rotation
c. Classic discogenic history-factors that worsen the pain
i. Sitting> standing> lying
ii. Arising from seated position
iii. First 20-30 minutes of day
iv. Coughing, sneezing, straining (Valsalva maneuver)
v. Lifting weight out in front of body
vi. Twisting
vii. Bending at waist
3. Anular tear
a. Common entity, often mistakenly diagnosed as lumbar strain
b. Mean age-probably early in fourth decade
c. Location of pain-not below sacroiliac region
d. Discogenic history (see above)
e. Often "locked" in flexion with acute attacks
f. No neurologic signs (nonradicular)
S6 HislDly and Past Medical HislDly
g. Diagnostic studies generally normal (except discogram)

h. Response to treatment-generally improved with passive extension, side glid-
ing, proper body mechanics
4. Paramedian protrusions and herniations
a. Most common herniation
b. Mean age-40 years; unusual after age 70
c. Location of pain
i. Variable percent of back and lower extremity pain-larger protrusions
generally associated with peripheral pain.
ii. Dermatomallocation is best prediction of which root is involved.
d. Relationship of pain to position, movement, activities, time of day
i. Patients have discogenlc history (see above).
ii. Occasionally pain increases with ipsilateral weight bearing in standing
and/or sitting.
iii. Patients are most comfortable in supine or lateral decubitus position with
hips and knees flexed.
iv. Patients with very large paramedian herniations are very uncomfortable
in standing and extension.
e. Neurologic symptoms and signs
i. Patients may note radicular pain or sensory changes.
(a) Radiculopathy with abnormal change in strength or sensation
(b) Radicular pain with no objective abnormalities (only subjective) in
strength or sensation
ii. 90-95% involve L5 or S1 roots.
iii. Calf cramps may occur with S1 radiculopathy on occasion.
f. Diagnostic studies-over 80% have abnormal imaging and electrodiagnostic
testing results.
g. Response to treatment
i. Pain centralizes with extension or side gliding.
ii. Pain peripheralizes with flexion activities or manipulation.
iii. Pain diminishes significantly with epidural injection procedure.
h. Time course of pain: > 90% improve within 12 weeks, but recurrences are
common.
5. Lateral and foraminal herniations
a. Frequently missed diagnosis-accounts for 10% of all lumbar surgical proce-
dures
i. 60% involve L4-L5.
ii. 30% involve L3-L4.
iii. < 10% involve L5-S 1 (contrast with paramedian protrusions and hernia-
tions).
b. Mean age-60 years
c. Onset of pain is usually spontaneous (cause rarely identifiable).
d. Time course of pain
i. Recurrences are not common once symptoms resolve.
ii. Contrast with paramedian protrusions and herniations.
e. Location of pain
i. Lower extremity pain is almost always present.
ii. Patient can usually identify a specific location, allowing a dermatome to
be delineated.
iii. Most patients do not have significant back pain.
f. Relationship of pain to position, movement, activities, time of day
History and PastMedical History 57
i. Patient may not have discogenic history (see page 37).

ii. Pain is worst with standing or walking erect.
iii. Patients are often uncomfortable in bed; many sleep sitting.
iv. Sitting usually affords relief.
v. Pain with Valsalva maneuver is atypical.
g. Neurologic complaints
i. Neurologic symptoms are frequent and occur in a radicular distribution.
ii. Bilateral complaints are rare and sphincter disturbances nonexistent.
h. Diagnostic studies
i. Magnetic resonance imaging (MRI)
ii. Computed tomography (CT), especially if fine (3-mm) cuts are obtained
iii. Almost never seen on myelography alone because the lateral recesses
and foramina are poorly visualized
iv. 50% seen on CT myelography
v. Usually seen on CT discography
i. Response to prior treatments
i. Generally more resistant to mobilization, centralization, and traction
than other disc presentations.
ii. Traction may temporarily worsen pain in 10-20% of patients.
6. Upper lumbar protrusions and hemiations
a. Mean age-55 years (higher than for patients with paramedian L4-S1 hernia-
tions)
b. Patients with prior L4-S 1 fusions are at significant risk.
c. Location of pain relates to level of involved disc.
i. LI-L2, L2-L3: groin, anterior thigh, back
ii. L3-L4: extension to knee and medial leg
7. Sequestered disc hemiatlons and disc fragments
a. Often diagnosed at time of surgery
b. According to literature, MRI has diagnostic accuracy of 85%.
c. Suspect sequestered disc in patients with discogenic history when:
i. Discomfort during Valsalva maneuver or lifting abruptly resolves.
ii. Back pain decreases and lower extremity pain increases.
8. Cauda equina syndrome
a. Background information
i, Acute cauda &quina syndrome Is stnl considered a surgical emergency.
(a) Must always be a consideration in patient with back pain.
(b) Outcome may not change even with immediate surgery.
ii. 0.0004% of all back pain patients
iii. Tumors are responsible for 50% of cauda equina syndromes.
iv. Central L3-L4 and L4-L5 discs represent most benign cases
b. History
i. The most common complaint is urinary retention.
ii. Other complaints may include:
(a) Bladder incontinence
(b) Bowel incontinence
(c) Sexual dysfunction
(d) Diminished perineal sensation
(e) Bilateral lower extremity neurologic complaints or pain
B. Other conditions associated with radiculopathy or radicular pain
1. Lumbar stenosis
a. History is the absolute key to diagnosis.
58 History and PastMedical History
i. Examination and electrodiagnostlc testing remain normal until late in

course of disease.
ii. Imaging has high false-positive rate.
b. Age-as early as fourth decade but uncommon before age 55
c. Medical background-history of significant prior disc or facet joint degenera-
tive disease is common.
d. Onset of pain
i. Spontaneous, insidious
ii. Gradual progression-sudden changes in symptoms require an explanation
other than stenosis (e.g., herniated nucleus pulposus, tumor).
e. Location of pain
i. "Pain" is a word generally not used by patients with stenosis.
ii. Central canal stenosis-symptoms are generally noted bilaterally, fairly sym-
metrically, but in nonspecific distribution.
iii. lateral or foraminal stenosis-symptoms are generally noted unilaterally in a
fairly specific dermatomal distribution.
f. Relationship of pain to position, movement, activities, time of day
i. Activities involving extension, which narrows the foramina and spinal
canal, are associated with increased symptoms.
ii. Symptoms: walking> standing> lying
iii. Sitting is often asymptomatic and relieves symptoms.
iv. Valsalva maneuver should not affect symptoms in pure stenosis.
v. Flexion relieves symptoms.
(a) Sitting is comfortable until late in course of disease; bicycling and
long car rides are well tolerated.
(b) While walking, relief is obtained with positions that increase lumbar
flexion, e.g., squatting, stooping, going uphill, leaning on walker or
cart.
vi. Nocturnal lower extremity paresthesias and pain have been noted in pa-
tients with congestive heart failure and stenosis (Vesper's curse).
g. Progression of disease
i. This condition gradually advances over several years unless other condi-
tions, such as disc disease, intervene.
ii. Initially symptoms occur only with walking long distances.
iii. Patients must sleep sitting or flexed after significant progression.
iv. Late in the course of disease patients walk with kyphotic posture and
spend most of their time sitting.
h. Associated neurologic symptoms
i. Particularly in central stenosis, symptoms may be nonfocal and neuro-
logic examination may be normal.
ii. Main symptoms are sensory.
(a) Vague dysesthesias
(b) Coldness
(c) Vague sense of weakness or "giving way"
(d) Bizarre symptoms (e.g., water trickling down legs)
iii. Regardless of nonfocal nature, neurologic symptoms limit walking-called
pseudoclaudication or neurogenic claudication)
iv. Very late in disease patients note focal weakness or numbness or sphinc-
ter disturbances.
v. Unlike vascular claudication, patients with stenosis are generally com-
Hislory and Post Medicol Hislory S9
fortable on exercise bicycles because they are in flexion, which increases

the size of the central canal.
i. Diagnostic studies
i. All patients should have CT/myelography or MRI to support clinical
findings.
ii. Beware of the significant number of false positives.
j. Response to prior treatment
i. Flexion exercise regimens may provide transient relief only.
ii. Chairs and corsets that place the patient in flexion may provide relief.
iii. Epidural injections may provide some relief.
iv. Adequate decompressive laminectomy provides permanent relief.
2. Spondylolisthesis
a. Isthmic
i. Most often presents with symptoms in late childhood or adolescence.
ii. This diagnosis should be entertained in athletic children, especially
those involved in sports with significant lumbar extension and rotation
that stress the pars interarticularis (e.g., gymnastics, dance, martial arts,
and crew).
iii. LS-S1most commonly involved
iv. Location of pain-L5 or S1 dermatome
v. Minority of symptomatic patients have radicular symptoms
vi. In some cases, symptoms may result from stenosis exacerbated by in-
stability.
vii. Worsened with extension
viii. Spondylolysis often progresses to spondylolisthesis at time of adoles-
cent growth spurt-when the slip occurs.
b. Degenerative
i. Female-to-male ratio of 6: 1
ii. Age-onset on rare occasions at age 40; incidence increases with age.
iii. L4-LS most commonly involved
iv. Pain is most commonly of the unilateral radicular type, probably due to
resultant foraminal stenosis.
v. Bilateral calf pseudoclaudication is less common.
3. Tumors-multiple types of primary and metastatic tumors can cause radiculopa-
thy, polyradiculopathy, or myelopathy (see "Spinal tumors," page 45).
4. Herpes zost" radiculopathy
a. Incidence is 1-2 per thousand in general population.
i. Rare in children but increases with age
ii. 10 per thousand during ninth decade
b. Medical background
i. 6010 have history of cancer.
ii. 8010 of leukemia and lymphoma patients get H. zoster.
iii. 25010 of patients with Hodgkin's disease get H. zoster; incidence is
greater in patients who have had splenectomy, chemotherapy, or within
1 year of radiation therapy.
iv. No lasting immunity from prior episode
c. Onset and duration of pain
i. Always spontaneous
ii. Pain generally precedes vesicular lesions by a few days; skin lesions
may not appear for 3 weeks.
60 History andPast Meclical History
iii. Pain usually lasts through eruption period; scabs form by 1 week and
healing occurs within 1 month.
iv. 10-200/0 have postherpetic pain-more common in older population.
v. Systemic complaints are noted in 50/0 at onset (e.g., headache, fever,
adenopathy, nausea).
d. Location of pain and lesions
i. Almost always involves single, unilateral dermatome
ii. 2-100/0 get disseminated lesions and pain-usually in patients with history
of cancer.
iii. 500/0 involve thoracic roots; cranial nerves and cervical, lumbar, and
sacral roots may be involved.
e. No clear relationship of pain to position, movement, or activities
f. Associated neurologic symptoms
i. Most patients have dysesthesias initially; some have residual numbness.
ii. Up to 300/0 of patients develop weakness, according to the literature.
iii. Full paresis occurs within hours to days.
(a) 55010 recover fully.
(b) 300/0 recover significantly from weakness.
5. Diabetic radiculopathy
a. Patients are usually middle-aged or elderly.
b. Term has been used loosely and applied to diabetic plexopathy and amy-
otrophy.
c. Pain is universal; sensory as well as motor complaints are common.
d. Pain is generally constant, worse at night, and occasionally associated with
weight loss.
e. At times may be wrongly diagnosed when the true disorder is a lateral her-
niated nucleus pulposus.
6. Arachnoiditis
a. Studies reveal the nearly universal presence of adhesions and scar formation
in postoperative patients as well as in many patients with disc disease; most
are asymptomatic.
b. Medical conditions predisposing to symptomatic arachnoiditis
i. Disc space infections
ii. Subarachnoid hemorrhage
iii. Surgery-especially multiple surgeries
iv. Intrathecal drugs
v. Radiation therapy
vi. History of pantopaque myelography
c. History suggesting adhesions as cause of symptoms (both i and ii]
i. Reproduction of lumbar or lower extremity symptoms with long stride or
cervical and thoracic flexion
ii. Sitting, lifting, and Valsalva maneuvers are much less uncomfortable
[e.g., no discogenic history)
C. Sciatic neuropathy
1. A lesion involving the sciatic nerve or its branches should be considered in the
differential diagnosis of a neuropathic picture involving L5 and/or S1 symp-
toms and signs.
2. Trauma
a. Type of trauma
i. Blunt-fall or contusion
ii. Penetrating-injection, knife, fracture
Hisloty amiPastMedical Hisloty 61
iii. Traction-hip joint surgery

b. Clinical picture
i. Neurologic complaints and deficits are more common than pain.
ii. Peroneal division is more susceptible to trauma, probably because of its
more peripheral location.
3. Tumors
a. Sciatic nerve or its branches may be involved.
b. Variable degrees of pain and neurologic deficits may be present.
c. Symptoms do not relate to spinal posture or Valsalva maneuver.
d. Patient has no discogenic history (see page 37).
4. Compression neuropathies
a. Sciatic nerve
i. "Wallet" sciatica-controversial; pain caused by large wallet while sitting
ii. Piriformis syndrome
(a) Myofascial pain (see "Muscle-based pain, "next page)
(b) Pyomyositis of piriformis muscle-extremely rare
b. Compression of more distal branches
D. Facet joint pathology (facet syndrome)
I. History
a. Approximately 800/0 of patients have evidence of prior disc disease.
b. Onset often relates to increased axial loading and hyperextension activities
(e.g., overzealous press ups).
c. Pain with extension and ipsilateral side bending and rotation theoretically sug-
gest facet-based pain, but studies have not clearly supported this association.
d. Standing generally worsens pain compared with sitting, but no pseudoclau-
dication is present, as in lumbar stenosis.
e. Pain location
i. Predominantly in back
ii. Generally not distal to the buttock; rarely if ever below knee
f. No localizing neurologic symptoms
g. Dramatic response to facet manipulation suggests facet syndrome.
h. Relief during anesthetic phase of properly performed fluoroscopically
guided, contrast-enhanced facet injection is diagnostic.
2. Conditions causing facet pain
a. Osteoarthritis
i. Disc disease is almost universally present.
ii. Onset is generally gradual.
b. Instability
i. Spondylolisthesis-facet joint may be source of nonradicular pain
ii. Other causes
c. Acute subluxation
i. Controversial entity, may be difficult to distinguish from anular tear
ii. Acute onset of pain after sudden rotation or hyperextension
E. Muscle-based pain
1. Strains
a. Uncommon entity that is overdiagnosed
i. Muscle spasm or pain is often concomitant with primary condition (e.g.,
anular tear, facet syndrome).
ii. Lack of other physical findings may mislead the diagnostician to empha-
size secondary muscle pain instead of focusing on underlying primary
condition.
62 History and PastMedical Hislory
b. Pain with stretch or prolonged contraction of involved muscle

c. Acute lumbar paraspinal compartment syndrome
i. Rare entity
ii. Patients with constant severe pain after prolonged lumbar muscle con-
traction
2. Fibromyalgia (see Chapter 27)
3. Myofascial pain syndromes-piriformis syndrome (see Chapter 27)
F. Sacroiliac joint pain
1. General considerations
a. Incidence and clinical presentation are controversial, but sacroiliac joint is
involved in 400/0 of patients with chronic low back pain below belt line.
b. History
i. Nonspecific
ii. Onset-gradual or sudden
iii. Location of pain
(a) Commonly affects sacroiliac region and buttocks
(b) May cause posterior thigh or groin pain
(c) Infrequently causes lower quadrant and/or symphysis pubis pain
(d) Usually unilateral
(e) Relationship to position and movement varies, but most patients feel
best when reclining.
iv. Pain with Vaisalva maneuver has been described in poorly controlled studies.
v. Dysesthesias also have been described.
2. It is difficult to distinguish above history from either discogenic or facet pain.
3. Consider sacroiliac-based pain in following settings
a. From mid pregnancy to postpartum period
b. Possible rheumatic conditions involving positive HLAB27 marker Ie.g.,
ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome, inflammatory
bowel disease)
c. After trauma, especially motor vehicle accident
d. After extensive spinal fusion
G. Spinal fractures
1. Macrotrauma
2. Compression fractures
a. At least one-third are asymptomatic.
b. Overwhelming majority occur in people with osteoporosis.
i. Most common in postmenopausal women or women with early surgical
menopause
ii. Associated with prolonged corticosteroid use for systemic disorders (e.g.,
chronic obstructive pulmonary disease, systemic lupus erythematosus)
iii. In absence of clear etiology in younger patients [e.g., 40s, 50s), consider
malignancies such as multiple myeloma.
c. Onset
i. Usually but not always sudden
ii. Often caused by little or no perceived trauma
iii. May occur after cough or on toilet seat
d. Course
i. Symptoms generally resolve within 6 weeks.
ii. On occasion delayed posttraumatic vertebral collapse (Kummell's disease)
develops.
History and Past Medical History 63
iii. About 45010 of patients with osteoporotic compression fractures experi-
ence another fracture in the next 12 months.
e. Location of pain
i. Most frequently involved vertebrae are TIO, TIl, T12, and L1 with resul-
tant lumbar pain.
ii. Lumbar fractures may result in lower extremity pain and occasionally
neurologic symptoms.
f. Relationship of pain to position, movement, and activity
i. Increased pain with changing positions
ii. Generally worse in spinal flexion
3. Stress fractures
a. Consider this diagnosis in people involved in repetitive hyperextension, ro-
tational, and axial loading activities (e.g., gymnasts, dancers, runners).
b. Symptoms are aggravated by extension, rotation, and weight bearing.
c. Unilateral weight bearing with hyperextension may localize the side of the
fracture (right or left).
H. Rheumatic diseases (spondylitides-see Chapter 27)
1. Ankylosing spondylitis
2. Reiter's syndrome (reactive arthritis)
3. Psoriatic arthritis
4. Enteropathic arthritis
I. Spinal infections
a. Diagnosis must be made rapidly to avoid neurologic consequences of rapidly
expanding mass or seeding of central nervous system and sepsis.
b. Strongly consider possibility of spinal infection in immunosuppressed pa-
tients, after prior sepsis, and after spinal procedures.
c. Be suspicious when pain is constant, awakens the patient, or does not relate
well to position or movement
2. Epidural abscess
a. 30-40010 occur secondary to osteomyelitis or disc space infection.
b. Rarely may follow after epidural blockade, particularly with indwelling
catheter
c. Progression of symptoms-usually within 1 week
i. Spinal pain usually with fever
ii. Nerve root pain
iii. Weakness
iv. Paralysis
v. Central nervous system signs
vi. Sepsis
vii. Slowly progressive presentation, ranging from weeks to months, is less
common.
3. Vertebral osteomyelitis
a. More common during childhood
b. Average delay to diagnosis is 3 months.
c. Presentation
i. Most common symptom is back pain that increases with motion.
ii. Many patients have fever and sweats.
iii. Occasionally patients complain of sciatica, abdominal pain, malaise, or
weight loss.
64 Hislory and PastMedical Hislory
iv. Tuberculosis of spine has slower course; symptoms are often constitu-
tional, not necessarily pulmonary.
4. Disc space infection
a. Most occur after surgical or percutaneous procedures, but contiguous spread
from osteomyelitis is possible.
b. Complaints of local pain within few days of a procedure should raise suspi-
cion.
J. Spinal tumors
a. Average delay to diagnosis is 3 months.
b. Average age for primary malignant tumors is 50; for benign tumors, 20.
c. Be suspicious when pain is constant, unrelated to position, awakens the pa-
tient, or persists beyond 1 month despite treatment.
d. Weight loss, anorexia, dry cough, change of bladder or bowel habits, and
smoking history should raise suspicion.
2. Benign primary tumors
a. Osteoid osteomas and osteoblastomas occur under age thirty 900/0 of the
time.
b. Aspirin may provide dramatic relief for the above two tumor types.
c. Giant cell tumors often present with neurological symptoms/signs.
3. Malignant primary tumors
a. Multiple myeloma is most common.
b. No specific identifying characteristics
c. Be concerned when constitutional symptoms are present.
d. Neurologic signs, including sphincter disturbances, are not uncommon; of-
ten they cannot be explained by a monoradiculopathy.
4. Metastatic tumors
a. Any patient with back pain and history of cancer should be considered a
candidate for metastatic disease until proved otherwise.
b. Most common metastatic tumors are bronchogenic, breast, prostatic, and re-
nal.
c. Pain is most common presenting symptom.
i. Pain may present as in disc disease, starting with mild local complaints
and progressing to severe radicular complaints.
ii. Sudden increase in pain may reflect pathologic fracture or instability.
d. Neurologic complaints may signal irreversible spinal cord or cauda equina
compression and must be addressed rapidly.
e. Sudden deterioration of neurologic function may suggest ischemic insult
and carries worse prognosis.
K. Vascular-based pain
1. Vascular claudication
a. Most patients have history of smoking, diabetes mellitus, or hyperlipidemia.
b. Onset may be gradual or sudden.
c. Location of pain
i. May involve calves asymmetrically
ii. Leriche syndrome-buttock claudication and impotence due to aortoiliac
occlusive disease.
d. Relationship to position and activity
i. Increased work demands on lower extremity musculature worsen symp-
toms.
ii. Walking uphill increases symptoms.
Hislory ami PastMedical Hislory 65
iii. Claudication symptoms caused by cycling and walking are relieved by

cessation of activity (contrast with lumbar stenosis)
iv. Standing, sitting, and flexion do not reproducibly relieve symptoms.
2. Abdominal aortic aneurysm
a. Medical background same as for vascular claudication
b. Characteristics of pain
i. Localized to lumbar region
ii. Constant
iii. Gradually worsens
iv. Unrelated to motion
L. Viscerogenic
a. Pain from visceral disease is modified by state of activity of viscera.
b. Careful review of systems, including screening for constitutional symptoms,
is instrumental in detecting visceral disorders.
c. Symptoms do not relate to position or movement.
2. Urologic disorders
a. Prostatitis
b. Renal disease
c. Bladder and testicular conditions usually are not accompanied by back
pain.
3. Stomach and duodenal diseases
4. Pancreatic disease
5. Retroperitoneal disease radiates to back and at times to abdomen, groin, and
anterior thigh.
6. Gynecologic disorders
M. Nonorganic or psychogenic symptoms
1. Malingering-intentional misrepresentation of signs and/or symptoms
a. Potential secondary gain is evident.
b. Patient asks excessive questions about disability and legal issues.
c. Excessive emphasis on details of initiating accident
d. Patient is overly fearful of invasive tests or procedures.
e. Patient may seem more interested in details of condition than in actual
treatment.
2. Depression, anxiety, hysteria-unintentiona~ subconscious presentation of non-
physiologic signs or symptoms
a. Nonphysiologic history or pain diagram (numerous shaded areas and
nonanatomic distribution of symptoms)
b. Patient is unclear about relationship of symptoms to movement, activity,
and other factors.
c. Symptoms are consistently diminished on weekends or vacations despite
similar physical activity.
d. Symptoms of anxiety or depression are noted.
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6
I
The Physical Examination of the Spine
and Its Functional Kinetic Chain
Michael C. Geraci, Jr., M.D., P. T., Joseph T. Alleva, M.D., and
Frederick B. McAdam, M.D.
Key Points
• The entire functional kinetic chain must be examined when evaluating the lumbar
spine and pelvis. Isolated physical exam findings should be interpreted in the context
of global kinetic chain function.
• No lesion remains localized because of the kinetic chain. Dysfunctions and pathology
of the lumbopelvic region have profound effects the peripheral joints, and vice-versa.
• The foot and ankle as well as the pelvis are critical links for the function of the lumbar
spine.
• The screening portion of the exam, which looks at gross multilevel motion, should cue
the examiner to which areas require a detailed scanning exam.
• The quality of spine motion is often overlooked but is an essential part of the scanning
examination. Abnormalities in the quality and control of motion help the examiner to
determine areas of dysfunction that require further evaluation.
• It is essential to understand the 3-dimensional mechanics of pronation (loading) from
the foot to the head and neck. The examiner should look for pelvic translation in the
opposite direction of the lumbar motion.
• The examination of the spine should help confirm suspected pain generators as
suggested by history.
• A lateral lumbar shift is virtually pathognomonic of disc pathology in the form of a
focal disc herniation.
• Lumbopelvic and lower extremity muscle imbalances may predispose the patient to
segmental dysfunctions, and eventual focal disc herniation and spinal stenosis. They
also are central to recurrent lumbopelvic pathology when not identified and treated.
• Physical examination should provide insights into psychosocial issues such as pain
behavior, anxiety, and depression.
• Note: All figures in this chapter can be found in the Atlas section beginning on page
84.
I. Screening Examination
A. Overview
1. The primary care physician, physical therapist, athletic trainer, and spine spe-
cialist will find that this part of the examination is the basis for the overall
physical examination.
2. The quality as well as quantity of movement is assessed to identify a region of
dysfunction.
69
70 The Physical Examination of the Spine and lis Functional Kinetic Chain
3. The whole spine and its related kinetic chain structures are evaluated.
4. The sequence of the screening exam minimizes exam time and patient reposi-
tioning
B. Observation
1. Posture-note asymmetry of the shoulder (Fig. 2A), iliac crest (Fig. 2B), and
trochanteric heights (Fig. 2C) in the standing position. Correlate static findings
with subsequent functional testing.
a. The dominant shoulder is typically lower.
b. If iliac crest and trochanteric heights are low on the same side, this repre-
sents a true leg length discrepancy until proven otherwise.
c. Observe for "flat spots" in the alignment of spinous processes or segmental
straightening of a sagittal spinal curve.
i. Usually represent areas of dysfunction.
ii. May represent a compensation for pathology higher or lower in the
spine or pelvis.
d. Note any convexity or scoliosis in the frontal plane.
i. Follow the convexity for changes on flexion and extension.
ii, If the convexity is present only on flexion or extension, the problem
may be functional rather than structural.
iii. Correlate the side of lumbar convexity with the side of the low iliac
crest, if present.
2. Gait-the patient is observed from the posterior, anterior, and lateral views for
asymmetry of movements, taking particular note of any anterior or lateral
pelvic tilt. A lateral pelvic tilt (Trendelenburg sign) may indicate gluteus
medius weakness.
3. Standing balance-the patient should be able to stand on one lower extremity,
then cross the arms and finally close the eyes while maintaining unwavering
balance for a minimum of 15 seconds (Fig. 3).
4. Crouching fully with the heels kept on the floor with full knee and hip flexion
(Fig. 4). The patient is asked to take 4 steps in a duck-walking manner, which
will stress the hip and knee, ankle joints, and the menisci of the knee (Fig. 5).
5. Range ofmotion-quality and quantity are equally important.
a. Standing lumbar range of motion-recorded on STAR diagram (Fig. 6).
TABLE 1. Quick Reference Guide

Topic Section Figure Topic Section Figure
DuraI tension signs VI.D (pp 59-60) 35,36 Scan Exam 11 (p 54)
Femoral nerve VI.D.3 (p 60) 20 Schober'stest I1.C (p 54)
stretch (modified)
Kinetic chain VII (pp 60-61) Screening exam 1 (p 49-53) 2-21
Lumbopelvic Vl1.C (pp 60-61) Segmentalexami- 11.B (p 54)
rhythm nation-lumbar
Muscle imbalances lV (pp 55-56) 31-34 Shift-lumbar p 49
Neurologic exami- VI (pp 59-60) Springtest 1.B.12,f (p 53)
nation
Pelvic clock 111 (pp 54-55) 22-30 Symphysis pubis 1.B.9.b (p 53) 15
Piriformis muscle V.C (pp 57-58) 32,33 Thomas test lV.C (p 56) 34
(modified)
Sacroiliac tests 1.B.5.b (p 51) 8,9,11,12 Waddell's signs V.D (p 58)
The Physical Examination af theSpine and Its Functional Kinetic Chain 71
i. Flexion-record quantity by using number 1 in the STAR diagram to

represent a 25010 loss, 2 for 50010 loss, 3 for 75010 loss, and 4 for 1000/0
loss of motion. The quality should indicate that during flexion one ob-
serves a normal reversal of the lumbar lordosis. If the patient, on return
to upright posture, crawls up their legs with their hands, this indicates
clinical instability.
ii. Extension-quantity is recorded in the same manner as mentioned
above. When assessing the quality of extension, observe the ability of
the patient to translate the pelvis forward.
iii. Side-bending right and left-observe side-bending and rotation to oppo-
site sides (i.e., left side-bending produces right-sided fullness). The
quantity of side-bending is considered normal when the posterior axil-
lary fold falls in line with the lumbosacral junction in the midline [i.e.,
on right side-bending, the left posterior axillary fold should come di-
rectly over the lumbosacral junction).
iv. Rotation with extension right and left-this may stress the pars interar-
ticularis and zygapophyseal joints, as well as cause radicular symptoms
with foraminal stenosis, particularly with a lateral disc herniation. To
increase sensitivity of test, add translation (Fig. 7A).
v. One-legged standing with extension-this further stresses the pars inter-
articularis and zygapophyseal joints (Fig. 7B). This also helps differenti-
ate limitations from hip vs. spine pathology [i.e., If extension is better
on the left lower extremity than on both, the pathology most likely is in
the right hip.).
b. Sacroiliac joint motion tests
L Standing forward flexion test (Fig. B)-the thumbs are placed facing
each other, just under the posterior superior iliac spine (PSIS). The pa-
tient forward flexes the lumbar spine to the maximal amount, with the
knees straight. Motion restriction is recorded on the side that moves
more cephalad. This indicates iliosacral restriction when the ilium fails
to move because of restriction on the sacrum.
ii. Modified Gillet's test (Fig. 9A)-one thumb is moved to the correspond-
ing level of the sacrum while the other thumb remains under the PSIS
and the ipsilateral hip is flexed. A positive test for motion restriction is
seen when the thumb under the PSIS does not move or moves cephalad.
The thumb moves downward and somewhat laterally if the test is nega-
tive (Fig. 9B).
iii. Contra-lateral Gillet's test-thumbs are kept in the same position as the
modified Gillet's, however, the opposite hip is flexed. A positive test is
when the thumb over the sacrum does not move downward, stays level
or elevates in relationship to the thumb under the PSIS. A positive test
indicates restriction of sacral motion in relationship to the ilium.
c. Seated thoracic range of motion-the patient crosses the arms on the shoul-
ders, then rotates left and right, and finally sidebends left and right with
the examiner providing overpressure to the shoulders to note the endfeel of
translation, ease or bind.
d. Seated cervical range of motion-a STAR diagram is used to record gross
motion limitations and pain response (Fig. 10).
e. Seated upper extremity range of motion-the patient is asked to abduct
arms overhead and to touch the hands back-to-back. This test has three
major purposes: (1) to assess the ability of the thoracic spine to extend, al-
72 The Physical Examination ofthe Spine and lisFunctional Kinetic Chain
lowing full arm abduction and elevation; (2) to assess tightness of the pec-
toralis muscles, latissimus dorsi, and teres major; and (3) to screen for
shoulder, elbow, and wrist and hand dysfunctions.
f. Seated forward flexion test (Fig. 12}-the examiner places the thumbs fac-
ing each other under the PSIS, and the patient flexes forward from the
seated position. A positive test indicates motion restriction of the side that
moves most cephalad. This test more specifically identifies sacroiliac re-
striction or the sacrum's inability to move on the fixed ilium.
g. The sacroiliac motion tests (i.e., standing and seated forward flexion and
the modified Gillet's test) indicate the side of restricted motion, which is not
always the painful side [i.e., the side opposite the restriction may have rela-
tive hypermobility and become painful).
6. Seated neurologic examination
a. The deep tendon reflexes at the patellar and Achilles tendon are evaluated,
along with strength of the hip flexors, knee extensors, dorsiflexors, exten-
sor hallucis longus, and ankle plantar flexors (Table 2). A brief sensory
exam (Table 3), including proprioception, can also be performed at this
time. Clonus and plantar responses should be assessed in the presence of
hyperreflexia.
b. Seated Slump Test-patients are asked to put their arms behind them, palms
up, resting on the table (Fig. IIA), then to slump forward with rounded
shoulders and neck flexion (Fig. lIB). Finally the examiner assists straight
leg raising with dorsiflexion (Fig. II C). The patient often experiences symp-
toms in the posterior knee but will say that their hamstrings hurt. Ham-
string pain is normally higher in the midbelly or proximal and should not
be confused with the dural tension point behind the knee. Varying degrees
of radicular complaints may be reported, including symptoms in the neck,
mid and lower back, buttock, and lower extremity (goal: reproduce patient's
symptoms). Neck flexion (increasing neural tension) and extension (de-
creasing neural tension) may help distinguish adverse neural tension
from muscle tension.
7. Supine straight leg raise
a. Base test (Fig. 13}-goal is to reproduce the patient's symptoms. (An incli-
nometer can be used to quantify the SLR more accurately.)
i. Done while the patient is in the supine position.
TABLE 2. Commonly Tested Muscles During a Strength Exam with theirMechanism of Action
and Myotome(s)
Muscle Position Tested Action Myotome(s)*
Rectus femoris/iliopsoas Seated Hip flexion (t.t), L2. LJ. (L4)
Quadriceps femoris Seated Knee extension L2. LJ, L4
Tibialis anterior Seated Dorsiflexion L4, L5
Extensor hallucis longus Seated Great toe extension L5
Gastrocsoleus Standing on one leg Plantartlexion (L5), 51, 52
Peronei Side-lying Eversion L5. 51
Hamstrings Prone Knee flexion L5, 51
Gluteus maximus Prone Hip extension L5, 5 I, (52)
Gluteus medius/minimus Side-lying Hip abduction L5, 5 I, (52)
*Themyotomes in parentheses indicate anatomic variations depending on source used.

The Physical Examinalion o/llle Spine and lisFunclional Kinetic Chain 73
TABLE 3. Nerve Root level and Corresponding Dermatome

Root Level Corresponding Dermatome
L1 Upper thigh and groin
L2 Mid anterior thigh
L3 Medial femoral condyle
L4 Medial malleolus
L5 Dorsum of the foot at the Jrd metatarsal phalangeal joint
51 Lateral heel
52 Popliteal fossa
ii. The lower extremity is slowly raised with the knee completely extended.
Classically, reproduction of radicular symptoms at < 70° is believed to
indicate irritation of the sciatic roots. (However, if the patient's symptoms
are reproduced at a higher elevation, this should be considered positive.)
iii. Adding dorsiflexion, adduction, internal rotation, and/or neck flexion
may increase the sensitivity of the test and also helps to differentiate it
from tight hamstrings.
iv. Crossed straight leg raise is positive when leg raising produces con-
tralateral symptoms.
b. Crossed straight leg raise response-usually indicates focal disc herniation
or, less likely, sacroiliac dysfunction.
8. Supine lower extremity range ofmotion
a. Hip-flexion, internal and external rotation. The capsular pattern of limita-
tion, which involves hip flexion and internal rotation, indicates hip joint
dysfunction if pain or limited range of motion is present.
b. Knee-hyperextension of approximately 10· and full flexion with the heel
touching the buttock are normal.
c. Ankle-dorsiflexion and plantarflexion with inversion and eversion of the
subtalar joints are also assessed.
d. pt Toe Extension of - 65° is assessed with passive range of motion (This is
the degree necessary for normal ambulation.).
e. Calcaneal Eversion-passive range of motion with one hand introducing
calcaneal eversion while the other hand introduces triplanar midfoot mo-
tion (calcaneal inversion locks-up mid foot motion).
9. Supine landmarks-symmetry of the anterior superior iliac spine (ASIS) and sym-
physis pubis, as well as leg lengths, are assessed along the superior-inferior
axis. The leg lengths should be measured by noting symmetry of the inferior
border of the medial malleoli. Labeling of the side as short or long is based on
the side of motion restriction as determined by the standing and seated for-
ward flexion tests and modified Gillet's sign.
a. ASIS height (Fig. 14)
b. Symphysis pubic height (Fig. 15)
c. Leg lengths (Fig. 16)
10. Supine neurologic examination
a. Superficial cremasteric reflex-upper motor neuron lesion is suspected if
this reflex is absent or diminished bilaterally. Unilateral absence of the re-
flex may represent a lower motor neuron lesion between L1 and L2.
b. Superficial abdominal reflex-absence on both sides indicates upper motor
neuron lesion; unilateral absence indicates a lower motor neuron lesion
from T7 to L2 levels.
74 The Physical Examination 01the Spine and /Is Functional Kinetic Chain
11. Abdominal examination should be included to complete when examining the low
back.
12. Prone tests
a. "Leg lengths" (Fig. 18}-label the side long or short based on the side re-
stricted on the seated forward flexion test, as this is the most indicative
sign of sacral alignment in the prone position. A true difference in leg
length may also be represented if the iliac crest and trochanteric heights are
both low or high on the same side in the standing position.
b. Press-up (Fig. 19}-the patient is asked to come to full elbow extension with
the hands placed underneath the shoulders, maintaining the pelvis on the
table.
i. Any flat areas along the line of the spinous process may indicate areas
of dysfunction.
ii. Note any centralization or peripheralization of symptoms with repeated
movements.
c. Femoral Nerve Stretch Test (FNST) (Fig. 20}-performed while the patient's
knee is passively flexed so that the heel touches the buttock; can be further
stressed by adding hip extension. Make sure that the pelvis does not rotate
anteriorly by stabilizing over the ischium with the other hand.
d. Strength of the knee flexors and hip extensors are best evaluated in this
position.
e. Medial hamstring (L5) reflex (Fig. 2l}-checked in this position by crossing
the ankles and striking the medial hamstring with 3 fingers placed just
proximal to the posterior knee crease. The authors find this reflex easier to
elicit than the posterior tibial reflex.
f. Spring test-the palm of the hand, preferably using the pisiform, is placed
over each spinous process, over the thoracic and lumbar areas, while exert-
ing a compressive force from posterior to anterior.
i. Normal response-each segment responds with equal "spring" and no
pain.
ii. Abnormal response-stiffness or less "spring" relative to other segments,
with associated local muscle spasm. These symptoms, along with repro-
duction of pain, are suggestive of bone pain, internal disc disruption,
segmental dysfunction, or instability at that level.
g. Step-off deformity-most common at L5-S1 and L4-L5; when present, may
indicate a spondylolisthesis.
13. Side·lying
a. Hip abduction strength is then assessed.
b. Rectal exam-including coccyx and piriformis palpation.
II. Scanning Examination

A. Overview-the scanning examination is well-suited for the spine specialist or the
primary care practitioner with a special interest in musculoskeletal disorders. The
scanning examination is undertaken only at the regions where the screening exam
has identified limited range of motion or dysfunctional movement patterns.
B. Lumbar segmental exam
I. Seated flexion-palpate for asymmetry of the transverse processes, identifying
which is the most posterior from L1 through L4. At the L5 segment, palpating
over the lamina and recording the most posterior side are preferable because
the transverse processes are not readily palpable. It is also important to look for
tissue texture abnormalities at the corresponding dysfunctional segment, such
The Physical Examinatian af /heSpine and Its Functional Kinetic Chain 7S
as deep, fourth layer muscle spasm, which help to identify not only the dys-
functional segment but also the likely painful segment.
2. Prone position-the patient is checked again for asymmetry of the transverse
processes in the neutral position and finally on elbows in extension to check
the position of the transverse processes through an arc of motion.
C. Modified Schober's Test-can be performed in flexion with patient standing. A line is
drawn between the PSIS, and a distance of 10cm is measured above and a dis-
tance of Scm below the line to give a IS-cm span. On flexion, normal elongation
of 5 em or more is noted. This test helps to differentiate lumbar spine flexion,
which accounts for 400/0 of the forward flexion motion compared with 60% from
hip joint motion (i.e., if the patient's fingertips reach the lower shins on flexion
but only a 2 cm elongation is noted, then most of the motion occurred at the hips,
not the lumbar spine). At least a 2 em shortening on prone extension is normal.
III. Quality of Movement Assessment-Functional Assessment ofthe Kinetic Chain

A. Overview-well-suited to the spine specialist or primary care practitioner with a
special interest in musculoskeletal disorders.
B. The 3-D Functional Physical Examination: The Isolated Integration Approach
-Based on the work of Gary Gray, P.T. and his team reaction, Martin Lambert,
M.S., P.T., O.C.S., F.A.A.O.M.P.T., as well as the physicians and physical thera-
pists at Buffalo Spine a Sports Medicine, P.c.
-Six Basic Functional Tests (include in all spine physical examinations):
I. Standing One-legged Squat (Fig. 22A)
a. Calcaneal eversion, ankle dorsiflexion and subtalar joint pronation (loading).
b. Knee loads inward (not over the toes) or knee internally rotates, abducts and
flexes (loading).
c. Hip internally rotates, flexes and adducts (loading).
d. Look for early heel rise or lack of calcaneal eversion, indicating gastroc-
soleus tightness (Fig. 22B).
2. Step-downs (approximately 4" step + l : 2" to start)
a. Medial step-down-look for calcaneal eversion and loading of the ankle,
knee and hip of the extremity on the step as mentioned above. (Fig. 23)
b. Anterior step-down-evaluates ankle dorsiflexion (Fig. 24A)-100k for early
heel rise (Fig. 24B).
3. 3D Core Evaluation
a. Sagittal Plane (SP): flexion (Fig. 25A) / extension (Fig. 25B), and especially
evaluate translation of the pelvis in the opposite direction of motion.
b. Frontal Plane (FP): sidebending left (Fig. 26A) and right (Fig. 26B); look for
translation of the pelvis to the opposite side and loading of the same side
lower extremity.
c. Transverse Plane (TP): rotation left (Fig. 27A) and right (Fig. 27B)-loading
of the opposite lower extremity. NB: Make sure you evaluate whether the
shoulders rotate further than the pelvis, indicating lack of hip and/or pelvic
motion.
4. 3D Eccentric Control ofthe Core (This is done on one leg or, if necessary for balance,
toe touch on the opposite side. The heel is approximately 3-4" from the wall.)
a. SP: hands are placed behind the head, and the head and hands are touched
to the wall while standing on one leg (Fig. 28).
b. FP: side touches to the wall while standing on the outside leg (Fig. 29).
c. TP: Rotating left and right shoulders back to the wall while standing on one
leg (Fig. 30).
76 The Physical Examination of Ihe Spine and Its Functional Kinetic Chain
5. 3D S(apular Readion
a. SP: scapular posterior tilt with same side hip extension with arm overhead
reach on same side (Fig. 31A, 31B)
b. FP: load opposite hip with scapular downward rotation and then unload
same side hip with upward rotation of the scapula as arm goes overhead
(Fig. 32A, 32B).
c. TP: load opposite hip with scapular protraction, unload same side with
retraction of the scapula (Fig. 33A, 33B).
6. Unloaded Foot Evaluation
a. Calcaneal eversion will unlock the midfoot (Fig. 34A). Calcaneal inversion
will lock-up the mid foot, especially in transverse and frontal planes (Fig.
34B).
b. First metatarsal phalangeal joint extension with plantar flexion on the first
ray and dorsiflexion on the MTPjoint should be approximately 65°, which
is necessary for normal ambulation (Fig. 35A, 35B).
IV. Muscle Imbalan(es

A. Overview-this examination is well-suited to the spine specialist and primary care
practitioner with special interest in musculoskeletal disorders. An assessment of
muscle length is not performed in isolation but combined with assessment of
quality of motion. This approach ensures identification not only of muscles that
are tight but also of muscles that interfere with the quality of movement and tri-
planar muscle tightness.
B. Use the Six Basi( Fundional Tests and observe for musde imbalan(es:
1. Gastrocsoleus tightness
SP-early heel rise with one-legged squat or anterior step-down or SP core with
flexion note decreased ankle dorsiflexion.
FP-lack of calcaneal eversion with one-legged squat or medial step-down
TP-lack of subtalar joint pronation or lower extremity pronation with one-
legged squat or step-downs or opposite lower extremity to the direction of
transverse plane core.
2. Hamstring
a. Lateral
SP-increased knee flexion with SP core-flexion or knee over toes with ante-
rior step-down or one-leg squat.
FP-increased knee abduction valgus with FP core to same side or medial
step-down/one-legged squat.
TP-decreased lower extremity (esp, tibial) internal rotation with TP core to
opposite side or medial step-down/one-legged squat.
b. Medial
SP-increased knee flexion with SP core flexion
FP-decreased knee abduction (valgus) with FP core to same side
TP-increased lower extremity [esp, tibial) internal rotation with TP core to
opposite side or with medial stepdown/one-legged squat.
3. Psoas/Quadratus Lumborum
SP-decreased anterior pelvic translation or decreased hip extension with SP
core extension.
FP-decreased pelvic translation to opposite side or decrease sidebending to op-
posite side with FP core.
TP-decreased rotation to same side with TP core.
The Physical Examination 01the SpineandIts Functional Kinetic Chain 77
4. Quadriceps (esp, rectus femoris)

SP-decreased hip extension and knee flexion with SP core extension.
FP-decreased knee abduction with one-legged squat or step-downs, or with
same side FP core.
TP-decreased lower extremity internal rotation (esp. femur) with TP core ob-
served opposite leg to direction of pelvic rotation.
5. Short Hip External Rotators
SP-decreased hip flexion with one-legged squat or step-downs or posterior
pelvic translation with SP core in flexion.
FP-decreased sidebending of pelvis on opposite side with step-down or one-
legged squat or decreased pelvic translation.
TP-decreased hip internal rotation with one-legged squat or medial step-down
on the same side.
v. Special Considerations
A. Overview-this section describes parts of the physical exam often overlooked by the
practitioner when evaluating the low back.
B. Thoracolumbar junction
I. Anatomy and biom.chanics
a. The thoracolumbar junction is an anatomic transition area between the
lower thoracic and upper lumbar vertebrae. A progressive change in the
zygapophyseal joints from the coronal plane of the thoracic region to the
more sagittal plane of the lumbar region takes place, most commonly from
TID-TIl and Tl2-LI.
b. This area also marks an increase in the size of the vertebral body and verte-
bral discs from the thoracic to the lumbar regions.
c. Biornechanically, because of the variation in the thoracolumbar junction
zygapophyseal joints, rotation occurs mainly at the thoracic segments,
whereas sagittal ranges occur in the lumbar region. The thoracolumbar junc-
tion also serves as an "inflexion point"-the transition area between the nor-
mal thoracic kyphosis and lumbar lordosis.
d. Functionally, this inflexion point is believed to serve as an area of particular
vulnerability to stress and the development of segmental dysfunction.
However, this transition is also thought to be the reason why it is a common
site of injury for spinal trauma.
e. Finally, the thoracolumbar junction is often compared to a mortise joint be-
cause it is in closed pack position when extended. This becomes particularly
significant when discussing its clinical evaluation and pathoanatomy.
2. Clinical signiflcanc.-Malimvaara found an increase in the incidence of thoracolum-
bar pathology based on the level.
a. The uppermost levels revealed anterior degeneration [i.e., degenerative disc
disease, vertebral body osteophytosis, Schmorl's nodes).
b. TlI-T12 was characterized by both anterior and posterior degenerative
changes. Consequently, Tl2-L1 revealed posterior degeneration such as
zygapophyseal osteoarthritis.
c. Traumatic injuries at the thoracolumbar junction often involve the vertebral
bodies, usually resulting in compression and burst fractures secondary to
flexion moment at impact.
3. Evaluation of thoracolumbar Junction
a. History
78 The Physical Examination of the Spine ancllb Functional Kinetic Chain
i. Thoracolumbar junction discomfort has not been extensively studied.

ii. Maigne reports patients commonly relate the onset of pain to rotary
twisting motions without radiation into the lower extremities.
iii. Patients typically present with persistent pain after adequate treatment
for what appeared to be lumbosacral disease.
b. Physical examination. In addition to assessing the quality and quantity of
movement at that area, Maigne points out three ways of evaluating the tho-
racolumbar junction while the patient is prone:
i. Iliac crest point sign-reproduction of pain with palpation over the iliac
crest, which corresponds to the cutaneous emergence of the posterior
branches of the affected nerves.
ii. Skin rolling test-thickening and hypersensitivity of the skin and subcu-
taneous tissue in the gluteal and iliac crest region. This should be com-
pared contralaterally.
iii. Localized tenderness with translational movement of the spinous process
of T1 O-L1. Diagnosis may be confirmed with tenderness of the corre-
sponding zygapophysealjoint palpated 1 cm lateral to the spinous
process.
C. Piriformis muscle
1. Anatomy and biomechanics
a. Originates medially from the inner surface of the sacrum and exits the pelvis
through the greater sciatic foramen and attaches to the greater trochanter of
the femur.
b. The innervation is from the first and second sacral nerves.
2. Cbnical significance
a. Travell refers to the piriformis muscle as the "double devil": "It causes as much
distress by nerve entrapment as it does by projecting pain from trigger points."
b. Biomechanically, it torsions the sacrum anteriorly, as seen during the nor-
mal gait cycle.
3. History
a. Pain originating from trigger points in the piriformis muscle includes low
back pain, buttock pain, and posterior thigh pain. Typically this is aggra-
vated by prolonged hip flexion, adduction, and internal rotation.
b. Pressure on the sciatic nerve may cause paresthesias and/or numbness in the
calf and foot; however, true weakness rarely occurs.
4. Physical exam
a. In the supine position, observation alone may reveal external rotation of the
affected leg. The piriformis should be assessed above and below 90· of hip
flexion. Assess painfulness and limitation in these ranges of motion.
b. Reproduction of symptoms in combination with forceful internal rotation of
the flexed thigh is referred to as Freiburg's sign. Bonet's sign is positive if
the examiner adds adduction. The Pace maneuver assesses for weakness and
pain with resisted abduction and external rotation of the thigh. This is done
with the patient in the seated position. A more recent study modifies this
latter technique by having the patient perform Pace's task against gravity in
the side-lying position.
c. External palpation exam is classically described as placing the patient in the
0
side-lying position with the affected side up. The hip is flexed to 90 and an ,
imaginary line is drawn from the greater trochanter to the sacroiliac end of
the greater sciatic foramen. Tenderness may be present throughout the
The Physical Examination af the Spine and Its Functional Kinetic Chain 79
length of the piriformis, as described; however, Travell notes it to be more

medial and/or lateral.
d. If any doubt exists about the cause of tenderness, one should proceed to in-
ternal palpation by rectal or vaginal route. This is done in the same position
as above and also can be performed bimanually. Confirmation of position
can be accomplished by assessing for contractile tension in the muscle with
active abduction of the thigh.
D. Nonorganlc physical signs In low back pain
1. Overview
a. Nonorganic physical signs, as classically described by Waddell, function on
the premise that most physical exams of the patient with low back pain con-
tain some nonorganic elements.
b. Waddell standardizes a group of nonorganic signs and relates them to psy-
chological findings in an attempt to clarify clinical assessment. The presence
of nonorganic signs may aid in identification of patients who require a more
detailed psychosocial assessment.
c. Caution must be taken in overinterpretation of nonorganic physical signs.
d. A more recent study in patients with low back pain investigated the rela-
tionship between biomechanical variables (lumbar dynamometry), psycho-
logic tests and nonorganic pain behavior (Waddell scores). The results sug-
gested that poor performance on blomechanical testing in this population
may be a form of abnormal illness behavior and thus may not accurately re-
flect alterations of the neuromusculoskeletal function.
e. Nonorganic physical exam signs were originally described with chronic low
back pain patients. Recent studies demonstrate them to have poor predictive
validity with respect to the acute work related low back pain patient and re-
turn to work.
2. Physical examination. Five nonorganic physical signs are described by Waddell:
a. Tenderness-nonorganic tenderness may be either superficial or
nonanatomic. Superficial tenderness can be elicited by lightly pinching over
a wide area of lumbar skin. Nonanatomic pain is described as deep tender-
ness felt over a wide area rather than localized to one structure.
b. Simulation test-usually based on movement producing pain. Two examples
include axial loading, in which low back pain is reported on vertical loading
over the standing patient's skull by the examiner's hands, and rotation, in
which back pain is reported when shoulder and pelvis are passively rotated
in the same plane as the patient stands relaxed with feet together.
c. Distraction test-if a positive physical finding is demonstrated in a routine
manner, this finding is checked while the patient's attention is distracted.
Straight leg raising is the most useful distraction test. There are several vari-
ations to this test; most commonly, however, straight leg raise is done in the
supine position and then, while distracting the patient, in the sitting posi-
tion. This is commonly referred to as the "flip test." However, keep in mind
that biomechanically the two positions are very different.
d. Regional disturbances-regional disturbances involve a widespread area,
such as an entire quarter or half of the body. The essential feature of this
nonorganic physical sign is divergence of the pain beyond the accepted
neuroanatomy. Examples include give-way weakness in many muscle
groups manually tested and sensory disturbances, such as diminished sen-
sation to light touch, pinprick or vibration, that do not follow a dermatomal
80 The Physical Examination of/he Spine and lis Functional Kinetic Chain
pattern. Again, care must be taken not to mistake multiple root involvement
for regional disturbance.
e. Overreaction-Waddell reports that overreaction during the examination may
take the form of disproportionate verbalization, facial expression, muscle
tension, tremor, collapsing, and even profuse sweating. Analysis of multiple
nonorganic signs showed that overreaction was the single most important
nonorganic physical sign. However, this sign is also the most influenced by
the subjectivity of the observer.
VI. Neurologic Exam

A. Reflexes
1. Muscle stretch reflexes
a. Assessed when the tested muscle is relaxed and therefore can be done in
the sitting, supine, or prone position, depending on which muscle is
tested. Listed below are the common muscles tested and the roots they
represent:
i. Patellar (L3-L4)
ii. Achilles (S1)
iii. Medial hamstrings (L5)
2. Pathologic reflexes
a. Pathologic reflexes obviously indicate upper motor neuron damage and
therefore should not be neglected in routine exam of the back.
i. Plantar response (Babinski sign)
ii. Clonus
B. Manual muscle testing. Grading of muscle strength commonly utilizes the Oxford
Scale with muscles tested in the neutral position. Unfortunately, the test does not
assess muscles individually. For example, one can have normal strength with hip
extension with very little gluteus maximus activity and predominant hamstring
activity.
l. Grade O-no movement
2. Grade r-frace contraction without joint motion
3. Grade 2-joint motion with elimination of gravity
4. Grade 3-full range of motion against gravity alone
5. Grade 4-completely moves body part against gravity and some resistance
6. Grade 5-normal
C. Sensory exam. Comparing the patient's ability to detect sharpness from right to left
lower extremity is the most common form of sensory exam testing. Table 3 (page
73) lists the accepted areas to be tested within a dermatome as defined by the
American Spinal Injury Association.
D. Dural tension signs
I. Straight leg raising test or Lasegues' test (see Fig. 13)
a. Done while the patient is in the supine position.
b. The lower extremity is slowly raised with the knee completely extended.
Classically, reproduction of radicular symptoms at < 70° is believed to indi-
cate irritation of the sciatic roots. Adhering to this definition will probably
under diagnose lumbar radiculopathy.
c. Adding dorsiflexion, adduction, internal rotation and/or neck flexion may
increase the sensitivity of the test and also helps to differentiate it from tight
hamstrings.
d. Crossed straight leg raise is positive when the contralateral leg raising pro-
duces symptoms. Typically, this carries a poor prognosis with regard to con-
The Physical Examination of the Spine and /Is Functional Kinetic Chain 81
servative management. It may indicate a large focal disc herniation or a

fragmented disc.
e. Butler advocates "sensitizing additions" to stress and therefore to evaluate
parts of the sciatic nerve; for example, the addition of dorsiflexion/eversion
or inversion/plantar flexion to stress (or bias) the tibial and peroneal nerves,
respectively (Figs. 35 and 36).
2. Slump test (see Fig. 11)
a. A term originally coined by Maitland; another means of assessing sciatic ir-
ritation. Usually it is positive in lumbar focal disc herniations and less posi-
tive in stenotic patients.
b. Although there are modifications to this test, basically patients are tested for
symptoms in the seated position.
c. One knee is held extended, and the head is flexed while the patient assumes
a slumped posture and the hands are held behind the back.
d. A positive test is reproduction of the patient's symptoms.
3. Femoral Nerve Stretch Test (FNST) (see Fig. 20)
a. Originally described by Wasserman in 1919; carried out in the prone posi-
tion while passively flexing at the knee, approximating the heel to the but-
tock.
b. Pain along the anterior thigh is considered a positive test, or reproduction of
the patient's symptoms.
c. This potentially represents irritation of Ll-LJ and at times the 14 nerve root.
d. The addition of hip extension adds to its sensitivity.
e. An FNST can also reproduce sciatic symptoms, this often indicates an 14-5
focal disc herniation is present.
f. Neck extension may decrease symptoms or neck flexion may increase symp-
toms (head and neck off the end of the table).
g. Sidelying slump FNST can be used alternately along with sensitizing and re-
lieving maneuvers of flexion and extension of the head and neck (see Fig.
21).
VII. Kinetic Chain and the Lumbar Spine Exam

A. Overview
1. The kinetic chain refers to the fact that joints of the human body are linked to-
gether into a series so that motion at one of the joints is accompanied by mo-
tion at an adjacent joint. This is particularly true in the closed system whereby
the distal joint is fixed.
2. Discussion of all variations of the lower quarter and their influences on the
lumbar spine is beyond the scope of this chapter. This section is intended to
demonstrate the importance of the kinetic chain in low back pain and to draw
the reader's attention to common deviations.
B. Lower extremity-Donatelli discusses the potential consequences of excessive prona-
tion of the foot or pes planus.
1. In layman's terms, this is referred to as "flat foot" and is commonly caused by a
tight gastrocnemius.
2. Excessive pronation in a closed system leads to subsequent internal rotation of
the tibia, fibula, and femur.
3. Internal rotation of the femur may result in anterior innominate rotation, thus
increasing lumbar lordosis.
4. Altered muscle function may result (shortened iliopsoas, lengthened ham-
strings) as well as increased tension on the iliolumbar ligament.
82 The Physical Examination 01Ihe Spine and Its Functional Kinetic Chain
5. Intuitively, strain on the lumbar spine may become excessive with increased
tension to soft-tissue structures listed above.
6. In his review of common ballet injuries, Milan concluded that they had multi-
factorial etiology that primarily involved the interplay of compensatory biome-
chanics in the spine and lower extremity.
7. Gray's functional kinetic chain rehabilitation is based on the interplay between
the distal Achilles' tendon and proximal hip joint, and that foot/ankle mechan-
ics either turn on or turn off the hip musculature.
C. Lumbopelvjc rhythm
1. Refers to the normal synchronous and smooth motion taking place during for-
ward flexion of the lumbar spine, pelvis, and hips.
a. With forward bending, one should observe reversal of lumbar lordosis with
concurrent pelvic rotation about the hip, and posterior translation.
b. The majority of motion with respect to the lumbar spine occurs at L5-S 1.
c. Return to the erect posture should demonstrate the reverse of the above
process.
2. With forward bending, sacroiliac motion also occurs.
a. A small amount of sacral extension occurs at the base, moving slightly pos-
teriorly.
b. These motions can be monitored and were discussed above.
3. Finally, the iliolumbar ligament functions to stabilize the lumbosacral complex;
the inferior band tightens during extension, and the superior band tightens dur-
ing flexion.
a. Clinically, normal lumbopelvic rhythm can be disturbed by numerous fac-
tors, such as SI dysfunction, zygapophyseal restrictions, disc disease, and os-
teoarthritis.
4. Anterior pelvic tilt
a. Muscle imbalances are generally the cause of this common dysfunction.
b. Excessive knee flexion at heel strike increases patellofemoral forces. The in-
nominate must be able to rotate anteriorly under control; if this does not oc-
cur, excessive knee flexion results at heel strike.
5. Lateral pelvic tilt
a. Caused by weak or inhibited gluteus medius and minimus.
b. Tensor fasciae latae tightness results.
c. Piriformis tightness results as it substitutes for the inhibited hip abductors.
May lead to sciatic compression neuropathy.
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The Physical Examination 01the Spine and lisFunctional Kinetic Chain 83
II. Estridge M, Rouhe S: The femoral stretch test. Neurosurg 57:813-817,1982.

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13. Fritz JM, Weinner R, Hicks GE: The use of nonorganic signs and symptoms as a screening tool for re-
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20. Hirsch G, Beach G: Relationship between performance on lumbar dynometry and Waddell's score in a
population low back pain. Spine 16:1039-1 043, 1991.
21. Hollinshead S: Functional Anatomy of the Limbs and the Back, 6th ed. Philadelphia, W.B. Saunders,
1991, pp 217-301.
22. Hudgins WR: The crossed straight leg raise test. N Engl J Med 297:1127, 1977.
23. Humphry G: A Treatise on the Human Skeleton. Cambridge, MacMillan, 1958.
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1979.
30. Malimvaara A, Videman T: Facet joint orientation, facet and costovertebral joint osteoarthritis, de-
generative disc disease, vertebral body osteophytosis and Schmorl's nodes in the thoracolumbar junc-
tion in cadaveric spines. Spine 12:458-463, 1987.
31. Markolf K: Defamation of the thoracolumbar junction intervertebral joints in response to external
loads. J Bone Joint Surg 54A:51 1-533, 1972.
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33. Norkin C, Levangie P: Joint Structure and Function in Comprehensive Analysis, 2nd edition.
Philadelphia, F.A. Davis, 1992.
34. Oxland TR, Lin R, Panjabi MM: Three-D mechanical properties of the thoraco-lumbar junction.
Orthopaedic Research 10:573-580, 1992.
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37. Singer K: Variations at the human thoracolumbar transitional junction with reference to the posterior
elements. PhD Thesis, University of Western Australia, 1989.
38. Stagnara P, Maurov J: Reciprocal angulation of the vertebral bodies in a sagittal plane: Approach to
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39. Travell J, Simons D (eds): Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore,
Williams Et Wilkins, 1992, pp 181-214.
40. Urban LM: Straight leg raise: A review. J Orthop Sports Phys Ther 2:117, 1981.
41. Waddell G: Non-organic physical signs in low back pain. Spine 5:117-125,1980.
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3:39-46, 1980.
84 The Physical Exami/KJlion of !he Spine andlis Functional Kinelic Chain
ATLAS OF FIGURES
FIGURE 1 (Right). Lumbar shift.
FIGURE 2A (Below left). Posture evaluation. Shoulder height is measured

by placingthe hands on top of the acromion bilaterally.
FIGURE 21(Belownidle). Posture. Iliac crestheightis measured by plac-

ing the hands horizontal and coming inwardand then down on top of
the iliaccrest.
FIGURE 2( (Below""'), Posture. Trochanteric heightismeasuredby plac-

ing the hands horizontal and moving them inward and downward on
top of each trochanteric region.
FIGURE 3A. Standing balance- FIGURE 31. Standing balance- FIGURE 3(. Standing balance-
startingposition. advance to arms crossed. most difficult with arms crossed
and eyes dosed.
The Physical Examination 01theSpine and Its Functional Kinelic Chain 85
FIGURE 4. Crouchtest.
FIGURE 5A-(. Duck-walking. Startingwith crouch position, the patientadvances four steps in the so-called
duck-walking fashion.
F( )
,-~< ,~< "-,"
E+L-rotC) E( I (IB+R-rol
FIGURE 6. STAR diagram-lumbar

range of motion.
1 = 25%limitation
2 = 50%limitation
3 = 75%limitation
4 = 100% limitation
Use 1-3 dash lines forpatient's repart
of pain severity on a specific motion: FIGURE 7A. Lumbar extension. FIGURE 78. Lumbar extension.
- represents mild pain Rotation and translation are added One-legged standing increases the
= represents moderate pain ta stress the pars and zygapaphy- stress on the pars ana zygapaphy-
== represents severe pain seal joints. seal joints.
86 The Physical Examination of the Spineand Its Functional Kinetic Chain
fiGURE SA and I. Standing forward Aexion text.
fiGURE 10. STAR diagram-cer-

vical range of motion.
1 = 25% limitation
2 = 50% limita~on
3 = 75% lirnitotion
4 = 100% limitotion
- represents mild pain reparted by the
porient
= represents moderate pain reparted
by the patient
fiGURE 9l. Gillet'stest. fiGURE 91. Gillet's test- '= represents severe pain reported by
normal response. the patient
fiGURE Ill. Slumptest- fiGURE III. Slumptest- fiGURE 11 C. Slumptest-

stage I. stage II. stage III.
The Physical Examination oIlheSpine and /Is Functianal Kinetic Chain 87
FIGURE 13A and B (Above).

Straight leg rcise-ebose test.
FIGURE 14(RI,6t). Supine land-

mark-anterior superior iliac
spine height.
FIGURE 12A and B. Seated forward

flexion test.
FIGURE 15A. Supine landmark-

symphysis pubisheight-stage I,lo- FIGURE 15B. Supine landmark-
cate the symphysis pubisby placing symphysis pubis height--the index
the hand over the lower abdomen Rngers are then flexed at the distal FIGURE 16. Supine land-
so that the middle finger is on the interphalangeal joints ta observe mark-leg lengths. The thumbs
umbilicus and the heel of the hand the height and symmetry of the sym- are pleced just inferior ta the
overthe symphysis pubis. physis pubis. medial malleoli.
88 The Physical Examination 01theSpine and lis Functional Kinetic Chain
FIGURE 17A. Bridging, stage I. FIGURE 17B. Bridging, stage II.
FIGURE 19. Pronetest-press-up.
FIGURE 18. Prone test-leg lengths

meosured by placing thethumbs inferior
to the medial malleoli.
FIGURE 20A. Prone test-femoral nerve stretch, FIGURE 20B. Prone test-femoral nerve stretch,
stage I. stage II.
TIte Physical Examination 01"'e Spine and Its Functional Kinetic Chain 89
FIGURE 21. Prone test-medial hamstring (l5)

reflex.
FIGURE 22A. Standing one-legged
squat, rightkneeloads properly with
abduction (valgus).
FIGURE 23 (lth). Step-down:

Right medial step-down, pos-
terior view, showing proper
calcaneal eversion and subta-
lor joint pronation (loading).
FIGURE 221 (R,."". Standing

one-legged squat. left knee
loads poorly (knee overtoes).
FIGURE 241. Step-down: left

anterior-medial step-down.
Notethe early heel-rise on the
left, indicating tight gastroc-
soleus.
FIGURE 24A. Step-down: left ante-

rior step-down evaluates functional
ankle dorsi-flexion.
90 The Physical Examinatian 01theSpine and Its Functional Kinetic Chain
FIGURE 25A. Core: Sagittal plane

flexion. Note posterior translation of
pelvis as arms reach as far forward
as possible.
FIGURE 251. Core:Sagittal planeex·

tension. Noteanterior pelvic transla-
tion as arms reach overhead.
FIGURE 26A. Core: Frontal plane

left-side-bending. Note pelvic
translation to the right.
FIGURE 261. Core: Frontal plane

right-side-bending. Note pelvic
translation to the left.
FIGURE 27A. Core: Transverse

plane left rototion. Notepelvis and
shoulders more symmetrically.
FIGURE 271. Core: Transverse

plane rightrotation. Note howthe
shoulders have rotated farther
than the pelvis. This could be a re-
striction at the ankle, knee or hip
region.
The Physical Examination 01the Spineand Its Functional Kinetic Chain 91
FIGURE 28. Eccentric control of FIGURE 29. Eccentric control of FIGURE 30. Eccentric control of
thecore:SagiHal plane extension. the core: Frontal plane left side- thecore:Transverse plane left ro-
This requires control of psoasand bending. This requires control of tation.
abdominals. rightgluteus medius, abdominals,
erector spinae, as well as quan-
dratus lumbarum and psoas.
FIGURE 31A. Scapular Reaction:

SagiHaI planeAexion with loading
of right hip Aexion and scapular
anterior tilt with right arm exten-
sion.
FIGURE 311. Scapular Reaction:

SagiHal plane extension. Notethe
right hipextension, posterior scap-
ular tilt allowing rightarm Aexion.

Frontal plane left arm adduction
with left side-bending and scapu-
lar adduction and downward ro-
tation (loading).

Frontal plane right side-bending
allows fOr left arm abduction with
left scapular abduction and up-
ward rotation.
92 The Physical Examination 01the Spine and lis Functional Kinetic Chain

Transverse plane left rotation, left
arm horizontal adduction allows
for leftscapular abduction or load-
ing.

Transverse plane right arm hori-
zontal abduction allowing for
right scapular adduction.
FIGURE 34A. Unloaded Foat Eval-

uation: Left calcaneal eversion un-
locks the mid-foot motion in all
three planes.
FIGURE 341. Unloaded Foat Eval-

uation: Left calcaneal inversion
locks up themid footexcept for in-
version.
FIGURE 35A. Unloaded Foat Eval-

uation: Left ~rst metatarsal plantar
Rexion will allow for ~rst toe ex-
tension. Note lack of extension of
the ~ rst toe on theleft foot.
FIGURE 351. Unloaded Foat Eval-

uation: Right ~rst toe extension to
approximately 65° is considered
normal.
The Physical Examination of the Spine and Its Functional Kinetic Chain 93
FIGURE 36. Hamstring-Hamstring lengths.
FIGURE 37. Piriformis length-Below 90° of hip

flexion.
7
I
Clinical Presentation and Diagnostic Subsets
Carolyn A. Marquardt, M.D., Andrew J.Co/e, M.D., F.A.C.S.M.,
Stanley Herring M.D., F.A.C.S. M., Irene. M. Young, M.D.,
and Steve Stratton, PhD, PT, ATC
Key Points
• 80 0/0 of the population experiences an episode of low back pain at some point in their
lives.
• The course of low back pain is typically recurrent and is chronic more often than
usually believed. Although 950/0 of patients who have low back pain recover within
6 months, these same patients have a 70-900/0 recurrence rate of low back pain.
• No more than 2 days of absolute bedrest is appropriate as part of the treatment of
lumbar spine pain. Relative rest is more appropriate.
• Many nonspinal conditions can masquerade as low back pain or create symptoms
analogous to those commonly originating from the lumbar spine and vice versa.
• Not all abnormal findings on imaging of symptomatic patients correlate with the
source of pain. Therefore, the clinician must relate history, physical examination,
response to treatment, and the results of other ancillary tests to the imaged findings
to determine which of the abnormal imaged results are actually causing pain.
• A fluoroscopically guided, contrast-enhanced injection procedure may provide
diagnostic and therapeutic benefit and allow a patient's rehabilitation program to
progress more rapidly.
• The vast majority of low back pain can be managed nonoperatively.
• The majority of surgery is done for patients who have failed conservative care and
continue to have pain and dysfunction that are unacceptably disruptive of their
chosen lifestyle despite appropriate lifestyle modification. Even if a patient has failed
aggressive conservative care, surgery may not be indicated because of a poor psycho-
logic profile. the possibility of a poor surgical outcome, or various other reasons.
• Cauda equina syndrome is the only entity affecting the lumbar spine that requires
emergent operative intervention.
I. Background
A. Epidemiology
1. Each year in the United States 1 of every 2 adults experiences at least 1 day of
low back pain.
2. Lifetime prevalence: 60-900/0
3. Annual incidence of low back pain is 50/0.
4. Symptoms improve in
a. 450/0 of patients in 1 week
b. 85-900/0 within 6-12 weeks
95
96 Clinical Presenlalianand Diagnostic Subsels
5. Low back pain recurs in 70-900/0.

6. The pain becomes chronic in 400/0.
B. Background
1. Multiple etiologies of low back pain
a. Acute muscle strain
b. Lumbar disc herniation
c. Posterior element pain
d. Segmental/somatic dysfunction
2. Other conditions causing low back pain (see Chapter 8 for a detailed description
of these conditions). Many nonspinal conditions can masquerade as low back
pain or create symptoms analogous to those commonly originating from the
lumbar spine.
a. Sacroiliac joint pain-pain referral into the gluteal area similar to facet joint
pain
b. Piriformis syndrome-pain referral in the distribution of the sciatic nerve,
particularly an S1 distribution
c. Myofascial pain-pain referral can be radicular in quality and mimic a lum-
bar radiculopathy
d. Peroneal nerve entrapment at the fibular head-pain referral may mimic an
L5 radiculopathy
3. Consider psychological evaluation if
a. Objective findings and subjective complaints are discordant.
b. Psychological issues seem to interfere with patient's progression through
rehabilitation program.
c. Muscle relaxation training (biofeedback or self-hypnosis) may help rehabili-
tation.
II. Diagnostic Subsets

A. Acute muscle strain or contusion
1. Pathophysiology
a. Muscle injury can result from
i. Unaccustomed eccentric exercise
ii. Acute trauma
iii. Acute muscle strain
b. Tissue injury complex
i. Muscle tissue or thoracolumbar fascia may be involved
ii. Myofibrillar damage involving the Z-band and sarcomere disruption and
localized contracted tissue
iii. Delayed-onset muscle soreness after intense eccentric exercise may result
in strength deficits for at least 10 days.
iv. Regeneration of damaged muscle tissue takes longer than 10 days.
v. Deficits in strength and range of motion may persist even after pain has
resolved.
2. History
a. Method of presentation
i. Acute traumatic injury
ii. Tearing sensation while lifting or during traumatic event
iii. Repetitive overload
iv. Unaccustomed eccentric exercise
b. Clinical symptoms
i. Localized lumbosacral discomfort
Clinical Presenlalian andDiagnostic Subsets 97
ii. Delayed-onset muscle soreness

iii. Typically occurs 24-48 hours after eccentric exercise
iv. May occur to lesser degree after concentric exercise
v. Attributed to disruption of muscle proteins and subsequent inflammation
3. Physical Examination
a. Segmental hypomobility of the three-joint complex may result from muscle
spasm and guarding
b. Loss of active and passive segmental and combined motions
4. Recommended management
a. Relativerest « 3 days)
b. Anti-inflammatory medication at dose levels to achieve both anti-inflammatory
and analgesic effects
c. Physical therapy
i. Modalities to reduce inflammation and muscle spasm
(a) Ice and cold packs
(b) Electrical stimulation
ii, Regain tissue flexibility and segmental motion
(a) Manual therapy techniques
(b) Stretching techniques in "spine safe" position
iii. Regain muscular strength and postural control during static and dynamic
activities
(a) Dynamic lumbar spine stabilization training-optimal strength may
protect the spinal motion segment from acute dynamic overload and
chronic repetitive shear stress.
(b) Activity-, job-, or sport-specific training helps to minimize chance of
future recurrence.
(c) Ensure that patient can safely return to intended activity, job, or
sport.
iv. Active home program should be developed as soon as possible to help
patient become independent.
v. Consider plain x-rays if patient does not respond to conservative care;
MRI is reserved for recalcitrant cases.
B. Disc herniation
1. Background
a. Incidence is highest among adults 30-40 years old.
b. > 95% of lumbar disc herniations occur at L4-L5 or L5-S 1.
c. 75% of lumbar herniated discs resolve spontaneously within 6 months.
d. The cumulative risk of having a second proven herniated disc during the
next 20 years is 8C¥o.
e. Up to 70% of patients who undergo first-time surgery for disc herniation
complain of low back pain years later.
2. Pathophysiology
a. Nucleus pulposus-central gelatinous portion of the disc
b. Annulus fibrosis-outer portion of the disc organized in concentrically ori-
ented lamellae
c. Disc "herniation" occurs when nucleus pulposis extends through radial tears
in the annulus
i. Disc bulge-disc extends symmetrically and concentrically by >2mm be-
yond the adjacent vertebral bodies
ii. Disc protrusion-focal asymmetric extension of disc but the annular
fibers remain intact
98 Clinical Presenlation and Diagnostic Subsel5
iii. Disc extrusion-disc disrupts the outer annular fibers and may migrate
above or below
iv. Disc fragment-extruded disc loses its attachment and may migrate
above or below
d. Pain generation may be a result of discogenic chemical irritation or mechan-
ical nerve root impingement
3. History
a. Often acute injury occurring with flexion and rotation of lumbar spine
b. Typically, recurrent episodes of back pain occur first
i. Increasing numbers of episodes of greater intensity and duration
ii. Pain and paresthesias begin radiating into the leg.
iii. Back pain may become less severe as leg pain progresses
c. Back symptoms are more pronounced in patients with annular tear but no
protrusion of disc.
d. Leg pain is usually much more pronounced than back pain when herniation
of disc occurs.
e. Far lateral disc herniations create leg pain in a radicular pattern with little or
no back pain.
f. Symptoms are usually exacerbated by activities that increase intradiscal
pressure.
i. Sitting
ii. Standing
iii. Walking
iv. Bending
v. Lying prone (with forminal herniation)
vi. Lumbar extension (with foraminal herniation)
g. Symptoms typically alleviated:
i. Lying supine
ii. Lying in fetal position
iii. Lying prone (without foraminal herniation)
iv. Lumbar extension (without foraminal herniation)
a. Soft tissue inflexibility (muscle, fascia, ligament) due to muscle spasm or
tightness
b. Pain with flexion> extension
c. Lateral shift
d. Neurologic symptoms with nerve root impingement
e. Dural tension testing (straight or seated leg raise, femoral stretch)
5. Diagnostics
a. Plain films
i. Consider if no response to conservative care or "red flags"
ii. Rule out other conditions such as malignancy, fracture, spondylytic de-
fect
b. CT scan
i. Provides more bony detail of pars defects, fractures osteophytes, tumor
ii. Can evaluate discs in those who cannot undergo MRI (pacemaker,
cochlear implants, etc.)
iii. Addition of myelography for details of nerve root impingement
c. MRI
i. Provides the best detail for soft tissue such as disc, thecal sac, spinous
ligaments and bone marrow
Clinical Pl'lmIRlation and Diagnostic Subsets 99
ii. Asymptomatic disc herniation may occur.
(a) Abnormal disc findings have been present in one-third of asympto-
matic volunteers
(b) MRI findings should be correlated to the history and physical exam
iii. Severe back pain and leg pain may occur without documentation of disc
herniation on imaging due to chemical inflammatory mediators causing
a chemical radiculitis.
d. Electrodiagnostic testing
i. May help localize anatomic level of nerve impingement in multi-level
disease
ii. Assessment in the degree of nerve injury (axon loss) when formulating
treatment plan and prognosis
iii. May assist in surgical decision making in determining degree of nerve
injury and confirming neurological deficit
iv. Helps differentiate old verses new nerve injury in recurrent back pain af-
ter surgery
v. May identify other contributing sources of pathology such peroneal
nerve entrapment of the fibular head mimicking an 15 radiculopathy,
plexopathy or peripheral neuropathy.
a. Relative rest « 3 days)-absolute bedrest > 3 days does not reduce disability
or dysfunction.
b. Medication
i. Anti-inflammatory medications at dose levels to achieve both anti-
inflammatory and analgesic effects
ii. Muscle relaxants act primarily via the central nervous system but may be
useful as a sleep aid
iii. Narcotic analgesics may be considered in acute pain not fully responsive
to anti-inflammatory meds.
iv. Oral steroids in a tapering course for pain unresponsive to anti-
inflammatories or a static neurologic deficit
c. Physical therapy
i. Education
(a) Body mechanics-helps to protect injured structures and to prevent
further injury
(b) Function and role of spine in patient's life
ii. Modalities to reduce inflammation and muscle spasm
(a) Ice, cold packs, and electrical stimulation do not reduce inflammation
created by a herniated disc because they do not penetrate deeply
enough into the soft tissues; however, they may diminish reflex mus-
cle spasm that contributes to overall level of pain and dysfunction.
(b) Ultrasound penetrates deeply through soft tissues but should be used
with caution in the setting of an acute disc herniation because its
thermal effects may increase the inflammatory response and worsen
radiculopathy.
iii. Traction may be helpful for acute discogenic lumbar spine pain.
(a) Manual, mechanical, inversion, split-table, and autotraction tech-
niques are available.
(b) May reduce intradiscal pressure by 20-30%
(c) May exert effects by allowing vertebral body separation, decreasing
compressive forces on nerve roots by increasing neuroforaminal size,
100 Clinical Presenlation and Diagnostic Subsets
improving blood flow to the nerve roots, and stretching spinal mus-
culature
iv.Corsets
(a) May help by decreasing active range of lumbar spinal motion
(b) May help decrease intradiscal pressure
(c) May help by increasing proprioceptive awareness of lumbar spine po-
sition and maintaining "neutral spine" positioning
(d) May cause muscles that are "braced" to become weaker and decondl-
tioned through disuse
v. Regain tissue flexibility and segmental motion of lumbar spine elements
as well as all related kinetic chain components
(a) Manual therapy techniques
(c) Stretching techniques in neutral "spine safe" position
vi. Regain muscular strength and postural control during static and dynamic
activities of lumbar spine elements as well as all related kinetic chain
components
(a) Initial exercise position is determined by which motions
(i) Lessen radicular or extremity pain ("centralize" pain)
[ii] Do not significantly increase lumbar spine pain. Usually exten-
sion helps to centralize acute discogenic lumbar spine pain.
(iii) Note that pain caused by large central, paracentral, and foraminal
herniations may be exacerbated with extension-biased exercise
because central canal and foraminal diameters are decreased.
Therefore, neutral and/or slightly flexion-biased training may be
the least painful.
(b) Dynamic lumbar spine stabilization training
(i) Optimal strength and flexibility protect the injured spinal motion
segment from acute dynamic overload and chronic repetitive
shear stress.
[ii) Balanced strength and flexibility of related kinetic chain compo-
nents help to optimize spinal mechanics and visa versa. Poor
flexibility may cause excessive stress to be transmitted to the
lumbar motion segments and sacroiliac joints.
(c) Activity-, job-, or sport-specific training helps to minimize chance of
future recurrence.
(d) Ensure that patient returns safely to intended activity, job, or sport.
vii. Active home program should be developed as soon as possible to help
patient become independent.
d. Fluoroscopically guided, contrast-enhanced spinal injedlon procedure using both local
anesthetic and steroid
i. Provides both diagnostic and therapeutic benefit
ii. Consider imaging study before injection (MRI, CT, CT myelography) to
ensure absence of anatomic contraindications.
(a) Caudal or translumbar epidural approach acceptable for L4-L5 or
L5-S 1 herniated disc
(b) Selective nerve root (transforaminal) block may be helpful for a
foraminal herniation with primarily leg pain or when an epidural ap-
proach has relieved the low back pain component but the patient's
leg pain continues.
e. Surgery
i. Approximately 5-100/0 of patients with persistent sciatica require surgery.
Clinical Presentation and Diagnostic Subsels 101
ii. Consideration in patients who have had no response to conservative care

after six weeks with associated neurologic signs and leg pain that corre-
sponds to neuroimaging and/or electrodiagnostic testing
iii. Absolute indications include cauda equina syndrome or progressive neu-
rologic deficit
i v. Cauda equina syndrome
(a) Incidence is < 10f0 of patients with lumbar spine pain.
(b) Usually due to extrinsic pressure on cauda equina by massive central
herniated nucleus pulposus
(c) Less common causes include
(i) Epidural abscess
[ii] Epidural tumor
(iii) Epidural hematoma
(iv) Trauma
(d) Symptoms and signs may include
(i) Lumbar spine pain
[ii] Bilateral motor or sensory changes
(iii) Saddle anesthesia
[iv] Bladder dysfunction-Loss of control-urinary retention
(v) Bowel dysfunction-Frank incontinence with decreased rectal
tone on examination
(e) Recommended management
(i) Emergent advanced Imaging depends on availability: MRI, CT, or CT
myelography.
(ii) Emergent surgical decompression may arrest further neurologic pro-
gression and improve chance of neurologic recovery.
C. Internal disc disruption and nonraGKUlar lumbar spine pain
1. Background
a. Controversial diagnosis
b. Supporters emphasize the importance of chemical, immunologic, and neural
mediation of lumbar spine pain.
c. No external manifestations of the disease in the form of disc bulge, hernia-
tion, or loss of disc height.
d. Internal disc disruption is located centrally, but it is the unaffected, intact
outer fibers of the anulus fibrosus that become symptomatic.
2. History
a. Often acute injury caused by sudden trauma with excessive load
b. Limited regional referred pain
c. Generally, patients complain of unremitting, chronic lumbar spine pain.
i. Particularly sensitive to axial loads
ii. Minimally responsive to physical therapy
iii. Limited response to medication
3. Physkal Examination
a. Soft tissue inflexibility of the muscle, fascia, and ligaments
b. Muscle spasm or tightness
c. Segmental hypomobility
d. Loss of normal lumbopelvic rhythm
a. Initial treatment stages for internal disc disruption syndrome are similar to
those for acute disc pain.
i. Relative rest
102 Clinical Presentation and Diagnoslic Subsets
ii. Medication-theoretically, a tapering 2-week course (as opposed to the

usual l-week taper) oral steroids may allow an adequate dose to pene-
trate the disc and approach the purported site of inflammation.
iii. Physical therapy
(a) Education
(b) Modalities
(c) Traction-to provide segmental unloading
(d) Flexibility training-manual therapy techniques may be of some bene-
fit to segmental mobility.
(e) Strength training
(i) Helps to maintain newly reestablished motion segment mechanics
[ii] Best done with the spine unloaded
(iii) The aquatic environment may be particularly beneficial because
graded unloading of the lumbar spinal segments occurs at pro-
gressively deeper depths.
(0 Home program
b. Additional management considerations
i. Consider plain x-rays if patient does not respond to aggressive conserva-
tive care; is reserved for recalcitrant cases when other diagnostic possi-
bilities must be considered.
ii. Consider fluoroscopically guided, contrast-enhanced epidural injection
procedure for diagnostic and therapeutic benefit if
(a) No or minimal improvement with aggressive conservative care
(b) Increased symptoms with aggressive conservative care
(c) Note that benefit may be limited because the disruption syndrome
is located inside the disc and the steroid does not directly contact
this area.
iii. Discography or CT discography is considered diagnostic if concordant
pain is reproduced during testing of the suspected disc and adjacent discs
are not painful
(a) The use of discograms in predicting fusion success is controver-
sial.
(b) Some advocate fusion with failure of conservative care
(c) IDET (Intradiscal electrothermal therapy) may be a treatment op-
tion but remains controversial
D. Acute posterior element pain: facet (zygapophyseal) joint
1. Background
a. 15-400/0 of chronic low back pain is due to the facet joints
b. Facet joints are paired synovial joints
c. The synovium contain sensory fibers including mechanorecptors and noci-
ceptive fibers
d. The facet joint may cause both axial and lower extremity pain
2. History
a. Often acute injury occurring with extension and rotation of the lumbar spine
b. Usually related to a torsion load on the lumbar spine
c. Pain may include the spine and often refer into the buttocks or posterior
thigh but rarely goes beyond the knee
3. Physical Exam
a. No historical, physical, or imaging studies are diagnostic of facet joint pain-
the clinical diagnosis is one of exclusion.
b. Pain often reproduced with extension and rotation
Clinical Presentation and Diagnostic Sulnels 103
c. Site of maximal tenderness with associated articular and soft tissue restric-
tion
4. Diagnostics
a. Radiographic (plain films, MRI, CT, bone scan) evidence of facet osteoarthri-
tis is not predictive of a painful facet joint.
b. A normal radiographic evaluation (plain films, MRI, CT, bone scan) of a
facet joint is not predictive of a nonpainful facet joint.
c. Fluoroscopically guided, contrast-enhanced facet injection procedures may
serve to diagnose a painful facet joint by providing appropriate duration re-
lief during the anesthetic phase.
d. Response to intraarticular injection does not correlate with or predict clinical
results after solid posterior lumbar fusion and should not be used as a pre-
operative screening test.
a. Initial treatment stages for acute facet pain are similar to those for acute disc
pain.
i. Relative rest
ii. Medication
(a) Education-avoid prone positions because they may increase facet
loading.
(b) Modalities
(c) Traction
(i) 90/90 traction seems to be most effective because this position
unloads the facet joints.
[ii] Sustained static traction should be avoided because it often exacer-
bates symptoms, probably through stretching of the facet capsule.
(d) Corsets-neutral to slight flexion bias helps to unload the facet joints.
(e) Flexibility training-in a neutral to slightly flexion-biased position
(t) Strength training
(i) Flexion and neutral spine bias posture and exercise positions are
emphasized because they unload the facet joints.
[ii] Posterior pelvic tilt exercises help to decrease lumbar lordosis and
should be performed in multiple positions of functional activity.
(iii) Flexion and posterior pelvic tilt exercises theoretically decrease
facet joint compressive forces.
(iv) Contraindications to flexion exercise
• Lumbar spine hypermobility or instability
• Increasing lumbar spine pain
• Peripheralization of symptoms
(g) Home program
b. Consider fluoroscopically guided, contrast-enhanced injection procedure for
diagnostic and therapeutic benefit if
i. No or minimal improvement with aggressive conservative care
ii. Plateau or increased symptoms with aggressive conservative care
iii. Aggressive conservative care has failed and surgical decision making re-
quires more precise localization of pain generators.
c. Consider neurotomy if relief from local intraarticular facet injections is not
long lasting
i. Medial branch dorsal primary ramus blocks help to determine the correct
levels for neurotomy, when indicated.
ii. A series of medial branch blocks using local anesthetics of different du-
ration helps confirm a positive response
E. Segmental and somatic dysfunction
1. Background
a. Definition: an injury to one or more components of the motion segments
that results in a series of significant compensatory changes that cause
i. Lowered pain threshold
ii. Muscle hypertonus
iii. Segmental muscular atrophy
iv. Reduced range of motion
v. Segmental facilitation
(a) Clinical palpatory examination correlates strongly with the motor re-
flex threshold as determined by electromyography.
(b) The segments with lowered motor reflex threshold have been termed
facilitated segments.
(c) Facilitated muscles are predisposed to activity when other muscles are
at rest.
(d) In a startle response facilitated muscles are the first to fire and the
last to relax compared with segments that do not have characteristics
of facilitation.
(e) Facilitated segments are hyperresponsive to impulses reaching them
from other sources of the body, including cerebral centers.
[f Facilitated segments may be identified on physical examination.
b. Segmental dysfunction is probably a more appropriate diagnosis for the
most common types of lumbar injury typically classified as "sprain-strain."
c. Most lumbar spine injuries are not due to disc herniations or facet injury but
rather to segmental dysfunction.
d. Segmental dysfunction encompasses a spectrum of injuries to one or more
segment-related structures that result in a series of compensatory changes.
i. Multifidus muscle atrophy
ii. Decreased tissue compliance
iii. Decreased pain threshold (tenderness)
iv. Altered segmental motion (articular dysfunction)
v. Muscular imbalances
vi. Segmental facilitation
vii. Proprioceptive deficits
2. History
a. Often acute injury occurring with flexion and rotation of the lumbar spine
superimposed on a history of episodes of lumbar spine pain that usually re-
solved unremarkably within 3-5 days.
b. Lumbar spine pain with variable degree of regional referred pain
a. Soft tissue inflexibility of the muscle, fascia and ligament due to
i. Spasm or tightness
ii. Segmental hypo mobility
iii. Segmental muscle atrophy
iv. Atrophy of type 2 fibers
v. Internal structure abnormalities in type 1 fibers
b. Loss of normallumbopelvic rhythm
c. Increased lumbar lordosis
Clinical Presenlotion and Diagnostic Subse15 lOS
a. Initial treatment stages for segmental dysfunction are similar to those for acute
disc pain.
i. Relative rest
ii. Medication
(a) Education
(b) Modalities
(e) Traction helps to improve segmental mobility, particularly if manual
therapy techniques have had limited benefit.
(d) Flexibility training-segmental mobility
(i) Manual therapy techniques are of critical importance to enhance
segmental hypomobility, thus allowing more uniform segmental
motion and functional balance.
(ii) Compensatory segmental hypermobility may occur adjacent to
hypomobile segments and become tender and painful; they may
require treatment.
(iii) If significant hypermobility is suspected, flexion-extension x-rays
may be necessary to assess the degree of hypermobility.
(e) Strength training helps to maintain newly reestablished motion seg-
ment mechanics.
[f Home program
F. Spondylolysis, spondylolisthesis, andpars interarticularis injury
I. Background
a. Definitions
i. Derived from Greek words spondylos-vertebrae and olisthesis-slip or
slide
ii. Spondylolysis-fracture of the pars interarticularis
iii. Spondylolisthesis-anterior displacement of one vertebrae on another
b. Classification by different types
i. Dysplastic (CongenitaQ
(a) Due to dysplastic or axially oriented facets
(b) Associated with other anomalies such as spina bifida occulta or
kyphosis
ii. Isthmic
(a) Due to a lesion in pars interarticularis
[i) Subtype A: lytic-stress fracture of pars interarticularis
[ii] Subtype B: elongated but intact pars secondary to healed stress
fractures
(b) Usually presents in the first years of school
iii. Degenerative
(a) Due to longstanding segmental instability with remodeling of articu-
lar processes at affected level
(b) Degeneration of suppporting structures leads to loss of lumbosacral
locking mechanisms
iv. Traumatic-due to acute fractures in areas around pars interarticularis but
not of the pars interarticularis
v. Pathological-due to localized or generalized bone disease
vi. Postsurgical
(a) Due to surgical removal of too much supporting structure
106 Clinical Presenlatianand Diagnostic Subsets
(b) Removal of more than 50010 of a facet joint renders the segment un-
stable.
2. Epidemiology
a. Incidence in school age children is 4010, increasing to 6010 by adulthood
b. Pars defects have been found in 7.2010 of asymptomatic adults
c. Pars defects are twice as common in young males but high grade slips are 4
times more common in girls
d. Increased incidence of isthmic spondylolysis is associated with certain sports
including diving, gymnastics, wrestling and weight-lifting
e. Degenerative spondylolisthesis is most common at L4-L5 and more common
in women
3. History (The following discussion pertains to pars stress reaction and isthmic
spondylolysis or spondylolisthesis.)
a. Chronic dull, aching or cramping low back pain
b. Often located along the belt line
c. Exacerbated by rotation and/or hyperextension
d. Underlying history of chronic repetitive motions
a. Pain with extension
b. Symptoms can be accentuated by having the patient stand on one leg and
bend backward
c. Paraspinal muscle spasm
d. Tight hamstrings
e. Loss of lumbar lordosis
5. Diagnostics
a. Plain films (see chapter 14 for greater detail)
i. Pars defect may be seen on oblique, lateral, and anteroposterior
views.
ii. Flexion-extension views to evaluate instability
(a) >4mm of horizontal translation
(b) > II degrees of angulation of the motion segment compared to ad-
jacent segments
b. Bone scan with single-photon emission computed tomography (SPECT) is
the gold standard.
i. Increased sensitivity and specificity allow detection of pars defect with
normal xray in acute injury
ii. Even when plain films demonstrate a pars defect, bone scan can be
helpful in documenting acuity.
iii. Bone scan may remain "hot" for 18 months and longer, even after the
pars defect has healed, because of remodeling
c. CT scan helps to demonstrate whether the fracture site is well corticated.
i. Good cortication indicates an older fracture.
ii. Little to no cortication indicates that the fracture is probably acute.
d. MRI provides additional soft-tissue information.
i. Disc degeneration occurs more frequently in patients with spondylolis-
thesis than in normal controls.
ii. Less radiation exposure than a CT scan
a. Bracing-Ibased on isthmic spondylolysis in adolescent)
i. Type and duration of bracing remains controversial (see Chapter 13)
(a) Rigid polypropylene brace (modified Boston overlap brace)
Clinical Presenlation and Diagnostic Subsets 107
(b) Lumbosacral corset

ii. Several bracing protocols available (see Chapter 25)
b. Medication
c. Physical therapy
i. Education
ii. Modalities to control pain and muscle spasm
iii. Flexibility training program
[a] Initially use slight flexion bias with neutral spine position because
this position decreases stress on the posterior elements and may help
to decrease pain.
(bl Timing is controversial-begin when patient is pain-free and out of
brace; still in brace without pain; or still in brace with some pain.
(cl Particularly hamstrings
iv. Strength training
Ial Initially use a slight flexion bias with neutral spine position because
this position decreases stress on the posterior elements and may help
to decrease pain.
(b) Helps to maintain
• Segmental spinal mechanics
• Lower extremity kinetic chain strength balance
(cl Timing is controversial-begin when patient is pain-free and out of
brace; still in brace without pain; or still in brace with some pain.
v. Home program
d. Fluoroscopically guided contrast-enhanced Injections
i. Consider fluoroscopically guided, contrast-enhanced injection procedure
for diagnostic and therapeutic benefit if
(a] No or minimal improvement with bracing and aggressive conserva-
tive care
(bl Increased symptoms with aggressive conservative care
ii. Epidural or transforaminal injection for associated discogenic or radicu-
lar symptoms
iii. Injection of the pars defect is controversial for therapeutic value but may
be helpful in diagnostic localization in the anesthetic phase of the injec-
tion
iv. Facets at level of defect as the source of pain is controversial.
e. Surgery
i. Children
(a) Often required in slips of >50010 with associated neurologic symptoms
(b) Progression of a slip or persistent mechanical or neurologic symp-
toms
ii. Adults
(a] Neurologic dysfunction requiring decompressive surgery often re-
quires fusion
[b] Spondylolisthesis >25010, unstable with dynamic imaging and neuro-
logic deficit
G. Degenerative lumbar disease
1. Background
a. Morphologic changes in the three-joint complex in varying proportions
i. Disc
ii. Facet
iii. Vertebral bodies
108 Clinical Presenlation and Diagnostic Su&sels
iv. Supporting soft tissues

b. Resulting morphologic changes may create a constellation of symptoms and
signs that depend, in large part, on which structures are predominantly in-
volved.
i. Anular fibers of the disc and chemical or mechanical irritation of the an-
terior and dorsal spinal root
ii. Posterior longitudinal ligament and other pain-sensitive intracanal and
foraminal structures
iii. Facet joints and surrounding synovium and joint capsule
iv. Osteophytosis of the vertebral body endplates and facet joint articular
processes
v. Hypertrophy of ligamentum flavum
c. The resulting clinical picture may be modified by any associated chemical,
mechanical, or psychological factors.
2. History
a. Acute onset or slowly progressive increase in back or radicular symptoms
b. Frequent history of episodes of lumbar spine pain
c. Morning stiffness
d. Radiating lower extremity pain or paresthesias that worsen with particular
movements, depending on which parts of the three-joint complex are most
involved
i. Flexion-increased symptoms from anterior element involvement (e.g.,
herniated and/or desiccated disc)
ii. Extension
(a) Increased symptoms may occur (but not necessarily) because of pos-
terior element (facet) involvement.
(b) Facet or vertebral body endplate hypertrophy causes foraminal or
central canal narrowing and stenosis.
3. Physical Exam
a. Soft tissue inflexibility (muscle, fascia, ligament)
b. Muscle spasm or tightness
c. Compensatory lower extremity kinetic chain flexibility and strength im-
balances
d. Increase or decrease in normal lumbar lordosis, depending on relative in-
volvement of anterior versus posterior elements
4. Diagnostics
a. Plain films
i. AP/lateral views to evaluate degenerative changes, tumor, trauma
ii. Oblique view to evaluate facet degenerative changes, pars defect
iii. Flexion-extension and lateral bending to evaluate for gross instability
b. CT scan
i. The imaging modality of choice in older patients whose symptoms and
signs are likely due to osseous involvement
ii. Superior to MRI and Xray for trauma such as fracture
iii. Addition of myelography may give superior detail of osseous structures
of nerve root impingement compared to MRI especially in spinal stenosis.
c. MRI
i. Optimal evaluation of soft tissue
(a) Disc, end plate changes, ligaments, hematoma
(b) Spinal infection
(c) Bone marrow processes
(d) Tumor
Clinical PresenIDtian and Diagnostic Subsets 109
ii. Degenerative changes are found in the normal population and incidence
increases with aging, but do not necessarily correlate with pain
d. Electrodiagnostic testing
i. May help localize anatomic level of nerve impingement in multi-level
disease
ii. Assessment in the degree of nerve injury (axon loss) when formulating
treatment plan and prognosis
iii. May assist in surgical decision making in determining degree of nerve
injury and confirming neurological deficit
iv. Helps differentiate old verses new nerve injury in recurrent back pain af-
ter surgery
v. May identify other contributing sources of pathology such peroneal
nerve entrapment of the fibular head mimicking an L5 radiculopathy,
plexopathy or peripheral neuropathy.
e. Fluoroscopically guided, contrast-enhanced injection procedures for diag-
nostic and therapeutic benefit if
ii. Increased symptoms with aggressive conservative care
iii. Conservative care has failed and surgical decision making requires more
precise localization of pain generators
a. Initial treatment stages for lumbar degenerative disease incorporate the same
core elements as other aggressive conservative care programs.
i. Relative rest in a position that minimizes symptoms
ii. Medication (NSAIDs)-caution should be exercised because many patients
with lumbar degenerative disease are older and may have decreased renal
function or gastrointestinal contraindications.
(a) Education
(b) Modalities
(c) Traction
(i) To provide segmental unloading
[ii] To provide foraminal decompression
(d) Bracing
(i) May provide some relief
[ii] Flexion, extension, or neutral bias depends on which position
minimizes symptoms most.
(e) Flexibility training
(i) Use the patient's unique "neutral" spine position that minimizes
symptoms.
(ii) Avoidance of painful positions allows program progression.
(f) Strength training
(i) Initially use the patient's"neutral" spine position to minimize
symptoms.
[ii] Avoidance of painful positions allows program progression.
(iii) Helps to maintain
• Segmental spinal mechanics for activities of daily living
• Lower extremity kinetic chain strength balance
[iv] The aquatic environment may be particularly beneficial because
graded unloading of the lumbar spinal segments occurs at pro-
gressively deeper depths.
(g) Home program
H. Spinal stenosis
1. Definitions
a. Spinal stenosis-narrowing of the spinal canal
b. Clinical definition of neurogenic claudication
i. Radiating pain or parasthesias into buttocks and lower extremities
ii. Pain exacerbated by standing or walking
iii. Pain relieved by lumbar flexion
c. Radiologic evidence of canal narrowing
i. Central stenosis defined by sagittal diameter of < 11 mm
ii. Lateral recess stenosis-lateral to the central canal with a depth of
<3mm
2. Pathophysiology
a. Narrowing of the spinal canal
i. Soft tissue such as disc
ii. Osseous thickening of bone, facet joints or spondylolisthesis
iii. Ligamentum flavum thickening
iv. Association with DISH or Paget's disease
b. Speculation of venous congestion of the roots of the cauda equina
i. Requires involvement of> 1 level of stenosis
ii. Increase in symptoms with walking due to vasodilation
3. History
a. Slowly progressive pain increase in back and unilateral or bilateral legs
b. Walking distances can vary
c. Symptoms are relieved by lumbar flexion and/or sitting
d. Increase in symptoms walking downhill due to increased lumbar extension
e. Differentiate from peripheral vascular disease by the need to have to sit or
bend forward to relieve symptoms or the ability to tolerate cycling with
neurogenic claudication
a. Often difficult to stand upright and knees are bent slightly forward
b. Loss of lumbar lordosis
c. Neurologic examination is often normal although ankle jerks are commonly
absent
d. Dural tension testing is often normal
e. Evaluate peripheral vascular status
5. Diagnostics
a. Plain films
i. May show presence of shallow vertebral canal
ii. Degenerative spondylolisthesis is often present in >500/0 men with bilat-
eral claudication
iii. Structural lumbar scoliosis is present in >500/0 with unilateral claudica-
tion
b. CTscan-helpful for evaluation of osseus changes
c. CT myelogram-more definition of canal and nerve root filling defects
d. MRI-may be complimentary for more soft tissue definition
e. EMG
i. Multilevel changes may be present especially in lumbar paraspinals
ii. May be helpful in identifying affected root levels for spinal injections or
surgery
f. Dermatomal somatosensory evoked potentials (SSEPs) can be useful in local-
izing involved levels
Clinical Presenlatian and Diagnostic Subsets 111
6. Initial treatment stages for spinal stenosis incorporate the same core elements as
other aggressive conservative care programs.
a. Relative rest or restriction of activities
b. Medication
i. (NSAIDs): caution should be exercised because most patients with spinal
stenosis are elderly and may have decreased renal function and/or gas-
trointestinal contraindications
ii. Calcitonin-has been beneficial in up to 400/0 of patients with neurogenic
claudication
c. Physical therapy
i. Education
ii. Modalities
iii. Traction provides segmental unloading and foraminal decompression
iv. Bracing in a flexion bias may provide some relief
v. Flexibility training: initially use a slight flexion bias in "neutral" spine
position because spinal extension makes stenosis worse.
vi. Strength training helps maintain segmental spinal mechanics and lower
extremity chain balance
vii. The aquatic environment may be particularly beneficial because graded
unloading of the lumbar spinal segments occurs at progressively deeper
depths
VIll. Home program
d. Fluoroscopically guided, contrast-enhanced injection procedures for diag-
nostic and therapeutic benefit if
ii. Increased symptoms with aggressive conservative care
iii. Aggressive conservative care has failed and surgical decision making re-
quires more precise localization of pain generators.
e. Surgery
i. Recent studies of the natural history of spinal stenosis suggest that ob-
servation and aggressive conservative care may be an acceptable alterna-
tive to surgery
ii. The natural history of symptoms may not progress
iii. Currently available data preclude analysis of outcome predictors for
surgery. A meta-analysis of the literature, however, reported that 64010 of
patients treated surgically for lumbar spinal stenosis had good-to-
excellent outcomes.
iv. Indications
(a) Intolerable pain unacceptable for current lifestyle despite aggressive
conservative care
(b) Progressive neurologic deficit or cauda equina symptoms
I. Arti(ular dysfunction
1. Sauoilia( loint (SIJ)
a. Ba(kground
i. Movement abnormality of one pelvic bone on the other because of in-
crease or decrease in joint mobility
ii. Prevalence: 13-30010 of intraarticular SIJ pain
iii. Pathophysiology
(a) Unknown
(b) Possible factors
(i) Inflammation
112 Clinical Presenlatian and Diagnostic Subsets
(ii) Ligamentous or capsular tension

(iii) Compression or shear forces
(iv) Trauma
(v) Hyper- or hypomobility
(vi) Myofascial or kinetic chain imbalances
iv. No validated method to diagnose a painful SIJ dysfunction by
(a) History
(b) Physical examination
(c) Radiographic study
v. Presumptive diagnosis confirmed by intraarticular SIJ anesthetic injec-
tions using contrast and fluoroscopic guidance
b. History
i. Acute onset as with stepping off curb or lifting heavy object in twisted
position
ii. Severe pain over SIJ/buttock
iii. Sometimes referred pain into groin, buttocks, and lower extremity
c. Physical examination (see Chapter 6)
i. Pain over region of PSIS
ii. Standing/seated forward flexion test
iii. Possible pelvic asymmetry or leg length discrepancy
d. Recommended management
i. Relative rest
ii. Medication
(a) Education
(b) Modalities
(c) Traction-to help improve segmental mobility, particularly to comple-
ment manual therapy techniques
(d) Bracing-Sl.I belts
(e) Flexibility training-segmental mobility
(i) Manual therapy techniques are of critical importance to enhance
SIJ and segmental hypo mobility to allow more uniform segmen-
tal motion and functional balance.
(ii) Compensatory segmental hypermobility may occur adjacent to
hypomobile segments and require treatment.
(iii) Compensatory hypermobile segments may then become tender
and painful.
(t) Strength training helps to maintain newly reestablished motion seg-
ment mechanics.
(g) Home program
iv. Consider fluoroscopically guided, contrast-enhanced injection procedure
for diagnostic and therapeutic benefit if
(a) No or minimal improvement with aggressive conservative care
(b) Increased symptoms with aggressive conservative care
2. Coccydynia
a. Background
i. Defined symptomatically as pain in and around the coccyx because un-
derlying pathophysiology is unknown
ii. Frequency, natural history, and intra- and interrater reliability of the di-
agnosis are unknown.
iii. Etiology
Clinical Presenlation and Diagnostic Subsets 113
(a) Trauma-pressure over a prominent coccyx

(b) Localized pathology
(i) Intraosseous lipoma
[ii] Chordoma
(iii) Giant cell tumor
(c) Ligamentous inflammation
(d) Referred pain from lumbar disc
(e) Neuralgic state from irritated sacral nerve
(f) Neurosis
(g) In majority of cases, etiology is unknown.
iv. Imaging typically normal
b. Recommended management
i. Relieve pressure on coccyx area
(a) Sitting posture
(b) Cushion with sacral cutout often better then donut cushion
ii. Treat symptoms
(a) Physical therapeutic pain control modalities and manual therapy
techniques
(b) Medication
iii. Injection
iv. Surgery if aggressive conservative care fails-coccygectomy
3. Bertolotti's syndrome
a. Background
i. Pseudoarticulation of L5 transverse process to sacrum
ii. Rarely painful
i. Physical therapy
(a) Pain control modalities
(b) Manual therapy techniques
ii. Injection
iii. Surgery if aggressive conservative care fails-resection
4. Baastrup's disease
a. Background
i. Also known as "kissing spines"-uncommon cause of lumbar spine pain
due to impingement of adjacent spinous processes limits motion in ex-
tension. Periostitis may develop with repetitive trauma.
ii. Localized pain over interspinous ligament
(a) Extension exacerbates pain.
(b) Injection at site alleviates pain.
i. Physical therapy
(a) Pain control modalities
(b) Manual therapy techniques
ii. Injection
iii. Surgery if aggressive conservative care fails-outcome generally poor
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8
I
Pseudospine Pain:
Conditions that Mimic Spine Pain
Daniel Mazanec, M.D., F.A.C.P.
Key Points
• Pseudospine pain describes back and/or leg pain as the presenting symptom of an
underlying systemic (metabolic or rheumatic), visceral, vascular, or neurologic disease.
• Pseudospine pain is common and may require urgent, specific treatment, e.g.,
symptomatic abdominal aortic aneurysm.
• Clinically insignificant spinal imaging findings are common in older patients. Before
attributing symptoms to radiographic findings, a careful assessment for nonspinal
causes of back pain is important.
• Recognition of conditions associated with pseudospine pain requires appreciation of
key extraspinal diagnostic dues in the appropriate demographic setting.
I. Introduction
A. Definition: systemic (metabolic or rheurnatologic], visceral, vascular, or neurologic
disorders that may present with back and/or leg symptoms (Table 1).
B. Importance
1. Pseudospine conditions are common.
a. Prevalence of fibromyalgia in U.S. general population-2%.
b. Trochanteric bursitis as a cause of back pain in a family practice-25%.
2. Evaluation and treatment for many pseudospine conditions (e.g., abdominal
aneurysm, polymyalgia rheumattca/giant cell arteritis, malignancy) are urgent
and specific.
3. Clinically insignificant "abnormalities" (false-positives) are frequent on plain
radiographs, computed tomography (eT), and magnetic resonance imaging
(MRI). Careful clinical evaluation for mimics of spinal pain is critical before at-
tributing symptoms to imaging abnormalities.
II. Vascular: Abdominal Aortic Aneurysm

A. Epidemiology
1. 1-4% of population over 50 years of age; four-fold more common in men.
2. Familial tendency: increased risk in first-degree relatives of patients.
3. 10,000 deaths annually in U.S.-1-2% of all male deaths over 65 years of age
B. Etiology: atherosclerosis, hypertension
C. Signs and symptoms
1. Most asymptomatic
2. Pain-abdomen and/or back with radiation to hips and thighs. 12% ofpatients
have back pain. Abdominal symptoms may mimic GI disease.
3. Pulsatile abdominal mass
117
118 Pseudospine Pain: Conditions "'at Mimic SpinePain
TABLE 1. Pseudospine Pain-Diagnostic Keys

Condition Diagnostic Keys Condition Diagnostic Keys
Vascular Rheurnatologic (cont.)
Abdominal aortic Ageover 50 yr Diffuse idiopathic Age over 50-60 years
aneurysm Abdominal and back pain skeletal hyper- Thoracolumbar stiffnessor
Pulsatile abdominal mass ostosis (DlSH, pain
Forrestier's Rowing anteriorvertebral
Gynecologic disease) calcification
Endometriosis Woman of reproductive age
Piriformis syndrome Buttock and leg pain
Cyclic pelvic and back pain
Pain on resisted hip
Pelvic inflammatory Young, sexually active external rotation and
disease woman abduction
Systemically ill (fever, chills) Transgluteal or transrectal
Discharge, dysuria tenderness
Ectopic Missed period 3 or more wedgedverte-
pregnancy Abdominal and/or pelvic pain brae with endplate
Positive pregnancy test irregularities
Trochanteric bursitis, Pain or tenderness over
Genitourinary gluteal fasciitis greater trochanter
Prostitis Men over 30 years
Dysuria Metabolic
Low back and perineal pain Osteoporosis Woman over60 years
Nephrolithiasis Flankand groin pain Severe acute thoracic
Hematuria pain (fracture)
Severe weight-bearinq
Gastrointestinal pelvic pain (fracture)
Pancreatitis Abdominal pain radiating Aching dull thoracicpain,
to back relieved in supine
Systemic signs (fever, position (mechanical)
nausea,vomiting) Loss of height, increased
Elevated serum amylase thoracickyphosis
Penetratingor per- Abdominal pain radiating Osteomalacia Diffuse skeletal pain or
forated duodenal to back tenderness
ulcer Increased alkaline
phosphatase
Rheurnatologic
Fibromyalgia Young to middle-aged Paget's disease Bone pain: low back,
woman pelvic, tibia
Widespread pain Increased alkaline
Multiple tender points phosphatase
Disrupted sleep,fatigue Characteristic radio-
Normal radiographs and graphicappearance
lab values Proximal rnotor Older (over50 years)
Polymyalgia Ageover 50-60 years neuropathy Diffuse leg pain, worse
rheumatica Hip or shouldergirdle pain at night
(PMR) and stiffness Proximal muscle
Elevated ESR weakness
Dramatic response to low- Malignancy Ageover 50 years
dose prednisone Back pain unrelieved by
Seronegative spondylo- Younger male (AS, Reiter's) positional change-
arthropathies (anky- Lower lumbosacral pain night pain
losingspondylitis, Morning stiffness("gel") Previous history of
Reiter's, psoriatic, Improvement with activity malignancy
enteropathic] Radiographic sacroiliitis Elevated ESR
Pseudospine Pain: Conditions thatMimic SpinePain 119
D. Diagnosis
1. Physical exam
a. Supine with raised knees and relaxed abdomen
b. Palpable aorta> 3 ern suggests aneurysm
c. Sensitivity 680f0 overall; 91Ofo if patient girth <40 inches
2. Anteroposterior and lateral lumbar spine radiograph: curvilinear aortic calcifi-
cation in 700f0.
3. Abdominal ultrasound: sensitivity approaches 100°/0.
4. Abdominal CT: sensitive and can identify rupture or contained leak.
E. Complications
1. Rupture
a. Sudden onset or increase in pain.
b. Risk increases with aneurysmal size. If diameter is 3-4.4 em, rupture risk is
2. 1Ofo/year. If diameter is 4.5-5.9 em, rupture risk is 1O.20f0/year. Risk also in-
creases if rate of aneurysm growth is > 1 cm/year.
2. Atheroembolism
a. Blue toes, livedo reticularis
b. Hypertension, renal insufficiency
F. Management
1. All males screened with ultrasound at 65 years of age
2. Aneurysms> 6 em in diameter or increasing by > 1 cm/year: surgical resection
and graft replacement or endovascular repair.
a. Elective surgical mortality < 50f0.
b. With rupture, early surgery is key to survival.
3. Asymptomatic aneurysms < 5 em in diameter: monitor with ultrasound every
4-6 months.
III. Visceral Disorders

A. Gynecologic
1. Endometriosis: presence of endometrial glands and stroma outside the uterine
cavity. Endometrial implants are hormonally reactive.
a. Epidemiology
i. Women of reproductive age: mean 25-29 years. More common in
women with shorter menstrual cycles «27 days) and longer menses (> 7
days).
ii. Prevalence approaches 100f0.
b. Etiology: probable transplantation of endometrium to ectopic sites via retro-
grade menstruation. Probable role for growth factors in maintaining en-
dometrial implant viability.
c. Signs and symptoms: pelvic pain, 25-670f0; back pain, 25-31%; noncyclic ab-
dominal pain, 25-390f0; dyspareunia, 250f0; infertility, ? 10-150/0.
d. Diagnosis
i. Physical examination is often unremarkable or nonspecific.
ii. CA-125 may be elevated.
iii. Laparoscopy is the gold standard.
iv. Transvaginal ultrasound for endometriomas.
v. MRl may be useful in assessing response to treatment; nonspecific.
e. Treatment
i. Estrogen/progesterone (oral contraceptives)
ii. Danazol (testosterone analogue)-pain relief in up to 900f0
iii. GnRH analogues
120 Pseud05pine Pain: Conditions thot Mimic SpinePain
iv. Surgery: risk of recurrence-250J0 in 18 months.

v. Analgesics and nonsteroidal antiinflammatory drugs
2. Pelvic inflammatory disease: infection and inflammation of female genital tract be-
yond cervicitis, including one or more of the following: endometritis, salpingi-
tis, oophoritis, peritonitis.
a. Epidemiology
i. Young (mean age: 25 years) sexually active women
ii. Multiple sexual partners
b. Etiology
i. Ascending infection: endocervix to upper urogenital tract
ii. Common organisms: Neisseria qonorrhoeae, Chlamydia trachomatis,
Haemophiius influenzae
iii. Risk factors: intrauterine device (IUD), douching
c. Signs and symptoms
i. Lower abdominal, back and/or pelvic pain
ii. Vaginal discharge, leukorrhea
iii. Dysuria, urgency, frequency
iv. Fever, leukocytosis
d. Diagnosis
i. Clinical diagnostic criteria 90% specific.
ii. Laparoscopy helpful in confirming mild cases.
e. Treatment
i. Broad antibiotic coverage, emphasizing N. qonorrhoeac and Chlamydia:
cefoxitin and doxycycline.
ii. Treat sexual partners.
3. Ectopic pregnancy: pregnancy with implantation outside uterus, most commonly in
fallopian tube.
a. Epidemiology: risk factors include pelvic inflammatory disease (360J0), previ-
ous abdominal or pelvic surgery (260J0), IUD use (IOO/o).
b. Signs and symptoms
i. Signs and symptoms of pregnancy: missed period (680J0), breast tender-
ness, morning sickness.
ii. Abdominal pain (99.30/0), unilateral in 330J0-may mimic upper lumbar radicu-
lopathy with radiation to thighs.
iii. Adnexal tenderness (980J0), unilateral adnexal mass (540J0).
c. Diagnosis
i. Positive pregnancy test (830J0)
ii. Nonclotting blood on culdocentesis (950J0)
iii. Ultrasound
d. Treatment: laparotomy
B. Genitourinary
J. Prostatitis: inflammation-infectious or noninfectious-of the prostate gland.
a. Classification
i. Acute bacterial prostatitis-50J0
ii. Chronic bacterial prostatitis-5%
iii. Nonbacterial prostatitis-su-snco
iv. Prostadynia-300J0
b. Epidemiology: men over 30 years of age; lifetime prevalence, 500/0.
c. Etiology
i. Bacterial: associated with urinary tract infection-Escherichia coli or
Enterobacter
ii. Nonbacterial-??? Chlamydia
Pseuclospine Pain: Conditions fha, Mimic SpinePain 121
d. Signs and symptoms

i. Bacterial: acute febrile illness with lower back and/or perineal pain, abdomi-
nal pain, dysuria. Chronic bacterial prostatitis associated with relapsing
urinary tract infection and less acute presentation.
ii. Nonbacterial: similar symptoms but less acute presentation
iii. Tender, boggy prostate gland
iv. Increased white blood cells in prostatic secretions
e. Diagnosis
i. Urinary tract infection
ii. Prostatic fluid white blood cells
f. Treatment
i. Prolonged antibiotic therapy: trimethoprim-sulfamethoxazole, 4-16
weeks, or ciprofloxacin, 30 days
ii. Sitz baths, prostatic massage
2. Nephrolithiasis: kidney stones
a. Epidemiology: common-30f0 prevalence in U.S.
b. Etiology
i. Types: struvite, calcium oxalate, uric acid, calcium phosphate
ii. Risk factors: hypercalcemia, hypercalcuria, hyperuricemia, urinary pH
abnormality
i. Flank pain with radiation to groin
ii. Fever and chills with complicating infection
iii. Abdominal symptoms: ileus, nausea, vomiting
iv. Costovertebral angle tenderness
v. Microscopic hematuria
d. Diagnosis
i. Plain radiographs-opaque: calcium, cystine; radiolucent: urate
ii. Intravenous pyelography
iii. Urine culture to exclude infection
e. Treatment
i. Hydration, analgesics
ii. If stone does not pass-lithotripsy
iii. Surgery
C. Gastrointestinal
I. Pancreatitis
a. Epidemiology: chronic pancreatitis more common in men aged 35-45 years
at onset.
b. Etiology
i. Alcohol abuse
ii, Hepatobiliary disease: cholelithiasis
iii. Hereditary
iv. Drugs: thiazides, sulfonamides, furosemide, estrogen
v. Infection: mumps, salmonella, streptococci
i. Acute midepigastric abdominal pain, radiating through to back-900f0
ii. Nausea and vomiting
iii. Fever
iv. Ileus: hypoactive bowel sounds, abdominal tenderness
v. With chronic disease, malabsorptive symptoms
d. Diagnosis
i. Elevated serum amylase
122 P5fllIdospine Pain:Conditions thatMimicSpine Pain
ii. Elevated amylase/creatinine clearance ratio

iii. Ultrasound or abdominal CT in selected cases
e. Treatment: supportive medical therapy; no oral ingestion; IV fluids; anal-
gesics
f. Complications: pseudocyst, shock, chronic pancreatitis
2. Penetrating or perforated duodenal ulcer
a. Signs and symptoms: clinical features, including abdominal pain with radia-
tion to the back, resemble acute pancreatitis.
b. Diagnosis
i. Abdominal radiograph demonstrating free air
ii. Upper endoscopy
IV. Rheumatologic Disorders

A. Fibromyalgia: chronic musculoskeletal pain syndrome, characterized by widespread
pain and multiple tender points in reproducible locations on physical examina-
tion. Frequently associated with fatigue, stiffness, subjective swelling, and pares-
thesias.
1. Epidemiology
a. Common: prevalence 2.00/0; in women 3.40/0.
b. 70-900/0 women; mean age at diagnosis 34-55 years.
c. Association with psychologic disorders: somatization, depression (current or
past history), anxiety
2. Etiology-unknown, several hypotheses
a. Muscle hypoxia-ragged red fibers, but no consistent, reproducible histologic
abnormality
b. Psychosomatic disorder: affective spectrum disorder; associated with depres-
sion and anxiety in some patients.
c. Sleep disturbance: 60-800/0 of patients; alpha intrusion in non-REM sleep
d. Neurotransmitter abnormality: low serotonin levels, low norepinephrine lev-
els, elevated substance P levels
3. Signs and symptoms
a. Diffuse musculoskeletal pain, typically including posterior neck, upper and lower
back
b. Fatigue
c. Disturbed nonrestorative sleep
d. Subjective swelling and paresthesias
e. Frequent headaches, pain in temporomandibular joint
f. Irritable bowel syndrome (500/0)
g. Tender points: localized excessive tenderness to palpation (important to
demonstrate "negative" control points-mid forehead or anterior thigh)
4. Diagnosis
a. American College of Rheumatology proposed diagnostic criteria in 1990
L History of widespread pain (at least 3 months)
ii. Pain in 11 of 18 tender point sites on digital palpation (palpation pres-
sure approximately 4 kg-enough to blanch examiner's finger nail)
b. Presence of second clinical disorder does not exclude diagnosis of fi-
bromyalgia.
c. Laboratory (i.e., erythrocyte sedimentation rate, C-reactive protein, blood
count) and radiographic studies are normal. Decreased cervical lordosis due
to muscle tightness or spasm is a soft sign.
d. Corroborative features-disturbed, nonrestorative sleep and fatigue.
PseuJospine Pain: Canclitians /hat Mimic Spine Pain 123
e. Differential diagnosis: polymyalgia rheumatica (PMR), hypothyroidism,

