1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 MUSCULOSKELETAL DISORDERS IN THE WORKPLACE: ISBN-13: 978-0-323-02622-2 PRINCIPLES AND PRACTICE ISBN-10: 0-323-02622-2 Copyright © 2007, 1997 by Mosby Inc., an affiliate of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail:
[email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’. Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose of formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, and to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher
Library of Congress Cataloging-in-Publication Data Musculoskeletal disorders in the workplace: Principles and practice / [edited by] Margareta Nordin, Gunnar B.J. Andersson, Malcolm H. Pope. —2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 0-323-02622-2 1. Musculoskeletal system—Diseases. 2. Occupational diseases. I. Nordin, Margareta. II. Pope, M. H. (Malcolm Henry), 1941- III. Andersson, Gunnar, 1942[DNLM: 1. Musculoskeletal Diseases—therapy. 2. Biomechanics. 3. Human Engineering. 4. Musculoskeletal Diseases—prevention & control. 5. Occupational Diseases—etiology, WE 140 M9854 2006] RC925.5M8783 2006 616.7—dc22 2006043830
Acquisitions Editor: Rolla Couchman Project Manager: Bryan Hayward
Printed in United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 1
Foreword Workers’ health priorities are now driven by demographics. All of the First World Nations are facing a future with a rapidly diminishing work force, an aging population, and a growing number of pensioners. The prevention and efficient management of work place injuries and disabilities has become a priority. Medical professionals work in an increasingly specialized world brought on by an explosion of knowledge, the demand from society for "the very best" in services, and the need for expertise to keep pace with technological change and innovation. Modern medical history, in particular, is replete with examples of sudden bursts of information that challenged the growth of new domains and abilities. The period of World War II saw an explosion of medical knowledge, rapidly dividing General Surgery into numerous subspecialties. Similarly, the 1970s was a critical period in orthopaedic surgical practice as many subspecialties developed that allowed greater expert use of modern technology. Occupational orthopaedics is a relatively young specialty that is still evolving rapidly. As in sports medicine, we have learned that it is not sufficient to examine and treat injuries alone. After recovery, an injured football player is expected to return to the game and perform at his previous level of athletic ability. The injured industrial worker is also expected to return
to his or her previous level of performance, accomplishing a particular task within a reasonable time frame. Although the average orthopaedic surgeon may be well-versed with the conditions of the gridiron, he or she may not be familiar with the requirements and limitations of the industrial playing field. In industrial medicine, it is not only necessary to "fix" the worker; one must have an idea about how to fix the workplace to prevent further injury. Like sports medicine, the management and prevention of industrial injury demands a dedicated and knowledgeable cadre of physicians, surgeons, and therapists who are able to apply modern knowledge and expertise to a successful medical program. This volume brings together chapters authored by the most knowledgeable group of surgeons, physicians, scientists, ergonomists, and therapists currently addressing the prevention and management of workplace injury. The editors have assembled a most versatile and practical tool for the many allied-health professionals involved with work-related injuries. This updated text will have a strong impact within industry and on the management of patients well into the 21st century. Victor H. Frankel KNO, MD, PhD Professor of Orthopaedic Surgery, NYU President Emeritus, Hospital for Joint Diseases
v
Contributors K. N. An, Ph.D. John and Posy Krehbiel Professor of Orthopaedics Maylo Clinic College of Medicine Orthopaedics Biomechanics Lab Rochester, MN 55905
Amit Bhattacharya, Ph.D., C.P.E. Professor Biomechanics-Ergonomics Research Laboratories Department of Environmental Health University of Cincinnati Medical College Cincinnati, OH 45267-0056
Gunnar B. J. Andersson, M.D., Ph.D. Professor and Chairman Department of Orthopaedic Surgery Rush-PresbyterianSt. Luke’s Medical Center Chicago, IL 60612
Anthony M. Buoncristiani, M.D., L.T. Orthopaedics Department Naval Medical Center San Diego, CA 92134
Thomas J. Armstrong, Ph.D. Professor Industrial and Operations Engineering Director Center for Ergonomics University of Michigan Ann Arbor, MI 48109-2117 Federico Balagué Médecin Chef Adjoint Division of Rheumatology, Physical Medicine and Rehabilitation Hôpital Cantonal 1708 Fribourg Switzerland and Adjunct Associate Professor Department of Orthopaedic Surgery New York University School of Medicine New York, NY 10014 Michele Crites Battié, Ph.D. Professor Department of Physical Therapy University of Alberta Edmonton, Alberta T6G 2G4 Canada Jane Bear-Lehman, Ph.D., OTR, FAOTA Associate Professor New York University Steinhardt School of Education Occupational Therapy Department New York, NY 10012 David P. Beason, M.S. Research Engineer Laboratory Manager McKay Orthopaedic Research Laboratory University of Pennsylvania Philadelphia, PA 19104
Linda Carroll, M.D. Associate Professor Department of Public Health Sciences University of Alberta Edmonton, Alberta T6G 2E1 Canada J. David Cassidy, M.D. Department of Public Health Sciences University of Alberta Edmonton, Alberta T6G 2E1 Canada Christine Cedraschi Division of General Medical Rehabilitation & Multidisciplinary Pain Center Division of Clinical Pharmacology and Toxicology Geneva University Hospitals 1211 Geneva 14 Switzerland Mark S. Cohen, M.D. Department of Orthopaedic Surgery Rush-PresbyterianSt. Luke’s Medical Center Chicago, IL 60612 Pierre Côté, D.C., Ph.D. Scientist Institute for Work and Health Toronto, Ontario M5G 2E9 Canada
Craig J. Della Valle, M.D. Assistant Professor of Orthopaedic Surgery Rush-Presbyterian-St. Luke's Medical Center Chicago, IL 60612 James A. Dewees, M.S., C.P.E., C.E.E.S. ERGO Accommodations Inc P O Box 499 Union, KY 41091-0499 Jiri Dvorak, M.D., Ph.D. Department of Neurology Schulthess Hospital 8008 Zurich Switzerland Ulf Eklund M.D. Orthopedic Surgeon Department of Orthopedics Molndal Hospital Molndal, Sweden Freddie H. Fu, M.D. Department of Orthopaedic Surgery University of Pittsburgh Pittsburgh, PA 15203 Douglass Gross, Ph.D. Assistant Professor Department of Physical Therapy University of Alberta Edmonton, Alberta T6G 2G4 Canada Robert Gunzburg, M.D., Ph.D. Senior Consultant Department of Orthopaedics Centenary Clinic 2018 Antwerp Belgium
Benjamin Crane, M.D. Resident Department of Orthopaedic Surgery Rush University Medical Center Chicago, IL 60612
Daniel J. Habes, M.S.E., C.P.E. Industrial Engineer Industrial Hygiene Section Hazard Evaluations and Technical Assistance Branch Division of Surveillance, Hazard Evaluations, and Field Studies National Institute for Occupational Safety and Health Cincinnati, OH
James N. DeBritz, M.D. Assistant Instructor Department of Orthopaedics Georgetown University Hospital Washington, DC 20007
Robert H. Haralson, III, M.D., M.B.A. Executive Director of Medical Affairs American Association of Orthopaedic Surgeons Rosemont, IL 60018
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Contributors
Rudi Hiebert, B.S. Interim Director Musculoskeletal Epidemiology Unit Occupational & Industrial Orthopaedic Center NYU Hospital for Joint Diseases New York, NY 10014 Beat Hintermann, M.D. Chief Orthopaedic Clinic University of Basel Kantonsspital CH-4410 Liestal Switzerland David M. Kalainov, M.D. Clinical Assistant Professor Department of Orthopaedic Surgery Northwestern University Chicago, IL 60611 Dennis D.J. Kim, M.D. Associate Professor Department of Physical Medicine and Rehabilitation Montefiore Medical Center Bronx, NY 10467 Stephan Konz, Ph.D., P.E. Professor Department of Industrial Engineering Kansas State University Manhattan, KS 66506 Vicki Kristman, B.Sc., M.Sc. Ph.D. Candidate, Epidemiology Department of Public Health Sciences University of Toronto Research Associate Institute for Work & Health Toronto, Ontario M5F 2E9 Canada Shrawan Kumar, Ph.D., D.Sc., F.Erg.S., F.R.S.C. Professor Department of Physical Therapy Faculty of Rehabilitation Medicine University of Alberta Edmonton, Alberta T6G 2G4 Canada Marianne Magnusson, R.P.T., Dr.Med.Sci. Senior Lecturer Liberty Safe Work Research Centre Department of Economy and Technology Halmstad University SE-301 18 Halmstad Sweden Paul H. Marks, M.D. Associate Professor Department of Surgery University of Toronto Toronto, ON M4Y 1H1 Canada Ronald Moskovich, M.D. Assistant Professor Department of Orthopaedic Surgery NYU Hospital for Joint Diseases New York, NY 10003
Margareta Nordin, Dr.Sci. Professor Departments of Orthopaedics and Environmental Medicine School of Medicine New York University Program Director Program of Ergonomics and Biomechanics Graduate School of Arts and Science New York University Director Occupational and Industrial Orthopaedic Center (OIOC) NYU Hospital for Joint Diseases New York University Medical Center New York, NY 10014 Mooyeon Oh-Park, M.D. Clinical Associate Professor Department of Rehabilitation Medicine Montefiore Medical Center Bronx, NY 10467 Rita M. Patterson, Ph.D. Associate Professor and Deputy Director Orthopaedics Biomechanics Laboratory Division of Research Department of Orthopaedic Surgery and Rehabilitation University of Texas Medical Branch Galveston, TX 77555 David I. Pedowitz, M.S., M.D. Chief Resident Department of Orthopaedic Surgery University of Pennsylvania Philadelphia, PA 19004 Anthony Petrizzo, M.D c/o Ronald Moskovich, M.D. 301 East 17th Street New York, New York 10003 Derek Plausinis, M.D. Shoulder & Elbow Surgery Fellow Department of Orthopaedic Surgery NYU Hospital for Joint Diseases New York, NY 10003 Malcolm H. Pope, Dr.Med.Sci., Ph.D. Professor Liberty Safework Research Centre Department of Environmental & Occupational Health Foresterhill Aberdeen, Scotland AB 25 2ZD United Kingdom Laura Punnett, Sc.D. Professor Department of Work Environment University of Massachusetts Lowell Lowell, MA 01854 Robert G. Radwin, Ph.D. Professor and Chair Department of Biomedical Engineering University of Wisconsin Madison, WI 53706
David Rempel, M.D., M.P.H. Professor School of Medicine –Ergonomics Program Division of Occupational and Environmental Medicine University of California, San Francisco Richmond, CA 94804 Michiel Reneman, Ph.D, P.T. Center for Rehabilitation University Medical Center Groningen University of Groningen P.O. Box 30002, 9750 RA Haren The Netherlands Per A.F.H. Renström, M.D., Ph.D. Professor Department of Molecular Medicine and Surgery Section of Orthopaedics and Sports Medicine Karolinska Hospital SE-171 76 Stockholm Sweden Mana Rezai, H.B.Sc., D.C., M.H.Sc. Candidate Research Associate Institute for Work & Health University of Toronto Toronto, Ontario M5G 2E9 Canada Tonu Saartok, M.D., Ph.D. Department of Surgical Sciences Section of Sports Medicine Karolinska Institute SE-171 76 Stockholm, Sweden G. James Sammarco, M.D. The Center for Orthopaedic Care, Inc. Cincinnati, OH 45219-2906 Peter Sheehan, M.D. Director Diabetes Center of Greater New York Cabrini Medical Center New York, NY 10003 Ali Sheikhzadeh, Ph.D., C.I.E. Research Assistant Professor Departments of Orthopaedic Surgery and Environmental Medicine New York University School of Medicine Associate Director of Research Occupational and Industrial Orthopaedic Center NYU Hospital for Joint Diseases New York, NY 10014 Mary-Louise Skovron, Dr. PH. Group Director, Pharmaco-epidemiology Global Epidemiology Bristol–Myers Squibb 311 Pennington-Rocky Hill Road Pennington, NJ 09534
Contributors
Louis J. Soslowsky, Ph.D. Professor of Orthopaedic Surgery and Bioengineering Vice Chair for Research Director, McKay Orthopaedic Research Laboratory University of Pennsylvania Philadelphia, PA 19104 Dan M. Spengler, M.D. Professor and Chair Department of Orthopaedics and Rehabilitation Vanderbilt Orthopaedics Institute Nashville, TN 37232 Marek Szpalski, M.D. Associate Professor and Chair Department of Orthopaedics IRIS South Teaching Hospitals Free University of Brussels 1190 Brussels Belgium James B. Talmage M.D. Occupational Health Center Cookeville, TN 38501
Ross Taylor, M.D. Coastal Orthopaedic Associates Conway, SC 29526 Victor Valderrabano, M.D., Ph.D. Human Performance Laboratory and Orthopaedic Department University of Calgary Calgary, Alberta T2N1N4 Canada also Orthopaedic Department University Hospital of Basel 4031 Basel Switzerland Tapio Videman, M.D., D.Med.Sci. Professor Faculty of Rehabilitation Medicine University of Alberta Edmonton, Alberta T6G 2G4 Canada Sherri Weiser, Ph.D. Research Assistant Professor of Environmental Medicine Occupational & Industrial Orthopaedic Center NYU Hospital for Joint Diseases New York, NY 10014
Sam W. Wiesel, M.D. Professor and Chair Department of Orthopaedic Surgery Georgetown University Medical Center Washington, D.C. 20007 Harriët Wittink, Ph.D., M.S., P.T. Head Physical Therapy Professional Master Program Hogeschool Utrecht 3508 AD Utrecht The Netherlands Joseph D. Zuckerman, M.D. Professor and Chair Department of Orthopaedic Surgery NYU Hospital for Joint Diseases New York, NY 10003
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CHAPTER
1
Introduction to Epidemiologic Concepts in Musculoskeletal Disorders Mary Louise Skovron and Rudi Hiebert
The literature on the epidemiology of occupational musculoskeletal disorders is often confusing because of conflicting evidence on the importance of various potential risk or causal factors. This chapter describes basic epidemiologic methods so the reader can evaluate critically the published literature on occupational musculoskeletal disorders. Most examples are drawn from the literature on occupational low back pain, but the reader should be aware that similar methodologic standards must be applied to the literature on upper extremity disorders. Epidemiology is the study of the distribution and determinants of diseases and injuries in human populations. It consists of a developed methodology for testing scientific hypotheses in groups of individuals rather than in a laboratory setting. With knowledge of the intrinsic strengths and limitations of the design and execution of studies reported in the literature, it is possible to evaluate the strength of the evidence derived from these studies and even to make sense of conflicting results from different studies on the same topic. In this chapter we present an overview of the basic terminology used in epidemiology and the characteristics and generic strengths and limitations of analytic (hypothesis testing) study designs, with an emphasis on observational study designs. There are several types of epidemiologic studies. Descriptive epidemiology is a means of monitoring the health of a population, identifying health problems, and compiling information that can be used for the development of causal hypotheses. Analytic epidemiology is a set of epidemiologic study methods used to test specific hypotheses.
Health Administration (OSHA) by employers, workers’ compensation records, records of visits to the workplace health facility, and surveys of the work force.11 In clinical practice, the simple case count is usually derived by chart review (retrospectively) or by enrollment of patients seen during a given period (prospectively). The frequency of the disorder can also be expressed as a proportionate ratio, a ratio of cases of a particular disorder to cases of all disorders in the population of interest. In 1985 for example, occupational back injuries accounted for 26% of all closed compensation cases in a sample of nine states. By itself, numerator data cannot provide useful information regarding the risk or probability of acquiring the disorder. The case frequency has to be related to the underlying population that could have potentially developed the disorder. For example, the U.S. Bureau of Labor Statistics estimated 303,750 OSHAreportable occupational injuries involving the back in 2003.4 Without reference to the number of people at risk, it is not possible to estimate the risk of back injury in the population or to test hypotheses regarding risk factors for occupational back injury. For this reason, rates are used when the objective is to assess the risk of the disorder or determinants of disorders or their outcomes.
Rates and ratios Rates describe the frequency of a disorder or disorder per unit size of the population per unit time of observation. The rates commonly used in epidemiology are morbidity and mortality rates. The general form of a morbidity or mortality rate is
MEASURES OF DISORDER FREQUENCY The fundamental strategy of epidemiology is the analysis of relative and absolute measures of frequency and a comparison of the characteristics of individuals with and without disorder. The most obvious measures of frequency are case counts and their variations, which are often referred to as numerator data. They describe the frequency of the disorder without reference to the underlying population at risk. Examples of sources of case count data include back injury reports to the Occupational Safety and
Number of cases × 10 0 (1000, etc.) per unit time Number of persons at risk The most frequently used morbidity rates in epidemiologic research are the incidence rate and the prevalence rate. The incidence rate is based on new cases of a disorder or disorders (or new disorder events), whereas the prevalence rate is based on existing cases. Because they are based on new versus existing cases,
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Introduction to epidemiologic concepts in musculoskeletal disorders
incidence and prevalence rates have different uses and different limitations. In a sense, the incidence rate is a rate of change, the frequency with which people change from healthy to injured, sick, or disabled. Therefore the appropriate denominator is the population at risk of acquiring the disorder (i.e., those who are free of the disorder at the start of the time interval). The incidence rate may be quantified in a number of ways, for example, as the number of new events per 1000 persons per year, when the population is stable and the number of new events is counted each year. Alternatively, it may be quantified as the number of new events per 1000 person-years, as is done in prospective studies where a fixed population is followed until the disorder, the end of the study, or loss to follow-up occurs. In practice, although the best denominator for incidence rates is the number of people free of the disorder at the start of the time interval, surveillance incidence rates (and prevalence rates) that are based on case reports often use the total population derived from census data or from work-force estimates. The U.S. Bureau of Labor Statistics’ estimate of 303,750 OSHA-reportable occupational injuries involving the back represents an incidence of 3.46 new cases per 1000 workers.4 The prevalence rate is the number of existing cases of a disorder in a given population in a given time period. For example, the 1-year prevalence of disabling back pain is as high as 25%.14 Point prevalence is the number of cases per unit population at one moment of counting, for example, all persons receiving disability because of back pain in the work force of a metropolitan electrical utility company on January 1, 2005, expressed per 1000 population. For point prevalence, the unit of time is often not expressed because the period of time is effectively instantaneous. Period prevalence is the number of cases existing at one time or another during a definable time interval such as 1-year, 5-year, or lifetime prevalence. Some epidemiologists do not express prevalence as a rate because in practice it is often derived from surveys that are difficult to assign to a specific time interval. A number of factors other than the risk factor under study may affect the incidence and prevalence rates. These include demographic characteristics of the underlying population, most obviously age distribution6 because age is known to be associated with the onset of almost all disorders. Gender and ethnicity distributions must also be taken into account when incidence rates are interpreted. Other influences can distort the apparent incidence rate, including certain company policies, workers’ compensation claims, and health care system influences that affect the likelihood of seeking medical attention, of being diagnosed with a given disorder or disorders, or of having the disorder reported. These factors should be considered when measures of disorder frequency are evaluated, particularly when changes are assessed over time or different populations are compared. To eliminate the effects of differences in these factors, the rates may be adjusted or standardized algebraically. The adjusted rates express the risk of acquiring the disorder in the populations being compared as if they had the same age, sex, and ethnicity distributions. Alternatively, if it is not necessary to have a single summary index of disorder risk, the morbidity rates within population strata defined by age, sex, and ethnicity may be compared. The number of existing cases of a disorder or disorders at any time is a function of both the rate of new cases (incidence) and the duration of that disorder. Therefore, when a population is
stable and the duration of a disorder is also stable, it is possible to estimate prevalence from incidence and vice versa according to the following approximation: ~ incidence × duration Prevalence ~ Thus a change in prevalence may reflect changes in the incidence rate, duration, or both. For example, the prevalence of low back pain in a population may change because of alterations in individual, work-related, or other environmental risk factors affecting incidence rate or because treatment changes alter the duration of back pain episodes and risk of chronicity. It is occasionally the case that improved treatment extends the duration of a disorder, with the result that the prevalence increases in the face of a decreasing incidence, as occurred some decades ago with Down syndrome. The survival of infants with Down syndrome improved because of improved medical and surgical management of their associated disorders. The prevalence of Down syndrome increased, although the incidence declined as a result of prenatal screening programs.
DESCRIPTIVE EPIDEMIOLOGY The first step often undertaken in epidemiology is development of the descriptive epidemiology of a disorder or disorders. Descriptive epidemiology supports the development of causal hypotheses but does not in itself support conclusions about disorder causality or about any hypotheses. In descriptive epidemiology the frequency of a disorder in the population is characterized in terms of person (e.g., age, sex, ethnicity-specific incidence rates, economic, behavioral, occupational, and other factors), place (rural versus urban, type of housing, national variations, type of industry, job requirements), and time (long-term trend, seasonality, occasionally day of the week or time of day). The need to explain variation in descriptive studies drives the formulation of causal hypotheses. Drawing on current available information from various fields (such as anatomy, physiology, psychology, behavioral science, etc.), specific hypotheses are developed by inductive reasoning to explain observed patterns of variation and then evaluated using specific study designs to test these hypotheses. Studies that test specific hypotheses are called analytic. As the results of hypothesis-testing (analytic) studies are accrued, they are added to the basis for causal inference, depending on their strengths and generalizability, and hypotheses are supported, modified, or negated. In interpreting the evidence from all scientific sources, the rules of causal inference are applied.7 Briefly, the hypothesized cause must be demonstrated to have preceded the disorder by a length of time sufficient to allow disorder development and expression (time sequence of events). The disorder should be more common in those with the hypothesized cause than in those without it (increased risk in those exposed to the hypothesized cause), and as the intensity or duration of exposure to the hypothesized cause increases, the frequency of the disorder should increase (dose-response relationship). The association between the hypothesized causal factor and the disorder should be consistently demonstrated in methodologically sound studies and should be biologically plausible. In addition, the specificity of an association (i.e., the extent to which the hypothesized
Chapter 1
causal factor is associated with only one disease or disorder) adds weight to a causal hypothesis, but it is not necessary for causal inference; for example, cigarette smoking is accepted as a cause of lung cancer, although the association is not specific. Cigarette smoking is also associated with a number of other cancers, obstructive pulmonary disorder, heart disorder, and a variety of disorders, including osteoporosis, low back pain, and, in particular, herniated intervertebral disks.
ANALYTIC EPIDEMIOLOGY Analytic, or hypothesis-testing, epidemiology relies on two types of study designs: observational and experimental. In observational studies, exposure to the hypothesized causal factor and development of the disorder in the population under study occur in the natural course of events; the investigator does not cause them to occur. The study is designed and executed to maximize the extent to which it can be seen as a natural experiment, that is, the extent to which all extraneous sources of variation are eliminated and only the exposure to the putative cause and the frequency of disorder vary between populations being compared. It is often the case that once substantial observational evidence has accrued, causality is widely accepted. However, it is desirable in etiologic epidemiology and almost universally required in evaluations of treatment that the final test of the hypothesis is in interventional or experimental studies. In experimental studies, the investigator causes individuals or groups of individuals in the population to receive the treatment in question. To demonstrate ethically the causal role of a risk factor for which there is only observational evidence, the investigator would prevent exposure to the risk factor for a group of people. In both types of interventional design strategies, a comparison group that does not receive the intervention is necessary. All other factors that might influence the outcome of the study (potential confounding factors) can be eliminated or controlled by the investigator. Because the conditions of the study are much more under control of the investigator, interventional studies can more closely approximate true experiments than can observational studies. When such studies are well designed and executed, they provide very strong support (or negation) for a hypothesis. All analytic study designs have potential problems of internal and external validity that must be solved by the investigator either in the study design or in the data analysis. Internal validity is the extent to which a study is a true test of the specific hypothesis, that is, the extent to which all possible biases of measurement or information and all possible confounding variables are eliminated as explaining the observed study result. External validity is the extent to which the study results can be generalized to the population of interest, namely, whether the study subjects are representative of the population at risk. If the potential validity problems have been solved in either the design or analysis of the study, the study evidence is strengthened. Because it is not possible to study the entire universe of potentially eligible subjects, epidemiologic studies are conducted on samples of the population of interest. Even a study of an entire city or the work force of a company constitutes a sample. The method of sampling should not introduce selection biases. For example, a volunteer study is potentially susceptible to selection
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Analytic epidemiology
bias because the health behavior and health status of people who volunteer for research are well documented to be better than those of refusers. No characteristics of the individuals should affect the likelihood of selection for the study, including their knowledge of the question at issue; their beliefs about the risk factors or about the cause of the disorder being studied; or any characteristic such as age, sex, or education that could be independently associated with both the disorder and the hypothesized causal factor. It is important for the internal validity of the study results that the information collected is accurate and complete. If there is inaccuracy (measurement error) in the information collected, the ability to detect the association of interest is reduced. If the accuracy of the information is worse for one exposure group than for another, the effect on the study results may not be predictable. For this reason, an evaluation of the accuracy (or validity) of measurements is necessary for any study. Research reports should describe the validity of the sources of information. Questionnaires or reporting methods that have been validated in the study population or in similar populations or circumstances should be used. The problem of validity of information is particularly important in research on occupational musculoskeletal disorders because the methods of both case diagnosis13 and measurement of work exposure17 have substantial limitations. Before specific study designs can be discussed, the term confounding must be defined. Confounding occurs when the study results can be explained by a factor extraneous to the hypothesis being tested. A potential confounding factor must be associated with both the disorder in question and the hypothesized causal factor. That is, the proportion of persons with the disorder having the confounding exposure must be different from the proportion of persons without the disorder with the confounding exposure. It is also necessary that the proportion of those with the hypothesized causal factor who have the confounding exposure are different from the proportion of those not exposed to the hypothesized causal factor who have the confounding factor. For example, a study that found an association between job satisfaction and the risk of occupational back injury could be confounded by the physical requirements of work if heavy work was a risk factor for back injury and was also associated with lack of job satisfaction in the studied population. Potential confounding factors can be eliminated in the design of the study by restricted or matched sampling or, in the data analysis phase, by stratified or multivariate analysis, for example. If in the study just described the statistical analyses controlled for physical requirements of work or if the researchers conducted an exploratory analysis and found no association between job satisfaction and the physical requirements of work, the potential for confounding would be eliminated. In experimental studies, potential confounding should be successfully eliminated by truly random blind assignment of subjects to the different treatments under study. Comparability of the treatment groups should be confirmed by presentation of the baseline characteristics of each group on entry to the study. Confounding invalidates a study as a test of the hypothesis. The study’s results cannot be taken as evidence of causality or efficacy of treatment. Lack of generalizability, as opposed to confounding, does not invalidate a study’s results but merely restricts inference to populations similar to those under study.
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Introduction to epidemiologic concepts in musculoskeletal disorders
Observational study designs are applicable in both clinical and etiologic epidemiology. In etiologic epidemiology the researcher tests whether a hypothesized factor is a determinant or cause of disorder in previously healthy people, whereas in clinical epidemiology one tests whether particular characteristics, risk factors, or clinical interventions are determinants of the prognosis or outcome. The classic observational analytic study designs are the cohort study, the case-control study, and the cross-sectional study.
Risk factor present
Target population
Risk factor absent
Figure 1.1
Disease or outcome does not occur
Sample
Cohort study (Prognostic study) The cohort study is the observational design that, when well designed and executed, produces the soundest results in terms of incidence rates and disorder etiology or prognostic determinants of all the observational study designs. The hallmark of a cohort study is that a population initially free of the outcome of interest is identified and characterized with respect to the hypothesized risk factor, important covariates, and potential confounders. The population is observed for a period of time adequate for development of the disorder, and the new cases (incident cases) are recorded. Rates of disorder development are compared between those exposed and those not exposed to the hypothesized risk factor. A study of prognostic factors related to return to work after episodes of absence due to work-related low-back-pain sickness is an example of a cohort study. The cohort consisted of all those first presenting to an occupational health clinic at a large municipal transportation agency for medical clearance for sick leave from work because of a complaint of work-related low back pain. These individuals were asked to complete a questionnaire on function, pain, satisfaction with work, and beliefs about pain. The occupational physicians conducting the sickness absence clearance examinations included assessment of gain, posture, and distribution of painful symptoms specific for back pain. Participants in the study were followed for 3 months, at which time the participant’s return to work status was determined. To identify which factors best predicted return to work, rates of return to work were compared between those with high and low scores on clinical signs and symptoms, function, pain, work satisfaction, and pain beliefs. Predictors that showed large differences in rates of return to work were interpreted as being strongly predictive.12 Cohort studies can be prospective in nature, meaning that a disorder-free population or group is initially identified and then subsequently tracked over time (Fig. 1.1). This same model can also be used with historical records. Employment records, for example, can be used to identify a group of new employees at a company. Job status and medical records can then be linked to these employment records to identify work exposures and the development of the disorder of interest. Studies that use historical records are called retrospective. Loss to follow-up is a potential problem in cohort studies. If a substantial proportion of subjects are lost to the study for any reason, for example, having moved out of the region, it would be expected that fewer cases of the disorder in question would arise in the study than originally planned. The number of study cases may ultimately be too small to yield stable estimates of the incidence rates and, consequently, estimates of the relative risk.
Disease or outcome occurs
Disease or outcome occurs Disease or outcome does not occur
Cohort study.
In this case, the observed relative risk would need to be very large to support the causal hypothesis. For example, consider a cohort study examining the causal role of occupational repetitive motion in carpal tunnel syndrome. New workers hired in 1985 through 1990 are enrolled and followed forward for 10 years, with information on new cases of carpal tunnel syndrome coming from the company medical department records. If 30% of the workers retire, take disability pensions, die, get another job, or leave the company for other reasons, there is a substantial loss to follow-up. A bias in loss to follow-up occurs if the workers who leave the company are those with the highest exposure to repetitive work movements and those who leave because upper extremity problems consistent with preclinical carpal tunnel syndrome are making it more difficult for them to do the job. The observed relative risk is an underestimate of the true relative risk because the detected incidence of carpal tunnel syndrome among those with repetitive-motion jobs is lower than the true incidence and the detected incidence among those not exposed is not affected. Biased loss to follow-up leading to underestimates of incidence in the unexposed would produce an inflated observed relative risk. High proportions lost to follow-up or higher proportions lost in one exposure category than another (selective loss to follow-up) leave open the possibility of biased loss to follow-up with consequent distortion of the study findings. Another form of selection bias can occur. This bias, called selective survival or selective attrition, occurs when people who have both the exposure and the disorder have a different probability of dropping out of the population available to be included in the study than do people who are not exposed and get the disorder. This type of bias can easily occur in cross-sectional and case-control studies. It can also occur in a particular variant of the cohort study called the prevalent cohort study. For example, a prevalent cohort study examining occupational repetitive motion as a risk factor for carpal tunnel syndrome that enrolled workers who were first employed between 1985 and 1990 and were still actively employed in 2005 could be affected by selective attrition if carpal tunnel syndrome by and large developed within 15 years of employment and workers tended to leave the company when carpal tunnel syndrome developed.
Chapter 1
Some diseases or disorders take many years to develop after the initial exposure to the presumed causal factor or take many years of exposure. The duration of time between the time of exposure to the presumed causal risk factor and the development of disease or disorder is called latency. Another problem concerns the prevalence of the disorder in the population. If a disorder is rare, many thousands of subjects may be required to identify and collect enough cases where the disorder occurs to be suitable for statistical analysis. Consequently, the cohort study design is not optimal in situations where the disorder of interest is both very rare and also has a long latency period. It can be more efficient in terms of time and the number of subjects studied to address the hypothesis by means of a case-control study, as described in the next section.
Case-control study The essential feature of the case-control study that differentiates it from the other observational study types is that individuals are selected for the study on the basis of the presence of the disorder in question (cases) and compared with individuals selected for the study on the basis of the absence of the disorder under study (control subjects). The presence or absence of the hypothesized causal factor is then ascertained in both case and control subjects. Although this appears on its face to be a simple undertaking, case-control studies present a number of methodologic challenges that must be solved for the study results to be valid (Fig. 1.2). A study of ergonomic risk factors for work absence due to onset of low back pain–related sickness conducted among Baltimore City workers is an example of a case-control study.10 Two hundred cases of absence due to back pain–related sickness were identified from the city’s occupational health department. Four hundred individuals without back pain but matched on gender, job classification, and department served as control subjects. In-person interviews were conducted to collect data on demographics, work history, psychosocial and work organization characteristics,
Risk Factor present? Disease present? Yes
Yes Sample
Cases No
Population Yes No
Sample
Controls No
Figure 1.2
Case-control study.
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Analytic epidemiology
and ergonomic factors related to work. Data on these factors were categorized. To analyze these data, the ratio of those exposed to the risk factor to those not exposed was calculated once for those with back pain and again a second time for those without back pain. A risk factor was interpreted to be associated with the back pain when the ratio of having the risk factor was higher among those with back pain as compared with those without back pain. Case-control studies frequently suffer from information biases. For example, if information on exposure to the risk factor of interest comes from a different source for case and control subjects, biased exposure information is possible. Recall bias, in which a case subject is more or less likely to recall an event in the past than is a control subject, is also possible. There is also the problem of unbiased recall failure, in which subjects are asked to recall events or conditions that took place so long ago they cannot be remembered. Establishing that exposure to the factor of interest took place long enough before the outcome to be a biologically plausible determinant is difficult for certain types of hypotheses; for example, a case-control study examining preexisting degenerative disk disorder as a determinant of chronicity (symptom duration greater than 6 months) in workers with chronic back pain could not establish that the disk problem predated chronicity based on clinical or imaging examinations at the time of study. These problems are avoided if the case-control study uses exposure or prognostic information that was recorded, for example, in medical or prescription records, long enough before the disorder condition being studied to be a biologically plausible cause and to obviate recall problems. Well-designed and well-conducted case-control studies may provide evidence as robust as that of cohort studies at considerably less cost and in considerably less time. However, because of the difficulty in avoiding the problems just described, casecontrol studies often produce weaker causal evidence than do cohort studies.
Cross-sectional study Cross-sectional studies simultaneously ascertain exposure to risk factors (or the presence of prognostic factors) and the presence of the disorder or outcome in question in a population sampled without regard to the presence of either. This type of sampling is sometimes called naturalistic sampling. In contrast to a cohort study, which follows subjects over time and ascertains incidence, a cross-sectional study ascertains conditions present at the moment of study, that is, the prevalence of the disorder or outcome in question at the time of the study. The estimates of relative risk derived from cross-sectional studies are therefore estimates of prevalence relative risk. Population-based crosssectional studies of low back pain often address, among other factors, the association of the type of work (occupation, physical requirements, and so forth) with low back pain (Fig. 1.3).2 Cross-sectional or survey studies are often undertaken because, unlike case-control studies, they require few a priori decisions with regard to the selection of subjects and, unlike cohort studies, it is not necessary to wait for the study outcome. These advantages are offset by their susceptibility to some of the problems of both cohort and case-control studies. When uncommon
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Introduction to epidemiologic concepts in musculoskeletal disorders
Risk factor present disease present
Risk factor present disease absent Study population
Sample Risk factor absent disease present
Risk factor absent disease absent Figure 1.3
Cohort Study
Feature Selective Survival Recall bias Loss to follow-up Time sequence of events Time to complete Expense
+ + − + − −
CaseControl Study + − + − + +
CrossSectional Study − − + − + +/−
Cross-sectional study.
disorders or exposures are being studied, a large number of people must be included, as in cohort studies. If information on exposures or on determinants of interest is collected at the time of the study rather than from previously existing records, there can be recall biases, recall failure, and problems in establishing the time sequence of events, just as in case-control studies. Nevertheless, for relatively common disorders (outcomes) and risk factors (determinants), cross-sectional studies may be a useful first step in exploring a hypothesis. Because of their many limitations, however, cross-sectional studies rarely produce robust results for evaluating the importance of causal or prognostic factors. When the literature on a problem consists predominantly of cross-sectional studies, it is often the case that the analytic epidemiology of that problem is in its infancy. Until recently, much of the epidemiologic information on occupational low back pain was derived from descriptive and cross-sectional studies.16 In the past 5 or 6 years there has been a substantial advance in the quantity and quality of observational analytic studies of work-related back pain. The epidemiologic investigation of upper extremity disorders began later than that of low back pain. Consequently, knowledge of the risk factors for work-related upper extremity disorders is less developed. The intrinsic strengths and limitations of the basic observational study designs are summarized in Table 1.1.
Experimental study designs: clinical trials The distinction between observational and interventional study designs is that in observational designs the investigator does not
Randomize
Patients
Table 1.1 Strengths (+) and limitations (-) of the observational study designs
Eligible
Experimental treatment
Successes/ Failures
Agree
Figure 1.4
Standard treatment Ineligible
Refuse
cause the exposure to the causal factor or treatment for the purposes of the study, whereas in interventional designs the investigator does cause subjects to be exposed to different factors or treatments. Observational study designs are susceptible to treatment assignment biases in which the treatment the patients receive is influenced by certain patient characteristics (e.g., lifestyle or clinical severity) that can confound the results. Clinical trials, in which the treating physicians or the investigators control which treatment patients receive, are also susceptible to such biases. For this reason, randomized controlled trials, where only chance influences which treatment eligible patients receive, are the preferred method of evaluating therapeutic interventions. The validity of randomized controlled trials depends on all the methodologic features described for the observational study designs and more. The study must be confined to those patients who have agreed to participate. Comparisons of treatment outcomes in patients who agree to participate with those in patients who refuse to participate are not valid. Assignment of patients to treatments must be done by using accepted methods of randomization, which are described in the report, and the resulting comparability of the treatment groups on important covariates should be described, usually in a table summarizing the baseline characteristics of the treatment groups. On the occasions when, by chance, randomization does not result in comparable groups, potential confounding must be controlled in the statistical analysis. Figure 1.4 is a schematic representation of appropriate design in a randomized controlled trial. Ordinarily, in randomized trials the treating physician and the patient are blind to which treatment group the patient has been assigned. If this is not possible, assessment of the study
Successes/ Failures
Randomized control trial.
Chapter 1
outcome should be done by an independent evaluator to avoid observer and participant biases in assessing the outcome. This is particularly important when the outcome being assessed is subjective. Information should be collected in the same way and with the same frequency in all treatment groups. Eligibility and exclusion criteria should be described and be appropriate to the question being addressed. Treatments should be clearly described, and patient compliance, dropouts from the study, and complications should be described and equivalent in both groups. Finally, the outcomes studied should be appropriate to the treatment or condition in question. A number of general health status assessment measures are used, for example, the SF-36, a standardized multidimensional assessment instrument that includes functional capacity, pain, locomotion, mental status, and affect. There are numerous assessment instruments for back pain disability, including the Oswestry,5 the Roland-Morris questionnaire,15 the Quebec Back Pain Disability Scale,8 the MaineSeattle back pain disability questionnaire,1 and others.3
STATISTICAL ISSUES Methods of analysis The statistical analysis of any study result should be appropriate to the hypothesis and to the structure of the data collected. When, for instance, the study examines the difference in Oswestry scores associated with a conditioning program as compared with usual care for subacute low back pain, comparisons of the mean scores in the treatment groups may be appropriate. If it is necessary to control for pretreatment differences between the groups, the analysis uses multivariate methods such as analysis of covariance or multiple regression. Occasionally, because of the statistical characteristics of the outcome being assessed, it may be necessary to transform it (e.g., log transformation, square root transformation) and analyze the transformed variable. It is often the case that the outcome variable distribution or the conditions of the study do not conform to the requirements of the usual statistical hypothesis tests such as t-tests, analysis of covariance, and regression analysis. In these cases, a nonparametric method of statistical analysis such as the Wilcoxon method is appropriate. When the hypothesis addresses the relative frequency of an event such as a back injury rate, a ratio can be formed consisting of the risk of development of the disorder among those exposed to the risk factor compared with the risk of the disorder among those not exposed to the risk factor. This ratio is called a relative risk. When the relative risk is 1, then the risk of the disorder is the same among those exposed to the risk factor as those not exposed. However, when the relative risk diverges from 1, then the risk is not the same between the exposed and unexposed groups. This is interpreted as evidence for an association between the risk factor and the disorder. The relative risk may be adjusted for important covariates or to eliminate potential confounding. Relative risks can be calculated only in those studies where the entire study population is tracked or a representative sample is identified, as would be the case in a cohort study. A relative risk cannot be calculated in situations where the study sample is not representative (e.g., as would be the case in a
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Statistical Issues
case-control study). Instead, an alternative to the relative risk needs to be used. The odds ratio is a measure of association that, in certain circumstances, can be used to estimate relative risk. The odds ratio is the ratio of the odds of the disorder in those exposed to the odds of the disorder in those unexposed. It also has valuable statistical properties because it can be estimated by using logistic regression. The effects of confounding variables can be controlled or the simultaneous effects of several causal variables or covariates can be estimated by using multiple logistic regression. Another measure of association can be found in studies that examine the rate of the development of a disorder in a population over time. In these studies, the risk of developing a disorder within a cohort changes for each point in time. As members of the cohort develop a disorder, the total number of individuals in the cohort still free of the disorder becomes smaller and the calculation of risk changes. A survival curve shows the cumulative proportion of cohort members remaining free of the disorder on the vertical axis and time on the horizontal axis (Fig. 1.5). Typically, survival curves show an exponential relationship between cumulative proportion remaining free of the disorder and time. We can examine whether the survival experience is different between members of a cohort with different exposure profiles by using statistical tests specific for this type of analysis, such as the log-rank test.9 Hazard is a term that expresses the rate of change of the cumulative proportion surviving with time. In prognostic studies it is possible to compare whether the rate of change of survival (hazard) is different between exposure groups. A useful property of hazards is that this term can be modeled using logistic regression techniques. The Cox proportionate hazards model is used to evaluate differences in hazard between exposure groups. The hazard ratio is interpreted much like the relative risk or odds ratio. When the hazard ratio is equal to 1, then the survival experience is interpreted to be the same among exposure groups. When the hazard ratio is not equal to 1, the interpretation is that there is an association between exposure to the risk factor and survival experience related to the disorder of interest.9 An advantage of survival analysis is that all study subjects contribute information for as long as they remain in the study. The reader should be aware, however, that if the number of dropouts during the course of the study is substantial, estimates of the hazard ratio toward the end of the follow-up period are based on relatively small numbers and are consequently unstable.
Estimates and confidence limits Research is conducted on a sample of persons or other units of observation drawn from a target population. The results of any given study are estimates of the true means, proportions, relative risks, and so forth in the population from which the samples were drawn. The precision of a study estimate of the population value, or parameter, of a measurement is described by the standard error of estimate. The standard error (SE) is the square root of the ratio of the variance (s2), or variability of the measurement in the sample, to the number of subjects (N) in the study. For example,
SE mean =
s2 N
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Introduction to epidemiologic concepts in musculoskeletal disorders
Percent returning back to any work
100%
75%
50%
Figure 1.5 Return to any work from sick absence because of nonspecific low back pain (n = 225). (From Hiebert R, Skovron ML, Nordin M: Work restrictions and outcome of nonspecific low back pain. Spine 28(7): 722-728, 2003. Reprinted with permission.)
25%
0% 0
90
180
270
364
Time lost from work because of LBP (in days) No restrictions Some restrictions
Variance is affected by a number of factors, including interindividual variability, intraindividual variability (such as diurnal variations), and instrument variability. Designing or executing a study to reduce any of these components reduces the variance of the measurement, thus reducing the standard error and increasing the stability of the estimate of the population parameter. The larger the number of subjects on whom the estimate is based, the smaller the standard error and the more confident we can be in its representation of the population parameter. Because sample results are estimates of population parameters, it is increasingly becoming the standard of reporting to describe the precision of the estimates as a range within which the population parameter probably lies. This is the confidence limit around the estimate and is by convention expressed as the 95% confidence limit. For example, the 95% confidence limit for a mean is approximated by 95% confidence interval = mean ± 2(SEmean)
Statistical hypothesis testing Because there is always sampling error, estimates may be expected to vary from sample to sample. Consequently, study results must be subjected to statistical hypothesis testing; that is, study results must be tested to determine the probability that the observed results from a specific study could have occurred by chance alone. The statistical hypothesis test evaluates the null hypothesis that the observed study results occurred because of sampling error when there was no true association in the population from which the study subjects were sampled. The probability of making this type of error is designated as alpha (α). If the observed association is large enough that this kind of error is improbable, the null hypothesis is rejected. The investigators then accept the alternative hypothesis, that the observed estimates of relative risk
or differences between treatments reflect the true situation in the population from which the samples were drawn. By convention, the cutoff for rejecting the null hypothesis is usually set at 0.05. Then if the probability (p value) that the observed results are due to sampling error is less than 0.05, that is, less than α, the null hypothesis is rejected and the results are declared statistically significant. Thus, statistically significant results are simply results that we have decided, within an acceptable margin of error, probably did not occur by chance. Further, the larger the observed association relative to the underlying variability of the outcome being measured, the more likely that it will be declared statistically significant.
Statistical power and sample size Statistical hypothesis tests actually involve two probabilities. The probability of making a type I error by incorrectly rejecting the null hypothesis, that is, by declaring an observed association to be statistically significant when in fact it is the result of sampling error, is referred to as α, as described in the preceding paragraph. There is also the probability of incorrectly accepting the null hypothesis; that is, declaring that the study results are due to sampling error (not statistically significant) when in fact they reflect a true association in the population from which the study subjects were drawn. This is the type II error and its probability is beta (β). The complementary probability that a study will be able to correctly reject the null hypothesis when it is false, that is, correctly detect an association when there is one in the population at large, is referred to as statistical power (1 – β). Table 1.2 illustrates the different conditions and possible results of a statistical hypothesis test. In the planning phase of research the investigators should make a determination of how strong an association would be clinically significant, that is, how large an estimated relative risk
Chapter 1
Table 1.2 Population conditions, statistical hypothesis test results, error types, and designations Hypothesis Test Result
Population Condition
Accept null hypothesis NULL HYPOTHESIS TRUE No association NO ASSOCIATION Correct Reject null hypothesis Type I error (alpha) Association exists
NULL HYPOTHESIS FALSE ASSOCIATION EXISTS Type II error (beta) Correct
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References
result should be specified, the plan of statistical analysis determined, and the necessary number of study subjects defined. Study management should avoid the introduction of differential loss to follow-up, unblinding, and other potential problems. The statistical analysis should be appropriate to the structure of the data and to the hypothesis. Finally, although the discussion should place the study in the context of other work and what is already known about the question, the specific conclusions should not go beyond what was actually tested.
REFERENCES or how big a difference between treatments. Because the validity of the study requires that it be a true test of the research hypothesis, it is important to design the study so that a clinically significant association will have a good chance of being declared statistically significant, that is, so that the study has sufficient power to detect a clinically significant association. The larger the sample size, the more power the statistical test has to detect associations; in other words, as expected differences or relative risks get smaller, the number of subjects studied must increase to have adequate power to test the hypothesis. Conversely, with very large numbers of study subjects it is possible to declare trivial associations statistically significant. When studies with small sample sizes report results that are not statistically significant, they should also report how large an association would have been required for there to have good power to detect it. The reader should also evaluate whether the observed difference and its upper confidence limit, although not statistically significant, are clinically significant. When studies with huge numbers of subjects report statistically significant results, the reader should decide whether the differences are trivial in clinical terms, even though they are statistically significant.
1.
2.
3.
4. 5. 6. 7. 8. 9. 10. 11.
SUMMARY
12.
The validity of clinical research depends on a number of factors. The hypothesis must be formulated specifically enough to be testable. The appropriate study subjects should be eligible, and there should not be differential participation. The information collected should be appropriate to the hypothesis and accurate. The study design and information sources should avoid potential information biases. Potential confounders should be eliminated in the study design or controlled in the statistical analysis. At the time the study is designed, a clinically significant hypothesized
13.
14. 15.
16. 17.
Atlas SJ, Deyo RA, van den Ancker M, Singer DE, Keller RB, Patrick DL: The Maine-Seattle back questionnaire: a 12-item disability questionnaire for evaluating patients with lumbar sciatica or stenosis: results of a derivation and validation cohort analysis. Spine 28(16):1869-1876, 2003. Bernard BP, ed: Musculoskeletal disorders and workplace factors: a critical review of epidemiologic evidence for work-related musculoskeletal disorders of the neck, upper extremity, and low back. U.S. Dept. of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention. Cincinnati, OH, 1997, National Institute for Occupational Safety and Health. Bombardier C: Outcome assessments in the evaluation of treatment of spinal disorders: summary and general recommendations. Spine 25(24):3100-3103, 2000. Bureau of Labor Statistics, US Labor Department, Annual Survey 2003, Tables R19, 22. Fairbank JC, Pynsent PB: The Oswestry Disability Index. Spine 25(22):2940-2952; discussion 2952, 2000. Gyntelberg F: One-year incidence of low back pain among male residents of Copenhagen aged 40-59. Danish Med Bull 21:30-36, 1974. Kelsey JL, Thompson D, Evans AS: Methods in observational epidemiology. New York, 1986, Oxford University Press. Kopec JA, Esdaile JM, Abrahamowicz M, et al: The Quebec Back Pain Disability Scale: measurement properties. Spine 20(3):341-352, 1995. Lee E: Statistical methods for survival data analysis. Belmont, CA, Lifetime Learning Publications, 1980, Wadsworth Inc. Myers AH, Baker SP, Li G, et al: Back injury in municipal workers: a case-control study. Am J Public Health 89(7):1036-1041, 1999. National Research Council and the Institute of Medicine. Musculoskeletal disorders and the workplace: low back and upper extremities. Panel on Musculoskeletal Disorders and the Workplace. Commission on Behavioral and Social Sciences and Education. Washington, DC, 2001, National Academy Press. Nordin MN, Skovron ML, Hiebert R, et al: Early predictors of delayed return to work in patients with low back pain. J Musculoskel Dis 5(2):5-27, 1997. van den Hoogen HM, Koes BW, van Eijk JT. On the accuracy of history, physical examination, and erythrocyte sedimentation rate in diagnosing low back pain in general practice. Spine 20:318-327, 1995. Praemer A, Furner S, Rice DP: Musculoskeletal conditions in the United States. Rosemont, IL, 1999, American Academy of Orthopaedic Surgeons. 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(2): 141-144, 1983. Skovron ML: Epidemiology of low back pain. Baillieres Clin Rheumat 76:559-573, 1992. Winkel J, Mathiassen SE: Assessment of physical work load in epidemiologic studies: concepts, issues and operational considerations, Ergonomics 37:979-988, 1994.
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2
Psychosocial Aspects of Work-Related Musculoskeletal Disorders: Clinical Implications Sherri Weiser
Until recently, attempts to unravel the mystery of work-related musculoskeletal disorders (MSDs) concentrated on the physical demands of the job and the physical vulnerabilities of the worker. It became clear that this problem did not easily lend itself to reductionistic approaches. Although certain physical loads and tasks have been associated with the development of musculoskeletal problems, the strength of these associations has been disappointingly weak.29 Furthermore, a determination of physical vulnerability before injury is nearly impossible. Even when a physical defect such as disk herniation has been established in conjunction with a report of pain, the correspondence with actual disability is often low. Like all human conditions, MSDs can be infinitely complex. A thorough understanding of these disorders requires a consideration of influences beyond the physical. The worker’s psychologic attributes and social reality may have significant bearing on the onset, progression, and outcome of occupational MSDs. A biopsychosocial perspective offers much in the way of understanding these disorders. Adoption of the biopsychosocial model in pain and disability research has resulted in the identification of specific psychologic and social aspects of MSDs. Recently, this research has been summarized in a number of excellent review articles and treatment guidelines, conclusions from which are discussed. The biopsychosocial model implies not just the inclusion of psychologic and social considerations but a new perspective on the part of all stakeholders involved in the prevention and treatment of MSDs. This chapter describes how to achieve the goal of preventing and treating the disorder in practical terms.