Parkinson's disease, osteomalacia, chronic fatigue and immunodeficiency
syndrome (CFIDS).
5. Treatment: treatable not curable
a. Patient education: a real condition that, although painful and disturbing,
does not deform or cripple; treatable.
b. Improve quality of sleep: cyclobenzaprine, tricyclic antidepressants in low
evening dose
c. SSRI (fluoxetine) in AM with tricyclic HS
d. Nonnarcotic analgesics: acetaminophen, low-dose nonsteroidal antiinflam-
matory drugs, tramadol
d. Aerobic exercise
e. Stretching and strengthening exercises
f. Trigger point injections
g. Alternative therapy: acupuncture, SAM-e, massage therapy
h. Natural history: despite treatment, 900/0 still symptomatic at 3-year followup.
Only 30/0 in full remission.
B. Polymyalgia rheumatica (PMR): clinical syndrome in older patients of proximal hip
and shoulder girdle pain and stiffness associated with elevated sedimentation rate
and typically dramatically responsive to low doses of prednisone.
I. Epidemiology
a. Prevalence increases with age: 53/100,000 over age 50, > 100/100,000 over
age 70. Onset under 50 years rare.
b. Women affected 2-4 times more frequently than men.
c. Caucasians much more commonly affected than African Americans.
2. Etiology: unknown
a. Often abrupt onset of shoulder, neck and upper back, hip, lower back, buttock,
and thigh pain and stiffness.
b. Morning stiffness (gelling) often more bothersome than pain.
c. Mild tenderness to palpation and pain on motion of shoulders and hips.
d. Synovitis (wrists, knees, sternoclavicular joints) occasionally present.
4. Diagnosis
a. Age > 50 years
b. Hip, shoulder girdle pain and stiffness> I month duration
c. Erythrocyte sedimentation rate (ESR) by Westegren method> 40 mm/hr
d. Dramatic, prompt response to low-dose prednisone
e. Exclude other disorders with similar clinical features
i. Fibromyalgia-normal ESR
ii. Myositis-weakness (not present in PMR)
iii. Viral syndrome-duration < I month
iv. Parkinson's disease-normal ESR, insidious onset, cogwheeling
v. Multiple myeloma-monoclonal spike
5. Complications: giant cell arteritis (temporal arteritis) associated with PMR in up
to 40-500/0 of cases. Look for new-onset headache, jaw claudication, visual
change (diplopia, visual loss), scalp tenderness, systemic signs.
6. Treatment
a. Prednisone, IS mg daily; expect response within I week or doubt diag-
nosis.
b. One-third of patients require long-term, low-dose (5 mg or less) treatment.
c. In selected cases, methotrexate may be steroid-sparing
124 Pseudospine Pain: Conditions thatMimic Spine Pain
C. Seronegative spondyloarthropathles (SNSA): group of rheumatic disorders characterized

by inflammatory spinal disease, enthesitis, diverse extraspinal manifestations, and
striking association with HLA-B27.
1. Classification
a. Ankylosing spondylitis (AS)
b. Reactive arthritis (Reiter's syndrome)
c. Psoriatic spondyloarthropathy
d. Enteropathic arthropathy
2. Epidemiology
a. Age: generally less than 40 yrs at onset.
b. Sex: AS (3:1) and Reiter's predominantly male; equal ratio for psoriatic and
enteropathic.
c. Association with HLA-B27 (% positive)
AS 90
Reiter's 60-80
Psoriatic 50
Enteropathic 50
d. 6-8% of normal Caucasians are B27-positive; AS occurs in approximately
5% of B27 positive persons. 1-2% of healthy African Americans are B27
positive. SNSA is less common in African Americans.
3. Etiology
a. Role of B27: ?enhanced susceptibility to infectious trigger; molecular mim-
icry-antigenic similarity between B27 and triggering microorganism.
b. Reactive arthropathy-triggers:
i. Genitourinary: Chlamydia trachomatis
ii. Gastrointestinal: Salmonella, Shigella, Yersinia, Campylobacter
iii. Reactive arthritis is more frequent and severe in HN infected individuals.
Association is based on increased frequency of sexually transmitted in-
fections such as chlamydia in HN-positive individuals.
a. Spinal (Axial)
i. Insidious onset of dull, deep, aching back pain In the gluteal or parasacral area
ii. Morning stiffness in the back which improves with physical activity
iii. Loss of spinal mobility: decreased lumbar lordosis, decreased forward
flexion (modified Shober test), decreased chest expansion
b. Peripheral arthritis: typically lower extremity large joints
c. Disease specific findings (extraarticular)
i. Psoriatic spondyloarthopathy: psoriasis
ii. Enteropathic arthropathy: abdominal pain, diarrhea with or without
blood
iii. Reiter's syndrome: conjunctivitis, urethritis, circinate balanitis, kerato-
derma blenorrhagicum
iv. AS: iritis (25%), aortitis (1-4%), apical pulmonary fibrosis (1%)
d. Enthesopathy: achilles tendonitis (heel pain)
5. Diagnosis
a. Clinical features suggestive of inflammatory back pain: insidious onset of
pain, morning stiffness, improvement with activity
b. History of iritis, inflammatory bowel disease, psoriasis, family history of AS
c. Elevated ESR (75%)
d. HLA B-27 if pre-test probability of diagnosis is 50-75%. Avoid if symptoms
are vague and not characteristic
Pseudospine Pain: Conditions thatMimic SpinePain 125
e. Radiographic features: sacroiliitis, vertebral body squaring, bridging syn-

desmophytes; bone scan more sensitive than plain films.
6. Complications
a. Spinal fracture or dislocation
b. Cauda equina syndrome
c. Bony ankylosis of spine in dysfunctional position
7. Treatment
a. Nonsteroidal antiinflammatory drugs
b. Extension exercise program to ensure satisfactory posture as fusion occurs
c. Methotrexate or sulfasalazine for active, aggressive disease
D. Diffuse idiopathic skeletal hyperostosis (DISH, Porrestier's disease): probable variant of
osteoarthritis characterized by exuberant ossification of spinal ligaments.
I. Epidemiology
a. More common with increasing age (> 50 years), observed in 10% of spine
films in elderly.
b. Twice as common in men as in women.
c. Caucasians much more commonly affected than African Americans.
2. Etiology: unknown, not associated with B27; may be increased in diabetics.
a. Back stiffness (80%) > back pain (50-60%); pain is typically thoracolumbar.
b. Dysphagia as result of large cervical osteophytes in up to 20%.
4. Diagnosis: radiographic
a. Flowing anterior calcification along 4 contiguous vertebrae
b. Preservation of disc height
c. No sacroiliac involvement
d. Normal ESR or C-reactive protein
e. Age and absence of sacroiliac involvement help to distinguish from
spondylitis.
5. Treatment: course is typically benign; patients often asymptomatic.
a. Active exercise program optimizes range of motion.
b. Simple analgesics (acetominophen) relieve pain.
c. Rarely surgical removal of osteophytes is required for treatment of dys-
phagia.
E. Piriformis syndrome: buttock and leg pain (pseudosciatica) resulting from compres-
sion or inflammation of sciatic nerve as it courses under or through piriformis
muscle in buttock.
I. Epidemiology: no particular group at risk.
2. Etiology: sciatic nerve compression at the sciatic notch by the piriformis muscle.
Minor trauma to piriformis may result in muscle contraction or inflammation.
a. Pseudosciatica-buttock and leg pain
b. Low back pain-50%
c. Dyspareunia-23%
d. Piriformis muscle tenderness (transrectal or transgluteal)
e. Pain on resisted external rotation and abduction of hip
f. Pain on internal rotation of hip
4. Diagnosis
a. Distinguish from lumbar radiculopathy-nerve tension tests
b. Distinguish from sacroiliitis-radiographs
5. Treatment
126 Pseudospine Poin: Conditions thatMimic Spine Pain
b. Piriformis stretch exercise program

c. Transgluteal or transrectal glucocorticoid muscle injection
d. Rarely, surgical section of piriformis muscle
F. Trochanteric bursitis, gluteal fascRtls
1. Epidemiology
a. Common: up to 25010 of patients evaluated for back pain
b. Female predominance-vsoo
2. Etiology: typically unknown. Look for mechanical causes: leg length difference,
abnormal gait, muscle tightness, osteoarthritis of the hip or spine; occasionally
trauma.
a. Gluteal and leg pain-64%
b. Pain lying on affected side or with crossed legs-50%
c. Local trochanteric tenderness, frequently with iliotibial band tightness and
tenderness
4. Diagnosis
a. Look for clinical features.
b. Exclude hip disease, lumbar radiculopathy, septic bursitis (rare).
5. Treatment
b. Local corticosteroid injection
c. Physical therapy exercise program
d. Correction of mechanical abnormality (e.g., heel lift)
V. Metabolic Disorders
A. Osteoporosis: generalized loss of bone mass with resultant risk of fracture. Most
common fracture sites include vertebrae, distal radius (Colles' fracture), and hip.
1. Epidemiology
a. Females at much higher risk; female-to-male ratio vertebral fracture, 7{1;
hip fracture, 2{1
b. Caucasians and Asians at higher risk than African Americans.
c. Risk increases with increasing age; peak bone mass at age 30 with steady
decline thereafter. Women experience accelerated bone loss at menopause
for 5-7 years.
d. Other common risk factors: heredity (English, Northern European), leanness,
hyperthyroidism (including iatrogenic), steroid therapy, excessive alcohol
consumption, amenorrhea, lifelong calcium deficiency, lifelong inactivity,
smoking.
e. Presence of a vertebral fracture increases the risk of a subsequent fracture
4-5 fold
2. Etiology: multifactorial; bone resorption exceeds formation.
a. Low peak bone mass-heredity, calcium deficiency
b. Excessive bone loss-estrogen deficiency (menopause), hyperparathyroidism,
immobilization
c. Reduced bone formation-corticosteroids, calcium deficiency
3. Signs and symptoms: asymptomatic until fracture occurs.
a. Vertebral compression fractures may be asymptomatic; progressive loss of
height and increasing thoracic kyphosis may be first manifestations.
b. Acute vertebral fracture pain: severe, immobilizing; usually resolves in 6-12
weeks.
c. Chronic mechanical spine pain: consequence of wedge fractures and in-
Pseuclospine Pain:Conditions /hat Mimic Spine Pain 127
creased kyphosis with paraspinal muscle strain and fatigue; increased with
prolonged standing, relieved rapidly in supine position.
d. Pelvic stress fracture: weight-bearing parasacral or groin pain.
4. Diagnosis
a. Plain radiographs insensitive: 25-300/0 of bone mass lost before osteopenia
becomes visible.
b. Bone densitometry: dual energy x-ray absorptiometry (DEXA)-accurate and
precise (I - 2%).
i. Osteoporosis defined as T score = - 2.5 (standard deviations below peak
adult bone mass)
ii. Spinal degenerative change may confound spinal bone density measure-
ment; consider hip measurement
iii. Repeat BMD measurement in 2-3 years to assess disease progression
c. Laboratory evaluation for secondary causes-chemistry profile, complete
blood count, thyroid-stimulating hormone in most patients. Serum testos-
terone in men. Serum PTH, urinary calcium, and creatinine selectively.
5. Treatment of osteoporosis
a. Optimize calcium intake.
i. Premenopause-1200 mg/day
ii. Postmenopause-1500 mg/day
b. Weight-bearing exercise: walking
c. Vitamin D 400-800 Units/d
d. Pharmacologic agents
i. Estrogen
ii. Diphosphonates-alendronate, risidronate
iii. Calcitonin
iv. Raloxifene-selective estrogen receptor modulator
e. Treat secondary causes (e.g., iatrogenic hyperthyroidism), if possible.
6. Treatment of vertebral compression fracture.
a. Limited bedrest-prolonged bedrest promotes further bone loss, cardiovascu-
lar deconditioning, and muscle atrophy
b. Adequate analgesia-opioids if necessary
c. Bracing to facilitate earlier ambulation
d. Supervised physical therapy after 8-12 weeks to improve function,
strengthen spinal extensors, improve posture
e. Consider vertebroplasty or kyphoplasty for persistent pain. Kyphoplasty may
offer longer term benefit for improved spinal mechanics and vertebral height
restoration.
B. Osteomalacia: disorder of bone metabolism characterized by defective mineraliza-
tion of organic matrix (osteoid).
I. Epidemiology: no characteristic age group or sex.
2. Etiology
a. Vitamin D deficiency: decreased GI calcium absorption with resulting
hypocalcemia and secondary hyperparthyroidism; vitamin D promotes min-
eralization.
i. Patients with lack of adequate sun exposure (inadequate vitamin D syn-
thesis)-elderly or chronically ill in nursing homes.
ii. Patients with malabsorptive disorders-Crohn's disease with bowel resec-
tion, sprue, scleroderma.
iii. Patients with renal disease-impaired hydroxylation of vitamin D.
iv. Patients with hepatic disease-impaired hydroxylation of vitamin D.
128 PseuJospine Pain: Conditions that Mimic SpinePain
b. Inadequate calcium and phosphorus at mineralization front

i. Phosphate malabsorption with excessive aluminum-containing antacid
consumption
ii. Renal tubular disorders with phosphate wasting
c. Abnormal matrix-unmineralizable
d. Drugs: fluoride, disodium etidronate, phenytoin, phenobarbital
a. Skeletal pain: back pain (90%), ribs, long bones of the legs
b. Skeletal tenderness to palpation
c. Antalgic, waddling gait (47010)
d. Radiographic: osteopenia (50010) and pseudo fractures (Looser's lines)
e. Laboratory: elevated alkaline phosphatase (94010), low calcium (47010), low
phosphate (530/0), low vitamin D [25-(OH) metabolite] (29010).
4. Diagnosis
a. Tetracycline-labelled, nondecalcified bone biopsy-decreased mineralization
front, wide osteoid seams.
b. Distinguish from osteoporosis, multiple myeloma.
5. Treatment: address underlying cause (e.g., supplemental vitamin D in cases of
vitamin D deficiency).
C. Paget's disease: focal disorder of excessive bone resorption associated with disorganized
bone formation. Pagetic bone is structurally weak, highly vascular, and enlarged.
1. Epidemiology:
a. 3010 of adults over 40 years old; 10010 over 80 years old
b. Rare in African Americans
c. Slight male predominance
2. Etiology: unknown; viral-like inclusions in osteoclasts suggest possibility of
slow virus infection.
a. 80010 of patients are asymptomatic.
b. Bone pain-deep, aching, constant; back pain (10-40%); may be difficult to dis-
tinguish pagetic source of spine pain from coexisting osteoarthritis.
c. Joint pain-accelerated degenerative joint disease from juxtaarticular pagetic
bony enlargement and irregular subchondral support.
d. Nerve root entrapment-hearing loss, spinal stenosis.
e. Deformities: enlarged skull, bowing of long bones, exaggerated spinal lordo-
sis, kyphosis.
4. Diagnosis
a. Radiology
i. Osteolytic phase: early, lytic lesions; in the skull-osteoporosis circum-
scripta.
ii. Mixed phase: lytic, blastic-appearing, sclerotic enlarged bone with wide,
coarse trabeculae, cortical thickening, and bone overgrowth; "cotton-
wool" appearance.
iii. Characteristic locations: skull, pelvis, vertebrae ("picture-frame" appear-
ance), tibia.
iv. Bone scan more sensitive.
b. Laboratory
i. Elevated alkaline phosphatase (osteoblastic activity)
ii. Elevated urinary hydroxyproline (osteoclastic activity)
iii. Levels can be used to monitor response to treatment.
Pseuclospine Pain: Conditions that Mimic SpinePain 129
5. Complications
a. Pathologic fracture
b. Sarcomatous degeneration-lOfo
c. High-output congestive heart failure
d. Immobilization hypercalcemia
6. Treatment
a. Asymptomatic disease generally not treated.
b. Nonspecific treatment: analgesics, NSAIDs for bone or joint pain.
c. Specific treatment
i. diphophonates drugs of first choice: alendronate, pamidronate, rise-
dronate, tiludronate, etidronate
ii. Calcitonin
iii. Mithramycin
D. Proximal motor neuropathy (diabetic polyradiculopathy, diabetic amyotrophy)
1. Epidemiology
a. Age of onset typically over 50 years
b. Mild, often recent-onset diabetes (Type II)
c. Men more commonly affected
2. Etiology
a. Neural ischemia or infarction. Some biopsies also reveal perivascular inflam-
matory infiltrate.
b. Metabolic: deficiency of myoinositol
a. Unilateral or bilateral leg pain, though diffuse, may resemble sciatica; typically
worse at night.
b. Proximal muscle weakness-quadriceps-difflculty climbing stairs
c. Proximal muscle wasting.
d. Weight loss may antedate onset.
4. Diagnosis
a. Demonstration of diabetes: glucose, hemoglobin Ale.
b. Electromyogram: acute and chronic polyradicular denervation.
c. Distinguish from disk herniation and radiculopathy, polymyositis, hip dis-
ease, or inflammatory plexopathy (increased ESR)
5. Treatment
a. Natural history: maximum weakness in 4-6 weeks, then stable. Resolution in
most patients in 1-3 years.
b. Strict glucose control.
c. For transient symptomatic relief: amitryptyline, gabapentin, mexilitene, cap-
saicin
VI. Malignancy
A. Epidemiology
1. At least 75010 of patients are over 50 years of age.
2. Previous history of malignancy in 30010.
3. Less than 1010 of all patients with back pain presenting for evaluation.
S. Etiology
1. Two-thirds metastatic: breast, lung, prostate, kidney most common.
2. Myeloma is most common primary spinal malignancy.
3. Nonspinal malignant back pain: intrapelvic tumors, retroperitoneal lym-
phadenopathy, renal cell cancer, pancreatic cancer.
130 PseuJospine Poin: Conditions that Mimic Spine Pain
C. Signs and symptoms

1. Constant back pain unrelieved by positional change.
2. Night pain.
3. Weight 10ss-1O Ibs/3months.
4. Retroperitoneal lymphadenopathy may produce pain typically relieved with for-
ward flexion.
D. Diagnosis
1. Erythrocyte sedimentation rate (ESR) is best screening test; elevated in at least
80010 of back pain patients found to have malignancy.
2. Serum and urine immunoelectrophoresis for monoclonal protein (myeloma).
3. Serum calcium, alkaline phosphatase-elevated in up to 50010.
4. Prostate-specific antigen (PSA)-if > 10.0 ng/ml strong, suggestive of metastatic
prostate cancer.
5. Lumbar radiograph-only 65010 sensitive.
6. CT or MR highly sensitive (95010) for malignancy; MR preferred because it im-
ages more of spine.
7. Bone scan highly sensitive (99010) but may be normal in myeloma.
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9
I
The Use of Medications for Low Back Pain
Jerome Schofferman, MD
Key Points
• Most patients with low back pain severe enough to see a physician will need
medications at some point in the treatment continuum.
• Nonsteroidal anti-inflammatory drugs have been proven useful for acute low back
pain and flares of chronic low back pain, but their role in chronic low back pain is not
well established.
• Muscle relaxants may be useful for up to 10 days in acute low back pain but are rarely
indicated for longer periods.
• Opioid analgesics are appropriate for moderately severe to severe acute low back pain
and in very well selected patients with severe chronic low back pain that is refractory
to other treatments.
• Adjunctive medications such as antidepressants, anticonvulsants, and others play
important roles in specialized situations such as neuropathic pain.
I. General Medication Issues

A. Part of an overall treatment plan with rehabilitation
a. Exercise, body mechanics training, psychotherapy, functional restoration
B. Multiple reasons to consider pharmacological pain management
1. Quality of medical care
2. Ethics of medical care
3. Business growth and development
a. Satisfied patients refer other patients
b. Dissatisfied patients complain to friends, family, referring doctors
4. Legal issues
a. Legislators mandating pain management
b. Fifth vital sign
c. Avoid malpractice suits for inadequate attempts at pain management
C. All medications have risk(s). Use requires considering risk to benefit ratio.
D. Multiple factors determine choice of drug including:
1. Patient factors
a. Age
b. Concurrent medical problems
c. Concurrent medications
d. Etiology of pain
e. Severity of pain
f. Prior experience with analgesics and other drugs
2. Medication factors
a. Proven efficacy of particular medication
b. Relative risks of a particular medication
133
134 The Use of Medications lor Low Back Pain
3. Acute versus chronic pain

a. Medications and dosing intervals useful for acute pain may not be appropri-
ate for chronic pain.
E. Essential concepts
1. Dosing Intervals
a. Pain contingent ("pm"): medication taken when pain appears or increases
i. Generally less effective.
ii. May require larger doses.
iii. Wide swings in blood, tissue, brain levels.
iv. Useful for rescue doses for "breakthrough pain."
b. Time contingent dosing.
i. Dosing interval determined by analgesic half-life of the drug.
ii. Generally more effective analgesia.
2. Ceiling effect: maximum analgesic dose; increasing above this dose does not
increase analgesia.
a. NSAIDs have a ceiling effect
b. Opioids do not have a ceiling effect
II. Categories of Medications

A. The multiple categories of medications that may be useful for the treatment of
LBP are shown in Table 1.
III. Analgesics
A. Peripherally acting analgesics
1. Aspirin (ASA)
a. Analgesic, anti-pyretic, anti-inflammatory (after days to weeks)
b. Prototype analgesic
c. Effective for mild and occasionally for moderate pain.
d. Progressive analgesia with increasing dose to a maximum of 1000 mg. 650
mg will last 4 hours; 1000 mg usually provides 6 hours of analgesia.
e. Side effects (especially GIl with long-term use may limit applicability.
2. Acetaminophen (APAP)
a. Analgesic and antipyretic; not anti-inflammatory.
b. Effective for mild and occasionally moderate pain.
c. Minimal side effects. Fears of hepatic damage probably inflated. At doses of
4 grams per day or less, hepatic abnormalities occur rarely. Concomitant use
of alcohol and fasting may predispose to hepatic damage.
d. CAUTION: APAP is combined with many opioids (codeine, hydrocodone, oxy-
codone], so patients may inadvertently consume larger amounts of APAP if
they are taking large amounts of combination products.
e. Progressive analgesia with progressive dose to a ceiling of 1000 mg. A dose
Table I. Categories ofMedications Potentially Useful for LIP

Most Useful Sometimes Useful
Nonsteroidal anti-inflammatory drugs Muscle relaxants
Opioid analgesics Sedative-hypnotics
Antidepressants Glucocorticosteroids
Anticonvulsants Stimulants
Antihistamines
The Use of Medications for Low Bocle Pain 135
of 650 mg provides about 4 hours of analgesia. A dose of 1000 mg provides

up to 6 hours of analgesia.
3. (Non-aspirin) Nonsteroidal anti-inflammatory drugs (NSAlDs)
a. Anti-inflammatory, analgesic, and antipyretic
b. Most commonly prescribed drugs
c. IMPORTANT: Anti-inflammatory effects and analgesic effects may be dis-
cordant. Analgesia occurs in painful conditions not associated with inflam-
mation (e.g., headache). Analgesia occurs with single doses long before there
is any effect on the inflammatory cascade.
d. Evidence for efficacy: Cochrane review
i. Small but significant benefit vs, placebo for acute LBP.
ii. No good evidence for efficacy in chronic low back pain.
iii. No single NSAID proven better than any others. For unclear reasons, al-
though the mechanisms of action of NSAIDs appear to be the same, it
has been observed repeatedly that some patients respond to some of the
NSAIDs and not to others. The chemical class of the NSAID does not cor-
relate with whether or not the patient will respond. Therefore, serial trials
of 3 or 4 different NSAIDs are indicated before giving up. A trial should
last at least 10 to 14 days.
e. Mechanism(s) of action. Probably multiple.
i. Inhibition of prostaglandin synthesis by inhibition of the enzyme cyclo-
oxygenase (COX). There are at least two COX enzymes, COX-I and COX-
II. COX-II is responsible for inflammation and? pain. COX-I is responsi-
ble for gastric mucus production and renal blood flow. Many of the
undesirable effects of NSAIDs are due to inhibition of COX-I.
ii. Multiple others
f. Risks and medical complications
i. Risk Factors
(a) Age> 60
(b) History of ulcer or other GI diseases
(c) Significant medical illness, especially liver disease, hypertension,
congestive heart failure, renal disease
(d) Other meds: anticoagulants, glucocorticosteroids
ii. Risks
(a) GI bleeding, ulcer, perforation. May occur without warning; dyspep-
sia (300/0 of patients on nonspecific COX inhibitors, poor correlation
with endoscopic mucosal lesions)
(i). If dyspepsia occurs, stop NSAID and it will usually dissipate. If
NSAID is very helpful and choice is to continue, use a COX-II in-
hibitor. If dyspepsia continues, may add omeprazole or equivalent
drugs. Cimetidine, ranitidine, misoprostol far less effective.
(b) Hepatic enzyme elevation not uncommon, but usually reversible
when drug is stopped. True chemical hepatitis occasionally. Liver fail-
ure very rare, but does occur. Most often abnormalities reverse to
normal soon after drug is stopped.
(c) Renal: Edema, exacerbation of hypertension, both not unusual. Renal
insufficiency, nephritis, proteinuria, and worse quite rare. Increased
risks include age >60, pre-existing renal insufficiency, diuretic use,
hypovolemia, serious medical illnesses. Most often abnormalities re-
verse to normal soon after drug is stopped.
(d) Bleeding due to platelet inhibition. Not seen with COX-II drugs. ASA
136 The Use 01Medications for Low Baclc Pain
and older NSAIDs alter platelet function. ASA irreversibly binds

platelet COX for the life of platelet. NSAIDs bind COX reversibly for
as long as the NSAID is present. Mixed COX NSAIDs must be discon-
tinued a week before surgery or other intraspinal interventions.
(e) Central nervous system. Probably more common than generally rec-
ognized. Some deterioration of cognitive function may occur in up to
200/0 of the elderly on naproxen or ibuprofen. Most common: tinni-
tus, headache, hearing changes. Less often: depression, cognitive dys-
function (more common in elderly?, psychosis. Usually clear when
drug is stopped
(f] Bronchospasm in aspirin sensitive patients.
(g) Skin: rashes, photosensitivity.
g. Choice of NSAIDs
i. By expected use, especially drug dose and duration (Table 2)
(a) Acute pain, pain contingent use: drug with rapid onset of action;
ibuprofen, naproxen, rofecoxib, etc.
(b) Chronic pain, time contingent use: drugs with once or twice daily
dosing. Rofecoxib, celecoxib, many others.
ii. Response to therapeutic trial. If no benefit in 10 to 14 days, this drug not
likely to work. Try 2 or 3 others; if no benefit, abandon NSAIDs.
Table 2. NSAIDs: Dosing Suggestions

Generic Name Brand Name Starting Dose Maximum Dose
Shorter Half-life
Aspirin 650 mg q6h 4000 to 6000 mg
Ibuprofen Motrin 600 mg q6h 3600 mg
Ketoprofen Orudis 50 mg q6-8h 300 mg
Flurbiprofen Ansaid 50 mg q6h 300 mg
Intermediate Half-life
Diflunisal Dolobid 1000 mg once, then 1500 mg
500 mg bid
Choline salicylate Trilisate 1500 mg bid 4000 mg
Sulindac Clinoril 100 mg q12h 400mg
Naproxen Naprosyn, others 375 mg q8-12h 1250 mg
Diclofenac Voltaren 50 mg q6-8h 225 mg
Nabumetone Relafen 500 to 750 mg bid 2000 mg
Etodolac Lodine 400 to 600 mg bid 1200 mg
Long Half-life
Rofecoxib Vioxx 25 mg daily 50 mg per day
(up to 5 days)
Celecoxib Celebrex 200 to 400 mg per day 600 mg for short
term use
Nabumetone Relafen 1000 to 1500 once/d 1500 mg
Oxaprozin DayPro 1200 mg once/day 1200 mg
Piroxicam Feldene 20 mg q24h 40 mg
Modified from multiple sources, including: Portenoy R. In: IASP Committee on Refresher Courses (eds],
Pharmacotherapy of cancer pain. IASP Refresher Course on Pain Management. Adelaide, Australia. April 1,
1990, pp 10 1-112; and Miyoshi HR. Systemic nonopioid analgesics. In: Loeser JD (I'd). 3'd edition. Lippincott
Williams Et Wilkins. Philadelphia, 2001.
The Use of Medications for LowBack Pain 137
iii. Costs: also consider costs of treating complications.

iv. Convenience: once or twice daily dosing preferred. Increases compliance.
v. Patient risk factors. Generally avoid these drugs in frail elderly or med-
ically ill. Consider APAP unless true inflammation present.
vi. Drugs' relative risk and efficacy factors. In general, there is no evidence
that any NSAlDs are more effective than others. Choice is more likely
based on the above factors.
vii. COX-II "controversy." Are the COX-II specific NSAlDs preferable to the
traditional NSAlDs? Two drugs available (rofecoxib, celecoxib): more in
pipeline. Have become most popular NSAlDs. Lower risk of GI and vir-
tually no risk of coagulation problems. Convenient with once daily dos-
ing. Expensive. Good choice in higher risk patients. Not clear if benefit
outweighs costs in low risk patients.
h. Patient monitoring
i. Low risk patients: check CBC, LFT, RFT, UtA after about 3 months of
chronic treatment. Again at 6 months and once to twice per year there-
after.
ii. Higher risk patients: Check after I month and then at least quarterly
thereafter.
iii. In any patient, stop the NSAlD if there is no clear improvement in pain
or function.
RECOMMENDATIONS REGARDING GASTROINTESTINAL SIDE EFFECTS OF NSAlDs

• Use the lowest dose of NSAlD that is effective for that patient.
• Be sure the NSAlD is effective before continuing therapy.
• It is not appropriate to place all patients on prophylactic therapy.
• In patients who at are high GI risk, consider COX-II drug and/or prophylaxis with
omeprazole, but only if drug is quite effective.
• Treat uncomplicated dyspepsia by discontinuing the NSAlD. If continued NSAlD
therapy is necessary, use COX-II drug and consider omeprazole.
RECOMMENDATIONS REGARDING USE OF NSAlDs

• Usually drug of first choice for mild to moderate acute pain
• Generally more effective when used in a time contingent manner
• No good data to help select one NSAlD versus another
• Moderately effective for acute low back pain
• No good data for chronic low back pain
• Therapeutic trial of 10 to 14 days; may need to try two or three drugs
• Screen for side effects by periodic clinical and laboratory screening
• COX-II specific drugs for higher risk patients
• Not good drugs for frail elderly or patients with serious medical problems
B. Centrally acting analgesics (opioid analgesics)

1. Overview
a. Well established for cancer pain and acute pain of many types.
b. Remains somewhat controversial for treatment of chronic "non-cancer" pain.
c. Over past few years, may have become standard of care.
d. 1994 surveyed 1912 physicians; multiple specialties; averaged 9 to 44 pa-
tients on long-term opioids. But has the pendulum swung too far?
2. Barriers to rational opioid use
a. Bias
b. Lack of physician education
138 The Use01Medications for Low Back Pain
3. Potential controversies: long-term opioid analgesic therapy (LTOAT)

a. Toxicity
i. No significant organ toxicity seen in long-term reviews. No reason to
avoid opioids for fear of producing organ toxicity.
b. Side EHeets. Common; usually abate over time or readily treatable.
i. Sedation. Common at initiation of treatment. Usually improves or com-
pletely dissipates. A problem for some patients. Can usually be treated
with methylphenidate.
ii. Nausea and/or vomiting. Due to stimulation of chemoreceptor trigger
zone. Common at initiation of treatment, but usually dissipates. May re-
quire treatment with hydroxyzine 25 mg qsh, prochlorperazine 10 mg
qsh, or haloperidol 0.5 to 1.0 mg q8h.
iii. Cognitive impairment. Surprisingly uncommon. Studies show pain itself
impairs cognition and effective pain control with opioids improves it.
iv. Constipation. A chronic problem. Almost always requires adjunctive
treatment with DSS, Senokot, Dulcolax, among others.
v. Itching. Not an allergic response. May be related to histamine release
and may respond partially to anti-histamines.
vi. Sweating. Can be a chronic problem.
vii. Myoclonic jerks. Often occur at night; often responds to clonazepam.
e. Addiction
i. Definition: continued use of a psychoactive substance despite harm (bio-
logic, psychological, social). Implies loss of control.
ii. Rare in treatment of pain unless there was pre-existing addictive dis-
ease. Pseudo-addiction may be more common. Defined as drug seeking
due to inadequate analgesic pain control.
iii. Often confused with dependence, defined as a physiologic state induced
by the chronic use of a psychoactive substance, and associated with an
abstinence syndrome upon abrupt termination or rapid decrease in that
substance. Dependence will occur in most patients on LTOAT, but it is
not a reason to withhold opioid treatment.
d. Tolerance. Common at initiation of treatment. Rarely progressive. More com-
mon is "pseudo-tolerance," which I define as increasing need for the opioid
analgesic due to either increase activity and function or to disease progression.
e. Fear of sanctions. Treatment of pain now a national priority. LTOAT is good
medical care in well selected patients. Need to perform regular follow-ups
and "good faith exams," and have adequate chart notes that document in-
formed consent (need not be a contract), compliance, response, side effects.
f. EHieaey. This is the major issue. Do opioids administered long-term provide
adequate analgesia? The answer is yes-for a small number of well selected
patients. Many published articles specifically related to spine including:
i. Jamison: Randomized open label comparison of oxycodone 5 mg qid to
continuous release morphine to naproxen. Found better pain control, im-
proved mood, but no better function. Study limited by fixed dose regi-
mens.
ii. Schofferman: Prospective I year evaluation of 33 patients with chronic
refractory low back pain. There were 5 unable to tolerate LTO, leaving
28 who completed trial period. Of the 28, 7 had no benefit and 21 had
good relief. There were significant improvements in pain and function
that persisted at one year in the LTOAT successes compared with the
The Use 01 Medications lor Low Back Pain 139
drop-outs and failures. Improvement was sustained at one year. Overall

treatment success was 21 of 33 patients.
4. Clinical (versus pharmacological) classification of opioids by potency
a. Weak: codeine, dihydrocodeine, pentazocine, hydrocodone. These drugs may
have a ceiling effect.
b. Potent: morphine, meperidine, methadone, levorphanol, hydromorphone,
fentanyl, and others. These drugs do not have a ceiling effect. Although one
drug may be more potent than another on a milligram for milligram basis,
equivalent analgesia can be obtained from each with proper dosing. Some
patients may respond better to one opioid than another, and therefore serial
trials may be necessary.
5. Selection of patients for LTOAT
a. Well established patient
b. Well defined structural or neuropathic pathology
c. Pain and impairment consistent with pathology
d. No significant psychopathology
e. No history of addictive disease
f. No serious medical conditions that might interfere with therapy
g. Good response to therapeutic trial
6. Choice of opioid for long-term treatment. There are at least five opioids well
suited for chronic use-continuous release forms of morphine, oxycodone, and
fentanyl or the long-acting drugs methadone and levorphanol. IMPORTANT:
Meperidine (Demerol) is virtually never indicated for long-term use. There is the
potential for accumulation of its very toxic metabolite, normeperidine, which is
neurotoxic and can produce agitation, tremors, confusion, and seizures.
Pentazocine is not a good choice either. Higher incidence of psycho mimetic
side effects. Partial antagonist may precipitate abstinence syndrome if given to
patient already on other opioids.
a. Morphine
i. Continuous release (MS-CR) preferred for chronic pain. Brand names in-
clude MS-Contin, Oramorph, and Kadian
ii. Available as 15, 30, 60, 100, 200 mg sizes
iii. Duration of analgesia: 8 to 12 hours depending on brand of drug and pa-
tient factors
iv. Immediate release morphine (MS-IR) for rescue doses for breakthrough
pain (liquid or tablets available).
b. Oxycodone
i. Continuous release. Brand name is Oxycontin
ii. Available as 10, 20,40,80 mg sizes.
iii. Duration of analgesia: 8 to 12 hours
iv. Very, very expensive
v. Immediate release oxycodone for rescue doses for breakthrough pain.
Available as 5, 15, 30 mg sizes.
vi. Has become the "drug du jour" of abuse; not usually seen in pain pa-
tients, but in true "addicts." Deaths reported from IV use or inhalation of
crushed Oxycontin.
c. Methadone
i. Long-acting drug
ii. Very inexpensive
iii. Takes 5 to 7 days to reach steady state.
140 The Use 01Medications lor Low Back Pain
iv. Metabolites may contribute to analgesia.

v. Available as 5 and 10 mg sizes; a 40 mg wafer is available on special
order.
d. Fentanyl
i. Continuous release through transdermal patch. Brand name is
Duramorph.
ii. Available as 25, 50, 75, and 100 micrograms per hour sizes
iii. One patch lasts 3 days
e. Levorphanol
i. Long-acting drug. Brand name is Levodromoran.
ii. Available only as 2 mg size.
iii. Duration of analgesia: 6 to 8 hours
7. Intrathecal opioids (ITO). Reserved for patients with effective analgesia with
oral or transdermal opioids, but in whom side effects limit their use.
IV. Muscle Relaxants

A. Overview.
1. One of the most frequently prescribed drugs for acute low back pain.
2. Muscle spasms may be a primary problem in acute low back pain, although the
muscle pain and spasm are usually precipitated by an anulus tear or other
problem.
3. Muscle spasm is rarely if ever the cause of chronic low back pain, but may con-
tribute to the overall pain and impairment.
4. Muscle relaxant drugs do not appear to selectively relax tight muscles. Most
drugs appear to act via a central effect.
a. Most muscle relaxants are sedating.
5. There appears to be a high incidence of dependence on muscle relaxants when
they are used for long periods of time.
B. Efficacy
1. Demonstrated to be better than placebo in acute low back pain.
a. Up to 10 to 14 days
b. Cyclobenzaprine and baclofen have most support in better studies.
2. No adequate comparisons between drugs in literature.
3. No data to demonstrate any effect in chronic low back pain.
e. The muscle relaxants used most commonly are shown in Table 3.
D. Detrimental effects
1. Sedating
2. Physical dependence with a withdrawal syndrome upon abrupt discontinuation.
3. Rebound insomnia patients who take muscle relaxants at night.
Table 3. Commonly Used Muscle Relaxants

Generic name Brand Name Common Doses
Cyclobenzaprine Flexeril 10 mg @hs to 10 mg tid
Carisoprodol Soma 350 mg tid and h.s.
Baclofen Lioresal 10 mg to 20 mg q6h
Methocarbamol Robaxin 500 mg to 750 mg tid
Chlorzoxazone Parafon forte 250 mg to 500 mg tid
Orphenadrine Norflex 100 mg bid
The Use ofMedications for Low Bad, Pain 141
E. Possible role in "fibrositis"

1. Diagnosis itself is controversial.
2. Cyclobenazprine may reduce the pain, improve the sleep, and decrease the
number of tender trigger points.
a. May be due to the fact that cyclobenzaprine is a tricyclic compound similar
in structure to amitriptyline and efficacy is due to the improved sleep or
analgesic effects of amitriptyline.
F. Empiric guidelines based on literature review
1. Muscle relaxants may be useful for 5 to 7 days for acute low back pain.
2. Probably best to combine with NSAID.
3. Discontinue muscle relaxant after 10 to 14 days.
4. Recent data suggest botulinum toxin A injections may be useful.
5. Use physical therapy and massage to treat muscle spasm after the acute phase
has passed.
SUMMARY OF THE USE OF MUSCLE RELAXANTS

• Efficacy fairly well established for acute low back pain; may be useful up to 14
days.
• No efficacy demonstrated for chronic low back pain.
• No good comparative data; best data support cyclobenzaprine and baclofen.
• Muscle relaxants are sedating and may produce dependence, especially with long-
term use.
V. Sedative-Hypnotics
A. Overview
1. Limited role in low back pain
2. Not analgesic
3. May produce dependence with prolonged use
a. Worsened insomnia when drug is stopped
4. Sleep produced is not physiologic
B. Sleep disturbance
1. Common in chronic pain
a. Multifactorial: pain, depression, sleep mechanics, sleep surface
2. Sedating antidepressants better choice in most instances
3. Ambien best choice of hypnotic
a. Closest to normal sleep
b. Least likely to produce dependence or rebound insomnia
VI. Antidepressants
A. Overview
1. Useful drugs for
chronic low back pain; no indication in acute low back pain
a. Promote sleep
b. Improve pain, especially extremity pain
i. IMPORTANT: Mechanism of action for pain control NOT related to pres-
ence or absence of depression.
ii. Noradrenergic tricyclic drugs preferred (nortriptyline, amitriptyline, de-
sipramine)
c. Treat depression
B. Mechanism of action
1. Block presynaptic reuptake of monoamine neurotransmitters such as serotonin
or norepinephrine, thereby increasing their action at the postsynaptic receptor
142 The Use of Medications for Low Bock Pain
sites. Knowing the relative potency for neurotransmitter or receptor blockade of

each antidepressant allows the clinician to predict the side effect profile and is
shown in Table 4.
a. Norepinephrine appears more important for pain control.
b. Some drugs act on other bio-amines such as dopamine.
2. Also may block other receptor sites, which accounts for other benefits and
many of the side effects.
C. Side effects common. May interfere with compliance if medication is not titrated
carefully. Type varies with the specific drug or drug class (Table 5).
1. May be used to patient's advantage
a. Antihistamine effect is sedating. May help with sleep.
D. Efficacy
1. Low back pain without depression
a. Definitely effective compared with placebo.
b. About 50% of patients get 25% reduction in low back pain.
c. Nortriptyline has best data to support its use.
2. Low back pain and depression
a. Efficacy probably established. Nortriptyline, amitriptyline, desipramine, dox-
epin, imipramine all probably equal.
3. Neuropathic leg pain
a. Noradrenergic drugs most effective.
b. 1/3 of patients get 50% relief.
4. Depression (primary or secondary)
a. Definitely effective
i. No difference in efficacy or side effects between paroxetine, fluoxetine,
and sertraline for treatment of depression.
ii. Serial trials may be necessary. About 20% of patients need to change
SSRls before finding best one.
iii. May be less drug-drug interactions with citalopram.
b. Antidepressants most effective when combined with psychotherapy.
E. Specific drugs
1. Tricyclic antidepressants
a. Specific drugs
i. Nortriptyline: high efficacy; moderately sedating
ii. Amitriptyline: high efficacy, highly sedating; perhaps best choice for
pain plus sleep disturbance in otherwise healthy patient
iii. Desipramine
b. Side effects
i. Sedation. Especially useful if there is sleep disturbance.
ii. Dry mouth
Table 4. Biochemical Activity of Commonly Used Antidepressants

Norepinephrine Serotonin Alpha-adrenergic
Amitriptyline 1 2 )
Doxepin 2 1 2
Desipramine ) 0 1
Nortriptyline 2 <1 1
Fluoxetine o ) 2
Trazodone 0 1 2
The Use ofMedications forLow Bock Pain 143
Table S. Relative Side ERects of Commonly Used Antidepressants

Sedation Insomnia Orthostasis Anticholinergic·
Amitriptyline 3 0 3 3
Doxepin 3 0 3 2
Desipramine 1 1 1 1
Nortriptyline 2 0 1 1
Fluoxetine 0 2 0 0
Trazodone 3 0 2 0
Scale: 0 is no effect, 1 is mild, 2 is moderate, 3 is major.
"Anticholinergic side effects include blurred vision, dry mouth, sinus tachycardia, constipation, urinary reten-
tion, and memory dysfunction.
Based on Potter WZ, Rudorfer MY, Husseini M. The pharmacologictreatment of depression. N Engl J Med
1991 ;325:633-642.49.
iii. Weight gain

iv. Orthostatic hypotension
v. Urinary retention. May be helped with addition of Urecholine.
vi. Constipation
vii. Cardiac conduction changes. Avoid use in patients with cardiac disease.
If any doubt, obtain cardiology consult.
viii. Sexual dysfunction
c. Dosing guidelines (nortriptyline, amitriptyline, desipramine)
i. Initial dose: 10 mg at bedtime
ii. Titrate upward in 10 mg increments every 3 to 5 nights as tolerated to
50 mg. Then titrate in 25 mg increments.
iii. Goal is at least 50 mg and preferably 75 to 100 mg. May stop at lower
dose if effective with respect to target symptom (sleep, pain, depression).
iv. Measure blood level morning after (especially desipramine, but also nor-
triptyline) if any question of absorption or toxicity.
2. Selective serotonin reuptake inhibitors (SSRIs)
a. Drugs
i. Fluoxetine (Prozac)
ii, Citalopram (Celexa)
(a) Very few if any drug interactions
iii. Paroxitine (Paxil)
iv. Sertraline (Zoloft)
v. Others
b. Common side effects (no difference among drugs)
i. Weight loss (especially fluoxetine); occasionally weight gain
ii. Sexual dysfunction
iii. Nausea
iv. Headache
c. Dosing guidelines (for fluoxetine, citalopram, paroxitine).
i. Begin at 10 mg (or 20 in very robust patients) in morning.
ii. Increase to 20 if no response in 2 to 4 weeks.
iii. Usual dose is 20 to 40 mg per day in single dose.
3. Other antidepressants
a. Bupropion (Wellbutrin)
i. "Energizing" antidepressant
144 The Useof Medications forLow Back Poi"
ii. Often useful in patients on potentially sedating drugs such as opioids,

anti-epileptics, etc.
iii. Also useful to help patients to stop smoking.
iv. Be sure to use sustained release form.
v. Wellbutrin-SR 150 mg daily; usually in morning
b. Ventazaline (Effexor)
i. Gaining more favor.
ii. May be effective for pain.
iii. Effective for depression and sleep disturbance
iv. Start at 38.5 mg at bedtime for one week. Then increase to 75 mg at bed-
time.
c. Trazadone
i. Only use may be for sleep.
ii. No significant analgesia
iii. Fair at best for depression
iv. Dose is 50 to 150 mg at bed time.
d. Many others
SUMMARY OF USE OF ANTIDEPRESSANTS FOR LBP

• Definitely useful when pain and depression coexist.
• Tricyclic antidepressants appear most useful for pain.
• For axial skeletal pain alone, studies are mixed, but sufficient number suggest
enough benefit to try.
• Definitely useful for some patients with neuropathic pain.
• Start at low doses and titrate up slowly.
• SSRIs, buproprion, ventazaline most useful for depression
• No therapeutic serum range established for treatment of pain.
VII. Anticonvulsants
A. Overview
1. Often very useful for neuropathic pain.
a. Damaged nerves from surgery; or prolonged compression from spinal steno-
sis or HNP
b. Arachnoiditis
2. Not usually useful for low back pain.
B. Most useful drugs
1. Gabapentin (Neurontin)
a. Equally efficacious with nortriptyline with less side effects
b. Never shown to be useful for nociceptive low back pain, but used too often
for this type of pain.
c. Side effects: sedation, ataxia
d. Dosing: Begin at 300 mg at bedtime; increase in 300 mg twice daily for 5
days, then 300 mg every 8 hours. Pause at 900 mg per day, which usually is
the minimum effective dose. If no response after 2 weeks, titrate up to max-
imum dose of 3600 mg per day.
e. Pill sizes: 100,300,400,600 mg
2. Clonazepam (Klonopin)
a. Useful for
i. Neuropathic pain
ii. "Myoclonic" jerks, a possible side effect of opioids
iii. Substitution detoxification from other benzodiazepines
The Use ofMedications far Low Boclc Pain 145
b. Side effects: sedation

c. Dosing: Begin at 0.5 to 1.0 mg at night; gradually increase dose to a maxi-
mum of 6 mg per day for neuropathic pain
3. Topiramate (Topamax)
a. Sometimes useful for neuropathic pain
b. Side effects: sedation, weight loss, kidney stones
c. Dosing: Begin at 25 to 50 mg at night. Titrate upward over 6 weeks to a
maximum dose of 400 mg per day in two divided doses.
4. Carbamazepine (Tegretol)
a. Begin at 100 mg twice daily
b. Increase by 100 to 200 mg every 2-3 days until pain control or side
effects.
c. Target dose is about 600 mg per day.
i. Periodically measure blood level.
ii. Target level: 5 to 10 micrograms/ ml. Toxicity may be seen above 8 mi-
crograms; benefit to toxicity has a narrow range. Start to measure at 400
mg per day.
d. Side effects
i. Nausea and vomiting
ii. Sedation
iii. Small but real risk of bone marrow suppression
5. Valproate
a. May be useful for neuropathic pain
b. Begin at 250 mg twice daily and increase 125 to 250 mg per day each week.
Maximum daily dose is 2500 mg per day.
c. Monitor blood levels and adjust to maintain dose of 50 to 100 micro-
grams/ml measured before morning dose.
d. Drowsiness may limit usefulness.
C. Occasionally useful
a. Phenytoin (Dilantin). I have been disappointed with this drug for neuro-
pathic pain.
b. Mexilitine
VIII. Antihistamines
A. Antihistamines are often used in pain management, although there are usually
better choices. Most often, the side effects are responsible for the efficacy.
B. Analgesic properties
1. Mechanism of action not known, but some direct and adjuvant analgesic ac-
tion shown for hydroxyzine, diphenhydramine.
2. Most often used in conjunction with opioids.
a. "Opioid sparing" effect; but is this of any value?
b. Hydroxyzine 75 to 100 rng 1M is equi-analgesic to morphine 8 mg.
i. No evidence for analgesia or opioid sparing at lower doses.
c. Case reports of responses to diphenhydramine 50 mg orally every 6 h
C. Hypnotic properties
1. Diphenhydramine often used to induce sleep in the elderly, but this may not
be safe. May cause confusion, disorientation.
D. Antiemetic
1. Somewhat effective for nausea.
2. Hydroxyzine and diphenhydramine
3. Part of benefit of prochlorperazine is its anti-histamine effect.
146 The Use of Medications for LowBacle Pain
E. Anti-histamine
1. Anti-pruritic. Decreases itching; may be effective for opioid-induced pruritus.
a. Opioid-induced histamine release and itching.
F. Anxiolytic
a. Probably minimally effective, but there are more specific drugs
SUMMARY OF THE USE OF ANTIHISTAMINES

• At commonly used oral doses, there is minimal enhancement of analgesia or opioid
sparing
• Antihistamines may cause sedation and deterioration of mental performance, espe-
cially in the elderly.
IX. Stimulants
A. Available medications
1. Methylphenidate
a. Useful to treat opioid-induced sedation. 10 to 20 mg twice daily with grad-
ual dose increase.
b. Can be useful as an antidepressant.
c. Probably acts synergistically with opioids.
2. Amphetamines
a. Shown to act synergistically with opioids for analgesia.
3. Caffeine
a. 65 mg enhances analgesia of over the counter analgesics to a meaningful
degree.
b. Direct analgesic effect as well.
B. Possible usefulness
1. Co-analgesic
2. Stimulant
3. Antidepressant
C. Mechanism of action
1. Not well established.
X. Miscellaneous Drugs
A. Capsaicin cream
1. Useful for neuropathic pain
2. Occasionally useful for focal nociceptive pain
B. Lidoderm transdermal patch
1. 50fa transdermal patch placed over painful area
2. May work best for neuropathic pain, but occasionally helpful for very focal no-
ciceptive pain
3. Worn 12 hours on, 12 hours off
C. Glucocorticosteroids
1. Useful for severe flairs of low back pain
2. I prefer prednisone over Medrol dose packs (dose too low; duration too short);
dexamethasone may be good alternative.
a. Begin prednisone at 20 mg every 8 hours for 3 days; then taper off over
about 14 days to O.
XI. Clinical Vignettes

A. 34-year-old worker hurts his back lifting at work. He has moderate to severe low
back pain, but no neurological deficit.
The Use of Medications for Law BacIc Pain 147
1. Sees M.D., who prescribes carisoprodol and recommends bed rest.

2. Sees second M.D. because pain is still severe, who prescribes MS-Contin and
nortriptyline.
3. Both doctors could have done better.
a. First doctor could have prescribed an NSAID and a short-acting opioid such
as hydrocodone, encouraged activity.
b. Second doctor over-reacted. If pain control poor, at this early stage, use a
short-acting more potent opioid such as oxycodone. Too soon to use an
antidepressant for pain.
B. 46-year-old woman has had chronic low back pain and seen many doctors. She
has low back pain, muscle spasms, poor sleep, and poor function. Falls asleep dur-
ing day.
1. Current medications: Dalmane for sleep, Ativan for muscle spasms, Neurontin,
Vioxx, and Vicodin for pain.
2. Recommend:
a. Discontinue Dalmane (excess daytime sedation, long half-life), Neurontin (no
evidence for neuropathic pain), and Vicodin (poor choice for chronic pain).
b. Try a time contingent continuous release or long-acting opioid for nocicep-
tive pain.
c. Try a sedating antidepressant such as nortriptyline or amitryptiline for pain
and sleep.
C. 57-year-old man with chronic low back pain. His primary care M.D. faxes over his
lab tests; he is slightly anemic and has slightly elevated Lf'Is. You have been pre-
scribing Vicodin for periodic use, but note he has been taking 8 to 10 per day. His
is also taking Tylenol over the counter for his abdominal pain and headaches.
1. He may be drinking excessively (anemia, abnormal lab).
2. He is taking excess quantities of acetaminophen (650 mg in each Vicodin over
the counter).
3. Recommend
i. Refer to chemical dependence physician.
ii. Stop Vicodin and use oxycodone plain.
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1 - - - - - - - -10
Physical Therapy Options for Lumbar
Spine Pain
Cary C. Bucko, M. PT, Jeffrey L. Young, M.D., M.A., F.A.C.S.M.,
Andrew 1. Cole, M.D., F.A.C.S.M., Steven A. Stratton, Ph.D., PT, ATC,
andJoel M. Press, M.D., F.A.C.S.M.
Key Points
• Rehabilitation of the primary site of injury and secondary sites of dysfunction
optimizes outcome by restoring function and minimizes the chance of recurrence.
• Prolonged bedrest decreases muscle strength, flexibility, cardiovascular fitness, bone
density, and disc nutrition; it also increases spinal segmental stiffness and depression.
Therefore, no more than 2 days of absolute bedrest is recommended for non-specific
low back pain. Relative rest is preferred.
• Failure of conservative care is the most common reason for surgical intervention for
low back pain. If the quality of conservative care is not optimal, more patients may be
selected for surgical intervention.
• Rehabilitation programs must be customized for each patient's lumbar spine dysfunction.
Customized rehabilitation programs improve outcome.
• A comprehensive rehabilitation program corrects soft-tissue inflexibilities and
improves strength, endurance, and power in the involved spinal segments and the
entire kinetic chain.
• A comprehensive rehabilitation program ensures that rehabilitation progresses beyond
the absence of symptoms; absence of symptoms does not necessarily imply normal
function, nor does normal function require the absence of pain symptoms.
• No one component of the rehabilitation program should be used in isolation but rather
in concert with other appropriate components.
• Protracted passive treatment places the patient in a dependent role and becomes
counterproductive to proceeding with participatory function-oriented and ultimately
independent care.
I. Background
A. Epidemiology of lumbar spine pain-implications
I. 60-90% lifetime incidence and 5% annual incidence.
2. Peak incidence at 40 years old; 12-26010 children and adolescents experience
low back pain.
3. 90% of cases resolve without medical attention in 6-12 weeks; 40-50% of pa-
tients are symptom free within 1 week; and 75010 with sciatica have relief of
pain at 6 months.
4. 70-90% of patients have recurrent episodes.
5. Despite symptomatic improvement, anatomic and functional adaptive changes
151
152 Physical Therapy Options forLumbar Spine Pain
may increase the chance of reinjury. The musculoskeletal demands of certain

activities may precipitate an episode of low back pain (LBP).
a. A comprehensive rehabilitation program must be initiated immediately so
that all aspects of the injury complex are thoroughly rehabilitated and func-
tion improves rapidly and safely.
b. The rehabilitation program must be based on an understanding of the
unique biomechanical stresses placed on the lumbar spine and its entire ki-
netic chain.
B. Why rehabilitate?
1. To resolve most rapidly the clinical symptoms and signs created by primary
lumbar spine injury so that active treatment can be initiated and the deleterious
effects of inactivity minimized.
a. Prolonged bedrest decreases muscle strength, flexibility, cardiovascular fit-
ness, bone density and disc nutrition; it also increases spinal segmental stiff-
ness and depression.
i. Complete bed rest results in a loss of 1- 3% of muscle strength per day or
10-1 5% per week. Therefore, no more than 2 days of absolute bedrest is rec-
ommended for nonspecific LBP.
ii. Relative rest allows short periods of rest between activities and helps to
minimize the deleterious effects of inactivity.
b. Encourage independence as soon as possible.
2. To optimize outcome by restoring function, returning to activity, and minimiz-
ing the chance of recurrence by rehabilitating both the primary site of injury
and secondary sites of dysfunction.
a. Up to 700/0 loss in trunk musculature strength after 6 months of lumbosacral
pain.
b. Rehabilitation continues beyond resolution of symptoms so that all other as-
pects of the injury complex are fully rehabilitated, including normalized
flexibility, strength, power, and endurance. However, it should be noted that
residual pain alone should not preclude the end of rehabilitation.
c. The single best predictor for new injury during activity is history of a previ-
ous injury.
d. Rehabilitation after lumbar spine injury may help to
i. Decrease intensity and duration of pain
ii. Decrease days lost from work or sport
iii. Increase productivity
3. To create a prehabilitation program based on the rehabilitation program so that
optimal physiologic and biomechanical fitness can be maintained and risk of
future injury minimized.
4. To minimize the need for surgical intervention.
a. Failure of conservative care is probably the most common reason for surgi-
cal intervention for LBP.
b. If the quality of conservative care is not optimal, more patients may be se-
lected for surgical intervention.
i. Programs that provide passive treatment only, such as modalities (e.g.,
ultrasound, electrical stimulation) and manipulation, are suboptimal.
(a) An exercise training component and body mechanics must be part of
a comprehensive rehabilitation program
(b) An optimal program teaches proper ergonomics and gives flexibility,
strength, and endurance to maintain the spine in the most optimal
biomechanical position during activity.
Physical Therapy Options lor Lumbar Spine Pain 153
ii, If a Physical Therapist is trained only in one or few physical therapeutic

techniques, all patients, no matter what the source of spine pain, receive
the same treatment ("cookie cutter" approach).
(a) Rehabilitation programs must be customized for each patient's indi-
vidual dysfunction.
(b) Customizing optimizes opportunity for successful rehabilitation out-
come.
II. Factors Influencing Rehabilitation Program Design and Progression

A. Few lumbar spine physical examination tests define the precise structure or struc-
tures that have been injured or cause pain.
B. The initial assessment is really a functional diagnosis because it is based on his-
tory, physical examination, and recognition of specific reproducible patterns of
painful motion.
C. Initial treatment techniques seek to minimize pain by avoiding painful patterns of
movement and expanding nonpainful patterns.
D. Reduction of pain is an important guide for measuring treatment success. If the pa-
tient fails to progress or reaches a plateau during rehabilitation, reevaluation is
imperative. Use of a Visual Analog Scale to self-report pain may be a helpful indi-
cator.
1. Further diagnostic testing (imaging, electrodiagnostic testing) may be required
so that specific pain control techniques can be used and the rehabilitation pro-
gram advanced.
a. Change of physical therapy techniques
b. Addition or change in oral medication
c. Fluoroscopically guided, contrast-enhanced diagnostic and therapeutic
spinal injection procedure (e.g., facet, selective nerve root, epidural, or
sacroiliac joint injection). If done under fluoroscopic guidance with anes-
thetic and contrast enhancement, the injection is both diagnostic (precisely
placed local anesthetic anesthetizes the presumed painful structure) and thera-
peutic (the steroid and possibly the anesthetic decrease or eliminate pain).
Often, experienced physical therapists can assist the physician in determin-
ing where to initiate the injection process.
2. Distinguish between low back pain and low back pain disability syndrome.
a. Low back pain disability syndrome is a product of painful musculoskeletal
injury and the patient's adaptation [i.e., psychosocial overlay is significant).
b. For this syndrome, consider psychological intervention in addition to physi-
cal therapeutic treatment.
III. Physiologic Basis of Rehabilitation

A. Muscle isthe largest Internal organ-approximately 400/0 of the human body.
I. Skeletal muscle is one of the target organs for comprehensive rehabilitation
programs.
2. Both muscular strength and endurance need to be developed.
3. Energy metabolism
a. Adenosine triphosphate (ATP) is the body's major energy store.
b. Two major metabolic pathways for ATP liberation
L Anaerobic pathway provides energy during short (seconds), intense ac-
tivity.
ii. Glycolytic/glycogenolytic system is important in first 1.5 minutes of in-
tense exercise and causes lactic acid production.
154 Physical Therapy Options lorLumbar Spine Pain
c. Oxidative system is most important for longer activity.

B. Types ofmuscular contractions and strength
1. Isometric
a. Despite muscular activity, there is no motion.
b. Useful during motions that require stabilization (e.g., holding a weight at
waist level, neither lowering or raising it).
2. Concentric
a. Muscle length is shortened during contraction.
b. Useful for accelerating motions (e.g., extending the knee while wearing an
ankle weight).
3. Eccentric
a. Muscle length is increased during contraction.
b. Useful for decelerating or controlling motions (e.g., slowly lowering an ankle
weight from knee level to the ground).
4. Isokinetic
a. Muscular contraction at constant velocity
b. Artificially created by special types of exercise machinery
c. Little proven relevance to real conditions
5. Plyometric
a. Contraction sequence during which rapid, eccentric contraction precedes
concentric contraction.
b. Especially useful for sports-specific rehabilitation; rarely used otherwise
(e.g., a high jumper lowers himself stretching his quadriceps and gluteal
musculature before accelerating up to the bar-theoretically to increase ulti-
mate force production).
6. Strength
a. Maximal force that can be generated during a single contraction (1 RM =
repetition maximum).
b. Force generation: eccentric contraction> isometric contraction> concen-
tric contraction.
7. Power
a. Amount of force generated per unit of time
b. Although strength is commonly discussed, power is the more important pa-
rameter, especially from a functional standpoint.
C. Aerobic fitness
1. Oxygen consumption (V02 ) increases in proportion to the intensity of exercise.
2. V0 2 is the product of cardiac output and arteriovenous oxygen difference
(AV02d).
3. V0 2 max (maximal oxygen consumption) is the best indicator of aerobic fit-
ness; it is the highest level of oxygen consumption achieved during exercise.
4. Individuals who are more fit recover more quickly from muscular injury.
5. Aerobic fitness may confer some protection against development of LBP.
6. Acute response to resistance (strengthening) exercises involves a much higher
blood pressure response than aerobic exercises, because of increased intramus-
cular pressure, increased peripheral vascular resistance, and use of the Valsalva
maneuver during lifting and straining activities.
7. The acute response to stretching exercises does not include significant escala-
tion of cardiorespiratory activity.
D. Exercise training
I. Specific Adaptation to Imposed Demand (SAID) Principle: the human body re-
sponds to given demands with specific and predictable adaptations.
Physical Therapy Options lor Lumbar Spine Pain lSS
a. Strength training causes development of larger, stronger muscles.
b. Aerobic endurance training increases oxidative capabilities of skeletal
muscle.
c. Flexibility exercises improve connective tissue pliability.
2. Exercise training parameters
a. Intensity: how difficult it is to exercise, typically in reference to the patient's
maximal effort.
i. For aerobic training effect, this is typically 40-85% of V0 2 max.
ii. For strength training, it is typically 25-95% of 1 RM.
b. Duration: how long the exercise session lasts.
i. For aerobic training, duration typically exceeds 15 minutes of continu-
ous exercise.
ii. Strength training sessions can last for hours because the lifting periods
are interspersed with breaks.
c. Frequency: how often exercise sessions are done.
i. For aerobic training, typically 3-6 times/week.
ii. For strength training, typically 3-5 times/week.
iii. Flexibility exercises may be done daily.
d. Mode: how the exercise is performed.
i. For aerobic exercise, patients with LBP may use eliptical trainers, stair
climbers, treadmills,aquatic-based exercises or other minimal impact
loading exercises.
ii. For strength training, patients may use elastic cords, free weights, ma-
chines, and the weight of their own body to perform isometric contrac-
tions.
E. Flexibility training for muscle
1. Increases the available range of motion of a joint or series of joints, makes the
patient feel less stiff, makes activities of daily living more comfortable, and
theoretically reduces biomechanical stresses placed through the joints.
2. Initial elastic stretch aligns collagen fibers; it reverses as soon as stretching
load is removed.
3. Further load elongates the collagen fibers. If applied for a prolonged period, the
fibers deform and retain a portion of the lengthened state.
4. Stretching should be maintained for at least 30 seconds so that a pulling, not
tearing, sensation occurs.
5. Rapid, high-force stretches result in tissue recoil but no prolonged tissue elon-
gation.
6. Overzealous stretching results in muscular soreness for> 24 hours
7. Warming of the area to be stretched improves collagen distensibility.
8. Upper and lower hamstring stretches (Figs. 1 and 2)
a. Use of a stretch cord facilitates the lower hamstring stretch while maintain-
ing the lumbar spine in a biomechanically stable position.
b. An example of a gastrocnemius stretch may be seen in Figure 3.
9. Flexibility usually improves over 1-2 months. If flexibility does not improve
adequately and noncompliance has been ruled out, consider persistent nerve
root or dural irritation as underlying cause of continued inflexibility.
F. Strength training
1. No single best method to improve strength.
a. All methods use some type of overload.
b. Increases in strength are associated with increases in cross-sectional area of
skeletal muscle and muscle hypertrophy.
156 Physical Therapy Options for Lumbar Spine Pain
FIGURE I. Hamstring stretch for the upper hamstring fibers.
c. More effective when muscle groups are rotated from session to session.
i. Arm and chest muscles are trained on alternate days from leg and back
muscles.
ii. Healthy men increase strength by 20-400/0 over 2-4 months.
iii. Apparent increases in strength during first 2 weeks of training are related
to neuromuscular retraining and more efficient recruitment of muscle
groups rather than to muscular hypertrophy, which occurs later.
(al Make sure the patient continues with home program.
(bl Make sure the patient has actually increased strength adequately be-
fore attempting safe return to activity.
d. Most regimens are based on a percentage of the 1 or 10 RM lifted.
i. At the outset 1-3 sets of lifting weight 8-12 times/week.
ii. Resistance increases no more than lO0f0/week.
FIGURE 2. Hamstring stretch to include the lower fibers. A towel or stretch cord facilitates keeping the
back in a protected position.
FIGURE 3. Gastrocnemius muscle stretch. Note that the knee joint is

extended. Isolated saleus stretch requires that the knee be bent while
the ankle is passively dorsiflexed.
2. Failure to progress may relate to

a. Improper technique
b. Too few (inadequate training intensity) or too many (excessive muscular fa-
tigue) lifts per session
c. Continued neurogenic strength loss
G. Aerobic training
1. If activity level is reduced beyond 1 week, aerobic conditioning decreases; V0 2
max decreases by 250/0 with 3 weeks bedrest.
2. 10-200/0 increases in V0 2 max with exercise training of 8-12 weeks duration is
common. Improvement in submaximal parameters and subjective increase in
endurance is typically observed earlier.
3. Exercise training effects
a. Improved metabolism of free fatty acids
b. Reduced body fat
c. Increased insulin sensitivity
d. Increased muscle blood flow
e. Increased maximal cardiac output
f. Increased V0 2 max
g. Lower heart rate for given level of exertion
h. Reduced blood lactate accumulation for given sub maximal level of exertion
i. Lower minute ventilation at submaximal level of exertion
4. Failure to improve aerobic fitness over 6-8 weeks commonly due to
a. Infrequent exercise sessions
b. Exercising at too Iowan intensity
c. Exercising for too short a period per session
IV. Rehabilitation Program

A. Rehabilitatian principles apply to all spine disorders in the acute, subacute, and
chronic settings for both nonoperative and surgical patients.
158 Physical Therapy Optionslor Lumbar Spine Pain
I. A comprehensive rehabilitation program ensures that rehabilitation progresses

beyond the absence of symptoms; absence of symptoms does not necessarily
imply normal function. Normal function can exist with pain as well.
a. A comprehensive rehabilitation program corrects soft-tissue inflexibilities and
improves strength, endurance, and power in the involved spinal segments and
entire kinetic chain. All supportive muscle groups must be trained as well.
b. The program also provides education and training for posture, body me-
chanics, and proprioception as well as supervised return to activity.
c. Patient education and understanding allow for the patient to be an active
participant in the rehabilitation process.
2. No one component ofthe rehabilitation program should be used in isolation but rather in con-
cert with other appropriate components.
B. Acute phase
I. Education and protection of injured tissue
a. The most important component of any back care program, including acute
injury
b. Proper body mechanics for movement and activities of daily living (e.g.,
sit/stand, bathe, toilet, drive)
c. Natural history of spine injury.
2. Physical modalities: little benefit ifused in isolation; help to control pain and in-
flammation while the spinal injury is given a period of relative rest.
a. Superficial cold (cryotherapy)
i. Decreases spasm, pain, and capillary blood flow.
ii. Skin cooled quickly but rate of cooling directly proportional to thickness
of overlying fat: 20-30 minutes.
iii. Cryotherapy Is preferable for acute spine Injury because both superficial heat
and cold control pain and spasm, but cryotherapy also decreases acute
inflammation.
iv. Contralndlcatlons
(a) Cold hypersensitivity
(i) Cold urticaria
[ii] Raynaud's phenomenon
(iii) Cryoglobulinemia
[iv] Paroxysmal cold hemoglobinuria
(b) Anesthetic skin
(c) Circulatory compromise
b. Superficial heat
i. Decreases spasm and pain but increases arterial and capillary blood
flow.
ii. Heating pads, hydrocollator, and whirlpool baths penetrate to a depth of
2 cm or less. Any deeper response to superficial heat is due to reflex
pathways.
iii. Contralndlcatlons
(a) Inability of patient to report sensation of pain
(b) Anesthetized areas
(c) Bleeding diathesis
(d) Regions of compromised circulation
(e) Acute inflammation
(tl Regions of acute trauma
c. Deep heat (diathermy)
i. Decreases spasm and pain, increases collagen distensibility (helping to
improve flexibility).
Physical Therapy Options far Lumbar Spine Pain 159
ii. Ultrasound most commonly used; microwave and shortwave rarely used
because of increased risks, equipment cost, and limited portability.
iii. Usually used for subacute or chronic injury if a heat modality is required.
iv. Contraindications
(a) Acute injury
(b) Fluid-containing cavities
(i) Uterus
[ii] Testes
(iii) Eyes
(c) Open physeal growth plates
(d) Unhealed fractures
(e) Region of acute disc herniation with radiculopathy
(f) Joint replacement containing methyl methacrylate
d. Therapeutic electrical stimulation
i. Decreases spasm, edema, pain, inflammation, and atrophy; increases cir-
culation to help remove inflammatory byproducts.
(a) High-voltage pulsed galvanic stimulation (HVPGS)
(b) Interferential electrical stimulation
(c) Minimal electrical noninvasive stimulation (MENS)
(d) Transcutaneous electric nerve stimulation (TENS)-usually used for
chronic pain but may also relieve acute pain.
(e) Percutaneous Neuro Treatment
ii, Best used during acute phase of rehabilitation
iii. Little benefit if used in isolation
iv. Contraindications
(a) Active bleeding sites
(b) Eyes
(c) Carotid sinus
(d) Cardiac pacemakers and defibrillators
(e) Mucus membranes
(f) Areas with metal close to skin
(g) Anesthetic areas
(h) Incompletely healed wounds
e. Accuscope and low energy lasers
i. Accuscope uses electricity to affect tissue healing.
ii. Low-energy lasers use monochromatic, coherent light to affect tissue
healing.
iii. Both modalities await well-controlled prospective studies to determine
mechanism of action and efficacy.
3. Medications: permit early and more rapid progression of rehabilitation by de-
creasing pain and/or inflammation.
a. Nonsteroidal antiinflammatory drugs (NSAIDs): studies do not specifically
demonstrate efficacy for low back pain.
b. Nonnarcotic and narcotic: acetaminophen plus NSAID enhances analgesia.
i. Narcotics for more severe acute pain-at adequate dose for pain relief on
time-contingent basis.
ii, Prolonged use of narcotics rarely indicated.
c. Muscle relaxants
i. Studies show short-duration, limited efficacy for low back pain.
ii, Central effect causes lethargy that may inhibit ability to participate in re-
habilitation.
d. Corticosteroids: pain relief from antiinflammatory action, oral or injected.
160 Physical Therapy Options forLumbar Spine Pain
4. Manual therapy techniques

a. Help to modulate pain; provide early controlled motion and stress to injured
lumbar spine segments.
b. Stimulation of mechanoreceptors and other nociceptive structures may help
to modulate pain and alter state of muscle contraction.
5. Mechanical therapy-traction
a. May provide pain relief by intervertebral distraction, stretching muscle and
other soft-tissue structures, and providing period of relative rest.
i. If symptoms are discogenic, traction may be applied in the prone position.
ii. If pain primarily involves posterior element, apply traction in supine po-
sition to unload posterior elements.
b. Types of traction
i. Horizontal split-table traction: traction force at least 25010 of body weight
to distract vertebral bodies.
ii. Auto traction: patient controls amount and direction of traction force.
iii. Inversion gravity traction: potential side effects include hypertension,
tachycardia, gastrointestinal reflux, and berry aneurysm rupture.
iv. Home pelvic traction may be applied with a 90/90 supine traction unit.
6. (orsets
a.
Help to control available range of motion.
b.
Provide proprioceptive feedback.
c.
Provide warmth to underlying soft-tissues.
d.
Decrease intradiscal pressure.
e.
Have significant potential for dependence; patients should be weaned as
rapidly as possible.
f. May decrease risk of future work-related injury if used properly and with
appropriate education.
7. Therapeutic exerdse: begins during acute phase because of deleterious effects of
prolonged bedrest. Determine initial movement pattern on basis of presumed
pathology, pain pattern, and pain centralization.
a. Extension bias-most commonly used with discogenic pathology; symptoms
decrease with repetitive extension on motion pattern testing and pain cen-
tralizes with extension (Fig. 4).
FIGURE 4. Spine extension exercise from prone position.

Physical Therapy Options for Lumbar Spine Pain 161
i. Extension exercises may reduce intradiscal pressure, allow anterior mi-

gration of nucleus pulposus, and increase mechanoreceptor input, thus
activating the pain gate mechanism.
ii. May increase symptoms in patients with large central herniation, forami-
nal stenosis, or foraminal herniation.
iii. Cardiovascular fitness may be initiated with aquatic stabilization train-
ing, eliptical machine, or other aerobic activity that places spine in neu-
tral to extension bias.
b. Flexion bias-most commonly used with posterior element pain; symptoms
decrease with repetitive flexion on motion pattern testing and pain central-
izes with flexion.
i. Flexion exercises may reduce facet joint compressive forces and provide
stretch to lumbar musculature, ligaments, and myofascial structures.
ii. May increase intradiscal pressure and exacerbate discogenic symptoms.
iii. Cardiovascular fitness may be initiated with aquatic stabilization train-
ing, stationary bicycle in slight lumbar flexion, stair climbing, or other
aerobic activity that places spine in neutral to flexion bias.
c. Neutral bias-most commonly used to treat central canal stenosis especially
when flexion or extension activities increase symptoms.
C. Subacute phase
Achieve full, pain-free range of motion of injured and adjacent motion segments
of lumbar spine and its kinetic chain.
Injury to ligaments, tendons, joint capsules, and fasdae may restrain motion and cause
pain. The mechanical properties of these tissues is determined by histologic com-
position (cells, fibers, and ground substance). The proportion of each determines
the tissue's mechanical properties. Collagen is the primary structure common to all
these tissues.
1. Myofasdal system
a. Fascia absorbs shock, transmits mechanical force, and exchanges metabo-
lites from fibrous elements to the circulatory and lymphatic systems. It sepa-
rates and supports muscles, allowing independent muscle function as well as
coordinated multimuscular function.
b. Loss of normal fascial gliding and increased cross-linking of fibers results in
loss of myofacial system mobility and secondary loss of spinal segmental ar-
ticular mobility and lower extremity flexibility.
c. Myofascial release techniques apply pressure and shear forces to fascial lay-
ers, improving elasticity and freedom of movement and decreasing pain.
2. Manual soft-tissue techniques that increase soft-tissue distensibility along lines of
physiologic stress promote proper alignment of collagen fibers during remodel-
ing and healing.
a. Provide graded tensile or compressive loads to connective tissue
i. Massage
ii. Fascial-tendon stretching
iii. Traction
3. Joint mobilization
a. Restores optimal joint mobility by applying forces at individually targeted specific motion
segment levels (versus connective tissue and myofascial system techniques
that restore soft-tissue mobility).
b. Graded I-V depending on depth and force of applied load.
i. I, II-oscillations within the painfree range of motion.
ii. III, Iv-larger-amplitude forces that move joint into restricted range of
motion and provide stretch.
162 Physical Therapy Options For Lumbar Spine Pain
iii. V-Low-amplitude, high-velocity manipulation that takes the joint to end

range of physiologic motion.
c. Benefit from mobilization and manipulation appears substantiated in the lit-
erature for specific subsets of patients with LBP.
d. No data support the role of repetitive long-term soft-tissue or articular mo-
bilization or manipulation for spine pain.
e. Manipulation may help certain subsets of patients to progress more rapidly
in the rehabilitation program.
f. Manipulation should never be used in isolation but rather in concert with other appropri-
ate rehabihtation components.
g. Protracted passive treatment places the patient in dependent role and be-
comes counterproductive to proceeding with participatory function-oriented
and ultimately independent care.
4. Exercise: dynamic lumbar stabilization training.
a. Goals
i. To control pain.
ii. To gain dynamic control of segmental spine and kinetic chain forces-
particularly torque.
iii. To optimize soft-tissue repair and regeneration.
iv. To eliminate repetitive motion segment injury and minimize chance of
acute dynamic overload.
b. Concepts
i. Neutral spine is the initial training position.
(a) Least painful and most biomechanically sound posture (Figs. 5 and 6).
(b) Loose-packed position that decreases tension on ligaments and joints.
(c) Allows more balanced segmental force distribution between disc and
facet joints.
(d) Close to the center of reaction and allows movement into flexion and
extension quickly.
(e) Provides the greatest functional stability with axial loading.
ii. Muscle "fusion" is an engram (cortically preprogrammed automatic multi-
muscular movement patterns activated without conscious control) for
neutral spine position.
(a) Developed through specific set of stabilization exercises.
(b) Allows patient to recruit spinal muscular stabilizers quickly and auto-
matically.
iii. Flexibility training allows patient to assume neutral position so that
strength can be developed to help maintain correct neutral position dur-
ing both static and dynamic conditions.
iv. While maintaining neutral position, exercises progress from static (e.g.,
supine or prone) to dynamic (e.g. standing, jumping, other motions).
v. Graded challenges to neutral position are created first by gravity, then by
therapist or assistive devices (e.g., Swiss ball) (Figs. 7-12). There is a sig-
nificant concentration on exhibiting adequate stability at each phase of
training before progressing on to the next most challenging level.
(a) These challenges progress from predictable to unpredictable (simulat-
ing, e.g. a blind side hit during football).
(b) Activity-specific retraining occurs by breaking down required motion
into individual component motions; the neutral position is trained for
each. Finally, the components are reassembled so that the entire mo-
tion uses dynamic stabilization techniques.
FIGURE 5. Left, Example of poor posture: cervicol copitolextension, increased cervical lordosis, retruded
mandible, rounded shoulders, increasedthoracickyphosis, increased lumbar lordosis, lockedknees, and
weightover heels.
FIGURE 6. Right, Correct neutral spine posture.
5. Cardiovascular fitness provides necessary aerobic and anaerobic fitness required

for activities and should be continued into subacute phase.
a. Cross-training in neutral spine position helps to maintain fitness while pro-
tecting healing motion segment.
b. Training for total body muscle strength, endurance, and power, specific
for demands of the patient's activity, should be combined with the spine
stabilization-strengthening program.
D. Other rehabilitation options
1. Aquatic rehabditation
a. Nonagitated water and whirlpool baths may allow relaxation of muscle but
are not efficacious as independent treatments for LBP.
b. Advantages of the aquatic environment
i. Graded elimination of gravitational forces allows training with comfort-
able and adjustable axial loads
ii. Challenges vertical posture because of refractive alteration of propriocep-
tive cues, which is depth-dependent
iii. Controls velocity because of water resistance, viscosity, buoyancy, and
training devices
iv. Increases range of training positions because of buoyancy
v. Enhances psychological outlook
vi. Attenuates pain, probably because of hydrostatic pressure, temperature,
and turbulence
164 Physico/Therapy Options for Lumbar Spine Pain
FIGURE 7. Abdominol strengthening exercise FIGURE 8. Neutral spine exercise in side-lie position.
while maintaining neutral lumbar and cervical
spine. Spine flexion > 30° is of no benefit for
abdominal muscles because the hip flexor mus-
cles are the major muscle group activated.
FIGURE 9. Neutral stabilization exercise. Hip FIGURE 10. Hip abductor strengthening with knees ex-
abductor strengthening with knees bent. tended.
FIGURE 11. Bridging exercise while maintaining

neutral spine position with a gym ball.
FIGURE 12. A and B, Progressively more advanced lumbar stabilization exercises

Ph)f5icol Therapy Options lor Lumbar Spine Pain 165
vii. Increases margin of error

viii. Earlier intervention during aerobic conditioning
ix. Speeds postoperative course
x. Potentially decreases risks of postoperative complications
c. Rehabilitation environment: land or water?
i. Dry to wet
(a) Minimizes dry risks associated with
(j) Axial and gravitational loads
(ij) Decreased bone density
(iii) Strength and proprioceptive deficits
(b) Establishes supportive environment
(c) Meets functional goals sooner
(d) Develops new activity
(e) Return to prior activity
(f) Earlier postoperative intervention
ii. Wet to dry
(a) Increases tolerance to axial and gravitational loads
(b) Increases challenge to strength deficit
(d) Increases challenge to proprioceptive deficit
iii. Wet only
(a) Dry environment exacerbates symptoms.
(b) Leads to exclusive preference for aquatic medium.
iv. Dry only
(a) Infectious disease (e.g., urinary tract infection, hepatitis) with incon-
tinence
(b) Certain skin infections
(c) Fear of water
(d) Chemical allergy
d. Contraindications
i. Fever
ii. Cardiac failure
iii. Urinary infections
iv. Bowel or bladder incontinence
v. Open wounds
vi. Infectious diseases
vii. Contagious skin conditions
viii. Excessive fear of water
ix. Uncontrolled seizures
x. Colostomy bag or catheter used by patient
xi. Cognitive or functional impairment that creates hazard to patient or oth-
ers in pool
xii. Severely weakened or deconditioned state that poses safety hazard
xiii. Extremely poor endurance
xiv. Severely decreased range of motion that limits function and poses safety
hazard
2. Other rehabilitation models
a. Various other rehabilitation models have been developed to treat LBP.
b. The superiority of anyone technique has not been scientifically validated.
c. Physical therapists familiar with various models and techniques can mix and
match techniques as needed for optimal rehabilitation. This avoids "cookie
cutter" approach that lessens chance of successfully rehabilitating patients
with different causes of LBP.
166 PhY5ical Therapy Option51or Lumbor Spine Pain
d. Partial list of models currently being used to treat LBP

i. Osteopathic model
ii. Norwegian model
iii. Australian model
iv. Cyriax model
v. Mennell model
vi. North American Institute of Manual Therapy (NAIOMT)
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,--------11
Manipulation
John J. Triano, D.C., Ph.D.
Key Points
• Interest in and utilization of spinal manipulation are growing.
• Evidence suggests that these procedures may be useful to control symptoms and
improve function for acute and subacute patients and for chronic patients with flare-
up.
• Back and leg pain patients may benefit provided there are no red flags and the patient
has pain that limits activity.
• On the average, the number of treatment sessions to maximum improvement for an
episode of back/leg pain is 8 with a range from 1 to 40.
• Major contraindications include undiagnosed loss of function (bowel, bladder, motor).
• One in 7 will experience a self-limiting minor soreness or increase of discomfort
within 24 hours of the initial treatment.
• Severe complications are very rare and consist of fracture (costal/vertebral) and cauda
equina syndrome.
• Evidence suggests that the skill in performance of procedures may affect outcomes.
I. Background
A. Medical interest in spinal manipulation as a remedy for some patient lower back
problems has grown rapidly in the past decade. Failure of the classical
pathoanatomical model of disease to adequately predict appropriate intervention
for back pain coupled with the growing use of chiropractic services independent
of medical recommendation drives this new attention.
B. The modern era of manipulation for spine related disorders began in 1975 with
the first scientific conference sponsored by the National Institutes of Health.
During the intervening three decades, more fundamental and clinical information
has accumulated on the appropriate use of spinal manipulation than ever before.
Although practiced in most countries in some form, the discussion of spinal ma-
nipulation continues to evoke strong emotional reactions by proponents and op-
ponents alike.
C. Two facts remain evident. First, evidence now supports the use of spinal manipu-
lation under far more circumstances than opponents often acknowledge and far
less than the claims of its extreme enthusiasts. Second, there are occasional, actu-
ally rare, severe complications when procedures are performed by unskilled
providers or under inappropriate conditions. However, the epidemiological data
are far less onerous than ardent opponents imply.
D. Like most debates, the practical truth for application of spinal manipulation lies
between the extremes of opinion. Current data suggest a prudent approach to be a
trial of manipulation for patients that meet the following criteria.
169
170 Manipu/ation
1. No red flag risks of serious illnesses such as primary spine tumor, metastatic
disease, spinal infection, or systemic disease.
2. No signs of progressive neurologic deficit to include loss of bowel or bladder
control and lower extremity neurologic deficit.
3. No clear evidence showing superiority of alternative treatments, for example,
epidural steroid injection for patients where primary radicular leg pain predom-
inates.
II. Applications
A. Disorders
1. Considerable confusion persists regarding the diagnoses best treated with ma-
nipulation. Much of the confusion resides with the persistent effort to tie treat-
ment to pathoanatomical terms and the development, only recently, of biome-
chanical knowledge of manipulable lesions and of treatment effects.
Traditionally, successful triage of patients relies more on descriptive character-
istics of patient presentations similar in nature to the classifications proposed
by the Quebec task force.
2. Matters are complicated further by the fact that the consensus on terminology
related to the manipulable lesion continues to evolve. Current terminology
more often is based on clinical discipline. Most frequently used terms include
joint dysfunction, subluxation, and functional spina/lesions (FSLj, a term that
follows from the logic of the smallest component of the spine retaining com-
plete functional characteristics being the functional spinal unit (FSU).
3. Primary disorder. The FSL may appear as a primary disorder associated with local
or remote symptoms. It is characterized by the findings listed below. Such pa-
tients often present with acute or chronic back complaints considered as having
mechanical back pain without abnormality on imaging.
4. Co-morbidity. The FSL may also present as a dysfunctional comorbid or compli-
cating factor along with other pathology including disc bulge or protrusion, de-
generative disease and spondylosis, facet syndrome, spondylolisthesis, and
sprain/strain injury. Indeed, many patients with these disorders are benefited
symptomatically with manipulative procedures.
B. Diagnosis
1. Signs and Symptoms of the isolated FSL
a. Local back pain with or without pseudoradicular pain
b. Focal sensitivity to manual pressure
c. Local muscular hypertonicity with or without tender points
d. Limited joint compliance in mid-range position and / or end-range limita-
tions with pain on overpressure testing
e. Reproduction of symptoms with joint compliance or end-range motion testing
f. Local soft tissue edema
g. Altered local skin turgor, temperature, or color
2. FSL concurrent with other pathology may present as an isolated FSL described
above or as an irritation to the coexisting pathology with consistent signs and
symptoms.
3. Provocative testing
a. Physical maneuvers-application of controlled forces and moments to the
suspect joint that give comfort and relieve symptoms. Such maneuvers may
guide the selection of treatment procedures that match patient needs.
b. Joint blocks may be helpful in identifying the pain generator and quelling
local inflammatory responses that may be interfering with patient recovery.
Manipulation 171
c. Manipulation under joint analgesia (MUlA)-application of manipulation

procedures within the window of analgesia after performing a joint block
procedure. MUlA may be useful in managing patients where the sensitivity
of the joint prevents direct manipulation or where underlying chronic in-
flammation aggravated by weight-bearing activity is suspected.
4. Therapeutic Trials
a. Manipulation, like all other therapy, must be performed using sufficient
threshold, dosage, and duration.
i. Threshold is defined as application of the necessary and sufficient joint
load to effect a change in its behavior and symptoms. Threshold levels
are a function of patient joint stiffness and soft tissue viscoelastic prop-
erties. Assessment of tissue condition to guide application of the proce-
dures is a skill developed through experience.
ii. Effective dosage varies with patient cooperation on reducing aggravating
factors, performing recommended exercises to gain stability and condi-
tion severity. Initial treatment dosage generally is 2 to 3 sessions per
week.
iii. Duration, similar to dosage, is affected by patient cooperation, presence
of other pathology or degenerative change, and condition severity. As a
broad indication, patients are expected to respond with clinically signifi-
cant improvement within 2 weeks of initiating care.
iv. Across the literature, the average number of treatment sessions to maxi-
mum improvement is 8 with a range of approximately 1 to 40.
C. Imaging
1. Diagnostics. The primary use for imaging is the determination of other significant
pathology or structural anomaly that may influence the procedure selection,
modification, or treatment prognosis.
2. The isolated FSL has no characteristic, independent radiographic findings.
D. Indications
1. Persistent acute or subacute lower back pain with or without radiation to the
lower extremities
2. Flare-up of a previously stable chronic condition
3. Significant reduction in activities at work or of daily living
4. Physical findings consistent with Sections II, B, 1 and 2.
E. Contraindications
1. Few patients may not receive treatment with appropriately selected proce-
dures.
2. Specific contraindications include:
a. Cauda equina syndrome
b. Undiagnosed loss of bowel or bladder control
c. Undiagnosed progressive neurologic deficit
d. Severe osteoporosis
e. Endocrine disorders with systemic bone weakening effects
f. Primary or metastatic tumor
g. Procedures consistent with unstable motion
F. Complications
I. A number of common, self-limiting reactions «24 hours) occur in up to 12.5%
of cases after the initial treatment.
2. The most frequent is the development of new pain or discomfort in the region
where treatment is applied.
3. Local use of ice 15 minutes, q 1 hour, PRN controls musculoskeletal reaction.
172 Manipulation
4. Non-musculoskeletal reactions occur on an infrequent «SOlo) basis including

nausea, fatigue, and abnormal cutaneous thermal sensations.
5. Severe complications are extremely rare and consist of bony fracture (costal or
vertebral) or cauda equina syndrome. The world medical literature reveals 26
cases of cauda equina, 73010 occurring with manipulation under anesthesia.
These complications can be avoided through adequate diagnostic work up,
proper procedure selection, and modification of treatment methods.
III. Mechanisms
A. Functional spinal lesion (FSL)/subluxation/joint dysfunction
I. Overview
The FSL is defined as a local, uncontrolled mechanical response (a buckling
event) to a spine load affecting the functional spinal unit (FSU). Symptoms are
generated by altering the stress distribution within the joint structures during
normal activities and the development of local inflammatory and neurogenic
pain responses. The identity of the tissue that has been stressed by the buckling
event determines the clinical findings. FSLs often are symptom-producing sub-
components of degenerative disease, disc herniation, sprain/strain injury, and
other pathoanatomical entities.
a. Local eHeds. Local mechanical overload triggers a biochemical cascade
through excitation of neurogenic or non-neurogenic pain mechanisms.
i. Neurogenic pain is triggered through the release of neural stimulating
peptides including substance-P and II-amino acid neuropeptides. The
neurogenic inflammatory response that results causes further sensitiza-
tion to spine motion and loading.
ii. Non-neurogenic pain arises from release of vasoactive substances (e.g.,
bradykinin, serotonin, histamine, prostaglandins). Nerve ending sensiti-
zation lowers the response threshold again leading to sensitization to
spine motion and loading.
b. Remote eHects. Symptoms may arise at distal sites, including abdominal or leg
symptoms through two mechanisms.
i. Inflammatory processes or direct mechanical irritation of peripheral
nerve roots may occur that set up radicular symptoms.
ii. Central sensitization and somatic reflexes may set up spasm or secondary
hyperalgesia and myotendinoses that promote chronicity.
2. Biomechanical stability. Stability of the spine during function requires the system
to accommodate an extreme range of postures and loads while minimizing
stresses transmitted through the FSU tissue structures. Dynamic structural con-
trol is maintained by two sets of muscle operating in parallel: large torso mus-
cles traversing multiple articulations and smaller intrinsic spinal muscles.
a. Multi-articular (extrinsic) torso muscles-abdominal and flank muscles of the
torso and pelvis initiate and control trunk movements and transmit loads
between the upper body and the lower extremity.
b. Intrinsic spinal muscles-small muscles traversing one to two FSUs are re-
sponsible for maintaining local intervertebral coordination and biomechani-
cal stability that minimizes the tissue stress.
c. Intrinsic and extrinsic torso muscle coordination-failure to adequately time
recruitment that couples local intervertebral function within the FSU to pos-
tural tasks results in local development of sudden or cumulative overload.
d. Factors known to affect the muscular timing under dynamic loads include:
i. Fatigue
ii. Overload
Manipulation 173
iii. Rapid loading

iv. Vibration
3. Buckling events
a. Biomechanical studies demonstrate that under circumstances of loading the
FSU at its balance point, critical loading can be achieved under physiologi-
cal loading conditions.
b. Buckling is defined as a disproportionate displacement for the load applied
or task being performed. Its effect is to create local stress concentration
within the affected tissues of the FSU. Studies show buckling of individual
motion segments in flexion, lateral bending, and rotation or in combination.
Regional buckling of the lumbar spine as a unit has also been recorded.
c. The total local displacement observed during a buckling event is dispropor-
tionate to the task demand but often remains within the boundaries of nor-
mal range of joint motion.
d. Damage to just one disc potentiates buckling:
i. Damage lowers the threshold critical value of load required to cause
buckling.
ii. Damage allows the buckling vertebral system to reach maximum range
of motion under lower loading conditions.
e. Buckling has been observed, by chance, at the time of injury during fluoro-
scopic monitoring of the lumbar spine in weight lifters.
f. Biomechanical factors known to facilitate buckling include:
i. Prolonged static posture followed by an incremental load over the bal-
ance point.
ii. Rapid loading on the order of 500 pounds per second.
iii. Vibrating environments.
g. Post-buckling mechanical behavior remains biologically functional under a
new configuration of mechanical equilibrium and increased stress within the
FSU.
B. Manipulation procedures: Fundamentally, these procedures apply controlled loads
(forces and moments), while the patient remains passive, to alter mechanical be-
havior of the FSU and internal stress distributions. The purpose is to restore nor-
mal function and reduce symptoms associated with the FSL. The field of spinal
manipulation often has been treated incorrectly by the literature as being homo-
geneous. A few authors have attempted to segregate the procedures selected for
study by using categorical names such as Diversified, Gonstead, or Maitland
methods. Such classification, cumbersome in like manner to the naming of new
surgical techniques, is not helpful for clarifying manipulation mechanics or clini-
cal applications. A new classification system recently has been proposed that cen-
ters on the biomechanical characteristics of the procedures and the properties of
the tissues most affected by them. Modem methods incorporate both manual and
instrumented methods to mechanically augment procedural performance.
1. Classifications. Table 1 groups modem treatment methods commonly used into
biomechanical categories, type of procedure, application, loading method, and
speed (frequency or load rise time).
a. Unloaded spinal motion
i. Continuous passive motion (Fig. 1)
ii. Flexion distraction
b. Mobilization
c. High velocity, low amplitude procedures
i. Manual (Fig. 2)
ii. Mechanically assisted
174 Manipulation
Table 1. Classification of Manipulation Procedures

Frequency or
Category Type Application Loading Method Load Rise Time
Unloaded spinal
motion
Continuous passive Mechanical Periodic 0.03-0.53 Hz
motion (CPM)
Flexion-distraction Manual Periodic 0.05-0.50 Hz
Mobilization Manual Periodic 0.50-2.00 Hz
High velocity, low
amplitude ma-
nipulation pro-
cedures (HVlA)
Manual Manual Impulse 32-140 msec
Mechnicallyassisted
CPM' Manual + Periodic + impulse Superimposed
mechanical
Impulse hammers Manual + Impulse <20 msec
mechanical
Classification of procedures can be made according to quantifiable biomechanical parameters including
whether the procedure uses mechanical devices or manual application, involvesapplying periodic or transient
loads, and the frequency or rise time of load application. 'CPM may be combined with other procedures. The
resulting load superimposes impulse or mobilization procedures onto the CPM frequency. (Reprinted, with
permission, from Triano 2001, reference 24.)
(a) CPM motion assisted (Fig. 3)

(b) Impulse hammer devices (Fig. 4)
2. TIssue"characteristic dependent manipulation eHeets. The biomechanical effects of ma-
nipulation procedures appear to reflect an interaction between the primary tis-
sue properties (viscoelasticity and stiffness) and the modes of application (Fig.
5). Effects are apparent from studies of load magnitudes, speeds, and interseg-
mental displacement responses reported in the literature.
a. Affecting viscoelastic changes, for example, to alter local edema, requires
slower procedures that permit time-dependent shifts in fluid volume between
tissue compartments. Such procedures induce broad motions across a num-
ber of FSU segments.
FIGURE I. Continuous passive motion of the lumbar spine induces motion of the spine while in non-weight
bearing postures. Simple flexion-extension motion is depicted as an example of motion in the cardinal planes.
Combined motions may also be induced.
Manipulation 175
FIGURE 2. A high velocity, lowam-

plitude manual manipulation ap-
plied to the lumbosacral junction,
FIGURE 3. Mechanically assisted

manipulation to the lumbosacral
'oint can be used to modify spinal
Ioads acting on the target joint by
combining theseparate procedures:
passive motion with high velocity,
lowamplitude procedure,
FIGURE 4. Mechanically assist using an

impulse hammer device designed to pro-
duce very short duration impulse load, in
this case, to the lumbosacral articulation,
176 Manipulation
ADcul'" Vtlodty
FIGURE 5. Manipulation procedures plotting th~parameter of angular velocity against tissue resistance to ap-
plied loads as a function of viscoelastic and stiffness characteristics.
b. Affecting changes that rely on stiffness properties, as in intra-articular me-

chanical stress distributions, require more rapid methods than do not allow
sufficient time for fluid transfer between compartments. Such methods en-
hance relative motions between FSU elements.
3. Theoretical effects, both biomechanical and clinical, predicted by the theoretical
model described in III, B, 2 are supported by biomechanical observations of the
load amplitudes, rates, and resulting intersegmental displacements in cadaver
and in-vivo human studies. Clinical effects are supported by observations of the
biomechanical and clinical actions of continuous passive motion.
IV. Skill Mastery

A. Skill in performance is believed to be associated with clinical effectiveness. Studies
show that medical providers instructed but not practiced in procedures are unable
to perform them skillfully and that the clinical outcomes are not improved with
their use.
B. The performance of spinal manipulation/adjusting is a bimanual task requiring
high-levels of sensory/motor coordination under complex and varied conditions.
C. As a motor act, manipulation techniques consist of postural and motion sequenc-
ing. Consensus processes define the following characteristics of a skillful manipu-
lation:
1. Fast
2. Forceful
3. Comfort
4. Confident
5. Precise
D. Skilled performance can be evaluated by measurement of mechanical parameters
related to procedural force/moment amplitude, speed, and duration.
V. Outcomes
A. Over 50 randomized trials of spinal manipulation and a score of meta-analyses
have now been completed. Control groups have included watchful waiting, exer-
cise, physiological therapeutics, and medication.
Manipulation 177
B. Effect sizes may be used to combine the results of studies with disparate outcome
measures. Effect sizes greater than 0.3 indicate that the change in clinical status as
a result of treatment clinically relevant.
1. Acute low back pain-effect sizes from various studies range from 0.4 to 1.0.
2. Acute sciatica-a single study suggests an effect size of approximately 0.5.
3. Chronic low back pain-the range of effect size from the literature is 0.3 to 0.8.
References
I. Ashton-Miller JA, Schultz AB. Biomechanics of the Human Spine. In: Mow Ve, Hayes We, eds. Basic
Orthopedic Biomechanics, 2nd ed. Philadelphia: Lippincott-Raven, 1997:353-393.
2. Bronfort G. Chiropractic versus general medical treatment of low back pain: A small scale controlled
clinical trial. Am J Chiro Med 1989;2:145-150.
3. Bronfort G. Efficacy of manual therapies of the spine. Thesis/Dissertation, Vrije Universiteit, EMGO
Institute, 1997, 1-186.
4. Bronfort G. Spinal manipulation: Current state of research and its indications. Neurol Clin 1999;17:
91-111.
5. Cohen E, Triano JJ, Mcgregor M, Papakyriakou M. Biomechanical performance of spinal manipulation
therapy by newly trained vs. practicing providers: Does experience transfer to unfamiliar procedures?
J Manip Physiol Ther 1995;18:347-352.
6. Cohen J. Statistical Power Analysis for the Behavioral Sciences, 2nd ed. 1988,8-14.
7. Haldeman S. Presidential address, North American Spine Society: Failure of the pathology model to
predict back pain. Spine 1990;15:718-724.
8. Haldeman S, Carey P, Townsend M, Papadopoulos C. Arterial dissections following cervical manipula-
tion: The chiropractic experience. Can Med Assoc J 2001 ;165:905-906.
9. Haldeman S, Kohlbeck FJ, Mcgregor M. Unpredictability of cerebrovascular ischemia associated with
cervical spine manipulation therapy. A review of sixty-four cases after cervical spine manipulation.
Spine 2002;27:49-55.
10. Haldeman S, Kohlbeck FJ, Mcgregor M. Risk factors and precipitating neck movements causing verte-
brobasilar artery dissection after cervical trauma and spinal manipulation. Spine 1999;24:785-794.
11. Haldeman S, Rubinstein SM. Cauda equina syndrome in patients undergoing manipulation of the
lumbar spine. Spine 1992;17: 1469-1473.
12. Haldeman S, Rubinstein SM. Compression fractures in patients undergoing spinal manipulative ther-
apy. JMPT 1992;15:44-48.
13. Haldeman S, Rubinstein SM. The precipitation or aggravation of musculoskeletal pain in patients re-
ceiving spinal manipulative therapy. J Manip Physiolog Ther 1993;16:47-50.
14. Mcgregor M, Haldeman S, Kohlbeck FJ. Vertebrobasilar compromise associated with cervical manipu-
lation. Top Clin Chiro 1995;2:63-73.
15. Mootz RD, Haldeman S. The evolving role of chiropractic within mainstream health care. Top Clin
Chiro 1995;2:11-21.
16. Pickar JG. Response of muscle proprioceptors to spinal manipulative-like loads in the anesthetized
cat. J Manip Physiol Ther, in press.
17. Rechtien JJ, Andary M, Holmes TG, Wieting JM. Manipulation, massage, and traction. In: Delisa JA,
Gans BM, eds. Rehabilitation Medicine: Principles and Practice, 3rd ed. Philadelphia:
Lippincott-Raven, 1998:521-552.
18. Schultz AB. Biomechanics of the human spine and trunk. In: Skalak R, Chien S, eds. Handbook of
Bioengineering. New York: McGraw-Hill, 1987:41.9-41.17.
19. Senstad 0, Leboeuf-Yde C, Borchgrevink C. Frequency and characteristics of side effects of spinal ma-
nipulative therapy. Spine 1997;22:435-441.
20. Spitzer WO, LeBlanc FE, Dupuis M. Scientific approach to the assessment and management of activity-
related spinal disorders. A monograph for physicians: Report of the Quebec Task Force on Spinal
Disorders. Spine 1987;12:S1-S59.
21. Triano J. The mechanics of spinal manipulation. In: Herzog W, ed, Clinical Biomechanics of Spinal
Manipulation. New York: Churchill Livingstone, 2000:92-190.
22. Triano J. Biomechanics of spinal manipulation. Spine 2001;1:121-130.
23. Triano J. Managing geriatric spine patients. In: Bougie J, Morganthal P, eds, The Aging Body. McGraw
HiIl,2001.
24. Triano J. Manipulative therapy in the management of pain. In: Tollison CD, Satterthwaite JR, Tollison
JW, eds. Clinical Pain Management: A Practical Approach, 3rd ed, Lippincott Williams Et Wilkins,
2002:109-119.
25. Triano JJ. Biornechanical analysis of motions and loads during spinal manipulation. Thesis/dissertion,
University of Michigan, 1998, 1-164.
178 Manipulation
26. Triano JJ, Erwin M, Hansen DT. Costovertebral and costotransverse joint pain: A commonly over-
looked pain generator. Top Clin Chiro 1999;6:79-92.
27. Triano JJ, McGregor M, Hondras MA, Brennan Pf', Manipulative therapy versus education programs
in chronic low back pain. Spine 1995;20:948-955.
28. Triano JJ, McGregor M, Skogsbergh DR. Use of chiropractic manipulation in lumbar rehabilitation. J
Rehabil Res Dev 1997;34:25-36.
29. Triano JJ, Schultz AB. Loads transmitted during lumbosacral spinal manipulative therapy. Spine 1997;
22:1955-1964.
30. Triano JJ, Rogers CM, Combs SB, et al. Quantitative feedback vs. standard training for cervical and
thoracic manipulation. JMPT, in press.
3 I. Triano JJ, Rogers CM, Combs SB, et al. Developing skilled performance of lumbar spine manipulation.
JMPT, in press.
1 - - - - - - - -12
Return-to-Work and Functional
Optimization Programs
Keith Wahlberg, M.A. T.P., P. T.A., Mark Sontag, M.D.,
Andrew J. Cole, M.D., F.A.CS.M., Robert P. Wilder, M.D., F.A.S.CM.,
and Steven A. Stratton, Ph.D, P. T., A. r.c
Key Points
• Clinicians treating low back pain should strive to return workers to employment as
soon as safely possible because retum-to-work rates of workers with low back injury
are 50% at 6 months of disability, 25% at 1 year, and 0% at > 2 years.
• Factors predictive of delayed recovery from work-related injuries include chronic pain
(> 3 months); accelerating pain symptoms; failed treatment programs; "limited"
objective physical signs; high levels of emotional arousal, including stress, anger, and
depression; excessive consumption of medications affecting the central nervous
system; and unrealistic treatment goals or expectations.
• The physician helps to provide effective and timely return to work by thoroughly
understanding the physical demands of the injured worker's job and how low back
injury and pain impair function; by communicating with all parties about medical
issues and eventual return to work; by developing an appropriate treatment plan; by
effective use of resources; and by timely initiation of referrals to other providers.
• Functional capacity evaluations may be used to measure a patient's ability to perform
the physical demands of a job.
• Functional job analysis identifies the maximal physical demands necessary to perform
a job safely by evaluating the maximal forces (both dynamic and static) required to
lift, carry, push, and pull with safety; the maximal tolerances and frequencies of
specific postures and movements; and the metabolic expenditure required to perform
specific tasks. This information may help the clinician and employer to establish
treatment goals, to structure modified or light-duty jobs, and to identify safety risks
using industry standards.
• Employment screening uses functional testing of essential physical demands of a job
to ensure that the potential employee is capable of safely performing a job that has
been conditionally offered.
• Work hardening programs are interdisciplinary and, use conditioning tasks that are
graded for progressive improvement of the injured worker's biomechanical, neuro-
muscular, cardiovascular, metabolic, and psychological function. Work hardening
provides a transition between acute care and return to work by addressing issues of
productivity, safety, physical tolerance, and behavior.
• Functional restoration programs are comprehensive, multidisciplinary programs that
help decrease the disability of workers with chronic low back pain who have
demonstrated multiple barriers to recovery including deconditioning, lack of
179
180 RehJm-lo-Workand Functional Optimization Programs
motivation, psychologic dysfunction, and secondary gain issues. An interdisciplinary

approach is essential.
I. Background
A. Frequency oflow back pain
I. Low back pain affects approximately 85% of all persons in the Western world
at some point in their lives.
2. Low back pain is second only to upper respiratory infections as the most fre-
quent reason for medical attention.
3. It is the most frequent cause of limited activity/disability in those under 45
years old.
4. It is the third most frequent cause of limited activity/disability in those 45-64
years old.
B. Epidemiology
1. Incidence of low back pain in industry
a. 2010 of all employees in U.S. have compensable back injury each year.
b. 35% of sedentary workers and 47% of laborers sought medical treatment for
low back pain over a IO-year period.
c. 19010 of all workers' compensation claims are related to back injury.
2. Return-to-work rates of injured worker
a. 50010 at 6 months of disability
b. 25010 at 1 year of disability
c. 0010 at greater than 2 years of disability
C. (ost related to industrial injury
I. Total cost to industry in U.S. is estimated at up to 25-100 billion dollars annu-
ally.
a. Direct medical costs are estimated at greater than 23 billion.
b. Medicolegal costs are estimated at 5 billion.
c. Indirect costs (e.g., productivity loss, disability payments, replacement
worker wages) are estimated at up to 2.4 X direct costs.
2. Average cost per claim is greater than $6800; median cost per claim is less than
$400. Thus a relatively small number of claims contribute the most to overall
expenses.
3. Back injury accounts for 41 % of overall workman's compensation costs.
4. 10010 of cases of low back injury account for 79010 of the cost.
D. Need for objective findings
1. Prompted by the economic magnitude of the problem.
2. Because clinicians rely on patient's subjective complaints due to the complexity
of the spinal unit and the discrepancies of actual spinal diagnosis.
3. Estimates are that 50% of those disabled by low back pain have no objective
findings.
4. To objectify spinal function and dysfunction and attempt to quantitate true ab-
normalities.
E. Back pain in industry
I. Back pain is multifactorial in nature
a. This nature must be acknowledged in order to analyze and objectively mea-
sure spinal function.
b. Low back injury must also be analyzed on the basis of physical, psychoso-
cial, and legal issues.
c. Industry requires uniformity in testing of the many variables.
d. Emphasis on objective parameters appears to facilitate recovery from low
back injury.
Relum-Io-Worlc and Fundianal OpIimization Programs 181
e. Ergonomic changes, worker pre-selection, and a more informed management

appear to be prerequisites in reducing industrial low back injury.
f. Focusing on strength alone is also a gross simplification of this complex
problem.
g. Biomechanical studies offer great insight into the stress and torque on the
lumbar spine during manual material handling.
2. Risk factors for injury in industry
a. Worker
i. History of previous low back injuries
ii. Worker's strength, agility, and endurance are poorly matched to the
physical demands of the job.
iii. Poor general health.
b. Psychological factors
i. Poor employee-supervisor relationship
(a) Psychosocial factors playa tremendous role in low back injury and
recovery.
(b) Boeing Aircraft employee study found correlation between incidents
of low back injury and poor appraisal ratings 6 months prior to injury.
(c) Richard Deyo found that psychosocial and demographic factors such
as education, prior back pain episodes, and a feeling of "always being
sick" were better predictors of outcome than the physical parameters
of examination and the type of PT used.
c. Poor job satisfaction
i. Magora found that employees not satisfied with their occupation, place
of employment, or social status had a higher incidence of low back pain
vs. the control group.
ii. Magora also showed that those who perceived a high degree of responsi-
bility and mental concentration along with feelings of tenseness and fa-
tigue were more likely to develop back pain.
iii. A high scale 3 on the Minnesota Multiphasic Personality Inventory
(MMPI) indicated a tendency toward somatization and denial of emo-
tional distress.
iv. Previous history of depression or anxiety disorders
3. Work factors
a. Excessive lifting requirements
i. The amount of weight appears to be correlated to the development of low
back pain.
ii. Jobs with lifting loads greater than 25 lbs. are associated with an in-
creased risk of back injury .
iii. Greater than 33010 of low back injuries are correlated to lifting
iv. Often a dichotomy exists between what an individual can actually per-
form and the perception of such.
v. A compressive force on the spine of greater than 6000 newtons leads to
a ax greater incidence of low back injury compared with compressive
force of 3500 newtons. 58
vi. Apparent relationship exists between low back pain and jobs requiring
heavy lifting, with the highest prevalence of low back pain in nurses,
truck drivers, and heavy industry workers. 52
b. Frequency of lifting
i. Those lifting frequently are most likely to be injured.
ii. Those lifting rarely are 2nd most likely to be injured.
iii. Those lifting occasionally seem less likely to be injured.
182 Relum-Io-Worlc and Functional Optimization Programs
c. High frequency of bending and twisting

i, Successful lifting requires coordination, proprioception, pulmonary fit-
ness, training, experience, intelligence, flexibility of the extremities and
spine, trunk and extremity strength, and endurance.
ii, Because of the complexity of spinal disability, both physical and psycho-
social factors must be considered in unison.
d. Incentive quotas in material handling jobs
i. Improper lifting is the most frequent cause of low back injury.
ii. Gunnar Andersson has demonstrated that the distance an object is away
from the body influences the stress on the back more than the actual
method used to lift.
iii. Sudden unexpected maximum physical efforts are related to low back in-
jury.
iv. Magora also hypothesized that unexpected maximum motion is more
prone to injury than controlled rehearsed motion.
e. Long work hours that do not allow physical recovery
f. Environmental factors such as excessive heat and cold
g. Vibrational exposure and static work postures also correlate to the develop-
ment of low back pain.
h. Poor implementation of effective safety programs (see Table 1)
II. Current trends in injury prevention

A. Appropriate matching of the employee's physical capacity to the physical demands
of the job through screening programs provided after the worker has been hired.
1. Ergonomic controls
a. Snook found that only ergonomic changes were successful in reducing in-
juries vs. pre-placement screening and education.
b. Snook also suggested designing the job to fit the capabilities and limitations
of the worker.
c. Ergonomic changes are often expensive and cumbersome to incorporate into
the workplace.
2. Administrative controls
a. Safety education consisting of proper bending and lifting techniques, al-
though scientific review has not yet demonstrated its preventative value.
b. Programs directed at changing management's perspective of the injured
worker have been extremely successful at reducing low back costs.
c. Compared with a back school injury prevention program, the management at-
titudinal program reduced injuries while the back school had no effect.
Table I. factors Aftecting Manual Materials Handhng Activities

Work Variables Task Variables Environmental Variables
Physical factors: age, sex, The load: mass, size, shape, Heat load
anthropometry strength, etc. stability, coupling, etc.
Physiological factors: aerobic The work place: space, Noise
power, anaerobic power, obstacles, etc.
endurance, etc.
Psychological factors: attitudes Temporal aspects Vibration
towards work, job satis-
faction, etc.
Training and experience Complexity Work surface: geometry, stability,
traction, etc.
Relum-ID-Worlc and Functional Optimization Programs 183
d. The Chelsea Back Program of structural, technological, and attitudinal

changes in management reduced total cost per back injury claims by 75% .
e. Incentives for low injury rates
f. On-site health and fitness promotion
i. Lee Cady's description of firefighters demonstrated that the most physi-
cally fit had the least number of low back injuries.
ii. In his 14-year follow-up study promoting health and fitness, Cady
found:
(a) 16% increase in physical work capacity
(b) Slight increase in spinal flexibility
(c) No clear increase in muscular strength
(d) Decrease in smoking
(e) Decrease in disabling injuries
(tl 25% decrease in workman's compensation costs
3. Factors predictive of delayed recovery from work-related injuries (and therefore
requiring more intensive intervention)
a. Chronic pain (greater than 3 months)
b. Pain symptoms that are accelerating
c. Failed treatment programs, "limited" objective physical signs
d. High levels of emotional arousal including
i. Stress
ii. Anger
iii. Depression
e. Excessive consumption of medications affecting the central nervous system
f. Unrealistic treatment goals or expectations
III. Worker's compensation systems

A. Background
1. State law usually governs how the system is run
a. Systems that involve attorneys are usually open-ended and revolve around
settlements that trade continued medical benefits for money.
b. Systems that do not involve attorneys tend to give more money to insurance
carriers in directing medical care by controlling reimbursement.
2. Role of the physician and other health care providers is twofold:
a. To provide effective medical care
b. To administer compensation benefits
B. Types of coverage by employers
I. Self-insured employers that do not subscribe to state laws
a. Usually open to litigation
b. Tend to playa more active role in injury reduction
2. Self-insured employers that subscribe to state laws and administer their own
benefits
a. Tend to take a more proactive role in injury prevention
b. Usually accommodate injured workers at light duty positions and work
closely with medical providers
3. Self-insured employers that subscribe to state laws and use third party to ad-
minister benefits
a. Tend to playa proactive role in injury reduction
b. May tend to lose contact with medical providers and injured worker
c. Medical providers and employer are protected from litigation in some
states.
184 Relum-Io-Work and Functional Optimization Programs
4. Coverage provided by insurance company based on premiums paid by employer

a. Promotes poor communication among employer, medical providers, and em-
ployee, leading to poor efforts at case management by employer to reduce
injuries.
b. Medical providers and employer are protected from litigation in some states.
C. Inherent problems ofworker's compensation system
1. Difficult cases can be products of system.
a. Secondary gain in litigious systems
b. Symptom magnifiers are typically patients who feel forced into proving their
injury or pain.
2. Poor understanding of the cause of pain, particularly in the absence of defini-
tive diagnostic tests
a. Unsuccessful return-to-work efforts by medical providers who have poor un-
derstanding of job.
b. Ineffective case management and poor communication between parties in-
volved usually lead to lengthy rehabilitation.
i. Poor medical follow-through
ii. Delays in medical care due to insurance reimbursement
iii. Poor communication between the medical provider and employer ham-
pers final return-to-work efforts.
iv. Poor motivation during rehabilitation may be caused by situational de-
pression and anxiety.
c. Deteriorating financial status
d. Change in family roles at home
e. Loss of control regarding future
f. Deteriorating employer relationships
D. Physician's role in managing the case is paramount to help provide effective and
timely return-to-work.
I. Understanding the physical demands of the injured worker's job
2. Thorough understanding of low back injury and pain and how they impair
function
3. Effective communication with all parties about medical issues and eventual
return-to-work
4. Manage case by
a. Effective use of resources
b. Timely referrals to other providers
c. Developing treatment plan
E. Other medico-legal aspects ofevaluations
1. In California, it is unlawful to practice discriminative hiring based on latent or
potential disability
2. Rejecting a job applicant on the basis of a potential back problem requires the
following criteria:
a. The applicant must be unable to do the specific job.
b. All or substantially all of the excluded people must be unable to safely and
efficiently perform the job.
c. There is identifiable and substantial immediate danger with a substantial de-
gree of risk.
3. Pre-employment screening is illegal in California because it is deemed discrimi-
natory based on latent or potential disability.
4. Once a person is hired, pre-placement screening is legal.
5. Chaffin's techniques using isometric strength testing and matching of job to
lifting capabilities once a worker is hired are legally defensible.
Relum-fo-Work and Functional Optimization Programs 185
IV. Evaluation Techniques

A. Strength
1. Isometric strength testing (Fig. 1)
a. Definition: static measure of maximal voluntary contraction with muscle at
fixed length
i. Simple strain gauge-demonstrates peak force (low tech, cost of device
$300)
ii. Computerized equipment-demonstrates peak and mean force over 5 sec-
onds (high tech, cost of device $50,000)
b. Advantages of isometric testing
i. Reliability and reproducibility have been well established.
ii. Strain gauge is simple and easy to administer
c. Concerns regarding isometric testing
i. Hanson, using biomechanical analysis, calculated compressive loads on
the L3 vertebral body of 5000-10,000 newtons during isometric testing
squat and torso lifting.
ii. The above loads caused vertebral endplate failure in vitro.
iii. Hansson also noted isometric testing of trunk flexors/extensors caused
significantly less load on the L3 vertebral body.
iv. Zeh analyzed 1000 volunteers testing isometric strengths! and found that
5010 could not continue testing and that 0.05010 developed an injury.
v. Zeh recommended less exertions, which reduced the probability of injury
while providing an accurate assessment of isometric strength.
FIGURE I. Low-tech isometric strength testing device.

(Reproduced by permission from Cady LD, Bischott DP,
O'Connell ER et al. Strength and Rtness and subsequent
back inuries in RreRghters. J Occup Med 1979; 21(4.):
271. © Am. College of Occupational Medicine.)
186 Relum-to-Work and Functional Optimization Programs
d. Indications
i. Objective quantification of manual muscle test
ii. Quick assessment of relative strength in work-related posture
iii. Screening for controlled effort or symptom magnification by examining
coefficients of variation
e. Contraindications
i. Acute injury
ii. Discogenic pain
iii. Joint or spinal instability
iv. Moderate to severe cardiovascular disease or hypertension
f. Correlation between low back pain rates and isometric strength
i. Chaffin showed a correlation between incidence rates of low back pain
and increased lifting strength requirements.
ii. A following study revealed a greater incidence of back pain when loads
exceeded subject's isometric lifting capacity.
iii. Chaffin actually reduced low back injuries by selecting workers on the
basis of their isometric strength and putting them in jobs where their
strength exceeded the lifting requirements.
iv. Battie and Bigos found no correlation between isometric strength and in-
jury, yet they didn't match job demands and strength.
g. In conclusion, since there is no demonstrated difference in static back ex-
tensor strength among workers performing a wide variety of jobs:
i. Isometric strength testing may be a useful tool in pre-placing workers.
ii, Currently no scientific study shows isokinetic or isoinertial technologies
that are predictive of subsequent back injury.48
2. Isokinetic testing
a. Definition: dynamic measure of strength while the speed of the body seg-
ment is held constant
b. Measures: computer-controlled hydraulic or electric motors that control various
parameters (e.g., range of motion, velocity, concentric or eccentric loading)
c. Mechanisms of isokinetic testing
i. Cybex: provides sagittal and torsion strength testing
ii. Kincom: uses an attachment to the extremity dynomometer that can be
used for back testing
iii. Biodex: uses an attachment to their existing extremity system
iv. Lido: provides a sagittal strength tester and allows the patient to sit or
stand.
d. Indications
i. Commonly used to compare strength between extremities
ii. Comparison with normative data (not widely accepted).
e. Contraindications
i. Acute injury
ii. Discogenic pain
iii. Joint or spinal instability
iv. Danger of causing injury due to high forces generated at extremely high
and low speeds.
v. Moderate to severe cardiovascular disease or hypertension
f. Advantages of isokinetic testing (Fig. 2)
i. Dynamic testing theoretically recreates functional lifting better than sta-
tic testing, although this premise is not scientifically proven.
Relum-Io-Work andFunctional Oplimizalion Programs 187
FIGURE 2. LIDO back isokinetic sys-

tem. Courtesy of Loredon.
ii. Lifting is actually isoinertial rather than isokinetic.

iii. Isokinetic testing has been proven safe, and the data are reliable and re-
producible.
iv. Isokinetic testing allows for curve analysis.
(a) Hypothesis is that curve variability distinguishes maximal effort from
submaximal effort in trunk and lift testing.
(b) Hope is that by computerizing strength testing malingerers may be
distinguished from those injured.
(c) May help distinguish between those providing a full effort and those
who are not.
v. Evaluation of variability of isokinetic curves as an indicator of effort by
Rowland and Hazard
(a) Clinical observation of the subject using isokinetic equipment is more
accurate than analyzing curve variability.
(b) Extremely difficult to discriminate between submaximal effort sec-
ondary to pain, malingering, and fatigue.
vi. Conclusion regarding isokinetic technology
(a) It is safe, repeatable, and the data are reproducible.
(b) It is extremely costly.
(c) Has not been scientifically shown to infer greater capacity than avail-
able isometric technologies.
(d) It is not specifically job related, as people do not lift isokinetically.
(e) It does appear, however, that quantifying trunk strength using isoki-
netic technologies facilitates low back injury recovery.
188 Relum-to-Work and Functional Optimization Programs
3. Isotonic testing
a. Definition: dynamic measure of strength or exercise during which weight re-
mains constant despite velocity
b. Measures: traditional weight training or lifting boxes (functionally more
valid testing and exercise method).
c. Indications
i. When controlling force is clinically indicated
ii. Progressive loading to allow structural adaptation
d. Contraindications
i. Poor spinal dynamic or structural stability
ii. Excessive loading through acutely injured disc despite good stability
iii. Immediate postoperative tendon repair
iv. Immediate postoperative spinal fusion
4. Isoinertial strength testing
a. Two basic approaches
i. Low tech approach
(a) Stover Snook used lifting boxes filled with lead shot or bricks.
(b) Thomas Mayer introduced progressive isoinertial lifting evaluation
(PILE).
(c) Minimal cost to both approaches
ii. High tech approach uses computerized isoinertial testing devices that can
cost more than $50,000 per machine.
iii. Factors in isoinertial testing
(a) Both approaches are repeatable, reproducible." safe to administer,
and relatively easy to use, especially the low tech approach.
(b) Despite closely replicating job related spinal motion, isoinertial test-
ing is a poor predictor of low back pain, although it can reduce low
back disability time.v
(c) Disability time reduction using both approaches may be related to ac-
tual objectification of function.
(d) Objectifying function gives the patient direct feedback about recovery
and can serve as a motivator.
5. Motion analysis
a. Definition: real-time measure of movement of spine in either two or three
dimensions
b. Measures
i. Hand-held goniometer
ii. Bubble and computerized inclinometers
iii. Three-dimensional electronic goniometers fixed to patient's spine
iv. Two and three-dimensional video motion analysis systems
c. Indications
i. Objective quantification of range of motion of spine in acute and chronic
injuries
ii. Electronic goniometer and video analysis are effective tools in functional
job analysis.
iii. Computerized models provide coefficients of variation.
iv. Electronic goniometer and video analysis systems can determine effects
of pain on velocity of movement.
d. Contraindications: none.
6. Summary of testing devices; isometric, isokinetic, and isoinertial
a. All are relatively safe, easy to use, and provide reproducible data."
Relum-Io-Wonc andFunctional Optimization Programs 189
b. Costs of high-tech isokinetic and isoinertial appear prohibitive.

c. Costs of isometric and low-tech isoinertial devices quite reasonable.
d. Only isometric and isoinertial techniques are actually job related.
e. Only isometric strength testing has been proven to be predictive of future
low back injury.
V. Functional Capacity Evaluation

A. Definition: quantitative measurement using a specific set of activities to assess an
individual's maximal safe ability to perform a series of functional activities. Focus
on whole-body tasks that incorporate the impaired region. In the lumbar spine,
this includes activities such as lifting at different heights, bending, reaching,
twisting, pulling, sitting tolerance, standing, walking, and crouching (Fig. 3).
B. Potential benefits offunctional assessment
1. Shifts the present inordinate importance on subjective complaints to more ob-
jective findings or functional parameters.
2. Would include objective analysis of patient's condition and subsequent recovery.
3. Would allow determination of spinal deficits and their rapid correction through
objective analysis of the spinal unit.
4. Would increase biomechanical and psychological understanding of the spine
through assessment of spinal function.
5. Help to legitimize the qualified worker and identify the malingerer or those
concerned with secondary gain.
Name _
Date of injury _
Description of injury _
Employer, _
Insurance carrier _
Attorney _
Case manager _
Referring physician. _
History:
Job description:
• Length of employment, number of hours worked per shift, maximal weights lifted at various heights, and fre-
quencies that they are lifted
• Amount or frequency of whole body movement and agility such as stooping, kneeling, crouching, bending,
reaching overhead, reaching forward, standing and walking
• Statements about the level of activity the employer is willing to accommodate in temporary and permanent
positions.
Evaluation summary
Performance during testing:
• Cooperation-maximal or submaximal effort
• Lift evaluation-maximal amount lifted and carried, reason testing was terminated, use of correct body me-
chanics, complaints of pain, objective signs of pain and fatigue
• Whole body movement and agility-ability to move in and out of different positions; ability to sustain pro-
longed postures such as standing, sitting; effects of fatigue and deconditioning on performance
Recommendations:
Statements should be made about how injury has impaired worker's ability to perform functional tasks.
Recommended therapies should be based on prognosis for improvement, given performance during testing.
Specific return-to-work prescription should list maximal weights and frequencies for lifting and maximal fre-
quencies for whole body movement.
FIGURE 3. Sample functional capacity evaluation (FeE).