THE BIOPSYCHOSOCIAL MODEL The notion of a link between the mind and body has existed throughout history. It was Walter Canon,2 however, who substantiated this idea with his scientific explanation of the “fight or flight” response. His research identified the organism’s physical reactions to psychologic stress. Selye24 later showed how these responses, if left unchecked, can over time cause severe damage
to vulnerable organs and body systems and may even cause death. Today, the relationship between the mind and the body is studied extensively. Psychologic factors have been shown to affect a spectrum of diseases involving virtually all bodily organs and systems.8 First described by Engel in 1977,5 the biopsychosocial model extends beyond mind and body to include the impact of social factors on illness. Influenced by models of stress and illness, Engel concluded that any illness must be viewed from a multidimensional perspective that takes biologic, psychologic, and social factors into consideration.5 Furthermore, these factors are not independent, as a medical model would suggest, but interrelated. It was by understanding this perspective, Engel believed, that physicians would be prepared to take on the complexities of health and illness. The biopsychosocial model soon became the prevailing view among those involved in pain research. In 1965 the gate control theory outlined the channels of pain transmission through neurologic pathways.19 This theory further asserted that pain transmission may be modulated by cognitive and affective states. This model was fundamental in explaining the disparities between physical findings and the phenomenologic experience of pain. The gate control theory laid the groundwork for modern approaches to treating chronic pain. In 1992, Waddell28 presented a detailed analysis of low back pain with the use of a biopsychosocial model (Fig. 2.1). The many levels on which pain is experienced are defined in the model. The physical injury is interpreted cognitively, resulting in a corresponding emotion. A man who believes that he has a herniated disk, for example, is more apt to be anxious and depressed than a man who believes that he has a sprain. The man with the “herniated disk” may also display more avoidance behavior initially than the man who believes he sprained his back. This process takes place within a social context that is constantly providing feedback and modifying the individual’s response. Waddell also pointed out that feedback loops exist among all levels in the model and that a change in one component affects the others. If the man with the supposed herniation sees a physician and is assured that the problem is only a sprain, his belief has changed. As a result, his affect and pain behavior will change,
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Psychosocial aspects of work-related musculoskeletal disorders
Social environment
PSYCHOLOGIC AND PSYCHOSOCIAL FACTORS ASSOCIATED WITH MSDs Illness behavior
Affective
Cognitive
Sensory
Figure 2.1 A cross-sectional analysis of the clinical findings and assessment of low back pain and disability at one point in time. (From Waddell G: Biopsychosocial analysis of low back pain. In M Nordin, TL Vischer, eds: Common low back pain: prevention of chronicity. London, 1992, Bailliere Tindall.)
and nociception may be experienced as less severe. These feedback loops are particularly important in chronic low back pain, wherein the original injury is often resolved. In these cases, psychologic and social variables are even greater determinants of functional status than in cases of acute back pain when nociception is responsible for much of the illness behavior. Occupational musculoskeletal injuries are clearly amenable to biopsychosocial analysis. They either occur at work or are believed to be its result. The cognitive, affective, behavioral, and social elements of such an injury are therefore inextricably related to the workplace. Injuries or disorders that did not occur at work may also be considered work-related if attitudes or beliefs about work affect recovery. If an injured worker fears that returning to work will exacerbate an injury, for example, recovery may be delayed. Recently, a number of studies have demonstrated the impact of psychologic and social factors on occupational musculoskeletal injuries. What has emerged is evidence that these factors have as much, and in some cases more, predictive value as physical and environmental factors. The main findings from recent critical review articles and current studies are discussed below. Most of the articles refer to nonspecific disorders of the spine; research has centered on these conditions because they account for most of the associated costs and suffering caused by the disorder. Some reviews include the upper extremities as well. To date, no high quality study of workrelated lower extremity injuries that explores psychosocial factors has been found.
Psychologic factors refer to cognitions or beliefs about pain and disability and affective or emotional responses, whereas psychosocial factors reflect an individual’s perceptions of others and the environment. Recent systematic evidence-based reviews have concluded that even when measured early in the injury, both these factors are stronger predictors than physical factors of outcomes such as work status. The Clinical Guidelines for the Management of Acute Low Back Pain, published in 2001, state that in addition to social and economic factors, psychologic factors play an important role in the development of chronic low back pain and disability and influence a patient’s response to treatment and rehabilitation.30 Specifically, beliefs that activity and work will make pain worse (fear-avoidance beliefs) and that the patient is not responsible for the pain or treatment along with behaviors intended to communicate that the patient is in pain (illness behaviors) are associated with poor outcome. Using strict inclusion criteria, in 2001 Koes et al13 published a comparison of clinical guidelines for the management of low back pain from 11 different countries that appeared from 1994 until 2000. They found that in most regards the content of the guidelines appeared to be quite similar and that all recognized the importance of psychologic and psychosocial factors, including work perceptions, in the development and maintenance of low back pain. Indeed, the New Zealand Guidelines for assessing acute low backpain, updated in 2003, likewise finds good agreement that beliefs, mood states, and behaviors, such as those identified by Waddell et al,29 consistently predict poor outcome.21 One of these is the belief that work will make the pain worse, evidence for which is so compelling that investigators have labeled this risk factor one of the “yellow flags.” Yellow flags are defined as factors that may increase the risk of developing or perpetuating long-term disability and work loss associated with low back pain. The New Zealand group recommends their assessment as early as 2 weeks after injury. Occupational health guidelines for low back pain were published in 2001. Although the effect size was small, strong evidence was found that psychosocial factors are associated with the risk of onset of low back pain in symptom-free workers. In the workplace, psychosocial factors are stronger predictors of care seeking and disability than clinical symptoms or physical work demands. Specifically, negative work perceptions were risk factors for symptom reports, health care utilization, and work loss. The most important factors associated with delayed recovery and response to treatment were beliefs that work caused the pain and expectations about recovery.29 A comparison of international occupational low back pain guidelines shows them in complete agreement that the early assessment of these risk factors was important if the patient exceeds the expected recovery time.25 Other reviews of factors affecting low back pain outcomes show similar results but call for more stringent scientific investigation of the interrelationships. For example, Hoogendoorn et al10 reviewed the literature and found that low workplace social support and low job satisfaction were related to reports of
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What is the relationship between psychosocial factors and work-related MSDs
back pain, but most studies failed to adjust for psychosocial work characteristics and physical load at work. Crook et al4 determined from their review that among other factors, psychologic distress and work environment characteristics were important prognostic factors. They noted, however, that most studies failed to investigate interactions among psychologic, social, and physical variables. Likewise, Pincus et al23 noted a lack of rigorous prospective studies that evaluated the role of psychologic factors in the development of chronicity. Of 25 publications, only 6 met their acceptability criteria for review. Depression, distress, and to a lesser extent somatization were the psychologic factors most strongly linked to low back pain disability. Catastrophizing by disabled workers as a coping strategy received weak support. The role of coping in conjunction with psychologic factors remains unclear. Although there are fewer studies on upper extremities than on back pain, thus far similar factors seem to be related to both disorders. In another review article, higher levels of perceived job demands and stress were the psychosocial factors most consistently linked to upper extremity disorders. Epidemiologic reviews revealed also that psychosocial factors unrelated to work, such as general worry/psychologic tension, depression/anxiety, general coping style, and response to pain, are likewise associated with both back and upper extremity disorders.15 Systematic reviews on this topic have not, however, been conducted. An interesting study by Ijzelenberg et al11 investigated whether individual, work-related physical, and psychosocial risk factors involved in the occurrence of musculoskeletal complaints also determined musculoskeletal sickness absence. Using a crosssectional study design and self-administered questionnaire, investigators collected data on individual and work-related risk factors and the occurrence of musculoskeletal complaints and musculoskeletal sickness absence among 373 employees of laundry-works and dry-cleaning businesses. Results show that both work-related physical factors and psychosocial factors showed strong associations with low back pain and upper extremity complaints. Workrelated physical factors did not influence sickness absence, however, whereas psychosocial factors showed some associations with it. This finding supports the notion that illness behaviors such as work absence are modified by cognitive and affective responses to physical symptoms in neck and back disorders. Linton15 systematically reviewed numerous studies of variable methodologic quality that looked at the effects of various psychologic factors on neck and back pain and concluded that there is a clear link. Prospective studies indicate, furthermore, that psychologic variables are related to the onset of pain and to all of its phases: Certain factors such as distress, anxiety, cognitive functioning, and pain behavior were found to be significant at all stages from acute to chronic pain. Still, psychologic factors account for only a portion of the variance, underscoring the importance of a multidimensional view. Luo et al16 found a variety of factors, including general stress, depression, and anxiety, to be associated with neck pain disability. Carroll et al3 confirmed the role of depression as a risk factor for pain onset. They followed a population-based random sample of adults and assessed them at 6 and 12 months. Controlling for demographic and socioeconomic factors, health status, comorbid medical conditions, and injuries to the neck or low back,
they found an independent and robust relationship between depressive symptoms and onset of a pain episode. They concluded that depression is a strong and independent predictor for the onset of an episode of intense and/or disabling neck and low back pain.
WHAT IS THE RELATIONSHIP BETWEEN PSYCHOSOCIAL FACTORS AND WORK-RELATED MSDs? There are a number of ways to explain the effect of psychosocial factors on MSDs. Perhaps the most straightforward explanation is that workers who are depressed or dissatisfied at work simply report more symptoms and disability than those who are content at their jobs. Distress in life and work may cause extra attention to be paid to symptoms, and therefore the signs are experienced as more troubling. This does not imply that workers are intentionally making more of symptoms than is warranted but that they are more likely to notice symptoms that can distract them from their daily routines. Another popular explanation is that stress results in increased muscle tension, causing spasms and ischemia, a painful condition resulting from oxygen reduction and the release of painproducing chemicals. Over time this pain may cause more distress, leading to a chronic cycle of stress and pain. Some laboratory studies have demonstrated an increase in muscle activation under stress,18 but findings have been inconsistent among patients with chronic pain. This may be because stress-induced muscle tension has a role in the development of chronic pain, but once patients are chronic their reactivity to stress becomes altered in ways that are unclear at present. The National Research Council and the Institute of Medicine reviewed evidence for the relationship between psychologic and physical factors and concluded that data exist to support a direct role of the central nervous system.20 This may help to explain how psychologic processes such as attention and emotion influence pain and its tolerance, an explanation supported by studies showing that pain is linked to a tendency to somatize or focus on symptoms.17 Other theories mentioned in the review include physiologic changes that occur under stress and result eventually in musculoskeletal pain. Stress hormones may facilitate the transmission of painful stimuli; physically stressful work tasks are associated with an increased release of stress hormones and slower recovery times. One reason for this may be that stress hormones affect the health of muscles, tendons, and ligaments and impede inflammatory or immune responses. Other factors such as behavior or life-style may moderate the effects of stress on muscle tension and biochemical changes. The concept of “work style” has been proposed to define how individuals interact with work demands.6 Originally proposed to explain work-related upper extremity disorders, work style is defined as cognitive, behavioral, and physiologic components of the stress response expressed behaviorally in movement, posture, and activity. Workers who respond to physical or psychologic workplace demands with a “high-risk” work style display excessive attempts to cope with stress and are susceptible to its negative
15
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Psychosocial aspects of work-related musculoskeletal disorders
consequences such as continuous arousal or reactivity. Similarly, Marras et al18 found that characteristic ways of responding to the environment were predictive of spinal loading. During a lifting task, introverts tend to exhibit muscle coactivation and alteration in movement patterns higher than those of extroverts. Stress-related behaviors such as these have been linked to symptom severity, functional limitations, and work disability.9 It is clear that the relationship between psychologic distress and physical responses is not simple. More research is needed to develop detailed models of the stress–pain relationship. Although various pathways have been proposed, there is a need to understand causal pathways and interactions among stresses and responses. Most likely there is no simple explanation of this relationship, and these proposed pathways are not mutually exclusive but work together in an ongoing dynamic way to result in MSDs. It is possible also that the stress pathways discussed here have variable influences in different stages of pain. What began as pain related to muscle tension, for instance, may over time develop into neuropathic pain. In addition, more clarity is needed in defining outcome measures, because different factors may moderate stress and physical complaints, sick absences, and disability.
PSYCHOSOCIAL INTERVENTIONS FOR MSDs
Physicians should share with distressed patients information about treatment philosophies and their possible outcomes. At the very least, physicians should be aware of the treatment philosophy of any facility to which they are referring patients, ideally one that adheres to current guidelines for the treatment of acute low back pain. The occupational health guidelines for the management of low back pain summarize recommendations for physicians to minimize the likelihood of chronic problems29: ● Reassure the worker and provide adequate information about the self-limiting nature and good prognosis of lower back pain. ● Advise the worker to continue normal activity and work or to return to them as soon as possible, even if there is still some pain. ● Because most workers with lower back pain manage to return to more or less normal duties quite rapidly, consider temporary adaptations of work duties or hours only when necessary. ● If a worker fails to return to work within 2-12 weeks (different guidelines vary considerably about the time scale), refer him or her to a gradually increasing exercise program or multidisciplinary rehabilitation (exercises, education, reassurance, and pain management following behavioral principles). These rehabilitation programs should be embedded in an occupational setting.
Most individuals at risk for MSDs can be effectively managed by their usual treatment provider, without the need for referral to a psychologist. Appropriate information and advice from the physician can reduce anxiety and improve patient satisfaction with care. Every encounter with health care professionals and medical management systems provides an opportunity for intervention. Waddell28 astutely observed the powerful effects a physician can have on the patient. Information that is vague, incomplete, or incomprehensible to a lay person can render the patient confused, helpless, and afraid. In the mind of a patient, the diagnosis of a herniated disk, for example, can be a sentence to disability. Diagnostic film results are often held up as proof by patients fearful of permanent disability. It is the health care provider’s responsibility to explain the implications of any diagnosis in terms the patient can understand. In the case of disk herniation, the patient needs to know that pain and disability are often self-limiting and that many people with this condition maintain their usual life-styles. Making sure that the patient has a realistic picture of the diagnosis and the prognosis is the first step. Patients who seem overly distressed can be questioned about other life circumstances. When the injury is work related, questions about work are particularly important. Often, patients feel residual anger toward the employer, sometimes believing that it is the employer’s responsibility to make sure they get well. Even if not responsible for their injuries, patients who understand the normal course of low back pain and are encouraged to take responsibility for their recovery from the onset may be spared the ordeal of becoming a compensation failure. Primary health care professionals have a responsibility also to make appropriate referrals. Information given by the physician can be reinforced or contradicted by secondary caregivers. One of the major causes of distress, contradictory information can lead to endless doctor shopping and prolongation of recovery.
Based on the conclusion that active care is superior to passive therapy, treatment guidelines recommending active and goal-oriented physical therapy should be the first course of treatment. Research has shown that the specific type of exercise prescribed is less important that the overall therapy philosophy. The objective should be to increase gradually the individual’s capacity for work with a balanced strength, flexibility, and cardiovascular program. Specific goal setting ensures that improvement is monitored, whereas positive feedback rewards productive behavior. The easiest program to implement early in treatment, a behavioral approach pioneered by Fordyce,7 consists of time-contingent care in which medication levels, exercise goals, and duration of treatment are preset and not determined by the patient. The idea is to provide environmental contingencies that reinforce “well” behavior and ignore “pain” behavior. In a benchmark study, Fordyce7 compared this approach with traditional care in which patients were told to “let pain be your guide.” Subjects with back pain for less than 10 days were randomly assigned to one of the two protocols and were followed at 6 weeks and 9 to 12 months after treatment. Although no differences were noted at 6 weeks, long-term follow-up showed significantly greater improvement in functioning for the treatment group. Like MSDs, physical therapy may be viewed from a biopsychosocial perspective. In contrast to passive modalities, an active approach shifts the responsibility to patients and provides techniques that they can use themselves to maintain fitness. As such, it increases the patient’s sense of control and may be instrumental in changing negative beliefs about pain. With improvement, the patient’s fears of returning to work should subside. After 2 weeks, patients who are not achieving weekly goals should be referred for a psychosocial evaluation. If warranted, they can begin a multidisciplinary program that addresses psychosocial issues. By their very nature these types of programs address physical, psychologic, and social concerns simultaneously.
Chapter 2
A multidisciplinary approach in treating patients with chronic pain is fairly standard,31 but the application of a biopsychosocial model in the acute and subacute phases of treatment as well is gaining popularity.
EVIDENCE No randomized controlled studies have assessed the use of psychologic interventions alone for MSDs, and high-quality studies that assess the effectiveness of multidisciplinary care for
Onset of pain • Explain the biopsychosocial model • Address concerns about pain, including the course, diagnosis, and prognosis • Emphasize the patient's role in recovery • Make appropriate referral if indicated
Four weeks after • Address concerns again, old and new • Address social factors again • Reinforce patient's role in recovery again • Refer for multidisciplinary evaluation and possible treatment Figure 2.2
●
Evidence
occupational MSDs in general are few. Nonetheless, in line with international opinion, expert panels have recommended the use of multidisciplinary team management for episodes of acute low back pain that is unresolved between 2 and 6 weeks, when patients risk chronic disability. Evidence clearly shows that multidisciplinary teams or networks are effective in managing chronic back pain,14,22,27 but their effectiveness for returning chronic patients to work remains unclear. Some studies showed good outcomes for chronic low back pain patients who are highly motivated to return to work,1 but randomized trials have yet to be done.
Two weeks after • Address concerns again, old and new • Address social factors including attitudes about work, as well as family and friends' responses to pain • Reinforce patient's role in recovery again • Make appropriate referral if indicated
Seven weeks after • Address concerns again • Address social factors again • Reinforce patient's role in recovery • Refer for multidisciplinary evaluation and treatment
Application of the biopsychosocial model: general guidelines for primary health care providers.
17
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Psychosocial aspects of work-related musculoskeletal disorders
Karjalainen et al12 conducted a Cochrane review of multidisciplinary programs for subacute low back pain patients. They concluded that “there is moderate evidence of positive effectiveness of multidisciplinary rehabilitation for subacute low back pain and that a workplace visit increases the effectiveness.” This endorsement is guarded because the only two articles that fit their inclusion criteria were only of moderate quality. However, more support for this treatment in the subacute phase was provided by van den Hout et al.26 In a randomized study, they showed that adding training in problem solving to a graded activity program improved outcome. The Work Loss Data Institute considered but did not recommend multidisciplinary or cognitive-behavioral treatment for upper extremity pain due to lack of studies.32 New studies should consider other MSDs as well. Future research would benefit also from a comprehensive multivariate causal model that would allow the assessment of interactions among psychologic, social, and physical variables. Adjustments for workload could be made when studying the effects of other factors; such a model would also permit an understanding of how these risk factors emerge during the transition from acute to chronic problems.
SUMMARY Traditional treatments for occupational MSDs have fallen short of expectations. The biopsychosocial model goes beyond physical factors to include psychologic and psychosocial elements that affect the worker before and after an injury. Investigations into the practical application of this model are most convincing. Studies have shown that psychosocial factors are at least as important as and often more important than physical factors in determining disability. Programs that have attempted to prevent injury or chronicity associated with occupational low back pain have flourished when they include a biopsychosocial framework. Though more research is needed, it is suggested that our best option is for primary health care providers and all health care practitioners to apply a biopsychosocial model in the same fashion for all MSDs that do not respond to traditional care (Fig. 2.2). Because we all share the burden of disability, we must all share in the solution. Much can be done by all medical professionals to make this process easier and more successful for everyone. For physicians, establishing a good rapport with the patient, giving clear and intelligible information, encouraging an active approach to treatment, and making appropriate referrals at the first sign of delayed recovery can go a long way toward reducing occupational MSDs. Physical therapists can follow a behavior model of active care that encourages patient responsibility for outcome and reinforces function over pain.
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Crook J, Milner R, Schultz IZ, Stringer B: Determinants of occupational disability following a low back injury: a critical review of the literature. J Occup Rehabil 12(4):277-295, 2002. Engel GL: The need for a new medical model. Science 196:129-136, 1977. Feuerstein M: Workstyle: definition, empirical support, and implications for prevention, evaluation, and rehabilitation of occupational upper-extremity disorders. In SD Moon, SL Sauter, eds: Beyond biomechanics: psychosocial aspects of musculoskeletal disorders in office work. Bristol, PA, 1996, Taylor & Francis, pp. 177-206. Fordyce WE: Acute back pain: a control group comparison of behavioral vs. traditional management methods, J Behav Med 9:127-140, 1986. Goleman D, Gurin D, eds: Mind body medicine: how to use your mind for better health. New York, 1993, Consumer Reports Books. Haufler AJ, Feuerstein M, Huang GD: Job stress, upper extremity pain and functional limitations in symptomatic computer users. Am J Ind Med 38(5):507-515, 2000. Hoogendoorn WE, van Poppel MN, Bongers PM, Koes BW, Bouter LM: Systematic review of psychosocial factors at work and private life as risk factors for back pain. Spine 25(16):2114-2125, 2000. Ijzelenberg W, Molenaar D, Burdorf A: Different risk factors for musculoskeletal complaints and musculoskeletal sickness absence. Scand J Work Environ Health 30(1):56-63, 2004. Karjalainen K, Malmivaara A, van Tulder M, et al: Multidisciplinary biopsychosocial rehabilitation for subacute low back pain among working age adults. Cochrane Database Syst Rev (3):CD002193, 2000. Koes BW, van Tulder MW, Ostelo R, Burton K, Waddell G: Clinical guidelines for the management of low back pain in primary care: international comparison. Spine 26(22):2504-2513, 2001. Koopman FS, Edelaar M, Slikker R, Reynders K, van der Woude LH, Hoozemans MJ: Effectiveness of a multidisciplinary occupational training program for chronic low back pain: a prospective cohort study. Am J Phys Med Rehabil 83(2):94-103, 2004. Linton SJ: A review of psychological risk factors in back and neck pain. Spine 25(9):1148-1156, 2001. Luo X, Edwards CL, Richardson W, Hey L: Relationships of clinical, psychologic, and individual factors with the functional status of neck pain patients. Value Health 7(1):61-69, 2004. Main CJ, Wood PL, Hollis S, Spanswick CC, Waddell G: The distress and risk assessment method: a simple patient classification to identify distress and evaluate the risk of poor outcome. Spine 17(1):42-52, 1992. Marras WS, Davis KG, Heaney CA, Maronitis AB, Allread WG: The influence of psychosocial stress, gender, and personality on mechanical loading of the lumbar spine. Spine 25(23):3045-3054, 2000. Melzack R, Wall P: Pain mechanisms: a new theory. Science 150:971-979, 1965. National Research Council and the Institute of Medicine: Musculoskeletal disorders and the workplace: low back and upper extremities. Panel on Musculoskeletal Disorders and the Workplace. Commission on Behavioral and Social Sciences and Education. Washington, DC, 2001, National Academy Press. New Zealand Guidelines Group: New Zealand acute low back pain guide. Wellington, NZ, October 2004, Accident Compensation Corporation. Patrick LE, Altmaier EM, Found EM: Long-term outcomes in multidisciplinary treatment of chronic low back pain: results of a 13-year follow-up. Spine 29(8):850-855, 2004. Pincus T, Burton AK, Vogel S, Field AP: A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine 27(5):E109-E120, 2002. Selye H: The stress of life. New York, 1956, McGraw-Hill. Staal JB, Hlobil H, van Tulder MW, et al: Occupational health guidelines for the management of low back pain: an international comparison. Occup Environ Med 60(9):617, 2003. van den Hout JH, Vlaeyen JW, Heuts PH, Zijlema JH, Wijnen JA: Secondary prevention of work-related disability in nonspecific low back pain: does problem-solving therapy help? A randomized clinical trial. Clin J Pain 19(2):87-96, 2003. van Tulder MW, Ostelo RWJG, Vlaeyen JWS, Linton SJ, Morley SJ, Assendelft WJJ: Behavioural treatment for chronic low-back pain (Cochrane Review). In The Cochrane Library, Issue 3. Chichester, UK, 2004, John Wiley & Sons, Ltd. Waddell G: Biopsychosocial analysis of low back pain. In M Nordin, TL Vischer, eds: Common low back pain: prevention of chronicity. London, 1992, Bailliere Tindall. Waddell G, Burton AK: Occupational health guidelines for the management of low back pain at work: evidence review. Occup Med (2):124-135, 2001. Waddell G, McIntosh A, Hutchinson A, Feder G, Lewis M: The clinical guidelines for the management of acute low back pain. In Low back pain evidence review. London, December 2001, Royal College of General Practitioners. Weiser S, Cedraschi C: Psychosocial issues in the prevention of chronic low back pain: a literature review. In M Nordin, TL Vischer, eds: Common low back pain: prevention of chronicity. London, 1992, Bailliere Tindall. Work Loss Data Institute: Disorders of the neck and upper back. Occup Environ Med 60:618-626, 2003.
CHAPTER
Neck
3
CHAPTER
3a
A Review of the Epidemiology of Neck Pain in Workers: Prevalence, Incidence, and Risk Factors Pierre Côté, Linda Carroll, J. David Cassidy, Mana Rezai, Vicki Kristman, and the Scientific Secretariat of the 2000-2010 Bone and Joint Decade Task Force on Neck Pain and Its Associated Disorders*
In the past half century, the nature of work has rapidly changed. Once dependent mainly on manufacturing and resource extraction, the economy of industrialized countries increasingly relies on the service sector. This new reality has transformed the nature of work injuries and disability. The shift from manufacturing and resource-based jobs to the service industry led to a sharp reduction in acute and fatal injuries but contributed to the current epidemic of musculoskeletal disorders (MSDs).45 Today MSDs are the most burdensome ailments that affect the health and reduce the productivity of workers.56 Neck pain is one of the most prevalent MSDs in the workingage population48 and a leading source of disability and health care utilization among adults.18,19 During any 6-month period, 54% of adults suffer from neck pain and 4.6% experience significant activity limitations because of neck problems.18 Contrary to popular belief, most adults with neck pain do not experience complete permanent resolution of their discomfort; in fact, it follows an episodic course marked by periods of remission and exacerbation.20 Each year between 14.6% and 18.0% of adults develop a new episode of neck pain,20,21,48 which causes a new episode of disability in 600/100,000 adults annually.20 The etiology of neck pain in workers is complex and multifactorial. Its hypothesized risk factors include demographics, psychosocial and work-related issues, and poor general health.5,7,16,17,20 Although the etiologic contribution of work receives increasing attention, most studies remain cross-sectional and can be used only to hypothesize about the causes of neck pain.5,7 Understanding its etiology in workers is necessary to develop, test, and implement prevention strategies to reduce its burden.
PURPOSE The purpose of this chapter is to review and appraise the recent literature on the epidemiology of neck pain in workers. Specifically, we review the literature to answer the following questions: 1. What is the prevalence of neck pain in workers? We define prevalence as the proportion of workers with neck pain
*Eugene J. Carragee, Jaime Guzman, Scott Haldeman, Sheilah Hogg-Johnson, Lena Holm, Eric Hurwitz, Margareta Nordin, Paul M. Peloso, and Gabrielle van der Velde.
during a specific period of time; its measurement is useful to quantify the burden of a condition in a defined population. 2. What demographic, socioeconomic, health- and workrelated, psychosocial, and societal factors are associated with prevalent neck pain in workers? We refer to “associated factors” to describe variables that are correlated with neck pain in cross-sectional studies. Although these cannot be used to draw causal inferences about its etiology, they are useful to describe the potential risk factors for neck pain. 3. What is the incidence of neck pain in workers? We use the term incidence to describe the average risk of developing neck pain during a time period. A measure of incidence is not only useful to describe the proportion of the workers who will develop a new episode of neck pain during a specific time period but also necessary to quantify the etiologic contribution of risk factors. Incidence is measured from cohort studies. 4. What are the risk factors for neck pain in workers? Risk factors are things that may contribute to on help predict neck pain. We have collected information on risk factors—variables that increase or reduce risk—from case-control and cohort studies.
METHODS We wrote this chapter in collaboration with the members of the scientific secretariat of the 2000-2010 Bone and Joint Decade Task Force on Neck Pain and Its Associated Disorders. The Task Force includes a multidisciplinary scientific secretariat of 12 clinicians and methodologists representing rheumatology, orthopedic surgery, physical and rehabilitative medicine, neurology, physiotherapy, health psychology, chiropractic, epidemiology, clinical epidemiology, and biostatistics. A main objective was to complete a systematic search and critical review of the scientific literature on neck pain and its associated disorders. The literature reviewed in this chapter was critically appraised by members of the Task Force using a standardized critical appraisal methodology.
Definition of neck pain We define neck pain as soft tissue disorders of the cervical spine/shoulder area, including disk lesions and radiculopathy that are experienced by workers. Our definition does not assume a causal link between work and neck pain. It includes neck pain that is caused or aggravated by work, that which interferes with work, and symptomatic neck pain that does not result in disability.
Literature search Having developed our literature search strategy in collaboration with a library scientist (see Acknowledgments), we applied it to two electronic databases: MEDLINE and Embase ( January 1997 to October 2003). For the purpose of this chapter, we used a restricted portion of the exhaustive search undertaken by the Task Force. Our search was based on specific key words (neck pain, neck injury, pain, injury, epidemiology, incidence, prevalence,
26
Chapter 3a
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Prevalence, incidence, and risk factors of neck pain in workers
workplace, worker, work, meta-analysis) and text words (neck pain, cervical pain, neck ache, whiplash, pain, ache, sore, stiff, discomfort, neck, occupational, work-related, review, literature synthesis, literature review). All search terms were limited to the English and French languages and adult subjects. We excluded duplicate articles.
Article selection Each citation found in the search was screened by rotating groups of three Task Force scientific secretariat members to assess its relevance to the epidemiology of neck pain in workers. For the purpose of this review, articles were deemed relevant if they passed the following inclusion and exclusion criteria:
Inclusion criteria 1. Studies that report results relevant to neck pain in workers with or without its associated disorders, which might include radiating arm pain, upper thoracic pain, headache, and temporomandibular joint disorder pain; 2. Studies that examine the prevalence, incidence, risk, and/or prevention of neck pain with or without its associated disorders; 3. Studies of the risk or prevention of neck pain that include at least 20 human subjects at risk for neck pain with or without its associated disorders.
Exclusion criteria 1. Studies that do not include human subjects with neck pain with or without its associated disorders; 2. Studies of neck pain due to fracture, dislocation, tumor, skin lesions, throat disorders, inflammatory disorders, cervical myelopathy, and spinal cord injury; 3. Studies concerning radiating arm pain, upper thoracic pain, headaches, temporomandibular joint disorder, and thoracic outlet syndrome not associated with neck pain; 4. Opinion papers, letters to the editor, traditional narrative reviews, and papers without scientific data; 5. Single-case reports of workers with neck pain with or without its associated disorders; 6. Studies using cadavers or nonhuman subjects, such as crash test dummies, animals, or laboratory simulations; 7. Biomechanical studies without human subjects with neck pain.
to assist reviewers in understanding the impact of bias on the study results and to abstract information. Rotating pairs of scientific secretariat members independently conducted these in-depth reviews of each article, and the remaining members read the studies. The two reviewers presented their critical appraisal to a larger group of members for discussion of the scientific merit of the study. The members decided by consensus whether a study was scientifically admissible or inadmissible, the latter being one in which methodologic flaws were judged to have fatally biased the results and therefore made the paper’s conclusions scientifically invalid.
Data synthesis Each research question was answered by a best-evidence synthesis,52,53 which consists of assembling and qualitatively synthesizing the best evidence relevant to it. We described the strength of evidence for risk factors by adapting a methodology that has been used to rank studies on breast cancer, whiplash injuries, and mild traumatic brain injuries.4,13,19 The methodology distinguishes among three phases of studies. Phase I studies are hypothesis-generating investigations that descriptively explore associations between potential risk factors and disease outcomes. Phase II studies are extensive exploratory analyses that focus on particular sets of risk factors or attempt to discover which ones predict the development of neck pain. Phase III studies are large confirmatory studies of explicit prestated hypotheses that allow for focused examinations of the strength, direction, and independence of the proposed relationship between a risk factor and the development of neck pain. We present the prevalence and incidence of neck pain with 95% confidence intervals. Where these figures were not reported in the article but sufficient information was provided, we computed these estimates and report our computations. We describe the cross-sectional associations between various risk factors and neck pain as positive or negative. We report odds ratios, relative risks or hazard rate ratios, and 95% confidence intervals to describe associations between risk factors and neck pain obtained from case-control or cohort studies. When these estimates did not appear in the paper, they were computed from sufficient data. Confidence intervals for prevalence and incidence rates were calculated using the standard confidence interval formula around proportions described by Kuzma.37 All other analyses were performed using SAS.49
RESULTS
Critical review of the literature
Selection and critical appraisal of articles
All articles meeting the inclusion and exclusion criteria were critically reviewed using standard criteria and computerized critical review forms. Modified for the purpose of the 2000-2010 Task Force, the forms were similar to the ones used by the Quebec Task Force on Whiplash-Associated Disorders and the Best Evidence Synthesis on Traumatic Mild Injury (Appendix 3a.1).12,55 These criteria prompt the reviewers to appraise the methodologic merit of a study by focusing on selection bias, information bias, and confounding. Rather than provide a rating scale for determining scientific acceptability, the forms are used
The results from the literature search and selection of articles are summarized in Figure 3a.1. Overall, we retrieved 162 publications, including 152 articles from the literature search and 10 from our files. Of the 159 nonduplicate articles, 45 met the inclusion criteria and were reviewed. Fifteen articles were excluded by the scientific secretariat after they were appraised as scientifically inadmissible.10,11,15,26,31-34,36,40,41,43,61,63,64 Of the 30 accepted articles, 18 were cross-sectional studies that reported on the prevalence and factors associated with neck pain,1-3,22-25,28-30,39,42,44,46,47,58-60 and 10 reported on its incidence
Chapter 3a
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Results
1. Literature search Medline
Embase
Personal files
109
43
10
Librarian
162 articles
159 non-duplicate articles
2. Screening Scientific secretariat Inclusion criteria
114 irrelevant 45 relevant articles
3. Review Scientific Critical appraisal secretariat
15 rejected
30 articles accepted and reviewed Figure 3a.1
Results of literature search and selection of articles included in the review.
and risk factors.6,8,27,35,38,50,51,54,57,62 Two studies reported crosssectional and prospective results.9,14
Neck pain in general working populations Prevalence We accepted four cross-sectional studies that described the prevalence of neck pain in samples of workers from the general population, in this case in Europe.9,14,23,46 The source population for these studies varied from registers of general practitioners in the United Kingdom to age cohorts of workers under the supervision of occupational physicians in France, workers who participated in periodical health surveys in the Netherlands, and 34-year old workers in Sweden. Overall, these studies suggest that neck pain is highly prevalent and a common source of activity limitations. In the United Kingdom, 34% of workers reported that they experienced neck pain in the preceding year (Table 3a.1).46 During the same period, 11% of workers limited their activities because of neck pain. Overall, 20% of surveyed workers had experienced neck pain in the preceding week. In Sweden, the 1-year prevalence of neck pain was 44% and 61% in 34-year-old men and women, respectively (Table 3a.1).9 In this cohort, 26% of men and 43% of women reported symptoms that lasted more than 1 month. In France during 1990, the prevalence of chronic neck/shoulder pain lasting for at least 6 months and associated with functional limitations was 7.8% in men and 14.8% in women (Table 3a.1).14 In 1995 this same study reported that the prevalence of chronic neck/shoulder pain had increased slightly to 9.5% in men and 17.6% in women.
Factors associated with neck pain All four studies reported that the prevalence of neck pain increases with age and is more common in women (Table 3a.1).9,14,23,46 In Sweden, self-employed males had a higher prevalence of neck/shoulder symptoms in the past month than other workers.9 In the United Kingdom, workers with musculoskeletal comorbidities were more likely to report neck pain. Palmer et al46 reported that the prevalence of neck pain in the preceding week was higher in those with shoulder, elbow, wrist-hand, hip, and knee pain. Similarly, neck pain was more common in workers who had experienced troublesome low back pain in the preceding year and in those who suffered from frequent headaches, fatigue, or stress.9,46 Barnekow-Bergkvist et al9 found that workers with better flexibility of the cervical spine (rotation) reported fewer neck/shoulder symptoms in the preceding month. Three studies reported that ergonomic, physical, and psychosocial factors at work are associated with neck pain (Table 3a.1). Two studies reported on its association with lifting. In Sweden, the prevalence of neck symptoms in the preceding month was lower in workers who performed repetitive or heavy lifting,9 whereas in contrast, Palmer et al46 reported that lifting increased it. Among U.K. workers, the prevalence of neck pain was found to be higher also in workers who reached overhead for more than 1 hour per day and in those exposed to hand and arm vibration.46 Using a keyboard for 4 hours or more in an average working day was positively associated with neck pain in women but not in men.47 A positive association between monotonous work, high decision latitude, and prevalent neck/shoulder symptoms was found among female workers in the Swedish sample.9 Finally, Dutch adult workers who reported a combination of mentally and physically demanding work and those performing heavily
27
Swedish student aged 16 years in 1974
Workers under the supervision of occupational physicians from France in 1990 and 1995
Registers of 163 general practitioners in 34 general practices in England, Scotland, and Wales and members of the British armed services in 1997-1998
Dutch workers who participated in the periodical occupational health surveys between 1982 and 1993
Cassou et al, 200214
Palmer et al, 200146
De Zwart et al, 199723
(−), negative association; (+), positive association; CI, confidence interval.
Inclusion: active workers aged 16-64 years Sample size = 44,486
Regular pain or stiffness in the neck
Not applicable
1-year prevalence: Men: 44% (36-52) Women: 61% (51-71) Prevalence of symptoms > 1/month: Men: 26% (19-33) Women: 43% (33-54) Point prevalence: Men: 1990: 7.8% (7.3-8.3) 1995: 9.5% (8.9-10.1) Women: 1990: 14.8% (14.0-15.6) 1995: 17.6% (16.7-18.5) 1-year prevalence: 34% (33-35) 1-year prevalence of neck pain interfering with normal activities: 11% (10-12) 1-week prevalence: 20% (19-21)
Men: Age (+); shoulder pain (+); elbow pain (+); wrist-hand pain (+); hip pain (+); knee pain (+); low back pain (+); headaches (+); tiredness/ stress (+); working overhead (+); heavy lifting (+); use of keyboard for > 4 hours/day (−); hand-arm vibration (+) Women: Age (+); shoulder pain (+); elbow pain (+); wrist-hand pain (+); hip pain (+); knee pain (+); low back pain (+); headaches (+); tiredness/stress (+); working overhead (+); use of keyboard for > 4 hours/day (−); heavy lifting (+); hand-arm vibration (+) Prevalence varies with occupation Prevalence is higher in women than men Men: Age (+); mentally and physically demanding work (+); heavy physically demanding work (+) Women: Age (+); mentally and physically demanding work (+); heavy physically demanding work (+)
Men: Lifting (−); self-employed (+); worrying (+); neck lateral rotation (−) Women: Monotonous work posture (+); lifting (−); high decision latitude (+); hand grip performance (−); neck lateral rotation (−) Age (+); women (+)
●
Chronic neck pain: self-report of neck/ shoulder pain lasting at least 6 months with functional limitations confirmed by clinical examination Neck pain measured with Standardized Nordic Questionnaire
Neck-shoulder pain measured with Standardized Nordic Questionnaire
Associated factors (95% CI)
Chapter 3a
Inclusion: workers born in 1938, 1943, 1948, or 1953 who underwent an annual medical examination Exclusion: Individuals not employed in 1995 Sample size = 16,950 Inclusion: individuals aged 16-64 years Sample size = 12,907
Inclusion: 34-year-old subjects in 1992 who worked at least 16 hours/week at time of survey Exclusion: maternity/paternity leave, students, long-term sick leave Sample size = 238
Prevalence (95% CI)
BarnekowBergkvist et al, 19989
Case definitions
Source population
Study
Inclusion/exclusion criteria
Studies of prevalence and factors associated with neck pain in workers
Table 3a.1
28 Prevalence, incidence, and risk factors of neck pain in workers
Chapter 3a
demanding work were more likely to report regular pain or stiffness in the neck.23
Incidence Three cohort studies, two conducted in France and one in the United States, provided information about the incidence of neck pain in samples of workers from the general population. The studied populations included workers under supervision of French occupational physicians/medical departments in the early 1990s14 and those covered by the Washington State Department of Labor and Industries state fund (including employees of selfinsured employers) between 1990 and 1998.51 These studies suggested that a significant proportion of the working population experiences a new episode of neck pain each year. These cohort studies offered insights about the “high-risk” groups for the development of an episode of neck pain. In France the 6-month incidence of neck pain among workers with no prior history was 17.4%, whereas it was 44.4% in those who reported a past history of neck disorders.38 Between 1990 and 1995, 12.5% female French workers and 7.3% of male French workers developed chronic neck pain (Table 3a.2).14 In Washington State, 40.1 per 10,000 full-time equivalent workers covered by the state fund developed neck pain.51 However, the reported incidence was only 5.1 per 10,000 full-time equivalent employees in self-insured firms.
Risk factors for neck pain Four phase II studies reported on factors associated with the development of neck pain in general working populations. Three Swedish studies described risk factors for developing neck pain in the past year, and one French study reported on the risk factors for chronic neck pain. In a Swedish cohort of 16-year-old student-workers, bench press performance was negatively associated with the development of neck/shoulder pain 18 years later (Table 3a.2).9 In other words, workers who performed better while bench pressing when 16 years of age in 1974 were protected against developing neck/shoulder pain in 1992. In another study, Fredriksson et al27 found that the development of neck/shoulder pain was associated with physical and psychosocial factors at work, specifically high physical work load for men and frequent hand movement for women. The authors found, moreover, that physical and psychosocial risk factors frequently interact and modify their effects on the incidence of neck/shoulder pain in workers. A third Swedish study found that both physical and psychosocial risk factors contribute to workers seeking health care for neck/shoulder pain.57 A previous episode of neck pain that persisted for more than 3 months and a nonfixed salary strongly predicted seeking health care for this symptom. The risk factors as well as the strength and the direction of association varied between men and women, suggesting that the etiology has a gender-specific component.57 For men, exposure to psychosocial factors such as high job demands or high time pressure reduced the risk of seeking care (Table 3a.2). In women, however, exposure to other psychosocial risk factors such as high degree of hindrance with work increased the risk of seeking care for neck/shoulder pain. Tornqvist et al57 also reported that workers with multiple risk factors were more likely to seek care. In France, the risk of developing chronic neck pain and disability was associated with sociodemographic variables, workplace
●
Results
psychosocial factors, comorbidities, and health risk behaviors (Table 3a.2). In their large cohort, Cassou et al14 found that increasing age, repetitive work, and high job demands were associated with chronic neck pain. Moreover, workers with depressive symptoms and those suffering from MSDs in the preceding year were more likely to develop chronic neck pain.
Neck pain in specific occupational groups Prevalence Twelve cross-sectional studies described the prevalence and factors associated with neck pain in samples of health care workers, including dental personnel, physical therapists and nurses,1-3,22,24,39,58-60 music and nursery school teachers,25,44 and blue collar workers (sewage workers, spinning industry, forestry, and scaffolding).28-30,42 The available evidence suggests that the prevalence of neck pain varies across occupations and tends to be higher for health care workers (Table 3a.3). Among these workers, the 1-year prevalence of neck pain varies from 45.8% in nurses to 47.6% in physical therapists, 64% in dentists, and 72% in dental hygienists (Table 3a.3).1,2,22,39,58-60 In Sweden, it is estimated that 50% of dental hygienists experience neck pain in the preceding week, whereas in Norway, 22.6% of nursing aides report that they experienced intense neck pain in the preceding 2 weeks.2,24 The prevalence of chronic neck pain is 9% among the nursing staff of Greek hospitals.3 In Sweden, most music teachers (59%) experience neck pain every year, and 30% experience an episode each week.25 Similarly, one fourth to one third of Japanese nursery school teachers report neck pain each month.44 Interestingly, except for sewage workers the prevalence of neck pain is lower in industrial, forestry, and construction workers than in health care workers or teachers. In Austrian sewage workers, the annual prevalence of neck pain is 52.4%, and 20.9% of workers suffer from neck pain each day.28
Factors associated with neck pain In health care workers, the presence of neck pain was associated with demographic, ergonomic, and workplace factors. Among nurses, neck pain was more common in older workers and in those with moderate/high physical or psychologic demands.39,58-60 Nurses and nursing aides who worked long hours reported neck pain more frequently.24,39,58-60 Although neck pain was more common in those who worked under strenuous back postures, it was less so in those who used mechanical lifts or received ergonomic training.3,24,39,58-60 In physical therapists, neck pain was positively associated with the pace of work and the type of practice.22 The association between neck pain and physical/psychologic variables was observed also in Japanese nursery school teachers, among whom it was more common in those with poor supervisor support and in those caring for young children.44 Similarly, male Swedish music teachers with low social support and women teachers with high psychologic demands were more likely to report neck pain.25 Neck pain in blue collar workers was associated with age, physical work, and psychologic demands.28,30
Incidence of neck pain Five cohort studies describe the incidence of neck pain in specific occupational groups, including industrial/service companies,6,8
29
Inclusion: individuals living in Sweden in 1993, without a diagnosis of MSD in 1969 and below age 59 in 1993 Sample size = 484
Individuals from Stockholm, Sweden who participated in the REBUS-69 study in 1969
Fredriksson et al, 200027 Nested casecontrol study Phase II
Cases: neck/shoulder Not applicable pain defined by a questionnaire reporting consultation with a physician, physiotherapist, chiropractor, osteopath, or other medical professional or sick leave for more than 7 consecutive days between 1970 and 1992 Neck/shoulder pain defined as pain lasting at least 7 consecutive days during the last year Controls: Individual matched on age, gender, and index year
5-year incidence: Men: 7.3% (6.8, 7.8) Women: 12.5% (11.7, 13.3)
Incidence (95% CI)
Men: Year of birth 1938 vs. 1953 OR = 2.0 (1.6, 2.6); year of birth 1945 vs. 1953 OR = 1.5 (1.2, 1.9); repetitive work before 1990 OR = 1.3 (1.0, 1.7); awkward work OR = 1.3 (1.1, 1.7); high job demand OR = 1.2 (1.0, 1.4); depressive symptoms OR = 1.3 (1.0, 1.8); MSD in past year OR = 1.5 (1.3, 1.8); sporting activities OR = 0.8 (0.7, 0.9); smoking OR = 1.2 (1.0, 1.4) Women: Year of birth 1938 vs. 1953 OR = 1.5 (1.2, 2.0); year of birth 1945 vs. 1953 OR = 1.6 (1.3, 2.0); year of birth 1948 vs. 1953 OR = 1.2 (1.0, 1.5); repetitive work in 1990 OR = 1.3 (1.0, 1.6); repetitive work before 1990 OR = 1.2 (1.0, 1.5); high job demand OR = 1.2 (1.0, 1.4); depressive symptoms OR = 1.5 (1.2, 1.9); MSD in past year OR = 1.7 (1.5, 2.0) Risk factors in the past 5 years. Men: High physical workload index OR = 2.2 (1.1, 4.6); frequent hand/finger work during leisure time OR = 2.1 (1.0, 4.5) Significant interactions: Work with vibrating tools and frequent hand movements; frequent hand work during leisure time and high perceived workload; frequent hand work during leisure time and work with vibrating tools; precision work during leisure time and high physical workload Women: Frequent hand movements at work OR = 1.5 (1.0, 2.3) Significant interactions: High perceived workload and low influence over work condition; high perceived workload outside work and low influence over work conditions; frequent hand work during leisure time and high perceived workload; frequent hand work during leisure time and high physical workload; precision work during leisure time and few possibilities of development; precision work during leisure time and low influence over work conditions
Men: Bench press performance at 16 years old (OR = 0.30 (0.09-0.85))
Risk factors (95% CI)
●
Chronic neck pain: self-report of neck/ shoulder pain lasting at least 6 months with functional limitations confirmed by clinical examination
Neck-shoulder pain measured with Standardized Nordic Questionnaire
Case definitions
Chapter 3a
Cassou et al, 200214 Cohort study Phase II
16-year-old Inclusion: 34-year-old subjects in Swedish student- 1992 who worked at least workers in 1974 16 hours/week at time of survey Exclusion: maternity/paternity leave, students, long-term sick leave Sample size = 238 Workers under Inclusion: workers born in 1938, 1943, the supervision 1948, or 1953 who underwent of occupational an annual medical examination physicians from Exclusion: individuals not employed France in 1990 in 1995 and 1995 Sample size = 16,950
BarnekowBergkvist et al, 19989 Phase II
Inclusion/exclusion criteria
Studies of incidence and risk factors associated with neck pain in workers
Study, design, Source and phase population
Table 3a.2
30 Prevalence, incidence, and risk factors of neck pain in workers
Workers covered by the Washington State Department of Labor and Industries State Fund and employees of self-insured employers between 1990 and 1998 Workers in the municipality of Norrtälje, Sweden from Sept 1, 1994 to June 30, 1997
Silverstein et al, 200251 Cohort study
Inclusion: workers aged 20-59 years who worked more than 17 hours/ week and had worked at least 2 months during the past year Exclusion: seeking health care for neck, shoulder, or low back disorders during the 6 months before enrollment Sample size = 1903
Inclusion: accepted State Fund claims for specific diagnostic or treatment codes. Of the self-insured claims, only those with more than 3 days of lost time were included. Sample size = 392,925
Inclusion: at least 1 year of employment Exclusion: workers with sick leave for more than 3 months in the previous year, pregnancy, temporary work contract, or retirement within the following 12 months Sample size = 511
Men: Suffered from neck or shoulder symptoms > 3 months earlier in life: RR = 4.4 (2.7-7.1); work with vibrating tools: RR = 1.6 (1.0-2.3); nonfixed salary RR = 1.9 (1.1-3.1); high demands RR = 0.7 (0.4-1.0); high time pressure RR = 0.5 (0.3-1.0); high creativity/low routine work profile RR = 0.6 (0.4-1.0); high quantitative demands RR = 0.2 (0.1-0.9); low demands in relation to competence RR = 1.5 (1.0-2.4) Women: Suffered from neck or shoulder symptoms > 3 months earlier in life: RR = 4.1 (3.0-5.7); repetitive hand/finger movements RR = 1.6 (1.2-2.2); nonfixed salary RR = 2.0 (1.0-4.2); nightshift/shift work including night work RR = 1.3 (1.0-1.8); long working hours RR = 0.7 (0.5-0.9); solitary work RR = 1.8 (1.2-2.9); job strain RR = 1.4 (1.1-2.0); high degree of hindrances at work RR = 1.4 (1.0-1.9)
Among 311 workers Not applicable without prior neck pain: 6-month incidence: 17.4% (13.3-22.0) 6-month incidence of disorders that lasted > 30 days: 1.3% (0.0-3.3) Among 27 workers with a prior history neck pain: 6-month incidence: 44.4% (25.5-64.7) 6-month incidence of disorders that lasted > 30 days: 11.1% (2.4-29.2) Cumulative incidence Not applicable (per 10,000 FTE): State fund: 40.1 (39.6, 40.6) Self-insured employers: 5.1 (4.9, 5.3)
Cases were those who Not applicable sought treatment for neck-shoulder disorders Controls were randomly from the population register Control group = 1511
Accepted claims for nontraumatic neck soft tissue disorders with the neck as the primary site of injury
Neck disorder (ache, pain, discomfort) in the past 6 months defined by questionnaire and body diagram Neck disorder for more than 30 days
●
CI, confidence interval; MSD, musculoskeletal disorder; OR, odds ration; RR, relative risk.
Tornqvist et al, 200157 Case-control study Phase II
Hospital, warehouse, office, and airport workers recruited from medical departments in France in 1991
Leclerc et al, 199938 Cohort study
Chapter 3a Results 31
Source population
Dental personnel (dentists, dental hygienists, and dental assistants) from the public health services in the county of Blekinge, Sweden
Nursing staff from six hospitals in Athens, Greece between 2000 and 2001
Physical therapists registered in the state of Victoria, Australia
Norwegian nurse’s aides in 1999
˚Akesson et al, 19991 ˚Akesson et al, 20002
Alexopoulos et al, 20033
Cromie et al, 200022
Eriksen, 200324
Neck pain measured with the Standardized Nordic Questionnaire Chronic neck pain is pain lasting > 3 months Neck pain measured with the Standardized Nordic Questionnaire
Neck pain measured with the Standardized Nordic Questionnaire
Case definitions
Inclusion: vocationally active Neck pain measured Exclusion: sick leave because with the Standardized of illness or pregnancy Nordic Questionnaire Sample size = 6485
Exclusion: therapists not living in Australia Sample size = 536
Inclusion: at least one year of experience in current job Sample size = 351
Exclusion: personnel on leave (other than sick leave) and specialist dentists Sample size = 244
Inclusion/exclusion criteria
2-week prevalence: Any pain: 53.5 % (52.3-54.7) Intense pain: 22.6% (21.6-23.6)
1-year prevalence: 47.6% (43.3-51.8)
1-week prevalence: Hygienists: 50% (33, 67); male dentists: 31% (16, 45); female dentists: 27% (12, 42); general practice dental assistants: 17% (10, 24); specialist dental assistants: 16% (4, 27) 1-year prevalence: Hygienists: 72% (56, 87); male dentists: 64% (49, 79); female dentists: 64% (47, 80); general practice dental assistants: 46% (37, 55); specialist dental assistants: 34% (19, 49) Prevalence at 5-year follow-up for females. 1-week prevalence: Hygienists: 41%; dentists: 38%; dental assistants 31% 1-year prevalence: Hygienists: 73%; dentists: 54%; dental assistants 62% 1-year prevalence: 47% (42-52) Prevalence of chronic neck pain: 9% (6-12) Prevalence of sick leave: 5% (3-7)
Prevalence (95% CI)
Male (+), private practice (+), sports physical therapy (+), manual techniques (+), sedentary work (+), repetitive tasks (+), large number of patients/day (+), few rest periods (+), rest periods (+), work when injured (+), mobilization/manipulation (+), other manual treatment (+) Female (+), marital status/single (+), working >36 hours/week (+), working in old people’s home (+)
Strenuous back posture (+); moderate/bad perceived general health (+)
Not applicable
Associated factors (95% CI)
●
Study
Studies of prevalence and factors associated with neck pain in specific occupations
Chapter 3a
Table 3a.3
32 Prevalence, incidence, and risk factors of neck pain in workers
Molano Workers from a scaffolding company in the et al, 200142 Netherlands from June to September, 1998 Ono et al, Nursery school teachers in a Japanese city, 200244 in October, 1995
Workers from the spinning industry in Lithuania in 1996 Forestry workers from Norway
Exclusion: male workers, nurses, supervisors Sample size = 959
Inclusion: job involving heavy lifting or working while bent over Sample size = 255 Inclusion: production workers Sample size = 363 Inclusion: manual workers, machine operators, and administrative workers who worked for at least 10 months/year during the previous 5 years Sample size = 835 Inclusion: all workers Sample size = 323
Friedrich Sewage workers from Vienna, Austria et al, 200028
Gamperiene and Stigum, 199929 Hagen et al, 199830
Inclusion: all music teachers Sample size = 208
FjellmanMusic teachers in two Wiklund counties of Sweden in 2000 et al, 200325
1-year prevalence: 27% (22, 32)
1-year prevalence: 27.7% (21.9, 33.5)
1-year prevalence: Cumulative: 59% (52-66) Men: 52% (43-61) Women: 67% (57-77) 1-week prevalence: Cumulative: 30% (24-36) Men: 26% (18-34) Women: 36% (26-46) Lifetime prevalence: 67.5% (61.6-73.3) 1-year prevalence: 52.4% (46.0-58.5) 1-week prevalence: 25.7% (20.3-31.3) Point prevalence: 20.9 (15.8-26.0) 1-year prevalence: 16.5% (12.4, 20.8)
Neck/shoulder pain in Not applicable the previous month greater than grade 3/5 on a self-reported scale
Neck pain measured with the Standardized Nordic Questionnaire
Neck pain measured with the Standardized Nordic Questionnaire Neck/shoulder pain for at least 30 days in previous 1 year measured with the Standardized Nordic Questionnaire
Neck pain measured with the Standardized Nordic Questionnaire
Neck pain measured with the Standardized Nordic Questionnaire
Continued
10 years of experience (+); caring for children aged 0 (+); holding/lifting a child/material exceeding 20 kg (+); poor supervisor support (+)
Not applicable
Age (+); physical work (+); low intellectual discretion (+); high psychologic demands (+)
Not applicable
Age (+)
Men: Low social support (+); lifting (+); playing guitar (+) Women: High psychologic demands (+); teaching at 5-12 schools/week (+)
Chapter 3a ●
Results 33
Registers of 163 general practitioners in 34 general practices across Britain in 1997-1998
Palmer et al, 200146
Inclusion: at current job for at least 1 year Exclusion: nurses with non-work related injuries within a 3-month period before onset of workrelated neck pain Sample size = 1163
Inclusion: workers aged 16-64 years employed in nonmanual occupations Exclusion: manual occupations Sample size = 4889
Inclusion/exclusion criteria
(−), negative association; (+), positive association; CI, confidence interval.
Trinkoff et al, Licensed registered nurses from Illinois and 200259 Lipscomb New York state in 1999-2000 et al, 200239 Trinkoff et al, 200358 Trinkoff et al, 200360
Source population
Study
Neck pain measured with the Standardized Nordic Questionnaire Case: neck pain lasting ≥ 1 week and ≥ 3/5 in intensity Symptoms: neck pain without full definition of a case
Neck pain measured with Standardized Nordic Questionnaire
Case definitions 1-week prevalence: Men: Keyboard: 14.8% (12.3-17.4) No keyboard: 13.8% (12.0-15.6) Women: Keyboard: 22.9% (20.3-25.4) No keyboard: 18.3% (16.3-20.3) 1-week prevalence of disability among workers with neck pain: Men: Keyboard: 26% (18-34) No keyboard: 33% (26-39) Women: Keyboard: 33% (27-39) No keyboard: 37% (31-42) 1-year prevalence: Cumulative: 45.8% (43.0-48.7) Case: 20.4% (18.1-22.8) Symptoms: 25.4% (22.9-27.9)
Prevalence (95% CI)
Age (+); mechanical lifting devices (−); training on adjustment of work station (−); training on recognizing workplace hazards (−); working long hours (+); moderate and high physical demands (+); psychologic demands; dependents (+); working long hours (+)
Not applicable
Associated factors (95% CI)
●
Studies of prevalence and factors associated with neck pain in specific occupations—cont’d
Chapter 3a
Table 3a.3
34 Prevalence, incidence, and risk factors of neck pain in workers
Chapter 3a
municipal office workers,35 teaching hospital employees,50 female nurses from acute care hospitals,54 and workers from a large forestry industry.62 Overall, the evidence suggests that the incidence of neck pain varies across occupational group, tending to be higher for those working in hospitals and offices (Table 3a.4). In England, female nurses working in acute care hospital settings developed neck pain at a rate of 17% per year.54 In Canada, 40.5% of employees at a teaching hospital who were asymptomatic in 1996 reported to have experienced an episode of neck pain in the preceding week when followed up a year later.50 In Finnish municipal office workers, the annual incidence of neck pain with or without radiations was 34.4%. Approximately 13% had local neck pain only, and 14.4% had radiating pain without neck pain. The annual incidence of workers reporting both local and radiating neck pain was 6.7%.35 The incidence of neck pain was lower among workers in industrial/service and forestry sectors. In workers from 34 industrial/service companies located throughout the Netherlands, the 3-year incidence of neck pain was 14.4%.6,8 The overall 3-year incidence among Finnish forestry workers was a similar 15.6%62: 9.2% developed mild neck pain, and 6.4% developed severe pain.
●
Relevance
neck pain; specifically, we found its incidence to be higher for nurses and office workers.35,50,51 Studies that quantified the role of risk factors supported that neck pain is more common in workers with high quantitative job demands, low coworker support, repetitive work, nonfixed salary, increased sitting time, poor ergonomics, previous musculoskeletal pain, and depressive symptoms.5,8,14,27,35,54,57 Although we identified several risk factors for neck pain, it is important to note that only one phase III study was designed specifically to test their independence.5,8 This finding indicates that very few risk factors can be considered well established. Efforts should be devoted to designing phase III studies to confirm the results of cross-sectional observations and phase II (exploratory) studies. Moreover, future studies should pay attention to interactions among individual, psychosocial, and workplace risk factors. The growing body of evidence supporting the role of psychosocial and workplace factors in the etiology of neck pain must not be considered in isolation. Because it is very likely that the risk factors for the development of neck pain and disability vary across occupations, as demonstrated in our review, future studies should ensure that the risk profiles of various occupations are explored.
Risk factors for neck pain Two phase II and one phase I study examined the risk factors for neck pain in specific occupational groups (Table 3a.4). Among Finnish municipal workers, females and those with poor keyboard position were more likely to develop neck pain.35 In English female nurses, a new episode of neck pain was associated with previous neck and low back pain and with various physical aspects of care such as moving and transferring patients.54 Only one phase III study supported the observation that physical and psychosocial factors contribute to the development of neck pain.5,8 In their cohort study of industrial and service workers from the Netherlands, Ariens et al5,8 demonstrated that high quantitative job demands, low coworker support, and prolonged sitting are independent risk factors for a new episode of neck pain.
SUMMARY Neck pain is endemic in workers. Our best evidence synthesis demonstrates that it is highly prevalent and a common source of disability. By far, most neck pain in workers is nontraumatic. Its etiology is consequently multifaceted, and although occupational factors may be important contributors to its development, they are neither sufficient nor necessary. This reality clearly emphasizes that the development of an episode of neck pain cannot be attributed entirely to the physical and psychosocial environment of a workplace. Our review of cross-sectional studies supports the view that neck pain is more common in various subgroups of workers. It is more prevalent among older workers, women, and those with musculoskeletal comorbidities.1,2,14,23,24,28,30,39,46,54,57-60 Moreover, it varies significantly across occupations and is associated with ergonomic, physical, and psychosocial factors.3,5,8,9,14,22,23,25,27,30,35,39,44,46,54,57-60 Evidence from case-control and cohort studies confirms that certain occupations pose higher risk of developing an episode of
RELEVANCE Our review has important implications for prevention. First, intervention must target clearly modifiable risk factors. Second, the multifaceted etiology of neck pain highlights the importance of designing preventive interventions focused on multiple rather than individual risk factors. Current research has not yet identified the “necessary” causes for neck pain and disability, and very little is known about the interrelationships among risk factors. Multimodal interventions targeting multiple modifiable risks such as workplace and psychosocial factors may thus prove more promising than one-dimensional approaches targeting a specific one. Finally, the complex etiology of neck pain suggests that the roles of economic and legal factors, work organization, and health care access and delivery are important and must be studied as well.14
ACKNOWLEDGMENTS We are indebted to Emma Irvin and Stephen Greenhalgh, research librarians, for their expertise and guidance with the literature search. The Bone and Joint Decade Task Force on Neck Pain and Its Associated Disorders is supported by a grant to the University of Alberta from the National Chiropractic Mutual Insurance Company and the Canadian Chiropractic Protective Association, Jalan Pacific Inc., Länsförsäkringar Wasa, and the Insurance Bureau of Canada. This article was made possible also through the financial support of the Workplace Safety and Insurance Board of Ontario. Dr. Côté is supported by the Canadian Institutes of Health Research through a New Investigator Award and by the Institute for Work & Health by the Workplace Safety and Insurance Board of Ontario. Dr. Carroll is supported by a Health Scholar Award from the Alberta Heritage Foundation for Medical Research. Dr. Cassidy is supported by an endowed research chair from the University Health Network. Vicki Kristman is supported by a Doctoral Training Award from the Canadian Institutes of Health Research in partnership with the
35
Shannon Employees of a teaching hospital in Hamilton, et al, 200150 Cohort study Ontario, Canada from 1995 to 1997
Korhonen Finnish municipal office workers in et al, 200335 Cohort study 1998-1999 Phase II
Inclusion: workers who worked Neck pain measured by a modified at least 20 hours per week Standardized Nordic Questionnaire and worked at their current Cases were defined as regular or job for at least 1 year prolonged neck pain, with episodes that Exclusion: workers who had another lasted for at least 1 day during the paid job for any substantial previous 12 months on at least amount of time, received a work one of 3 follow-up measurements disability payment for neck pain in the preceding year, and had prolonged neck pain during the year before baseline Sample size = 977 Inclusion: full-time Incident cases were healthy subjects at employees working on baseline (those who reported local or video display units for radiating neck pain for less than 8 days more than 4 hours/week during the preceding 12 months) who Sample size = 180 reported at follow-up local or radiating neck pain for at least 8 days during the preceding 12 months. Question for local neck pain was: “Estimate the total number of days you have had local neck pain (not radiation) during the preceding 12 months: 0 days, 1-7 days, 8-30 days, >30 days but not daily, and daily.” Healthy was defined as 0-7 days, and 8 or more days defined incident neck pain. Inclusion: workers still Neck pain measured by question: “In the employed by the hospital past week, how often have you suffered at the end of the study from neck and/or shoulder pain?” Exclusion: physicians Sample size = 173
High quantitative job demands RR = 2.14 (1.28, 3.58); low coworker support RR = 2.43 (1.11, 5.29); sitting > 95% of the time RR = 2.34 (1.05-5.21)
Incidence of an episode of neck pain in the previous week: 40.5% (33.1, 47.8)
Not applicable
1-year incidence: Female OR = 2.9 (1.3-2.7); poor keyboard Local or radiating neck position OR = 2.1 (1.0-4.5) pain: 34.4% (12.5-41.3) Local and radiating neck pain: 6.7% (3.0-10.3)
1-year incidence: 5.7% (4.3, 7.2) 3-year incidence: 14.4% (12.2, 16.6)
Incidence (95% CI) Risk Factors (95% CI)
Workers from 34 industrial/service companies located throughout the Netherlands from 1994 to 1997
Case definitions
Ariens et al, 20018 Ariens et al, 20015 Cohort study Phase III
Inclusion/exclusion criteria
Source population
Study
●
Studies of incidence and risk factors associated with neck pain in specific occupations
Chapter 3a
Table 3a.4
36 Prevalence, incidence, and risk factors of neck pain in workers
Exclusion: workers with rheumatoid arthritis and part-time workers Sample size = 5180
Viikari-Juntura Workers from a large forest industry et al, 200162 Cohort study enterprise in Finland Phase II from 1992 to 1995
CI, confidence interval; HR, hazard ratio; OR, odds ratio; RR, relative risk.
Inclusion: working at same job throughout the study Exclusion: agency staff, student nurses, and community nurses Sample size = 587
Smedley Female nurses from two acute et al, 200354 Cohort study hospitals in the Phase II south of England
Radiating neck pain measured by a modified version of the Standardized Nordic Questionnaire Mild pain: 8-30 days in previous year Severe pain: >20 days in previous year
Neck pain measured with the Standardized Nordic Questionnaire
Cumulative 3-year incidence: Mild pain: 9.2% (7.9, 10.5) Severe pain: 6.4% (5.3, 7.5)
2-year incidence of neck pain: 34% (30-38)
Previous neck pain: > 1 year before baseline HR = 1.6 (1.1-2.3); < 1 year before baseline HR = 2.8 (2.0-3.9) Duration of previous neck pain: < 1 week HR = 1.7 (1.1-2.5); 1-4 weeks HR = 2.3 (1.5-3.3); > 4 weeks HR = 2.6 (1.7-4.0) Previous low back pain: >1 year before baseline HR = 1.8 (1.2-2.7); < 1 year before baseline HR = 1.9 (1.4-2.7). Duration of previous low back pain: 1-4 weeks HR = 1.8 (1.2-2.7); > 4 weeks HR = 2.3 (1.6-3.3) Assisting patients to mobilize > 4 times/shift HR = 1.6 (1.1-2.3); moving patients around > 4 times/shift HR = 1.6 (1.1-2.4); transferring patients in/out bath HR = 1.4 (1.0-2.0); washing or dressing patients while on chair > 4 times/shift HR = 1.7 (1.1-2.8); washing or dressing patients while on bed > 4 times/shift HR = 1.6 (1.0-2.5) Not applicable
Chapter 3a ●
Relevance 37
38
Chapter 3a
●
Prevalence, incidence, and risk factors of neck pain in workers
Canadian Institute for the Relief of Pain and Disability (formally known as the Physical Medicine Research Foundation) Woodbridge Grants and Awards Program and by the Institute for Work & Health by the Workplace Safety and Insurance Board of Ontario.
25.
26.
27.
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Slavin RE: Best evidence synthesis: an intelligent alternative to meta-analysis. J Clin Epidemiol 48(1):9-18, 1995. Smedley J, Inskip H, Trevelyan F, Buckle P, Cooper C, Coggon D: Risk factors for incident neck and shoulder pain in hospital nurses. Occup Environ Med 60(11):864-869, 2003. Spitzer WO, Skovron ML, Salmi LR, et al: Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash” and its management [see comment]. [Erratum appears in Spine 20(21):2372, 1995.] Spine (8 Suppl): 1S-73S, 1990. Stewart WF, Ricci JA, Chee E, Morganstein D, Lipton R: Lost productive time and cost due to common pain conditions in the US workforce [see comment]. JAMA 290(18):2443-2454, 2003. Tornqvist EW, Kilbom A, Vingard E, et al: The influence on seeking care because of neck and shoulder disorders from work-related exposures. Epidemiology 12(5):537-545, 2001. Trinkoff AM, Brady B, Nielsen K: Workplace prevention and musculoskeletal injuries in nurses. J Nurs Admin 33(3):153-158, 2003.
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39
Appendix 3a.1
GENERAL METHODOLOGIC ISSUES USED FOR ALL STUDY DESIGN 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Research question is clearly stated Source and target population identified and described Inclusion criteria described and appropriate Exclusion criteria described and appropriate Number of excluded or refusals (before study) reported Withdrawals (during study) reported, explained, and reasonable Withdrawals equal in groups Statistical analyses appropriate Adjustment for important variables measured at entry into study Results verifiable from raw data
CRITERIA FOR THE APPRAISAL OF THE METHODOLOGIC QUALITY OF CROSS-SECTIONAL STUDIES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Similar sampling procedures for all subjects Similar ascertainment of exposure for all subjects Similar referral and diagnostic procedures for all subjects Diagnostic criteria for disease (clear, reliable, and valid) Characteristics of subjects at enrollment reported All aspects of exposure measured (level, dose, duration, etc.) Coexposures measured Recall bias controlled Data collection valid and reliable Selection bias considered Analyses controls for confounding factor
CRITERIA FOR THE APPRAISAL OF THE METHODOLOGIC QUALITY OF COHORT STUDIES 1. Zero time identified 2. Baseline comparability reported (including confounding variables)
3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.
Same data collection for all cohorts Important baseline variables measured, valid, and reliable All aspects of exposure measured (dose, level, duration) Exposure adequately measured (previous, at entry, during study) Regular follow-up periods Coexposures monitored Duration of follow-up adequate Outcome(s) defined and measurable Outcome(s) valid Blind assessment of outcome(s) Analyses controls for confounding
CRITERIA FOR THE APPRAISAL OF THE METHODOLOGIC QUALITY OF CASE-CONTROL STUDIES 1. Similar population sources for cases and controls (time, place, potential for exposure) 2. Referral and sampling independent of exposure 3. Random selection of controls 4. Diagnostic criteria for cases clear, precise, and valid 5. Date of diagnosis for case operationally defined 6. Ascertainment of disease adequate for cases and controls 7. Comparison of cases and controls at enrollment reported (including confounding variables) 8. All aspects of exposure measured (level, dose, duration, etc.) 9. Exposure adequately measured (same in all groups, blinded) 10. Coexposures measured 11. Recall bias controlled 12. Data collection valid and reliable 13. Analysis according to level of exposure 14. Effect of matching assessed
CHAPTER
3b
Biomechanics of the Cervical and Thoracic Spine Jiri Dvorak and Malcolm Pope
BIOMECHANICS OF THE NECK The biomechanics of the cervical spine is determined by the shape of the vertebral bodies and the orientation of the zygapophyseal joints and can accordingly be divided into three sections: ● Upper cervical spine: occiput, atlas, axis; ● Lower cervical spine: C2-C3 to C7; ● Cervical-thoracic junction: C7 to the third thoracic vertebra (Fig. 3b.1). The primary aim of the clinician treating a patient with neck pain is to find the region or even segment responsible for pain symptoms. Because the intersegmental nerve root anastomosis
Upper cervical spine
C2
makes it almost impossible for a patient suffering from neck pain to localize the exact origin of pain,11,12,26 the clinician must base the diagnosis on functional and palpatory examinations of the cervical spine. To do this correctly requires analysis and interpretation of normal and disturbed motion patterns based on a knowledge of clinical biomechanics and an understanding of developmental anatomy. The natural aging process results in many changes in the cervical spine that must be taken into account in the clinical assessment, especially as related to range of motion. It is well established that range of motion decreases with age, mainly in the middle and lower segments of the cervical spine.4 This is due to the ongoing transformation process of the intervertebral disk and the development of uncovertebral joints14,29; later it may also be due to development of osteoarthritis of the zygapophyseal joints. In the first two decades of life, the uncovertebral spaces of the lower part of the cervical spine begin to undergo a lifelong transformation into uncovertebral joints. This transformation is a response to the compressive force of the weight of the head, which the upright posture of the body requires the cervical spine to support (Fig. 3b.2).14,28,29 The result is the formation of lateral tears of the disk annulus beginning in the second decade of life (Fig. 3b.3). These lateral tears continue to develop into the medial center part of the disk until, in the third decade, complete transverse tears commonly occur (Fig. 3b.4).28 The resulting space in the middle of the intervertebral disk partially takes over the function of the zygapophyseal joints during the second and third decades. (At this stage, the nucleus pulposus dries out, appearing on radiographs as a narrowing between the vertebrae of the lower cervical spine, which provides a convenient way for the clinician to monitor these changes.) This new space within the disk significantly reduces the loadabsorbing function of the intervertebral disk in the cervical spine. To support the load of the head, a transformation of the uncovertebral joints starts to occur.28 Instead of the original pointed shape, the uncovertebral processes now become flat
C3
C4
C5
Lower cervical spine
C6
C7
Th1
Th2
Cervical-thoracic junction
Th3
Figure 3b.1
Sections of the cervical spine.
Figure 3b.2 Drawing of the uncovertebral joints. (From Luschka H: Die Halbgelenke des menschlichen Körpers. Berlin, 1858, Reimers.)
42
Chapter 3b
●
Biomechanics of the cervical and thoracic spine
Figure 3b.3 Frontal section of the cervical spine of a 9-year-old child. Remnants of cartilage are still present. The arrow points to a space in the lateral part of the intervertebral disk at level C3-C4.
with a shape like that of a cow horn (Fig. 3b.5) and take over the load of the cranial vertebrae. The overall result is a natural transformation of the structure and shape of the uncovertebral processes that is probably responsible for much of the decreased range of motion that accompanies aging and must be taken into account in any clinical assessment of the cervical spine. In the first two decades of life, the surfaces of the articular processes are covered by a thin layer of cartilage, with the uneven surfaces filled in by a synovial fold in the joint capsule. This synovial fold has been described by Penning and Töndury21 as meniscoid. It is found within the entire cervical spine (Fig. 3b.6) and again degenerates or atrophies with increasing age.
UPPER CERVICAL SPINE: OCCIPUT/C2 The upper cervical spine, which consists of the occiput, atlas, and axis, is responsible for most of the axial rotation and some of the flexion-extension and lateral bending of the head. In addition to allowing large rotations, it must be stable enough to support the weight of the head and protect the delicate spinal cord and intervertebral arteries from injury and is therefore quite a complicated structure. Possible motion in the atlantooccipital and atlantoaxial joints is determined by the orientation of the articular processes. The occipital condyles are an oval-shaped bean-like form with a sagittal orientation of the joint axis of 28 degrees on average (Fig. 3b.7).8,10 The frontal orientation of the joint axis (Fig. 3b.8) averages 124 degrees in males and 127 degrees in females.9,27 The motion axis of the atlantooccipital joints was described by Knese9 (Fig. 3b.9). The atlantooccipital joints are described as a spheroid articulation. They are connected with a tight joint
Figure 3b.4 Frontal section of the cervical spine of a 33-year-old man. In the three lowest segments, each intervertebral disk shows a complete transverse tear; however, the upper two levels have only lateral tears. (From Töndury G, Theiler K: Entwicklungsgeschichte und Fehlbildungen der Wirbelsäule, ed 2, Stuttgart, Germany, 1990, Hippokrates-Verlag.)
capsule that limits the movements possible. The dominant movement in the atlantooccipital joint is flexion and extension of approximately 22 to 24 degrees, according to the author. Lateral bending, again according to the author, is between 5 and 10 degrees. The idea of axial rotation in this joint has long been rejected; however, newer investigations by Dvorak et al7 showed axial rotation in both in vitro and in vivo studies. A summary of movements possible in the atlantooccipital joint is shown in Table 3b.1. The atlantoaxial joint consists of four joint spaces: the two atlantoaxial lateral joints, the atlantoaxial median joint (between the anterior arch of the atlas and the dens axis), and a joint between the posterior surface of the dens and the transverse ligament, which is connected to the anterior joint space. From the medial part arises a large synovial fold in the lateral atlantoaxial joint (Fig. 3b.10).4 This joint capsule is loose, which allows for a great deal of motion. It is here that most of the axial rotation occurs. The movements possible in the atlantoaxial joints are summarized in Table 3b.2. Motion within the upper cervical spine, especially in the atlantoaxial joint, is mainly limited by ligaments that, with exception of the tectorial membrane, consist of nonstretchable collagen fibers.24,25 The tectorial membrane, which consists of elastic fibers, inserts at the great occipital foramen and distally joins the posterior longitudinal ligament. The biomechanical properties of the tectorial membrane have been studied by Oda et al,17 who documented their large elasticity.
Chapter 3b
●
Upper cervical spine: occiput/C2
Figure 3b.5 Cow horn-like shapes (arrows). Changes of the uncovertebral disks at the C4-C5 and C5-C6 levels of the same subject at the age of 47 years (A) and 49 years (B). At the same level on the lateral views, anterior and posterior osteophytes are starting to form (C and D) and narrow the intervertebral foramen at the C5-C6 level (E and F).
A
B
C
D
E
F
43
44
Chapter 3b
●
Biomechanics of the cervical and thoracic spine
Frontal orientation of joint axis 124°
Figure 3b.8 Frontal orientation of the occipital condyles according to Stoff. (From Stoff E: Verh Anat Gesch Jena 70:575, 1976.)
Y-axis
Figure 3b.6 Parasagittal section of the intervertebral joints (zygapophyseal joints) at the level of C4 and C6. The articular processes show an inclination of approximately 45 degrees. The arrow points to the synovial folds in between the intervertebral joint surfaces, which have been described by Penning and Töndury as meniscoid. (Courtesy Professor Doctor W. Rauschning, Uppsala, Sweden.)
Z-axis
X-axis
Figure 3b.9 Possible joint axis of the upper cervical spine according to Knese. (From Knese KH: Z Anat Entwickl 114:67-107, 1949.)
Table 3b.1 Possible movements in the atlantooccipital joint according to different authors Occipto-C1 joint Fick (1904) Poirer and Charpy (1926) Werne (1957)30 Penning (1978)20 Dvorak et al (1985) Clark et al (1986) Dvorak et al (1987)3 Penning and Wilmink (1987)22 Panjabi et al (1988)19
Figure 3b.7 Sagittal orientation of the occipital condyles is 28 degrees on average. (From Ingelmark BE: Acta Anat (Basel) 6:1-48, 1947.)
Flexion/extension (total) rotation Side bending (one side) (one side) Axial 50
30-40
0
50 13 35 — 22.7 —
14-40 8 10 — — —
0 0 0 5.2 4.8 4
— 24.5
— 5.5
1 7.2
Chapter 3b
A Figure 3b.10
●
Upper cervical spine: occiput/C2
B
Dissection of normal left atlantoaxial meniscoid from a fresh cadaveric specimen (A); the surface is covered with meniscoid (B).
The cruciate ligament (Fig. 3b.11) has the important function of restricting potentially dangerous anterior gliding of the atlas during flexion movement of the head while still allowing the atlas to turn freely around the dens during axial rotation. It consists of two main parts: a horizontally oriented transverse ligament and vertically oriented longitudinal fibers. The transverse ligament inserts at the medial portion of the lateral mass of the atlas. The caudal fibers are occasionally fixed at the base of the dens and may additionally stabilize the dens (Fig. 3b.12). At the level of the dens is a thin layer of cartilage covering
Table 3b.2 Summary of possible motions at the atlantoaxial joint according to various authors
C1-C2 joint Fick (1904) Poirer and Charpy (1926) Werne (1957)30 Penning (1978)20 Dvorak et al (1985) Clark et al (1986) Dvorak et al (1987)3 Penning and Wilmink (1987)22 Panjabi et al (1988)19
Flexion/ extension (total)
Side bending (one side)
Axial rotation (one side)
0
0
60
11 10 30 — 10 —
— 0 10 — — —
30-80 47 70 32.2 14.5 43.1
— 22.4
— 6.7
40.5 38.9
the transverse ligament,5 which allows the ligament to move more freely and protects it from damage caused by friction. The transverse ligament consists exclusively of collagen fibers with an interesting fiber orientation similar to a folding lattice (Fig. 3b.13). This allows extensive stretching of the ligament during axial rotation without damage to the fibers. In vitro experiments show failure of the transverse ligament to occur between 170 and 700 N.5 The main limiting structures for the upper cervical spine are the alar ligaments. Consisting exclusively of nonstretchable collagen fibers, the alar ligaments connect the dens axis with the occipital condyles and the anterior arch of the atlas (Fig. 3b.12).1,3,13 Occasionally, a loose connection is also found between the basis of the dens axis and the anterior arch of the atlas3; this has been described by Von Barrow as the atlantodental anterior ligament. According to Werne,30 alar ligaments are of great importance in limiting axial rotation (Fig. 3b.14), a belief that has been confirmed by newer investigations.5,18 In conjunction with the tectorial membrane, the alar ligaments also limit flexion of the occiput. During lateral bending (Fig. 3b.15), the alar ligament is responsible for forced rotation of the second vertebra.5,30 The apical ligament has no functional meaning and is actually a rudiment of the chorda dorsalis.10 Clinical analysis of upper cervical spine motion can be done through the use of functional radiographs. In the anteroposterior view, lateral bending can be assessed.23 Physiologic movements, gliding of the atlas in bending direction, and forced rotation of the axis are presented in Figure 3b.16 as seen on functional radiographs. Axial rotation is currently assessed through measurements of functional computed tomography and may in the future be tested by functional magnetic resonance imaging (Fig. 3b.17).2,6
45
46
Chapter 3b
●
Biomechanics of the cervical and thoracic spine
Clivus
Dura Jugular foramen
Tectorial membrane Hypoglossal canal Transverse occipital ligament Alar ligament Cruciate ligament
Atlantooccipital articulation
Atlantoaxial articulation
Posterior longitudinal ligament
Transverse ligament
Figure 3b.11 Ligaments of the upper cervical spine, posterior view. (From Lang J: Klinische Anatomie der Halswirbelsäule. New York, 1991, Georg Thieme Verlag.)
LOWER CERVICAL SPINE The anatomic structures of the motion segments of the lower cervical spine are different from those in the upper cervical spine. Their particularities include the uncovertebral joints, which support part of the axial load once the intervertebral disk loses its elasticity due to age-related transformations.14,28,29 The articular processes of the cervical spine are inclined approximately 45 degrees from the horizontal plane (Fig. 3b.18), with steeper inclinations in the lower segments. The transverse processes hide and protect the spinal nerve and vertebral artery.
Anterior atlantodental ligament Alar ligament (atlantal portion)
Alar ligament (occipital portion) Transverse ligament Figure 3b.12 Drawing of the ligaments of the upper cervical spine (axial dissection). (From Dvorak J, Froehlich D, Penning L, Baumgartner H, Panjabi MM: Spine 13(7):748-755, 1988.)
The motion segments are connected and stabilized by ligaments, anteriorly by the anterior longitudinal ligament (Fig. 3b.19) and dorsally by the posterior longitudinal ligament. The density of nociceptive and mechanoreceptive innervation of the posterior longitudinal ligament is high in comparison with other cervical spine ligaments and the disk.16 This results in a very sensitive ligament that indirectly controls the innervation of neck muscles through nociceptive and mechanoreceptive reflexes.32 The laminae are connected by the strong ligamentum flavum, which consists almost exclusively of elastic fibers and is a major limiting structure in flexion movement. The dominant motion in the lower cervical spine is flexionextension. Different parameters can be measured with flexionextension x-ray views, including segmental rotation, translatory movement, and the location of the center of rotation (Fig. 3b.20).7 Because a significant motion difference exists between actively and passively performed movements, the use of passively performed radiographs has been recommended in diagnosing segmental instability, such as can occur after trauma (Fig. 3b.21).6,7 The first description of the center of rotation in healthy adults came from Penning and Töndury’s measurements21 of flexion and extension radiographs. The center of rotation has been determined with computer-assisted methods7 and has confirmed Penning and Töndury’s findings (Fig. 3b.22). Table 3b.3 shows the relevant data on flexion-extension movements of healthy adults for in vitro and in vivo examinations. Table 3b.4 presents data on rotation, translation, and center of rotation as measured by computer-assisted methods on a healthy population.7 Lysell15 described the so-called top angle, or segmental arch, as being flat at the level of C2 and steep at the lower cervical spine. Motion of the upper segments during flexion-extension is therefore fairly horizontal, whereas motion of the lower segments is more like that of an arc (Fig. 3b.23).
Chapter 3b
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Lower cervical spine
Figure 3b.13 The orientation of the collagen fibers of the transverse ligament is similar to a folding lattice and allows extensive stretching of the ligament during flexion and axial rotation without damage to the fibers.
Figure 3b.14 Drawing of possible movements in the atlantoaxial joint during axial rotation of the head according to Werne. (From Werne S: Acta Orthop Scand Suppl 23:80, 1957.)
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Left lateral bending –∅z
y
Figure 3b.15 Function of the alar ligaments during side bending of the head. (From Dvorak J, Froehlich D, Penning L, Baumgartner H, Panjabi MM: Spine 13(7):748-755, 1988.)
Right lateral bending y y
y1
+∅z y1
C0
C1 +x
–x + ∅y
+∅y C2
Figure 3b.16 Forced rotation of the axis and gliding of the atlas in the direction of bending as seen from functional radiographs in the anteroposterior view. (From Reich C, Dvorak J: Manual Med 2, 1986.)
Figure 3b.17 Functional computed tomography of the upper cervical spine during axial rotation within the atlantoaxial and atlantooccipital joints.
Chapter 3b
Figure 3b.17
●
Lower cervical spine
Cont’d
Figure 3b.18 Orientation of the articular processes of the lower cervical spine in the frontal plane. (From White AA, Panjabi MM: Clinical biomechanics of the spine, ed 2. Philadelphia, 1990, JB Lippincott.)
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Biomechanics of the cervical and thoracic spine
Figure 3b.19 Ligaments of the anterior and posterior parts at the lower cervical spine. (From White AA, Panjabi MM: Clinical biomechanics of the spine, ed 2. Philadelphia, 1990, JB Lippincott.)
D
G F
A C B E D
H I
G. Facets F. Capsular ligament
E. Intertransverse ligament A. Anterior longitudinal ligament
I. Interspinous and superspinous ligaments
B. Anterior one-half annulus fibrosus C. Posterior one-half annulus fibrosus
H. Ligamentum flavum
D. Posterior longitudinal ligament
Y RX
BY BZ
+Y AY
+RY AZ
+RX +X +Z
+RZ CRY Z X
CRZ
Figure 3b.20 Parameters for measurement of segmental motion using computer-assisted methods. RX is the rotation about the x-axis; CRY and CRZ are the centers of rotation of the Y and Z rotations, respectively; AY, AZ, BY, and BZ are the translations of point A in the Y and Z directions and point B in the Y and Z directions, respectively.
Chapter 3b
A
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Lower cervical spine
B
D
C Figure 3b.21 Female, aged 51, 1 year after injury to the cervical spine. The examination has been performed during active and passive motion (A-D) and measured according to Penning’s method (E and F).
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Biomechanics of the cervical and thoracic spine
35
Figure 3b.21 Cont’d According to the functional diagram, there is a significant difference in segmental motion, especially as related to segments C3-C4 and C6-C7. Drawing the vertebral bodies on a transparent paper (G) makes the difference obvious. (From Dvorak J, Froehlich D, Penning L, Baumgartner H, Panjabi MM: Spine 13(7):748-755, 1988.)
Hypermobile 30 25
Passive
20 15 10 5 0 C1/C2
C2/C3
E
C3/C4
C4/C5
C5/C6
C6/C7
Average + 2 STDV Average + 1 STDV Average Average – 1 STDV Average – 2 STDV Z.A., F, 51y
35 30 25
Active
20 15 10 Hypomobile
5 0 C1/C2a
C2/C3a
F
C3/C4a
C4/C5a
Average + 2 STDV Average + 1 STDV Average Average – 1 STDV Average – 2 STDV Z.A., F, 51y
Active
Active Passive
Passive
Hypermobile
G
Z.A., f, 51Y
C5/C6a
C6/C7a
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53
Table 3b.4 Averages and standard deviations of rotations, translations, and coordinates of center of rotation as measured by computer-assisted methods Parameter* C1-C2 C2-C3 C3-C4 C4-C5 C5-C6 C6-C7 RX (deg) Male RX (deg) Female AZ (mm) AY (mm) BZ (mm) BY (mm) Penning
Dvorak
Figure 3b.22 Determination of the center of rotation by graphic method (Penning, 1960) and by using computer-assisted methods on a normal population. (From Dvorak J, Schneider E, Saldinger P, Rahn B: J Orthop Res 9:828-834, 1991.)
CRZ (mm) CRY (mm)
15.4 6.1 12.9 3.4 –3.8 1.6 6.2 2.3 –1.4 1.4 8.1 3.0 –4.1 4.2 30.0 5.6
11.7 3.1 12.3 3.0 2.4 0.9 1.8 0.8 6.9 1.7 3.0 1.3 4.0 3.5 9.4 4.8
16.0 2.5 18.3 4.7 3.2 1.0 2.3 1.0 8.5 1.8 3.6 1.2 4.3 2.7 9.7 3.4
20.1 2.8 22.1 3.9 3.6 1.2 2.9 0.7 10.0 1.9 4.2 1.0 6.0 2.2 10.4 2.8
21.5 3.9 24.1 4.0 2.9 1.1 3.2 0.8 9.8 1.9 4.3 1.0 6.4 1.8 12.9 2.5
21.0 4.0 21.8 3.5 2.0 0.9 3.1 0.8 8.4 1.9 3.9 0.9 6.4 2.5 17.2 2.1
*See Figure 3b.20 for definitions.
Table 3b.3
Summary of flexion-extension movements of healthy adults in vivo and in vitro
Flexion/Extension (Total) C2-C3 C3-C4 C4-C5 C5-C6 C6-C7
Dvorak (1988) (In Vivo/Passive)
Dvorak (1988) (In Vivo/Active)
10.0 15.0 19.0 20.0 19.0
12.0 17.0 21.0 23.0 21.0
White and Panjabi
(1978)31
8.0 13.0 12.0 17.0 16.0
Penning (1978)20 (In Vivo/Active) 12.0 18.0 20.0 20.0 15.0
C2
C4
C7
Figure 3b.23 Segmental arch of the top angle according to Lysell.9 The flatter the articular surfaces, the flatter the top angle of the motion segments and vice versa.
Left bending
Neutral
Right bending
Figure 3b.24 Coupled axial rotation during lateral bending of the head. (From White AA, Panjabi MM: Clinical biomechanics of the spine, ed 2. Philadelphia, 1990, JB Lippincott.)
Chapter 3b
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Biomechanics of the cervical and thoracic spine
Table 3b.5a Values of main lateral bending according to various authors Main side bending (one side)
Moroney (1988) (in vitro FSU)
C2-C3 C3-C4 C4-C5 C5-C6 C6-C7
4.7 4.7 4.7 4.7 4.7
Table 3b.5b Values of coupled axial rotation according to various authors
White and Penning (1978)20 Panjabi (in vivo/active) (1978)31 6.0 6.0 6.0 6.0 6.0
10.0 11.0 11.0 8.0 7.0
Coupled axial rotation (one side) C2-C3 C3-C4 C4-C5 C5-C6 C6-C7
Dvorak (1987)3 (in vivo/passive) 3.0 6.5 6.7 7.0 5.4
Penning (1978)20 (in vivo/ active) 3.0 6.5 6.8 6.9 5.4
White and Panjabi (1978)31 9.0 11.0 12.0 10.0 9.0
FSU, functional spinal unit.
Lateral bending of the cervical spine is normally coupled with axial rotation to the same side.15,31 This means that the spinal processes are moving in a direction opposite the motion (Fig. 3b.24). This coupled motion is of clinical importance because palpation of the spinal processes can serve as an indirect indicator of disturbed function in motion segments. The lateral bending of the cervical spine below the first cervical vertebra has been variously reported by different researchers. According to Penning,20 the lateral bending is 35 degrees, whereas White and Panjabi31 reported between 4 and 10 degrees per motion segment. Axial rotation, as measured with functional computed tomography, is between 3 and 7 degrees,2,22 but an in vitro study19 showed a higher result, between 8 and 12 degrees. Tables 3b.5a and 3b.5b summarize the segmental motions for lateral bending with coupled axial rotation according to various authors.
10. 11. 12. 13. 14. 15. 16. 17. 18. 19.
20. 21.
REFERENCES
22. 23.
1. 2.
Cave AJE: On the occipito-atlanto-axial articulations. J Anat (Lond) 68:416, 1934. Dvorak J, Hayek J, Zehnder R: CT-functional diagnostics of the rotatory instability of upper cervical spine. Part 2. An evaluation on healthy adults and patients with suspected instability. Spine 12:726-731, 1987. 3. Dvorak J, Panjabi MM: Functional anatomy of the alar ligaments. Spine 12:183-189, 1987. 4. Dvorak J, Antinnes JA, Panjabi M, Loustalot D, Bonomo M: Age and gender-related normal motion of the cervical spine. Spine 17(105):5393, 1992. 5. Dvorak J, Schneider E, Saldinger P, Rahn B: Biomechanics of the craniocervical region: the alar and transverse ligaments. J Orthop Res 6:452-461, 1988. 6. Dvorak J, Froehlich D, Penning L, Baumgartner H, Panjabi MM: Functional radiographic diagnosis of the cervical spine: flexion/extension. Spine 13(7):748-755, 1988. 7. Dvorak J, Panjabi MM, Novotny JE, Antinnes JA: In vivo flexion/extension of the normal cervical spine. J Orthop Res 9:828-834, 1991. 8. Ingelmark BE: Üeber den cranicervicalen Übergang beim Menschen. Acta Anat (Basel) 6:1-48, 1947. 9. Knese KH: Kopfgelenk, Kopfhaltung und Kopfbewegung des Menschen. Z Anat Entwickl 114:67-107, 1949.
24.
25. 26. 27. 28. 29. 30. 31. 32.
Lang J: Craniocervical region, osteology and articulations. Neuroorthopedics 1:67-92, 1986. Lang J: Klinische Anatomie der Halswirbelsäule. New York, 1991, Georg Thieme Verlag. Lang J, Bartram CT: Ueber die Fila articularia der Radices ventrales et dorsales des menschlichen Rückenmarkes. Gegenbaurs Morphol 128:417-462, 1982. Ludwig K: Üeber das Lig. alare dentis. Z Anat Entwickl Gesch 116:442, 1952. Luschka H: Die Halbgelenke des menschlichen Körpers. Berlin, 1858, Reimers. Lysell E: Motion in the cervical spine. An experimental study on autopsy specimens. Acta Orthop Scand Suppl 123:1-61, 1969. Mendel T, Wink CS, Zimny ML: Neural elements in human cervical intervertebral discs. Spine 17(2):132-135, 1992. Oda T, Panjabi MM, Crisco JJ, Bueff HU, Grob D, Dvorak J: Role of tectorial membrane in the stability of the upper cervical spine. Clin Biomech 7(4):201-207, 1992. Panjabi M, Dvorak J, Crisco JJ, Oda T, Wang P, Grob D: Effects of alar ligament transection on upper cervical spine rotation. J Orthop Res 9:584-593, 1991. Panjabi MM, Dvorak J, Duranceau J, Yamamoto I, Gerber M, Rauschning W, Beuff HU: Three-dimensional movements of the upper cervical spine. Spine 13(7):726-730, 1988. Penning L: Normal movement of the cervical spine. AJR Am J Roentgenol 130: 317-326, 1978. Penning L, Töndury G: Entstehung, Bau und Funktion der meniskoiden Strukturen in den Halswirbelgelenken. Z Orthop 98:1-14, 1964. Penning L, Wilmink JT: Rotation of the cervical spine: a CT study in normal subjects. Spine 12:732-738, 1987. Reich C, Dvorak J: The functional evaluation of craniocervical ligaments in sidebending using x-rays. Manual Med 2, 1986. Saldinger PF: Histologische Untersuchung des kraniozervikalen Bandapparates im Hinblick auf Weichteilverletzungen der Halswirbelsöule. Diss. med., Bern, 1987 (Leitung J. Dvorak). Saldinger PF, Dvorak J, Rahn BA, Perren SM: Histology of the alar and transverse ligaments. Spine 15:257-261, 1990. Simmons E, Marzo J, Kallen F: Intradural connections between adjacent cervical spinal roots. Spine 12(10):964-968, 1987. Stoff E: Zur Morphometrie des oberen Kopfgelenks. Verh Anat Gesch Jena 70:575, 1976. Töndury G, Theiler K: Entwicklungsgeschichte und Fehlbildungen der Wirbelsäule, ed 1. Stuttgart, Germany, 1958, Hippokrates-Verlag. Töndury G, Theiler K: Entwicklungsgeschichte und Fehlbildungen der Wirbelsäule, ed 2. Stuttgart, Germany, 1990, Hippokrates-Verlag. Werne S: Studies in spontaneous atlas dislocation. Acta Orthop Scand Suppl 23:80, 1957. White AA, Panjabi MM: The basic kinematics of the human spine. Spine 3:12-20, 1978. Wyke B: Neurological mechanisms in the experience of pain. Acupunct Electrother Res 4:27-35, 1979.
CHAPTER
3c
Evaluation of the Neck Ronald Moskovich and Anthony Petrizzo
Neck, or cervical spine, pain with concomitant disability is a common presentation among injured workers. Neck pain, however, is less prevalent than low back pain as a cause of worker absenteeism and represents less than 2% of all workplace injuries. The 1-year prevalence rate of non–work-related neck pain in most industrialized countries is approximately 20%; the prevalence of neck pain during a 1-month period in the United Kingdom is reported to be 14%.21 In a cohort of patients with neck pain, almost half had persistent neck pain 1 year later.10 Overall, back pain is commonly cited as the second leading cause of absenteeism in workers and the primary cause of workers’ compensation claims. In the Saskatchewan working age population, 10% experience severe neck pain, with up to 5% having neck pain that severely affects their activities of daily living.4 Most of these injuries are diagnosed as either a strain or sprain. For these types of milder neck injuries, analogous to the lower spine, it is a challenge to determine the precise pathoanatomic diagnosis before the initiation of therapy.
STANDARD EXAMINATION Evaluation of the cervical spine requires a history, using standard interviewing principles; a physical examination, focused on elimination of the pertinent negatives; and utilization of functional assessment scales to measure the impact of cervical dysfunction on common daily activities. This crucial assessment of the history with specific questions is used to rule out or determine the need for an urgent workup, a static and/or dynamic physical examination, laboratory studies, and further diagnostic and prognostic evaluations. Although the approach to a patient injured at work should not differ from that of a patient who injured his or her neck during recreational activity, patients referred for work-related cervical spine injury have another aspect added to their evaluation and assessment: critical return of the patient to pre- or near preinjury function to resume prior income-related activities as soon as possible.
DISABILITY EXAMINATION The critical distinction between a standard medical examination and a disability examination or impairment evaluation, lies not only in obtaining the information, but what to do once pertinent information is obtained (Table 3c.1).5 For example, once it is determined that a patient fell at work and is diagnosed and treated for the neck injury, the patient must be further evaluated for his or her ability to attend work and function in the workplace, albeit with possible job modifications.
This is referred to as a disability evaluation or examination. A more comprehensive overview of a disability evaluation is described below.5
IMPAIRMENT EVALUATION An impairment evaluation is another type of assessment tool regarding injury in the workplace. The distinctive contribution of an impairment evaluation is the measure of functional loss or derangement of any body part, organ, or organ system. Another purpose of an impairment evaluation is to measure, define, and determine the status of the patient’s (claimant’s) general health at a particular point in time. Establishing impairment can be accomplished using different objective methods, based on guidelines set by the American Medical Association.3 A diagnosis-related estimate is an impairment method based on eight diagnosis-related categories (i.e., muscle atrophy, guarding, asymmetric motion) for each of the three spinal regions. A second approach in the diagnosis-related estimate method is the diagnosis of a fracture or dislocation of the spine that, after appropriate tests and treatment has been rendered, requires no further verification. Impairment can also be documented based on assessment of the patient’s range of motion (ROM). This method is based on loss of active range of motion (AROM) in addition to an accompanying diagnosis and a spinal nerve deficit. The AROM approach is usually reserved for instances when a diagnosisrelated estimate is not applicable.3 Interestingly, the ability to participate in work activity is not included in calculating impairment percentages. The impairment evaluation is performed after the patient is determined to have achieved the highest possible level of recovery but before they return to work-related activity. Any deviation from predetermined normal criteria or from the patient’s prior health status is translated into an impairment rating. Impairment can then be converted to impairment percentages, which reflect the degree to which the impairment decreases the individual’s ability to perform activities of daily living. The development of an impairment rating is based on clinical decision making, whereas its purpose usually is to determine financial remuneration to the claimant by a third party.5
Table 3c.1 1. 2. 3. 4. 5. 6. 7. 8.