190 Relum-to-Worlc and Functional Optimization Programs
6. Would reassure the worker of his capacity to perform work tasks before return-
ing to the actual job site.
7. Following the normative data collection, pre-placement screening could be in-
stituted to prevent injuries (Fig. 4).
C. Measures: various manual and computerized testing protocols
1. Evans and Kagan developed a functional rating scale for chronic low back pa-
tients that quantifies the patient's level of activity and relative personal inde-
pendence.
D. Indications
1. To measure a patient's ability to perform the physical demands of a job
2. To determine the need for additional general physical therapy or more intensive
rehabilitation programs such as work hardening
3. To determine a patient's ability to perform general categories of work to assist
in vocational retraining programs
a. Sedentary, up to 10 # of lifting
b. Light, up to 25# of lifting
c. Medium, up to 50# of lifting
d. Heavy, up to 100# of lifting
e. Very heavy, over 100# of lifting
4. To document objectively the psychosocial influences that affect performances
a. Controlled effort "malingering"
b. Excessive disability for secondary gain
c. Inappropriate illness behaviors of psychogenic origin
Test Score Job Demand

(pounds) (pounds)
Static 0 F C 0 F C
Pushingshoulder 60 30 12 100 50 20
Pullingshoulder 80 40 16 90 45 18
Liftingknuckle 90 45 18 100 50 20
Liftingankle 80 40 20 100 50 20
Dynamic
Liftingwaist height 40 20 8 100 50 20
Liftingchest height 20 10 4 50 25 10
Carrying 50 25 10 100 50 20
Whole body movements
Standing Occasional Frequent
Walking Occasional Frequent
Silting Occasional Occasional
Crouching Frequent Frequent
Stooping Occasional Occasional
Kneeling Occasional Not required
Crawling Occasional Not required
Bending Frequent Frequent
Climbing Occasional Not required
Reachingoverhead Occasional Occasional
Reachingforward Occasional Occasional
FIGURE 4. Performanceon functional capacity evaluation vs. job demand. (0 = occasional-up to 33% of
day; F = frequent-up to 66% of day; and C = constant-up to 99% of day.)
Relum-Io-Worlc and Functional Optimization Programs 191
E. Contraindication: excessive pathology that could lead to further Inlury

F. Components
1. Maximal objective strength
2. Tolerance levels to specific activities, positions, and repetition (i.e., coordina-
tion, pace)
3. Cardiovascular or endurance requirements
4. Safety (see Table 2)
G. Strength vs. endurance
1. Low back sufferers have weaker trunk muscles vs. weakness as a result of pain.
a. Low back pain sufferers show decreased isometrically tested strength of the
trunk muscles.
b. Low back pain sufferers show weaker trunk muscles when tested dynami-
cally.
c. Nachemson and Lindh report no difference in isometric abdominal or trunk
strength when comparing low back pain sufferers and an age-matched con-
trol group.
2. Biering-Sorenson
a. They published two studies stating trunk strength alone is a poor predictor
of low back pain.
b. They also demonstrated that isometric back endurance is significant in pre-
dicting the first episode of back pain in men."
3. Nicholaisen and Jorgensen
a. They found no difference in abdominal and back strength between back pain
patients and normals.
b. They also found decreased endurance of trunk muscles in low back pain suf-
ferers. 26,44
4. Conclusion: reduced trunk muscle endurance might force the spine to perform
functional activities in an uncoupled, unprotected way, making injuries more
likely.
5. Extensive controversy exists about the relationship between trunk strength and
low back injury.
a. Chaffin's concept of matching worker strength and job strength demands us-
ing pure isometric strength testing has merit.
b. Additional investigation regarding isometric strength vs. isometric en-
durance is needed in light of recent studies.
H. Outcomes
1. Patient is healed and able to return to work without restrictions.
2. Patient is moderately impaired and able to return to work without restrictions
after completing a work hardening program.
TABLE 2. States of Whole-Body Strength Testing·

Criterion Isometric Isokinetic Isoinertial
Repeatable Excellent Excellent Excellent
Safe Good Excellent Excellent
Easy to Use Excellent Excellent Good
Cost Medium High Low
Job-related Good ? Good for lifting
Predictive Good ? ?
From Gary Herrin, University of Michigan Center for Ergonomics, Ann Arbor, MI, 1990.
192 Retum-Io-Work and Functional Oplimizalion Programs
3. Patient is significantly impaired and has the potential to return to work without
restrictions but needs additional general physical therapy to increase functional
level before work hardening.
4. Patient is significantly impaired and has the potential to progress in a work
hardening program but does not have the potential to return to work without
restrictions.
5. Patient is impaired and incapable or returning to work without restrictions but
employer is willing to accommodate.
6. Psychosocial influences prevent accurate assessment and will most likely affect
effectiveness of further rehabilitation.
VI. Functional Job Analysis

A. Definition and purpose
1. The process of identifying the maximal physical demands necessary to perform
a job safely in terms of maximal forces ( both dynamic and static) required to
lift, carry, push, and pull with safety.
2. To determine maximal tolerances and frequency of specific postures and move-
ments.
3. To determine metabolic expenditures required to perform specific tasks.
B. Indications
1. To establish treatment goals.
2. To assist employer in structuring modified or light-duty jobs.
3. To identify safety risk using industry standards.
C. Contraindications: none.
D. Timing in overall rehabilitation program
I. Early during acute phase for injuries of minimal severity
2. Before FCE, for injuries of moderate-to-severe complexity, when work harden-
ing may be indicated
E. Types and techniques
1. Interview with qualified personnel who have considerable knowledge of job
2. On-site analysis for a more objective measurement
a. Force gauges and weight scales to quantify static and dynamic forces
b. Observation of task over long periods of time (hour, day, or week) to deter-
mine maximal frequencies of movement and postures
c. Ergonomic analysis of job forces (vertical, horizontal, center of mass, veloc-
ity of movement, acceleration, compression forces within the body) using
scientific formulas
VII. Employment Screening

A. Definition and purpose: functional testing of the essential physical demands of a job
to ensure that the potential employee is capable of safely performing the job that
has been conditionally offered.
1. Indications-should be used for any job that poses any risk of injury.
2. Contraindications
a. When medical screening reveals significant health risks
b. Test protocols that have poor validity [i.e., do not test workers performing
actual job tasks) may be basis for litigation if used to deny employment.
3. After timing-conditional offer of employment has been made
B. Historically, pre-employment histories and physical exams were used to screen
potential employees.
1. Although previous histories of low back pain predisposes one to additional low
Relum-Io-Worlc ana Functional Optimization Programs 193
back pain, prospective employees can distort their own history to facilitate em-
ployment.
2. 7-8010 of those prone to develop low back pain can be screened via pre-
employment history and physical exam (Rowe).
3. Chaffin and Snook were unable to identify susceptible workers with pre-
placement exams.
4. Pre-placement radiographs of the lumbar spine were used during the 1950s
and 1960s.II,24,40
a. Other studies showed pre-employment radiographs alone were not predic-
tive of future low back injury.33,41,47,49
5. Height, weight, and body frame have not been predictive of subsequent low
back injury.
6. Although psychological factors are not good predictors of low back injury,
they can certainly playa role in recovery.
C. Association between low back pain and spinal stenosis
I. Association between low back pain and L4-5 disc space narrowing and spurs
was shown by Frymoyer.
2. The pain from a herniated nucleus pulposus that is not responsive to non-
operative care may be caused by spinal stenosis.
3. Although plain radiographs are not predictive of low back injury, spinal cord
diameter might be a predictive factor in low back injury.
VIII. Physical Therapy (for injuries of low-to-moderate severity)

A. Functional job analysis provided by therapist or employer is useful tool in identi-
fying physical demands of job.
B. Baseline functional objective testing specific to physical demands of job should
be used to develop appropriate treatment goals, length of treatment programs,
and eventual outcome.
C. Treatment program should include instruction in correct posture and body me-
chanics to optimize function by reducing pain with activity.
D. Appropriate timing of referrals to more intensive rehabilitation programs is essen-
tial.
I. Functional restoration occurs 3-4 times faster in work hardening programs.
2. Premature referrals to work hardening programs may mean discharge at levels
below maximal medical improvement.
a. Increased pain
b. Inability to progress in rehabilitation program
IX. Work Hardening Program

A. Definition and purpose: work hardening programs are interdisciplinary and use con-
ditioning tasks that are graded for progressive improvement of the injured
worker's biomechanical, neuromuscular, cardiovascular, metabolic, and psycho-
logical function by using a series of real or simulated work activities. Work hard-
ening provides a transition between acute care and return-to-work and addresses
the issues of productivity, safety, physical tolerance, and behavior. Work harden-
ing is a highly structured, goal oriented, individualized treatment program de-
signed to maximize ability to return-to-work. In addition to general conditioning
and strengthening, emphasis is placed on job-specific simulation activities with
the goal of returning an injured worker to the workplace.
B. Team members
I. Physician
194 Relum-Io-Woric ana Functional Optimization Programs
2. Physical therapist
3. Occupational therapist
4. Vocational therapist
5. Psychologist
6. Case manager
7. Patient
C. Therapeutic ,Heds
1. Uses graded functional tasks, aerobic conditioning, body mechanics training,
and various treatment modalities to decrease pain.
2. Education about extent of injury, methods for self-treatment, and prognosis for
full recovery are used to promote realistic goal setting and allow patients to
return-to-work even with some discomfort.
3. Mental health counseling in group and individual settings helps to address situ-
ational depression, anxiety, and fear about effects of the injury and return-to-
work.
4. Group setting helps to promote healthy social interaction, worker identity, and
worker traits.
D. Indications
1. Functional capacity evaluation that demonstrates significant impairment that
prohibits a safe return to work.
2. Improved opportunity for worker to return safely to regular or modified duty.
3. Timely referral so that injured worker will reach the goals of the program at
discharge
1. Psychological screening shows excessive inappropriate illness behaviors or ten-
dencies to self-limit performances to the point that expected progress will not
occur.
2. Incomplete medical work up or treatment
3. Serious health risks that may outweigh benefit of the program
F. Program content
I. Daily program that is usually progressive in hours (up to 8) and activity over
4-6 weeks
2. Scheduled daily activities designed to address specific areas of impairment
3. Weekly testing in areas of impairment; in long programs, usually interim and
final FCEs
4. Exit FCE with specific recommendations for return-to-work and documentation
of injured worker's performance during program.
G. Outcome measures
I. Purpose: to measure the effectiveness of treatment program
2. Statistics regarding norm of percent improvement per diagnosis should be used
by physician to time referral.
3. Statistics regarding pre-and post-FCE scores and successful return-to-work per-
centages should be used by the physician to select appropriate referral sources.
4. Statistical outcome measures
a. Length of time between date of injury and entrance into program
b. Initial score on FCE
c. Length of program
d. Percent of patients that met treatment goals
e. Final score on FCE
f. Percent functional improvement for men and women based on pre-and-post
FCE scores
Relum-Io-WatIc: andFunctional Optimization Programs 195
g. Percent returned to work

i. Same job without restrictions
ii. Same job with restrictions
iii. Different job
iv. Did not return to work
v. Did not complete program
X. Functional Restoration
A. A small subset of patients progress to chronic low back pain and associated dis-
ability despite proper and thorough attempts to diagnose and treat identifiable
pathology. Once it is clear that a given patient's pain cannot be diagnosed and/or
cured, quantification of function becomes essential to assess rehabilitation needs
and eventual readiness for work. Two key factors of the patient with chronic low
back pain confound efforts to stem disability:
1. No objective method exists to measure pain
2. The correlation between a patient's report of pain and observed physical capac-
ity deteriorates with chronicity.
B. Definition: functional restoration is a comprehensive, multidisciplinary program in-
tended primarily to correct disability in the patient with chronic low back pain
who has demonstrated multiple barriers to recovery, including deconditioning,
lack of motivation, psychologic dysfunction, and secondary gain issues. An inter-
disciplinary approach is essential and integrates physical therapy, occupational
therapy, vocational rehabilitation, psychology, nursing, and the physician. Unlike
work hardening, functional restoration is a physically directed program.
C. Indications
1. Persistent disability despite completion of proper primary and secondary work-
up and treatment
2. Presence of barriers to recovery
a. Deconditioning
b. Lack of motivation
c. Psychological dysfunction
d. Secondary gain issues
3. Mutually agreed upon work goals (established by patient and physician)
4. Willingness to participate and comply
5. Insurance authorization
D. Elements
1. Quantification of physical function
2. Physical reconditioning of injured functional unit
3. Work simulation and whole body coordination training
4. Cognitive-behavioral disability management
5. Fitness maintenance program with outcome assessment using objective criteria
E. Program content
1. Initial medical evaluation
a. Ensure patient has been properly evaluated to rule out surgically correctable
cause for pain and disability.
b. Screen for medical problems that may preclude rehabilitative progress.
c. Exercise tolerance testing for patients greater than 40 years old or with sig-
nificant cardiovascular risk factors.
2. Quantification of physical function
a. The deconditioning syndrome affecting patients with chronic back pain may
result in trunk stiffness, weakness, intolerance for aerobic exercise, and loss
196 Return-to-Worlc and Functional Optimization Programs
of speed and coordination required for activities of daily living. A detailed

quantitative functional evaluation measures the results of such decondition-
ing as it affects the spine, thus assisting the clinician in prescribing appro-
priate rehabilitation and monitoring.
b. Trunk range of motion
i. Allows clinician to judge significance of small variations from antici-
pated value and to track rehabilitative progress.
ii. Inclinometers help to separate hip motion component from lumbar spine
component.
iii. Sagittal
iv. Coronal
v. Rotation
c. Trunk strength
i. Isokinetic measurements allow the preselection of a fixed speed of mo-
tion and distance moved to isolate torque as the only variable.
ii. Hips and lower extremities are stabilized so that only torques generated
in the thoracolumbar functional unit are measured.
iii. Differences in trunk strength between normal and patient populations
have been demonstrated.
iv. Trunk strength can be improved.
v. Trunk strength deficits may exist independently of symptoms and in-
crease risk of recurrent injury.
d. Whole body task performance
i. Movement of whole body task performance represents the interactions of
multiple functional unit links in the biomechanical chain.
ii. Optimal physical capacity involves the highest possible functioning of
each functional unit involved in a task and a relearning of coordination
and agility linking the functional units to provide optimal safety and ef-
ficiency.
iii. Multiple tests of varying complexity to examine a single task [i.e., lifting)
(a) Isometric lifting
(b) Isokinetic lifting
(c) Isoinertial lifting
iv. Positional and activity tolerance (i.e., sitting, squatting, kneeling, walk-
ing, carrying, climbing).
3. Assessment of symptom self-reports-pain and disability
a. Millen visual analogue scale
b. Oswestry pain questionaire
c. Pain drawing
4. Psychological evaluation
a. Personality features-MMPI
b. Disability coping scale-Millon Behavioral Health Index
c. Depression-Beck Depression Inventory
d. Self-perception, family dynamics-patient interview
5. Vocational assessment
a. Employment history and aptitudes
b. Goals
c. Litigation status
d. Interpersonal work behavior
6. Phases of rehabilitation
a. Initial reconditioning phase
Relum-Io-Worlc and Functional Optimization Program5 197
i. Up to 12 appointments over 4-6 weeks

ii. Supervised stretching, aerobic and light work simulation exercises for 2
hours twice/week
iii. Focus: improving mobility, overcoming neuromuscular inhibition and
pain sensitivity, and measuring cardiovascular endurance.
b. Comprehensive phase
i. 10 hours/day, 5 days/week, 3 weeks
ii. Vigorous stretching and aerobics classes
iii. Progressive resistive exercises twice a day under supervision of physical
therapist
iv. Daily work-simulation of tasks, lifting drills, and position-tolerance
training exercises similar to work hardening
v. Classes on goal setting, work issues, stress management, and interper-
sonal skills development under direction of psychologist
vi. Active return-to-work planning monitored by vocational therapist
vii. Patient will not be permitted to complete this phase of functional
restoration without a work plan and will be terminated if he or she re-
fuses to make such a plan.
c. Follow-up phase
i. 1 and If, days/week, up to 6 weeks
ii. Reconditioning, work hardening, and vocational counseling continue.
iii. Allows integration of improvement and behavioral changes generated
during intense phase with return-to-work.
iv. At end of follow-up, patient receives appropriate work release from med-
ical director with functional limitations as indicated
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Relum-Io-Wo,* and Functianal Optimization Programs 199
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,--------13
Bracing for Low Back Pain
Michael W. Wo/~ M.D., Michael M. Weinik, D.O.,
and Ian B. Maitin, M.D.
Key Points
• Proper orthotic prescription requires knowledge of the biomechanics of the thoraco-
lumbar spine and general principles of bracing, including their indications and
limitations.
• Spinal orthoses utilize the principle of three-point pressure control. The corrective
component is typically and ideally located midway between the opposing forces.
• Spinal orthoses may be used as an adjunctive treatment for various conditions that
can cause low back pain, including vertebral fractures, facet joint arthritis, degener-
ative intervertebral discs, scoliosis, neuromuscular disease, spinal cord injury, and
myofascial and ligamentous injuries.
• Spinal orthotic prescriptions for uncomplicated low back pain should be discouraged.
• Prescription of a spinal orthotic should be made only after careful clinical assessment,
including a detailed history and extensive physical examination. Ancillary testing
helps the clinician to choose an orthotic that best meets the biomechanical demands of
the lumbar spine disorder. Diagnostic imaging may not be needed in all cases.
• Prescription of spinal orthoses should be accompanied by specific activity restrictions
to help ensure protection from injury progression.
• Lumbar spinal orthoses should be considered for short-term use as part of a compre-
hensive rehabilitation program; exceptions include spinal metastasis and severe cases
of osteoporosis.
• When indicated, the patient may perform therapeutic exercises while wearing the
orthosis. In certain cases, such as acute spondylolysis or acute compression fracture,
the patient should not exercise even while wearing an orthosis until adequate healing
is ensured.
• No lumbar orthosis provides absolute spinal immobilization. Rather, they partially
limit spinal motion.
• Variations in body habitus (i.e., obesity) may render an appropriately selected orthosis
ineffective.
• A poor response to bracing warrants a reevaluation of the diagnosis, treatment plan,
and orthotic prescription.
• To prevent psychological dependence, patients should be weaned from their orthosis
rapidly, when clinically appropriate.
• Like any prescriptive treatment, spinal orthotics involve the potential for abuse and
noncompliance. The appropriateness of any prescribed orthosis may vary as the
patient's condition changes over time.
Illustrations by T. Cate Nguyen-Trate, M.D.
201
202 Bracing for Low Bade Pain
• Long term use of lumbar orthoses should be discouraged in most cases secondary to
potential adverse effects, including possible loss of strength of core body musculature,
psychological dependence, and decreased spinal mobility.
• Scientific literature has not conclusively demonstrated that lumbar supports
significantly prevent low back injuries in the industrial population.
I. Goals of Spinal Orthotic Prescription

A. Truncal support and control spine position by use of external forces.
B. Restriction of gross spinal and segmental motion.
C. Partial unloading of spinal segments (anterior vs. posterior).
D. Stabilization of spine when soft tissues cannot adequately perform this function
[ie., fractures).
E. Proprioceptive feedback and postural control.
F. Reinforcement of proper body ergonomics.
G. Warmth to underlying soft tissues.
H. Compression or cushioning of paravertebral soft tissues by design.
I. Apply corrective forces to abnormal curvatures.
II. Indications for Use of Spinal Orthotics

A. Spondylolisthesis
B. Spondylolysis with or without spinal instability
C. Degenerative intervertebral disc, including herniation
D. Rheumatic diseases
E. Severe osteoporosis
F. Vertebral compression fractures
G. Chronic muscle weakness
H. Pain that is not responsive to therapeutic exercise
1. Scoliosis
J. Spinal cord injury
K. Neuromuscular disease
III. Principles of Orthotic Mechanism of Action

A. Range of motion (ROM) is restricted by a 3-point pressure system that provides
spinal support by means of opposing forces.
B. Increases proprioception secondary to increased cutaneous input.
I. Results in enhanced awareness of pelvis and spine and improved posture.
2. Prevents motion into painful positions.
C. Reflexive muscle relaxation through body heat containment by the orthosis.
D. Soft-tissue swelling and edema control by compression of paravertebral soft tissues.
E. Increased trunk support aids weak abdominal muscles and increases intraabdomi-
nal pressure (lAP), thus mechanically unloading the intervertebral discs.
I. Increased lAP reduces the tension on the posterior spinal muscles.
2. Nachemson et al. found an inflatable corset to decrease intradiscal pressure by
25-300/0.
F. Improved posture; more balanced load distribution through lumbar spine and pelvis.
H. Possible decrease in muscle strength and endurance with long term use (contro-
versial).
IV. Types of Orthoses

A. Flexible orthoses
I. Lumbosacral Corsets (Fig. 1)
a. Corsets are soft, flexible spinal orthoses constructed from fabric (e.g., can-
Bracing for Low Bocle Pain 203
FIGURE I. Added support is provided by

anterior and/or vertical stays.
vas, Neoprene, elastic) that encircle the lumbosacral or thoracolumbosacral

trunk.
b. Added support is provided by addition of posterior rigid or semi-rigid verti-
cal stays.
c. Corset closure and/or compression is achieved with buckles, Velcro, or
laces.
d. The lumbar spine is restricted and supported by means of cylindrical pres-
sure on the truncal soft tissues.
e. Functions to reduce spinal motion and provide benefit via proprioceptive
feedback.
f. Truncal muscles weakened by disuse, paralysis, injury (blunt or surgical), or
multiple pregnancies can be supported by a tightly fastened corset, thus re-
ducing discomfort.
g. Lantz et al. found that a corset can limit spinal motion by as much as two-
thirds.
h. For optimal control of the thoracolumbar spine, the corset should extend
from the xiphoid process to the symphysis pubis anteriorly and from just be-
low the scapula to the apex of the buttocks (men) or the gluteal crease
(women) posteriorly.
i. For adequate support, the corset length should be at least 16 inches, with the
posterior vertical stay running the entire length. The corset should fit snugly
over the iliac crests and accommodate the contour of the buttocks.
j. Corsets are usually prefabricated in various sizes and designs.
2. Lumbar belts (Fig. 2)
a. Fabric or elastic lumbar support belts reduce repositioning error in patients
with low back pain.
i. Enhanced cutaneous input results in improved proprioception and im-
proved posture.
ii. Reduced trunk motion
b. Increase in intraabdominal pressure (lAP) is controversial. The majority of
studies do not find it to be significantly affected by bracing. However, some
204 Bracing forLow Bock Pain
fI
.
FIGURE 2. Lumbar belt.
studies report fabric lumbar belts increase the lAP and may decrease the
load on the spine by up to 500/0.
c. A lumbar belt provides improved proprioception and increased stability of
the trunk with decreased ROM. Rotation and side-bending can be limited by
up to 600/0 and lumbar flexion by up to 400/0.
d. Research has not strongly confirmed protection from injury or any enhanced
lifting ability while wearing a lumbar belt.
e. Majority of literature has demonstrated that the use of lumbar supports
and/or education has not resulted in reduced incidence of low back pain or
sick time in industrial workers.
f. With acute injury, a lumbar belt support can facilitate traditional means of
pain control (ice and medications), and the patient should be weaned in 2-4
days.
g. Indicated for low back pain associated with degenerative disc disorders and
acute flexion injuries.
3. Sacroiliac joint (SIJ) belts (Fig. 3) and corsets (Fig. 4)
a. 5IJ corsets are usually made of cloth with adjustable side laces or cinch
down-straps and are of a low-profile, low-riding design.
b. 5IJ belts are usually made of a nonstretch canvas, leather, or nylon cloth
with a width of 2.5-3 inches and a cinch or Velcro closure.
c. 5IJ corsets are contoured garments that should be worn snugly over the
anatomic curves of the buttock and anterior pelvis.
d. 5IJ belts are aligned directly superior to the greater trochanters for proper fit.
e. 5IJ belts and corsets restrict motion through the sacrum and innominates
through compression.
B. Rigid arthoses
1. Chairback brace (Fig. 5)
a. Consists of a short spinal brace made of a plastic or aluminum frame with
an inferior pelvic and superior thoracic band joined by two midaxillary an-
terior abdominal upright supports, and two posterior parspinal uprights.
Bracing lorLow Bade Pain 205
FIGURE 3. Sacroiliac jointbelt.
b. Biomechanics are based on a 3-point pressure system.

c. Functions to control lumbosacral flexion/extension and some lateral motion
It immobilizes the lumbar spine in a neutral position.
2. Knight brace (Fig. 6)
a. Similar to the chairback brace with increased rigidity from additional lateral
supports that extend from the axilla to the greater trochanter.
b. More effective restriction of lateral motion.
FIGURE 4. Sacroiliac joint corset.

206 Bracing lorLow Baele Pain
FIGURE 5. Chairback brace.
3. Williams flexion brace (Fig. 7)

a. Consists of a pelvic band, abdominal apron, and oblique lateral uprights.
b. Limits lumbosacral extension and lateral flexion but allows flexion.
4. Taylor brace (Fig. 8)
a. Thoracolumbar orthosis (TLSO)
b. Consists of a pelvic band with two posterior uprights joined by a short
transverse bar that attach to the shoulders via axillary straps. Anteriorly, has
abdominal support via apron or corset.
c. Functions to restrict flexion and extension in the region of the thoracolum-
bar junction.
FIGURU. Knight brace.

Brac;ng lor Low Back Po;n 207
FIGURE 7. Williams Aexion brace.
5. Knight-Taylor brace (Fig. 9)

a. Combines the features of a Knight and Taylor brace.
c. Provides flexion/extension and lateral flexion control.
6. Jewett hyperextension brac. (Fig. 10)
a. Consists of a lateral frame attached to sternal, suprapubic, and thoracolum-
bar pads.
b. Provides flexion control while maintaining a hyperextended posture.
c. Utilizes a 3-point system consisting of anteriorly directed forces from a pos-
FIGURES. Taylor brace.

208 Bracing forLow Back Pain
FIGURE 9. Knight-Taylor brace.
terior thoracolumbar pad and posteriorly directed forces from sternal and
suprapubic pads.
d. Hyperextension increases lumbar lordosis and stabilizes the spine through
locking of the facet joints, thus restricting lateral and rotary movement.
e. Caution should be used when prescribing this orthosis in patients with
spondylolysis or spondylolisthesis. If facet joint arthritis is present, even a
properly adjusted Jewett brace may prove uncomfortable.
7. Cruciform anterior spinal hyperextension brace (CASH) (Fig. 11)
a. Variation of the hyperextension brace with an anterior horizontal and verti-
cal bars forming a large cross.
FIGURE 10. Jewett hyperextension brace.

Bracing for Low 8cIck Pain 209
FIGURE 11. Cruciform anterior spinal hyperextension brace.
b. The CASH brace is lighter than a Jewett brace and is usually easier to don and
doff.
c. The CASH brace is better designed to accommodate large breasts and allows
axillary pressure relief.
d. The CASH brace is not easily fitted for patients with large or protuberant ab-
domens.
FIGURE 12. Custom-molded

thoracolumbosacralorthosis.
210 Bracing for Low Back Pain
8. (ustom-molded thoracolumbosacral orthosis (TLSO) (Fig. 12)

a. Custom-molded body jacket that controls flexion, extension, lateral and ro-
tatory movement.
b. Provides the highest degree of immobilization and control of all spinal orthoses.
c. Fabricated in polypropylene from cast of the patient's torso, thus providing a
total-contact orthosis. Less intimate fitting, custom-measured, prefabricated
orthoses are also available.
d. Total-contact orthosis provides pressure distribution over a wide area, thus
reducing the likelihood of localized pressure problems and skin ulceration.
e. Lightweight, easier to clean, and relatively easy to don and doff, thus allow-
ing for bathing and frequent skin inspection. Because of the simplicity of its
design, with one molding and Velcro closures, a plastic TLSO is less likely to
be adjusted or modified by the patient.
f. A polypropylene nsa can be uncomfortable in hot and humid conditions.
g. A custom-molded Tl.Su increases the intracavitary pressure, thus decreasing
the load on the intervertebral disc. It also provides a rigid cylinder, restrict-
ing motion at painful segments.
h. Indicated for the treatment of spinal fractures or low back fusions. Allows
for early mobilization and rehabilitation.
9. Raney jacket (Fig. 13)
a. Custom-fitted, z-piece acrylic lumbosacral orthosis that holds the lumbar
spine in slight flexion and posterior pelvic tilt, potentially increasing inter-
foraminal space and limiting spine extension.
b. Side-lacing system joining anterior and posterior shells provides adjustable
fit with slight weight fluctuations. Closed, foam-padded shells cushion bony
prominences of spine.
c. Lower profile than full-size thoracolumbosacral orthosis and therefore most
appropriate for lower lumbar pathology.
d. Must be custom-fitted by certified orthotist.
FIGURE 13. Raney jacket.

BlUeing for Low Bock Pain 211
10. Pneumatic decompression brace

a. Custom fit, low profile, adjustable pneumatic vest with anterior/posterior
channels and adjustable lumbar support.
b. Provides lumbar support and decompression. May offload 300/0-500/0 of
body weight from the lumbar spine onto the iliac crests.
c. Indicated for mechanical low back pain with/without radicular pain, such
as intervertebral disc disorders (discogenic pain), facet syndrome, foraminal
stenosis and stable spondylolisthesis.
d. Use multiple times daily (20-30 minutes/ TID) as needed for relief or during
functional activity. Avoid full time use.
v. Specific Treatment Plans

A. Spondylolysis
1. Treatment goals
a. Maintain alignment of the fracture segments.
b. Facilitate healing of the acute injury.
2. Proposed orthotic mechanism of action (MOA)
a. Unload the posterior elements.
b. Restrict motion between the fracture segments.
3. Preferred orthosis-rigid orthosis in 0° of flexion (listed below in order of pref-
erence)
a. Boston overlap brace-provides excellent unloading, restriction of range of
motion, and is extremely lightweight. May be uncomfortable if fit is not in-
timate and/or used in hot and humid conditions.
b. Raney jacket-reduces lumbar lordosis and holds the patient in posterior
pelvic tilt. Thus, limiting lumbar extension and unloading posterior ele-
ments.
c. Williams flexion brace-provides good limitation of lumbar extension.
d. Chairback orthosis-provides good control of lumbosacral motion in the
planes of extension and side-bending. It is heavier, less comfortable, and
more difficult to fit.
4. Duration of treatment
a. 3 to 6 months; brace should be worn at all times (may be removed for short
periods with restricted activity, as for personal hygiene).
b. Duration depends on degree of symptoms/pain and compliance with activity
restriction. May discontinue after this time if asymptomatic and repeat bone
scan with SPECT is negative.
c. Some studies have shown controversial results: patients braced early did
better than asymptomatic patients treated with activity restriction, relative
rest, and no bracing.
5. Considerations
a. If a bone scan reveals no increased activity at the fracture site, potential for
additional healing is remote.
b. Follow-up imaging such as CT scan to see if there is bone remodeling at
fracture site (vs. well corticated) or complete healing. Another consideration
is bone scan with SPECT.
c. May consider a less restrictive orthotic that still offers enough support to
minimize pain so that rehabilitation can be advanced more efficiently.
B. Spondylolisthesis
1. Treatment goals
a. Control and minimize pain.
212 Bracing for LowBocle Pain
b. Decrease translation between spinal segments if spondylolisthesis is unstable

on bending radiographs.
2. Proposed orthotic MOA
a. Restrict spinal motion through 3-point restraint principle.
b. Antilordotic lumbosacral orthosis. May reduce shear stress at the involved
segment.
3. Preferred orthosis
a. Low-profile, molded lumbosacral orthosis-maximal motion control through
total-contact; often less comfortable.
b. Semirigid designs-more comfortable than total-contact designs but also less
restriction of spinal motion.
c. Chairback brace-good restriction of motion but difficult to achieve comfort-
able fit.
a. If spondylolisthesis is symptomatic but not unstable, brace may be worn as
pain dictates on as-needed basis.
b. If spondylolisthesis is unstable and/or neurologic deficits are present, the or-
thosis should be worn during all waking hours.
5. Considerations
a. Establish the direction of instability (increased translation) with bending
films (flexion, extension, and side-bending) to establish anterolisthesis,
retrolisthesis, or laterolisthesis.
b. Brace to limit this motion.
e. Disc degeneration
1. Treatment goal
a. Decrease intradiscal pressure
b. Improve posture and reduce spinal motion
a. Cylindrical compression of the abdomen to increase intraabdominal pressure.
b. This proposed MOA remains quite controversial; extensive research both
supports and denies this claim.
c. Reduce stress/pressure on lumbar disc.
a. Soft corset [i.e., cloth, elastic, neoprene)
b. Pneumatic lumbar vest-provides support and decompression
a. Indeterminate time
b. Use on as-needed basis depending on symptom severity, activity level and
aggravating factors
D. Myofascial pain and muscular strain
1. Treatment goals
a. Reduce pain and increase/maintain mobility, reduce deconditioning sec-
ondary to inactivity.
b. Decrease muscle tension and spasm.
c. Control edema if present.
a. Decrease muscle spindle and Golgi tendon organ activity through compres-
sion, warmth, and proprioceptive feedback.
b. Mild compression of soft tissues to decrease edema of strained paravertebral
musculature.
Bracing for Low Baclc Pain 213
a. Neoprene or elastic low-profile corset without stays or inserts.
b. Lumbar belt
a. On as-needed basis, usually limited to the acute pain phase (usually 1-2
weeks).
b. When pain complaints decrease enough to resume daily activities, wean use
of the orthosis promptly.
5. Considerations
a. Orthotic prescription is generally discouraged for simple injuries.
b. Short term use may be indicated in some instances for treatment goals listed
above.
c. Patient should begin exercises as soon as pain allows even while wearing
orthosis.
E. Sacroihac joint dysfunction
1. Treatment goal
a. Restrict motion between the sacrum and the innominate and at the pubic
symphysis.
b. Reduce pain
a. Compression of the joints of the pelvic ring.
b. Reduce motion
3. Preferred orthosis-nonelastic sacroiliac joint belt with D-ring and Velcro
closure.
a. On as-needed basis, particularly during acute pain period.
b. During periods of ambulation and sitting.
c. Supplemented and eventually replaced by a dynamic hip girdle musculature
stabilization program as pain and healing allow.
5. Considerations
a. Useful in conditions of connective-tissue disease, traumatic shear injuries,
sacral ala or stress fractures, infections, or inflammatory sacroilitis.
b. Suboptimal outcome may result from improperly fitted orthosis. SIJ belts
should be fastened snugly just superior to the greater trochanter and level
with the pubis.
F. Compression fractures
1. Treatment goals
a. Initial pain control and allow for early mobilization
b. Restrict motion at the fracture segment and at the segments immediately
above and below.
c. Unload the anterior column.
d. May help reduce progression of kyphosis.
a. Prevent flexion of thoracolumbar spine with a 3-point restraint system.
b. Reduce/restrict load on anterior column.
a. Molded polypropylene TLSO, such as a bivalved total contact TLSO. With
lower lumbar involvement, consider the addition of a unilateral thigh cuff and
lockable hip joint to improve control of flexion in the lower lumbar segments.
b. Hyperextension orthosis, such as a Jewett or CASH brace, may restrict mo-
214 Bracing for Low Sock Pain
tion equally well and be more comfortable for treatment of thoracolumbar

fractures.
c. Addition of a cervical extension (CnSO) is useful in cases of upper thoracic
injuries (Tl-T6).
a. Average 6-12 weeks, as pain requires (may be up to 4 months).
b. With severe osteoporosis, may need to extend the spinal immobilization for
several additional months.
5. Considerations
a. Indicated-anterior column fracture with intact posterior column and no
neurological deficits.
b. Compression fractures with loss of 400/0 or more vertebral body height
are potentially more unstable and warrant more extensive orthotic man-
agement.
c. May experience activity limitations for up to 1 year and some discomfort for
up to 2 years. Nonoperative treatment with bracing usually has similar func-
tional outcome to surgically treated patients after 2 years.
G. Osteoporosis
1. Treatment goals
a. Reduce incidence of compression fractures
b. Reduce severity of compression fractures
a. Unload anterior spine with use of hyperextension orthoses
b. Reduce/restrict flexion of thoracolumbar spine
3. Preferred othosis.
a. CASH brace
b. Posture Training Support orthosis
H. Lumbar facet-related pain
1. Treatment goals
a. Unload posterior elements
b. Restrict motion of painful facet joints
a. Limit spine extension from either a slightly flexed or neutral position.
b. Unload posterior elements
a. Soft corset orthosis with either posterior steel stays or molded plastic insert
posteriorly
b. Pneumatic decompression brace (chronic cases only)
a. Orthosis is to be worn while standing and bending during acute phase only.
b. Generally 2-3 weeks
5. Considerations
a. More recalcitrant posterior element pain may require more extensive bracing
(Such as a pneumatic decompression brace, chairback or semirigid orthosis
set in neutral or slight flexion).
I. Pregnancy
1. Treatment goals-accommodate skeletal changes associated with pregnancy.
a. Increased lumbar lordosis.
b. Elongated and weakened abdominal musculature.
c. Ligamentous laxity and hypermobility due to the effects of relaxin.
Bracing lor Low Back Pain 215
a. Support a protuberant abdomen, thus reducing the strain of paraspinal and

abdominal musculature.
b. Restrain motion of hypermobile joints
a. Low-profile cloth corset orthosis with steel posterior stays
b. "Iwata Obi"-matemity wrap style support
4. Considerations
a. Custom fabrication may be necessary in patients with recurrent low back
pain and SIJ pathology.
b. Do not attempt to encircle the protuberant abdomen.
J. Orthoses in the workplace
1. Treatment goals
a. Improve posture and body ergonomics during lifting and other functional
activities.
b. Reduce injuries and lost time from workplace.
a. Provide enhanced cutaneous input and proprioception to encourage de-
creased lumbar flexion and increased hip flexion during lifting activities.
Certain movements may produce discomfort.
b. Decreasing forward flexion encourages lifting closer to the trunk and center
of gravity, thereby lessening load on the spine.
c. Controversy exists regarding whether lumbar belts and corsets signifi-
cantly increase lAP, provide support of the spine and alter intradiscal
pressure.
a. Heavy-duty, elastic lumbar corset with adjustable suspenders and Velcro
closure.
b. Lumbar belt of nonstretch material of at least 4 inches width and with either
Velcro or buckle closure.
a. Some controversy exists. Some studies suggest that long term use has been
associated with secondary deconditioning, while others have demonstrated
no significant decrease of trunk strength and endurance.
b. Consider intermittent limited duration of use when possible. Consider core
body strengthening exercises if prolonged use is anticipated.
5. Considerations
a. Scientific literature has not conclusively demonstrated that either education
and/or lumbar supports significantly prevent low back injuries in the indus-
trial population.
b. The US Occupational Safety and Health Administration (OSHA) and the US
National Institute for Occupational Saftey and Health (NIOSH) do not con-
sider back supports to be personal protective equipment for the prevention
of low back injuries.
VI. Compliance and Wearing GuideHnes

A. Comphance
1. Patient compliance is a significant variable in the success of any orthotic pre-
scription.
2. Issues of cosmesis, comfort, fit, and function should be addressed prior to or-
thotic prescription.
B. Orthotic check-out
216 Bracing for Low Back Pain
1. Check the orthosis to ensure that it is fabricated as prescribed and functions as

desired.
2. Check the fit in sitting, standing, and lying positions.
3. For corsets with steel stays, confirm that the steel stays conform to the contour
of the spine, buttocks, and pelvis.
4. For corsets with molded plastic inserts, confirm that the inserts are well molded,
properly oriented, and seated in the pocket.
5. For rigid orthoses, confirm that the orthosis is well molded and set in the de-
sired degree of flexion or extension.
6. Confirm that the rigid orthosis is not compressing the patient at pressure-
intolerant locations such as the pubic symphysis, breasts, axilla, or groin (while
seated).
C. Wearing schedule
1. A rigid orthosis should be worn on the initial fitting for 20-30 minutes and
then evaluated by the physician for areas of undue pressure, as evidenced by
persistent redness of skin after removal of the orthosis.
2. Once a proper fit is ensured and regular wearing schedule initiated, the skin
should be carefully inspected daily by the patient for areas of undue pressure.
3. Corset or soft-wrap orthoses are generally well tolerated in initial wearing peri-
ods and can be worn as long as tolerated.
D. Comfort concerns
1. Rigid orthoses can be fabricated with ventilation holes for wearing in warm or
humid conditions.
2. Foam padding or liner can be added to a rigid orthosis to protect bony promi-
nences and increase comfort.
3. Wearing a cotton T-shirt or thin tube-top beneath an orthosis can help to ab-
sorb perspiration.
4. Talc or antifungal powder also helps to absorb perspiration and reduces the
likelihood of developing a fungal infection.
E. Adverse eHeets ofprolonged bracing
1. Controversy still exists about whether more prolonged orthotic wearing may
weaken musculature and contribute to inactivity-related osteoporosis.
2. Psychological dependence
a. Prescribing an orthosis without appropriate explanation and justification
may lead the patient to believe that a relatively minor condition is very seri-
ous and cause psychological dependence on the orthosis.
b. The patient should be given an estimated duration of use rather than linking
use to level of discomfort.
c. When the orthosis is no longer required, a weaning schedule should be
developed.
3. Posttreatment flexibility deficits-in an effort to immobilize certain vertebral
segments, prolonged spinal orthotic prescription may cause shortening of the
overlying myoligamentous structures with resultant capsular and soft-tissue
contractures.
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1 - - - - - - - -14
The Lumbar Spine: Imaging Options
Andrew J. Cole, M.D., F.A.C.S.M., Kenneth B. Heithoff, M.D., and
Richard J. Herzog, M.D.
Key Points
• Imaging studies do not determine whether a particular structure is painful or is the
source of a patient's pain.
• The optimal imaging study to order and its interpretation must be correlated with a
patient's history, physical examination, response to treatment, and other ancillary
tests. This approach improves diagnostic specificity and selection of the most appro-
priate nonsurgical or surgical treatment options.
• Abnormal imaging findings are found in asymptomatic people. In fact, 340/0 of
asymptomatic people have abnormal computed tomography (CT) scans, and 20-250/0
of asymptomatic people have abnormal magnetic resonance imaging (MRI) scans.
• Not all abnormal imaging findings in symptomatic patients correlate with the source
of their pain. Therefore, the clinician must relate patients' histories, physical exam-
inations, responses to treatment and the results of other ancillary tests to the imaged
findings to determine which of the abnormal imaged results are actually causing pain.
• Plain films provide information about basic osseous structure and the integrity and
alignment of the lumbar spinal motion segments; they help to guide selection of
subsequent imaging.
• The strength of CT resides in its superb demonstration of osseous anatomy, and the
strength of MRI resides in its excellent characterization of soft-tissue anatomy.
• If discogenic pain is suspected, MRI is the test of choice.
• If multisegrnental bony stenosis is thought to be causing a patient's symptoms, CT
provides the best osseous definition.
• MRI with and without gadolinium-DTPA contrast may be beneficial for recurrent or
new symptomatology.
• Both CT and MRI are frequently ordered as complementary studies in cases of spinal
trauma and tumor.
• Single-photon emission computed tomography (SPECT) imaging increases the sensi-
tivity and specificity of a bone scan, particularly when performed to evaluate for a
pars stress reaction or pars stress fracture.
I. Why Order an Imaging Study of the Lumbar Spine?

A. To provide precise anatomic information
1. Must be correlated with the patient's history, physical examination, response to
treatment, and other ancillary tests.
a. Imaging studies provide information about the anatomy of the imaged struc-
tures at a single moment in time.
b. Imaging studies do not determine whether a particular strudure ispainful oristhe source
of a patient's pain.
219
220 The Lumbar Spine: Imaging Options
2. Helps to confirm the clinical diagnosis.

3. More precise imaging information allows greater therapeutic specificity.
B. To help make a diagnosis so that the most effective treatment can be determined.
1. Emergent imaging of a patient with a suspected unstable fracture helps to de-
termine whether the fracture is unstable and the type of surgery that may be re-
quired for stabilization.
2. Imaging a patient who does not improve with physical therapeutic treatments
may localize a suspected disc herniation. The imaging findings help to deter-
mine what type of selective injection procedure would be most effective.
C. To help make a diagnosis so that return to work and sport can be determined. For
example, imaging of a young football player with an acute spondylolysis helps to
determine whether he will be able to return safely to contact sports.
D. To assess the effect of both nonsurgical and surgical treatment techniques.
1. Imaging of a lumbar spine fusion helps to determine whether or not the fusion
has begun, is complete, or has failed. Fusion integrity determines the intensity
of physical therapy and work.
2. Imaging of a lumbar osteomyelitis can help to determine whether chemother-
apy has been successful.
II. Types of Lumbar Spine Imaging Studies (Table 1)

A. Plain films
1. Why toorder
a. Usually the first imaging study ordered due to
i. Availability to most physicians
TABLE 1. Radiographic Studies and Disease Categories ofthe Lumbosacral Spine

Spinal
Herniated Stenosis Hemato-
Nucleus (Osteo- Spondylo- Spondylo- logic
Radiographs Pulposus arthritis) listhesis arthropathy Tumor Disorder Trauma Other
Plain films 1 1 1
Radiation: (Motion) (Sacroiliitis)
2.5 rads
Bone scan 2 2* 2 4 4
Radiation: (Meta- (Hemoglo-
0.15 rads static) binopathy)
Computed 2 2 3 3 4* 3 3*
tomography (Cortical [Intra- (Retroperi-
Radiation: destruction) spinal) toneum)
13 rads
Magnetic 3 2 3* 2 2
(Intra-
Radiation: None spinal)
Myelogram 4 5*
Radiation: (Dropped
6-7 rads metastases)
(Normal
background)
Radiation:
0.6 rads/year
Numbers include sequence of radiographic studies used for diagnosis.
"Best method.
"Costs include mean technical and professional fees.
Adapted from Borenstein DG, Weisel SW, Boden SO: Radiographic evaluation. 1n Low Back Pain. Philadelphia.
W.B. Saunders. 1989, pp 114-115, with permission.
The Lumbar Spine: Imaging Options 221
ii. Speed
iii. Easy to obtain
iv. Reasonable cost
v. Type of information obtained
vi. Helps to determine the next imaging study to be ordered, if needed.
b. Demonstrate basic osseous structure, integrity and alignment of the lumbar
spinal motion segments (Figs. 1- 5).
c. Specific information gained from plain films
i. Unisegmental or multisegmental involvement-disc degeneration
ii. Acute and/or chronic-chronic changes include decreased intervertebral
disc height, vacuum phenomena, end-plate remodeling with ridging and
sclerosis, and spinal malalignment (Fig. 6).
iii. Congenital, developmental, and/or acquired
(a) Transitional vertebrae
(b) Scoliosis and kyphosis
(c) Stenosis
(d) Scheuermann's disease
iv. Alignment and stability or progression
(a) Spondylolysis and spondylolisthesis (see Fig. 5)
(b) Scoliosis and kyphosis
(c) Postoperative results
v. Posttraumatic deformities in alignment and osseous integrity-
compression fracture (Fig 7)
vi. Destructive and erosive
(a) Primary and/or metastatic disease
(b) Infection
(c) Metabolic
(d) Spondyloarthropathies
vii. Other
(a) Paget's disease
(b) Diffuse idiopathic skeletal hyperostosis (DISH)
2. When toorder
a. With no complicating factors, patients between 20 and 50 years old may not
initially require plain films.
b. Patients younger than 20 and older than 50 years
c. No response to conservative care
d. History of trauma (fracture)
e. Known cancer
f. Pain at rest or night pain (malignancy)
g. Unexplained weight loss (malignancy)
h. Corticosteroid use (pathologic fracture)
i. Drug or alcohol abuse (disc space infection)
j. Temperature> 38° C (infection)
k. Neurologic loss
I. Suspicion of spondyloarthropathy
m. Suspicion of spondylolysis or spondylolisthesis
n. Medicolegal requirements and concerns
o. Workman's Compensation claim or assessment
3. Sensitivity and specificity
a. In general, low sensitivity and specificity
b. High sensitivity and specificity
i. Acute fracture or dislocation
222 The Lumbar Spine: Imaging Option5
ii. Chronic spondylolysis and spondylolisthesis

iii. Scoliosis and kyphosis
iv, Gross degenerative changes
v. Some benign bony lesions
(a) Hemangiomas
(b) Bone islands
(c) Osteoid osteoma
(d) Paget's disease
(e) Osteoblastoma
c. Relatively insensitive for diagnosing early spinal infection or tumor since
40-600/0 of bone mass must be lost before a plain radiographic abnormality
is seen.
d. Insensitive and non-specific for
i. Disc herniaton
ii. Marrow infiltration-myeloma
4. Views to obtain and what to look for
a. Anteroposterior (AP)-standing view (see Fig. 1)
i. Five lumbar vertebrae
(a) Lumbarization of S1
(b) Sacralization of L5
ii. Morphology and alignment and symmetry of vertebrae, spinous and
transverse processes, pedicles, facets and lamina
(a) The position of the spinous processes may indicate that the vertebral
body has rotated but also may represent a normal variant. This may
not be correlated with scoliosis.
(b) Lytic and sclerotic lesions of the posterior elements or transverse
processes best seen on AP view (e.g., osteoid osteoma).
(c) Altered pedicle morphology is seen with metastatic disease ("winking
owl" sign).
(d) A pars interarticularis defect appears as an oblique line just inferior
to the pedicles and is seen in the presence of spondylolysis.
b. Lateral view of entire lumbar spine-standing (see Fig. 2)
Morphology of vertebral bodies, pedicles, spinous processes and interverte-
bral disc spaces; lumbar lordosis.
i. Intervertebral disc space height normally increases from Ll-L2 to L4-L5.
Generally, L5-S 1 intervertebral disc and foramina are smaller than those
above.
ii. Degenerative disc changes (See II.A.l.c.ii.) are easily seen.
iii. Compression fractures are observed.
iv. Abnormal spinal alignment may be observed including antero- or
retrolisthes due to acute or chronic degenerative conditions.
c. Coned-down lateral view (see Fig. 3)
Provides more accurate information about the L5-S 1 interspace and bony
elements because the x-ray beam is centered through this interspace and not
through the middle of the lumbar spine, as for the lateral view of the entire
lumbar spine.
d. Left and right oblique views (see Fig. 4)
Morphology of the facet joints and pars interarticularis.
i. Facet joint degenerative changes
ii. Pars interarticularis defect (fracture) can be observed and appears like a
collar on a Scotty dog. (see Fig. 5) The Scotty dog silhouette is formed by
The Lumbar Spine: Imaging Oplions 223
-Twelfth rib
pinous process of L2
-1----r-L3 pedicle
Facet joint
et;lh;7l..l\=7.:i~~:::;~Superior facet of L4
\, Inferior facet of L3
First sacral foramen
A
FIGURE I. Anteroposterior radiographof the lumbar spine. A, Film tracing. 8, Anteroposterior (A-P) normal
plain Rim. Fig. 1A adapted from Magee.16
Pedicle of--*--j~
L2
Intervertebral
Spinous disc
process L2
~:;:::::::=::;;:""Superior
articulating
surface of L3
.------.."--Inferior
articulating
surface ofL3
Transverse
rAocessof
A
FIGURE 2. Lateral radiograph of the lumbar spine. A, Film tracing. 8, Lateral normal plain Rim. Fig. 2A
adapted from Finneson BE: Low Back Pain. Philadelphia, J.B. Lippincott, 1993, pp 54-55.
FIGURE 3. Cone lateral plain Rim radiographof thelumbarspine.
FIGURE 4. Left posterior oblique radiograph of the lumbar spine. A, Film tracing. B, Left posterior oblique
plain Rim. Fig. 4A adopted from Magee. 16
FIGURE S. A, Lytic spondylolysis and spondylolisthesis. B, The lateral plain ~Im of a patientwithGrade I lytic
spondylolisthesis of L5-S1 shows a lytic defectin the pars interarticularis (arrow)and a 10%spondylolisthe-
sis of L5 on S 1. C, Theobliqueplain ~Im shows a defect in the pars interarticularis (arrow). Theneckof the
"Scottie dog" isdisrupted. The14 pars interarticularis has a normal appearance (open arrow head). Fig 5A
adapted from Magee. 16
FIGURE 6. Chronic degenerative changes-

plain ~Im. On a coned down lateral ~Im (A),
the L4-L5 motion segment shows a vacuum
phenomena in the disc (large black arrow),
endplateremodeling withlarge anterior ridges
(curved arrows), and minimal retrolisthesis
(openarrow). A standinglateral ~Im (8) shows
multilevel degenerativedisc disease with large
posterior spurs, small anterior osteophytes,
endplate remodeling, and moderately severe
disc space narrowing at L2-L3, L3-L4, and
L4-L5. An anteroposterior (A-P) ~Im (e) shows
moderately severe scoliosis convexto the left,
severe disc space narrowing of the right side
of the L2-L3 and L3-L4 discs with erosion of
the inferior endplate of l2 by the superiorend-
plate of L3 because of right lateral translation
of the L2 vertebra, and a vacuum sign in the
L3-L4 disc. Inscoliosis, the disc space narrow-
ing occurs earliest and is most severe on the
concave side of the curve. Note that the curve
reverses and isconcaveon the left at L4-L5, re-
sulting in sclerosis and severe disc space nar-
rowingon the left (arrow).
FIGURE 7. A lateral plain Rim showsa compres-

sion fracture of the superior endplate of II with
moderate anterior wedging of the vertebral. The
posteriorcolumn is intact.
the bony elements as seen in the oblique projection. The appearance of a

"decapitated" Scotty dog occurs when a spondylolisthesis is present.
5. Special views
a. Postoperative AP and lateral views-ordered at set intervals to follow the
progress of fusion incorporation after transverse process and anterior inter-
body bony fusions
b. Flexion and extension lateral views
i. Determine whether instability is present. Instability is suggested if on
standing flexion and extension views there is > 4.0 mm of horizontal
translation or > 110 of angulation at the involved level compared with
the adjacent motion segment (Fig. 8).
ii. To follow postoperative fusions for continued or new instability
c. AP lateral side-bending films-to determine whether lateral instability is pre-
sent in patients with scoliosis
B. Tomography (see Table 1)
1. Background
a. Prior to CT and MRI, the imaging test of choice when plain films were not
adequate.
b. Radiation dose is usually significantly greater than with standard CT.
2. When and why to order
a. When CT and/or MRI not available.
b. When the patient is not suitable for CTor MRI.
i. Claustrophobia
ii. Ferromagnetic metal implants or debris
iii. Unable to remain in supine position
228 The Lumbar Spine:Imaging Options
FIGURE 8. Instability-plain films. A, The neutral lat-

eral film shows a Grade I lytic spondylolisthesis of
L4-l5 with severedegenerative disc space norrowing
of the L4-l5 disc and gas within the L4-l5 disc (ar-
row). B, TheAexion lateralfilm showsnarrowingof the
anterior aspect of the disc space and an increase in
the degree of spondylolisthesis (arrow). C, Theexten-
sionviewshowswideningof the anterior aspect of the
disc and a reduction in the spondylolisthesis (arrow).
c. To assess the amount, extent, and integrity of postoperative spinal fusion.
d. Facilitates detection of horizontal fractures and tumors.
C. Bone scan (see Table 1)
1. Background
a. Assess function and tissue metabolism of organs by using a radionuclide
(99mTc) that emits radiation in proportion to its attachment to target struc-
ture. The 99mTc is targeted to specific tissues by attachment or chelation to a
biologically active radiopharmaceutical. For bone scanning, the 99mTc is usu-
ally attached to a diphosphonate derivative (methylene diphosphate [MDP]
or hexose diphosphate [HOP]) that is absorbed to hydroxyapatite matrix.
b. Excellent for detection of bony abnormalities
c. Normally osteoblast and osteoclast activity is balanced.
d. A disturbance in this balance can create an abnormality on bone scan.
i. Increased osteoblastic activity results in increased concentration of ra-
dionuclide tracer.
ii. Interruption of blood flow creates a decrease or absence of tracer ("cold
spot").
iii. Decreased metabolic activity can create a decrease or absence of tracer.
2. Technique
a. Radiopharmaceutical tracer
i. Technetium-99m-MDP or HOP most commonly used for suspected bony
pathology.
(a) 6-hour half-life
(b) Emits gamma rays
(c) Low radiation exposure
ii. Gallium-67 (67Ga) most commonly used to evaluate for infection.
(a) Binds to plasma transferrin, then localizes to sites of infection by sev-
eral mechanisms, including uptake by migrating polymorphonuclear
leukocytes.
(b) Used to detect vertebral osteomyelitis and sacroiliac septic arthritis.
(c) Used to distinguish osteomyelitis from other causes of positive bone
scans (e.g., bony nonunion, infarction, prosthetic complications).
b. Images obtained by scintillation cameras that detect gamma ray production.
i. Especially useful when plain film changes lag behind increased bony ac-
tivity.
(a) Plain film changes associated with osteomyelitis may lag 10-14 days
behind onset of infection
(b) Bone scan becomes abnormal within 24 hours.
ii. Large field-of-view cameras survey entire skeleton (e.g., metastatic disease).
iii. Spot views evaluate smaller areas in more detail.
iv. Single-photon emission computed tomography (SPEO)
(a) Tomographic (CT-Iike) bone imaging technique that offers improved
image contrast and more accurate lesion localization than planar
bone scan but not image resolution (the clarity of the image is not
improved with SPECT).
(b) Especially helpful when more accurate localization of skeletal lesions
within large and/or anatomically complex bony structures is required,
because SPECT can visualize separately bony structures that would
overlap on planar images (e.g., separating vertebral body, facet and
pars interarticularis lesions).
(c) Supplements but does not replace planar bone imaging.
(d) SPECT imaging increases the sensitivity and specificity of bone scan
for detection of lumbar spine lesions by 20-500/0 over planar tech-
nique.
(e) Cost of SPECT study may equal or exceed cost of CTor MRI study.
c. Images may be obtained in three phases
i. Immediate flow study
(a) Essentially an angiogram that tracks vascular spread of the injected
radionuclide over multiple sequential images.
(b) Observe for perfusion abnormalities of suspect tissue.
(c) Aids in detection of lesions with increased perfusion (e.g., with os-
teoid osteoma and acute fractures).
ii. Immediate static blood pool study
(a) Observe for abnormal pooling of radionuclide tracer in suspect tissue.
(b) Increased blood pooling (hyperemia) seen (e.g., with osteoid osteoma,
acute fractures and cellulitis).
iii. Delayed static study (2-4 hours after injection)
(a) Observe for abnormal accumulation of radionuclide in areas of active
bone remodeling.
(b) Increased uptake seen (e.g., with pars stress reaction, acute spondylo-
lysis, acute compression fracture, osteomyelitis).
3. Clinical applicatians
a. Pars stress reaction, acute or subacute spondylolysis, stress fractures, and acute frac-
tures (Figs. 9 and 10)
i. May be difficult to detect on plain films.
ii. With bone scan, the lesion can be detected within 72 hours of fracture.
iii. SPECT imaging increases sensitivity and specificity.
iv. A healing acute spondylolysis or compression fracture may continue to
be abnormal on bone scan for up to 2 years. Usually more rapid resolu-
tion of abnormal bone scan is seen in younger patients.
(a) In essence, the bone has healed before the bone scan becomes normal
because of continued remodeling.
(b) Serial bone scans may be ordered if clinical decision-making will be
influenced by the amount of healing that has occurred.
fIGURE 9. Radionuclide bone scan-delayed

static study. This patient with a unilateral lytic
spondylolisthesis shows increased activity of
the left pars interarticularis of l5 on the right
posterioroblique (RPO) view(arrow).
FIGURE 10. Coronal SPECT image

of the same patientas Figure 9 is
markedly positive with area of in-
creased uptakeat the pors interar-
ticularis (arrow).
(c) Bone scans may be performed at three to four month intervals. The
intensity of the tracer at the lesion site typically diminishes over time.
(d) Interval scanning can also be used to evaluate the natural history of a
spondylolysis or compression fracture.
b. Facet osteoarthritis and facet pain syndromes
i. There is a strong correlation between increased uptake in the articular
facets on SPECT images and morphologic changes of osteoarthritis.
ii. An abnormal SPECT scan may help to select patients for intraarticular
facet injection procedures because abnormal increased facet uptake on
SPECT images has been shown to be predictive of a favorable response to
facet injection.
c. Failed lumbar spine surgery syndrome
i. By 1 year after surgery a well-healed fusion mass has, at most, mildly in-
creased intensity on bone scan.
(a) Pseudarthrosis has increased activity
(b) Abnormal SPECT images may be of significant value in detecting
painful pseudarthrosis.
ii. Increased uptake may be seen in spinal motion segments directly adja-
cent to fusion because of spondylolysis and/or facet joint osteoarthritis.
d. Primary and metastatic disease: 10-400/0 of patients with metastatic disease and
normal plain films have abnormal bone scans.
i. Bone scanning is highly sensitive for most metastases.
ii. However, in some cases of multiple myeloma or purely lytic metastases
from aggressive tumors, the lack of a significant osteoblastic response
can diminish sensitivity.
iii. Increased bone scan activity is seen in these conditions when a fracture
occurs.
e. Infection
i. Osteomyelitis
ii. Septic arthritis
iii. Discitis
f. Generalized bone disease associated with metabolic abnormalities
g. Osteoneuosls
h. Sacroiliac lolnt-spondylarthropathies
D. Myelography (see Table 1)
1. Background
232 The Lumbor Spine: Imaging Options
a. Long considered the gold standard to evaluate neural compression.

b. Contrast injected into the subarachnoid space outlines the dural sac and
nerve roots.
c. Dynamic test measuring ability of CSF to flow by an extradural lesion.
i. Visualization of the spinal canal in flexion, extension, side-bending,
extension-rotation, and weightbearing may result in dynamic nerve root
impingement that may be missed on routine static CTor MRI.
ii. Imaging can occur while patient is in pain-provoking position to see if
abnormal spinal morphology can identify potential source of pain.
d. 24010 of asymptomatic volunteers found to have an abnormal filling defect
on myelography.
e. Now performed as a same-day outpatient procedure.
f. Rarely used as an imaging test in isolation; is usually combined with a post-
myelographic CTstudy.
g. Study of choice to evaluate for disc herniation and/or arachnoiditis in post-
operative spines with metal hardware in place.
h. Useful for evaluating severe spinal deformities and post-operative patients
with metal hardware in place.
i. Useful for the few preoperative patients in whom questions remain about
equivocal CT or MRI findings.
j. Useful when clinical findings are compelling and not adequately explained
by CT or MRI.
k, Unable to differentiate disc herniation from bony, malignant, infectious, or
other extradural lesions.
2. Technique
a. Usually outpatient procedure
b. Usually combined with postmyelographic CT
c. 10-15 ml of water-soluble, nonionic contrast medium injected through 22-
gauge needle into subarachnoid space. Water-soluble contrast now used:
i. Fewer side-effects than oil-based contrast (Pantopaque) (e.g., seizures,
nausea, vomiting, and arachnoiditis).
ii. Equal imaging detail as Pantopaque.
d. Complications
i. Headache-680f0
ii. Nausea and vomiting-380f0
iii. Back pain-260f0
iv. Seizures-O.40f0
e. Views obtained (Fig. 11)
i. Anteroposterior view demonstrates
(a) Conus medullaris
(b) Cauda equina
(c) Dural nerve root sleeves
ii. Bilateral oblique views demonstrate nerve roots surrounded by nerve root
sheath.
iii. Lateral prone view demonstrates relationship subarachnoid space and
dura to posterior aspect of vertebral bodies and intervertebral discs.
f. Lesion locations
i. Extradural-may interrupt contrast column by displacing the dura and
the normal course of thecal sac and subarachnoid contents.
(a) Herniated disc
(b) Osteophyte
(c) Abscess
FIGURE 11. Myelography. The A-P Rim (A) shows mild scoliosis con-
vex to the left and on extradural defecton the left at L3-L4 due to
recurrent discherniation. There isassociated nonRlling of the left L4
nerveroot(arrow). There isbiconvex narrowing of the thecalsocat
L4-l5 without amputation of the l5 nerveroot sheathsdue to cen-
tral bulging of the L4-l5 disc. 8, The left posterior oblique Rim
demonstrates a left L3-L4 extradural defectand the nonRlling of the
left L4 nerveroot (arrow). C, Thelateral prone Rim showsindenta-
tionof the thecal soc at bath L3-L4 and L4-l5 resulting from poste-
rior disc protrusions.
(d) Hematoma
(e) Tumor
ii. Intradural-extramedullary-alters thecal sac and dural spatial relation-
ship.
(a) Neurofibromatosis
(b) Meningioma
(c) Dropped metastasis
iii. Intramedullary-causes expansion of spinal cord and usually symmetric
obliteration of subarachnoid space.
(a) Spinal cord tumor

(b) Vascular malformation
(b) Syringomyelia
3. Clinical applications (see page 243)
E. Computed tomography (a) (see Table 1)
1. Background
a. Provides excellent osseous detail of osteophytes, fractures, and the location
and extent of neoplastic or infectious bony destruction and extension to ad-
jacent soft tissues.
i. Visualize vertebral body and posterior elements.
ii. Can detect bone destruction before changes are visible on plain radio-
graphs.
b. Soft tissue seen in graded shadings helps to distinguish between ligaments,
nerve roots, free fat, and herniated disc material.
c. CT is at least as sensitive and specific in diagnosing herniated lumbar disc as
myelography.
d. The addition of myelography to the CTstudy may demonstrate additional
pathologic conditions.
e. Use of CT and myelography together exceeds the value of either alone.
i. Improved evaluation of neural compression by bone and soft tissue
f. Axial CTimages sometimes unable to demonstrate foraminal disc hernia-
tions, ventral facet hypertrophy, and endplate osteophytes.
i. Multiplanar reformatted images help demonstrate.
g. 34010 of asymptomatic people have abnormal CTscans.
a
h. Advantages of (Table 2)
i. Performed as outpatient procedure
ii. Noninvasive
iii. Limited ionizing radiation exposure
(a) To adjacent structures that are not being imaged.
(b) Dose increases with high-resolution slow speed scanning.
iv. Total imaging time relatively short
v. Relatively low cost
vi. New spiral technology allows multiplanar images to be obtained quickly
and easily.
vii. Although new scanning techniques may decrease examination time, res-
olution may also be compromised.
TABLE 2. atO-Myelography vs. MRI

CT/MPR MRI
Discdegeneration + ++
Discherniation + ++
Facet arthropathy ++ +
Infection + ++
Intrathecal pathology -/+ ++
Myelopathy + ++
Paravertebral pathology + ++
Postoperativespine + ++
Spondylosis/spondylolisthesis ++ ++
Stenosis ++ ++
Structural alignment ++ +
Trauma ++ ++
Tumor evaluation + ++
Examination of choice, + +; Additional information, +; No role. -.
a
i. Advantages compared with MRI
i. Direct imaging of cortical bone to detect bony trauma, stress fractures
(pars interarticularis defects), or tumor invasion.
ii. Open scanner format-little difficulty for c1austraphobic patients.
iii. CT-myelography useful when MRI contraindicated.
(a) Cardiac pacemaker or defibrillator
(b) Cochlear or ocular implants
(c) Some intracerebral aneurysm clips
(d) Metal life-support system being used
(e) Medication pump
(f1 Ferromagnetic metal fragments embedded in eye or spinal canal
j. Disadvantage of a
i. Ionizing radiation exposure
ii. Slightly restricted field of view
iii. Poor delineation of intrathecal anatomy and pathology
k. Relative contraindication to CT-pregnancy
2. Technique (Fig. 12)
a. X-ray source generates cross-sectional images.
b. CT images are representations of differential x-ray attenuation by tissue.
Attenuation determined by tissue's electron density.
c. Spatial and contrast resolution depend on
i. Energy of x-ray source
ii. Slice thickness
iii. Field of view
iv. Scanning matrix
d. Optimization of soft tissue vs. osseous structures is accomplished with a va-
riety of pre- and postprocessing computer software programs.
e. AP and lateral "scout" radiographs assess for
i. Transitional segmentation
ii. Spinal alignment abnormalities
(a) Lytic or degenerative spondylolisthesis
(b) Retrolisthesis
(c) Kyphosis
(d) Hyperlordosis
iii. Disc space narrowing
iv. Spondylotic changes
f. Routine examination includes 5-mm thick with a 2-mm overlap slice thick-
ness or contiguous 3-mm thick sections to produce high-resolution axial
and multiplanar (sagittal and coronal) CTimages (see Fig. 12).
i. Axial images from mid S1 sacral segment to L3 pedicle
ii. Additional images obtained depending on
(a) Clinical history
(b) Information provided by requesting physician
(c) Results of scout view
iii. Reformatted images are obtained using bone and soft-tissue windows to
include
(a) Entire neural foramen
(b) Central spinal canal
g. New spiral CT technology provides more rapid imaging capabilities of the
lumbar spine, which may be helpful for imaging patients whose pain pre-
vents them from remaining still for prolonged periods of time. May slightly
compromise both spatial and contrast resolution.
FIGURE 12. Normal lumbar spineanatomy-CT/MPR. On the axial (A) and sagiltal(B) images, there is excel-
lent delineation of thethecal sac (straight black arrows), dorsal rootganglia (curved black arrows) in the neuro-
foramen, and the posterior margin of thediscovertebral joints (curved white arrows). (Figure continued.)
h. Image quality depends on patient immobility to prevent artifact formation.

i. Faster scanners allow an entire routine examination to be performed in
under 20 minutes.
ii. Not difficult for most patients to maintain a single position for this
amount of time.
i. Contiguous sagittal and coronal reformatted images provide evaluation of
the lumbar spine in complementary orthogonal planes.
j. Software programming produces two sets of images
i. Images emphasizing soft-tissue detail
ii. Images emphasizing bony detail
3. Clinical applications (see page 243)
FIGURE 12. (Continued). On the axial (e) and sagittal (0) images, there is excellent delineation of the facet
joints (curved black arrows). The neuroforamen (straight whitearrows) are optimally demonstrated on the
sagittal images. Thecurved white arrows demonstrate the l5 pars interarticularis.
F. Magnetit resonante imaging (MRI) (see Table 1)

1. Batkground-uses a magnetic field, not ionizing radiation, to obtain direct multi-
planar images with excellent soft-tissue contrast.
a. Excellent anatomic resolution of MRI allows more precise description of disc
morphology. Tears of the anulus fibrosus can be imaged.
b. Imaging test of choice (which may be supplemented when used with gado-
linium DTPA, an intravenous contrast agent) for
i. Detecting both intradural and extradural spinal tumors, spinal infections
ii. Detecting intramedullary abnormalities such as syringomyelia, myeloma-
lacia, neoplasms, and demyelination
iii. Distinguishing recurrent disc herniation from postoperative scar
b. Comparison of MRI with CT and myelography
i. MRI is more sensitive and specific than CT for diagnosing a herniated
lumbar disc.
(a) MRI as accurate in detecting sequestered and far lateral (extraforami-
nal] disc herniations.
ii. MRI and CT-myelography both detect spinal stenosis of the central canal,
lateral recess, and neuroforamen if higher resolution MPRF are used.
(a) But MRI also detects associated disc degeneration in significantly
more cases.
iii. MRI comparable to CT-myelography for detection of routine lumbar de-
generative changes
(a) Osteophytosis
(b) Disc bulges
c. MRI abnormalities detected in 22010 of asymptomatic subjects under 60 and
57010 over age 60, 98010 prevalence of degenerative disc findings at one level
(decreased signal intensity on T2 images) in those over age 60.
i. Normal nonpainful degenerative changes of the lumbar spine must be

recognized so that imaging findings are not misinterpreted.
ii. Imaging findings must always be correlated with the patient's history, physlcalex-
amlnatlon, response to aggressive conservative care, and other test results.
d. Advantages of MRI
i. Performed as outpatient procedure
ii. Noninvasive
iii. No ionizing radiation used
iv. Exquisite soft-tissue detail possible
v. Direct multiplanar images possible so that images in all planes have bet-
ter resolution (clarity)
vi. Visualization of intrathecal neural elements
vii. Extremely sensitive to marrow abnormalities
(a) Infection
(b) Metastatic disease
(c) Nondisplaced vertebral body fracture
(d) Sacral insufficiency
e. Disadvantages of MRI
i. Claustrophobic patients have difficulty due to small diameter of imaging
"tunnel."
(a) Sedation with medication may help.
(b) Preprocedure patient education helps.
ii. Longer scan time than CT
iii. Cost may be higher than CT
iv. Contraindicated in patients with
(a) Cardiac pacemaker and defibrillator
(b) Cochlear and ocular implants
(c) Some intracerebral aneurysm clips
(d) Ferromagnetic metal-life-support system being used
(e) Medication pump
(0 Ferromagnetic metal fragments embedded in eye or spinal canal
(g) Nonferromagnetic implants near the intended imaging site can create
artifact causing significant image degradation.
(h) Pregnancy-some consider a relative contraindication in first trimester.
2. Technique (Fig. 13).
a. MR image is created by radio waves of a specific radiofrequency (RF) pulsed
into the body after the patient is placed in an external strong magnetic field
(the MR magnet). Causes the nuclei of atoms (primary hydrogen) with an
odd number of protons to absorb energy and achieve a higher energy state.
b. When RF pulse is terminated, the excited nuclei release energy and return to
a lower energy state
i. Nuclear magnetic resonance is the characteristic absorption and release of
this energy.
ii. Relaxation is the process of returning from the excited to the equilib-
rium state and is characterized by two independent time constants,
T1 and T2.
(a) T1 (longitudinal relaxation time) reflects the time required for protons
excited to a higher energy state by the MR magnet to return to their
equilibrium state.
(b) 12 (transverse relaxation time) reflects the time required for protons
that have been excited by an externally applied RF into a direction
The Lumbar Spine: Imaging Oplians 239
FIGURE 13. Normol lumbar spine anatomrMRI. On the

sagittal Tl-weighted image (AI, there is excellent delineation
of the vertebral bodies, intervertebrol discs, thecal sac, lower
thoracic cord, and conusmedullaris (curved white arrow).The
high signal intensity of thevertebral bodies isdue to the fat in
the cancellous marrow. There is not a well-deflned interface
between the posterior outer anular flbers (straight white ar-
row) and the cerebrospinal Ruid. (Figure continued.)
perpendicular (transverse) to that initially created by the MR magnet

to lose their transverse magnetization.
(c) II and T2 are intrinsic physical properties of tissue.
iii. MR signal intensity depends mainly on the II, T2, and proton density
(number of mobile hydrogen ions) of the tissue being evaluated.
iv. Pulse sequences (spin echo and gradient echo are the most commonly used)
are the methods used to obtain MR data and depend on several scanning
parameters that are determined before scanning (Table 3).
(a) Repetition time (TR)-the time between RF pulses.
(b) Echo time (TE)-the time between the application of the RF pulse and
the recording of the MR signal.
v. By varying the scanning parameters (TR and TE), the relative contribu-
tion of the II, T2, and proton density of the tissue determines image
contrast
vi. n-weighted image-emphasizes the II properties of a tissue (see Table 3)
(a) Short TR (400-600 ms) and a short TE (15-30 ms)
TABLE 3. Image Weighting Parameters

Proton Density
T1 Spin Density T2
TR 400-600 ms 1500-2000 ms 1500-4000 ms
TE 15-30 ms 15-30 ms 60-120 ms
FIGURE 13. (Continued). On the sagittal proton-density-

weighted image (B), increasedsignal intensity in the disc is iden-
ti~ed along with increased signal intensity of the cerebrospinal
Ruid. This results in improved delineation of the posterior anular-
posterior longitudinal ligament complex (arrow). On the sagittal
T2-weighted image (q, increased signal intensity in the disc is
identi~ed along with a linear horizontal area of decreased signal
intensity inthecenterof thediscrepresenting the intranuclear cleft
(arrows). Thereis increased signal intensity in the cerebrospinal
Ruid creating a myelographic effect and providing an excellent
CSF-extradural interface. On the sagittal Tl-weighted image (D)
through the neuroforamen, there is excellent delineation of the
dorsal root ganglia (straight white arrows) positioned subjacent
to the vertebral pedicles. Theposterolateral margin of the discs
(curved white arrows) is well delineated. (Figure continued).
(b) Best to evaluate structures containing fat, subacute or chronic hemor-

rhage, or proteinaceous fluid because they have a high signal inten-
sity on Tt-weighted images (Table 4).
vii. Proton-density or spin-density-weighted image reflects the absolute number of
mobile hydrogen ions in the tissue (see Table 3).
(a) Long TR (I,500-2,OOO ms) and short IE (I 5-30 ms)
(b) Best to evaluate spinal ligaments and facet morphology (see Table 4)
viii. T2-welghted image-emphasizes the T2 properties of a tissue; depends on
the state of tissue hydration and biochemical environment (see Table 4).
FIGURE 13. (Continued). On the axial Tl-weighted image IE), there is excellent delineation of the individual
nerveroots(long whitearrow) in the thecal sac. The presenceof fat in the epidural space and neuroforamen
provides an excellent soft-tissue interface to evaluatenerveroots(shortblackarrows), ligaments, and osseaus
elements.
(a) Long TR (1,500-4,000 ms) and a long IE (60-120 ms)

(b) Best to evaluate tissues rich in free or extracellular water such as
cerebrospinal fluid, cysts, necrotic tissue, fluid collections, interverte-
bral discs, and neoplasms because they have a high signal intensity
on Tz-weighted images (see Table 4).
ix. Mineral rich tissue (e.g., cortical bone) contains few mobile protons and
has very low signal intensity on all pulse sequences.
x. Gas has no mobile hydrogen ions and therefore generates no MRI signal.
xi. Image quality is affected by signal-to-noise ratio, slice thickness, field
of view, and size of acquisition, display matrices, and magnetic field
strength.
TABLE 4. nssue and Bady Fluid Signal Intensity an Il- and T2-Weighted Images
Tissue or Body Fluid n-Weighted T2-Weighteel Proton Density
Cortical bone Low Low Low
Tendons and ligaments Low Low Low
Fibrocartilage Low Low Low
Hyaline cartilage Intermediate Intermediate Intermediate
Muscle Intermediate Intermediate Intermediate
Benign neoplasm Low-intermediate Low-intermediate Low-intermediate
(occasionally high)
Malignant neoplasm Low-intermediate Intermediate-high Intermediate
(occasionally low)
Free water (CSF) Low High Intermediate
Proteinaceous fluid (abscess) Intermediate High Intermediate
Adipose tissue High Intermediate-high Intermediate
Hemorrhage Variable Variable Variable
Adapted from Herzog RJ: Selection and utilization of imaging studies for disorders of the lumbar spine. In
Herring SAled): Low Back Pain. Philadelphia, W.B. Saunders, 1991, p 14, with permission.
xii. Motion artifact also affects image quality.

(a) With MRI patient movement degrades all images in a spin sequence
vs. CT, where only a single image is affected
(b) Fast-scanning methods (gradient echo and fast spin-echo imaging)
decrease scan time so that patient discomfort and motion during the
study are minimized.
(i) The information obtained from gradient echo sequences is differ-
ent from standard Tt- and Tz-weighted sequences and is there-
fore not a simple replacement for a standard spin-echo sequence.
(ii) Referred to as a T2* (gradient echo), this contrast is different from
the standard T2 contrast obtained on spin-echo sequences.
c. Standard MRI examinatian af the lumbar spine (Table 5) (see Fig. 13)
i. Sagittal n-weighted sequence optimally evaluates
(a) Spinal anatomy
(b) Medullary bone
(c) Discovertebral joints
(d) Neural foramen
(e) Facet joints
(f) Conus medullaris
(g) Epidural space
ii. Axial n-welghted sequence optimally evaluates
(a) Thecal sac
(b) Epidural sac
(c) Facet joints
(d) Ligamentum flavum
(e) Nerve roots
(f) Neural foramen
(g) Paraspinal soft tissues
iii. Axial T2-weighted sequence optimally evaluates
(a) Thecal sac contents
(b) Disc contour
TABLE 5. Standard MRI Examination of the Lumbar Spine

Sagittal Tl-weighted sequence optimallyevaluates Axial T2-weighted sequence optimallyevaluates
Spinal anatomy Thecal sac contents
Medullary bone Disc contour
Discovertebra1joints Paravertebral soft tissues
Neural foramen Epidural space
Facet joints Facet joints
Conus medullaris Axial Tl-weighted sequence optimallyevaluates
EpiduraI space Thecal sac
Sagittal T2-weighted sequence optimallyevaluates Epidural space
Discdegeneration and herniation Facet joints
Marrow edema Ligamentum flavum
Abnormal fluid accumulations Nerve roots
Extradural masses Neural foramen
Intrathecal disease Paraspinal soft tissues
Sagittal proton density sequence optimallyevaluates
Posterior anular-posterior longitudinal ligament complex
Ligamenta flava
Central canal
Neural foramen
Facetjoints
Posterior elements
(e) Paravertebral soft tissues

(d) Epidural space
(e) Facet joints
iv. Sagittal T2-welghted sequence (with fat saturation) optimally evaluates
(a) Disc degeneration and herniation
(b) Marrow edema
(c) Abnormal fluid accumulations
(d) Extradural masses
(e) Intrathecal disease
(f) Spinal cord
(g) Conus medullaris
(h) Nerve roots
v. Sagittal proton density sequence optimally evaluates
(a) Posterior anular-posterior longitudinal ligament complex
(b) Ligamenta flava
(c) Central canal
(d) Neural foramen
(f) Posterior elements
vi. depending on the suspected pathology before the study, abnormalities
discovered may require further imaging, special sequences and planes of
view may be obtained.
d. Sagittal slice thickness is 4-5 mm with an interslice gap of 0.5-1.0 mm
e. Contiguous axial images with a thickness of 3-4 mm and an interslice gap
of 0.5-1.0 mm obtained from L2-L3 or L3-L4 disc level to the sacrum.
3. Clinical applications (see below)
III. Clinical Applications

A. Background
1. The decision to order an imaging study and which one to order should be based on the following:
a. An understanding of the natural history of spinal diseases and the degenera-
tive cascade
b. History
c. Physical examination
d. Response to treatment
e. Prior test results
2. Plain films may help to guide selection of next imaging test.
a. CT and/or CT myelography may be most helpful if osseous abnormality sug-
gested.
i. Trauma
ii. Facet arthrosis
iii. Spondylolysis
vi. Spondylolisthesis
v. Multilevel stenosis
b. MRI may be most helpful if an abnormality suggested
i. Disc
ii. Thecal sac
iii. Epidural space
iv. Neural elements
v. Paraspinal soft tissue
vi. Bone marrow abnormalities
3. Advanced imaging studies should be ordered if the information they provide
will directly affect the care of the patient.
4. The transformation of diagnostic data into useful clinical information depends

directly on the level of expertise of the physician interpreting the study.
5. The preimaging probability that a patient truly has a specific disease fre-
quently determines whether the findings on a particular imaging study will
be acted on.
6. In some locations the equipment required to perform the imaging study of
choice for a particular problem is not available, and the clinician may have to
"make the best" of the situation.
B. Degenerative lumbar "disease"
1. Background
a. Do not focus on isolated pathology (e.g., an L4-L5 herniated disc); rather, make
sure to evaluate all components of each imaged motion segment.
b. Plain film abnormalities are of limited value for evaluating disc degenera-
tion and are of little predictive value for determining the cause of spinal or
radicular pain. Plain film changes associated with degenerative disc disease
(see Fig. 6) include
i. Decreased disc height
ii. Bony sclerosis
iii. Gas within disc space ('vacuum phenomenon")
iv. Calcification within the disc space
v. Vertebral body endplate osteophytosis
2. Disc herniation
a. MRI and CT provide excellent delineation of disc herniation.
i. However, MRI can detect pathoanatomic and chemical changes within
the disc prior to changes in disc contour.
ii. On an MRI spin-echo T2-weighted sequence, the signal intensity of the
disc is related to the state of hydration and biochemical environment of
the nucleus pulposus and the inner anular fibers.
iii. Normally a loss of the high signal intensity in the disc is seen on the T2-
weighted images as the disc gradually degenerates and the disc becomes
a more fibrocartilaginous structure.
iv. Not unusual to detect decreased signal intensity in disc levels that are
asymptomatic
v. Asymptomatic disc herniations are relatively common.
b. Myelography, an invasive study, is rarely indicated for evaluation of disc
abnormalities because of the excellent sensitivity, specificity and accuracy of
MRI and CT.
b. Morphology and terminology ofdisc herniation (Fig. 14)
i. Anular tear (synonym: fissure): a cleft or separation between fibers of the
anulus, extending circumferentially, radially, or horizontally through one
or many layers of the anular lamellae (Fig. 14A).
(a) Probably the necessary step in development of a disc herniation.
(b) MRI can detect these tears before a herniation occurs.
(c) Routine CT and CT myelography cannot detect anular tears.
ii. Disc protrusion (one type of disc herniation; disc herniation is a general term
describing focal displacement of disc material beyond the normal confines
of the disc.): a focal contour abnormality of the outer anular disc fibers
caused by the displacement of nuclear material that is contained by the
outer anulus or the posterior longitudinal ligament (Fig. 14B).
(a) The location of the protrusion in the axial plane is described as cen-
tral, right central (synonym: right paracentral), left central (synonym:
left paracentral), subarticular zone foraminal, or extraforaminal.
FIGURE 14A-I. Morphology and terminology of the disc herniation-diagram and MRI. A, Sagittal T2-
weighted image showing a highsignalintensity anular tear (block arrow). B, A contained high signal inten-
sity(lise protrusion at L4-L5 (arrow). (Figure con/inued.)
(b) The location of protrusion in the sagittal plane is described as discal,

suprapedicular, infrapedicular, or pedicular.
(c) Both MRI and CTICT myelography can detect.
iii. Disc extrusion (one type of disc herniation; disc herniation is a general
term describing a focal displacement of disc material beyond the normal
confines of the disc): penetration of the disc material through the outer
anulus. If the disc material does not penetrate the posterior longitudinal
ligament complex, it is considered a subligamentous extrusion. If it pen-
etrates through the posterior longitudinal ligament, it represents a
transligamentous extrusion (Fig. 14C).
246 The Lumbar Spine: Imaging Oplions
FIGURE 14(. An extruded disc at L5-S1 on proton density MRI. Theextruded disc material extendswell be-
yond the torn anulusand posterior longitudinal ligament (arrows). (Continued below.)
FIGURE 14D. There is a large complex

sequestered discherniation at the L5-S1
level which consists of a large broad-
based extruded central component
(small black arrow on sagittal image
[top] and open arrowhead on the axial
image [bottom]), and a superimposed,
high signal intensity sequestered Frag-
ment on the right which extends cau-
dallyto the inFerior aspect of the Sl ver-
tebral body and produces severe
compression of the right S1 nerve roat
and rightsideof thethecalsac (largear-
rows). (Continued on next page.)
FIGURE 14E. Bulging disc-MRI. There is dehydration, disc space narrowing and circumferential bulging of
the L4-L5 disc (arrow), and degenerative dehydration and disc space narrowing at L5-S1.
(a) Both MRI and CT/CT myelography can detect.

(b) MRI may determine whether the disc material is contained by the
outer anulus.
iv. Sequestered dis( fragment (synonyms: free fragment, displaced disc): disc
material separates from its disc of origin (Fig. 14D).
(a) May migrate cranial or caudal to the disc space.
(b) Usually initially generates increased signal intensity on T2-weighted
images compared to the degenerated disc of origin.
v. Bulge: symmetric extension of the anulus beyond the margins of the ver-
tebral body endplates (Fig. 14E).
c. After a disc has herniated, the disc material within the disc space continues to
degenerate, and low signal intensity on spin-echo T2-weighted images is seen.
i. Foci of high signal intensity on Tz-weighted images representing fluid-
filled fissures and granulation tissue within the degenerating disc also
may be seen. These foci of high signal intensity should not be confused
with an inflammatory process.
ii. No prospective study has determined the length of time necessary for a
normally hydrated disc to become degenerated after it herniates.
Therefore, itisnot possible to date the elad o((urrente ofadis( herniation unless a
prior MRI study isavailable for (omparison.
d. Vertebral body endplate degenerative changes occur in response to altered
discovertebral joint mechanics. Altered discovertebral joint mechanics occur
as a result of disc degeneration and herniation (Figs. 6, 15, and 16).
i. CT, however, is more accurate than MRI in the evaluation of the location
and size of endplate ridges.
(a) CT permits accurate delineation of the location endplate ridges in re-
lation to neural structures.
(b) CT helps to differentiate osteophytes from disc material.
ii. Schmorl's nodes represent extension of the intervertebral disc into the
adjacent vertebral body (see Figs. 6 and 15).
(a) Due to compressive loading of the disc with extension of disc mater-
ial through an endplate defect.
FIGURE 15. Schrnorl's Nodes-MRI. There are

multilevel Schrnorl's nodesinvolving theT12-L 1
through L3-L4 endplates. (Open arrowheads).
Schmorl's nodes may be seen as an isolated
finding or, as in this case, multilevel. This 31-
year-old male has advanced degeneration of
the L4-L5 and L5-S1 discs with broad-based
bulging, dessication, and discspace narrowing
(arrows).
(b) The vast majority are asymptomatic.

(c) Sagittal MRI images demonstrate extension of disc material through
the endplate of an adjacent vertebral body.
(d) CT also demonstrates Schmorl's nodes as a lucent endplate defect
with a surrounding rim of sclerosis.
3. Facet arthrosis
a. As the discovertebral joint degenerates and its functional mechanics change,
the facet joints may share increasing loads. The increased loads placed on
the facet joints may induce facet degeneration.
b. CT is best at evaluating facet bony degenerative changes and facet joint ori-
entation (see Fig. 16).
i. Early bony erosions
ii. Cystic changes
iii. Bony proliferation
iv. Facet capsular calcification
v. Facet joint vacuum phenomenon
c. MRI can be helpful to visualize (see Fig. 15).
i, Articular erosion
ii. Facet hypertrophy
iii. Joint effusions
iv. Capsular hypertrophy
v. Facet joint cysts
4. Spinal stenosis
a. Local, segmental or generalized narrowing of the central spinal canal or
neuroforamina by bony or soft-tissue elements that may encroach on the
neural structures.
i, Narrowing may involve bony canal alone, dural sac, or both.
ii, The degenerative changes most often associated with stenosis include
(a) Osteophytosis of the vertebral body endplates
(b) Hypertrophy and bony proliferation of the facet joints
(c) Hypertrophy of the ligamenta flava
(d) Hypertrophy of the anterior facet capsules
iii. Initial size of the central spinal canal and neural foramen is an important
factor in determining whether degenerative changes cause neural im-
pingement or compression.
FIGURE 16. lumbar facetorlhrosis. On the axial proton-density-weighted imageof the MRI examination (AI,
degeneration of the left facetIOoint is identi~ed with narrowing of the articularcartilage(shortarrow)and os-
teophytic ridging ofthedorsa surfacelIong arrow)of the left superiorarticularprocess. On the a /MPR eval-
uation of the lumbar spine IBI, there is excellent delineotion of subehrondral cystic changes (blackarrow) in-
volving the facet joints.
b. Purpose ofMRI and a isnot just to demonstrate that stenosis ispresent but also to de-
fine the relative contributions ofeach component ofthe stenotic process.
c. Types ofstenosis
i. Congenital stenosis is present neonatally.
ii, Developmental stenosis is a growth disturbance of the posterior elements in-
volving the pedicles, laminae, and facet joints that cause decreased vol-
ume of the central spinal canal or neural foramina.
(a) Relative stenosis-midline sagittal diameter of < 12 mm (measured from
the middle of the posterior surface of the vertebral body to the junc-
tion point of the base of the spinous process and the laminae).
(i) Reserve capacity of the spinal canal is reduced.
[ii] Small disc herniation or mild degenerative changes may cause
symptomatic stenosis.
(b) Absolute stenosis-midline sagittal diameter of < 10 mm.
iii. Acquired stenosis is the narrowing of the central spinal canal or the neural
foramina by degenerative changes of the discovertebral joints, facet
joints, and ligamenta flava (Fig. 17).
FIGURE 17. Neuroforaminal canal stenosis ot the l5-S 1 disc level-cT/MPR. On the axial image (Al, the
spondylotic ridges (straight arrow) are identified, projecting into the right neuroforaminal canal. (Figure
continued.)
fIGURE 17. (Continued.) The sagittal (8 and C) and

coronal (D) reconstructed images optimally delineate
the degree of stenosis secondary to the degenerative
ridging (curved arrows).
d. Both CT and MRI can accurately assess the degree of central canal narrow-
ing (see Fig. 17).
i. CT better demonstrates osseous proliferative changes that may be nar-
rowing the subarticular and lateral recesses. Helps with presurgical plan-
ning, ensuring that the structures causing the stenosis are adequately de-
compressed while those that are not contributing to the stenosis are
preserved so that the chance of postoperative instability is minimized.
ii. MRI allows noninvasive measurement of the cross-sectional area of the
thecal sac-a measurement that may have the best correlation with a pa-
tient's stenotic symptoms. Previously, invasive imaging (myelography or
CT-rnyelography) was needed to determine the degree of narrowing of
the thecal sac.
e. Foraminal stenosis may be an important cause of radicular symptoms and the
most common cause of failed low back surgery. Multiplanar CT helps to
demonstrate accurately (see Fig. 17).
i. Osteophytes projecting from the posterolateral margin of the vertebral
body endplates that may narrow part or all of the neural foramina.
Location and size of osteophytes help to guide selection of spinal injec-
tion procedures and, when required, help with surgical planning.
ii. Facet degenerative changes may also narrow the neural foramina, central
spinal canal, and lateral recesses.
f. Far-out (extraforaminal) stenosis at L5-S 1 causes compression of the L5 nerve
root after it exits the neural foramen.
i. Seen most commonly in elderly patients with scoliosis and younger pa-
tients with isthmic spondylolisthesis.
FIGURE 18. Multilevel degenerative changes of the lumbar spine-MRI. On the sagittal proton-density-
weighted imoge (A), multilevel degenerative changes are identified. A degenerativeanterolisthesis is present
at tne L3-L4 disc level (short straightarrow), causing moderately severecentralcanal stenosis (curved black
arrow). On the sagittal T2-weighted image (B), discdegeneration and decreased signal intensity are identi-
~ed at all disc levels. Increased signal intensity of the cerebrospinal Auid facilitates the evaluation of the de-
gree of multilevel central canal stenosis (arrows).
ii. Neural compression occurs between the base of the L5 transverse process
and the sacral ala.
iii. Optimally delineated by CTwith multiplanar reformatted images.
g. Degenerative spondylolisthesis can cause both central and neuroforaminal steno-
sis (Figs. 18 and 19).
i. Most frequently involves the L4-L5 disc level.
ii. Middle aged or elderly patients
iii. Degenerative changes of the disc and sagittally oriented facet joints pre-
dispose to anterolithesis.
iv. Rarely progresses beyond grade I slip because the neural arch remains
intact.
v. Stenosis of the central canal, and subarticular and lateral recesses is
caused by the anterolisthesis as well as proliferative changes of the fol-
lowing:
(a) Anteromedial margins of the facet joints
(b) Hypertrophy of the ligamenta flava
(c) Posterior anular bulging
vi. Both MRI and CT can be used to assess the orientation and associated
degenerative changes of the facet joints.
FIGURE 19. Degenerative spondylolisthesis-

CT. The hallmark of degenerative spondylolis-
thesis on axial CT imagesisseveredegenerative
facet disease with marked erosion of the facet
joints and marked overgrowth and defarmity of
the facets resulting in ventral subluxation of the
intactneuralarch of the craniad vertebral body.
This is invariabl)' associated with thickening of
the ligamentum Aavum which may be marked.
These changes lead to varying degrees of cen-
tral canal stenosis which is often severe (A),
since interestingly, mostpatients with degenera-
tive spondylolisthesis present with symptoms of
claudication due to the central spinal stenosis
rather than back pain due to the facet degener-
ation. Hypertrophic overgrowth of the superior
articular facets leads to subarticular stenosis
(small arrow). Associated central bulging of the
disc, when present, may contribute to both cen-
tral and subarticular stenosis (open arrow). The
majority of the visualized disc on axial CT im-
ages, however, isdue to theanterolisthesis ofthe
vertebra above, resulting in an anteroposterior orientation of the posteriormargin of the disc (opposing ar-
rows). B, Synovial cysts with calciRcation are rarelyfaund in porients with degenerativespondylolisthesis. The
association is so common that when synovial C)lsts with colcilicotion are noted on axial CT images, the di-
agnosis of underlying degenerative spondylolisthesis mustbe strongly suspected. Thesynovial cystwithcal-
cification (arrow) shown in (B) results in moderate subarticular stenosis at l4-l5 on the leftand moderately
severecompression of the thecal sac. The high density of the lesion indicates calciRcation and therefore is
consistent with the diagnosis of synovial cystwith calciRcation. Cclcilicofion in these lesions is best demon-
strated by CT. MRI cannot easilydifferentiate between focal thickening of the ligamentum Rovum and a sy-
novial chondroma since they may be equally low signal intensity. Note the typical changes of degenerative
spondylolisthesis in thispatientas describedin (A) above. Inthispatientthe apporent "discprotrusion" isen-
tirely due 10 the anlerolislhesis of l4 on l5 (small arrows).
C. Spinal trauma
1. Vertebral trauma
a. Initial evaluation includes routine plain film studies, sometimes followed by
flexion and extension views to assess spinal alignment and stability.
Severity and extent of injury determine the type of films ordered.
b. Roles of MRI and CT are complementary.
i. CT provides excellent delineation of fractures and deformation of the
vertebral bodies or posterior elements.
(a) Demonstrates the degree of fracture healing; healing fracture defor-
mities is a dynamic process, and remodeling of vertebral bodies can
be demonstrated on serial CT studies.
(b) Demonstrates residual bony malalignment.
(e) Cl-myelography best to demonstrate a posttraumatic pseudomeningo-
cele.
ii. MRI is optimal in evaluating the spinal cord, thecal sac, and conus medullaris.
(a) Demonstrates posttraumatic arachnoid cysts.
(b) Demonstrates myelomalacia.
(c) Demonstrates hematoma.
(d) Demonstrates disc herniation.
2. Isthmic spondylolysis (Figs. 5, 9, 10, and 20)
a. A stress fracture of the pars interarticularis usually due to cumulative micro-
trauma of the pars interarticularis; usually bilateral and most often involves
the L5 pars interarticularis.
b. Occasionally secondary to acute extension injury
i. Athletics
ii. Motor vehicle accident
iii. Industrial trauma
c. Fracture of the pars may cause back pain but also is frequently detected in
asymptomatic individuals.
d. Plain films may demonstrate a pars defect that is longstanding and mani-
fested by bony sclerosis that is visible at the fracture site.
e. Pars stress reactions may occur before a complete stress fracture, reflecting
increased bone turnover.
i. SPECT bone scan and MRI with fat saturation are the most sensitive test
to detect stress reactions and early stress fractures of the pars (see page
229).
ii. Stress reactions have been associated with onset of back pain.
f. After fracture present for a short time, bone resorption or hypertrophy at the
fracture site can be visualized on CT with multi planar reformatted images.
i. CTimage slices should be orthogonal to the fracture so that it is visualized.
ii. Image slices that are directly through the pars defect may not reveal the
presence of the bony defect.
g. Fragmentation and hypertrophy of the pars interarticularis can cause steno-
sis of the central spinal canal or neural foramina; best visualized with CT.
h. Lateral erect flexion/extension views may demonstrate instability (abnormal
spinal motion) associated with the spondylolysis.
i. Spondylolysis is associated with increased incidence of disc degeneration and
herniation at the level of the spondylolysis and at the adjacent disc level.
ii. MRI can detect disc degeneration, anular tears, and herniation.
iii. CT can detect disc herniation.
j. Bone scan detects only the osseous abnormalities and cannot demonstrate
discal abnormalities or stenosis.
FIGURE 20. Isthmic spondylolysis. On the G/MPR examination, axial (A) and sagittal (B) images demon-
stratespondylolytic defects (arrows) involving the L5 pars interarticularis. On the sagittal Tl-weighted image
of the MRI examination (e), the spondylolytic defect(curved arrow) involving the L5 pars interarticularis is
difficult to delineate. There isexcellent delineation of thecephalocaudalnarrowing of the intervertebral canal
and compression of the l5 nerveroot (straight arrow).
3. Isthmic spondylolisthesis (see Figs. 5, 9, 10, and 20)

a. When there is anterior displacement of the superior vertebral body.
i. Usually involves the L5 vertebral body with respect to the S1 vertebral
body.
(a) Degree of slip graded I-V depending on the degree of anterior dis-
placement of the L5 vertebral body with respect to the S1 vertebral
body.
(b) 1-<25% IV-~ 75-< 100%
11-25-<50% V->100%
I1I-50-<75%
ii. Lateral erect plain films are obtained to measure the amount of anterolis-
thesis. Flexion/extension views may demonstrate instability (abnormal
spinal motion) associated with the spondylolysis or spondylolisthesis.
iii. Fragmentation and hypertrophy of the pars interarticularis can cause
stenosis of the central spinal canal or neural foramina.
256 The Lumbar Spine: Imaging Oplions
(a) Neural foraminal stenosis may be due to the anterolisthesis, hypertro-

phied pars interarticularis, osteophytes projecting from the vertebral
endplates, disc/soft-tissue encroachment, or decreased disc height.
(b) Bony changes are best visualized with CT, whereas soft-tissue
changes are best visualized with MRI.
D. Spinal tumors
t. Plan films: first imaging study to order but relatively insensitive for detection
of osseous metastases.
a. 40-50% of vertebral body cancellous bone destroyed before abnormality de-
tected on plain films.
b. Pedicle destruction frequently seen before vertebral body destruction be-
cause pedicle contains higher percentage of cortical vertebral bone. But
metastases almost always involve the vertebral body first.
c. Main value of plain films is to detect fracture or malalignment of the spinal
column secondary to infiltrative or destructive process
2. Helpful to classify as
a. Intramedullary
b. Intradural-extramedullary
c. Extradural
d. Osseous
3. Intravenous gadolinium-DTPA helpful to highlight neovascularization and thus
delineate a tumor mass.
4. MRI optimal examination for suspected tumor; CT helps to assess degree of os-
seous destruction and risk of fracture.
5. MRI (Fig. 21)
a. Evaluates all potential sites of tumor involvement.
b. Particularly sensitive to invasion or destruction of cancellous bone of verte-
brae with extension into central spinal or paravertebral soft tissue.
c. Gadolinium-DTPA can help to separate viable from necrotic tissue before
biopsy performed.
d. Osseous metastatic deposits to the vertebral marrow are detected by abnor-
mal signal intensity in bone marrow on spin-echo or STIR sequences.
6. Bone scan can survey entire skeleton for metastatic disease. Sensitivity of bone
scan and MRI similar except with multiple myeloma, where MRI is more sensi-
tive. However, MRI provides superior spatial resolution and specificity.
E. Infection
1. MRI is the best examination.
2. Typically involves disc space and contiguous vertebral bodies via hematoge-
nous spread from a remote site.
a. Begins in endplate and then spreads to adjacent disc and vertebral body.
b. Sensitivity, specificity, and accuracy MRI comparable to bone scan and gallium
scan combined. Advantage of MRI is that it can also determine whether the in-
flammatory process extends beyond the margins of the disc and bone.
c. MRI can detect presence of a focal abscess.
3. Findings on MRI
a. Sagittal Tt-weighted image demonstrates confluent decreased signal inten-
sity in the vertebral bodies and intervertebral disc.
b. Sagittal Tz-welghted image demonstrates increased signal intensity in the disc
and the vertebral bodies and poor delineation of the vertebral body endplates.
c. Inflammatory changes in the paravertebral soft tissues.
4. MRI with gadolinium DTPA used for initial evaluation of epidural abscess; if
MRI findings inconclusive, a Cl-myelogram may help.
The Lumbar Spine: ImagingOptions 257
FIGURE 21. Pathol~ic compression fractures involving the 12and LA vertebral bodieson protonsdensity (A)
and T2-weighted (8) midline sagittal images. There is diffuse in~ltration of multiple vertebral bodies from II
to l5. Involvement of the posterior cortexof LA encroacheson the central spinalcanal (arrow).
5. MRI with gadolinium-DIPA helpful for reevaluation of patients with spinal in-
fection undergoing treatment.
a. MRI response may lag behind therapeutic response.
b. Determines extent of healing.
c. May help to separate infectious from noninfectious discitis during immediate
postoperative period.
F. Postoperative evaluation
1. The reason for the initial surgery and the type of surgical procedure help to de-
termine which imaging studies would be most appropriate.
2. Prior disc surgery with recurrent discogenic symptoms
a. MRI optimal method to detect presence of discal abnormality.
b. MRI specificity limited during first 6 months after surgery; commonly iden-
tifies abnormal morphology of posterior disc margin in asymptomatic pa-
tients.
c. After 6 months, MRI with and without gadolinium-DIPA can detect abnor-
mal disc material, recurrent herniated disc, and postoperative scar (Fig. 22).
i. Gadolinium-DIPA causes scar to enhance.
(a) Frequently present at operative site
(b) Intermediate signal intensity on Tt-weighted image
(c) Poorly marginated
(d) Little mass effect
ii. Recurrent disc does not enhance with gadolinium-DIPA.
(a) Usually contiguous with disc space
(b) Well marginated
FIGURE 22. Sequestered disc fragment-postoperative MRI examination. On the axial Tl-weighted image
{AI, there is a large soft tissue extradural mass (arrows) interposed between the right lateral margin of the
thecal sac and the rightfacet joint. Themass extends throughthe right neuroforamen. After the administra-
tion of Gd-DTPA, on the repeat axial Tl-weighted image (B), a large sequestered disc fragment (long ar-
rows) with lowsignal intensity is now identiReCl surrounded by enhancinggranulation tissue (shortarrows),
demonstrating highsignal intensity.
(cl Iso-or hypointensity on T1-weighted sequence compared with disc of

origin
ld) Iso- or hyperintensity on T2-weighted sequence
iii. Other possible sources of pain may also be visualized.
(a) Foraminal, central canal or lateral recess stenosis
(b) Arachnoiditis
(c) Disc infection
(d) Epidural abscess
(e) Pseudomeningocele
3. Prior decompressive procedure to corred spinal stenasis with recurrent stenotic symptoms
a. Important to evaluate for the degree of
i. Osseous regrowth
ii. Residual or recurrent stenosis
iii. Postoperative instability
b. Both MRI and CTcan be useful.
c. CT determines the degree of
i. Osseous stenosis, especially of the subarticular and lateral recesses
ii. Foraminal stenosis
d. MRI determines the degree of
i. Thecal sac compression at the stenotic level
ii. Foraminal stenosis
4. Prior fusion
a. Plain film sensitivity and specificity, including flexion and extension views,
to detect pseudoarthrosis are poor.
b. CT with sagittal and coronal reformatted images as well as 3-D reformations
optimally evaluates solidity of a fusion, particularly posterolateral or inter-
transverse process fusion masses.
c. Both MRI and CT can be used to evaluate an interbody fusion; continuous
bone bridging is present if the fusion is solid.
5. Postoperative infection- MRI with gadolinium-DTPA is imaging study of choice.
a. Bone scan does not provide the same degree of specificity and spatial resolu-
tion.
b. If MRI is inconclusive, CT-myelogram may be helpful.
c. Gallium and labeled white all studies
6. Posterior instrumentation and hardware
a. MRI and CT images degraded due to ferromagnetic and metallic hardware,
respectively.
i. On MRI, most metallic constructs generate a large amount of artifact un-
less they are composed of a nonferromagnetic material such as titanium.
ii. On CT, artifacts are a problem particularly if the area of interest is at the
level of pedicular screws, but CTusually provides better images than MRI
for this patient population.
b. Extent and amount of artifact influenced by the instrumentation's
i. Size
ii. Position
iii. Orientation
iv. Composition
G. Spondyloarthropathies
I. Usually plain films are adequate, but not sensitive to detection of early disease
2. CT optimally evaluates for
a. Osseous erosions
b. Bony proliferations
c. Joint space narrowing
d. Enthesophytes that may form at the insertion of the anterior facet capsule
and can cause foraminal stenosis.
IV. Terminology
A. Disc morphology (see Fig. 14)
I. Normal: no degenerative changes; all discal tissues are within the disc space.
Degenerative changes or bulging may be clinically insignificant, but, when
deemed so, the disc should be designated as degenerated or bulging.
2. Annular tear (synonym: fissure): a cleft or separation between fibers of the anu-
Ius, extending circumferentially, radially, or horizontally through one or many
layers of the anular lamellae (Fig. 14A).
3. Disc protrusion (one type of disc herniation; disc herniation is a general term de-
scribing focal displacement of nuclear material beyond the normal confines of
the disc.): a focal contour abnormality of the outer anular disc fibers caused by
the displacement of nuclear material that is contained by the outer anulus or
the posterior longitudinal ligament (Fig. 14B).
4. Disc extrusion (one type of disc herniation; disc herniation is a general term de-
scribing focal displacement of disc material beyond the normal confines of the
disc.): penetration of the disc material through the outer anulus. If the disc ma-
terial does not penetrate the posterior longitudinal ligament complex, it is con-
sidered a sub-ligamentous extrusion. If it penetrates through the posterior lon-
gitudinal ligament, it represents a transligamentous extrusion (Fig. 14C).
5. Sequestered disc fragment (synonyms: free fragment, displaced disc): disc material
separates from its disc of origin (Fig. 140).
6. Bulge: symmetrical extension of the anulus beyond the margins of the vertebral
body endplates (Fig. 14E).
B. Location 01 displaced discaltissue in axial plane
1. Central zone: between the sagittal planes through the medial edges of the facets.
If disc material is predominantly the right or left of the bisector of the central
zone, it is termed
a. Right central zone (synonyms: right paracentral)
b. Left central zone (synonyms: left paracentral)
2. Subarticular zone (synonyms: lateral recess): the zone, within the vertebral canal,
defined sagittally by the planes of the medial edges of the pedicles and medial
edges of the facets and coronally by the planes of the posterior surfaces of the
vertebral bodies and the anterior surfaces of the superior facets.
3. Foraminal zone (synonyms: pedicle zone, lateral zone): the zone between planes
passing through the medial and lateral edges of the pedicles.
4. Extraloraminal zone (synonyms: far lateral zone, far out zone): the zone beyond a
sagittal plane through the lateral edges of the pedicles, having no well defined
lateral border.
Acknowledgments: The authors thank Marcus G. Calahan, B.A., for helping to pre-
pare the manuscript. The authors also thank T. Siemers, M.D., for reviewing the
manuscript and K. Heitoff, M.D., for providing figures to supplement the text.
References
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1 - - - - - - - -15
Electrodiagnostic Medicine
Joel M. Press, M.D., andJeffrey L. Young, M.D., M.A.
Key Points
• Electrodiagnostic studies give dynamic information about muscle and nerve function,
whereas radiographic studies look at static anatomy.
• Electromyography (EMG) and nerve conduction studies (NCS) give information about a
specific nerve or muscle that is injured or not functioning properly. They do not give
information about what is causing pain but may point the clinician in the right
direction.
• EMG and NCS are an extension of the history and physical examination, which need
to be included in the report. Electrodiagnosis is a complete examination, not simply a
test, and must be interpreted in accordance with the entire clinical picture.
• A normal electrodiagnostic examination does not necessarily mean normal function or
that the patient's complaints have no physiologic basis. It may mean that the sensi-
tivity and specificity of the exam cannot reveal a definable problem by available
techniques.
• EMG and NCS are examiner-dependent and vary with the technique, ability, and
thoroughness of the examiner. All electrodiagnostic studies are not equal in terms of
the quality or accuracy of the report.
• Different electrodiagnostic laboratories have different normalized values.
• The yield of EMG and NCS is improved when tests are meticulously performed. Tech-
nical error is the most important factor leading to incorrect conclusions about the data
obtained.
• In most cases EMG and NCS should be performed no sooner than 21 days after injury
or onset of signs and symptoms.
I. General Electrophysiology Anatomy, Physiology, and Terminology

A. Afferent-carrying inward to a central organ or section, as nerves that conduct im-
pulses from the periphery of the body to the brain or spinal cord.
B. Amplitude-with reference to an action potential, the maximal voltage difference
between two points, usually a baseline-to-peak or peak-to-peak measurement. The
amplitude gives information about the number of intact functioning axons. Severe
nerve injury can decrease the amplitude of the response.
C. Antidromic-propagation of an impulse in the direction opposite to physiologic con-
duction; e.g., conduction along motor nerve fibers away from the muscle and con-
duction along sensory fibers away from the spinal cord.
D. Axon-usually the long process of a nerve fiber that generally conducts impulses
away from the body of the nerve cell.
E. Axonotmesis-nerve injury characterized by disruption of the axon and myelin
sheath, but with preservation of the supporting connective tissue, resulting in ax-
onal degeneration distal to the injury.
263
264 Eledrodiagnostic Medicine
MWAVE
Stimulate
Wrist
Below elbow
NxNe elbow
Axilla
SUpraclavicular fossa
-----.J)o mV
5ms
FIGURE 1. The Mwaveor motor wave recordedwith surfaceelectrodes over theabductor digiti quinti elicited
by electric stimulation of the ulnar nerveat several levels. TheMwave is a compound actionpotentialevoked
from a muscle by a single electric stimulus to itsmotor nerve. Thelatency, commonly calledthe motorlatency
or baseline-to-peak amplitude ofthe first phase. (Reprinted with permission from theAAEM GlossaryofTerms
in Clinical Electromyography. Muscle Nerve lO(No. 8S):Gl-G60, 1987.)
F. Compound muscle action potential (CMAP)-the summation of nearly synchronous mus-

cle fiber action potentials from a muscle, commonly produced by stimulation of
the nerve supplying the muscle either directly or indirectly. The size of this poten-
tial (e.g., amplitude) is determined by the number of functioning axons. A de-
creased CMAP indicates that an injury has occurred to the specific muscle or the
nerve supplying that muscle (Fig. 1).
G. Compound nerve action potential (CNAP)-the summation of nearly synchronous nerve
fiber action potentials recorded from a nerve trunk, commonly produced by stimu-
lation of the nerve directly or indirectly (Fig. 2).
H. Conduction velocity-speed of propagation of an action potential along a nerve or mus-
cle fiber. The nerve fibers studied (motor, sensory, autonomic, mixed) should be
specified. A decreased conduction velocity usually reflects some injury to the myelin
sheath; for example, slowing of the conduction velocity across the elbow due to
compression of the ulnar nerve in the cubital tunnel or retrocondylar groove.
I. Distal latency-interval between the onset of a stimulus and the onset of a response.
A delayed distal latency also reflects injury to the myelin sheath and a delay in
the transmission of the neural signal at the distal part of the nerve. In carpal tun-
nel syndrome, the median nerve distal latency is prolonged (see Fig. I).
J. Dermatome-areas of sensation on the skin supplied by a single spinal segment.
K. Efferent-directed away from a central organ or section, as nerves that conduct im-
pulses toward the periphery of the body from the brain or spinal cord.
L. Electromyography-strictly defined, the recording and study of insertion, sponta-
neous, and voluntary electric activity of muscle.
M. Evoked potential-electric waveform elicited by and temporally related to a stimulus,
most commonly an electric stimulus delivered to a sensory receptor or nerve or
applied directly to a discrete area of the brain, spinal cord, or muscle (Fig. 3).
Electrodiagnostic Medicine 265
COMPOUND SENSORY NERVE ACTION POTENTIALS
Slimulale MEDIAN NERVE ULNARNERVE
Elbow
Elbow
~ ----_J\.
WIllI -\-.I'v ..~
-Mr-+
..J:
11111
50 ,.v ..J:
11111
2O,.V
FIGURE 2. Compound sensory nerveaction potential recorded with surfaceelectrodes in a normalsubject. A

compound nerveaction potential isconsideredto have been evoked from afferent ~bers ifthe recordingelec-
trodes detect activity in only a sensory nerveor in a sensorybranch of a mixed nerve. Thecompound sen-
sory nerveaction potential has been referredto as the sensoryresponseor sensorypotential. (Reprinted with
permission from the MEM Glossary of Terms in Clinical Electromyography. Muscle Nerve 10(No.
8S):G1-G60,1987.)
N. Mixed nerve-a nerve containing both motor and sensory fibers, e.g., tibial nerve.
O. Motor nerve-a nerve containing only fibers to the muscle, e.g., suprascapular
nerve.
P. Motor unit action potential-action potential reflecting the electric activity of a single
anatomic motor unit. It is the compound action potential of muscle fibers within
the recording range of an electrode.
Q. Myotome-groups of muscles innervated by a single spinal segment.
R. Neurapraxia-failure of nerve conduction, usually reversible, due to metabolic or
microstructural abnormalities without disruption of the axon.
S. Neurotmesis-partial or complete severance of a nerve,with disruption of the axons,
their myelin sheaths, and the supporting connective tissue, resulting in degenera-
tion of the axons distal to the injury site.
T. Orthodromic-propagation of an impulse in the direction the same as physiologic
conduction, e.g., conduction along motor nerve fibers toward the muscle and con-
duction along sensory nerve fibers toward the spinal cord.
u. Sensory nerve-a nerve containing only sensory fibers, e.g., saphenous nerve.
II. Use of EMG and NCS in the Clinical Setting
A. Localization of processes, e.g., compression neuropathies
B. Extent of injury
C. Age of injury, e.g., chronic vs. acute
D. Type of nerve fiber affected, e.g., motor, sensory, mixed
E. Pathology of nerves vs. muscle vs. neuromuscular junction
F. Prognosis
266 Electrodiagnostic Medicine
SHORT-LATENCY SOMATOSENSORY EVOKED

POTENTIALS
MEDIAN NERVE
NR
C4' - Fz
FIGURE 3. Evoked potential tracings from

the median nerve. The different peaks of
C4' - EP2 the evoked potentials are assessed and
compared side to side and against nor-
mal values. (Reprinted with rermission
from the AAEM Glossary 0 Terms in
Clinical Electromyography. Muscle Nerve
lO(No. 8S):Gl-G60, 1987.)
CSS - Fz
EP
EP1 - EP2
~:="::::::=:::::~====== ] ~.5~V
I I
N=1024 30 40 ma
o 10 20
III. Risks Involved with EMG and NCS (all minimal if proper precautions taken)
A. Patient discomfort (often depends on tester patience)
B. Transmissible diseases-Jakob-Creutzfeldt, hepatitis, AIDS
C. Anatomic structural injury-vessels, nerve, viscera
D. Bleeding-anticoagulation, coagulopathy
E. Endocarditis-valvular heart disease
F. Electrical injury-leakage current, applied current
G. Patient paraphernalia-catheters, intravenous lines, pacemakers
IV. Basic Physiology

A. Resting membrane potentiol
1. Influenced by diffusion and sodium (Na)-potassium (K).
2. Na + primarily kept extracellular.
3. K+ primarily kept intracellular.
4. Protein anions-nondiffusable, help to maintain gradient.
5. Approximates equilibrium potential of K+.
B. Creation of action potential (nerve)
1. Transmembrane potential> threshold> > depolarization.
2. Activation of Na + (fast) and K+ (slower) channels.
3. Accommodation to prolonged stimulation with slow rise time.
4. Repolarization and hyperpolarization along the course of the nerve signal sent
down the axon.
EledroJiagnostic Medicine 267
5. Na+ channels influenced by calcium (Ca++); hypocalcemia results in in-

creased nerve excitability.
C. Transmission along a nerve
1. Velocities range from 0.5-100 m/sec.
2. Nerve conduction velocity (NCV) = flx) myelination and fiber diameter.
3. Myelin-insulator that decreases membrane capacitance 50-fold. More myelin
means faster NCV; demyelination results in slower NCV, i.e., tardy ulnar palsy.
4. Nodes of Ranvier-site of action potential propagation.
5. Saltatory conduction causes increased conduction velocity.
D. Neuromuscular junction
I. Specialized synapse between motor nerve terminal and sarcolemma.
2. Increased Ca+ + influx after nerve impulse.
3. Presynaptic release of previously synthesized acetylcholine "quanta."
4. Postsynaptic receptor on muscle membrane has acetylcholine sensitive channels.
5. Muscle contraction occurs in response to action potential effect at neuromuscu-
lar junction.
E. Muscle contraction
I. Excitation/contraction coupling.
2. Depends on Na+, K+, and Ca++-metabolic imbalances of any of these can
cause muscle firing abnormality.
3. Tetanic contraction stronger than maximal twitch.
4. Twitch speed and tension are greater in type II fibers (short burst types of activities).
V. Chronology ofChanges with Nerve Injury

A. Compression of nerve tissue may induce structural damage to nerve fibers, impair
intraneural blood flow, create intraneural edema, and cause axonal transport block.
S. Electrodiagnostic changes occur from the onset of compression or damage to a
nerve, although the ability to detect such changes is limited.
C. Clinically apparent weakness may be recognized electrophysiologically as a re-
duced recruitment pattern on maximal voluntary contraction.
D. Electrophysiologic hallmark of findings of axonal degeneration are the sponta-
neous single muscle fiber discharges called positive sharp waves and fibrillation poten-
tials (Figs. 4 and 5).
E. Positive sharp waves are first noticeable in paraspinal muscles within 1-10 days
after loss of axon function.
F. By 14-18 days, positive sharp waves can appear in the limb muscles, beginning
proximally and spreading distally, becoming evident throughout the involved
myotome.
G. By 18-21 days, all muscles in the involved myotome have abnormalities, includ-
ing positive sharp waves and fibrillation potentials.
H. Larger amplitude positive sharp waves (about 200 microvolts) are usually suggestive
of an acute injury to the involved nerve, whereas smaller amplitude positive sharp
waves (100-150 microvolts) may be more indicative of a subacute or chronic injury.
1. Positive sharp waves and fibrillations normally disappear if the radiculopathy resolves
(does not become chronic), although they can persist indefinitely in some cases.
J. When reinnervation occurs, long-duration, large-amplitude polyphasic motor unit
potentials are seen.
K. Over time (years) these polyphasic potentials may normalize or persist.
VI. Nerve Conduction Studies

A. NCS are performed to look at the ability of a specific nerve to transmit an impulse
down an axon from one area to another.
268 Electrodiagnoslic Medicine
POSITIVE SHARP WAVE
~~OO~V
10 rns
TRAIN OF POSITIVE SHARP WAVES
FIGURE 4. A positive sharp wave is a biphasicaction potential initiated by needle movement and recurring
in a uniform, regularrattern. A "train"of suchwaves can be recorded from a damaged area of Rbrillating
muscle Rbers. One 0 the hallmarks of axonal degeneration. (Reprinted with permission from the AAEM
Glossary of Terms in Clinical Electromyography. Muscle Nerve WINo. 8S):G1-G60, 1987.)
B. Specific areas of different nerves are studied based on the accessibility of the
nerve and the propensity for block in conduction to occur along a given segment.
C. NCS can give information about the overall function of the entire nerve or the
function of only a specific segment.
D. Both motor and sensory nerves can be studied.
FIBRILLATION POTENTIAL
~~~V
100 rna
FIGURE 5. Fibrillation potential. A fibrillation potential istheelectric activity associated with a spontaneously con-
tracting (Rbrillating) muscle Rber. One ofthe hallmarks ofaxonal degeneration. (Reprinted with permission from
the AAEM Glossary ofTerms in Clinical Electromyography. Muscle Nerve 10(No. 8S):G1-G60, 1987.)
E. NCS are helpful
I. When a compression neuropathy is contemplated (e.g., carpal tunnel syndrome,
ulnar neuropathy at the elbow, peroneal neuropathy at the fibular head).
2. To evaluate for peripheral neuropathy, which can affect motor fibers, sensory
fibers, or, most commonly, both.
3. To give more information about the degree of nerve injury in radiculopathy.
F. Technically, NCS are done by stimulating a nerve at one point and measuring how
long it takes an impulse to travel to an electrode pick-up some distance down the
nerve. Sensory responses are picked up over the sensory nerve, e.g., sural nerve
for sural nerve potential. Motor responses are picked up over a muscle, e.g., the
abductor pollicis brevis for the median nerve potential. The size of the evoked re-
sponse is also noted and gives information about the physiologic health of the
nerve.
G. H-reflexes and F-waves are special types of conduction studies that give information
about nerve conduction in proximal sections of nerves, which are difficult to as-
sess by standard NCS techniques.
\. H-reflexes are the electrophysiologic analog to the Achilles' muscle stretch re-
flex. The If-reflex study measures afferent and efferent conduction mainly
along the S1 nerve root and is used in localizing nerve compromise at that
level. H-reflexes would be absent in an S1 radiculopathy but present in an L5
radiculopathy, assuming normal neural function otherwise.
2. F-waves can be performed on any nerve and, when abnormal, suggest some al-
teration in function along the course of that nerve. They are obtained when
there is some suggestion of a block in nerve conduction, usually somewhere
proximally along a nerve, e.g., lumbosacral plexus injury.
H. When NCS are abnormal, they give information that a specific nerve is not con-
ducting impulses in the measured area. This information needs to be correlated
with the clinical picture because it mayor may not be the cause of the patient's
symptoms or signs.
l. A good electrophysiologic report should give information about the NCS in terms
not only of whether it is normal or abnormal but also of the degree of abnormality
in nerve conduction velocity, evoked potential amplitude, and nerve latency and
how this abnormality correlates with the patient's history and physical examination.
It should give information about what entities have been ruled out by the studies.
J. Sources of error in nerve conduction studies
1. Temperature
2. Inadequate or excessive stimulation
3. Improper placement of electrodes
4. Tape measuring error
5. Age
6. Anomolous innervation
7. Volume conduction of impulse to nearby nerve
8. Improper electrode montage setup
9. Improper filter settings
10. Involuntary muscle contractions
VII. Needle Examination

A. Needle electromyography (EMG) is probably the single most useful electrodiagnos-
tic study in evaluating patients with low back complaints for evidence of nerve
injury. EMG is particularly useful in localizing a nerve injury to a specific root
level; for accuracy, various muscles in a multisegmental distribution that are in-
nervated by different peripheral nerves need to be studied.
270 ElecIroJiagnostic Medicine
B. EMG evaluates only motor (muscle) fibers for axonal loss.

C. EMG studies are not always abnormal even if true nerve injury exists.
1. Weakness with a normal EMG can be due to neurapraxia or conduction block,
in which the nerve is not conducting normally but no axonal injury has oc-
curred.
2. If only a few axons degenerate, the lesion may be missed by random sampling
of the muscles.
3. Timing of the EMG is important. If the exam is performed more than 4-6
months after symptoms have occurred, reinnervation by collateral sprouting
has probably halted the occurrence of positive sharp waves and fibrillation po-
tentials. If performed less than 2-3 weeks after onset, positive sharp waves and
fibrillations have not yet appeared.
D. Besides radiculopathy, EMGs are also abnormal when significant nerve injury has
occurred, i.e., peripheral neuropathy or compression neuropathy. Muscle diseases
(e.g., myopathy, muscular dystrophies) also are detected by abnormalities on EMG.
E. EMGs are performed with very fine needles (euphemistically called pins). The pins
are placed into different muscles (determined by the examiner on the basis of
which muscles are most appropriate to examine). The pins are moved short dis-
tances in different directions, sometimes in different parts of a muscle, to look for
abnormalities on a display screen in insertional activity, spontaneous activity, and
the activity of the motor units observed as the patient voluntarily contracts and
relaxes his or her muscles. (Figs. 6 and 7).
F. EMG of paraspinal muscles is important in the needle examination of a patient
being evaluated for radiculopathy. Paraspinal positive sharp waves and fibrilla-
tions indicate that the site of the lesion is proximal to the posterior primary ra-
mus, eliminating the concern of a possible plexopathy.
G. Of all patients with positive EMG findings in radiculopathy 3 weeks or longer af-
ter the onset of symptoms, about 70% have abnormalities in the paraspinal mus-
cles and 900/0 in the peripheral nerve distribution in the extremities.
RECRUITMENT PATTERN
Voluntary Contraction
Week
~.
~~~Y
0.51
FIGURE 6. Recruitment and interference pattern. Recruitment refers to the successive activation of the same
and new motorunits withincreasing strength of voluntary muscle contraction. The interference pattern is the
electric activity recorded from a muscle with a needle electrodeduring maximal voluntary effort. (Reprinted
with permission from the MEM Glossary of Terms in Clinical Electromyography. Muscle Nerve 101No.
8S):G l-G60, 1987.)
Eleclrodiagnostic Medicine 271
INSERTION ACTMTY
FIGURE 7. Insertional activity in a normal subject. Insertion activity is the electric activity caused by insertion
or movement ofa needleelectrode. The amount ofactivity may bedescribed as normal, reduced,or increased
[prolonged]. (Reprinted with permission from the AAEM Glossary of Terms in Clinical Electromyography.
Muscle Nerve 10(No.8Sj:G1~60, 1987.)
H. Abnormalities in the paraspinal muscles in patients who have had back surgeries
can be difficult to interpret because scar tissue alone may cause abnormalities in
positive sharp waves and fibrillations.
I. An abnormal EMG is indicative of axonal loss to the nerve supplying a specific
muscle. This information still needs to be correlated with the history, physical ex-
amination, and any imaging studies.
J. A good EMG report describes whether any abnormality exists, which level or lev-
els are most likely involved, how significant the degree of axonal loss is, the rela-
tive acuity or chronicity of the findings, and how this information correlates with
the clinical picture.
K. The degree of positive sharp waves and fibrillations seen in a given muscle has
not been proved to correlate quantitatively with the degree of clinical symptoms
or with prognosis.
L. Single fiber EMG is a specialized type of study that looks at isolated muscle fibers
(as opposed to standard EMG, which looks at small groups of muscle fibers) to see
how certain parameters change with time. These parameters can give information
about subtle nerve injuries that standard EMG cannot detect. They are not used in
routine electrodiagnostic studies. They may be considered for patients with post-
polio syndrome or motor neuron disease.
VIII. Somatosensory Evoked Potentials (SEPs)

A. Because of the insensitivity of routine electrodiagnostic studies to detect radicu-
lopathies that primarily involve sensory nerve fibers, SEPs have been investigated.
B. SEPs are elicited by electrical stimulation of a sensory nerve or a mixed motor
and sensory nerve or the skin innervated by a specific nerve (Figs. 8 and 9).
1. Nerves are selected by their dermatomal distribution.
2. Recordings are made with surface and needle electrodes from the spine and/or
scalp.
3. Varying degrees of success have been noted with SEPs in patients with sus-
pected lumbar radiculopathy.
4. They reflect primarily the integrity of dorsal column pathways as the elicited
response travels through these fibers.
C. Limitations
I. SEPs can be abnormal in patients with no symptoms at all.
2. SEPs reflect only nerve fibers that carry position and vibration senses.
272 Eleclrodiagnostic Medicine
FIGURE 8. Somatosensory evoked potential of the median nerve using a 4-channel technique. Note where
the stimulation occursand where evoked potential latencies are recorded from. (Reprinted with permission
from the AAEM Glossary ofTermsin Clinical Electromyography. Muscle Nerve 1O(No. 8S):Gl-G60, 1987.)
FIGURE 9. Somatosensory evoked potential of the tibial nerve. Note where the stimulation occursand where
evokedpotential latencies are recorded from. (Reprinted with permission from the AAEM Glossaryof Terms
in Clinical Electromyography. Muscle Nerve 10(No. 8S):Gl-G60, 1987.)
3. Short segments of nerve injuries may not produce detectable changes in the latency
when the latency measured is over the entire or significant length of the nerve.
4. SEP amplitudes vary widely in normal subjects and from side to side in the
same patients.
5. SEP potentials from the spine are technically difficult to record and are absent
in up to 400/0 of normal patients.
6. SEPs, like H-reflexes and F-waves in standard electromyography, give no infor-
mation about the specific site of the lesion; they indicate only that some abnor-
mality exists in somatosensory pathways between the point at which the stimu-
lus is applied peripherally and the point at which the response is recorded in
the central nervous system.
D. Purpose-assessment of afferent conduction in specific nerve roots (a technique
known as dermatomal SSEP) may help in disorders affecting the posterior roots,
such as lumbosacral spinal stenosis or possibly multiple sclerosis.
1. A dermatomal SSEP is done by applying a stimulus to a region of the skin that
represents the autonomous zone of a particular nerve root. A mixed nerve
study is done by applying the stimulus to a specific motor or sensory nerve.
The clinical utility of both is unclear, and the value of either compared with the
other is unclear.
2. Sensitivity/specificity-studies are mixed, but it is not widely accepted that the
diagnosis of radiculopathy can be based on SEP abnormalities alone.
IX. When to Order an Electrodiagnostic Test in Patients with Low Back Pain
A. To establish or confirm a clinical diagnosis if some doubt exists or findings of the
physical exam are not consistent.
B. To localize nerve lesions:
1. Root level (radiculopathy)
2. Plexus level (lumbosacral plexus, e.g., metastatic disease, retroperitoneal
hematoma)
3. Peripheral nerve (e.g., meralgia paresthetica, tarsal tunnel syndrome, peroneal
nerve entrapment at the fibular head).
e. To determine the extent of nerve injury and to differentiate neurapraxic lesion
from axonal injury.
D. To correlate findings on anatomic studies (radiologic injury). May guide surgery or
serve as adjunct to selective nerve blocks.
E. To assist in prognosis. Paucity of positive sharp waves and fibrillations in acute
lumbosacral radiculopathy with proper timing of the exam portends an excellent
prognosis for return of muscle strength.
F. To guide patient management. When the patient is treated for a specific problem
without timely improvements, EMG and NCS may find missed diagnoses that may
change treatment plan.
X. When Not to Get an Electrodiagnostic Test in Patients with Low Back Pain
A. In the first 2-4 weeks after the onset of symptoms, because many findings are
harder to detect if testing is done too early.
B. In unequivocal radiculopathy, because EMG and NCS add nothing to treatment
plan if clinical situation is clear.
C. If previous high-quality study resulted in no change in symptoms, any change in
further electrophysiologic studies is highly unlikely.
D. Findings will not change medical or surgical management because of extreme ill-
ness or patient's refusal of treatment.
E. Anticoagulated patient has significant oozing with any needle penetration.
274 Electrodiognoslic Medicine
XI. Checklist for Evaluating the Electrodiagnostic Report