Goals of a disability examination5
Establish a diagnosis Quantify impairment Determine if examinee is capable of performing specified tasks Determine if examinee can attend work Determine if examinee can work in the occupational environment Determine if worker poses a threat to others in the workplace Make a recommendation regarding job modifications Extrapolate into the future a. Recommend treatment(s) b. Derive a time course c. Specify how treatment(s)/time will change points 1 through 7
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Evaluation of the neck
EVIDENCE-BASED MEDICINE In recent years, there has been a shift by research and evaluative bodies to apply evidence-based medicine (EBM) techniques and outcomes as a foundation for clinical decision making.11 The U.S. Agency for Health Care Policy and Research (AHCPR), which convenes expert multidisciplinary nonfederal panels to develop clinical practice guidelines for specific conditions and treatments, has similarly embraced the EBM perspective: Comprehensive evaluation of the results from randomized control studies is the best available scientific evidence on which to base clinical decision making. The working goal of the AHCPR’s musculoskeletal panel is to determine a model for the clinical utility of various diagnostic and therapeutic interventions for low back pain.5 This model for evaluating low back pain, although not interchangeable for cervical issues, has sound principles that can be effectively applied to treat cervical spine disorders. The AHCPR promotes a change in the former paradigm for treating acute low back pain, from focusing care exclusively on the pain itself to improving patients’ activity tolerance once all red flags for critical disorders have been eliminated.1 It is our suggestion that the low back pain model, although not a blueprint for management, can be applied to effectively treat cervical disorders as well. The fact that this approach could be advantageous for both clinician and patient, at minimum, underscores the importance and necessity of excluding red flags through the history and physical examination. The fact that the patient would now be more focused on movement behavior, and perhaps earlier than with prior treatment paradigms, underscores an added relevance to work-related injury cases. An interest in consistent and well-substantiated assessment and treatment paradigms are not limited to clinical medicine settings. A landmark U.S. Supreme Court ruling, in 1993, amended the Federal Rules of Evidence to require experts giving medical depositions to have reliable data to substantiate their testimony.2 Since that ruling, concepts supporting and policies enforcing EBM have expanded through input from epidemiology, outcomes research, policy makers, and clinicians. To adopt an evidencebased approach for the care of patients with neck problems, it is important that practicing clinicians understand the process of critically evaluating the accuracy of individual studies in the literature, know the natural history of cervical spine disorders, and be able to use that knowledge and their clinical experience as a check-and-balance to their practice decisions.
HISTORY Interview A description of the injury and of the precipitating events provides indispensable information for the treating physician. The inciting incident can be acute in onset or chronic with a progressing debility. Documentation must include how and when the precipitating event occurred as well as its duration. The history should begin with the identification and essential demographics of the patient: age, sex, race, and occupation. The chief complaint(s) should be recorded, at least initially, in
the patient’s own words. History of the present illness should include the location, duration, and concise description of symptoms and the timing, setting, any aggravating or relieving factors, and associated manifestations and prior treatments, to include their effects. It is important to establish whether or not there is a relationship between the injury and symptoms and the patient’s work activities and/or work setting. This part of the history may require close attention to draw subtle but meaningful information from the patient, in part because their pain or discomfort can make this information difficult to convey or because they may not be aware of the relationship. From this type of detailed dialogue with the patient, a statement of the probability that the injury is work-related is developed. The primary cause of many injuries can be obvious, whereas causes or etiologies of the injuries require deeper evaluation. Patients commonly present with neck complaints after a vehicular injury, a fall, or rough sport contact. Workers who perform overhead activities or who carry loads that could strain the neck muscles may also develop debilitating neck or arm pain. The symptoms of cervical disease can radiate cephalad to the skull or caudal to the extremities, where repetitive light to moderate work activity may be poorly tolerated and reveal underlying existing pathologies. The presence of a radicular component to the patient’s pathology necessitates documentation of the nature and sources of each of the symptoms. The patient’s prior medical history and a review of systems provide an account of his or her general state of health. A thorough musculoskeletal history should be done to establish the presence or absence of overall joint pain, stiffness, swelling, arthritis, gout, and low back pain. All illnesses and surgeries should be recorded. A history of gastrointestinal diseases, specifically gastritis and ulcerative disorders, should be taken, because patients with cervical ailments may require treatment with nonsteroidal antiinflammatory drugs. Specific hereditary predisposing conditions for inflammatory arthropathies, such as rheumatoid arthritis, psoriatic arthritis, and ankylosis spondylitis, may be discovered in the review of family history. Details of tobacco smoking should also be incorporated into the history. Positive associations between current smoking and nonspecific back pain were found in 18 of 26 studies in men and 18 of 20 studies in women.3 Any history of accidents, at work or home, or occupational exposures must be explored, because they can reveal risky habits or hazardous conditions. Relevant workers’ compensation issues should begin to emerge through the history, but their presence or impact may continue to be revealed during care of the patient. A comprehensive psychosocial history is a valuable but often overlooked part of the evaluation. Nonphysical or psychosocial factors such as job or life satisfaction can affect disability status and treatment outcome. Key features of this review include the patient’s life-style, home situation, and vocational and recreational activities. Notably, a history of mental illness, in particular depression and anxiety, must be addressed. Patients may be reticent to disclose such information, so its importance and practical function for treatment and recovery should be carefully and objectively expressed to the patient and, if necessary, sensitively probed. Finally, a list of the patient’s current medications, including prescription, herbal, holistic, over-the-counter, and “borrowed” must be reviewed.
Chapter 3c
Table 3c.2
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Physical examination
Red flags in cervical spine evaluation
Tumor
Osteomyelitis
Spinal cord compression
Trauma
Age > 50 Cancer history Unexplained weight loss Nocturnal pain
Intravenous drug abuse History of immunosuppression History of fever, night sweats History of urinary tract infection or skin infection
Bowel/bladder dysfunction Gait dysfunction, balance problems Fine motor dysfunction, clumsiness Arm pain, weakness
Trauma in patient < 50 years Low velocity trauma in patient > 50 Corticosteroid use
Modified from Clinical Practice Guidelines, AHCPR.
Red flags After inquiring about the presenting complaint, it is appropriate to focus on “red flags,” the presence of which command urgent evaluation. These red flags include a history of trauma, tumor, or infection, among others. Patients should be questioned regarding changes in any bowel and bladder habits, specifically an inability to fully empty the bladder, a feeling of fullness after urinating, and any history of bladder or bowel incontinence. Again, these may be difficult questions for patients, and they should understand that even quite minimal changes in these behaviors may be important to follow-up if they occur with any frequency or intermittency. Even though a neurologic examination will be done, it is important to question the patient about noticing any loss of manual dexterity as well as the development of headaches. Patients should be specifically questioned regarding recent fever, weight loss, night sweats, and nocturnal pain. Table 3c.2 identifies some of the more common red flags.
PHYSICAL EXAMINATION Inspection The physical examination typically begins with a general visual inspection of the patient’s health and conditioning. It is important to inspect the skin for general and isolated color changes. Warmth and redness are common physical findings with acute musculoskeletal strain. Posture is examined for asymmetry in positions such as lateral bending or rotation and the presence of abnormal sagittal and coronal curves. Ambulation should be observed for an ataxic broad-based gait, commonly seen in myelopathy, and any inability to heel-walk or toe-walk, seen with motor weakness and ability to accomplish tandem gait (walk on a straight line), which may be compromised in myelopathy or cerebellar disorders.
Range of motion A regional evaluation of the spine is part of the overall assessment. The spine has four normal sagittal curves. There is a fixed sacral kyphosis and a primary thoracic kyphosis that are apparent at birth. Cervical lordosis develops when the infant can maintain an upright head posture. The next curve, which typically develops once a child starts to walk, is the lumbar lordosis. Between each
of the sagittal curves is a transition zone where alignment is neutral relative to the vertical sagittal axis of the body. The cervical spine is well balanced in the sagittal plane so that C1 and C7 should be centered over the weight-bearing axis, and a plumb line should descend through T12 and continue caudally through the anterior portion of S1. The cervical lordotic curve normally ranges from 25 to 50 degrees with an apex at C4 (Fig. 3c.1). Assessment of cervical ROM is important from a functional and diagnostic perspective. ROM should be assessed with an inclinometer and recorded during the examination. Inclinometers can be mechanical or electronic, and the use of even a simple home-made device is preferable to a “guestimation.” An inclinometer can easily be made by punching a small hole through the center point of a protractor, passing a string through the hole and through a washer (to act as a weight), and tying the string in a loop. The loop of string indicates the degree of inclination on the protractor scale. A plastic scoliosis protractor can be used or a paper protractor downloaded from www.eece.ksu.edu/∼hkn/ files/protractor.pdf and pasted onto a card for use. C1, C2, and C7 are atypical vertebrae with respect to morphology and function, whereas C3 to C6 are commonly described as typical cervical vertebrae. The atlantooccipital joint acts as a pivot for the flexion/extension motion of the cranium, with 13 degrees average flexion/extension and 8 degrees lateral bending, allowing only a few degrees axial rotation.6 The atlantoaxial complex (C1-C2) has a total axial rotation of approximately 80-90 degrees, coupled with a flexion and extension of approximately 10 degrees and minor lateral bending. The prominent motion of the subaxial cervical spine is flexion/extension with some segmental rotation, the latter being both facilitated and constrained by the alignment of the apophyseal joints and the presence of the uncinate processes. The C5-C6 interspace is generally found to have the greatest range of flexion and extension motion of the subaxial spine.6 Subtle secondary motion, or coupled motion, of the cervical spine occurs in response to the primary motion. The coupled pattern of the cervical spine occurs with motion in the axial, sagittal, or coronal plane, for example, the direction of axial rotation in the subaxial spine is such that the spinous processes rotate into the convexity of the spine on side bending. AROM is performed by the patient at the instruction of the examiner and is one of the cornerstones in the determination of functional limits, assessment of improvement, and demonstration of disability when evaluating permanent impairment.5 AROM is performed by the patient alone on instruction by
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Evaluation of the neck
Figure 3c.1 Lateral radiographs of the cervical spine of various individuals of different ages. Clockwise from top left: A 16-year-old girl with normal cervical spine lordosis and normal disk space. A 46-year-old woman with mild loss of the normal cervical lordosis, noted in the mid-upper cervical spine. A 51-year-old woman with multilevel cervical spondylosis manifesting as narrowing of the intervertebral disk spaces at C4-C5 and C5-C6 with endplate changes and marginal osteophytes. A 73-year-old woman with advanced spondylosis and a frank reversal of the normal cervical lordosis as a result of marked multilevel diskogenic degenerative changes.
the examiner. In passive range of motion (PROM), the patient is assisted by the examiner to reach the maximum range. Often, PROM allows for more ROM in all planes. In the absence of pain, PROM can be performed to the anatomic barrier, whereas AROM is typically hindered by a physiologic barrier created by extant pathology or patterns of disuse not related to the presenting symptoms. ROM of the cervical spine is performed by having the patient rotate the head to the right and to the left. End points of motion should be symmetric. The patient should
be able to bend the head to the right and left, as though attempting to touch the ear to the shoulder but keep the shoulder from rising at the same time. This motion is also referred to as side or lateral bending. Flexion/extension ROM is assessed by having the patient flex or touch the chin to the chest and then extend or bend the neck backward. Neck extension is generally restricted and may be painful for patients with cervical stenosis or nerve root compression, although the opposite may also occur. All these motions should be recorded in degrees using a goniometer
Chapter 3c
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Neurologic examination
or, preferably, an inclinometer. Spurling’s test (see below) may be administered at this time.
Palpation While the patient is lying down, a thorough palpatory assessment of muscle tension, tenderness, and tissue texture abnormalities from spasm or contracture of the superficial anterior and posterior musculature must be performed. The examination of the neck with the patient seated and the examination of the upper thoracic spine are often integrated. The sternocleidomastoid muscle runs obliquely from the mastoid process of the skull to the lateral border of the sternal notch and may be injured in sudden hyperextension injuries of the cervical spine. The trapezius muscle originates from the inion and the spinous processes from C1 (atlas) to T12 (last thoracic vertebra); it flares out to insert on the clavicle, acromion, and spine of the scapula. Spasm in this muscle can best be palpated on the lateral aspect of the neck. The scalene muscles are palpable in the anterior paratracheal area. They originate on the transverse processes of the cervical vertebrae and insert bilaterally on the first and second ribs. These muscles function to laterally flex the neck (side bend) and help the attached ribs elevate during forced inspiration. Within this region, three anatomic sites of neural compression have been implicated in thoracic outlet syndrome: between the anterior and middle scalenes, between the clavicle and first ribs, and between the pectoralis minor and the upper ribs. The levator scapula originates on the rib’s posterior tubercles and inserts on the upper medial border of the scapula. This muscle is tender to palpation when in spasm. Anomalous cervical ribs may be palpated and can be confirmed radiologically; they may be involved in thoracic outlet obstruction but usually exist only as an anatomic anomaly. The cervical spine has an abundant supply of superficial and deep interconnected lymphatics to return the lymph to the vascular compartment in the thorax. Palpation of the cervical lymph nodes can elicit tenderness in adenopathy caused by tumor or infection.
NEUROLOGIC EXAMINATION The neurologic examination provides both direct and indirect methods of determining damage to the spinal cord and nerves by examination of their sensory, motor, and reflex distribution. The aim is to identify an anatomic level for possible neurologic deficit.
Sensory examination and dermatome testing The sensory component for each spinal nerve originates in a dermatome, a segmental portion of the skin. Each cutaneous innervation generally follows the distribution of the underlying muscle innervation (Fig. 3c.2). However, there are exceptions and variations to this generalization in the cervical spine. The suboccipital nerve (dorsal ramus of C1) exits the spine between the skull and C1 and has no cutaneous distribution. The dorsal branch of C2 is the greater occipital nerve, which distributes
Figure 3c.2 The cervical dermatomes are indicated. The C5 to T1 dermatomes are expressed in the upper extremity and develop as the embryonic limb bud does, extending from the trunk.
cranially upto provide sensation to the vertex of the scalp. The lesser occipital nerve of the cervical plexus (ventral ramus of C2) supplies sensation to the skin of the scalp behind the ear as well as the skin of the ear. Pathologic conditions affecting the C2 nerve result in occipital neuralgia. The dorsal ramus of C3 (third occipital nerve) distributes cutaneous sensation to the upper neck and scalp. The dorsal rami (sensory) of C4-C6 provide sensation to the posterior neck in a cephalad to caudal direction. The cutaneous nerves of the upper limb, on the other hand, are derived from branches of the brachial plexus, and thus each one is comprised of more than one nerve root.24 The dermatomal pattern in the extremities is patterned on orderly embryologic limb development. Clinical differentiation between dermatomal sensory loss and a peripheral nerve deficit helps distinguish cervical radiculopathy from other neurologic problems. The upper lateral cutaneous nerve of the arm is the termination of the lower branch of the axillary nerve. Its cutaneous distribution is the lower half of the deltoid muscle and the long head of the triceps brachii. The sensory branches of the radial nerve are the posterior cutaneous nerve of the arm that distributes to the middle third of the back of the arm, the posterior cutaneous nerve of the forearm, and the superficial branch of the radial. All the above arise from the posterior cord of the brachial plexus. The lateral cutaneous nerve of the forearm distributes into the lower lateral and the anterior surface of the arm. This nerve is the cutaneous branch of the musculocutaneous nerve which arises from the lateral cord of the brachial plexus. The medial cutaneous nerve of the arm provides sensation to the posterior surface of the lower third of the arm, as low as the olecranon, and the medial cutaneous nerve of the forearm covers the ulnar aspect of the forearm down to the hand. These are sensory branches of the ulnar which arises off the medial cord of the brachial plexus. The shoulder receives its cutaneous sensation proximally from the cervical plexus, specifically from the supraclavicular nerves of C3 and C4.
Motor strength examination The dorsal and ventral rootlets at each level unite to form a mixed spinal nerve. The motor roots arise from the anterior horn
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C4 Dorsal scapular n. Suprascapular n.
Axillary n. Radial n. Median n. Ulnar n.
C8
rior ste Po
T1 l T2 ia ed M Medial Long pectoral n. thoracic n.
To subscapularis teres major latissimus dorsi
Medial cutaneous nerves to the arm and forearm
Figure 3c.3 Diagram of the brachial plexus. There is a complex interconnection of nerve tissue. Note the differentiation between the nerve roots, which arise segmentally, and the ultimate peripheral nerves, which are usually an amalgam of two or more nerve roots.
cells and thus lie ventral to the sensory rootlets; they exit the spinal cord through the foramen above the named cervical vertebrae and carry their fibers to the striated muscles. Because there are eight cervical nerves and seven cervical vertebrae, the C8 nerve root exits below the C7 body. From C5 to T1, these nerves separate and recombine to form the brachial plexus where the fibers are reconfigured into trunks, divisions, and cords before finally forming independent branches (Fig. 3c.3). The resulting nerves are thus of mixed root origin and are named musculocutaneous, axillary, radial, median, and ulnar, innervating muscles in the upper extremity. Evaluation of the efferent nerves is achieved by testing the muscles they innervate. Motor strength is objectively evaluated using a six-point grading system (Table 3c.3). Testing begins with assessment of the patient’s breathing. The phrenic nerve (C3-C5) is the motor nerve to the diaphragm, although it also contains many sensory and sympathetic fibers. If the patient is breathing adequately without the use of accessory musculature, the diaphragm is functionally intact.19 The C5 nerve root innervates the deltoid muscle, and along with C6 it also innervates the biceps muscle. The C6 nerve root also innervates the wrist extensors. The C7 motor distribution includes the triceps muscle, the wrist flexors, and finger extensors.
Table 3c.3
Reflex examination
C7
l era Lat
Musculocutaneous n.
C5 C6
Lateral pectoral n.
These demonstrate the overlapping character of upper limb innervation (Fig. 3c.4).
Evaluation of motor strength15
5 - Normal 4 - Able to overcome moderate resistance (not symmetric to contralateral side) 3 - Able to accomplish full range of motion against gravity 2 - Able to accomplish full range of motion with gravity eliminated 1 - Only trace muscle contraction 0 - Flaccid
Pathologic alterations in the basic stretch reflexes are important findings in neurologic disease. Deep tendon reflexes are a misnomer, because they are actually muscle stretch reflexes initiated by excitation of the afferent muscle spindle fibers. These 1a afferent fibers synapse directly onto the proximal dendrites and soma of the motor neurone, completeing the reflex arc, resulting in a reflex muscle contraction. These monosynaptic reflexes are helpful for localizing the level of pathology in the cervical spine or nerve root and for differentiating a lower motor neuron lesion from an upper motor neuron lesion. Although some examiners grade the intensity of reflexes on a scale of 0 to 3, we believe it is more realistic to grade them as absent or present, because there are variable individual reactions to reflex testing. Deep tendon reflexes can be influenced by age, metabolic factors, and anxiety levels in the patient. Brisk, or hyperreflexic responses, however, may be abnormal findings on reflex testing. Typically, upper motor neuron lesions involve the spinal cord and cause hyperreflexia. Lower motor neuron lesions depress reflexes. For example, the nerve of C5 mediates the biceps reflex and that of C6 can be tested through the brachioradialis reflex and C7 through the triceps reflex (Table 3c.4 and Figs. 3c.5, 3c.6, and 3c.7).
Long-tract signs After injury to the corticospinal tract of the spinal cord, abnormal reflexes, or long-tract signs, can be elicited that are not typically found in normal individuals. These reflexes suggest the presence of lesions proximal to the anterior horn cells and represent clinical signs of myelopathy. Below are select examples. ● Clonus is elicited by the examiner rapidly dorsiflexing the ankle and maintaining slight pressure while counting the pulsed contractions on resistance. Greater than four beats of clonus is considered abnormal. ● Lhermitte’s sign (a.k.a. the barber’s chair phenomenon) is a symptom of radiating shock-like sensation down the back with neck flexion. ● Babinski’s sign is an abnormal reflex elicited by stroking the lateral border of the plantar surface of the foot with a blunted pointy object, which elicits dorsiflexion of the great toe with fanning and dorsiflexion of the small toes (Fig. 3c.8). A normal response is plantar flexion of all toes. A positive Babinski sign indicates damage to the corticospinal tract or injury to the spinal cord. ● Oppenheim’s sign is indicative of disease of the pyramidal tract and is performed by sliding the pointed back of the reflex hammer up the crest of the tibia. A positive test elicits a response similar to a positive Babinski sign; the great toe extends whereas the small toes flex and splay. ● Hoffman’s sign is a pathologic reflex elicited by flicking and flexing the distal phalanx of the patient’s middle finger. When the sign is present, there is prompt adduction of the thumb and flexion of the index finger on the ipsilateral side (Fig. 3c.9).
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B
A
C
D
E
F
G
Figure 3c.4 Testing a full array of individual muscles permits the examiner to form an accurate assessment of the affected nerve roots and to assess whether the injury is due to a specific peripheral nerve injury. Comprehensive examination is necessary because of the overlapping neural supply to individual muscles. A: infraspinatus (suprascapular nerve; C5, C6): external rotation of the upper arm at the shoulder. B: deltoid (axillary nerve; C5, C6): abduction of the upper arm. C: biceps brachii (musculocutaneous nerve; C5, C6) flexion of the supinated forearm. D: triceps (radial nerve; C6, C7, C8): extension of the forearm at the elbow. E: bracioradialis (radial nerve; C5, C6): flexion of the forearm at the elbow with the forearm in neutral rotation. F: extensor carpi ulnaris (posterior interosseous nerve; C7, C8): extension and abduction of the hand at the wrist. G: extensor digitorum (posterior interosseous nerve; C7, C8): extension of the fingers at the metacarpophalangeal joints.
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H
I
J
K
L
M
Figure 3c.4 Cont’d H: Flexor carpi radialis (median nerve; C6, C7): flexion and abduction of the hand at the wrist. I: abductor pollicis brevis (median nerve; C8, T1) abduction of the thumb at right angles to the palm. J: flexor digitorum profundus I and II (anterior interosseous nerve; C7, C8): flexion of the distal phalanges of the index and middle fingers. K: third and fourth palmer interossei (ulnar nerve; C8, T1): finger adduction by the patient on the left as the examiner pulls a card. L: dorsal interosseous muscle (ulnar nerve; C8, T1): abduction of the fingers. M: abductor digiti minimi (ulnar nerve; C8, T1): abduction of the little finger.
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An inverted brachioradialis reflex is elicited by tapping the brachioradialis tendon and observing ipsilateral finger flexion. In the finger escape sign, the patient is asked to hold his or her fingers in an extended and adducted position. If the two ulnamost digits drift into abduction and flexion within 30-60 seconds, the patient is deemed to have a positive finger escape sign. In a grip and release test, the patient should be able to rapidly make and release a fist 20 times within 10 seconds.
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A scapulohumeral reflex is elicited by tapping the vertebral border of the scapula at the tip of the scapula spine or the base of the inferior angle. A normal response should be retraction of the scapula by the rhomboid muscles (C4-C5). Absence of retraction is abnormal. A pectoralis reflex is an indication of hyperreflexia. The reflex is present when tapping the pectoralis tendon elicits flexion of the elbow or dorsiflexion of the wrist (Fig. 3c.10).
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Table 3c.4
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Muscle nerve root origins
Upper extremities
Root level tested
Nerve foramen
Pectoralis Biceps Brachioradialis Triceps
C5-T1 C5-C6 C5 C7 (C8)
— C4-C6 C5-C6 C6-C7
Figure 3c.6 The brachioradialis reflex is tested by a direct tap on the muscle tendon.
Figure 3c.5 Biceps reflex: Support the forearm with the patient’s elbow at a right angle and apply light tension to the biceps tendon with your thumb, which should then be hit lightly with the reflex hammer.
Figure 3c.7 The triceps reflex can be more easily elicited if the arm is supported so that the forearm hangs freely or by supporting the arm in the horizontal gravitational plane.
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Specialized physical tests
Figure 3c.8 A positive or extensor plantar response, also known as a Babinski sign. The sole is scratched from the lateral aspect of the heel forward and then medially across the ball of the foot.
The distraction test is an example of a provocative maneuver that can relieve symptoms of spondylosis or radiculopathy. While the patient is sitting or lying down, the palm of the examiner’s dominant hand is placed under the base of the skull and the nondominant hand placed under the chin. The head is gently distracted, increasing the pressure to about 5-7 kg. A positive sign provides symptomatic relief of neck or arm pain. An axial compression test is a provocative maneuver intended to elicit the neck or arm pain a patient may be experiencing intermittently. This is performed by placing up to 5-7 kg of pressure on the top of the head, preferably while the patient is sitting. A positive response precipitates or increases the patient’s symptoms. A distraction test can be performed after this test to attempt to provide some relief. Spurling’s sign is a maneuver to provoke symptom radiation. The patient laterally flexes and extends the neck (rotating the head to the symptomatic side), after which the examiner applies axial compression to the spine. A positive result causes pain or tingling that starts on the ipsilateral side of the neck or shoulder and radiates distal to the elbow (Fig. 3c.11). Spurling’s test has been shown to have a sensitivity of 30% and a specificity of 93% when confirmed with electrodiagnostic studies.17 Pronator reflex (a.k.a., ulnar reflex) is produced by tapping the volar aspect of the distal radius, or alternatively the styloid process of the ulna, with the forearm in a neutral position and the elbow flexed. The normal response is forearm pronation and adduction of the hand. The pronator reflex represents a muscle stretch reflex of the pronator teres that would make it helpful in evaluating C6 and C7 root lesions.14 The Valsalva maneuver is a provocative test that exacerbates arm pain when a patient bears down or coughs. These symptoms result from the increase in intrathecal pressure.
Figure 3c.9 Hoffman’s sign is positive or present if the act of flicking (flexing) the distal phalanx of the index or middle finger (black arrow) elicits a flexion of the thumb (white arrow) and/or other fingers.
Chapter 3c
Figure 3c.10 Position of the examiner’s fingers over the pectoralis tendon to test for a pectoralis reflex.
Tests for thoracic outlet syndrome include maneuvers that are presumed to tighten the thoracic outlet, such as arm hyperabduction, the “elevated arm stress test,” or the Adson test, all of which may provoke the patient’s typical symptoms of pain and/or paresthesia or affect the radial pulse. The Adson test, also called Adson’s maneuver, is performed with the patient in a sitting position. The patient’s hands rest on the thighs, the examiner palpates both radial pulses as the patient rapidly fills his or her lungs by deep inspiration, and, holding his or her breath, hyperextends the neck and turns the head toward the affected side. If the radial pulse on that side is decidedly or completely obliterated, the result is considered positive. In the Allen test, which is sometimes also described in the literature as the Adson test, the arm in which the patient is experiencing symptoms is raised and rotated while the head is turned away from the affected side. If the strength of the pulse is reduced in either of these two tests, it indicates compression of the subclavian artery. All the above are nonspecific tests. If they are positive, however, there may be an indication to perform further studies.
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Evaluating the impact of neck pain
Figure 3c.11 Spurling’s test: Hold the patient’s neck in extension for a few moments. Typical symptoms of brachialgia may be elicited, and if not, the test can be augmented by adding a lateral tilt of the head toward the symptomatic side as shown above. These maneuvers increase the degree of foraminal compression.
EVALUATING THE IMPACT OF NECK PAIN The standard history and physical examination provide objective findings that support subjective complaints to develop an overall assessment of cervical spine disorders. This “standard” examination does not often assess the impact of the disability on a patient’s life quality. Functional scales can be potentially useful to measure the impact of disease on the performance of common daily activities. Defining a standard evaluation for functional disability is difficult, because functional activity can be influenced by many factors independent of symptoms and signs such as age, psychologic ability to cope with disease, and the demands of professional activity.8 Well-validated instruments for evaluating neck dysfunction are widely available (Table 3c.5). For individual patient follow-up evaluation, the Patient-Specific
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Table 3c.5 Standard instruments for evaluating neck dysfunction Medical Outcomes Study 36-Item Short Form Health Survey Neck Disability Index18 Copenhagen Neck Functional Disability Scale12 Northwick Park Neck Pain Questionnaire13 Patient Specific Functional Scale22 Neck Pain and Disability Scale23
Functional Scale has high sensitivity to change and thus represents a good choice for clinical use.16 The MOS 36-Item Short Form Health Survey (SF-36), developed for the Medical Outcomes Study, is an example of a traditional scale for functional assessment.20 This questionnaire has demonstrated an overall usefulness in the general reporting of musculoskeletal ailments; however, it does not report on specific neck pain or disability. The Neck Disability Index is a 10-item questionnaire designed to assess pain-related limitations in activities of daily living. The test is scored as a percentage of maximal pain and disability. The scale is categorized by activity; however, some questions are not pertinent for all patients. The Copenhagen Neck Functional Disability Scale is a 15-item questionnaire requiring yes, no, or occasional as responses. The Northwick Park Neck Pain Questionnaire has nine five-part questions requiring responses of 0-4. The Patient Specific Functional Scale is unique in that it requires the patient to generate a specific list of problems emphasizing the limitations most affecting the patient. The Neck Pain and Disability Scale is a unique 20-item questionnaire in which a visual analog scale is assigned to each discomfort. The 20 items measure intensity of pain and its interference with the vocational, recreational, social, and functional aspects of living and the impact of emotional factors.
SPECIAL TESTS Imaging studies of the spine After the development of a working pathologic and anatomic diagnosis, appropriate imaging studies should be selected to demonstrate and confirm the diagnosis. Routine spinal imaging is not recommended during the first month of symptoms except in the presence of red flags.
Radiographs Plain radiography is the most widely available modality for imaging the cervical spine. The cervical (C) spine series consists of anteroposterior and lateral views to visualize the entire cervical spine and an open-mouth odontoid view to assess the odontoid and C1-C2 joint (Figs. 3c.12 and 3c.13). A swimmer’s view may be required to assess the cervicothoracic junction if the C7-T1 level is obscured by the patient’s shoulders on the lateral cervical radiograph. Lateral flexion and extension radiographs should also be obtained in patients with a history of trauma and patients with extensive degenerative disease. These radiographic views permit assessment of cervical alignment, degenerative changes, assessment of bony architecture in the vertebral bodies, and gross evaluation of the soft tissues. Oblique radiographs can be used to assess encroachment of the neural foramina (Fig. 3c.14). Radiographs should be the first-line diagnostic modality for patients presenting with neck pain when any of the following red flags are present: recent significant trauma or recent mild trauma in patients over 50, prior cancer or recent infection, neck pain worse at night or worse with rest, and history of intravenous drug abuse or corticosteroid use. Radiographs are the least sensitive of the imaging modalities in predicting symptomatology once tumor, trauma, or infection is excluded. A cervical sprain or strain leave no direct radiographic
Figure 3c.12 Lateral and anteroposterior radiographs of the cervical spine of a 34-year-old patient who had a disk herniation at C6-C7 with a clinical radiculopathy. The plain lateral film shows narrowing of the C5-C6 disk space (arrow) with a bony bar between the two vertebrae. That was not appreciated on the MRI. Note also the loss of cervical lordosis. The C5-C6 uncovertebral joint is indicated by an arrow on the anteroposterior radiograph.
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evidence, nor does a herniated disk. Although the presence of degenerative disk disease can be visualized on radiographs, it cannot predict symptoms or disability status.9 As much as 25% of the population has radiographic degenerative changes by age 50, and 75% have degenerative changes by age 70.7 It is the strength of this literature that persuades against the use of routine cervical spine radiographs alone to evaluate disability.
Computed tomography
Figure 3c.13 Open mouth view: A frontal view of the atlantoaxial (C1-C2) joint can be obtained radiographically with the patient’s mouth open as the teeth no longer obscure the direct view. In this example, both right and left C1-C2 facet joints are clearly seen, the dens is clearly visualized equidistant from both facet joints, and a partial view is even obtained of the occipitocervical articulations.
Figure 3c.14 Oblique cervical radiograph: The right-sided neural foramina can be clearly visualized. The black arrow indicates the right C4-C5 intervertebral or neural foramen; the C5 nerve root traverses the foramen. The small osteophytes arising from the right C3-C4 uncovertebral joint (joint of Luschka) are identified by the white arrow. The mild foraminal stenosis can be appreciated when comparing the foraminal dimensions with the normal adjacent foramina.
Computed tomography (CT) is a noninvasive diagnostic modality that provides excellent visualization of the cervical bony anatomy, helps evaluate osseous pathology, and assesses the integrity of the spinal canal. When CTs are supplemented with myelography, one can also evaluate soft tissue structure and impingement of nerve elements. That being said, studies directly comparing magnetic resonance imaging (MRI) and CT myelogram with respect to identifying pathology can yield conflicting results. However, general consensus points to the advantage of the CT myelogram in identifying osseous pathologies such as fractures, osteophytes, and bony foraminal encroachment. MRI studies better demonstrate soft tissue impingement, spinal cord edema, and myelomalacia. The ability of current multiplanar CTs has greatly enhanced the detail of the spine but also escalates the risk of false positivity. Scans can be reconstructed electronically in any desired plane to better visualize pathoanatomy (Fig. 3c.15).
Figure 3c.15 Midsagittal reconstructions of the cervical spine of a 56-year-old man who has an os odontoideum. Note the very short dens (odontoid process) that results in multiplanar atlantoaxial instability. The anterior ring of C1 (arrow) is normally aligned in neutral; there is posterior C1-C2 subluxation in the extended position and marked anterior C1-C2 subluxation in flexion. Note the marked anterior reposition of the C1 ring in flexion resulting in the posterior arch of C1 approaching the C2 body and causing severe spinal stenosis.
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Three-dimensional multiplanar CTs are extremely useful to demonstrate the complex anatomy of fractures and spinal deformity, be it congenital or other (Fig. 3c.16).
Magnetic resonance imaging MRI uses radiofrequency pulses within a strong magnetic field to produce an image without the use of ionizing radiation. MRI is a potentially useful modality for evaluating spinal cord pathology in the presence of brachialgia. MRI is also an excellent imaging modality to assess the soft tissues in the cervical spine and their contribution to compression of the nerves and spinal cord (Figs. 3c.17, 3c.18, and 3c.19). MRI provides excellent visualization of the spinal cord for masses or lesions and cysts as well as for the myelomalacia seen in chronic compression and edema seen in various acute pathologies. Spinal pathology, such as diskitis or local abscess, can be well identified with MRI. However, many of the abnormalities seen on MR images may be incidental, resulting in the potential for over-diagnosis. Nevertheless, in the presence of many of the red flags for pathology, MRI provides indispensable information that can rapidly help confirm or rule out serious clinical problems.
Myelography Myelography uses nonionic contrast injected intradurally to indirectly visualize soft tissues in the canal. Filling defects are an
A
Figure 3c.16 Three-dimensional reconstruction of the cervical spine of a child with a congenital hemivertebra (arrow). There is also a split or butterfly vertebra at C5.
indicator of spinal cord or nerve root compression. Plain myelography is typically enhanced with the addition of a CT. Myelography is a good test for patients in whom spinal root or cord compression is suspected and for patients who have received metallic
B
Figure 3c.17 Cervical magnetic resonance imaging (MRI) of a 26-year-old woman who has a large C6-C7 disk herniation. (A) Sagittal MRI. (B) The axial image through the C6-C7 disk (D) shows the large herniation (H) and the compressed spinal cord (SC).
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A
B Figure 3c.18 Cervical magnetic resonance imaging (MRI) of a 34-year-old woman who had a left C7 radiculopathy. (A) Midsagittal and parasagittal MRIs show the apparently small disk herniation. (B) Axial MRI at C5-C6 demonstrates normal anatomy, whereas at C6-C7 there is a large disk herniation (white arrow) extending into the left neural foramen and compressing the C7 nerve root. Note the normally patent right-sided neural foramen.
implants, which render an MRI ineffective. Myelographic studies also permit acquisition of (dynamic) images of the spinal cord and nerves taken with the neck flexed, extended, laterally tilted, or rotated (Fig. 3c.20). Soft tissue or bony impingement on the neural elements may be demonstrated in positions other than neutral. Note that there are now MRI scanners that also permit a full range of movement and the opportunity to obtain dynamic scans.
Barium swallow Visualizing swallowed radiographic contrast fluoroscopically can demonstrate mechanical compression on the esophagus from anterior osteophytes and differentiate dysphagia from other pathologies.
Bone scans A bone scan uses the technique of scintigraphy (diagnostic technique of recording the distribution and uptake of radioisotopes
injected into various body systems) to gauge the chronicity of a bony lesion such as a fracture, neoplasm, or a focus of osteomyelitis and to monitor disorders affecting bones. Scintigraphy is a very sensitive imaging modality; however, it is not very specific. The bone scan detects the distribution of a radioactive agent injected throughout the venous system. After injection, a scintillation camera detects the radioisotope’s distribution in the body, most importantly its concentration in the skeleton. Areas of increased metabolic activity are imaged as increased isotope uptake on a full body scan.
Electrodiagnostic studies Examination by electrodiagnostic methods is useful to document radiculopathy and to confirm nerve root impingement. These studies additionally facilitate the diagnosis of peripheral
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A
B Figure 3c.19 Cervical magnetic resonance imaging (MRI) of a 51-year-old man who had cervical myelopathy. (A) The sagittal scans show multilevel spinal stenosis. T1- and T2-weighted scans are shown. (B) Axial scans through the disks show central spinal stenosis from C3-C4 to C6C7 with spinal cord compression.
entrapment syndromes and peripheral neuropathy. The tests commonly include needle electromyography, nerve conduction studies, and somatosensory evoked potentials.
Electromyography Measuring the electrical activity of muscle fibers at rest and when active provides diagnostic information on the degenerative or healthy status of muscles and their innervation and distinguishes neurogenic from myopathic disorders. The electromyographic evaluation in chronic cervical radiculopathy shows a
partial denervation pattern that manifests as increased amplitude and a longer duration of the motor unit potential. Fibrillations, or small-amplitude, single muscle fiber potentials, may also be present but are nonspecific and usually seen in the acute stage. Insertional activity from movement of the electrode is normal in electromyographic studies, but if it persists after electrode motion ceases, it is described as prolonged insertional activity and can be a sign of radiculopathy. When these tests are done within the first 2-3 weeks after injury, the results are falsely negative as it takes time to develop denervation.
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Figure 3c.20 Cervical myelogram. (A) Lateral (left) and anteroposterior (right) views of the cervical spine of a 56-year-old man with neck and arm pain and early signs of cervical myelopathy. Compression of the thecal sac is well seen on the lateral view at the C4-C5 and C5-C6 levels when his neck is extended. The anterior-posterior view demonstrates a paucity of contrast at those levels and truncation of the exiting nerve roots. Normal nerve root filling is noted at C6-C7 and distal levels. (B) Postmyelogram axial computed tomography images clearly demonstrate bilateral foraminal stenosis at C4-C5, whereas at C6-C7 the nerve root sleeves can be seen to fill well with the contrast (arrow).
Nerve conduction studies Using nerve conduction studies to evaluate how well nerves transmit electrical signals provides an assessment of the overall condition of both individual nerves and whole nerve structures. Measured electrical parameters are usually the signal amplitude and signal onset latency. These measured values are then compared with established normal parameters to determine the site of a compression. Nerve conduction studies are useful to evaluate acute and chronic peripheral entrapment neuropathies that mimic radiculopathy. Nerve conduction velocity and latency changes are not typically found in cervical radiculopathy unless there is extreme demyelinization of axons. The F-wave response tests electrical conduction through motor roots (Table 3c.6). The F-wave is recorded after maximal stimulation of a motor nerve. The amplitude, shape, and latency should change with each stimulation. Clinical parameters usually evaluated are response time, or latency. Because the F-wave is dependent on the integrity of the entire motor unit, it can assess proximal neuropathies. Another parameter with which to document nerve abnormalities is through the recording and measurement of sensory nerve action potentials. Abnormal sensory nerve action potentials are noted with damage to the nerve from the dorsal root ganglion while they are normal in pure radiculopathy, as the presumed lesion is proximal to the sensory ganglion. In patients with sensory deficit in the hands, recordings of sensory nerve action potentials make a differentiation between lesions of dorsal roots and peripheral nerves possible.
Somatosensory evoked potentials Somatosensory evoked potential recordings can be used to evaluate the integrity of the central nervous system and peripheral sensory neurons. Because most peripheral nerves in the upper extremity carry fibers from multiple roots, somatosensory evoked
potentials are not specific in elucidating spinal root dysfunction but can be useful in determining spinal cord abnormality that affect cord pathways.
Laboratory screening Laboratory studies provide valuable clinical evidence for patients presenting with atypical neck complaints or those suspected of tumor or infection. A complete blood count with differential can help detect a response to infection, blood dyscrasias, and medication side effects. The erythrocyte sedimentation rate and C-reactive protein are categorized as acute phase reactants commonly used in orthopedics to detect evidence of an infection or a connective tissue disorder. Although both indices serve the same primary function, clinicians often use them simultaneously, because the C-reactive protein is quicker to respond to either improvement or worsening of a clinical course. A comprehensive metabolic panel, including Ca+, phosphorus, uric acid, alkaline phosphatase, and acid phosphatase, can help detect metabolic bone disease.
CONCLUSION Evaluation of the cervical spine in workplace injuries requires a multidimensional workup that facilitates, first, ruling out serious pathology before initiating therapy for the work-related injury and, second, evaluation of the patient’s work setting relative to the patient’s recovery process for a rapid and safe return to work activity. The trend in evaluating cervical spine injuries increasingly involves more emphasis on EBM to guide treatment. Using EBM as a guide facilitates a rapid evaluation with concise elimination of red flags for spinal pathology. Returning to work
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Table 3c.6
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Evaluation of the neck
Nerve and main root supply of muscles Spinal roots
Spinal accessory nerve Trapezius C3, C4 Brachial plexus Rhomboids C4, C5 Serratus anterior C5, C6, C7 Pectoralis major Clavicular C5, C6 Sternal C6, C7, C8 Supraspinatus C5, C6 Infraspinatus C5, C6 Latissimus dorsi C6, C7, C8 Teres major C5, C6, C7 Axillary nerve Deltoid C5, C6 Musculocutaneous nerve Biceps C5, C6 Brachialis C5, C6 Radial nerve Long head Triceps Lateral head C6, C7, C8 Medial head Brachioradialis C5, C6 Extensor carpi radialis longus C5, C6 Posterior interosseous nerve Supinator C6, C7 Extensor carpi ulnaris C7, C8 Extensor digitorum C7, C8 Abductor pollicis longus C7, C8 Extensor pollicis longus C7, C8 Extensor pollicis brevis C7, C8 Extensor indicis C7, C8 Median nerve Pronator teres C6, C7 Flexor carpi radialis, C6, C7 Flexor digitorum superficialis C7, C8, T1 Abductor pollicis brevis C8, T1 Flexor pollicis brevis C8, T1 Opponens pollicis C8, T1 Lumbricals I and II C8, T1 Anterior interosseous nerve Flexor digitorum profundus I and II C7, C8 Flexor pollicis longus C7, C8 Ulnar nerve Flexor carpi ulnaris C7, C8, T1 Flexor digitorum profundus III and IV C7, C8 Hypothenar muscles C8, T1 Adductor pollicis C8, T1 Flexor pollicis brevis C8, T1 Palmar interossei C8, T1 Dorsal interossei C8, T1 Lumbricals III and IV C8, T1 Abductor digiti minimi C8, T1
See Figure 4
activity or to normal daily activities, in general, is therapeutic; if necessary, they can be modified to minimize exacerbations and maximize productivity. Once neck pain shifts from acute to subacute or chronic, there exists a comprehensive panel of tests and studies that help to continue to delineate pathology and further guide patient treatment.
REFERENCES 1.
A 2. 3.
B
4.
C
5. 6. 7.
D
8.
E
9. 10. 11.
F G
12. 13. 14. 15. 16.
H I
17. 18. 19. 20.
J
21.
22.
23.
24.
K L M
Adapted from Medical Research Council: Aids to the examination of the peripheral nervous system. London, 1980, Her Majesty’s Stationary Office.
Bigos S, Bowyer OR, Braen GR, Brown K, Deyo R, Haldeman S, et al: Acute low back problems in adults. Rockville, MD, 1994, Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services. Bigos SJ, McKee JE: Data-driven Daubert defendable care code—activity paradigm and reliable data for back problems. Semin Spine Surg 15:68-90, 2003. Cocchiarella L, Andersson GBJ: Guides to the evaluation of permanent impairment. AMA Press, 2004. Co^té P, Cassidy JD, Carroll L: The Saskatchewan Health and Back Pain Survey. The prevalence of neck pain and related disability in Saskatchewan adults. Spine 23:1689-1698, 1998. Demeter S, Anderson G: Disability evaluation. St Louis, MO, 2003, Mosby. Dvorak J, Panjabi MM, Novotny JE, Antinnes JA: In vivo flexion/extension of the normal cervical spine. J Orthop Res 9:828-834, 1991. Friedenberg ZB, Miller WT: Degenerative disc disease of the cervical spine, J Bone Joint Surg Am 45:1171-1178, 1963. Goldberg MS, Scott SC, Mayo NE: A review of the association between cigarette smoking and the development of nonspecific back pain and related outcomes. Spine 25:995-1014, 2000. Gore DR, Sepic SB, Gardner GM: Roentgenographic findings of the cervical spine in asymptomatic people. Spine 11:521-524, 1986. Hill J, Lewis M, Papageorgiou AC, Dziedzic K, Croft P: Predicting persistent neck pain: a 1-year follow-up of a population cohort. Spine 29:1648-1654, 2004. Holland JP, et al: How to critically evaluate the clinical literature on low back problems: the foundation for an evidence-based approach to care. Semin Spine Surg 15:54-67, 2003. Jordan A, et al: The Copenhagen Neck Functional Disability Scale: a study of reliability and validity. J Manip Physiol Ther 21:520-527, 1998. Leak AM, et al: The Northwick Park Neck Pain Questionnaire, devised to measure neck pain and disability. Br J Rheumatol 33:469-474, 1994. Malanga GA, Campagnolo DI: Clarification of the pronator reflex. Am J Phys Med Rehabil 73:338-340, 1994. Medical Research Council: Aids to the examination of the peripheral nervous system. London, 1980, Her Majesty’s Stationary Office. Pietrobon R, Coeytaux RR, Carey TS, Richardson WJ, DeVellis RF: Standard scales for measurement of functional outcome for cervical pain or dysfunction: a systematic review. Spine 27:515-522, 2002. Tong HC, Haig AJ, Yamakawa K: The Spurling test and cervical radiculopathy. Spine 27:156-159, 2002. Vernon H, Mior S: The Neck Disability Index: a study of reliability and validity. J Manip Physiol Ther 14:409-415, 1991. Wagner R, Jagoda A: Spinal cord syndromes. Emerg Med Clin North Am 15:699-711, 1997. Ware JE Jr, Sherbourne CD: The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 30:473-483, 1992. Webb R, Brammah T, Lunt M, Urwin M, Allison T, Symmons D: Prevalence and predictors of intense, chronic, and disabling neck and back pain in the UK general population. Spine 28:1195-1202, 2003. Westaway MD, Stratford PW, Binkley JM: The patient-specific functional scale: validation of its use in persons with neck dysfunction. J Orthop Sports Phys Ther 27:331-338, 1998. Wheeler AH, Goolkasian P, Baird AC, Darden BV: Development of the Neck Pain and Disability Scale. Item analysis, face, and criterion-related validity. Spine 24:1290-1294, 1999. Woodburne RT, et al: The Netter Collection of Medical Illustrations: Volume 8 Musculoskeletal System. New Jersey, 1997, Novartis Pharmaceutical Corporation.
CHAPTER
3d
Treatment Options for Disorders of the Cervical Spine James N. DeBritz and Sam W. Wiesel
As with any pathophysiologic condition, treatment of neck pain depends on the proper diagnosis. Neck pain has multiple etiologies (Table 3d.1) that may result from trauma as well as from chronic atraumatic conditions. Understanding these etiologies requires detailed knowledge of both the anatomy of the cervical spine and its relationship to neurovascular structures as well as comprehension of the natural history of cervical spondylosis and myelopathy. Diagnosis of neck pain can be more easily accomplished by dividing clinical complaints into several main categories, including axial neck pain, neck pain with an associated radiculopathy, and neck pain with signs and symptoms of myelopathy. Once the proper diagnosis is established, treatment can be directed in a focused and individualized manner. This chapter summarizes some of the most common cervical spine disorders to aid in their diagnosis. The reader is instructed on how a pertinent history, directed physical examination, and diagnostic findings can be used to establish a diagnosis. Treatment options are discussed in detail, and finally a diagnostic and treatment algorithm is presented that integrates the information into a usable format.
ANATOMY A detailed understanding of the osseous and soft tissue structures of the neck is a prerequisite to fully understand the pathophysiology of neck pain and cervical spine disease. Once a pathologic process temporarily or permanently distorts the normal anatomy of the neck, a compensatory response may occur that often presents to the individual as pain. With the exception of C1, each cervical vertebra articulates with the adjacent vertebra through the facet, or zygapophyseal, joints. These are gliding joints characterized by capsules and synovial membranes in addition to ligamentous support. The facet joints are innervated by the dorsal ramus of the associated nerve roots. Axial neck pain can be produced by facet joint injections in asymptomatic individuals, providing evidence that it can originate from the facet joints themselves.2 This information can be used to direct treatment in certain cases, as discussed. The amphiarthrodial joints that join each vertebral body through intervertebral disks play an important role in the pathologic process of the spine as well. Although varying in size depending on the level of the spinal column, all intervertebral disks are identical in their structural organization. The internal portion of the disk is comprised of the nucleus pulposus that is contained around its periphery by the annulus fibrosus.
Table 3d.1 Causes of neck and neck-related pain syndromes Localized neck disorders Osteoarthritis (apophyseal joints, C1-C2-C3 levels most often) Rheumatoid arthritis (atlantoaxial) Juvenile rheumatoid arthritis Sternocleidomastoid tendinitis Acute posterior cervical strain Pharyngeal infections Cervical lymphadenitis Osteomyelitis (staphylococcal, tuberculosis) Meningitis Ankylosing spondylitis Paget disease Torticollis (congential, spasmodic, drug involved, hysterical) Neoplasms (primary or metastatic) Occipital neuralgia (greater and lesser occipital nerves) Diffuse idiopathic skeletal hyperostosis Rheumatic fever (infrequently) Gout (infrequently) Lesions producing neck and shoulder pain Postural disorders Rheumatoid arthritis Fibrositis syndromes Musculoligamentous injuries to the neck and shoulder Osteoarthritis (apophyseal and Luschka) Cervical spondylosis Intervertebral osteoarthritis Thoracic outlet syndromes Nerve injuries (serratus anterior, C3-C4 nerve root, long thoracic nerve) Lesions producing predominantly shoulder pain Rotator cuff tears and tendinitis Calcareous tendinitis Subacromial bursitis Bicipital tendinitis Adhesive capsulitis Reflex sympathetic dystrophy Frozen shoulder syndromes Acromioclavicular secondary osteoarthritis Glenohumeral arthritis Septic arthritis Tumors of the shoulder Lesions producing neck and head pain with radiation Cervical spondylosis Rheumatoid arthritis Intervertebral disk protrusion Osteoarthritis (apophyseal and Luschka joints, intervertebral disk, osteoarthritis) Spinal cord tumors Cervical neurovascular syndromes Cervical rib Scalene muscle Hyperabduction syndrome Rib-clavicle compression From Wiesel SW; Neck pain, ed 2. Charlottesville, VA, 1992, The Michie Company, pp. 60-61.
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Figure 3d.1 Cross-sectional view showing the cervical nerve root, dorsal and ventral primary rami, recurrent meningeal or sinuvertebral nerve, and sympathetic plexus. Note the proximity of the disc space, vertebral artery, and facet joints. (From Rao R: Instr Course Lect 84A(10):1872-1881, 2002.)