1. Specific question answered?
2. Clinical findings consistent with your evaluation?
3. Limb temperature monitored and recorded?
4. Cool limbs warmed?
5. Individual measures reported?
6. Presence of partial or complete conduction block described?
7. Normal values provided?
8. Sufficient evaluation to document problem?
9. Sufficient data to rule out alternative diagnoses?
10. Appropriate negative findings described?
11. Interpretation consistent with clinical findings?
(Source: From Albers-ref. # 19.)
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67. Weichers DO: Radiculopathies. Phys Med Rehab State Art Rev 3:713, 1989.
68. Wiens JJ, Saal JA: Rehabilitation of cervical spine and brachial plexus injuries. Phys Med Rehabil
State Art Rev 1:583-595, 1987.
69. Weinstein SM, Herring SA: Nerve problems and compartment syndrome in the hand, wrist and fore-
arm. Clin Sports Med 11:161, 1992.
70. Weintraub JR, Madalin K, Wong M, et al: Achilles tendon reflex and the H response. Muscle Nerve
I 1:972, 1988.
7 I. Wilbourne AT: The value and limitations of electromyographic examination in the diagnosis of
lumbosacral radiculopathy. In Hary RW [ed]: Lumbar Disc Disease. New York, Raven Press, 1982,
pp 65-109.
72. Wilbourne AJ, Aminoff MJ: The electrophysiologlc examination in patients with radiculopathies and
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73. Young A, Getty CMJ, Jackson A, et al: Variations in the pattern of muscle innervation by the L5 and
SI nerve roots. Spine 8(6):616, 1983.
74. Young A, Wynn PCB: The assessment and management of the failed back. Part I. Int Disabil Stud 9:
21,1987.
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1978.
.-------------16
I
Inieclion Procedures
Susan 1. Dreyer, M.D./ Paul Drerh!ss, M.D.,
Andrew 1. Cole, M.D., F.A.C.S.M., and Robert E. Windsor, M.D.
Key Points
• Selective injections into the lumbar spine and proximal lower extremity provide the
practitioner with diagnostic information about the precise pain generator(s).
• Selective injection produces a controlled and focused blockade of a particular anatomic
structure. This technique requires skillful needle placement (under fluoroscopic control)
and use of small quantities of local anesthetics to prevent diffuse anesthetic spread and
loss of diagnostic specificity.
• Selective spinal and lower extremity injections can provide significant analgesia and
are often an important part of successful nonoperative management of spinal
disorders.
• lntraarticular corticosteroids provide potent, local antiinflammatory effects and may
relieve pain sufficiently to allow the patient to participate more fully in a compre-
hensive rehabilitation program.
• All injection procedures require thorough patient assessment to determine appropri-
ateness of the injection.
I. Introduction
A. Purpose
1. Accurate diagnosis of the precise cause of low back pain is complicated by the
frequency of overlapping clinical signs and symptoms and lack of strict corre-
lation between imaging studies and presentation. Often advanced imaging stud-
ies, such as magnetic resonance imaging (MRI), reveal no obvious anatomic de-
fects despite symptoms that limit a patient's activities. In addition, false-positive
imaging results increase with the age of the patient. In both cases, selective
spinal injections can provide a more precise diagnosis, which can be used to
optimize the treatment plan.
2. Selective injections are based on the principles of regional anesthesia. If pain is
relieved by anesthetizing a specific anatomic structure, one assumes that struc-
ture to be the pain source. Selective injections precisely place aliquots of local
anesthetic at the nerve supply to an anatomic region or within an anatomic
cavity, such as a joint or bursa, to block all afferent nociceptors in that region.
If corticosteroids are added to the local anesthetic, selective injections may pro-
vide therapeutic benefits beyond the temporary effect of the local anesthetic.
Intraarticular injections with steroids may relieve inflammation and its result-
ing discomfort when joints have not responded to traditional measures, such as
oral medications, rest, and physical therapy.
B. Pharmacology
1. Local anesthetics inhibit transmission of nerve impulses by blocking the intracel-
211
278 In;edion Procedures
lular sodium channel. They prevent nerve depolarization by binding within the
sodium channels and impairing sodium influx. Only preservative free local
anesthetics should be used for spinal injections because of the potential for in-
advertent subarachnoid spread.
a. Udocaine (Xylocaine) is the most versatile and widely used of the local anes-
thetic agents. It has a short onset of action (1-15 min) and a short duration of
action (1-2 hrs). Lidocaine has a high therapeutic index compared with other
local anesthetic agents. Typically, concentrations of 0.5-2010 are used for injec-
tion; quantities for intraarticular and selective spinal injections are far below
the toxic dose (400 mg lidocaine epidurally or 250 mg intravascularly).
b. Bupivacaine (Marcaine) is another widely used local anesthetic. Compared with
lidocaine, bupivacaine has a slower onset (5-20 min) and a longer duration
of action (2-5 hrs). Bupivacaine is commonly administered in concentrations
of 0.125-0.75010. The higher concentrations have the shortest onset of action
but are not recommended for epidural injections because of the risk of car-
diac arrest. Bupivacaine is more cardiotoxic than lidocaine, and cardiotoxic-
ity is exaggerated by accidental intravascular injection. Toxic doses are in
the range of 100-200 mg, depending on the site of extravascular injection;
80 mg given intravascularly may be toxic.
2. Corticosteroids are potent antiinflammatory agents. The following compounds
have prominent glucocorticoid (antiinflammatory) actions with relatively low
mineralocorticoid activity.
a. Betamethasone sodium phosphate and betamethasone acetate (Celestone). Each ml of
Celestone combines 3 mg of betamethasone sodium phosphate, a highly sol-
uble glucocorticoid with a rapid onset, with 3 mg of the relatively insoluble
acetate salt for extended activity. It is approved for intraarticular or soft-
tissue injection to provide short-term adjuvant therapy in osteoarthritis,
tenosynovitis, gouty arthritis, bursitis, epicondylitis, and rheumatoid arthri-
tis. It has been commonly used in epidural administration. Typical intraartic-
ular doses range from 0.25-2 ml, depending on the size of the joint.
b. Dexamethasone (Decadron phosphate) is a short-acting glucocorticoid with a
rapid onset of action. It is approved for intraarticular or soft-tissue injection in
short-term adjuvant therapy of osteoarthritis, tenosynovitis, gouty arthritis,
bursitis, epicondylitis, and rheumatoid arthritis. Typical doses are 0.5-6 mg.
c. Methylprednisolone acetate (Depo-Medrol) is a poorly soluble form of methyl-
prednisolone that provides a sustained antiinflammatory effect. This gluco-
corticoid is approved for intraarticular or soft-tissue injection in short-term
adjuvant therapy of osteoarthritis, tenosynovitis, gouty arthritis, bursitis,
epicondylitis, and rheumatoid arthritis. Single dose vials are available in 40
and 80 mg strengths and have been used for epidural administration. These
formulations without methylparaben lessen the potential for arachnoiditis
from the preservative if the injection is inadvertently placed into the sub-
arachnoid space. Typical intraarticular and soft-tissue doses are 4-80 mg,
depending on the size of the bursa or joint.
d. Triamcinolone hexacetonide (Aristospan) is another insoluble glucocorticoid with
a sustained antiinflammatory effect that lasts several weeks. Typical intraar-
ticular doses are 2-20 mg. It is approved for intraarticular or soft-tissue in-
jection for short-term adjuvant therapy in osteoarthritis, tenosynovitis,
gouty arthritis, bursitis, epicondylitis, and rheumatoid arthritis. It is also
commonly used for epidural administration. Dermatologic side effects, such
as fat atrophy and hypopigmentation, are reported more frequently with tri-
amcinolone than with other long-acting corticosteroids.
Injection Procedures 279
C. Potential complications. Due to their invasive nature, all injections carry some risk of
complications. Patient selection requires that the potential benefit of any injection
exceed its potential risk. Sterile technique and a skilled injectionist familiar with
both procedure and patient reduce the incidence of complications.
1. General considerations include the possibility of several types of adverse reactions.
a. Vasovagal reactions are the most common complication associated with injec-
tion therapy. Feeling of faintness can be minimized by adequate hydration.
A declining pulse rate should signal the physician to reassess the patient's
status and ensure no other intervention such as a cool cloth, N fluids, eleva-
tion of the feet, or atropine are needed.
b. Bleeding is a risk with any procedure that punctures the epidermis. If the re-
gion is highly vascular or if the patient has compromised coagulation, the
risk of bleeding increases. Bleeding into a confined space with nearby
pressure-sensitive structures may cause serious consequences.
c. Infection is uncommon if percutaneous procedures are performed with sterile
technique. Infection is more likely to result from inadequate site preparation
or use of contaminated equipment. Infections are usually superficial, but
deep infections, such as a septic joint or epidural abscess, may result on rare
occasions if these regions are entered. In addition, a local infection may
spread to distal sites. Therefore, sterile technique is imperative for all injec-
tions.
d. Local tissue damage may occur any time a needle punctures the skin. If the in-
jection is technically difficult, multiple passes of the needle or inadvertent
contact with periosteum, ligament, tendon, or muscle increases chances of
regional tissue trauma. Fluoroscopy helps to lessen the risk of tissue damage.
e. Allergic reactions are a risk for all medications and may occur in response to
either topical agents used to cleanse the skin or injected medications and
contrast agents. An appropriate history and consideration of premedication
in highly sensitive individuals helps to minimize such risks. All injectionists
should be prepared to deal with an unanticipated allergic reaction.
2. Local anesthetics may cause confusion, convulsions, respiratory arrest, seizures,
and even death if inadvertent intravascular injection occurs. These risks are
greatest in the head and neck regions where unintentional intraarterial injec-
tion may reach the cerebral circulation. All local anesthetics have a cardiac-
depressant effect, and they have the potential to trigger malignant hyperther-
mia and hypersensitivity reactions, including anaphylaxis. Appropriate
selection of agents and adjustments of dose are essential for patients with de-
creased renal or hepatic function as well as for patients with reduced levels of
plasma esterases.
3. Corticosteroids are an important therapeutic modality. They provide potent anti-
inflammatory effects, but they also carry risks of potentially serious side effects.
a. General. Corticosteroids have many potential adverse effects. In general,
short-term use is associated with far fewer complications than long-term
use. Corticosteroids may mask signs of infection or unmask a new infection.
In addition, vaccination with live viruses should be avoided during cortico-
steroid use because of steroid-induced immunosuppressive effects. Average-
to-large doses may precipitate dangerous changes in fluid balance, electro-
lyte levels, and blood pressure in susceptible patients. Although uncommon,
corticosteroids may cause hypersensitivity reactions. Especially at high
doses, they may precipitate or aggravate peptic ulcer disease. Adrenal sup-
pression generally occurs only with long-term therapy-not with single injec-
tions. Steroid-induced psychosis is dose-related and is more common with
280 Injection Procedures
doses that exceed 40 mg of prednisone or the equivalent. Rarely, a single

steroid dose, either oral or parenteral, may produce avascular necrosis, but
this problem is more common with higher doses or prolonged therapy.
Similarly, the risk of osteoporosis increases with increased dose and duration
of steroid use. An autoimmune response, called a steroid flare, sometimes
occurs within 4-24 hours after injection. A steroid flare, which is thought to
result from a local response to the steroid crystals, presents as a hot, red, and
very painful joint almost immediately after the injection. Early onset helps
to distinguish the steroid flare from an infected joint. Improved formulation
of long-acting steroid preparations has generally decreased the incidence of
steroid flare.
b. Local. Local reactions depend, in part, on the route of administration. Re-
peated subcutaneous or intramuscular injections of corticosteroids into the
same site may cause atrophy. Dermal and subdermal injections may cause
hypopigmentation. Intraarticular injections cause both local and systemic
effects. Patients must be cautioned against overusing joints in which they
experience symptomatic improvement but in which inflammation persists.
Unstable joints should not be injected. Excessive numbers of intraarticular
injections may damage joint tissues. Tendon rupture has occurred after in-
jection of corticosteroids in weight-bearing joints.
D. Side eHects. The most common side effect after injection therapy is pain at the in-
jection site. This discomfort is typically short-lived and may be minimized by the
local application of cold. Other side effects are related to the agents injected.
E. Patient selection. Injection therapy is generally reserved for patients with moderate
to severe pain who do not respond to traditional, conservative treatments such as
oral medications, physical or manual therapy, rest, and time. Although no studies
indicate the optimal time for injections, they are generally used only after several
weeks of conservative therapy have failed. Furthermore, the diagnostic or thera-
peutic benefit should be greater than the potential risk for any given patient.
a. Bleeding tendencies. Generally, patients who have a bleeding diathesis are not
candidates for injections. Those patients on anticoagulant therapy which can
be temporarily suspended should reach an INR of < 1.2 prior to the injection.
On rare occasion, the potential benefit justifies substitution of heparin as an
anticoagulant and discontinuing this agent immediately before injection.
b. Infection. Injections are contraindicated in the presence of local or systemic
infections because of the risk of spreading the infection.
c. Unstable medical conditions. The injection techniques described in this chapter
are elective procedures that provide diagnostic and therapeutic benefit for
non-life-threatening conditions. Medically unstable patients should have
their illnesses treated appropriately prior to elective injections.
2. Precautions
a. Platelet-inhibiting drugs. To minimize the risk of bleeding, some clinicians rec-
ommend withholding all aspirin-based products and newer platelet inhibit-
ing drugs for 7-10 days before an injection and all nonspecific nonsteroidal
antiinflammatory drugs for 2-3 days. The newer cyclooxygenase 2 inhibit-
ing anti-inflammatory drugs (e.g. valdecoxib, celecoxib, rofecoxib) do not
affect bleeding time and need not be stopped prior to an injection.
b. Medication hypersensitivity. Patients with a known drug hypersensitivity should
not receive that medication in a parenteral form. Exceptions may be made if
the reaction was mild and the potential benefit is high. In such cases, one
should premedicate with histamine blockers and corticosteroids and use the
smallest possible dose along with careful monitoring. Appropriate resuscita-
tive equipment and medications must be readily available. Premedication is
commonly employed prior to radiologic procedures when there is a history
of allergic reactions; however, premedication has never been proven to pre-
vent life threatening anaphylactoid reactions.
c. Concomitant medical dlnesses. Patients with diabetes mellitus may experience a
decline in blood sugar control after injections of corticosteroids. Patients
with congestive heart failure, renal failure, hypertension, or significant car-
diac disease may decompensate clinically after corticosteroid injections be-
cause of effects on fluid and electrolyte balance. Such decompensation is
uncommon following spinal injection therapy when small doses of cortici-
steroids are used. Appropriate monitoring and adjustments of medication
regimens help to minimize these effects. Spinal injections are sterile proce-
dures and patients with mitral valve prolapse generally do not need antibi-
otic prophylaxis before the procedure.
II. Specific Blocks

A. Epidural Steroid Injections (ESls). ESls include various procedures that involve injecting
corticosteroids into the epidural space of the vertebral column for diagnostic or ther-
apeutic purposes. Fluoroscopy to confirm epidural injection is strongly advised but
not universally accepted. Studies show that up to 400/0 of blind (nonfluoroscopic) in-
jections miss the epidural space. The injectionist may erroneously perceive epidural
placement at an inadequate depth of tissue penetration, especially when soft-tissue
planes are abundant. An absent or thin ligamentum flavum may result in inappropri-
ately deep injections into the subarachnoid space with serious consequences. The
epidural space is highly vascular, and inadvertent vascular injections are not uncom-
mon, despite failure to aspirate blood. Thus, fluoroscopic visualization and confirma-
tion with a contrast agent are recommended to ensure that the medication is properly
placed within the epidural space and that flow occurs to the target location.
1. Type ofinjection
a. Caudal. For caudal ESIs, a needle is placed in the sacral hiatus, near the supe-
rior portion of the gluteal cleft, and passed into the epidural space. If suffi-
cient volume is injected, the medication spreads cephalad from the caudal
epidural space to the lumbar epidural region. Caudal epidural injections are
typically performed with the patient lying prone. With fluoroscopic visual-
ization of the bony anatomy one notes the widely variable sacral hiatus,
which on rare occasions may be absent. Furthermore, fluoroscopic visualiza-
tion of injected contrast medium allows confirmation of cephalad spread.
Even in experienced hands, blind caudal ESIs fail in 400/0 of patients to de-
liver medication to the epidural space.
b. Translumbar. The lumbar epidural space can be approached directly by intro-
ducing a needle into the interlaminar space between spinous processes, pass-
ing it through the interspinous ligament and ligamentum flavum into the
epidural space. Alternatively, a paramedian approach directs the epidural
needle through the interspinous space just lateral to the interspinous liga-
ment. Interlaminar lumbar ESIs are commonly performed in the lateral decu-
bitus, prone, and sitting positions. Even in experienced hands, without fluo-
roscopic guidance as many as 200/0 of interlaminar epidural injections do not
reach the epidural space. In 9-100/0 of injections, venous penetration may
occur despite a negative aspiration for blood.
c. Transforaminal. Transforaminal or selective ESIs injections instill the medica-

tion along the desired nerve root. This procedure requires fluoroscopic visu-
alization of the regional bony anatomy to allow proper direction of the nee-
dle. In addition, contrast medium should be injected to document adequate
periradicular and epidural flow. Transforaminal epidural injections are typi-
cally performed in the prone or oblique positions. Transforaminal injection
may be the best means of reaching the ventral epidural space.
2. Indications and proposed mechanism of action
a. General
i. ESIs are an accepted treatment for radicular pain. The rationale for their
use is supported largely by numerous uncontrolled trials in which
33-77010 of injected patients report relief from pain. As with all therapeu-
tic interventions, the success of the injection depends on both technique
and patient selection. Obviously, proper localization of the injectant into
the epidural space is paramount to success. Fluoroscopic visualization
and contrast enhancement greatly facilitate this goal. Normal saline or
local anesthetics are the usual vehicle for delivery of the corticosteroid to
the epidural space.
ii. Pain relief from a single injection generally declines over time. Some
clinicians propose a series of three ESIs, regardless of return of pain, but
the benefit of this series is unproved. We prefer to treat each patient in-
dividually, and we repeat the procedure only if it was originally benefi-
cial and the radicular pain has partially returned. No studies address the
maximal safe number of injections per year, but to minimize the risks of
large doses of corticosteroids, most injectionists limit a patient to 3-4
ESIs per year.
iii. Radicular pain, characteristically burning, cramping, lancinating or
shooting, radiates into the distal extremity along a band. The pain radia-
tion does not necessarily mimic dermatomal distributions, nor does it
typically involve the entire extremity. Epidural steroids are believed to
work through their potent antiinflammatory effects. Acute disc injuries
release phospholipase A2 , a potent proinflammatory enzyme. In addition
to chemical irritation, a herniated disc may press on an exiting nerve
root. Periradicular swelling from the pressure of the actual herniated disc
produces significant discomfort when the nerve root is placed under trac-
tion with concomitant inflammation. Corticosteroids may relieve pain by
reducing the edema and subsequent deformity.
iv. Epidural steroids are also used to treat discogenic pain from anular rents
or herniations that release the proinflammatory enzyme, phospholipase
A2 • This chemical irritant may cause epiduritis (inflammation of the ven-
tral dural sac and root sleeve); pain may respond to the potent antiin-
flammatory effects of ESIs. The pain of epiduritis may be more somatic
in nature, i.e., deep, aching quality perceived in the back and proximal
extremity. When used for discogenic pain, ESIs work best when there is
an acute flare rather than in long standing or post discectomy pain.
v. Another mechanism proposed for the palliative actions of ESIs is direct
blockade of nociceptive nerves. Methylprednisolone has been shown to
inhibit nociceptive axons directly, much like a local anesthetic.
b. Caudal. The caudal approach to epidural administration of medication is pre-
ferred by some clinicians because of the lower risk of inadvertent dural
puncture and therefore of subarachnoid injection. The dural sac generally
ends between S1 and S2. Caudal ESls are also a convenient route by which
lumbosacral nerve roots can be bathed when a translaminar approach is ill
advised because of previous surgery, trauma, or congenital abnormalities.
The caudal injection requires sufficient injectant volume to ensure adequate
cephalad spread to the desired lumbosacral level. The total volume injected
determines the spread. Generally, a volume of 6-10 ml reaches the L5 level,
and 15 ml reaches the L4 level. Excessive volume may cause intracranial
complications from sudden shifts in epidural pressure and toxicity if a local
anesthetic is used as the vehicle.
c. Translumbar. The translaminar approach to the lumbar epidural space is prob-
ably the most widely used technique for ESI. The choice of the interlaminar
space depends on the level of the suspected disorder. Volumes injected range
from 2-10 ml, including 40-120 mg depot methylprednisolone or 6-18 mg
of betamethasone mixed with lidocaine, bupivacaine, and/or normal saline.
d. Transforaminal. Transforaminal spinal injections can limit the spread of injec-
tant to a single spinal nerve root or advance the needle tip slightly more me-
dial position to provide epidural spread. If the appropriate nerve root sleeve
is injected and there is adequate spread along the sleeve, the patient should
obtain temporary relief. This diagnostic information becomes important
when imaging studies demonstrate multiple sites of potential pathology. To
maintain the diagnostic specificity of the block, small volumes of injectant,
generally 1-3 ml, should be administered slowly. Epidural spread to the ad-
jacent level may occur with as little as 2 ml if the needle is positioned to fa-
vor medial and cephalad rather than caudal periradicular flow. Alternatively,
larger volumes may produce more diffuse spread with improved ventral
epidural spread. In one small study, pain relief of at least 1 week's duration
after transforaminal ESI prognosticated a favorable response to surgery. In
the same study, patients with radicular pain for 6 months or longer, who did
not obtain relief for at least 1 week, were unlikely to obtain significant relief
from surgical intervention.
a. Technical. ESls are contraindicated in regions where the epidural space is al-
tered or eliminated. Specifically, epidural injections should be avoided at the
level of congenital anatomic anomalies or previous surgery. In addition, one
should not use ESls in patients with systemic infections. Penetration of in-
fected skin should be avoided to reduce spread of infection and potential
epidural seeding. Patients with a bleeding diathesis and patients who are
anticoagulated should not undergo ESls because of the increased risk of
bleeding and epidural hematoma formation.
b. Steroid-related. ESls may cause systemic corticosteroid effects. Patients at risk
for medical decompensation from fluid retention, such as those with severe
congestive heart failure or poorly controlled hypertension, should not un-
dergo ESls. ESls also may unmask an infection or interfere with blood glu-
cose control.
4. Risks
a. Dural pundure and subarachnoid injections. Inadvertent dural puncture reportedly
occurs in 0.1-5010 of all epidural injections. It may result in persistent spinal
fluid leak that imposes tension on intracranical structures; this complication
is manifested by a headache when the patient assumes an upright posture. In
general, postdural puncture headaches respond to rest in the supine position,
adequate hydration, and analgesics. Occasionally they require repair by an
autologous epidural blood patch. Significant problems may occur if the injec-
tionist fails to recognize the subarachnoid position and injects medications
intended for the epidural space into the intrathecal space. Respiratory depres-
sion may result from unintentional spinal anesthesia, and intrathecal injec-
tion of medications with preservatives may cause arachnoiditis and pain.
b. Intravascular injections. Inadvertent intravascular injections may cause local
anesthetic toxicity, including seizures, cardiac arrest, and death.
Intravascular injection of corticosteroids may cause burning, pain, and even
anaphylactic reactions.
c. Infection. Strict adherence to aseptic technique is critical to avoid superficial
and deep infections from ESIs. Epidural steroids suppress the adrenal system
for 2-3 weeks and thus may unmask a systemic infection or allow it to
spread. Development of an epidural abscess is heralded by increased back
pain, fever, and leukocytosis. An epidural abscess requires rapid investiga-
tion, decompressive surgery, and antibiotic treatment to minimize the risk of
permanent neurologic sequelae.
d. Bleeding. Epidural bleeding with resultant hematoma formation is a signifi-
cant risk in patients with coagulopathies or altered bleeding states.
Unrecognized arteriovenous malformations also may cause bleeding compli-
cations after epidural blockade. Relaxation of the patient to avoid venous
distention from Valsalva maneuvers and placement of the epidural puncture
in the less vascular midline region reduce the risk of venous puncture.
Injection of contrast agent further confirms extravascular location before in-
stilling the active medications.
e. Bladder dysfunction. Bladder dysfunction, with decreased awareness of disten-
tion, may result from prolonged local anesthetic blockade of the sacral roots.
Overdistention of the bladder may weaken the detrusor muscle with persis-
tent symptoms.
f. Neurologic comphcations. Neurologic complications can result from direct pene-
trating trauma to the spinal nerves or spinal cord by the epidural needle,
neurotoxicity of medications injected, ischemia, or compression from a
hematoma or abscess.
5. Side eHects. The side effects of ESIs include adverse reactions to the injected
medications, as discussed in section IC (page 279). Occasionally, patients may
experience a transient increase in back and radicular pain after ESIs.
6. Technique
a. General. ESIs are best performed under fluoroscopic visualization and with
contrast enhancement to avoid inadvertent soft-tissue, subarachnoid, or in-
travascular injections. Fluoroscopy and contrast also ensure appropriate
spread to the side and level of the targeted ventral epidural space. Unrecog-
nized venous cannulation occurs in 7-9010 of epidural injections. Light con-
scious sedation may improve patient tolerance for the procedure but requires
additional monitoring for problems associated with sedation. Written in-
formed consent should be obtained before injection.
b. Caudal. Caudal ESIs are performed with the patient prone on the fluoroscopy
table. The skin over the sacrum and coccyx is cleansed with a surgical
preparation such as povidone-iodine (Betadine), and the region is sterilely
draped. Local anesthesia is achieved by infiltrating the skin, subcutaneous
tissues, and sacral hiatus with less than 5 ml of lidocaine 1-2010. Next, a
20-25-gauge, 3.5-inch spinal needle is advanced through the sacrococcygeal
ligament and into the sacral canal; its position is confirmed by lateral and
anteroposterior fluoroscopic visualization and by subsequent injected con-

trast medium. Epidural steroid (6-18 mg of betamethasone or 40-120 mg of
depot methylprednisolone) is injected in a diluent, such as lidocaine (1-20/0)
and/or normal saline, to a usual volume of approximately 10 ml,
c. Translumbar. The authors recommend fluoroscopic visualization during lum-
bar ESls with the patient in the prone position or lateral decubitus position.
The skin over the lumbar spine is cleansed with a surgical preparation such
as povidone-iodine (Betadine), and the area is sterilely draped. The inferior,
ipsilateral aspect of the lamina corresponding to the site of pathology is then
identified and visually confirmed. After skin and subcutaneous tissue anes-
thesia is achieved with local infiltration of lidocaine, an epidural needle is
inserted to the ligamentum flavum. Using a loss-of-resistance technique, the
needle is slowly advanced in a controlled fashion, as with a Bromage grip.
Lateral fluoroscopic images can help guide depth of injection. When loss of
resistance is noted, the needle should be in the epidural space. The position
is confirmed by epidural pattern of contrast flow under fluoroscopy. Typical
medication for a lumbar ESI includes 6-18 mg of betamethasone or 40-120
mg of depot methylprednisolone in 3-8 ml of lidocaine, bupivacaine, and/or
normal saline.
d. Transforaminal. Selective, transforaminal ESls are placed directly along the
lumbosacral nerve root and epidural space in the neural foramen. The pa-
tient is positioned prone on the fluoroscopy table, and the skin over the in-
volved level is prepared sterilely and draped. The lumbar nerve roots exit the
spinal canal just inferior and medial to the mid position of the ipsisegmental
pedicle on AP imaging. Needle placement above the nerve root and below
the pedicle is confirmed by a slow injection of 1 ml of contrast medium,
which should spread both peripherally along the nerve root and centrally
along the pedicle to the epidural space. If the transforaminal injection is for
diagnostic as well as therapeutic purposes, the injectionist must take utmost
care not only to ensure adequate spread along the nerve root but also to pre-
vent excessive spread to other levels. Transforaminal ESls generally involve
only small volumes, e.g., 1-2 ml of steroid and 1-4 ml of local anesthetic.
B. Zygapaphyseal (facet) joint injections. Injections into the zygapophyseal joints [z-joints]
or around their nerve supply were developed to localize and treat low back pain
emanating from these paired, posterior synovial joints. It is well established that
the lumbar z-joints can produce low back pain. Presently, diagnostic blockade of
the joint is the only reliable means of establishing in which patients low back
pain emanates from zygapophyseal joints. Knowledge of the precise pain gen-
erator helps to guide therapeutic intervention and potentially prevents unneces-
sary surgery.
I. Types
a. Intraarticular. Injections into the lumbar z-joints are analogous to the more
common peripheral joint injections. Both require a thorough knowledge of
the regional anatomy and injection techniques. Both are used to block pain
from the involved joint and, if steroids are injected, to relieve presumed in-
flammation. However, unlike their peripheral counterparts, lumbar z-joint
injections require fluoroscopy to ensure an intraarticular injection.
b. Medial branch blocks. Medial branch blocks can exclude or implicate the lum-
bar z-joint as the source of low back pain. The nerve supply to the lumbar
z-joints is via the medial branches of the dorsal rami at the level of the spe-
cific joint and the level above. For example, the L4-L5 z-joint is innervated
286 Injedion Procedures
by the medial branches of the L3 and L4 dorsal rami, which innervate pri-
marily the z-joint and a segmental multifidus muscle. Thus, anesthesia of
these nerves blocks the z-joint without interrupting sensation from other im-
portant nociceptors, such as the ventral root, disc, or ligaments.
c. Radiofrequency neurotomies. Radiofrequency neurotomies denervate the lumbar
z-joint in patients in whom the z-joint is the proved pain generator and
more conservative forms of treatment have failed to bring relief. The medial
branches innervating the joint are targeted, as for medial branch nerve
blocks. However, instead of injecting a local anesthetic, as for a temporary
block, the nerve is coagulated by application of radiofrequency current. This
technique results in long-lasting (months to years) denervation.
2. Indications
a. General. The ability of intraarticular z-joint and medial branch blocks to di-
agnose pain of z-joint origin has been confirmed both clinically and neuro-
anatomically. Controlled studies have not established the efficacy of intra-
articular steroid injections or radiofrequency neurotomies for treatment of
the lumbar z-joint, although uncontrolled studies consistently report benefits
from both procedures. Joint injection procedures are associated with a
placebo response of 350/0, and one should not overinterpret favorable re-
sponse to a single block. However, if the pain is relieved repeatedly using
two comparative blocks with anesthetics of different durations, and if
longer-duration anesthetic agents provide long-lasting relief, the blocked z-
joints are implicated as the source of low back pain.
b. Intraarticular. Although a large number of uncontrolled studies report relief of
low back pain by intraarticular z-joint steroid injections, two controlled
studies indicate that the beneficial effects are not attributable to cortico-
steroids. Instead, both control and treated groups of patients (vehicle or ac-
tive steroid injection) had significant and lasting benefit. Despite certain de-
sign flaws, the controlled studies remain superior to uncontrolled reports. In
summary, present knowledge indicates that intraarticular lumbar z-joint in-
jections, although not a panacea for low back pain, may be of benefit in cer-
tain cases. Further studies are needed to establish their efficacy. In addition,
the effects of lavage or intraarticular manipulation on the joints should be
explored further.
c. Medial branch blocks. Medial branch blocks are an important diagnostic tool.
Pain that is reproducibly relieved by this means probably emanates from the
blocked joints. Medial branch blocks are performed with local anesthesia;
thus their effect is temporary. For unknown reasons, patients who respond
favorably occasionally achieve long-lasting relief of their chronic low back
pain. Medial branch blocks may be used to prognosticate response to medial
branch neurotomies.
d. Radiofrequency neurotomies. Various methods of denervating lumbar z-joints
have been used, but none have been subjected to rigorous controlled trials.
Achievement of long-lasting pain relief with localized denervations is an at-
tractive concept, but adequately controlled research must establish the utility
of such procedures.
3. Contralndlcatlons to z-joint injections are the same as the generalized contraindi-
cations to injection procedures listed in section IE (page 280).
4. Risks. The risks of z-joint injections include general risks of bleeding, infection,
local tissue damage, allergic reaction, or drug adverse effects, as discussed in
section IC. Poorly placed injections may cause subarachnoid spread of local
anesthetics and subsequent spinal anesthesia. In addition, radiofrequency neu-

rotomies carry the risk of dysesthetic pain or radicular pain from a misplaced
lesion. Careful electrical stimulation testing before lesioning combined with ex-
cellent technique minimizes the chance of misplaced denervations.
5. Side eHeds. The most common side effects from lumbar z-joint injections are
from injected medications or local pain at the injection site.
6. Te(hniqu8
a. General. Precise localization of z-joint injections requires fluoroscopic imag-
ing and confirmation of position with contrast medium. There are no reli-
able, palpable landmarks for lumbar z-joint injections. Only through radio-
graphic visualizations can one ensure that the needle has reached the desired
location within the joint or at the medial branches of the appropriate dorsal
rami. In addition to confirming location, an injection of contrast medium
identifies inadvertent venous cannulizations that may occur despite negative
aspiration for blood. Lumbar z-joint injections require informed consent,
sterile field preparation, and sterile technique. For the anxious patient, light
sedation may improve patient tolerance for the procedure but requires addi-
tional monitoring. Patients undergoing diagnostic injections should not re-
ceive intravenous or oral analgesic agents.
b. Intraarti(ular. Lumbar intraarticular z-joint injections are performed with the
patient positioned obliquely on the fluoroscopy table or prone if a C-arm
is available. Rotating either the patient or C-arm brings the target joint
line into view. The injectant is typically lidocaine (1-20/0) or bupivacaine
(0.5-0.750/0) with or without addition of a long-acting steroid, such as depot
methylprednisolone or betamethasone. The capacity of the lumbar z-joints is
generally 2 ml or less.
c. Medial branm blocks. The target for medial branches of the primary dorsal rami
that innervate the lumbar z-joints lies at the junction of the subjacent trans-
verse process and the base of the superior articular process as viewed antero-
posteriorly. On oblique imaging, the target point is in the "eye" of the Scotty
dog. Each lumbar z-joint is innervated by the ipslsegmental medial branch of
the dorsal ramus and the level above. Because of the inferior course of the
medial branch, the target locations are at the base of the transverse process of
the involved joint and the transverse process below. Each medial branch
should be injected with no more than 0.5 ml of anesthetic. The patient is re-
examined for pain relief after blockade of the selected nerves. A pain diary
kept for the next 6-72 hours helps to determine the response.
d. Radiofrequen(y neurotomies. The target location for medial branch radiofre-
quency neurotomies is identical to that for medial branch blocks. Placement
of the radiofrequency probe tangential to the nerve optimizes the overlap of
the elliptical bum and the nerve. The nerve is electrically stimulated before
application of the heating current in an attempt to reproduce usual discom-
fort and to confirm lack of radicular pain or extremity motor stimulation.
Once the physician is satisfied with the probe's position, injection of a small
amount of local anesthetic (0.5 ml of lidocaine [1-20/0]) improves patient tol-
erance to the lesioning current. Light sedation is also beneficial.
C. Hardware. Placement of a local anesthetic block along orthopedic hardware, such
as fusion plates and screws, provides selective blockade of nociception from a tar-
get area.
I. Indi(ations. Hardware blocks are used to determine whether a piece of hardware
that has migrated or loosened is responsible for the patient's pain. Local anes-
thetics applied around the hardware block nociception from that region. One
should avoid voluminous injections that may spread to nearby structures and
result in loss of specificity for the blocked area.
2. Contraindlcations. Contra indications to hardware injections are the same as the
generalized contraindications to injection procedures listed in section IE (page
280).
3. Risks. As with all injections, hardware blocks carry the risk of bleeding, infec-
tion, local tissue damage, allergic reactions, and local anesthetic toxicities. In
addition, altered regional anatomy and scarring pose an increased risk of inad-
vertent subarachnoid injections or contact with a nerve root. Placebo response
to injections is not uncommon; any positive analgesic response may need to be
confirmed with subsequent blocks by local anesthetics of different duration.
4. Side eHects. A temporary increase in lumbar discomfort is the primary side effect
associated with hardware blocks.
5. Technique. The proposed site of pain is identified before the procedure. Informed
consent is obtained, and the patient is positioned prone on the fluoroscopy
table. The skin is sterilely prepared and draped. Next, skin anesthesia over the
involved segment is achieved, and a 22-25-gauge, 3.5-inch spinal needle is
placed with fluoroscopic guidance at the proposed site of pathology. Contrast
medium may be injected to ensure that the needle is extravascular and that no
undesired tracking occurs. Once the needle is correctly positioned, 1-3 ml of lo-
cal anesthetic is injected to anesthetize the region. The patient is reexamined
within 15-20 minutes to determine whether an analgesic response has oc-
curred. The absence of pain implicates the blocked structure as the pain source.
D. Discography. Discography combines radiographic imaging of the internal architec-
ture of the disc and provocative injections to determine whether a given interver-
tebral disc is the source of pain.
1. Indications. Lumbar discography is a controversial diagnostic procedure to iden-
tify painful discs and examine their internal anatomy. It is unique in that it
evaluates both pathoanatomy and symptomatology. Traditional imaging studies
cannot reveal whether an anatomic lesion is painful, and computed tomogra-
phy, bone scans, myelography, or radiographs cannot reliably identify internal
disc disruption. Magnetic resonance imaging may reveal degenerative disc
changes, but such changes are common in the general population and not
unique to painful discs. Discography is often used to confirm abnormal internal
disc architecture and the pain-producing status of a given disc when surgical
intervention is considered. Proponents argue that it is especially useful for es-
tablishing the primary source of discomfort from multiple degenerative discs.
Discography is commonly used to test the structural integrity of a disc adjacent
to a planned surgical fusion, and it may confirm suspected far lateral or recur-
rent disc herniations that are difficult to visualize with traditional imaging
studies. In addition, discography may be used before chernonucleolysis.
2. Contraindications. Discography is contraindicated in a patient with a known infec-
tion, severe allergic reaction to contrast agents, bleeding diatheses, or an unsta-
ble medical condition. In addition, candidates must be able to communicate
with the injectionist about their pain. Patients with significant pain behavior or
secondary gain have been shown to produce nondiagnostic disco grams.
3. Risks. Potential complications of discography include allergic reactions to the
radiopaque contrast agent or local anesthetic, neural injury from needle contact
with ventral root, superficial skin infections, and disc space infections. There
has been concern over potential damage to normal discs, but animal studies
have not demonstrated significant damage after discography and human discs
examined either after surgical removal or at post-mortem examination fail to
show inflammation or other structural changes as a result of discography. The
risk of allergic reactions is minimized through appropriate preprocedure screen-
ing and prompt medication of suspected reactions. The risk of infection is re-
duced by strict adherence to sterile technique. In addition, several studies sug-
gest that prophylactic intravenous or intradiscal antibiotics may be of benefit.
A two-needle technique appears to reduce the risk of discitis, presumably by re-
ducing the risk of tracking skin flora. Overall, the risk of disc space infection
ranges from less than 0.5% to 2.7%. Skilled technique and slow advancement
of the needle in the region of the nerve root helps to avoid neural injury. A
conscious patient can notify the injectionist of early radicular pain, allowing
the needle to be redirected.
4. Side effects. The most common side effect is that of increased discomfort after
the procedure, but adverse reactions to either the local anesthetic, contrast
agent or antibiotic may also occur. There are also attendant risks of sedation or
light anesthesia.
5. Technique
a. The patient is evaluated for potential contraindications before discography,
and informed consent is obtained. Discography is performed in either a radi-
ology suite or operating room under sterile conditions with light sedation.
Patients must be conscious and able to communicate fully with the injec-
tionist about their pain. The procedure is performed by alternating oblique,
anteroposterior, and lateral views to facilitate placement of the 22-25-gauge,
6-8-inch discography needle into the geometric center of the disc. Skin and
subcutaneous anesthesia is obtained through infiltration of a local anesthetic
before needle placement.
b. Once the needles are placed in the desired discs, 0.5-3 ml of normal saline
or contrast is injected into each disc until firm resistance or significant pain
occurs. Intradiscal pressure is measured. During the injection, the patient is
observed for pain behavior and questioned about the location, intensity, and
similarity of any pain provoked. Painful discs are then injected with 0.5 ml
of lidocaine 1%, and the presence or absence of analgesia is noted. A posi-
tive analgesic response further supports discogenic pain; however, lack of a
response does not exclude a discogenic pain source. After pain provocation,
if saline was initially injected, 0.5-1 ml of radioopaque contrast is injected
into each disc, and anteroposterior and lateral films of the resulting nucleo-
gram are recorded. The disc appearance is recorded. The needles are re-
moved, the puncture sites dressed, and the patient sent for computed tomog-
raphy of the lumbar discs to define further the spread of contrast material
within the disc nuclei.
c. A positive discogram requires reproduction of the patient's usual pain and
an abnormal nucleogram, In addition, at least one additional control disc in-
jection should be free of concordant pain response. This control disc injec-
tion guards against false-positive responses.
E. Sacroiliac joint. The sacroiliac joint (SIJ) can cause pain through nociceptors in and
around the joint. However, clinical acceptance of this joint as a source of low back
and buttock pain has been both endorsed and denied. Recent literature strongly
indicates that the SIJ can cause back and referred pain.
I. Indications
a. There are no pathognomonic signs of SIJ pain. Injection of the SIJ should be
considered in cases of chronic low back and buttock pain not attributable to
other causes. Specifically, tumor, infection, and painful herniated disc
should be excluded before considering SIJ injections. Injection of the SIJ
with a local anesthetic provides diagnostic information. If the pain is re-
lieved by such injections, especially if relief is reproducible, it probably em-
anates from the injected SIJ. Pain that is not relieved by local blockade sug-
gests a different etiology.
b. There are no controlled studies of the therapeutic benefits of SIJ injections
with corticosteroids, but SIJ injections are likely analogous to corticosteroid
injections in peripheral joints for control of chronic inflammation and pain.
Pain from inflammatory sources (e.g., inflammatory arthropathies or os-
teoarthritis) that is not relieved by conservative measures may respond fa-
vorably to intraarticular SIJ injections of corticosteroids.
2. Contraindications. General contraindications that apply to injection therapy (infec-
tion, acute fracture, tumor, bleeding diathesis, unstable medical condition, and
allergic reactions to local anesthetics or steroids) apply to SIJ injections as well.
3. Risks. Risks associated with SIJ injections include bleeding, infection, local tis-
sue damage, and allergic reactions.
4. Side eHeets. Side effects associated with corticosteroid and local anesthetic injec-
tions are discussed on page 279; they pertain to injection in the SIJ as well.
5. Technique
a. Sacroiliac joint injections are performed under sterile conditions with fluoro-
scopic imaging after informed consent is obtained. Most of the SIJ is inac-
cessible to direct posterior penetration with a needle. The SIJ is most easily
entered at its inferior extent. The patient is positioned in a prone to slightly
oblique position with the uninvolved side up to visualize the posterior, cau-
dal portion of the joint. Once joint entry is perceived, position is confirmed
by spread of contrast medium superiorly along the joint margin. Next, a
local anesthetic. generally 1- 2 ml of lidocaine (1-2010) or bupivacaine
(0.25-0.75010), is injected alone or with a corticosteroid preparation such as
betamethasone or depot methylprednisolone. After the procedure, the patient
is reexamined for pain relief. Total volume should be limited to 2-2.5 ml.
b. All intraarticular corticosteroid injections carry the risk of significant sys-
temic absorption, and repeat doses should be limited to avoid adrenal sup-
pression and iatrogenic Cushing syndrome. No rigorous clinical trials have
established the limit of frequency and number of injections. Nonetheless,
most practitioners limit the number of injections to 3 per year at intervals of
no more than every 3 weeks.
F. Sacrococcygeal injedions. The sacrococcygeal joint is a rudimentary intervertebral disc
at the junction of the sacrum and coccyx. This region is covered by the sacrococ-
cygeal ligaments. Patients suffering chronic coccygeal pain may have a chronic
strain of sacrococcygeal ligaments or pain from the rudimentary disc.
1. Indications. The sacrococcygeal ligaments can be infiltrated with local anesthetic
and corticosteroids in cases of refractory coccygeal pain.
2. Contraind'lCations. The general contraindications to injection therapy (infection,
acute fracture, tumor, bleeding diathesis, unstable medical condition, and allergic
reactions to local anesthetics or steroids) also apply to sacrococcygeal injections.
3. Risks. Risks associated with sacrococcygeal injections include bleeding, infec-
tion, local tissue damage, and allergic reactions.
4. Side eHeds. The side effects of corticosteroid and local anesthetic injections (dis-
cussed on page 279) also pertain to injection into the sacrococcygeal ligaments.
5. Technique. After informed consent is obtained, the patient is positioned prone,

and under lateral fluoroscopy the sacrococcygeal junction is imaged. A 25-
gauge needle is inserted down to the periosteum, and the region is infiltrated
with 2- 3 ml of local anesthetic alone or in combination with a corticosteroid.
The rudimentary disc also can be entered in the midline and injected. Care must
be given to avoid passing through the disc toward anterior structures.
G. Lower extremity injedions. Selective injections of the lower extremity can assist the
practitioner in the differential diagnosis of low back pain, radicular pain, periph-
eral nerve entrapments, and referred joint pain. Hip pain and axial back pain may
present with overlapping features. Relief of pain after a fluoroscopically guided
intraarticular hip injection indicates that therapy should be directed at the hip
pathology. Similarly, relief of lower extremity pain with a peripheral nerve block
of the peroneal nerve at the fibular head or the tibial nerve at the tarsal tunnel
points to a nonradicular source. Localizing the source of the pain in this fashion
focuses the treatment on the appropriate structure and eliminates the need for a
potentially costly trial-and-error approach to care.
1. Indications
a. The hip joint can be infiltrated with local anesthetic and corticosteroids in
cases of refractory buttock, hip, medial knee, and groin pain in which the
possibility of intraarticular hip pathology exists. Pain from osteoarthritis
may occur before visible radiographic changes.
b. Patients with pain and paresthesias in the leg and dorsal foot may suffer
from peroneal nerve entrapment or L5 radiculopathy. Nerve conduction
studies and electromyography often can be used to distinguish the two con-
ditions. At times a double crush injury to both the root and peripheral nerve
is suspected. Selective root blocks and peripheral nerve blocks at the entrap-
ment site, usually the fibular head, help to distinguish the relative contribu-
tions of the two sites of pathology.
c. In a similar fashion, pain and numbness in the foot due to tarsal tunnel syn-
drome vs. S I radiculopathy may be explored with electrodiagnostic studies
and selective injections.
2. (ontraindications. The general contraindications to injection therapy (infection,
acute fracture, tumor, bleeding diathesis, unstable medical condition, and aller-
gic reactions to local anesthetics or steroids) also apply to lower extremity in-
jections.
3. Risks. Risks associated with lower extremity injections include bleeding, infec-
tion, local tissue damage, and allergic reactions.
4. Side eHeds. The side effects of corticosteroid and local anesthetic injections (dis-
cussed on page 279) pertain.
5. Technique. Intraarticular hip injections are best carried out under fluoroscopic
guidance. After informed consent is obtained, the patient is positioned supine
and a 22- or 25-gauge spinal needle is passed just anterior and superior to
the greater trochanter into the joint capsule. Alternately, an anterolateral ap-
proach may be used taking care to avoid the more medial neurovascular bun-
dle. Position is confirmed with injection of a contrast agent and visualization
of an intrarticular pattern. Peripheral nerve injections, such as the peroneal or
tibial nerves, are best accomplished with electrodiagnostic localization of the
nerve rather than fluoroscopy. Adjusting the electrodiagnostic needle to max-
imize the amplitude of the response and to minimize the stimulating current
ensures placement adjacent to the nerve and thereby allows a specific anes-
thetic block.
292 In;ection ProceJures
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1 - - - - - - - -17
Psychological Considerations
J. David Sinclair, M.D. F.R.CP.(C)
Key Points
• Pain is an unpleasant [and always both] sensory and emotional experience associated
with actual or potential tissue damage or described in terms of such damage.
• 30% to 50% of people who seek treatment in primary care do not have specific
diagnosable disorders, and for up to 80% of people complaining of back pain no
anatomical basis for pain can be found.
• Physical disability is more closely associated with psychological factors than with
medical diagnosis: finding of a World Health Organization study of more than 26,000
subjects in 14 countries.
• Psychological factors playa critical role in patient recovery from injury or illness.
Ignoring either the physical or the psychological components in diagnosis and
treatment is a prescription for failure, patient disappointment, and third party
dissatisfaction.
• Questions about the emotional aspects of the low back pain patient can be considered
a state-of-the-art component of the initial evaluation.
• Patients in whom pain could not be traced to a significant structural pathology have
been shown to be much more likely to have encountered childhood abuse and conflict,
parental job stress, or a difficult divorce. This constellation of circumstance creates a
diathesis toward the development of chronic pain.
• The chronic low back pain patient's [often unconscious] aim is to confirm his or her
identity as a painful suffering person. It is as unreasonable to expect him or her to
[spontaneously] relinquish that identity [and sometimes career] as it is to expect the
physician to do so.
• One of the main problems physicians who treat low back pain face is that a patient's
developmental experience, personality, and emotional nature that are profoundly
influencing his or her experience of pain are unknown when he or she walks through
the door.
• Assessments using the Million Clinical Multaxial Inventory of patients awaiting
admission to an outpatient chronic pain treatment program revealed that 66% of the
subjects were diagnosed with a personality disorder.
• Once identified, the high risk/problem patient can be assumed to be untreatable in a
one-on-one doctor patient therapeutic alliance. (see Managing Difficult Patients).
I. Scope of Problem
A. Epidemiology
1. Pain is a ubiquitous symptom that is essential for survival.
2. Pain has been identified, second to respiratory infections. as the most common
reason for seeking medical care. 50% to 75% of people have an episode of back
pain at some time in their adult lives. 14% of these have back pain lasting
297
298 Psychological ConsiJeralions
longer than two weeks. 18010 to 22010 indicate their pain was "severe" to "excru-
ciating."
3. More important than prevalence, however, is impact. Chronic and acute recur-
rent pain is the presenting symptom in over 80 million office visits to physi-
cians each year.
4. In the U.S., 2010 of national work force sustains a work-related back injury lead-
ing to compensation each year.
5. Back pain was the most common factor causing time off from work for people
under 45 years of age during 1969-1970.
6. Between 1957 and 1976, the rate of disability from back pain increased at a
rate fourteen times faster than the U.S. population and is growing at a discem-
ably higher rate than the aggregate of all other categories of disability.
7. Workers injured for the first time and those who have had more severe prob-
lems in the past are at greater risk for future problems than those who had pre-
vious episodes with relatively little trouble.
8. Occupations that require handling materials are at especially high risk for in-
jury.
B. Financial cost
1. The annual costs of chronic pain have been estimated to exceed $125 billion.
2. In various studies back pain accounts for about 20010 of all claims and back in-
jured patients are more likely to have multiple claims.
3. The 1986 Bigos study revealed that the cost of back injuries was three times
higher than for non-back-related injury claims.
4. 1990s data from the Workers Compensation Back Pain Claims Study show that
the "average cost per industrial back injury in the U.S. is now more than
$24,000.00".
5. Surgical cost data indicate a cost of more than $168,000.00 for lumbar fusion.
II. Psychological Considerations

A. About Pain
1. Chronic pain patients whose damages or pathologies are similar one to another
report marked differences in severity, quality, and impact of their pain. This in-
dicates that in chronic pain there is no relationship between damages and pain.
2. As a consequence of dubious reliability, sensitivity and specificity and utilty of
many common examinations and tests, there are large numbers of patients for
whom either we are unable to demonstrate objective findings or we are identi-
fying objective abnormalities in asymptomatic individuals.
3. In the brain, there are no pain fibers and no pain pathways.
4. Pain has profound emotional meaning and cognitive significance.
5. No particular stimulus is painful. Whether or not a stimulus will be perceived as
painful depends on the nature of the stimulus, the situation in which it is expe-
rienced, memories, present emotions, and assigned meaning [which predicts the
future].
6. The experience of pain is more akin to hunger or thirst than to vision or hear-
ing; i.e., more akin to a need state than a sensation.
7. A complex perception, an experience, pain is not as its nominalization might
imply: a thing that can be surgically excised or pharmacologically "killed."
8. Anatomical pathology cannot be thought of simplistically in terms of it being
"the pain generator."
9. Patients who transition from acute back pain to chronic pain undergo a trans-
formation that has a psychological, not an anatomical basis.
Psychological Considerations 299
B. A Common Chronic Back Pain Scenario

1. Patient has seen multiple doctors, who have asked the patient pretty much the
same questions. Monthly, patient becomes more irritable and edgy.
2. The advice of the psychologist or psychiatrist is invoked. Patient feels disap-
pointed, rejected, and angry. Patient feels marginalized by the physician send-
ing him or her to "the shrink." Patient knows he or she is not "crazy" or imag-
ining the pain and knows he or she is not a drug addict but does need
analgesics to control symptoms. The psychological consultant will leave with
few helpful recommendations.
3. Finally patient is sent home with a new set of prescriptions, an appointment for
an office visit, and the sequence begins anew.
4. All the repetitiously somatically focused questions and examinations direct pa-
tient's thoughts to notice and to think about symptoms more than he or she has
before.
5. In addition, he or she now begins to notice all the other bodily feelings that
previously went unnoticed.
6. Noticing bodily feelings and paying attention to them magnifies them. They be-
come more frequent and more noticeable, and soon patient begins to answer
more doctors' questions affirmatively.
7. Patient is referred for another consultation in what feels to him or her [and
third parties] like a never ending cycle (see The Natural History of Chronic Back
Pain).
C. The Natural History of Chronic Back Pain
1. Awareness and interpretation of symptoms.
2. Help seeking.
3. Diagnostic uncertainty.
4. Patient frustration.
5. Doctor shopping.
6. Multiple costly and often invasive tests and treatment.
7. Suggestion of psychological causation and/or malingering.
8. Increased symptom reporting, pain behaviors and help seeking.
9. Increased psychological distress.
10. Transformation from acuity to chronicity: consolidation of abnormal illness
behavior.
D. Pain Suffering and Illness Behavior
1. An important distinction is the distinction between pain and suffering.
Suffering is psychological distress.
2. Waddell found that the most important psychological feature in a study of
chronic low back pain and disability was increased bodily awareness. It seemed
to be the hieroglyphic for depression and anxiety and completely overshad-
owed psychological measures of personality traits or fears and beliefs about ill-
ness in its contribution to psychological distress.
3. Increased awareness and reporting of bodily function appears to be a much
more powerful clinical concept than theories of hypochondriasis as they relate
to chronic pain.
4. We recognize that the patient is ill, not only by what he or she tells us but also
by changes in the whole pattern of behavior that we recognize as "illness be-
havior."
5. Overt illness behaviors include guarding, bracing, rubbing, grimacing, and
sighing and are usually carried over into the physical examination part of the
evaluation.
300 Psychological Considerations
6. The signs of illness behavior are most simply illustrated by the pain drawing.
a. The way patients draw their pain is strongly influenced by emotional dis-
tress, and the patient's drawing communicates both physical information
about the pain and psychological information about his or her response to
pain.
b. In Wiltse's scoring system, each of the following rates a score of one. A total
score of one is normal; five or more reflects abnormal illness behavior.
i. Writing anywhere.
ii. Unphysiologic pain pattern.
iii. Unphysiologic sensory change.
iv. More than one type of pain,
v. Both upper and lower areas of body involved.
vi. Marking outside body.
vii. Unspecified symbols.
7. A number of symptoms have been identified as being more closely related to
psychological distress than to anatomical or pathological mechanisms.
a. Pain at the tip of the tail bone.
b. Whole leg pain.
c. Whole leg numbness.
d. Whole leg giveaway.
e. Complete absence of any periods of the normal variations and remission
with time.
f. Intolerance or reactions to every treatment due to it aggravating pain or
causing severe side effects or subjective complaints.
8. Six important physical signs readily incorporated into a routine physical exam-
ination point toward psychological distress.
a. Dramatic displays of distress or smiling while describing excruciating pain
or disproportionate verbalization or cringing are examples of overreaction to
examination that are associated with the psychological component of the
experience of pain.
b. Tenderness that is superficial (i.e., to light touch) or nonanatomic.
c. Production or accentuation of low back pain on gentle vertical loading over
the patient's skull (doctor's hands resting on patient's head) or passive rota-
tion (pelvis rotated en-bloc with upper body) with the patient standing (no
reason for back to hurt).
d. Complaints of pain during authentic physical examination maneuvers that
the physician modifies to eliminate the possibility of pain. For example,
when the patient is supine and the raised straight leg is lowered to a level
just below the level where pain was produced, plantar flexion of the foot is
carried out.
e. Cogwheel type of giveaway of any muscle group,
f. A stocking or glove type of sensory disturbance in the absence of a meta-
bolic neuropathy.
E. Psychological Testing
I. Some simple questions introduced in the course of history taking can illuminate
most of the important psychological determinants of chronic pain. They open the
psychological door without "psychologizing" the patient. (see Patient Specifics)
a. How have you changed what you do on a daily basis (household chores,
recreation, etc)?
b. Do you think this pain problem is temporary or permanent?
c. What is it about your pain problem that worries you the most?
d. Is there some aspect of your problem that frightens you?

e. Do you believe something has been missed?
f. Do you believe you'll be back to work soon?
g. How would you rate your chances of returning to work?
h. What is it that stops you from being active?
i. How are things at home?
j. Are you functioning sexually?
k. How has your pain problem changed your wife's/husband's/children's life?
1. What was it like in your house when you were growing up?
m. Has your pain problem affected the quality of your relationship with your
spouse (one way or the other)?
n. Has your pain problem caused you to seek legal help?
o. What coping skills would you call on if your present condition were as good
as it gets?
p. The CAGE Inventory. A "yes" answer to any 2 of the 4 questions triggers an
alcohol abuse evaluation:
i, Have you ever felt you should cut down on your drinking?
ii. Have you ever felt annoyed by others criticizing your drinking?
iii. Have you ever felt guilty about your drinking?
iv. Have you ever had a drink on rising in the morning: an eye opener to
treat a hangover or the jitters with "the hair 0' the dog that bit yuh"?
2. A disability index that can be incorporated into the history taking is the
Waddell Index of Disability. Beyond the obvious indication of disability, symp-
toms revealed can identify a distressed perceptual apparatus which together
with cognitive factors underpins inappropriate behavior. Using the Waddell
Index the severity rating can be obtained by assigning one point to each "yes"
answer to obtain a score out of nine; the higher the score the greater the pa-
tient's disability. A score over five is considered significant. The nine parame-
ters described are:
a. Pain with sitting less than 30 minutes.
b. Pain with traveling less than 30 minutes.
c. Pain with standing less than 30 minutes.
d. Pain with walking less than 30 minutes.
e. Pain with heavy lifting.
f. Need for help with foot wear.
g. Sleep disturbance because of pain.
h. Social life restriction because of pain.
i. Sex life restriction because of pain.
3. The most specific and powerful cognitive factor yet identified to explain
work loss due to low back pain is fear avoidance beliefs about work [activ-
ity].Fear theory and avoidance behavior focuses specifically on the patient's
belief about how physical activity and work would or might affect his or her
back pain.
4. Prospective studies have linked job satisfaction to future pain reports.
5. Romano, Turner, and Sullivan have published Indications for Psychological
Evaluation of Chronic Pain Problems. These basic indicators can assist the pri-
mary care physician in detecting patients for whom referral for testing is ap-
propriate when on-site testing is not available.
a. Pain
i. Persists beyond normal expected healing time without clear evidence of
ongoing nociception from physical defect.
ii. Significantly disrupts normal functioning in one or more of the follow-

ing areas:
(a) Ambulation.
(b) Self care.
(c) Home care.
(d) Recreational activities.
(e) Marital or family relationships.
(m Social activities.
b. Patient exhibits sign or symptoms of significant psychological distress; e.g.,
depression or anxiety.
c. Disability greatly exceeds that expected on the basis of physical findings.
d. Patient excessively uses the health care system; patient persists in seeking
tests or treatments which are not indicated on the basis of the physical find-
ings.
e. Excessive or inappropriate use of opioid or sedative hypnotic medications;
use of alcohol or illicit substances for pain control.
6. Primary care physicians treating chronic low back pain patients should be
aware of the prevalence of personality disordered patients within the chronic
pain population.
a. Example: A Dayton Ohio Wright State University School of Medicine
Department of Psychiatry chronic pain study in a family practice setting
finds nearly two thirds of participants are diagnosed borderline personality
disorder (BPD) according to a highly structured interview.
i. Self harm behavior is the behavioral specialty of individuals with BPD.
Repeated "accidents" are prevalent in the chronic pain population.
ii. The combination of mood disorder and impulse disorder commonly seen
in chronic pain patients is particularly suggestive of BPD.
b. Patients with any personality disorder are resistant to treatment and change
slowly.
F. Psychological Tests
1. The objective testing of psychological functioning is accomplished through
psychological testing.
2. A volume of research confirms that attempts to view pain patients within the tra-
ditional mental health framework prove to be neither valid nor clinically useful.
3. With the availability of self-administered, computer scored, and interpreted
psychological testing the initial primary care evaluation of back pain patients
can include objective psychological data.
4. This data will significantly enhance the primary care physician's ability to di-
rect therapy and prevent disability by identifying high risk patients. It will sup-
port the need for comprehensive treatment with objective evidence of psycho-
logical functioning.
5. Because of the biphasic nature of pain (has both physical and psychological
components) physicians must exercise caution in the choice of the psychologi-
cal test instrument to ensure that it is specific for pain and proven effective in
clinical practice.
6. Psychological Instruments Commonly Used
a. Rowland-Morris Disability Questionnaire and the Oswestry Disability
Questionnaire
i. Brief questionnaires to provide an economical office assessment specific
for function in individuals with back pain.
ii. High scores on the Oswestry test or any comparable disability index
and behavior judged inappropriate by the Self Reported Pain Drawing

and the Waddell test indicate that further psychological tests are war-
ranted.
b. Beck Depression Inventory
i. Self administered.
ii. 21 multiple choice check-off questions.
iii. Takes 15 minutes.
iv. May alert the physician to a mood disorder as well as the possibility of
suicide.
c. Short-Form Health Survey (SF-36)
i. Patient rated health status scale.
ii. Evaluates functioning and well-being in chronic disease.
iii. Used to determine the degree of functional impairment and changes in
overall wellness following treatment of patients with pain.
iv. Is indicated in any treatment program that purports to demonstrate evi-
dence of efficacy as perceived by the patient.
v. Can be used to compare general and specific populations differentiating
the health benefits produced by a wide range of different treatments and
in screening individual patients.
d. Symptom Check List 90, Revised (SCL 90-R); a good screening measure for
psychopathology in psychiatric and medical patients; not statistically
normed on patients in pain.
e. Minnesota Multiphasic Personality Inventory (MMPI)
i. Developed in 1943; updated several times.
ii. Thought to be the most frequently utilized psychological test instrument
in the world.
iii. Prior to introduction of newer pain specific tests instruments was the
best test available to psychologists.
iv. Takes a long time to complete;
v. Requires a clinical psychologist to interpret.
vi. Was statistically normed on psychiatric patients not patients in pain.
f. Millon Behavioral Health Inventory (MBHI)
i. A personality inventory designed to assess psychological coping factors
related to the physical health of adult medical patients.
ii. Psychometric norms based on medical rather than psychiatric patients;
not statistically normed on patients in pain.
g. Fear Avoidance Beliefs Questionnaire
i. Measures fear of pain and re-injury and subsequent avoidance of activi-
ties which might cause pain.
ii. Fear of pain and avoidance of activity can playa significant role in
maintaining a painful condition.
h. Battery for Health Improvement (BHI)
i. Has helped to address the shortcoming in psychological testing that looks
at patients as if life began at the time of the illness or injury and that
failed to look at personality development and pre injury/illness psycho-
logical functioning.
ii. Helps gain a comprehensive picture of the patient both pre and post in-
jury/illness.
iii. The only psychological test that is statistically normed on physical reha-
bilitation patients as well as a large community sample.
i. West Haven Yale Multidimensional Pain Inventory
i. Identifies patients as adaptive copers, interpersonally distressed or dys-

functional.
ii. Statistically normed on chronic pain patients.
j. Pain Patient Profile (P-3)
i. Easily administered by secretary or office nurse.
ii. Takes 15 minutes of patients time.
iii. Immediately interpreted by computer software with clinical summary
available to physician within minutes.
iv. Identifies patients who are experiencing emotional distress; assesses how
an individual's psychological functioning may be influencing his or her
pain symptoms and measures the degree or intensity of psychological
distress.
v. Included in the computer generated test interpretation is:
a. A bar graph that shows the intensity of Depression, Anxiety, and
Somatization.
b. A validity index is included that assesses the magnification of symp-
toms, inadequate reading comprehension and random responding.
vi. Is statistically norrned on national samples of patients in pain as well as
the general population.
III. Patient Specifics

A. Maladaptive Patient Beliefs that Interfere with Success in Treatment
1. Regarding physicians and health care.
a. Something has been missed regarding the diagnosis.
b. A doctor somewhere can be found who will remove the pain.
c. The pain would be completely cured if some doctor found the time and took
the interest to find the real problem.
d. Has never been thoroughly examined for the cause of the pain.
e. Surgery is the only answer left to overcome the pain.
2. Regarding medication.
a. Pain medications will probably always be required.
b. The most relief from pain is obtained by the use of medications.
3. Regarding the system.
a. Feels cheated or victimized.
b. Feels he or she deserves a pension.
4. Regarding being active
a. Exercise could make the cause of the pain much worse.
b. Permanent damage could result from being too active.
5. Regarding work.
a. If the pain continues at the current level, work will be impossible.
b. A person can't work while in pain.
c. Return-to-work requires complete removal of the pain.
d. Return-to-work will result in re-injury.
e. Return-to-work will result in being fired.
f. His or her work is too heavy/repetitive/stressful etc.
g. Working ever again is impossible.
6. Miscellaneous beliefs
a. Family should provide preferential treatment and be solicitous when he or
she is in pain.
b. Pain is frightening.
c. People don't believe he or she has pain.
d. The amount of pain patient feels is completely out of his or her control.
B. Shortcut to Recognizing Problem Patients
1. Your "gut reaction" to patient.
2. Patient not proficient in English
a. Difficulty following
i. Instructions for activity.
ii. Reasoning about medication use.
b. Cultural attitudes may cause "inexplicable" non compliance.
3. A gait that caricatures a painful limp.
4. Time off work:
i. Off work 6 months-500f0 chance of return to work (RTW) in lifetime.
ii. Off work 1 year-lOOfo chance of RTW.
iii. Off work 2 or more years-virtually no chance of RTW.
5. Job dissatisfaction.
6. Patient perceives work as "too heavy" (see Patient Specifics Regarding Work).
7. Disabled spouse.
8. Workers injured for the first time and those who have had more severe prob-
lems in the past are at greater risk for disability than those who have survived
previous episodes of pain with relatively little trouble.
9. Deactivated and withdrawn life style.
10. Notable verbal behavior:
i. Emotional (affective) and evaluative words for pain; e.g., frightful, depress-
ing, sickening, unbelievable, horrendous, soul-destroying, punishing, ex-
cruciating, crippling.
ii. Patient adds a catalog of all his or her problems to the answer to each
question.
iii. Sighing and moaning.
iv. Fault finding/angry patient.
v. End-of-appointment request for opioid medication.
11. Misuse or abuse of alcohol, medications or recreational drugs.
C. Managing Difficult Patients
1. Having recognized the problem, call for help: refer for evaluation and manage-
ment to a comprehensive multidisciplinary team (usually a pain management
facility).
2. Advantages of pain clinic
a. Patient can be monitored 8-24 hours/day for:
i. Malingering.
ii. Detoxification.
b. Ideal for noncompliant patient.
c. Allows partial control over negative family reinforcement of pain behavior.
d. Allows collection of data needed for claim closure.
e. Removes patient from primary care physician's practice; as a result:
i. Time and emotional energy savings occurs when "high maintainance"
patient displaced from the practice.
ii. Stress of being the "bad guy" responsible for claim closure is avoided.
iii. Risk of lawsuit is minimized by not engaging high-risk patient.
3. When referral is not available the following actions can be very helpful:
a. Explain the difference between acute and chronic pain to patient.
b. Reassure patient that you know the pain isn't "all in his or her head."
c. Treat on the basis of the paradigm that everything that is appropriate for acute
pain is probably inappropriate for the patient experiencing chronic pain.
d. Explain test results and describe what you believe is contributing to the
pain.
e. Place improved function ahead of symptom resolution as a therapeutic goal.
f. Use time contingent schedules for medication and mobilization. Pain contin-
gent schedules label pain as dangerous as well as aversive.
g. Recognize that your relationship with the patient is a powerful therapeutic
tool.
h. Reassure yourself that it is the patient, not you, who has the problem. You
can show him or her the tools but he or she must ultimately take responsi-
bility for doing what is necessary to get better.
i. If opioid medication (including acetaminophen with codeine and also the
non opioid carisoprodol) is being used have patient sign an opioid contract
and provide a clear description of what you accept and do not accept in re-
gard to behaviors related to opioids.
j. If you are initiating the use of opioid medication, be clear with the patient
and in your notes that this is a trial that has functional improvement as its
goal. It is a bridge that for chronic noncancer pain is almost never a safe
long term strategy.
k. Talk to claims managers to help facilitate moving treatment toward rehabili-
tation, IME or claim closure.
4. Don't
a. Fall into the either/or trap of pain being either somatogenic or psychogenic.
b. Continue opioids beyond the healing phase after injury just because pain
persists.
c. Give up on the patient. A commitment to care can prevent doctor shopping
and iatrogenic injury.
d. Use PRN schedules for medication or activity. PRN schedules are a prescrip-
tion for chronic pain and disability.
References
1. Berne E: Games People Play. New York, Grove Press, 1964.
2. Bigos SJ, Crites Battle M: Acute care to prevent back disability. Clin Orthop 221:121-130,1987.
3. Bigos SJ, Spengler OM, Martin NA, et al: Back injuries in industry: A retrospective study. II: Injury
factors. Spine 11:246-251, 1986.
4. Bigos SJ, Spengler OM, Martin NA, er al: Back injuries in industry: A retrospective study. III:
Employee-related factors. Spine 11:252-256, 1986.
5. Cassel EJ: The Nature of Suffering and the Goals of Medicine. New York, Oxford Press, 1991.
6. Cats-Baril W, Frymoyer JW: Identifying patients at risk of becoming disabled due to low back pain:
The Vermont Rehabilitation Engineering Center predictive model. Presented at the Eastern Orthopedic
Association for Spinal Research, Boston, MA, October, 1988.
7. Frank J: Persuasion and Healing. New York, Random House Inc, 1963.
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9. Frymoyer JW, Cats-Baril W: Predictors of low back pain disability. Clin Orthop and Related Rsch
221 :90-97, 1987.
10. Frymoyer JW: Predicting disability from low back pain. Clin Orthop and Related Rsch 279:101-9,1992.
11. Gatchel RJ et al: Predicting outcome of chronic back pain using clinical predictors of psychopathol-
ogy: a prospective analysis. Health Psycho I 14:5, 1995.
12. Hadjipavlou A: Low back pain: disability and psychological assessment. Cdn J of CME, Jun/Jul 1991.
13. Hazard RG et al: Early predictors of chronic disability after occupational low back injury. Spine 21: 8,
1995.
14. Hudziac JJ: Clinical study of the relation of borderline personality disorder to Briquet's Syndrome
(Hysteria), Somatization disorder, antisocial personality disorder, and substance abuse disorders. Am J
Psychiatry 153: 1598-1606, 1996.
15. IASP Task Force on Pain in the Workplace. Fordyce WE (I'd): Back pain in the workplace. Seattle,
lASP Press, 1995.
16. Kirkady-Willis WH: Managing low back pain. New York, Churchill Livingston, 1983.
17. Ormel J et al: Common mental disorders and disability across cultures. JAMA 272: 22, 1994..
18. Roland M, Morris R: A study of the natural history of back pain. Part I: Development of a reliable and
sensitive measure of disability in low-back pain. Spine 8:141-144, 1983.
19. Romano JM et al: Presented at 14th Annual Pain and Suffering Symposium. The Foundation of
Medical Excellence, Vancouver Be, May 2001.
20. Sansone RA: Borderline personality disorder: the enigma. Primary Care Reports. 6(26): 219-226, 2000.
21. Schofferman J: Low back and neck pain: Psychological predictors of chronicity. J Musculoskel Med
December 2000.
22. Shelton JL: The Low Back Pain Handbook: A practical guide for the Primary Care Physician. Phila-
delphia, Hanley Et Belfus, 1997.
23. Sternbach RA: Pain Patients: traits and treatment. New York, Academic Press, 1974.
24. Tollison CD:Pain and behavioral medicine; psychological testing Part II. Newsletter of The Nat. Forum
of Indep. Pain Clinicians Winter, 2002.
25. Turk DC: Evaluation of pain and dysfunction. J Disability 2: 1-20, 1991.
26. VonKorff M, Ormel J, Keefe FJ, Dworkin SF: Grading the severity of chronic pain. Pain 50:133-149,
1992.
27. Waddell G, et al: Normality and reliability in the clinical assessment of low back pain. Br Med J 384:
1, 1982.
28. Waddell G, et al: Assessment of severity of low back pain disorders. Spine 9: 204-208, 1984.
29. Waddell G, et al: Chronic low back pain, psychological distress and illness behavior. Spine 9: 209-213,
1984.
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1992.
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work and item selection. Med Care 30:473-483, 1992.
1 - - - - - - - -18
Surgical Options for Lumbar Spine Pain
Thomas 1. Puschak, M.D., Paul A. Anderson, M.D.,
John H. Peloza, M.D., and Andrew J. Cole, M.D.
Key Points
• Only 1-3% of patients with degenerative conditions of the lumbar spine require
lumbar spine surgery.
• Approximately 97% of painful lumbar spine conditions resolve satisfactorily with
aggressive conservative care.
• Absolute indications for lumbar spine surgery include progressive neurologic deficit
and cauda equina syndrome.
• Relative indications for lumbar spine surgery include pain refractory to aggressive
conservative care that results in significant functional loss.
• Surgery is not a cure.
• The best surgical outcome occurs when surgery is combined with superb rehabilitation.
• Successful surgical outcome depends in great part on selecting patients who have an
appropriate surgical lesion that has been precisely diagnosed; normal or near normal
psychologic profile; realistic outcome expectations; and a plan for return to a
functional lifestyle.
• The vast majority of lumbar spine surgery is performed because of failure of
conservative care. However, if the quality of conservative care is poor or the
rehabilitation program is not customized for each patient's unique spinal condition,
the number of patients who fail conservative care and then receive surgery increases.
I. Terminology
A. Laminectomy Surgical procedure to remove the lamina portion of the vertebra (Fig. J)
B. Hemilaminectomy Procedure to remove one-half of the lamina to one side of the
midline
C. Discectomy Procedure to remove a portion (usually only the herniated part) of a
disc (Fig. 2)
D. Facetectomy Procedure to remove some part or all of the facet joint
E. Foraminotomy Enlargement of the intervertebral foramen by removing bone
and/or soft tissue
F. Laser discectomy Use of light energy to dissect tissue; theoretically, causes less tis-
sue destruction
G. Laparoscopy Technique using fiberoptic instruments for spinal surgery that allows
a closed abdominal surgical approach, thus avoiding the need for laparotomy
H. Endoscopy Technique using fiberoptic instruments for spinal surgery that allows a
closed percutaneous posterior and retroperitoneal approach to the lumbar spine,
thus avoiding the need for open spinal surgery
I. Fusion Surgical procedure to render a whole spinal segment immobile by bridging
the segment with bone (Fig 3)
309
310 Surgical Options for Lumbar SpinePain
FIGURE 1. laminectomy. (From Reulan H-J: Neurosurgical operations. In BauerK, Kerschbaumer F, Poisel S
(ads): A~as of SpinalOperations. New York, Thieme, 1993, p 344, with permission.)
FIGURE 2. Discectomy. (From Bauer R, Kerschbaumer F, Poisel S: Approaches. In BauerK, Kerschbaumer F,

Poisel S (ads): A~as of Spinal Operations. New York, Thieme, 1993, p 72, with permission.)
Surgical Options for Lumbar Spine Pain 311
0
FIGURE 3. 360 anteriorand posterior interbody fusion with instrumentation. A, Lateral view. B, Anterior view.
J. Instrumentation Orthopedic metallic implants that stabilize the motion segment

(Fig 3); examples include
a. Bone screws c. Plates e. Wires
b. Rods d. Hooks f. Interbody cages
II. Surgical Indications

A. Absolute
1. Cauda equina syndrome
a. Surgical emergency-outcome may be affected by delay in performing
surgery.
b. Variable neurologic loss of motor and/or sensory function
i. Symptoms or signs of urinary retention may be the first patient com-
plaint.
ii. May include loss of bowel and/or bladder control
2. Progressive loss of motor function-static loss of motor control is relative surgi-
cal indication; significant percentage of patients respond to aggressive conserv-
ative care.
B. Relative
1. Static motor loss-consider surgical intervention if motor function does not im-
prove with aggressive conservative care, whether or not the motor loss is asso-
ciated with pain.
2. Intractable pain that causes debilitating functional loss-consider surgical inter-
vention if aggressive conservative care fails.
C. Other situations in which to consider surgical intervention
1. Neoplasm
2. Infection
312 Surgical Options lor Lumbar Spine Pain
3. Congenital condition
4. Deformity
a. Idiopathic d. Congenital
b. Iatrogenic e. Degenerative
c. Posttraumatic
III. Patient Selection

A. Absolute surgical situations Except for highly unusual circumstances, all patients
with absolute surgical indications undergo an appropriate surgical procedure.
B. Relative surgical situations Various factors affect surgical outcome and therefore pa-
tient selection for surgery.
1. Physician factors
a. Precise diagnosis-history, physical examination, imaging studies, ancillary
testing (electrodtagnostic studies, fluoroscopically guided, contrast-enhanced
injection procedures) are consistent.
b. Technical competence of the surgeon
c. Quality of aggressive pre- and postoperative conservative care
2. Patient factors
a. Physical parameters that may decrease surgical suitability
i. Limitations in strength
ii. Poor flexibility
iii. Poor aerobic condition
iv. Poor awareness of body mechanics
b. Psychological factors
i. Psychological predisposition toward chronic pain
ii. Childhood developmental risk factors (presence of 3 or more portends a
poor surgical outcome)
(a) Physical abuse (d) Neglect
(b) Sexual abuse (e) Chemically dependent parents
(c) Abandonment
iii. Depression
iv. Substance abuse
v. Secondary gain
(a) Legal
(b) Financial
(c) Social
IV. Surgical Options

A. Surgical treatment is based on patient's symptoms, neurologic findings, and imag-
ing studies.
B. Several broad groups of surgical conditions exist:
I. HNP
2. Stenosis
3. Instability
4. Chronic LBP
5. Deformity
C. HNP
I. Indications
a. Failure of conservative modalities
i. Medication-NSAIDS, narcotics, oral steroid
ii. Physical therapy
Surgical Options lor Lumbar Spine Pain 313
iii. Injection-ESI vs. selective block

iv. Time
2. Timing
b. Emergent-immediate
i. Cauda equina syndrome
ii. Delay beyond 24 to 48 hours worsens outcome
iii. Varied motor/sensory loss
iv. Bowel/bladder loss
b. Urgent-2 to 14 days
i. Progression of motor loss
ii. Uncontrollable pain
c. Elective-patient's choice
i. Intractable pain-failed conservative care
ii. Functional loss due to pain
iii. Static motor loss
3. Surgical options
e. Lumbar discectomy-GOLD STANDARD
i. Open
[a] Laminotomy and wide exposure
(bl Aggressive discectomy
ii. Microdiscectomy
[a] Smaller incision
(bl Limited muscular dissection
(cl Only herniated fragment removed
(d] Can be outpatient procedure
iii. Open vs. microdiscectomy
(al Several studies show no significant difference except that microdis-
cectomy decreases hospital time and may allow earlier return to
work.
iv. Complications
[a] Reoccurrence 5-10010
(bl Dural Tear 1-3010
(c) Infection 1-2010
v. Results
[a] 90-95010 excellent and good
(b) 5-10010 Reoperation Rate
vi. Conclusion-both are effective techniques with comparable results. In
cases of cauda equina syndrome with a large HNP, open discectomy
should be considered to minimize surgical traction of already compro-
mised nerve roots.
b. Endoscopic discectomy
i. Percutaneous via cannula
(a) >90010 good outcomes-experienced surgeons
Ib] Steep learning curve-has limited this technique's acceptance
c. Chemonucleolysis (chymopapainl-controversial
i. Proteolytic enzyme-hydrolyzes peptide bonds of proteoglycans in the
nucleus
ii. Intradiscal pressure decreased-glycosaminogIycans bind less water
iii. Complications-rare but catastrophic
[a] Transverse myelitis-.004%
(b) CNS hemorrhage .026010
314 Surgical Options for Lumbar Spine Pain
[c) Capillary rupture after accidental intrathecal injection

[d] Anaphylaxis-IOfo. Higher in blacks and women
(el Screening-RAST
iv. Results-70 to 800f0 good
v. Conclusion-effective technique in selected patients; however, risks have
limited its use in the US in the past 10 years
d. Automated Percutaneous Lumbar Discectomy (APLDl
i. Nucleus removed through cannulated system
ii. Intradiscal pressure reduced
[a] Herniated fragment not removed
iii. Complications-rare
iv. Results-poor
(a) ChatteIjee-710f0 satisfactory results
v. Conclusion-although safe, low success rate
e. Ablative procedures-heat ablation of nucleus
i. Laser discectomy-percutaneous fiberoptic
ii. Radiofrequency probe
iii. Results-NO literature support
D. Lumbar Stenosis
I. Indications-similar to HNP
a. Failure of conservative modalities
i. Medication-NSAIDs, narcotics, Neurontin
ii. Physical therapy
iii. Injection-ESI vs. selective block
iv. Bracing-not proven
v. Time
2. Timing
a. Emergent-immediate
i. Cauda equina syndrome-can occur with
(a) acute HNP in face of pre-existing
(bl stenosis
b. Urgent-days to weeks
i. Progression of motor loss
ii. Uncontrollable pain
c. Elective-patient's choice
i. Intractable pain-failed conservative care
ii. Functional loss-due to pain, motor/sensory loss
iii. Static motor loss
3. Preoperative Clearance
a. Medical evaluation of comorbidities
i. Cardiac-stress test, catheterization if needed
ii. Pulmonary-PFTs
iii. Diabetes-evaluation by primary MD
b. Nutritional evaluation
c. Encourage smoking cessation
d. Weight loss "pep talk"
4. Surgical options
a. Selection of levells)
i. Based on preoperative imaging and symptom pattern
[a] CT myelogram
(bl MRI
ii. All regions of stenosis should be addressed

(a) Central
(b) Lateral recess
(c) Foramen/extraforaminal (osteophyte)
iii. Multiple levels-effort should be made to decompress all stenotic levels
unless contraindicated
b. Traditional laminectomy
i. Removal of spinous processes
ii. Removal of lamina-take care to spare pars
(a) Addresses central stenosis
iii. Partial facetectomy-<500f0
(a) Addresses lateral recess stenosis
iv. Foramenotomy
(a) Addresses foramenal stenosis due to superior articular process
v. Advantages
(a) Good visualization
(b) Wide neuro decompression
vi. Disadvantages
(a) May lead to instability
(b) Pars-broken or too thin
(c) Facet->500f0 removed
(d) Disk-if discectomy required weakened anterior column
(e) May increase progression of scoliosis
c. Limited laminectomy/laminotomy (fenestration)
i. Spinous process/interspinous ligament-preserved
ii. Lamina-partial excision
iii. Ligamentum flavum-excised
iv. Partial facetectomy-through laminotomy window
v. Advantages
(a) Preserves stability
(b) Reduces risk of slip
(c) Reduces risk of scoliosis progression
vi. Disadvantages
(a) More technically demanding
(b) Less visualization-especially in lateral recess and foramen
(c) May lead to incomplete decompression
d. Lumbar laminoplasty-limited information
e. Lumbar fusion
i. Indication in stenosis
(a) Degenerative spondylolisthesis (see below)
(b) Iatrogenic injury to pars
(c) Isolateral scoliosis
ii. Advantages
(a) Allows more aggressive decompression
(b) Correct deformity
iii. Disadvantages
(a) Surgical morbidity
(b) Adjacent segment changes
f. Postoperative management
i. Thigh high TEDS/SCDS
ii. Suction drain-surgeon choice
316 SurgicCll Options for Lumbar Spine Pain
iii. No bracing
iv. Out of bed postop day # 1
v. Walking exercise postop day # 1
vi. Aerobic conditioning/PT in 6 to 12 weeks
g. Results of decompression
i. 75 to 95010 improvement
ii. Results diminish for 10 years by 10 to 20010
(a) Progression of degeneration
(b) Comorbidities
(e) Joint arthritis
(d) Bone regrowth
(e) Instability
h. Complications
i. Linked to age and comorbidities
ii. Medical risks
(a) Cardiac-HTN, CAD, MI
(b) Pulmonary-pneumonia, embolism
(c) Infection 2010
(d) Dural tear 4010 (more likely in revision surgery)
(e) Instability 10010
(f Bony regrowth-40% without fusion
i. Conclusions
i. Traditional laminectomy
(a) Congenital stenosis
(b) Stiff/immobile spine-narrow disk spaces
(c) Surgeon's preference
ii. Laminotomy-fenestration
(a) Unilateral symptoms
(b) Stenosis confined to facet-disk level
(e) Associated instability-role not defined
E. Lumbar stenosis with degenerative spondylolisthesis
1. Indications/timing/medical evaluation-same as for stenosis
2. Decompression vs. decompression and fusion
a. Decompression alone-no prospective studies
i. Limited laminotomy-role unclear
(a) Unilateral radiculopathy "stiff spine"
b. Decompression and arthrodesis-strong literature support
i. Arthrodesis addresses the instability
ii. Decompression addresses the stenosis
c. Instrumentation-improves fusion rates but does not significantly affect out-
come in short term
d. Solid fusion-provides best long term outcome
3. Decompressive procedures-covered in lumbar stenosis section
a. Traditional laminectomy
b. Limited laminotomy-fenestration
4. Posterolateral fusion-GOLD STANDARD (Fig. 4)
a. Indications
i. Preoperative structural integrity
(a) Degenerative spondylolisthesis
(b) Scoliosis and/or kyphosis
(c) Recurrent stenosis above previous fusion
Surgical Optian51or Lumbar SpinePain 317
FIGURE 4. Degenerative spondrlolistheSiS. A, Flexion-extension x-rays demonstrate anterior translation at

L4-5. B, Sagittal {left} and axia (rigM MRI illustrate stenosis as well as spondylolisthesis. C, PostopAPand
lateral x-royafter laminectomy and fusion L4-5.
(d) Revision decompression-excessive bony resection

(e) Multiply recurrent HNP-relative
ii. Intraoperative structural alterations
(a) Aggressive facetectomy->500l0 both facets
(b) Radical disk excision
(c) Removal of pars
b. Instrumentation
i. Goals of hardware
(a) Correct deformity
(b) Stabilize spine
(c) Improve fusion rate
(d) Reduce rehab time
(e) Reduce need for external immobilization
ii. Types of instrumentation
(a) Nonsegmental-rarely used (Harrington)
(i) Longer fusion needed
[ii] Distraction-"t1at back"
(iii) Sacral fixation-poor
(b) Segmental-pedicle screws
(i) Torsional stability
(ii) Improved sacral fixation
(iii) Shorter fusion lengths
[iv] Maintains lordosis
(v) Increases fusion rates
(vi) Intact posterior elements not required
(vii) Pedicle-strongest part of osteopenic vertebrae
c. Postoperative management
i. Thigh high TEDS/SCDS
ii. Suction drain-surgeon choice
iii. Bracing-only multisegment fusion with significant osteopenia
iv. Out of bed postop day # 1
v. Walking exercise postop day # 1
vi. Walking 15-30 minutes bid 1 week postop
vii. Stationary bike/swim exercise-4-6 weeks postop
viii. Aerobic conditioning/PT in 6 to 12 weeks
d. Results
i. Short term (2 years)
(a) Decompression-75 to 900/0 good/excellent
(b) Decompression and fusion-75 to 900/0 good/excellent
(c) Decompression and instrumented fusion
(i) 75-80010 good/excellent
ii. Long term (successes drop 15 to 20010 over time)
(a) Recurrent stenosis
(b) Same level-bony overgrowth
(e) New level-progression of degenerative cascade
(d) Inadequate index decompression
(e) Pseudarthrosis
(f) Hardware failure
iii. Outcomes best if:
(a) Spinal canal/roots adequately decompressed
(b) Surgery done for radiculopathy or neuro-claudication rather than
LBP
(c) Less than 3 comorbidities

e. Complications
i. Medical (less than 5010)
(a) Cardiac
(b) Pulmonary embolus-D. 1010
(c) Pneumonta-i too
(d) Confusion
(e) Mortality 0.6010
ii. Intraoperative (Jess than 10010)
(a) Inadequate decompression
(b) Wrong level
(c) Inadequate operation
(d) Dural tear
iii. Postoperative (less than 1DOlo)
(a) Infection
(b) Instability
(c) Fusion failure-lO to 300AJ
(d) Implant failure
(e) Neurologic deficit
(I') Epidural hematoma
5. Posterior lumbar interbody fusion (PLIF)
a. Indications (Fig. 5)
i. Anterior column weight bearing deficiency
ii. Failed posterolateral fusion
iii. Deformity
(a) Coronal-asymmetric disk collapse
(il Unilateral PLIF
(b) Sagittal-kyphosis correction
iv. Severe foraminal stenosis
(a) Allows facet disarticulation
(b) Radical excision of foraminal disk
(c) Extraforaminal osteophyte excision
v. Gross instability-isthmic spondylolisthesis
(a) 5 to 15 mm translation
vi. Multiply recurrent HNP-relative
b. Advantages
i. Increases fusion surface area
ii. Favorable biomechanics-graft under compression
(a) Restore anterior column weight bearing
iii. Excellent decompression
(a] Aggressive facet/disk excision
[b] Foraminal distraction
iv. Deformity correction-coronal and sagittal
c. Disadvantages
i. Technically difficult-compared with posterolateral
[a] Blood loss
[b] Nerve retraction
ii. Epidural fibrosis
d. Interbody devices
i. Allograft-fresh frozen tibia shaft
[a) Surgeon contours-avoid making graft too small
(i) Fracture
320 Surgical Options frK Lumbar Spine Pain
FIGURE S. Isthmic spondylolisthesis. A, Preoperotive loteralx-roy shows anterior translation L5-1 and pars
defectat L5. B, Preopsagittal MRI shows severeforaminal stenosis of exiting L5 nerveroot. C, Postop APand
lateralx-royafter decompression and L5-1 fusion. A PLiF IBrantigan cagel was performed and augmented
with a posterolateral instrumented fusion. The edges of the radiolucent Brantigan cage are marked with
Radiopaque dots seen in the L5-1 diskspace.
(ii) Subsidence
(iii) Graft migration
(b) Advantage-inexpensive
(c) Disadvantage-fiddle factor
ii. Manufactured
(a) Allograft
(b) Carbon fiber
(c) Metallic-cylindrical. box
(d) Advantages-instrumentation
[e] Disadvantages
(i) Expensive
(ii) Dependent on stock availability
e. Most techniques require adjunctive pedicle screw instrumentation
f. Complications
i. Neurapraxia-1.5 to 4Gb
ii. Durallaceration-I.50/0
iii. Graft migration-D.3 to 2.40/0
iv. Epidural fibrosis
v. Epidural bleeding
g. Conclusion-PLIF allows improved biomechanical stability of posterior
constructs by addressing all three columns of the spine. It can allow for
aggressive decompression of foraminal stenosis not achievable with
standard posterior decompression techniques as well as correct coronal
and sagittal deformity. We recommend this technique as an adjunct to
posterolateral fusion and decompression rather than a "stand alone"
technique.
F. Degenerative scoliosis with stenosis
I. Etiology-asymmetric degenerative disc collapse
2. Symptoms
a. Back pain-arthritis, muscle fatigue from imbalance
a. Leg pain
i. Stenosis
ii. Radiculopathy-nerve impingement in concavity
(a) Lateral listhesis
3. Natural history
a. 1O-2D percent of patients progressive--f to 6 degrees/year (average 3
degrees/yrl
4. Evaluation
a. Plain films
i. AP/lateral standing-coronal/sagittal balance
ii. Side bending films-flexibility of curve
iii. CT myelogram-best for stenosis evaluation
iv. MRI-poor study due to obliquity of cross section
b. Clinical-visual assessment of sagittal/coronal balance
i. Monitor height serially
ii. Bone density often osteoporotic
5. Treatment
a. Nonoperative
i. Similar to other degenerative disorders
ii. Most patients do not require surgery
iii. Temporary bracing with Boston overlap or TLSO
b. Operative
i. Indications
(a] Progressive pain
[b] Progressive deformity
[c] Sagittal and/or coronal imbalance
ii. Goals
[a) Pain reduction
(bl Prevent progression
(e) Restore balance-coronal/sagittal
iii. Surgical options

(a) Decompression
(b) Decompression and fusion
(c) Try to include entire curve
(d) Anterior/posterior fusion
c. Decompression alone
i. Stenosis with a "stiff' well balanced curve
d. Posterior decompression with instrumented fusion
i. Stenosis with flexible or progressive curve
(a) Corrects with good coronal and sagittal balance
e. Anterior-posterior fusion
i. Rigid scoliosis with sagittal and/or coronal imbalance
f. Complications-VERY HIGH
i. Pseudarthrosis-5 to 20010
ii. Residual pain-5 to 15010
iii. Thromboembolism-1 to 20010
iv. Neural injury-1 to SOlo
v. Mortality-1 to 5010
vi. Infection-SOlo
g. Postoperative management
i. Early mobilization
ii. TEDS/SCDS
iii. Bracing-osteopenia or hardware failure risk
iv. Rehab services-OT/PT/physiatry
G. Chronic discogenic low back pain
1. Vast majority of patients respond well to aggressive conservative care. Surgery
should be a last option after exhausting conservative measures. Chronic LBP is
often associated with significant psychosocial issues that can prevent successful
surgical outcomes.
2. Indications
a. Intractable back pain-failed aggressive conservative care >6 months
b. Accurate diagnosis of pain generator-very difficult
i. CT myelogram-usually negative
ii. MRI-"black disk"-decreased hydration
(a) Annular tear-HIZ lesion
(b) Questionable prognostic value
iii. No neurologic compromise
iv. Discography-controversial
(a) Dye extravasation
(b) Concordant pain on pressurization
(c) Negative control levels
(d) False positives in somatosizers
v. No more than two painful disks
vi. Normal psychiatric evaluation
vii. Beware of secondary gain
3. Anterior lumbar interbody fusion (AUF) (Fig 6)
a. Indications
i. Anterior column discogenic pain
ii. Anterior column structural incompetence
iii. Instability or collapse on x-ray
iv. Painful disk anterior to posterior fusion
v. Intact posterior elements
FIGURE 6. Anterior lumbar interbody fu-

sion (AUF). A, Postop AP x-ray. B, Postop
lateral x-ray.
324 Surgica/Oplians for Lumbar Spine Pain
b. Principles
i. Restore native disk height
ii. Re-tension annulus
iii. Graft under compression
iv. Graft or cages-maintain stability
c. Interbody options
i. Disk spacers-allograft rings, Harms cage, Pyramesh
ii. Threaded cages-Ray, BAK, LT
iii. Cages and spacers both unstable in extension
d. Complications
i. Vascular/visceral injury 1-2010
ii. Neurologic injury 3%
iii. Traction radiculopathy 0%
iv. Pseudarthrosis 5-10010
v. Infection < 10010
vi. Graft migration or collapse SOlo
vii. Sympathetic injury 2-5010
(a) Retrograde ejaculation
viii. Graft donor site pain 100/0
ix. Malposition of graft 3-5010
e. Conclusion-AUF allows removal of the painful disc and tensioning of the
annulus. Threaded cages have increased immediate postoperative stability as
long as the posterior elements are intact. Recently, the use of AUF cages as
a stand alone device has lost some favor due to cage subsidence and
pseudarthrosis. With the advent of biologic implants such as BMP, the indi-
cation for stand alone AUF may expand.
4. Posterolateral fusion
a. Indications-same as above
b. Techniques/results/outcomes-discussed above
c. Advantages
i. Common technique with established learning curve
ii. No risk to viscera or great vessels
iii. No risk of epineural fibrosis-as in PUF
iv. May transmit less stress to adjacent segment than AP fusion
d. Disadvantages
i. Not operating on pain generator (annulus)
ii. Paraspinal muscle fibrosis/denervation
iii. Lower fusion rate than AP fusion
iv. Residual motion through disc complex
(a) Even under solid fusion
v. Longer operative time
e. Conclusion-may have a role in treatment of discogenic pain; however, the
limitations of not directly operating on the pain generator (disc), residual
disc motion, and fusion rates should be considered.
5. Posterolateral fusion with PUF
a. Advantages
i. Distraction across disc space
ii. Anterior column support
iii. Graft under compression
iv. Improved fusion rate than posterolateral alone
b. Disadvantages
i. Longer operative time
ii. Increased blood loss
iii. Nerve root traction-potential for neurapraxia
c. Conclusion-addition of PLIF to posterolateral fusion addresses the collapse
and instability of the degenerative disc, however, the increased operative
time, blood loss, and muscle stripping must be considered when planning
this approach.
6. Anterior-posterior (AP) fusion
a. Indications
i. Degenerative disc disease-very controversial
ii, Rigid deformity-kyphosis or scoliosis
iii. "Flat back" syndrome
iv. Pseudarthrosis
v. Epidural scarring-unable to perform PLIF
b. Advantages
i. High fusion rate
ii, Correction of sagittal deformity
c. Disadvantages
i. Prolonged OR time
ii. Increased blood loss
iii. Longer hospitalization
iv. Ileus
v. Infection
vi. Expensive
b. Conclusion-a very technically and medically demanding procedure. Very ef-
fective in obtaining a solid fusion with good alignment. Surgeons should
have strict indications for determining when AP fusion is necessary due to
its significant risks and costs.
H. Bone Grafting
1. Fusion biology
b. Osteogenesis-bony producing cells
b. Osteoinduction-stimulates bone growth
c. Osteoconduction-scaffolding
2. Autograft-GOLD STANDARD
a. Structural or cancellous
b. Provides all three aspects noted above
c. Best fusion rates
3. Disadvantages
a. Donor site morbidity
i. Pain
ii. Infection
iii. Hematoma
iv. Structural defect (anterior iliac)
v. Meralgia paresthetica
vi. Cluneal neuroma
vii. Superior gluteal artery injury
b. Increased operative time
c. Increased blood loss
I. Bone graft extenders
1. Allograft
a. Osteoconduction-excellent
b. Osteoinduction-poor
c. Osteogenesis-none
326 Surgical Options forLumbar Spine Pain
d. Disease transmission
(a) HN transmission x 2 since 1980
e. Structural allograft
i. Fibula, humerus, femur, tibia
ii. Manufactured-machined dowels, cages
iii. Advantages
(a) Structural strut support
(b) Medullary space-pack autograft
iv. Disadvantage
(a) Processing
(b) Fatigue failure
(c) Size/contour
v. Incorporation
(a) Creeping substitution
(b) Slow-especially cortical bone
(c) Initial loss of strength
(d) Need instrumentation?
f. Crushed cancellous allograft
i. Croutons or chips
ii. Expands volume of autogenous graft
2. Demineralized bone matrix (DBM)
a. Preparation
i. Demineralization-acid treatment
ii, Fat removal-solvents
iii. Lyophilization
iv. End product
(a) Non-collagenous proteins
(b) Type I collagen
(e) <0.01010 osteoinductive growth factors (BMP, TGFB)
b. In vivo actions
i. Enchondral new bone formation
ii. Osteoconduction-primary effect
iii. Osteoinduction-weak
c. Available products
i. Grafton-gel, putty, flex sheets, matrix
ii. Osteofll-shydrogel carrier
iii. Dynagraft-sgel, matrix putty
iv. Allomatrix-putty
d. Important considerations
i. Carriers-i.e., glycerol
(a) Renal failure in rats
ii. Product preparation
iii. Significant product variability
e. Results
i. Animal data suggest efficacy
ii. Little human evidence for efficacy
3. Platelet derived growth factors (PDGF)
a. Theory
i. Platelets contain PDGF, TGFB, IGF, VEGF
ii. Fibrin clot-scaffold
iii. Require concentration from whole blood
Surgical Option51or Lumbar Spine Pain 327
iv. Animal models-effective extender
v. Humans-no published data
b. Important considerations
i. "Workability" of products
ii. Cost
iii. Preoperative blood draw
iv. No BMPs
c. No human studies in spinal fusion
4. Ceramics
a. Mechanism of incorporation
i. Osteoconductive
ii. Porosity
iii. Resorption over time
iv, Replacement with new bone
b. Available products
i. Pro Osteon-coral/hydroxyapatite
ii. Osteoset-calcium sulfate
iii. Vitoss
iv. Collagraft-HA/Ca3(P04)2/collagen
c. Important considerations
i. Structural integrity
(a) Decreases quickly with resorption
(b) Supplemental fixation
ii. Within cages
(a) Osteoinductive material and cells still needed
(b) Bone marrow aspirate-supplement to ceramics? Studies pending
d. Results-Efficacy demonstrated in scoliosis and posterior lateral fusion
5. Summary-elements of spinal fusion require bone producing cells (osteogenesis)
stimulated to produce bone (osteoinduction) in a structured scaffolding (osteocon-
duction). Autogenous graft is still the gold standard, as it includes all three essential
functions. The current role of graft expanders should be to help increase the vol-
ume of graft material and hopefully enhance osteoconduction and osteoinduction.
J. Osteoinductive growth factors
1. Discovery-Marshall Urist (1965)
a. Osteoinductive proteins-human bone extract
b. Family of growth factors
i. BMP-bone morphogenetic protein
2. Refined-growth factors cloned
a. rhBMP-2
b. BMP-7-osteogenic protein-I (OP-I)
3. BMP-2
a. Animal studies-excellent bone formation
b. Human studies-results equal to autograft
c. Availability-not in US, potentially late 2002
4. OP-I/BMP-7
a. Osteoinductive protein
i. Member of TGFB superfamily
ii. Pure differentiation/growth factor
b. Canine spine model
i. OP-1 groups superior at 4,8, and 12 weeks
ii. Intramembranous ossification
328 Surgical Optians lor Lumbar Spine Pain
c. Rabbit spine model

i. OP-I overcame effect of nicotine
d. US pilot spine study-underway
e. Available in Europe/Australia
5. Conclusion-exciting future potential especially in cases of pseudarthrosis,
metabolic bone disease, steroid dependence, osteoporosis, and smokers. May
eventually help decrease indications for bone graft harvesting, but "not ready
for prime time" currently.
Selected Reading
1. Ahn UM, Ahn NU, Buchowski JM, et al. Cauda equina syndrome secondary to lumbar disc herniation:
A meta-analysis of surgical outcomes. Spine Jun 15 2000, 25(12) 1515-1522.
2. Atlas SJ, Keller RB, Chang Y, et al. Surgical and nonsurgical management of sciatica secondary to a
lumbar disc herniation: Five-year outcomes from the Maine Lumbar Spine Study. Spine 2001, 26(10)
1179-1187.
3. Atlas SJ, Keller RB, Robson 0, et al. Surgical and nonsurgical management of lumbar spinal stenosis:
Four-year outcomes from the Maine Lumbar Spine Study. Spine (United States), Mar 1 2000, 25(5)
556-562.
4. Boden SO, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in
asymptomatic subjects: A prospective investigation. JBJS 72A:403-408, 1990.
5. Boden SO, Martin GJ Jr, Morone MA, et al: Posterolateral lumbar intertransverse process spine
arthrodesis with recombinant human bone morphogenetic protein 2/hydroxyapatite-tricalcium phos-
phate after laminectomy in the nonhuman primate. Spine 24: 1179-1185, 1999.
6. Boden SO, Zdeblick TA, Sandhu HS, et al. The use of rhBMP-2 in interbody fusion cages definitive
evidence of osteoinduction in humans: preliminary report. Spine 25:376-381. 2000.
7. Carragee EJ, Tanner CM, Khurana S, et al. The rates of false-positive lumbar discography in select pa-
tients without low back symptoms. Spine 25:1373-1381, 2000.
8. Carragee EJ, Tanner CM, Yang B, et al. False-positive findings on lumbar discography reliability of
subjective concordance assessment during provocative disc injection. Spine 24:2542, 1999.
9. Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percuta-
neous lumbar discectorny and microdiscectomy in the treatment of contained lumbar disc herniation.
Spine 20:734-738, 1995.
10. Fischgrund JS, Mackay M, Herkowitz HN, et al. 1997 Volvo Award winner in clinical studies.
Degenerative lumbar spondylolisthesis with spinal stenosis: A prospective, randomized study compar-
ing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine
(United States), Dec 15 1997, 22(24) 2807.
11. Gogan WJ, Fraser RD. Chymopapain. A IO-year double-blind study. Spine 17:388-394, 1992.
12. Herkowitz HN, Kurz LT. Degenerative lumbar spondylolisthesis with spinal stenosis. A prospective
study comparing decompression with decompression and intertransverse process arthrodesis. J Bone
Joint Surg Am (United States), Jul 1991,73(6) 802-808.
13. Holt, EP: The question of lumbar discography. JBJS 50A:720-726, 1968.
14. Kahanovitz N, Viola K, McCulloch J. Limited surgical discectomy and microdiscectomy: A clinical
comparison. Spine 14:79-81, 1989.
15. Katz IN, Stucki G, Lipson SJ, et al. Predictors of surgical outcome in degenerative lumbar spinal
stenosis. Spine (United States), Nov 1 1999, 24(2 J) 2229-2233.
16. Kinoshita T, Ohki I, Roth KR, et al. Results of degenerative spondylolisthesis treated with posterior de-
compression alone via a new surgical approach. J Neurosurg (United States), Jul 2001, 95(1 Suppl) 11.
17. Kuslich SO, Ulstrom CL, Griffen SL: The Bagby and Kuslich method of lumbar interbody fusion:
History, techniques and two-year follow-up results of United States prospective multicenter trial
study. Spine 23:1267-7279, 1997.
18. Martin GJ Jr, Boden SO, Titus L, Scarborough NL. Experimental posterolateral lumbar spinal fusion
with a demineralized bone matrix gel. Spine 23:159-167.
19. Mirzayan R, Panossian V, Avedian R, et al. The use of calcium sulfate in the treatment of benign
bone lesions. A preliminary report. J Bone Joint Surg 83-A: 355-358, 2001.
20. Mitlak BH, Finkelman RD, Hill EL, et al. The effect of systemically administered PDGF-BB on the ro-
dent skeleton. J Bone Miner Res 11(2) 238-247, 1996.
21. Nordby EJ, Fraser RD. Chemonucleolysis in the Adult Spine: Principles and Practice, ed JW Frymoyer.
Philadelphia: Lippincott-Raven, 1997, 1989-2008.
22. Patel TC, Vaccaro AR, Truumees E, et al: A safety and efficacy study of OP-I (rhBMP-7) as an adjunct
to posterolateral lumbar fusion. 15th Annual Meeting NASS New Orleans, 2000.
23. Philips FM: OP-l (BMP-7) for spinal fusion. Fourteenth Annual Contemporary Update on Disorders of
the Spine. Whistler, British Columbia, 2002.
24. Pritchett JW. Bortel DT: Degenerative symptomatic lumbar scoliosis. Spine 18(6): 700-703. 1993.
25. Ransford AO. Morley T, Edgar MA, et al: Synthetic porous ceramic compared with autograft in scolio-
sis surgery. A prospective, randomized study of 341 patients [published erratum appears in J Bone
Joint Surg Br 1998 May; 80(3):562] [see comments]. J Bone Joint Surg Br (England) 80:13-18,1998.
26. Ray CD.Threaded titanium cages for lumbar interbody fusions. Spine 22:667-680, 1997.
27. Sassard WR, Eidman OK, Gray PM. Augmenting local bone with Grafton demineralized bone matrix
for posterolateral lumbar spine fusion: Avoiding second site autologous bone harvest. Orthopedics
23: 1059-1064; discussion 1064-1065,2000.
28. Tullberg T, Brandt B, Rydberg J, Fritzell P. Fusion rate after posterior lumbar interbody fusion with
carbon fiber implant: One-year follow-up of 51 patients. Eur Spine J 5(3):178-182, 1996.
29. Urist MR. Bone: Formation by autoinduction. 1965. Clin Orthop (United States), Feb 2002, (395) 4-10.
5;117-115,1980.
31. Walsh TR, Weinstein IN, Spratt KF, et al. Lumbar discography in normal subjects. JBJS 72: 1081-1088,
1990.
32. Yong-Hing K, Kirkaldy-Willis WHo The pathophysiology of degenerative disease of the lumbar spine.
Orthop Clin North Am (United States), Jul 1983, 14(3) 491-504.
,--------19
Failed Low Back Surgery Syndrome
Key Points
• Do not assume that the original diagnosis was correct. The surgery may have
addressed only part of the problem or a problem that was not a cause of the patient's
main complaints.
• Assume that psychological factors are an issue-if not before, then after the "surgical
failure."
• "You cannot make the diagnosis if you do not think ofit"-or attempt to rule it out.
• Postoperative assessment usually requires multiple methods of evaluation; doubtful
cases are often best seen by a multidisciplinary team.
• Measure treatment gains by improved function-not just by subjective reporting.
• Be aware that surgery is often "the big placebo." Many patients appear to have early
postoperative success and then fail-often as the time arrives to move out of the sick
role.
• Second (or more) surgeries are even more likely to fail. A definitive diagnosis and a
patient environment that promotes healing are essential before reoperation.
• The cost of reassessment may be high, but postoperative failure exacts other kinds of
high costs. Insist that all studies be done well; quality may vary.
I. Introduction
A. Scope of problem
1. 200,000-250,000 surgeries per year in U.S. for low back pain
2. Estimate: 30,000-40,000 failed lumbar surgeries per year (some studies
higher)
3. Lifetime prevalence of lumbar surgery in U.S. is 3-4010 of population
B. Indications for initial surgery or reoperation (back, herniated nucleus pulposus)
1. Pain
a. Back
b. Leg
2. Fracture
3. Instability
a. Spondylolisthesis
b. Degenerative segment
4. Neurologic loss
a. Radiculopathy
b. Cauda equina
5. Medical
a. Tumor
b. Infection
331
332 Failed Low Back Surgery Syndrome
C. Success rate
1. Least successful dealing with low back and axial pain
2. Approximately 50% of patients report back pain relief after excision
3. Sciatica relief is 75-80%
4. 15% fall into true "failed" category
5. As many as 40% have persistent complaints of some significance
D. Reasons for failure
1. Wrong diagnosis
2. Wrong surgical plan or technique
3. Recurrence of problem
4. Patient factors (wrong patient)
5. Postoperative management errors
6. Neurologic injury
7. Postoperative complications
II. General Considerations for Reasons for Failure

A. Wrong patient-due to fail because of associated factors
1. Psychological
2. Secondary gain
3. Lack of motivation
4. Already settled into chronic pain mode
B. Wrong diagnosis
1. Missed stenosis
2. Multilevel involvement; extent of painful levels underestimated
3. Problems at unrecognized levels (beware of thoracic and thoracolumbar level
disc masquerading as lumbar pain)
4. Instability unrecognized; failure to fuse
5. Pseudoradiculopathy (mechanical low back pain with lower extremity nerve
entrapment)
C. Wrong surgery-misidentification of planned surgical level during procedure (par-
ticularly in patients with transitional or atypical number of lumbar vertebrae)
1. Failure to decompress stenosis adequately
2. Neural injury
3. Improper screw placement
D. Inadequate postoperative rehablhtation
1. Overuse of long-term medications
2. Failure to push postoperative physical reconditioning (in balance with time re-
quired for postoperative healing)
E. Neural injury or chronic neurogenic pain
F. Risk fadors for postoperative pseudoarthrosis
1. Smokers
2. Osteopenia
3. Increased number of levels of surgical fusion
G. Medical risk fadors
1. Diabetes
2. Peripheral neuropathy
3. Addiction or alcohol abuse
4. Osteopenia or osteoporosis
5. Smoker
6. Obesity
7. Poor general health
Failed Law Back Surgery Syndrome 333
III. Initial Approach to Failed Surgery Patients

A. History
1. Allow extra time to evaluate initially
2. Essential to have prior records
3. Preoperative vs. postoperative complaints
4. Did surgery help initially? Period of relief followed by recurrence may indicate:
a. Recurrence of herniated nucleus pulposus
b. Development of lateral stenosis
5. Was there a new problem immediately after surgery?
a. Infection
b. Pseudo meningocele
c. Intraoperative nerve injury
6. Current medication usage and issues of dependency
7. Careful assessment of psychological status
8. Vocational status and workers' compensation
9. Legal involvement
a. Personal injury
b. Malpractice
10. Other secondary gain
a. Family
b. Social relationships
11. Back vs. leg pain
12. Postoperative systemic complaints (often subtle)
a. Fatigue
b. Irritability
c. Bladder
d. Fever
e. Sweats
f. Decreased appetite or weight loss
13. Past medical history-systemic risk factors
14. Unusual pain patterns (reflex sympathetic dystrophy [RSD1/sympathetic
mediation/complex regional pain)
a. Swelling
b. Burning
c. Hypersensitivity
d. Color changes in painful limb
15. Postoperative rehabilitation (aerobic, flexibility, strengthening, body mechan-
ics, manual physical therapy)
16. Evaluate postsurgical testing and results
a. Computed tomography (CT)
b. CT/myelogram (most useful-hardware present-artifact on other scans)
c. MRI and gadolinium
d. Injections
i. Caudal epidural
ii. Selective epidural
iii. Hardware
e. Electrodiagnostic
f. Radiographs (include flexion-extension)
17. Relieving and exacerbating positions and activities
a. Anterior spinal column and related structures (herniated nucleus
pulposus)-typically flexion aggravates pain
334 Failed Law/JQclc Surgery Syndrome
b. Posterior spinal column and related structures (facet, stenosis,

spondylolisthesis)-typically extension aggravates pain
c. Spinal pain generators, some central discs-worse in extension
B. Physical examination
1. Observe closely for pain behavior as warning of associated problems
2. Careful neurologic exam for focal localizing findings
3. Evaluate for potential major joint problems as referral source
a. Hip
b. Knee
c. Low back
d. Shoulder
e. Neck
4. Palpation at surgery site
a. Hematoma
b. Local fluid
c. Abscess
d. Pseudomeningocele
5. Examination of extremity for sympathetic or RSD-type changes
6. Palpation for Tinel's-peripheral nerves for pseudoradiculopathy
7. Screening for neural tension signs
a. Straight leg raise
b. Adson's test
8. Long tract signs
a. Babinski's sign
b. Clonus
c. Hoffman's sign
9. Vascular assessment
a. Diabetics
b. Elderly patients
c. Known vascular disease
10. Local soft tissues
a. Psoas muscle
b. Iliotibial band
c. Gluteal muscles
C. Diagnostic testing
1. Potential testing in failed spinal surgery patients requires careful consideration.
Test usefulness may be altered as a result of surgery (e.g., postoperative scar-
ring on MRI masquerading as herniated nucleus pulposus).
2. Postsurgical patients present new diagnostic categories (e.g., fibrosis, scarring,
pseudomeningocele),
3. Testing is primarily a form of confirming a clinical diagnosis. More than ever
the "big picture" must make sense. False-positives are frequent.
D. Laboratory screening
1. Rule out infection-high percentage of false negatives
2. Complete blood count
3. Sedimentation rate-often not reliable
4. Other lab work usually based on clinical assessment from patient history and
review of systems
E. Radiographs
1. Flexion-extension films evaluate instability
2. Oblique films
Failed Law Bacle Surgery Syndrome 335
a. Rule out postoperative facet fracture
b. Pars fracture
3. Lateral film
a. Assess for disc space collapse (stenosis risk)
b. Endplate changes (discitis)
c. Spondylolisthesis (postoperative instability + slip)
4. Anteroposterior film
a. Evaluate lateral slip
b. Pedicle irregularities
5. Evaluate broken hardware
IV. Imaging Studies

A. Magnetic resonance imaging (MRI)
I. Particularly helpful when used with gadolinium for diagnosing
a. Recurrent or residual herniated nucleus pulposus
b. Fibrosis and scarring
2. Limited value to assess any level with instrumentation or fusion because of
artifact
3. More likely to miss stenosis in following cases
a. Lateral recess
b. Intravertebral canal
c. Far lateral stenosis
4. Good imaging for
a. Neural structures
b. Psoas abscess
c. Infection in disc space
d. Arachnoiditis
B. Computerized axial tomography (CAT)
I. Helpful to evaluate for missed spinal stenosis
2. Excellent to assess fusion integrity
3. Herniated nucleus pulposus (HNP)
4. Fibrosis or scar vs. HNP-Iess reliable
5. Facet fracture-helpful to confirm radiographs
6. Insist on multiplanar reformatted imaging-visualizes intervetebral and lateral
canals in greater details
C. Myelography
I. Generally less used since advent of MRI
2. Of particular value when combined with CT scan to assess levels with postoper-
ative instrumentation; contrast agent (dye) may decrease ability to see lateral
and intervertebral canals
3. Arachnoiditis
a. Allows visualization of root clumping
b. Older oil-based dyes likely cause of arachnoiditis
4. Evaluate and assess extent of pseudomeningocele
5. Lower reliability when used alone for evaluation of herniated nucleus pulposus
at L5-S I level vs. other levels (more likely to underestimate extent)
D. Bone scan
I. Nonspecific nature leads to limited value in postoperative settings
2. Consider to rule out infection-limited value
E. Gallium scan-to rule out infection. Usually of limited value in this setting.
336 Failed Low Bode Surgery Syndrome
V. Electrodiagnostic testing
A. Nerve conduction studies (NCS)
1. Assess for peripheral nerve injury masquerading as radiculopathy (pseudo-
radiculopathy)
a. Peroneal nerve at fibular head
b. Tibial nerve and tarsal tunnel
c. Tibial nerve at popliteal space
d. Femoral nerve at inguinal canal
e. Saphenous nerve-thigh
2. Particular points
a. New postoperative weakness
b. High-risk peripheral nerves from
i. Surgical trauma (roots)
ii. Positioning (ulnar, brachial plexus)
iii. Postoperative compression boots (peroneal)
3. Screen for missed peripheral neuropathy-associated with high rate of post-
operative failure
a. Diabetes
b. Alcohol
c. Idiopathic
4. H-reflexes-evaluate integrity of S1 root
B. Electromyography (EMG)
1. Useful to assess new vs. old neurologic changes
2. Identification of involved root
3. Assess reinnervation patterns of recovery in cases of neurologic loss
4. Paraspinal findings less reliable in postoperative settings-peripheral muscles
more reliable
C. Somatosensory-evoked potentials (SSEPs)
1. Helpful to assess root and CNS pathways
2. Evaluate pure sensory involvement
3. Unable to assess new vs. old nerve involvement
4. More hardware/user-sensitive than EMG or NCS
VI. Injections
A. Diagnostic blocks
1. Allows more precise assessment of pain generators than anatomic findings of
imaging studies
2. Requires technical skill, particularly with blocks at prior fusion levels; fusion
mass gets in way
3. Epidural block alone is nonspecific
4. Should be done under fluoroscopic guidance with contrast for accuracy
8. Selective nerve root blocks (SNRBs)
1. Useful as both diagnostic and therapeutic tool (block single root; use local
anesthetic and corticosteroid)
2. Effective block may be limited by fibrosis, scar, or significant stenosis (use
fluoroscopic guidance; observe contrast flow along nerve)
3. May be difficult to do under fusion mass
4. Failure to relieve patient symptoms in anesthetic phase leads to concern about
nerve as pain generator
C. Facet blocks
1. Fluoroscopic guidance with contrast
Failed Low Back Surgery SynJrome 337
2. Patient typically worse in lumbar extension in facet synovitis
a. Prolonged standing
b. Walking
c. Overhead work
d. Lying prone
3. May see postoperatively after
a. Disc space narrowing or settling
b. Emphasis on extension exercises during rehabilitation phase
4. Also occurs at levels above prior fusion due to
a. Shift
b. Mechanical stress-longer lever arm increases forces
5. May be done more selectively by blockade of joint innervation (medial
branch/dorsal primary ramus block)
D. Sympathetic blocks
1. Rule out sympathetically mediated pain
2. Verify by change in limb temperature after block
3. When pain pattern of RSD is suspected, a series of blocks may be valuable for
treatment
E. Hardware blocks
I. Useful after instrumentation when loose hardware or hooks are suspected pain
generator
2. Bursa may develop at site of loosening
F. Peripheral blocks
1. When peripheral nerve is suspected as pseudoradicular source
2. Lower extremity
a. Peroneal-fibular head/popliteal
b. Tibial-popliteal space (ankle-tarsal tunnel)
c. Femoral-groin and inguinal canal
d. Saphenous-adductor's (Hunter's) canal
e. Sural-calf or ankle
f. Superficial peroneal-calf or ankle
3. Upper extremity
a. Median
b. Radial
c. Ulnar
VII. Diagnostic Categories

A. Psychological factors
1. Multiple potential issues
2. Probably the primary reason that patients who otherwise had careful pre-
operative assessment fail surgery
3. Preoperative risk factors are often ignored or seen as minor concerns
4. Depression: major risk factor for the development of chronic pain; often easily
treatable
5. Medication abuse: overuse of narcotics without true specialist monitoring of-
ten only heightens pain complaints
6. Screening tests have a role but are secondary to trained psychiatric interview
a. Pain drawing
b. Minnesota Multiphasic Personality Inventory
c. Beck's Depression Inventory
d. Millon Inventory
338 Failed Low Back Surgery Syndrome
7. Preoperative treatment and early psychological support can promote positive

outcome
8. Must be aware of risk due to
a. Conversional disorders
b. Factitious syndromes
c. Secondary gain issues
9. Recent focus: patient at risk to "get well" because of factors in early develop-
ment (poor inner ability to heal)
10. High risk
a. Physical abuse as a child
b. Psychological abuse as a child
c. Sexual abuse as child
d. Adult children of alcoholics
e. Children forced into caregiver role early in life
11. Preexisting alcohol abuse/pain use may inhibit recovery
12. Preoperative psychological assessment suggested for all spinal surgery
a. Particularly when surgery primarily for pain vs. other reasons
b. Pain longer than 3-6 months
13. Psychological assessment essential for all failed surgery, if not a factor pre-
operatively, likely to become one postoperatively
14. Tricyclic medications may be of combined benefit
a. Neurogenic pain
b. Sleep disturbance
c. Depression
d. Myofascial pain
B. Spinal stenosis
1. Failure often due to inadequate decompression
2. Major cause of recurrent or residual back and leg pain-missed stenosis
3. May be missed on common preoperative studies
a. Myelography (lateral/foramina!)
b. Some MRI studies
c. Lower-quality CT
4. Best evaluated on multiplanar reformatted CT scans; better able to see en-
trance and exit zones
5. Be suspicious if plain radiographs show marked disc space narrowing or spurs,
with no report of foraminal assessment at surgery
6. Many surgeons prophylactically do foraminal decompression with surgery for
herniated nucleus pulposus because of expected narrowing of disc space and
resultant stenosis
7. Harder to manage nonsurgically than herniated nucleus pulposus-bony com-
pression is not reabsorbed
8. More common: age >50 years
9. Pain worsens with prolonged standing, walking, or lying prone
10. Pain relieved with
a. Sitting
b. Leaning forward
c. Lying in fetal position
11. Exam: pain increased with lumbar extension, flexion well tolerated; straight
leg raising test may be negative in sitting position but positive in supine posi-
tion (spine flexed vs. extended)
Failed Low Bade Surgery Syndrome 339
C. Chronic radiculopathy
1. Patient with residual postoperative pain in typical nerve root distribution
2. Must exclude persistent nerve compression
3. Pain may be due to persistent chemical or inflammatory pattern as result of
local release of disc enzymes (phospholipase A2)/local chemical irritants, nitric
oxide
4. Concern of waiting too long for surgery in patient with significant preopera-
tive neural changes vs. attempt to manage nonsurgically-neural injury may
become chronic despite treatment
5. Electrodiagnostic testing helpful to assess extent of injury
6. Selective nerve block may be helpful to assess pain localization; relief with
corticosteroid
7. Intraneural fibrosis: "sick nerve syndrome," neuropathic pain
8. Persistent unexplained peripheral pain-overlaps with other pain syndromes
a. RSD/complex regional pain
b. Arachnoiditis
c. Fibrosis or scar
d. Peripheral nerve involvement
9. Generally seen as due to combination of peripheral neurologic and CNS fac-
tors
10. Dorsal root ganglion (DRG) may have modulating effect-at risk of injury with
invasive spinal procedures
11. Increased peripheral neural excitability, loss of CNS modulation, peptide
release-all likely factors
12. Sometimes respond to membrane-stabilizing drugs
a. Tricyclics
b. Antiseizure medications
c. Calcium channel blockers
d. Alpha blockers
e. Neurontin
f. SSRIs
13. Often patient does clinically worse with long-term narcotic use because of
a. Depression
b. Dependency
c. Decreased endorphins
d. Pattern of relief followed by rapid withdrawal patterns with shorter-
acting agents; pain and withdrawal effects during day begin to blend
together
14. Best managed by substituting non narcotics-may see short-term pain increase
during detoxification phase (up to 6-8 weeks)
15. Peripheral stimulation seems to be of some benefit, but research data are con-
troversial
a. Transcutaneous electrical nerve stimulation (TENS)
b. Acupuncture
16. Must assess psychological factors as source of pain resistance in conjunction
with peripheral factors
D. Recurrent disc herniation
1. May occur in 5-15% of patients with prior laminectomy or discectomy
2. Typically period of postoperative recovery followed by sudden return of
symptoms
340 faileJ Law Baele Surgery syndrome
3. May be influenced by surgical techniques

a. Removal of facet leading to instability
b. Micro approach with less aggressive removal of nuclear material
4. MRI most valuable assessment tool when combined with gadolinium-allows
more reliable separation of disc material vs. fibrosis or scar
5. Does not necessarily require reoperation; may be treated initially as original
herniated nucleus pulposus
6. Some surgeons favor fusion at second surgery for same level herniation; need
to assess in context with other factors
a. Age
b. Problems at other levels
c. Medical status
d. Vocational status
7. Protect against flexion loading in early postoperative period
8. Pain worsened by
a. Sitting
b. Bending
c. Driving
9. Pain relieved by
a. Walking
b. Changing positions
10. Physical exam
a. Poor flexion tolerance
b. Neurologic deficits
E. Epidural fibrosis and scarring
I. May lead to chronic neurogenic type pain
2. Iatrogenic-result of surgical intervention
3. Likely represents
a. Chronic nerve tethering
b. Loss of normal vascularity
c. Mass effect
4. Enhanced pain when combined with stenosis, instability of spine; seen on MRI
(especially with gadolinium; probably most reliable technique), CT (combined
with myelography or alone)
5. Treat pain directly or associated complications
6. Surgery to remove scar-likely to increase long-term scarring, with risk of
worsening pain
7. Treatment
a. TricyclicsfneurontinfSSRIs
b. Nonnarcotic medications
c. Flexibility for lower extremities (hamstring and neural stretching)
F. Neurogenic pain
I. May fall into various patterns
2. Many experts debate the physiologic nature of chronic pain of neurologic type;
patterns difficult to separate
3. In making such a diagnosis, it is important to separate causes that are poten-
tially reversible vs. "management mode" [i.e., missed stenosis with residual
nerve compression vs. RSD)
G. Instability
I. Segmental instability-loss of general support structures at spinal level
a. Discogenic changes
Failed Low Back Surgery Syndrome 341
b. Incision of ligamentous structures

c. Removal of lamina
2. When more widespread, surgeon may see significant postoperative instability
with "slip"-spondyIolisthesis at postoperative levels
3. More common to see gross postoperative instability in elderly patients after
widespread decompression for stenosis in setting of marked degenerative disc
disease or osteopenia
4. May require reoperative fusion; again of concern in older patients
5. Slip may also occur laterally
6. Postoperative tests-radiographs with flexion and extension
7. Significant portion of postoperative failures may represent low-grade instability
combined with nerve tethering or traction
a. Fibrosis
b. Scarring
8. Likely also accentuated by
a. Loading of involved level during activity
b. Prolonged postural demand
H. Reflex sympathetic dystrophy/complex regional pain syndrome
1. Multiple names
a. Causalgia
b. Sympathetically mediated pain
c. Sudeck's atrophy
2. Active neurophysiologic debate: sympathetic system vs. visceral afferents
3. Often associated with seemingly minor extremity injury
4. Classic pattern may include
a. Changes in color or temperature of limbs
b. Skin changes
c. Swelling
d. Marked sensitivity to touch
e. Atrophy
f. Changes in sweat pattern
g. Spread to opposite limb
5. Likely due to combination of central and peripheral neural input
6. May respond to sympathetic blockade through
a. Medication
b. Injection
7. Recent research suggests that C-fiber neuropeptides spread through visceral af-
ferent system
8. May exist in less than full blown phenomenon, leading to failure of recognition
(low-grade RSDj
I. Infection
1. Multiple manifestations-some subtle, others overt
2. Superficial skin infections common in early postoperative setting
3. Deeper infections may present with constitutional complaints of subtle nature
or may appear simply as persistent low back pain and failure to improve
4. Laboratory tests
a. Complete blood count
b. Sedimentation rates are often normal; hence of limited value
5. Other screening tests-gallium scan, MRI, CT, etc., also often normal
6. May see
a. Discitis
342 Failed Law Back Surgery Syndrome
b. Deep soft-tissue abscesses

c. Deep wound inflammation changes
7. Some infections by chronic low virulent organisms
a. Diphtheroids
b. Polymicrobial
8. Others more typical manifestations (suspect staphylococci)
a. Fever
b. Elevated lab tests
c. Increased blood cultures
d. Chills
e. Sweats
f. Malaise
g. Weight loss
9. Review early postoperative records
a. Wound closure
b. Healing problems
10. Particular risk: patients with instrumentation
11. Cannot treat infection with hardware present
12. Best diagnosed by operative cultures
13. Treat with 4-6 weeks of intravenous antibiotics; choice based on cultures
J. Pseudomeningocele
1. Postoperative complication
2. Pain changes with position
3. Headache
4. Visualized by
a. MRI
b. CT scan combined with myelography
K. Arachnoiditis
1. Nerve clumping or scarring-intrathecal
2. Postoperative complication
3. Risk increased after oil-based myelography
4. May cause back/extremity symptoms
5. Often worse at night
6. Diagnosis
a. MRI
b. Myelogram
c. Myeloscopy (direct visualization)
7. Relative surgical contraindication; treat nonsurgically
8. Typically treated as neurogenic pain
9. May respond to nerve membrane-stabilizing drugs
a. Tricyclic antidepressants
b. Antiseizure medications
c. Calcium channel blockers
d. Neurontin
e. SSRIs
10. Patient may be candidate for implantable epidural stimulator
L. Facet fracture
1. Potential postoperative complication
2. May present as localized pain
3. More common with wider surgical decompression
4. May lead to lumbar instability
Failed LawBack Sul'flB'Y Syndrome 343
5. Typically worse with

a. Spinal extension
b. Extension and rotation
6. Diagnose by
a. Plain radiograph
b. CTscan, if plain radiographs are negative
7. Usually presents as increase in pain after initial early recovery (new pain)
8. Usually relieved by flexion
9. Usually exacerbated by extension
10. Treatment may require immbolization or brace; in patients with significant
pain and no response to bracing, consider fusion
M. Pseudarthrosis
1. Postfusion complication with clinical or radiologic evidence of failed bony
fusion
2. Persistent pain, clearly related to activity
3. Must look for other causes so that failed surgery does not become a quest to do
fusion and "solve" pain problem
4. Best evaluated on multiplanar CT
5. Flexion and extension radiographs in addition to anteroposterior, lateral, and
oblique views, may be helpful
6. May be visualized on tomograms
7. Rule out other reasons for bony failure
a. Osteoporosis
b. Metabolic bone disease
8. Risk of fusion reported as significantly greater in smokers
9. May require refusion if all other possibilities assessed first
References
1. Burton CV, Kirkaldy-Willis WH, Yong-King K, et al: Causes of failure of surgery of the lumbar spine.
Clin Orthop 157:191, 1981.
2. Burton CV: How to avoid the failed back surgery syndrome. In Cauthen JC (eds): Lumbar Spine
Surgery. Baltimore, Williams Et Wilkins, 1983.
3. Deen JG, Zimmermann T, Lyons M, et al: Analysis of early failures after lumbar decompressive
laminectomy for spinal stenosis. Mayo Clin Proc 70:33-36, 1995.
4. Dubner R: Neuropathic pain: New understanding leads to new treatments. Am Soc Pain J 2:8-11,
1993.
5. Fager CA, Friedburg, ST: Analysis of failures and poor results of lumbar spine surgery. Spine 5:87-94,
1980.
6. Fromm GH: Physiologic rationale for the treatment of chronic pain. Am Pain Soc J 2: 1-7, 1993.
7. Jonsson B, Annetz M, Sjoberg C, Stromquist B: A prospective and consecutive study of surgically
treated lumbar spinal stenosis. Spine 22:2938-2944, 1997.
8. Kirkaldy-Willis WH: Managing Low Back Pain. New York, Churchill Livingstone, 1983.
9. Pheasant Jf', Dyck P: Failed lumbar disc surgery: Cause, assessment and treatment. Clin Orthop
164:93, 1982.
10. Saal JA, Dillingham MF, Gamburd RS, et al: The pseudoradicular syndrome: Lower extremity periph-
eral nerve entrapment masquerading as lumbar radiculopathy. Spine 13:926-930, 1988.
11. Schofferman L: Occult infections causing persistent low back pain. Spine 14:417-419, 1989.
12. Schofferman L: Diphtheroids and associated infections as a cause of failed instrument stabilization
procedures in the lumbar spine. Spine 16:356-358, 1991.
13. Schofferman J, Anderson D, Hines R, et al: Childhood psychological trauma correlate with unsuccess-
fullumbar spine surgery. Spine 17(Suppl):S138-5 144, 1992.
14. Schofferman J, Anderson D, Hines R, et al: Childhood psychological trauma and chronic refractory
low back pain. Clin J Pain 9:260-265, 1993.
15. Schott GD: Visceral afferants: Their contribution to "sympathetic pain." Brain 117:397-413, 1994.
16. Taylor V, Devo R, Ciol M, et al: Patient oriented outcomes from low back surgery." A community
based study. Spine 25(9):2445-2542, 2000.
344 Failed LowBack Surgery Syndrome
17. Weber H: Lumbar disc herniation: A prospective study of prognostic factors including a controlled
trial. J Oslo City Hosp 28:91-113,1978.
18. Weinstein IN, Wiesel SW: The Lumbar Spine-International Society for the Study of the Lumbar
Spine. Philadelphia, W.B. Saunders, 1990.
19. Wenger, M: Mariani L, Kalbarczyk A, Goroger U: Long-term outcome of 104 patients after lumbar
sequestrectomy according to Williams. Neurosurgery 49(2):329:334, 200l.
20. White AH, Rothman RR, Ray CD: Lumbar Spine Surgery: Technique and Complications. St. Louis,
Mosby, 1987.
,--------20
Chronic Pain Programs
Peter B. Polatin, M.D., Robert Gatchel, PhD.,
Donald Hinnant, PhD., and C. David Tol/ison, no.
Key Points
• Chronic pain involves interrelated biologic, sensory, psychological, behavioral, and
environmental factors.
• Chronic pain is persistent and does not respond to conventional medical care.
• Treatment of chronic pain requires a biopsychosocial model that helps the patient to
improve function without necessarily diminishing or curing the pain.
• The patient is referred to a chronic pain program when persistent pain significantly
limits or interferes with physical, psychological, and vocational or social functioning.
• If issues related to chronic pain significantly impede the progression of treatment,
referral can be made before treatment and testing are complete.
I. Introduction
A. Definition: Chronic pain is persistent pain that continues beyond the usual course of
an acute disease or injury. Often an arbitrary period of 6 months is used to desig-
nate pain as chronic. Guidelines recently published by the Agency for Health Care
Policy and Research of the United States Department of Health and Human Services
define chronic low back pain as having a duration of 3 months. In contrast to acute
pain, chronic conditions may be caused and reinforced by primary and secondary
gain factors (e.g., financial award) in addition to social and psychological factors.
Responses to chronic pain usually involve atypical behavioral, affective symptoms,
and pathophysiologic changes. Chronic pain does not serve a protective or biologi-
cal purpose, although it may have an ego protective psychodynamic function, and
creates severe psychological, social, economic, and health problems.
B. Incidence
1. In 1987, the National Center for Health Statistics reported 10 million physician
visits for low back pain over a 3-year period.
2. Fourteen percent of the adult population have chronic low back pain.
3. 1.4 billion work days are lost because of chronic low back pain.
4. One or two percent of the entire work force in North America (U.S.A. and
Canada) will file a workers' compensation claim for low back disability at some
time during their employment, and more than 1% of the work-age population
is disabled by low back pain.
5. Total annual costs associated with back pain have been estimated at over $50
"Not all health plans cover integrated treatment services for chronic pain, and the clinician may have
to modify treatment goals as a result of such limitations.
345
346 Chronic Pain Program5
billion/year. One-third of the costs are for medical care, whereas two-thirds are
for compensation and work loss. Approximately 33% of all healthcare and in-
demnity costs under workers' compensation go to occupational low back pain.
II. Early Detection

A. Variable symptoms and nonspecific diagnosis
I. Symptom magnification and "non-organic" (Waddell) signs
a. Tenderness
i. Superficial
ii. Widespread
iii. Nonanatomic
b. Simulated rotation: Back pain reported when shoulders and pelvis are pas-
sively rotated with patient relaxed, feet together.
c. Simulated axial loading: Low back pain reported when downward pressure is
applied to head while patient is standing.
d. Straight leg raising during distraction vs. formal testing
i. Pain improves when patient is distracted.
ii. Pain reaction decreased during straight leg raises when patient is seated.
iii. Pain reaction decreased during straight leg raises when patient is seated
as muscles, foot, or knee examined.
e. Sensory
i. Regional
ii. Nondermatomal
f. Motor
i. Regional
ii. Nonmyotomal
g. General reaction or overreaction (objective examiner should attempt to
avoid influences such as personal bias and cultural factors)
i. Crying out
ii. Extreme guarding
iii. Sweating
iv. Collapsing
2. Inconsistent physical examination
3. Inconclusive diagnostic data
B. Poor response toprior treatment
I. Lack of response to treatment that is usually effective (e.g., relative rest, med-
ications, physical therapy, injections)
2. Exacerbation of symptoms with attempts at physical therapy or intolerance of
therapeutic exercise
C. Psychological factors
I. History of psychiatric illness
a. Depression
b. Hypochondriasis
c. Somatization disorder
2. History of emotional or physical abuse as child or adult
3. Personality disorder
a. Antisocial
b. Passive-dependent
c. Borderline
4. Misinterpretation of symptoms as indicative of "cognitive distortion" (catastroph-
ization)
Chronic Pain Progroms 341
a. Patients with diagnosis of bulging disc or degenerative disc disease, for ex-
ample, have a tendency to catastrophize and misinterpret their potential for
improvement.
b. Such patients are often fearful of physical activity and restorative therapy
because of their extreme pain sensitivity and associated anxiety.
5. Sense of entitlement (e.g, I was injured on "their" job)
6. Tendency toward doctor shopping
7. Concrete or magical thinking: "if only the doctor could find the problem or
give me the right medication"
8. History of or current substance abuse or dependence
9. Subnormal intellectual ability
10. Patients who refuse to take personal responsibility for recovery
a. Noncompliant
b. Reject treatment that may temporarily increase pain or discomfort
11. Psychological evaluation indicating high probability for chronic pain
syndrome, emotional disorder. or both
D. Vocational factors
1. Job dissatisfaction
2. Heavy work
3. Dangerous work
4. Boring work
5. Poor work history
a. Multiple jobs over relatively short time
b. Terminations
c. Excessive absenteeism
d. Poor performance evaluations
e. History of work-related injuries
6. Brief term of employment at time of injury
7. Perception of "unconcerned employer"
8. Employer policy of "no light duty" or "1000/0 rule" before return to work
9. Individual with few or no transferable skills after injury
E. Social factors
1. Disabled spouse
2. Codependency
a. Spouse or significant other reinforces illness behavior.
b. Spouse defends or excuses detrimental behavior (e.g., substance abuse).
c. Spouse takes dominant or powerful role in patient's problems.
3. Dysfunctional family
a. Substance abuse problems
b. Physical abuse
c. Psychological abuse
d. Chronic disruptive family interactions
4. Cultural reactions to illness and injury
5. Family history of chronic disability and ingrained pattern of chronic illness in
family structure
F. Other factors
1. Risk factors
a. Obesity
b. Smoking
c. Other health problems
2. Litigation
348 Chronic Pain Prograrm
3. Problems with insurance coverage

a: Preexisting condition
b. Denial of work-related injury
c. Denial of authorization
d. Unfavorable managed care decision for treatment
4. Workers' compensation
a. Getting lost in the system
b. Insurers that do not provide for vocational rehabilitation or retraining
c. Premature assessment of "maximum medical improvement" or "permanent
and stationary" status
5. Lack of coordination between treating physicians and other health professionals
III. Criteria for Referral to aChronic Pain Program

A. Persistent pain that does not respond to traditional conservative treatment or sur-
gical intervention
B. Psychological evaluation of pain patient demonstrates psychopathology, poor cop-
ing skills, extreme pain behavior, motivational problems, psychosocial or voca-
tional complications
C. Moderate-to-severe impairment of physical ability and/or functional status
D. Dependence on potentially harmful medications, need for detoxification, alcohol
or illicit drug abuse
IV. Types of Pain Treatment Programs

The International Association for the Study of Pain (IASP) has specified four levels of
pain clinics.
A. Modahty-oriented clinics (level I) provide specific interventions for chronic pain, such
as biofeedback, nerve blocks, accupuncture, or physical therapy. They do not pro-
vide overall management of chronic pain or perform interdisciplinary evaluations.
The possible types of modality-oriented programs are practically endless. Some
programs may offer legitimate services, whereas others may use techniques that
border on "quackery."
B. Pain clinics (level II) diagnose and manage chronic pain in an outpatient setting
and may specialize in a particular diagnosis or area of the body (syndrome-
oriented programs).
C. Multidisdphnary pain clinics (level III) contain a number of different disciplines of
health care specialists who offer different therapeutic assessments and interven-
tions and operate as a team.
D. Multldisdphnary pain centers (level IV) also offer a multidisciplinary assessment and
treatment approach and are affiliated with a major medical center offering oppor-
tunities for teaching and research. Functional Restoration, a sports medicine ap-
proach to the disability associated with chronic back pain and other musculo-
skeletal syndromes, is an important variant of the multidisciplinary approach,
with documented outcomes of up to 85% return to work for patients who com-
plete the program.
There is an important distinction to be made between unidisciplinary, multi-
disciplinary and interdisciplinary care. Unidisciplinary treament refers to a single
discipline of therapy, such as a physical therapy, accupuncture, medication man-
agement by a physician, or chiropractic care. Multidisciplinary treatment involves
the input of a number of different medical disciplines, but not necessarily in a co-
ordinated way in which regular communication between the health care providers
takes place. In interdisciplinary treatment, all of the providers are "under one
Chronic Pain Programs 349
roof' and collaborate regularly about each patient's treatment plan and progress
to date (see further discussion below).
V. Models of Chronic Pain

A. The biomedical model of pain: dates to the seventeenth century and was originally for-
mulated by Descartes. Pain results from a specific disease state that is traceable to
specific pathological biological processes. Once the underlying problem or cause
has been identified in the lumbar spine, a diagnosis will be made and lead to ap-
propriate treatment and cure. The pain is considered to result from ongoing physi-
cal injury or disease and to be related to sensory input through stimulation of spe-
cific nerve fibers triggered by tissue-damaging thermal, mechanical, or chemical
stimuli.
1. Certain chronically painful medical conditions may be treated appropriately
within the biomedical model (e.g., headaches, arthritis, and cancer during exac-
erbation).
2. Patients with chronic low back pain often adhere to the biomedical model as
they continue to search for a specific cause, diagnosis, and cure. This model of-
ten leads to doctor shopping and multiple referrals to various specialists.
Patients also may be tempted to pursue unorthodox treatment and often deplete
significant economic resources.
3. Clinicians utilizing this model tend to dichotomize pain into the "organic'{for
which a pain generator can be found) and the "psychogenic" (which defies clin-
ical diagnosis).
B. Chronic pain model: Chronic pain involves a complex interaction of biological, sen-
sory, cognitive, emotional, behavioral, economic, and environmental factors.
Within this conceptual framework, it is accepted that pain may persist without
demonstrable nociceptive input or pathophysiologic disturbance. The "gate control
theory" of Melzack and Wall hypothesized central nervous system mechanisms
whereby the dorsal horns of the spinal cord regulate the transmission and inten-
sity of efferent nociceptive input to the central nervous system. Incoming pain im-
pulses, according to this model, are modifiable by chronic stimulation and psy-
chological mechanisms via afferent reflex arcs. Subsequent research has focused
on the role of psychosocial factors in chronic pain syndromes (see below).
C. Operant behavioral model
1. Initially developed by Wilbert Fordyce in 1968, behavior modification tech-
niques are applied to the actions or behaviors of patients with chronic pain.
2. Pain behavior is viewed as learned behavior maintained by environmental in-
fluences. Central to this approach is the theory that when the subjective experi-
ence of pain manifests in behavior such as grimacing, limping, and groaning,
such behavior is systematically reinforced by attention, medications, sympathy,
and other factors in the environment that maintain pain behavior.
3. Treatment seeks to identify objective pain behaviors and to eliminate them
through application of behavioral modification techniques.
D. Biopsychosocial model: This model utilizes physiological, biological, cognitive, affec-
tive, behavioral, and social factors and their interplay to explain a patient's self
report of pain. These include such things as determinants of self report of pain
(social and cultural conditioning, coping skills, reinforcement, emotional distress,
and beliefs about illness), compliance, and secondary gain. Pain transcends the
confines of a physical symptom and reflects overall suffering as created by de-
moralization and depression; pain sensitivity and reactive neuromuscular inhibi-
tion; limitation of personal, social, and work activities; and increased utilization
350 Chron;c Pa;n Programs
of medication and other health care services. As suffering increases, so does illness
behavior and refractoriness to medical interventions. The treatment of chronic
pain is therefore most effectively delivered by an interdisciplinary team of special-
ists utilizing a biopsychosocial approach (Table 1).
VI. Outpatient Chronic Pain Programs

A. Indications for outpatient treatment
1. The patient can attend the pain program by commuting, residing in a motel, or
making some other arrangement that allows for frequent attendance.
2. The evaluation of the patient's pain does not indicate the need for 24-hour su-
pervision, and the patient is found to be medically and psychologically stable.
3. No evidence suggests that the patient is abusing potentially harmful prescrip-
tion or nonprescription medications, alcohol, or other substances.
4. The patient is willing to comply with self-management activities provided by
the treatment team.
5. The patient's pain is not sufficiently severe to warrant hospitalization, and the
medical evaluation has clearly ruled out any significant pathological process or
injury that requires closer supervision or further diagnostic evaluation.
B. Advantages and disadvantages ofoutpatient programs
I. Advantages
a. Reduced costs
b. Opportunity to apply self-management recommendations in natural setting
c. Most patients can remain with family members, whose input about the pa-
tient's compliance and pain in general may be an important component of
ongoing assessment.
d. Changes in treatment plans are easier and more adaptable to home, social,
and work environment.
e. Light-duty work, retum-to-work program, vocational rehabilitation, or other
vocational endeavors may be implemented.
TABLE I. Medical vs. Blopsychosodal Model

Medical Model Biopsychosocial Model
Focuses on disease or injury. Focuses on interaction of biologic, sensory, cognitive,
emotional, behavior, economic. and environmental
factors.
Pain is directly related to disease or injury Recognizes importance of cognitive and illness
behavior and operant influences on such behavior.
Physician is responsible. Focuses on a systems approach to treat pain.
Emphasizes peripheral pain mechanism. Focuses on a systems approach to treat pain.
Reductionistic approach to pain treatment relies
entirely on physical assessment and treatment Accepts the role of central mechanisms that affect
modalities. peripheral nociception as well as allows the
possibility of pain in the absence of nociception.
Most useful for acute pain. Emphasizes self-management in treatment.
Considers the patient equally responsible for
managing pain.
Accepts the existence of pain even when underlying
cause cannot be determined.
Most useful for chronic pain.
f. Does not reinforce the "sick" role, which implies dependence on medical sys-
tem or doctors for daily care.
g. Flexible scheduling of treatment and changes in treatment protocol as
well as tapering of visits and reintegration into vocational system and
community.
h. Most high-quality outpatient programs provide the same interdisciplinary
staff and treatment approaches as an inpatient program.
2. Disadvantages
a. Patients often have difficulty with transportation, family obligations, and/or
financial resources for lodging if they reside too far from the pain manage-
ment center.
b. No opportunity to observe and monitor the patient's behavior accurately and
exactly after the course of therapy or to determine compliance with self-
management activities.
c. No capacity for 24-hour observation and control of patient's environ-
ment.
d. No provision of optimal control measures such as those necessary for detox-
ification or changing medications.
e. No control of possible environmental contingencies or reinforcers that help
to maintain pain behavior through secondary gain and other variables that
may undo much of what is taught or reinforced in the treatment program on
a daily basis.
VII. Inpatient Pain Programs

A. Inpatient comprehensive pain programs
1. Provide full range of coordinated interdisciplinary services for pain manage-
ment that are intended to prepare patients for painful procedures such as
surgery.
2. Provide preoperative and postoperative pain management techniques and fol-
low through with additional pain management problems.
3. Primary goal: to provide full continuum of pain control throughout hospitaliza-
tion and reintegration into community.
a. Typically include discharge into outpatient program for postacute care with
continuation of interdisciplinary approach.
b. Additional services may include work hardening, vocational services, or
other programs developed for the patient's particular needs.
B. Indications for inpatient treatment
1. The patient's pain must be incapacitating.
2. Potential medical complications or concomitant medical conditions that require
24-hour supervision and management.
3. Chemically dependent patients who require detoxification under 24-hour super-
vision.
4. Prior outpatient program failure and exhaustion of all available health care re-
sources for pain.
e. Advantages and disadvantages ofinpatient programs
1. Advantages
a. Control over environmental factors (e.g., social-behavioral reinforcement in
home).
b. Prevents patient from engaging in activities that may perpetuate pain condi-
tion or cause harm.
c. Requires patient to engage fully in therapeutic environment.
352 Chronic Pain Programs
d. Allows 24-hour behavioral observation that may be helpful in certain cir-

cumstances.
i. Suspicion of malingering
ii. Noncompliant behavior
iii. Illicit or inappropriate drug use
e. Allows provision of further diagnostic testing or hospital-based services
when necessary.
2. Disadvantages
a. Cost and lack of coverage by many managed care plans.
b. Reinforces the "sick" role and medical necessity of remaining in the hospital.
c. Dissimilarity to home environment, where opportunities for self-management
can be practiced, creates an artificial environment that may not encourage
application of coping skills taught in the program.
VIII. Basic Principles of Treatment

A. Multidisciplinary vs. interdiscipnnary models
1. The term interdisciplinary represents a model that incorporates democratic shar-
ing of information and philosophy and integration of therapeutic modalities
without deference to an arbitrary hierarchy. This approach requires continued
effort towards effective communication. The team consists of a group of core
professionals who share a common philosophy and conceptualization of the
patient in pain. Continued efforts are made to synthesize clinical evaluations
and plan of care. Treatment is based on the combined observations and ex-
pertise of the entire team rather than individual opinion. Most current and
effective chronic pain programs use this approach, which incorporates the
biopsychosocial model.
2. The term multidisciphnary generally notes clinical involvement of a group of
specialists, each performing a specific type of therapy germane to their train-
ing. Often this approach leads to serial consultations or poorly integrated
treatment. A major problem is the possibility of multiple philosophies in treat-
ing a particular problem such as chronic back pain. A more devastating side
effect is the fact that patients may become confused when confronted with
various philosophies and treatment, goals and expectations, all of which lead
to poor outcome. The delegation of responsibilities and quality of communi-
cation among team members is compromised.
B. Self-management
1. The self-management approach places the primary responsibility on the pa-
tient with the chronic pain.
2. The health care practitioners involved in the patient's treatment consider a
"cure" as inappropriate. The primary goal is to increase function; the sec-
ondary goal is to eliminate or diminish the pain as much as possible.
3. The therapist acts as teacher or coach, with the main purpose of assisting the
patient in the use of self-management skills. The patient must accept the fact
that the greatest degree of improvement and relief comes with a written con-
tractual agreement between patient and program staff. For self-management
to be effective, the biopsychosocial model must be incorporated. The patient
must be taught that all pain involves a combination of biologic and psycho-
logical as well as social-environmental factors.
4. Patients with chronic pain may be resistant to understanding the psychologi-
cal components of their pain experience. However, education can be highly
effective in demonstrating the interrelationship of mental factors with pain
and physiologic processes. Cognitive-behavioral techniques teach patients to
identify and then abort their catastrophizing, psychophysiologic arousal, and
dysfunctional "pain behaviors" such as guarding, limping, moaning and
avoidance of physical activities. Patients learn that these behaviors, when
unchecked, lead to a regressive pain cycle and prevent a healthy adaptation to
a chronic condition.
5. Treatment should address family issues, sexual difficulties, financial problems,
and vocational issues. When significant pain reduction is unrealistic, coping
mechanisms are taught that enable the patient to improve function and quality
of life.
6. The chronic pain patient is expected to become an active participant rather
than depend on medical professionals. The patient is encouraged to develop a
sense of control, which frequently leads to a reduction in reliance on the health
care system.
C. Education
1. Patient education is a critical component of chronic pain management. Most
patients are confused and frustrated about their condition, and may have heard
conflicting messages from various health care providers. Many have reacted to
implications that they have bulging discs, arthritis in the spine, or "no objective
findings." The patient's emotional reaction demands extensive education in
conjunction with treatment. In fact, many patients will not subject themselves
to an active physical rehabilitation program unless they are convinced and re-
assured about the nature of their condition, pain, and safety.
2. Group presentations are led by various team members and cover a wide variety
of topics. Involvement of spouse or family member is often crucial in achieving
patient compliance and ensuring that the family and others understand the na-
ture of the treatment and their role in the patient's problem. Important group
topics:
a. Various causes of pain
b. Understanding diagnostic issues and types of appropriate treatment
c. Self-management techniques for pain
d. Cognitive-behavioral coping skills
e. Medications
f. Stress management
g. Body mechanics
h. Anatomy
i. Insurance system, worker's compensation, disability, Social Security
j. First aid and preventive behavior for back pain
k. Emotional and psychological issues of chronic pain
I. Reestablishing restorative sleep habits
3. Family members are taught that they are an extension of the treatment team.
For example, they are taught that they may reinforce the patient's pain behav-
ior and dependency or correctly assist the patient in practicing self-management
techniques. Spouses and other family members can reinforce and participate in
the patient's self-management regimen.
IX. Therapeutic Options and Program Components

A. Medical director: Most programs have an identified medical director or codirectors,
who are physicians of various specialties, and work closely with a clinical director
(often a medical psychologist).
1. The program physician is responsible for obtaining a detailed history and phys-
ical examination as indicated. Although most patients have already been thor-
oughly evaluated, it is not uncommon for a patient to be referred to the pain
program for diagnosis and treatment.
2. The physician involved in an interdisciplinary program recognizes that the tra-
ditional medical model is inappropriate; improving function is the primary
goal, whereas pain reduction is secondary.
3. Medical management requires that the physician listen to patients' complaints,
particularly their frustration with the medical system for not curing their pain.
Physicians must emphasize the multi modal approach and enlist the patient's re-
sponsibility for taking an active role in the treatment process.
B. Medical consultants: The pain physician may rely on various specialists for assistance
in the treatment of chronic low back pain. Many pain programs have a formal in-
terdisciplinary medical advisory committee. Members of this committee may serve
as consultants, review the program's outcomes, and provide support for its growth
and survival.
C. Physical therapy
1. The efficacy of an active physical therapy program for treatment of low back
pain has been well established. The use of passive modalities offers little for the
patient with chronic back pain. Short-term pain-relieving modalities may be
used on occasion during an exacerbation or as an initial preparation for graded
participation into a more active protocol. The most effective therapeutic exer-
cises include flexibility training, lumbar stabilization exercises, therapeutic
aquatics, and other active techniques.
2. Many patients with chronic back pain have developed a deconditioning syn-
drome. The positive effects of an active physical therapy program include phys-
iologic, physical, and psychological components. Physiologic improvement is
related to cardiovascular conditioning and improved blood flow. Stress and de-
conditioning lead to ischemia in the muscles, which increases the propensity for
pain. When the patient improves and is capable of aerobic activities, exercise
increases beta-endorphin levels in the blood and cerebral spinal fluid. The ef-
fect of beta-endorphins is powerful; they decrease depression. give the patient
an overall feeling of well-being, diminish the need for medication, and thus
help to establish patient self-confidence and to decrease the patient's perception
of disability.
3. Physical therapy should emphasize body mechanics, ergonomics, and postural
training. Many chronic pain programs provide jobsite ergonomic analysis and
prevention programs in addition to the treatment of chronic back pain. Chapter
8 reviews the role of physical therapy in the treatment of low back pain.
D. Occupational therapy
1. Occupational therapy focuses on functional tasks, body mechanics, and safe ac-
tivity. Adaptation techniques for more physically impaired and/or elderly pa-
tients may include reaching, physical support devices, and structural modifica-
tions for the home.
2. Occupational therapists perform a detailed analysis of the patient's aptitudes,
intelligence, and work capacity.
3. Occupational therapy often addresses the financial, legal, and work-related bar-
riers to recovery. As patients approach program completion, return-to-work is-
sues, job changes, ergonomics, and referral to vocational rehabilitation services
may be indicated. Many patients fear reinjury or failure at their previous occu-
pation and possible loss of worker's compensation or financial security if their
return to work is unsuccessful.
Chronic Pain Pf09rams 355
E. Vocational counseling: Many comprehensive pain centers provide vocational services,

including work hardening. An interdisciplinary approach is crucial for rehabilita-
tion of the injured worker. The counselor works as a case coordinator and media-
tor between employer and patient. Patients incapable of returning to their former
occupation are referred to vocational rehabilitation.
F. Psychology
1. Psychologists who specialize in pain management must have additional train-
ing in medicine and rehabilitation. The pain psychologist should have a work-
ing knowledge of anatomy and physiology, neurology, physical medicine and
rehabilitation, spinal diagnostics, and other areas of medicine. The psychologist
must be capable of answering questions and responding appropriately to pa-
tients' inquiries about medical problems.
2. Psychological services include techniques such as psychological evaluation, re-
laxation training, biofeedback, and cognitive-behavioral therapy. Psychological
testing may be conducted before entry into the program and is often helpful as
a component of treatment planning and outcome measurement. Behavior modi-
fication, self-management techniques, and supportive services such as family
counseling and education are provided.
4. Psychotherapy may be performed as a component of treatment with some pa-
tients, but the primary role of the psychologist is to provide goal-directed in-
struction in self-management techniques, behavior modification, education, and
individual and group therapy.
5. Group therapy is a potent technique when provided with an emphasis on edu-
cation. Didactic group classes explain stress management, anatomy and physi-
ology, the nervous system and pain, the effects of pain on the emotions, and
dealing with work- and family-related issues.
G. Nursing
1. Pain nurses are an essential component of the program and have the major re-
sponsibility for the total well-being of the patient. Often nurses are responsible
for monitoring every patient's physical-medical condition and communicating
directly with the attending physician.
2. In inpatient programs, nurses overlap their traditional roles with those of other
therapists. For example, nurses provide education, group therapy, and counseling.
3. Professional organizations, such as the American Society of Pain Management
Nurses, have contributed to improved management of acute and chronic pain.
H. Ergonomics: Specialists trained in ergonomics are a common component of a com-
prehensive pain management program. Computerized instrumentation and analy-
sis of body mechanics are often performed. The degree of dysfunction and indi-
vidual capacity to return to work are addressed. The ergonomist provides an
analysis of job requirements and recommendations for jobsite modifications that
help to minimize the chance for reinjury or recurrent pain.
I. Biofeedback: Chronic pain programs provide relaxation training and biofeedback,
which may be a highly effective tool for diagnosis as well as treatment.
1. Biofeedback, particularly electromyographic (EMG) biofeedback with surface
electrodes and sophisticated computer systems, is used to identify postural
problems, muscle asymmetry, guarding, and other reactive pain behaviors.
Patients may practice walking, bending, lifting, and other physical activities
while EMG levels are monitored to allow for therapeutic change in technique
and safe practice of body mechanics. Portable EMG biofeedback equipment
may be used for postural and gait training while patients carry out their normal
physical and/or work activities.
356 Chronk Poin Programs
2. Various biofeedback techniques, such as EMG, thermal/temperature (blood

flow), skin conductance (galvanic skin response), and brain-wave patterns
(electroencephalography) may be used to teach stress reduction and relaxation
techniques. Psychologists and technicians with specialized training in biofeed-
back evaluate patients and select the most appropriate technique to help ame-
liorate the patient's physiological stress and symptoms. Such self-control skills
are a powerful method for improving self-confidence, reducing stress and pain
reactions, and learning how to prevent or abort overreactions to episodic in-
creases in pain. Stress control with biofeedback may help to teach patients how
to break the pain-tension cycle.
J. Medications: The patient with chronic pain frequently presents on a variety of med-
ications. It is very difficult initially to determine whether any or all of them have
been effective and, therefore, it may be necessary to taper many or all medications
before making any assessment. This may take some time and require supervised
detoxification.
1. The use of narcotics for the treatment of chronic nonmalignant pain has be-
come an acceptable option, so long as the patient demonstrates a commitment
to a functional life style and does not escalate the dose or manifest drug seek-
ing behavior. However, many pain programs adhere to a philosophy of limited
or no use of narcotic medication, and seek to utilize adjunctive medication in
coordination with refined self regulatory skills.
2. Nonsteroidal antiinflammatory medications may be effective.
3. Antidepressant medications, particularly the tricyclics, may be of value. They
have a positive effect on the serotonergic system that may decrease pain and
help to improve the quality of sleep. Improved sleep is critical because most
chronic pain patients have a nonrestorative sleep pattern that facilitates in-
creased muscle pain, soreness, fatigue, and irritability. Antidepressants are ef-
fective with patients who are not clinically depressed; the dosage is usually
lower than the dosage used for depression.
4. Anticonvulsants may be effective for the control of neuropathic pain, but must
be monitored closely for side-effects, and should be introduced carefully and
with close medical superivision.
x. Duration of Treatment
A. Program intensity. Historically many chronic pain programs have had a highly struc-
tured treatment protocol and time frame for completion of the program. With the
current emphasis on reduced costs, managed care, and outpatient treatment, pain
centers have developed more individually tailored programs. Patients may attend
an outpatient program on a full-day or half-day basis, depending on diagnosis,
degree of dysfunction, and work obligations. However, injured workers under-
going treatment for low back pain typically are involved in a full-day treatment
schedule.
B. Program frequency. Some patients with back pain can be successfully treated with a
less intensive program, coupled with part-time and modified duty work release.
Elderly or unemployed patients may be appropriately treated with several weekly
visits and implementation of a home-based protocol.
C. Discharge criteria
1. Patients are assessed with pre- and posttreatment physical and self-report
measures. Discharge should be determined by attainment of specific physical,
behavioral, and psychological goals established upon entry into the program.
Physical measures may include improvement in strength, range of motion,
aerobic capacity, and overall ability to function at a higher level. Injured work-
ers who are successfully treated must be capable of resuming functional status
appropriate for a job. Subjective measures of successful treatment and dis-
charge decision making are based on self-report measures of pain, sleep distur-
bance, depression, and other common problems. Additional indications for dis-
charge include appropriate use of medication and demonstrated ability to
resume a healthier lifestyle.
2. After discharge an opportunity for maintenance should be provided to enable
patients to continue physical therapy and attend a support group. It is unrealis-
tic to expect that most patients will be able to manage pain effectively without
occasional professional support. A weekly support group emphasizes relapse
prevention and maximizes coping skills. The American Chronic Pain Association
provides support, information, and assistance for patients who wish to establish
a group in their area.
3. At discharge, the program director provides the primary care physician with a
report of the patient's progress, pertinent suggestions about medications, other
recommendations, and assistance for patients who wish to establish a group in
their area. The referring physician should have a clear agreement with the pa-
tient about responsibilities for continued pain management and what is ex-
pected in the event of a flare-up. In some instances the pain program physician
agrees to manage the chronic patient's medications and pain-related problems.
4. There should be a defined end point for treatment. If a patient is going to suc-
cessfully integrate the goals of therapy into an adaptive lifestyle, he or she will
do so within 3 to 6 months. Those patients who fail to progress, as demon-
strated by lack of achievement of defined goals within that period of time, may
require discharge or a change of focus to less intensive palliative care (med-
ication management). In some cases, patients require stabilization in a mental
health setting prior to embarking on pain management. In others, the secon-
dary gain issues must be resolved before the patient will benefit from further
treatment.
XI. The Unsuccessful Patient

A. Prevention of treatment failure may be avoided by pre-treatment screening and
strict admission criteria. The intensity of the pre-admission evaluation varies
greatly among pain programs. Many patients referred for pain management are
labeled "difficult" or "unmotivated" or carry other negative descriptions. Pain pro-
grams are expected to treat patients who, by definition, have failed all reasonable
types of treatment and have significant psychological overlay.
B. Early detection of the patient at high risk for failure is important for cost contain-
ment, prevention of staff frustration, and preservation of a positive therapeutic
milieu.
C. At the beginning of the treatment program, it should be clearly explained to the
patient that progress probably will fluctuate and that exacerbations of pain are
likely. The patient should be prepared for possible setbacks with physical and
cognitive-behavioral coping strategies. Self-management techniques should be
practiced and evaluated throughout treatment.
D. Short- and long-term goals and measures of progress are critical. When the pa-
tient does not meet goals and/or progress as expected, team intervention is indi-
cated. If the program is too regimented or inflexible, noncompliance will be ram-
pant and failure at too high a risk. By the same token, lack of therapeutic
leadership and a "laissez faire" attitude of limited expectations will create a poor
milieu where patients fail to reach their expected goals. Continuous reevaluation
and modification of the treatment protocol helps to improve outcome.
E. When a patient does not respond to treatment, team decision making and appro-
priate referral or discharge arrangements should be made. Some patients may ben-
efit from referral to an alternate treatment program or specialist if they are unwill-
ing to participate or need psychiatric treatment, a chemical dependency program,
or modified outpatient treatment. The difficult or noncompliant patient may need
to be reevaluated by the psychologist. Often counseling helps to resolve issues re-
lated to the patient's failure and allows successful treatment. In some cases, com-
pensation or litigation secondary gain issues need to be resolved before therapeu-
tic progress can be made, but true chronic pain is never "cured by a verdict" or a
"green-back poultice."
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,--------21
Implantables: Neurostimulation and
Intrathecal Drug Delivery Systems
Ray M. Boker, M.D., andAndrew J. Cole, M.D., F.A.C.S.M.
Key Points
• Optimal candidates for neurostimulation (NS) and intrathecal drug delivery systems
UDDS) are patients in whom:
• More conservative therapies have failed.
• An observable pathology exists that is concordant with the pain complaint.
• Further surgical intervention is not indicated.
• No serious untreated drug habituation exists.
• Psychological evaluation and clearance for implantation has been obtained.
• No contraindications to implantation exist.
• A screening test has been successful.
• Patients who have lIffIf'optJtItic pain in an appropriate anatomic distribution respond best
to neurostimulation (NS).
• Patients who have nociceptive pain in an appropriate anatomic distribution respond best
to Intrathecal Drug Delivery Systems (IDDS).
• Patients who fail neurostimulation may be candidates for intrathecal drug delivery
systems.
• NS and IDDS are expensive procedures that should be performed only after
appropriate patient screening and only by physicians specifically trained and
dedicated to performing the procedure.
• Long-term outcome studies indicate that NS can produce a 500/0 or greater reduction in
pain.
• Long-term outcome studies for IDDS are not available.
• Complication rates for NS and IDDS are very low when performed by physicians
specifically trained and dedicated to their use.
• Both procedures are usually completely reversible.
I. General Concepts
A. Pain classifications (may exist alone or in combination; one usually predominates)
1. Neuropathic pain
a. Definition
i. Pain resulting from trauma or disease evoked injury to the peripheral
nerves, posterior roots, spinal cord, or brain.
b. Pain description
i. Burning
ii. Lancinating
iii. Electrical
361
362 Imp/anlables: Neurostimulation and Inlrathecal Drug Delivery Syslems
FIGURE 1. Indications for neurostimulation and Intrathecal drug delivery systems.
c. Examples
i. Direct nerve root injury-radiculopathy
(a) Battered root syndrome
(b) Perineural fibrosis
(c) Intrafascicular fibrosis
(d) Adhesive arachnoiditis
ii. Peripheral deafferentation
(a) Phantom limb pain
(b) Sympathetic mediated pain syndrome
(c) Herpetic neuralgia
(d) Diabetic polyneuropathy
iii. Central deafferentation-thalamic stroke
2. Nociceptive (somatic) pain
a. Definition:
i. Pain resulting from nociceptor activation in response to the destruction
(or threatened destruction) of tissue.
ii. Results from mechanical, thermal, or chemical trauma to peripheral noci-
ceptors
b. Pain description
i, Dull
ii. Aching
iii. Throbbing
iv. Boring
Implanlablss: Neurostimulation and Inlrathecal Drug Delivery SyslflmS 363
c. Examples
i. Mechanical low back pain
(a) Discogenic pain
(b) Joint pain
(i) Zygapophyseal (facet) joint
[ii] Sacro-iliac joint
ii. Pseudarthrosis
iii. Osteoporosis
iv. Musculoskeletal trauma
3. Combined nociceptive/neuropathic components
a. Examples
i. Failed back surgery syndrome (FBSS)
ii. Idiopathic chronic pain syndrome
iii. Cancer pain (may include only nociceptive or neuropathic components,
but often includes both)
B. Algorithm for chronic pain management
I. Primary interventions
a. Activity modification
b. Medications
i. Nonsteroidal anti-inflammatory drugs (NSAIDs)
ii. Non-narcotic analgesics
c. Physical therapy
i. Passive
ii. Active
d. Mobilization / manipulation
e. Accupuncture
2. Secondary interventions
a. Injections
i. Diagnostic
ii. Therapeutic
b. Medications
i. Antidepressants
(a) Tricyclics (TCAs)-amitriptyline, nortriptyline
(b) Selective serotonin reuptake inhibitors (SSRIs)-Prozac, Paxil, Zoloft,
etc.
(c) Others-Wellbutrin, Effexor, etc.
ii. Anticonvulsants-Neurontin, Gabatril, Tegretol, etc.
iii. Muscle relaxants
iv. Class 3 narcotics-hydrocodone, propoxyphene, etc.
c. Primary surgical intervention
d. Psychological intervention
3. Tertiary interventions
a. Medication
i. Class 2 narcotics
(a) Extended release formulations of: morphine, oxycodone, fentanyl.
(b) Immediate release formulations of: morphine, oxycodone, methadone.
b. Secondary and salvage surgical intervention
c. Multidisciplinary chronic pain program
d. Neurostimulation and intrathecal drug delivery system
C. False perceptions regarding implantable technologies
I. Fear of complications from implantation-Too invasive'
364 Implanlables: Neurostimulation ond Inlrathecal Drug Delivery Syslems
a. "Spinal cord stimulator" and "morphine pump"connote high risk procedures,

though complication rate islow.
2. Fear of creating drug-addicted patient with IDDS-"Too strong"
a. roDS may even be used in appropriate patient with history of treated addic-
tion since drug is contained and controlled
3. Fear of cost burden for managed care system-"too expensive"
a. Less expensive over several years than large doses of oral class 2 opiates
D. Psychological assessment-strongly encouraged prior to consideration of implant of NS or IDDS
I. Purpose
a. Exposes psychological factors that should be addressed in treatment
b. Suggests specific treatments that may help resolve psychological risk factors
c. Facilitates patient selection for specific pain therapies
d. Provides clues to evaluate the patient's response to a screening test or treat-
ment.
2. Assessment tools
a. Minnesota Multiphasic Personality Inventory (MMPI)
b. Symptom Checklist 90 (SCL-90)
c. Multidimensional Pain Inventory
d. Coping Strategies Questionnaire
e. Presurgical Psychological Screening (PPS)
II. Neurostimulation
A. Description of system
I. Each neurostimulation system consists of:
a. One or two leads which deliver electrical stimulation to the spinal cord or
targeted peripheral nerve
b. An extension wire which conducts electrical stimulation from the power
source to the lead
c. A power source which generates the electrical stimulation
2. Two types of neurostimulation systems
a. Completely internal (surgically implanted)-the power source (battery) and
lead(s) are surgically implanted.
b. Both internal and external components-a radio-frequency receiver and
leads are implanted, and the power source is worn externally with an an-
tenna over the receiver.
3. The neurostimulation system is typically implanted in a two-stage procedure,
separated by a trial screening period lasting approximately 3 to 10 days.
B. Mechanism of pain control/potential benefits of system
I. Electrical activation the body's pain inhibitory system (Melzack and Wall's
"gate theory" of pain)
a. Stimulates pain-inhibiting nerve fibers, masking the sensation of pain with a
tingling sensation (paresthesia).
2. Goal of neurostimulation is reduction NOT elimination of pain.
a. Improve pain relief (a majority of patients may experience at least 50 per-
cent reduction in pain)
b. Increase activity levels
c. Reduce use of narcotic medications
3. NS may also lead to reduced hospitalizations and surgical procedures, reduced
health care costs, greater independence, and improved quality of life.
C. Indications: Neuropathic pain
I. Pain locations
Implanlables: Neuroslimu/alian andIntrathecal Drug Delivery Syslems 365
a. One or both lower extremities

b. Not for primary back (axial) pain
2. Pathology
a. Failed Back Surgery Syndrome (FBSS)
i. Often mixture of nociceptive/neuropathic components
ii. Best neurostimulation candidate has radicular (neuropathic) pain> axial
(nociceptive) pain.
iii. Advances in neurostimulation technology are blurring this distinction.
(a) Dual lead placement with greater coverage of back pain
(b) Longer eight electrode arrays which cover both leg and back pain ar-
eas
b. Direct nerve root injury-radiculopathy
i. Battered root syndrome
ii. Perineural fibrosis
iii. Intrafascicular fibrosis
c. Adhesive arachnoiditis
d. Peripheral deafferentation
i. Sympathetic mediated pain syndrome, complex regional pain syndrome
(eRPS, RSD)
ii. Diabetic polyneuropathy
iii. Phantom limb pain
iv. Herpetic neuralgia
3. Patient selection criteria (Fig. 2).
a. More conservative therapies have failed.
FIGURE 2 Screening algorithm for neurostimulation.

366 Implanla&les: NfHlrostimulotion and Inlralhecal Drug Delivery Syslems
b. An observable pathology exists that is concordant with the pain complaint.

c. Further surgical intervention is not indicated.
d. No serious untreated drug habituation exists.
e. Psychological evaluation and clearance for implantation have been ob-
tained.
f. No contraindications to implantation exist.
g. A screening test has been successful.
D. Medical contraindicatlons
I. Absolute
a. Coexisting stimulator [e.g., pacemaker, implanted cardiac defibrillator)
b. Pregnancy
c. Cancer as cause of the pain problem
d. Drug addiction-psychological patterns include
i. Hoarding
ii. Theft
iii. Substance abuse (e.g., alcohol)
iv. Multiple provider prescriptions
v. Drug-seeking behavior
e. Death anticipated within 1 year due to concurrent medical condition
2. Relative
a. Anticoagulation therapy-must be temporarily reversed
b. Severely compromised cardiac status-must be medically cleared
c. Psychopathology
d. Failure to respond to appropriate ongoing psychological and/or medication
intervention
e. Stable pain state > 1 year
f. Poor intellectual capacity
i. Patient must be able to understand and use technology.
ii. Family member may assist.
E. Choice ofsystem
I. Implanted epidural lead-The lead is a small conductor with a set of electrodes
that delivers electrical stimulation to the spinal cord or the peripheral nerves.
a. Number of leads
i. One lead for unilateral pain pattern
ii. Two leads for bilateral pain, complex pain pattern, or unilateral pain
with significant back pain component.
b. Types of leads (Table I)
i. Percutaneous lead most commonly used-quadripolar (4 electrodes) or
octapolar (8 electrodes) with cylindrical electrode design for delivering
stimulation
ii. Surgical lead (laminectomy-introduced) less commonly used-quadripolar
leads with plate electrodes to create multiple stimulation combinations
and a broad area of paresthesia
2. Power source
a. Types
i. Internal (subcutaneous) implantable battery with direct communication
with epidurally placed leads
ii. Single use-lasts 1-5 years depending upon usage, battery type.
iii. Rechargeable-not yet available, but battery will be recharged via com-
munication with external charger.
iv. Externally worn battery communication via radio frequency (RF) with
Implanlables: Neurostimulation andIntrathecal Drvg Delivery Syslems 367
Table" Pros and Cons ofPenutaHous and Surgical Lead Placement

Percutaneous Lead Surgical Lead
Cost Higher Less
Complications/risk Higher Less
Recovery Longer Shorter
Stimulation strength Greater Less
Stimulation stability More stable Morevariable
Need for revision Infrequent More frequent
subcutaneously implanted radio receiver in direct communication with

epidurally placed leads
b. Choice of power source
i. Internal (subcutaneous) implantable battery preferred when appropriate
(a) Better choice if battery replacement predicted to be infrequent
(> 18-24 months)
(b) Greater surgical costs and morbidity associated with battery replacement
than with RF system
(c) $8,000-12,000 for each battery replacement every 18 months to 5 years
(depending on level of use)
(d) Cosmesis-excellent patient acceptance because all components are inter-
nal and therefore not visible
ii. Externally worn battery
(a) Better choice if < 18 months of battery life predicted because of heavy
energy demand
(b) Lower overall cost / risk: no surgical battery replacement costs or mor-
bidity
(c) $1400 maximum cost for annual 9-volt battery replacement; lower if
rechargeable batteries are used
(d) Cosmetically less appealing
F. Implantation
I. Stage I: Percutaneous lead placement and intraoperative test stimulation
a. In an outpatient/day surgery setting, the physician places and positions the
percutaneous lead through a needle, so that the stimulation pattern covers as
much of the patient's pain pattern as possible. (Fig. 3).
b. The lead is connected to the screener (temporary power source) to enable the
implant team to conduct intraoperative test stimulation. The screener is used
to set amplitude, pulse width, rate, and lead selections.
c. As the lead is positioned and electrode selections are changed, the patient
provides feedback about the location and intensity of paresthesia. This give-
and-take between patient, physician, and other members of the implant team
is critical to locating the best lead position and electrode selections for that
patient.
d. The lead should be adjusted so that paresthesia covers the painful area as
fully as possible (sweet spot).
e. Some clinicians choose to implant a lead temporarily for the screening test.
Leads implanted using a temporary implantation protocol are typically re-
moved within 10 days.
f. If lead placement and intraoperative test stimulation is successful, the next
step is the screening test period.
g. If the stimulation achieved is unsatisfactory to the patient during the proce-
368 Implantables: Neurostimu/ation and Intrathecal Drug Delivery Syslems
FIGURE 3. Vertebral level of lead placement for typical pain patferns.
dure itself and the patient does not wish to continue, the temporary screen-
ing lead is removed, and the patient can be evaluated for other therapies.
2. Stage II: Screening test period
a. Purpose
i. Evaluation of the impact of stimulation on the patient's pain and daily
life
ii. A low-cost means of evaluating the effectiveness of the therapy
iii. Exclusion of non-responding patients prior to system implantation
iv. Identification of lead position and stimulation parameters
v. A method of demonstrating efficacy to both third-party payers and re-
view organizations
vi. Opportunity for the patient to develop an understanding of the technol-
ogy and realistic expectations of the therapy.
b. Length of test period
i. Usually 3-10 days.
[a] During this time the patient is carefully educated and encouraged to
try different parameter settings to optimize and fully "test" neu-
rostimulation.
c. Screening assesment
i. Did the stimulation continue to "cover" the painful area with paresthe-
sia?
ii. Was the paresthesia an agreeable sensation?
iii. Did the paresthesia relieve the patient's pain during activities which typi-
cally provoke pain?
Implontables: NeurosHmulaHon ana Inlralhecal Drug Delivery Syslems 369
iv. What percentage pain relief was achieved with stimulation? (Was it
50-700/0 or greaterr)
v. Did activity levels rise consistent with pain reduction?
vi. Was the patient capable of understanding the technology and operating
the screener?
d. Screening test conclusions
i. If the patient responds positively to a neurostimulation system during the
test period, a complete neurostimulation system is implanted.
ii. If the patient does not respond positively to neurostimulation during the
screening test period, the lead is removed.
(a) Consider !DDS, or
(b) Consider referral to chronic pain facility for long-term management.
3. Stage III: Implantation of permanent internal or external power sources
a. Place or access lead(s)
i. Percutaneously place new leadls] through small incision, or
ii. Access previously percutaneously placed lead(s), or
iii. Place surgical lead(s) via thoracic laminectomy approach.
b. Form subcutaneous abdominal pocket and implant programmable power
source or radio receiver
i. Internal power source-battery implanted
ii. External power source-radio receiver implanted
(a) Antenna and power source positioned over receiver to be worn on
patient's belt
c. Connect internal power source or radio receiver to leadls] via percutaneously
tunnelled extension wire.
4. Stage IV: Postoperative follow-up
a. Patient follow-up in 7-10 days, opportunity to:
i. Adjust stimulus parameters
ii. Provide further patient education
b. Rechecks
i. 4 weeks after placement
ii. 6 months after placement
iii. 1 year after placement
iv. Annually
v. At end of battery life for implantable battery (1-5 years)
G. Long-term outcome
1. With 20-year follow-up, 50% of patients report ~ 50% pain relief.
2. 58% reported reduction or elimination of analgesic intake.
3. 54% of patients < 65 years old were working at follow-up vs. 41010 pre-
operatively.
4. Implantation does not negatively affect-and may improve-return to work.
H. Complications
1. Lead migration or breakage-occurs in up to 25% of percutaneously placed
leads
a. Lead revision or replacement required
b. If recurrent, consider surgically placed lead
2. Failure of device to provide continuous levels of pain relief despite multiple re-
programming attempts
a. Remove lead and power source
b. Consider referral to chronic pain facility for long-term management
3. Infection « 5% of cases)
370 Implontables: Neurostimulotion ond Intrathecal Drug Delivery Syslflms
a. Remove device
b. Treat infection
c. Reimplant when infection clears
4. Neurologic injury « 1Ofo of cases]
a. Remove device
b. Appropriate surgery
c. Consider referral to chronic pain facility for long-term management
5. Mechanical device failure (rarel-replace defective components
III. Intrathecal Drug Delivery System

A. Description ofsystem (Fig. 4)
1. An implantable, programmable drug delivery system is used to treat pain, spas-
ticity, and cancer.
2. It consists of the following components:
a. An implantable, programmable pump placed abdominally in a subcutaneous
pocket
b. An intrathecal catheter which is tunneled under the skin and connected to
the pump
c. An external programmer
3. Medication is delivered from the pump reservoir, through the catheter, and into
the CSF at constant or variable flow rates.
B. Mechanism ofpain control and potential benefits ofIDDS
1. Mechanisms
a. Chronic Pain
i. Opioids inhibit the release of substance P and other neurotransmitters by
binding to opioid receptors in the brain and spinal cord.
b. Spasticity:
i. Baclofen decreases muscle tone directly, resulting in less spasticity.
2. Potential benefits
a. Intrathecal drug delivery delivers drug directly to the CSF, resulting in much
smaller effective doses.
FIGURE 4. Medtronic Synchromed EL intrathecal drug deliv-

ery system.
Implantable5: Neuro5timulation and Intrathecal Drug Delivery SyJtem5 371
i. Effective intrathecal dose is 1/300 oral morphine dose.

ii. Reduced drug dosage equates to greater effect to side effect ratio.
b. Reduced risk of infection compared to the long-term use of external systems.
c. Internal system usually does not restrict daily activities.
d. Programmable system allows adjustment of doses non-invasively, minimiz-
ing patient discomfort.
e. Advanced programming options allow delivery of medication at variable
rates throughout the day.
e. Indications: nociceptive and/or neuropathic pain
1. Chronic intrathecal infusion of morphine for chronic, intractable pain of malig-
nant and/or benign origin
a. Pain location
i. Lumbar axial and/or radicular pain
b. Pathology
i. FBSS
ii. Osteoporosis
iii. Cancer
iv. Musculoskeletal trauma
v. Chronic pseudarthrosis
vi. Idiopathic chronic pain syndromes
c. Patient selection criteria
i. Failure of oral/transdermal opiate use for pain control or untoward side
effects at therapeutic level
ii. More conservative therapies have failed.
iii. An observable pathology exists that is concordant with the pain com-
plaint.
iv. Further surgical intervention is not indicated.
v. No serious untreated drug habituation exists.
vi. Psychological evaluation and clearance for implantation has been ob-
tained.
vii. No contraindications to implantation exist.
vm. A screening test has been successful.
2. Other uses for implantable drug delivery systems
a. Chronic infusion of baclofen for severe spasticity of spinal or cerebral origin
b. Chronic intravenous infusion of clindamycin for the treatment of os-
teomyelitis.
c. Chronic intravascular infusion of chemotherapy for the treatment of cancer:
i. Floxuridine (FUDR), doxorubicin, methotrexate, cisplatin
D. Medical contraindicatlons
1. Absolute
a. Pregnancy
b. Allergy to proposed medications to be used with IDDS
c. Drug addiction-psychological patterns include:
i. Hoarding
ii. Theft
iii. Substance abuse, e.g., alcohol
iv. Multiple provider prescriptions
v. Drug-seeking behavior
d. Death anticipated in < 3-6 months (not cost-effective)
2. Relative
a. Anticoagulation therapy-must be temporarily reversed
372 Implanlables: NeurostimulGtion ancllnlrathecal Drug Delivery SyslemS
b. Severely compromised cardiac status-must be medically cleared

c. Psychopathology
d. Failure to respond to appropriate ongoing psychological and/or medication
intervention
e. Age
f. Desire for pregnancy
i. Medications can cause amenorrhea
E. Implantation
1. Stage I-trial drug delivery
a. Setting: Inpatient or outpatient, depending upon the type of trial per-
formed
i. Inpatient trial more common
b. Method: Intraspinal or epidural morphine is administered via a lumbar
puncture or percutaneous catheter
i. Bolus injection, or
ii. Continuous infusion (more common)
2. Stage II-screening period (evaluation of trial drug delivery)
a. Occurs immediately after injection (bolus), or during the period of drug
infusion (catheter)
b. Purpose
i. Evaluation of the impact of intrathecally delivered medication on the
patient's pain and daily life
ii. Low-cost means of evaluating the effectiveness of the therapy prior to
implantation
iii. Exclusion of non-responding patients prior to system implantation
iv. Identification of drug and dosage parameters
v. A method of demonstrating efficacy to both third-party payers and
review organizations
vi. Opportunity for the patient to develop an understanding of the technol-
ogy and realistic expectations of the therapy.
c. Length of trial period
i. Usually 1-7 days.
d. Trial assessment
i. Did the medication adequately relieve the patient's pain during activities
which typically provoke pain?
ii. What percentage pain relief was achieved? (Was it 50-70 % or
greater?)
iii. Did Activity levels rise consistent with pain reduction?
iv. Were there a lack of serious medication side-effects, or were the side-
effects well controlled?
(a) Urinary retention
(b) Nausea, vomitting
(c) Pruritus
e. Screening trial conclusions
i. If the patient responds positively during the trial period, a permanent
system is implanted.
ii. If the patient does not respond positively during the screening test
period, the catheter (if present) is removed.
(a) Consider referral to chronic pain facility for long-term manage-
ment
Implantables: Neurostimulation ancllntralhecal Drug Delivery Systems 373
3. Stage III-implantation of permanent system

a. Percutaneously place new intrathecal catheter through small incision, or
access previously placed catheter
b. Form subcutaneous abdominal pocket and implant programmable pump
c. Connect subarachnoid (intrathecal) catheter to programmable pump.
d. Fill pump reservoir with drug to be used, and program pump.
4. Stage IV-post-operative follow-up
a. Patient follow-up in 7-10 days, opportunity to:
i. Adjust medication dosing parameters
ii. Provide further patient education
b. Rechecks
i. 4 weeks after placement
ii. At end of battery life for implanted programmable pump (3-5 years)
c. Pump refills as needed-anticipated in 60-90 days, depending on drug con-
centration and patient use
i. Pump refills performed percutaneously as outpatient procedure under
local anesthetic.
F. Long-term outcome
1. No studies assess long-term outcome.
2. For chronic pain, additional medicationls) can be used when morphine alone is
not sufficient to control pain.
a. Bupivacaine (marcaine)
b. Other opiates
i. Hydromorphone
ii. Meperidine
c. Clonidine
G. Complications
I. Tachyphylaxis (drug tolerance)
a. 100% prevalence-patient requires larger doses of narcotic to achieve same
result.
b. Usually slow occurring, and is treated with gradual increases in medication
dose.
2. Infection « 5% of cases)
a. Remove device
b. Treat infection
c. Reimplant when infection clears
3. Neurologic injury « 1% of cases)
a. Paraparesis or paraplegia
i. Catheter tip granuloma
ii. Idiopathic
b. Management
i. Appropriate surgery, including removing or revising catheter and drug
delivery system
ii. Consider referral to chronic pain facility for long-term management
4. Mechanical device failure (rare)-replace defective components
IV. Crossover: Combined NS and IDDS

A. On exceedingly rare occasions both procedures may be used simultaneously for the benefit of
conditions having both nociceptive and neuropathic pain components. Patients must meet all
preimplant criteria for each implant.
374 Implantables: Neurostimulalion ami Inlralhecal Drug Delivery Syslllms
v. Who performs the procedure?

A. Physicians spedahzing in pain management
1. Anesthesiologists
2. Physiatrists
3. Neurologists
4. Neurosurgeons
5. Orthopedic surgeons
References
I. Barolat G, et al: Mapping of sensory responses to epidural stimulation of the intraspinal neural struc-
tures in man. J Neurosurg.1993;78:233-239.
2. Bell G, Kidd 0, North R: Cost-effective analysis of spinal cord stimulation in treatment of failed back
surgery syndrome. J Pain Symptom Mgmt 1997;13(5):286-295.
3. Burchiel K, et al: Prospective, multicenter study of spinal cord stimulation for relief of chronic back
and extremity pain. Spinel 996;2 1(23):2786-2794.
4. Burchiel K, et al: Prognostic factors of spinal cord stimulation for chronic back and leg pain. J
Neurosurg 1995;36:1101-1111.
5. Burchiel KJ, Johanes TJ: Management of Postherpetic Neuralgia with Chronic Intrathecal Morphine.
San Francisco, American Pain Society, 1992.
6. Daniel MS, Long C, Hutcherson WL, et al: Psychological factors and outcome of electrode implanta-
tion for chronic pain. Neurosurgery 17:773-777, 1985.
7. Devulder J, DeCovenaer L, Raleigh G, et al: Spinal cord stimulation in chronic pain therapy. Clin J
Pain 6:51-56, 1990.
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infusion. Appl Neurophysiol 50:425-426, 1987.
9. Holsheimer J: Computer modelling of spinal cord stimulation and its contribution to therapeutic
efficacy. Spinal Cord.1998:36,53 1-40.
10. Krames E: Intraspinal opioid therapy for chronic nonmalignant pain: Current practice and clinical
guidelines. JPSM (6):333-352, June 1996.
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Pain Symptom Manage 8:36-45, 1993.
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thetic dystrophy. Neurosurg 1997;40(3):503-509.
13. Kumar K,Toth C, Nath R: Spinal cord stimulation for chronic pain in peripheral neuropathy. Surg
Neurol 1996;46(4):363-369.
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Pump Delivery System. Adelaide, Australia, International Association for the Study of Pain, 1990,
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Surg Neurol 1998;49: 142-144.
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17. North R, Kidd 0, Lee M, Piantodosi S: A prospective, randomized study of spinal cord stimulation
versus reoperation for failed back surgery syndrome: Initial results. Stereotact Funct Neurosurg
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1 - - - - - - - -22
Percutaneous Intradiscal Therapies
Ray M. Baker, M.D., and Andrew J. Cole, M.D., F.A.C.S.M.
Key Points
• Patients with ongoing low back or lower extremity pain resulting from uncomplicated
anular tears or contained disc herniations, who have failed to improve despite at least 6
months of comprehensively applied non-operative care, are candidates for
percutaneous intradiscal therapy.
• Patients with axial (low back) pain > radicular may pain respond to Intradlscal
electrothermal therapy (lDET).
• Patients with radicular pain > axial pain may respond to percutaneous disc
decompression (PDD).
• Patients with well maintained disc height (:f:500/0) may respond to these therapies.
• Provocation discography is an integral part of the patient selection process, and
must be properly performed.
• The science of percutaneous intradiscal therapies is still in its infancy.
• The precise therapeutic mechanisms of action of both IDET and PDD are unknown.
• Technology and basic science in the area of percutaneous intradiscal therapies is
rapidly advancing, and patient selection criteria are evolving.
• Although many still view both technologies as experimental,
• 2-3 year outcome data for lDET support:
• Maintained benefits over time.
• No advancement of disc deterioration.
• Low complication rates when performed by physicians specifically trained and
dedicated to its use.
• Similar outcome data for PDD are unavailable.
I. History of percutaneous disc therapies

A. Chemonudeolysls using chymopapain
1. Rationale
a. Chemical dissolution of disc nuclear material via enzyme.
b. Decreased disc volume, decreased intradiscal pressure, decreased posterior
anular pressure.
c. First performed in 1963.
2. Problems
a. Ongoing enzymatic action, over-decompression, disc collapse, lumbar insta-
bility.
b. Higher than acceptable complication rates.
i. 55 catastrophic events in first 100,000 cases.
(a) Transverse myelitis
(b) Paraplegia
(c) Anaphylactic reaction (0.50/0)
375
376 Percutaneous IntraJiscol Therapies
B. Automated percutaneous lumbar discectomy (APLD)

1. Rationale
a. Uses cutting probe with suction applied to decompress the nucleus, de-
creased intradiscal pressure, decreased size of contained disc herniation.
b. APLD first performed in 1975.
2. Problem
a. Large probe, cumbersome and expensive equipment.
b. Questionable efficacy.
C. Percutaneous laser discectomy (PLD)
1. Rationale
a. Vaporization of nuclear material, decrease in intradiscal pressure.
b. YAG laser first used for disc decompression in 1991.
2. Problem
a. Large amount of heat is generated.
i. 'Over-decompression' can occur.
ii. Risk to surrounding tissue (spinal nerves).
iii. Gas build-up, rapid and dangerous increase in intradiscal pressure.
b. Very expensive equipment to purchase or lease.
D. IDEl and Nucleoplasty
1. Designed to address concerns with prior technologies.
a. More controllable heating I ablation.
b. Increased patient safety.
c. Less cumbersome design.
d. Less expensive equipment.
II. Intradiscal Electrothermal Therapy-IOET

A. Introduction
1. A typical IDET system consists of:
a. An introducer needle (Fig. 1)
b. A navigable catheter with an 'active' tip.
c. A generator used to produce and control the heating of the catheter tip.
2. Technique
a. The catheter is threaded internally around the disc until the desired portion
of the disc is covered.
i. The objective is to place the catheter circumferentially across the painful
portion of the anulus fibrosis, across the radial fissure, and parallel to
any circumferential fissures (Fig. 2a).
FIGURE 1. Lateral view of correct Oratec

IDEI introducer placement.
Percutaneous Inlradiscol Therapies 377
FIGURE 2. Sagittal section of discshowing (AI representation of leftposterolateral circumferential ~ssures and
correctOratec SpineCath placement; (8) representation of thermal lesion during treatment.
b. The catheter is then connected to the generator and is heated to a set tem-
perature over a defined period of time (Fig. 2b).
B. Rationale
I. Lumbar intervertebral discs can generate pain.
a. The posterior anulus is innervated with nociceptors.
b. Direct posterior disc manipulation at surgery results in pain.
2. Internal disc disruption (IDD) is thought to be the most common cause of
chronic low back pain. (Fig. 3)
a. Prevalence of IDD at least 400/0 in patients with chronic low back pain.
i. IDD may result in pain through:
(a) Mechanical sensitization of posterior anular nociceptors.
(b) Chemical sensitization of posterior anular nociceptors.
3. Precise therapeutic effectls) not established; however, proposed mechanisms of
action include:
a. Heating collagen to > 60· C results in contraction, stiffening and strength-
ening of the collagen against mechanical nociception.
b. Denaturation or deactivation of inflammatory/degradative enzymes or other
chemicals, reduction of chemical nociception.
c. Application of direct thermal energy, coagulation of intradiscal/posterior an-
nular nociceptive pain fibers.
FIGURE 3. Cross-section of disc with right postero-

lateral anular tear.
378 Perculaneous Intradi5CQ1 Therapies
C. Indications
1. Low back pain
a. Axial pain> radicular pain.
2. Provocation discography proven painful internal disc disruption.
3. Pain despite at least 6 months of comprehensively applied non-operative care.
4. Surgery as the sole other therapeutic option.
5. Posterior mechanical (facet or sacro-iliac joint) pain has been excluded.
D. Patient selection
1. Properly performed provocation discography with reproduction of the patient's
usual pain at the target disc.
a. Provocation discography is a technically demanding procedure that should
be performed only by experienced clinicians using both International
Association for the Study of Pain (IASP) and International Spine Injection
Society (ISIS) criteria and protocols.
2. Concordant pain reproduction of at least moderate intensity.
3. Non-painful 'normal' controls in at least one and preferably 2 adjacent discs.
4. Post-discography CT revealing a grade 3 or greater anular tear (Dallas discogra-
phy classification).
5. Disc height :j: 500/0 (preferably 800/0) of normal.
6. Pearls
a. Patients with disc defects confined to one quadrant of posterior anulus re-
spond better.
b. Discs with a single discrete tear respond best.
c. At most, 2 levels should be treated. Three level 'positive' discograms are
considered an indeterminate result.
d. Previous surgery is not a contra-indication, as long as all other criteria are
met.
1. Specific
a. Indeterminate results of provocation discography
i. Atypical or 'nonconcordant' pain production with stimulation of target
disc.
ii. More than 2 positive discs.
iii. No asymptomatic disc upon pressurization (negative control level).
b. Primary radicular pain.
c. Spinal stenosis.
d. < 500/0 disc height remaining.
e. Sequestered or extruded disc fragment at target level.
f. Spondylolisthesis at target level.
g. Mechanical instability at target level.
2. General
a.Medical or psychological instability.
b. Bleeding diathesis.
c. Evidence of active infection.
d. Pregnancy.
e. Patient unwilling or unable to consent to the procedure.
F. Post-procedure care
1. Patients wear a lumbar corset for 6-8 weeks following the IDET procedure.
2. Sitting is limited to 30-45 minutes at a time for the first 6 weeks.
3. Sedentary duty allowed at 1-3 weeks after the procedure, but sitting longer
than 30 minutes at a time is avoided.
Perculaneous Inlradiscal Therapies 379
4. Driving is prohibited for the first 5 days, then only 20-30 minutes at one time
for the first 6 weeks.
5. Riding as a passenger acceptable for up to 45 minutes in a comfortable seat.
6. Lifting is limited to to lbs. for the first 6 weeks.
7. Bending or twisting is avoided for the first 6 weeks.
8. Walking 20 minutes daily after the first week. Advance walking to 20 minutes
twice daily as tolerated.
9. No manipulation or massage through the treated disc levels for the first 6 weeks.
to. Stretch exercises for legs may be done (gently) after the first week.
11. No swimming for the first 6 weeks.
12. A program of graded resumption of activity, with attention to back care, com-
mencing at approximately 8 weeks, as tolerated, supervised by a physical ther-
apist or physiatrist if required.
G. Outcomes (see tables 1and 2)
1. Most studies show:
a. 20-300/0 of patients achieve excellent results (>800/0 pain relief)
b. 500/0 of patients with moderate pain relief (:j: 2 point drop in VAS)
H. Risks and Complications
1. 1 case report of cauda equina syndrome.
2. 1675 IDET procedures performed by 5 spine specialty centers.
a. 6 nerve root injuries reported.
b. 6 post-IDET disc herniations (2-12 months post-treatment).
c. 19 cases of catheter breakage
d. 8 cases of superficial skin bum.
e. 1 case of bladder dysfunction.
III. Percutaneous Disc Decompression--Nucleoplasty

A. Introduction
1. A typical POD system consists of:
a. An introducer needle
Table 1. IDEl Published Studies

Number Follow-up Compli-
Study Design of Patients Period R.sults cations
Saal JA, SaalJS. Spine Case series 25 6 months 80% improved; mean VAS None
25:3,2000 reduced from 7.3 to 3.6
Saal JA, SaalJS. Spine Prospective 62 Mean of Mean reduction in VAS of None
25:20,2000 case series 16 months 3.0; Mean change in
SF-36 Physical Function
of 20; Mean change in
SF-36 Bodily pain of 17.
Karasek M. BogdukN. Casecontrol 53 (35 active 12 months 23% complete relief of None
Spine 25:20, 2000 study treatment) pain; 60% had >50%
reduction in pain.
Singh,V.Pain Physician Original case 21 6 months >50% pain reduction in None
3:4,2000 study 67% of patients
Mauer P, Squillante D Original case 78 12-24 Decrease in VAS:j: 2 in 71% None
NASS 2001 study months of patients
Saal JA, SaalJS Prospective 58 Minimum Decreasein VAS :j: 4 in None
Spine 2002 case series 24 months 50% of patients; 83%
of Workers Comp pts
returned to work.
380 Perculaneous Inlradiscal Therapies
Table 2. IDEl Poster and Paper Presentations

Number Follow-up Compli-
Meeting Design of Patients Period Results cations
SaalJA,SaalJS, Derby R. Case series 56 6-12 50-75% 'successful' None
North American Spine months outcomes
Society, 1998
Davis T, Delamarter R, Retrospective 60 12 months 37% satisfied with proce-
et al, North American dure; 50010 dissatisfied.
SpineSociety, 2001
Thompson K, Eckel T. Retrospective 100 2 year 80010 satisfied. VAS de-
NorthAmerican Spine creased from 6.7 to 3.6.
Society,2oo1
Wetzel FT, Andersson G, Prospective 78 2 year 880f0 of patients "definitely"
et a1. North American cohort and "probably" would
SpineSociety, 2001 repeat the procedurefor
the same results. VAS
decreased from 5.3 to 3.3.
Carragee E, Khurana S, Prospective 18 (active) 12 months No significant difference
et a1. North American controlled between "declined
SpineSociety, 2001 series surqery" control and
activelDET groups.
Shadid E,Derby R, et al. Prospective 115 1-2 years Average NRS dropped from
North American Spine caseseries (mean 18 7.45 to 6.08; "1/3 better,
Society, 2001 months) 1/3 the same, 1/3 worse";
> 500/a would not repeat
the procedurefor the
same result.
b. A navigable bipolar radio-frequency wand

i. Ionized vapor 'plasma' layer ablates tissue.
ii. Heat from bipolar RF source secondarily coagulates soft tissue.
iii. Process is termed coblation = coagulation + ablation.
iv. Relatively low temperatures are used (40-70" C)
c. A generator used to produce and control the heating of the wand's tip.
2. Technique (Figs. 4 and 5)
a. The wand is advanced into the disc, through the introducer, using ablation mode.
b. The wand is then slowly removed as the nuclear material is coagulated.
c. This process is repeated forming multiple coblation 'channels' by passing the
wand at different angles.
d. The concept is to remove a portion of the nucleus, thereby reducing intradis-
cal pressure and thus reducing pressure applied to the posterior anulus.
B. Rationale
1. Contained lumbar discs herniations can generate pain.
a. Mechanical and/or chemical irritation of adjacent spinal nerve.
b. Discogenic pain-same rationale as for IDET
i. The posterior anulus is innervated with nociceptors,
ii. Direct posterior disc manipulation at surgery results in pain.
2. Precise therapeutic effect(s) not established; however, proposed mechanisms of
action include:
a. Decrease in intradiscal pressure from removal of nuclear material, decrease
in size of contained disc herniation.
b. Denaturation or deactivation of inflammatory/degradative enzymes or other
chemicals, reduction of chemical nociception,
Percutaneous Inlradiscol Therapies 381
FIGURE 4. Sagittal section of disc showing correctplacement of Arthrocare Coblation wand.
FIGURE 5. Closeup of Arthrocare Coblation wand.

382 Percutaneous Inlrodiscal Therapies
c. Application of direct thermal energy, coagulation of intradiscal/posterior an-

nular nociceptive pain fibers.
C. Indications
1. Radicular lower extremity pain
a. Radicular pain > axial pain.
2. Provocation discography proven painful internal disc disruption/contained disc
herniation.
3. Pain despite at least 6 months of comprehensively applied non-operative care.
4. Surgery as the sole other therapeutic option.
5. Posterior mechanical (facet or sacroiliac joint) pain has been excluded.
D. Patient selection
I. Properly performed provocation discography with reproduction of the patients
usual pain at the target disc.
a. Provocation discography is a technically demanding procedure that should
be performed only by experienced clinicians using both International
Association for the Study of Pain (IASP) and International Spine Injection
Society (ISIS) criteria and protocols.
2. Concordant pain reproduction of at least moderate intensity.
3. Non-painful 'normal' controls in at least one and preferably 2 adjacent discs.
4. Post-discography CT revealing a grade 3 or greater anular tear (Dallas
Discography Classification) or contained disc herniation.
5. Disc height :j: 500/0 of normal.
6. Patients with disc defects confined to one quadrant of posterior anulus respond
better to PDD.
7. At most, 2 levels should be treated. Three level 'positive' discograms are consid-
ered an indeterminate result.
8. Previous surgery is not a contraindication, as long as all other criteria are met.
1. Specific
a. Indeterminate results of provocation discography
i. Atypical or 'nonconcordant' pain production with stimulation of target disc.
ii. More than 2 positive discs.
iii. No asymptomatic disc upon pressurization (negative control level).
b. Spinal stenosis.
c. < 500/0 disc height remaining.
d. Sequestered or extruded disc fragment at target level.
e. Mechanical instability at target level.
2. General
a. Medical or psychological instability.
b. Bleeding diathesis.
c. Evidence of active infection.
d. Pregnancy.
e. Patient unwilling or unable to consent to the procedure.
F. Post-procedure care
I. Days 1-3
a. Rest for 1-3 days in position of comfort.
b. Restrict sitting or walking to 10-20 minutes.
c. No driving.
2. After 1 week
a. Begin walking 20 minutes per day; progress as tolerated to 1 hr/day over 3
weeks.
Perculaneous InlracJiscal Therapies 383
3. First 2 weeks
a. Lifting limit of 5-10 lbs.
b. No bending or twisting.
c. No swimming.
4. After 2-3 weeks
a. Begin abdominal brace exercises with back flat against floor.
5. First 6 weeks
a. Do not use treadmill or Stairmaster.
6. After 6-8 weeks
a. Begin formal physical therapy.
7. First 12 weeks
a. No manipulation through or adjacent to treated levels.
b. No traction.
G. Outcomes
1. Limited data available
a. Case reports.
b. Case series with 3 month post-procedural outcomes.
i. 86% of patients reported up to 50% reduction in pain at 3 months.
ii. No complications were reported.
2. Outcomes are promising, but placebo controlled studies are needed for valida-
tion.
H. Risks and complications
1. Too early for full assessment.
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3. Chen yc, Lee SH, Date E, Carragee E. Histology findings of discs and neural tissues status post percu-
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4. Chen Yf', Lee SH, Date E, Carragee E. Nucleoplasty (volumetric tissue ablation and coagulation of the
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study. ISIS 9th Annual Scientific Meeting, 200 I.
5. Choy DS. Percutaneous laser disc decompression (PLDD): Twelve years experience with 752 proce-
dures in 518 patients. J Clin Laser Med Surg 16(6): 325-331,1998.
6. Coppes M, Marani E, Thomeer R, et al. Innervation of 'painful' lumbar discs. Spine 1997; 22:
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plasty for back pain due to internal disc disruption. Spine 2000; 25:2601-2607.
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ment for internal disc disruption. Proceedings of the 14th Annual Meeting of the North American
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11. Lee C, Wetzel FT. Andersson G, et al. Two year post treatment evaluation of pain levels and location
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New Orleans, October 25-28, 2000, P 168.
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13. Maurer P, Squillante D. Is IDEI effective treatment for discogenlc low back pain? A prospective co-
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Annual Scientific Meeting, 2001 and Proceedings of the 16th Annual Meeting of the North American
Spine Society, Seattle, October 31-Nov 3, 2001, P 127.
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15. Saal JA, Wetzel FT, Saal JS et al. IDEI - related complications: A multi-center study of 1,675 treated
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North American Spine Society, Seattle, October 31-Nov 3, 2001, P 187.
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tradiscal thermal catheter: A pilot study. Proceedings of the 13th Annual Meeting of the North
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,--------23
The Lumbar Spine and Sports
Christopher J. Standaert, M.D., Stanley A. Herring, M.D.,
Andrew J. Cole, M.D., and Steven A. Stratton, Ph.D., P. T., A.T.C.
Key Points
• A comprehensive rehabilitation program based on an understanding of the unique
biomechanical stresses placed on the lumbar spine and its entire kinetic chain by any
given sport must be initiated immediately after injury to resolve the clinical symptoms
and signs created by the primary lumbar spine injury and any secondary sites of
dysfunction. Active treatment can then be initiated to help minimize the deleterious
effects of inactivity.
• The single best predictor for a new injury during athletic activity is history of a
previous injury.
• The severity and duration of a sports-related lumbar spine injury are influenced by
multiple factors, including history of prior injury, the athlete's age, the specific type of
injury, the level of competition, the demands of the athlete's particular sport, the time
of season at which the injury occurred, the treatment applied, and any equipment
involved.
• Sports-specific retraining occurs by breaking down the gross motions required for
performing a given sports skill into their individual component motions and training
the athlete to maintain optimal spinal positioning for each. The components are then
progressively reassembled so that the entire sporting motion occurs, using dynamic
stabilization techniques.
• Dynamic, multi-planar core stabilization techniques that are specific to the demands of
the athlete's sport are central to the rehabilitation of an athlete with a lumbar injury.
• Create a prehabilitation program based on the rehabilitation program so that optimal
physiologic and biomechanical fitness can be maintained and risk of future injury
minimized once an athlete returns to sports activities.
I. Background
A. Epidemiology of lumbar spine sports injuries
1. Very frequent site of injury in gymnastics, football, weightlifting, wrestling,
dance, rowing, swimming, and golf.
2. Less frequent but significant site of injury in skating, tennis, baseball, track and
field sports, cycling, and basketball.
3. High level sports participation in adolescents and young adults is associated
with a greater incidence of low back pain and structural abnormalities on
imaging studies.
4. Recreational sports participation in adults is not necessarily associated with a
higher incidence of low back pain and may be protective for risk of disc hernia-
tion.
5. Time lost from sports participation
385
386 The Lumbar Spine and Sports
a. Football-up to 300f0 of professionals lose playing time due to lumbar spine

pain.
b. Tennis-380f0 of men's professional tennis tour players missed at least one
tournament because of back pain.
c. Baseball-50f0 of disability list days in Major League Baseball due to back in-
juries.
6. Exact incidence and prevalence reported for specific athetic injuries can vary
significantly depending on numerous factors, including the definition of "in-
jury" used in a particular study. As such, numbers reported here and elsewhere
need to be viewed in the overall context of the study of athletic injury.
B. Epidemiology oflumbar spine pain--lessons for those treating athletes
1. 60-90% lifetime prevalence of lumbar spine pain in adults.
2. Up to 50% lifetime prevalence of lumbar pain by age 15.
3. 5-20% annual incidence of lumbar spine pain.
4. Peak incidence at 40 years old.
5. 40-50% are symptom-free within 1 week.
6. Up to 90% resolve without medical attention in 6-12 weeks.
7. 75% with sciatica have relief of pain at 6 months.
8. 60-80% of adults have recurrent low back pain after an initial occurence.
9. 25-30% of adolescents have recurrent lumbar pain.
10. Symptoms may improve, but structural changes may persist.
a. Anatomic and functional alterations may increase the chance of reinjury
b. Some anatomic alterations occur with greater frequncy in young athletes
(e.g. spondylolysis).
c. The musculoskeletal demands that sports activity creates may precipitate
more significant bone and soft tissue injuries than are seen in the general
population.
II. Fadors Influencing Iniury, Rehabilitation, and Return to Sport

A. Potential sites ofinjury
1. Musculotendinous unit (strain)
2. Ligamentous structures (sprain), including zygopophyseal joint capsule
3. Disc
a. Acute tear in anulus fibrosis
b. Herniation posteriorly! posterolaterally of nucleus pulposis
c. End plate disruption! extrusion of nucleus pulposus (Schmorl's node)
4. Vertebrae
a. Acute traumatic fracture
b. "Fatigue" fracture (e.g., isthmic spondylolysis)
c. Apophysitis or ring apophyseal injuries
5. Zygopophyseal joints
6. Pelvis (associated with low back pain)
a. Sacro-iliac joint
b. Sacral stress fracture (particularly in runners)
c. Proximal hamstring! attachment site
d. Hipjoint
7. Always consider potential medical causes of symptoms (e.g., ankylosing
spondylitis, neoplasms), particularly when symptom onset is non-traumatic or
associated with other joint or constitutional symptoms
B. Type ofinjury
1. Macrotraumatic due to a direct blow. For example, the hockey player who sus-
The Lumbar Spine and Sports 387
tains a transverse process fracture due to a direct check from an opponent to
the lumbar spine.
2. Macrotraurnatic due to an indirect blow. For example, the football player tack-
led at the thighs who sustains a lumbar spine injury, such as an anular tear.
3. Microtraumatic (repeated exposure to sub-catastrophic forces). For example, the
gymnast with facet pain or spondylolysis due to repetitive extension move-
ments.
C. Risk factors potentially associated with an increased frequency oflow back pain or lumbar injury
in athletes (some controversial)
1. Prior lower extremity injuries
2. Decreased endurance
3. Relative strength imbalance in lower extremities or lumbo-pelvic musculature
4. Leg length discrepency
5. High number of hours of training per week
6. Prior low back injury
7. Incomplete rehabilitation of a prior injury
8. Psychological issues due to stressful life events
Note: Injury patterns in athletes tend to be sport and position specific. Anthro-
pomorphic features that may be a factor in injury for some athletes may actually
be beneficial in the performance of other sports.
D. Age
1. The aging athlete
a. The number of older individuals and of those participating in sports is in-
creasing. There will be about 70 million individuals aged 65 or older in the
United States by 2030.
b. Exertional injuries in older individuals are related to degenerative changes
more frequently than are those that occur in younger individuals.
c. Multiple age-related changes occur that affect the musculoskeletal system
and may influence lumbar spine injury and rehabilitation.
i. Reduction in bone density. This makes older individuals more susceptible
to insufficiency fractures or compression fractures.
ii. Loss of strength. Age-related declines in lean muscle mass and muscle
cross-sectional area occur along with muscle atrophy due to loss of mus-
cle fibers, particulary type II fibers. The percentage of type II muscle
fibers decreases from 600/0 in sedentary young men to below 300/0 by 80
years old and is associated with declines in strength, which can diminish
by 300/0 between ages 50 and 70 and up to 300/0 per decade after that.
iii. A decrease in V0 2max of 50/0-150/0 per decade after age 25.
iv. Decreased neurophysiologic function, including changes in the vestibu-
lar, visual, and somatosensory systems.
v. Decreased postural stability.
vi. Decreased joint flexibility, particularly after age 30.
d. The body remains responsive to specific exercise into the 90s in healthy in-
dividuals. Strength training in the elderly has been associated with improved
strength, functional performance, bone density, resting metabolic rate, sleep
quality, and balance as well as reduced pain and disability from athritis,
body fat, and central adiposity.
2. The younger athlete
a. Young children and adolescents form the largest group participating in
sports.
b. Vulnerable growth regions
i. Physeal plates
ii. Joint surfaces
iii. Sites of major musculotendinous insertions
iv. Apophyses
c. Bony injuries tend to occur with overuse rather than soft tissue injuries (e.g.,
adult patellar tendinitis tends to express itself as Osgood-Schlatter disease in
the growing athlete).
d. Adolescence often associated with a marked increase in training hours and
intensity, particularly as level of competition increases.
e. Skill levels are generally lower in younger athletes.
f. Inconsistency and variability of coaching, training, and equipment may be
additional risk factors for injury.
g. Increasing maturity, size, and competitiveness result in increasing collision
forces with potential for more severe traumatic injury
h. Rates of severe spinal trauma much higher in adolescents and young adults
than in older individuals
E. Level ofcompetition
1. Occasional recreational athlete
2. Competitive recreational athlete
3. Club-level athlete
4. Institutional athlete-high school
5. Institutional athlete-university or college
6. Professional athlete or performing artist
7. Olympic athlete
8. The physiological and psychological needs vary among these athletic populations.
a. Highly competitive athletes require alternative training regimens during
their rehabilitation programs to maintain peak flexibility, strength, and
aerobic conditioning. Recreational performers may be more flexible in this
regard.
i. VOzmax can be maintained for up to 15 weeks with a reduction in train-
ing frequency of up to 66% if training duration held constant.
ii. Combined reduction in training frequency and duration that results in a
70% decrease energy demand can maintain VOzmax over 4 weeks.
iii. Maintaining the intensity of training is crucial to the retention of
VOzmax during periods of reduced activity.
b. Competitive recreational, club, institutional, professional, and Olympic ath-
letes require a specific training schedule and goals to compete or perform ef-
fectively during their particular athletic season. The occasional recreational
athlete's needs are usually not as time-dependent.
c. Specific patient goals are met by tailoring the work-up and rehabilitation
program to the level of athletic demand and needs of the individual athletes.
d. Changes in training routines and sport-specific mechanics require close co-
operation among physician, patient, therapist, trainer, and coach.
e. For professional athletes, performing artists, and very elite level athletes,
practitioners need to remember that these are really occupational injuries
that may have significant implications on future income and psychosocial
functioning; aspects of managing injured workers may readily apply to their
care. For some, the stakes are very high.
F. TIming ofsporting season
1. Preseason phase
2. Competition phase
The Lumbar Spine anJ Sports 389
a. Early phase
b. Middle phase
c. Late phase
3. Off-season phase
4. Training techniques, duration, intensity, and repetition vary during different
parts of the season and predispose the athlete to different types of lumbar spine
injuries.
G. Equipment
1. Designed to prevent a specific injury.
2. May fail and result in a lesser, same, or greater degree of injury.
3. May create a new set of unanticipated injuries at the same site or at another
location in the kinetic chain.
4. May change sporting technique in ways that offset some of the gains made in
protection from injury.
III. Rehabilitation Program Design and Progression

A. Basic principles
1. Utilize an understanding of the unique biomechanical stresses placed on the
lumbar spine and its entire kinetic chain by any given individual sport.
2. An accurate diagnosis of the acutely injured structure (the tissue injury com-
plex) is extremely helpful in planning a rehabilitation strategy. It may be nec-
essary to obtain advanced imaging earlier in elite athletes than would normally
be the case in order to appropriately plan care.
3. Understand the nature of the injury, the healing process, and the effects of
treatment.
a. Prolonged bed rest or immobilization results in decreased muscle strength,
flexibility, cardiovascular fitness, and bone density along with neural, vas-
cular, and other changes in local and systemic function.
b. Potentially deleterious effects on disc nutrition, spinal segmental mobility,
and the psychological state of the athlete may occur with injury and in-
activity.
4. Assess the entire functional kinetic chain for sites of additional injury, over-
load, or dysfunction that may be impacting the more acutely injured tissue or
global function.
5. Rehabilitation should be goal directed and comprehensive. Goals should in-
clude:
a. Resolution of the clinical symptoms and signs created by the primary injury
so that active treatment can be initiated and the deleterious effects of in-
activity minimized.
b. Restoration of optimal function and minimization of the chance of recurrent
injury by rehabilitating both the primary site of injury and any secondary
sites of dysfunction elsewhere in the kinetic chain.
c. Normalization of flexibility, strength, and endurance with the specific de-
mands of the athlete's sport in mind.
d. Restoration and optimization of cardiovascular fitness.
e. Assessment of skill technique and biomechanics.
6. Progression of activity must ultimately include sports-specific retraining for the
entire kinetic chain.
7. Dynamic multi-planar lumbar stabilization is an essential component of care in
the rehabiltiation of spine injuries in athletes.
B. Dynamic multi-planar lumbar ("core") stabilization training
390 The Lumbar Spine and Spom
1. Concepts
a. The spine and trunk serve three primary functions in sports:
i. Force generation
ii. Force transfer (e.g., from the lower extremities to the upper extremities in
throwing or golf)
iii. Force re-acquisition (e.g., deccelerating the arm after releasing a ball
when throwing)
b. Neutral spine-the initial training position that is the least painful and most
biomechanically sound.
c. "Core" muscles-for the spine, those muscles that stabilize the lumbar motion
segments during static and dynamic tasks (e.g., multifidi, transversus ab-
dominus, obliquus internus abdominus).
d. Train through progressive loading.
e. Muscle fusion-engram (cortically preprogrammed automatic multimuscular
movement patterns activated without conscious control) for neutral spine po-
sition is developed through a specific set of stabilization exercises so that the
athlete can recruit the spinal muscular stabilizers quickly and automatically.
2. Static to dynamic progression
a. Exercises progress from static (e.g., supine and/or prone) to dynamic (e.g.,
rotating, jumping).
b. Graded challenges to the neutral position are created first by gravity, then
by the therapist and or assistive devices (e.g., a Swiss ball).
c. Base of support goes from stable (floor, mat, etc.) to unstable (ball, foam roll,
etc.)
d. Challenges progress from predictable to unpredictable (simulating, for exam-
ple, a blindside hit during football).
e. Initial exercises are done with a closed kinetic chain and then progress to an
open kinetic chain.
3. Sports specific
a. The neuromuscular system is extremely specific in its response to exercise
(e.g, speed of motion, range of motion used, force generated).
b. Training needs to simulate sports-specific activities.
i. Appropriate motions.
ii. Appropriate speed of muscular contraction or joint motion.
iii. Appropriate force required.
iv. Expected perturbations of motion.
c. A thorough understanding of the motions required for a given sport is nec-
essary to plan rehabilitation.
4. Multi-planar stabilization
a. Establish a strong, effective "core" before advancing to exercises out of neu-
tral position.
b. Train the athlete to maintain spinal mechanics in all planes of motion re-
quired for sport while moving at speeds and against resistance that are nec-
essary for sports competition.
c. Sports simulation with supervision and re-training of appropriate mechanics
is essential.
IV. Failure to Progress

A. An athlete's inability to progress in terms of either pain resolution or physical
functioning should prompt an immediate re-assessment of the diagnosis and treat-
ment regimen.
The Lumbar Spineand Sporn 391
B. Further diagnostic testing [e.g., imaging, electrodiagnostic testing) may be re-

quired to clarify or confirm the diagnosis so that specific pain control techniques
can be utilized and the rehabilitation program advanced.
C. Re-assess physical therapy or training program.
1. Appropriate techniques for the correct problem
2. Pacing. The program may be advancing more rapidly than the athlete or in-
jured tissue is able to adapt. If so, back up to the previously tolerated level,
ensure that adequate time for appropriate healing has been allowed, and start
again.
3. Undiagnosed confounding factors affecting the kinetic chain.
4. Compliance. Is the athlete doing what they are supposed to be doing (either too
little or too much)?
D. Is there a need to alter the medical treatment being administered?
1. Addition or change in oral medication
2. Is there a need for a local injection (e.g., zygopophyseal joint, epidural, or
sacroiliac joint injection)? If done under fluoroscopic guidance with contrast
enhancement, the injection is both potentially diagnostic (the precisely placed
local anesthetic anesthetizes the presumed painful structure) and therapeutic
(the steroid, and possibly the anesthetic, decreases or eliminates pain that is
mediated by inflammation).
E. Is surgical intervention necessary to best progress function?
F. Distinguish between low back pain and low back pain disability. The disability
that results from injury is a product of both the painful musculoskeletal injury and
the athlete's adaptation to it (i.e., psychosocial overlay is significant).
1. Obtain a thorough social history that may provide clues to concurrent psycho-
logical issues.
2. Consider psychological intervention in addition to physical therapeutic treatment.
a. Assessment and/ or treatment through an experienced clinical psychologist
b. Medications
3. Psychological issues due to stressful life events have a direct relationship to in-
jury prevalence.
G. Athletes cannot always regain the level of function required to return to competi-
tion after an injury. In some circumstances, return to play after injury may pose
significant risks to the athlete such that continuation in the sport is not advisable.
V. Return to Play
A. Criteria
1. No symptoms or signs of the clinical injury
2. Negative provocative testing of the injury site
3. Full pain-free range of motion
4. Normal flexibility
5. Normal strength and strength balance
6. Good general fitness
7. Normal sports mechanics
8. Ability to demonstrate sports-specific skills
9. Fully informed about risks of future injury and disability
10. Properly instructed about proper warm-up, flexibility, and strength programs,
proper use of ice and heat, and reporting any increase in pain.
B. Depending on level of sports participation (e.g., high school vs. professional) and
time of the season the injury occurs, some flexibility in the criteria is possible and
should be based on sound clinical judgment.
392 The Lumbar Spine andSports
VI. Sport-specific Lumbar Spine Injuries

A. Noncontact sports
1. Baseball! Softball
a. Epidemiology
i. 5-8% of time loss/disabled list days in collegiate and professional base-
ball from low back pain/injury
ii. Upper extremity injuries most common
b. Biomechanics
i. Infielders
(a) Seek assistance for low back pain more commonly than other posi-
tions.
(b) Approximately 100 ground balls per practice, repeatedly bending
over.
(c) Sudden extreme twisting through lumbar spine, including off-balance
bending and lifting.
(d) Proper fielding mechanics are protective of the lumbar spine.
ii. Hitters
(a) Trunk stabilization important in transfer of power from lower ex-
tremities to arms.
(b) Trunk musculature needs to respond to subtle and rapid changes in
balance and position.
(c) Low back pain may prevent appropriate trunk rotation and diminish
power and bat control.
iii. Pitchers
(a) In baseball, the pitching motion represents a "controlled fall" off of
the mound and is associated with significant truncal rotation and lat-
eral flexion
(b) The lumbar spine, trunk, and hips transfer and amplify ground reac-
tion forces as they pass from the lower extremities to the shoulder
and, ultimately, to the ball.
(c) Maintaining proper trunk position during the throwing motion allows
for optimal arm positioning and may help prevent shoulder and up-
per extremity injuries.
(d) Truncal range of motion, strength, endurance, and muscular coordi-
nation are all important in maintaining appropriate throwing me-
chanics.
(i) Deficiencies in these areas can lead to decreased pitch velocity
and accuracy or musculoskeletal injury.
[ii] Fatigue of the trunk musculature may result in increased lumbar
lordosis. This places the shoulder and arm relatively posteriorly in
the throwing motion, resulting in a higher ball release point and
increased torsional forces through the lumbar spine.
iv. Catchers-low back pain uncommon
c. Rehabilitation considerations
i. The trunk predominantly acts to transfer force from the lower extremities
and to allow for appropriate postioning of the upper extremities in hit-
ting and throwing.
ii. Rehabilitation of disc and facet injuries seeks to minimize the forces
placed across the lumbar spine by correcting flexibility and strength
deficits, improving the mechanics and sequencing of each motion re-
The Lumbar Spine and Sporn 393
quired, and providing the endurance required to complete a game or

practice session while maintaining proper spinal mechanics.
iii. Work on the individual components of a particular motion in isolation
and then reassemble the primary motion. Players may do best with re-
moval from play and without being allowed to continue to practice with
their old motion patterns
2. Golf
a. Epidemiology
i. Amateur-lumbar spine most common injury.
ii. Professional-lumbar spine first or second most common injury.
iii. 290/0 of professional golfers report a history of lumbar spine pain.
iv. 900/0 of tournament level golfers have previous cervical or lumbar in-
juries.
v. More than twice the number of downswing injuries compared with back-
swing injuries because the club during downswing covers the same range
of motion as the backswing but roughly three times faster.
b. Biomechanics
i. Coordination of trunk musculature essential for efficient movement and
force transfer from the lower extremities.
ii. The lumbar spine is subject to significant lateral bending, shear, com-
pressive, and torsional forces during the golf swing.
iii. The golf swing develops a peak lumbar compression load of more than 8
times body weight in both amateur and professional golfers; running, by
comparison, produces peak lumbar compression loads of 3 times body
weight.
iv. Forces generated are greater in amateur than professional golfers and
muscular activity is also relatively increased in amateur golfers com-
pared with professional golfers, both likely reflective of worse mechanics,
muscular coordination, and consistency in amateur golfers.
v. During the "classic" golf swing, the hips tum almost as much as the
shoulders; this minimizes the torsional forces generated across the lum-
bar spine.
vi. The "modern" golf swing uses a large shoulder tum while restricting the
amount of hip rotation to build torque in the muscles of the back and
shoulders, ultimately resulting in greater club head angular velocity. At
the end of follow-through, the spine assumes a reverse C position, caus-
ing hyperextension and rotation of the lumbar spine. However, the mod-
em swing also significantly increases the torsional forces generated
across the lumbar spine and may result in a greater number of lumbar
spine injuries.
i. Retrain the golfer to use a "classic" swing instead of a "modem" swing to
help reduce torsional forces generated across the lumbar spine (i.e., re-
duce the disassociation between shoulder and pelvic rotation).
ii. Increase club length to minimize the amount of lumbar spine and hip
flexion required when addressing the ball.
iii. Use golf shoes without spikes so that the sole of the foot can rotate dur-
ing the swing, which may minimize the amount of torque developed
through the lumbar spine.
iv. Retrain the golfer to use increased elbow and wrist deviation during the
394 The Lumbar Spine and Spor1s
backswing to minimize the amount of spinal rotation required to position

the club at full backswing (transition).
v. Coordinated trunk motion, consistency, strength, flexibility, and en-
durance are all important in maintaining appropriate swing mechanics
and reducing loads across the lumbar spine.
vi. It may be helpful to retrain the golfer's swing in an isolated fashion,
eliminating the use of a golf club outside of the therapeutic arena while
participating in rehabilitaition.
3. Gymnastics
a. Epidemiology
i. Low back pain is extremely common, affecting up to 85% of gymnasts.
ii. Spine and trunk account for 12-19% of injuries reported.
iii. For the relative amounts of time spent in each, injuries occur much more
frequently during gymnastics competition than during training.
iv. The frequency of injuries in general, including lumbar spine injuries, in-
creases significantly when training exceeds 15-20 hours per week.
v. Competitive female gymnasts have a 5-fold increase in the prevalence of
spondylolysis on radiographs compared with females in the general pop-
ulation (11-14% vs. 2.3%).
vi. Disc abnormalities on MRI are more common in elite gymnasts when
compared with either non-athletes or swimmers.
vii. Former elite-level gymnasts aged 25-43 do not appear to have a greater
frequency of low back pain than controls.
b. Biomechanics
i. Facet joint: increased loads during extension and combined extension
and rotation; loading further increased with disc degeneration.
ii. Spondylolysis: believed to represent a fatigue fracture of the pars interar-
ticularis from repeated stress associated with repetitive extension and
coupled torsional motions of the lumbar spine.
iii. Herniated disc: repetitive torsional forces coupled with flexion create ex-
cessive posterior anular stress predisposing to anular disruption and disc
herniation.
iv. Herniated disc associated with an apophyseal rim lesion: can be seen in
the skeletally immature gymnast.
v. Schmorl's nodes: likely due to axial loads through the disc space; dis-
rupts nutrient flow to the nucleus and may result in premature degenera-
tion). May be associated with high axial loads at impact on dismounts.
i. Accurate diagnosis crucial in planning care given fairly high risk of sig-
nificant structural injury (as is the case for adolescent athletes in general).
ii. Comprehensive rehabilitation should include spinal and lower extremity
range of motion and progression through multi-planar dynamic stabi-
lization work for the lumbar spine given the tremendous range of motion
and combined spinal movements required for the sport.
iii. Optimize mechanics and the relative strength of the trunk and proximal
lower extremities to allow for performance of skills with reduced forces
applied to the spine.
4. Dance
a. Epidemiology.
i. Lumbar spine is 2nd most common site of injury among ballet and aero-
bic dancers, following foot and ankle injuries.
The Lumbar Spine anJ Sparn 395
ii. Lumbar spine injuries in professional ballet have the greatest cost in
terms of time lost from active participation in dance.
iii. Lumbar spine injury frequency is increasing in ballet dancers.
iv. Most dance injuries are related to overuse.
b. Biomechanics: ballet
i. Turnout, the core of ballet technique, requires bilateral 80-90° external
rotation of the hips. It is maintained during all training sessions and
most dance sequences. Its purpose is aesthetic and functional. Turnout
allows for easy initiation of multiplanar movements and allows the leg to
be raised higher (extension) because the externally rotated greater
tochanter can clear the acetabular rim during flexion and abduction.
Frequently the dancer uses compensatory lumbar hyperextension to de-
crease the tension on the iliofemoral ligament so that the dancer feels
less hip capsule strain. The abdominal muscles are not easily engaged in
this position, thus minimizing the effect of an important lumbar protec-
tive mechanism. In addition, the lumbar facet joints may bear increased
loads while in this extended position.
ii. Arabesque position is maintained by standing on one leg while posteri-
orly extending the contralateral leg to 90°. It is frequently maintained for
long periods and is also a landing position during large, powerful jumps.
The lumbar spine becomes hyperextended in this position, even when us-
ing good body mechanics. The abdominal muscles are once again in a
mechanically disadvantaged position to help control lumbar spine forces,
and the facet joints may become suddenly loaded during the axial com-
pression forces generated during a landing.
iii. Lifting injuries can occur in male dancers who lift with poor lumbar me-
chanics or who set their partner down too far from their own center of
gravity. Unintended lumbar flexion or hyperextension may result.
iv. Modern and jazz techniques require more off-balance and forceful tor-
sional movements that cause increased dynamic stresses through the
lumbar spine.
i. Correct compensatory hyperextension errors in technique in order to
minimize stress to the posterior elements of the spine.
ii. Emphasize core stabilization.
iii. During dance reintegration training, initially eliminate arabesque and
other movements that require lumbar hyperextension while retraining
the dancer to use techniques that are more protective of the lumbar
spine.
5. Racquet sports
a. Epidemiology
i. 38% of men's professional tennis players missed at least one tournament
due to lumbar pain.
ii. Roughly 9% of competitive junior tennis players have a history of lum-
bar spine injury.
iii. There appears to be no significant increase in low back pain in recre-
ational tennis players compared with controls.
b. Biomechanics
i. The serve (and overhead) likely places the greatest load on the lumbar
spine. During the toss, the lumbar spine initially hyperextends and ro-
tates away from the net and then laterally flexes. The shoulders and
trunk subsequently rotate as the trunk flexes forward toward the net.
Significant compressive, shear, and torsional forces are likely imparted to
the disc by this mechanism.
ii. The forehand groundstroke generally involves 90 degrees of axial rota-
tion. Poor mechanics may create increased torque across the lumbar
spine if the shoulders rotate ahead of the hips.
iii. The one-handed backhand uses less trunk rotation than the forehand be-
cause the dominant hitting shoulder is already facing the net. The two-
handed backhand requires greater rotation than the one-handed back-
hand as the nondominant shoulder must rotate more completely during
follow-through.
iv. Elite tennis players show significantly greater trunk strength in lateral
flexion on their non-dominant side. This may be related to the need for
powerful lateral trunk flexion out of the hyperextended and rotated posi-
tion in serving. It is unclear if this is an appropriate adaptive imbalance
to allow for high level function or if this potentially represents a "patho-
logical" imbalance related to low back pain.
c. Rehabihtation considerations
i. During the serve and overhead, it may be helpful to train the player to
flex the knees instead of hyperextending the lumbar spine.
ii. During the forehand and backhand, train the player to keep the shoulders
more aligned with the hips to minimize excessive rotation across the
lumbar spine.
iii. As with other sports, it is essential to train the athlete to perform indi-
vidual trunk motions with appropriate mechanics, coordination, strength,
and endurance of the required musculature. Maximize trunk strength and
endurance through multi-planar work that mimics the service or ground-
stroke motion desired.
6. Bicycling
a. Epidemiology
i. Studies indicate 2.7-15% of cyclists have had lumbar spine pain, and
63% have reported buttock and ischial tuberosity pain.
ii. 72% of the 1986 Hawaii Iron Man Triathlon reported having lumbar
spine pain or sciatica.
iii. A study on 92 triathletes reported that 32% of the athletes experienced
low back pain in the prior year. Bicycling was believed to be a potential
major risk factor for low back pain in triathletes.
b. Biomechanics
i. A short stem/tube length and/or a handlebar position that is too high re-
sults in increased lumbar lordosis and consequently increased loads
across the facets.
ii. An elongated stem/tube length and/or a handlebar position that is too
low results in a more flexed lumbar spine position and consequently in-
creased loads across the disc.
iii. If the bike seat is too high, the rider laterally flexes the lumbar spine to
the pedal. A rider with a leg length and/or strength discrepancy laterally
flexes to the short and/or stronger leg side.
iv. High performance cyclists flex their hips and make their pelvis horizon-
tal with a relatively neutral spine position while placing more weight on
their upper limbs in order to improve aerodynamics. Paravertebral mus-
cles contract proportionately with pedalling intensity while abdominals
The Lumbor Spine and Spam 397
are relatively relaxed. This may result in a reduction in intra-abdominal
pressure often associated with spinal stabilization.
v. Hip flexion angle tends to vary more with different bike models and cy-
clist postitions than does lumbar lordosis in elite cyclists.
vi. Mountain biking may allow for a more neutral alignment of the lumbar
spine, but places increased axial loads and vibration exposure to the
lumbar spine due to repetitive impact from cycling on uneven surfaces
and over obstacles.
c. Rehabilitation (onsiderations
i. Optimal seat height, seat position, and stem/tube length must be precise
to minimize lumbar loads and optimize lumbar function.
ii. If the rider rocks from side to side, seat height should be lowered.
iii. If the rider has a significant leg length discrepancy, a build-up can be
placed between the shoe and cleat.
iv. Anterior inclination of the saddle may decrease lumbar lordosis and re-
lieve back pain.
v. Training of spinal muscles should emphasize the extensors in a neutral
position for high-performance cyclists.
vi. Road shock may be minimized by using larger tires, decreasing tire infla-
tion pressure, and adding a suspension system to the bicycle.
7. Running
a. Epidemiology
i. Annual incidence of low back pain about 8010 for track and field athletes.
ii. Back, pelvis, and hip injuries are a greater problem for jumping athletes
than other track and field sports, and a relatively more common problem
in distance runners than in sprinters (in whom hamstring strains are the
dominant injury).
b. Biomechanics
i. 2000 Newtons of force (approximately 2.5 times body weight) at heelstrike,
ii. Lumbar disc height decreases 3.2 mm over 6-km run and 8.0 mm over a
19-km run.
iii. Running shoes, surface, distance, and duration of run correlated with
disc height changes.
iv. Impact loads through lower extremity that reach the spine are attenuated
by normal ankle, knee, hip, and sacroiliac joint function and the mus-
cles that support these joints. Therefore, any mechanical or muscular
dysfunction may limit force attenuation and increase cyclic lumbar
spinal loading.
v. There is prominent rotation of the pelvis associated with a counter-
rotation of the upper trunk as a runner moves through the gait cycle.
The lumbar spine rotates anteriorly with forward limb movement during
swing phase and laterally flexes to the weight bearing side at heel strike.
Any condition that impairs spinal mobility (e.g., disc degeneration, facet
arthropathy) may alter normal motion, diminish appropriate force trans-
fer, and be a contributing factor to ongoing pain.
vi. The lumbar spine is relatively flexed during the period of midsupport and
relatively extended at heel strike and toe-off.
vii. Downhil\ running is associated with greater lumbar extension and thus
may increase the load to the zygopophyseal joints and dynamical1y nar-
row intervertebral foramina. Zygopophysealjoint pain and radicular
pain, respectively, may result.
viii. Uphill running increases lumbar flexion and anterior pelvic tilt, limit-
ing hip flexion and possibly resulting in a relative increase in disc loads
that may create or exacerbate discogenic pain.
ix. Anterior pelvic tilt has been associated with an increased risk for ham-
string injury and increased pelvic obliquity has been associated with
iliotibial band syndrome.
i. Optimize flexibility, strength, and strength balance throughout the en-
tire lower extremity and appropriately treat concurrent lower extremity
injuries so that impact loads can be maximally attenuated before reach-
ing the lumbar spine.
ii. Optimize thoracolumbar mobility and pelvic motion in order to allow
for appropriate spinal rotation.
iii. Address strength, endurance, and relative balance of trunk, pelvic, and
hip musculature.
iv, Consider correcting a leg length inequality in the runner with lumbar
spine pain that has not responded to aggressive conservative rehabilita-
tion techniques.
v, Runners with facet pain or symptomatic foraminal stenosis should
avoid downhill and faster runs that result in increased lumbar exten-
sion and facet loads and foraminal narrowing.
vi. Runners with discogenic pain should avoid uphill runs that increase
lumbar flexion and disc loads.
vii. Appropriate footwear and training surfaces may be helpful in force at-
tenuation, as well.
8. Swimming
a. Epidemiology
i. Repetitive microtrauma is the primary cause of lumbar spine injury.
ii. If the average competitive swimmer trains 5000 yards freestyle per day,
5 days per week, using 15 strokes per pool length, and breathes every
other stroke, 600,000 arm movements, 300,000 cervical spine rotations,
and 600,000 lumbar rotatory movements result per year.
iii. A competitive breastroke swimmer may be exposed to over 1,000 repet-
itive flexion/ extension motions of the lumbar spine daily.
iv. In elite Japanese swimmers, the lumbar spine was found to be the most
common site of injury; 37.1% had chronic lumbar spine pain. However,
the shoulder is usually recognized as the most common site of injury in
competetive swimmers.
v. Low back pain seems to be more common in swimmers whose main
stroke is breaststroke or butterfly.
vi. Significant structural injuries of the lumbar spine (e.g., disc herniation
or spondylolysis) appear to be relatively uncommon in swimmers when
compared with other athletes involved in higher impact sports, such as
gymnasts.
b. Biomechanics
i. Butterfly and breaststroke accentuate lumbar extension and require
repetitive flexion/extension movements, potentially increasing the risk
of zygopohyseal joint pain and spondylolysis.
0
ii. Freestyle and backstroke both require significant body roll (up to 160
per stroke in freestyle) that likely contributes significantly to power
The Lumbar Spine and Sports 399
generation from the armstroke by utilizing the trunk musculature.

Novice swimmers tend to have less body roll than elite swimmers.
iii. Flip turns can increase disc loads and exacerbate discogenic pain.
iv. Poor stroke mechanics may alter spine positioning and increase loads to
spinal structures. For example, a hand entry position in freestyle that crosses
over midline results in excessive compensatory lateral lumbar flexion and
(coupled) lumbar rotation, increasing zygopophyseal and anular stress.
v. Peripheral joint dysfunction may cause abnormal lumbar spine mechan-
ics and exacerbate lumbar spine pain. Decreased active shoulder range of
motion due to rotator cuff tendinitis may lead to increased trunk flexion
and rotation for both the pull and recovery phases of freestyle.
i. Optimize stroke mechanics. This will vary by stroke, but efforts should be
made to maintain spinal alignment, optimize body roll in freestyle and
backstroke, and ensure appropriate arm positioning. This will minimize
stress placed across the lumbar spine.
ii. Use freestyle as a means of training during the rehabilitation of breas-
troke or butterfly swimmers with posterior element-based pain.
iii. Excellent motion and dynamic stabiltiy of the glenohumeral joint are es-
sential to maintain body position.
iv. Excellent strength and endurance of the hips, lower extremities, and
trunk musculature allow appropriate development of propulsion without
altering trunk and upper extremity mechanics.
iii. Apply strapping tape in a basket weave formation across the lumbar
spine while the swimmer is in neutral spine position. This tape provides
increased lumbar spine proprioceptive feedback to help the swimmer
maintain the neutral spine position during pool training sessions.
B. Contact sports
1. Football
a. Epidemiology
i. Up to 300/0 of football players lose playing time due to lumbar spine
pain.
ii. 270/0 of college football players complain of lumbar spine pain.
iii. Up to 500/0 of interior lineman have been noted to have spondylolysis,
although the prevelance in college football players as a whole is closer to
150/0.
iv. The majority of football injuries in general are due to direct contact/
acute trauma.
v. Hyperflexion injuries may result in vertebral body fractures, while direct
blows cause fractures of the spinous and transverse processes.
b. Biomechanics
i. The forces attained when collegiate players hit a blocking sled are ap-
proximately 3000 N for impact, 8500 N for peak compression at L4/5,
and 3300 N for peak antero-posterior shear. These forces exceed those
determined to cause pathologic change in the intervertebral disc and the
pars interarticularis. Thus, discogenic or bony injury may result from
macrotraumatic or cumulative microtraumatic forces.
ii. Repetitive flexion, extension, and torsional stresses coupled with repeti-
tive collisions with other players and the ground increase the likelihood
of lumbar spine injury.
400 The Lumbar Spine and Sporls
c. Rehabihtation considerations
i, Emphasize core training in position of function for a given player.
ii. Multi-planar, dynamic stabilization work is important given the range of
motion, speed, and force generating or dissipating functions of the mus-
culoskeletal system required for these athletes.
2. Basketball
a. Epidemiology
i. The lumbar spine accounts for about 8-12010 of injuiries in high level
basketball players.
ii. The more common lumbar injuries seem to consist of contusions,
"sprains or strains," or facet mediated pain, although disc injuries,
spondylolysis, and transverse process fracture have all been reported.
iii. The injury rate in general has been reported to be significantly higher in
female basketball players when compared with males, although limited
data suggest the rates are similar for lumbar injuries.
iv. Time loss from lumbar injuries appears to be relatively low compared
with that for lower extremity injuries.
b. Biomechanics
i. Contact and collision stress the lumbar spine.
ii. Running associated with lumbar lateral rotation, flexion, and extension
in concert with rapid acceleration, deceleration, and sudden changes in
direction puts all parts of the lumbar spine at risk.
iii. Non-uniform loading of the intervertebral disc and posterior elements
occurs when a player lands off balance during a rebound, body contact
shifts the player's center of gravity, and leaning, holding, and hand and
body checking throw the player off balance.
i. Balance is crucial for maintaining postural stability in basketball players.
Due to the multi-planar motions, high speeds, and frequent flexion and
rotational motions required, multi-planar dynamic lumbar stabilization
with unstable surfaces and postural challenges may be a useful compo-
nent in training.
ii. Train spine-neutral landing positions after jumping to help distribute im-
pact loads more evenly.
iii. Throwing and catching with a weighted ball utilizing dynamic stabiliza-
tion techniques may be helpful in rehabilitation for all positions.
3. Soccer
a. Epidemiology
i. The incidence of lumbar spine pain in soccer players has been reported
to be as high as 14010, although the percentage of overall injuries related
to the lumbar spine is generally less than this.
ii. Most injuries in soccer players are traumatic in nature and affect the
lower extremities.
iii. Acute vertebral fractures are extremely rare in soccer, although spondy-
lolysis has been reported.
b. Biomechanics
i. Lumbar spine injuries during kicking usually occur during long-distance
kicks because of excessive trunk flexion during follow-through-
especially if the kick was initiated from a position of trunk extension.
Posterior element loading may occur during backswing with too much
hip extension.
The Lumbar Spineand Sports 401
ii. Lumbar spine injuries during dribbling are usually due to feinting. Feinting
requires quick lateral movements, resulting in rapid changes in direction
and speed. Such quick changes may increase lumbar spinal loads.
iii. A chest trap is particularly stressful to the lumbar spine because the
trunk is extended, then recoiled into flexion on ball contact to achieve
adequate ball deceleration.
iv. Throw-ins require lumbar spine movement from end-range extension
through adequate flexion. A long lever arm is used because the arms are
held overhead. Lumbar spine injuries result from these end-range posi-
tions, transition from end-range positions, or ineffective deceleration af-
ter ball release.
c. Rehabilitation considerations.
i. Adequately rehabilitate the more common lower extremity injuries so that
effective motion and force transfer are maintained in the lumbar spine.
ii. Core stabilization to include trunk and hip rotation, dynamic training to
stabilize the trunk in kicking, and multi-planar work to prepare for the
wide range of spinal motions and sudden changes in direction associated
with this sport may be helpful.
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1r----------24
Low Back Pain During Pregnancy
Avital Fast, M.D.
Key Points
• About 50% of pregnant women complain of low back pain.
• About 20% of pregnant women suffer from posterior pelvic pain.
• Radiculopathy due to herniated lumbar disc should be considered in women with
neurologic deficits.
• Rest and pelvic support combined with specific exercises may bring relief.
• Acetaminophen may be prescribed for pain relief. Nonsteroidal antiinflammatory
drugs (NSAIDs), especially if prescribed after the 32nd week of pregnancy, may lead to
failure of closure of the ductus arteriosus.
I. Introduction
Low back pain (LBP) commonly occurs during pregnancy. Frequently, the patient is
told that backache is expected and that it is an integral part of normal pregnancy and
will dissipate after delivery.
II. Prevalence
The scope of the problem has been investigated in various studies. Self-reporting sur-
veys were conducted during pregnancy or immediately after delivery.
A. About 50% of pregnant women complain of LBP. One-third of women suffering
from backache consider the pain severe.
B. In about one-half of women with backache the pain radiates to the buttock or into
the thigh. In most women the pain does not radiate below the knees.
C. Up to 30% of pregnant women complain of nocturnal backache. The pain may in-
terfere with sleep. Sleep studies clearly demonstrate disrupted sleep architecture
during pregnancy.
D. The incidence of back pain increases during the fifth to seventh month (Fig. 1).
E. About 20% of pregnant women complain of posterior pelvic pain. This is accom-
panied by "catching of the leg" upon ambulation.
III. Diagnosis
A. History
1. Location of pain: In most symptomatic women the pain may be limited to the
low back. In about one-half of women with LBP the pain radiates unilaterally
or bilaterally into the buttocks and thighs. In most women the pain does not ra-
diate below the knees. At times the pain in the low back area may radiate into
the lateral aspect of the proximal thigh and into the inguinal region.
2. Activities that aggravate symptoms: The pain may be aggravated by prolonged
standing and walking. House chores that require prolonged standing and stoop-
ing tend to aggravate the pain. The pain subsides upon sitting or lying down.
405
406 Low Back Poin During Pregnancy
28
24
I
Q.
'5
20
16
I
Z
::J 12
2 3 4 5 6 7 8 9
Month When Pain Started
FIGURE 1. Histogram shows thedistribution of onsetof back pain invarious months of pregnancy. (From Fast
A, ShapiroD,Ducommun EJ, et 01: low back pain in pregnancy. Spine 12:368-371, 1987, with permission.)
3. Multiparous women tend to complain of more severe pain.

4. Women with a history of back and pelvic pain during previous pregnancies are
at a higher risk to develop these symptoms in subsequent pregnancies.
5. Among women with severe backache during pregnancy, up to two-thirds may
continue to suffer from back pain after delivery.
6. The prevalence of backache during pregnancy tends to be higher as maternal
age increases.
7. No correlation has been found between maternal height or weight, weight gain
during pregnancy, or weight of the infant and the development of backache.
8. A study of people with sciatica found that women who had proven sciatica had
significantly more children than women in the control group. No such differ-
ence was found in men who raised their children as sole parent. This study sug-
gests that pregnancies leading to live births may be a risk factor for the devel-
opment of sciatica. The risk of sciatica increases with subsequent births.
9. Posterior pelvic pain occurs almost exclusively in relation to pregnancy. The
patient may complain of pain in the sacroiliac joint region, gluteal region, and
occasionally the symphysis pubis region. Patients with pelvic pain may have
difficulty ambulating due to a feeling of "catching of the leg" in which the pa-
tient has difficulty moving the leg forward during ambulation At times, they
cannot ambulate without assistive devices and may have difficulty in activities
of daily living.
B. Physical examination
I. In most women the neurologic examination remains normal. Dural tension
signs [i.e., positive straight leg-raising or popliteal compression test) are nega-
tive.
2. The patient may have tenderness to palpation over the symphysis pubis.
3. Sacroiliac compression tests may be positive.
Low Bock Pain During Pregnancy 407
4. Pressure applied downward over the flexed knee, while the patient is lying
supine with one leg flexed at the hip and knee to 90° and the other leg in
extension is an important tool to identify patients with posterior pelvic
pain.
5. Patients suffering from posterior pelvic pain following pregnancy may have
difficulty with active straight leg raising.
6. Gait dysfunction may be observed with a positive Trendelenburg gait or diffi-
culty taking a step forward.
IV. Potential Pathophysiologic Mechanisms

A. Hyperlordosis
1. Increasing weight gain during pregnancy rapidly leads to postural adjustments,
resulting in the position typically described as "pride of pregnancy."
2. Increased lumbar lordosis during pregnancy is likely to affect the load distribu-
tion in the motion segment and to alter the pressure distribution in the inter-
vertebral discs and posterior joint complex. This may lead to abnormal stresses
and strain and may playa role in the production of pain.
3. There is still no consensus in the literature about the potential role of lumbar
lordosis in the pathogenesis of low back pain.
4. Extensive radiologic reviews fail to show increased lumbar lordosis in nonpreg-
nant patients with idiopathic low back pain. Similar studies have not been con-
ducted in pregnant women.
5. Some researchers deny the presence of hyperlordosis during pregnancy.
B. Muscle insuHiciency
1. The protruding abdomen stretches the abdominal muscles and renders them
weak by altering their length-tension relationship.
2. As the woman gains weight, she adopts the hyperlordotic posture to prevent a
shift in the center of gravity and to maintain truncal stability.
3. The posture affects the length of the abdominal and paraspinal muscles and
may render them less efficient.
4. The weakened muscles may not withstand daily demands and thus may playa
role in the production of pain.
c. Pelvic instability
1. The increased levels of relaxin, a hormone secreted by the corpus luteum, "soft-
ens" the pelvic ligaments and renders the pelvic ring, including the sacroiliac
joints, less stable. This mechanical instability may lead to pain.
2. The pain, which may be acute, results from stretching of the capsule and liga-
ments around the sacroiliac joints. These structures are richly innervated by un-
myelinated nerves that provide nociceptive input.
3. Sacroiliac joint pain referral maps, obtained after administration of irritant so-
lutions into the sacroiliac joints, coincide with pain distribution patterns ob-
served during pregnancy.
4. An excellent study measuring the blood relaxin levels in pregnancy demon-
strated significantly higher relaxin levels in women who were most function-
ally limited by low back and pelvic pain.
D. Vascular-induced pain
1. The vascular system may playa role in nocturnal pain production.
2. As pregnant women sleep on their back, the vena cava may become completely
obstructed by the enlarged uterus.
3. Obstruction may increase pressure within the lumbar vertebrae, slow or stop the
venous flow, and lead to anoxia of the neural elements [i.e., roots).
408 Low Back Pain During Pregnancy
E. Myofasdal pain syndrome

1. No studies in the literature establish the prevalence of myofascial pain syn-
drome during pregnancy.
2. Our clinical experience indicates that it may be rather common.
V. Differential diagnosis
A. Herniated lumbar disc
1. Incidence: the incidence of herniated lumbar discs during pregnancy is
1:10,000. This incidence may be on the increase due to a greater number of
women who get pregnant at an older age.
2. History
a. The pain may be worse when the patient is sitting and standing and relieved
when the patient lies down.
b. The pain may radiate to the legs; leg pain may be worse than back pain.
3. Physical examination
a. Weakness in myotomal distribution and sensory changes in dermatomal dis-
tribution may be found.
b. In posterolateral herniation the straight leg-raising test may reproduce the pain.
4. Management
a. Bed rest
b. Analgesic medication (acetaminophen and, when appropriate, NSAIDs)
i. Acetaminophen may be considered safe throughout pregnancy.
ii. A number of NSAIDs, including aspirin, have been shown to lead to pre-
mature closure of the ductus arteriosus and pulmonary hypertension in
susceptible infants.
iii. NSAIDs, therefore, should be limited strictly to the first 32 weeks of
pregnancy.
iv. The physician is advised to consult with the obstetrician before prescrib-
ing medication.
c. In patients with progressive neurologic deficits and/or cauda equina syn-
drome [i.e., compromised sphincteric function), MRI studies should be done
and surgical intervention considered.
B. Symphysiolysis pubis
I. History
a. Groin pain aggravated by weight bearing and thigh movements is the major
complaint.
b. The pain may radiate into the thigh.
c. Occasional unpleasant clicking may be felt during ambulation.
d. Symptoms usually appear at the end of the first trimester or at the beginning
of the second trimester.
2. Location: pain is located over the symphysis pubis and groin.
3. Physical findings
a. A tender area and a gap may be felt between the pubic bones.
b. The pain may increase during active or passive thigh movements, while ris-
ing from sitting to standing, and during ambulation.
c. At times, the pain may be so severe that it interferes with the patient's abil-
ity to ambulate.
4. Management
a. Decreased physical activities combined with rest should be recommended.
b. A pelvic belt may prove helpful during ambulation; it should be worn just
proximal to the greater trochanters.
Low Bade Pain During Pregnancy 409
5. Prognosis: within several weeks after delivery the pelvis becomes more stable
and the symptoms may subside.
C. Transient osteoporosis ofthe hlp
1. Incidence: rare disorder of unknown etiology; may be underdiagnosed.
2. History
a. Pain commonly occurs in the third trimester.
b. Onset of pain may be sudden or gradual.
c. Pain is localized to hip and groin areas and may radiate to lateral thigh.
d. The pain may be severe and prevent the patient from ambulating.
a. The pain increases on weight bearing.
b. The patient may demonstrate a Trendelenburg gait (lateral limp during the
stance phase).
4. Diagnosis
a. The diagnosis can be established with an anteroposterior supine pelvic
radiograph.
b. Significant osteoporosis of one or both hips may be observed.
c. Occasionally the femoral neck and acetabulum may be osteoporotic.
5. Management
a. The patient should not be allowed to ambulate; weight bearing increases the
pain and may lead to subcapital fractures.
b. Rest is advocated.
c. Crutch walking may protect the osteoporotic hip.
6. Prognosis: excellent.
a. Within several months after delivery the symptoms may subside altogether.
b. The local osteoporosis also disappears.
D. Osteonecrosis ofthe femoral head
1. Incidence: rare.
2. Etiology
a. May be related to excessive cortisol production in late stages of pregnancy.
b. Increased intra osseous pressure also may playa role.
3. History
a. Symptoms usually appear in the third trimester.
b. The patient complains of groin or hip pain aggravated by weight bearing.
c. Pain may radiate to the thigh, knee, and even back.
d. Initial complaints may resemble those of pelvic instability.
a. Groin pain during passive hip range of motion, especially rotation.
b. Positive Patrick's test.
5. Diagnosis
a. Osteonecrosis can be identified on plain radiograph of the hip.
b. Magnetic resonance imaging also may help to establish the diagnosis.
6. Management
a. Basically similar to osteonecrosis in nonpregnant patients.
b. The hip joint may be aspirated and protected from weight bearing [i.e.,
crutch walking).
7. Prognosis: guarded
a. If the osteonecrotic segment is small, the segment may revascularize and the
hip may recover.
b. In large osteonecrotic segments, the area may collapse and the femoral head
will become deformed.
410 Low Bacle Pain During Pregnancy
c. Patients with a deformed femoral head develop early severe osteoarthritic

changes and may require femoral head replacement.
E. SacroUiac joint dysfunction, pelvic insuHiciency, posterior pelvic pain
I. May be a most common reason for low back pain and discomfort during preg-
nancy.
2. Etiology: may be related to excessive mobility of pelvic joints and altered stress
distribution through pelvic ring.
3. History
a. Posterior pelvic pain overlying the sacroiliac joint area; may be unilateral or
bilateral.
b. Pain may radiate into the gluteal area or thigh.
c. Pain does not radiate below the knee.
d. Pain is related to weight bearing, interfere with activities of daily living
mostly ambulation. Sitting may be comfortable.
e. At night, however, the patient may notice pain while turning in bed.
a. Normal neurological examination.
b. No dural tension signs.
c. Normal spinal range of motion.
d. Positive provocation tests may duplicate the pain.
e. Iliac compression test and Patrick's test are usually positive.
f. Posterior pelvic provocation test has been recently described.
i. The patient lies supine with one hip flexed to 90° and the ipsilateral knee
in full flexion.
ii. Pressure is applied over the flexed knee while the examiner stabilizes the
pelvis by applying pressure over the contralateral anterior superior iliac
spine.
iii. The test is positive if it reproduces the pain.
5. Management
a. The patient should be advised to avoid prolonged ambulation and to wear a
nonelastic trochanteric belt.
b. The belt should be strapped around the pelvis during ambulation; it should
be located proximal to the greater trochanters and distal to the sacroiliac
joints.
c. Exercises to strengthen muscles that may contribute to the stability of the
pelvis should be recommended.
d. Strong gluteal, piriformis, and hamstring muscles may promote pelvic stabil-
ity and enhance the patient's ambulation capacity.
VI. Exercises During Pregnancy

A. The spine literature clearly indicates that general physical fitness has protective ef-
fects against backache. Should the pregnant woman participate in sports activities?
B. Contraindications to fitness exercises during pregnancy
I. Hypertension (eclampsia)
2. Diabetes mellitus
3. History of premature labor or delivery
4. Placenta previa
5. Threatened abortion
6. Post date
7. Multiple gestation
LowBack Pain During Pregnancy 411
C. Potentially negative physiologic eHecls of moderate-to-severe exercises during preg-

nancy
I. Exercise-induced hyperthermia, especially during the first trimester, may lead
to abortion or congenital abnormalities, particularly of the central nervous sys-
tem, heart, spine, and urogenital systems.
2. Intense exercises lead to significant increase in catecholamines. This increase,
combined with blood flow shunting and decrease in stroke volume, may lead to
fetal hypoxia.
3. Fetal bradycardia has been documented during intense exercises.
4. Women who continue intense exercises throughout pregnancy may gain less
weight and deliver small-for-date infants.
5. Musculoskeletal injuries may be sustained during weight-bearing activities in
late stages of pregnancy because of impaired maternal balance and "softening"
of connective tissues.
D. Recommendations for exerases during pregnancy
1. Exercises should be mild to moderate (walking, bicycling). Pulse monitoring
may help to define the intensity of the exercise. Subjective feelings of fatigue
and stress also determine whether the exercises should be discontinued.
2. Continuous exercises should not last more than 15 minutes.
3. The pulse rate should not rise beyond 140 beats per minute.
4. The core temperature should be kept at less than 38° C. Exercising in a well air-
conditioned room may help dissipate the heat.
5. Non-weight-bearing activities are preferred during the late stage of pregnancy.
6. The intensity of exercises should be decreased in the late stage of pregnancy.
Brisk walking renders the same cardiovascular benefits with less risks than run-
ning.
7. Contact sports, scuba diving, and water skiing should be strictly avoided.
8. Exercising at anaerobic pace should be avoided throughout pregnancy.
9. Any woman who starts exercising during pregnancy should consult her obste-
trician and engage a physical therapist with experience in exercises during
pregnancy.
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Gynecol 71 :495-498, 1988.
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Am J Obstet Gynecol 119:867-876, 1974.
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Med 16:163-169, 1984.
1 - - - - - - - -25
Children and Adolescents
Steven J. Anderson, M.D.
Key Points
• Complaints of back pain in children and adolescents should be taken seriously.
• An appropriate clinical evaluation of back pain in children and adolescents should be
expected to yield a specific diagnosis.
• The possibility of a serious, underlying medical condition needs to be considered and
ruled out in all young patients with back pain.
• An appreciation of spinal anatomy and biomechanics underlies the clinical evaluation
and rehabilitation of mechanical and traumatic back disorders.
• Applying "adult" diagnostic criteria to pediatric patients with back pain increases the
likelihood of inaccurate or missed diagnoses.
• The most obvious spinal symptom or physical finding is not always the cause of the
pain, e.g., muscle spasm, scoliosis.
• A symptomatic spondylolysis is not always evident on plain radiographs and a
spondylytic defect on radiographs is not always symptomatic.
• A lumbar disc can be injured and cause pain without being herniated or causing
radiculopathy.
• Appropriate treatment and rehabilitation of mechanical back problems in young
patients has the potential to reduce the high morbidity of back problems in the adult
population.
I. Overview
A. Adults vs. Children
1. Incidence of back pain
a. Adults
i. 60-800/0 experience at least one episode of low back pain.
ii. Time loss from work: 93 million days annually.
iii. Most common cause for limitation of activity under age 45 years.
iv. Most costly medical problem for age group 30-60 years.
b. Children and adolescents
i. True incidence not known; many cases self-limited or not reported.
ii. In selected athletic populations, incidence may be 10-50%.
2. Common diagnoses
a. Adults
i. Degenerative disease, osteoarthritis
ii. Disc degeneration; disc herniation
iii. Radiculopathy
iv. Combined anterior segment and posterior element disease; multilevel dis-
ease
v. Functional; psychosomatic
413
414 Children andAdolescenls

i. Developmental conditions (spondylolysis); growth-related conditions
(Scheuermann's kyphosis)
ii. Segmental dysfunction (less degenerative or multilevel disease; less
structural abnormality)
iii. Greater chance for establishing specific diagnosis
3. Treatment
a. Adults
i. Therapies must address the consequences of years of dysfunction and
cumulative trauma.
ii. More likely to need surgery when irreversible structural changes occur
(disc herniations, stenosis).
iii. Secondary gain issues may complicate assessment and response to treat-
ment.
i. Soft-tissue injury and spinal dysfunction are more responsive to exercise
and conservative therapy; structural or degenerative change in adult
population may be more "fixed" and less reversible with conservative
treatment.
ii. Fewer complications from multilevel disease and/or concurrent medical
problems.
iii. Fewer secondary gain issues.
B. Current level of care in chndren and adolescents
1. More medical attention is directed toward back pain due to "serious" conditions
such as tumors, infections, rheumatologic disorders, major structural abnormal-
ities, and acute trauma. Such conditions usually have obvious symptoms, phys-
ical findings, and radiographic changes and the pain does not go away with
rest.
2. Less medical attention is directed toward cases of back pain with nonspecific
physical findings and normal radiographs in an otherwise healthy, active out-
patient population.
3. Medical education and training programs place disproportionate emphasis on
the most serious (and most rare) causes of back pain and cases that require in-
patient management or subspecialty care.
4. The more common outpatient causes of back pain receive less attention from
traditional spine specialists (spine surgeons, neurosurgeons] and less attention
in the medical literature and in medical education programs.
5. When the evaluation of back pain goes only far enough to rule out the more
serious conditions, the vast majority of patients suffering from back problems
go undiagnosed and untreated.
6. Physician anxiety, sense of inadequacy, and/or indifference to dealing with
back problems encourages the proliferation of nonorthodox care and alterna-
tive therapies for patients with back problems.
C. Attitudes and behaviors contributing to suboptimall"el of back care in children and adolescents
1. Assuming that "children heal faster" or will "outgrow" the problem.
2. Assuming that the absence of pain implies the absence of spinal dysfunction.
3. Attributing pain solely to psychosocial or environmental factors.
4. Abandoning work-up once serious underlying medical conditions have been
ruled out.
5. Applying "adult" treatment model for treatment of children, i.e., bed rest, anal-
Children andAdolescenls 415
gesics, muscle relaxants, spinal manipulation, standardized exercise programs.