Both the nucleus pulposus and the annulus fibrosus share a similar composition and are comprised mainly of water, proteoglycans, and collagen. They differ, however, in their organization and in the type of collagen present. Type II collagen is found in the nucleus pulposus, and type I collagen is present in the annulus. The cervical intervertebral disks are wedge-shaped to accommodate the uncinate processes and the corresponding joints of Luschka, a bony articulation between the vertebral bodies. The blood supply and innervation of the intervertebral disks of the cervical spine have been well defined. Branches of the sympathetic plexus and the ventral nerve root form the sinuvertebral nerve that innervates the intervertebral disk, supplying portions of the annulus, the posterior longitudinal ligament, the periosteum of the vertebral body and pedicle, and the adjacent epidural veins (Fig. 3d.1). In a review of clinical findings of cervical diskography, Grubb and Kelly5 showed a correlation between reliable patterns of pain and each cervical disk. These pain patterns and axial pain patterns produced by facet joint injections are summarized in Figures 3d.2 and 3d.3, respectively. In addition to the major articulations of the cervical spine and their innervations, the soft tissue structures of the cervical spine and the neck play an important role in neck pain. The vertebrae are bound together by many ligaments. The anterior longitudinal ligament and the weaker posterior longitudinal ligament bind the vertebral bodies along the anterior and posterior surfaces, respectively, and run from the skull to the sacrum. The segmental denticulate configuration and intricate association with the intervertebral disk is characteristic of the posterior longitudinal ligament, and a prolapsed nucleus pulposus is most likely to be permitted lateral to these expansions. The ligamentum flavum is a strong elastic ligament that connects the laminae of each of the vertebrae and runs from C2 to the lumbosacral interval. A continuation of the supraspinous ligament, the ligamentum nuchae, runs from C7 to the occiput and along with the interspinous and intertransverse ligaments serves to stabilize further the spinal column architecture.
Muscles in the neck are divided into anterior and posterior groups. Anterior muscles are comprised mainly of the strap muscles and the sternocleidomastoid. The neck musculature forms several distinct layers posteriorly. From dorsal to ventral
Figure 3d.2 Axial pain patterns provoked during discography at each cervical level. A: level between second and third cervical vertebrae; B: level between third and fourth cervical vertebrae; C: level between fourth and fifth cervical vertebrae; D: level between fifth and sixth cervical vertebrae; and E: level between sixth and seventh cervical vetebrae. (From Rao R: Instr Course Lect 84A(10):1872-1881, 2002.)
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Acute herniated disk
will usually reveal only some local tenderness lateral to the bony spine. The loss of motion in individual patients is variable and tends to correspond directly with the intensity of the pain. True muscular spasm, defined as continuous muscular contraction, is rare, except in severe cases of torticollis in which the head is tilted to one side. Because radiographic studies in neck strain are usually normal, plain films are generally not warranted on the first office visit. If the pain persists for more than 2 weeks, however, a radiograph should be obtained to rule out other more serious causes of neck pain such as instability or neoplasia.
Treatment
Figure 3d.3 Composite map of axial pain patterns produced by injections into the facet joints at the second through seventh cervical levels. (From Rao R: Instr Course Lect 84A(10):1872-1881, 2002.)
are the trapezius and levator scapulae, splenius and longissimus, semispinalis, and suboccipital muscles. These muscles assist in scapular rotation (trapezius and levator scapulae) and rotation, flexion, and extension of the neck. Strain of these muscles can also contribute to neck pain.
The prognosis for patients with cervical strain is excellent because the natural history of this disorder is complete resolution of all symptoms over a period of several weeks. Therapy consists primarily of rest and immobilization, often with the use of a soft cervical orthosis. Certain medical interventions such as antiinflammatory agents and/or muscle relaxants may aid in the acute phase of pain management, but they do not appear to alter the natural course of the syndrome. Although no good randomized, prospective, clinical trials have studied their efficacy, trigger point injections do seem empirically to work well. The purpose of a trigger point injection is to decrease inflammation in a specific anatomic area, with apparently superior results the more localized the trigger point. These injections can be repeated at 1- to 3-week intervals.
ACUTE HERNIATED DISK NECK SPRAIN The condition of nonradiating neck pain with a concomitant loss of motion has been referred to incorrectly as neck sprain. Correctly termed cervical strain and one of the most common neck disorders, this often occurs in the absence of a distinct traumatic episode. Most commonly, the pain is located in the middle to lower part of the neck, and although the pain is not secondary to trauma, its onset can be acute. The pain associated with cervical strain is often a dull ache that is exacerbated by movement. In addition, a component of referred pain may be involved. This is not, however, true radicular pain secondary to mechanical compression of a nerve root. The pain is referred generally to other mesenchymal structures derived from a similar sclerotome during the process of embryogenesis. The most common referral patterns include the posterior of the shoulder, the occipital area, the scapular region, and the anterior chest wall, also known as cervical angina pectoris. The source of the pain is most commonly believed to be the ligaments and musculature of the cervical spine.14 As previously illustrated, however, both facet and disk disease can contribute to axial neck pain and should be considered as a source of the inciting complaint (Figs. 3d.2 and 3d.3). Once the precise location, frequency, and quality of the pain have been determined, careful questioning should then address the presence, if any, of subtle long-tract signs, including bowel or bladder dysfunction and gait abnormalities, to avoid missing the diagnosis of myelopathy. Physical examination of the patient
A herniated disk results when the nucleus pulposus protrudes through the fibers of the surrounding annulus fibrosus and occurs around the fourth decade of life while the nucleus pulposus remains gelatinous. Stookey15 and Rothman and Marvel13 described three types of soft disk herniations (Fig. 3d.4), with the posterolateral herniation being the most common due to the anatomy of the posterior longitudinal ligament, as previously mentioned. Herniations occurring posterolaterally produce predominantly motor signs and symptoms. As opposed to those in the lumbar region, disk herniations occurring centrally may cause myelopathy because of the presence of the cord in the cervical region. The most common levels for herniation are at the C6-C7 and C5-C6 levels. Those at the C7-Tl and C3-C4 levels are uncommon, and those at the C2-C3 level are extremely rare. Interestingly, not every disk herniation is symptomatic. The presence and severity of symptoms depend on the individual’s spinal reserve capacity, the presence or absence of associated inflammation, the size of the herniated fragment, and the presence of concomitant disease processes such as uncovertebral joint osteophytes. In general, a herniated disk affects the nerve root of the next lowest cervical level: A C3-C4 disk affects the C4 nerve root, a C4-C5 disk affects the C5 nerve root, and so on. The radicular symptoms then correspond to the involved nerve root. In addition, as previously stated, a herniated disk may cause some long-tract signs because of the presence of the spinal cord at the cervical level.
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Figure 3d.4 Types of soft disk herniations. (From Boden SD, et al: The aging spine: essentials of pathophysiology, diagnosis, and treatment. Philadelphia, 1991, WB Saunders.)
Most patients have symptoms consisting primarily of arm pain. Although it may begin in the neck region, the pain radiates down into the shoulder, arm, forearm, or hand along a clearly defined dermatome. The onset of pain may be gradual, although acute tearing or snapping sensations may occur. The arm pain may vary in intensity from a dull cramping pain in the arm with
use to pain so severe as to preclude use. In addition, attacks of sharp pain may radiate into the hand and fingers with associated paresthesias. Pain severe enough to awaken the patient at night is common. The differential diagnosis of radicular pain must be considered. Pathologies that range from tumors to nerve entrapment syndromes share the common trait of mechanically compressing a nerve root and imitating radicular symptoms. Other neurologic diseases can masquerade as a radicular process, however, and should also be contemplated. Classic differential diagnoses include a Pancoast tumor, which is an apical lung tumor often accompanied by Horner syndrome because of disruption of the sympathetic chain, and thoracic outlet syndrome, which can be diagnosed on physical examination. Physical examination may reveal some decreased motion of the neck that may be so severe as to manifest as frank torticollis. Any maneuver (such as the Valsalva maneuver) that stretches the involved nerve root may recreate the pain pattern. Spurling’s test, in which the neck is extended, may often make the pain worse by further narrowing the involved intravertebral foramina. Additionally, coughing, shoulder abduction, and axial compression tests are often positive in patients with compression radiculopathy. The axial compression test is performed by pressing down on a patient’s head while he or she is either sitting or lying down. A positive finding consists of worsening or reproduction of radicular symptoms. The shoulder abduction relief test is positive if radicular symptoms are decreased when a seated patient elevates one hand above the head with the elbow flexed and the shoulder abducted to 90 degrees. An axial manual traction test is performed with the patient supine. A positive finding consists of a decrease or complete absence of radicular symptoms when 20 to 30 pounds of axial traction is applied. The finding of a neurologic deficit on physical examination greatly aids in the diagnosis, although in the setting of a chronic radiculopathy, the neurologic examination may be normal. Because subjective sensory changes are often difficult to interpret, the neurologic examination must show a diminution of reflexes, motor weakness, or atrophy to be significant. Henderson et al6 found a diminished deep tendon reflex in 71% and a demonstrable motor deficit in 65% of 846 patients with cervical radiculopathy. The specific motor and deep tendon reflex changes noted depend on the cervical nerve root that is compressed by the herniated disk. Because the C3 and C4 nerve roots do not have a uniquely testable reflex or motor innervation, involvement of these roots corresponds to sensory changes in their respective dermatomes. The remaining cervical nerve roots do exhibit testable motor and reflex changes in addition to sensory deficits in their corresponding dermatomes (Table 3d.2). The specific motor innervation of the individual nerve roots allows the examiner to pinpoint the level of disease with good accuracy. Because plain films are most often normal they are nondiagnostic, leaving the clinician to rely on the history and physical examination to arrive at the diagnosis of an acute herniated cervical disk. Occasionally, disk space narrowing is seen at the involved interspace, or oblique films may show foraminal narrowing. Plain films are useful primarily for ruling out other causes of arm and neck pain, such as instability and neoplasia. Other diagnostic tests, such as electromyography (EMG) or myelography, are not useful as screening tests and should be
Chapter 3d
Table 3d.2
Neurology of the upper extremity
Disk
Root
Reflex
Muscles
Sensation
C4-C5
C5
Biceps reflex
C5-C6
C6
C6-C7
C7
Brachioradialis reflex (biceps reflex) Triceps reflex
Deltoid Biceps Wrist extension Biceps
Lateral arm Axillary nerve Lateral forearm Musculocutaneous nerve Middle finger
C7-T1
C8
T1-T2
T1
Wrist flexors Finger extensions Triceps Finger flexion Hand intrinsics Hand intrinsics
Medial forearm Med. Ant. Brach. Cutaneous nerve Medial arm Med. Brach. Cutaneous nerve
used more to confirm diagnoses based on a detailed history and physical examination. In addition, the routine use of computed tomography (CT) or magnetic resonance imaging (MRI) is not warranted. These sensitive studies may reveal herniated disks that are clinically insignificant: In a study of 63 asymptomatic individuals, 10% showed evidence of cervical disk herniation on MRI.1
Treatment The primary mode of treatment for an acute herniated disk is rest and immobilization. A cervical orthosis greatly improves the chance that the patient will remain at rest. The collar must fit properly and hold the head in a neutral to slightly flexed position. If the neck is held in hyperextension, the patient often is uncomfortable and therefore noncompliant in its use. Once the acute pain starts to subside, the patient should be weaned slowly from the orthosis and should likewise increase activity gradually. If the patient complies with the rest and immobilization, the use of analgesics is often not necessary, although a brief course of analgesic medicine may occasionally be required in severe cases. Benzodiazepines and muscle relaxants can act as central nervous system depressants but as such have a limited role in the treatment of acute herniated disk disease. Drug therapy does, however, have an important role in combination with rest and immobilization. Evidence now suggests that herniated disks are capable of eliciting an immune response characterized by the secretion of cytokines such as interleukin-1, interleukin-6, nitric oxide, and prostaglandins, which have multiple effects on tissues, including direct stimulation of nerve ending and sensitization of nociceptors.7 By inhibiting the production pathway of some of these mediators, antiinflammatory medications such as nonsteroidals have a role to play in symptomatic relief. Many such medications can have adverse gastrointestinal side effects but can generally be well tolerated for brief periods. The patient should be educated on these side effects, however, and should be instructed to stop taking the medication immediately if side effects occur. Routine use of oral systemic
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Cervical degenerative disk disease
steroids is not necessary but may prove useful in the more refractory cases. In this case, a tapering dose schedule over a period of 7 days can be used. Injections of local anesthetic and steroid into the cervical epidural space may provide some pain relief. This again is based on the premise that inflammation plays a significant role in the production of radicular symptoms. This procedure, however, requires considerable experience and technical competence and carries with it a risk of complications. Some authors have had limited success with this procedure, but we do not routinely use cervical epidural steroids. The prognosis for patients with an acute herniated cervical disk is generally very good. If patients are compliant with the rest and immobilization program as outlined, most are able to return to work within a period of 1 month, at least under light duty conditions. Indications for surgical intervention in the treatment of an acute herniated disk include persistent radicular pain unresponsive to at least 3 months of conservative therapy, progressive neurologic deficit, static neurologic deficit in the presence of radicular-type pain, and radiographic studies such as CT or MRI with a myelogram confirmatory of clinical signs and symptoms (Fig. 3d.5). Diskectomy for pain relief has been shown to be greater than 90% effective when performed for the proper diagnosis.
CERVICAL DEGENERATIVE DISK DISEASE Cervical degenerative disk disease can produce cervical spondylosis in isolation or in concert with a number of syndromes, including myelopathy, radiculopathy, myeloradiculopathy, and associated visceral or vascular encroachment. Radiculopathy secondary to spondylosis is not discussed separately because it does not significantly differ from radiculopathy secondary to acute herniated disk disease as previously described.
Spondylosis The human cervical spine has a high degree of mobility and flexibility. It has paid the price for this mobility with an almost universal propensity for degenerative change. Cadaveric studies have revealed that nearly everyone will demonstrate some degree of degenerative change in the cervical spine by age 55. Cervical spondylosis is a term used to describe the chronic process of degenerative changes that occur as part of natural aging. These include changes in the vertebral body, intervertebral disk, uncovertebral joints of Luschka, zygapophyseal joints, ligamentum flavum, dura, and soft tissues. The primary cause of cervical spondylosis appears to be agerelated changes that occur in the intervertebral disks, including loss of annulus fibrosus elasticity, desiccation of the nucleus pulposus, and narrowing of the disk space with or without associated disk rupture. Narrowing of the disk space creates excessive motion between vertebral segments, causing secondary changes such as osteophyte formation, facet joint and ligamentum flavum hypertrophy, inflammation of synovial joints, and possibly microfractures. Ultimately, spinal canal and lateral recess stenosis may result. These changes are seen in varying degrees in patients with spondylosis and to a lesser extent in asymptomatic
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JS
C5
A
B
Figure 3d.5 Magnetic resonance images of a 45-year-old man with unilateral C6 radiculopathy. (A) Midsagittal view showing more pathologic anatomy than a parasagittal view of the unaffected side (arrows). (B) Parasagittal view of the affected side showing hard disk pathology (arrow). (From Boden SD, Rothman RH, Wiesel SW, Laws ER, Boden SD: The aging spine: essentials of pathophysiology, diagnosis, and treatment. Philadelphia, 1991, WB Saunders.)
elderly individuals and can produce a variety of clinical signs and symptoms depending on the severity. However, not everyone has clinically symptomatic complaints. Friedenberg and Miller4 showed a lack of correlation between symptoms and degenerative changes seen on plain radiographs of the cervical spine. These changes become clinically significant only when directly related to symptoms. Historically, the typical patient with cervical spondylosis is over 40 years of age and has a complaint of neck ache. Referred pain patterns discussed above include shoulder pain, suboccipital referred pain, occipital headaches, intrascapular pain, anterior chest wall pain, or other nonspecific symptoms such as blurred vision and tinnitus. Physical examination of a patient with cervical spondylosis often reveals little in the way of objective clinical findings. Neurologic findings are generally normal in isolated spondylosis without radiculopathy or myelopathy. Some decrease in motion of the cervical spine may be evident. Point palpation may reveal some tenderness along the midline of the neck and in areas of referred pain. Plain radiographs are obtained primarily to rule out more serious causes of neck pain. Plain films in the anteroposterior, lateral, and oblique planes reveal varying degrees of change, including disk space narrowing, osteophyte formation, foraminal narrowing, facet degeneration, or instability patterns. Once again, these changes do not directly correlate with the presence or severity of clinical symptoms.
Treatment The mainstay of therapy for patients with cervical spondylosis is conservatism. In the presence of acute exacerbation of symptoms
against a background of chronic disease, rest and immobilization are generally beneficial. Aspirin or other nonsteroidal antiinflammatory medications may be helpful also for an acute exacerbation and may be needed on a chronic basis to abate symptoms. As previously described, trigger point injections may be of value also both diagnostically and therapeutically. A soft cervical orthosis may assist in resting and immobilizing the cervical spine. Cervical isometric exercises and changes in the patient’s daily activities such as work habits, sleeping positions, and automobile driving may be useful adjuvant therapies in the treatment of these chronic patients. In this patient population, the use of manipulative techniques and traction protocols should not be performed.
Spondylosis with myelopathy When the previously described degenerative changes of the cervical spine become so severe as to impinge on the spinal cord, a pathologic process termed myelopathy is produced. Spinal cord and nerve root compression produces myeloradiculopathy. Having been described already in detail in relation to acute herniated disk disease, radiculopathy is not addressed here. Those patients with developmental cervical stenosis are more prone to the development of spondylitic myelopathy at a younger age. Etiologic factors in the reduction of canal reserve volume include hypertrophy of the ligamentum flavum, facets, lamina, and dura with redundant annulus fibrosus; foraminal osteophyte compression of radicular vessels; vertebral osteophyte cord compression; tethering of the cord by dentate ligaments; and ossification of the posterior longitudinal ligament or ligamentum flavum.
Chapter 3d
A reduction in volume of the spinal canal can result in direct canal compression and intrinsic or extrinsic ischemia. Edward and LaRocca3 demonstrated that development of myelopathy with spondylosis is almost certain with canal diameters of less than 10 mm. Patients with canals 10-13 mm in diameter are at risk, and those with canals 13-17 mm are myelopathic prone. Myelopathy rarely develops with canal diameters greater than 17 mm. In addition to these static considerations, dynamic changes in the cervical spine may result in myelopathy. Penning and van der Zwaag described the pincer mechanism in 1966. In this mechanism, the spinal cord becomes compressed between the anterosuperior margin of the lamina of the inferior vertebrae and the posteroinferior osteophyte (i.e., hard disk disease) of the superior level. Flexion of the spine causes stretching of the cord over vertebral body osteophytes, with extension possibly resulting in retrolisthesis of one vertebral body on another or buckling of the hypertrophied ligamentum flavum. All these dynamic changes can cause compression of the cord as it passes through the cervical canal. Clinically, most patients are between 40 and 60 years of age when initially seen, with males affected more often. Myelopathy develops in fewer than 5% of patients with cervical spondylosis. Although a history of trauma may occasionally be given, the onset is more often insidious. Acute myelopathy generally reflects a central soft disk herniation producing a high-grade block. The natural history is one of deterioration initially, followed by a plateau in deficit lasting for several months. The exact clinical picture is variable, with a patchy distribution of deficits. This distribution depends on the number of levels involved and the severity of cord impingement at each level. Typically, patients have a gradual onset of numbness and paresthesias with associated weakness and clumsiness. Often, a history of difficulty writing is elicited. Lower extremity symptoms may precede those in the upper extremity and include gait disturbances, peculiar leg sensations, weakness, hyperreflexia, spasticity, and clonus. Upper extremity findings that may initially be unilateral often progress bilaterality. These include hyperreflexia, a brisk Hoffmann sign, and muscle atrophy, particularly of the hand intrinsics. Abnormalities in micturition are seen in approximately one third of cases and connote a more severe cord impingement. Sensory changes are a less reliable sign of myelopathy. Spinothalamic tract signs may be seen with disturbances in pain and temperature sensation in the upper extremities, thorax, or lumbar region. These may be characterized by a stocking-glove distribution. Dorsal column function can be affected with resultant vibratory and proprioceptive disturbances. Impingement on the dorsal division of the nerve root may produce unusual dermatomal sensory changes. In the event of a severe myelopathy, one of several spinal cord syndromes may develop. These include (1) Brown-Sequard syndrome with ipsilateral motor dysfunction, contralateral pain, and temperature dysfunction one to two levels below the motor involvement; (2) central cord syndrome with upper extremity involvement greater than lower extremity involvement; (3) transverse lesion syndrome, which occurs most commonly with involvement of the posterior columns, spinal thalamic tracts, and corticospinal tracts; (4) brachialgia cord syndrome with upper extremity radicular symptoms and long-tract signs; and (5) motor
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Rheumatoid arthritis
system syndrome with corticospinal tract involvement and weakness of both the upper and lower extremities. The differential diagnosis for patients with cervical spondylitic myelopathy includes such disorders as multiple sclerosis, amyotrophic lateral sclerosis, spinal cord tumors, syringomyelia, disk herniation, intracranial lesions, low-pressure hydrocephalus, and subacute combined degeneration. Each of these should be ruled out with appropriate history, physical examination, and diagnostic studies. Plain radiography in these patients generally demonstrates typical degenerative findings, including spinal canal narrowing by prominent posterior osteophytes, variable foraminal narrowing, disk space narrowing, facet joint arthrosis, and instability. MRI can demonstrate structural and parenchymal changes (Fig. 3d.6). The myelogram also is valuable in demonstrating the typical washboard appearance (Fig. 3d.7) with multiple anterior and posterior dye column defects. The posterior defects are produced by facet joint arthrosis and ligamentum flavum buckling.
Treatment Studies looking at the natural history of cervical spondylitic myelopathy are inconsistent and often difficult to compare because of the lack of a universal classification system. Some common factors, however, can be identified. The age at onset and duration of symptoms before the onset of treatment are prognostic factors. Increased age at diagnosis and delay in treatment for longer than 1 year indicates a poor prognosis. Most patients in these series had periods without progression, or plateau phases, interspersed with periods of rapid deterioration. Some patients had a steady progression of the disease with resultant severe disability. Conservative therapy rarely reverses the myelopathy, although in a patient who is a poor surgical candidate because of concomitant medical conditions, conservative measures such as immobilization and rest with a cervical orthosis are viable options. In general, however, management of patients with myelopathy requires surgical decompression of the spinal canal and prevention of further spinal cord impingement and vascular compromise. Progression of the myelopathy after surgical decompression is uncommon. Both anterior and posterior surgical procedures have been reported to lead to improvement in the myelopathy of patients with cervical spondylosis.
RHEUMATOID ARTHRITIS Approximately 2% to 3% of the general population is affected with rheumatoid arthritis. Of these, 86% show radiographic evidence of cervical spine disease, and 60% have clinical signs and symptoms of cervical spine involvement reflecting the erosive inflammatory changes characteristic of this systemic disease process. The clinical variable that is the most consistent indicator of cervical spine involvement is the presence of hand deformities.11 Involvement of the cervical spine consists of three distinct syndromes: atlantoaxial instability, basilar invagination, and subaxial instability. Although atlantoaxial instability is the most common of these syndromes, Ranawat et al12 showed that they tend to occur in combination. They found that 60% of patients had atlantoaxial instability, 16% had basilar invagination, and 60% had subaxial instability. Risk factors for the development
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Figure 3d.6 (A) A sagittal 500-ms TR/17-ms TE image in a patient who sustained a cervical extension injury. Note the disruption of the anterior longitudinal ligament at multiple levels (solid white arrows) and the traumatic disk herniations (open arrows). Pinching occurs at the C5-C6 level (black arrows). (B) A parasagittal 500-ms TR/17-ms TE image shows anterior longitudinal ligamentous disruption (arrows) and prevertebral soft tissue swelling. (C) The midline sagittal 2000-ms TR/30-ms TE 7-mm image demonstrates ligamentous disruption (white arrows), prevertebral edema (e), and pinching at C5-C6 (black arrows). The canal compromise appears more serious on this 7-mm sagittal image, most likely because of a partial volume effect from the lamina laterally. (D) A 2000-ms TR/60-ms TE midline sagittal image shows similar findings, again with prevertebral edema (e), ligamentous disruption (white arrows), and some increase in signal intensity of the spinal cord at the site of compression (black arrows). (E and F) 2000-ms TR/90- and 120-ms TE images with similar findings, although the increased signal intensity within the spinal cord secondary to edema is more obvious on those more T2-weighted scans. The absence of any significant focal areas of decreased signal intensity indicates a relative absence of intramedullary hemorrhage (contusion) and a more favorable prognosis. Despite the initially severe neurologic deficit, this patient eventually recovered significant function. (From Modic MT, Masaryk TJ, Ross JS: Magnetic resonance imaging of the spine, ed 2. St. Louis, 1994, Mosby Year Book.)
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3 4 5 6 B Figure 3d.7 (A) Lateral roentgenogram of a 43-year-old man with complaints of left shoulder pain, gait abnormality, and leg weakness. He had mild spondylotic changes and a congenitally narrow cervical canal (12 mm). (B) Lateral myelogram showing significant extradural defects at C3-C4, C4-C5, and C5-C6. (C) A computed tomography myelogram shows large uncovertebral spurs (arrows) plus soft disk material protruding at C3-C4. (D) Severe spinal cord flattening at C4-C5 from the disk and an osteophytic ridge. (From White AH, Schofferman JA: Spine care, vol. 2. St. Louis, 1995, Mosby Year Book.)
of atlantoaxial instability include prolonged systemic steroid use, long disease duration, older age, and erosive peripheral joint involvement. Patients with cervical spine involvement secondary to rheumatoid arthritis often have occipital neuralgia caused by compression of the greater occipital branch of C2. This gives the typical complaint of headaches when upright that is relieved by
recumbency. Range of motion may be limited, and crepitation or sensations of frank instability may be present, in which case Lhermitte’s sign may be elicited with motion. Neurologic changes can be variable and are often difficult to interpret in rheumatoid patients, who may have severe involvement of the upper and lower extremities. Physical examination should be performed very carefully to rule out upper motor neuron signs, such as
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hyperreflexia and spasticity, and the presence of abnormal reflexes, such as the Babinski and Hoffmann signs. Brainstem involvement by compression of the invaginated dens and/or associated pannus can result in symptoms of vertebrobasilar insufficiency. Other nonspecific findings may include the onset of bowel or bladder incontinence or retention, development of spasticity, and a change in ambulatory status. Evaluation of patients with any of these clinical symptoms should first begin with plain radiographs of the cervical spine. Common findings include osteopenia, facet erosion, disk space narrowing, and subluxation of the lower cervical spine (step ladder). Clinical management and operative indications can be defined by five radiographic measurements: (1) the anterior atlantodens interval, (2) the posterior atlantodens interval, (3) the McGregor line, (4) the Ranawat measurement, and (5) the Redlund-Johnell measurement10 (Fig. 3d.8). Basilar invagination occurs with upward migration of the odontoid process into the foramen magnum with resultant brainstem impingement. Radiographic evaluation includes a measurement of the distance from the tip of the odontoid to beyond the MacGregor line. This is seen on the lateral view of the cervical spine and represents a line drawn from the tip of the hard palate to the posterior base of the foramen magnum. Normally, the dens should not protrude more than 4.5 mm above this line. Protrusion more than 8 mm in females or 9.7 mm in males may be an indication for surgery. A CT may be helpful in determining radiographic landmarks, which tend to become more diffuse in the rheumatoid patient. Subaxial subluxations are also evaluated on dynamic flexion-extension views of the spine. Significant subluxation is defined as translation of one vertebral body on another of 3.5 mm or more or disk space angulation of 11 degrees or more.
Treatment Most of these patients can be managed conservatively despite the fact that cervical spine involvement may develop in a significant number. The mainstay of nonoperative therapy is a hard cervical orthosis (Philadelphia collar), which produces symptomatic relief without actually affecting the atlantoaxial interval. Medical treatment of these patients plays a crucial role in nonoperative management. Medications such as oral steroids, methotrexate, leflunomide, and other disease-modifying antirheumatic drugs are administered under the supervision of a rheumatologist.
Prognostically, these patients tend to do very well with conservative measures, and only a small percentage die of medullary compression from significant atlantoaxial disease. Atlantoaxial disease gradually worsens with time, with only 2% to 14% of patients exhibiting progressive neurologic symptoms. To summarize, surgical intervention should be considered in the presence of (1) more than 3.5 mm of mobile subaxial subluxation on flexion-extension views, (2) atlantoaxial subluxation greater than 8 mm in the presence of spinal cord compression on flexion-extension radiographs, or (3) cranial settling indicative of basilar invagination in the presence of radiographic evidence (MRI) of cord compression. Additionally, in the absence of these findings, the presence of a progressive neurologic deficit is a strong indication for surgical intervention.
HYPEREXTENSION INJURIES (WHIPLASH) Most hyperextension injuries to the cervical spine result from rear-end automobile accidents, which cause acceleration hyperextension injuries in the drivers of the struck cars. Falls and sports injuries contribute to the remainder of the hyperextension injuries. This injury has great economic considerations. The term whiplash injury was introduced by H. E. Crowe in 1928, and since that time it has become a major source of litigation potential. The pathophysiology behind a hyperextension injury involves the soft tissues of the neck region.9 Usually, the driver of the struck automobile is relaxed and unaware of the incipient collision. When struck from behind, the automobile accelerates forward acutely. If no headrest is present, the driver’s head is thrown back and the neck forced into hyperextension as the torso continues onward with the automobile. The sternocleidomastoid, scalenes, and longus coli muscles are extended beyond their elastic limit and are severely stretched or torn. Tears of the longus coli muscles may be associated with a concomitant tear of the sympathetic trunk and result in Homer syndrome. Further hyperextension may result in injury to the larynx or esophagus with subsequent hoarseness or difficulty in swallowing, respectively. Injury to the anterior longitudinal ligament may result in hematoma formation with cervical radiculitis or injury to the intervertebral disk. Furthermore, when the head is thrown backward, the jaw generally lags behind, resulting in injury to the temporomandibular joint as the jaw falls open. When the head recoils forward, the skull may strike the driver’s wheel or windshield, resulting in a head injury.
Figure 3d.8 (A) Measurement of anterior atlantodens interval and posterior atlantodens interval. (B) The Ranawat method for measurement of vertical setting. (C) The Redlund-Johnell method for measurement of vertical setting. (From Monsey RD: J Am Acad Orthop Surg 5:240-248, 1997.)
Chapter 3d
Hyperextension injuries in elderly patients with preexisting cervical spondylosis may acutely compress the spinal cord as the already limited spinal reserve volume is overcome. This cord compression can take the form of a frank paralysis or a central cord syndrome. Patients with a hyperextension injury are generally examined 12 to 24 hours after the initial traumatic event. It is at this point that the patient starts to feel stiffness in the neck and pain at the base of the neck made worse by motion. The pain becomes progressively worse, and eventually the slightest head or neck movement elicits severe pain. The anterior cervical musculature may be tender to palpation, and the patient may have hoarseness, dysphagia, or pain with chewing or opening the mouth. Pain may radiate into both shoulders and arms and upward into the base of the skull. Other pain patterns may include the anterior of the chest, interscapular region, and vertex of the skull. The potential for a closed-head injury even in the absence of visible head trauma should not escape the examiner. Concussion can occur secondary to mechanical deformation during the acceleration-deceleration phase of the injury. This may result in headache, photophobia, mild transient confusion, fatigue, tinnitus, or transient concentration abnormalities. Physical examination must be complete from head to toe so that other associated injuries are not overlooked. The potential for a “chance fracture” of the lumbar spine exists if the patient was wearing a lap seatbelt. The head should be examined for any evidence of a closed-head injury. A unilateral dilated pupil may suggest an injury to the sympathetic chain as it travels along the longus coli muscles with resultant Horner syndrome. It may also indicate significant intracranial pathology in a patient with an altered level of consciousness. Temporomandibular joint tenderness should be assessed as well as suboccipital tenderness, which may indicate that the head struck the top of the seat. A careful and thorough neurologic examination should be performed. Again, particular attention should be paid to elderly patients, who may have baseline spinal stenosis secondary to cervical spondylosis with resultant cord injury or central cord syndrome. If any objective neurologic deficit is identified, further diagnostic tests, including CT and/or MRI, are necessary. CT is better at providing bone detail, whereas MRI is better at demonstrating soft tissue disruption such as intervertebral disk protrusion. In most cases of hyperextension injury, only soft tissue disruption occurs. Plain radiographs should be obtained, however, to rule out unsuspected facet dislocations, facet fractures, odontoid fractures, or spinous process fractures. In most cases, these films are normal or may show some straightening of the cervical spine. As noted, other diagnostic studies such as a head CT should be obtained as the history and physical findings dictate.
Treatment Treatment involves primarily rest and immobilization. Rest consists of a soft cervical orthosis that assists in relieving muscle spasms and prevents quick movements of the head. Collar wear beyond 2 to 4 weeks should not be encouraged, because this may result in weakening of the neck musculature and, in turn,
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development of a long-term psychoneurosis. Strict bed rest may be necessary for 3 to 5 days if the symptoms are severe. Heat in the form of hot soaks or heating pads may be useful. Although narcotics should be avoided, medical therapy in the form of nonnarcotic analgesics, nonsteroidal antiinflammatory medications, and muscle relaxants is helpful. Activity should be restricted according to symptom severity. Characteristically, improvement should occur after 2 weeks of treatment as outlined earlier. If improvement does not occur, an additional 2 weeks of rest and immobilization should be prescribed with the addition of home cervical traction. Lowweight traction consisting of 7 to 10 pounds for 20 to 30 minutes per day generally gives symptomatic improvement. Persistence of symptoms past 4 weeks should alert the physician to search for another etiology. If headaches persist, a CT of the head should be obtained to rule out a closed-head injury. If arm or shoulder pain persists, CT of the spine and/or EMG should be performed. In general, symptoms should be resolving by 6 weeks, although complete resolution may take as long as 1 year.8 Persistence of symptoms beyond 6 weeks of severity equal in intensity to that in the initial period may alert the physician to secondary gain from pending litigation, and compensation neurosis should be suspected. Before assigning this diagnosis, the physician should certainly rule out any significant pathology by a careful history, physical examination, and appropriate diagnostic testing. The physician should not, however, over-treat the patient and encourage a retreat into a life of incapacitating neck pain. The point at which the patient is able to return to the work force depends on both the severity of the hyperextension injury and the type of work involved. Patients performing heavy manual labor may require 3 to 4 weeks of treatment before returning to work, whereas those in less demanding positions may be able to return after only 2 weeks. Limitations on the work performed should consist of no lifting of objects heavier than 50 pounds, no bending, and no prolonged periods of stooping. These restrictions should remain in effect for the first 3 weeks that the patient has returned to work. Depending on the severity of the injury, the prognosis is generally good for complete recovery. Occasionally, a 5% to 10% disability rating is appropriate in an honest patient in whom symptoms persist during hard manual labor.
CERVICAL SPINE TREATMENT ALGORITHM The goal for patients with neck pain is to obtain an accurate diagnosis and administer the correct therapy at the appropriate time. The previously presented clinical entities have been organized into a standardized approach,16 a graphic display of which is presented in the form of an algorithm in Figure 3d.9. The algorithm aids in establishing the proper diagnosis and guides in the delivery of the proper treatment. A summary of treatments categorized by pathology is listed in Table 3d.3. The algorithm begins with evaluation of those patients seen for neck pain with or without associated arm pain. Patients with a history of trauma and associated fractures and/or dislocations are excluded. The first task is a thorough medical history and physical examination to rule out the presence of cervical myelopathy, as discussed earlier.
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Figure 3d.9
Treatment options for disorders of the cervical spine
Cervical spine algorithm. (From Wiesel SW, et al: Neck pain. Charlottesville, VA, 1988, The Michie Company.)
Chapter 3d
Table 3d.3 Treatment options for cervical spine pathology Neck sprain
Spondylosis
Hyperextension/ whiplash Rest Soft orthosis Moist heat Activity modification Physical therapy NSAIDs Rheumatoid arthritis
Rest Soft orthosis Activity modification NSAIDs Muscle relaxants Trigger point injections Acute herniated disk Rest Soft orthosis NSAIDs Oral steroids Epidural injections ↓ Diskectomy
Rest Soft orthosis Activity modification Isometric exercises NSAIDs Trigger point injections Spondylosis with myclopathy Rest/immobilization (nonoperative candidate)
Hard orthosis Steroids/DMARDs
↓ Surgical decompression
↓ Surgical fusion
DMARDS, disease modifying antirheumatic drugs, NSAIDs, nonsteroidal antiinflammatory drugs.
If a myelopathic process is confirmed, surgical intervention should be considered in a timely fashion. The best results are obtained with only one- to two-motor unit involvement and relatively short duration of symptoms. Further studies, including myelography or MRI, should be performed to define precisely the neural compression. Adequate surgical decompression should then be performed. If cervical myelopathy is ruled out, most patients should then be started on a course of conservative management. Regardless of the etiology of the neck pain, all patients are treated equally in this regard. Initially, this nonoperative management consists primarily of immobilization and drug therapy. A well-fitted soft cervical collar should be worn for 24 hours per day to prevent awkward positioning and movements during sleep and while awake. In addition, antiinflammatory medications, analgesics, and muscle relaxants will improve patient comfort. Most patients will symptomatically improve with this protocol within approximately 10 days and should then start to be weaned over the next 2 to 3 weeks. Additionally, their level of activity should be gradually increased, and they should start a series of exercises aimed at strengthening the paravertebral musculature. If the condition remains unimproved, patients should continue full-time collar wear and pharmacologic management. If no significant improvement in symptoms is seen after 3 to 4 weeks, a trigger point injection at the point of maximum tenderness should be considered. This is performed with a combination of 10 mg of corticosteroid and 3 to 5 ml of 1% lidocaine. If this is likewise not successful at 4 to 5 weeks, a trial of home cervical traction may be considered. For patients with neck pain, a total period of 6 weeks of conservative management should be pursued. Most patients respond to this program and return within 2 months to their previous life-styles. If, on the other hand, the symptoms fail to resolve within 6 weeks of conservative therapy, the patients are
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then divided into two groups depending on whether neck or arm pain (brachialgia) is the predominant complaint. For those patients whose main complaint is neck pain and for whom conservative therapy for 6 weeks has failed, plain radiographs, including flexion-extension films, should be obtained. Several of these patients will have evidence of instability, the criteria for which include horizontal translation of one vertebra on another of 3.5 mm or an angular difference of 11 degrees between adjacent vertebrae. Most of these patients do well with nonoperative management consisting of education and bracing, but those who do not may require segmental spinal fusion. A second group of patients have changes characteristic of degenerative disease. Radiographic findings include osteophyte formation, loss of intervertebral disk height, narrowing of the neural foramina, and zygapophyseal joint osteoarthritis. As previously mentioned, degeneration of the cervical spine may be a normal part of the aging process. The difficulty arises in determining which of the degenerative changes are clinically significant. The most significant change has been found to be narrowing of the intervertebral disk height, particularly at C5-C6 and C6-C7. Treatment of these patients consists primarily of antiinflammatory agents, support braces, and trigger point injections. During quiet periods, isometric exercises should be used. Reexamination is necessary to monitor for the development of myelopathic symptoms or signs. Most patients who have normal plain films receive a preliminary diagnosis of neck strain. After failure to improve with conservative therapy, these patients should have a thorough medical evaluation and a bone scan to rule out infection, neoplasia, or inflammatory arthritis as the etiology of the neck pain. If this workup proves negative, they should then undergo psychosocial evaluation and receive treatment, if appropriate, for depression or substance dependence, both of which can frequently be found in patients with neck pain. If the psychosocial findings prove normal, the patient is considered to have a diagnosis of chronic neck pain. Treatment therefore consists of thorough education and support, detoxification from narcotics, and institution of an exercise program. Antidepressant agents may prove to be useful, and frequent reevaluations are necessary to avoid overlooking any serious pathologic process. Other large groups of patients in this algorithm are those in whom arm pain is the predominant symptom. The etiology of this pain may be either direct pressure from a herniated disk or inflammation about a nerve on hypertrophic bone (hard disk disease). Other causes of extrinsic compression of the vascular or nervous structures supplying the upper extremity, including pathologic processes of the chest and/or shoulder region, may imitate brachialgia also and must therefore be ruled out. A thorough history and physical examination, including an Adson test, shoulder examination, and Tinel’s test of the carpal, cubital, and ulnar tunnels, should be performed, with additional appropriate studies possible, based on the results. If an Adson test is positive, vascular studies and EMG should be performed to evaluate causes of thoracic outlet syndrome. Compression of the brachial plexus may occur secondary to vascular structures, cervical ribs, muscular or fibrous bands, or neoplastic processes. Additionally, an apical lung carcinoma can cause brachial plexus compression with or without Horner syndrome from sympathetic chain involvement (Pancoast tumor).
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If plain films of the chest and shoulder are negative and fail to reveal a source of extrinsic compression, EMG studies should be performed. If these indicate peripheral nerve compression, surgical decompression at the site should be performed. In the presence of radicular symptoms, a myelogram or MRI should be performed, and if the results are consistent with the neurologic deficit, history, and physical findings, surgical decompression of the nerve root should be undertaken because conservative treatment results in persistent symptoms. This algorithm is applicable to all patients with nonspecific neck or arm pain and provides a rational approach to the therapeutic and diagnostic sequence of events. The goal of this approach must always be to treat appropriately the etiology of the pain while avoiding unnecessary tests and therapeutic interventions and, most importantly, to minimize the chance of overlooking other serious pathologic processes.
REFERENCES 1.
2. 3. 4. 5. 6.
7.
8.
CONCLUSION
9. 10.
This chapter summarizes some of the major pathologic processes that affect the cervical spine. A detailed description of the anatomy and of the pathophysiology is provided to aid in the understanding of these clinical entities. In addition, the clinical workup of each disease process is discussed, covering the presenting signs and symptoms, corresponding physical examination, and pertinent diagnostic studies. A special emphasis is placed on the treatment of cervical spine disease, which is individualized for each pathologic process. Finally, a treatment algorithm is presented that provides a coherent clinical decision-making process combined with a standardized approach to treatment of cervical spine disease.
11. 12. 13. 14. 15. 16.
Boden SD, McCowin PR, Davis DO, Dina TS, Mark AS, Wiesel S: Abnormal magneticresonance scans of the cervical spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg 72(8):1178-1184, 1990. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns. I. A study in normal volunteers. Spine 15:453-457, 1990. Edward WC, LaRocca SH: The developmental segmental sagittal diameter in combined cervical and lumbar spondylosis. Spine 10:43-49, 1985. Friedenberg ZB, Miller WT: Degenerative disc disease of the cervical spine. J Bone Joint Surg 45A:1171-1178, 1963. Grubb SA, Kelly CK: Cervical discography: clinical implications of twelve years of experience. Spine 25:1382-1389, 2000. Henderson CM, Hennessy R, Shuey H: Posterolateral foraminotomy for an exclusive operative technique for cervical radiculopathy: a review of 846 consecutively operated cases. J Neurosurg 13:504-512, 1983. Kang JD, Stefanovic-Racic M, Mcintyre LA, Georgescu HI, Evans CH: Toward a biochemical understanding of human intervertebral disc degeneration and herniation: contributions of nitric oxide, interleukins, prostaglandin E2 and matrix-metallo-proteinases. Spine 22:1065-1073, 1997. McNab I: Acceleration injuries of the cervical spine. J Bone Joint Surg 46A:1797-1799, 1964. McNab I: The whiplash syndrome. Orthop Clin North Am 2:289-403, 1971. Monsey RD: Rheumatoid arthritis of the cervical spine. J Am Acad Orthop Surg 5:240-248, 1997. Oda T, Fujiwara K, Yonenobu K, Azuma B, Ochi T: Natural course of cervical spine lesions in rheumatoid arthritis. Spine 20:1128-1135, 1995. Ranawat CS, O’Leary P, Pellici P, Tsairis P, Marchisello P, Dorr L: Cervical spine fusion in rheumatoid arthritis. J Bone Joint Surg 61A:1003-1010, 1979. Rothman RH, Marvel JP: The acute cervical disc. Clin Orthop 109:59-68, 1975. Rothman RH, Marvel JP: The spine, ed 4. Philadelphia, 1999, WB Saunders. Stookey B: Compression of spinal cord and nerve roots by herniation of nucleus pulposus in the cervical region. Arch Surg 40:417-432, 1940. Wiesel S: Neck pain, ed 2. Charlottesville, VA, 1992, The Michie Company.
CHAPTER
3e
Workplace Adaptation Thomas J. Armstrong
The deviation of neck, shoulder, and elbow postures from neutral positions is associated with adverse health effects such as fatigue and chronic muscle, tendon, and nerve disorders. The effects of these disorders range from minor discomfort and degraded performance to disability. Available data suggest that the time at onset of adverse effects decreases with increasing exertion duration, frequency, and force. This does not mean, however, that some postures can or should be maintained indefinitely without interruption. Also, it does not mean that brief exposures to extreme postures are not desirable. The relationship between certain work activities and adverse health effects is referred to as the “dose-response” relationship (see Chapter 1). The dose-response relationship provides insight into how work can be designed to minimize the risk of possible adverse health effects or to facilitate the return to work of persons in whom an adverse effect may have developed. Unfortunately, sufficient data are not yet available to specify job designs that provide a specific level of risk. For example, it cannot be said how many times a group of workers can exert a horizontal force of 50 N to engage the bit of a powered screwdriver weighing 15 N at an elevation of 1.5 m before unacceptable health effects would develop in a given fraction of them. It is extremely important that the work equipment and procedures be evaluated at all stages of design and implementation. Workplace adaptation entails three basic steps14: 1. Evaluation of the proposed or existing job; 2. Specification of adaptations; 3. Evaluation of adaptations. It may be necessary to repeat one or more of these steps one or more times to achieve a desired level of control.
EVALUATION Evaluation entails documentation of the process, equipment, procedures, and environment and assessment of stressors, including posture, force, duration, and frequency.1,7 The documentation is performed from available job descriptions, time studies, workplace inspections and measurements, equipment specifications, and interviews with workers and supervisors. This information is then used to identify stressful postures and forces necessary to reach, hold, and use work objects and the duration and frequency of these exertions. Tables 3e.1 and 3e.2 and Figures 3e.1 and 3e.2 illustrate evaluation summaries of two jobs: claims processor and assembler. An assessment of stressful postures and forces entails examining each step of the operation for extreme neck, shoulder, and elbow
postures and forces (Fig. 3e.3). These elements should be recorded along with their duration, frequency, and cause. For example, in the claims processor job described in Table 3e.1, extreme reaches to the workers’ side are required 80 times per day to get unfinished files and 80 times per day to put aside finished files. Workers must reach over the files and rotate their forearms to use the keyboard 6 hours per shift. In the assembler job described in Table 3e.2, the workers must reach for parts beside and behind them 2400 times per 8-hour shift; they must elevate their elbow above shoulder height and rotate their forearm 14,400 times per shift, and so forth. The analysis should also include an inspection of infrequent or irregular elements. For example, in the claims processor job (Table 3e.1), 3 of 10 claims are set aside to await additional information that must be retrieved by telephone. In the assembler job (Table 3e.2), 1 of 12 screws is defective and requires additional movements and time to replace. By their very nature, it may be hard to identify irregular elements from existing job descriptions or observations. Often they are identified via worker and supervisor interviews.
SPECIFICATION OF ADAPTATIONS The causes of the physical stressors should be apparent from the work evaluation. The tabulation of stressors and their causes illustrated in Tables 3e.1 and 3e.2 provide a systematic format for developing possible adaptations. This format also provides insight into how the overall stressfulness of the job is affected by the proposed control measures and how one adaptation may affect other stressors. For example, in Table 3e.1 it can be seen that the claims processors are exposed to 2 hours of a stressful shoulder-neck posture per day to hold the phone handset. It can also be seen that a headset or a bracket attached to the handset could reduce this exposure. Yet another adaptation might be passing uncompleted files to another worker who does all the phoning; however, this solution could result in increased keyboard times and other undesirable effects. Reaching for documents is associated with cart location and design. It follows that locating the carts close to the workers’ side and modifying them with a fold-down side would reduce reaching. Because these reaches occur an average of only once every 3 minutes, it can be argued that this work element is by itself unlikely to produce adverse health effects; however, it can also be argued that when combined with other factors, this reaching could result in an adverse effect or could aggravate an existing case. An analysis of the low cost associated with parking the carts close to the workers versus the possible cost of medical treatment and lost work for disabled workers would support locating carts close to the workers. Such an analysis would probably also support a modification of the cart with drop sides. Workplace adaptations may involve modification of ● Work processes; ● Work standards; ● Design of methods; ● Workplace layout; ● Equipment; ● Training.