(This model is not necessarily appropriate for adult patients either.)
6. Little or no emphasis on prevention in young patients. Despite epidemic levels
of disease in adults, children are not regularly exposed to preventive strategies
(back school, spine education, flexibility, and trunk-strengthening exercises).
D. Recommendations for Improving back care for children and adolescents
1. Take complaints of back pain seriously.
2. Continue to pursue the diagnosis even after more serious or life-threatening
causes have been eliminated.
3. Recognize that recommendations for prolonged rest or inactivity do not solve
dynamic problems associated with mechanical back pain.
4. Recognize that inattention to back problems may lead a patient to seek treat-
ment that is unorthodox, unproved, or potentially unsafe.
5. Encourage further research that addresses risk factors, diagnosis, treatment, and
prevention of low back pain in children and adolescents.
E. DiHerentlal diagnosis
1. Frequency of diagnosis depends on patient age, practice setting, and specialty
orientation of practitioner; i.e., what causes back pain in children and adoles-
cents depends on who you ask and where they work.
a. Age-related diagnostic patterns
i. Younger children (age 10 and under) present with more medical causes
of back pain (infections, tumors).
ii. Older children and adolescents tend to have greater proportion of trau-
matic and mechanical disorders.
b. Diagnostic patterns related to practice settings and practitioner biases
i. Hospitals and emergency departments deal with more traumatic causes
of back pain and a higher proportion of serious underlying medical prob-
lems and/or surgical conditions.
ii. Office orthopedic setting deals with spinal deformity, acute trauma, de-
velopmental conditions, and surgical problems.
iii. Office rehabilitation and sport medicine practice sees mechanical,
overuse trauma, developmental conditions.
iv. Primary care office may see all of above plus a higher portion of non-
spinal conditions presenting with back pain.
2. Biases and deficiencies in the medical literature
a. Likelihood of a spine-related topic or diagnosis being published in the litera-
ture is based on the specialty of treating physician: orthopedic
neurosurgeon> >rehabilitation/sports medicine> >primary care physician.
b. Therefore, the majority of information in the literature is based on the small-
est minority of problems and heavily biased toward surgical or hospitalized
patients.
c. This chapter addresses these biases and provides information representative
of the back problems likely to be seen and managed by a primary care
physician.
3. Differential diagnosis of back pain in children and adolescents (Table I).
II. Anatomy and Function

A. Basic function ofspine
1. Supports weight
2. Linkage system between upper and lower extremities
416 Children ond Adolescenls
Table 1. Differential Diagnosis of Back Pain In Chddren and Adolescents

Trauma Developmental abnormalities Neoplasm
Vertebral compression fracture Spondylolysis Muscle
Vertebral endplate fracture Spondylolisthesis Spinal canal
Transverse process or spinous Scheuermann's kyphosis Vertebral column
process fracture Scoliosis Osteoid osteoma
Facet fracture or dislocation Aneurysmal bone cyst
Soft-tissue injury Inflammatory disorders Eosinophilic granuloma
Discitis Giant cell tumor
Mechanical disorders Disc space calcification Leukemia
Postural Vertebral osteomyelitis Osteoblastoma
Overuse syndrome Sacroiliac joint infection Osteochondroma
Disc protrusion or herniation Rheumatologic disorders
Facet syndrome or arthropathy Juvenile rheumatoid arthritis Nonspinal disorders
Reiter's syndrome Iliac apophysis avulsion/fracture
Psoriatic arthritis Hip
Inflammatory bowel disease RenaI disorder
Pelvic/gynecologic disorder
Retroperitoneal disorder
Conversion reaction
B. Functional elements ofthe spine: 3-joint complex made from anterior and posterior
segments.
1. Anterior segments
a. Anatomy: vertebral body, vertebral endplates, intervertebral discs.
b. Function: support weight, absorb shock.
c. Unique pediatric aspects: vertebral endplate and ring apophysis (growth cen-
ter) are more susceptible to failure (fracture, collapse, displacement) during
growing years.
d. Clinical correlate: anterior segments are stressed with lifting, bending for-
ward; sitting, straining, axial loading, lying supine.
2. Posterior segments
a. Anatomy: vertebral arches, spinous and transverse processes, inferior and
superior facets, pars interarticularis.
b. Function: protect neural structures, control motion, protect disc from rota-
tion and shear force.
c. Unique pediatric aspects
i. Pars interarticularis is most susceptible to failure (fracture) during grow-
ing years.
ii. Apophyseal growth centers on spinous and transverse processes are more
susceptible to injury (fracture, avulsion) during growing years.
d. Clinical correlate: posterior elements are stressed with back extension, back
rotation, standing, walking, running, lying prone.
3. Interaction between functional spinal units
a. The 3-joint motion complex works in series with adjacent units to carry out
movement and support functions of spine.
b. Interaction between and within the 3-joint complexes allows isolated joint
abnormalities to affect motion and/or load bearing at adjoining segments.
C. Stability and motion
1. The geometric configuration of the bony elements of the spine confers little sta-
bility. Soft-tissue structures (muscles and ligaments) are essential for spinal
support and stability.
Children andAdolescents 417
2. The geometry of the spine is quite specific in dictating the amount and type of
motion available.
3. The presence of the rib cage in the thoracic spine limits excessive motion and
provides significant support for the spine.
4. The lumbar spine has greater weight-bearing demand than cervical or thoracic
spine but less external protection and support.
D. Pathogenesis ofspinal injury-principles
1. Normal integrated spinal function requires a "balance" between
a. Bony and soft-tissue elements
b. Anterior segments and posterior elements
c. Load-bearing and motion-controlling elements
2. Imbalances, asymmetries, and/or overload to the functional elements of the
spine may lead to injury (Table 2).
a. Imbalances between bony and soft-tissue elements may occur during peri-
ods of rapid growth due to the disproportionate growth rate of bone, liga-
ment, and muscle.
b. Overload may occur if training and activity demands are not adjusted for
the tolerance of immature structures (e.g., vertebral endplate, pars inter-
articularis).
3. Passive structures (disc, vertebral endplates, facet joints) are the structures
most often injured.
4. The forces acting on these passive structures are modulated by active struc-
tures (muscles).
5. Ironically, the structures that are injured (facet joints, pars, discs) have little
control over the forces that cause injury. Furthermore, the structures that
appear to be the source of symptoms (muscles) are usually not primarily
injured.
6. Generally speaking, posterior structures are more susceptible to repetitive or
excessive extension.
7. Anterior structures are more susceptible to repetitive compression, flexion,
and/or torsion.
8. Pain and inflammation from injury result in abnormal motion as well as dys-
function of active structures necessary to maintain normal forces in the in-
jured areas.
Table 2. PathogHesis of Traumatic and Mechankal Back Pain

Injury may occur if:
1. A load-bearing structure (disc, vertebral body) is subjected to excessive load.
2. A motion-controlling structure (facet joint, pars interarticularis) is subjected to excessive motion.
3. A load-bearing structure is subjected to excessive motion.
4. A motion-controlling structure is subjected to excessive load.
Applied Stress
Structure Function Excessive Load Excessive Motion
Disc, vertebrae Load-bearing + ++
Facet, pars Control, motion ++ +
+ = risk of injury.
418 Children andAdolescents
9. Injury to one part of a 3-joint complex leads to abnormal function in other

joints at the same level and may eventually extend to adjacent levels; for ex-
ample:
a. Facet joint degeneration with capsular laxity may lead to segmental insta-
bility with increased shear stress at disc or even disc disruption.
b. Disc narrowing may increase compressive forces on facet joints and lead to
accelerated degenerative changes at facet joints.
c. Restricted mobility at one level may put increased demand for motion at
adjacent levels in order to compensate.
10. A potential benefit of early recognition and treatment of spinal dysfunction
is to minimize progression toward multilevel disease and spinal degenera-
tion.
E. Added risks as a result ofgrowth and skeletal immaturity
1. Increased susceptibility of growing tissues to injury-pars interarticularis, verte-
bral endplates, apophysis. Clinical examples: spondylolysis, spondylolisthesis,
Scheuermann's kyphosis.
2. Disproportionate growth rates of soft tissues-ligaments, musculotendinous
units-and bony elements contribute to possible imbalances of bony and soft-
tissue structures. Clinical examples: lumbar facet syndrome, postural or "me-
chanical" back pain.
3. Extrinsic factors leading to excessive demand and overload
a. Examples that may contribute to injury
i. Improper training (too much, too soon, too fast)
ii. Improper equipment
iii. Improper technique
iv. Inappropriate amount and type of activity
v. External sources of motivation leading to overuse (pressure to ignore
warning signs of injury or "push through the pain")
b. Extrinsic factors have an amplification effect on intrinsic risk factors; i.e.,
patients with poor flexibility, poor trunk strength, and poor posture (intrin-
sic risk factors) may be at increased risk of injury if they also employ inap-
propriate training methods, equipment, techniques, and criteria for continu-
ing to participate (extrinsic risk factors).
F. Treatment implications based on underlying anatomy and biomechanics
1. Successful treatment is contingent on an accurate diagnosis and an apprecia-
tion of the specific biomechanical abnormalities that lead to injury.
2. After identifying the biornechanical abnormalities, the goal of treatment for
mechanical spine disorders should be to restore normal segmental motion, nor-
mal soft-tissue extensibility [joint capsules, ligament, muscle), normal strength
and coordination of trunk stabilizing musculature, normal posture, and normal
mechanics for motion.
III. Clinical Evaluation

A. History
1. Mode of onset
a. Antecedent illness (e.g., fever, viral syndrome, skin rash, abdominal pain)
b. Antecedent injury (specify mechanism-flexion, extension, rotation)
c. Change in activity level (type of activity, quantity, intensity, technique, and
rate of change)
2. Nature of pain
a. Location (confirm with pain diagram)
Children and Adolescents 419
b. Radiation
c. Quality (sharp, dull, aching, throbbing, tight)
d. Constant or intermittent
3. Severity of pain
a. Limitation of activities
b. Presence at night
c. Response to medication or other treatment modalities
4. Relation of pain to posture and activity (AS=tends to cause more pain with
anterior segment disease; PE=tends to cause more pain with posterior element
disease)
a. Sitting AS
b. Standing PE
c. Walking PE
d. Running PE
e. Forward bending AS
f. Arching PE
g. Lifting AS
h. Twisting AS/PE
i. Lying down
i. Prone PE
ii. Supine AS
j. Cough, sneeze, strain AS
5. Neurologic changes
a. Paresthesias
b. Weakness, clumsiness, limp, foot drop
c. Bowel or bladder dysfunction
6. Associated symptoms
a. Musculoskeletal: other areas of bone, joint, or muscle pain, swelling, re-
stricted motion.
b. General medical: fever, malaise, headache, weight change, anorexia, rash.
c. Medical conditions that may be associated with or cause back pain.
i. Urologic-urolithiasis, pyelonephritis, glomerulonephritis.
ii. Gynecologic-ovarian tumor, ovarian cyst, uterine myoma.
iii. Gastrointestinal-appendicitis (with psoas irritation), pancreatitis (sec-
ondary to Kawasaki's disease), inflammatory bowel disease (with abscess,
fistula, megacolon).
iv. Systemic infections-brucellosis, Q fever, influenza, encephalitis, pneumo-
nia, tuberculosis.
v. Spondyloarthropathies-ankylosing spondylitis [juvenile], Reiter's, psori-
atic disease.
vi. Hematopoietic disease-sickle cell, leukemia, lymphoma.
7. Previous work-up and response to treatments
8. Pain diagram
9. Past medical history
a. Medical conditions, hospitalizations, surgeries
b. Prior spine problems (including diagnostic tests, treatments, and outcomes)
B. Physical exam
I. Inspection and observation
a. Standing posture (observe from back and side)
i. Scoliosis, kyphosis, lordosis
ii. Pelvic obliquity
420 Children and Aclolescenls
iii. Leg length discrepancy

iv. Muscle definition, spasm, atrophy
b. Range of motion (look for asymmetries, restriction, lumbar shift)
i. Spine: flexion, extension, lateral bending, rotation
ii. Hip and lower extremity: flexion, extension, internal rotation, external
rotation; flexibility of hamstrings and hip flexors
2. Palpation
a. Posterior elements: facet joints, spinous process, transverse processes
b. Paraspinous musculature
c. Iliac crest (iliac crest apophysis may be open up to age 25 years and may be
tender with traction injury)
d. Sacroiliac joint
e. Sciatic notch
f. Check for local tenderness in all referral areas: groin, hamstring, calf.
g. Abdominal exam, pelvic/rectal exam (with specific indications)
3. Neurologic (basic screen-more detailed testing is warranted if abnormalities are
present on initial neurologic screening)
a. Deep tendon reflexes, long tract signs
b. Motor testing
i. Tibialis anterior-L4
ii. Extensor digitorum longus-Ls
iii. Peroneal longus-S 1
c. Sensory: light touch, pinprick, 2-point discrimination
d. Signs of nerve root irritation or dural tension
i. Straight leg raising, Lasegue's sign
ii. Bowstring test
4. Gait
a. Stride length
b. Posture
c. Limp
C. Radiographic and laboratory evaluation
1. Plain films
a. Lumbar spine series: standing anteroposterior, lateral, bilateral obliques, spot
view
i. Indications for plain films in children and adolescents: acute trauma
(flexion/ compression injury), bony tenderness on exam, back pain with
constitutional symptoms (weight loss, fever); obvious malalignment or
structural deformity (scoliosis, kyphosis).
ii. Risks of ionizing radiation: minimized by shielding most sensitive struc-
tures (eyes, thyroid, breasts, gonads) and by modem equipment (high-
speed film, special grids, collimation of x-ray beam).
iii. Interpretation: note overall spinal alignment, shape of vertebral bodies,
disc space narrowing, facet alignment and symmetry, pars defects, con-
genital variations such as hemivertebrae, sacralization, or lumbarization
of vertebrae, spina bifida occulta.
b. If indicated:
i. Flexion-extension views of spine (for instability)
ii. Views of sacroiliac joints, pelvis, hips (for rheumatoid disease or hip
dysplasia)
2. Computed tomography (CT)
a. Best for detailing bony abnormalities (endplate fracture, compression frac-
ture, congenital bony abnormalities, pars defects, infection, tumor, or spinal

canal diameter after fracture).
b. CT not as helpful if soft-tissue abnormalities (disc, nerve root) are suspected.
3. Magnetic resonance imaging
a. Best for defining soft-tissue abnormalities (disc protrusion, extruded disc
fragments, nerve root or cord compression, cord masses or tumors).
b. Not as helpful for detailing bony abnormalities.
4. Bone scan
a. Helpful in confirming suspected pars interarticularis lesion; also sensitive for
showing other active bone pathology (fracture, apophysitis, infection).
b. Single-photon emission computed tomography (SPECT) is more sensitive and
more specific than planar bone scan; SPECT scan is preferred for scinti-
graphic imaging of the spine in children and adolescents.
c. Gallium scan: best for suspected soft-tissue disorders such as discitis,
5. Myelography
a. Fewer indications with availability of MRI.
b. Still may be used in planning surgical intervention.
6. Discography
a. Used for confirming degenerative or incompetent disc.
b. Studies suggest MRI may be as accurate with less invasiveness and radiation
exposure; however, MRI does not provide information about pain reproduc-
tion or precise nuclear morphology.
7. Laboratory (indicated when suspicious of medical problem such as tumor, in-
fection, or arthritis)
a. Complete blood count with differential, erythrocyte sedimentation rate, C-
reactive protein, antinuclear antibody, rheumatoid factor, calcium, HLA-B27,
P04, alkaline phosphatase, urinalysis
b. Selected cultures, biopsy, aspirations as indicated
c. Electrodiagnostic studies: electromyogram, nerve conduction velocity, so-
matosensory evoked potentials
D. Diagnostic algorithm
Three questions that help focus the evaluation of back pain, identify the causes,
and help plan treatment: (1) Is the problem medical or mechanical? (2) If mechani-
cal, does the problem involve the anterior segments or the posterior elements? (3)
What special considerations apply to the patient?
1. Medical vs. mechanical
a. Characteristics of medical back problems
i. Examples: tumors, infections, rheumatologic disorders.
ii. Onset: tend to come on without specific injury or change of activity.
iii. Symptoms: pain tends not to vary with changes of posture or activity
nor does pain remit with rest; may have night pain; may have constitu-
tional symptoms (fever, weight change, skin rash, multiple joint or organ
system involvement)..
iv. Exam: evidence of concurrent medical problems or systemic disease
v. Treatment: minimal response to modalities, analgesics, therapeutic exer-
cise or rest.
b. Characteristic of mechanical back problems
i. Examples: disc disease, facet syndrome, spondylolysis.
ii. Onset: often occurs in relation to trauma or specific physical activity.
iii. Symptoms: vary in relation to activity or posture; can usually find some
position of comfort.
422 Chi/Jren andAclolescent5
iv. Exam: localized findings; pain can be reproduced with stress applied to
affected structure; usually no signs of other medical problems.
v. Treatment: responds to relative rest (avoidance of pain-causing activity);
improves with unloading affected structure.
2. Anterior segment vs. posterior element
a. Characteristics of anterior segment problem
i. Symptoms: worse with sitting, bending, lifting, coughing, sneezing,
straining, lying supine.
ii. Exam: restricted or painful forward flexion; possible lumbar shift.
b. Characteristics of posterior element problem
i. Symptoms: worse with standing, walking, running, arching (trunk exten-
sion), lying prone.
ii. Exam: restricted or painful extension or extension with rotation.
3. Special considerations: factors that influence risk of injury and have bearing on
treatment
a. Extrinsic
i. Sport: type of sport, level of competition, intensity, position played,
equipment
ii. Training: duration, intensity, technique, coaching
b. Intrinsic
i. Individual: age, maturation, level of fitness, general health status, past
injury history
ii. Anatomy: alignment (spine, pelvis, lower extremity), flexibility, strength,
joint mobility, anatomic variations (leg length discrepancy, transitional
vertebrae, spina bifida occulta)
iii. Psychological and emotional factors
4. By using this framework to analyze the history, physical examination, and
imaging studies, the cause of the back pain and treatment options should be
more clear.
IV. Posterior Element Problems

A. Pars interarticularis lesions-definition of terms
1. Spondylolysis-unilateral or bilateral radiographic defect of pars interarticularis.
2. Pars stress reaction-positive bone scan in pars interarticularis; without visible
defect on radiograph.
3. Spondylolisthesis-anterior slippage (usually L5 on S I) due to bilateral pars inter-
articularis defects.
4. Incidence
a. Radiographic pars defects
i. 4.2-5.8% in adult white Americans
ii. 6.4% in white males; 2.3% in white females
iii. 2.8% in black males, 1.1% in black females
iv. 50-60% in Eskimos
v. 32-50% in patients with Scheuermann's kyphosis
b. Higher among athletes in particular sports, e.g., football, weight lifting, div-
ing, pole vault, baseball pitching, dance, gymnastics
c. Explaining the variation in reported incidence and prevalence of spondylo-
lysis: not all patients with lesion on radiograph are symptomatic; not all
patients with symptomatic pars lesion have radiographic defect.
5. Etiology and natural history
a. Lesion does not appear radiographically until school age (5-6 yrs).
Children andAdolescenls 423
b. ~ 90% occur at L5 level.

c. Runs in families (genetic etiology?).
d. Seen with repetitive hyperflexion and extension of spine and with selected
sports activities (seen more frequently in gymnastics, diving, ballet, football
blocking, weight lifting, jumping tennis serve-traumatic etiology?).
e. Slippage (when it occurs) is most common at ages 9-13.
f. Spondylolysis lesion differs from other fatigue fractures in that
i. It develops at earlier age.
ii. Onset of pain does not always correlate with development of radi-
ographic lesion.
iii. There may be a hereditary predisposition.
iv. Callus formation or periosteal reaction is usually not seen. as part of
healing response
v. Defect tends to persist while other stress fractures tend to heal.
6. Symptoms-pain pattern
a. Well-localized; usually at level of belt line
b. Worse with extension, twisting, standing, walking
c. Better with sitting, flexion, lying supine
a. Hyperlordotic posture, tight hip flexors and hamstrings, weak or poorly
toned abdominal muscles
b. Pain with lumbar extension, positive one-legged standing extension test
c. Posterior element tenderness, paraspinous muscle spasm; palpable step-off
(with spondylolisthesis)
d. Relief of pain with trunk flexion or knee-chest position
e. Usually no localizing neurologic signs
8. Radiographs
a. When pars interarticularis defect is evident on plain films, it is usually best
seen on oblique projections; occasionally on lateral view.
b. Pars interarticularis may be elongated but not interrupted.
c. Spina bifida occulta on anteroposterior view raises suspicion for associated
spondylolysis.
d. Bone scan may indicate whether pars defect is acute or chronic; may also
identify pars stress reaction when plain film is normal.
e. SPECT scanning may enhance sensitivity and specificity for diagnosis of
spondylolysis.
i. Bone scan may positive in a unilateral, bilateral, or pseudo-bilateral pat-
tern
f. Grading spondylolisthesis
i. Taillard method: slippage is graded as percentage of forward slippage of
L5 on S I.
ii. Meyerding method: grades slippage in quarters. Grade I =0-25%;
grade II = 25-50%; grade III = 50-75%; grade N = 75-100%.
9. Treatment for pars stress reaction and spondylolysis (The following is a summary of a
previously published treatment regimen. Other successful regimens are included
in the referenced articles.)
a. Rest, activity modification
i. For some patients, simply avoiding pain-causing activities may be ade-
quate; e.g., elimination of repetitive extension (running) or elimination
of extreme extension (e.g., back walk-overs, back dives, Arabesque).
ii. If avoidance of selected activities over 4-6 weeks is not enough to elirni-
424 Children andAdo/escenls
nate pain, more global restrictions may be necessary (e.g., complete rest
or bracing).
iii. Rationale for bracing
(a) Provides external support to limit painful motion.
(b) Protects for purposes of healing (different studies show bony healing
rates from 18010 [Steiner, Micheli, 1985] ,40% [Jackson, Wiltse, 1981],
57010 [Sys, Michielsen, Bracke, Martens, Verstreken, 2001]).
iv. Types of braces
(a) Lumbosacral corset-with or without stays
(b) Thoracolumbosacral orthosis (TISO) (e.g., Boston overlap brace)
v. Utilization
(a) Lumbosacral corset best for intermittent use as postural reminder or
to provide added external support during selected activities.
(b) Boston overlap brace: consider for patients with spondylolysis with
positive bone scan when pain does not subside with conservative
measures (Table 3).
b. Before patient resumes activities, must correct abnormalities of flexibility
(especially hip flexors and hamstrings); postural correction.
c. Physical therapy program may be used to teach and train in proper body
mechanics and posture, as well as teach and supervise flexibility and trunk
stabilization exercises (especially abdominals); then monitor gradual return
to activities.
Table 3. Suggested Bracing Protocol

Protocol for use of Boston overlapbrace
Indications:
1. Acute spondylolysis 2. Lumbar disc disease
a. Pain uncontrolled with rest and conservative a. Degenerative or bulging disc (without radiculop-
measures athy); refractory to conservative measures
b. Positive bone scan/SPEer scan b. Central disc protrusion
c. Evidence of slippage (spondylolisthesis c. Disc protrusion with segmental hypermobility
d. Young age (before peak adolescent
growth spurt
Weeks Hours/Day in Brace Activity Level Physical Therapy
1-4 23.5+ ADLs; no extra or unnecessary Assist with brace adjustment;
activity. no extra exercises.
5-8 23.5+ ADLs, moderate aerobicactivity Upperand lowerextremity
as tolerated in brace (cycling, flexibility and strengthening;
stair machine, walking) trunk isometric (in brace).
9-12 20+ ADLs, moderate to strenuous Progressive strengthening and
(out of brace for aerobic aerobics in brace; may do neu- conditioning (supervised, out
exercise and physical tral spine aerobics out of brace of brace) trunk stabilization
therapy) (swim, cycle) out of brace; start in neutral;
progress to full ROM
13+ Benin weaning in 1-2 ADLs out of brace first; then Supervise and monitor wean-
hour increments; increase increase aerobic activity out ing from brace; progressive
time out of brace over 4-6 of brace; continue with "neu- trunk stabilization; supervise
weeks tral" aerobics while gradually resumption of sport-specific
starting a running program. skills.
ADLs = activitiesof daily living; ROM = range of motion.
d. Treatment is aimed at pain reduction and restoring normal, pain-free func-
tion; documentation of bony healing is not necessary before return to
sports.
10. Treatment for spondylohsthesls-similar to spondylolysis, but must also closely
monitor for progressive slippage
a. Under age 10, follow lateral radiograph every 6 months (slip usually occurs
during adolescent growth spurt).
b. With 25% slip but no symptoms: monitor for symptoms to develop; full
activities are permissible if patient remains clinically stable.
c. With 2: 50% slip but no symptoms: restrict from high-risk sports.
d. With 2: 50% slip with symptoms: rest, body jacket; fusion if symptoms
progress.
e. Any slip with persistent symptoms (> 1 year), nerve injury, progressive
slippage: consider fusion z decompression.
B. Lumbar facet syndrome
1. Etiology and pathogenesis
a. Secondary to repetitive and/or forceful extension.
b. Controversy exists about whether pain comes from facet joint capsular in-
flammation or trauma/arthritis of facet joint surface.
c. Seen in same population at risk for spondylolysis.
2. Symptoms
a. Low back pain at level of waist; worse with extension.
b. Pain may be unilateral or bilateral; usually does not radiate.
a. Hyperlordotic posture, tight hip flexors, hypermobile spine
b. Restricted or painful lumbar extension
c. Tenderness over facet joint and surrounding soft tissues
4. Radiographs
a. Plain films are usually normal
b. May see nonspecific changes in facet joints, including facet joint tropism
(asymmetric planes of motion) or facet subluxation.
c. SPECT imaging may show increased uptake in facet joint (as distinct from
pars interarticularis).
d. Plain films or MRI may reveal disc space narrowing or disc degeneration
(these changes may be the source of some of the patient's symptoms and
may contribute to some of the added stress on the facet joints).
5. Treatment-relative rest (minimize extension), antiinflammatory medication
and modalities, exercise to decrease lumbar lordosis and strengthen ab-
domina Is.
6. Differential diagnosis
a. The diagnosis of "facet syndrome" in an adolescent should not be made until
spondylolysis has been ruled out.
i. A normal plain film with obliques rules out chronic spondylolysis.
ii. A negative bone scan/SPECT scan rules out acute spondylolysis.
b. Other causes of posterior element pain pattern
i. Lateral disc herniation (extrusion of disc material lateral to the nerve
root or into the neuroforamen).
ii. Foraminal stenosis (due to extruded disc fragment, neurofibroma, con-
joint nerve root, or spondylolisthesis)
iii. Osteoid osteoma (in lamina, facet, or pediclel-radiograph shows ovoid,
sclerotic lesion with central nidus.
426 Chilclren and Adolescents
iv. Atypical disc (central disc protrusion)

(a) Typical disc protrusion is paracentral in location.
(b) Atypical disc protrusion causes bulging of the anulus or protrusion in
the midline or central part of the disc; this is atypical because the
wall of the central portion of the disc is reinforced by the posterior
longitudinal ligament.
(c) A central disc protrusion, in the author's experience, may be seen
more commonly in individuals with segmental hypermobility.
v. Anterior Segment Problems

A. Disc disease in children and adolescents
1. Incidence
a. 2010 of all documented disc herniations
b. 10% of all causes of back pain under age 21
c. Reported in weight lifters, gymnasts, rowers, football players, wrestlers
d. Recognition of early disease enhanced by more sensitive diagnostic methods
(MRI)
2. Etiology and pathogenesis
a. Disc is well adapted to tolerate compression; however, disc does not tolerate
torsion or shear forces.
b. In skeletally immature patients, acute flexion/compression injury is more
likely to cause vertebral endplate fracture or intravertebral herniation of nu-
clear contents (Schmorl's nodes) rather than a paracentral disc herniation,
which may be seen in adult patients.
c. A displaced vertebral apophyseal fracture may clinically mimic a disc pro-
trusion or may be seen in combination with disc protrusion.
3. Symptoms-pain pattern
a. Paracentral low back; with or without radicular pain
b. Worse with flexion, twisting, sitting, coughing, straining
c. Better with standing, extension, lying prone
4. Physical exam
a. Sciatic scoliosis (lumbar shift), decreased or painful lumbar flexion (idio-
pathic scoliosis is not a cause of back pain).
b. Palpation may reveal tenderness in paraspinals, sciatic notch, or with ante-
rior translation of vertebrae.
c. May have dural tension signs or focal neurologic deficits; however, the
presence of such changes is not required to make the diagnosis of disc
injury.
5. Radiographs
a. Plain films: may see endplate fracture, Schmorl's node (cystic appearing lu-
cency contiguous to vertebral endplate); rarely see disc space narrowing in
young patient with early disc disease.
b. MRI: provides better detail of soft-tissue anatomy than plain films or
CT; MRI shows early degenerative changes in disc, disc protrusions,
disc herniations, extruded disc fragments, and neural compression or
displacement.
c. Myelography: still used for preoperative planning but has minimal role in
the initial evaluation of back pain in young patients because of the in-
creased quality and availability of MRI.
6. Treatment (progresses successively in stages outlined below)
a. Relative rest, modify activity (restrict lifting, bending, twisting, and pro-
longed sitting in nonsupportive chair).
b. Control pain, spasm, and inflammation.
i. Modalities: ice, electrogalvanic stimulation
ii. Medication: nonsteroidal antiinflammatories (minimize use of analgesics
and "muscle relaxants")
iii. Initial exercise: press-ups, extension exercises; lumbar traction
c. Mobilization of restricted soft tissues and joints
d. Flexibility-especially for hamstrings, hip flexors, lumbodorsal fascia
e. Training to restore normal and optimal mechanics; postural correction, spine
education
f. Stabilization (train trunk musculature to function as a corset for the spine-
help to support load and control motion)
i. Selective strengthening of trunk stabilizers to decrease shear and tor-
sional forces on disc.
ii. Emphasis on abdominals, obliques, hip extensors.
iii. Start with isometric exercises and exercise in neutral spine position; then
progress to exercises involving increasing degrees of trunk extension,
flexion, and rotation.
iv. Equipment for stabilization: free weights, tubing, pulleys, gym ball, wa-
ter exercise.
g. Restore and maintain general strengthening and conditioning.
h. Equipment options
i. Lumbar roll
ii. Lumbar corset
iii. Spinal orthosis
iv. Orthotics to correct lower extremity biomechanics or leg length differences
v. Supervised return to functional activities or sports; advance slowly as
symptoms allow.
7. Surgical indications
a. Persistent and/or progressive neurologic deficit.
b. Pain and/or dysfunction refractory to all conservative measures combined
with reliable confirmation of which disc(s) is (are) causing the pain and
how surgery will favorably alter the forces acting on the disc(s) that are
injured.
B. Differential diagnosis ofanterior segment conditians
I. Scheuermann's disease [juvenile kyphosis)
a. Incidence
i. 0.4-8.3010 of population
ii. Most common in boys aged 13-17
b. Diagnostic criteria
i. Wedging of 3 or more vertebrae by at least 5°.
ii. Kyphosis> 35°.
iii. "Classic" Scheuermann's occurs most commonly at T7-TlO.
iv. Thoracolumbar Scheuermann's occurs at Tl2-LI.
c. Symptoms
i. Apical (i.e., maximal point of curve) back pain; worse with flexion.
ii. Pain more common in thoracolumbar Scheuermann's.
iii. Low back pain in classic Scheuermann's is uncommon unless there is a
spondylolysis secondary to lumbar hyperlordosis.
d. Physical exam
i. Increased thoracic kyphosis
ii. Increased lumbar lordosis
iii. Acute angulation of thoracic spine seen with forward flexion
428 Children and Adalescenls
iv. Prominent scapula, tight pectoralis muscles, forward head/neck position

v. Scoliosis present in 33%
vi. Neurologic exam usually normal
e. Radiographs
i. Irregular vertebral endplates
ii. Narrowing of vertebral endplates
iii. Schmorl's nodes (due to presumed disc herniation through vertebral
endplate)
iv. Persistent anterior vascular grooves
v. Anterior wedging of intervertebral spaces
(a) 5° wedging of 3 or more adjacent vertebral bodies in "classic"
Scheuermann's
(b) One or more wedged vertebra in thoracolumbar Scheuermann's
f. Differential diagnosis
i. Postural round back (distinguished by normal radiograph)
ii. Vertebral compression fracture
iii. Discitis, vertebral osteomyelitis, vertebral neoplasm
g. Treatment
i. For kyphosis < 35° or thoracolumbar involvement
(a) Lumbar flexion exercises
(b) Flexibility exercises for anterior soft tissues, pectoralis muscles
ii. For kyphosis> 45°, use brace (Milwaukee or TLSO)
iii. For kyphosis> 60°, apply surgical fusion and/or instrumentation
2. Discitis
a. Incidence-average age of occurrence 6 years (range: 1-18 years)
b. Etiology-Staphylococcus aureus most common
c. Symptoms
i. Abrupt onset back pain
ii. Radiation of pain to abdomen, hip, lower extremities
iii. Fever, malaise, irritability
iv. Symptoms do not follow mechanical pattern.
d. Physical exam
i. Restricted range of motion
ii. Limp
iii. Refusal to sit, walk, or move
e. Radiographs
i. Early changes-decreased disc space height
ii. Late changes-decreased disc height, erosions on vertebral endplates with
sclerosis
iii. Early detection by bone scan, gallium scan, and/or MRI
f. Laboratory
i. Elevated erythrocyte sedimentation rate, white blood cell count
ii. Blood culture should be obtained but may be negative.
iii. Needle biopsy-positive 20-500/0
g. Treatment
i. Intravenous antibiotics
ii. Bed rest, immobilization
3. Vertebral osteomyelitis
a. Symptoms
i. Presentation similar to discitis but in older population
ii. Does not follow mechanical pattern for back pain
Children and Adolescenls 429
b. Physical exam
i, Tenderness, spasm along spine
ii. Pain with percussion
iii. Splinting, guarding
iv. Possible kyphotic deformity
c. Radiographs
i. Lytic lesions, possible vertebral collapse on plain films
ii. Bone scan, MRI scan-positive early
d. Laboratory
i. Elevated erythrocyte sedimentation rate, white blood cell count
ii. Positive blood culture in 50010
iii. Positive PPO with tuberculosis
iv. Consider biopsy to establish diagnosis.
e. Treatment
i. Bed rest, immobilization in brace
ii. Intravenous antibiotics
iii. Possible surgical drainage
iv. Possible surgical fusion
4. Neoplasms
a. Most common forms
i. Benign: osteoid osteoma, fibrous dysplasia, osteoblastoma, aneurysmal
bone cyst, eosinophilic granuloma, giant cell tumor, hemangioma
ii. Malignant: Ewing's sarcoma, osteosarcoma, leukemia, lymphoma,
metastatic neuroblastoma, rhabdomyosarcoma, Wilm's tumor
b. Symptoms
i. Insidious onset of pain; night pain
ii. Pain not associated with activity; not relieved with rest (not mechani-
cal)
iii. Constitutional symptoms: fever, malaise, weight loss
c. Physical exam
i. Tenderness to palpation or percussion over spine.
ii. May see localized kyphosis or scoliosis.
d. Radiographs
i. Plain films-osteolytic bone destruction, thinning or fracture of cortical
margin, pathologic vertebral compression fracture.
ii. Bone scan-helpful in making early diagnosis and in localizing lesions.
iii. CT{MRI-to assess tumor morphology and to assess adequacy of spinal
canal if vertebral collapse or neurologic deficit is present.
e. Treatment-referral to specialist
5. Scoliosis
a. Definition: lateral curvature of the spine; most obvious on anteroposterior
radiography; scoliosis involves a 3-dimensional rotational deformity.
b. Classification
i. Idiopathic-650f0 of all patients
(a) Infantile-less than 3 years
(b) Juvenile-4-12 years (girls), 4-14 years (boys)
(c) Adolescent-greater than age 12 (girls); greater than age 14 (boys)
ii. Congenital skeletal abnormalities-150f0 of all patients
(a) Vertebral (e.g., myelomeningocele, hemivertebrae)
(b) Extravertebral (e.g., rib coalition)
iii. Neuromuscular-lOOfo of all patients
430 Children and Aclalescenls
(a) Neuropathic (e.g., cerebral palsy, spinal cord injury, tumors, poliomyelitis)
(b) Myopathic (e.g., muscular dystrophy)
iv. Scoliosis with neurofibromatosis-SOfo of patients
v. Mesenchymal disorders
(a) Congenital (e.g., Marfan's, Ehlers-Danlos syndromes)
(b) Acquired (e.g., rheumatoid arthritis)
vi. Trauma
(a) Fractures of vertebral body
(b) Surgical insult (e.g., laminectomy, thoracoplasty)
(c) Radiation
vii. Osteochondrodystrophies (e.g., diastrophic dwarfism, mucopolysacchari-
doses, multiple epiphyseal dysplasia)
viii. Infection of bone (e.g., osteomyelitis, tuberculosis)
ix, Metabolic disorders (e.g., osteomalacia, osteogenesis imperfecta)
x. Lumbosacral disorders (e.g., spondylolysis, spondylolisthesis, sacroiliac
anomalies)
xi. Tumors of vertebral column or spinal cord (see above)
c. Incidence
i, 20f0 of population has curve ~ 10°
ii. 0.2-0.30f0 have curves > 20°
iii. 0.1 0/0 have curves> 40°
iv. Higher incidence in girls than boys-especially for more severe curves
d. Etiology (theories on cause of idiopathic scoliosis)
i. Central nervous system abnormalities
ii. Hormonal and growth factors
iii. Abnormal proteoglycans
iv. Abnormal platelets and calcium metabolism
v. Abnormal skeletal muscle
vi. Genetics
e. Natural history
i. Factors associated with increased risk of progression
(a) Female gender
(b) Size of curve at time of presentation
(c) Skeletal immaturity
ii, SOOfo of curves < ISo do not progress
f. Symptoms
i, Pain due to scoliosis is rare; presence of pain should suggest diagnosis
other than idiopathic scoliosis.
ii. Respiratory compromise-only with most advanced cases.
g. Physical exam
i. General inspection
(a) Body habitus, Tanner stage (sexual maturation), syndromic features
(b) Skin lesions, pigmentary changes
(c) Cardiac exam, mitral valve prolapse murmur
(d) Hand/foot abnormalities
ii, Spinal inspection
(a) Obvious malalignment or curvature of spine
(b) Asymmetric shoulder height
(c) Asymmetric scapula
(d) Asymmetry in space between arm and body
(e) Rib hump with forward flexion
Children and Aclolescenls 431
iii. Common curve patterns (for idiopathic scoliosis)

(a) 900/0 single thoracic curve, convex to the right
(b) 800/0 thoracolumbar curve, convex to the right
(c) 700/0 of single lumbar curves, convex to the left
(d) 900/0 of double curves are right thoracic, left lumbar
(e) Appearance of left primary thoracic curve raises possibility of under-
lying neurologic or neoplastic cause.
h. Radiographs
i. Definition of terms
(a) "Cobb angle"-angle at intersection of lines drawn parallel to the
most steeply inclined vertebra at each end of the curve. The degree of
error in these measurements is 5_10° when performed by "experts."
(b) Curve location-determined by the level of the apical vertebra of the
curve (e.g., thoracic-above TIl; thoracolumbar-TII-TI2; lumbar-LI
or below).
(c) Direction of curve-named for convex side (same as side of rib
hump).
(d) Risser scale-measures degree of skeletal immaturity by looking at
progression of ossification of iliac crest from anterior to posterior;
Risser stage I = immature; Risser stage IV= mature.
ii. Standard views
(a) Standing anteroposterior (to include pelvis) and lateral (to evaluate
kyphosis).
(b) 1400 36 inch film is optimal.
iii. Additional views
(a) Oblique views of lumbar spine useful if back pain is present (to rule
out spondylolysis).
(b) Supine side-bending views can determine the degree of flexibility of
curve.
iv. Radiation exposure
(a) Average patient has 22 radiographs during course of treatment.
(b) Most sensitive tissues to ionizing radiation include breast, bone mar-
row, thyroid, eyes, ovaries, and testes.
(c) All radiation-sensitive tissues, except marrow, can be shielded.
(d) Posteroanterior projection may reduce radiation to breast, abdomen,
and thyroid when compared to anteroposterior projection; must allow
for magnification effect.
(e) Radiation exposure limited by modem equipment, e.g., high-speed
film, rare earth screens, special grids, collimation of x-ray beam.
i. Treatment
i. Options
(a) Exercise: no proved benefit; may decrease or control mechanical
pain.
(b) Electrospinal stimulation: good patient acceptance; questionable re-
sults with curves> 30°.
(c) Bracing: Cervicothoracolumbosacral orthosis (CnSO); Milwaukee
brace.
(d) Surgery: spinal fusion with instrumentation.
ii. Treatment and monitoring recommendations
(a) 15-20° curves: follow with repeat radiograph every 6-12 months
during rapid growth.
432 Children and Adolescents
(b) 30-45° curves or documented interval progression of 6-7°: CTLSO

(bracing).
(c) > 50°: surgery.
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1 - - - - - - - -26
Elderly Patients
Robert G. Viere, M.D.
Key Points
• The most common cause of back pain in the elderly is degenerative spondylosis of the
spine.
• Insufficiency fractures above T8 are less common in osteoporosis, and evaluation for
other etiologies should be undertaken.
• Patients with osteoporosis who receive increased dosage of corticosteroids are at risk
for a cluster of multiple compression fractures and should be braced at initiation of
high-dose corticosteroids.
• Spinal stenosis should be actively treated, and no assumptions should be made that
"it's just old age."
• Osteoporosis should be prevented by building peak bone mass in early life and treating
hormone deficiencies.
• Surgical treatment of insufficiency fractures requires overcorrection of kyphotic de-
formity, or it is doomed to failure-it should be undertaken only for progressive
deformity and neurologic loss.
• Newer medications (transdermal estrogen, selective estrogen receptor modulators, 3rd
generation biphosphonates, and slow release fluoride) hold promise for the future.
I. Introduction
A. Back pain is a condition that effects the majority of people at some time during
their lives.
B. In 1990, it is estimated that the direct costs of spinal disorders exceeded 23 billion
dollars.
C. Approximately 25010 of all visits to physical therapists were due to back-related
problems.
D. Among the elderly, the most common causes come under the categories of degen-
erative, neoplastic, or metabolic disorders of the spine.
II. Degenerative Conditions of the Spine

A. Definition: spondylosis is the term used to describe degeneration of the lumbar
spine.
B. Epidemiology
I. Yearly prevalence in the 15-20010 range.
2. Chronic back pain present in 3-7010 of adult population.
3. Lifetime prevalence exceeds 70010 in all industrialized countries.
4. 1010 of U.S. population is chronically disabled by back pain.
5. No strong relationship between height, weight, body build, and low back pain.
6. Heavy work, lifting, static work postures, bending and twisting, and vibration
are work factors associated with low back pain.
431
438 Elderly Palienls
7. By age 50, 97% of all lumbar discs have some degenerative changes.
8. Physical fitness is not a predictor of risk of acute low back pain, but the physi-
cally fit have a lower risk of chronic low back pain.
C. Sped'ic conditions
1. Disc herniations
a. Definition: a protrusion of a portion of the nucleus pulposus through the
fibers of the anulus of the intervertebral disc.
b. Epidemiology
i. The prevalence of herniated lumbar discs is 1-3 % with a lifetime history
of sciatica in 22.4% of 45-54-year-olds.
ii. Operation rates vary from country to country; the rate per 100,000 is
100 in Great Britain, 200 in Sweden, 350 in Finland, and 450-900 in
the U.S.
iii. 95% of all operations are at L4-L5 or L5-S1.
iv. The mean age is 40-45 years; male:female ratio equals 2: 1.
v. Much less common in patients over 65 years.
c. Clinical features
i. History of sciatica-pain radiating in the distribution of a lumbar der-
matome below the level of the knee.
ii. Positive straight leg-raising (SLR) test
(a) Below 30°, straight leg raising is highly predictive of herniated nu-
cleus pulposus (HNP).
(b) Above 50°, its diagnostic significance decreases.
iii. Contralateral SLR is highly specific for herniation.
iv. Certain clinical signs have predictive value in diagnosing a large disc
herniation; order of decreasing importance:
(a) Reflex asymmetry
(b) Motor weakness
(c) Sensory loss
d. Imaging studies
i. Magnetic resonance imaging (MRI) most sensitive and specific tool.
ii. Myelography with computed tomographic (CT) scanning has> 92% sen-
sitivity and > 90% specificity.
e. Treatment
i. Nonoperative
(a) Bed rest-2 days for patients with back pain, up to 7 days for patients
with sciatica.
(b) Progressive increase in activity-McKenzie extension exercises, aero-
bic (low-impact) exercise programs.
(c) Epidural cortisone injections: of short-term benefit but no proved
long-term benefit.
(d) As noted in previous chapters, aggressive physical therapy can also
be of benefit in the elderly; surgical consideration should be given for
patients who fail nonoperative management.
ii. Surgical
(a) Approximately 60% pain-free in long-term follow-up.
(b) 87% satisfied with care vs. 68% in nonoperative group.
(c) 5-15% need further surgery.
2. Spinal stenosis
a. Definition: no universally accepted definition; however, generally de-
fined as < 100 mm3 of area for the dura available in the neural canal.
EIJer/y Patients 439
Confirmation of diagnosis requires myelographic evidence of obstruction

to distal flow of contrast material or MRI evidence of compression of
cauda equina.
b. Epidemiology: affects approximately 100/0 of population over the age of 65
to varying degrees.
i. Cardinal symptom is pseudoclaudication or neurogenic claudication
(94%), provoked by standing or walking.
ii. Description of pain (93%), numbness (63%), weakness (43%).
iii. Symptoms into bilateral legs (69%) accompanied by back pain (65%).
iv. Site: whole limb, 78%, above knee only, 15%; below knee only, 7%.
v. Ankle reflexes reduced or absent in 43%.
vi. Knee reflexes reduced or absent in 18%.
vii. Objective muscle weakness in 37%.
viii. Electromyogram (EMG) abnormal in 920/0.
ix. Symptoms made better by adopting flexed posture.
x. True vascular claudication is muscle pain of cramping quality without
paresthetic quality, provoked by walking and relieved by standing.
xi. Cycling provokes vascular claudication but is generally well tolerated
by stenotics.
xii. Extended posture in lumbar spine exacerbates symptoms.
xm. Symptoms may wax and wane in intensity.
d. Diagnostic studies
i. CT/myelography is gold standard.
ii. MRI shows contributions from disc lesions, hypertrophied ligamentum
flavum, and facet capsules.
iii. MRI with high-resolution CTscan may significantly decrease the need
for myelography.
e. Treatment
i. Nonoperative
(a) Lumbar flexion exercises: flexion increases the size of the neural
canal and therefore alleviates the patient's neurologic symptoms to
some degree.
(b) Low-impact aerobic conditioning is important to build endurance in
the available muscles. Bicycling may be of benefit to patients with
stenosis in deterring the onset of neurogenic claudication, because it
tends to put the patient in a flexed posture through the lumbar
spine, which increases the size of the neural canal and allows more
vigorous exercise.
(c) Epidural cortisone injections give symptomatic relief but long-term
benefits are unclear.
(d) Calcitonin has been shown to reduce symptoms of stenosis in recent
studies and may be helpful in patients who medically are not candi-
dates for other options. Doses are similar to those used in osteo-
porosis.
ii. Surgical
(a) Lumbar laminectomy and foraminal decompression have approxi-
mately 85% rate of significant improvement in symptoms.
(b) Reoperation rate is 15-200/0;
(c) If stenosis is due to instability (spondylolisthesis or degenerative
scoliosis), concomitant fusion is necessary.
440 Elderly Patienls
3. Degenerative spondylolisthesis
a. Definition: the anterior slippage of one vertebra onto the next lower vertebra
due to degenerative changes in the facet joints and/or intervertebral disc at
the same level.
b. Epidemiology
i. 100/0 of women over the age of 60 have a first- or second-degree slip.
ii. L4-L5 most common level, followed by L3-L4.
iii. Five times more common in women over 40 years old.
iv. Sacralization of L5 is four times more common than in general population.
v. Slippage seldom exceeds 25-300/0.
i. Primarily low back pain due to facet arthrosis.
ii. Progression may lead to symptoms of spinal stenosis due to neural com-
pression at level of slippage.
iii. Leg pain may be primary complaint in approximately 400/0 characterized
by pseudoclaudication.
iv. EMG changes in approximately 400/0, of which 800/0 involve the root be-
low the slip.
d. Treatment
i. Nonsurgical
(a) Exercise programs: flexion exercises, aerobic conditioning, trunk
strengthing, and stabilization exercises
(b) Bracing: intermittently to control symptoms during exacerbations.
(c) Medications: nonsteroidal antiinflammatory drugs and analgesics for
short periods.
(d) Facet joint and epidural blocks may give symptomatic relief of un-
known long-term efficacy.
ii. Surgical
(a) Necessary in approximately 10-15010 of patients with degenerative
spondylolisthesis.
(b) Patients presenting with neurologic complaints do better than pa-
tients with only low back pain.
(c) Patients treated with decompression and fusion do better than pa-
tients with decompression or fusion done alone, dependent of the
degree of mobility of listhesis.
4. Degenerative adult scoliosis (Fig. 1)
a. Definition: sometimes called collapsing scoliosis and/or senescent lumbar
scoliosis.
b. Epidemiology
i. Prevalence approximately 60/0 in patients 60 years of age.
ii. 320/0-38010 prevalence in patients with osteoporosis or osteomalacia.
i. Low back pain
ii. 900/0 of degenerative scoliosis cases may have symptoms indicative of
spinal stenosis.
iii. Pain aggravated by spinal extension.
iv. Sitting down less likely to relieve symptoms than in typical stenotic
patients.
v. Need to support body weight on arms to get relief.
vi. May occur as a complication of decompression for spinal stenosis.
vii. Curves tend to be of lower magnitude than in idiopathic curves with as-
Elderly Patients 441
FIGURE I. A 70-year-old patient who had

undergone previous decompression from
L3 through L5 for spinal stenosis presented
with degenerative scoliosis not previously
present and recurrent stenosis at the L3-4
level. Thehallmark of collapsing or degen-
erative stenosis is the increased incidence
of lateral translation, as seen here at the
L3-4level.
sociated degeneration but are more likely to have lateral translation

they are less likely to have significant rotational component.
viii. Discography can be helpful in selecting levels to be fused in patients
with idiopathic scoliosis and back pain. However, discography has no
role in diagnosing degenerative scoliosis, because the pain is generally
not reproduced by discography.
ix. Myelographic defects most commonly seen within the compensatory
lumbosacral curve in idiopathic scoliosis patients and tend to be in the
concavity of the primary curve in patients with degenerative scoliosis.
d. Treatment
i. Nonsurgical-covered in Chapter 10; however, specific modalities that
can be useful include:
(a) Nonsteroidal antiinflammatory medications
(b) Flexion exercises as well as general aerobic conditioning
(c) Braces and corsets used temporarily during acute exacerbation
(d) Treatment of coexistent osteoporosis or osteomalacia
ii, Surgical
(a) Nerve root symptoms and spinal stenosis are major indications.
(b) Decompression alone only for patients in whom disease is limited to
one nerve root and facets can be preserved.
(c) Incorporation of all levels with rotary subluxation, disc space nar-
rowing, and wedging into the fusion.
(d) Important to maintain or obtain lumbar lordosis, even if it requires
concomitant anterior fusion.
(e) 85-900/0 good results in adult scoliosis if above criteria followed.
(tl Treatment of concominant compression fracture with kyphoplasty
or vertebroplasty to prevent progressive collapse.
III. Neoplastic Conditions of the Spine

A. General Considerations
1. Metastatic lesions are much more common than primary spine tumors in the
elderly.
442 EkJeny Patients
2. In patients over the age of 21, over 700/0 of primary spinal neoplasms are ma-
lignant.
B. Primary Tumors
1. Presentation
a. Most consistent complaints (840/0) are back pain.
b. Pain tends to be progressive, unrelenting, and unrelated to activity. Pain at
night is common.
c. Approximately 400/0 of patients present with weakness. Usually focal in na-
ture.
2. Benign tumors:
a. Much less common in the elderly.
b. Hemangioma most common.
i. Occurs in 10- 120/0 of all people.
ii. Rarely symptomatic.
c. Other primary tumors include osteochondroma, osteoblastoma, giant cell tu-
mor, and aneurysmal bone cyst, all of which are uncommon in the elderly.
3. Malignant tumors:
a. Multiple myeloma and solitary plasmacytoma
i. Most common malignant primary spinal tumor.
ii. Incidence of 2-3 per 100,000, with plasmacytoma accounting for only
30/0 of all plasma cell neoplasms.
iii. Patients with solitary plasmacytoma may have prolonged survival de-
spite eventual progression to myeloma.
iv. Prognosis for survival in disseminated myeloma is poor.
(a) 5-year survival rate of 18%.
(b) Spinal column involvement denotes an even worse prognosis.
v. Solitary plasmacytoma of the spine has approximately a 600/0 5-year,
disease-free survival rate.
vi. Treatment of solitary plasmacytoma is irradiation.
vii. Surgery is reserved only for rare refractory cases or where pathologic
vertebral fracture requires surgery for progressive deformity.
viii. Need to consider in the diagnosis of patients who present with vertebral
compression fractures.
b. Chordoma
i. Relatively rare but found predominantly in patients in Sth and 6th
decades of life.
ii. Tends to occur in the suboccipital or sacrococcygeal regions of the
spine.
iii. Surgical extirpation with wide margins is the only curative procedure.
iv. Newer radiation treatment with Proton beam radiation allows high dose
directed treatment with sparing of adjacent neurologic structures, but
its availability is limited.
c. Other primary malignant tumors include osteosarcoma, which may occur in
pagetoid bone; chondrosarcoma; and Ewing's sarcoma, all of which are rare.
C. Metastatic tumors
1. Diagnosis
a. Axial skeleton is the third most common site of metastases, after lung and
liver; lumbar spine most common area in the spine.
b. Prognosis is more dependent on tumor type, location, or extent of metas-
tases.
c. Most common symptom is back pain unrelated to activity.
EIJerIy Patients 443
d. Approximately 8- 100/0 of time, metastatic lesion with neurologic involve-

ment is presenting symptom of cancer.
e. The most common tumor metastatic to the spine is breast followed by lung,
prostate, GI tract, and kidney (Table I).
2. Treatment options:
a. Radiation and chemotherapy
i. The majority of spinal metastases are radiosensitive.
ii. Even patients with neurologic involvement should be given radiation
as initial prescription, except for very specific circumstances outlined
below.
iii. Bracing can be performed to maintain spinal alignment while radiation
therapy is ongoing. The majority of bony lesions heal after radiation.
b. Surgery is reserved for specific indications:
i. Tumor known to be non-radiosensitive.
ii. Progressive neurologic deficit while undergoing radiation therapy.
iii. Neurologic deficit due to deformity or fracture caused by tumor and not
to tumor itself.
iv. Patient with limited life span who would not be able to be functional
without surgical stabilization to decrease pain or stabilize spine.
IV. Metabolic Conditions of the Spine

A. Osteomalacia
1. Definition: generally described as a group of diseases denoted by a decrease in
the primary mineralization of newly formed bone matrix or osteoid.
2. Pathophysiology
a. Trabeculae are irregular and thinned.
b. Areas of lightly stained osteoid are present due to a defect in primary miner-
alization related to defects in vitamin D intake or metabolism.
3. Clinical features
a. Osteopenia on radiograph with coarsened trabecular pattern.
b. Looser's zones or pseudofractures present on radiograph are typically bilat-
eral and symmetrical.
c. In vitamin D deficiency, calcium and phosphate levels are decreased; alka-
line phosphatase is increased; parathyroid hormone is normal or increased,
and urinary calcium and phosphorus are decreased.
4. Differential diagnosis
a. Vitamin D deficiency
i. Less common today due to vitamin D supplementation; more common in
colder northern climates due to decreased sunlight.
Table 1. Estimated New Cases for Major Sites of Cancer and 'ercent of
Spinallnvolvement-Most Comman Tumors
Site No. of Cases % Spine Involvement
Lung 149,000 10-30
Colon/rectum 140,000 20-30
Breast 123,000 50-70
Prostate 90,000 50-80
Urinary tract 60,500 10-25
444 EIcler/y Polienls
ii. Diets high in phytate or lignin, which bind bile acids, can decrease vita-
min D absorption.
iii. Increased in elderly, particularly those who are housebound or institu-
tionalized.
b. Gastrointestinal malabsorption
i. Most common cause of vitamin D deficiency in the U.S.
ii. Can be seen in sprue, gluten-sensitive enteropathy, regional enteritis, or
patients who have had resection or bypass of the small intestine (espe-
cially Bilroth II procedures).
c. Liver disease
i. Complication of chronic biliary ductal and hepatocellular disorders. Bile
acids are necessary for vitamin D absorption.
ii. Liver major site of 25-hydroxylation of vitamin D3 with active form of
vitamin.
iii. Liver disease can lead to decreased vitamin D absorption due to de-
creased bile production.
iv. Cholestyramine therapy may add considerably to risk of osteomalacia.
v. Severity of liver disease, on lab evaluation, does not correlate with de-
velopment of osteomalacia.
d. Anticonvulsant drugs
i. Most commonly seen with phenobarbital or phenytoin.
ii. Also may be seen with primidone and acetazolamide.
e. Renal osteodystrophy
i. Secondary hyperparathyroidism
ii. Abnormal vitamin D metabolism-decreased l-hydroxylation of 25-0H-D
to I, 25(OH)2 (vitamin 03)
5. Treatment
a. Vitamin D deficiency states can generally be cured by intake of 1,600 IU
(400 IU is RDR) per day.
b. Need to provide active metabolite I, 25 dihydroxy vitamin D3 in renal os-
teodystrophy.
c. Dosages in the range of 5,000-10,000 IU/week are required for patients with
osteomalacia on anticonvulsant medications.
d. Dosages from 2,000-10,000 IU may be needed in liver disease.
B. Pagel's Disease
1. Definition: disease characterized by excessive and abnormal remodeling of
bone; named after Sir James Paget.
2. Pathophysiology
a. Thickened and disordered trabecular pattern termed "mosaic."
b. Active phase is associated with aggressive bone resorption followed by ex-
cessive and disorganized bone formation, leading to dense sclerotic but bio-
mechanically weak bone (Fig. 2).
3. Clinical features
a. Increased frequency with age-approximately 1O-110f0 of patients over age
80.
b. Predilection for the axial skeleton.
c. May be mono- or polyostotic
d. Presents with local pain and tenderness.
e. May present with increasing size of involved bone (e.g., increased hat size).
f. May lead to pathologic fracture with resulting pain or angulation as well as
stiffness and osteoarthritis of joints.
Elderly Patienls 445
fiGURE 2. Sagittal MRI of a 64-year-old woman with

Paget'sdisease.TheLA vertebrashows a biconcave type
of insufficiency fracture pattern as well as the circumfer-
ential enlargement of the vertebral body, which is com-
mon in Paget'sdisease.
g. Neuromuscular complaints common: muscle weakness, paralysis, and incon-

tinence may result from enlargement of involved vertebrae causing spinal
stenosis or fracture of mechanically weak vertebrae.
h. Compression of cranial nerves in their foramen not uncommon.
i. Congestive heart failure may occur due to hyperemia and increased blood
flow in involved bone.
j. Etiology unclear-possible viral cause postulated.
k. Associated with a form of osteosarcoma-has bad prognosis.
4. Laboratory findings
a. Increased alkaline phosphatase and hydroxyproline levels in serum
b. Increased hydroxyproline levels in urine.
c. Serum calcium and phosphorous levels generally normal.
d. The key to making the diagnosis is clinical suspicion. In rare cases, biopsy
may be necessary.
5. Treatment
a. Diphosphonates-20 mg/kg/day for 1 month; lower dosages for long-term
suppression. Risedronate (third generation biphophonate) effective against
Paget's Disease at 40 mg per day. Pamidronate given intravenously can be
effective for patients unable to tolerate oral therapy.
b. Calcitonin-1.5-2.0 IU/kg/day in divided doses; relapses occur with discon-
tinuation of treatment.
c. Mithramycin-15-25 J.Lg/kg/day intravenously for 10 days for cases of im-
pending paraplegia without fracture.
d. Surgery reserved for cases of progressive spinal stenosis or impending para-
plegia due to vertebral expansion or vertebral fracture.
e. Pretreatment for period of time preoperatively with diphosphonate
etidronate decreases blood flow and makes surgery safer in elective decom-
pression of spinal stenosis.
446 Elderly Patients
f. New diphosphonates under investigation at this time with more selective de-
crease in bone resorption.
C. Osteoporosis
1. Definition: generalized decrease in bone mass, with the remaining bone being
histologically and chemically normal.
2. Epidemiology
a. Affects 15-20 million U.S. citizens and causes 1.5 million fractures an-
nually.
b. In 1991, approximately 10 billion dollar cost.
c. 50% of women over age 65 and 90% over age 75 have radiographic evi-
dence of osteoporosis.
d. Fractures above T8 less likely with osteoporosis; need to consider other
causes.
e. T8, 112, Ll, and L4 most common vertebral fractures.
f. 25% of women over 50 suffer one or more compression fractures, most often
precipitated with weight on outstretched arms.
g. Most common in white women (17.1/1O,OOO/year), followed by white men
(9.9/10,000/year).
h. One standard deviation decrease in lumbar bone mineral density comparable
to 12-year increase in age.
L 400/0 prevalence of vertebral fractures by age 85-89, 65% of which do not
come to attention of physician.
3. Pathophysiology
a. Normal bone structure.
b. Osteoclasts produce excessively deep cavity or osteoblasts fail to fill normal
resorption cavity.
c. Excessive osteoclast activity may lead to perforation and loss of entire tra-
beculae so that osteoblasts have no remaining scaffold on which to form
bone.
4. Major causes of generalized osteoporosis (Table 2). Proposed risk factors for
postmenopausal women (Table 3).
5. Clinical features:
a. Osteopenia
b. Compression fractures
i. 3 patterns
(a) Anterior wedge compression
(b) Biconcave
(c) Crush pattern
Tobie 2. Molor Couses ofOsteoporosis

Senile and postmenopausal states Endocrine states Deficiency states
Medication Hyperthyroidism Scurvy
Steroids Hyperparathyroidism Malnutrition
Thyroid hormones Cushing's disease Calcium deficiency
Heparin Acromegaly Alcoholism
Antacids containing aluminum Pregnancy Chronicliver disease
Isoniazid Diabetes Anemic states
Hypogonadism
Eklerly Patients 447
Table 3. Proposed Risk Factors for Low Bone Mass In Postmenopausal Women
Femalegender Nu11iparity
White or Asian ethnicity Alcohol abuse
Positive family history High sodium intake
Low calcium intake Cigarettesmoking
Early menopause High caffeine intake
Oophorectomy High protein intake
Sedentarylifestyle High phosphate intake
ii. Treatment
(a) Bed rest
(b) Pain management with local or systemic analgesia
(c) Bracing to improve comfort
(d) Patient reassurance
(e) Treatment of underlying osteoporosis, osteomalacia, or neoplasm
(f) Calcitonin nasal spray (Miacalcin) can help with bone pain and stim-
ulate production of new bone.
iii. Surgical treatment
(a) Progressive kyphotic deformity with neurologic deficit
(b) Imperative that surgery correct deformity to bring weight-bearing ac-
cess posterior to instrumentation to make it load-sharing and not
load-bearing (Fig. 3).
(c) Kyphoplasty can be helpful in acute compression fracture with spinal
canal compromise to prevent progressive kyphosis.
(d) Vertebroplasty for patient with subacute fractures with continued
pain. Be aware of risks!
iv. Radiologic assessment
(a) Conventional radiographs-300/0 of skeletal calcium must be lost.
(b) Radiogrammetry--measuring thickness of metacarpal or phalangeal
cortical bone thickness; no information about trabecular bone.
(c) Radiographic absorptiometry:
(i) Single-photon absorptiometry (SPA)
• Confined to appendicular skeleton.
• Cannot differentiate between cortical and trabecular bone.
• Correlates to some degree with osteoporotic fractures.
(ii) Dual-photon absorptiometry (DPA)
• Dual-energy scanning eliminates need for constant path length.
• Measure cortical and trabecular bone, but cannot differentiate
between them.
• Used to measure bone mass in central skeleton or total body
mineral and fat content.
(iii) Dual-energy x-ray absorptiometry (DEXA)
• Modem upgraded version of DPA.
• Reduced examination time.
• Improved reproducibility.
• Most common technique used today.
• Aortic calcification and intervertebral arthrosis both falsely in-
crease measurement; lateral DEXA scanning of spine helps
eliminate this problem.
448 EIJer/y Patients
FIGURE 3. A and B, A 77-year-old woman presentedwithocute cauda equino syndrome secondoryto con-
tiguous osteaporotic fractures of the crush variety. The anteroposteriorview showsthe lateral translation of
l2 on l3 as the twovertebral bodies collapseintoeach other. Thelateralviewshows crushfractures withpro-
gressive collapseof the inferior aspect of l2 and the superior aspect of l3 withassociated localized kypho-
sis. C,Sagittal MRI showsretropulsion of bone intothe spinalcanal causing severespinalstenosis at the l2-L3
level. Dand E, Anteroposterior and lateralveiwstakenapproximate!>, 6 months postoperatively showthe sur-
gical reconstruction, which consisted of anterior decompression of the neural canal and osteotomy at the
l2-l3 level, bringingthe patientback intoa lordotic posture.Thelateralviewshowscomplete removal of the
pedides of l3. With the osteotomy, the l2 and l3 vertebral bodies take on the appearance of a singleverte-
bra. In patientswith osteaporosis, sagittal alignmentmustbe correctedduring the reconstruction.
(d) Quantitative computed tomography

(i) Only method that can separate trabecular and cortical bone com-
partments.
(ii) Only method that can give a true density estimate (in milligrams
per cubic centimeter).
(iii) Vertebral body most common site of use; uses reference density
substances as controls
Elderly Patients 449
(e) Quantitative ultrasonography

(i) Uses ultrasound velocity and attenuation measurements.
[ii) Measures confined to appendicular skeleton.
(iii) Questionable accuracy.
v. Nonoperative therapeutic options
(a) Prevention
(i) Direct relationship between weight-bearing exercise and bone
mass.
[ii] 1,500 mg calcium for adolescents, 1,000 mg for premenopausal
women, and 1,500 mg for postmenopausal women.
(iii) Replacement of deficient sex hormones.
(iv) Vitamin D supplementation-BOO ill in elderly.
(v) Evaluate patients at risk: premenopausal women with bone den-
sity one standard deviation below mean should consider receiv-
ing estrogen therapy; estimate rate of bone loss.
(b) Estrogen
(i) Accelerated bone loss in first 6-10 years after menopause but loss
related to low estrogen may continue for 20 years. Typically after
the 6-10 year period, the rate of loss returns to the pre-
menopausal level.
[ii] Prolonged amenorrhea in young women should be treated.
(iii) Begin soon after menopause.
(iv) Need 0.625 mg of conjugate estrogen to retard bone loss.
(v) Transdermal beta estradiol, 0.1 mg, has been shown to retard
bone loss.
(vi) May decrease incidence of cardiovascular disease by up to 500/0.
(vii) Contraindicated in patients with history of breast cancer or uter-
ine cancer.
(viii) Medroxyprogesterone acetate, either cycled through days 11 to
21 or used continuously, eliminates increased risk of endometrial
cancer.
[ix] With continuous medroxyprogesterone, spotting general stops
after 2-6 months.
(x) May cut the incidence of fracture by 500/0 if begun in early
menopause.
(xi) Annual mammography and physician exam.
(c) Calcium
(i) 1,500 mg in postmenopausal women.
[ii) Calcium citrate with better bioavailability.
(iii) Generic brands may have less bioavailability.
(iv) Use with 400-BOO IU of vitamin D.
(d) Calcitonin
(i) Decreases loss of trabecular bone but may not reduce cortical loss.
(ii) May be useful in patients who cannot take estrogen.
(iii) Nasal forms are also available.
[iv] Resistance less common if given nasally or not continuously.
(e) Biphosphonates
(i) Etidronate given 14 days on, 76 days off, has been shown to in-
crease spinal bone density and decrease fractures.
[ii] Etidronate also inhibits bone formation, and cannot be used con-
tinuously because it causes osteomalacia.
(iii) Impair osteoclasts' ability to resorb bone.
450 Elderly Patients
(iv) New biphosphonates (risedronate, alendronate) have been shown

to be effective in increasing bone mass. Major side effects are
GI-once weekly dosing may help.
(v) Pamidronate can be given intravenously 30 mg every 3 months
for patients who can not tolerate oral therapy.
(vi) Raloxifene (selective estrogen receptor modulator) has estrogen
like effects without stimulating breast or uterine tissue.
• Inhibit bone resorption at much lower dosages than inhibit
bone formation.
• Can be used continuously.
• Alendronate has just recently been approved by FDA for treat-
ment of osteoporosis.
(f) Sodium fluoride
(i) New slow-release fluoride plus continuous calcium citrate has
been shown to increase bone density and inhibit vertebral frac-
ture.
(ii) Side effects no higher than in placebo groups.
vi. Surgery
(a) Surgery should be reserved for patients who present with progressive
deformities and impending neurologic loss due to collapsing osteo-
porotic fractures.
(b) The goals of surgery should be decompression of neural elements and
stabilizing of the vertebral column.
(i) Requires getting the spine back into a normal balanced align-
ment.
[ii] Surgery should not be attempted unless the surgeon is prepared
to achieve this goal.
V. Medication Issues
A. Elderly comprise 12% of U.S. population but consume 33% of all prescription
drugs.
B. Incidence of adverse drug reactions is higher in persons over 65 years of age due
to the decreased renal function and higher incidence of liver disease, both pre-
medication and related to medication use.
C. Risk factors for falling-attention to and modification of can decrease risk of
falling.
1. Postural hypotension
2. Use of sedatives
3. Use of at least 4 prescription drugs
4. Impairment in arm strength, or range of motion, or ability to move safely in
transfers
5. Diazepam, diltiazem, diuretics, and laxatives: found to be risk factors for multi-
ple falls.
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,--------------27
I
Myofascial Pain, Fibromyalgia, and Soft
TIssue Causes of Low Back Pain
Joanne Borg-Stein, M.D., and Muhammad B. Yunus, M.D.
Key Points
• Myofascial pain syndrome (MPS), or regional fibromyalgia, is characterized by regional
musculoskeletal pain and localized area(s) of tenderness (trigger points) on digital
palpation that reproduce the pain complaint.
• Fibromyalgia syndrome (FMS) is defined as a chronic painful condition with widespread
musculoskeletal aching, accompanied by multiple widespread tender points.
• Both MPS and FMS are common conditions and frequently present with low back or
neck pain. FMS can be diagnosed reliably by widespread pain and tender points, as
delineated by American College of Rheumatology criteria.
• Patients with both MPS and FMS usually have other symptoms besides musculo-
skeletal pain, such as fatigue, poor sleep, headaches, and paresthesias. These are more
common in FMS that in MPS.
• Regional pain may also be caused by local pathology in the bone, disc, or soft tissues.
Common causes of regional soft tissue pain include: gluteus bursitis, ischial bursitis,
sacroiliac sprain, sacrococcygeal sprain, trochanteric bursitis, piriformis syndrome,
iliotibial band tendinitis, and iliopsoas bursitis/tendinitis.
• Acute trauma or mechanical overload may initiate or trigger MPS or regional soft
tissue pain. It is likely that mechanisms of symptoms in chronic MPS and FMS involve
aberrant central pain mechanisms. Psychological factors, poor sleep, physical trauma,
and muscle deconditioning are other factors that amplify chronic pain in both MPS
and FMS.
• Management of MPS and FMS includes firm diagnosis, reassuring patients about the
benign nature of both conditions (despite much genuine pain based on a biophysiologic
mechanism), emotional support, use of physical therapy, encouraging cardiovascular
fitness exercises, cognitive behavioral therapy in relatively difficult cases, local injection
of trigger points with lidocaine, use of simple analgesics, various tricyclic agents (TCAs),
and a combination of selective serotonin reuptake inhibitors in the morning and TCAs in
the evening. A multidisciplinary approach has been found to be helpful.
• Management of local soft tissue pain includes specific diagnosis, correction of muscle
imbalance and mechanical abnormalities, stretching tight muscles, strengthening weak
muscles, intralesional corticosteriod injection in cases of acute inflammation, and
education on appropriate sports specific training to avoid recurrence.
I. Myofascial Pain Syndrome

A. Definitions
1. Myofascial pain is defined as pain that originates from myofascial trigger
points, either alone or in combination with other pain generators.
453
454 Myolascial Pain, Fibromyalgia, and Soft Tissue Causes of Law Bac/e Pain
2. Myofascial trigger points are discrete areas of focal tenderness within a muscle
that reproduce the patient's pain and may have a characteristic referral pattern
when palpated.
3. Some clinicians prefer the term regional soft tissue pain as a clinically useful term
that encompasses pain and localized tenderness not only in muscles but also in
other contiguous soft tissues, such as ligaments and tendons.
B. Clinical features
1. Symptoms
a. Patients experience localized or regional deep aching sensation. Low back
pain may be associated with pain in the gluteal areas and thighs. Similarly,
neck pain may be accompanied by pain in the trapezius, and periscapular
muscles, with or without spread to the upper extremities.
b. Pain is usually chronic.
c. Frequently, associated autonomic dysfunction may occur, including abnor-
mal sweating, lacrimation, dermal flushing, and vasomotor/temperature
changes.
d. Cervical myofascial pain may be associated with neuro-otologic symptoms
including imbalance, dizziness, and tinnitus.
e. Functional complaints include decreased work tolerance, impaired muscle
coordination, stiffjoints, fatigue, and weakness.
f. Later stages can be compounded by sleep disturbance, mood changes, and
stress.
g. Nonmusculoskeletal symptoms, such as poor sleep, fatigue, and paresthesias
may be present but are less common in MPS than in FMS (Table I).
a. Begin with a careful general medical examination, including neurological
and musculoskeletal examination.
b. Analyze posture, biomechanics, and joint function.
c. Localized tenderness on palpation in the area of the pain with pain recogni-
Table 1. Comparison of Various Features of Fibromyalgia Syndrome and Myofasaal

Pain Syndrome Based on Evaluation ofAvadable Data
Features Fibromyalgia Syndrome Myofascial Pain Syndrome
Musculoskeletal pain Widespread Regional
Tender points Multiple, widespread Few, regional
Referred pain + ++
Taut band Similar to normal controls Similar to normal controls
Twitch response Probably similarto normal controls Similar to normal controls
Fatigue ++++ ++
Poor sleep ++++ ++
Paresthesia +++ ++
Headaches +++ ++
Irritable bowel ++ +
Swollen feeling in tissues ++ +
+ =24% or less; + + = 25-49%; + + + = 50-74%; + + + + = 75-100% of patients.
FromYunus MB: Fibromyalgia syndrome and myofascial pain syndrome:Clinical features, laboratory tests,
diagnosis, and pathophysiologic mechanisms.In Rachlin ES (ed): Myofascial Pain and Fibromyalgia. St. Louis,
Mosby, 1994, pp 3-29.
Myolaseial Pain, Fi&romyolgia, and Salt Ti_ Causes 01Law Back Pain 4SS
tion by the patient are the two most reliable signs. With training and time, a
skillful examiner should appreciate a "rope like" nodularity to the taut band
of muscle.
d. Referred pain on palpation of the tender/trigger point is often present. Pain
may radiate to the buttocks or lower extremities. Several common muscles
that may have trigger points are illustrated in Figure 1.
e. Neurologic and joint examinations should be normal; mildly restricted range
of motion (ROM) may be secondary to pain and muscle shortening.
Significantly decreased ROM of the cervical or lumbar spine (that does not
substantially improve after trigger or tender point injections) and neurologic
deficit suggest joint or disc disease.
3. Perpetuating or triggering factors
a. Trauma, including repetitive occupational trauma
b. Poor posture and ergonomic factors
c. Mechanical overload, e.g., from leg length discrepancy
d. Psychological factors: anxiety, stress, depression, poor coping skills
e. Poor sleep
C. Laboratory tests
1. Routine blood tests, such as complete blood count (CBC) and chemistry profile,
are normal.
2. Radiologic exam (x-rays, CT scan, MRI) is normal; mild osteoarthritis or disc
bulge may be coincidentally found.
3. Order MRI or CT scan only if pathology in bone, disc, or soft tissue is suspected
clinically.
4. Controlled studies of muscle biopsy in MPS show normal results.
D. Diagnosis
1. Regional musculoskeletal pain with localized tenderness on palpation (with or
without referred pain)
2. Significant arthritis and disc degeneration with or without nerve root compres-
sion usually can be ruled out clinically and, if necessary, by radiologic investi-
gations.
3. Pelvic and intraabdominal causes of low back pain can be ruled out by proper his-
tory, physical examination, and laboratory (including radiologic) investigations.
E. Differential diagnosis
I. Differential diagnosis includes overlapping causes of regional musculoskeletal
pain. Differential diagnosis should include (but is not limited to) the following:
a. Joint disorders: zygapophyseal joint disorder, osteoarthritis
b. Neurologic disorders: radiculopathy, entrapment neuropathy, metabolic my-
opathy
c. Inflammatory disorders: polymyalgia rheumatic a
d. Discoqenic disorders: degenerative disc disease, annular tears, protrusion,
herniation
e. Visceral referred pain: Gl, cardiac, pulmonary, renal
f. Mechanical stresses: postural dysfunction, scoliosis, leg length discrepancy,
poor body mechanics
g. Fibromyalgia or widespread chronic pain.
h. Psychological disorders: depression, stress, anxiety
F. Pathophysiologic mechanisms
1. Acute regional pain following trauma is probably caused by inflammatory
products [e.g., serotonin, potassium, bradykinin, and prostaglandins) with acti-
vation of nociceptors.
456 Myolascial Pain, Fibromyalgia, and Soh Tissue Causes of Low SackPain
fiGURE I. Common myofascial triggerpoints which cause lowback, buttock, and leg pain. (From Travell JG,
Simons DG, Simons LS: Myofascial Pain and Dysfunction, The Trigger Point Manual: Volumes 1 and 2,
Williams & Wilkins, 1999 and 1992, with permission.)
Myolasciol Pain, Fibromyalgia, and Salt Tissue Causes 01LowBack Pain 457
2. Chronic pain most likely results from centralization of acute peripheral pain, a
process referred to as central sensitization. Neurotransmitters (e.g., substance P,
NMDA, glutamate and nitric oxide) at the dorsal hom of the spinal cord, and
perhaps higher pathways, cause hyperexcitation of neurons with self-sustained
neuroplastic changes.
3. Recent research suggests the hypothesis of a pathological increase in release of
acetylcholine by the nerve terminal of an abnormal motor endplate resulting in
sustained depolarization, and abnormal muscle shortening and contracture.
4. Pain may be amplified by other factors, including psychological disturbance
(e.g., anxiety, stress, depression, poor coping skills), poor sleep, physical
trauma, mechanical overload, and muscle deconditioning.
G. Management
1. Pharmacologic:
a. NSAIDs: simple analgesics such as acetaminophen or low dose non-steroidal
anti-inflammatory drugs (NSAIDs).
b. Tramadol: This is a good option for moderate pain. This drug binds mu
opioid receptors weakly and inhibits reuptake of serotonin and norepi-
nephrine. It is a combination of weak opioid and inhibitor of serotonin
and norepinephrine. It is also available in a combination tablet with
acetaminophen.
c. Antidepressants: Tricyclic antidepressant agents such as low dose amitrypti-
line (10-50 mg) in the evening improve sleep and help pain. A combination
of a low-dose tricyclic agent in the evening and selective serotonin reuptake
inhibitor such as fluoxetine in the morning is a useful combination in more
severe cases.
d. Alpha-2 adrenergic agonists: Clonidine and tizanidine may be useful in low
doses, especially in the evening.
e. Botulinum toxin: Botulinum toxin A is emerging as a promising but expen-
sive agent for injection of trigger/tender points in cervical and lumbar myo-
fascial pain.
2. Non-Pharmacologic:
a. Discussion of diagnosis and its probable cause. Emphasize that the pain is
real and based on a pathophysiological mechanism.
b. Reassurance about the benign nature despite much pain.
c. Correction of posture, mechanical, and ergonomic factors at work or recre-
ation.
d. Stress reduction: Stress reduction techniques including meditation, progressive
relaxation training, and biofeedback are often incorporated into treatment.
e. Acupuncture
f. Massage, transcutaneous nerve stimulation, and ultrasound
g. Exercise: Encourage cardiovascular fitness through physical exercise
h. Stretch-and-spray techniques involves passively stretching the involved
muscle after application of a vapocoolant spray (e.g., fluorimethane). in 2-3
parallel, unidirectional sweeps. Allow 1 minute or so for rewarming, stretch
the muscle again, and repeat spraying several times until full muscle length
is achieved.
i. Trigger/tender point injection: Inject tender or trigger points with 1 ml of
1% lidocaine after accurate localization and pain reproduction. Advise post-
injection stretching and rest of the area for 24-48 hours to avoid post-injection
flare. Local application of ice for a few hours following injections usually
helps to prevent such a flare.
458 Myolascial Pain, Fibromyalgia, and Soft Tissue Causes 01Low Bacle Pain
II. Fibromyalgia Syndrome

A. Definition
I. Fibromyalgia syndrome (FMS) is characterized by widespread musculoskeletal
aching and multiple tender points at many locations. (See Diagnosis.)
2. A concomitant disease, such as rheumatoid arthritis (RA), osteoarthritis, or hy-
pothyroidism, does not rule out FMS. A satisfactory treatment of these diseases
has modest effect on the clinical picture of FMS. For example, a patient with
FMS and RA will continue to have widespread pain, fatigue, and multiple ten-
der points despite effective treatment of concomitant RA. Similarly, treating
hypothyroidism helps fatigue only to some degree.
B. Clinical features
1. Symptoms
a. Musculoskeletal pain and stiffness in a widespread location, usually involv-
ing neck, back, shoulder, and pelvic girdles as well as all of the extremities.
b. Patients may present with pain in one or two regions-e.g., low back or neck
(the most common areas)-but direct questioning reveals pain in many other
areas.
c. Peak age: 30-60 years
d. Gender: 900/0 of patients are women.
e. Other common symptoms (Table 2) are general fatigue, poor sleep, and
morning fatigue. Paresthesia is present in about one-half of cases, usually in
the extremities, and may mimic nerve root compression. Associated condi-
Table 2. Symptoms in Fibromyalgia Syndrome Based on Several Relatively Large Series

of Well-defined Patients Seen in Rheumatology Chnics
Symptoms % Frequency (Mean)· % Frequency (Range)
Musculoskeletal pain
Pain at multiple sites 100 100-100
Stiffness 78 76-84
"Hurt all over" 64 60-69
Swollen feeling in soft tissues 47 32-64
Nonmusculoskeletal
Fatigue (most times of the day) 86 75-92
Morning fatique" 78 75-80
Poor sleep' 65 56-72
Paresthesia 54 26-74
Associated symptoms
Self-assessed anxiety 62 48-72
Headaches 53 44-56
Dysmenorrhea 43 40-45
Irritable bowel syndrome 40 30-53
Restless legs syndrome 31§
Self-assessed depression 34 31-37
Sicca symptoms 15 12-18
Raynaud's phenomenon 13 9-17
Female urethral syndrome 12§
• Mean values derived from percentage figures reported in multiple studies.
t Morning fatigue is a sensitive indicator of nonrestorative sleep.
• Based on the question, "Doyou sleep well?," or a similarquestion,
§ Based on a single study.
Adapted from Yunus MB, Masi AT: Fibromyalgia, restless legs syndrome, periodic limb movement disorder
and psychogenic pain. In McCarty OJ Jr, Koopman WJ [eds]: Arthritis and Allied Conditions: A Textbook of
Rheumatology, Philadelphia, Lea Et Febiger, 1992, pp 1383-1405.
Myofascial Pain, Fibromyolgia, anJ SaltTissue Causes 01Low 8cH:1c Pain 459
tions, e.g., headaches, irritable bowel syndrome, and restless legs syndrome,
are common.
2. Signs
a. Examination of joints and nervous system is normal (despite symptoms of
swollen feeling in joints and numbness).
b. Range of motion of the cervical and lumbar spines may be slightly restricted
because of pain.
c. The most characteristic finding of diagnostic value is the presence of wide-
spread tender points. (See Diagnosis and Fig 2.)
d. Diffuse soft-tissue tenderness on palpation of the cervical, thoracic, and lum-
bar spine areas (including ligaments and paraspinal muscles) may be present.
e. Note: Diffuse tenderness "everywhere" does not necessarily indicate severe
psychological disturbance.
C. Laboratory tests
1. Complete blood count, chemistry profile, (BUN, creatinine, albumin, liver en-
zymes) erythrocyte sedimentation rate, rheumatoid factor, x-rays of joints and
spine, and bone scan are normal; antinuclear antibody is present in 100AJ (simi-
lar to normal controls). However, CBC and chemistry profile may be ordered to
Anterior Posterior
-----1
2-----+e
"'--_---3
FIGURE 2. Locotions of nine bilateral tender 5---1-- ~..._+---4
point sites to be palpated for testing American
College of Rheumatology criteriaforclossifico-
tion of FMS: (1) occiput (at the suboccipital
muscle insertion); (2) lowcervical (at the ante-
rior intertransverse spaces over C5-C7); (3)
trapezius (mid upper border); (4) supraspina- 6---'"
tus (abovethe scapular spine near medial bor-
der); (5) second rib (just lateral to costochon-
dral junction on upper surfaceof second rib);
(6) lateralepicondyle); (7) gluteal (upperouter 8--+-/11
quadrant); (8) greater trochanter (posterior to
trochanteric prominence); and (9) ~nee (medial
fat pad proximal to jointline). (From Yunus MB,
MasiAT: Fibromyalgia, restless legssyndrome,
periodic limb movement disorder and psy-
chogenic pain. In McCarty DJ Jr, Koopman
WJ (eds): Arthritis and Allied Conditions: A
Textbook of Rheumatology. Philadelphia, Lea
& Febiger, 1992, pp 1383-1405, with per- t .
mission.)
460 Myolascia/ Pain, Fibromya/gia, and Soh Tissue Causes af LowBack Pain
monitor drug therapy (NSAIDs, for example) and detect anemia that may con-
tribute to fatigue.
2. None of the several neuroendocrine tests found to be abnormal by controlled
studies (see Biophysiologic mechanisms) is of practical value for diagnosis.
Decreased glucose metabolism in the caudate nucleus, thalamus, and cortex
was found by photon-emission computed tomography.
3. Controlled studies show normal muscle biopsy, electromyography, and nerve
conduction studies.
4. Sleep electroencephalogram (EEG) studies may be requested to confirm clinical
suspicion of sleep disorders, such as periodic limb movement disorder, REM-
behavior disorder, and sleep apnea. Alpha intrusion into stage 4 delta wave is
seen in about 400/0 of patients, but these studies should be ordered only if there
is clinical suspicion of the above disorders.
D. Diagnosis
1. FMS is not a diagnosis of exclusion.
2. American College of Rheumatology Criteria: widespread aching (pain in right side
of body, left side of body, above waist, below waist, and in axial skeleton [cervi-
cal, thoracic, lumbar spine and chest wall]) and presence of 11 tender points
among 18 pose of uniform classification; they are also helpful in clinical practice.
3. Patients with characteristic symptoms (Table 2) but fewer tender points [e.g.,
8- 10) may be diagnosed with FMS in the clinical setting.
4. Several conditions may mimic FMS (Table 3), but their concomitant presence
does not exclude FMS.
E. Biophysiologic mechanisms
1. Significant peripheral pathology is absent.
2. Pain is best explained by an aberrant central pain mechanism; pain is not "all
psychological." Recent studies suggest central sensitization as the most impor-
tant CNS aberration.
Table 3. Presenting Features ofFibromyalgia Syndrome with Confounding

Diagnosis and Key Points ofDifferentiation
Presenting Features Confounding Diagnosis DiHerentiating Points'
Joint pain and swelling Arthritis Objective joint swelling
Diffuse muscular aching Polymyalgia rheumatica Increased erythrocyte sedimentation
and stiffness rate, decreased hemoglobin, weight
loss
Muscle fatigue, weakness Myopathy Objective weakness, increased muscle
enzymes
Fatigue. sensitivity to cold, Hypothyroidism Increased thyroxine, increased thyroid-
muscle pain stimulating hormone
Back pain and stiffness Ankylosing spondylitis Sacroiliitis
Sciatica-like pain Disc herniation Neurologic and radiologic findings of
disc herniation
Chest pain Cardiac or pleural pain Typical history of cardiac pain, pleural
rub; electrocardiographic. chest
x-ray. or other laboratory findings
of intrathoracic disease
*These points are characteristic of corresponding confounding diagnosis and absent in fibromyalgia syndrome.
Adapted from Yunus MR, Masi AT: Fibromyalqia, restless legs syndrome, periodic limb movement disorder
and psychogenic pain. In McCarty DJ Jr, Koopman WJ [eds]: Arthritis and Allied Conditions: A Textbook of
Rheumatology. Philadelphia, Lea Et Febiger, 1992, pp 1383-1405, with permission.
Myolascial Pain, Fibromyolgia, and Soft TiuueCauses of Law Back Pain 461
3. Controlled studies have shown an increase in cerebrospinal fluid (CSF), sub-
stance P (which mediates pain transmission), as well as a decrease in serum
serotonin (which mediates pain inhibition) and CSF 5HIAA (a metabolite of
serotonin). These findings may explain amplified pain and decreased pain
threshold in FMS.
4. Sleep abnormality has been objectively documented by EEG studies (see
Laboratory tests); disturbed stage-a sleep may explain reported decrease in
serum insulin like growth factor-l (IGF-I) (which reflects the integrated se-
cretion of growth hormone).
5. FMS is not a psychiatric condition; a psychological disturbance (anxiety, mental
stress, depression) is present in 30-400/0 of patients (generally similar to rheuma-
toid arthritis). Psychological factors seem to aggravate but not cause, pain. There
is no correlation between psychological status and other symptoms of FMS be-
sides pain (e.g., swollen feeling, paresthesia, and number of tender points).
6. Mechanisms of symptom production in FMS involve multiple interacting fac-
tors in a milieu of neuroendocrine dysfunctions (which may be induced or ag-
gravated by genetic predisposition, poor sleep, anxiety, depression, poor coping
skills, physical trauma, mental stress, or infection). (Fig. 3). The most important
neurological aberration is central sensitization, probably modulated by en-
docrine factors.
7. A subgroup of patients have significant anxiety, stress, or depression (about
30-400/0) and need focused treatment (see below).
7 '7
Genetic
Trauma Predisposition 0n om on
Heterogenous
Neuroendocrine-immune Dysfunction
FIGURE 3. Schematic represen-
tation of proposed model for bio-
physiologic mechanisms of FMS
t
Aberrant Central Pain
showsmultiple fadors that interact Mechanism
to amplify pain. Theprimary prob-
lem is currently believed to be in
the "box," i.e., a heterogeneous Fatigue _ Depression Pain
t Poor
neuroendocrine-immune aysfunc- Anxiety - _ sleep
tion. (Adopted from Yunus MB:
Toward a model of pathophysi-
/
Mental Physical
ology of fibromyalgia: Aberrant stress - - deconditioning
?SymJ~thetic !
central pain mechanisms with pe-
ripheral modulation. J Rheumatol
19:846-850, 1992, with permis- activlty- -Trauma
sion.)
t
?HYP!Xia- -Spinal
stress
Environmental
t
Poor
stimuli _ _ posture
Others _
Amplified Pain
(FIBROMYALGIA)
462 Myolascial Pain, Fibromyalgia, and Soft Tissue Causes 01Low Baclc Pain
F. Management
1. Make a firm diagnosis of FMS based on its own characteristics; avoid unnec-
essary investigations.
2. Educate patients regarding FMS.
3. Reassure patient that FMS does not cause tissue damage or crippling.
4. Demonstrate an attitude of understanding and empathy; this is crucial for suc-
cess in management; never imply that symptoms are "all psychological."
5. Elucidate probable mechanisms of pain to the patient in simple language (neu-
roendocrine dysfunction = chemical imbalance). Explain low serotonin and
how its deficiency causes pain. Significant psychological factors, if present,
should be explained as aggravating factors.
6. Recognize and address significant psychological factors, such as depression,
anxiety, mental stress (at home or work), and poor coping skills. Significant
depression or other psychiatric conditions require a larger dose of antidepres-
sant drug than the small dose prescribed for pain. A small minority of patients
may require referral to a psychiatrist for management of a severe psychiatric
disease.
7. Inquire about all aggravating factors that vary from patient to patient (Fig. 4);
individualize management.
8. Help patients to have restful sleep. Emphasize sleep hygiene (e.g., sleeping in a
comfortable, firm bed at the same time every day, avoiding caffeine, alcohol
or smoking in the evening, regular exercise early in the evening) and prescribe
a low-dose (10-50 mg) tricyclic agent in the evening (Table 4).
9. Encourage cardiovascular fitness. Exercises (e.g., brisk walking, swimming,
treadmill) should be increased gradually to attain desirable heart rate of 70-800/0
of age predicted maximum (220 minus age).
10. Prescribe physical therapy modalities (see Myofascial Pain Syndrome); physi-
cal therapy should be done initially under supervision in an institution 2-3
times/week for 3-4 weeks and then at home daily.
11. Promote behavioral modification through education including cognitive be-
havioral concepts. A psychologist may be consulted to encourage the patient
to assume self-responsibilities, change negative perceptions (e.g., "the pain is
going to cripple me and I can't do anything") to positive attitudes (e.g., I can
do my exercises without causing harm, and I can control my symptoms"), and
teach patients other coping skills.
12. A patient may be referred for relaxation techniques-se.g., electromyographic
biofeedback or hypnotherapy.
13. Inject the 1-4 most symptomatic tender points with 0.5-1 ml. of 10f0 lidocaine,
using a 27-guage needle at each site. Ask patient not to use the injected areas
for 24-48 hours to avoid postinjection flare. Injections can be repeated every
4 weeks if necessary.
14. Recommend acetaminophen and low-dose NSAIDs in mild cases.
15. Prescibe low-dose centrally acting drugs in moderate and severe cases; in-
crease dose to optimally tolerable level (Table 4).
16. Prescribe an SSRI (Table 4) in the morning and a tricyclic agent (TCA) in the
evening (both in low doses) if single agent does not help; combination works
better than either alone. However, keep the doses of both drugs low (e.g., flu-
oxetine 20 mg, amitriptyline <50 mg), since side effects ofTCA may be ac-
centuated. If in doubt, order serum tricyclic levels.
17. Educate patients about side effects of TCAs (particularly sedation, dry mouth,
and possible urinary retention) and SSRls (particularly gastrointestinal and
sexual side effects). SSRls may disrupt sleep if prescribed at hs or evening.
Myolascial Pain, Fibromyalgia, and Soh Tissue Causes 01LowBock Pain 463
pm""lImel
Netgtwmpnggw··
FIGURE 4. Various hostand environmental factors mayaggravate symptoms of FMS and shouldbe addressed
forcomprehensive management. The relative impartance of thesefOctors variesfrom patientto patient. (From
Yunus MB: Fibromyalgia syndrome: A guide to managementoptions to diminish pain-improve quality of
pain. Consultant, in press, 1996, with permission.)
18. Refer individual cases for cardiovascular fitness exercises and relaxation tech-
niques as necessary.
III. Soft TIssue Causes of Regional Low Back, Gluteal, or Leg Pain
A. Gluteal Bursitis
I. Location
a. Gluteal bursa lies under the gluteus maximus muscle
2. Etiology
a. Overuse (e.g., new exercise on a hip extension machine)
b. Leg length difference
c. Local trauma
d. Abnormal gait
e. Muscle tightness
a. Posterior gluteal and proximal thigh pain
464 Myofascial Pain, Fibromyolgia, and Soh Tissue Causes af Law Back Pain
Table 4. Centrally Acting Pharmacologic Agents Commonly Presulbed

In Flbromyalgla Syndrome-
Daily Dase Reuptake Inhibition Side EHects
Drugs Ronge(mg) Serolonin Norepinephrine Anticho/inelflic Sedation
Tricyclic agents
Amitriptyline 10-100 +++ + +++++ ++++
Doxepin 10-100 +++ + +++++ ++++
Imipramine 10-100 +++ ++ ++++ +++
Desipramine 10-100 ++ +++++ ++ +
Nortriptyline 10-100 +++ +++ ++ ++
Cyclobenzaprine 10-40 +++ + ++++ ++++
Triazolopyridine
derivative
Trazodone 25-200 ++ 0 + +++
SSRls
Fluoxetin 10-60 ++++ 0 + 0
Paroxetine 10-40 +++++ 0 + 0
Sertraline 25-150 ++++ 0 + 0
Atypical
antidepressants
Venlafaxine 25-100 +++ ++ + 0
Nefazodonet 50-400 +++ + + 0
Atypical opioid
Trarnadol" 150-400 + + 0 0
• Although drugs in this list are labeled as "antidepressants" (except cyclobenzaprine and trarnadol], the dose
used in FMS to control pain is generally lower than the usual antidepressant dose; patients with significant
depression require a larger dose of the antidepressant medication. All drugs should be started in a low dose
and increased gradually.
"Nefazodone also blocks 5HT2 receptors.
*Tramadol also weakly binds to opioid flo receptors.
SSRls = selective serotonin reuptake inhibitors.
From Yunus MB: Fibromyalgia syndrome: A guide to management options to diminish pain-improve quality
of pain. Consultant, 1996, with permission.
b. Pain with lying on affected side

c. Superior gluteal tenderness
4. Treatment
a. NSAIDs
b. Local lidocaine and corticosteroid injection
c. Physical therapy stretching, strengthening program with modalities as
needed for symptom control
d. Correction of biomechanical abnormality (e.g., heel lift, stretch tight muscles)
8 . Trochanteric bursitis
1. Location
a. Trochanteric bursa overlying the greater trochanter of the femur.
2. Etiology
a. Overuse (e.g., increased running/training on uneven surface)
b. Look for muscle tightness of the tensor fascial lata, iliotibial band. Look for
knee/ankle/foot malalignment such as pes planovalgus.
c. Trauma: fall on lateral hip girdle
d. Abnormal gait with weakness of hip abductors
e. Abnormal hip biomechanics: osteoarthritis
3. Signs and symtoms
a. Lateral gluteal/hip girdle and leg pain, with referral to the lateral knee.
Myolascial Pain, Fibromyalgia, aOO Soft Tissue Causes 01Law Back Pain 465
b. Pain on affected side with lying
c. Local trochanteric and iliotibial band tightness and tenderness.
4. Treatment
a. NSAIDs
b. Relative rest/cross-training (performing other types of sports) during acute
pain
c. Local lidocaine and corticosteroid injection to trochanteric bursa
d. Physical therapy exercise program
e. Biomechanical correction: (e.g., heel lift, foot orthotics)
C. Ischial tuberosity bursitis (ischiogluteal bursitis)
1. Location
a. Inferior gluteal area directly over the ischial tuberosity
2. Etiology
a. Excessive pressure on the ischial tuberosity with sitting
b. Trauma
a. Pain directly over the ischial tuberosity region with sitting
b. Local tenderness to palpation over the ischial tuberosity
c. Possible tight hamstring muscles
d. Possible referred pain into the posterior proximal thigh
4. Treatment
a. Unload the affected area with less time sitting
b. Provide gel or foam cushion with cut out area for pressure relief under the
ischial tuberosity
c. NSAIDs
d. Local corticosteroid injection
e. Stretching of the gluteal and hamstring muscles
D. Piriformis syndrome
1. Location
a. Piriformis muscle originates medially from the inner surface of the sacrum
and exits the pelvis passing laterally to attach to the greater trochanter of
the femur.
2. Etiology
a. Tight piriformis muscle
b. Abnormal spinal or pelvic mechanics
a. Pain with palpation of the piriformis muscle either externally or by internal
exam (rectal or vaginal route)
b. Pain with provocative dynamic piriformis testing (see Chapter 6)
c. Patients may present with low back, buttock, or posterior thigh pain. If there
is also entrapment of the sciatic nerve, pain and paresthesias may be re-
ferred into the calf and foot.
4. Treatment
a. Local stretching to the piriformis muscle
b. Local trigger point injection to piriformis
c. Fluoroscopically or EMG guided botulinum toxin injection to the piriformis
may be considered for severe recurrent cases.
d. Physical therapy for massage, stretching, and correction of underlying bio-
mechanical abnormalities
E. Psoas bursitis/iliopsoas tendinitis
1. Location
466 Myolascial Pain, Fibromyalgia, anclSolt Tissue Causes 01LowBack Pain
a. The psoas originates from the anterolateral upper lumbar vertebrae and in-
serts on the lesser trochanter of the femur.
2. Etiology
a. Tightness and shortening of the iliopsoas muscle.
a. Patients present with pain either in the upper lumbar region or inguinal area
or both.
b. Look for tight psoas muscle with hip flexion contracture and limited hip ex-
tension. Pain may also radiate to the anterior proximal thigh.
c. Pain to palpation over the iliopsoas muscle insertion region or over the
psoas bursa.
d. Pain to palpation proximally in the upper lumbar area lateral to the verte-
bral bodies.
4. Treatment
a. Physical therapy for stretching and strengthening
b. Specific home stretching program for tight hip flexors
c. In more difficult cases, diagnostic psoas bursography followed by local cor-
ticosteroid injection
d. NSAIDs
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1 - - - - - - - -28
Complex Regional Pain Syndrome
Way Yin, M.D.
Key Points:
• The terms "causalgia" and "reflex sympathetic dystrophy" are now obsolete. New
evidence suggests that complex regional pain syndrome (CRPS) may be caused by a
central mechanism (from the brain or spinal cord), but the precise mechanism by
which CRPS develops remains unknown.
• Symptoms of CRPS often involve non-dermatomal burning pain, swelling, skin color
changes, joint stiffness, abnormal sweating, and extreme skin sensitivity.
• Diagnostic criteria for CRPS may include a constellation of patient symptoms and
objective findings on physical examination.
• There are no diagnostic laboratory or imaging tests that are pathognomic for CRPS.
• Optimal treatment may involve a combination of medications, physical therapy, and
contrast confirmed fluoroscopically guided interventions. The role of surgical sympa-
thectomy remains controversial. Spinal cord stimulation has been effective in
refractory cases.
• New evidence suggest possible preventative measures in certain clinical situations.
I. Definitions
A. Complex regional pain syndrome (CRPS): a constellation of symptoms and physical ex-
amination findings that apply to any specific region of the body (usually the ex-
tremities) that include aspects of:
1. Pain disproportionate to known injury
2. Hypersensitivity to touch
3. Constant burning pain
4. Edema
5. Vasomotor changes (alterations in regional blood flow)
6. Regional alterations in temperature
7. Abnormal sweating.
B. CRPS is subdivided (based on the presence or absence of major peripheral nerve
injury) as types 1 or II:
1. CRPS type II: diagnostic criteria for CRPS but with history of major peripheral
nerve injury.
2. CRPS type I: diagnostic criteria for CRPS without history of major peripheral
nerve injury.
a. Causalgia: an obsolete term previously used to describe many of the symp-
toms of CRPS associated with a history of major peripheral nerve injury.
"Causalgia" is now known as "CRPS type II."
3. Sympathetically maintained pain (SMP): a term used to describe a subset of
CRPS patients where symptoms are associated with abnormal function of the
sympathetic ganglia innervating the affected area. Not all patients with CRPS 1
469
470 Complex Regio/KII Pain Syndrome
have pure SMP. The SMP variant of CRPS I is different from CRPS II in that
there is no history of peripheral nerve injury. Also referred to, in older litera-
ture, as:
a. Reflex sympathetic dystrophy (RSD)
b. Algodystrophy
c. Sudeck's atrophy
d. Microcausalgia
e. Reflex algodystrophy
f. Causalgia
II. Historical Perspective

A. "Causalgia" was originally described in 1864 during the American Civil War.
Further descriptions occurred during World War I. The largest series of case stud-
ies arose from injuries suffered by soldiers in World War II. Additional case
studies were reported during the Vietnam Conflict. Cases consistent with the pre-
sent day definition of CRPS were originally described as a post-traumatic disorder
in 1877.
1. Sudeck made the first classical description of "RSD" in 1900 (Sudeck's dystrophy).
2. Numerous competing and ill-defined terms continue to be used in describing
CRPS in the literature.
3. A panel of international experts met in 1993 to standardize diagnostic criteria
and nomenclature.
a. Accumulated evidence demonstrates that SMP, causalgia, and RSD exhibited
significant symptom overlap, and that many of the features of these clinical
diagnoses did not involve reflexes or sympathetic abnormalities.
b. In 1994, the International Association for the Study of Pain (IASP) coined
the term "complex regional pain syndrome," or "CRPS."
i. "CRPS II" denotes the historical presence of injury to a major peripheral
nerve
ii. "CRPS I" encompasses all other varieties, including the subset of SMP.
4. The diagnostic criteria advocated by the !ASP have been further revised and re-
fined. Further work has gone into distinguishing CRPS from other syndromes such
as post-stroke pain and painful neuropathies (e.g., diabetic peripheral neuropathy).
B. The latest recommendations suggest that patients who meet specific diagnostic
criteria may simply be referred to as suffering from CRPS.
C. The distinction between CRPS types I and II remains valid from a taxonomic
standpoint.
III. Prevalence
A. CRPS may develop following any type of tissue injury, regardless of severity, in-
cluding:
1. Peripheral nerve injury (e.g., trauma, surgery, crush injuries, injury from injec-
tions)
2. Tissue trauma (e.g., sprains, fractures, lacerations, crush injuries, peripheral or
nerve root compression, surgical incisions, compartment syndromes)
3. Amputation
IV. Etiology
A. The mechanisms by which CRPS develop remain unknown. Why most patients
suffering major trauma to an extremity do not develop CRPS, while a minority de-
velop the syndrome after trivial injury, remains an enigma.
Complex Regional Pain Syndrome 471
B. There is a growing consensus that the clinical pathology associated with CRPS
may have origins in the central nervous system. The pain pathways and neu-
ropathophysiology involved are complex, but many basic observations support
the theory of a central mechanism.
1. A frequent finding in CRPS is autonomic dysfunction (swelling, abnormal sweat-
ing' color changes, temperature changes, changes in skin, nail, or hair growth).
Abnormalities of the sympathetic nervous system have long been suspected.
2. Sympathetic abnormalities in one limb of patients with CRPS may spread to the
contralateral limb, or even to a remote limb, suggesting a functional distur-
bance within the CNS.
3. Patients with CRPS will often exhibit normal sensation to cold and heat, but in-
creased sensitivity to cold-pain and heat-pain.
a. This finding suggests a peripheral disorder of pain receptors, or a selective
disturbance within the CNS.
b. The autonomic features of CRPS are often identical to autonomic failure in
some patients following stroke.
i. The autonomic failure after stroke occurs in the absence of pain.
ii. The pain and sensory features of CRPS are separate from (but may paral-
lel) the underlying autonomic abnormalities following stroke.
C. A peripheral mechanism may also be present.
1. Patients with CRPS demonstrate abnormal cutaneous blood vessel permeability.
2. An abnormal release of neuropeptides in response to decreased regional blood
flow, tissue hypoxemia, and tissue acidosis perpetuating abnormal vessel per-
meability has been postulated.
V. Psychological Aspects
A. Patients with CRPS, like other chronic pain conditions, may become clinically de-
pressed, dysthymic, and suffer degradation of normal coping mechanisms.
1. Emotional lability
2. Abnormal sleep patterns
3. Anhedonia
4. Weight gain, loss
5. Obsessional guarding of affected limb(s)
6. Psychomotor abnormalities
B. A minority of researchers argue that CRPS may represent a somatoform
pseudoneurologic illness.
1. Some patients meeting diagnostic criteria for CRPS have responded to placebo
injections or intravenous infusions.
2. As the fundamental mechanism of CRPS remains elusive, a tremendous range
of pathophysiologic and associated psychological issues may be present.
VI. Diagnosis
A. CRPS remains a clinical diagnosis.
B. Current lASP criteria (1994):
1. Presence of an initiating noxious event or a cause of immobilization.
2. Continuing pain, allodynia, or hyperalgesia with which the pain is dispropor-
tionate to any inciting event.
3. Evidence at some time of edema, changes in skin blood flow, or abnormal su-
domotor activity in the region of pain.
4. This diagnosis is precluded by the existence of conditions that would otherwise
account for the degree of pain and dysfunction.
472 Complex Regionol Pain Syndrome
C. Proposed IASP criteria (more specific), addressing diagnostic shortfalls of 1994

criteria:
1. Continuing pain which is disproportionate to any inciting event
2. Must report at least one symptom in each of the four following categories:
a. Sensory: reports of hyperesthesia
b. Vasomotor: temperature asymmetry and/or skin color changes and/or skin
color asymmetry
c. Sudomotor: edema and/or skin color asymmetry
d. Motor/trophic: decreased range of motion and/or motor dysfunction and/or
trophic changes.
3. Must display at least one sign in two or more of the following categories:
a. Sensory: hyperesthesia
b. Vasomotor: temperature asymmetry and/or skin color changes and/or skin
color asymmetry
c. Sudomotor: edema and/or skin color asymmetry
d. Motor/trophic: decreased range of motion and/or motor dysfunction and/or
trophic changes.
D. Diagnostic laboratory tests
I. The diagnosis of CRPS remains clinical, although several laboratory tests may
be useful in supporting (or refuting) the diagnosis.
a. The Quantitative Sudomotor Axon Reflex Test (QSART): a measure of sym-
pathetic axonal activity.
b. Resting sweat output (RSO): quantitative measure of sweat output, which is
proportional to sympathetic outflow.
c. Infrared thermometry: non-invasive measure of topical (skin) temperature,
useful for qualitative comparison between extremities.
E. Diagnostic sympathetic nerve blocks may help differentiate CRPS with a sympa-
thetically maintained pain component, but false-positive results in uncontrolled
single analgesic tests are high.
VII. Prevention
A. The cause of CRPS remains unknown, thus preventative measures and recom-
mendations are vague.
B. Some evidence indicates that free-radicals may be involved in the development
ofCRPS
1. In patients with acute fractures of the radius, one group of researchers found
that treatment with vitamin C reduced the development of CRPS.
C. In patients with a history of CRPS who require surgery on the affected limb:
I. Sympathetic blockade reduced the risk of CRPS developing after surgery.
2. Perioperative administration of calcitonin may prevent recurrence.
VIII. Treatment
A. The wide variety of potential clinical findings with potential central, sympa-
thetic, and peripheral pathophysiologic contributions culminating in CRPS
makes the definition of a single treatment intervention unrealistic.
B. An integrated approach towards treating the underlying pathology (if possible),
coupled with physical and occupational therapies for desensitization, improving
range of motion and strength, and addressing the psychological sequelae that
may accompany CRPS, represents the current accepted standard of care.
C. Some patients with SMP may benefit from a limited series of fluoroscopy-guided
Complex Regionol Poin Syndrome 473
sympathetic ganglion blocks, not only to define a predominant sympathetic com-
ponent to their CRPS, but also to alleviate pain during physical therapy.
D. Utilization of corticosteroids has been reported to provide long-term improvement
in patients with CRPS.
E. Patients with a proven SMP component may benefit from minimally invasive sur-
gical intervention (e.g., sympathetic ganglionolysis via chemical, thermal. laser, or
surgical ablation) targeted at the involved sympathetic ganglia.
1. Advancements in techniques of minimally invasive (percutaneous) nerve and
ganglionic lesioning with radiofrequency are encouraging, but no controlled or
large clinical series has been published using current diagnostic criteria for the
establishment of CRPS.
F. Long term follow-up of patients after surgical (open or video-assisted thoraco-
scopic) sympathectomy has raised questions regarding the efficacy and side-
effects of surgical sympathectomy. However, a carefully controlled clinical trial
comparing surgical intervention versus non-surgical or minimally invasive surgi-
cal intervention in patients with proven SMP has yet to be reported.
G. Several controlled studies have demonstrated long-term efficacy with the use of
spinal cord (or dorsal column) stimulation for the treatment of CRPS. However, the
reported broad range of efficacy likely reflects an inhomogeneous patient study
group. A single randomized double-blind clinical trial has demonstrated remarkable
efficacy with intravenous clodronate. Other bis-phosphonates have not demonstrated
clinical efficacy.
IX. Making aReferral

A. It is best to refer early if CRPS is suspected.
I. Select an evidence-based multidisciplinary pain management practice with ac-
cess to the following:
a. Physical and occupational therapy
b. Pharmacologic therapy
c. Psychological therapies
d. Interventional therapies
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,--------29
Lumbar Whiplash
Richard Seroussi, M.D.
Key Points
• Low back pain is a very common symptom after motor vehicle trauma and is the
second to third most prevalent problem after neck pain and headache.
• The management of low back injuries after whiplash parallels that of other forms of
low back pain diagnosis and treatment, with an emphasis on the prevention of long-
term disability and functional loss.
• Ifthe diagnostic work-up is complete and the patient's symptoms persist after 2 years,
the patient will most likely not respond to further conservative care.
• Imaging studies must be understood in terms of their limitations, and must always be
interpreted within a clinical context, rather than as isolated and absolute indicators of
injury.
• There is strong clinical and epidemiologic evidence of low back injury after motor vehicle
trauma, even among those who have had low-property ("low impact") damage injuries.
• The weight of the evidence, in more contemporary literature on whiplash, actually
does not support a healing effect from claim settlement. Numerous studies document
physical symptoms, most commonly neck pain, headache, and back pain long after
claim settlement.
I. Introduction
A. Scope of the problem
1. Neck pain after motor vehicle trauma is 'ar more studied than low back pain.
2. However, low back pain isavery common symptom after motor vehicle trauma, considered
the second to third most prevalent problem after neck pain, in competition with
headache.
B. Reviewo' the evidence 'or low back injury after motor vehide "soft-tissue" trauma
1. Chnical data
a. Strong clinical and epidemiologic evidence of low back injury after motor
vehicle trauma, including among those who have had low-property ("low
impact") damage injuries.
b. Patients often complain of low back pain a few hours or days after impact.
2. Imaging studies
a. Imaging mayor may not be revealing for a source of injury, similar to non-
traumatic causes of low back pain.
b. In the absence of or with mild radiculopathy, an annular tear may be sus-
pected, and may be revealed by a correlative "high intensity zone" on MRI
scan, but there is an emerging controversy about the absolute reliability of
this finding.
c. Bone scan with SPECT may suggest facet injury, but is likely not a sensitive
study.
475
476 Lumbar Whiplash
d. Thus, only a very small proportion of imaging studies in isolation can pro-
vide definitive evidence for specific injury, and clinical correlation is critical.
e. Exceptions where imaging reliably predicts the clinical picture might include
the rare case of a disc extrusion seen on MRI scan.
3. Biomechanics
a. The biomechanics of lumbar injury after motor vehicle crash exposure are
not yet well defined.
b. The biomechanics of neck injury are only recently becoming understood,
with the aid of high-speed digital instrumentation:
i. Recent studies have shown that there is actually an S-shaped curve of the
neck within 50 milliseconds after rear impact collision, with hyperflexion
of the upper neck combined with hyperextension of the lower neck.
ii. This may well be the mechanism for cervical facet injury, rather than a
uniform hyperextension of the neck (which occurs after 100 millisec-
onds), classically assumed to be the mechanism of whiplash injury for
over 70 years.
c. Experimental disc injury, in the form of a surgically applied outer annular
"rim lesion" in sheep ultimately leads to facet degeneration, likely from a
combination of biomechanical and biochemical factors.
4. Post-mortem evidence
a. Autopsy studies of the lumbar facet joints reveal injury to the articular carti-
lage and capsule of these joints, in the setting of negative x-rays.
b. Autopsy studies of the cervical region after motor vehicle trauma, in the set-
ting of normal post-mortem x-rays, where the cause of death was typically
blunt head trauma rather than neck injury, reveal:
i. Cervical "rim lesions," i.e., tears in the outer annulus, likely due to shear
or distraction injury across the motion segment.
ii. Cervical facet injury.
c. An excellent post-mortem neck study by Taylor and Twomey in 1993 showed
no such injuries among a control group who had non-traumatic cause of
death.
d. Schmorl's nodes have been documented at autopsy among motor vehicle
trauma victims, most notably in the T8-L 1 region, significantly in the ab-
sence of postmortem x-ray findings, and more common among motorcy-
clists. Axial compression is a proposed mechanism of injury.
C. A practical approach
1. Use clinical judgment to screen whether the patient is reliable.
2. If so, accept the injury and treat it like any other injury of the lower back.
3. Try to understand the patient in terms of an overall clinical puzzle, not neces-
sarily with all the pieces in place.
4. The puzzle analogy holds especially true for imaging, which lags behind more
reliable but less practical diagnostic tools such as controlled selective spinal in-
jections.
II. Diagnostic Approach

A. General principles
1. A good maxim is "treat the patient, not the scan." Current imaging modalities,
including MRI scanning, really require clinical correlation, and may not reveal
underlying injury. It is also well known that MRI scanning can reveal imaging
"abnormalities" among those without back pain.
Lumbar Whiplash 477
2. In the absence of neurologic findings, do not pursue extensive and expensive
diagnostic work-up early after injury. Exceptions to this rule apply, and clinical
judgment remains paramount.
B. Specific pain generators
I. Discogenic and radicular pain
a. Except in the rare cares [i.e., about 1O-150,b of time) of disc extrusion or severe
neuroforaminal compression, MRI viewed in isolation cannot reliably predict
the clinical picture, including instances of radicular pain and radiculopathy.
b. An advanced annular tear with a high intensity zone seen on T2-weighted
MRI scans may suggest the presence of a painful disc, but Carragee and oth-
ers have challenged the reliability of this imaging finding. Ultimately, even
the HIZ must be placed within a clinical context when it is detected on MRI.
2. Facet and sacroiliac joint mediated pain
a. Sacroiliac joint pain and facet-rnediated pain are not routinely revealed by
conventional imaging including MRI.
b. For example, facet arthropathy on CT does not correlate with response to di-
agnostic spinal injections.
c. Some evidence that bone scan with SPECT is helpful.
L SPECT likely is fairly specific, but not sensitive.
ii. Confirmatory diagnostic injections directed at the facet joint or sacroiliac
joint may also be needed.
d. Disc and facet dysfunction and pain likely co-exist and interact, as revealed
in post-mortem studies, animal models of injury, and clinical studies based
on the use of diagnostic spinal injections.
III. General Treatment Principles

A. There is no clear evidence that low back injury after motor vehicle trauma is fun-
damentally different than injury from non-traumatic causes and from other forms
of trauma such as occupational injury.
B. Similar to the neck, there may be a greater prevalence of lumbar facet injury
rather than disc injury in the setting of motor vehicle trauma, but no definitive
study has addressed this issue.
C. Therefore, in the absence of data suggesting otherwise, treatment protocols devel-
oped from the study of other causes of low back pain and radiating pain are likely
applicable.
D. This general rule of thumb is reasonable when considering overall treatment ap-
proach to low back pain after motor vehicle trauma.
E. There are some specifics to the treatment of the patient with a history of motor
vehicle trauma, specifically "whiplash," and these will be specifically addressed at
the end of this section.
IV. Acute Treatment

A. Judiciously address the four R's: Rest, reassurance, restridions, and range ofmotion.
B. Correct use of these guidelines helps minimize the effect of what one might call
the 5 D's:
I. Depression
2. Deconditioning
3. Disability
4. Dependence on opioid pain medicine
5. Dysfunctional relationships.
478 Lumbar Whipla5h
C. Rest
1. Clinical LBP research is clearly steering us to limit or eliminate the prescription
of bed rest after an episode of low back pain.
2. Although intuitively appealing. prolonged bed rest has not been validated in
numerous studies for low back pain.
D. Reassurance
I. Reassurance is good advice: most patients recover but the clinician should
avoid an approach which implies full recovery for all patients.
2. Based upon one's initial evaluation. close follow-up may be indicated in first
few weeks after acute injury to allow further workup and treatment prescription
for patients who are not gradually recovering.
3. Note that several studies document at least 20-30% chronic symptoms two
years after injury, including low back pain.
a. If symptoms persist after 2 years, they will most likely not respond tofurther conserva-
tive care.
b. The presence of symptoms has been prospectively tracked for up to 15 years
after motor vehicle trauma and found to be persistent.
c. Individual exceptions are always noted. and newer treatments such as facet
joint neurotomy may offer hope and were not accounted for in earlier
prospective epidemiologic studies.
E. Restrictions
1. Work restrictions likely reasonable If acute flare-up has not resolved within afew days.
a. Should be prescribed short-term, as minimal as possible while still protecting
patient from further aggravation of symptoms.
b. A few weeks follow-up is needed to ensure restrictions are minimized and
possibly revised.
2. Risk factors for delayed. partial. or full disability after whiplash including em-
ployment in heavy manual labor. pre-existing psychological problems, reduced
cervical mobility and the long-term presence of intrusive physical symptoms on
a whiplash functional scale.
3. Studies from the occupational medical literature are documenting early return to
work with restrictions is protective against long term disability and should be
widely adopted. even in settings where employers state "no light duty exists."
F. Range of motion
1. Limiting range of motion for lower back not carefully studied after MYA-
caused LBP.
2. However, rigid range of motion limitations are generally likely not agood idea since pro-
longed bed rest also detrimental.
3. Whiplash literature isnow replete with evidence that soft cervical collar to restrict neck ROM
isactually harmful and not helpful for recovery from acute whiplash.
4. Spinal manipulation may be most efficacious when used to treat acute injury to
help restore a patient's function to pre-morbid status. When it is used. manipu-
lation should be incorporated into a comprehensive rehabilitation program.
with coordination among clinicians.
V. Sub-Acute Treatment (8to 12 weeks)

A. The principles of this type of care are similar to those for low back pain not
caused by motor vehicle trauma.
B. Increased attention to the avoidance of the 5 D's. as listed above should be done.
Emerging disability in particular may be treatable at this stage, with the avoidance
of its long-term devastating effects.
C. Increased commitment to diagnosis and treatment if the patient is not recovering.
Lumbar Whiplash 479
D. Interventions should be graded from the minimally invasive and less expensive to
more invasive/expensive options, both for diagnosis and treatment.
E. If acute surgery was not indicated, a graded hierarchy of care might be as follows:
I. Diagnosis
a. Advanced imaging including possible MRI scan or bone scan with SPECT to
be considered, but only if clinically indicated.
b. Electrodiagnostic testing in the setting of suspected nerve injury without
good imaging correlation.
c. Fluoroscopically-guided, contrast-enhanced diagnostic spinal injection pro-
cedures.
2. Treatment
a. Anti-inflammatory medications and muscle relaxants.
b. Physical therapy, spinal manipulation, massage.
c. Sensible advice to stay active but to not "overdo it," especially excessive
lifting, bending, and twisting activities.
d. Light-duty work prescription, as needed only.
e. Minimally invasive care such as percutaneous neuromodulation therapy, or
more specialized medications.
f. Fluoroscopically guided, contrast-enhanced therapeutic spinal injections.
g. Surgical consultation, if appropriate, and generally only if the patient has
been reliable and compliant with care.
F. If not recovering or if disability is emerging, consider an appropriate consultation.
VI. Chronic Treatment (Greater than 3 to 6 months)