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Table 3e.1 Sample documentation and analysis of “claims processor” job for identifying and controlling shoulder and neck stressors TITLE Claims processor STANDARD Complete 80 claims per day EQUIPMENT Computer, keyboard, 13-inch color monitor and claim processor software Desk Staple remover Stapler Telephone with handset Adjustable-height chair Carts for holding files METHOD 1. Get file from cart—place on lap in front of keyboard 2. Remove staples 3. Sort documents 4. Perform keystrokes to open file 5. Perform keystrokes to update file 6. Call for information as necessary—3 calls per 10 claims 7. Perform keystrokes to close file 8. Staple documents 9. Stamp and date file 10. Place finished file in cart 11. Note: occasionally claims processor cannot finish file and will set it aside at the front of desk until someone calls back with necessary information MATERIALS Files weighing 5-50 N ENVIRONMENT Inside overhead fluorescent lights with diffusers
Work processes refer to the technologies used for completing the work objectives. In the claims processor example (Table 3e.1), the technologies are keyboards and telephones. Alternative technologies include scanners and electronic mail. In the assembler example (Table 3e.2), the technologies include threaded fasteners; alternative technologies include clips and adhesives. Work standards refer to the quantity and quality of work produced in a given time. In the claims processor example, the standard is 80 claims per 8-hour shift; in the assembler example, the standard is 2400 motor assemblies per 8-hour shift. The work standard is an important factor in how many times per day workers must assume a given posture or exert a given force. Reducing work standards is generally considered an adaptation of last resort; however, it may be shown that the lost productivity is more than offset by the reduced cost of medical treatment and lost work for a disabled worker. Work methods refer to the procedures or sequence of movements used to perform the job. In the assembler example, the method entails getting motors from a bin, placing them on the line, and driving six screws. A methods change to reduce reaching would be to unload one corner of the bin and then rotate it 90 degrees so that the workers are always working from the
WORKER Skilled male and female keyboard operators Fifth percentile female to 95th percentile male stature ERGONOMIC STRESSORS Stressor POSTURE Reaching for unfinished files (80 times per shift) Reaching over file on lap to use keyboard (6 hr/shift) Looking down at file (4 hr/shift) Extending the neck to see monitor through bifocals (2 hr/shift) Reaching to put aside finished files (80 times per shift) Inward forearm rotation and wrist deviation to position hands over keyboard (6 hr/shift) Holding phone between neck and shoulder (2 hr/shift) Proposed Adaptation Provide access for carts so that it can be positioned to minimize reaching Provide adjustable tray to hold file above keyboard Provide corrective lenses that do not require worker to extend neck Investigate variable geometry keyboard to reduce forearm rotation Provide headset for phone Investigate adjustable keyboard holder Investigate wrist rest Provide adjustable monitor holder Stressor FORCE Lifting files weighing up to 50 N from cart to lap (80 times per shift) and from lap to cart (80 times/shift) Proposed Adaptation Provide access for cart so that it can be positioned to minimize reaching Investigate drop side for cart
corner closest to them. A methods change may also require an equipment change and worker training. Workplace layout refers to the position of equipment and work objects in the workplace. In the claims processor example, the workplace layout includes the position in space of the carts with files, the keyboard, the monitor, the phone, and the active file with respect to the worker. Adaptations include repositioning the carts to reduce reaching, adding equipment to allow repositioning of the keyboard, and supplying adjustable document and monitor holders. In the assembly example, adaptations include equipment to reposition the parts bin and adjustment of the suspender so that the tool can be positioned to minimize reaching. Anthropometric data may be used to estimate reach distances.3,11 Average link length proportions can be used with population stature data to estimate vertical, horizontal, and lateral reach limits (Fig. 3e.4). Caution should be used in interpreting reach predictions based on link length data. A reach distance based on average proportions and a given percentile stature may correspond to a different percentile reach. Work locations should be made as adjustable as possible to accommodate individuals and should be tested with user trials.8,12,14 Reach data for U.S. civilian populations are available from U.S. National Health surveys.13
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Table 3e.2 Sample documentation and analysis of “assembler” job for identifying and controlling shoulder and neck stressors TITLE Assembler STANDARD Assemble 2400 motor assemblies per 8-hour shift EQUIPMENT Assembly line (1 m above floor level) Power screwdriver suspended above line Rack and bin for holding parts METHOD 1. Get motor assembly from bin (weight, 40 N) and position on subassembly 2. Get handful of screws with one hand 3. Get screwdriver with other hand 4. Position screw in screwdriver × 6 5. Drive screw (1 of 12 screws is defective and must be backed out and replaced) ENVIRONMENT Inside overhead fluorescent lights with diffusers WORKER Males and females Fifth percentile female to 95th percentile male stature ERGONOMIC STRESSORS Stressor POSTURE Reaching for motor assemblies located to side and behind worker (300 times/hr)
Equipment refers to hardware such as tools to drive fasteners or shape and smooth surfaces, containers, jigs, fixtures for holding parts, and seating to support the worker. A proposed adaptation in the claims processor example includes modification of the cart; adjustable holders for the keyboard, monitor, and files; and a headset for the phone. In the assembly example, equipment changes include an in-line screwdriver with articulating arm, an indexing assembly line, and a turntable for the parts bin. Training entails instructing workers on the hows and whys of arranging and performing their work. In the claims processor example, it should be explained to the workers where they should position the carts and why this is necessary to prevent possible shoulder problems. Follow-up training and evaluations should be performed to determine whether the workers understand and follow the specified procedures. If procedures are not followed, further evaluations should be performed to determine why they are not followed. The design of adaptations should draw on all available resources. Available resources vary from one situation to another, depending on the size and type of industry. Possible resources include ● Job designers, such as engineers, facilities people, and setup people; ● Safety and health personnel, such as doctors, nurses, industrial hygienists, and safety personnel; ● Supervisors;
Reaching for parts located to side and behind worker (300 times/hr) Reaching for screwdriver located overhead (300 times/hr) Driving 1800 screws/hr with pistol-shaped driver requires elevation of elbow and forearm rotation Reaching upstream and downstream to keep up with production line (50% of time, but 90% of time when bad screws are encountered) Proposed Adaptation Position trays close to worker and production line to minimize reaching Unload trays one corner at a time and then rotate tray 90 degrees to minimize reaching Adjust tool suspender to minimize tension and locate tool as close as possible to point of use Investigate use of in-line tool with articulating arm to control torque Investigate indexing production line in which work object stops until released by worker Position work object as close to edge of production line as possible to minimize reaching Investigate quality control program to avoid defective screws that take extra motions to try and to reject Stressor FORCE Lifting motor assemblies weighing 40 N from bin (300 times/hr) Pulling down power tool into work position (300 times/hr) Proposed Adaptation Investigate small hoist or air balancers to facilitate transferring motors to line (See above recommendations for tool suspender)
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Workers or work representatives; Purchasing; Sales and technical representatives from suppliers; Catalogs, brochures, and technical specifications; Scientific papers, books, and magazines.
In general, the team approach is the most effective way to mobilize the resources necessary to develop and implement workplace adaptations. On occasion, however, the problems are conspicuous and the solution is clear so organizing a special team is not merited. Development of adaptation is not an exact process. Consequently, all adaptations should be evaluated to ascertain their effectiveness.
EVALUATION OF ADAPTATIONS Ideally, adaptations should be evaluated in terms of their effects on upper limb disorders. Unfortunately, such evaluations are difficult. Upper limb disorders develop over long periods of time. To determine the effect of a given adaptation on the occurrence of disorders would require identification of a group of several hundred workers, implementation of the adaptation in a random subset of these people, and some kind of comparison adaptation in the others.6 The population would then have to be tracked for
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Figure 3e.1 (A) Illustration of a claims processor job. (B) Major stresses include reaching for documents, holding the telephone, reaching for the keyboard, looking down at documents, and reaching to get and put aside documents. (C) Possible claims processor job interventions include an adjustable document holder (a), adjustable monitor holder (b), adjustable keyboard holder (c), drop-side cart (d), headset for phone (e), and optically correct glasses (f).
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1 or more years. Unfortunately, such studies are extremely difficult and expensive. It is difficult to find large groups in which adaptations can be randomly assigned. Work activities are generally dictated by production schedules that may cause the work population to shrink or swell. In addition, non–health-related factors may cause a turnover in the work population. Although evaluation of health patterns is an important means of identifying workers and jobs that merit further evaluation and assessing an overall program, in most cases it provides only limited feedback about specific adaptations. Adaptations can be evaluated by using the same methods that were used for the initial job evaluations. This analysis should begin as the adaptations are developed on paper and continue through the prototype, pilot testing, and implementation phases.8 In some cases it may be possible to identify and evaluate other jobs at that work site or other work sites where the proposed
adaptations have already been implemented. In other cases it may be necessary to develop prototypes and conduct pilot testing on a small number of the proposed interventions. Worker feedback can be obtained through interviews; however, care should be taken to avoid leading questions.9 The questions should be structured in such a way as to provide guidance on how to enhance the adaptation. For example, one of the proposed adaptations for the assembly job was the use of another tool and locating it to minimize reaching. In this case, workers could be permitted to try several tools and then rank them in order of preference. They could also be asked to try the tools at several locations and rate them on a scale of 0 to 10 where 0 is “too low,” 5 is “just right,” and 10 is “too high.”2,12 Even though these measures do not ensure that future shoulder, neck, or elbow problems will not develop, they do provide a basis for selecting a work configuration that minimizes stress on the worker.
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Figure 3e.2 (A) Work station layout for an assembler. (B) Proposed interventions for the assembler example include using a narrower conveyor to reduce reaching over line “dead space,” using an indexing line so that the worker does not have to “chase” the assemblies, and using a smaller box of parts mounted on a turntable to reduce reaching to the side and behind the worker.
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Neck deviation
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Figure 3e.3 Shoulder and neck stressors include extreme neck, shoulder, and elbow postures and force. (Modified from Armstrong TJ: Hand Clin 553-565, 1986.)
Discomfort patterns can also be used to evaluate work designs before and after they are implemented.4,5,10 Workers are shown pictures of the body and asked to identify and rate areas of discomfort. Discomfort patterns provide information about many parts of the body, as well as those parts likely to be affected by the stress of concern and the proposed adaptation. Often, the variation from within and between workers is considerable, and rigorous statistical conclusions may not be possible.
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The available data are not yet sufficient to develop design specifications that can be used to achieve a given level of risk of neck, shoulder, and elbow disorders; however, the data do provide insight into some of the things that can be done to reduce risk. Control of disorders entails three basic steps: (1) evaluation of
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Figure 3e.4 (A) Average link length proportions can be used with population stature data to estimate vertical, horizontal, and lateral reach limits. (B) The outer arc represents maximum reach without bending. The inner arc represents maximum reach without bending and not flexing the shoulder more than 30 degrees to minimize loads on shoulder tissues.
Chapter 3e
the job to determine the frequency, duration, and cause of extreme reaches and forces; (2) specification of adaptations; and (3) evaluation of the adaptations. It may be necessary to repeat these steps before the desired level of control is achieved. Development of workplace adaptations should be integrated into an ongoing program that includes health surveillance, job surveys, evaluation of affected workers and jobs, medical management, training, and a team approach with participation from all levels of the organization.
5.
6. 7.
8.
9. 10.
REFERENCES
11. 12.
1. Armstrong TJ: Ergonomics and cumulative trauma disorders. Hand Clin 2(3):553-565, 1986. 2. Armstrong TJ, Punnett L, Ketner P: Subjective worker assessments of hand tools used in automobile assembly. Am Ind Hyg Assoc J 51(12):639-645, 1989. 3. Armstrong TJ, et al: Repetitive trauma disorders: job evaluation and design. Hum Factors 28(3):325-336, 1986. 4. Corlett EN, Bishop RP: The ergonomics of spot welders. Appl Ergonom Mar:23-31, 1978.
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References
Harms-Ringdahl K: On assessment of shoulder exercise and load-elicited pain in the cervical spine. Biomechanical analysis of load-EMG-methodological studies of pain provoked by extreme position. Scand J Rehab Med Suppl 14:1-40, 1986. Hennekens CH, Buring JE, Mayrent SL, eds: Epidemiology in medicine. Boston, 1987, Little, Brown. Keyserling WM, Armstrong TJ, Punnett L: Ergonomic job analysis: a structured approach for identifying risk factors associated with overexertion injuries and disorders. Appl Occup Environ Hyg 6(5):353-363, 1991. McClelland I: Product assessment and user trials. In JR Wilson, EN Corlett, eds: Evaluation of human work: a practical ergonomics methodology. New York, 1990, Taylor & Francis, pp. 218-247. McCormick E: Job and task analysis. In G Salvendy, ed: Handbook of industrial engineering. New York, 1982, John Wiley & Sons, pp. 2.4.1-2.4.21. Saldana N, et al: A computerized method for assessment of musculoskeletal discomfort in the workforce: a tool for surveillance. Ergonomics 37(6):1097-1112, 1994. Ulin SS, Armstrong TJ, Radwin RG: Use of computer aided drafting for analysis and control of posture in manual work. Appl Ergonom 21(2):143-151, 1990. Ulin SS, et al: Effect of tool shape and work location on perceived exertion for work on horizontal surfaces. Am Ind Hyg Assoc J 54(7):383-391, 1993. U.S. Department of Health, Education and Welfare: Weight and height of adults 18-74 years of age: United States, 1971-1974. Vital Health Stat 11(211), Hyattsville, MD, 1979, National Center for Health Statistics. Wilson JR: A framework and a context for ergonomics methodology. In JR Wilson, EN Corlett, eds: Evaluation of human work: a practical ergonomics methodology. London, 1990, Taylor & Francis, p. 6.
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Lower Back
4
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4a
Epidemiology: Incidence, Prevalence, and Risk Factors Michele Crites Battié, Tapio Videman, and Douglas Gross
The high prevalence and social and economic impact of low back pain and related disability are well recognized. Low back pain is one of four musculoskeletal conditions specifically targeted by the Bone and Joint Decade (2000-2010) initiative endorsed by the World Health Organization.15,106 Related to the workplace, back injury claims comprise the most expensive category of industrial injuries40,65 and are one of the most common causes of disability in adults under 45 years of age.24,90 In response to this problem, many workplace programs and medical services have been designed to prevent back problems or to minimize their negative consequences. Limited progress has been made, however, in alleviating this common condition and its consequences. When the underlying condition and risk factors for an ailment are understood, prevention and treatment strategies can be rationally based and well directed. In such situations, interventions are likely to be successful. Unfortunately, medical science still lacks information sufficient to guide the prevention and treatment of common back pain. Epidemiologic studies have sought to gain information that could be helpful in guiding these efforts. Epidemiology generally refers to the study of occurrence rates of diseases and especially factors associated with disease occurrence or nonoccurrence. A primary goal of such studies is to obtain information about the disease cause. However, challenges of the most basic nature have hindered epidemiologic studies of back problems.
CHALLENGES FACING EPIDEMIOLOGIC STUDIES OF BACK PAIN PROBLEMS Definition of the problem A central challenge of epidemiologic studies of back pain problems is that in the vast majority of cases the underlying pathology or condition is unknown.29,89 Current clinical examination methods rarely identify the underlying pathology of either acute or recurrent back pain in the absence of major trauma. Despite this reality, there is a tendency to approach back pain as though it were a specific disease or injury state. Miettinen and Caro67 cautioned that epidemiologic studies based solely on a complaint have limited value and that inferences to pathology can be misleading. A complaint is a voluntary behavior and as such can be influenced by a variety of factors other than physical pathology. Further problems encountered in studying any type of pain
include defining and quantifying the pain experience and controlling the effects of individual and cultural factors on pain perception and interpretation. Studies can be complicated also by uncertain reliability in a person’s recall of symptoms and by variations in how researchers define their presence.83 Back pain problems, moreover, are identified through numerous different reporting systems, primarily health surveys and symptom complaints noted in clinical or workplace settings. In North America, for example, in contrast to some other industrialized countries, pain in the workplace becomes known or registered through the filing of an incident report or workers’ compensation claim, and back pain is labeled a “back injury.” Taylor91 described a complex chain of events that leads to the production of industrial insurance and sickness data and makes it clear that the occurrence of back pain incidents registered in the industrial setting cannot be equated to the occurrence of morbidity. Failure to distinguish between studies of different back-related outcomes such as spine pathology, back symptom complaints, industrial injury claims, absenteeism, and long-term disability may lead to misleading generalizations and inaccurate conclusions. Along with different low back pain problem case definitions themselves are the influences and potential biases of the systems through which they are registered. An example of the potentially large effect of health system differences has been provided by Cherkin et al,23 who compared rates of back surgery in 11 developed countries and examined the association between these rates and the number of neurologic and orthopedic surgeons per capita. They found that the rate of back surgery was at least 40% greater in the United States than in any of the other countries investigated and more than four to five times that of England and Scotland. They also found that the rate of back surgery was positively correlated with the number of surgeons per capita (Fig. 4a.1).
Assessment of occupational and other relevant exposures In addition to the challenges posed by definitions, influences, and biases involved in back pain are the methodologic challenges of measuring occupational and other relevant exposures. Occupational exposures that appear frequently on lists of suspected risk factors are vehicular vibration and physical loading involving heavy lifting, bending, twisting, and sustained nonneutral postures. Virtually all inhabitants of developed countries are exposed to these factors during leisure time and work. Exposure is therefore a matter of degree and requires reliable valid methods of measurement. Unfortunately, practical tools to identify and quantify the different exposures in epidemiologic studies of large populations are not fully developed. Further complicating measurement is that for many outcomes such as structural changes of the spine, data are needed on lifetime loading rather than simply on current conditions. Most studies have used the job title as an indicator of occupational loading. This simple method of estimating occupational exposure can be highly inaccurate. The activities and environments of persons with similar job titles can vary substantially, and the loading profiles of workers who remain in one occupation for many years can change greatly. Moreover, most persons
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1.2 Back surgery rate (as compared to the United States)
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hold several different types of jobs during their working years, and their current positions may poorly reflect the physical loading experienced over their working lives. It has also been shown that workers in sedentary jobs tend to engage in more physically loading leisure-time activities than do workers with physically heavy jobs, which can confound attempts to investigate the effects of occupational loading.50 Conceptually, studies designed with the aim of understanding the effects of physical loading on back pain problems should be assessing total loading exposures both within and outside the work environment. Such studies are very seldom performed. Identifying factors associated with risk can give clues about causation, but an understanding of the basis for associations is required to formulate optimal prevention strategies. Leino58 showed that greater exercise activity was associated with fewer back symptom reports and back findings, for example, and Videman et al95 found that former elite athletes had significantly fewer back pain complaints than did nonathletes. If exercise has a protective effect and decreases the risk of back symptoms or spine pathology, then exercise participation could be expected to help prevent back pain. Exercise is also a marker for other healthy life-style behaviors, as well as higher education, higher life satisfaction, and lower occupational physical demands and psychosocial problems,85 all of which can affect back pain reporting. Because physical loading from certain forms of exercise and sports can increase spine pathology, exercise itself may not be directly beneficial and may even have some harmful effects on the spine, so that the apparent benefits are produced instead by factors not associated with exercise. If this were the case and exercise were only a risk indicator, exercise without other changes in life-style would be unlikely to decrease back troubles. Before interventions are planned, it would be important to sort out whether exercise is a beneficial factor or only an indicator of “healthier” life conditions. An odd paradox exists in perceptions of the effects of physical loading at work and at leisure. Physical loading associated with work and with leisure or sport activity share many dimensions
such as frequency, intensity, and duration, yet adaptation to loading, which is an expected result of regular exercise, receives little attention in studies of occupational loading. It is often stated that one reason for disability is that work demands exceed the capacity of the worker. The level of physical demands over prior months, however, is a primary determinant of individual capacity, which should include an adaptation of strength to routine daily work demands, as is the case with exercise training. Yet perhaps the greatest challenge in studies of the association between workplace exposures and back pain incidents and “injury” claims in the developed countries of the world is the injury model commonly used to explain the presence of back pain. Under the injury model, occupational physical loading exposures are believed to be primarily responsible for damage to the back and related pain. This belief naturally leads to greater attribution of symptoms to occupational exposures as workers search for possible causes of their problem. Attributing back pain to work activities may be further enhanced within a workers’ compensation system that offers clear benefits to causation lying with work. These inherent problems to studying back pain reporting in the workplace and its association with work activities greatly complicate, and in some cases may invalidate, study findings and their interpretation.
Causation versus exacerbation Another unresolved issue is that of back pain causation versus exacerbation. Certain occupational exposures, like heavy materials handling in bent and twisted postures, awkward sustained postures, or other forms of physical loading, play a role in the conditions underlying back symptoms that is not well understood. Whether physical loading contributes to the pathology underlying common back pain or simply exacerbates symptoms from an already present underlying condition is a matter of current controversy.
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Incidence and prevalence
high estimates, whereas low back pain that is defined as prolonged or disabling yield estimates toward the lower end of the range. What is clear is that back pain problems are ubiquitous in the general adult population. Work-related low back pain must be viewed against this high baseline. Whether or not a back “injury” has occurred at the workplace, back pain among workers is common, and many believe that their work is to blame. This is a natural and expected consequence of beliefs fostered by the injury model that back pain problems are the result of structural damage caused by physical demands. Further complicating the determination of occurrence rates is the recognition that back pain cannot be neatly categorized as acute or chronic. Instead, it is a fluctuating condition characterized by recurrences or exacerbations of varying severity and pain-free periods.103 In many cases an underlying condition appears to influence propensity for symptoms and occasional flare-ups loosely related to a variety of individual and environmental factors. This recurrent variable nature of back pain within individuals commonly leads to misclassification of the presence or absence of contributing conditions and influences occurrence rates and observed associations with suspected risk factors. Also important to the incidence and prevalence of low back pain reporting in the workplace are significant overall trends in industrial injury reporting. The mix of industrial injury claims has changed dramatically over past decades, with increasing dominance of back and other ill-defined musculoskeletal complaints over traumatic accident-induced injuries. Ostry78 clearly depicted this trend in a summary of short-term work loss claims from 1952 to 1996 in British Columbia. He presented the relative number of claims attributable to strains, which includes the categories of back strain, overexertion, and other strains and sprains, as compared with claims for impact (falls, slips, blows from objects, and so forth) and other miscellaneous injuries (Fig. 4a.2). During the years studied, a dramatic decline occurred in the proportion
Some evidence suggests that routine physical loading exposures, such as seen in occupations with heavy physical demands, may have a modest role in influencing underlying pathology and a role in exacerbating such pathology. Videman et al99 controlled for spine pathology and found that a history of back symptoms was correlated with physical loading. This finding supports the belief that loading exacerbates symptoms from existing conditions. The same study found that annular tears were more commonly found in subjects who engaged in occupations involving heavy physical loading, which suggests that it can lead also to increased risk of some structural failures. The role of occupational loading in degenerative changes and pathology, however, appears to be considerably less than previously thought.
INCIDENCE AND PREVALENCE As mentioned previously, there are no standard definitions for determining the presence or absence of back pain problems in the general population; instead, various definitions and methods for collecting such data are used. This leads to wide variations in prevalence and incidence estimates. A systematic review of the scientific literature from 1966 to 1998 presenting data on the prevalence of low back pain yielded point prevalence estimates from 12% to 33%, 1-year prevalence estimates from 22% to 65%, and lifetime prevalence estimates from 11% to 84%.102 Another review of the literature on low back pain prevalence estimated the point prevalence specifically in North America at 5.6%, but similarly broad ranges were noted in prevalence estimates as in the aforementioned review.63 These wide ranges are influenced by many factors, not the least of which is the definition of low back pain used in terms of pain severity, duration, and associated disability. Responses to such questions as “Have you ever had low back pain?” result in
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of impact injuries from over 80% of all injury claims in the late 1960s to slightly over 30% in 1996. Conversely, claims for strains rose from approximately 10% of all injury claims to 50%. Overall, in recent years occupational injury and illness rates in North America have shown a downward trend. The U.S. Survey of Occupational Injuries and Illnesses, generated by employer workplace incident logs, revealed a decline in nonfatal injuries in private industry from a high of 9.2 cases per 100 full-time workers in 1978 and 1979 to a low of 6.6 cases per 100 full-time workers in 1997, the last year for which data were analyzed.30 Similar trends were observed in Ontario, Canada from 1993 to 1998, where a 29% reduction in lost-time compensation claims was seen.72 The reasons for the decline are unclear. It has been speculated that it could be due to more effective prevention or treatment programs that influenced incidence or time loss, greater reluctance by employees or employers to report incidents, or changes in criteria for the diagnosing of some of these conditions by health care providers.12 The reduction may be due also to shifts in dominant industries and more generalized economic, social, cultural, or legislative trends that have affected injury reporting. Of the approximately 5.7 million injuries reported in 1997, representing 93% of all injuries and illnesses documented in employer records, however, the category of “strains, sprains, and tears” accounted for a disproportionately large share of cases with days away from work. Nearly half of these involved the back.30 Looking specifically at low back pain claims and associated disability and costs in North America, a downward trend has been noted since the late 1980s. Using a large sample of claims from the privately insured U.S. workers’ compensation market, Hashemi et al44 examined length of disability for low back pain claims and associated costs during the period of 1988 to 1996. As in previous studies,88 the distribution in terms of disability and costs was highly skewed. Depending on the year, 4.6-8.8% of claims with a disability duration lasting over 1 year accounted for 78-90% of the total disability days and 65-85% of the claims costs. Over the study period from 1988 to 1996, the mean length of disability decreased by 61%, whereas the mean and median cost per claim decreased by 41% and 20% respectively, suggesting that the most influential changes occurred through a reduction in long-term disability claims. Concurrently, a 34% decrease in the annual low back pain claim rate was reported in the United States from Bureau of Labor and Statistics data between 1987 and 1995, although it was noted that the trend was not monotonic. There was a sharper decrease in costs, one of 58%. Yet in 1995 the rate of low back claims in the United States was 1.8 per 100 employees, still representing a major health problem in the workers’ compensation system.71 These changes in back incident and claims rates seem to be a part of the larger trend for declines in all work-related injury and illness reporting. In Washington state, for example, there was a decrease of approximately 24% in the incidence rate of back claims from 1989 to 1996 and a similar decrease of 27% in all claims during the same period.44 Although a significant variation exists among industry sectors, Yamamoto107 reported a trend for a decline in the number of recognized occupational low back pain cases in Japan as well. In a large study of over 730,000 claims initiated from 45 U.S. states in 1989, available through a Liberty Mutual Insurance Company database, back-related claims constituted 16% of all
claims and 33% of all costs.104 Medical costs were overshadowed by indemnity costs that represented nearly 66% of total claims costs. These figures are similar to those from other studies reported from the United States at around the same time88 and somewhat lower than figures from Australia from the early 1990s.77
RISK FACTOR ASSOCIATIONS Structural pathology and tissue injury Back pain is commonly used as a synonym for spinal illness or, in the case of the workplace, spinal injury, although it is obvious that they are not the same and that the causal factors for the underlying pathology and reporting of back pain can be different. Some pain could originate from a metabolic disturbance such as muscle fatigue, which could be expected to recover fully without remaining identifiable pathology. Physical loading exceeding the tolerance of a structure produces a structural pathology with pain. This true injury and other factors, such as severe degeneration or infections, could lead to irreversible pathologic conditions, the symptoms of which could be triggered by routine or “physiologic loading.” This could be one explanation for the result that previous history of back pain is one of the most consistent predictors of later back pain.13 Commonly used “disability” scores estimate avoidance of defined functions due to back pain (the modifying effect of reported physical loading on pain). The correlations of underlying illness with sickness absenteeism, permanent disability pension, and use of health care due to back pain, however, are generally low.
Clinical relevance of spine pathology Studies of factors associated with the pathology of spinal structures have received relatively little attention, although the disk has been commonly thought to be responsible for most back symptoms and has been a primary target for diagnostic and therapeutic interventions related to spinal disorders. Knowledge of the macropathoanatomy and micropathoanatomy of the spine is consequently limited with respect to painful conditions. For example, we do not know the clinical value of osteophytes, disk space narrowing, disk bulges, end-plate changes, intervertebral foramina and spinal canal anthropometry, or facet joint degeneration. In the past decade even our understanding of the clinical relevance of disk herniation and annular ruptures has changed. Some studies have shown an association between disk pathology and back pain reporting, but degenerative findings are also common among asymptomatic subjects.14,16,99,105 Certain mechanisms have been suggested to explain associations between disk pathology and back pain. Full annular ruptures reaching innervated disk structures could be associated with back pain through several mechanisms. Annular tearing can lead to disk herniation with nerve compression, has been shown to produce pain by biochemical effects, and is the pathology allowing nerve ingrowth into the disk.5,33,34,76 Disk degeneration could make the disk mechanically incompetent, allowing abnormal motion between neighboring disks and leading to pain in innervated structures in the functional unit.73 Several other structures in the spine, such
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as muscles and tendon insertions, are possible sources of back pain. The condition underlying most back pain remains unknown, however, and the structural changes mentioned are currently of little clinical value.
Hereditary influences on disk degeneration There has been a dramatic paradigm shift over the past decade with respect to determinants of disk degeneration and pathology. This shift is clearly depicted by the contrasting conclusions of two reviews on the topic of “degenerative disk disease” written a decade apart. After an extensive review of the literature in 1992, Frymoyer35 concluded, “Among the factors associated with its occurrence are age, gender, occupation, cigarette smoking, and exposure to vehicular vibration. The contribution of other factors such as height, weight, and genetics is less certain.” A decade later in 2002, Ala-Kokko1 concluded, “Even though several environmental and constitutional risk factors have been implicated in this disease, their effects are relatively minor, and recent family and twin studies have suggested that sciatica, disk herniation and disk degeneration may be explained to a large degree by genetic factors.” Traditionally, degeneration of the spine has been viewed as an outcome of the accumulation of lifetime mechanical insults and injuries imposed on normal aging changes. During the 1990s the dominant effect of hereditary factors became clear, but the traditional view still maintains wide support.1,35 The traditional view, however, makes it difficult to explain the very high concordance in degenerative signs observed in lumbar spine magnetic resonance images in monozygotic twin pairs highly discordant for occupational exposures. In a study of determinants of disk degeneration in 115 pairs of identical twins, occupational physical loading explained from 0 to 7% of the variance in disk degeneration in the lumbar spine and age (ranging from 35 to 70 years) below 10%, whereas the combined effect of genes and shared environmental factors accounted for 30-60% of the total variance in disk degeneration.11 The observed significant individual differences at all ages in the degree of disk degeneration support a conclusion that there are crucial individual differences in predisposition to this problem. Using a classic twin study, Sambrook et al84 reported that heritability estimates explained 74% of the variance of the “overall score of disk degeneration” of the lumbar spine. The results from these twin studies suggest that heredity has a dominant role in disk degeneration compared with the importance of all commonly suspected adulthood exposures. The role of genetics has been confirmed additionally in several studies identifying gene forms associated with disk degeneration.4,51-53,97 It is likely that more genes associated with disk degeneration and symptoms will be found over the coming years, enhancing our chances to investigate so-called gene-environment interactions and leading to better understanding of the etiopathogenesis of disk degeneration.
Occupational and other influences on disk degeneration Most epidemiologic studies in the area of common spinal disorders have been of back symptoms, and the literature related to the epidemiology of spine pathology is limited. In an exceptional study of musculoskeletal findings based on 1000 consecutive autopsies, the occurrence rate of “spondylitis deformans”
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increased linearly from 0 to 72% between the ages of 39 and 70 years.45 Although these findings relate to people and work conditions around the turn of the century and the definition of “spondylosis” is not clearly stated, the rapid linear increase is notable. In a review article, Miller et al68 reported a similar increase in grades II to III disk degeneration from 0% at age 20 to about 90% at age 70 years. The authors also concluded that radiographic data are corroborated by macroscopic findings. Frymoyer et al37 compared the radiographs of three groups of men between the ages of 18 and 55 years: men with no history of back pain, men with moderate back pain, and men with severe back pain. In these three groups the frequency of Schmorl’s nodes, claw spurs, disk heights at the L3-L4 and LS-S1 levels, the disk vacuum sign, and transitional vertebrae were similar. The radiographic findings that differed in the three groups were traction spurs and/or disk space narrowing between L4 and L5, but these findings did not correlate with occupation, occupational lifting, or whole-body vibration. Specifically with respect to driving and associated whole-body vibration, findings have been somewhat conflicting, but the current weight of evidence suggests no notable effect on disk degenerative findings. Arguably the most well-controlled study to date on the subject did not find lumbar disk degeneration or pathology to be associated with lifetime driving.9 Riihimaki82 found that concrete reinforcement workers had a relative risk of 1.8 for disk “space narrowing as compared with house painters and a relative risk of 1.6 for ‘spondylophytes’.” They concluded that heavy physical work enhanced the degenerative process in the lumbar spine. An autopsy study of 86 subjects by Videman et al99 showed that occupations that involved sitting, standing, and walking without heavy physical loading were associated with the least degeneration. Workers with heavy physical loading had the highest incidence of annular ruptures, and sedentary work was associated with the highest degree of general disk degeneration. Studies using magnetic resonance imaging reported risks of 0.35 and 0.57 at the age of 20 years among asymptomatic and symptomatic subjects and 0.09 among asymptomatic subjects at the age of 11 years.79,86 In addition, Boos et al17 demonstrated histologically verified annular tears in a group of subjects aged 11-16 years and endplate cartilage pathology among 3 to 10 year olds. The adjusted disk signal intensity reflecting the water content of nucleus pulposus has been shown to change rapidly in early years between the ages of 9 and 77 years.68,98 Obviously, degeneration begins before individuals are exposed to workplace factors. All adults have disk degeneration, and only the degree of spine degeneration varies. That degenerative changes are present already in childhood further underlines our limited understanding of the etiology of spinal degeneration. Many researchers have studied spine degeneration based on radiography, which provides good measures of disk space narrowing and annular insertions to vertebrae (osteophytes), although its overall relevance for the intervertebral disk is not clear. A study of more than 15,000 adults did not show that heavy work was associated with spine degeneration in radiographs, although men had more degenerative signs than women. Lawrence56 reported that lumbar disk degeneration was most common in persons with physically heavy tasks compared with more sedentary workers, but only in men. Hult49 showed the
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prevalence of disk degeneration to be nearly 100% by age 59 in workers with heavy physical work, and similar degenerative findings were noted about 10 years later among those engaged in light work. Interestingly, however, important differences between the groups with heavy and light physical work were observed at baseline, and firm conclusions about the relative role of occupational physical loading on disk degeneration cannot be made. Conflicting findings in the scientific literature and failure to identify a dose-response relationship have not led to a convincing demonstration of the primacy of workplace factors in causing anatomic abnormalities.10,96
SUMMARY In principle, the determinants of all degenerative processes are similar. A function of individual constitutional factors, including genetics, they are modified by behaviors and extrinsic exposures. As studies progress in the area of spinal degeneration and structural variation, genetic influences appear to play a dominant role. Occupational exposures, representing different loading conditions, alone appear to have only modest affects on disk degeneration and pathology. Virtually all humans are exposed to the types of physical activities that have been suspected of accelerating lumbar degeneration during either work or leisure, with exposure being simply a matter of degree. Their influences vary due to recovery times, adaptation level, and stage of degeneration, among other factors. It is likely also that there are as yet unknown factors contributing to degeneration. In the end, both environmental and constitutional factors have some role in all degeneration, and only their relative magnitudes vary.21
Work-related back pain reporting Industrial back “injury” incident reports and claims filing involve specific definitions of back problems to be distinguished from structural pathology, symptom complaints solicited on surveys, or problems identified through health care visits. Most developed countries have systems for filing complaints of work-related injuries and illnesses with their own sets of rules, costs, and benefits. In discussing such systems in the United States, Hadler41 emphasized that filing a complaint forces the person to conform to the workers’ compensation paradigm. He stated, “By definition, work task description is causal. By inference, the illness is a manifestation of major structural damage.” As we have discussed, both of these assumptions are highly controversial. We found 13 prospective longitudinal studies that investigated predictors of industrial back pain reports.13,19,22,31,38,46,48,55,69,70,81,83,93 Early studies focused largely on physical factors, whereas more recent research attempted to account for other factors influencing back pain reports. Chaffin and Park22 performed some of the earliest prospective research in this area. In the early 1970s, they conducted a study of back incident reports in 411 men and women who engaged in manual lifting in their work at an electronics manufacturing company. The study focused on the effects of occupational lifting and mismatches between individual strength and job requirements. They reported an association between low back pain and jobs
with higher lifting strength requirements. They also found a higher incidence of back pain reporting in persons who demonstrated less strength on isometric strength testing than that deemed necessary to meet job demands, as compared with those whose strength met or exceeded demands, although the association was not statistically significant. Limitations of this study were that only 25 low back incidents were reported and controls for other factors influencing back pain reports were not undertaken. Cady et al19 later reported on physical fitness as an indicator of risk in 1652 firefighters over a 3-year period. Fitness was defined by a composite score based on aerobic capacity, strength, and flexibility measures. They found that firefighters with low “fitness” levels were about nine times more likely to report a back injury than those in the “most fit” group. The few injuries reported among the highly fit were the most serious, however, in terms of cost. Again, the effects of age, previous back pain, and other potentially confounding factors were not reported, making interpretation of the results difficult. Isokinetic lifting strength was investigated as a predictor of low back injury claims among nurses in a study by Mostardi et al,70 who concluded that lifting strength was a poor predictor of subsequent back symptoms and injury reports. Another prospective study of back injury reports in nurses reported by Ready et al81 reached similar conclusions about isometric lifting strength and other general fitness parameters. The factors that discriminated most between the nurses who did and did not report subsequent back injuries were previous receipt of compensation, smoking status, and poorer job satisfaction. In the Boeing study, a prospective cohort study of industrial back pain complaints in 3020 aircraft manufacturing workers, isometric lifting strength, maximal aerobic capacity, and lumbar range of motion were among the factors that were not associated with subsequent complaints. Other than having had current or recent back problems at the onset of the study, the strongest predictors of future back pain reports were negative perceptions of the workplace, including low job task enjoyment and social support and emotional distress.13 The only factor from the baseline physical examination that was strongly associated with future reporting was back pain elicited on straight leg raise testing, which probably represents another aspect of recent or current back problems also known to influence future risk.7 Yet in multivariable analysis, considering the numerous suspected risk factors under investigation, less than 10% of the variance in the reporting of work-related back pain was explained. The study findings underline the multifaceted nature of back pain reporting in industry and the limited predictive ability of most suspected risk factors. A later extension of the Boeing study looked specifically at back incident reports that resulted in the formal filing of industrial insurance claims. Lower job satisfaction and a poorer employee appraisal rating by the employee’s immediate supervisor were associated with back injury claims. Given the findings of the earlier analysis of back incident reports, this result was not surprising. A more notable finding of the later analysis was that these psychosocial factors were similarly associated with non–back injury claims as well. It would appear that certain psychosocial factors may predispose to the filing of injury claims, but the study did not provide evidence of significant differences between those who filed back injury claims and those who filed other types of injury claims.9 Such findings caution against
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stereotyping persons who file back injury claims as being distinctly different from those filing other injury claims with respect to “preinjury” psychosocial factors. As Leavitt57 stated, “The unfortunate problem is that stereotypes have consequences. Doubts raised by labels often shape evaluation and treatment of industrial workers in problematic ways, to the extent that their integrity and status as patients is challenged.” Since the Boeing study, researchers have continued to search for risk indicators and have expanded the investigation more fully into multiple domains including the physical, social, and psychologic. Numerous potential risk indicators, including exposure to repetitive trunk rotation, low supervisor support, and lack of control over work duties, have been reported. Many of these indicators have been found through exploratory studies, however, and few results have been taken to the next crucial stage of confirmation or replication in a separate cohort. Exploratory investigations have many inherent risks, including observing statistically significant associations by chance that do not actually exist or are biologically implausible.2 More trust can be placed in findings that have been validated through confirmation studies. Although confirmation studies in this area of research are rare, six indicators have been reported in multiple studies to increase the probability of future back pain reports: low job satisfaction,13,48,55,81,83 heavy physical work requirements,31,38,55,69 low social support at work,13,93 previous low work performance ratings,13,55,93 smoking status,8,81,93 and previous history of low back problems.13,83,93 The magnitudes of each of these associations have been relatively low, with odds or rate ratios typically ranging between 1.5 and 3.0 and accompanied by confidence intervals approaching 1.0. It is clear also that individual worker strength levels do not predict future injury.7,69,70,81 Although the above results have been substantiated in multiple investigations, it is unknown whether the associations observed indicate causal relationships, especially regarding the psychosocial and physical indicators. Although theories abound for how both psychosocial and physical stressors could result in reports of back pain, it is possible that indicators from within one domain influence indicators within the other. It has been theorized that individuals with higher workloads may be more likely to have lower job satisfaction.27 Alternatively, individuals under psychologic stress may be exposed to altered biomechanical forces through changes in posture or movement strategies.66 Further research is required to clarify the potential interactions arising between physical and psychosocial indicators. One study in which interaction effects between predictor variables were studied found independent effects of both psychosocial and physical variables, possibly indicative of unique effects for each.55 Although some work has been done to elucidate which factors are associated with industrial back pain reporting, the practical value of predictive models or preemployment screening for identifying specifically who will or will not experience or report symptoms is questionable. The magnitude of associations for individual predictor variables and overall predictive accuracy of created models has been relatively low, and practical difficulties arise when attempting to apply results from large samples to individual workers. Additionally, attempts at prevention based on knowledge of suspected risk factors such as workplace ergonomic modification have been largely unsuccessful.26,64,94 In fact, authors of one systematic review evaluating the effectiveness
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of multiple prevention strategies stated, “The results concerning prevention for subjects not seeking medical care are sobering. Only exercises provided sufficient evidence to conclude that they are an effective preventive intervention.”60
Subsequent disability Evidence suggests that back symptoms have always been present to some degree among humans and likely always will be. Episodes of these symptoms are, however, typically manageable and relatively short-lived. A systematic review of the prognosis of acute (<3 weeks) low back pain indicated that the prognosis of this condition is largely positive.80 Although back pain is a recurring phenomenon, most individuals recover from episodes quickly and experience little disability. The vast majority (68-86%) of individuals off work due to back pain returns to work within 1 month, and further improvements are seen for up to 3 months. In the small minority experiencing pain and disability for 3 consecutive months, however, little further improvement in important clinical outcomes is seen. Although some chronic back pain sufferers are able to cope with their pain and continue to work, a portion remains off work and experiences extended time loss.20 Within the workplace, it has been reported that approximately 10% of back injury claimants with extended work loss account for approximately 10% of back-related industrial insurance costs.88 Long-term disability is therefore the outcome that poses the greatest threat to the individual and the greatest cost to society. Disability is typically represented in the work environment as absenteeism. An examination of factors associated with illness absenteeism led Backenheimer6 to conclude that “absence behavior is, in considerable measure, a cultural and social phenomenon.” He claimed also that “a biological frame of reference is too narrow to explain the condition of being ill.” There is now a large body of evidence that these notions apply also to absenteeism and disability from back problems. Great variability is observed in back pain disability and work loss durations among nations and disability systems that would not be expected if disability were purely a biologic phenomenon.47,100 Long-term back pain disability is a relatively new phenomenon in the history of Western civilization, and its dramatic growth since World War II suggests that factors other than physical pathology are influencing its development. This is not to say that many working people do not genuinely experience back pain or that severe symptoms do not cause physical limitations of some duration. On the contrary, numerous health surveys indicate that back symptoms are extremely common in both developed and Third World countries.3,75,101 What appears to have changed in many societies, however, is the public perception of back pain as an “injury” or medical problem and its effect on work life in terms of disability. One striking example of the tremendous growth in back pain disability seen in many of the developed countries comes from the U.S. Social Security Disability Insurance System, where from 1957 to 1976 the incidence of disability awards increased by approximately 270%, a rate 14 times that of the population growth (Fig. 4a.3).87 Similarly striking increases in the incidence of disability awards have occurred in Finland, Sweden, and England.74 Although there is some evidence that the increasing
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Figure 4a.3 Social Security Disability Insurance awards by diagnosis: percent increase from 1957 to 1976. (From Fordyce WE: Back pain, compensation, and public policy. In JC Rosen, LJ Solomon, eds: Prevention in health psychology. Hanover, NH, 1985, University Press of New England.)
trends have leveled or reversed, disability associated with back pain remains widespread.71 Factors other than just the presence of back symptoms influence back symptom reporting and long-term disability. Multiple literature reviews have been published examining what factors are related to prolonged disability or work loss.25,59,92 Consistently, a multifactorial model of disability incorporating factors from physical, social, psychologic, and occupational domains is advocated. Of likely importance to the onset and persistence of disability are cultural norms; socioeconomic conditions, including unemployment rates and opportunities for compensation; and physical and psychosocial work environments.25,54,59,101 Many studies seeking to identify predictors of prolonged disability have enrolled subjects already in subacute or chronic states, however, thus confounding results and reducing generalizability to more acute cases. The authors of a systematic review of acute back pain prognosis reported identifying only one study of high methodologic quality that included a clinically relevant predictor.80 Clearly, further research is needed to accurately identify acute back pain patients at risk of developing chronic conditions. Compensation availability appears to affect the length of disability in the case of both surgical intervention32,43 and conservative care.39,42 However, Leavitt57 noted that most studies citing an association between compensation and back pain reporting and disability failed to take into account the effects of physical demands of the job; these can affect the outcome and differ significantly between compensation and noncompensation groups. He attempted to disentangle the effects of these factors and found that work-related back symptom reports were associated with more time loss than were non–work-related back symptoms, even after controlling for the degree of physical job demands. In addition, a related literature synthesis by Loeser et al62 concluded that when all other factors are held constant, the existing economic studies imply a positive relationship between the level of wage replacement benefits and both the incidence and duration of workers’ compensation claims. The relative effect of benefit
level appeared to be greater on claim duration than on claim incidence. This suggests that a key issue for workers’ compensation systems to contend with may be determining an optimal wage replacement ratio. Inappropriate medical management has been implicated also as a contributor to the growing disability problem. The rise in disability and increasing health care costs and utilization despite advances in medical technology led Frymoyer and Cats-Baril36 to raise the question, “Have medical professionals of all types become part of the problem rather than part of the solution?” Erroneous back pain beliefs of both health care professionals and the general public, including frequent suspicions of and investigations for major pathology and fear-avoidant beliefs in cases of simple back pain, appear to influence back pain disability.61 In regards to the desynchrony between current evidence-based treatment guidelines and popular opinions, Deyo28 stated, “The new back pain guidelines represent such a substantial shift from the traditional approach that the public will need to be re-educated.” Indeed, a recent public reeducation attempt through a social marketing campaign in Victoria, Australia, which portrayed the positive prognosis of back pain and conveyed the importance of staying active, was effective in altering beliefs and reducing workrelated disability.18
CONCLUSION AND IMPLICATIONS Back pain continues to be a major burden for developed countries. Since the earlier version of this chapter was written for the first edition of this book, further epidemiologic studies have been undertaken in an attempt to understand the prevalent and costly condition of low back pain. Because they substantially alter the conceptualization of occupational back pain, several discoveries are particularly noteworthy. First, lumbar spine degeneration, long considered a consequence of the accumulation of mechanical insults and injuries,
Chapter 4a
mainly from occupational exposures, has been found to be influenced in large part by heredity. The clinical implications of these findings include an altered conceptualization of the etiology of lumbar spine degeneration. Medical imaging findings that were once commonly attributed to occupational exposures can no longer be explained as such. Current evidence suggests that the role of occupational loading exposures is relatively minor in comparison with genetic influences. Second, the search for risk indicators has continued to result in inconsistent findings, identifying relatively small roles for environmental factors in explaining work-related back pain reporting and associated disability. These findings are contrary to earlier views that ascribed back pain incidents to excessive occupational physical loading requirements (either peak or repetitive). Thus it is not currently possible to predict which workers will experience back pain in a given occupation and which will experience delayed recovery. Finally, although the global experience of work-related back pain reporting and associated disability varies markedly by country or jurisdiction, over the past decade or so, for which figures are available, there has been an overall decline in some countries. This decline comes after many decades of growth. Recent trends in North America indicate that incidence and disability related to back injury claims, and time loss claims in particular, have declined over the past 10 years or so that data have been analyzed. However, this decline is part of one observed in all industrial injury and illness claims. The phenomena of work-related back pain incident reports, claims, and disability are influenced by socioeconomic, cultural, and broad legislative and jurisdictional factors. When comparing incidence and prevalence figures between nations and jurisdictions, great variations are thus observed. For this reason, the role of dominant paradigms through which back pain is viewed, particularly as it pertains to work, and the systems through which persons file related complaints must be acknowledged. Such factors constitute inherent biases in studies of the role of occupational exposures that must be recognized in planning epidemiologic studies and interpreting resulting data.
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Hashemi L, Webster BS, Clancy EA: Trends in disability duration and cost of workers’ compensation low back pain claims (1988-1996). J Occup Environ Med 40:1110-1119, 1998. Heine J: Uber die Arthritis deformans. Virch Arch Pathol Anat 260:521-663, 1926. Hemingway H, Shipley MJ, Stansfeld S, Marmot M: Sickness absence from back pain, psychosocial work characteristics and employment grade among office workers. Scand J Work Environ Health 23:121-129, 1997. Hestbaek L, Leboeuf-Yde C, Manniche C: Low back pain: what is the long-term course? A review of studies of general patient populations. Eur Spine J 12:149-165, 2003. Hoogendoorn WE, Bongers PM, de Vet HC, Ariens GA, van Mechelen W, Bouter LM: High physical work load and low job satisfaction increase the risk of sickness absence due to low back pain: results of a prospective cohort study. Occup Environ Med 59:323-328, 2002. Hult L: Cervical, dorsal and lumbar spinal syndromes; a field investigation of a non-selected material of 1200 workers in different occupations with special reference to disc degeneration and so-called muscular rheumatism. Acta Orthop Scand Suppl 17:1-102, 1954. Ilmarinen J, Louhevaara V, Korhonen O, Nygard CH, Hakola T, Suvanto S: Changes in maximal cardiorespiratory capacity among aging municipal employees. Scand J Work Environ Health 1(17 Suppl):99-109, 1991. Jones G, White C, Sambrook P, Eisman J: Allelic variation in the vitamin D receptor, lifestyle factors and lumbar spinal degenerative disease. Ann Rheum Dis 57:94-99, 1998. Kawaguchi Y, Kanamori M, Ishihara H, Ohmori K, Matsui H, Kimura T: The association of lumbar disc disease with vitamin-D receptor gene polymorphism. J Bone Joint Surg Am 84A:2022-2028, 2002. Kawaguchi Y, Osada R, Kanamori M, et al: Association between an aggrecan gene polymorphism and lumbar disc degeneration. Spine 24:2456-2460, 1999. Krause N, Frank JW, Dasinger LK, Sullivan TJ, Sinclair SJ: Determinants of duration of disability and return-to-work after work-related injury and illness: challenges for future research. Am J Ind Med 40:464-484, 2001. Krause N, Ragland DR, Fisher JM, Syme SL: Psychosocial job factors, physical workload, and incidence of work-related spinal injury: a 5-year prospective study of urban transit operators. Spine 23:2507-2516, 1998. Lawrence JS: Rheumatism in coal miners. III. Occupational factors. Br J Ind Med 12:249-261, 1955. Leavitt F: The physical exertion factor in compensable work injuries: a hidden flaw in previous research. Spine 17:307-310, 1992. Leino PI: Does leisure time physical activity prevent low back disorders? A prospective study of metal industry employees. Spine 18:863-871, 1993. Linton SJ: A review of psychological risk factors in back and neck pain. Spine 25:1148-1156, 2000. Linton SJ, van Tulder MW: Preventive interventions for back and neck pain problems: what is the evidence? Spine 26:778-787, 2001. Linton SJ, Vlaeyen J, Ostelo R: The back pain beliefs of health care providers: are we fear-avoidant? J Occup Rehab 12:223-232, 2002. Loeser JD, Henderlite SE, Conrad DA: Incentive effects of workers’ compensation benefits: a literature synthesis. Med Care Res Rev 52:34-59, 1995. Loney PL, Stratford PW: The prevalence of low back pain in adults: a methodological review of the literature. Phys Ther 79:384-396, 1999. Maher CG: A systematic review of workplace interventions to prevent low back pain. Aust J Physiother 46:259-269, 2000. Maniadakis N, Gray A: The economic burden of back pain in the UK. Pain 84:95-103, 2000. Marras WS, Davis KG, Heaney CA, Maronitis AB, Allread WG: The influence of psychosocial stress, gender, and personality on mechanical loading of the lumbar spine. Spine 25:3045-3054, 2000. Miettinen OS, Caro JJ: Medical research on a complaint: orientation and priorities. Ann Med 21:399-401, 1989. Miller JA, Schmatz C, Schultz AB: Lumbar disc degeneration: correlation with age, sex, and spine level in 600 autopsy specimens. Spine 13:173-178, 1988. Mooney V, Kenney K, Leggett S, Holmes B: Relationship of lumbar strength in shipyard workers to workplace injury claims. Spine 21:2001-2005, 1996. Mostardi RA, Noe DA, Kovacik MW, Porterfield JA: Isokinetic lifting strength and occupational injury. A prospective study. Spine 17:189-193, 1992. Murphy PL, Volinn E: Is occupational low back pain on the rise? Spine 24:691-697, 1999. Mustard C, Cole D, Shannon H, Pole J, Sullivan T, Allingham R: Declining trends in work-related morbidity and disability, 1993-1998: a comparison of survey estimates and compensation insurance claims. Am J Public Health 93:1283-1286, 2003. Nachemson A: The future of low back pain research. In JW Frymoyer, SL Gordon, eds: New perspectives on low back pain. Illinois, 1989, AAOS. Nachemson AL: Problemets omfatting. In Ont i ryggen, orsaker, diagnostik och behandling. Stockholm, 1991, SBU, pp. 18-28.