A. More specialized medications such as gabapentin or the judicious use of opioids.
B. Increased emphasis on more specialized invasive approaches such as spinal injec-
tions, possible facet neurotomy, surgery if appropriate, etc.
C. Behavioral approaches for chronic pain management.
D. Permanent activity modifications, such as retraining to a lighter duty job.
VII. Issues Specific to Whiplash

A. Psychological issues
I. The weight of the evidence is that physical pain in a chronic setting often leads
to reactive depression, and does not stem from pre-existing depression, at least
in the setting of whiplash and/or low back pain.
a. An antecedent history of or tendency towards depression may worsen the
ability to cope with chronic pain, and clinical judgment remains paramount
when formulating an individual treatment plan.
2. For neck pain, a randomized controlled trial of facet neurotomy has docu-
mented that resolution of psychological dysfunction, including depression
and anxiety, will accompany resolution of pain, without psychological inter-
vention.
3. The question of whether pain counseling makes sense is thus raised.
a. This should be evaluated on an individual basis, at the discretion of the care
provider.
b. However, knowledge of this literature is important to keep in mind when ad-
dressing psychological issues.
4. Post-traumatic stress disorder (PTSDj occurs with some frequency after motor
vehicle trauma, including in the setting of so-called "soft-tissue injury," docu-
mented for both adults and children.
a. Counseling for PTSD should be strongly considered among patients with lin-
gering symptoms.
480 Lumbar Whiplash
b. Overall, PTSD is not adequately screened for among clinicians.

c. PTSD likely more common among patients who have had repeated motor
vehicle crash exposures.
B. Role of litigation
1. A traditional view has been that claim settlement in the setting of litigation
somehow helps to heal patients with whiplash injury.Note the famous quote by
H. Miller in an article titled "Accident Neurosis," published in the British
Medical Journal in 1961:
A compensation neurosis is a state of mind born out offear, kept alive by
avarice, stimulated by lawyers, and cured by a verdict.
2. The weight of the evidence, in more contemporary literature on whiplash, actu-
ally does not support a healing effect from claim settlement. Numerous studies
document physical symptoms, most commonly neck pain, headache, and back
pain long after claim settlement.
3. There likely is a small subset of patients who are focused on secondary gain
and litigation.
a. Careful screening of such patients, clear guidelines and open communication
between care provider and the patient are critical.
b. Screening for emerging disability should be done frequently.
c. Behavioral signs, Waddells', should not be used for medicolegal evaluation
of malingering but rather as a screen for a psychological component of the
patient's lower back pain experience.
C. Chronic whiplash syndrome
I. "If it's sprain/strain, what's causing the pain?"
a. Specific pain generators
i. Most chronic LBP, with or without a radiating component, likely stems
more from joint injury, rather than a primary "muscle sprain."
ii. Nonetheless, myofascial pain may coexist with pain from underlying
joint injury. (See other chapters.)
iii. Based on research studies employing controlled fluoroscopically-guided,
contrast-enhanced diagnostic spinal injections, the most common
anatomic sources of LBP are likely the intervertebral disc (with or with-
out radiculopathy), the facet joint, and the sacroiliac joint.
b. Central sensitization
i. Similar to other forms of chronic pain, in the setting of chronic whiplash,
"central sensitization of pain" likely occurs.
ii. This refers to a central nervous system amplification in the processing of
nociceptive inputs.
iii. Some literature documents a positive relationship between fibromyalgia
and chronic whiplash. This may be no more than a labeling of one ex-
treme of the pain centralization phenomenon, documented for chronic
whiplash as well as for other long-standing painful conditions.
iv. The treatment of chronic pain syndromes should focus on preventing as-
sociated conditions such as disability, depression, deconditioning, and
withdrawal from community.
v. These associated conditions often accompany the central sensitization
phenomenon, although causal mechanisms remain unclear.
2. Problems with documenting impairment
a. Current methods of impairment are likely biased toward radiculopathy, from
disc injury and/or stenosis.
i. Imaging studies generally have a poor ability to document discogenic,
Lumbar Whiplash 481
facet-mediated pain and sacroiliac joint pain. Fluoroscopically guided,

contrast-enhanced selective spinal injections may be impractical and ex-
pensive to obtain, but are often needed for diagnostic confirmation
ii. There is often an absence of neurologic signs such as weakness and/or
sensory loss, associated with low back pain conditions that do not in-
clude radiculopathy, and current impairment systems are often based on
the presence of neurological loss.
b. Clinical radiculopathy may have poor or incomplete correlation to MRI.
c. Impairment rating exam may not be reliable among different practitioners,
especially range of motion assessments.
d. A system of impairment oriented towards functional loss with respect to
daily activities may ultimately lead to a more rational approach.
3. Problems with the validity of chronic whiplash syndrome, according to some
authors.
a. Dr. Robert Ferrari believes that the biopsychosocial model of chronic whiplash
largely negates the presence of long-term physical injury after whiplash.
b. Two Lithuanian studies are cited as evidence that chronic whiplash syn-
drome is a construct based on a culture which compensates for injury after
motor vehicle trauma and which allows for litigation to achieve such com-
pensation.
i. Lithuania is a country apparently without a system of compensation or
of litigation after whiplash, and thus forms an ideal setting for testing
this hypothesis.
ii. These studies involved both retrospective and prospective analyses of co-
horts of Lithuanian subjects who had a motor vehicle accident. Subjects
were questioned about the presence of neck pain and headache, without
specific reference to the known history of antecedent motor vehicle
trauma.
iii. The prevalence of neck pain and headache for this cohort was compared
to a cohort of subjects who did not have an antecedent history of motor
vehicle trauma.
iv. No significant difference in the rates of both neck pain and headache
were found between these two populations.
v. The authors thus feel that chronic whiplash syndrome does not have a
solid foundation as a physical injury.
c. Criticism of the Lithuanian studies has been as follows:
i. These studies used as their basis a cohort of subjects exposed to a mo-
tor vehicle crash, a fraction of whom reported injury after such expo-
sure.
ii. Other authors have stated that there is not significant statistical power
with this experimental design given that only a minority of these motor
vehicle crash-exposed subjects sustained acute injury.
iii. In addition, only a small proportion of Lithuanian subjects in the motor
vehicle crash-exposed groups were female, a gender with higher risk for
chronic whiplash syndrome.
d. Perhaps the most elegant critique of the Lithuanian studies stems from a
study done in Sweden by Berglund and others.
i. As a refinement of the Lithuanian study design, these researchers com-
pared rates of chronic neck pain between subjects who did and did not
report acute whiplash, among those exposed to a motor vehicle crash
(MYCI 7 years previously.
482 Lumbar Whiplash
ii, For each of the two MVC-exposed groups, they also employed control
groups of subjects without histories of MVC exposure.
iii. Seven years after MVC exposure, the authors found an approximate 400/0
rate of chronic neck pain among MVC-exposed patients who reported
acute whiplash, as compared to a range of 11% to 15010 rates of chronic
neck pain for the other three groups.
4. There likely is some validity to the biopsychosocial model, which suggests that the
clinician should avoid "disabling" the acutely injured patient. However, the weight
of the epidemiologic evidence points to organic and partially treatable chronic joint
injury after whiplash for a minority-but not insignificant-fraction of patients.
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tomic impairment visible on lumbar magnetic resonance imaging. Spine 25:819-828, 2000.
3. Bennett RM: Emerging concepts in the neurobiology of chronic pain: Evidence of abnormal sensory
processing in fibromyalgia, Mayo Clin Proc 74:385-398, 1999.
4. Berglund A, Alfredsson L, Cassidy JD, et al: The association between exposure to a rear-end collision
and future neck or shoulder pain: A cohort study. J Clin Epidemiol 53: 1089-1094, 2000.
5. Berglund A, Alfredsson L, Jensen I, et aI: The association between exposure to a rear-end collision
and future health complaints. J Clin Epidemiol 54:851-856, 2001.
6. Borchgrevink GE, Kaasa A, McDonagh D, et al: Acute treatment of whiplash neck sprain injuries.
A randomized trial of treatment during the first 14 days after a car accident. Spine 23:25-31,1998.
7. Buskila D, Neumann L, Valsberg G, et aI: Increased rates of fibromyalgia following cervical spine
injury. A controlled study of 161 cases of traumatic injury. Arthritis Rheum 40:446-452, 1997.
8. Carragee EJ, Paragioudakis SJ, Khurana S: 2000 Volvo award winner in clinical studies: lumbar high-
intensity zone and discography in subjects without low back problems. Spine 25:2987-2992, 2000.
9. Cocchiarella L, Andersson GBJ. Guides to the Evaluation of Permanent Impairment, Fifth Edition:
American Medical Association Press, 200 I.
10. Cooper JE, Tate RB, Yassi A, Khokhar J: Effect of an early intervention program on the relationship be-
tween subjective pain and disability measures in nurses with low back injury. Spine 21:2329-2336, 1996.
I I. Cusick JF, Pintar FA, Yoganandan N: Whiplash syndrome: Kinematic factors influencing pain pat-
terns. Spine 26:1252-1258, 2001.
12. de Vries AP, Kassam-Adams N, Cnaan A, et al: Looking beyond the physical injury: Posttraumatic
stress disorder in children and parents after pediatric traffic injury. Pediatrics 104: 1293-1299, 1999.
13. Dreyfuss P, Halbrook B, Pauza K, et al: Efficacy and validity of radiofrequency neurotomy for chronic
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15. Fahey V, Opeskin K, Silberstein M, et al: The pathogenesis of Schmorl's nodes in relation to acute
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16. Ferrari R, Kwan 0, Russell AS, et al: The best approach to the problem of whiplash? One ticket to
Lithuania, please. Clin Exp Rheumatol 17:321-326, 1999.
17. Ferrari R, Schrader H: The late whiplash syndrome: A biopsychosocial approach. J Neurol Neurosurg
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18. Fishbain DA, Cutler R, Rosomoff HL, Rosomoff RS: Chronic pain-associated depression: Antecedent
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19. Freeman MD, Croft AC, Rossignol AM, et al: A review and methodologic critique of the literature re-
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management. Spine 22:2911-2918,1997.
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33. Main CJ, Waddell G: Behavioral responses to examination. A reappraisal of the interpretation of
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307:647-651,1993.
35. Mealy K, Brennan H, Fenelon GC: Early mobilization of acute whiplash injuries. Br Med J (Clin Res
Ed) 292:656-657, 1986.
36. Miller H: Accident neurosis. BMJ 1:19-25, 1961.
37. Moore RJ, Crotti TN, Osti OL, et al: Osteoarthrosis of the facet joints resulting from anular rim lesions
in sheep lumbar discs. Spine 24:519-525, 1999.
38. Norris SH, Watt I: The prognosis of neck injuries resulting from rear-end vehicle collisions. J Bone
Joint Surg [Br] 65:608-611, 1983.
39. Obelieniene D, Schrader H, Bovim G, et al: Pain after whiplash: A prospective controlled inception
cohort study [see comments]. J Neurol Neurosurg Psychiatry 66:279-283, 1999.
40. Pettersson K, Toolanen G: High-dose methylprednisolone prevents extensive sick leave after whiplash
injury. A prospective, randomized, double-blind study. Spine 23:984-989, 1998.
41. Radanov BP, Sturzenegger M, Di Stefano G: Long-term outcome after whiplash injury. A 2-year
follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial find-
ings. Medicine (Baltimore) 74:281-297, 1995.
42. Rosenfeld M, Gunnarsson R, Borenstein P: Early intervention in whiplash-associated disorders:
A comparison of two treatment protocols. Spine 25: 1782-1787, 2000.
43. Sapir DA, Gorup JM: Radiofrequency medial branch neurotomy in litigant and nonlitigant patients
with cervical whiplash: A prospective study. Spine 26:E268-273, 2001.
44. Schofferman J, Wasserman S: Successful treatment of low back pain and neck pain after a motor
vehicle accident despite litigation. Spine 19:1007-1010, 1994.
45. Schrader H, Obelieniene D, Bovim G, et al: Natural evolution of late whiplash syndrome outside the
medicolegal context [see comments]. Lancet 347:1207-1211, 1996.
46. Schwarzer AC, Wang SC, O'Driscoll D, et al: The ability of computed tomography to identify a painful
zygapophysialjoint in patients with chronic low back pain. Spine 20:907-912,1995.
47. Squires B, Gargan MF, Bannister GC: Soft-tissue injuries of the cervical spine. 15-year follow-up.
J Bone Joint Surg Br 78:955-957, 1996.
48. Suissa S, Harder S, Veilleux M: The relation between initial symptoms and signs and the prognosis of
whiplash. Eur Spine J 10:44-49,2001.
49. Swartzman LC, Teasell RW, Shapiro AP, McDermid AJ: The effect of litigation status on adjustment
to whiplash injury. Spine 21:53-58, 1996.
50. Taylor JR, Twomey LT: Acute injuries to cervical joints. An autopsy study of neck sprain. Spine 18:
1115-1122,1993.
51. Twomey LT, Taylor JR, Taylor MM: Unsuspected damage to lumbar zygapophyseal (facet) joints after
motor-vehicle accidents [see comments]. Med J Aust 151:210-212,215-217,1989.
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tion for chronic low back pain. Spine 24: 1937-1942, 1999.
53. Waddell G, McCulloch JA, Kummel E, Venner RM: Nonorganlc physical signs in low-back pain. Spine
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,--------30
Traumatic Iniuries of the Lumbar Spine
Craig C. Col/ewart, M.D.
Key Points
• Usual mechanism of injury is a fall or vehicular accident.
• Check cervical and thoracic spine, pelvis, knees, and feet for associated fractures.
• Obtain good quality anteroposterior (AP) and lateral radiographs of the lumbar spine.
Caution: a TI2 fracture may be hidden by the liver and an underexposed lateral
radiograph. Repeat as needed.
• Perform complete neurologic exam, including rectal exam.
• Four fracture patterns: compression, burst, chance, and dislocation.
• Treatment options: observation and symptomatic care, bracing, or surgical fusion.
• Treatment goals: to maintain spinal alignment and to preserve function.
• Referral should be made for all unstable fractures and for all fractures with a neuro-
logic deficit.
I. Epidemiology
A. At least 77,000 spinal fractures per year in the U.5.-50% between TI2 and L2.
B. Approximately 5010 suffer neurologic deficit.
C. Majority occur between the ages of 16-64 years.
D. Many involve the use of intoxicating substances.
II. Etiology
A. Most fractures are caused by excessive flexion of the spine; for example, a vehicu-
lar accident in which the body is forcibly thrown forward, but the pelvis is re-
strained by a lap belt.
B. Extension injuries are rare.
C. Excessive compression may also cause fracture (e.g., a fall with the victim landing
on the buttocks).
D. Other excessive forces may combine to produce a fracture-distraction, rotation,
and shear.
E. Gunshot wounds.
F. Pathologic processes may weaken spine and predispose to fracture (e.g., osteo-
porosis, metastatic carcinoma).
III. Anatomic Considerations (see Chapter 2)

Unique anatomic features of the thoracolumbar spine (TI2-Ll) predispose it to a high in-
cidence of fracture.
A. It is the junction between the relatively immobile thoracic spine (stabilized by the
thoracic ribs) and the mobile lumbar spine (surrounded by soft tissues).
B. It is the junction between the kyphotic (forward curved) thoracic spine and the
lordotic (reverse curve) lumbar spine.
485
486 Traumatic Injuries 01theLumbar Spine
e. Change in facet orientation from the coronal plane (thoracic spine) to the sagittal
plane (lumbar spine) predisposes the thoracolumbar junction to rotation and flex-
ion strain.
IV. Associated Injuries

The same excessive force that produces a spinal fracture may injure other areas.
A. Noncontiguous spinal fractures-100f0 of patients will suffer an additional fracture.
1. The fracture may produce a neurologic deficit.
2. Roentgenograms of the cervical spine (AP/lateral, odontoid) and the thoracic
spine (AP/lateral) are a mandatory part of the initial evaluation.
B. Lower extremity and pelvic fractures
I. The foot (e.g., calcaneus) and knee (e.g., tibial plateau) are particularly suscepti-
ble; fractures may occur in up to 100/0 of patients.
2. Less commonly, the sacroiliac joint may be fractured or disrupted.
e. Viscera
1. Evaluation should be made for injury to the spleen, liver, duodenum or pan-
creas, diaphragm, and aorta.
2. Such injuries are uncommon but may result from excessive flexion/
compression of the abdominal contents at the time of injury.
V. Clinical Diagnosis
A. Neurologic exam (see Chapter 6)
1. A complete neurologic exam should be performed, including upper and lower
extremities and motor, sensory, and reflex testing.
2. Particular attention should be given to anal sphincter tone and perineal sensation.
B. Spine
1. The patient should be turned to the side, with care not to allow twisting be-
tween the shoulders and hips ("log rolling"), i.e., they stay in the same plane.
2. The spinous processes should be palpated for tenderness.
3. Observe for ecchymosis.
4. Percuss to elicit pain.
e. Radiographs
I. AP and lateral views of the spine are mandatory.
2. For best results, center beam at the level of the fracture.
3. The density of the liver may obscure a fracture at the T12 level.
4. It is vitally important to repeat films as needed so that all portions of each ver-
tebra can be seen.
VI. Classification and Treatment

A. The purpose of fracture classification is to determine if the fracture is stable.
Stability dictates treatment.
B. A stable spinal fracture is one that is capable of allowing the patient to assume
most activities of daily living without significant risk of causing (further) neuro-
logic injury or deformity.
e. Denis divided a vertebra into three structural columns (Fig. 1):
1. Anterior column
a. Anterior longitudinal ligament
b. Anterior half of disc and vertebra
2. Middle column
a. Posterior longitudinal ligament
b. Posterior half of disc and vertebra
TroumaticInjuries of the Lumbar Spine 487
FIGURE 1. Theanterior (8), middle

(e), and posterior (D) columns are
illustrated.
Sll =supraspinous ligament
Pll =posterior longitudinal ligament
All =anterior longitudinal ligament
3. Posterior column
a. Supra/interspinous ligament
b. Pedicles, facets, lamina, spinous processes
D. A fracture involving one column is stable, whereas a fracture involving two or
three columns is unstable.
1. Extrapolating his three column theory, Denis found that fractures usually fit
into one of four patterns:
a. Compression (Fig. 2)
i. Due to excessive flexion of the spine.
ii. Involves only anterior column; thus it is stable.
iii. Because neurologic elements are located in the middle and posterior
columns, compression fracture is not associated with neurologic in-
jury.
iv. AP radiograph may appear nearly normal, whereas the lateral view
shows wedging or compression of the normally square vertebra.
v. Compression of more than 200/0 should arouse suspicion that the frac-
ture is an unstable burst fracture, and CT scan should be obtained to
check for fracture of the middle and posterior columns.
vi. Treatment is symptomatic (see Chapter 13).
vii. A lightweight corset or brace may be beneficial for pain control (see
Chapter 13).
viii. Bending and lifting activities should be restricted for 6-12 weeks.
ix. Prognosis is good.
b. Burst (Fig. 3)
i. Due to excessive flexion and compression of the spine.
488 Traumatic Injuries 01 !heLumbar Spine
FIGURE 2. Compression fracture (arrowl-only involves

anterior column.
ii, Involves anterior, middle, and sometimes posterior columns (2-3

columns) and is thus an unstable injury.
iii. Approximately 500/0 of patients have a neurologic deficit.
iv. AP radiograph reveals widening between the pedicles, whereas the lat-
eral film shows wedging of more than 200/0.
v. CT scan is useful to determine the details of bony anatomy.
vi. Treatment goals are to preserve or improve neurologic function and to
maintain or improve spinal alignment.
(a) Surgical decompression is usually necessary to treat neurologic
compression.
(b) Spinal alignment concerns may be treated by surgical fusion or ap-
plication of a rigid, total contact brace.
vii. Prognosis is related to various factors, such as age of patient, degree of
neurologic injury, and associated injuries.
c. Chance (Fig. 4)
i. Due to an excessive flexion-distraction force.
FIGURE 3. Burst fracture (arrowl-involvement of anterior

and middle columns. May also involve posterior column.
Traumatic Injuries of /heLumbor Spine 489
FIGURE 4. Chance fracture---disruption of ligamentsof an-

terior, middleand posterior columns.
ii. All three columns are involved; this is an unstable fracture.

iii. Many have an associated neurologic deficit.
iv. A radiograph in the lateral view shows spinous processes, facets, and
vertebrae being pulled apart, whereas the AP view may show minimal
changes.
v. Treatment requires a total contact, rigid brace or surgical fusion.
vi. Prognosis is usually good.
d. Fracture dislocation (Fig. 5)
i. High-energy injury with multiple forces involved.
ii. All columns are disrupted; highly unstable.
iii. High incidence of neurologic injury.
iv. Radiograph reveals loss of spinal alignment with dislocation of vertebrae.
FIGURE S. Fracture dislocation

(arrows).
490 Traumatic Injuries ollhe Lumbar Spine
v. Nearly all such fractures require surgical stabilization.

vi. Prognosis is related to various factors, such as age of patient, degree of
neurologic injury, and associated injuries.
e. Other
i. Isolated fractures of the spinous processes or transverse processes involve
one column and are therefore stable.
ii. Plain radiographs show the fracture.
iii. Make sure that the fracture is isolated and not a sentinel for a burst frac-
ture.
iv. Treatment is symptomatic.
v. Prognosis is good.
References
1. Bohlman HH: Treatment of fractures and dislocations of the thoracic and lumbar spine. J Bone Joint
Surg 67A: 165-169, 1985.
2. Denis F: The three-column spine and its significance in the classification of acute thoracolumbar
spinal injuries. Spine 8:817-831,1983.
3. Denis F, Armstrong GW, Searls K, et al: Acute thoracolumbar burst fractures in the absence of neuro-
logic deficit: A comparison between operative and nonoperative treatment. Clin Orthop 189:142-149,
1984.
4. Frymoyer JW, Ducker TB, Hadler NM, et al [eds): The Adult Spine: Principles and Practice. New York,
Raven Press, 1991, pp 1269-1329, 1331-1352.
5. Gupta A, el Masri WS: Multilevel spinal injuries: Incidence distribution and neurological patterns. J
6. Keenen II, Antony J, Benson DR: Noncontiguous spinal fractures. J Trauma 30:489-491,1990.
7. Stauffer ES (ed): Thoracolumbar Spine Fractures Without Neurologic Deficit. Rosemont, IL, American
Academy of Orthopedic Surgeons, 1993.
r------------31
I
Independent Medical Examinations and
Disability Evaluations
Richard Paul Bonfiglio, M.D., and Ronald Lee Bonfiglio, M.D.
Key Points
• Eligibility for worker's compensation medical and disability benefits after work-related
injury or illness is primarily based on medical information and analyses provided by
physicians. Treating physicians are often requested to provide impairment determin-
ations or assessments of injured workers suitability for return-to-work. When treating
physicians are unable or unwilling to provide sufficient information for vocational
and compensation determinations, independent medical evaluations and disability
evaluations are often requested. Because so much is based on physician reports, the
evaluator should make every effort to provide accurate, useful information. Thus, the
primary goal should be to provide an unbiased, objective, reproducible patient
assessment.
• In addition, the evaluation should meet the system requirements for disability assess-
ment. The physician should also recognize the vocational implications of an injured
worker's ongoing medical concerns.
• Independent medical evaluations are used by compensation systems to provide a
patient assessment by an unbiased practitioner. These evaluations are particularly used
when the injured worker's recovery seems delayed or there are other areas of potential
dispute.
• Often physicians also are asked to provide testimony to support the results of their
evaluations. Thorough assessments and accurate documentation of results aid the
physician in providing such testimony.
I. Introduction
A. Definitions
1. Independent medical evaluation-an evaluation usually provided by a physician not
giving direct care to the patient undergoing assessment; needs to be thorough;
conclusions most important; content should be same regardless of referral
source; however, compensation system may require more information and
analysis than are found in a routine medical report.
2. Disabihty/impairmentevaluation-assessment of an individual's limitations; serves
as basis for determinations by worker's compensation system.
3. Impairment-alteration in normal physiologic process that is evaluated by med-
ical means; American Medical Association guidelines provide systematic ap-
proach to measurement of permanent impairment.
a. Impairment determinations-based on medical evaluation, especially physical
findings.
491
492 Independent Medical Examinatians and Disability Evaluations
b. Combined values chart-used to determine total impairment by combining

results from individual limitations.
c. Limitations-impairment determination may not accurately estimate impact
of physical limitation on work capabilities; in addition, pain perception can-
not be adequately quantified.
d. Statutes-for some impairment determinations, especially with amputations,
the determination may be prescribed in compensation statute.
4. Disability-reflects impairment but includes impact of impairment on daily func-
tion, especially in work setting; should take into account claimant's vocation,
age, transferrable skills, and education.
a. Vocational considerations-as an example, the impairment determination for
a violinist and a truck driver, each with complete amputation of the left,
nondominant little finger, should be the same, but the disability would be
much greater for the violinist than the truck driver.
b. Transferrable skills-disability greater for worker who has done only manual
labor and has no transferrable skills, training or education for alternate
work, especially less physically demanding work.
S. Historical perspective
I. 1910-1920: Development of first state worker compensation systems.
2. 1934: Mixter and Barr recognize correlation between radiculopathy and disc
protrusion.
3. 1980s: Increasing recognition of cumulative trauma disorders-conditions rec-
ognized as compensible without a single precipitating event.
C. Context-physician should recognize the background that leads to need for inde-
pendent medical evaluation.
I. Patient-recognizes relationship between proving disability and continued ben-
efits.
2. System-attempts to be fair and equitable; "no fault" approach to handling injuries.
3. Employer-attempts to limit all costs, but must recognize worker's compensa-
tion, disability payments.
4. Insurance carrier-passes on costs but must be competitive with sales.
5. Managed care-additional control and limitation of medical payments.
6. Peers-disability evaluations often viewed as not providing medical care.
D. Indications for disability evaluations
I. Suitability of claimant for return-to-work
2. Provision of compensation/disability benefits
3. Ongoing medical and rehabilitative needs
4. Prognosis for future-medical needs and vocational outcome
5. Causality-relationship between ongoing symptoms and impairments and origi-
nal compensation claim
E. Potential referral sources
I. Physicians-especially by those not wanting to get involved.
2. Attorneys-may represent claimant or employer/insurance company; need medical
opinion supportive of their position, preferably backed with medical evidence.
3. Case managers-usually paid by insurance companies or directly by employer;
interested in timely return-to-work and case closure.
4. Employers-interested in cost savings and getting employees back to work.
5. Unions-want to protect rights of members but may also be paying disability
benefits.
6. Insurance companies-pass along costs of compensation but prefer reduced ex-
penses to increase competitiveness.
Independent Medical Examinations and Disability Evaluations 493
7. Worker's compensation system-needs basis for compensation awards.

8. Long-term disability carriers-provide compensation for medical conditions lim-
iting capabilities for return-to-work.
II. System Constraints

A. Adversarial system-especially if claim denied (employer does not recognize injury
or medical condition as work-related).
B. "All-or-none"-injury or illness usually compensable if it stems from the person's
work; preexisting conditions or multiple episodes of injury can complicate deter-
minations.
C. Potential for testimony-physicians performing independent medical evaluations
can anticipate providing testimony occasionally, especially via deposition; the fre-
quency is quite variable and depends on the compensation system and local legal
practices.
D. Questions of physician's motivation-especially by physician peers and attorneys.
E. Variations in system needs
I. Percentage impairment/disability system-based on predetermined scale of
impairment/disability assessment.
2. Wage loss determination system-benefits based on inability to return-to-work.
F. Musculoskeletal and neurological system diseases most significant symptom is pain.
1. Evaluator cannot quantify or even varify presence or absence of patient's pain.
2. Pain is a very personal experience and can have a variable impact on patient's
life.
3. Pain experience can be significantly impacted by previous painful conditions,
patient's satisfaction with life and work, and other nonmedical issues.
III. System Expedations

A. Reliability-trust in findings.
B. Objectivity-lack of bias related to specific case referred.
C. Reproducible evaluation-findings consistent between examinees and with other
examiners.
D. Accuracy-correct information in reports, especially recommendations and calcu-
lations.
E. Timeliness-in scheduling of patients and report preparation.
IV. Potential Sources of Bias

A. Patient-perceived need to demonstrate disability to sustain medical and economic
benefits.
B. Physician-results from past patient experiences, personal philosophies about pain,
work, ambiguities in diagnosis, management, and prognosis.
C. Case manager-most interested in timely case closure.
D. Attorney-represents interests of one of the involved parties but not necessarily
focused on an equitable outcome.
E. Employer-increasing interest in cost savings with less interest in impact on indi-
vidual workers.
V. Vocational Considerations
A. Job demands-provision of accurate evaluation by independent physician signifi-
cantly enhanced by recognizing vocational implications.
I. Physical expectations-routine physical demands of claimant's regular job.
a. Lifting-usually considers weight of materials moved from floor to waist level
494 Independent Medical Examinations and Disability Evoluotions
and frequency of lifts; additional lifting and overhead lifting required for
some jobs; repetitive lifting, especially with awkward loads or twisting most
often associated with spine injuries.
b. Carrying-considers weight and frequency of moving materials; a bulky or
awkward object may also be a factor because it can impede use of proper
body mechanics and posture.
c. Bending-most significant when concomitant with lifting.
d. Stooping-most significant in jobs that frequently require awkward positions.
e. Crawling-most significant in jobs that frequently require awkward posi-
tions.
f. Static positions-maintaining a consistent position can be a significant con-
tributing factor to development of cumulative trauma disorders; becoming
increasingly important as companies attempt to increase worker productiv-
ity, especially in service industries.
g. Overhead activities-lifting and reaching overhead are particularly difficult
for injured workers with shoulder or neck disorders.
h. Bimanual activities-performance of tasks using both upper limbs requires
sufficient strength, balance, and dexterity.
i. Dexterity-ability to manipulate objects and tools to accomplish work tasks.
j. Repetitive activity-increasing productivity increases strain, especially on a
worker's upper limbs.
2. Cognitive expectations-problem-solving abilities and ability to learn new job tasks
becoming increasingly important in industry for individual worker to increase
productivity and reduce likelihood of injury.
3. Interpersonal skills-ability to interact with peers and customers.
B. Pathomechanics of injury-implications for return-to-work and recurrence.
1. Material handling (lifting, carrying)-most common cause of spine injuries
among injured workers.
2. Twisting and bending-contributing factors to spine injuries, especially when
associated with lifting.
3. Static postures-increased stress on musculoskeletal structures; muscle fatigue
may contribute to injury.
4. Repetitive exertions-increasingly recognized as major factor with cumulative
trauma disorders; probably also significant with spine disorders.
5. Falls-less common cause of injury. but associated length of time off work and
cost of individual claims greater than average of other causes of injury.
6. Safety issues-cardiovascular demands and working at heights are examples of
potential safety concerns for occupations such as police officers and iron workers.
VI. Ergonomic Factors

A. Job expectations-work performance expectations may lead to the worker's use of
improper technique.
1. Static' positions-maintaining a static posture contributes to development of
pain.
2. Repetition-repeated tasks, especially if forceful exertions are needed, contribute
to development of cumulative trauma disorders.
B. Tools-many workplace tools are not designed to accommodate the worker or have
limited tolerances outside of use by "average" worker; cumulative trauma fre-
quently results.
I. Gloves-their use requires increased force for gripping and object manipulation.
2. Vibration-common in workplace and enhances musculoskeletal trauma, includ-
ing upper limb cumulative trauma disorders and spine conditions, especially at
frequency of 5-6 Hz.
C. Environmental conslderations-work-setting factors can increase the likelihood of
worker injury.
1. Cold exposure-increases soft-tissue and muscle tightness and decreases pe-
ripheral nerve conduction.
2. Heat and humidity-increase cardiovascular work demands.
VII. Definitions from Americans with Disabilities Act

A. Essential job functions-job duties that are core to performance of a job.
B. Reasonable accommodations-job modifications that can be provided to facilitate
performance by a worker with a disability.
C. Transferable skills-ability to perform comparable job, based on past work expe-
rience and training.
VIII. Clinical History

A. Verification of historical information is important. Patient typically serves as the pri-
mary source of historical information; thus patient bias or memory limitations
may impede performance of an independent evaluation.
1. All available medical records should be reviewed for comparison.
2. Discussion with treating physicians or other health care providers, when possi-
ble, may be necessary to resolve apparent, significant discrepancies.
B. (omponents-may vary depending on nature of injury or illness.
1. Onset ofinjury or illness
a. Description of inciting episode, especially as it pertains to possible patho-
mechanics and pathophysiology.
b. Contributing factors to injury, including repetitive trauma, influence of
work setting (e.g., productivity incentives).
2. Past pain history-context of current pain problem as it compares with previous
pain experiences is helpful.
3. Underlying medical conditions that may increase impact of work trauma or delay
recovery, such as underlying diabetic peripheral neuropathy or spine osteo-
arthritis in an injured worker with a lumbosacral radiculopathy.
4. Previous diagnostic testing, including laboratory work, radiologic assessment, and
electrornyographic evaluations; recognize that previous abnormalities do not
necessarily correlate with persistent symptoms.
5. Previous treatment regimens, including surgeries, medications, and therapies, and
their effectiveness.
6. Persistent symptoms, with particular attention to a thorough description of pain;
the pain description should include the quality of the pain, its duration, incit-
ing factors, relieving factors, radiation, and associated symptoms.
a. Providing pain description choices is sometimes necessary (e.g., sharp,
aching, burning, pressure, throbbing, electrical).
b. Pain rating scale also helpful, including current level and previous 3D-day
range (for instance, pain rated zero to ten with zero being absence of pain
and ten being the most pain the individual had ever experienced).
7. Relationship of ongoing symptoms to initial trauma; temporal relationship to onset
most common factor.
8. Risk factors for chronicity should be assessed.
a. Poor work performance may be most significant correlation with individu-
als developing long-term disabling work-related conditions.
496 Independent Medical Examinations and Disability EYalualions
b. Limited interpersonal skills may impede return-to-work and getting through

the health care system.
c. Substance abuse interferes with effectiveness of many aspects of treatment.
d. History of childhood abuse, more commonly reported by individuals with
chronic pain than by general population, may influence their way of view-
ing pain experience.
e. Interpersonal conflicts may slow recovery process, especially when signifi-
cant other involved.
f. Recurrent injuries-some workers prone to injuries; cumulative effect of re-
peated trauma may slow recovery.
g. Learning disorders are more common among individuals with chronic pain;
may be related to greater tendency to perform heavy manual work that
makes injury more likely; may also increase difficulty of successfully navi-
gating the health care system to receive most effective treatment.
IX. Examination
A. Observation during history taking should initiate examination and serve as basis for
initial diagnostic impression; remaining examination should focus on confirming
these impressions.
B. Pain behavior-facial grimacing and other signs associated with pain help to delin-
eate the patient's pain experience.
C. Posture, physique, and body mechanics provide information about impact of pain on
patient.
D. Gait pattern analysis demonstrates protection of painful body parts, weakness, and
exaggeration of symptoms. Tandem walking, toe-and-heel walking, and walking
in reverse may clarify or accentuate findings.
E. Musculoskeletal system examination should include involved body part and all other
potentially involved structures and a general survey of musculoskeletal structure.
1. Spine examination
a. Inspection-description of scars, especially adherence to underlying struc-
tures, abnormal curves or step-off, evidence of inflammation or infection.
b. Range-of-motion evaluation should be repeated to determine consistency.
c. Palpation-attempt to identify tender structures and presence or muscle
tightness or guarding.
2. Limb joints
a. Inspection-evidence of inflammation, including calor, rubor, effusion.
b. Range of motion-determine flexibility and instability.
c. Palpation-identification of involved structures.
F. Neurologic examination
I. Muscle stretch reflexes-best elicited when patient performs motor activity with
agonist muscle.
2. Motor evaluation-evaluation of strength, flexibility (especially for two-joint
muscles), and atrophy.
3. Sensory evaluation-vibratory sensation especially useful for diagnosing under-
lying peripheral neuropathies.
4. Cognitive evaluation-especially important in identifying safety concerns, such
as impulsivity and impaired safety judgment, for patients returning to poten-
tially dangerous jobs.
G. Review of diagnostic testing
1. Comparison of testing results versus historical information and examination
findings.
Independent Medical Examinations andDisability Evaluations 497
2. Recognition of frequency of false positive and negative results.

3. Need for correlation between test results and clinical findings and recognized
pathological conditions.
4. Recognition of testing limitations.
a. Radiolucency of pain-pain cannot be identified on any testing.
b. Structural abnormalities may not correlate with physiological impact of
condition.
X. Evaluation Conclusions
A. Diagnoses-based on compilation of historical information, examination findings,
and review of available records; should include most likely diagnostic explanation
for findings and differential diagnosis; potentially contributing and underlying
conditions should be included.
B. DiHerentiation of physica~ cognitive, psychologica~ and malingering components of pain expe-
rience.
C. Causality-relationship of ongoing disability to recognized injury or illness; may be
difficult to determine with cumulative trauma disorders or when a history of mul-
tiple traumatic episodes is provided; extent of ongoing symptoms and impairment
does not directly correlate with extent of initial trauma.
D. Prognosis-including medical stability, need for ongoing care, and potential for
return-to-work; determination of maximal medical improvement for many com-
pensation systems (benefits, especially medical, may terminate).
1. Potential for additional injury or condition deterioration with retum-to-work.
2. Recurrent injury potential with exposure to same initiating ergonomic factors.
E. Projections
1. Physical capabilities-ability to perform physical demands of work.
2. Job description review and determination of suitability of injured worker for
the position.
F. Calculations
1. Impairment-most often based on American Medical Association Guidelines.
2. Costs of care-relationship of condition to need for ongoing services.
G. Legitimacy
1. Enhancement of findings intentionally or unintentionally by the patient sec-
ondary to pain experience or desire for secondary gain.
2. Practitioner must compare historical and examination findings with recognized
clinical conditions.
3. Waddell signs are example of distinguishing tool for demonstrating patient
pain experience amplification.
4. Development of increased examination testing sensitivity and specificity allows
the clinician to distinguish patient malingering (feigning disability).
XI. Team Evaluation Components and Team Considerations

A. System requirements and recognition may allow for other health care providers to
supplement physician evaluation.
1. Therapists
a. Physical capacity testing-evaluation of patient's ability to perform physical
tasks.
b. Work capacity testing-determination of patient's ability to perform work
tasks.
c. Identification of specific core job expectations.
d. Provision of guidelines for alternate job development.
498 InclepencJent Medical Examinations andDisability Evaluations
2. Vocational specialist
a. Delineation of patient's vocational interests-particularly helpful with
chronic pain patients.
b. Achievement testing-identifies patient's past performance with learning.
c. Aptitude testing-identifies patient's areas of strength for new learning.
d. Transferable skills-injured worker's abilities that may be useful in alternate
job development.
e. Identification of job market availability for positions within patient's trans-
ferrable skills.
3. Psychologist
a. Interpersonal skills-determination of most effective way to motivate patient.
b. Mood and affect-often influence outcome.
c. Intellectual ability-ability to learn new material.
d. Stress management-determination of patient's most effective strategies for
dealing with stress related to pain and return-to-work.
XII. Documentation Considerations

A. Precision and accuracy-clinician should strive for developing an articulate approach
to providing information, especially via written reports.
I. Dictation and transcription-should not introduce significant or recurrent typo-
graphical inaccuracies.
2. Consistency-standard formats help to ensure thoroughness.
3. Proofreading-reduces errors and enhances future performance.
4. Eponyms-need for accuracy.
5. Abbreviations-should be either defined or obvious based on context.
6. Format-should facilitate review by non clinicians, especially sections related to
analysis and conclusions.
7. Any component of any report developed for compensation system may need to
be defended via medical testimony and clinician should document and prepare
accordingly.
B. Teaching setting considerations-any apparent lack of consistency must be addressed.
C. Note taking-needs to enhance final report.
I. Patient forms may streamline history taking, but care must be taken not to in-
troduce bias.
2. Encapsulation and recapitulation of historical information to patient may im-
prove report quality and patient comfort with report accuracy.
D. Enhancing objectivity
I. Attitude adjustment-practitioner should attempt to limit biases that can affect
accuracy of evaluations.
2. Role-understanding the extent and expectations of the evaluation.
a. Adjudicator-physician usually not required to make ultimate decisions
about compensability.
b. Reporter of facts-only physician can accurately delineate impact of medical
conditions.
3. Differentiating malingering-actual feigning of disability from symptom exag-
geration.
4. Refining examination techniques.
a. Developing measures to assess patient credibility, such as Waddell signs.
b. Reviewing evaluation outcome, including comparing reports and depositions
without regard to referral source.
XIII. Testimony Considerations

A. Recognizing physician role
1. Honest opinions-patient particularly has the right to expect honest physician
opinions.
2. Not adjudicator-although medical opinion serves as a basis for determina-
tions, compensation system is final adjudicator of claimant's benefits.
3. Thoroughness-medical intervention must provide sufficient information for
accurate system determinations.
4. Objectivity-compensation system effectiveness based on practitioner's objec-
tivity.
B. Preparation
1. Intensity of testimony experience can be reduced by accurate preparation.
2. Review all available materials.
a. Own reports-especially important to be familiar with calculation and esti-
mations.
b. Other medical reports-particularly valuable to recognize opposing opinions.
c. Depositions-especially those of individuals with opposing opinions.
d. Recognizing discrepancies, especially related to conclusions, but also sig-
nificant typographical errors, such as side of involvement.
3. Notes of key facts, especially dates and result of significant diagnostic tests
and treatments.
4. Meeting with attorney-obtaining background information, especially about
testimony needs.
C. Recognizing key issues-areas likely to be covered during testimony, especially areas
of potential contention.
1. Causality-relationship of ongoing symptoms to alleged injury or illness.
2. Extent of impairment-most significant in compensation systems that base
claimant compensation on impairment/disability determinations.
3. Maximal medical improvement-claimant has reached maximal level of func-
tioning after medical and rehabilitative care; ongoing treatment services usu-
ally not warranted.
4. Medical condition stability-likelihood of long-term deterioration.
5. Contributory negligence-usually not an issue in "no fault" worker's compen-
sation systems, but may be a factor if product liability is an issue or injury is
based on non-work-related factors or inappropriate worker behavior.
XIV. Marketing Considerations

A. Medical documentation serves as the physician's greatest marketing tool.
B. Content of reports is of greatest importance, especially meeting the system needs
by providing answers to questions that underlie compensation system determi-
nations.
C. Timeliness-immediate feedback of findings greatly enhances value of evalua-
tions.
XV. Summary
A. Evaluations should be objective, reliable, thorough, accurate, precise, consistent,
and timely.
B. Practitioner should recognize system needs and constraints.
C. Appropriate documentation enhances the quality of independent evaluations and
serves as the basis for testimony.
500 Independent Medical Examinatians andDisability Evaluatians
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1r-----------32
Assessing Impairment of the Lumbar Spine
Terrence P. Glennon, M.D., and Charlotte H. Smith, M.D.
Key Points
• Impairment is an alteration in an indfvidual's health status as determined by medical
means; due to a loss, loss of use, or derangement of any body part, organ system or
organ function.
• Disability is an alteration in an individual's capacity to meet personal, occupational, or
social demands.
• Handicap is a barrier to full functional activity that may be overcome by compensating
in some way for the causative impairment.
• Impairment rating is a medical assessment of the individual's health status, usually used
by legal or administrative organizations, to assist in determining compensation for
injury. It is obtained by medical assessment of the patient's history and medical
records, examination of the patient, and translation of the data into an impairment
percentage by use of an appropriate set of guidelines.
I. Background
A. Overview
1. AMA Guides: The AMA Guides was first published in book form in 1971 in re-
sponse to a public need for standardized, objective approach to evaluating
medical impairments.
2. Since then, the Guides has undergone four revisions, incorporating available
scientific evidence, prevailing medical opinions, and technological advances in
diagnosis and treatment in response to specific requests from user groups.
3. The Guides were written by a panel of physicians, who were encouraged to use
the latest scientific evidence from their specialty, and where evidence was lack-
ing, develop a consensus view.
4. A 1999 survey indicated that 40 of 51 jurisdictions (50 states and the District of
Columbia) use some version of the Guides in workers' compensation cases be-
cause of statute, regulations or by administrative/legal practice. The Guides is
also used in Canada, Australia, New Zealand, South Africa and European coun-
tries for different applications.
a. Various editions of the Guides are used in differentjursidictions. There are
significant differences in the methodologies of the different editions of the
Guides. Most jurisdictions currently use the 3rd, 4th, or 5th editions.
b. Note that some states require use of a different impairment rating methodol-
ogy. Physicians should contact the workers compensation agency of their
state to determine which edition of the Guides to use or if another method-
ology is mandated.
c. The information in this chapter reflects impairment rating techniques de-
503
504 Assessing Impairment 01the Lumbar Spine
scribed in the AMA Guides, noting differences between various editions of

the Guides where appropriate.
d. There are significant differences between AMA Guides editions (Table I).
B. Definitions
1. Impairment: an alteration in an individual's health status as determined by med-
ical means; due to a loss, loss of use, or derangement of any body part, organ
system or organ function.
2. Disability: an alteration in an individual's capacity to meet personal, occupa-
tional, or social demands.
3. Handicap: a barrier to full functional activity that may be overcome by compen-
sating in some way for the causative impairment.
4. Distindion between impairment and disabihty: the left fifth digit of two patients is am-
putated. They have exactly the same impairment, but one is a truck driver, who
may have no disability, and the other is a violinist, who may be totally disabled.
5. Maximal medical improvement (MMI): when a condition has been optimally treated,
medically or surgically, so that no further improvement is expected in the con-
dition or the patient's function.
6. Impairment rating: a medical assessment of the individual's health status, usually
used by legal or administrative organizations, to assist in determining compen-
sation for injury.
7. Whole person impairment: degree of impairment expressed as a percent of the
whole body.
a. Strictly interpreted, assessment of impairment is a purely medical determina-
tion of the deviation from an individual's normal health status.
Determination of employability or any other assessment of function is a de-
termination of disability.
b. Determination of impairment typically yields a percentage of impairment or
an assessment of the degree of abnormality of the body, usually due to a
specific injury.
c. An impairment rating is ordered after completion of treatment for a particu-
lar injury (maximal medical improvement). Some states mandate perfor-
mance of an impairment rating to signify the end of treatment and to quan-
tify the alteration in the individual's health status. The appropriate time to
assess impairment is determined by the regulations under which the individ-
ual patient is covered.
d. The impairment rating typically may be performed by any qualified and
trained professional, including the treating physician.
e. Permanent vs. temporary impairment
i. Permanent impairment is expected to last indefinitely. One such definition is
that the condition will not significantly change for 1 year.
Table 1. DiHerences Between Various Editions of the AMA Guides

Area 3 RD Editian 4 TH Editian 5TH Editian
Date written: December 1988/ June 1993 November 2000
February 1989
Length: 254 pages 339 pages 613 pages
Chapters: 14 total 15 total 18 total
Significant differences Uses range of motion Uses diagnosis-related Uses diagnosis-related
in lumbar spine impair- model (ROM model) estimates model (DRE estimates model (DRE
ment: model) model)
Assessing Impainnent of theLumbar Spine 50S
ii. Temporary Impairment is not expected to last indefinitely. Typically, only

permanent impairment is assigned a rating.
iii. Maximal medical improvement. Usually, an impairment rating is per-
formed only when a condition has been optimally treated and no fur-
ther improvement is expected. Often, this is a precondition of assigning
impairment; otherwise, the impairment would change as the condition
improved. The residual impairment at that point is considered to be
permanent.
f. Total vs. partial impairment
i. Total impairment implies that the body is completely impaired. The term is
more typically applied to disability, with total disability implying that
the patient is unfit for gainful employment.
ii. Partial impairment implies that only a portion of the body is impaired; this
degree of impairment can be described as a percentage.
(a) The most common type of impairment that requires a rating is per-
manent, partial impairment. A temporary impairment rarely requires
a rating, because it changes with time or treatment. Most injuries
leave a residual partial rather than total impairment, and the objec-
tive measurement of percentage of impairment is needed by adminis-
trative organizations.
(b) Clinical judgment. All decisions are subject to clinical judgment, such as
whether the impairment discovered at assessment may be due to the
injury that is stated as the cause. The results of the medical examina-
tion are subject to the same judgment, such as whether the abnormal-
ities are truly pathophysiologic.
(c) Impairment report. The impairment rating serves as the medical sum-
mary of the injury in question. A well-performed and well-written
impairment summary may be the only document that reports the
medical ramifications of injury. As such it should be accurate, objec-
tive, reproducible, and comprehensive. In some states, the impairment
rating is directly linked to the amount of benefit received by the in-
jured worker. Although a disability assessment is probably more ap-
propriate for this purpose, the practitioner should find out from the
administrative body exactly how the impairment rating will affect
each patient.
II. Sources of Impairment

A. Impairment may be assigned to any organ system of the body, such as the diges-
tive, respiratory, or musculoskeletal system.
B. This chapter focuses on the musculoskeletal system, specifically as it relates to the
lumbar spine.
I. Impairment may include the spine itself as well as any resultant impairment to
the limbs due to lumbar spine injury.
2. Abnormalities of the neuromuscular system (e.g., permanent radiculopathy)
caused by injury to the lumbar spine are included in the assessment.
3. The specific technique for determining impairment varies depending on which
edition of the AMA Guides is used.
III. Typical lumbar spine impairment evaluation

A. Either the range of motion Model or the diagnosis-related estimates model is used (de-
pending upon which version of the AMA Guides is required.)
506 Assessing Impairment of the Lumbar Spine
1. The typical evaluation starts with a comprehensive review of the medical record
to ensure that the findings on the examination match the findings on the previ-
ous medical reports. In addition, knowledge of the history determines which
findings will be included in the impairment calculations.
2. The general history and physical examination focus on the systems of the body
with reported symptoms and related dysfunction.
3. Impairment related to specific disorders of the system is derived from instruc-
tion or reference tables and recorded. This portion of the impairment is directly
related to objective findings from various tests or surgical procedures.
4. Range-of-motion of the involved region of the spine is assessed according to
instructions provided in the required reference, and impairment for restriction
of motion is calculated if utilizing the Range of Motion Model.
5. Lastly, the above impairment values are summarized to arrive at the final rating
in terms of whole person impairment.
B. Range ofMotion Model of lumbar spine impairment is determined by combining im-
pairment classified in three major categories: (1) specific disorders of the lumbar
spine, (2) loss of range of motion of the lumbar spine, and (3) persistent residual
neurologic deficits.
1. Specific disorders (vary according to the edition of the Guides used). Impairment
is assigned according to the diagnostic category in which the predominant
pathology falls. Impairment may be assigned in the following categories, de-
pending on the reference used:
a. Fractures (of vertebral body or posterior elements)
b. Intervertebral disc or other soft-tissue lesions
c. Spondylosis
d. Spondylolisthesis
e. Spinal stenosis
f. Segmental instability
2. Loss of range of motion
a. As with other regions of the musculoskeletal system, loss of range of motion
is associated with impairment of the lumbar spine.
b. Loss of range of motion is interpreted as an alteration in the structure of the
body and is translated into an impairment percentage.
3. Neuromuscular deficits
a. Weakness in a radicular distribution is rated by the value of the radiculopa-
thy and the degree of weakness
b. Each nerve is assigned a certain value, depending on the degree of impair-
ment due to loss of the nerve.
c. The degree of nerve loss is then assessed. For example, a complete nerve in-
jury is 1000/0 loss of the nerve's value. Partial nerve injuries account for a
lesser percentage of loss of nerve function. The partial amount of nerve
function loss is multiplied by the value of the nerve.
d. Sensory loss is similarly rated.
4. Total whole person impairment is calculated by combining (not adding) the impair-
ments due to (I) specific disorders of the lumbar spine, (2) loss of range of mo-
tion in the lumbar spine, and (3) persistent residual neurological deficits, using
the Combined Values Chart found in the AMA Guides.
5. The ROM Model is used exclusively in the 3rd edition of the AMA Guides.
6. The ROM Model is used only in certain circumstances in the 4th and 5th editions
of the AMA Guides (when it is not feasible to assign a DRE Category.l
7. The AMA Guides 5th edition states that the ROM Model is used:
Assessing Impainnent of the Lumbar Spine 507
a. When the impairment is not caused by an injury, or

b. When an individual's condition is not well represented by a DRE category,
c. When an individual has an injury or alteration of motion segment integritiy
at more than one level in the same spinal region, or
d. When an individual has recurrent pathology,
e. If statutorily mandated in a particular jurisdiction.
f. The reason for using the ROM method under these circumstances must be
carefully supported in writing.
C. Diagnosis-Related Estimate Model oflumbar spine impairment uses diagnosis-related categories
that consider:
I. Presence or absence of clinical findings (symptoms, signs and diagnostic test
results) including:
a. Muscle spasm
b. Muscle guarding
c. Asymmetry of spinal motion
d. Nonverifiable radicular root pain
e. Reflexes
f. Atrophy
g. Radiculopathy
h. Electrodiagnostic verification of radiculopathy
i. Alteration of motion segment integrity
j. Cauda equina syndrome
k. Urodynamic test abnormalities.
2. Assignment of Lumbar Spine DRE Category (Table 2).
3. The DRE Model is the preferred method of assigning lumbar spine impairment in
both the 4th and 5th editions of the AMA Guides (unless it is not clinically feasible.)
4. In a small number of instances, both the ROM or DRE methods can be used.
5. The 5th edition of the AMA Guides states that the individual be evaluated by
both methods and that the higher rating be awarded.
6. The 4th edition of the AMA Guides states that if impairment cannot be assigned
using the DRE Model, then the ROM method should be used to assign the DRE
category that is closest in impairment percentage to the percent determined by
the ROM Model.
7. The 3rd edition of the AMA Guides does not use the DRE Model. Impairment is
determined solely by the ROM Model.
8. Differences in the DRE Categories and definitions between the 4th and 5th edi-
tions of the AMA Guides.
a. There are significant differences in the DRE Categories definitions and
methodologies used in the 4th and 5th editions of the AMA Guides.
b. The appropriate edition of the AMA Guides should be consulted with close
attention to the text and tables related to the DRE Categories for lumbar im-
pairment.
IV. Procedure for Assessment of Impairment

A. General concepts ofimpairment raling
1. Performance of an impairment assessment should be guided by an appropriate
reference. This discussion assumes that the examiner will have direct access to
such a guide and is not intended to replace it. Different states and different
agencies mandate the use of different editions of the AMA Guide to the
Evaluation of Permanent Impairment or other references.
2. Impairment is expressed as a percentage.
Table 2. Lumbar Spine Diagnosis-Related Estimate (DRE) Categories (AMA Guhles, Sill ed1tlon)
% Impairment
DRE Category (Whole Person) Description
I 0% No significant clinical findings
11 5-8% Findings compatible with a specific injury; finding may
include significant muscle guarding/spasm, asymmetricloss
of ROM, nonverifiable radicular complaints; no alteration
of the structural integrity; no significant radiculopathy
Or
Clinically had a significant radiculopathy + imaging study
with HNP that correlates with the previous radiculopathy,
but no longer has the radiculopathy following conservative
treatment
Or
Fractures: (1) < 25% compression of one vertebral body; (2)
posterior element fracture without dislocation that has
healed without alteration of motion segment integrity;
(3) spinous or transverse process fracture with displace-
ment without a vertebral body fracture, not disrupting the
spinal canal.
1lI 10-13% Significant signs of radiculopathy (such as dermatomal pain
± derrnatomal sensory loss, loss of relevant reflexles], loss
of muscle strength or unilateral measured atrophy) may be
verified by electrodiaqnostic finding
Or
Historyof HNP that correlates with the radiculopathy, or
individualswho had surgery for radiculopathy but are now
asymptomatic
Or
Fractures: (1) 25-50% compression of one vertebral body;
(2) posterior element fracture with displacement disrupting
IV 20-23% Lossof motion segment integrity (defined by ~ 4.5 mm of
translation of one vertebra on another or angular motion
> 15 degrees at Ll-2, L2-3, and LJ-4, > 20 degrees at
L4-5, and> 25 degrees at L5-S1; may have near com-
plete loss of motion of a motion segment due to develop-
mental fusion or successful or unsuccessful attempt at
surgical arthrodesis
Fractures: (1) > 50% compression of one vertebral body
without residual neurological compromise.
V 25-28% Meets criteria for DRE categories 111 and IV; both + radicu-
lopathy and alteration of motion segment integrity;
+ significant lower extremity impairment (atrophy, loss of
reflexes, pain ± sensory changes within an anatomic
distribution, or + EMG finding and alteration of spine
motion segment as defined in IV)
Or
Fractures: (1) > 50% compression of one vertebral body
with unilateral neurological compromise
3. Impairment is calculated by organ system. In the case of the musculoskeletal

system, it is calculated by regions of the body (limbs and trunk). Regional im-
pairment may be calculated in terms of a limb or other body part and later con-
verted to impairment of the whole person.
4. After all regional calculations are performed, they are combined to yield a sin-
gle impairment percentage that represents whole person impairment (WPI).
Assessing Impairment of!he Lumbar Spine 509
5. For example, impairment of the thumb may first be calculated in terms of im-
pairment of the hand, then as impairment of the upper extremity, and finally as
impairment of the whole person.
6. When impairment of different regions is combined, the percentages are not
simply added. If they were, the total could easily surpass 1000/0. Therefore, a
formula or table (such as the Combined Values Chart) is used to combine the
values from different regions.
7. Range of motion is often used as an assessment of the residual function of an
injured portion of the body. Range-of-motion measurements of any joint are
generally repeated until at least three measurements are within the appropriate
margin of error (100/0 or 5°).
a. A maximum of 6 measurements may be taken.
b. If no 3 consecutive measurements are within the acceptable margin of error,
the measurement is discarded, and no impairment is assigned. Such incon-
sistent measurements are not likely to reflect the true range of motion; thus
impairment should not be assigned on such a basis.
c. Different versions of the AMA Guides have various consistency and validity
criteria requirements for range of motion impairment. The specific Guides
edition should be consulted for guidance in the required methodology.
B. Find out whi(h referen(e isrequired for the assessment.
1. The reference should be specified by the organization requesting the impair-
ment assessment. Many state workers' compensation systems require a specific
reference.
2. The ideal reference and measurement process produces the same impairment
percentage if performed by two different examiners or by the same examiner at
two different times. Such a reference is still being sought.
C. Obtain all pertinent medi(al re(ords.
1. Hospital, office, or emergency center notes
2. Radiographic films and reports, therapy records, procedure notes, operative
notes
D. S(hedule adequate time for record review, patient history and physical examination,
review of relevant data and report dictation. Complex cases that are new to the
examiner may take up to 2 hours for:
1. Complete record review, including relevant radiological, electrodiagnostic, and
ancillary tests
2. Patient interview and examination
3. Range-of-motion assessment
4. Impairment calculation
3. Report dictation
E. Assign pathology to a spedfi( disorder (ategory.
1. The predominant pathology of the spine should be identified by
a. Imaging studies
i. Magnetic resonance imaging
ii. Myelography
iii. Plain radiographs
b. Surgical findings or procedures performed
c. Physical examination findings
i. Impairment is assigned specifically for the pathology that is believed to
account for the patient's symptoms. Additional measures, such as range
of motion, mayor may not be combined with this value, depending on
the specific pathology and which edition of the Guides is used.
ii. It is essential that the rater include in the report a description of how the
impairment was calculated.
F. Range-of-motlon measurement of the lumbar spine:
I. Because the joints of the lumbar spine are not superficial enough to allow direct
access to standard goniometric measurement and because there is no "contralat-
erallimb" for comparison, the spine must be assessed in a different manner.
2. Inclinometers, which use a bubble inside a ring of viscous fluid (much like a
carpenter's level), are used to measure the change in the angle of a specific site
on the body compared with baseline position.
3. To measure flexion and extension of the lumbar spine
a. Locate the landmark for the upper margin of the lumbar spine, which is the
TI2 vertebral spinous process.
i. Mark the L4 spinous process.
ii. L4 is the spinous process located at a line intersecting the upper margins
of the iliac crests.
iii. Count upward from L4 to TI2.
iv. Place the upper inclinometer over the TI2 spinous process. The feet of
the inclinometer should straddle the spinous process.
v. Set the grid on the inclinometer to the "zero" mark.
b. Locate the landmark for the lower boundary of the lumbar spine, the
sacrum.
i. Count down from L4 to S1.
ii. Place the lower inclinometer over S1. Both feet of the inclinometer may
be placed securely on the sacrum.
iii. Set the grid on the inclinometer to the "zero" mark.
c. Measure lumbar flexion and extension.
i. With the inclinometers held securely in place, ask the patient to bend
forward as far as possible, keeping the knees straight and the feet about
one shoulder-width apart.
ii. Record the new readings on both upper and lower inclinometers.
iii. Ask the patient to extend back as far as possible, and record the read-
ings from the inclinometers.
iv. The difference between the readings on the inclinometers is the total
amount of motion of the lumbar spine (e.g., 112 flexion minus S1 flex-
ion = total lumbar flexion of L1 through L5).
v. Example:
(1) 112 initial reading: 0°
(2) S1 initial reading: 0°
(3) 112 reading after flexion: 110°
(4) S1 reading after flexion: 50°
(5) Total lumbar flexion = 60°
vi. Ensure that 3 consecutive measurements are within the acceptable mar-
gin of error.
vii. Choose the largest of the 3 measurements to represent the range of mo-
tion.
viii. Compare this measurement to the normal values for lumbar flexion and
extension from the appropriate table in the guide, and assign the appro-
priate percentage of impairment (if any) to this particular range-of-
motion measurement.
ix. For lumbar flexion, the rating may also depend on the total sacral flex-
ion recorded.
Assessing Impairment of the Lumbar Spine 511
4. To measure lateral flexion 01 the lumbar spine

a. At the T12 vertebra, hold the inclinometer flat against the back to prepare to
measure motion in the coronal plane.
b. With the feet of the inclinometer on either side of the spinous process and
the inclinometer level, mark a line on the skin at each foot, representing the
level landmark.
c. Do the same at S1.
d. Ask the patient to bend laterally to the left, and record the measurement on
each inclinometer. The patient should keep both feet on the ground.
e. As with the previous measurements, the true lateral flexion of the lumbar
spine is the difference between the recordings of the upper and lower incli-
nometers.
f. Find the corresponding impairment percentage for the range of motion mea-
sured.
g. Follow the same procedure for right lateral flexion.
5. Use the straight leg raise (SLR) as across-check maneuver.
a. Assessment of range of motion of the lumbar spine has a validity criterion
in addition to the requirement the 3 consecutive measures be within 5° or
100/0 .
b. Straight leg raise (SLR) is measured for each leg, with a single inclinometer
over the tibia, until 3 consecutive measures are within validity range. If 6
measures are performed and 3 consecutive measures are not consistent, this
measurement is thrown out along with the corresponding lumbar flexion/
extension measures.
c. This maneuver is passive, i.e., the examiner moves the patient's leg to the
point of maximal range.
d. For each leg, the largest of the 3 ranges is used.
e. The measurement for the more restricted of the two legs is used for compari-
son.
f. When lumbar flexion is assessed, a measurement of sacral flexion is also ob-
tained (the lower inclinometer measurement). The maximum of the 3 consec-
utive measures should be used.
g. A measurement of sacral extension has already been obtained.
h. The largest sacral flexion and extension values should be added together.
The sum represents the total excursion of the pelvis over the hip in the
sagittal plane.
i. The total range of motion of the more restricted of the two hips likewise rep-
resents the total excursion of the hip within the pelvis in the sagittal plane.
j. The theory is that the values in e. and h. (above) should be relatively similar,
since they both represent the total range of the hip-pelvis articulation. If
they are not, it is suggested that full lumbar flexion/extension may not have
been assessed, and therefore are invalidated.
k. Therefore, the more restricted (tighter) of the two SLR measures has to be
within 10° of the total sacral range of motion for the lumbar range of mo-
tion measurements to be valid. If the more restricted SLR measurement is
more than 10° larger than the total of sacral flexion and extension, the lum-
bar flexion and extension measures are discarded.
G. Impairment due to neurologic dellat
1. General issues
a. The typical neurologic deficit in lumbar spine injuries is radiculopathy,
which may involve motor or sensory deficits in a radicular distribution.
512 Aueuing Impairment of /he Lumbar Spine
b. Diagnosis depends on corroboration with the history of the injury, the spe-
cific disorder of the spine and its anatomic location, results of eletromyo-
graphic testing, and the physical examination at the time of impairment as-
sessment.
c. The degree of deficit is multiplied by the value of the nerve root involved to
obtain the degree of impairment due to the radiculopathy.
d. This impairment is typically given in terms of impairment of the lower limb
affected by the radiculopathy. Therefore, the value needs to be combined
with other impairment of the involved lower limb, converted into impair-
ment of the whole person, and combined with impairment values from other
regions of the body, including the spine itself.
e. Other means of testing may provide information about whether the nervous
system is intact. However, the clinical examination should guide how the re-
sults are used in the impairment rating. For example, if electromyography
and nerve conduction velocity testing (EMG/NCV) show residual denervation
or slowing of nerve conduction velocity but the clinical examination reveals
normal strength, the impairment rating should reflect the patient's normal
strength. The results of objective tests, however, may be used to corroborate
the findings on the clinical assessment in the presence of an abnormality, as
in confirming evidence of weakness on the clinical examination.
2. Motor deficits
a. Motor deficits are graded according to the distribution of the weakness and
its severity. The weakness must be in a distribution that corresponds with
the source of the radiculopathy.
b. The severity of the weakness is assessed by standard manual muscle testing.
c. The grading scheme for weakness is as follows:
i. Complete range of motion against gravity and full resistance
ii. Complete range of motion against gravity and some resistance or re-
duced fine movements and motor control
iii. Complete range of motion against gravity only without resistance
iv. Complete range of motion with gravity eliminated
v. Slight contractibility but no joint motion
vi. No contractibility
d. The above may be recognized as the standard rating scale for manual muscle
testing, from grade 5 to O. Each of these grades is assigned a percentage
range for deficits (which varies between the different Editions of the AMA
Guides.)
e. The following are examples of the relative values for the motor roots:
i. L-3 200/0
ii. L-4 340/0
iii. L-5 370/0
iv, S-1 200/0
f. The impairment for degree of weakness is multiplied by the value of the mo-
tor root to obtain the impairment, in terms of the lower limb, for weakness
due to radiculopathy (Fig. I).
Motor Impairment = Motor Grade Deficit % x

Relative Value % of Nerve
FIGURE I. Rating impairment due to motor deficits.

Assessing Impairment of /he Lumbar Spine S13
3. Sensory deficits
a. Sensory deficits are more difficult to assess objectively. To establish impair-
ment, sensory loss must be documented as objectively as possible and must
not consist only of subjective report of sensory abnormality or asymmetry.
b. Sensory rating scale is as follows:
i. No loss sensation or no spontaneous abnormal sensations
ii. Decreased sensation, with or without pain, that is forgotten during activ-
ity
iii. Decreased sensation, with or without pain, that interferes with activity
iv. Decreased sensation, with or without pain, that may prevent activity (mi-
nor causalgia)
v. Decreased sensation with severe pain, which may cause outcries as well
as prevent activity (major causalgia)
vi. Decreased sensation with pain, which may prevent all activity
c. Each of the above categories of sensory deficit are assigned a range of per-
centage impairment (that varies between different editions of the AMA
Guides.)
d. The impairment for degree of sensory loss is multiplied by the value of the
nerve root to obtain the impairment, in terms of the lower limb, for sensory
loss due to radiculopathy (Fig. 2).
4. Chronic pain
a. Chronic pain as a diagnostic entity cannot be rated as impairment.
b. Chronic pain as a result of loss of nerve function may be rated as loss of
sensation with pain in the above section.
c. However, because chronic pain cannot be measured objectively or accurately
at this time, it cannot be rated.
5. Calculations and Sample Case (performed according to the AMA Guide to the
Evaluation of Permanent Impairment, 3rd ed.)
a. Patient history
i. 43-year-old male dock worker
ii. Lifting injury with L4/L5 herniated discs 18 months previous; diagnosed
by MRI/EMG
iii. Laminectomy and discectomy 3 weeks after injury due to progressive
neurologic deficit (left foot drop)
iv. Operative findings: large herniated nucleus pulposus at L4-L5 with se-
questered fragment
v. Postoperative recovery: persistent back pain, inability to do many
household tasks, some resolution of left lower extremity weakness
vi. Postoperative rehabilitation program completed
vii. Patient at maximal medical improvement (MMI)
b. Physical exam
i. Some pain with lumbar flexion
ii. Negative neural tension signs
iii. Motor exam on left
(a) Ankle dorsiflexion: 3/5
Sensory Impairment = Sensory Rating Deficit DID x Relative

Value DID of Nerve
FIGURE 2. Rating impairment due to sensorydeficits.

514 Assessing Impairment 01theLumbar Spine
(b) Ankle eversion: 2/S

(c) Ankle inversion: 3/S
(d) Hip abduction: 4/S
iv. Sensory exam
(a) Consistent diminished sensation to pinprick vs. touch over left lat-
eral leg and dorsal web space between digits 1 and 2 of the foot
(b) Sensation otherwise intact
v. Range-of-motion (ROM) measures
(a) Lumbar flexion: 4So
(TI2 ROM = 7So minus SI ROM = 30°)
(b) Lumbar extension: 20°
(TI2 ROM = 40° minus SI ROM = 20°)
(c) Lumbar right lateral flexion: 20°
(d) Lumbar left lateral flexion: 2So
(e) SLR right: 7So
(0 SLR left: 8So
(g) Total sacral flexion and extension: SOO
(S1 flexion [30°] + S1 extension [20°] = SOO)
(h) SLR validity criteria met? No
(total sacral excursion [SOO] must be within
10° of the tighter SLR [7S0] to be valid)
(i) Left ankle dorsiflexion: 10°
vi. Calculatlan af Impairment using the ROM Model
(a) Specific disorders
(i) Table 49, Section II-E, Surgically treated
disc lesion with residual symptoms: 100/0
(b) Range of motion
[i] Lumbar flexion: Invalid
(ii) Lumbar extension: Invalid
(iii) Lumbar right lateral flexion: 1%
(iv) Lumbar left lateral flexion: 0%
(c) Restriction of left ankle dorsiflexion is considered to be a product of
the neurologic deficit and is taken into consideration in the tables
that rate motor loss. Therefore, no additional impairment is assigned
for loss of range of motion of this joint.
(d) Total impairment for range of motion loss: 1010
vii. Neurologic deficit
(a) Motor exam
(i) The average motor grade of the LS innervated muscles listed is
3/S.
(ii) 3/S strength equates to SO% impairment of involved nerve
root.
(iii) Motor function of the LS nerve root is assigned a maximum of
37% impairment.
(iv) SO% times 37010 = 18.S% or 19010 impairment of the lower ex-
tremity.
(b) Sensory exam
(i) This loss of sensation is rated as decreased sensation without
pain, category no. 2, or 2S% impairment of the nerve root.
[ii] Maximal impairment for loss of sensation for the LS nerve root
is SOlo.
Assessing Impairment 01the Lumbor Spine 515
(iii) 25% times 5% = 1.25% or 1% impairment of the lower extrem-

ity.
(e) Combining the above values for motor and sensory loss yields a to-
tal of 20% impairment of the lower extremity.
(d) Because there is no other impairment of the limb, the above value is
converted into terms of the whole person. The total is 8% WPI.
viii. Final calculation: the following categories of impairment have been calcu-
lated:
(a) Summary of findings:
(b) Specific disorders: 10%
(c) Range of motion: 1%
(d) Neurologic loss: 8%
(e) These values are combined in order of decreasing value:
(i) 10% combined with 8% yields 17%.
[ii] Note that the combination yields a value that is less than the
sum of the two numbers.
(iii) It is important to use the Combined Values Chart to combine
any values when indicated rather than adding them.
(iv) 17% combined with 10/0 yields 18%.
(t) The patient has a permanent partial impairment rating of 18% due
to injury to the lumbar spine.
6. Calculations and Sample Case (performed according to the AMA Guide to the
Evaluation of Permanent Impairment, 5th ed.)
a. Patient history
i. 25-year-old male
ii. Lifting injury with Left L5-S 1 herniation with Left S1 radiculopathy; di-
agnosed by MRI
iii. Underwent discectomy 3 months after injury due to progressive neuro-
logic deficit and failure to respond to conservative treatment.
iv. Operative findings: large posteriorlateral herniated nucleus pulposus at
L5-S1
v. Postoperative recovery: improved and returned to work without restric-
tions after 4 months of rehabilitation
vi. Patient at maximal medical improvement (MMI)
b. Physical exam
i. Full range of motion of the lumbar spine
ii, Negative neural tension signs but loss of the Achilles reflex
iii. Motor exam normal
iv. Sensory exam normal
c. Calculation of impairment using the DRE Model
i. Meets criteria of "history of herniated disk at the level and on the side
that would be expected from objective clinicalfindinqs, associated with
radiculopathy, or individuals who had surgery for radiculopathy, but are
now asymptomatic. "
ii. Qualifies for DRE Lumbar Category III (I 0-13010 Impairment of the Whole
Person)
d. Final calculation:
e. Summary of findings:
i. Symptoms, physical findings and imaging studies are all consistent with
a symptomatic herniated disk.
ii. Most symptoms have been resolved with surgical treatment.
516 Assessing Impairment of the Lumbar Spine
iii. The evaluator may award any whole person percentage of impairment
from to-130/0.
iv. The patient has a permanent partial impairment rating of toO/o due to in-
jury to the lumbar spine.
7. Report Generation
a. The final report should represent a self-contained, complete summary of the
case relative to the injury in question.
i. It should summarize all medical history, objective testing, and results of
the physical examination.
ii. It should contain a complete record of all calculations performed in ref-
erence to the impairment rating, including any hand-written worksheets
used to record or calculate data in reference to the impairment.
iii. Specific table numbers used in the calculation should be cited.
iv. The reference should be cited.
v. Specific information required by the requesting agency should be in-
cluded, such as whether the patient is at the point of MMI and the spe-
cific definition of MMI. If the patient is not at MMI, recommendations
for further treatment may be indicated.
vi. Be clear, complete, and concise.
b. Fair treatment of the patient depends on an objective, accurate assessment
of his or her medical condition upon maximal recovery from injury.
References
I. Brand RA. Lehmann TR: Low-back impairment rating practices of orthopedic surgeons. Spine 8:75-77.
1983.
2. Clark WL, Haldeman S. Johnson P. et al: Back impairment and disability determination. Spine 13:
332-341.1988.
3. Engelberg AL (ed): Guides to the Evaluation of Permanent Impairment. 3rd ed, Milwaukee. WI.
American Medical Association. 1984.
4. Guides to the Evaluation of Permanent Impairment. 3rd ed (revised). Milwaukee, WI. American
5. Guides to the Evaluation of Permanent Impairment, 4th ed. Milwaukee, WI. American Medical
Association. 1993.
6. Guides to the Evaluation of Permanent Impairment. 5th ed. Milwaukee. WI, American Medical
Association. 2000.
,--------33
Workers' Compensation
Tom Mayer, M.D.
Key Points
• Work-related causation represents entry into workers' compensation system.
• Workers' compensation is a compromise:
1. Employer receives limited liability for negligence suits.
2. Employee receives statutorily mandated medical and indemnity benefits.
• Medical endpoint is determined by physician on basis of maximal medical
improvement or similar concept.
• Permanency awards, based on evaluation of disability and impairment, increase role of
physician gatekeeper.
• Major differences exist between handling of medical benefits in workers'
compensation and handling of general health care.
I. General Issues
A. Causation
1. Work-relatedness must be demonstrated for entry into workers' compensation
system.
a. Specific major traumatic incident, such as fall from a height, is observed in
minority of cases.
b. Single minor traumatic incident, observed or not, occurs in most cases (for
example, lifting a box and feeling a "pop").
c. Repetitive or cumulative trauma is reported in minority of incidents, but fre-
quency is increasing, particularly in upper extremities.
2. Aggravation of preexisting condition, even if only 1% attributable to the industrial
incident, is generally considered 1000/0 covered.
a. Includes additional conditions that may be caused by the industrial accident
or its direct sequelae.
i. Primary area of injury covered in report (e.g., low back, shoulder).
ii. New area may be accepted if reported as consequence of treatment (e.g.,
sexual dysfunction after anterior lumbar fusion, arm fracture after leg
gives way because of sciatica).
iii. Other medical problems must be investigated for exercise clearance or
preoperative evaluation (e.g., hypertension or diabetes discovered in pre-
operative blood tests); only temporary treatment is permitted in such
cases.
b. Disputes frequently arise over claims of aggravation of preexisting condi-
tions.
3. Intervening injuries
a. Defined as second documented injury subsequent to industrial accident.
517
518 Worlcers' Compensalion
b. If area of primary industrial injury is involved, insurance carriers almost in-

variably argue over who is responsible for sequelae of injury.
c. If a second industrial accident is covered by a second insurer, carriers may
divide responsibility and sort out cost after case closure.
d. If second injury is a personal compensation injury, dispute may result in ter-
mination of benefits until legal agreement is achieved or medical documen-
tation specifies degree to which each accident is at fault.
4. Determining work-relatedness
a. Observed accident on the job is usually considered prima facie evidence.
b. All systems hold injured worker responsible for reporting industrial acci-
dents within specific period (10 or 30 days common).
c. Definition of "on the job" may be extended to activities "occurring in the
course of employment" (e.g., lifting suitcases at airport on business trip, slip-
ping in the parking lot, auto accident driving to lunch in company car).
Causation disputes are common under such circumstances.
d. State-mandated administrative mechanisms are usually in place with specific
procedures available to resolve disputes.
B. History of workers' compensation
1. Originated in 1880s in Otto von Bismarck's Germany.
a. Developed from military traditions dating back to pirates and Roman era.
b. Employing military institution was responsible for welfare of soldier injured
in line of duty without regard to negligence.
c. Concept extended to industrial setting that supported military expansion
[i.e., "blood and iron").
d. British model evolved from English Poor Laws, which were based more on a
welfare model.
i. Still operative in England and many Commonwealth countries.
ii. Many hybrids exist in Europe.
2. Implicit contract between employer and employee
a. Employee receives specific benefits after industrial accident.
i. Indemnity benefits; wage continuance during period of temporary total
disability.
ii. Medical benefits if specifically designed to ameliorate effects of injury.
iii. Permanency award: possible compensation for permanent effects of in-
jury (developed later and expanded).
b. Employer benefits
i. Employer not subject to risk of litigation for negligence.
ii. Employer liability limited by statute.
c. "Rules of the road" mandated by specific jurisdictions, with frequent efforts
by either employers or employees to modify rules.
3. American developments
a. Concept accepted as preferable to "lottery system" of suits for negligence af-
ter 1900 in large eastern industrial states.
b. 42 states had workers' compensation laws by 1920.
c. Hastened by World War 11.
d. Slower acceptance in rural or agrarian states; Mississippi was last state to
adopt workers' compensation (1949).
e. 50 separate state-mandated programs.
f. Several federal programs cover different groups of federal employees or in-
dustries; historically termed national in scope, but with many inconsisten-
Wor*ers' Compensation 519
cies (for example, railroads operate under federal program, whereas airlines
and buses do not).
e. Employee indemnity benefits
1. Wage continuance benefits
a. Almost always tied to a period of temporary total disability (TID).
b. Waiting period of 1-4 weeks before weekly benefits commence is common,
but payment is often retroactive.
c. Wage continuation benefit usually set at 60-75% of demonstrated preinjury
weekly pay; generally tax-exempt.
d. Take-home pay occasionally exceeds preinjury wage, creating disincentives
to recovery.
e. Workers' compensation benefit occasionally supplemented by short-term
disability (STD) policy, either employer-provided or personally held, which
may increase financial disincentive to recovery.
f. Certain jurisdictions allow payment at discretion of employer, but employee
may have modified compensatory right to sue for negligence, pain, and suf-
fering.
2. Termination of temporary benefits
a. Failure to prove causation
b. Reaching medical endpoint
c. Reaching medical endpoint by noncompliance or abandonment of treatment
d. Reaching statutory limit on temporary benefits
i. Long ITO periods expanded in most jurisdictions during prosperity after
World War II.
ii. Current trend restricts TID periods to 2-5 years from previous range of
10 years to lifetime.
e. Other employer-provided or disability benefits may be tied to medical end-
point, but reporting system between workers' compensation medical
providers and other disability policies may be inadequate.
3. Permanency awards
a. Compensates for permanent injuries in lieu of litigation.
b. Obvious injuries handled by scheduled award (e.g., loss of eye or limb).
c. Unscheduled awards for injuries with variable outcomes handled by disability
determination.
i. Common with musculoskeletal soft-tissue injuries and psychological
problems.
ii, Disputes common and usually handled by administrative procedures.
4. Death benefits
a. Generally paid by scheduled award.
b. May be paid as lump sum or lifetime weekly benefit.
D. Employee medical benefits
1. Medical benefits provided for specific injury arising during course of employ-
ment. Covers all acute, hospital, surgical, and rehabilitation expenses designed
a. To return injured employee to work or
b. To terminate period of TID.
2. Medical benefits driven by specific socioeconomic outcomes to be achieved un-
til medical endpoint.
3. Medical benefits provided for secondary conditions aggravated by industrial
accident. Also includes temporary care for unrelated medical conditions if nec-
essary to provide primary care (e.g., surgery) to specific injured area.
520 Workers' Compensolion
4. Employee's choice ofphysician is usual feature of most workers' compensation

venues.
a. Employer may have option to mandate health provider in first 30 days with
patient choice thereafter.
b. Current trend is away from unlimited free choice to a limited number of
physicians.et
c. Change of treating physicians now will frequently require administrative
procedure involving state agency and/or insurance carrier.
E. Medical endpoint
1. History: disputes arose because of conflicting determinations of medical endpoint.
a. Extreme employee position defined endpoint as full symptomatic relief (e.g.,
painless state).
b. Extreme employer position defined endpoint as absence of objective evi-
dence of disease or injury progression (e.g., stable pulmonary status, healed
fracture).
2. Endpoint determination became one of major disputed areas.
a. Attorneys represented injured worker.
b. Insurance carriers and their attorneys represented employers.
c. Complex administrative procedures generally incomprehensible to injured
workers without assistance.
d. Significant "friction costs" often benefit supporting parties.
3. Selection ofphysician asjudge of medical endpoint
a. Concept of medically determined endpoint-maximal medical improvement
(MMI) or maximal medical recovery (MMR) results when "all reasonable ef-
forts designed to improve or cure the condition" (not including palliative
treatment) have been exhausted.
b. Permanent and stationary (PEtS) endpoint results when condition reaches a
medically stable plateau at which it is not anticipated to change more than
1-5010 (depending on venue) over the ensuing 3-12 months (ranges depend
on statute).
c. Determination of endpoint is usually the responsibility of designated "treat-
ing doctor" selected by the patient.
i. Adverse determination may cause injured worker to "shop" for more
sympathetic physician.
ii. Creates built-in disincentive for physician to do other than patient's bid-
ding; counteracted by carrier role as payer.
iii. Employer representative (insurance carrier) frequently uses independent
medical examination (lME) to document medical endpoint and combat treat-
ing doctor's opinion.
iv. Adversarial system polarizes physician opinions. Many treating doctors
become known as "employee-oriented," whereas search for predictability
leads to network of "employer- or insurance-oriented" doctors.
F. Disabdity evaluation
1. Disabihty types
a. Temporary total disability (TID): immediate postinjury period until medical
endpoint.
b. Temporary partial disability (TPD): same time period, but injured employee
continues working to some degree, either part-time or light duty, receiving
all or part of preinjury wage.
c. Permanent total disability (PTD): determination of permanency of medical
endpoint with the perception that patient will be "totally disabled."
Worlcers' Compensation 521
i. In some venues, implies that person can perform no useful activities.

ii. Generally requires demonstration of "inability to work."
iii. Sets up antiproductivity incentive for injured workers, with highest
awards given for lowest demonstrated physical capability.
d. Permanent partial disability (PPD): most common permanency award, usu-
ally with monetary payment geared to:
i. Wage loss (demonstrated and/or predicted)
ii. Inability to work (demonstrated and/or predicted)
iii. Permanent impairment with or without disability-related modifying fac-
tors (e.g., education, skills, age)
2. Demonstration of disability leads to monetary awards.
a. Weekly benefits
b. Lump sum benefits
c. Major contest between adversaries
i. Employee and representative generally attempt to maximize award.
ii. Employer and carrier generally attempt to minimize award.
iii. Other factors, such as employer reluctance to have employee return to
work, may lead to higher awards ("buy-out" concept).
G. Impairment evaluation
1. Nonmedical concept designed to use medical expertise to resolve financial
issues.
a. Physician is deemed a "disinterested third party" who provides evidence in
contest between employee and employer.
b. Contest generally adjudicated by state agency.
2. Temporary vs. permanent impairment
a. Impairment is considered temporary prior to medical endpoint.
b. Residual impairment after medical endpoint is determined to be permanent.
c. Medical endpoint assumes adequate rehabilitation to resolve all temporary
(correctable) impairment before final impairment evaluation.
3. Nonmedical event
a. Scheduled awards determine payments for certain specific events.
b. For nonscheduled awards, there is no gold standard for determination of im-
pairment.
c. System administrators seek to minimize variance in numerical impairment
ratings to achieve predictability.
d. Numerical impairment rating sought for ease of administration; considera-
tions include:
i. Fairness
ii. Convenience and timeliness
iii. Accuracy and validity
iv. Cost
4. Impairment rating systems for achieving standardized resolution
a. American Medical Association Guides to the Evaluation of Permanent
Impairment (4th edition, 1994)
b. Social Security System
c. Minnesota Impairment Guides
H. Administrative systems
1. Workers' compensation involves 50 U.S. state jurisdictions and District ofColumbia.
a. State administrative agencies
b. Workers' compensation law and administrative rules governing worker bene-
fits, employer behaviors, employee safety, and procedures for resolving disputes
522 Workers' Compensalion
c. Administrative contest rarely spills over into courts in state-mandated

systems.
2. Reporting of injury
a. Forms for reporting injury are vital.
b. No benefits without timely reporting.
3. Common administrative disputes covered by state agency
a. Temporary indemnity benefits to injured worker
b. Right to medical treatment ordered by treating doctor
c. Choice of treating doctor
i. Trend is to limit free and unrestricted choice (and change) of treating
doctor.
ii. Right to costly medical care with unproved outcomes (e.g., spine surgery)
also restricted by managed care oversight.
d. Determination of medical endpoint
e. Permanency award
4. Federal systems
a. Generally more complex, bureaucratic, and cumbersome, with historical
framework and strong political constituencies; often related to bitter indus-
trial turmoil during latter 19th century.
b. Sample federal systems
i. FELA: covers railroad workers; essentially a minimally regulated, per-
sonal injury, compensation system.
ii. FECA: covers most federal employees.
iii. AAFES: covers Army and Air Force Exchange civil employees.
iv. Jones Act, Longshore Act: covers merchant marines, offshore oil workers,
dock workers, tugboat employees in a relatively high-cost system com-
bining workers' compensation and personal injury characteristics.
c. Part of Department of Labor functions as "insurance carrier" for FECA em-
ployer agency.
II. Medical Care in Workers' Compensation ys. in General Health

A. (opayment
1. No copayment by worker to health provider in workers' compensation
2. Frequent copayment by patient in general health care
3. If copayment were instituted in workers' compensation, patient might not be
motivated to seek health care in view of potential disincentive of indemnity.
a. Conversely, presence of indemnity allows for some coercion of employee to
seek effective outcome-oriented medical care or be identified as refusing or
abandoning care.
b. Payment of premium
i. Worker has no responsibility for payment of premium for workers' com-
pensation benefit.
ii. Employer is covered by payment of premium to limit liability for em-
ployer negligence.
iii. Employee covered incidentally.
4. Employee pays for health benefit in general health care.
a. Health benefit not currently mandatory for many employers and may be ab-
sorbed entirely by employee.
b. Many employees carry no health insurance or have limited coverage.
i. Tempts employee to cost-shift certain problems into workers' compen-
sation.
ii. Even if employer provides health benefit, employee may be responsible

for copayment for part of benefit (e.g., family benefit).
iii. Even without copayment in general health care, provision of health ben-
efit is seen by employees as direct benefit in lieu of increased salary.
B. Indemnity provision
I. Indemnity provided during period of TID under workers' compensation.
2. No similar benefit linked to medical care under general health provision.
a. Employers may provide short and/or long-term disability (SID/LID) benefit
coverage.
b. STD or LID benefits provided by employer are generally not linked to med-
ical care provision, although treating doctor must document disability for
such policies.
c. STD/LID and general health insurance carrier are usually different.
i. SID/LID carriers require minimal authentication from physician of per-
sistence of disability.
ii. May be incentive for SID/LTD carrier to provide effective treatment for
reduction of disability.
iii. However, general health insurance carrier has no compensatory benefit
to provide effective care aimed at specific socioeconomic outcomes (e.g.,
return to work, case closure, reduction of impairment).
C. Medi(al payments
1. Under workers' compensation, payments vary from state to state. Any and all
"reasonable and necessary" treatment is provided.
a. Fee schedules
b. Usual and customary fees limitation
c. Preferred provider contracts possible but slow to develop because of choice
of physician issue.
2. Under general health provision medical care is significantly restricted.
a. Medical payments vary according to premium paid.
b. Medical payments vary according to coverage approved under contract.
c. Choice of physician and coverage may be significantly restricted by premium.
d. Although preferred provider contract is easier to implement in general health
care, there is no socioeconomic basis for limiting or rationing care; hence
faster growth of premiums in general health care as high technology and ac-
cess expand.
D. Rehabilitation requirements
I. Under workers' compensation, rehabilitation requirements vary from state to
state and in federal jurisdictions by statute.
a. Small number of states carry mandatory vocational rehabilitation.
b. Vocational rehabilitation usually mandated after medical endpoint.
c. Often medical and vocational rehabilitation are poorly coordinated.
2. Under general health care, rehabilitation requirements vary greatly.
a. Depends on coverage, varying from policy to policy.
b. Opinion of managing physician determines recommendation for rehabili-
tation.
c. Lack of socioeconomic goals in general health care limits incentives for re-
habilitation to productivity.
d. Lack of link between indemnity and medical care in SID and LID policies
tends to prolong indemnity.
3. Workers' compensation has built-in return-to-work requirements. Return to
work not an issue in general health care.
524 Worlcers' Compensation
E. Medical claims processing

1. Medical fee disputes-workers' compensation has established adjudicative
process usually lacking in general health.
2. Medical treatment disputes
a. Workers' compensation relies on socioeconomic outcomes as basis for deter-
mining treatment requirements.
b. General health treatment often determined by patient satisfaction, policy
coverage, and doctor-patient persistence.
3. Claims processing
a. Workers' compensation requires consideration of return-to-work ability for
case closure.
b. In general health care, return to work (e.g., degree of disability) is irrelevant.
4. Medical care after medical endpoint
a. In workers' compensation, limitation of future medical treatment may be ne-
gotiable as part of permanency award.
b. In workers' compensation, future palliative treatment (narcotics, return to pal-
liative modalities) may continue indefinitely, if permitted by state or contract.
c. Policy coverage limits medical care under general health, with no specific
medical endpoint determination usually necessary.
5. Insurance reserve requirements
a. Workers' compensation includes future medical costs, attorney fees, indem-
nity benefits, and friction costs.
b. Reserve requirements in general health care relate only to medical consider-
ations.
III. Medical Benefits and Special Considerations

A. Goals oftreatment
1. Specific socioeconomic outcomes important in workers' compensation
a. Return to work
i. Employer may not want to rehire employee.
ii. Americans with Disability Act (ADA) may influence employer behavior.
iii. Impairment, handicap, and disability may determine vocational potential.
iv. Tests of functional capacity, work capacity, or work tolerance may help
to determine employee match to demands of specific job.
v. Permanently modified work may be available from large employers; perma-
nent light duty (as opposed to transitional light duty) is rarely successful.
b. Decreased utilization of health care
i. Limitation on future surgical intervention
ii. Limitation on future palliative care for ongoing pain and suffering
c. Case closure
i. Employer desires earliest possible case closure to avoid both indemnity
and health benefit utilization.
ii. Small number of injured workers absorb most of indemnity and medical
cost.
iii. Deconditioning and psychological involvement increase as chronicity in-
creases.
iv. Contest over permanency award underlies contest over case closure.
v. Employer and insurance carrier tactics to achieve early case closure may
paradoxically expand cost through patient resentment, exacerbating pre-
vious job dissatisfaction.
d. Recurrent injury
i. May occur in presence of unresolved employer-employee conflict [i.e.,
inadequate vocational rehabilitation).
ii. May occur in presence of inadequate physical capacity to match job de-
mands (i.e., inadequate medical rehabilitation).
iii. May be covered by state-mandated "second injury fund."
iv. May result in apportioned permanency award.
v. Multiple injuries may be followed by state agency and lead to fraud in-
vestigation.
2. Managed care
a. More likely to be based on socioeconomic outcomes than patient satisfaction
or perceived symptom relief.
b. Growth limited by problem of choice of physician in adversary system.
c. Pilot programs are ongoing.
i. 24-hour coverage: functions like SID/LID.
ii. Nonsubscriber status: no mandate for workers' compensation.
B. Nonoperative treatment issues
1. Acute injury: primary care
a. Shortly after injury, symptom control is the goal.
b. Primary care generally involves passive modalities.
i. Narcotic medications
ii. Bedrest
iii. Gentle stretches
iv. Manipulation and mobilization
v. Temperature modalities (e.g., heat, diathermy, ultrasound)
vi. Massage
vii. Cold application
VIII. Transcutaneous electric nerve stimulation, other electric stimulation
c. Necessity for primary care terminates in 8-12 weeks.
i. Patients may have incentive to prolong passive modality care.
ii. Extended primary care enhances deconditioning and debilitation as
well as progression of psychological problems.
2. Poslacute phase: secondary care
a. Concept of reactivation to prevent ongoing deconditioning.
b. Generally managed by single allied health discipline (e.g., physical therapy,
occupational therapy).
c. Programmatic care (e.g., work conditioning or work hardening) may be de-
sirable in certain cases, but not appropriate for many injured workers in this
stage for various reasons.
d. Often involves eclectic mixture of modalities and active exercise, combining
symptom control and reactivation (depending on acuity of injury).
e. Secondary care most effective in posta cute period, generally 2-6 months af-
ter injury, to prevent deconditioning; less effective after deconditioning and
psychosocial barriers to recovery become established.
3. Postoperative phase
a. If surgery is performed within first few months, secondary care may be ap-
propriate.
b. If surgery is performed in chronic phase of injury after deconditioning, de-
bilitation and psychosocial barriers to recovery have already been created;
tertiary care is indicated.
526 Workers' Compensalion
4. Chronic phase: tertiary care

a. Generally involves complex mixture of physical and psychosocial barriers to
recovery
i. Physical deconditioning
ii. Results of permanent soft-tissue scarring or surgical procedures
iii. Psychosocial barriers to recovery include drug dependence, preexisting
psychological trauma, and depression.
b. Usually involves medically directed interdisciplinary team approach with:
i. Physical therapists and/or
ii. Occupational therapists and/or
iii. Psychologists and/or
iv. Rehabilitation specialists and/or
v. Nurses
c. Expense and effectiveness of tertiary care may be disputed.
d. Individualized treatment plans geared to needs of patient in terms of dura-
tion, frequency, and intensity of services are becoming more common.
C. Surgical care-effectiveness measured by socioeconomic outcomes.
1. If it facilitates earlier return to work (e.g., fracture repair, disc excision), surgi-
cal care achieves desirable status.
2. Surgery may increase perceived impairment.
a. May lead to higher impairment and disability awards.
b. May lead to increased pain behaviors if postoperative rehabilitation is inade-
quate.
c. May be used by claimant to enhance permanency claims and entry into
other social welfare systems (e.g., Social Security Disability Income,
Supplemental Security Income, long-term disability).
3. Multiple surgery
a. Failed spine surgery syndrome is well recognized.
b. In repetitive trauma syndromes of upper extremity (e.g., thoracic outlet syn-
drome, reflex sympathetic dystrophy), psychosociomedical component not as
well recognized.
c. Psychosocial recovery barriers or inadequate medical or vocational rehabili-
tation is almost always associated with multiple or repeat surgery.
d. Multiple surgery has poor outcome in workers' compensation.
D. Psychalogical factors
1. Psychiatric diagnoses increase with increasing chronicity.
a. Preexisting psychiatric disorders are definite risk factor for developing
chronicity in workers' compensation injury.
i. Affective disorders (e.g., depression, anxiety)
ii. Personality disorders (axis II in DSM-N-TR categorization)
iii. Childhood psychological trauma (rape, incest, neglect, and physical
abuse)
iv. Substance abuse
b. Various job dissatisfaction factors significantly affect development of
chronicity.
i. Job stress
ii. Problems with supervisor or coworkers
iii. Sexual harassment
iv. Conflict between job and home demands
c. Financial or family stressors
d. Socioeconomic issues
i. Permanency award contest
ii. Extraneous litigation (e.g., personal injury, divorce)
iii. Other financial secondary gain (e.g., disability policies, wage replacement
exceeds preinjury wage)
iv. Indemnity benefit allows one family member to stay home while spouse
works or allows laid-off union member to resume job while another re-
ceives benefits.
e. Relief of obligation to work
i. Stressed worker may need "vacation."
ii. Most individuals obtain self-esteem from working.
iii. Certain groups at higher risk (e.g., housewives leaving home for the first
time, immigrant workers, people unable to maintain long-term employ-
ment, older workers approaching retirement).
E. Multidisciphnary consultation
1. Necessary when unrelated medical condition appears as consequence of treat-
ment for work-related injury or is aggravated by work-related injury.
2. Relationship to industrial accident always an issue.
a. Must be carefully documented medically.
b. May require administrative dispute resolution.
3. Consultation to document work-relatedness usually accepted after dispute re-
solved.
a. Treatment for such conditions usually problematic.
b. Short-term treatment to facilitate surgical or rehabilitation plan often permitted.
F. Failure to complete treatment
1. Noncompliance
a. Treating doctor's perception is paramount.
b. Treating physician obligated to report noncompliance.
i. In some venues, failure to document may result in fines and penalties for
treating physician.
ii. Timeliness of reporting medical endpoint is major issue.
c. Must distinguish noncompliance from other failures to complete treatment
plan.
d. Noncompliant behaviors are usualIy risk factor for chronicity.
e. Noncompliance often associated with other psychiatric diagnoses (e.g., per-
sonality disorders, substance abuse).
2. Abandonment of treatment
a. Patient "disappears,"
b. Injured worker has explicit obligation to participate in appropriate medical
treatment as condition for receiving indemnity benefits in most venues.
c. Abandonment of treatment usually results in determination of MMI by treat-
ing doctor and little or no permanency. Note: Failure to document may sub-
ject treating doctor to fines or penalties in some venues.
d. Late doctor shopping may be result of patient's attempt to prevent termina-
tion of indemnity benefits.
e. IME may be used for case closure if treating doctor fails to provide timely
documentation.
3. Refusal to accept treatment
a. Common in cases of high-risk, invasive diagnostic and surgical procedures.
b. May be confused with noncompliance and/or abandonment of treatment.
c. Tests limits of coercion to achieve socioeconomic outcomes in workers' com-
pensation.
528 WorlreT5' Compensation
d. Generally acceptable in primary nonoperative and surgical care.

e. Generally not acceptable in postoperative rehabilitation or tertiary care re-
quiring patient's active cooperation.
f. Refusal of remaining medical options leads to early determination of MMI or
PEtS.
i. Impairment determination may be estimated at level patient would have
reached by cooperating with treatment.
ii, Disability (work tolerance) may be enhanced, leading to greater intensity
of adversarial procedures with widened areas of dispute over permanency
award.
iii. Often involves multiple IMEs with "dueling doctors."
References
t. Beals R, Hickman N: Industrial injuries of the back and extremities: Comprehensive evaluation-an aid
in prognosis and management. J Bone Joint Surg 54A:1593- 1611, 1972.
2. Brand R, Lehmann T: Low back impairment rating practices of orthopaedic surgeons. Spine 8:75-78,
1983.
3. Clark W, Haldeman S, Johnson P, et al: Back impairment and disability determination: Another at-
tempt at objective reliable rating. Spine 13:332-341, 1988.
4. Franklin G, Haug J, Heyer N, et al: Outcome of lumbar fusion in Washington State Workers'
Compensation. Spine 19:1897-1903, 1994.
5. Greenwood J: Socioeconomic factors in back pain and compensation systems. In Mayer T, Mooney V,
Gatchel R (eds): Contemporary Conservative Care for Painful Spinal Disorders. Philadelphia, Lea Et
Febiger, 1991, pp 155-166.
6. Mayer T., Gatchel R: A prospective two-year study of functional restoration in industrial low back in-
jury. JAMA 258:1763-1767,1987.
7. Mayer T, Gatchel R: Functional Restoration for Spinal Disorders: The Sports Medicine Approach.
Philadelphia, Lea Et Pebiger, 1988.
8. Mayer T, Mooney V, Gatchel R; Contemporary Care for Spinal Disorders; Concepts, Diagnosis and
Treatment. Philadelphia, Lea Et Febiger, 199 t.
9. Mayer T, Polatin P, Smith B, et al: Spine rehabilitation: Secondary and tertiary non operative care.
Spine 20:2060-2066, 1995.
to. Polatin P, Kinney R, Gatchel R, et al.: Psychiatric illness and chronic low back pain: The mind and the
spine-which goes first? Spine 18:66-71, 1993.
1 - - - - - - - -34
What to Do When There Is Nothing
Left to Do
Christopher 1. Standaerf, MD
Key Points
• Ensure that the diagnostic evaluatian is appropriate, being neither deficient nor
excessive for a given patient.
• Ensure that the treatment provided has been appropriate for the diagnosis; use the
assistance of experienced practitioners in other fields if necessary (surgeons, non-
operative specialists, psychologists).
• Ensure the accuracy of diagnostic and treatment steps performed either personally or
with the assistance of an experienced practitioner in the appropriate field (e.g,
musculoskeletal radiologist, electromyographer).
• Distinguish between impairment and disabdity, pain and suffering, and hUrl and harm.
• The cognitive shift from continued attempts at a "cure" to managing the patient's
symptoms and chronic impairment is essential.
• Help the patient adapt to a chronic impairment by providing medical information and
access to available support services, avoiding abandonment of the patient, and
encouraging appropriate behaviors and interactions between patients, their social
units, and their health care providers.
I. "Nothing Left to Do" Is Not the Same as "Done Everything Possible·

A. Do no harm. If a treatment poses a potential for substantial harm to the patient and
the chance for significant improvement is low, the procedure is generally inappro-
priate for that patient.
B. Extensive passive treatment that is providing minimal to no long-term change in
a patient's condition may actually be detrimental. Excessive reliance on passive
care (applied by others to the patient but requiring little patient action) may result
in an external shift in the patient's "locus of control," leaving the patient with lit-
tle sense that he or she is capable of controlling problems independently. Passive
coping styles have been related to the perpetuation of chronic pain and disability.
C. Beware of performing too many tests.
1. The usefulness of a positive result is highly dependent upon the pre-test expec-
tation that the result will be positive.
2. The odds of a false-positive result increase substantially with either an increas-
ing number of tests performed or a very low prevalence of true disease in the
population studied.
3. Realistic expectations are important in coping with chronic impairment. An ex-
cessive quest to identify a "curable" problem may make it difficult to establish
a sense of what is actually realistic.
529
530 What to Do When There Is Nothing Left to Do
II. Make Sure That There Really is "Nothing Left to Do"

A. Diagnostic accuracy
1. Has an accurate diagnosis been established? For example, diagnosing a patient
with low back pain due to a lumbar disc herniation can be problematic;
lout of 5 individuals under 60 and lout of 3 individuals over 60 who have
never had low back pain will have a disc herniation on an MRI of their lum-
bar spine.
2. Make sure that the diagnosis is based upon a sound correlation between his-
tory, physical examination, imaging studies, additional diagnostic procedures,
and an appropriate, if not ideal, response to treatment applied.
B. If no clear diagnosis has been established, as is often the case for patients with low
back pain, have appropriate diagnostic steps been taken to exclude clinically rele-
vant diagnostic possibilities?
I. Appropriate imaging studies may, but not necessarily should, include the fol-
lowing:
a. Plain radiographs including standing flexion/ extension views to exclude
instability
b. MRI (magnetic resonance imaging)
c. Planar bone scan with SPECT (single photon emission computed tomogra-
phy) imaging of the lumbar spine
d. CT (computed tomography) myelogram with flexion/ extension views
2. Fluoroscopically guided, contrast- enhanced, selective spinal injections
3. Electrodiagnostic evaluation
4. Assessment for alternative medical or non-spinal causes of pain, e.g., multiple
myeloma, inflammatory spondyloarthropathy, vascular insufficiency
5. Psychological evaluation
C. Make sure that the diagnostic studies performed actually show what the reports say they do.
1. Review all films personally andl or with an experienced radiologist who has
been given a full history and knows what to look for.
2. Repeat a study if any of the following apply:
a. The study is of insufficient quality to answer the question for which it was ob-
tained.
b. A crucial study cannot be found.
c. There are significant questions about the validity of the study.
d. There has been a substantive change in the clinical scenario since the prior
study was performed and there may potentially have been a structural
change.
D. Have the appropriate procedures been performed correctly?
I. Whenever possible, obtain and read operative, procedural, and relevant clinic
notes.
E. Is the study sufficient to substantiate the clinical conclusion drawn?
1. For example, it is not accurate to state that the diagnosis of spondylolysis has
been excluded in a female gymnast with low back pain based upon negative
plain films.
F. Has the patient received the correct treatment for the problem?
1. Be extremely familiar with the treatment methods applied.
2. Have an appropriate specialist answer this question if necessary.
G. Has the patient seen specialists in non-operative and operative care to have thor-
oughly explored approprHlt. diagnostic and treatment options, potentially including eval-
uation at a multi-disciplinary pain clinic? Again, "appropriate" does not mean "all
possible."
What to Do When There Is Nothing Left to Do 531
III. Adapting to Chronic Impairment

A. A cognitive shift away from the desire for a "cure" is essential for patients, their
family, and the physician. The goal is to teach patients to manage the symp-
toms and functional limitations in a way that allows for maintenance of quality
of life.
I. The psychological characteristics of the patient and the greater social construct
in which he or she lives playa crucial role in the patient's ability to make this
transition.
2. Health care providers often must provide their patients and their patients' fami-
lies with the tools necessary to make this transition, including information on
the appropriate cognitive, physical, and social resources that may help them.
B. Distinguish between three central sets of terms
1. Impairment vs. disabihty
a. Impairment refers to a loss or alteration of a specific physical or psychological
function, such as an inability to dorsiflex the foot after a severe L-5 radicu-
lopathy.
b. DisabiKty refers to an inability to perform an activity or function within the
range of normal for that individual or equivalent peers as a result of an im-
pairment, such as an inability to perform as a professional dancer due to an
inability to dorsiflex the foot.
c. Disability is determined by multiple factors other than impairment, including
motivation, fatigue, pain, and external physical barriers to function.
d. Recognize when the degree of dlsabihty isbeyond that expected based upon the degree
ofimpairment; this implies that other factors are affecting the individual's
ability to function optimally.
2. Pain vs. sunering
a. Pain is a psycho-physiologic phenomenon that involves nociception and the
individual's experience of the sensation. To some degree or another, pain is
a universal occurrence.
b. Sunering is a purely psychological reaction to a specific circumstance or state
and is dependent upon multiple internal and external factors, including ex-
pectation.
c. Suffering is not a mandatory consequence of pain.
3. Hurt vs. harm
a. Hurt, or the perception of uncomfortable sensations or direct nociception,
does not necessarily reflect underlying tissue damage, particularly in the set-
ting of chronic pain.
b. Harm, in the physiological sense, implies that a structural injury or change
has occurred.
c. Patients with chronic pain need to understand that not all uncomfortable or
negative sensations that they perceive are the result of "harm" to their bod-
ies. These patients generally need to be encouraged to advance their func-
tional abilities in the presence of ongoing discomfort.
C. How does a patient "live with it"?
I. Education about the problem, biomechanics, and natural history.
a. Realistic expedatlons, including potential for exacerbation or recurrence, may
help with a better sense of control.
b. "Catastrophizing" has been associated with persistent pain and disability.
A better understanding of the problem may help reduce this.
c. Provide the patients with the tools to manage "flares" of symptoms effec-
tively.
532 What 10 Do When There /5 No/hing Leh 10 Do
2. Modification of physical activity

a. Specific activities may not be possible or may pose significant risk of re-
injury.
b. Patients should be directed toward more appropriate activities that allow
them to achieve similar goals and an equivalent degree of satisfaction.
3. Environmental adaptations (layout, ergonomics, etc.) and assistive devices may
limit the disability associated with a specific impairment.
4. Psychological support for the patient and the family
a. Approaches vary depending upon individual and family dynamics.
b. The sense of loss that accompanies injury-related impairment is dependent
upon the perspective of the individual.
c. "Resolution" of the sense of loss does not necessarily occur, and adaptations
to chronic impairment can take place over an extended period of time.
d. Work towards "adjustment" to impairment with maintenance of behaviors
congruent with the degree of impairment (e.g., minimize excessive internal
perceptions, external manifestations, and familial re-enforcement of dis-
ability).
5. Allow patients to experience the emotions associated with chronic injury and
impairment and adequate time in which to do so.
6. Provide appropriate medical care, information, and resources without adding to
the patient's sense of disability, neglecting legitimate concerns, or abandoning
the patient.
7. Ultimately, it is the patients' responsibility to choose the way in which they ap-
proach their life.
References
I. Boden SO, Davis DG, Dina TS, et al: Abnormal magnetic-resonance scans of the lumbar spine in
asymptomatic subjects. J Bone Jt Surg 72-A:403-408, 1990.
2. Campbell IN: Nerve lesions and the generation of pain. Muscle Nerve 24:1261-1273, 2001.
3. Gatchel RJ, Adams L, Polatin PB, Kishino NO: Secondary loss and pain-associated disability:
Theoretical overview and treatment implications. J Occupat Rehabil 12:98-110, 2002.
4. Kirby RL: Impairment, disability, and handicap. In Delisa JA, Gans BM: Rehabilitation Medicine:
Principles and Practice. Philadelphia, JB Lippincott, 1993, pp 40-50.
5. Kleinman A: The Illness Narratives: Suffering, Healing, and the Human Condition. New York, Basic
Books, 1988.
6. Linton SJ: A review of psychological risk factors in back and neck pain. Spine 25:1148-1156,2000.
7. Rohe DE: Psychological aspects of rehabilitation. In Delisa JA, Gans BM: Rehabilitation Medicine:
Principles and Practice. Philadelphia, JB Lippincott, 1993, pp 131- I50.
8. Stanton-Hicks M, Baron R, Boas R, et al: Complex regional pain syndromes: Guidelines for therapy.
Clin J Pain 14:155-166, 1998.
,--------35
Evidence-Based Medicine
Robert 1. Gatchel, Ph.D., and Stanley A. Herring, M.D.
Key Points
• Rapidly rising healthcare costs and limited healthcare resources have contributed to an
increased interest in evidence-based medicine and treatment outcomes.
• Monitoring treatment outcomes provides data for payors, improves individual practices,
and serves as a foundation for clinical research.
• In an individual practice, evidence-based medicine depends upon a comprehensive
anatomical, biomechanical, and psychosocial assessment.
• Outcomestudy designs have different levels of methodological rigor, and each individual
study design category should be assessed for specific factors such as clinical meaning-
fulness, thoroughness of followup data, sample size, and other areas that affect the value
of the research.
I. Introduction
A. Low back pain economics
1. Rapidly rising costs for medical care, disability and lost productivity.
2. Allocation of healthcare resources is limited-cost containment is now a central
component of healthcare policy. Often, cost effectiveness is confused with low-
est cost care.
3. These factors have contributed to an increased interest in evidence-based
medicine.
4. Physicians are now being monitored for effectiveness of treatments they pro-
vide, as well as patient satisfaction with their treatment. Many times, a "score
card" is maintained by third party payors in order to monitor practitioner's
efficacy.
5. However, given the current status of the spine literature, evidence-based guide-
lines are not standards of care, and overall effectiveness does not equal efficacy
for the individual patient.
B. Reasons to monitor treatment outcomes using evidence-based medicine
I. To provide objective data to third party payors in order to demonstrate treat-
ment effectiveness. Such data can also be utilized to market the clinical effec-
tiveness of a practice. There is now evidence for safety, efficacy, and cost-
effectiveness of evidence-based guidelines for the management of acute low
back pain in primary care
2. As a means of monitoring quality assurance in one's own practice. Regular
evaluation of treatment outcomes allows the practitioner to ascertain whether
there is any "slippage" in the quality of care being provided.
3. For those interested in contributing to the medical literature, such evidence-
based outcomes serve as a foundation for publication or presentation of data
at conferences.
533
534 Eviclence·8aseJ Medicine
C. Current practice and treatment of patients with low back pain.