75. Nayha S, Videman T, Laakso M, Hassi J: Prevalence of low back pain and other musculoskeletal symptoms and their association with work in Finnish reindeer herders. Scand J Rheumatol 20:406-413, 1991. 76. Olmarker K, Rydevik B, Nordborg C: Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots. Spine 18:1425-1432, 1993. 77. Osti OL, Cullum DE: Occupational low back pain and intervertebral disc degeneration: epidemiology, imaging, and pathology. Clin J Pain 10:331-334, 1994. 78. Ostry A: The history of injury and industrial disease rates in British Columbia from 1950 to 1996. Can J Public Health 91:36-40, 2000. 79. Paajanen H, Erkintalo M, Kuusela T, Dahlstrom S, Kormano M: Magnetic resonance study of disc degeneration in young low-back pain patients. Spine 14:982-985, 1989. 80. Pengel LH, Herbert RD, Maher CG, Refshauge KM: Acute low back pain: systematic review of its prognosis. BMJ 327:323, 2003. 81. Ready AE, Boreskie SL, Law SA, Russell R: Fitness and lifestyle parameters fail to predict back injuries in nurses. Can J Appl Physiol 18:80-90, 1993. 82. Riihimaki H: Low-back pain, its origin and risk indicators. Scand J Work Environ Health 17:81-90, 1991. 83. Rossignol M, Lortie M, Ledoux E: Comparison of spinal health indicators in predicting spinal status in a 1-year longitudinal study. Spine 18:54-60, 1993. 84. Sambrook PN, MacGregor AJ, Spector TD: Genetic influences on cervical and lumbar disc degeneration: a magnetic resonance imaging study in twins. Arthritis Rheum 42:366-372, 1999. 85. Sarna S, Sahi T, Koskenvuo M, Kaprio J: Increased life expectancy of world class male athletes. Med Sci Sports Exerc 25:237-244, 1993. 86. Smith F, Jeffrey J, Porter RW: unpublished data. 87. Social Security Statistical Supplement (1977-1979), HE 3.3/ 3:979. Washington, DC, 1979, Government Printing Office. 88. Spengler DM, Bigos SJ, Martin NA, Zeh J, Fisher L, Nachemson A: Back injuries in industry: a retrospective study. I. Overview and cost analysis. Spine 11:241-245, 1986. 89. Spitzer WO: Scientific approach to the assessment and management of activity-related spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 12(Suppl):S12-S15, 1987. 90. Stewart WF, Ricci JA, Chee E, Morganstein D, Lipton R: Lost productive time and cost due to common pain conditions in the US workforce. JAMA 290:2443-2454, 2003. 91. Taylor PJ: International comparisons of sickness absence. Proc R Soc Med 65:577-580, 1972. 92. Truchon M, Fillion L: Biopsychosocial determinants of chronic disability and low-back pain: a review. J Occup Rehab 10:117-142, 2000. 93. Tubach F, Leclerc A, Landre MF, Pietri-Taleb F: Risk factors for sick leave due to low back pain: a prospective study. J Occup Environ Med 44:451-458, 2002. 94. van Poppel MN, Koes BW, Smid T, Bouter LM: A systematic review of controlled clinical trials on the prevention of back pain in industry. Occup Environ Med 54:841-847, 1997. 95. Videman T, et al: Elite sport as a predictor of back-related outcomes. American College of Sports Medicine Annual Meeting, Seattle, 1993. 96. Videman T, Battié MC: The influence of occupation on lumbar degeneration. Spine 24:1164-1168, 1999. 97. Videman T, Leppavuori J, Kaprio J, et al: Intragenic polymorphisms of the vitamin D receptor gene associated with intervertebral disc degeneration. Spine 23:2477-2485, 1998. 98. Videman T, Nummi P, Battié MC, Gill K: Digital assessment of MRI for lumbar disc desiccation. A comparison of digital versus subjective assessments and digital intensity profiles versus discogram and macroanatomic findings. Spine 19:192-198, 1994. 99. Videman T, Nurminen M, Troup JD: 1990 Volvo Award in clinical sciences. Lumbar spinal pathology in cadaveric material in relation to history of back pain, occupation, and physical loading. Spine 15:728-740, 1990. 100. Volinn E: The epidemiology of low back pain in the rest of the world. A review of surveys in low- and middle-income countries. Spine 22:1747-1754, 1997. 101. Waddell G: 1987 Volvo Award in clinical sciences. A new clinical model for the treatment of low-back pain. Spine 12:632-644, 1987. 102. Walker BF: The prevalence of low back pain: a systematic review of the literature from 1966 to 1998. J Spinal Disord 13:205-217, 2000. 103. Wasiak R, Pransky GS, Webster BS: Methodological challenges in studying recurrence of low back pain. J Occup Rehab 13:21-31, 2003. 104. Webster BS, Snook SH: The cost of 1989 workers’ compensation low back pain claims. Spine 19:1111-1115; discussion 1116, 1994. 105. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N: A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 9:549-551, 1984. 106. Woolf AD, Pfleger B: Burden of major musculoskeletal conditions. Bull World Health Org 81:646-656, 2003. 107. Yamamoto S: A new trend in the study of low back pain in workplaces. Ind Health 35:173-185, 1997.
CHAPTER
4b
Clinical Biomechanics of the Spine Malcom H. Pope
The spine is an important structure with many conflicting functions. The first function, mobility, provides the motion necessary for the activities of daily living. The second function is one of support for the body segments and any load moments that are applied by the worker. The third function is housing, in which the spinal cord and nerve roots are protected. The last function is control, with the muscles acting through the vertebrae to precisely control the posture.
FUNCTIONAL SPINAL UNIT The functional spinal unit (FSU) consists of two adjacent vertebrae, the interposed vertebral disk, and adjoining ligaments. The motion segment can be divided into anterior and posterior components. The anterior components are the vertebral bodies, the disk, and the attached ligaments; all the remaining structures are posterior components.19 The FSU is a structure in which the disk acts as a spring, the facet joints as a pivot, and the posterior ligamentous complex as another spring. Experiments have shown that the FSU exhibits coupled motion in which vertical translation also results in complex movements in other directions. The anterior elements of the FSU have a support function and a function of impact absorption, whereas the posterior elements control motion.
Anterior portion The major structural part of the anterior portion of the FSU consists of the vertebral bodies. These bear mainly compressive loads and are progressively larger caudally as the weight of the upper body increases (Fig. 4b.1). Therefore, the vertebral bodies in the lumbar region are bigger than those in the thoracic and cervical regions. Compressive strength concomitantly gradually increases from the cervical spine down to the lumbar spine. Overall, the vertebrae are six times stiffer than the disks, three times thicker than the disks, and suffer half the deformation of the disks. The vertebrae are very important in shock absorption. Under compression, endplate deformation precedes the expelling of hematopoietic contents from the vertebrae themselves. The vertebrae are an expression of Wolff’s law inasmuch as the trabeculae are oriented to resist the vertical compression forces and tensile forces through the spinous and transverse processes caused by muscle and ligament attachments. There is a zone of relative weakness anteriorly because of a lack of trabeculae.
Compressive failure, particularly in an osteoporotic individual, occurs in this region. The other major component of the anterior portion of the FSU is the intervertebral disk. The function of the disk is to distribute loads and restrain excessive motion. The disk is composed of the annulus fibrosus and nucleus pulposus. The annulus is made up of a series of sheets of collagen fibers, with the fibers of one sheet at a 30-degree angle relative to the neighboring sheet. Mathematical models show that with removal of the nucleus, interval stresses ensue as a result of the compressive forces being carried through the annulus. The inner portion of the disk, the nucleus pulposus, is rich in hydrophilic glycosaminoglycans in young adults, but with age the nucleus pulposus becomes progressively less hydrated. Animal experiments have shown that disks are avascular structures and that endplate permeability decreases with age, thereby decreasing disk nutrition. Motion is beneficial for intervertebral disks. Solute transport and metabolism are both improved by spinal motion, and intermittent motion is less effective than continuous motion. Aging usually results in disk degeneration. Degeneration of a disk reduces its proteoglycan content and thus its hydrophilic capacity. As the disk becomes drier, its elasticity and its ability to store energy and to distribute loads gradually decreases. Most disk herniations occur in the fourth decade of life, and herniations are found in 15 to 30 of autopsy specimens. The intervertebral disk exhibits creep, which means that the disk continues to deform under a constant load. This timedependent behavior comes from the fluid flow of the disk under an applied load and from the inherent viscoelastic behavior of the collagen and proteoglycan matrix. Time-dependent behavior has been demonstrated both in vivo by Keller et al8 and in vitro by Kazarian.7 The studies of Eklund and Corlett3 and Krag et al10 indirectly measured the change in overall height of the subjects. The diurnal loss was about 17 mm. Kazarian7 noted that a degenerate disk had a higher rate of deformation and the creep curve stabilized sooner. Virgin17 was the first to suggest that the nucleus pulposus acts hydrostatically to pressurize the disk and thus stabilizes the FSU. In a nondegenerate disk, nucleus pressure is redistributed as tension in the annulus layers. Normal disk pressure is about 1.5 times the compressive load divided by the cross-sectional area. Pressure is higher in the disk center and decreases toward the exterior. Nachemson15 reported that disk pressure is different in various positions or maneuvers (Table 4b.1). Andersson et al1 found in vivo that intradiskal pressure increased linearly with an increase in both trunk load and trunk moment. Disk pressure was found to be high in unsupported sitting but decreased significantly with the use of a backrest inclination greater than 110 degrees, with the use of lumbar supports, and with the use of armrests. The tensile stress in the annulus fibrosus due to disk pressure in the thoracic spine is less than that in the lumbar spine because the higher ratio of disk diameter to height in the thoracic disks reduces the circumferential stress.11
Posterior portion The posterior portion of the FSU has a primary role of guiding its movement. The type of motion possible at any level is
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C3 C4 C5 C6 C7 T1 T2 T3 T4 T5 Vertebral level
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T6
Messerer, 1880
T7
Perry, 1957
T8
Bell et al, 1967
T9 T10 T11 T12 L1 L2 L3 L4 L5
0
2000 (450 lbf)
4000 (900 lbf)
6000 (1350 lbf)
8000 (1800 lbf)
Compression strength in newtons (pound force) Figure 4b.1 Vertebral compression strength at a slow loading rate. (Modified from White AA, Panjabi MM: Clinical biomechanics of the spine. Philadelphia, 1991, WB Saunders.)
determined by the orientation of the facets of the FSU to the transverse and frontal planes. This orientation changes throughout the spine (Fig. 4b.2). Other structures that influence motion of the spine are the rib cage, which limits thoracic motion, and the pelvis. The cervical spine, the most mobile region of the spine, affords the head a
large range of motion, which is necessary for the activities of daily living. Except for the facets of the two uppermost cervical vertebrae (C1 and C2), which are parallel to the transverse plane, the cervical facets are oriented at 45 degrees to the transverse plane and are parallel to the frontal plane (Fig. 4b.2). The loadbearing function of the facets at all spinal levels is significant.
Chapter 4b
Load (N)
Supine (awake) Supine (semi-Fowler) Supine (traction, 500 N) Sitting (unsupported) Standing (relaxed) Coughing Straining
250 100 0 700 500 600 600
Functional spinal unit
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joints play an important role in resisting shear forces. In addition, Farfan5 showed that 40% of the torsional strength of the FSU come from the facet joints, and Lorenz et al12 suggested that 25% of the axial load bearing is from these structures.
Table 4b.1 Loads on the L3 disk calculated from intradiskal pressure measurements in a 70-kg man Position, Maneuver
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Ligaments The spine ligaments function in conjunction with other elements of the FSU as stabilizers and check reins. They are tensile elements that can fatigue, and they do contain pain fibers. The overall load deflection curve on the FSU is nonlinear, being reflective of ligament behavior. Extension loads the anterior ligaments and flexion loads the posterior elements. During flexion, the interspinous ligaments have the greatest strain, followed by the capsular ligaments and the ligamenta flava, whereas in extension the anterior longitudinal ligament bears the greatest strain. During lateral flexion, the contralateral transverse ligament is strained the greatest, followed by the ligamenta flava and the capsular ligaments. The capsular ligaments bear the most
Load sharing between the facets and the disk varies with the position of the spine. The loads on the facets are very high, peaking at about 30% of the total load when the spine is hyperextended.9 They are also quite high during forward bending coupled with rotation.4 The facets through the vertebral arches and intervertebral
Cervical (C3-C7)
0˚ A
45˚
20˚ Figure 4b.2 Orientation of the facets of the intervertebral joints. (A) In the lower cervical spine the facets are 45 degrees to the transverse plane and are parallel to the frontal plane. (B) The facets of the thoracic spine are oriented at 60 degrees to the transverse plane and at 20 degrees to the frontal plane. (C) The facets of the lumbar spine are oriented at 90 degrees to the transverse plane and at a 45 degree angle to the frontal plane. (From White AA, Panjabi MM: Clinical biomechanics of the spine, 1991, JB Lippincott.)
Thoracic
B – 60˚
45˚ C
90˚
Orientation of the facets to the transverse plane
Orientation of the facets to the frontal plane
Lumbar
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strain during rotation. The ligamentum flavum, which connects two adjacent vertebral arches longitudinally, is an exception in its behavior because it contains a large percentage of elastin. The elasticity of this ligament is therefore very high. This allows it to contract during extension of the spine and elongate during flexion. In a neutral position, the ligamentum flavum is under tension as a result of its elastic properties. Because it is located at a distance from the center of motion in the disk, it prestresses the disk and thus adds to overall stability.
independently of the rest of the cervical spine, but motion below C1 involves the entire cervical spine. The facets guide the motion, and as a result flexion-extension is coupled with transverse translation, lateral flexion with rotation (Fig. 4b.4), and rotation with axial translation. In the thoracic region, rotation is associated with lateral flexion, especially in the upper thoracic region. In this case, the vertebral bodies generally rotate toward the concavity of the lateral curve.18 Coupling of rotation and lateral flexion occurs in the lumbar spine, with the vertebral bodies rotating toward the convexity of the curve.13
KINEMATICS KINETICS The range of motion of the spine varies from level to level. White and Panjabi19 summarized these data (Fig. 4b.3). Flexion and extension are about 4 degrees in the upper thoracic, about 6 degrees in the midthoracic, and about 12 degrees in the lower thoracic segments. This increases in the lumbar motion segments to a peak of 20 degrees at L5-S1. Lateral flexion varies from level to level quite markedly but is greatest in the lower thoracic segments and L3-L4 (8 to 9 degrees). In the upper thoracic segments the range is 6 degrees. Rotation is greatest in the upper segments of the thoracic spine (9 degrees). The range of rotation is minimal in the lumbar spine because of facet orientation. The lumbar spine is susceptible to injury from rotation. There have been reports of coupled motion throughout the spine. Coupling refers to a primary motion in one direction leading to a secondary motion in another. For example, C1 moves
0˚
10˚ 20˚
0˚
10˚
20˚
The basic building materials of the spine are the vertebral bodies, which take the loads of compression, shear, and bending, and the muscles which act as the building blocks in tension. The muscles position and stabilize the spine. Without muscles, the ligamentous spine buckles under loads of as small as 2 kg. In general, the muscle electrical activity electromyographic (EMG) amplitude is directly proportional to the moment arm of the muscle line of action from the center of rotation. We can investigate the role of muscle around the periphery through a free-body analysis in which, mathematically at least, the body is cut in two and the forces and moments are resolved across that cut surface. Forces are estimated from the electromyographic signals. In complex postures, very high antagonistic activity occurs. Loads are also produced by body weight, prestress from ligaments, and externally applied loads.
0˚
10˚ 20˚
OC - C1 C1 -2 2-3 3-4 4-5 5-6 6-7 C7 - T1 T1 - 2 2-3 3-4 4-5 5-6 6-7 7-8 8-9 9 - 10 10 - 11 11 - 12 T12 - L1 L1 - 2 2-3 3-4 4-5 L5 - S1
Figure 4b.3 A composite of representative values for type and range of motion at different levels of the spine. (Modified from White AA, Panjabi MM: Clinical biomechanics of the spine. Philadelphia, 1991, JB Lippincott.)
Flexionextension
Lateral flexion
Rotation
Chapter 4b
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Kinetics
Neutral: OCC – C1 1.3 Nm (0.6 – 1.5) C7 – T1 1.2 Nm (0.5 – 2.2)
Left lateral flexion
Neutral
Right lateral flexion
Figure 4b.4 Coupled motion during lateral flexion is depicted schematically. When the head and neck are flexed to the left, the spinous processes shift to the right, indicating rotation. The converse is also illustrated. (Modified from White AA, Panjabi MM: Clinical biomechanics of the spine. Philadelphia, 1991, JB Lippincott.)
Because the lumbar spine is the main load-bearing area and the most common site of pain, studies have focused on this region. Loads on the cervical spine are mainly produced by the weight of the head, the activity of the surrounding muscles, the inherent tension of adjacent ligaments, and the application of external loads. Investigations in vivo confirm that physiologic loads are lower than those on the thoracic and lumbar spines. However, quite large loads on the cervical spine have been calculated during neck flexion, particularly in the lower cervical motion segments. Harms-Ringdahl6 calculated the bending moments generated around the axes of motion of the atlantooccipital joint and the C7-T1 motion segment with the neck in flexion, neutral position, and extension (Fig. 4b.5). The load on the junction between the occipital and C1 was lowest during extreme extension and highest during extreme flexion. The load on the C7-T1 motion segment was low with the neck in the neutral position but tucked in (ranging from an extension moment of 0.8 Nm to a flexion moment of 0.9 Nm). The load increased substantially during slight flexion (reaching 6 Nm). Moroney et al14 studied subjects who resisted loads. Calculation of the maximum (compressive) reaction forces on the C4-C5 motion segment ranged from 500 to 700 N during flexion, rotation, and lateral bending and rose to 1100 N during extension. Body position also affects the magnitude of the loads on the lumbar spine. These loads are minimal during well-supported reclining, remain low during relaxed upright standing, and rise during sitting (Fig. 4b.6). Trunk flexion increases the load by increasing the forwardbending moment on the spine. The forward inclination of the spine also makes the disk bulge on the concave side of the spinal curve and retract on the convex side. Hence when the spine is flexed, both compressive and tensile stresses on the disk increase.1 Nachemson and Elfström16 and Andersson et al2 also showed that during relaxed unsupported sitting, the loads on the lumbar spine are greater than during relaxed upright standing. In this position the pelvis is tilted backward and the lumbar lordosis straightens the upper body, thereby creating a longer lever arm for the weight of the trunk.
Slight flexion: OCC – C1 1.4 Nm (0.8 – 1.7) C7 – T1 3.7 Nm (3.0 – 6.2)
Figure 4b.5 Extension and flexion moments around the axes of motion of the atlantooccipital (OCC-C1) joint and the C7-T1 motion segment (marked with Xs) are presented for five positions of the head: extreme flexion, slight flexion, neutral, head upright with the chin tucked in, and extreme flexion. Values shown are the medial and range for seven subjects: Negative values indicate extension moments. The arrows represent the force vectors produced by the weight of the head. (Modified from Harms-Ringdahl K: On assessment of shoulder exercise and load-elicited pain in the cervical spine. Biomechanical analysis of load-EMG-methodological studies of pain provoked by extreme position. Thesis, 1986, Karolinska Institute, University of Stockholm.)
Figure 4b.6 The relative loads on the third lumbar disk for living subjects in various body positions are compared with the load during upright standing, depicted as 100. (Modified from Nachemson A, Elfström G: Intravital dynamic pressure measurements in lumbar discs: a study of common movements, maneuvers and exercises. Stockholm, 1970, Almqvist & Wiksell.)
111
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A
B
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Clinical biomechanics of the spine
C
D
Figure 4b.7 Influence of backrest inclination and back support on loads on the lumbar spine in terms of pressure in the third lumbar disk during supported sitting. (A) Backrest inclination is 90 degrees, and disk pressure is at a maximum. (B) The addition of lumbar support decreases disk pressure. (C) Backward inclination of the backrest to 110 degrees but with no lumbar support produces less disk pressure. (D) The addition of lumbar support with this degree of backrest inclination further decreases the pressure. (E) Shifting support to the thoracic region pushes the upper part of the body forward, moves the lumbar spine toward kyphosis, and increases disk pressure. (Modified from Andersson GBJ, Ortengren R, Nachemson A: Clin Orthop 129:156-164, 1977.)
E
Disk pressure
The loads on the lumbar spine are lower during supported sitting than during unsupported sitting because part of the weight is supported by the backrest. Backward inclination of the backrest and a lumbar support further reduce the loads (Fig. 4b.7).2 Because user requirements vary, the kinds of chairs available also vary widely. Regardless of use, however, it is important to be able to adjust any chair to meet the basic anthropometric dimensions of the worker. A proper seat height is desirable and should be adjustable for the individual user. The seat surface should be 3 to 5 cm below the knee-fold when the lower limb is vertical. Foot supports can be used with higher chairs. The width of the seat should be sufficient to accommodate the user. It must be possible to use the backrest, so the seat pan should not be too deep. Pressure should be avoided on the back of the thigh near the knees. Lifting creates the highest loads on the lumbar spine, and these are the occupational exposures with the greatest incidence of low back pain injury reports. The key to prevention is to reduce the load moment, which means reducing either the magnitude of the load, the distance from the body, or both. Therefore, if objects of the same weight, shape, and density but of different sizes are held, the lever arm for the force produced by the weight of the object is longer for the larger object and the bending moment on the lumbar spine is greater (Fig. 4b.7).
REFERENCES 1.
2.
3. 4.
5. 6.
7.
8. 9. 10. 11. 12.
DISCUSSION
13. 14.
The spine has functions of load bearing, protection of neural elements, and mobility yet stability. The FSU, which is the basic unit, exhibits coupled motion. It is composed of the anterior components (vertebral body, disk, pedicles, and ligament), and the remainder make up the posterior elements. Motion, which is largely controlled by the facet, varies between regimes. Flexion-extension is high in the lumbar spine, but rotation is minimal. Loads in the spine are a function of body mass, muscle activity, prestress, and external loads. The latter is particularly important in the lumbar spine.
15. 16.
17. 18. 19.
Andersson GBJ, Ortengren R, Nachemson A: Intradiscal pressure, intra-abdominal pressure and myoelectric back muscle activity related to posture and loading. Clin Orthop 129:156-164, 1977. Andersson GBJ, Ortengren R, Nachemson A, Elfstrom G: Lumbar disc pressure and myoelectric back muscle activity during sitting. I. Studies on an experimental chair. Scand J Rehabil Med 6:104, 1974. Eklund JAE, Corlett EN: Shrinkage as a measure of the effect of load on the spine. Spine 9(2):189-194, 1985. El-Bohy AA, King AI: Intervertebral disc and facet contact pressure in axial torsion. In SA Lantz, AI King, eds: Advances in bioengineering. New York, 1986, American Society of Mechanical Engineers, pp. 26-27. Farfan HF: Mechanical disorders of the low back. Philadelphia, 1973, Lea & Febiger. Harms-Ringdahl K: On assessment of shoulder exercise and load-elicited pain in the cervical spine. Biomechanical analysis of load-EMG-methodological studies of pain provoked by extreme position. Thesis, 1986, Karolinska Institute, University of Stockholm. Kazarian L: Dynamic response characteristics of the human vertebral column: an experimental study of human autopsy specimens. Acta Orthop Scand Suppl 146, 1972. Keller L, et al: In vivo creep behavior of the normal and degenerated porcine intervertebral disc-a preliminary report. J Spinal Disorder 1(4):267-278, 1989. King AI, Prasad P, Ewing CL: Mechanism of spinal injury due to caudocephalad acceleration. Orthop Clin North Am 6:19, 1975. Krag MH, Cohen MC, Pope MH: Load-induced changes in human intervertebral disc height in-vivo: a new and closer look. Orthop Trans 9(3):516, 1985. Kulak RF, Schultz AB, Belytschko T, Galante J: Biomechanical characteristics of vertebral motion segments and intervertebral discs. Orthop Clin North Am 6:121, 1975. Lorenz M, Patwardhan A, Vanderby R: Load-bearing characteristics of lumbar facets in normal and surgically altered spinal segments. Spine 8:122, 1983. Miles M, Sullivan WE: Lateral bending at the lumbar and lumbosacral joints. Anat Rec 139:387, 1961. Moroney SP, Schultz AB, Ashton-Miller JA: Analysis and measurement of neck loads. J Orthop Res 6(5):713-720, 1988. Nachemson A: Lumbar interdiscal pressure. In MIV Jayson, ed: The lumbar spine and back pain. London, 1987, Churchill Livingstone, p. 191. Nachemson A, Elfström G: Intravital dynamic pressure measurements in lumbar discs: a study of common movements, maneuvers and exercises. Stockholm, 1970, Almqvist & Wiksell. Virgin WJ: Experimental investigations into the physical properties of the intervertebral disc. J Bone Joint Surg 33B:607-611, 1951. White AA: Analysis of the mechanics of thoracic spine in man. An experimental study of autopsy specimens. Acta Orthop Scand Suppl 127:1-105, 1969. White AA, Panjabi MM: Clinical biomechanics of the spine. Philadelphia, 1991, JB Lippincott.
CHAPTER
4c
Initial Evaluation of the Low Back Region
have some specific properties (sensitivity and specificity) as well as those depending on the prevalence of the disease considered (predictive value) in the population being evaluated. Basically, signs and symptoms (or any other test) with very high sensitivity allow the clinician to rule out the target disease when the test is negative. On the contrary, when the specificity of a test is extremely high, a positive result “rules in” the target disease.21
Marek Szpalski, Federico Balagué, Robert Gunzburg, and Dan M. Spengler
HISTORY
Although patient evaluation and management have been clearly improved by the explosive growth in technology over the past decades, the hallmark of patient assessment continues to reside in the fundamentals of the history and physical examination. The information provided in this chapter emphasizes the importance of these basic skills to attempt to motivate the reader to continue to improve and update this important knowledge area. The focus of this chapter is the clinical assessment of patients who seek an evaluation of low back pain, with an emphasis on occupational aspects. Another relevant aspect that has become increasingly important in the last decades is the point of view of the patients. An important volume of literature devoted to this topic has been reviewed recently. In their systematic review of qualitative and quantitative studies, Verbeek et al72 highlighted the major patient expectations, specifically diagnosis, instructions, and interpersonal management. This information is important for the individual clinician. It is important to remind the clinician that the variables elicited by history taking and through a clinical examination
Two reviews of patient histories reported that although 2% to 3% of the causes of low back pain are nonmechanical, these etiologies must be considered most seriously and diagnosed quickly.20,22 All the factors that might be relevant because of their association with increased risk of cancer, infection, or other complications should be included in the history.20 In a study of almost 2000 back pain patients, Deyo21 found that no cancer was identified among those under age 50 without a history of cancer, unexplained weight loss, or failure of conservative therapy (combined sensitivity of 100%). The elements suggesting a diagnosis of specific low back pain are commonly designated in the literature as red flags (Table 4c.1).6 Concluding that a patient suffers from “nonspecific low back pain” once the clinician has reasonably excluded red flags seems to be rather unsatisfactory for most health care providers, who do not believe nonspecific low back pain to be one condition.42 It has been shown, moreover, that a comprehensive medical assessment is not predictive of return to work after an episode of occupational low back trouble.34 For all patients who are examined for an evaluation of low back pain with or without sciatica, a history of the present illness should be completed, including information regarding the nature
Table 4c.1
Red flags for potentially serious conditions
Possible fracture
Possible tumor or infection
Possible cauda equina syndrome
Age over 50 or under 20 History of cancer Constitutional symptoms such as recent fever or chills or unexplained weight loss Risk factors for spinal infection: recent bacterial infection (e.g., urinary tract infection) intravenous drug abuse, or immune suppression (from steroids, organ transplantation, or human immunodeficiency virus infection) Pain that worsens when supine; severe nighttime pain
Saddle anesthesia Recent onset of bladder dysfunction such as urinary retention, increased frequency, or overflow incontinence Severe or progressive neurologic deficit in the lower extremity
From medical history: Major trauma such as vehicle accident or fall from a height Minor trauma or even strenuous lifting (in older or potentially osteoporotic patients)
From physical examination: Unexplained laxity of the anal sphincter Perianal/perineal sensory loss Major motor weakness: quadriceps (knee extension weakness); ankle plantar flexors, evertors, and dorsiflexors (footdrop)
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of symptom onset. The absence of sciatica or femoral nerve radicular pain makes a clinically important disk herniation very unlikely (sensitivity about 0.95 and specificity 0.88).21 In addition, the examiner should document various treatment approaches and the effects of the treatments on symptoms. The reason for the evaluation and any anticipated outcomes must be understood in advance by both the physician and the patient. If the evaluation is for an independent medical evaluation, for example, the patient needs to understand its purpose of providing an independent objective assessment for a third party and that treatment is not included. The evaluation may be to assist another physician in patient management or solely to provide an insurance company or a workers’ compensation carrier with a diagnosis and recommendations. When related to swirling litigation and compensation issues, a history must usually be more detailed than one obtained solely to diagnose symptoms and manage a patient. If a patient falls at home and seeks evaluation, for example, the history might be succinct and relate only the type and distance of the fall. In a contested on-the-job injury encounter, the details may be more important for dispute resolution. Was the fall witnessed? Did the employee return to work? For how long? Is an attorney involved? Who are the physicians or others who have evaluated the patient? Has the employee had a previous injury? Has an impairment been recorded previously? An interview with a patient who is involved in litigation can be facilitated by having the referring person summarize the outcomes desired from the consultation. In addition, a succinct summary of the events to date should be provided to serve as a template for review during the patient interview. Information provided by the referral source does not replace the need for a good history; it only highlights the issues from another perspective. The opening aspects of the history should focus on the present illness. The examiner must not lead patients into answers by the use of “closed” questions, such as “Does your back pain radiate to the posterior of your thigh, calf, and foot?” Patients may often answer yes to these questions even though they may not understand what was asked or the relevance. A much better strategy is to ask the patient to describe the pain. What makes the pain better or worse? These questions can amplify the pain drawing that is gathered before the history and physical examination.9 This tool is helpful to maintain in the patient’s file to compare over time or to establish the patient’s pain pattern at the time of evaluation. In addition, recording a few notes for later dictation, the physician should also observe the psychologic, physical, and emotional behavior of the patient throughout the interview and examination. Loss of eye contact, change in voice tone, or excessive movement on the examining table should be noted, because these nonverbal cues may be equally or more important than the actual words spoken. Signs suggesting a clinical depression should be noted also because depression can be commonly encountered as both a primary and a secondary disorder in patients complaining of low back pain. Slurred speech or an impressive knowledge of pain medications should be noted also to provide clues to potential alcohol or medication abuse, the latter of which is quite common in patients who complain of chronic back symptoms.9,61 Pain patterns should also be noted. Does the pain intensity stay the same throughout the 24-hour day, or is it better or worse
in the morning or in the evening? Is the pain predictable or erratic? Is the patient’s sleep pattern disrupted because of night pain? Although night pain can be associated with various forms of malignancy or inflammatory disorders, it can also reflect clinical depression or be associated with psychosocial issues. The relationship of various activities to the pain complaints should be discussed as well. Pain that increases with walking short distances yet disappears rapidly with sitting or lying can represent a typical pattern in a patient with lumbar spinal stenosis. A clinical diagnosis cannot be advanced solely on the basis of the pain pattern, however, because of the wide variability of clinical symptoms in most disorders that result in low back pain. When interviewing a patient with low back pain that has been present for more than 3 months, the physician should completely review the patient’s systemic symptoms, including fever, chills, night sweats, weight loss, and lethargy, along with any sources of infection, whether systemic or not, such as a localized cutaneous abscess. Gastrointestinal symptoms are relevant because such disorders can actually occur concomitantly with low back symptoms and because so many patients take large doses of salicylates or nonsteroidal antiinflammatory agents, which can lead to significant gastrointestinal bleeding.53 Genitourinary symptoms are reviewed also, because bladder dysfunction can be associated with pressure on the spinal cord or cauda equina. Although such symptoms are more commonly related to causes other than neural compression, an early recognition of a change in bladder habits may signal a subtle increase in pressure on the neural elements.5 When genitourinary symptoms are present, the physical examination should include a well-documented rectal examination. A cystometrogram and a urologic consultation may be necessary to clarify the nature of these problems.5 Female patients should be questioned regarding any changes in bleeding patterns or pain related to menstruation, and those with persisting back complaints should be evaluated by their gynecologists. Medications taken by the patient should also be recorded. If the patient has been taking multiple medications in the past for back pain, the associated clinical response should be noted. Other back treatment approaches, including the patient’s pain-free interval after an intervention such as steroid dose packs, epidural steroid injections, or physical therapy, should be noted as well. Psychosocial and economic issues associated with the low back symptoms should be reviewed. Life stressors, litigation, compensation, and other secondary gain parameters would likely not have “caused” the pain, but such issues can certainly maintain the chronicity of symptoms in specific cohorts of patients. A systematic review of psychologic factors as predictors of chronicity or disability highlight the limits of the available evidence, but the roles of distress/depressive mood and, to a lesser extent, somatization are underlined. As discussed in greater detail in Chapter 2, the role of coping strategies and fear avoidance deserve further research.52,73 In recent years a list of red flags and treatment matrices have been enlarged to include cognitive and behavioral approaches into the early management of acute low back pain. “Yellow flags” can be evaluated by means of six open questions that should be phrased in the health care provider’s own words: 1. Have you had time off from work in the past with back pain? 2. What do you understand to be the cause of your back pain? 3. What are you expecting will help you?
Chapter 4c
4. How are your employer, coworkers, and family responding to your back pain? 5. What are you doing to cope with back pain? 6. Do you think that you will return to work? When?40 Moreover, “blue” flags (psychosocial aspects of work) and “black” flags (employer-specific and global) aimed at evaluating other socioeconomic environmental factors have been described in the last few years.31 The past medical history should be completed to include any diagnostic assessments, treatment approaches not previously noted, and doctors or others who have evaluated or treated the patient for low back and other medical problems. The length of any pain-free interval after previous surgical procedures should also be documented. Short-term relief after major surgery may occur after procedures that may not have been clearly indicated. Other causes can include an operation performed at the wrong spinal level, an inaccurate diagnosis, an associated medical disorder with referred low back symptoms, and a pain-prone patient who tends to amplify symptoms. A comparison of the existing occupational health guidelines for the management of low back pain revealed that all the published guidelines distinguished specific and nonspecific cases and consistently recommended a clinical history to identify relevant physical and psychosocial workplace factors and a physical examination including neurologic screening. Red and yellow flags are highlighted by most of the guidelines.63
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Physical examination
patient and doctor. They must be understood in the context of the patient’s history and offer only a psychologic “screener,” not a complete psychologic assessment. Finally, they are not on their own a test of credibility or veracity, nor are they a reason to deny appropriate physical treatment.48 A study showed that with regard to return to work in patients with acute low back pain, the predictive value of the nonorganic symptoms or signs (independently or combined) was rather poor.28 The patient should be suitably attired for the examination to provide for privacy but also to facilitate a complete musculoskeletal evaluation. Together with a sheet for the supine and prone portions of the examination, the standard patient gown that is open in back is quite appropriate. The physical examination should be complete but also age and complaint related. Although not an essential portion of the examination in an 80-year-old patient with back pain after a minor fall, chest expansion, for example, is clearly important in a 20-year-old man with an insidious onset of low back pain over a long period of time. Decreased chest expansion (less than 2.5 cm) in such a patient could suggest the diagnosis of ankylosing spondylitis. A study showed that a screening system led by two physiotherapists resulted in a clinical and economic improvement in the care of those suffering from acute low back pain.49 The physical examination is divided into five components based on the position of the patient, beginning with the patient standing.
Patient standing PHYSICAL EXAMINATION A physical examination is one among many patient expectations72 that permits the physician to assess the patient and record the observations. Objective findings, including deep tendon reflexes and circumferential measurements of the calf and thigh to determine swelling or atrophy, represent the most important parameters. Less helpful, subjective, physical examination findings include supine straight leg raising (unless done in the sitting position as well) and range of motion, the least reliable of all determinants.3 Unfortunately, range of motion is still used, although to a lesser degree, for impairment ratings as suggested in the American Medical Association guidelines. Inappropriate physical examination findings are important to record also. A certain number of inappropriate physical signs have been described and are often referred to as “Waddell’s signs.” Too often, physicians consider the presence of three or more of these findings as an alert that the patient may be attempting to amplify them for secondary gain. It is important to note, however, that the presence of inappropriate physical findings does not exclude the presence of a pathologic process and may be due to factors other than attempted malingering. This illness behavior may be linked to fear of reinjury, misunderstanding of instructions, other psychologic issues, and other incident issues. The onus is therefore on the physician to recommend the appropriate diagnostic studies. Main and Waddell48 discussed the theoretical misunderstandings of the behavioral signs in clinical practice and in the medicolegal context. We reproduce here some of the authors’ conclusions and recommendations. As “behavioral responses to examination,” these signs are a form of communication between
The lumbar spine examination begins with the patient standing. The physician should observe the general configuration of the spine to detect any lateral curvatures, kyphosis, or excessive lordosis. Patients with lumbar paraspinous spasms frequently have a pelvic list that should be noted. In patients with lumbar disk herniation, it has been demonstrated that although not associated with the location of nerve root compression, the direction of lumbosacral scoliotic list is related to the side of disk herniation.64 In young adult males with low back pain, chest expansion should be measured with a cloth tape because expansion less than 2.5 cm suggests an inflammatory process such as ankylosing spondylitis. After observing the spine orientation in the erect patient, the physician should ask him or her to flex forward, a step particularly important in adolescents to detect early lateral curvatures of the spine. To assess the range of motion of the lumbosacral spine, the physician should stand behind the patient and observe the lumbar paraspinous muscles. Any eccentric contractions of the musculature suggest lumbosacral paraspinous spasms; limited motion without evidence of such eccentric contractions might suggest a lack of patient cooperation even though there are other possibilities (such as a congenital block or previous fusion). Forward and lateral flexion and extension of the lumbar spine should be observed. Normal patients should be able to bend forward nearly to touch their toes and to the sides to touch the fibular heads, but extension of the spine is extremely variable. In general, pain increased by flexion suggests lumbar disk abnormalities and pain with extension suggests degenerative changes involving posterior elements of the spine, lumbar spinal stenosis, or both. Occasionally, patients with lumbosacral paraspinous
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spasm can flex forward reasonably normally but have difficulty returning to the erect position. Such patients may accomplish this move in a two-phase recovery by flexing the knees and extending the hips without motion in the lower back. The true value and reliability of flexibility assessment is, however, dubious. The reliability of lumbar flexion and extension measured with an electronic inclinometer within a complete physical examination was evaluated in a group of normal volunteers. The intrarater and interrater reliability for flexion were, respectively, 0.48 and 0.56, whereas the same values for extension were 0.53 and 0.37, respectively.33 In older patients, the range of motion of the cervical spine should also be assessed because degenerative osteoarthritis of the cervical spine occasionally results in low back complaints. A study including 27 patients suffering from lower back pain and unilateral single nerve root symptoms, 14 patients with multilevel nerve root symptoms, and 10 control subjects showed that low back pain correlated significantly with restriction of anteroposterior spinal flexion measured with a computerized triaxial potentiometric analysis system.54 After observing the range of motion, the physician should percuss the spine to detect any localized tenderness, a subjective reaction. This test has little value if the patient has tenderness at multiple areas, but consistent localized tenderness over the midline of the spine may suggest inflammatory diskitis (or fractures, tumors, and so forth). The costovertebral angle should be palpated; tenderness in this area suggests a genitourinary problem such as pyelonephritis. Patients should next be asked to walk on their heels and then toes to assess the overall strength of the dorsiflexors (L5) and plantar flexors (S1) of the ankle. In particular, the extensor hallucis longus muscles should be observed when the patient is walking on the heels, because discrepancies can be detected between this act of walking and later passive strength testing. To assess and detect weakness of the triceps surae muscles, which are innervated primarily through the S1 nerve root, the physician should ask the patient to hop several times on the left foot, then on the right foot, and note any discrepancies in the two abilities. The patient should be observed also while walking in the examining room. Extreme staggering from side to side and other bizarre gait patterns suggest symptom amplification. Patients with true herniated disks often have a gait pattern slightly antalgic on one side but with no bizarre abnormalities.
Patient sitting The patient should next sit on the edge of the examining table so the physician can perform the knee and ankle reflex tests and determine the strength of the extensor hallucis longus muscle. This latter examination is critical in all patients complaining of back and leg pain because many have weakness of the extensor hallucis longus but not the tibialis anterior. Weakness of the extensor hallucis longus in a patient who complains of back and leg pain suggests involvement of the L5 nerve root. The extensor digitorum brevis muscle should be checked; however, some authors remain unconvinced that observation of this muscle has any diagnostic significance in patients with lumbar disk disease. Asymmetry is often observed in patients who have never had low back and/or leg pain.
Figure 4c.1 Sitting straight leg raise test. The patient leans back in the “tripod” sign, indicative of true sciatic tension.
The most important portion of the sitting examination is the distracting straight leg raise (SLR) test (Fig. 4c.1). The SLR test has shown to be adequate in healthy subjects when performed within a complete physical examination.33 During this lifting of an extended symptomatic leg in the sitting position, patients with herniated disks and true symptoms of sciatic tension arch backward and complain of pain in the buttock, posterior of the thigh, and calf. Patients who do not have true sciatic tension do not recognize this as a sciatic tension test and therefore have no symptoms. For the patient who complains of pain in the neck as well as the lower back, the strength and reflexes of the upper extremities can be evaluated while he or she is sitting.
Patient supine With the patient supine on the examining table, the physician uses a standard tape to measure the true length of the limbs from the anterior superior spine to the medial malleolus on both sides. Although significant discrepancies (more than 2.5 cm) in limb lengths can result in mild compensatory scoliosis and low back discomfort, these associations are uncommon. The physician should observe the thigh and leg muscles for early signs of atrophy. In addition, the physician should use a cloth tape to measure the circumferences of both thighs one handbreadth above the patella and those of both calves one handbreadth below the patella. Discrepancies greater than 2 cm again are probably significant and suggest muscle atrophy. For the standard ipsilateral SLR maneuver, the physician stands to the patient’s right, places the left hand on the patient’s patella to extend the knee, places the right hand under the os calcis, and then lifts the leg while keeping the knee extended (Fig. 4c.2). Because patients often describe their discomfort in different locations in the extremity, the objectivity of the test results are qualified. If the patient complains of radicular discomfort
Chapter 4c
Figure 4c.2 Supine straight leg raise (SLR) test. For maximum accuracy in identifying sciatic tension, this test must be compared with the sitting SLR test.
during the test, the limb should not be lifted any higher. At that moment, plantar flexion of the ankle should be performed as a distracting test. Because plantar flexion of the ankle should not increase back pain, exacerbation of pain may suggest amplification of symptoms by the patient. Dorsal flexion, on the contrary, should increase sciatic tension and pain (Fig 4c.3). The physician should perform the crossed SLR test also by lifting the nonsymptomatic extremity as in the ipsilateral SLR test. If the patient complains of discomfort radiating into the symptomatic extremity when the well extremity is lifted, this test is positive, almost invariably indicating lumbar disk herniation. During both the SLR test and the crossed SLR test, the patient must be allowed to state where the discomfort is occurring. Specifically, asking the patient whether lifting the well extremity causes pain in the symptomatic extremity invalidates the test. It is important to note that in patients with L4-L5 and L5-S1 disk herniations, the SLR test has very high sensitivity (95%) but lower specificity, whereas the cross SLR has much lower sensitivity (25%) but significantly higher specificity (90%).20
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Patrick’s test should then be performed bilaterally. In this test, the shear force applied across the sacroiliac joint helps detect early abnormalities. Many patients with osteoarthritis of the hip complain of buttock pain rather than the classic groin discomfort, causing the hip joint often to be overlooked because of the apparent back problem. Patients with abnormalities of the hip joint cannot tolerate Patrick’s test, however, because of the discomfort when the limb is fully externally rotated into the abducted position. While the patient is supine with the limbs extended, the physician should therefore gently rotate the lower extremity both internally and externally, a gradual rotation that reveals early irritability in the hip joint. If internal and external rotations cause pain, it may arise from that area. Brown et al14 reported on the clinical signs that may be helpful to distinguish between a hip disease and a spinal origin of pain: “the presence of a limp, groin pain, and limited internal rotation of the hips more often was associated with and predictive of a hip disorder than a spine disorder.” The abdomen should be examined by palpating the four quadrants to detect any intraabdominal masses. Abdominal lesions may erode into the lumbosacral plexus and cause symptoms identical to those of lumbar spinal stenosis or disk disease (Fig. 4c.4). The strength of the abdominal muscles should be assessed by having the patient flex the knees while keeping the feet flat on the table and then perform a sit-up. Patients who have extreme difficulty completing even one sit-up are theoretically excellent candidates for a vigorous rehabilitation program. In addition, the patient should be asked to hold the lower extremities 15 to 20 cm off the table. In general, a patient with an established herniated disk can easily perform this maneuver, so the primary value of this test is to assess the strength of the abdominal musculature rather than determine the likelihood of a disk herniation. With the patient supine, the motor strength of the iliopsoas, quadriceps, and hamstrings, along with Babinski’s reflexes and proprioception, should all be assessed. A sensory examination also should be performed and recorded. A study demonstrated significant elevations of warm, cool, and touch perception thresholds correlated with leg pain in patients with unilateral L5 or S1 nerve root pain. However, dermatomal quantitative sensory tests require some specific tools that are not part of the routine clinical equipment.54
Patient on side
Figure 4c.3 Dorsiflexion of the ankle during a straight leg raise test increases pain.
The supine patient is then asked to turn on one side and to raise and maintain the superior extremity against resistance by the physician (Fig. 4c. 5). In most patients, the gluteus medius is innervated primarily by L5, so patients with L5 radiculopathy often have weak abductors, as do patients with significant hip disease. The trochanter should be palpated to test for trochanteric bursitis. These same tests should be repeated with the patient lying on the opposite side. With the patient on one side, perianal sensation and but-tocks sensation also should be evaluated. All patients over the age of 40 and any patient suspected of a neurologic deficit should have a rectal examination. In males, anal sphincter tone and the size of the prostate may be assessed. Female patients with chronic back pain should have a pelvic examination by a gynecologist.
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A Figure 4c.4 on an MRI.
B (A) CT of a calcified arthrosynovial cyst (circled) causing left nerve root entrapment. (B) The same pathology is less obvious
Figure 4c.5
Gluteus medurs strength testing with the patient on the side and abducting against resistance.
Chapter 4c
Patient prone With the patient prone on the examining table, the lumbar spine, sacrum, and sacroiliac joints should then be reexamined for any localized tenderness. A reverse SLR maneuver can easily be accomplished by the physician simply by lifting both of the patient’s lower extremities off the table, although quite often just bending the knees in the prone position is enough to elicit pain in the L3 or L4 dermatome. The patient should next flex the knees 90 degrees so that the physician can observe internal and external rotation of the hips. In most patients, the amount of internal and external rotation is quite similar. Patients with femoral anteversion, however, have excessive internal rotation and limited external rotation and often experience discomfort in the low back area and buttocks while running. When the patient is prone, ankle jerks often are easier to reexamine and compare; the absence of one or both reflexes should be noted. Finally, the patient should extend first one lower extremity and then the other by using the gluteus maximus muscle. Increased low back discomfort during this maneuver suggests a more superficial myofascial source of the symptoms.
ADDITIONAL INVESTIGATIONS After careful history taking and physical examination (and only then), a number of technical examinations can be ordered based on the results. None of those examinations should be considered as a screening tool, “to see how they come out.” A specificity of low back pain is that in most cases a precise cause of nociceptor cannot be precisely determined despite the increasing sophistication of investigations. Specialized examinations should serve to confirm or pinpoint a suspected diagnosis, and the precision of each should be known. That precision can be determined by statistical measures of sensitivity (the proportion of subjects with the disease in whom the examination is positive), the specificity (the proportion of subjects without the disease in whom the examination is negative), the accuracy, and the predictive value. The two latter measures are not always available in all cases, and in the context of back pain the specificity of imaging is often poor due to a wide range of abnormal images that are asymptomatic. With more sophisticated examinations, more asymptomatic abnormal images are found. In contrast to severe osteoarthritis of the hip or knee, which does not affect everyone and is seldom asymptomatic, marked degenerative changes in the spine seem to affect nearly all human beings with aging and are often asymptomatic. The patient should be told the reason for which an examination is ordered and advised that it may show some meaningless “pathologic images” that are irrelevant to the present symptoms. Those incidental findings are usually nonsignificant and not what was suspected and researched. We all see patients coming with multiple radiology reports where statements about “black disk,” “bulging disk,” or “degenerative changes” have been strongly underlined or highlighted by the patient (or sometimes the doctor). Those misconceptions can lead patients to further impressions of seriousness and prolonged disability. Early and complex imaging
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Additional investigations
with precise description of nonsignificant abnormalities facilitates the “medicalization” of low back pain,12 and duration of disability is associated with its early increased use.47 Patients’ perceptions, expectations, and demands play a major role in the use of imaging modalities to diagnose low back pain. A myth common among patients is that radiographs will show the exact cause of their back pain,36 so they expect to have radiographs when seeing doctors for such complaints.43 They wish to have an x-ray examination ordered, moreover, and physicians’ attitudes are often correlated to patient wishes.77 It appears then that patient education is necessary, although physician education is perhaps even more acutely needed.74 Although many guidelines about diagnostic procedures in back pain have been published in several countries, multiple studies show that most are not followed in the United States,27,56 Canada,8 Norway,77 and Spain.29 All those studies reveal that physicians, mainly in primary care settings but also specialists, still order too many examinations that are of little use.
Plain radiograph Plain radiographs have been the standard (and only widely available) imaging technique in assessment of back pain for decades. They show the bony structures precisely, displaying spondylolysis, spondylolisthesis, deformities, tumors, fractures, and degenerative changes such as disk narrowing, disk vacuum, and traction osteophytes. The latter, however, appear to be a normal evolution of the spine and are very common in symptom-free middle-aged and aged subjects. Instability can be assessed on dynamic (flexion/extension/lateral flexion) radiographs, but the relation of radiologic “instability” to back pain is subject to discussion.65 For these reasons plain films have very low specificity and therefore low diagnostic precision38 and make no difference to the outcome for back pain,78 especially in elderly subjects.10,71 In the case of acute low back pain in a subject between 18 and 50 years of age, plain films are indicated only if there is a history of trauma, malignant disease, or symptoms of infection. In the case of neurologic symptoms, magnetic resonance imaging (MRI) (or computed tomography [CT] if it is unavailable) might be a better diagnostic tool. If no clinical improvement is observed after 6 weeks, plain films may be taken to help exclude a diagnosis of tumor, infection, spondylolysis or olisthesis, and osteoarthritis of the hip, and along with simple laboratory tests will rule out systemic diseases.37 Some studies suggest, however, that in the absence of red flags, radiographs should not be ordered even after 6 weeks of symptoms.41 In chronic low back pain, the same pathologies should be ruled out, but preferably by MRI.10
Myelography Until the advent of CT, myelography was the only examination that enabled physicians to assess spinal neural structures, the dural sac, and the roots. Myelography is still the only widely available examination permitting a dynamic view of the dural sac during flexion and extension in the upright posture (Fig. 4c.6). Given the decrease of the dural sac diameter during extension, some cases of
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stenosis can be underestimated during examinations like CT or MRI that are performed in a supine position. Although upright MRI is becoming available, it is very expensive, uncommon, and constrained in patient positioning and acquisition time, making it inappropriate for this kind of assessment in stenotic patients. Upright myelography examination appears useful also in the diagnosis of position-related disk herniations35 and those in the lateral recess where MRI may underestimate root compression in nearly 30% of cases.2 Indeed, some authors have demonstrated similar sensitivity and specificity in myelography and MRI.55 Myelography is an invasive procedure, however, and neurologic or infectious complications, although very rare, are possible. Combined with CT (myelo-CT), myelography still has a place in cases of strong clinical suspicion of stenosis or herniated disk not clearly demonstrated on other imaging modalities. It also enables the laboratory analysis of the cerebrospinal fluid to be performed to rule out a number of neurologic diseases.