1. Physicians often select a treatment option for low back pain based on their own
experience, local expert consensus, or patient and/or public expectations, and
not selected based on evidence-based medical outcome studies.
2. Physicians may not be aware of, or have access to, evidence-based outcome
studies.
3. The evidence-based literature regarding low back pain is often incomplete.
Practitioners must balance their own clinical expertise with the best external
evidence.
D. Where to find reviews of relevant reviews of clinical efficacy of treatment tech-
niques and assessment methods.
1. The Cochrane Collaboration Website (www.cochrane.org)
2. The North American Spine Society Website (www.spine.org)
II. Evidence-Based Medicine in Your Own Pradice

A. Comprehensive patient assessment.
1. Anatomical and biomechanical sources of pain can be of great importance
when deciding how to treat a patient with low back pain.
2. However, in many cases, there is a close interaction between physical and men-
tal health, making it important to consider the psychosocial aspects of your pa-
tient's symptoms.
a. Psychosocial, personality/emotional factors-depression, anxiety, fear, cop-
ing abilities, and other abilities.
b. Family dynamics.
c. Economic considerations; workers' compensation/disability.
d. Substance/medication abuse.
3. There are now brief structured psychosocial interviews for the primary care
physician.
a. Broad psychosocial screening
b. Screening for depression
B. When collecting outcome data, the use of a progressive screening procedure may
help so that all appropriate physical and psychosocial issues are addressed (Fig. I).
1. Initial comprehensive history. Often, the healthcare provider offers a brief social
screening, followed by a brief history of the problem, and then followed by
physical examination. Many important questions are often not addressed
(Gatchel and Oordt, in press).
a. Patient worries about the pain symptoms that were not really discussed with
the healthcare provider.
b. Relatedly, the patient often worried about serious disease or disability con-
cerning pain symptoms, without being told what the "red flags" or risks
were for these serious problems.
c. The healthcare providers rarely took the opportunity to explain what was
being looked for or "ruled out" during their evaluation.
d. Staying active was often recommended to patients without addressing how
to do so safely.
e. Healthcare providers rarely spent time identifying functional difficulties that
may be associated with pain syndromes, or the treatment strategies for over-
coming such difficulties.
f. Relatedly, physicians did not attempt to identify and address such difficul-
ties associated with performing work activities.
g. Although many patients were already performing self-care activities, physi-
Evidence-Based Medicine 535
INITIAL HISTORY INITIAL PHYSICAL EXAMINATION

Historyof presentinjury/illness Range-of-motion, Straightleg raising,
Past medicalhistory + Areas of tendemess, Neurological signs,
Review of systems Gait and posture,
Functional limitations Waddellnon-organic signs
I I
+
IADDITIONALDIAGNOSTICS, IF NEEDED I
t
FUNCTIONAL CAPACITYEVALUAnON (IF SAFETYALLOWS)
Range-of-motion, Isometric muscle strength testing, Liftingcapacity,
Cardiovascular and upper body endurance
~
IINTEGRATE WITH PSYCHOSOCIAL SCREENING I
t
INITIAL PSYCHOSOCIAL SCREENING MEASURES
SCl-90-R, 801-11, SF-36, Oswestryor Roland
and Morris Disability Questionnaire
I
i-
IF ELEVATIONS
t
IF NO ELEVATIONS
t t
CONSULTA PSYCHOLOGIST REFER TO CONSERVATIVE
REHABILITATION PROGRAM
" " IF PROBLEMS ENCOUNTERED
IF PATIENTIS TO BE ENTERED/RE·ENTERED INTO TREATMENTPROGRAM
I MPI, MBHI I
+
ITREATMENT PLANNINGI
FIGURE I. The step-wise approach to the biopsychosocial assessment of a patient with low back pain.
(ModiRed from the North American SpineSociety Compendium of OutcomeInstruments for Assessment and
Research of Spinal Disorders, 2001.)
cians missed opportunities to focus the visit on reinforcing such self-care,

but rather focused on simply the medical management of pain.
h. Diagnostic information provided to patients was often quite ambiguous,
leaving patients uncertain about what improvement meant or when it could
be expected.
536 Eviclence-Bosed Medicine
i. Current information about the natural progression of back pain was usually
not provided, and many patients were simply given overly optimistic prog-
noses.
j. Palliative care was usually prescribed, particularly the prescription of non-
steroidal anti-inflammatory medications, elementary advice about exercise,
and possible referral to physical therapy. Less frequently, opioids or muscle
relaxants were prescribed.
k. Rarely were recommendations written down, nor were patients given any
documentation of the recommendations.
2. Initial comprehensive physical examination.
a. Range of motion-particularly functional range of motion. Measuring true
range of motion may have little correlation with clinical outcome, but may
serve as a data-collecting tool.
b. Documentation of areas of tenderness.
c. Posture and gait assessment.
d. Neurologic examination.
e. Screening examination for other etiologies of low back pain (orthopedic or
medical).
f. Waddell signs suggesting pain amplification, which may be conscious
or unconscious. The presence of Waddell signs is not equivalent to
malingering.
3. Additional diagnostic tests, if needed.
4. A comprehensive functional capacity evaluation (FCE).
a. This test can be requested in order to obtain baseline data, if needed, to indi-
vidually tailor a treatment program for a patient.
b. An FCE performed early in the course of treatment may be most appropriate
in a multidisciplinary functional restoration program, and often is not or-
dered in patients seen in an individual practitioner's office.
c. An FCE may include such things as dual inclinometer range of motion, iso-
metric muscle strength testing, lifting capacity, and cardiovascular and up-
per body endurance assessment. Additional functional tests to address work-
specific capabilities may also be appropriate.
5. A screening process to "flag" obvious psychosocial distress.
a. Administration of simple paper and pencil tests such as the Beck Depression
Inventory (BDI-II), the Symptom Checklist 90-Revised (SCL 90R), the
Oswestry Low Back Pain Disability Questionnaire, the Roland and Morris
Disability Questionnaire, and the Medical Outcomes Study Short Form
Health Survey (SF-36).
b. Pronounced scale deviations on these instruments would alert the healthcare
provider to the degree of emotional distress or dysfunction, and could indi-
cate the need for a more thorough evaluation and consultation with a men-
tal health professional specializing in pain. The Structured Clinical Interview
for DSM diagnosis (SCID), Minnesota Multiphasic Personality Inventory-Il
(MMPI-II) or other tools can be utilized as appropriate.
III. Evidence-Based Medicine in the Published Uterature: The Five Outcome Study Designs (in
Descending Order of Methodological Rigor)
A. The Control-Outcome Study, which eliminates other factors that would explain the
change observed in the study. The randomized controlled trial (RCT) is the most
rigorous form of this study design.
B. The Single-Subject Study and Replicated Single-Subject Study
Evidence-Based Mec/icine 537
I. It is possible to isolate a particular treatment or future treatment that is respon-
sible for a therapeutic change in this type of study.
2. However, one cannot rule out the possibility that the observed effect of the
study was specific to the patient being evaluated unless there are additional
systematic replications of the study.
C. The Single-Group or Cohort Outcome Study
I. The results of treatment are reported on a group basis, rather than on an indi-
vidual basis, in this type of study.
2. Often, percentage of patients responding positively to a given intervention is
reported.
3. This experimental design has no control for other potentially mediating factors
that could be responsible for the observed results (such as specific physician
characteristics or selection bias in the type of patients treated).
D. The Systematic Case Study and the Multiple Systematic Case Study
I. Data are available from the initial baseline, as well as during the course of
treatment in this type of study.
2. This experimental design allows the observation of a time course for change
and response to treatment.
3. However, again, it is not possible to rule out other potential mediating factors
that may be responsible for treatment effects.
E. The Anecdotal Case Report
I. Little or nothing is controlled in this experimental design.
2. It is not possible to rule out other potentially mediating effects that may be re-
sponsible for treatment outcome.
F. Often, in management of spinal problems, less rigorous experimental designs are
initially employed to document the potential effectiveness of a treatment, and
these preliminary results may result in a more rigorously designed experimental
study, eventually leading ideally to a randomized controlled trial, if possible.
1. Even randomized controlled trials can vary greatly.
a. Check internal validity-the validity of an inference that there is a causal re-
lationship between two variables that are being evaluated (e.g., nonsystem-
atic administration of a treatment program or changes of the treatment pro-
tocol during the study are threats to internal validity).
b. Check external validity-the value of whether or not the presumed causal
relationship found in the study can be generalized to different types of pa-
tients and in different settings.
IV. further Evaluation of Study Design Categories (There Are Six Other Areas toAssess for
Any Study Design)
A. The degree of clinical meaningfulness of any treatment benefit that is obtained
(statistical significance does not always translate to clinical significance). For ex-
ample, a decrease in pain of 10 on a 100 VAS may be statistically significant, but
may be clinically non-meaningful in terms of patient relief.
S. The extent and thoroughness of followup data. It is important to get long-term
follow-up. Improvement maintained at I-year is more impressive than that mea-
sured immediately after treatment.
C. What percentage of the treated patient sample demonstrated a therapeutic effect
of intervention? For example, demonstrating that 900/0 of patients improved is
quite impressive.
D. The degree of change that was obtained in the study that was subsequently trans-
ferred to the patient's actual living environment. For example, if an improvement
538 Evidence-Bo5fld Medicine
in an FeE was found, did this transfer to return-to-work and other positive activi-
ties of daily living?
E. Reproducibility of the results as demonstrated by other investigators. The hallmark
of good evidence-based medicine is the demonstration that other independent
clinicians in other clinical sites can replicate the results.
F. The amount of change in the biophysiological response for which the intended
treatment was prescribed.
1. If a spinal fusion was performed, is there radiographic evidence for good
fusion?
2. If the patient had also reported pain, was there a clinically significant decrease
in pain after treatment?
3. If range-of-motion or strength was restricted, was there clinically significant
improvement in these functional measures?
4. If the patient was not able to work before surgery, can he/she now return to
work?
References
1. Beck AT, Ward CH, Mendelson M, et al: An inventory for measuring depression. Arch Gen Psychiatr
4:561-571.1961.
2. Gatchel RJ: Compendium of Outcome Instruments for Assessment and Research of Spinal Disorders,
LaGrange, IL, North American Spine Society, 2001.
3. Gatchel RJ. Matt-Maddrey A: Experimental design issues in clinical research of musculoskeletal pain
disabilities. Crit Rev Phys Rehab Med 12:90-10 I, 2000.
4. Gatchel RJ, Mayer TG: Occupational musculoskeletal disorders: Introduction and overview of the
problem. In: Mayer TG, Gatchel RJ, Polatin PB (eds.): Occupational Musculoskeletal Disorders: Function,
Outcome and Evidence. Philadelphia, Lippincott Williams Et Wilkins, 2000.
5. Gatchel RJ. Oordt M (in press): Clinical Health Psychology in the Primary Care Setting. Washington,
DC, American Psychological Association.
6. Health Behavior Information Transfer (HABIT), July 24, 2001, Volume 4, No. 10.
7. Herring SA: Tyrannized by evidence? Making outcomes work for our patients. Phys Sports Med
26:25-2B, October 199B.
B. McGuirk B, King W, Govind J, et al: Safety, efficacy, and cost-effectiveness of evidence-based guide-
lines for the management of acute low back pain in primary care. Spine 26:2615-2622, 2001.
9. Spitzer RL, Williams JBW, Kroenke K, et al: Utility of a new procedure for diagnosing mental disor-
ders in primary care: The PRIME-MD 1000 Study. JAMA 272:1749-1756,1994.
10. Staab JP, Evans DL: A streamlined method for diagnosing common psychiatric disorders in primary
care. Clin Cornerstone 3: 1-9. 2001.
,--------36
Basics of Personallniury Law
Douglas Phillips, J.D.
Key Points: Common Legal Terms

• Alternative Dispute Resolution (ADR): Alternatives to trial for resolution of legal disputes.
Includes mediation, arbitration, and settlement conferences.
• Bench Trial: A case heard and decided by a judge without a jury.
• Comparative Fault: A defense available to the defendant. Reduction of the plaintiffs
recovery in proportion to the percentage of negligence or fault attributed to the
plaintiff.
• Defendant: The party claimed by the plaintiff to be responsible for the plaintiffs
damages and from whom the plaintiff seeks some form of relief.
• Demand Letter: A letter from the patient's attorney to the defendant or their insurance
company expressly stating a legal right and an amount due as reasonable
compensation for injuries to person and/or property. Usually accompanied by the
treating physician's narrative report.
• Deposition: A form of discovery where the attorney asking for the deposition has the
right to ask questions and obtain answers from a party, witness, or expert while that
individual is under oath. Advanced notice is required to set a deposition. A court
reporter records the proceeding.
• Discovery: Procedure by which each party may obtain and examine documentary and
physical evidence from the opposing party. Each party may also question the opposing
party and its witnesses to discover relevant evidence to the claims in dispute. Evidence
or information may be obtained by the parties through interrogatories, requests for
production of documents, depositions, and an independent medical examination.
Information that can be obtained in discovery is broader in scope than what may be
admissible at trial
• Expert Witness: An individual who possesses specialized knowledge beyond the under-
standing of the ordinary person or juror. A person whose knowledge will aid a jury in
reaching a proper decision. Treating physicians and those hired by the defendant are
often expert witnesses.
• General Damages: Money damages for "pain and suffering," disability, or other
unquantifiable losses.
• Guardian Ad Litem: A person, often a lawyer, appointed by the court to represent the
interests of a minor. The guardian reviews potential settlements on behalf of a child to
ensure the child's best interests are being served. In most cases the court must approve
a settlement on behalf of a minor.
• Hearsay: Statements made out of court, by persons other than the person testifying. If it
is offered to prove the truth of what the witness heard, the evidence is not admissible.
An exception to the rule is a statement made for the purpose of medical diagnosis or
treatment, including description of medical history, past or present pain, sensations,
etc.
539
540 Basics 01Personal Injury Law
• Independent Medical Examination: May be required of a patient for "good cause" as

determined by the court. The defense has the right to have their own medical expert
examine and evaluate the plaintiffs injuries.
• Jury: A group of persons selected from a pool of citizens that have the power to decide
a question of fact in a civil case and award damages. In personal injury cases, either
party has the right to ask for a jury trial. With a six-person jury, five out of six jurors'
votes are needed for a verdict. With a twelve-person jury, ten jurors' votes are needed
for a verdict.
• Mediation: A procedure by which an impartial third person meets with all the parties
and attempts, in an informal setting, to find common ground for agreement to settle a
complaint or claim.
• Plaintiff: The party who requests damages and initiates a civil lawsuit.
• PrivDege: Communications made in confidence between persons, at times, are legally
protected from forced disclosure [e.g, attorney/client, doctor/patient, priest/penitent,
and husband/wife).
• Preponderance of Ihe Evidence: Degree of evidence necessary for a plaintiff to win a civil
case. On a scale of 1 to 100, more than fifty percent wins.
• Proximale (ause: Refers to a cause which leads directly, or in an unbroken sequence, to
a particular result. An element of negligence.
• Reasonable Medical (erlainly: Standard required of opinions of a doctor or other expert
concerning his/her patient's condition, diagnosis, or prognosis. A doctor's opinion
cannot be based on speculation or possibilities. Reasonable medical certainty means
"more probable than not" or "more likely than not."
• Special Damages: Fixed costs or expenses attributable to any injury or loss. These costs
can include past, present, and future wage loss; treatment costs; and other out-of-
pocket losses.
• Sialule of Umilalions: Laws enacted by every state which govern the time frame when a
lawsuit must be filed, and beyond which time the claim may be barred or dismissed.
• Subpoena: A legal document requiring a person to appear at a certain time and place to
give testimony at a deposition or trial. Subpoenae may be "quashed" (invalidated) by
motion to the court.
• Subpoena Duces Tecum: A legal document requiring a witness to produce documentary or
other tangible evidence such as medical records in their possession or control.
• Tori: French word meaning "wrong." Body of law that determines rights and liabilities
when a person is injured or property is damaged through negligent or intentional
conduct.
I. Basics of Personallnlury Law

A. Personal injury or tort law is intended to compensate your patient if sorneone's
negligence or intentional misconduct injures them.
B. Common personal injury cases
1. Motor vehicle accident
2. Product liability
3. Premises liability-"slip and fall"
4. Medical malpractice
C. Torts can be classified in three categories: negligence, intentional torts and strict
liability torts.
1. Negligence. Negligence is the failure to use reasonable care to avoid a foreseeable
(predictable) harm to a person, place or thing. An individual or entity will be li-
able if their unreasonable act or failure to act causes an injury, even if the
harm is unintentional.
Ba5;C5 of Per5Ol101Iniury I.Dw 541
a. Reasonable person standard. An adult is negligent if he or she fails to act the

way a person of ordinary intelligence and judgment would have acted in
similar circumstances.
b. Professional community standard. Professionals are held to a higher standard of
care due to their specialized training and experience. Professionals (lawyers,
doctors, architects, etc.) and individuals who practice "skilled trades" (car-
penters, electricians, etc.) may be found negligent if they do not exercise the
same degree of skill and knowledge normally exercised by other qualified
and competent members of the profession working in similar communities.
Expert witnesses are usually required to establish the standard of care.
2. Intentional tort. The "malicious" or "intentional" infliction of harm that results in
injury. It is usually a tort for which insurance coverage is not available or al-
lowed as a matter of public policy.
a. Assault
b. Battery
c. Fraud and misrepresentation
d. Harm to reputation (defamation)
e. Trespass
3. Strict (absolute) liability. The defendant is responsible for injuring another person
regardless of negligence or intent.
a. Product liability
b. Abnormally dangerous or ultra-hazardous activities
D. Proximate cause or causation. The cause which leads directly, or in an unbroken se-
quence, to a particular result.
E. Damages in a personal injury case
1. Special damages-actual costs.
a. Medical and hospitahzatlon bUls
b. Actual wages lost
c. Cost ofhousehold or nursing help, cost ofwheelchair or uutches, etc.
d. Costs to replace or repair damaged property
2. General damages-"pain and suffering"
a. Physical pain-past, present, future
b. Mental anguish-r'suffering"
i. Mental anguish may include:
(a) Fright
(b) Nervousness
(c) Grief
(d) Anxiety
[el Worry
(f) Shock
(g) Humiliation
(h) Indignity
(i) Embarrassment
OJ Apprehension
(k) Terror
ii. Mental anguish may continue to exist when pain is gone yet disfigure-
ment or a deteriorating physical condition continues to exist.
c. Loss of earning capacity
i. Loss of earning capacity is the difference between what the injured per-
son was capable of earning before the accident and injury and what that
same person is capable of earning afterward. Proven by testimony of
542 Basics 01 Persona/Injury Law
[a] physicians
Ib) vocational experts
(cl financial experts
ii. Proof of these damages must be to a level of reasonable certainty.
Speculation, estimation, and conjecture are not sufficient evidence to
prove these damages.
d. Disfigurement
e. Impairment
i. Physical
ii. Psychological
f. Loss of consortium
i. Consortium typically includes both tangible and intangible elements. The
tangible elements may be loss of support and service, such as household
help and intangible elements may be love, compassion, affection, and
sexual relations.
(a) Spousal claim for consortium
[b] Parents' claim for loss of child's consortium
(c] Child's claim for loss of parental consortium
ii. The extent of consortium claims vary by judicial jurisdiction
g. Loss of the enjoyment of life
i. Some jurisdictions have considered this a distinct element separate and
apart from pain and suffering.
II. Common Injuries in Personal Injury Cases

A. Soft tissue damage
B. Mechanical spine pain
C. Radiculopathy
D. Fracture
E. Lacerations
F. Peripheral joint injury
G. Head trauma
H. Post traumatic stress
I. Depression
1. Caused by pain
2. Caused by circumstances brought about by injuries
J. Degenerative joint disease
1. Asymptomatic before accident
2. Aggravated by accident
K. Myofascial pain syndrome
1. Fibromyalgia syndrome
M. Pre-existing condition
1. Some of the common injuries may be present before the motor vehicle accident.
a. The patient's attorney should provide the treating physician with records or
reports from prior physicians in order to establish the patient's condition just
prior to the accident.
III. Before a Lawsuit Is Filed in Court

A. Before a lawsuit is filed in court a patient's lawyer will likely:
1. Obtain relevant medical records, both past and present
2. Obtain witness statements regarding the accident and/or the effects of the in-
jury upon the patient
Basics 01Penonallnjury Law 543
3. Obtain a comprehensive report from the primary treating physician that in-
cludes, but is not limited to:
a. Description of patient's version of the accident
b. Medical history obtained from patient, including patient's complaints
c. Examination findings and test results
d. Diagnosis
e. Treatment administered
f. Physician's opinion on the causal relationship between the accident and the
patient's injuries
g. Whether patient had any prior health conditions which may have been af-
fected by the accident, and whether prior conditions, if any, altered the type
and duration of treatment provided by physician
h. Effect of the injuries on the patient's work and leisure activities
i. Physician's prognosis and estimate of future medical treatment and ex-
penses, if any
j. For multiple motor vehicle accidents with differing or overlapping injuries,
the patient's lawyer should request all pertinent medical records and provide
them to the treating physicians. The patient's doctor may rely upon these
records and the patient's history to apportion injury to each accident.
k. An analysis of any pre-existing conditions that were aggravated by acci-
dent.
\. An analysis of any prior asymptomatic conditions
i. The physician may rely upon the patient's history and/or medical records
in forming that opinion.
ii. The physician may always change that opinion if new information comes
to light.
4. Provide pertinent information to the insurance company for the negligent party
and engage in settlement negotiations
5. Consider Alternative Dispute Resolution (Mediation) if direct negotiation with
insurance company fails.
a. Usually a non-binding settlement process where a mediator facilitates settle-
ment negotiations
b. This process may diminish posturing by attorneys and insurance adjusters.
IV. Starting a Lawsuit

A. The plaintiffs attorney may need to file a lawsuit because:
1.Negotiations between the plaintiff and the defendants' insurance company are
unsuccessful:
a. Disagreement over the monetary value of the case;
b. Disagreement over which party bears responsibility for the injuries in dis-
pute.
2. The patient's condition remains unstable, precluding settlement discussions, but
the statute of limitations is near expiration.
a. Statute of limitations. Legislatively determined time period during which a
lawsuit must be brought. Usually 1 to 3 years.
B. A lawsuit begins when one person files a complaint in court against another.
1. The person bringing the suit is called the plaintiff or claimant.
2. The person or entity against whom the complaint is filed is called the defen-
dant.
C. The discovery process allows the parties to prepare for trial by gathering relevant
information from one another and from witnesses.
544 Basics 01Personal Injury /.Qw
1. Common methods of discovery

a. Interrogatories. Written questions by one party to the other.
b. Requests for Production. Requests of the opposing party for tangible documents
[i.e., medical records, reports, investigation).
c. Subpoena.
L A court order requiring non-parties to provide documentary evidence.
ii. A court order requiring a person to testify at a deposition or trial.
d. Depositions
i. A deposition is the pre-trial procedure during which a plaintiff, defen-
dant or witness answers questions asked by the opposing attorney about
the accident and the injuries the plaintiff suffered.
ii. Depositions are taken under oath. The questions and answers are tran-
scribed by a certified court reporter.
iii. If you are being deposed, you should be well prepared when answering
the questions. Review your patient's chart prior to a deposition.
iv. The patient's lawyer may, and often should, meet with you before the de-
position to discuss the expected nature of the questioning.
e. Independent medical examination (lME). Defendants for "good cause," may have
the plaintiff examined by a doctor of their choosing, but only for medical
"conditions in controversy."
i. If plaintiffs will not agree to an IME, good cause and conditions in con-
troversy will be determined by the court.
V. Trial Outcomes
A. Bench trial
1. All evidence presented only to a judge.
2. The judge determines:
a. Whether the defendant was negligent.
b. Whether damages should be awarded and in what amount.
B. Jury trial
1. Either party has a right to demand a jury trial.
2. Juries may be 12 person or 6 person.
3. 10 of 12 or 5 of 6 jurors must agree on a particular issue for there to be a jury
verdict.
4. If there is no consensus the judge will declare a "hung jury."
a. The plaintiff may retry the case.
5. Either party may ask the trial judge to alter the jury's verdict or for a new trial.
This request is seldom granted.
C. Standard of proof. Both judge and jury must make their decision based on a "pre-
ponderance of the evidence."
1. More likely than not
2. Better than 500/0 chance
D. Appeal. Either party may appeal the verdict rendered by a judge or jury.
1. An appeal is usually a request for a new trial made to a higher court. Examples
of possible appealable matters include errors interpreting the law by judges, or
a jury that has acted inappropriately during trial.
VI. Evidence in aTrial

A. Direct examination
1. Your patient, the plaintiff, will testify about the accident and his/her injuries.
The defendant may also testify,
8Gs;cs of Persona/Injury Law S4S
2. Lay witnesses (non-experts) may testify regarding the accident or the effects of
injuries upon the plaintiff.
3. The patient's doctor may testify as an expert witness about the patient's injuries
and the cause of those injuries.
a. The testimony will usually follow the form of the narrative report
4. The standard for expert testimony.
a. "To a reasonable degree of medical certainty" or "more likely than not."
Generally means a greater than 50% probability.
5. Experts are used in technical cases, such as medical malpractice.
a. A medical expert may testify to judges or jurors about the common proce-
dure for a certain treatment and whether a doctor failed to follow standard
rules, directly causing plaintiffs injuries.
B. Cross-examination
1. A lawyer will try to weaken the other party, or other party's witnesses, during
cross-examination, often referred to simply as "cross."
2. The attorney's goal during cross-examination is to make the party or witness
appear unreliable or unbelievable.
3. At the end of cross-examination the attorney who calls the witness to testify
can rehabilitate the witness with "redirect" questioning.
a. Asking questions that allow a more full explanation than was allowed on
cross.
b. Clarify issues made unclear during cross.
e. Medical records
1. Accurate documentation of objective findings as well as subjective reports of
symptoms
2. Commentary unrelated to treatment or the physical condition of the partient
should not be included.
D. Testimony at trial or deposition. It is appropriate and customary to charge the pa-
tient's attorney for preparation and testimony at trial. It is appropriate and cus-
tomary to charge the defendant if the defendant's attorney requires the physi-
cian's testimony.
1. Amount charged.
a. That which is customary in the community.
b. Amount which reflects lost income for time away from practice.
E. Videotaped depositions-alternative to testimony attrial
I. Physician's testimony is transcribed by a court reporter while physician is un-
der oath, videotape of testimony to be shown at a later date before the jury.
2. Often economically beneficial to patient if physician's testimony is not crucial
to case.
VII. Insurance Issues

A. If a patient has medical coverage through their own automobile insurance com-
pany the insurer must pay medical bills.
1. If reasonable (customary charges in the community)
2. If related to the injury-bills incurred directly as a result of injuries caused by
accident
B. If auto insurance refuses to pay
1. Patient's attorney may demand a hearing as determined by the insurance policy
provisions.
2. Patient's attorney may file a lawsuit to enforce the provisions of the insurance
policy.
546 Ba5;C5 01Perwnallnjury /.Qw
C. The treating physician's role

1. Provide a narrative report addressing "reasonable" and "related" issues.
2, Testify at the hearing or trial
References
1. Cocchiarella L, Andersson GBJ [edsl: Guides to the Evaluation of Permanent Impairment, 5th ed,
American Medical Association, 200 I.
2. Branton JL, Lovett JD: Damages; Volume 4. Knowles Publishing, Inc., 1987-1993.
3. Mauet TA: Fundamentals of Trial Techniques. Litlle, Brown and Company, 1992.
4. Injury Forum; Reviewed by Richard Seroussi, M.D.; Summary of Landmark Medical Research for
Legal and Medical Professionals; www.injuryforum.com.
5. Gross DJF, Webber CF: The Power Trial Method. Faegre Et Benson, LLP, 2001.
6. Adler RH: Common Legal Terms in a Personal Injury Case, December 1999.
7. Personal injury legal information on who is liable, gathering evidence, and filing claims;
www.nolo.com/lawcenter.
8. Basics of Personal Injury Law; www.mycounseI.com.
9. Personal Injury Litigation, Personal Injury Cases, Attorneys and Law Firms in the United States;
www.personalinjuryfyi.com.
10. Personal Injury Information Center; www.legalaidman.com.
.-----------37
I
Medical Malpractice Issues
Brenda Hight, J.D.
Key Points
• Guidelines for "medically necessary" care may conflict with a physician's recom-
mendations for care, or a capitation agreement may generate financial self-interest
concerns in conflict with patient care. The physician must serve as the patient's
advocate when managed care limitations abridge reasonable care. However, certain
gag clauses in managed care contracts may create a significant conflict of interest.
Read your contract carefully.
• Federal and state privacy laws require medical providers to provide the patient the
right to consent or authorize sharing of confidential health information, training of
personnel in the protection of confidentiality and uniform electronic records.
• E-medicine increases the physician's scope of practice, but also increases physician
responsibility for information, referrals, and purchases the consumer/patient may
make from the physician's electronic communications.
• An overview of the medical malpractice case informs the medical provider of the legal
framework of the lawsuit, responsibilities within the legal framework, and the respon-
sibilities of insurer and attorney.
• Insurance needs for the medical practitioner have expanded as medical practice has
taken advantage of the internet.
• Federal laws on emergency presentations of medically unstable patients may create
additional regulatory, civil, and criminal penalties for failure to treat the medically
unstable patient.
I. Ethical Issues for Physician Liabdity in Patient Care

A. Managed care changes challenges the physician/patient relationship. With the rapid growth
of cost-conscious healthcare delivery through managed care plans marketed by a
bewildering array of new healthcare entities, physicians and patients confront
unique legal issues arising from potential conflicts inherent in their new relation-
ships. In the past only the healthcare interests of the patient mattered.
I. Cost containment may cause a conflict in physicians' responsibilities to patients,
their own financial interest, and the provider and other plan participants'
interests.
2. Managed care directives to provide only umedically necessary care" may result in treat-
ment below community standards.
a. Plan utilization and pre-certification requirements may affect both type of
treatment and time frame for treatment.
b. Gatekeeper responsibilities may cause delay or total avoidance of specialist
intervention, which may further increase legal liability for patient manage-
ment.
547
548 Medical Ma/praclice 155l1es
3. State legislatures Imphdtly recognize the conflid. For example, Texas Insurance Code
§20A.25 and §2I.58A set guidelines for the review process:
a. The physician shall be the care giver.
b. Guidelines must have physician input.
c. Appeals of adverse determinations may be made by the patient or the
physician.
d. The appeal process initiated by the physician:
(I) Requires a written explanation of good cause for having a particular type
of specialty provider review the case.
(2) The denial shall be reviewed by a healthcare provider in the same or sim-
ilar specialty as typically manages the medical condition, procedure, or
treatment under discussion.
e. The utilization review plan should be reviewed by a physician in accordance
with practice standards developed with input from appropriate healthcare
providers.
B. What can the primary care provider do to address the challenges?
I. Recognize the dramatic change.
2. Ad as a case manager, matching patient needs and preferences to medical services.
3. Exercise the six Cs: choice, competence, communication, compassion, continuity
of care, and avoid conflict of interest.
4. Educate patients, making them aware of the potential for conflict between inter-
ests of patient, managed care organization, and physician.
a. Allow patient to participate in care discussion.
b. Disclose plan policies and guidelines.
c. Encourage patient to self-refer if utilization review does not comply with
what the physician believes to be appropriate care.
d. As a physician, participate in formulating utilization guidelines for patient
care.
C. The courts' review ofgatekeeper role emphasizes patient advocacy in managed care.
1. In Wickline v. State of California, 192 Ca. App. 3d 1630, 239 Cal. Rptr. 8 I6
(Cal. 1986), the healthcare organization, Medi-Cal, denied payment for addi-
tional hospitalization recommended by HMO physician. The court found the
physician personally liable for the denial of care because it believed that he
should have been more aggressive in convincing the HMO to pay for additional
hospitalization but found the HMO was not liable.
2. In Hand v. Tavera, 864 S.W.2d 678 (Tex. App.-San Antonio 1993, no writ), a
plan pre-certification physician was found liable for his decision to reject an-
other physician's recommendation for patient management in an emergency
room setting.
3. In Greene v. Tniet, 846 S.W.2d 26 (Tex. App.-San Antonio 1992, writ denied),
the court recognized the patient's right to know risks and hazards not defined
by informed consent regulations. Managed care guidelines limiting the use of
certain tests, procedures, or referrals would likely fall into this area of informed
consent.
4. Doctors should further be aware that the federal law under the Employment
Retirement Income Security Act of 1974 (ERISA), 29 U.S.C.A. §§ 100I et seq.,
exempts qualified health management organizations from all state law causes
of action but does not protect contracting physicians.? Many states have, how-
ever, enacted specific legislation to create a duty of ordinary care for health in-
surance carriers, health maintenance organizations or other managed care enti-
ties in allocating care. See, for example, Texas Civil Practices Et Remedies Code,
Medical Malpractice Issues 549
Chapter 88, Health Care Liability in which health maintenance organizations,
managed care entities and health insurance carriers are held to a duty of care in
making health care treatment decisions and creating liability for damages for
harm to an insured or enrollee arising from the failure to exercise such reason-
able care.
D. Any wOling provider laws (AWP) stress abmty tocompete.
1. Threatened or adualtermination from networks because of "excessive" treatment;
economically poor areas motivate physician care decisions."
2. Some states have responded by passing AWP laws designed to set reasonable
guidelines for physician admission into and termination from networks.
Reasonable restriction on the selection of treatment providers is enforceable.'
3. Some states have enacted laws holding managed care entities liable for injuries
arising from their care decisions.>
II. Overview ofFederal Privacy laws on Patient Care

A. Individually identifiable health information is now subject to privacy standards in
health plans, health care clearing houses, and health care providers that transmit
health care information in an electronic form in connection with certain transac-
tions. These regulations are under the Health Insurance Portability and Account-
ability Act of 1996 ("HIPPA").6 The Department of Health Et Human Services has
published fiduciary rules to protect confidentiality of individual health infor-
mation,? HIPPA protects confidentiality of personally identifiable health informa-
tion by regulating how health care providers transmit the information electroni-
cally and by providing the consumer/patient, through the health care provider, with
notice of the use of the personal health information and providing the patient with
the right to consent to the use or disclosure of the patient's personal health infor-
mation treatment, payment or health care operations or as long as it involves treat-
ment, payment or health care operations. The privacy rules require the following:
1. The covered entities will be required to establish internal procedures and prac-
tices to protect the privacy of health information including training employees
about privacy, receiving complaints from patients regarding privacy and desig-
nating a privacy officer at the health care entity to ensure that appropriate
safeguards are in place to protect health information.
2. Patient consent will be required for the routine use and disclosure of health in-
formation.
3. Covered entities are required to inform patients how their health information is
being used and to whom it may be disclosed. Disclosure from one covered
health entity of protected health information to a "business associate" (another
person or entity who on behalf of the covered entity performs or assists in a
function involving the use of health information) is permitted if they enter into
an arrangement or contract which sets out the permitted use of the health in-
formation and provides that the business associate will not use or further dis-
close the health information other than as permitted within the scope of the
contract and requires the business associate to report to the covered entity any
use or disclosure of the health information.
4. HHS may issue regulations and the Office for Civil Rights (OCR) may conduct
compliance reviews to determine whether the covered entities are complying
with the privacy rules. Full compliance is expected by October 2003.
B. The HIPPA privacy standards" include all individually identifiable health informa-
tion regardless of the manner in which such is stored including paper, hard copy
and/or electronic records. Each of the covered entities must provide to the patient
550 Medical Malpractice 155ue5
notice of the use of their health information and request consent or authorization
or give the patient another opportunity to permit or reject the use of this informa-
tion in the health care entities' operations. This material is more fully explained at
the government website for HIPPA.9
C. Health care entities are now required to provide publically posted language notify-
ing the patient of their medical information being used and disclosed and their
rights to access such information.
D. Personal health information that has been "de-identified" is not subject to HIPPA.
Information is considered de-identified when information that might provide iden-
tification of an individual has been removed, such as the names, geographic infor-
mation, telephone numbers, Social Security numbers, health benefits numbers and
other traceable information.'?
E. Each HIPPA covered entity must institute written policies and procedures and doc-
umentation requirements to address compliance with the notice of privacy prac-
tices and information being maintained and shared. I I
F. Each HIPPA entity must have a "privacy official" that is responsible for the devel-
opment of the policies and procedures for the use and disclosure of private health
information. Such person should also be the contact person for any patient who
has complaints or needs information."
G. HIPPA covered entities must train their employees on these information and pri-
vacy concerns. Health entities have been given until December 28, 2002 to imple-
ment the procedures required by these final regulations. Patients may not file law-
suits against health care entities and/or physicians for violations of these privacy
standards but may file a complaint through the federal government. HHS and its
enforcement arm may assess penalties for violating the privacy rules including a
fine of up to $50,000.00 and up to 1 year in prison for intentional disclosure of
personal health information. Disclosing personal health information with the in-
tent to sell the data is punishable with a fine of up to $250,000.00 and up to 10
years in prison. Final regulations establish new civil penalties of $100.00 per per-
son for unintentional disclosures and other violations (up to $25,000.00 per per-
son per year).
State laws that are stricter than HIPPA are permissible under federal law.
H. Violation of patient confidentiahty may result in lawsuits against the physician.
1. Most states have created a statutory physician/patient communications privi-
lege and privacy laws. See http://healthprivacy.org for discussion and re-
sources. The privilege prevents public disclosure of the patient's private medical
information and of communications between patient and physician during the
relationship, unless the patient waives the privilege. The waiver in Texas occurs
when the patient initiates court or administrative proceedings, whether against
a physician or any other defendant, to recover damages for any physical or
mental condition, including death.'? An express written waiver also terminates
the privilege. Without such a written waiver, however, the courts have had
some difficulty in determining when waiver occurs. The courts recently began
to address this issue by setting guidelines for when defense counsel may con-
tact the plaintiffs treating physicians.
2. When the patient is suing, can the treating doctor speak to opposing counsel?
A significant number of jurisdictions allow ex parte interviews of treating
physicians by defense counsel once the patient either expressly or implicitly
waives the physician/patient privilege. 14 However, physicians may find that ex
parte communications with lawyers adverse to their patients to be an ethical
violation of their code of conduct. See http://www.biethics.org.
3. A small number of states (South Carolina, Alabama, Kentucky, and Illinois) re-
strict communication during litigation. These jurisdictions do not allow private
interviews of treating physicians." Of the jurisdictions that strictly limit private
contacts between defense counsel and treating physicians, Illinois is most rep-
resentative. Treating physicians in Illinois may not speak with defense counsel,
even after their patient initiates suit. Defense counsel retains the option, how-
ever, of deposing a treating physician, if the physician is identified as either a
fact witness or expert by the patient.
4. Prudent practice requires familiarity with local rules. Physicians must know the
confidentiality law of their state. If the law of the jurisdiction does not prohibit
disclosure of relevant information once the patient initiates a claim or lawsuit,
documentary proof of the claim or lawsuit, such as a copy of the original peti-
tion, should suffice to establish both waiver of the privilege by a patient and
scope of the waiver by defining the nature of the claim.
I. E-medicine: Bto ( (Business to (onsumer) concerns 16
1. Electronic commerce has provided much greater geographic coverage for
physicians of patients and online communication of patient care. Physicians
who use the internet, particularly in doing business across state lines, must be
aware of potential violation of consumer statutes such as the Federal Trade
Commission and Stark provisions of the Social Security Act.'? These types of
laws regulate physician referrals to health care service and providers in which
the physician has a personal financial relationship. The laws prohibit a physi-
cian from making referrals to entities or providers with whom or with which
the physician has an indirect or direct financial relationship. Other false claims
acts, under both state and federal law, may ensnare a health care provider
through sponsoring or providing content online that directs a client/patient
to a specific health care service or provider. If "hits" or purchases occur from
that website or link, potentially the provider is at risk for violating the anti-
kickback statutes."
2. Traditional state regulation of physicians is challenged by internet medicine.
a. When does the physician/patient relationship arise?'?
b. If a consumer hits a website and checks links or follows advice and infor-
mation on that site or links to that site, has that created a patient relation-
ship?
3. State regulation of e-health care has been growing. Physician websites or other
health care web sites may be considered to be practicing medicine. Under
Chapter 22 of the Texas Administrative Code § 174.2, the practice of medicine
includes performing an act through any medium that is part of a patient care
service that would affect the diagnosis or treatment of a patient. The Federation
of State Medical Boards (FSMB) has proposed model legislation for "out of
state" licensure for physician practice when the physician is occasionally from
out of state.P It has been reported that already 20 states, including Texas,
Illinois, Montana and others, have implemented laws permitting out of state pa-
tient/physician contact and treatment for tele-medicine. Particular care must be
exercised in familiarizing oneself with the legal requirements in states where
the physician is prescribing medication and/or treating patients through either
telephonic or internet communication. The digitalized image could be wrong,
distorted, or even an incorrect patient. Who is at fault? The physician assuming
the care of a patient on e-cornmerce Business (physician) to Consumer (the "pa-
tient") basis may well assume the risk of the transmittal error. No known cases
are located at this time but the physicians needs to beware.
552 Medicol Malpractice Issues
III. Torts 101: The Basic Medical Negligence (ase

It is sometimes frightening to consider the unknown, especially the impact of a mal-
practice lawsuit on the physician's personal and professional life. As a practical mat-
ter, most physicians, either as student or resident, receive some education about basic
legal principles, but rarely do they receive enough information to assuage the anxiety
attack that often occurs when a patient threatens suit. This section gives the practi-
tioner a basic outline from the author's point of view of what to expect.
A. Basic concepts: duty, breach of duty, causation, and damages
1. The common law provides patients with legal recourse against their physicians
for injuries foreseeably caused by a deviation from reasonable and prudent
practice; however, the patient has the burden of proving malpractice through
the presentation of expert testimony. The complaining patient must establish,
by competent expert testimony, that (1) a deviation from reasonable practice
occurred and (2) the deviation foreseeably resulted in the patient's injuries.
Only when the physician commits an error obvious to a layman, such as oper-
ating on the wrong limb. is the patient allowed to forego the expert testimony
requirement.
2. Physician's testlmany required. Lawsuits cannot successfully get to a jury unless a
physician testifies under oath that the medical care in question was below the
reasonable and prudent medical practices of a similarly situated physician and
probably caused the injury.
a. Initial service. Prudent physicians immediately tum over the notice of suit or
petition to their insurance carrier in order to preserve their right to coverage
and a defense. Any papers accompanying the citation may be time-sensitive
and should be turned over immediately. Similarly, physicians should not en-
gage in independent investigation; rather. their obligation should be to in-
form the insurance carrier of the claim and to cooperate with the carrier's
investigation. It is the responsibility of physicians to meet with their ap-
pointed counsel and to cooperate and educate counsel about the care or
treatment in question and their understanding of the medical complaints of
the patient.
b. TIming. Doctors are often frustrated by the relative inaction at the beginning
of litigation. Frequently this is due to the fact that courts are reluctant to
force plaintiffs to show their hand. preferring to give them the opportunity
to discover and investigate fully their claims of negligence against the de-
fendants before forcing them to produce expert testimony and the precise
theories of their lawsuit. The physician, however. should expect the defense
counsel to come up with a preliminary evaluation of the lawsuit, but only
after counsel has been provided with the relevant medical records. Obtaining
such records can take time.
c. Cooperation and communication between physician and attorney result in bet-
ter outcomes. The attorney should report to the physician and the physi-
cian's carrier about significant developments in the lawsuit on a periodic ba-
sis, including evaluations of witnesses, their credibility, whether or not the
plaintiff's case has a greater chance of success than the defendant's in a
trial, and the approximate range of damages.
d. Deposition. The physician faces a deposition process that can be excruciat-
ingly difficult. Physicians are accustomed to being mobile and busy with
their practice all day long. Depositions take physicians away from their cus-
tomary environment. putting them in front of a lawyer intent on eliciting
responses that favor the plaintiff's version of events. These questions may be
Medical Malpractice IssUflS 553
leading and loaded with facts assumed by the lawyer. The skillful deponent
picks through the assumptions and responds to questions solely on the basis
of known facts. Speculation is not an appropriate answer.
e. Preparation. There is no substitute for adequate and intense preparation for the
deposition process. The physician should insist on visiting with counsel to
discuss the tactics of the plaintiffs attorney, details of the legal process, and
the nature of the claim from a legal perspective. The physician should pre-
pare emotionally to remain calm during the attorney's often accusatory
questioning. The plaintiffs attorney must and will question the physician
very carefully about all the decisions made and all damages that the plaintiff
sustained, because the attorney represents the interests of one who truly be-
lieves that he or she has been wronged. Some attorneys take inappropriate
advantage of the adversarial nature of the legal process, and the physician
should be ready to stand firm in the face of such excesses.
f. Mediation. Following the discovery phase of the litigation, the case will
likely go to mediation prior to trial. Many states have enacted statutes
mandating mediation. For example, Texas enacted the Alternative Dispute
Resolution Act, Tex.Civ.Prac, Et Remedies Code, Ann. §§ 154.00 1 et seq.
(Vernon's Pamp. 2001, which provides a non-binding opportunity for set-
tlement negotiation. Generally, the parties must appear before an impartial
mediator, either court-appointed or selected by agreement of the parties,
along with a representative with authority to settle. Clearly, not every
physician will want to go into mediation with consent. Nevertheless, if one
prepares well, mediation can be very valuable in resolving claims. If suc-
cessful, it eliminates uncertainty as well as the costs and sacrifices associ-
ated with the commitment to trial before a jury. In medical liability cases
in particular, both patients and doctors feel that they have been wronged,
and the sense of hurt is often a serious cloud in their perception of the
facts. Mediation gives the physician and his or her counsel an opportunity
to try to defuse much of the hurt that the patient may feel. Even if media-
tion does not result in settlement, it assists the physician in trial prepara-
tion; the plaintiff recognizes that the doctor is human and cared about the
patient but simply had to face the reality that some outcomes are not what
one wants or can prevent.
g. Trial. The physician must be present during a trial before six to twelve jurors,
depending on the jurisdiction. He or she must participate in what will be one
of life's more emotionally draining experiences. Nevertheless, a jury trial is a
method of resolving the dispute between the parties.
B. Overview ofstate law
1. Most actions are hmited tostatute rather than common law. For example, many states
require pre-hearing boards to determine whether there is merit to a medical lia-
bility claim. Other states have mandatory mediation prior to filing a suit. If suit
is filed, there are certain minimal requirements for proceeding on the part of
the plaintiff. For example, in Texas, article 4590i of the Tex.Rev.Civ.Stat.Ann.
(Vernon Pamp. 2000) controls healthcare liability. This statute replaces all com-
mon law causes of action, whether arising in contract or tort, and is designed
to limit healthcare liability to cases allowed under the statute based on (I) neg-
ligence or (2) failure to obtain informed consent of the patient. Other statutory
elements often found in state law are as follows:
a. Notice isrequired. Often before a suit is filed the provider must be given writ-
ten notice of a claim a certain number of days (e.g., 60 days) before the fil-
554 Medical Malpractice 1551185
ing of suit. Such notice also may trigger certain mandatory screening
processes required in some states, such as Florida.
b. AHidavit or bond required. A complaining patient or attorney must often file a
cost bond if they do not have an expert's written opinion establishing that
the plaintiffs treatment from defendant physician was below accepted stan-
dards of care and proximately caused the injury. See, for example, the Texas
statute, Article 4590i §13.01, which requires a $5000 bond or a written
statement by an expert similarly situated to the defendant physician which
sets out the appropriate treatment of a patient, how the physician deviated
below acceptable standards of care, and how that deviation caused injury.
c. Expert witness qualifications. The minimal qualifications of an expert medical
witness are often specified in state statutes. Generally, only similarly situ-
ated physicians can testify about the standard of care. This may not mean
that only a family practitioner can testify against a family practitioner
who is sued; it may mean that the witness must have a similar practice. In
other words, a board-certified internist could testify against a family prac-
titioner or anesthesiologist, if the anesthesiologist's practice is similar to
the internist's practice situation in the lawsuit, i.e., each practices pain
managment,
2. Arbitration agreements. Many state laws limit the right to arbitrate, requiring the
healthcare provider to give the patient notice of arbitration and often requiring
attorney representation. Such limitations basically emasculate any opportunity
to avoid suit by arbitration.
3. Healthcare referral fees, kkkbacks, and other remunerative practices are strictly prohibited.
Most states are clamping down on interaction among practitioners designed to
generate fee income from referrals. For example, under the Texas Health Et
Safety Code, any practice of securing or soliciting patients in exchange for a
referral fee or remuneration, particularly in the area of psychiatric care, mental
health, and chemical dependency treatment, is strictly forbidden. An offense
under this section is a class A misdemeanor unless the person has been previ-
ously convicted or is an employee of a governmental entity, in which event the
offense is a third-degree felony. Furthermore, a violation of this section can be
grounds for a disciplinary action (Id. at §161.092). Civil penalties may result
(Id. at §161.094). Federal counterparts exist in the Stark I and II.
4. Insurance claim fraud. There are now specific penal sanctions for knowingly pro-
viding false or misleading information in submitting a claim for payment for
healthcare rendered. Federal legislation also has been enacted to control and
detect fraud.
C. Insurance options
1. Be a sophisticated buyer of insurance. With the breadth of 2151 century medical prac-
tice, professional efforts may require more than a professional liability policy.
The physician needs to visit carefully with his insurance broker to determine if
his practice, including his internet usage for patient information, prescriptions,
and even patient care, requires additional insurance. At the very least, the
physician needs to consider whether he or she also needs to obtain advertising
and personal injury liability insurance. Professional liability policies do not al-
ways cover the physician for postings information or other activities that may
go on in the internet where the question of a physician/patient relationship
may not have been determined. Additionally, the physician should be careful to
purchase from financially secure companies.
a. Physicians should contact the Commissioner or Department of Insurance
Medical Malpractice l55l1eS 555
about the status of their potential professional liability insurance carrier and
whether it has been recently placed under any type of supervision or pur-
chased or sold because of questionable financial status.
b. Best's Review, an insurance industry magazine, annually publishes benefi-
cial information about the industry, including combined ratio (ratio of loss
and expenses to premium).
c. Physicians should use an independent insurance agent with long-term rela-
tionships in the insurance community to receive good information about
carrier solvency.
d. Insurance hopping-Le., changing carriers frequently-increases the risk of
gaps in coverage.
2. Insurance for health care providers
a. The focus of any provider should be to prevent the occurrence of problems,
rather than who will pay for them when they occur. As has been shown,
however, even the best laid plans may result in a lawsuit. Unless they are
large enough to be self-insured, the average health care provider relies upon
insurance coverage to defray the costs of litigation. A brief synopsis of each
type of relevant policy, along with potential coverage problems. is provided
below. Since coverage for director's and officer's is becoming a topic of in-
creased interest, an extended discussion is provided as to their liability.
b. The professionalliabilily insurance policy is generally a "claims made" policy. It
has many permutations. Nonetheless, certain aspects of the claims made
policy are fairly universal. The policy covers an act or omission before
or during the policy term. Claims made policies also provide what is re-
ferred to as retroactive coverage; the policy may cover only claims
arising out of acts or omissions after the specified retroactive date. The
physician should be aware that claims made policies are triggered by the
reporting of a claim. If that is a defined term in the policy, the insured
must specifically notify the carrier who is on the risk at the time that the
claim or suit is made. Some claims made policies require that both claim
and suit occur during policy period to respond to requests for coverage.
Because of their limited ability to respond to an event affecting a patient,
claims made policies also provide additional coverage through what is
called a "tail." This allows the insured physician to assert a claim on an
event during the policy period after the expiration of the policy period.
Such coverage always specifies a date at which the tail expires. The in-
surer charges more for a longer tail. Physicians must carefully consider
the possibility that a catastrophic injury may occur to a patient during
the term of one policy, with no suit or claim during the policy term. If
the injury is outside the retroactive date of ensuing policies, they may not
cover the claim. Such a situation may arise when the insured physician
identifies a potential claim in applying for or renewing coverage. The in-
surer may exclude the claim or charge an increased tail premium for writ-
ing the coverage. Thus, physicians may find themselves paying premiums
for professional liability insurance without coverage for a likely claim be-
cause it was not filed during the year of the injury and subsequent carri-
ers refuse to insure against it.
c. Commercial properly insurance: This type of insurance provides coverage to the
insured for direct property damage loss. Often, coverage is written for "all
risks." If it is, Y2K problems that cause actual property damage will almost
certainly be included.
SS6 Medical Malpraclice Issues
d. TIme element coverage: This insurance provides coverage for Business

Interruption Exposures and/or Extra Expense related to increases in operat-
ing expenses as a result of a "fortuitous" event. Business interruptions are a
given in Y2K scenarios, but computer failure is generally an excluded risk.
The question is, will the exclusion preclude coverage for failures in embed-
ded chips? Also, expect the "expected or intended" clause to come into play
in the majority of these claims. In other words, can anyone claim that the
Y2K bug is actually a "fortuitous" event, when the possibility of Y2K events
has been highlighted in the media for last few years?
e. Boiler and machinery insurance: This is valuable insurance that is really "Business
Equipment Protection." It insures against mechanical breakdowns of certain
machinery. Some boiler policies now provide coverage for computer equip-
ment. Depending on the wording of the policy, there is a possibility of cov-
erage for embedded-chip problems.
f. Commerdal general tlGbiUty (CGL): The CGL is generally intended to provide cover-
age for certain types of tort liability. In general, CGL provides coverage for
bodily injury or property damage to third persons. Claimants who produce
products with Y2K compliance problems may claim that their losses fall within
the "products hazard" clause of the policy. Expect battles over the existence of
"bodily injury" and "property damage" in these suits, as well as whether the
underlying acts of production negligence constituted an "occurrence."
g. Directors and oHlcers Insurance (D &0): D Et 0 insurance protects individual di-
rectors and officers of a company from claims asserted against them arising
from the performance of their duties. Some policies also provide coverage to
the company for the cost of indemnifying its directors and officers.
3. Physician consent clauses In professional habibty policies should be carefully considered.
a. Physicians can control settlement if their consent is required.
b. Some policies write a provision in their policy in which policy limits may be
reduced if the insured physician does not follow the carrier's advice to settle.
Read your policy carefully to see if such a condition is included in the clause
concerning consent to settlement.
D. Insurance obligations during suit
1. Read the pohcy and follaw Its conditions. When a letter arrives in which a patient has
made a claim for medical liability arising out of an alleged negligent act, the
letter should be forwarded immediately to the agent or insurance company.
Likewise, any petition or complaint should be forwarded along with any other
documentation received from an attorney concerning litigation. Every insur-
ance policy requires the cooperation of the physician and in fact may limit its
coverage if the physician fails to cooperate or to agree to a settlement recom-
mended by the insurer.
2. Insurer's obligations to protect the physician
a. The insurance carrier has obligations both to defend and thoroughly investi-
gate claims and to determine whether settlement is in the insured's best in-
terest. The insurance company usually reserves the right to appoint defense
counsel. However, if the physician wishes to have a specific counsel with ex-
perience in medical malpractice, the insurance company often may comply
with the physician's wishes, so long as the counsel agrees to abide by the re-
porting and compensation guidelines of the insurance carrier.
b. The insurance company's obligations arise from contract and from a com-
mon law duty of good faith and fair dealing because of the special relation-
ship between the insured and insurer.
Medical Malpractice Issues SST
c. The defense lawyer owes the physician unqualified representation. Whoever
selects counsel, the lawyer has the duty to represent the insured fully and
cannot compromise that interest in the event of a coverage dispute between
insured and insurer.
d. The duty to settle. The courts have created a common law duty to settle when
liability is probable. In Texas the duty to negotiate and settle claims is called
the Stowers Doctrine. The doctrine holds that when the liability of the in-
sured is reasonably clear and a settlement demand within the insurer's pol-
icy limits is made, the insurer has a duty to settle the case.22
3. The physician's cooperation, coupled with insurer's obligations, may limit personal liability.
If, in litigation, the physician has consented to settlement and the plaintiff
has made a demand within policy limits but the insurance company refuses
to settle or is unable to settle with the plaintiff within its policy limits, the in-
surance company may find itself in violation of the Stowers Doctrine and
other duties of good faith and fair dealing. The insurance company's failure
to settle when faced with a demand within policy limits may eliminate any
personal exposure to the insured for excess of policy limit payments.
Although this can be accomplished in various ways, as a general practice, the
physician may go to trial on a bad case with an ultimately adverse outcome
but escape payment of personal liability on the judgment in exchange for as-
signment to the plaintiff of rights against the insurance company for breach
of its duties to settle.
4. Physician exposure to personal liability, cannot be ignored. In today's climate of million
dollar jury awards, financial asset planning and estate planning should be part
of the physician's risk management of his practice. Assets may be placed into
different ownership to be sheltered from judgments exposing the practitioner to
liability excess of policy limits. This type of planning must be done on a life-
time basis, that is, planning early and regularly with appropriate legal and fi-
nancial consultants. Once a lawsuit is filed against an individual, and that indi-
vidual tries to "hide" assets, the original plaintiff may pursue not only the
original defendant and "trace" his assets, but may be able to sue the entity or
other individuals who accepted the assets. Criminal penalties are also possible.
This can be avoided by the physician setting up a life time estate and family
planning early. Currently any contributions to qualified retirement plans are
also exempt from any execution of judgments.
IV. Physician Uability of Patient Transfers [Antidumping]

A. The Emergency Medical Treatment and Active Labor Act (EMTALA), originally
signed into federal law in April of 1986 and codified at 42 U.S.c. §1395cc and
1395dd (1992), and state laws such as the Texas Transfer Laws, Texas Health a
Safety Code (§§241.001-244.0 14 and §§31 1.022-31 1.024) address patient transfer
requirements. Such laws establish guidelines to prevent discriminatory practices
against patients who cannot pay for care. A physician may be exposed to penal-
ties, fines, and civil liability to the patient if there is a violation. EMTALA is regu-
lated by the U. S. Department of Health a Human Services with the Centers for
Medicare and Medicaid Services administering and state survey and agencies and
officer of inspector general doing compliance.
B. Physicians who attend, who serve in the emergency department, or who are on
call are covered, as are hospitals that participate in the Medicare program and offer
emergency services, including facilities that share the same Medicare provider
number with the hospital.
558 Medical Malpractice Issues
c. EMTALA requirements
1. Notice to patients must be publically posted that the hospital and/or physicians
will not discriminate against patients who are presenting with emergency med-
ical conditions.
2. EMTALA requires a medical screening examination and if an emergency
medical condition is determined, the necessary stabilizing treatment or trans-
fer to an institution with the capability of stabilizing the emergency medical
condition.
3. Record keeping includes keeping a central log, a written policy on the EMTALA
requirements, and on-call physician list available in the emergency services
area and maintaining the records, including records of transfer for five years.
4. Under the 1994 regulations and interpretive guidelines issued in 1995 and
1998, EMTALA applies to (I) the entire physical hospital property, including
hospital owned ambulances; (2) it applies to all hospitals that offer emergency
services; and (3) it requires hospitals receiving inappropriate transfers to report
the receipt of an inappropriate transfer or face fines.
5. What is amedical screening examination? It is an exam to determine whether an
emergency medical condition exists that is provided to any person who comes
to the hospital requesting emergency services or who is requested by any rea-
sonable person acting on his behalf to have an emergency evaluation. The
medical screening examination must be provided by qualified medical person-
nel. The medical screening examination is not "triage" and it may not be de-
layed to inquire about available insurance or obtain prior authorizations.
6. How isan emergency medical condition defined?
a. The medical condition manifesting itself by acute symptoms of sufficient
severity including: severe pain, psychiatric disturbances, symptoms of sub-
stance abuse or absence of immediate medical attention could result in plac-
ing the persons health in serious jeopardy or serious dysfunction of bodily
organ or part.
b. A pregnant woman having contractions with inadequate time to effect a safe
transfer or transfer may pose a threat to the health and safety of either the
woman or the unborn child.
7. How do we define quaDfied medical personnel? Such person must be designated in the
hospital by-laws or rules and regulations, in writing, and approved by the gov-
erning board and generally should be physicians, nurse practitioners or physi-
cian assistant qualified to evaluate emergency medical conditions).
a. It may include a registered nurse with specialized training if it is within the
scope of their practice, they are properly supervised and have demonstrated
clinical competence.
8. What isstabilizing treatment? It is defined with respect to an "emergency medical
condition" to mean "to provide such medical treatment of the condition neces-
sary to assure, within reasonable medical probability, that no material deterio-
ration of the condition is likely to result from or occur during the transfer of
the individual from a facility or that [with respect to a pregnant woman having
contractions] the woman has delivered the child and the placenta." Stabilizing
treatment, it must be recalled, is to be provided to the person only if that per-
son has an emergency medical condition and it must be provided by qualified
medical personnel.
9. What is atransfer? Under interpretive guidelines, transfer means the movement,
including discharge, of a person outside of a hospital's facility at the direction
of any person employed by or affiliated or associated directly or indirectly with
the hospital, but does not include such a movement of an individual who
(i) has been declared dead, or (ii) leaves the facility without the permission of
any such person. Physicians must certify in writing, based on the information
available at the time of transfer, that the medical benefits are reasonably ex-
pected to outweigh the risks of transfer and to write down the summary of risk
and benefits upon which certification is based. Failure to do so could result
not only in fines to the hospital, but in fines to the physician as well. CMS and
surveyors from the state departments monitoring hospitals frequently cite the
lack of documentation and EMTALA violations. Another difficult issue on
transfers is determining what is an appropriate transfer. A receiving hospital
has no duty to accept a patient for whom the hospital does not have appropri-
ate treatment capability or available space and personnel. If a hospital refuses
a transfer, it likewise must establish, with written documentation, the appro-
priateness of the refusal.
10. Reporting: The tattle rule. Under the interpretive guidelines and the regulations
(42 C.F.R. 489.20(m)) the receiving hospital must report to CMS or the
local/state survey agency, any transfer "it has reason to believe" it received in
violation of EMTALA. If the receiving hospital fails to report a transfer in vio-
lation of EMTALA, it could face termination of provider status.
1 I. What are on-call physician duties? On-call physicians have now been targeted as
potential violators of EMTALA. They must respond to calls made from emer-
gency centers. If he has a good reason for not responding that also must be
documented.
12. What are the penalties and enforcement provisions of EMTAlA? The CMS regional of-
fices, the state agency contracting with CMS and the office of inspector gen-
eral are involved in the assessment of EMTALA violations, determination of
civil monetary penalties and program exclusion. Please note that with the im-
plementation of interpretive guidelines in 1995 and 1998, the physician is
clearly culpable for EMTALA violations and could also be excluded from
Medicare and be assessed civil monetary penalties of up to $50,000.00 per vio-
lation. A physician may be excluded from the Medicare program if the viola-
tion was found to be "gross or flagrant or is repeated" or presents imminent
danger to the patient's health, safety or well being, or unnecessarily places the
patient in high risk situations. Please see Cherukuria v. Shalala, 175 F.3rd 446
(6th Cir. 1999) in which a physician was unsuccessfully attacked for alleged
flagrant violations of EMTALA.
D. Amis-diagnosis is not the same as an improper transfer.
I. Holcomb v. Monahan, 30 F.3d 116 [I lth Cir. 1994), the Eleventh Circuit specifi-
cally approved a lower court decision in Holcomb v. Humana Medical Corp.,
831 F. Supp. 829 (M.D. Ala. 1993) dismissing an EMTALA action brought by
the survivors and estate of a patient who died of undiagnosed endometriosis af-
ter a hospital emergency department evaluation. The patient was discharged
without the diagnosis having been made. The court found that the EMTALA
emergency screening requirement required only that the hospital provide the
same level of care to all similarly situated patients-not that it make the proper
diagnosis.
2. In Stewart v. Myrick, 731 F. Supp. 433 (D. Kan 1990), Dr. Myrick saw Mr.
Stewart in the emergency department and instructed the patient to return for
testing the next day. The patient returned the following day but had not fol-
lowed physician instructions for GI testing and therefore was discharged to re-
turn at a later time. The patient then called the doctor twice but did not return.
Four days later the patient had extreme chest pains and collapsed, dying
shortly after arrival at the hospital. The court found that the case involved an
allegation of medical malpractice, due to mis-diagnosis, not patient dumping;
therefore, there was no EMTALA action, although medical negligence action
was possible.
V. Self-Referrals: Stark Iand II, and Anti-Kickback Statute

It is important to distinguish between the Federal Anti-Kickback Statute and Stark I
and II. Although both are federal acts aimed at preventing many types of "self-
referral," Stark I and II is aimed at specific types of services and clinics, whereas the
Federal Anti-Kickback Statute applies generally to all goods and services covered by
Medicare or Medicaid.
A. Federal antl-kldlback statute Codified at 42.U.S.C. section 1320a-7b(b), this criminal
statute prohibits various activities that are "illegal remunerations" for referrals.
Specifically, subsection b( 1) reads as follows:
Whoever knowingly and willfully solicits or receives any remuneration (including
any kickback, or bribe or rebate) directly or indirectly, overtly or covertly, in cash
or in kind-
(a) In return for referring an individual to a person for the furnishing or arranging
for the furnishing of any item or service for which payment may be made in
whole or in part under [Medicare or Medicaid].
(b) In return for purchasing, leasing, ordering or arranging for or recommending
purchasing, leasing or ordering any good, facility, service or item for which
payment may be made in whole or in part under [Medicare or Medicaid] shall
be guilty of a felony and upon conviction thereof, shall be fined not more
than $25,000 or imprisoned for not more than 5 years, or both.
Its scope is obviously broad, because it includes any type of medical service or
good for which payment may be made under Medicare, Medicaid or any similar
state payment method. On the other hand, its scope appears limited, because it
speaks of remuneration in exchange for referrals. That has caused some courts
(but not all) to find a requirement that the defendant knew he was violating the
law. See Hansletter Network v. Shalala, 51 F.Jd 1390 (9th Cir. 1995) (finding
corrupt intent a necessary element of the violation); but see U.S. v. Neufeld,
908 F. Supp. 491 (5. Dist. Ohio 1995) (finding corrupt intent unnecessary).
B. Stark Iand II Concerned that the apparent limitation of "remuneration in exchange
for referrals" might not be sufficiently clear to attack the types of behavior that
Congress deemed fraudulent or abusive, or that a court would find a corrupt intent
unnecessary, Congress passed 42 U.S.c. section 1395nn (Stark I), which took effect
January 1, 1992. Stark II, which took effect January 1, 1995, amends Stark I pri-
marily by expanding its scope. Stark I prohibits self-referrals to "clinical laborato-
ries." Stark II adds nine new categories of "designated health services" to be cov-
ered by the referral prohibitions and applied the billing prohibition (see definitions
below) to all types of payers.
1. The referral prohibition generally prohibits physicians from referring covered pa-
tients (i.e., Medicare or Medicaid) to any entity in which the physician or an
immediate family member has a financial or ownership interest for a designated
health service.
2. The billing prohibition generally prohibits an entity that performs a designated
health service from presenting a claim for payment to any person if the biller
knows or should know that the service results from a prohibited referral. This is
not merely a mirror image of the referral prohibition. The billing prohibition
does not apply only to bills submitted to Medicare or Medicaid; it prohibits

billing to any individual, insurance company, or third-party payor if the biller
knows or should know that the service results from a prohibited referral. Much
litigation is expected in this area.
3. Exceptions to prohibitions fall into three categories.
a. Owners lip and compensation arrangement
i. Physicians' services performed personally by (or under the direct super-
vision of) the referring physician or another physician in the same group
practice.
ii. Physicians' in-office ancillary services that are both (1) furnished person-
ally by (or under the direct supervision of) the referring physician or an-
other physician in the same group practice, in the same building as the
referring physician or the group practice uses for such services and (2)
billed by the physician or his/her group practice or by an entity wholly
owned by the physician or his/her group practice.
iii. Qualified HMO services performed for an enrollee.
a. Stock ownership in publicly traded stock or mutual funds: large entities listed on
the New York Stock Exchange, American Stock Exchange, or NASDAQ
with an average market capitalization of at least $75 million over the last
3 years.
c. Ownership or investment prohibitions
i. Hospitals in Puerto Rico.
ii. Rural providers, if substantially all of the designated health services fur-
nished by such entity are furnished to individuals residing in the area.
iii. Hospital ownership, if the referring physician is authorized to perform
services at the hospital, and he or she owns an interest in the hospital
itself, not just in a subdivision of the hospital.
4. Compensation arrangements not considered to violate the prolibitions
a. Office space rental, if by a written lease for at least 1 year at a fair market
value, not taking into account the value of any anticipated referrals.
b. Equipment rental, if by a written lease for at least 1 year at a fair market
value, not taking into account the value of any anticipated referrals.
c. Bona fide employment compensation paid to a physician or member of the
physician's family for identifiable services at a compensation that would be
reasonable even if no referrals are made to the employer.
d. Personal services if the payment arrangement is in writing, covers all ser-
vices to be provided by the physician or family member, extends for at least
1 year, and specifies a compensation that would be reasonable even if no re-
ferrals are made to the employer.
e. Services performed by a physician under a qualifying physician incentive
plan [i.e., a plan that allows payments to physicians to reduce or limit ser-
vices provided to a group enrolled with the plan). Such a plan must meet
two key requirements before it is exempt under this exception:
i. No specific payment is made to a physician or physician group as an in-
ducement to reduce or limit medically necessary services for a specific
individual enrolled with the plan.
ii, The plan must meet all regulations imposed by the Secretary of Health
and Human Services (HHS).
f. Payments by a hospital to a physician if the payments do not relate in any
way to designated health services.
g. Recruitment payments by a hospital to a physician to induce the physician
to relocate to the hospital's geographic area, but only if they meet the safe
harbors imposed by the Secretary of HHS.
h. Isolated transactions such as a one-time sale of a physician's property or prac-
tice, but only if they meet the safe harbors imposed by the Secretary of HHS.
i. Certain groups practice arrangements with a hospital for designated health
services billed by the hospital if they meet all of the following requirements:
i. they are for inpatient services under an arrangement that began before
December 19, 1989 and has continued since then.
ii. Substantially all of the hospital's patients receiving such designated
health services do so through this group.
iii. The agreement is in writing and is for reasonable compensation for the
services provided, without taking into account the volume or value of
any referrals, and would be reasonable even if no referrals were made.
iv. The arrangement otherwise meets the safe harbors imposed by the
Secretary of HHS.
j. Payments by a physician to a laboratory or other entity for clinical services
at fair market value.
VI. National Data Bank Issues

A. Congress enacted the Healthcare Quality Improvement Ad of 1986 (42 USA
§ 11101-11152) (HCQIA) to improve the quality of medical care and to restrict
the ability of incompetent doctors and dentists to move from state to state and
thereby evade discovery or disclosure of their damaging or incompetent perfor-
mance.P
1. HCQIA requires that "each entity (including an insurance company) which
makes payments under a policy of insurance, self-insurance, or otherwise in
settlement (or partial settlement) of, or in satisfaction of a judgment in, a med-
ical malpractice action or claim shall report ... information respecting the pay-
ment and circumstances thereof."24
2. Failure to report is subject to a civil penalty of up to $10,000.
3. Reparting regulations. Who reports? In 1993 the Department of Health and
Human Services (DHHS) promulgated a regulation that required "each person
or entity ... which makes a payment under an insurance policy, self insur-
ance policy or otherwise" to report. A court challenge resulted in a ruling that
the term "entity" in the statute was not broad enough to encompass payments
made by a person individually; therefore, only entities (not individuals) must
be reported to the National Practitioner Data Bank.->
B. National Data Bank resources. The Bank has a website, htt;p:/Iwww.npdbhipdb.coml
npdb.html and an 800 number, 1-800-767-6732, that provides entities and
healthcare practitioners with assistance in (1) filing complete and accurate medical
malpractice payment information and adverse action reports, (2) requesting data
bank information (other than legal interpretations of statutes and regulations, in-
formation about a practitioner, or assignment of data bank ID numbers), and (3)
complying with federal regulations and data bank policies and procedures. The
Data Bank is also expected to produce a revised Data Bank Guidebook is a good
resource for further information.
C. Scope of the ad
I. The act requires reporting for three types of actions:
a. Malpractice payments
b. Licensor actions
c. Adverse professional review actions
2. In each of these categories the reporting is mandatory for physicians, dentists,
and other healthcare providers who hold clinical privileges. It is voluntary for
adverse actions by health care entities.
b. What isreportable tothe Data Bank? Not included are actions that a hospital or
provider may take outside the reporting requirements, such as a hospital's
determination not to accept an application for appointment and clinical
privileges or an applicant's withdrawal of application before the board takes
final action. Neither of these actions is reportable. Voluntary leaves of ab-
sence by a practitioner for rehabilitation from substance abuse are also not
reportable. The litmus test is whether the action involves true peer review
and limitation of privileges, such as a preceptorship or requirements of re-
training. Likewise, a personal, voluntary decision by a physician not to per-
form certain procedures or not to renew certain privileges is not subject to
reporting.
b. Who may request information? Providers and practitioners may.
b. Sandions for faibng to report information to the Data Bank
i. An insurance company, self-insurer, or other person or entity that fails
to report information about a medical malpractice payment it makes on
behalf of a physician, dentist, or other healthcare practitioner in accor-
dance with Data Bank reporting regulations may be fined up to $10,000
per each unreported payment.
ii, Healthcare entities such as HMOs, hospitals, and group medical practices
that fail to report "adverse professional review actions" against the clini-
cal privileges of a physician or dentist may lose their immunity with re-
spect to such peer review processes for up to 3 years.
iii. State medical and dental associations that fail to comply with reporting
are subject to having their reporting duties reassigned to another quali-
fied entity.
D. Reporting lawsuit or claim settlements (or not)
1. No minimal threshold amount has been set by regulation (although a number of or-
ganizations have attempted to get such thresholds in place; therefore, any
amount paid on behalf of a practitioner must be reported within 30 days of
the date of initial payment. Waiver of debt is not considered a payment, nor
are attorney's fees, court costs, or other expenses of litigation.
2. The Data Bank Guidebook suggests that once a claim-" is made or suit filed,
any payment on behalf of a practitioner is reportable. However, the supplement
also states that "the secretary is appreciative of the fact that some medical mal-
practice claims, particularly those that are often referred to as 'nuisance or friv-
olous claims' and that may be settled for purely reasons of convenience, are
frequently settled for payments that do not reflect on the professional compe-
tence or conduct of the physician." In such cases the guidebook recommends
that the reporting entity indicate in the GOO-character narrative of item 38, sec-
tion C, payment information of the Medical Malpractice Payment Report, that
"there was no medical merit to the claim" and that "the practitioner in issue
had met the accepted standard of care in dealing with the patient."
3. Payments for corporations and hospitals are not reportable unless the named de-
fendant is a sole practitioner referred to as a "professional corporation." If
a practitioner is released prior to settlement, the Guidebook recognizes that
the payment made on behalf of the hospital would not be reportable because
payments made on behalf of organizations are not reportable to the Data
Bank.
E. Reporting dinical privilege actions

1. Professional review actians based on professional competence or professional con-
duct that adversely affects the clinical privileges of a practitioner for a period
of longer than 30 days and acceptance of a physician's or dentist's voluntary
surrender or restriction of privileges while under investigation for possible pro-
fessional incompetence or improper professional conduct must be reported to the
Data Bank. Hospitals and other healthcare entities may report such actions re-
garding other healthcare practitioners.
2. Restriction or denial of clinical privileges that occurs solely because a practi-
tioner does not meet the threshold eligibility criteria is not reportable to the
Data Bank.
Summary suspensions are reportable if the following criteria are established:
a. It is in effect for more than 30 days or imposed for a period of longer than
30 days.
b. It is based on professional competence or professional conduct of the practi-
tioner that adversely affects or could adversely affect patients.
c. It is the result of professional review action taken by a hospital or other
healthcare entity.
d. DHHS specifically requires summary suspensions to be considered "final,"
even though the matter may be under appeal. This is the only time that pro-
fessional review actions are reportable prior to being "truly final."
F. Confidentiality. The Data Bank materials are supposed to be confidential and limited
to those who have the right to make queries. Unfortunately, it is questionable that
the system is maintaining confidentiality. Data Bank information is requested rou-
tinely by hospitals for credentialing information. That information becomes part
of the credentialing file and is discoverable in any litigation. Although the Data
Bank has confidentiality provisions and monetary penalties for violating confi-
dentiality provisions similar to the civil money penalties imposed pursuant to
§1128A of the Social Security Act, 42 USC 13lOa-7a, such provisions may be ex-
tremely difficult to invoke.
G. Aprofessional practitioner iswell advised to request a self·query. Self-queries are free to
practitioners and allow them to discover who or what entities have requested in-
formation. Likewise, practitioners may want to protect themselves from disclosure
of such information by following suggested procedures that limit third-party
inquiry.
H. Consider the alternatives. In this time of regulation, reporting, and constant utiliza-
tion of quality controls, physicians owe themselves as well as their patients the
duty of self-evaluation and risk management. Physicians may be concerned about
the effects on their practice of reporting to the data bank, including continuing el-
igibility for hospital staff privileges, provider de-selection activities, and general
competitiveness. However, physicians must also be mindful of the risks of going
into a courtroom and being found negligent. The court finding and ultimate judg-
ment will be reported to the data bank, regardless of outcome. At that point, the
physician also has to deal with the consequent loss of time away from the office,
emotional anguish to self and family, and other personal losses associated with
going through a trial to a potentially adverse verdict. Physicians should utilize the
expertise of their counsel and their professional liability insurance carrier to eval-
uate and determine whether the case is appropriate for mediation or settlement
proceedings. The reporting agency, i.e., the insurance carrier, often takes into ac-
count the physician's private concerns about a data bank report and allows the
physician input into what is reported to the data bank. Clearly any reporting of
Medicol Malpractice Issues S6S
settlements will be reviewed by credentialing committees and selection commit-

tees; it is part of doing business in the United States and should be reviewed and
analyzed with a balanced. unemotional eye.
Endnotes
I. Ezekiel J. Emmanuel EJ, Dubler NN: Preserving the physician-patient relationship in the era of man-
aged care. JAMA273:32-329, 1995.
2. See the Supreme Court decision in Pegram v. Herdrich, 530 U.S. 211 (2000). In that case the patient
sued not only the doctor for malpractice but also the managed care entity for the decision to delay a
sonogram exam and send the patient to a distant sonography center (owned by the same owner as
the health care organization). While the patient won the medical liability case, the ERISA claim for
breach of fiduciary duty against the managed care entity was lost at the Supreme Court level. The
Court recognized the inherent conflict between the managed care organization incentives to ration
care but held that that was not in and of itself actionable.
3, Jiranek AI, Baker ST: Any willing provider laws: Regulating the health providers contractual relation-
ship with insurance company. Health Lawyer 7:4, Winter 1994-95. See also state statutes such as
California Health a Safety Code Division 105; Colorado R.S. Title 10, Art. 16 Health care coverage;
Louisiana Rev. Statutes Title 22 Insurance Chap. 4.
4. For a more comprehensive analysis of the impact of AWP statutes on healthcare provider relation-
ships with insurance companies, see Jiranek, AI, Baker, ST: Any willing provider laws: Regulating
the health providers contractual relationship with insurance company. Health Lawyer 7:4, 1994-95.
5. See, for example, Texas Civil Practices a Remedies Code Chapter 88 (2001); Chap. 215 Insurance,
Health Maintenance Organization Act 215 Illinois Civ. Statute 125/1-1 (2001); Tennessee Code Ann. §
56-32-201 Health Maintenance Organization Act of 1986.
6. Health Insurance Portability a Accountability Act, Pub. LJ04-191 (1996),45 e.F.R. 162 et. seq.
7. 65 Fed Reg. No. 250 at 82462 et seq.
8. Health care operations is defined to mean certain activities including but not limited to quality as-
sessment and improvement activities, competence or qualification of health care professions; profes-
sional review processes; underwriting or other activities related to the creation, renewal or replace-
ment of a contract of health insurance or benefits; conducting or arranging for medical review, legal
services, and auditing, including fraud, abuse and compliance programs; business planning and de-
velopment related to formulary development administration, development and improvement of meth-
ods of payment or coverage of policies; business management in general, administrative activities of
the HIPPA covered entity including implementation and compliance requirements of HIPPA privacy
standards, customer service, due diligence in connection with sale or transfer of assets and other mat-
ters. See http·/Iwww.hhs.gov!ocr!hiJ;Ula for the OCRguidance material.
9. www hcfa foy!hippa!hipaahm.htm
10. 45 e.F.R. §164.514(c).
II. 95 e.F.R. Sec. 164.530(i).
12. 45 e.F.R. § 164.530(a)(d) and I64.520(e).
13. See TEX. OCe. CODE ANN. §§ 159.003-.004 and TEX. HEALTH a SAFETY CODE ANN. § 24J.153;
TEX. R. EVID. 509(e) which provide exceptions to confidentiality as follows:"An exception to the
privilege of confidentiality in a court or administrative proceeding exists in a proceeding brought by
a patient against a physician, including a malpractice proceeding" or "in a civil action or administra-
tive proceeding, if relevant, brought by the patient or a person on the patient's behalf, if the patient
or person is attempting to recover monetary damages for a physical or mental condition including the
patient's death. The Rules of Evidence TEX. R. EVID. 509(e}(4) contains a similar provision: An ex-
ception to confidentiality or privilege exists "as to a communication or record relevant to an issue of
the physical, mental or emotional condition of a patient in any proceeding in which any party relies
upon the condition as a part of the party's claim or defense." However, neither the Occupations Code
nor Rule 509 explicitly addresses ex parte communication when an exception applies to physician-
patient confidentiality. A federal court in Texas has questioned whether such exparte communication
is improper, but several state courts have allowed it.
See Durst v. Hill sCountry Memorial Hospital, 2001 Tex. App. Lexis 8357 (decided December 2001 in
San Antonio court of Appeals); Rios v. Texas Dept. of Mental Health ft Mental Retardation, 58
S.W.3d 167 (Tex. App.-San Antonio 2001, no pet.): See also Hogue v. Kroger Store No. 107,875
S.W.2d 477, 481 (Tex. App.-Houston ltst Dist.] 1994, writ denied) (holding ex parte meeting between
patient's doctor and defense counsel not improper).
14. Langdon IJ. Champion, 745 P.2d 1371, 1373 (Alaska 1987), reaffirming Arctic Motor Freight, Inc. v.
Stover, 571 P.2d 1006, 1009 (Alaska 1977) and Trans-World Investments v. Drobny, 554 P.2d 1148,
1152 (Alaska 1976) (filing of suit); Green v. Bloodsworth, 501 A.2d 1257, 1260 (Del. Super 1985) [fil-
566 Medical Malpractice '"IIeS
ing of suit); Street v. Hedgepath, 607 A.2d. 1238, 1246-47 (D.C. App. 1992), adopting Sklagen v.
Greater Southeast Community Hospital, 625 F. Supp. 991, 992 (D.D.C. 1984) and Doe v. Eli Lilly ft
Co., lnc., 99 F.R.D. 126, 128 (D.D.C. 1983)(filing of suit); Orr v. Sievert, 292 S.E.2d 548, 550 (Ga. App.
1982) (filing of suit); Domako v. Rowe, 475 N.W.2d 30,34 (Mich. 1991) (execution of medical autho-
rization); Brandt v. Pelican, 856 S.W.2d 568, 660-62 (Mo. 1993) (deposition of treating physician);
Stempler v. Speidell, 495 A.2d 857, 864 (N.J. 1985) (filing of suit); Moses v. McWilliams, 549 A.2d
950,955-56,959 (Pa. Super 1988) (filing of suit); Lewis v. Roderick, 617 A.2d 119, 121-22 (R.I. 1992)
(filing of suit).
15. Felder v. Wyman, 139 F.R.D. 85, 88 (D.S.C. 1991) (interpreting South Carolina law); Romine v.
Medicenters of America, Inc., 576 So.2d 51, 54-56 (Ala. 1985); Roberts P. Estep, 845 S.W.2d 544, 547
(Ky. 1993).
16. The author gratefully acknowledges the thoughtful commentary by Patterson, J.A. (Tony), Barbara
Bennet and Robert Corrigan, "Emerging Issues in Electronic Health Law" Monograph 6, Nov. 2001
American Bar Association Health Law Section.
17. 42 U.S. § 1395nn (The Stark Law) and Texas Occupations Code Chapter 102 (2001) and the Florida
"Anti-kickback Statute § 456.054 FSA.
18. See Special Counsel for Health Care Fraud and Chief Privacy Officer DOJ at
http://www.cybercrime.gov/healthsp.htm.
19. The Uniform Electronic Transactions Act (UETA) and the Uniform Computer Information Transactions
Act (UCITA) are two proposed laws that various states may adopt to address electronic communica-
tions and their creation of contract or not. This is still a highly fact specific area of the law in evalu-
ating whether or not a physician/patient relationship may be created.
20. See, http://www.fsmb.orgltelemed/htm
21. The author gratefully acknowledges the thoughtful commentary by Patterson, J.A. (Tony), Barbara
Bennet and Robert Corrigan, "Emerging Issues in Electronic Health Law" Monograph 6, Nov. 2001
American Bar Association Health Law Section.
22. G. A. Stowers Furniture Co. v. American lndem. Co., S.W.2d 544 (Tex. Comm. App. 1929, holding ap-
proval).
23. Id. at § 11131(a)
24. Id. at § 11131(c)
25. American Dental Association v. Shalala, 3 F.3d 445 (D.C. Cir. 1993).
26. For example, a statutory 4590i claim letter.
I
Index
Page numbers in boldface type indicate complete chapters.
Abdominal examination, 73 Analgesics (Cont.)

Abdominal reflex, superficial, 73 peripherally acting, 134-137
Abdominal strengthening, 164 Anesthetics, local, 277-278
Abscess, epidural, 63 complications of, 279
Absorptiometry, of osteoporosis, 447 Aneurysm, abdominal aortic, 65, 117, 118, 119
Accessory process, 11 Ankle, supine range of motion of, 73
Accuscope, for low back pain, 159 Ankylosing spondylitis, 118
Acetaminophen, for low back pain, 134-135 Anterior external venous plexus, 21
Achilles tendon reflexes, 72 Anterior internal venous plexus, 21
Action potential Anterior longitudinal ligament, 15, 19
compound muscle, 264 Anterior segment, 9
compound nerve, 264, 265 pediatric, disorders of, 422, 426-432
creation of, 266-267 Anticonvulsants
Acute back pain syndrome, management of, 45 for chronic pain, 356
Acute pain, 39 for low back pain, 144-145
Acute pain syndrome, 40 for neuropathic pain, 45
vs. chronic pain syndrome, 42 osteomalacia from, 444
Adaptive mechanisms, in acute pain syndrome, Antidepressants
42 biochemical activity of, 142
Addiction, delta sleep role in, 43 for chronic pain, 356
Adenosine triphosphate, 153-154 for low back pain, 141-144
Adolescents. See Pediatric patients for myofascial pain syndrome, 457
Aerobic fitness, 154 side effects of, 142, 143
Aerobic training, 157 tricyclic, 142-143
Afferents, 263 for chronic back pain, 45
Affidavit, 554 for fibromyalgia syndrome, 462, 464
Age, in sports injury, 387-388 Antidromic, 263
Allergic reactions, in injection procedures, 279 Antiemetic agents, for low back pain, 145
Allograft, 325-326 Antihistamines, for low back pain, 145-146
Alpha-2 adrenergic agonlsts, for myofascial Anti-inflammatory agents, for disc herniation, 99
pain syndrome, 457 Anulus fibrosus
Alpha-Il agonists, for chronic back pain, 45 anatomy of, 10-11, 12, 13
Alternative dispute resolution, 539 biochemistry of, 30
American Medical Association Guides to the bulge of, 260
Evaluation of Permanent Impairment, in discogenic pain, 55-56
503-504 in flexion and extension, 21
Americans with Disabilities Act, 495 in flexion and torsion injuries, 23
Amplitude, 263 in internal disc disruption, 24-26
Amyotrophy, diabetic, 129 in mechanical pain, 25-26
Analgesics, 134-140 tears of, 37, 55-56, 97, 259, 377
centrally acting, 137-140 imaging of, 244, 245
561
568 Index
Anxiety, 65 Bladder dysfunction, epidural injection and,

in pain perception, 44 284
Any willing provider laws, 549 Bleeding, in injection procedures, 279, 284
Aorta, abdominal, aneurysm of, 65, 117, 119 Bleeding tendency, injection procedures in, 280
Appeal,544 Blood vessels, injection into, 284
Aquatic rehabilitation, 163, 165 Body pain diagram, 51
Arachidonic acid, in inflammation, J2 Body weight, in compression, 21-22
Arachnoiditis Bond, 554
in failed low back surgery syndrome, 342 Bone graft extenders, 325-326
radiculopathy in, 60 Bone grafting, 325
Arbitration agreements, 554 Bone scan, 220, 229-23 I
Artery(ies), 20- 21. See also specific artery of facet pain syndrome, 231
Articular dysfunction, 111-113 of failed low back surgery syndrome, 335
Aspirin, for low back pain, 134, 136 of infection, 231
Athletes. See Sports injuries of metastatic disease, 231
Autograft, 325 of osteoarthritis, 231
Axial rotation, 22--23 of pars interarticularis, 230, 231
Axon, 263 of pars interarticularis stress reaction, 254
Axonotmesis, 263 of pediatric back pain, 421
of spondylolisthesis, 106, 230
Baastrup's disease, 113 Botulinum toxin, for myofascial pain
Baclofen, for low back pain, 140 syndrome, 457
Ballet injury, lumbar effects of, 82, 394-395 Bracing
Base test, 72-73 compliance and wearing guidelines for,
Baseball, low back pain in, 392-393 215-216
Basivertebral veins, 21 goals and indications for, 202
Basketball, low back pain in, 400 for low back pain, 201-216
Battery for Health Improvement, 303 orthoses for, 202-211
Beck Depression Inventory, 303 for pediatric pars interarticularis defect, 424
Bedrest, 95,151,152 principles of, 202
in lumbar whiplash, 477-478 specific treatment plans for, 211- 215
Behavior, 40 for spondylolisthesis, 106- 107
illness. 299- 300 Bridging exercise, 164
operant, in chronic pain, 349 Bridging test, 88
pain, in disability evaluation, 496 Bupivacaine, 278
Beliefs, maladaptive, 304-305 Bupropion, for low back pain, 143-144
Belts Bursitis
lumbar, 203-204 gluteal, 463-464
sacroiliac joint, 204, 205 ischiogluteal, 465
Bench trial, 539, 544 psoas, 465-466
Bending trochanteric, 464-465
compression in, 22
in industry-related back pain, 182 Calcaneus, eversion of; 73
Bertolotti's syndrome, 113 Calcitonin
Betamethasone acetate, 278 for osteoporosis, 449
Betamethasone sodium phosphate, 278 for Paget's disease, 445
Bicycling, low back pain in, 396-397 for spinal stenosis, III
Biofeedback, in chronic pain program, 355-356 Calcium, for osteoporosis, 449
Biological response, 40 Capsaicin cream, for low back pain, 146
Biomedical pain model, 349, 350 Carbamazepine, for low back pain, 145
Biopsychosocial assessment, in evidence-based Cardiovascular fitness, in lumbar spine pain
medicine, 534-536 rehabilitation, 163
Biopsychosocial model, of chronic pain, Carisoprodol, for low back pain, 140
349-350 Cauda equina syndrome
Biopsychosocial paradigm, 41-42 disc herniation and, 101
Biphosphonates, for osteoporosis, 449-450 discogenic pain in, 57
Index 569
"Causalgia," 470. See also Complex regional Collagen (Cont.)
pain syndrome proteoglycans and, 30
Celecoxib, for low back pain, 136 Common law, 552
Central sensitization, in lumbar whiplash, 480 Comparative fault, 539
Ceramics, 327 Compensation neurosis, 480
Cervical spine, range of motion of, 71 Complex regional pain syndrome, 469-473
Chairback brace, 204-205, 206 causes of, 470-471
Chemical factors, in pain, 31-32 definition of, 469-470
Chemonucleolysis, 313-314 diagnosis of, 471-472
history of, 375- 376 in failed low back surgery syndrome, 341
Children. See Pediatric patients historical perspective on, 470
Chlorzoxazone, for low back pain, 140 neurophysiology of, 31
Choline salicylate, for low back pain, 136 prevalence of, 470
Chronic back pain syndrome, management of, prevention of, 472
45-46 psychological aspects of, 471
Chronic pain, 40 referral for, 473
definition of, 40, 345 treatment of, 472-473
impairment from, 513 Compression, 21-22
incidence of, 345- 346 injuries from, 24-26See also Fracture(s),
models of, 349-350 compression
natural history of, 299 in intervertebral disc, 12
prior treatment response in, 346 Computed tomography, 220, 234-236
psychological factors in, 298-299, 346-347 of degenerative lumbar disease, 108
social factors in, 347 of degenerative spondylolisthesis, 253
symptoms of, 346 of facet arthrosis, 248
treatment algorithm for, 363 of failed low back surgery syndrome, 335
vocational factors in, 347 indications for, 243
in workers, 40 of neuroforaminal canal stenosis, 250-251
Chronic pain programs, 345-358 of osteoporosis, 447
components of, 353-356 of pediatric back pain, 420-421
discharge criteria for, 356-357 of vertebral endplate degeneration, 247
inpatient, 351-352 of vertebral trauma, 254
multidisciplinary vs. interdisciplinary, 352 vs. magnetic resonance imaging, 234, 235,
outpatient, 350-351 237-238
referral criteria for, 348 Concentric contraction, 154
treatment in Conduction velocity, 264
duration of, 356-357 Contusions, 96-97
options for, 353-356 Core evaluation, 75-76, 90-91
principles of, 352-353 Corsets
types of, 348-349 for disc herniation, 100
unsuccessful, 357-358 for low back pain, 160
Chronic pain syndrome, 40 lumbosacral, 202-203
acute pain syndrome vs., 42 sacroiliac joint, 204
exacerbations of, 46 for zygapophyseal joint pain, 103
premature infants and, 43 Corticosteroid injections, 278
Chronic whiplash syndrome, 480-482 complications of, 279-280
Chymopapain, chemonucleolysis with, epidural, 283
375-376. See also Chemonucleolysis for low back pain, 159
Claim notice, 553-554 Corticosteroids
Claudication, 64-65 for disc herniation, 99
Clonazepam, for low back pain, 144-145 for internal disc disruption syndrome, 102
Coccydynia, 112-113 Cost containment, in malpractice, 547
Cognitive restructuring, 40 COX-II specific nonsteroidal anti-inflammatory
in pain perception, 45 drugs, 137
Collagen for chronic back pain, 45
in anulus fibrosus, 13 Cremasteric reflex, superficial, 73
570 Index
Cross-examination, 545 Disability (Cont.)

Crouch test, 70, 84 low back pain and, 40
Cruciform anterior spinal hypertension brace, types of, 520-521
208-209 vs. impairment, 504, 531
Cryotherapy, for low back pain, 158 Disability evaluation, 491-499
Cyclobenzaprine, for low back pain, 140, 141 documentation considerations in, 498
ergonomic factors in, 494-495
Daily routines, pain and, 51-52 indications for, 492
Damages, in personal injury case, 541-542 system constraints and expectations in, 493
Dance, low back pain in, 394-395 team member considerations in, 497-498
Data Bank Guidebook, 563 testimony considerations in, 499
Decompression vocational considerations in, 493-494
for lumbar stenosis with generative in workers' compensation, 520-521
spondylolisthesis, 316 Disability index, 30 I, 302-303
percutaneous discSee Percutaneous disc Disc degeneration, bracing for, 212
decompression Disc herniation, 25, 97-101
stenotic symptoms after, 258-259 bulge in, 247
Defendant, 539 diagnostic studies for, 98-99
Degenerative cascade model disc extrusion as, 245, 246, 260
as clinical model and predictor, 36-37 disc protrusion as, 244-245, 260
of lumbar spine pain, 33-38 patient history of, 55-56
stage I (dysfunction), 34 upper lumbar, 57
stage II (instability), 34-35 in elderly patients, 438
stage III (stabilization), 35-36 foraminal, 56-57
Degenerative disc disease imaging of, 244-248
collagen in, 28 incidence of, 97
imaging of, 2U, lateral, 56- 57
Degenerative lumbar disease, 107-109 morphology of, 244-247
in elderly, 437-441 myelography of, 233
electrodiagnosis in, 109 pathophysiology of, 97-98
imaging of, 244-253 patient history of, 98
Demand letter, 539 phospholipase A2 in, 32
Demineralized bone matrix, 326 physical examination of, 98
Demographic factors, in patient history, 50 in pregnancy, 408
Deposition, 539, 544, 552-553 recurrent, in failed low back surgery
videotaped, 545 syndrome, 339-340
Depression, 65 Schmorl's nodes in, 247-248
in failed low back surgery syndrome, 337 sequestered fragment as, 57, 246, 247, 260
low back pain and, 40 surgery for, 100-10 I, 312-314
neurobiology of, 43 terminology for, 244-247
in pain perception, 44 Disc space infection, 64
Dermatomal pain, 27 Discectomy, 309, 310
Dermatomes, 28, 264 automated percutaneous lumbar, 314, 376
nerve roots and, 73 endoscopic, 313
Dexamethasone, 278 lumbar, 313
Diabetes mellitus percutaneous lumbar, 376
neuropathy in, 129 Discitis, pediatric, 428
radiculopathy in, 60 Dlscogenic pain
Diathermy, for low back pain, 158-159 annular tear and, 55-56
Diclofenac, for low back pain, 136 cauda equina syndrome and, 57
Diffuse idiopathic skeletal hyperostosis, 125 chronic, surgery for, 322-324
Diffusion, in intervertebral disc, 2 I motor vehicle trauma and, 477
Diflunisal, for low back pain, 136 patient history of, 55-57
Diphosphonates, for Paget's disease, 445 protrusions and herniations and, 56-57
Direct examination, 544-545 traction for, 99-100
Disability, 2, 492, 503, 504 vs. myofascial pain syndrome, 455
Index 571
Discography, 288-289 Electromyography (Cont.)

pediatric, 421 risks of, 266
Discovery, 539 for spinal stenosis, III
Disectomy, laser, 309 Electronic medicine, 551
Distal latency, 264 Emergency medical condition, 558
Distraction test, in nonorganic physical signs, 79 Emergency Medical Treatment and Active
Documentation, in disability evaluation, 498 Labor Act (1992),557-560
Dorsal ramus, 19, 20 Emotional stress, childhood, in adult pain
Dorsal root ganglion perception, 43-44
anatomy of, 28-29 Emotions, 40
biochemistry of, 31 Employment screening, 192-193
Drugs Endometriosis, 118, 119-120
adverse reactions to, in elderly patients, 450 Endoscopy, 309
for chronic pain, 45-46, 356 Environmental factors, 3
injection procedure precautions for, 280-281 in chronic impairment, 532
intrathecal delivery ofSee Intrathecal drug in chronic pain syndrome, 41-42
delivery system in disability evaluation, 495
for low back pain, 133-147 in fibromyalgia syndrome, 462, 463
analgesics, 134-140 Enzymes, in nerve injury, 30
anticonvulsants, 144-145 Epidural fibrosis, in failed low back surgery
antidepressants, 141-144 syndrome, 340
antihistamines, 145-146 Epidural steroid injections, 281-285
muscle relaxants, 140-141 Erector spinae aponeurosis, 18, 19
sedative-hypnotics, 141 Ergonomic factors
stimulants, 146 in chronic pain program, 355
for myofascial pain syndrome, 457 in disability evaluation, 494-495
Duck-walking, 70, 84 Estrogen, for osteoporosis, 449
Duodenal ulcer, penetrating, 118, 122 Etodolac, for low back pain, 136
Dural puncture, injections and, 283-284 Evidence, 544-545
Dural sac, 19 preponderance of, 540
Dynamic stabilization training, 100 Evidence-based medicine, 533-538
factors in, 533-534
Eccentric contraction, 154 implementation of, 534-536
Efferents, 264 outcome study designs for, 536-538
E-health care, 551 Evoked potential, 264, 266
Elderly patients, 437-450 Exercise
degenerative spinal conditions in, 437-441 bridging, 164
drug reactions in, 450 extension, 160-161
falls in, 450 flexion, 161
metabolic spinal conditions in, 443-444 for myofascial pain syndrome, 457
neoplastic spinal conditions in, 441-443 during pregnancy, 410-411
Electrodiagnosls, 263-274 therapeutic, 160-161
in clinical setting, 265 training, 154-155
contraindications to, 273 Expert witness, 539, 554
for degenerative lumbar disease, 109 Extension, 21
for disc herniation, 99 in forward bending, 22
evaluation of, 274 injuries from, 23
for failed low back surgery syndrome, 336 lumbar spine, 71, 84
indications for, 273 measurement of, in impairment evaluation,
physiology for, 266-267 510
risks of, 266 Extension exercise, 160-161
terminology for, 263-266 Extensor hallucis longus muscle, strength
Electromyography, 264 examination of, 72
in clinical setting, 265 Extremities
for failed low back surgery syndrome, 336 lower
needle, 269-271 fractures of, 486
572 Index
Extremities (Cont.) Fibromyalgia syndrome (Cont.)

injections into, 291 aggravating factors in, 462, 463
for failed low back surgery syndrome, biophysiologic mechanisms of, 460-461
337 delta sleep role in, 43
in kinetic chain, 81-82 diagnosis of, 460
range of motion of, 73 signs of, 459
upper symptoms of, 458-459
injections into, for failed low back surgery treatment of, 462-463, 464
syndrome, 337 vs. myofascial pain syndrome, 454
range of motion of, 71-72 Flank pain, 121
"Flat foot," lumbar effects of, 81
Facet joint. See also Zygapophyseal joint Flexibility training, 155, 156, 162
anatomy of, 10. 12 for segmental dysfunction, 105
arthrosis of, imaging of, 248, 249 Flexion, 21
diseases of, 61 in forward bending, 22
fracture of, in failed low back surgery injuries from, 23
syndrome, 342-343 lumbar spine, 71
hypertrophy of. 37 measurement of, in impairment evaluation,
imaging of, 222, 224 510-511
osteoarthritis of, imaging of, 231 seated forward test of, 72, 86
synovitis of, 37 standing forward test of, 71, 72, 86
Facet joint pain, 102-104 torsion with, injuries from, 23, 24
bracing for, 214 Flexion exercise, 161
motor vehicle trauma and, 477 Flurbiprofen, for low back pain, 136
Facet pain syndrome, bone scan of, 231 Foot
Facet syndrome, 6 I pronation of, lumbar effects of, 81
pediatric, 425-426 unloaded evaluation of, 76, 92
Facetectomy, 309 Football, low back pain in, 399-400
Failed low back surgery syndrome, 331-343 Foraminotomy, 309
bone scan of, 231 Fracture(s)
categories of, 337-343 anatomy in, 485-486
diagnostic testing for, 334 burst, 487-488
elcctrodiagnosis for, 336 causes of, 485
imaging for, 335 chance, 488-489
injection procedures for, 336-337 classification of, 486-490
patient approach in, 333-335 compression, 62-63, 487, 488
patient history in, 333-334 bone scan of, 230
physical examination for, 334 bracing for, 213-214
radiographs for, 334-335 imaging of, 227
reasons for, 332 in osteoporosis, 127
scope of, 331 pathologic, 257
surgical indications in, 331 diagnosis of, 486
surgical results in, 332 epidemiology of, 485
Falls, in elderly patients, 450 facet, in failed low back surgery syndrome,
Family history, 53-54 342-343
Fear Avoidance Beliefs Questionnaire, 303 fatigue, 26
Federal Anti-Kickback Statute, 560 flexion and torsion and, 23
Federal privacy laws, on patient care, 549- 551 injuries associated with, 486
Femoral head, osteonecrosis of, in pregnancy, noncontiguous, 486
409-410 spinal, 62-63
Femoral nerve stretch test, 74, 81, 88 stable, 487, 490
Femur, internal rotation of, 81 stress, 63
Fentanyl, for low back pain, 140 of pars interarticularis, 254
Fibrillation potentials, 267, 268 subchondral, 23
Fibromyalgia syndrome, 118, 122-123, unstable, 488-490
458-463 vertebral endplate, 24, 25, 26
Index 573
Fracture-dislocation, 489-490 Heathcare Quality Improvement Act (1986),
Functional capacity evaluation, 189-192 562
Functional job analysis, 192 Hemilaminectomy, 309
Functional restoration, 195-197 Herpes zoster, radiculopathy from, 59-60
Functional restoration program, for chronic Hip
back pain, 46 abductors of, strength of, 74, 164
Functional spinal lesion, 172 flexors of, strength of, 74
biomechanical stability and, 172-173 forward flexion of, 82
manipulation for, 170-171, 173-176 short external rotator imbalances in, 77
Fusion, 309, 311 supine range of motion of, 73
anterior lumbar interbody, 322-324 transient osteoporosis of, in pregnancy, 409
anterior-posterior, 325 History, 49-65
lumbar, 315 components of, 50-55
posterior lumbar interbody, 319-321 in disability evaluation, 494, 495
posterolateral, 316-318, 324 in failed low back surgery syndrome,
with posterior lumbar interbody fusion, 333-334
324-325 in impairment evaluation, 513, 515
prior, imaging of, 259 in pediatric back pain, 418-419
F-waves, 268 in pregnancy-related low back pain,
405-406
Gabapentin, for low back pain, 144 of specific conditions, 55-65
Gait analysis Host factors, in fibromyalgia syndrome, 462,
in disability evaluation, 496 463
in physical examination, 70 If-reflexes, 268
Gastrocnemius muscle stretch, 155, 157 Hurt, vs. harm, 531
Gastrocsoleus muscle Hyperlordosis, in pregnancy, 4j07
strength examination of, 72 Hysteria, 65
tightness of, 76
Gastrointestinal disorders, 118, 121-122 Ibuprofen, for low back pain, 136
General damages, 539 Iliac crest, height of, 70, 84
Genetic factors, in chronic pain syndrome, 41, Iliocostalis lumborum muscle, 17, 18, 19
42 Iliolumbar ligament, 14
Genitourinary disorders, 118, 120-121 in lumbosacral complex stability, 82
Gillet's test, 71, 86 Iliopsoas tendinitis, 465-466
Glucocorticosteroids, for low back pain, 146 Imaging, 219-260. See also Bone scan;
Gluteal bursitis, 463-464 Computed tomography; Magnetic
Gluteal fasciitis, 126 resonance imaging
Gluteus muscles, strength examination of, 72 clinical applications of, 243-259
Golf, low back pain in, 393-394 of degenerative lumbar disease, 244-253
Gray ramus communications, 19 of degenerative spondylolisthesis, 252, 253
Guardian ad litem, 539 of disc herniation, 244-248
Gymnastics, low back pain in, 394 of facet arthrosis, 248, 249
Gynecologic disorders, 118, 119-120 of failed low back surgery syndrome, 335
indications for, 219-220
Hamstrings muscle of lumbar whiplash, 475
imbalances of, 76 of osteoporosis, 447-449
length of, 93 postoperative, 257-259
medial, reflex of, 74, 89 of spinal stenosis, 248, 250-253
strength examination of, 72 of spinal trauma, 254-256
stretch of, 155, 156 of spondyloarthropathy, 259
Handicap, 503, 504 of tumors, 256, 257
Harm, vs. hurt, 53 I types of, 220-243
Health Insurance Portability and Accountability of vertebral endplate degeneration, 247-248
Act (1996), 549-550 Impairment, 491, 503
Hearsay, 539 chronic
Heat, for low back pain, 158-159 adaptation to, 531-532
574 Index
Impairment (Cont.) Injection procedures (Cont.)

diagnostic accuracy in, 530 for disc herniation, 100
treatment appropriateness in, 529 epidural, 281-285
definition of, 504 for failed low back surgery syndrome,
in lumbar whiplash, 480-481 336-337
partial, 505 for internal disc disruption syndrome, 102
permanent, 504 lower extremity, 291
sources of, 505 for myofascial pain syndrome, 457
temporary, 505 with orthopedic hardware, 287-288
total, 505, 506-507 patient selection for, 280-281
vs. disability, 504, 531 pharmacology of, 277-278
whole person, 504-505 precautions in, 280-281
Impairment evaluation, 503-516 purpose of, 277
calculations in, 513-516 sacrococcygeal, 290-291
diagnosis-related estimate model for, 507, sacroiliac, 289-290
508 side effects of, 280
in disability evaluation, 491-492 specific blocks in, 281-291
procedure for, 507-516 for spinal stenosis, 111
range-of-motion model for, 506-507 for spondylolisthesis, 107
in workers' compensation, 521 zygapophyseal, 103, 285-287
Impairment rating, 503, 504, 507-508 Injury prevention, in return-to-work programs,
in workers' compensation, 521 182-183
Impairment report, 505, 516 Instability, 61
Implantables, 361-374. See also Intrathecal in failed low back surgery syndrome,
drug delivery system; 340-341
Neurostimulation imaging of, 227, 228
concepts about, 361-364 Instrumentation, 311
false impressions about, 363-364 posterior, imaging of
indications for, 362 Insurance
psychological assessment before, 364 boiler and machinery, 556
Incentive quotas, in industry-related back pain, commercial general liability, 556
182 commercial property, 555
Indemnity, in workers' compensation, 523 directors and officers, 556
Independent medical examination, 491-499, liability, 554-555
540, 544 during malpractice suit, 556-557
Indicationsfor Psychological Evaluation of in personal injury cases, 545-546
Chronic Pain Problems, 301-302 time element, 556
Industry-related back pain, 180-182 Insurance claim fraud, 554
Infection Internal disc disruption syndrome, 24, 25, 26,
bone scan of, 231 101-102
disc space, 64 Interrogatories, 544
epidural injection and, 284 Interspinales muscles, 16
in failed low back surgery syndrome, Interspinous ligaments, 14, 15
341-342 Intertransversarii Iaterales muscle, 16
in injection procedures, 279, 280 Intertransversarii mediales muscle, 16
postoperative, 259 Intertransverse ligaments, 14
spinal,63 Intervening injury, with industrial injury,
Inferior articular facet, 11 517-518
Inferior articular process, 11 Intervertebral disc
Inferior vena cava, 21 anatomy of, 10- 13, 19, 28
Inflammation biochemistry of, 29-30
in low back pain, 31-32 blood supply of, 21
vs. myofascial pain syndrome, 455 central zone of, 260
Injection procedures, 277-291 compression injuries to, 24, 25
complications of, 279-280 in degenerative cascade model, 36-37
contraindications to, 280 degradation of, 25
for degenerative lumbar disease, 109 displaced, in axial plane, 260
Index 575
Intervertebral disc (Cont.) Joints (Cont.)
extraforaminal zone of, 260 in disability evaluation, 496
extrusion of, 245, 246, 260 disorders of, vs. myofascial pain syndrome,
in flexion and torsion injuries, 2], 24 455
foraminal zone of, 260 mobilization of, in low back pain, 161-162
herniation ofSee Disc herniation Jury, 540
innervation of, 28 trial by, 544
internal disruption of, 24, 25, 26
isolated resorption of, 24, 25 Ketoprofen, for low back pain, 136
morphology of, 259-260 Kickbacks, statutes against, 560-562
pediatric, diseases of, 426-427 Kidney stones, 121
protrusion of, 244, 245, 260 Kinetic chain
sequestered, 246, 247, 260 lumbar spine examination and, 81-82
sports injury to, ]86 physical examination of, 75-76
subarticular zone of, 260 Knee, supine range of motion of, 7]
surgery on, recurrent discogenlc symptoms Knee flexors, strength examination of, 74
after, 257-258 Knight brace, 205, 206
terminology for, 259-260 Knight-Taylor brace, 207, 208
Intervertebral disc disease, nerve injury Kyphosis, juvenile, 427-428
mechanisms in, ]0
Intradiscal electrothermal therapy, ]75, Lamina
]76-379 anatomy of, 11
care after, ]78- ]79 in extension injuries, 2]
complications of, ]79 Laminectomy, ]09, ] 10, ] 15
contraindications to, ]78 limited, ] 15
history of, ]76 Laminotomy, ] 15
indications for, ]78 Laparoscopy, ]09
outcomes in, ]79 Laseques' test, 80
patient selection in, ]78 Laser, disectomy with, ]09
rationale for, ]77 Lateral flexion, 2]
system for, ]76-]77 Lawsuits, 542-544
Intrathecal drug delivery system, ]70-]7] in lumbar whiplash, 480
complications of, ]7] reporting of, 56]
contraindications to, 371-]72 Leg length, 87
implantation in, ]72-]7] prone tests of, 74
indications for, ]62, ]71 Levorphanol, for low back pain, 140
mechanism of, ]70-]71 Liability
neurostimulation with, ]7]-]74 personal, 557
outcomes in, ]7] strict (absolute), 541
system for, ]70 Lidocaine, 278
Ischial tuberosity bursitis, 465 Lidoderm transdermal patch, for low back pain,
Isoinertial strength testing, in workers' 146
compensation evaluation, 188 Lifting, in industry-related back pain, 181-182
Isokinetic contraction, 154 Ligaments, 13-15, 29. See also specific
Isokinetic testing, in workers' compensation ligament
evaluation, 186-187 Ligamentum flavum, 14-15
Isometric contraction, 154 Litigation, 542-544
Isometric testing, in workers' compensation in lumbar whiplash, 480
evaluation, 185-186 reporting of, 56]
Isotonic testing, in workers' compensation Liver disease, vs. osteomalacia, 444
evaluation, 188 Longissimus thoracis muscle, 16, 17, 18, 19
Low back pain
Jewett hyperextension brace, 207-208 biopsychosocial assessment of, 5]4-5]6
Job satisfaction, in industry-related back pain, biopsychosocial model of, 41-42
181 causes of, 96
Joints characteristics affecting, 2-]
anatomy of, 10, 11 clinical presentation of, 95-113
576 Index
Low back pain (Cont.) Magnetic resonance imaging (Cont.)

definitions in, 27 of postoperative discogenic symptoms, 257,
degenerative cascade model of, 27-38 258
discredited models of, 41 principles of, 238-239
economic costs of, 1,40, 180,298,533 proton-density, 240
environmental factors affecting, 3 of Schmorl's nodes, 248
epidemiology of, 1-4, 40-41, 95-96, of sequestered disc, 246
151-152, 180,297-298,386 Tt-weighted, 239-240
frequency of, 180 Tz-weighted, 240-242
incidence of, 1-2,4,40,345-346 tissue and body fluid signal intensity on, 241
nonorganic physical signs in, 79-80 of tumors, 256, 257
patient history of, 50-55 of vertebral trauma, 254
patient interviews in, 40-41 vs. computed tomography, 234, 235,
psychological factors affecting, 3 237-238
spinal pathology and, 41 vs. myelography, 237-238
subacute, 39 Malabsorption, vs. osteomalacia, 444
vs. low back pain disability syndrome, 153 Maladaptive mechanisms, in chronic pain
Low back pain disability syndrome, vs. low syndrome, 42
back pain, 153 Malignancy, 129-130
Lumbar arteryfiesl, 20-21 Malingering, 65
Lumbar muscles, in compression, 22 Malpractice, 547-564
Lumbar shift, 84 electronic medicine in, 551
Lumbar spine ethical issues in, 547-549
anatomy of, 9-21, 28-29 federal privacy laws in, 549-550
arteries of, 20- 21 insurance against, 554-556
biochemistry of, 29-31 insurance obligations during, 556-557
biomechanics of, 21 legal concepts in, 552-553
blood supply to, 20-21 managed care and, 547-549
examination of; kinetic chain and, 81-82 National Practitioner Data Bank issues in,
extension of, 84 562-565
forward flexion of, 82 negligence lawsuits in, 552-557
innervation of, 19,20 patient confidentiality violations in, 550-551
mechanical injuries to, 23-26 personal liability in, 557
muscles of, 16--19 physician liability in, 547- 549
range of motion of, 70-71 physician liability of patient transfers in,
rotation injuries of, 23, 24 557-560
segmental examination of, 74-75 self-referrals in, 560-562
standing range of motion of, 70-71, 84 state law in, 553-554
venous supply of, 21 Mamillary process, 11
Lumbar stabilization training, dynamic, Managed care
162-164 any willing provider laws in, 549
Lumbar veins, 21 patient advocacy in, 548-549
Lumbar vertebrae, 9-10, 11 physician-patient conflicts in, 547-549
Lumbopelvic rhythm, 82 primary care provider's role in, 548
Manipulation, 169-177
Magnetic resonance imaging, 220, 237-243 applications of, 170-172
of bulging disc, 247 classification of, 173-175
of degenerative lumbar disease, 108-109 high velocity, low amplitude, 173, 174, 175
of degenerative spondylolisthesis, 252 impulse hammer, 174, 175
of disc herniation, 245 under joint analgesia, 171
of extruded disc, 246 mastery of, 176
of facet arthrosis, 248, 249 mechanically assisted, 174, 175
of failed low back surgery syndrome, 335 mechanisms of, 172-176
image weighting parameters in, 239 mobilization, 173, 174
indications for, 243 outcomes of, 176-177
of lumbar spine, 239-241, 242-243 therapeutic trials of, 171
of pediatric back pain, 421 tissue-characteristic dependent, 174, 176
Index 577
Manipulation (Cant.) Muscles (Cant.)
unloaded spinal motion, 173, 174 conduction velocity of, 264
Manual materials handing, 182 contractions of, 154,267
Manual therapy, for low back pain, 160, 161 "fusion" of, 162
Marketing, in disability evaluation, 499 imbalances of, 76-77
Maximal medical improvement, 504 insufficiency of, in pregnancy, 407
McGill Pain Questionnaire, 51 manual testing of, 80
Mechanical pain Musculoskeletal examination, in disability
anulus fibrosus in, 25-26 evaluation, 496
pediatric, 417, 421-422 Myelography, 220, 231-234
Mechanical therapy, for low back pain, 160 for failed low back surgery syndrome, 335
Medial branch block, 285-286, 287 of pediatric back pain, 421
Mediation, 540, 553 vs, magnetic resonance imaging, 237-
Medical back pain, pediatric, 421 238
Medical care, in workers' compensation, 522-524 Myofascial pain syndrome, 453-457
Medical consultants, to chronic pain program, bracing for, 212-213
354 definition of, 453-454
Medical director, of chronic pain program, in pregnancy, 407
353-354 trigger points in, 454, 455, 456
Medical Malpractice Payment Report, 563 vs. fibromyalgia syndrome, 454
Medical personnel, qualified, 558 Myofascial system, physical therapy of, 161
Medical records, 545 Myotomal pain, 27
Medical screening examination, 558
Menopause, osteoporosis risk in, 446, 447 Nabumetone, for low back pain, 136
Mental illness, delta sleep role in, 43 Naproxen, for low back pain, 136
Metabolic disorders, I 18, 126-129 Narcotics
Metastatic tumors, in elderly patients, 442-443 for chronic pain, 356
Methadone, for low back pain, 139-140 for disc herniation, 99
Methocarbamol, for low back pain, 140 for low back pain, 159
Methylprednisolone acetate, 278 National Practitioner Data Bank, 562-565
Million Behavioral Health Inventory, 303 Negligence, 540
Minnesota Multiphasic Personality Inventory, lawsuits resulting from, 552-557
303 Nephrolithiasis, 118, 121
Mis-diagnosis, vs. improper transfer, 559 Nerve(s). See also specific nerve
Mithramycin, for Paget's disease, 445 anatomy of, 19, 20
Mixed nerve, 265 conduction velocity of, 264
Modality-oriented clinics, 348 injuries to, 267, 268
Morphine, for low back pain, 139 mechanism of, 30
Motion analysis, in workers' compensation transmission along, 267
evaluation, 188 Nerve blocks, 281-291
Motion segment, in degenerative cascade for failed low back surgery syndrome,
model,33 336-337
Motor deficit, impairment from, 512 local anesthetic, with orthopedic hardware,
Motor nerve, 265 287-288
Motor unit action potential, 265 medial branch, 285-286, 287
Motor vehicle accidents, lumbar whiplash from, Nerve conduction studies, 267-269
475-482 in clinical setting, 265
Mu narcotic receptor, in pain, 43 for failed low back surgery syndrome, 336
Multidisciplinary pain clinics/centers, 348-349 F-waves in, 268
Multifidus muscle, 16, 19 H-reflexes in, 268
Muscle relaxants risks of, 266
for disc herniation, 99 Nerve roots, 28
for low back pain, 140-141, 159 compression of, 28
Muscle stretch reflexes, examination of, 80 dermatomes and, 73
Muscle-based pain, 61-62 selective blocks of, for failed low back
Muscles. See also specific muscle surgery syndrome, 336
anatomy of, 15-19, 29 Neural arch, 11
578 Index
Neuroforarninal canal stenosis, imaging of, Nucleus pulposus (Cont.)

250-251 heat ablation of, 314
Neurogenic pain, in failed low back surgery Nursing, in chronic pain program, 355
syndrome, 340
Neurologic complications, epidural injection Occupational therapy, in chronic pain program,
and, 284 354
Neurologic deficits One-legged standing, in lumbar examination,
impairment from, 511-512, 514-515 71
vs. myofascial pain syndrome, 455 Operant behavioral model, of chronic pain, 349
Neurologic examination, 72, 80-81 Opioids
in disability evaluation, 496-497 for chronic pain, 45
supine, 73-74 controversies about, 138
Neurologic symptoms, associated with pain, 52 efficacy of, 138-139
Neuromuscular deficits, in impairment, 506 long-term therapy with, 138, 139
Neuromuscular junction, 267 for low back pain, 137-140
Neuropathic pain, 361-362 Orphenadrine, for low back pain, 140
neurostimulation for, 361, 364-365 Orthopedic hardware
Neuropathy injections with, for failed low back surgery
proximal motor, 129 syndrome, 337
sciatic, 60-61 local anesthetic block with, 287-288
Neurostimulation, 364- 370 Orthoses, 202-211
complications of, 369-370 compliance and wearing guidelines for,
contraindications to, 366 215-216
implantation in, 367-369 custom-molded thoracolumbosacral, 209,
indications for, 362, 364-365 210
intrathecal drug delivery system with, flexible, 202-204
373-374 rigid, 204-211
mechanism of, 364 in workplace, 215
outcomes in, 369 Osteoarthritis, facet joint, 61
screening algorithm for, 365 bone scan of, 23 I
system choice in, 366-367 Osteoinductive growth factors, 327-328
Neurotomy Osteomalacia, 127-128
radiofrequency, 286, 287 in elderly patients, 443-444
for zygapophyseal joint pain, 103-104 Osteomyelitis, vertebral, 63-64
Neutral spine posture, 162, 163, 164 pediatric, 428-429
New millennium theory, 42, 43-44 Osteonecrosis, femoral head, in pregnancy,
Nociceptive (somatic) pain, 362-363 409-410
intrathecal drugs for, 361 Osteoporosis, 126-127
Nonorganic signs/symptoms, 65, 79-80 bracing for, 214
Nonradicular pain, internal disc disruption causes of, 446
syndrome and, 10I-I 02 in elderly patients, 446-450
Nonsteroidal anti-inflammatory drugs of hip, in pregnancy, 409
for chronic pain, 356 imaging of, 447-449
dosage for, 136 medical treatment of, 449-450
gastrointestinal side effects of, 137 risk factors for, in postmenopausal women,
for low back pain, 135-137, 159 446,447
for myofascial pain syndrome, 457 surgery for, 447, 448, 450
risks of, 135- 136 Oswestry Disability Questionnaire, 302-303
for spinal stenosis, I II Overreaction, in nonorganic physical signs, 80
Norepinephrine, in pain, 43 Oxaprozin, for low back pain, 136
Nucleoplasty, 376 Oxycodone, for low back pain, 139
Nucleus pulposus
anatomy of, 10, 12 Paget's disease, 128-129
biochemistry of, 29-30 in elderly patients, 444-446
bulging of, imaging of, 247 Pain
in endplate fracture, 24, 25 biochemical interventions for, 32
extrusion of, 97, 98 biopsychosocial model of, 41-42
Index 579
Pain (Cont.) Pelvic insufficiency, in pregnancy, 410
daily routines and, 51-52 Pelvic pain, in pregnancy, 410
delta sleep role in, 43 Pelvis
inflammation in, 31-32 anterior tilt of, 82
neurobiology of, 43 forward flexion of, 82
neuro-processing of, childhood pain fractures of, 486
experiencesand,43-44 instability of, in pregnancy, 407
psychological factors in, 298-304 lateral tilt of, 82
vs. suffering, 53 I sports injury to, 386
Pain behavior, in disability evaluation, 496 Percutaneous disc decompression, 375,
Pain clinics, 348 379-383
Pain Patient Profile, 304 care after, 382-383
Pain perception contra indications to, 382
anxiety in, 44 indications for, 382
depression in, 44 outcomes in, 383
personality type in, 44-45 patient selection in, 382
Pancreatitis, 118, 121-122 rationale for, 380, 382
Pars interarticularis system for, 379-380, 381
bone scan of, 230, 231 Percutaneous intradiscal therapies, 375-383
imaging of, 222, 224 history of, 375-376
injury to, 105-107 indications for, 375
imaging of, 254 Percutaneous lumbar discectomy, 376
lesions of, pediatric, 422-425 automated, 376
stress reaction of, 254 Peripheral nerve blocks, for failed low back
pediatric, 422-425 surgery syndrome, 337
Patellar tendon reflexes, 72 Peronei muscle, strength examination of, 72
Patient Personal injury law, 539-546, 539-546
difficult, 305-306 basics of, 540-542
in surgical decision-making, 312 common injuries in, 542
Patient care evidence in, 544-545
federal privacy laws on, 549-551 insurance issues in, 545-546
physician liability in, 547-549 lawsuits in, 542-544
Patient confidentiality, violations of, 550-551 terminology for, 539-540
Patient education trial outcomes in, 544
in chronic impairment, 53I Personality types, in pain perception, 44-45
in chronic pain, 353 Pes planus, lumbar effects of, 81
Patient transfer, physician liability in, 557-560 Phospholipase A2 , in disc herniation, 32
Pediatric patients Physical examination
back pain in, 413-432 in evidence-based medicine, 536
anterior segment, 422, 426-432 of failed low back surgery syndrome, 334
care levels for, 414 in impairment evaluation, 513-514, 515
clinical evaluation of, 418-422 of myofascial pain syndrome, 454-455
differential diagnosis of, 415, 416 of pediatric back pain, 419-420
growth effects on, 418 of pediatric scoliosis, 430-431
mechanical, 421-422 of pregnancy-related low back pain,
medical, 421 406-407
pathogenesis of, 417-418 of spine, 69-82
posterior element, 422-426 Physical stress, childhood, in adult pain
spinal anatomy and function in, 415-418 perception, 43-44
suboptimal care for, 414-415 Physical therapist, in disability evaluation, 497
treatment of, 418 Physical therapy
vs. adult back pain, 413-414 for acute strains and contusions, 97
pain experiences in, in adult pain neuro- in chronic pain program, 354
processing, 43-44 for degenerative lumbar disease, 109
sports injury in, 387-388 for disc herniation, 99-100
Pedicles, 10, 11 for internal disc disruption syndrome, 102
Pelvic inflammatory disease, 118, 120 for low back pain, 151-166
580 InJex
Physical therapy (Cont.) Press-up test, 74, 88

for pediatric pars interarticularis defect, 424 Privileges, 540
programs for, 157-166 Professional community standard, 541
rationale for, 1'i2-153 Prone tests, 74, 88
in return-to-work programs, 193 Prostatitis, 118, 120-121
for sacroiliac joint dysfunction, 112 Proteoglycans, 30
for segmental dysfunction, 105 Provocative testing, 170-171
for spinal stenosis, 111 Proximate cause, 540, 541
for spondylolisthesis, 107 Pseudarthrosis, in failed low back surgery
for zygapophyseal joint pain, 103 syndrome, 343
Physician Pseudo meningocele, in failed low back surgery
in disability testimony, 499 syndrome, 342
liability insurance for, 554-556 Pseudosciatica, 125
in medical endpoint determination, 520 Pseudospine pain, 117-130
on-call duties of, 559 malignant, 129-130
patient transfer liability of, 557-560 metabolic, 118, 126-129
personal liability of, 557 rheumatologic, 118, 122-126
risk management by, 564-563 vascular, 117-119
in surgical decision-making, 312 visceral, 118, 119-122
in workers' compensation, 184 Psoas bursitis, 465-466
Piriformis muscle Psoas muscle, 15, 19
evaluation of, 78-79 imbalances of, 76
length of, 93 Psychogenic symptoms, 65
Piriformis syndrome, 125-126,465 Psychological disorders, vs. myofascial pain
Piroxicam, for low back pain, 136 syndrome, 455
Plaintiff, 540 Psychological factors, 3, 297-306
Platelet-derived growth factors, 326-327 in chronic impairment, 532
Platelet-inhibiting drugs, injection procedures in chronic pain, 298-299, 346-347
in, 280 in complex regional pain syndrome, 471
Plyometric contraction, 154 in evidence-based medicine, 536
Pneumatic decompression brace, 211 in failed low back surgery syndrome,
Poly myalgia rheumatica, 118, 123 337-338
Polyradiculopathy, diabetic, 129 in illness behavior, 299-300
Positive sharp waves, 267, 268 in implantables, 364
Posterior element, 9-10, 11 in industry-related back pain, 181
pediatric, disorders of, 422-426 in low back pain, 40, 96
Posterior longitudinal ligament, 15, 19 in lumbar whiplash, 479-480
Posterior longitudinal plexus, 20 in maladaptive beliefs, 304-305
Posture in managing difficult patients, 305-306
in disability evaluation, 496 in pain perception, 44
neutral spine, 162, 163, 164 in pain suffering, 299-300
physical examination of, 70, 84 in recognizing problem patients, 305
poor, 163 in workers' compensation, 526-527
Power, 154 Psychological stress, childhood, in adult pain
Preexisting conditions, work-related perception, 43-44
aggravation of, 517 Psychological testing, 300-304
Pregnancy Psychologist
ectopic, 118, 120 in chronic pain program, 355
low back pain in, 405-411 in disability evaluation, 498
bracing for, 214-215 Psychotherapy, in chronic pain program,
diagnosis of, 405-407 355
differential diagnosis of, 408-410
exercise for, 410-411 Quadratus lumborum muscle, 15, 19
pathophysiology of, 407-408 imbalances of, 76
prevalence of, 405, 406 Quadriceps muscle
Premature infants, chronic pain syndrome and, imbalances of, 77
43 strength examination of, 72
InJex 581
Racquet sports, low back pain in, 395-396 Return-to-work programs, 179-197
Radicular artery, 20 employment screening in, 192-193
Radicular pain, 27 functional capacity evaluation in, 189-192
motor vehicle trauma and, 477 functional job analysis in, 192
Radiculopathy, 27 functional restoration in, 195-197
arachnoiditis and, 60 injury prevention in, 182-183
chronic, in failed low back surgery manual materials handling in, 182
syndrome, 339 whole-body strength testing in, 191
conditions associated with, 57-60 work hardening program in, 193-195
diabetic, 60 workers' compensation evaluation in,
in ectopic pregnancy, 120 185-189
herpes zoster, 59-60 workers' compensation in, 182-183
lumbar stenosis and, 57-59 Rheumatic disease, radiculopathy in, 63
in lumbar whiplash, 480-481 Ring apophysis, II, 12
rheumatic disease and, 63 Rofecoxib, for low back pain, 136
spinal infection and, 63 Rotation
spondylolisthesis and, 59 in core evaluation, 90
tumors and, 59 injuries from, 23, 24
Radiopharmaceuticals, for bone scans, 229 lumbar spine, 71
Raney jacket, 210 Rowland-Morris Disability Questionnaire,
Range of motion 302-303
in lumbar whiplash, 478 Running, low back pain in, 397-398
measurement of, in impairment evaluation,
506-507,510-511,514 Sacral artery, median, 20
physical examination of, 70-72 Sacrococcygeal joint, injections into, 290-291
Reasonable medical certainty, 540 Sacroiliac joint
Reasonable person standard, 541 dysfunction of, 111-112
Reassurance, in lumbar whiplash, 478 bracing for, 213
Rectal examination, 74 in pregnancy, 410
Rectus femoris muscle, strength examination injections into, 289-290
of,72 in lumbopelvic rhythm, 82
Referrals range of motion of, 71
in disability evaluation, 492-493 Sacroiliac joint pain, 62
fees from, 554 motor vehicle trauma and, 477
self-, prohibitions against, 560-562 Scanning examination, of spine, 74-75
Referred pain, 27 Scapular reaction, 91, 92
neurophysiology of, 31 three-dimensional, 76
Reflex sympathetic dystrophy, See Complex Scheuermann's disease, 427-428
regional pain syndrome Schmorl's nodes
Reflexes, examination of, 80 after motor vehicle trauma, 476
Regional disturbances, in nonorganic physical in disc herniation, 247-248
signs, 79-80 Schober's test, modified, 75
Regional soft tissue pain, 454 Scintillation camera, 229
Rehabilitation Sclerotomal pain, 27
factors in, 153 Scoliosis, 2, 3
physiologic basis of, 153-157 degenerative
rationale for, 152-153 in elderly patients, 440-441
for sports injuries, 389-390 stenosis with, surgery for, 321-322
in workers' compensation, 523 myelography of, 233
Reiter's disease, 118 pediatric, 429-432
Relative rest, 95, 151, 152 Screening examination, 69-74
for acute strains and contusions, 97 Seat Slump Test, 72
for disc herniation, 99 Sedative-hypnotics, for low back pain, 141
for low back pain, 158 Segmental dysfunction, 104-105
Renal osteodystrophy, vs. osteomalacia, 444 Segmental facilitation, 104
Requests for production, 544 Selective serotonin reuptake inhibitors
Resting membrane potential, 266 for chronic back pain, 46
582 Index
Selective serotonin reuptake inhibitors (Cont.) Spine (Cont.)

for fibromyalgia syndrome, 462, 464 tumors of, 64
for low back pain, 143 Spinous processes, 11
Self-management, of chronic pain, 352-353 in extension, 21
Self-referral, prohibitions against, 560-562 Spondyloarthropathy
Sensory deficit, impairment from, 513 imaging of, 259
Sensory examination, 80 seronegative, 118, 124-125
Serotonin, in pain, 43 Spondylolisthesis, 2, 105-107
Short-Form Health Survey, 303 bone scan of, 230
Side-bending, 71 bracing for, 211-212
in core evaluation, 90 degenerative, 59, 105
Single-photon emission computed tomography, in elderly patients, 440
in bone scans, 229-230 imaging of, 252, 253
Sinuvertebral nerve, 19, 20 spinal stenosis with, surgery for, 316-319
Sleep, delta, in pain disorders, 43 dysplastic (congenital), 105
Slump test, 81, 86 imaging of, "Scotty dog" sign in, 222, 225,
Soccer, low back pain in, 400-401 227
Social factors, in chronic pain, 347 isthmic, 59, 105
Social history, 54 fusion for, 320
Socioeconomic factors, in workers' imaging of, 255-256
compensation, 524 pathological, 105
Sodium fluoride, for osteoporosis, 450 pediatric, 422, 423, 425
Softball, low back pain in, 392-393 postsurgical, 105-106
Somatosensory-evoked potentials, 271-273 traumatic, 105
dermatomal, 273 Spondylolysis, 105-107
for failed low hack surgery syndrome, 336 bone scan of, 230
Special damages, 540 bracing for, 211
Spinal canal arteries, 20 in elderly patients, 437-438
Spinal motion segment, in degenerative imaging of, "Scotty dog" sign in, 222, 225,
cascade model, 33, 36 227
Spinal stenosis, 110-111 isthmic, imaging of, 254, 255
acquired, 250-251 pediatric, 423-424
congenital, 250 Sports injuries, 385-401
decompression for, imaging after, 258-259 in aging athlete, 387
degenerative spondylolisthesis with, surgery competition level and, 388
for, 316-319 contact, 399-401
developmental, 250 epidemiology of, 385-386
in elderly patients, 438-439 equipment in, 389
in failed low back surgery syndrome, 338 factors in, 386-389
far-out (extraforaminal), 251-252 low back pain incidence in, 4
foraminal, 251 noncontact, 391-399
imaging of, 248, 250-253 rehabilitation programs for, 389-390
lumbar, radiculopathy in, 57-59 return to play after, 391
surgery for, 314-316 risk factors for, 387
types of, 250-252 sites of, 386
Spine timing in, 388-389
in disability evaluation, 496 treatment of, failure of, 390-391
fracture of, 62 -63 types of, 386-387, 391-401
infection of, 63 in young athlete, 387-388
neurologic examination of, 80-81 Sprains, 386
pediatric Spring test, 74
functional elements of, 416 Squats, standing one-legged, 75, 89
stability and motion of, 416-417 Standard of proof, 544
physical examination of, 69-82 Standing balance, 84
scanning examination of, 74-75 physical examination of, 70
screening examination of, 69-74 STAR diagram, 70-71, 84
supine landmarks for, 73, 87 Stark I and II, 560-562
Index 583
State laws, in malpractice, 553-554 Symptom Check List 90, Revised, 303
Statute of limitations, 540
Step-downs, 75, 89 Taylor brace, 206, 207
Step-off deformity, 74 Tenderness, 79
Stimulants, for low back pain, 146 Tendinitis, iliopsoas, 465-466
Stimulation test, in noncrganic physical signs, Tendons, deep reflexes of, 72
79 Testimony
Straight leg raise test, 80-81, 87 in disability evaluation, 499
crossed, 73, 80-81 legal,545
in impairment evaluation, 511 in malpractice, 552-553
supine, 72-73 Therapeutic electrical stimulation, for low back
Strains, 386 pain, 159
acute, 96-97 Therapeutic exercise, for low back pain,
bracing for, 212-213 160-161
Strength, 154 Thoracic spine, range of motion of, 71
Strength examination, 72 Thoracolumbar fascia, 19-20
Strength training, 155-157 Thoracolumbar junction
for degenerative lumbar disease, 109 evaluation of, 77-78
for internal disc disruption syndrome, physical examination of, 78
102 Three-dimensional physical examination,
for spondylolisthesis, 107 75-76
for zygapophyseal joint pain, 103 Tibialis anterior muscle, strength examination
Subarachnoid space, injection into, 283- of,72
284 Tissue damage, in injection procedures, 279
Subchondral postcapillary plexus, 21 Toe, extension of, 73
Subluxation, facet joint, 61 Tomography, 227, 229
Subpoena, 540, 544 Topiramate, for low back pain, 145
Subpoena duces tecum, 540 Torsion, flexion with, injuries from, 23, 24
Substance abuse, neurobiology of, 43 Tort, 540
Suffering intentional, 541
psychological factors in, 299-300 Traction
vs. pain, 531 for acute discogenic lumbar pain, 99-100
Sulindac, for low back pain, 136 for low back pain, 160
Superior articular facet, 11 for zygapophyseal joint pain, 103
Superior articular process, 11 Tramadol
Supraspinous ligaments, 14, 15 for fibromyalgia syndrome, 464
Surgery for myofascial pain syndrome, 457
for chronic discogenic pain, 322-324 Transverse process, 11
for degenerative scoliosis with stenosis, Trauma, 485-490. See also Fracture(s)
321-322 imaging of, 254-256
for degenerative spondylolisthesis with Trazodone
spinal stenosis, 316-319 for fibromyalgia syndrome, 464
for disc herniation, 312-314 for low back pain, 144
imaging evaluation after, 257-259 Treatment
indications for, 311-312 evidence-based medicine in, 533
for low back pain, 309-328 patient history of, 52
options for, 312-328 stabilizing, 558
patient selection for, 312 Trials, 544
for spinal stenosis, 11I, 314-316 malpractice, 553
terminology for, 309-311 Triamcinolone hexacetonide, 278
Swimming, low back pain in, 398-399 Trigger points, myofascial, 454
Sympathetic nerve blocks, for failed low back Trochanteric bursitis, 126, 464-465
surgery syndrome, 337 Trochanteric height, 70, 84
Sympathetic pain, neurophysiology of, 31 Tumors
Sympathetic trunk, 19 in elderly patients, 442
Symphysiolysis pubis, in pregnancy, 408-409 imaging of, 256, 257
Symphysis pubis, height of, 73, 87 metastatic, in elderly patients, 442-443
584 Index
Tumors (Cant.) West Haven Yale Multidimensional Pain

pediatric, 428-429 Inventory, 303-304
spinal,64 Whiplash, lumbar, 475-482
Twisting, in industry-related back pain, 182 Whole-body strength testing, 191
Williams flexion brace, 206, 207
Ultrasonography, of osteoporosis, 448 Wiltse's scoring system, 300
Women, pain experience of, childhood abuse
Valproate, for low back pain, 145 and, 43-44
Vascular-induced pain, 64-65 Work hardening program, 193-195
in pregnancy, 407 Work restrictions, in lumbar whiplash, 478
Vasovagal reactions, in injection procedures, Workers' compensation, 517-528
279 administrative systems for, 521-522
Veins, 2 I. See also specific vein disability evaluation in, 520-521
Ventazaline, for low back pain, 144 employee indemnity benefits of, 519, 523
Ventral ramus, 19, 20 employee medical benefits of, 519- 520
Vertebrae federal systems for, 522
anatomy of, 9-10, 11 general issues in, 517-522
anterior column of, 486 history 01',518-519
in flexion, 21 independent medical evaluation for,
middle column of, 486 491-499
osteomyelitis of, 63-64 medical benefits and special considerations
posterior column of, 487 in, 524-528
sports injury to, 386 medical care in, vs. in general health,
trauma to, imaging of, 254 522-524
Vertebral bodies medical endpoint in, 520
anatomy of, 9, 10, II, 19 in return-to-work programs, 183-184
blood supply of, 20 Workers' compensation evaluation, 185-189
innervation of, 20 medico-legal aspects of, 184
pathologic compression fracture of, 257 Workplace, 2, 3
venous supply of, 21 orthoses in, 215
Vertebral endplates Work-related low back injury, 517, 518
anatomy of, 11, 12
degeneration of, imaging of, 247-248 X-rays
fatigue fracture of, 26 of degenerative lumbar disease, 108
fracture of, 24, 25 of failed low back surgery syndrome,
Vertebral foramen, 11 334-335
Visceral injury, 486 indications for, 220-221
Visceral referred pain, vs. myofascial pain of pediatric back pain, 420
syndrome, 455 of pediatric pars interarticularis defect, 423
Viscerogenic pain, 65 of pediatric scoliosis, 431
Visual analog scale, 51 sensitivity and specificity of, 221-222
Vitamin 0 deficiency, 127-128 of spinal stenosis, 111
vs. osteomalacia, 443-444 of tumors, 256
Vocational counseling, in chronic pain views in, 222-227
program, 355
Vocational factors Zygapophyseal joint
in back pain risk, 3 anatomy of, 10, 13, 14, 19, 29
in chronic pain, 347 in extension injuries, 23
in disability evaluation, 493-494 in flexion, 21
in industry-related back pain, 181 in flexion and torsion injuries, 23, 24
Vocational specialist, in disability evaluation, injections into, 103, 285-287
498 for failed low back surgery syndrome,
336
Waddell Index of Disability, 301 pain in, 102-104
Waddell's sign, 40 sports injury to, 386

Low Back Pain Handbook. A Guide For The Practicing Clinician by Andrew J. Cole, M.D., F.a.C.S.M. and Stanley A. Herring, M.D., F.a.C.S.M. (Eds.)

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Low Back Pain Handbook. A Guide For The Practicing Clinician by Andrew J. Cole, M.D., F.a.C.S.M. and Stanley A. Herring, M.D., F.a.C.S.M. (Eds.)

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Publisher: HANLEY Et BELFUS, INC.

Library of Congress Control Number 2002114022

THE LOW BACK PAIN HANDBOOK, 2nd edition ISBN 1-56053-493-1

Last digit is the print number: 9 8 7 6 5 4 3 2 1

To the memory of Mary Ann and Earl Herring, my parents, whose

Thomas Agesen, M.D.

Joseph T. Alleva, M.D.

Paul A. Anderson, M.D.

Steven J. Anderson, M.D.

Ray M. Baker, M.D.

Nikolai Bogduk, M.D., Ph.D., D.Sc.

Richard Paul Bonfiglio, M.D.

Ronald Lee Bonfiglio, M.D.

Joanne Borg-Stein, M.D.

Cary C. Bucko, M.P.T.

Craig C. Callewart, M.D

Andrew J. Cole, M.D., F.A.C.S.M.

Susan J. Dreyer, M.D.

Paul Dreyfuss, M.D.

Avital Fast, M.D.

Robert J. Gatchel, Ph.D.

Michael C. Geraci, Jr., M.D., P.T.

Terrence P. Glennon, M.D.

Kenneth B. Heithoff, M.D.

Stanley A. Herring, M.D., F.A.C.S.M.

Richard J. Herzog, M.D.

Brenda Hight, J.D.

Donald W. Hinnant, Ph.D.

Gerald P. Keane, M.D.

Donald Liss, M.D.

Howard Liss, M.D.

Ian B. Maitin, M.D.

Gerard A. Malanga, M.D.

Carolyn A. Marquardt, M.D.

Tom Mayer, M.D.

Daniel Mazanec, M.D.

Frederick B. McAdam, M.D.

Scott F. Nadler, D.O.

Jeff Pavell, D.O.

John H. Peloza, M.D.

Douglas Phil\ips, J.D.

Peter Barth Polatin, M.D.

Joel M. Press, M.D.

Thomas J. Puschak, M.D.

Jerome Schofferman, M.D.

Richard Seroussi, M.D.

J. David Sinclair, M.D., F.R.C.P.(C.)

Charlotte H. Smith, M.D.

Mark J. Sontag, M.D.

Christopher J. Standaert, M.D.

Steven A. Stratton, P.T., Ph.D., A.T.C.

John J. Triano, D.C., Ph.D.

Robert Gerard Viere, M.D.

Michael M. Weinik, D.O.

Robert P. Wilder, M.D., F.A.S.C.M.

Robert E. Windsor, M.D.

Keith Andrews Wohlberg, M.A.T.P., P.T.A.

Michael W. Wolff, M.D.

Way Yin, M.D.

Irene An-Mel Young, M.D.

Jeffrey 1. Young, M.D., M.A., F.A.C.S.M.

Muhammad B. Yunus, M.D., F.A.C.P., F.A.C.R.

Andrew J. Cole, M.D., F.A.C.S.M.