Computed tomography
Figure 4c.6 Myelogram showing multiple level central degenerative stenosis (arrows). Myelogram remains the only widely available examination enabling dynamic and upright assessment.
A
CT is the first examination to provide axial and three-dimensional representations of the spine and the first noninvasive examination to provide a view of spinal neural structures. When it appeared in the 1970s, it was a true revolution. It has now been widely replaced by MRI for the assessment of neural structures but still remains the best examination for the visualization of bony elements. It is also the only examination available for claustrophobic patients or for those with pacemakers or ferrous metallic implants. CT also offers more precise views of calcified disk protrusions.24
B
Figure 4c.7 (A and B) Spondylolysis and olisthesis are best investigated by computed tomography. In this case the pars defect is partially filled by Gill’s nodules (ossified fibrous tissue), which when associated with a disk bulge provoke a lateral stenosis.
Chapter 4c
CT shows more precisely the patterns of fractures in trauma cases and investigates pars fracture in spondylolysis or olisthesis (Fig. 4c.7). In the case of spinal stenosis, if MRI allows a better view of neural elements, CT is still invaluable to investigate the osseous participation in the stenotic process. We believe that it complements MRI before surgical treatment of lumbar stenosis. Spiraled helical CT allows a three-dimensional view of long spinal segments and as such may be very interesting for the accurate description of deformities.
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Additional investigations
MRI has become the standard investigation tool for spinal disorders. The precision of this examination handicaps its specificity, however, because it demonstrates a high frequency of clinically irrelevant abnormal images without associated symptoms. Some studies have shown a prevalence of 28% of disk herniations, at an average age of 42, in asymptomatic subjects,11,39 up to 52% of
which presented at least one bulging disk.39 With MRI, degenerative intervertebral disk disease is present in one third of subjects between 20 and 39, over half of those between 40 and 59, and in nearly all subjects over that age.11 Apparently, a normal physiologic evolution of the decrease of disk hydrophilic properties, dark or black disks, appear in almost everyone. These findings underline that to avoid misunderstandings by patients, MRI results must be interpreted with great care and meticulously related to clinical presentation. Even in the presence of symptoms, the correlation between the severity of clinical findings and MR images of mild to moderate compression due to bulging or stenosis is poor.4 Keeping these limitations in mind, MRI is nevertheless the best tool to investigate compromise of neural elements of the spine. In spinal stenosis it is especially useful in determining the extent of the narrow canal. In presence of a suspicion of neural compression, the addition of MR-myelography, realized through specific acquisition sequences, complements the results of the standard MRI in many cases (Fig. 4c. 8,9).26
Figure 4c.8 Voluminous extruded disk herniation provoking a cauda equine syndrome. In this case magnetic resonance imaging is the examination of choice. The patient had a full recovery after surgery.
Figure 4c.9 Magnetic resonance image of a lytic spondylolisthesis showing root entrapment in the foramen. The root (A) is hampered by the disk bulge in the foramen (B) consecutive to the sliding and flattening of the disk.
Magnetic resonance imaging
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Because it is usually performed in the supine position, MRI may underestimate images of compression in position-related stenosis or sciatica, as is the case with neurogenic claudication. Devices enabling axial compression during supine MRI (or CT) appear to add useful information about the decrease of the spinal canal diameter that appears during upright weight-bearing positions76 and also to enable more precise surgical strategies to be performed.32 MRI is highly specific and sensitive also in the research of malignant and infectious spinal diseases, warranting the use of gadolinium-enhanced MRI in acute low back pain when one of those pathologies is suspected.30 The results in MRI investigation of back pain are more subject to caution. An example is the high intensity zone, the presence of which has appeared to show much promise as a marker of discogenic low back pain. The high intensity zone is a high T2 signal in the posterior and/or posterolateral annulus that seems to increase during axial loading.59 Some authors have found a high correlation of this finding with pain and annular penetration of the dye during diskography, which they believe demonstrates a very high positive predictive value.1,60 Other authors, however, have shown a high prevalence of high intensity zone in asymptomatic subjects,15 whose reaction to diskography is similar to that of symptomatic patients.20 The sensitivity of the sign is low,58 and although it seems that the high intensity zone may show an annular fissure, that fissure is not a reliable sign of painful disk disease. In patients without active symptoms, furthermore, annular disruption is a weaker predictor of future low back pain than psychologic distress.19
have proposed ultrasonic imaging combined with pain provocation by vibrations to diagnose internal annular tears,79 but this technique has not gained widespread acceptance. Investigation of nerve roots and facets has been abandoned due to the lack of accuracy.51 Those examinations do not play a major role in spinal imaging.
Diskography Provocative diskography, which aims at back pain reproduction, has been a controversial subject for many years. It has been considered by some authors to be the best indicator of discogenic pain and has been widely used to confirm surgical indications of fusion and, more recently, disk replacement. Even after positive diskography, however, fusion results remain unpredictable.75 Furthermore, the frequency of positive responses to diskography among asymptomatic subjects challenges the value of this examination as a predictor of clinically relevant discogenic pathology.16,18 Although diskography is indeed a good indicator of annular tears, the latter do not appear to predict a clinically relevant spinal pathology.16 Specificity of diskography appears low,17 and pain intensity during injection is influenced strongly by the patient’s psychologic factors and compensation claims.16 In any case, diskography has no place in the initial assessment of low back troubles.
Electromyography Radionuclide bone scan Radionuclide bone scan (isotopic) is a highly sensitive but poorly specific examination. Of the different radionuclides that can be used, technetium-99m is the most common in spinal indications because it is highly sensitive for malignant diseases and infections. Bone scans using markers such as gallium or marked leucocytes show better specificity for infections. Nearly 40% of subjects with spinal metastasis and normal plain films have a positive bone scan.50 The test might help also to determine whether a vertebral or pelvic fracture is recent or old. Single photon emission CT has been suggested as useful for identifying patients with facet joint disease more likely to benefit from facet injections.23 Single photon emission CT also reveals many abnormalities not detected on a standard radiograph,57 but here again one might wonder about the clinical relevance of those findings. Whereas either the planar bone scan or single photon emission CT reveals areas of increased bone turnover, these tests lack the specificity necessary to determine the true nature of the “lesion” and serve only as indicators for further studies in accordance with the clinical presentation.
Ultrasonography Ultrasonograms may be useful in cases of paraspinal soft tissue infections or tumors or to rule out other sources of lumbar pain, such as urinary tract calculus or kidney diseases. Some studies
Electromyography may be useful in specifying the level of symptomatic compression and ruling out peripheral neuropathies (diabetic, ethylic, or other). One must bear in mind that electromyography shows abnormal signals only several weeks after the occurrence of a nerve compression. Although interesting as an adjunct examination, electromyography is not an essential tool in the initial assessment of spinal troubles.
Mechanical testing The inability to correlate low back pain to anatomic findings and the difficulties in quantifying pain have directed much effort toward measurement of spinal performance through the assessment of function across various dimensions such as flexibility, strength, speed, endurance, and coordination. Goniometers and isokinetic and isoinertial dynamometric devices are currently used. Isoinertial testing seems to be the most physiologic and clinically relevant approach. Useful for prescribing musclestrengthening therapy precisely, it enables the physician to follow up on the patient’s progress and can also be used to assess the efficacy of diverse treatments.44,46,68 In certain pathologies like spinal stenosis, specific patterns of motion have been demonstrated,69 and early decrease of spinal function has been shown in subjects with Parkinson disease.13 The use of neural network technique analysis of motion patterns has enabled researchers satisfactorily to assign back pain patients to pathologic categories based on the Quebec Task Force classification.7 These tests can also provide insight into the maximum effort exerted by the subjects62,66 but
Chapter 4c
despite the hopes of their proponents are by no means back pain “lie detectors.” The measure of flexibility is of limited value in the assessment of the spine,70 and the current American Medical Association guidelines for evaluating disability, heavily based on spinal range of motion, can lead to irrelevant results.45 More elaborate protocols, based on more complex analysis of kinematic profiles, appear to be much more promising.25
Other diagnostic studies Laboratory evaluation should be recommended for patients who are not responding to treatment or who have severe pain. Although many of these tests are indicated in specific situations, a useful screening evaluation for patients with persistent symptoms should include a complete blood count, sedimentation rate, coagulation survey, sequential multiple analysis-18, and urinalysis. Patients who show diminished bone density should be evaluated more thoroughly with thyroid studies, protein electrophoresis, urinary calcium, and evaluation of parathyroid hormone levels. Should one proceed this far in the evaluation, a referral to an endocrinologist with an interest in calcium metabolism is clearly warranted. In young male patients suspected of having ankylosing spondylitis, an HLA-27 antigen study can be ordered.
DIFFERENTIAL DIAGNOSES When evaluating patients with complaints of low back pain, the physician must remain vigilant to identify those whose symptoms result from referred pain unassociated with the intervertebral Differential diagnosis disk or spinal nerves. In this of low-back pain time of intense focus on cost, the physician must also remain Trauma dedicated to a proper evaluaInfections tion for the patient and not Inflammations succumb to managed-care Neoplasms bureaucrats who are interested Developmental abnormalities primarily in the cost rather Metabolic diseases than the quality of care. Patients with low back pain Degenerative disorders represent an interesting group. Neurologic disorders A list of differential diagnoses Referred pain is provided in the box to the Psychological disorders right. Approximately 2% of Miscellaneous patients who come to a low back specialty clinic have evidence for neoplasms as the source of the symptoms.10 A list of suspected causes coupled with the knowledge of appropriate testing aid the physician in formulating a proper workup. A complete history and careful physical examination must underlie any assessment for low back pain. Physicians should remember that their most effective and readily available tools are their hands and brains. Only after this meticulous first stage has been completed can specialized examinations be ordered to answer precise questions and to confirm or eliminate specific pathologies.
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References
Evidence-based medicine principles apply to diagnostic investigations, but there are no screening tests for back pathologies. The poor specificity of the most common imaging techniques is inversely proportional to the frequency of their use. Radiographs and now MRI, which seem to be used almost as routine investigations in low back pain patients, provide a huge quantity of clinically irrelevant information. In a world in which health care resources are decreasing while the population ages and increasing technology costs demand further funding, physicians will be held accountable for unjustified practice costs. Patients should be educated and alerted that technology will not invariably uncover the precise reason of their pain, but physicians too require education, as the failed implementation of many guidelines painfully shows.
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Pincus T, Burton AK, Vogel S, Field AP: A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine 27:E109-E120, 2002. Pincus T, Griffin M: Gastrointestinal disease associated with nonsteroidal anti-inflammatory drugs. Am J Med 91:209-212, 1991. Quraishi NA, Taherzadeh O, McGregor AH, Hughes SPF, Anand P: Correlation of nerve root pain with dermatoma sensory threshold and back pain with spinal movement in single level lumbar spondylosis. J Bone Joint Surg 86B:74-80, 2004. Ramsbacher J, Schilling AM, Wolf KJ, Brock M: Magnetic resonance myelography (MRM) as a spinal examination technique. Acta Neurochir (Wien) 139:1080-1084, 1997. Rao JK, Kroenke K, Mihaliak KA, Eckert GJ, Weinberger M: Can guidelines impact the ordering of magnetic resonance imaging studies by primary care providers for low back pain? Am J Manag Care 8:27-35, 2002. Ryan PJ, Evans PA, Gibson T, Fogelman I: Chronic low back pain: comparison of bone SPECT with radiography and CT. Radiology 182:849-854, 1992. Saifuddin A, Braithwaite I, White J, Taylor BA, Renton P: The value of lumbar spine magnetic resonance imaging in the demonstration of anular tears. Spine 23(4): 453-457, 1998. Saifuddin A, McSweeney E, Lehovsky J: Development of lumbar high intensity zone on axial loaded magnetic resonance imaging. Spine 28(21):E449-E451, 2003. Schellhas KP, Pollei SR, Gundry CR, Heithoff KB: Lumbar disc high-intensity zone: correlation of magnetic resonance imaging and discography. Spine 21(1):79-86, 1996. Spengler DM, Loeser JD, Murphy TM: Orthopaedic aspects of the chronic pain syndrome. Instr Course Lect 29:101-107B, 1980. Spengler DM, Szpalski M: Newer assessment approaches for the patient with low back pain. Contemp Orthop 21:371-378, 1990. Staal JB, Hlobil H, van Tulder MW, et al: Occupational health guidelines for the management of low back pain: an international comparison. Occup Environ Med 60: 618-626, 2003. Suk KS, Lee HM, Moon SH, Kim NH: Lumbosacral scoliotic list by lumbar disc herniation. Spine 26:667-671, 2001. Szpalski M: The mysteries of segmental instability. Bull Hosp Jt Dis 55:147-148, 1996. Szpalski M, Federspiel CF, Poty S, Hayez JP, Debaize JP: Reproducibility of trunk isoinertial dynamic performance in patients with low back pain. J Spinal Disord 5:78-85, 1992. Szpalski M, Gunzburg R: Methods of trunk testing. Semin Spine Surg 10:101-111, 1998. Szpalski M, Hayez JP: Objective functional assessment of the efficacy of tenoxicam in the treatment of acute low back pain: a double-blind placebo-controlled study. Br J Rheumatol 33:74-78, 1994. Szpalski M, Michel F, Hayez JP: Determination of trunk motion patterns associated with permanent or transient stenosis of the lumbar spine. Eur Spine J 5:332-337, 1996. Szpalski M, Parnianpour M: Trunk performance, strength and endurance: measurement techniques and applications. In JN Weinstein, SW Wiesel, eds: The lumbar spine. Philadelphia, 1996, WB Saunders. Tress BM, Hare WS: CT of the spine: are plain spine radiographs necessary? Clin Radiol 41:317-320, 1990. Verbeek J, Sengers MJ, Riemens L, Haafkens J: Patient expectations of treatment for back pain: a systematic review of qualitative and quantitative studies. Spine 29: 2309-2318, 2004. Waddell G, McCulloch JA, Kummel E, Venner RM: Nonorganic physical signs in low back pain. Spine 5:117-125, 1980. Werner EL, Laerum E, Ihlebaek C: How is the general practitioner managing the back pain? Tidsskr Nor Laegeforen 122:1800-1803, 2002. Wetzel FT, LaRocca SH, Lowery GL, Aprill CN: The treatment of lumbar spinal pain syndromes diagnosed by discography: lumbar arthrodesis. Spine 19(7):792-800, 1994. Willen J, Danielson B: The diagnostic effect from axial loading of the lumbar spine during computed tomography and magnetic resonance imaging in patients with degenerative disorders. Spine 26(23):2607-2614, 2001. Wilson IB, Dukes K, Greenfield S, Kaplan S, Hillman B: Patients’ role in the use of radiology testing for common office practice complaints. Arch Intern Med 161(2):256-263, 2001. Yelland M: Diagnostic imaging for back pain. Aust Fam Physician 33:415-419, 2004. Yrjämä M, Tervonen O, Vanharanta H: Ultrasonic imaging of lumbar discs combined with vibration pain provocation compared with discography in the diagnosis of internal anular fissures of the lumbar spine. Spine 21(5):571-575, 1996.
CHAPTER
4d
Treatment Options Margareta Nordin, Federico Balagué, and Christine Cedraschi
More than 17 guidelines drawn from large evidence-based systematic literature reviews have been published in different countries on low back pain (LBP),8,79,96 a topic that the World Health Organization included in their report, the Bone and Joint Decade 2000-2010.38,59,98 LBP remains a common affliction that is debilitating for the patient and expensive for the working individual and for society.31,70 This chapter gives an overview of treatment modalities for returning an individual to work during the course of acute to chronic LBP. The focus is on LBP that is nonspecific, where causality cannot be established and which is treated by a structured evidence-based approach to prevent disability and chronicity.
SPECIFIC AND NONSPECIFIC LBP The classification for pain in the lumbar spine used by clinicians is “specific” or “nonspecific,” depending on which of more than 60 diagnoses applies.
TREATMENT MODELS Two treatment models are commonly used in treating back pain: the medical model and the biopsychosocial model. Modern medicine uses the classic scheme, which implies that an interaction between the patient and an exposure leads to an illness complex.99 This model works well in dealing with SLBP. The procedures are to 1. Recognize patterns of symptoms and signs by history and examination; 2. Identify underlying injury or disease by investigation and diagnosis; 3. Treat underlying injury or disease by specific intervention; 4. Expect the patient to recover. Preferably applied to NSLBP, the biopsychosocial model identifies factors associated with delayed recovery for return to activity and, most often, return to work. The model calls for identification of symptoms and signs outside the traditional medical field such as beliefs, high perception of disability, kinesophobia, depression, stress, job dissatisfaction, anxiety, somatization, or lack of control.22,94 These contributing factors are treated with nontraditional medical approaches such as cognitive behavioral therapy (CBT) or ergonomic or occupational intervention. The biopsychosocial model in occupational health care helps to 1. Recognize the nonspecific nature of the back pain; 2. Identify underlying psychosocial and/or environmental factors; 3. Treat these factors with appropriate interventions; 4. Empower the patient to assume responsibility for managing a condition with possibly frequent recurrence.
Specific low back pain The common feature for specific low back pain (SLBP), the diagnosis in up to 2% of all early back pain cases, is a causal link between a structural pathology and the described experience of the patient (see Chapter 4c). SLBP may result from systemic disease, infection, injury, trauma, cauda equine, or structural deformity. Additionally, nerve root pain, which occurs in about 5% of the individuals seeking care early, includes diagnoses such as a disk prolapse or spinal stenosis. These conditions are treated with or without surgery and should be referred to a specialist for determination of care.6,8,57
Nonspecific low back pain Nonspecific low back pain (NSLBP), which afflicts 85-90% of all individuals seeking care, is a diagnosis of exclusion: No precise structure is identified as the cause. NSLBP is attributable to common diagnoses such as lumbago, myofascial syndromes, muscle spasms, mechanical LBP, back sprain, and back strain. These conditions all include pain in the lumbar region that may or may not radiate to one or both thighs but not below the knee(s). The following International Classification of Diseases diagnostic codes are suggested to best represent NSLBP: lumbago (724.2) and sprains of the lumbosacral region (846.0-3/8-9, 847.2-3).24
The first occupational health guidelines for the management of LBP at work were published in 2001 (see also www.facoccmed. ac.uk).96 These guidelines are based on an extensive systematic review of the scientific literature primarily in terms of occupational settings or outcomes.
PATIENT EXPECTATIONS A patient approaches a physician with expectations and preconceptions. The patient expects diagnostic explanation, pain relief, referral for treatment, instructions for coping with pain and disability, and, in an occupational environment, help with sickness certification or light duty assignment. Some patients expect imaging or special tests and specific medication. In one cross-sectional study (n = 1942), for example, 77% of the responders believed that if back pain exists, a wrong movement could lead to a serious problem. Forty percent believed also that radiographs and imaging could always identify the cause of back pain.40 It takes time to explain inappropriate concepts and expectations. The first encounter addresses such misconceptions, whereas at subsequent visits the important concepts for recovery are discussed and reinforced.69,91 Evidence-based information educates the patient that selective treatments may take time; some treatments may pose higher risks, and the effects of new treatments
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are not entirely known. The patient and clinician discuss the proposed treatment and the prospect of harm when work is resumed and agree on a regimen including compliance and return to work. Patient education about treatment choice and expected outcome is a key factor for success.49,97
NATURAL HISTORY AND RECURRENCE OF NSLBP Acute NSLBP has a favorable prognosis. Some authors argue that NSLBP is a lifetime disease if recovery has not occurred during the first 3 months,10,84,92 as is true for a large subgroup of individuals.48 Von Korff et al93 found that 20% of the U.S. population suffers from chronic LBP each year and that about 30% of them suffer chronic pain over their lifetimes. Studies focusing on the natural history of LBP report that 80% of patients who consult a health care provider for acute NSLBP can expect to resume normal activities within 4 to 6 weeks. By 12 weeks, the rate of recovery rises to almost 90%. Compared with approximately 35% to 40% of patients with SLBP, 10% or fewer of NSLBP patients experience chronic pain and work incapacity.1,11,70 The recurrence rate in NSLBP varies considerably from 5% to 70%, with up to 2 years follow-up in studies of both general and specific occupational populations.18,92 Recurrence or episode rate is difficult to estimate, however, because the definition of an episode is not standardized in different studies.29 We diagnose recurrent NSLBP when the employee has returned to regular work pain free for at least 8 weeks since the previous episode.71
on exercises and NSLBP, the authors concluded that “exercise therapy is as effective as either no treatment or other conservative treatments” in 11 trials involving 1192 adults.1,45,88 A series of five to six manipulations in the acute stage of NSLBP reduces pain and disability for up to almost 3 weeks.4,8,14,33 Alternatively, the patient may have a short course in pain management involving five to six encounters with a therapist trained in the biopsychosocial approach.61 In a comparison of manipulation and pain management in patients with acute NSLBP, the outcomes at 3 months and 12 months were almost identical (difference 0 [95% confidence interval (CI), -1.3-1.4]), with a decrease in disability score of about 8.8/24 points.44 With the patient maintaining tolerable activity, manipulations and pain management in acute NSLBP are superior to all passive modalities (mobilization, diathermy, massage, heat) over the long term.21,33 Continued passive longterm treatment of NSLBP is harmful because it precludes patient involvement, increases fear that the condition is serious, decreases cardiovascular conditioning, and reinforces the role of sick person.94 For the employee seeking care, the message is sometimes difficult to understand, particularly if the injury or back pain started at work. “Why should I go back to work, where I was injured, if it may hurt my back?” he or she asks. This legitimate question needs to be answered in relation to the type of job involved and the availability of modified work for a limited period if necessary. The occupational health care provider is best placed to answer this question and to adapt the employee’s duties if necessary.
Self-care for acute NSLBP DURATION OF PAIN AND TREATMENT GOALS The following definitions of LBP and duration since onset are used and well accepted: The duration of acute NSLBP is 0-4 weeks and that of subacute NSLBP is 4-12 weeks.1,8,33 Although episode definition is not standardized, intermittent or recurrent NSLBP is diagnosed when the patient is pain free or almost pain free between the bouts of pain.1 Chronic NSLBP is defined as a duration of pain longer than 12 weeks.1,8,17,33 The most important goal for acute LBP is a continuum of occupational care and identification of factors to prevent chronicity during the first 3 months after the patient seeks help. Management in occupational medicine can make a difference by providing regular follow-up and using a multidisciplinary approach to reinforce return to work with temporary job accommodations or, in some cases, job change.
ACUTE NSLBP AND EVIDENCE FOR TREATMENT Because acute NSLBP is largely self-limiting, minimal or no medical interventions are recommended for most patients.1,26,33,67,88,95 The most important message is for the patient to keep as active as tolerable without bed rest.1,33,67,73,74,88 Specific exercises are not needed and may also have a negative effect. In two systematic reviews and a recent meta-analysis
Self-care implies that the NSLBP patient can control symptoms and engage in behaviors necessary to reduce or alleviate them. Playing an active role in recovery, the patient decides what behaviors are tolerable. The message to remain as active as possible cannot be overemphasized.1,88 Self-care techniques include (but are not limited to) stretching and/or walking or using heat and/or ice or relaxation techniques72 when convenient for shortterm relief. Written evidence-based information is helpful to reinforce the good prognosis of NSLBP, explaining the biopsychosocial factors influencing recovery and offering instructions for self-care.16 Company-specific information may have a better impact than a generic pamphlet.46,75 In summary, systematic literature reviews, randomized controlled trials, and meta-analysis of acute NSLBP show that selfcare in the form of maintained activity, education, and medication as needed is as effective as manipulation or a short course of pain management based on the biopsychosocial model. Bed rest and passive treatment should be avoided. If patients demand treatment, it is prudent to ask about their expectations and goals, educate them, and reinforce the positive prognosis. The natural history of acute NSLBP measured as return to work is altered only marginally by prescribed treatment at this early stage, but together with self-care it provides shortterm relief from pain. Patients should be followed until they resume work.
Chapter 4d
INTERVENTIONS FOR SUBACUTE NSLBP The interval of 4-12 weeks in the management of NSLBP has been called “the window of opportunity.” The occupational health care professional can become instrumental in preventing work disability and recommending alternative and more intensive regimens of evidence-based treatment. A clinical reevaluation at 4 weeks includes a careful orthopedic and neurologic examination along with imaging and other diagnostics if warranted to exclude any ongoing process in the spine.8,33 If the diagnosis remains NSLBP, screening for psychosocial factors is warranted.
Yellow flags “Yellow flags”56 indicate psychosocial barriers to recovery and predict poor outcomes related to occupational health care because the patient does not return to any kind of work.55 Yellow flags are employee misconceptions (that back pain is harmful or can be severely disabling), avoidance of movement or activity due to fear of pain, tendency toward depression, withdrawal from social interaction, or expectation of continued passive treatment rather than belief that active participation will help.55,61 Six open-ended questions are helpful for revealing yellow flags: 1. Have you had time off work in the past with back pain? 2. What do you understand to be the cause of your back pain? 3. What do you expect will help you? 4. How is your employer responding to your back pain? Your coworkers? Your family? 5. What are you doing to cope with your back pain? 6. Do you believe you will return to work? When?
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In one study from a primary care cohort (n = 800) over 5 years, not recognizing psychosocial issues early on has been shown to account for an increase of 10 consultations per year per patient.52
Blue flags In occupational health care it is also helpful to recognize so-called “blue flags” that are related to possible work problems. Initially proposed by Main and coworkers,7,65,66 blue flags represent occupationally related predisposing factors for delayed recovery and return to work. Blue flags include factors such as fear of losing one’s job, monotony at work, lack of job satisfaction, and poor relationships with peers and supervisors. Occupational health care professionals are particularly well placed to address these issues. Appropriate intervention such as CBT aims to strengthen the employee’s coping skills and problem solving. In collaboration with the occupational physician, a discussion with supervisors or a workplace visit can occur early in the course of back pain to prevent chronicity. An active approach combining patient participation with involvement by the health care provider, the management, and the union is beneficial.60,62,81
Management of NSLBP The management of subacute NSLBP treatment should proceed in a stepwise fashion from least to the most invasive treatment (Fig. 4d.1). There is weak to moderate evidence in randomized controlled trials for efficacy of a treatment regimen including exercise, behavioral therapy, and ergonomic intervention.33,70 The employee must be convinced to participate actively to prevent long-term chronicity and disability. Meaningful outcomes for the patient that need to be discussed are those of taking control of
Work disability in %
100
50
• Convey optimism • Stay active • Pain medication • Self care techniques • Follow-up • Pamphlet/information
0
1 month Acute
Figure 4d.1
• Convey optimism • Exercise • Pain medication • Psychological evaluation and possible cognitive behavoral treatment • Work conditioning program • Ergonomic and/or occupational intervention
>6 months
3 months Subacute
Suggested management of occupational nonspecific low back pain.
• Exercise • Aggressive pain management • Cognitive behavoral treatment • Multidisciplinary conditioning program with focus on return to work • Workplace intervention • Surgery (?)
Early chronic
Chronic
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the condition; feeling better; resuming activities, including work; and avoiding recurrences. Because compliance with regimens requires the patient’s active participation, management of subacute NSLBP is demanding. Compliance rates for different regimens have been reported to vary from 13% to 85%,2,61 and a patient’s decision to adhere to a treatment regimen is complex.50 Patients may prefer passive treatment that may delay the course of recovery.83 One study has shown, for example, that patient compliance with video watching for back education (70-80%) in a physical therapy practice was significantly higher than compliance with a more demanding exercise regimen (40-50%).2 Linton and Andersson61 indicated an adherence rate of 53% and 72% for six and four CBT sessions, respectively. Adherence appears to be influenced by both the type of treatment and its frequency. The stepwise active approach includes an exercise regimen or a CBT program as a single intervention or a combination of the two as a bimodal treatment if no recovery occurs.
Exercise regimens The message here is for the patient to “start moving” with or without help from a coach. There are many different types of exercise regimens for LBP, each with its own proponents. Exercise programs evaluated in randomized controlled trials include the McKenzie regimen, walking programs, Williams flexion exercises, endurance-strength-stabilization training, and other less frequently described regimens.23,27,43,47,54 Different types of exercises appear to be equally effective.1,87 A recent meta-analysis of five exercise studies involving about 800 patients resulted in pooled weighted difference decrease in pain of about two points (1.89 [95% CI, -1.13 to 4.91) on a scale of 100. Pooling four trials demonstrated an improvement of 1.07 (95% CI, -3.18 to 5.32) points on a scale of 100 for perceived functional outcomes.45 The authors concluded that the evidence is insufficient to refute or support the effectiveness of regimens involving exercise alone without a behavioral component.
Cognitive behavioral therapy CBT interventions include creative visualization, imagery, progressive muscle relaxation, problem solving, and other techniques. The clinician uses the components in various combinations to have the patient understand, accept, and take control of the back pain. Moderate to strong evidence indicates that CBT should be used early if biopsychosocial signs or symptoms are present, and strong evidence exists for using CBT in patients with chronic NSLBP.33,87,96 The European Guidelines 2005 stated, “We recommend cognitive-behavioural treatment for patients with chronic LBP,” and summarized as follows: There is strong evidence that behavioural treatment is more effective for pain, functional status, and behavioural outcomes than placebo/no treatment/waiting list control. There is strong evidence that a graded activity programme using a behavioural approach is more effective than traditional care for returning patients to work, and finally there is strong evidence that there is no difference in effectiveness between the various types of behavioural therapy.33
Combination therapy in occupational settings Three studies in occupational settings have found that a behaviorally oriented graded-activity exercise program provides moderate to excellent reduction of days lost at work. This type of program has been compared to usual care in the Netherlands and in Sweden.60,81,86 These studies had highly structured interventions with an unambiguous primary goal of returning the patient to work. A behaviorally oriented graded-activity exercise program includes the following components: 1. The occupational or treating physicians advise workers on ergonomics, prevention, and return to work schedules; 2. The clinicians also advise and communicate with interested parties such as health care providers and workplace representatives; 3. The programs use gradually progressive exercises adapted to patient needs; 4. The clinical team is trained, and all caregivers provide the same message to the patient to avoid ambiguity; 5. There is ample communication and discussion with the patient; 6. An ergonomic intervention such as a workplace visit or a discussion with the occupational physician may be included.60,62 The studies showed significant reduction in days of work loss. Lindstrom et al,60 for example, showed an average return to work in the intervention group at 10 weeks (standard deviation, 12.7) and in the control group at 15.1 weeks (standard deviation, 15.6). Staal et al80 showed an effect on work loss days (HR 1,9; CI, 1.2-3.2) at 50 days after randomization in favor of the graded-activity program. However, the results were not significant in early follow-up less than 50 days after treatment for the two interventions (an exercise program and a graded operant conditioning program). One randomized controlled trial in an occupational setting in the Netherlands added problem-solving therapy conducted by a trained therapist to a behaviorally oriented graded-activity exercise program for patients with subacute and chronic NSLBP. The combination group showed significantly favorable results, including fewer work loss days and fewer patients receiving disability pensions 1 year after the intervention.86 In all studies, self-reported pain and function were affected marginally.60,80,86 Usually measured by a pain score or visual analog scale, pain itself appeared not to be a major determinant for return to work. Possibly the highly structured positive environment in an occupational setting provides a better venue for problem solving, educating the patient, and monitoring progress.
Ergonomic intervention Using the Sherbrooke model of occupational/ergonomic intervention and clinical rehabilitation, Loisel et al62 found that a consultation with an occupational physician or a low-cost ergonomic intervention contributed the most to the success of return to work. In a follow-up study of cost effectiveness 6.4 years later, the same authors found that the Sherbrooke model yielded the highest savings in work loss days compared with standard care or rehabilitation alone.64 The authors assessed participatory ergonomics in workers
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suffering from subacute LBP (>6 weeks of work disability). Performed 6 months after the ergonomic intervention, the assessment included all parties: management, union, and afflicted worker. About half of the recommended ergonomic solutions were implemented with a substantial agreement among all respondents.63 The Cochrane review of multidisciplinary biopsychosocial rehabilitation concluded, “There is moderate evidence showing that multidisciplinary rehabilitation for subacute LBP is effective and that a work site visit increases the effectiveness.”53 These findings must be interpreted with caution, however, because the few studies reviewed contained methodologic flaws and need to be confirmed. Based on several studies of patients with chronic back pain, the European Guidelines 2005 recommend an occupational intervention.33
MULTIMODAL PROGRAMS FOR CHRONIC LBP Two recent reviews and one systematic Cochrane review of chronic NSLBP showed the importance of multimodal active programs.9,10,19,39,42 The Cochrane review covered 18 trials, including 1964 chronic NSLBP patients (Fig 4d.2).53,87 The comparison included treatment such as back training, exercise only, education, standard care, assessment by specialist with or without a nurse and/or advisement (oral and printed), waiting lists, and other factors. Like the European Guidelines 2005, the review concluded, “There is strong evidence that intensive multidisciplinary biopsychosocial rehabilitation for chronic NSLBP with a functional restoration approach reduces pain when compared with inpatient or out-patient nonmultidisciplinary treatments and moderate evidence when these programs are compared to usual care. There is contradictory evidence regarding global vocational outcomes.”42 The authors cautioned about the lack of definition concerning content, duration, and intensity of the programs but found that those longer than 100 hours of therapy with a focus on functional restoration seem to be more effective than less intensive programs or nonmultidisciplinary control groups. The review indicated significant and favorable results for pain ratings, functional status, employment status, and sick leave up to 60 months.
MANIPULATION Manipulation has been evaluated extensively for chronic LBP and studied less in the subacute phase. A recent pragmatic randomized trial, however, included 181 general practices in the United Kingdom with 1334 patients, most of whom had subacute NSLBP. Patients were randomized to groups of standard best care or manipulation, each with or without exercise, and followed for 1 year.85 Results on the Roland Morris disability questionnaire76-78 improved with a mean of 3.3 (standard deviation, 4.5) and 3.5 (standard deviation, 4.7) points out of a total score of 10 points at 3 and 12 months, respectively. A score change of 20% is deemed clinically significant.10 The difference between the groups was nonsignificant. Manipulation for chronic NSLBP was reviewed extensively by Assendelft et al,4 Bronfort and Bouter,13 and Cherkin et al.25 In a
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meta-analysis, Cherkin et al compared sham manipulation, traction, corset, bed rest, home care, topical gel, diathermy, massage, general practitioner care, analgesics, physical therapy, exercises, back training, no treatment, or some combination thereof. They found no evidence that spinal manipulation is substantially more or less effective than other conventional therapies for chronic NSLBP. The expected gain in pain reduction is 4-5 points (ranging from -4 to 12) on a 100-mm visual analog scale for pain of longterm duration and somewhat less for self-reported disability. These measures were reported for both the short and the long term.25 A UCLA study (n = 681) included about 50% patients with chronic NSLBP in a managed care health organization. The patients were randomized to chiropractic, medical, or physiotherapy care, and at a 6-month follow-up the results were comparable.51 Chiropractic care in combination with physical modalities or physical therapy modalities provided in combination with medical care did not produce clinically significant improvements in outcome.58 The European Guidelines 200533 recommend a short course of spinal manipulation/mobilization as a treatment option for chronic LBP. They also summarize the evidence for medication use as follows.
MEDICATION Nonsteroidal antiinflammatory drugs (NSAIDs) The usefulness of nonsteroidal antiinflammatory drugs (NSAIDs) was reviewed systematically by van Tulder et al,89 who highlighted the methodologic problems they encountered. Most of the published trials reported on acute LBP. In comparison with placebo, the authors found “conflicting evidence” that NSAIDs provided better pain relief, but patients on NSAIDs exhibited significantly less use of analgesics. There were no significant differences in terms of side effects. In the same review, “conflicting results” were found among studies comparing NSAIDs with paracetamol. Included in the same systematic review were six studies comparing NSAIDs with narcotic analgesics or muscle relaxants. The authors found “moderate evidence” that NSAIDs are not more effective than other drugs. van Tulder et al89 highlighted the impossibility of making any statement about the relative effectiveness of different NSAID types because no studies comparing the same two drugs for acute or chronic LBP were available.
Muscle relaxants Benzodiazepine and nonbenzodiazepine muscle relaxants, either isolated or combined with other drugs, have been extensively investigated in LBP. A systematic review of this literature was published by van Tulder et al.90 Limited evidence from one study favored diazepam (an intramuscular injection followed by 5 days of oral treatment) versus placebo. The authors found strong evidence both that oral nonbenzodiazepines are more effective than placebo for short-term pain relief and that both types of muscle relaxants are associated significantly more than placebo with central nervous system side effects. Because the number of high-quality studies comparing different muscle relaxants is
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Treatment options
Trial characteristics
Time since treatment
Pain record
Functional status
Days on sickness leave
Employment status
Intensive (>100h) daily MBPSR with functional restorative: Alsants 1994* v >100h inpatient rehabilitation
3 months 12 months
Bendix 1995:1* v < 30h outpatient rehabilitation
4 months 12 months 24 months 60 months
Bendix 1990 v usual care
4 months 24 months 60 months
Michel 1994* v usual care
4 months 12 months 24 months
Less intensive (<30h) once or twice daily outpatient MBPSR: Bazier 1997 v outpatient rehabilitation
At treatment completion
Bendix 1995:2* v <10h outpatient rehabilitation
6 months 12 months 24 months 30 months
Nichols 1991* v < 30h outpatient rehabilitation
6 months 12 months
Nichols 1992* v < 30h outpatient rehabilitation
6 months
Martapea 1989:2 v usual care
3 months 12 months 30 months 54 months
Other types of MBPSR: Martapea 1989:1 Inpatient MBPSR >108h (no functional restoration) v usual care
3 months 12 months 30 months 54 months
Juckel 1990 Sμ type MBPSR v waiting list
At treatment completion
Uritias 1989* Individualized inpatient MBPSR v usual care
12 months
–2 –1
0
1
Standardized mean difference
2
–2 –1
0
1
Standardized mean difference
2
0.1
1 Relative risk
10
–2 –1
0
1
2
Standardized mean difference
Figure 4d.2 Treatment effect sizes for 12 randomized comparisons of multidisciplinary biopsychosocial rehabilitation and a control condition. Bars represent standardized mean differences and 95% confidence intervals for comparison of intervention and control groups, except for employment status, where bars represent relative risks. Treatment effect sizes entirely to the left of the vertical line indicate statistically significant differences in favor of the intervention. *, High quality trial; I1, intervention 1 testing more than one multidisciplinary intervention; I2, intervention 2 testing more than one multidisciplinary intervention; MBSPR, multidisciplinary biopsychosocial rehabilitation.
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rather limited, it seems very difficult to make general recommendations in this area. There is strong evidence that combining tizanidine plus paracetamol or tizanidine plus NSAIDs is more effective for short-term pain relief than placebo plus paracetamol or plus NSAIDs. Two high-quality trials offer strong evidence that temazepam 50 mg 3 times a day is more effective than placebo for short-term pain relief and overall improvement. When the literature review was published, however, this drug was available only in some European countries and Mexico. Among the nonbenzodiazepines, there is moderate evidence that flupirtine and tolperisone are more effective than placebo for short-term improvement.90
Opioids Breckenridge and Clark12 and Fillingim et al35 independently showed that the use of opioids in chronic LBP patients was not predicted by pain intensity. Therefore, the factors influencing health care providers to prescribe opioids probably deserve more research.
Antidepressants The efficacy of antidepressants in chronic LBP was systematically reviewed by Staiger et al.82 Based on the seven studies reviewed, the authors concluded that tricyclic and tetracyclic antidepressants can produce moderate symptom reductions. Inhibition of norepinephrine reuptake seems important for the analgesic effect. Benefits appear to be independent of a patient’s depression. Selective serotonin reuptake inhibitors were evaluated in three studies that failed to show any analgesic effect. It remains unclear whether these drugs affect functional status.
Corticosteroids In their review, Atlas and Nardin5 stated that evidence supporting the use of oral corticosteroids is lacking. Because these drugs have potential significant side effects, the authors therefore advised against their use in patients with chronic pain.
SURGERY Chronic NSLBP would imply LBP without sciatica in patients with degenerative disk diseases.30 Although shown to be controversial, the diagnosis itself is usually made by provocative diskography at the level of the disk possibly causing the pain.19,20 An et al3 discussed disk degenerative progressive changes as part of normal aging. Studies today cannot confirm what starts and what influences progression if no trauma or disease is present. There is also debate about the disk as a pain source; from a clinical perspective, however, severe disk degeneration on several levels is shown to cause pain. Moderate to less visible disk degeneration changes are more debatable. The authors argued for investigating other sources of pain as well as its enhancers or modifiers. A systematic literature review in 1999 concluded that there was insufficient evidence for lumbar spine fusion in lumbar
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Surgery
spondylolysis and back pain.39 Three randomized trials have since shown that long-term benefits for surgery over 2 years is comparable with those of nonsurgical treatments.15,35,37 In a large randomized controlled study, Fritzell et al36,37 compared fusion with usual conservative care in patients (n = 294) with one- or two-level disk degeneration and pain duration of at least 1 year. The surgical group had a greater improvement in pain relief, function, depressive symptoms, and return to work at 1-year follow-up compared with those who had common conservative treatment prescribed by a physician. At 2-years follow-up, the difference between the groups had diminished, suggesting that the results of fusion are intermediary rather than long term. The heterogeneous therapy in the nonsurgical treatment may also have contributed to a less favorable result in the nonsurgical group. The nonsurgical group received a variety of treatments according to individual physician preferences such as acupuncture, physical therapy, injections, electrical stimulation, and CBT. The study did not have blinded evaluators. In a smaller randomized trial, 64 patients aged 25-60 years with NSLBP lasting longer than 1 year and evidence of disk degeneration at L4-L5 and/or L5-S1 at radiographic examination were randomized to either lumbar fusion with posterior transpedicular screws and postoperative physiotherapy or cognitive intervention and exercises.15 The cognitive intervention consisted of a lecture to help patients understand that ordinary physical activity would not harm the disk and a recommendation to use the back and bend it. This was reinforced by three daily physical exercise sessions for 3 weeks. The main outcome measure was the Oswestry Disability Index. At a 1-year follow-up visit to 97% of the patients, the Oswestry Disability Index was significantly reduced from 41/100 to 26/100 points after surgery, compared with 42/100 to 30/100 points after cognitive intervention and exercises. The mean difference between the groups of 2.3 points (-6.7 to 11.4; p = 0.33) was not significant. Improvements in back pain, use of analgesics, emotional distress, life satisfaction, and return to work were not different. Fear-avoidance beliefs and fingertip-floor distance were reduced more after nonoperative treatment, and lower limb pain was reduced more after surgery. According to an independent observer, the success rate was 70% after surgery and 76% after cognitive intervention and exercises. The early complication rate in the surgical group was 18%. The authors concluded that the main outcome measure showed equal improvement in patients with chronic LBP and disk degeneration randomized to lumbar fusion or cognitive intervention and exercises.15 The risk for the nonsurgical group was considerably lower, however, because no complications occurred. Although the evidence is less compelling than it might have been, in the future these patients may be offered surgery or CBT with similar results. This study needs to be confirmed by other and larger studies, but it may provide an alternative to surgery when expected outcomes from that treatment are uncertain. In a multicenter study from Great Britain,34 349 patients with chronic back pain lasting more than 1 year were randomized to surgery (spinal fusion) or to an intensive rehabilitation program for 5 days a week for 3 weeks continuously and followed for 2 years. The team included a physician, a physical therapist, and a psychologist. The program was individually tailored to each patient with progressive exercises and CBT to overcome fears and negative beliefs about back pain. Both groups reported
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reductions in disability, and the only primary outcome measure that marginally favored surgery was the Oswestry Disability Index, which showed a clinically insignificant decrease of about four points on a scale of 100 (-.1 [95% CI, -4.1 to -0.1; p = 0.045). No clear evidence emerged that primary spinal fusion was any more beneficial than intensive rehabilitation. Randomized controlled trials on novel technology such as artificial disks, electrothermal therapy, analgesic pumps, and implanted stimulators are lacking. One systematic literature review stated, “There is no evidence that disk replacement reliably, reproducibly, and over longer periods of time fulfills the three primary aims of clinical efficacy, continued motion, and few adjacent segment degenerative problems. Total disk replacement seems to be associated with a high rate of re-operations, and the potential problems that may occur with longer follow-up have not been addressed.”28 Arthroplasty and fusion or laminectomy have been compared in randomized clinical trials with similar outcomes.41,68 In these studies no nonsurgical groups were included for comparison, as is greatly needed. In patients with chronic NSLBP, the current evidence points to improved triage and a stepwise active approach in which the patient and clinician discuss goals, outcomes, and compliance with the proposed treatment.
COMPLICATIONS AND TREATMENT CHOICE
REFERENCES 1.
2.
3. 4.
5. 6. 7.
8.
9. 10. 11.
12.
We could not find any complications reported in therapies including exercise, CBT, or workplace intervention. The complication rate for spinal surgery varies by type from 2% to 15%, including instrument failure, prosthetic migration, infection, chronic pain, and neural injuries or/and pulmonary embolus. When advising a patient, this information can be used for education to help with choice of treatment.
13.
SUMMARY
17.
This chapter summarizes evidence-based management and treatment regimens for patients seeking care for LBP and diagnosed with NSLBP. In acute NSLBP there is strong to moderate evidence for self-care by taking over-the-counter medication and maintaining activity as tolerated or engaging in limited sessions of manipulative therapy. In subacute NSLBP, there is weak to moderate evidence for a graded activity program, including a combination of exercise and CBT. Strong evidence indicates that these programs reduce work absenteeism. In NSLBP of more than 12 weeks’ duration, a variety of regimens seems to be available with limited and similar efficacy on pain and disability reduction. There is weak to moderate evidence that interventions, including CBT, exercise, and education about chronic NSLBP, are as effective as surgery after 2 years of followup. Surgical indications for chronic NSLBP are ill-defined.
14.
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25.
26.
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ACKNOWLEDGMENT 29.
We thank Chaitrali Gore, M.S., for her excellent help with references and figures.
30.
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Fritzell P, Hagg O, Jonsson D, Nordwall A: Cost-effectiveness of lumbar fusion and nonsurgical treatment for chronic LBP in the Swedish Lumbar Spine Study: a multicenter, randomized, controlled trial from the Swedish Lumbar Spine Study Group. Spine 29:421-434, 2004. Fritzell P, Hagg O, Wessberg P, Nordwall A: Lumbar fusion versus nonsurgical treatment for chronic LBP: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group, 2001 Volvo Award Winner in Clinical Studies. Spine 26: 2521-2532, 2001. Garfin SR, Andersson G, Gronblad M, et al: The Bone and Joint Decade, 2000-2010, for prevention and treatment of musculoskeletal disorders. Spine 24(11): 1055-1057, 1999. Gibson JN, Grant IC, Waddell G: The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine 24:1820-1832, 1999. Goubert L, Crombez G, De Bourdeaudhuij I: Low back pain, disability and back pain myths in a community sample: prevalence and interrelationships. Eur J Pain 8: 385-394, 2004. Guyer RD, McAfee PC, Hochschuler SH, et al: Prospective randomized study of the Charite artificial disc: data from two investigational centers. Spine 4:252S-259S, 2004. Guzman J, Esmail R, Karjalainen K, et al: Multidisciplinary rehabilitation for chronic LBP: systematic review. BMJ 322:1511-1516, 2001. Hansen FR, Bendix T, Skov P, et al: Intensive, dynamic back-muscle exercises, conventional physiotherapy, or placebo-control treatment of low-back pain. A randomized, observer-blind trial. Spine 18:98-108, 1993. Hay EM, Mullis R, Lewis M, et al: Comparison of physical treatments versus a brief pain-management programme for back pain in primary care: a randomised clinical trial in physiotherapy practice. Lancet 365:2024-2030, 2005. Hayden JA, van Tulder MW, Malmivaara AV, Koes BW: Meta-analysis: exercise therapy for nonspecific LBP. Ann Intern Med 142:765-775, 2005. Hazard RG, Reid S, Haugh LD, McFarlane G: A controlled trial of an educational pamphlet to prevent disability after occupational low back injury. Spine 25: 1419-1423, 2000. Helmhout PH, Harts CC, Staal JB, Candel MJ, de Bie RA: Comparison of a high-intensity and a low-intensity lumbar extensor training program as minimal intervention treatment in LBP: a randomized trial. Eur Spine J 13:537-547, 2004. Hestbaek L, Leboeuf-Yde C, Engberg M, et al: The course of LBP in a general population: results from a 5-year prospective study. J Manip Physiol Ther 26:213-219, 2003. Heymans MW, van Tulder MW, Esmail R, Bombardier C, Koes BW: Back schools for nonspecific low-back pain. Cochrane Database Syst Rev, CD000261, 2004. Hiebert R: Factors influencing patient compliance with medically recommended care for work disabling, non-specific, low back pain during acute and subacute phases. Masters of Science (Sc.M.) thesis. Baltimore, 2004, Johns Hopkins School of Hygiene and Public Health, Department of Health Policy and Management. Hurwitz EL, Morgenstern H, Harber P, et al: A randomized trial of medical care with and without physical therapy and chiropractic care with and without physical modalities for patients with LBP: 6-month follow-up outcomes from the UCLA LBP study. Spine 27:2193-2204, 2002. Kapur N, Hunt I, Lunt M, et al: Psychosocial and illness related predictors of consultation rates in primary care—a cohort study, Psychol Med 34:719-728, 2004. Karjalainen K, Malmivaara A, van Tulder M, et al: Multidisciplinary biopsychosocial rehabilitation for subacute LBP in working-age adults: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 26:262-269, 2001. Kellet J: Support groups: caring about each other. Nurs Stand 5:46, 1991. Kendall NA: Psychosocial approaches to the prevention of chronic pain: the low back paradigm. Baillieres Best Pract Res Clin Rheumatol 13:545-554, 1999. Kendall NA, Linton S, Main C: Guide to assess psychosocial yellow flags in acute LBP: risk factors for long-term disability and work loss. Wellington Accident Rehabilitation and Compensation Insurance of New Zealand, 1997, National Health Committee. Koes BW, van Tulder MW, Ostelo R, Kim BA, Waddell G: Clinical guidelines for the management of LBP in primary care: an international comparison. Spine 26: 2504-2513, 2001. Kominski GF, Roby DH, Kincheloe JR: Cost of insuring California’s uninsured. Policy Brief: UCLA Cent Health Policy Res 1-6, 2005. Lidgren L: The bone and joint decade 2000-2010. Bull World Health Org 81(9):629, 2003.
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Lindstrom I, Ohlund C, Eek C, et al: Mobility, strength, and fitness after a graded activity program for patients with subacute LBP: a randomized prospective clinical study with a behavioral therapy approach. Spine 17:641-652, 1992. Linton SJ, Andersson T: Can chronic disability be prevented? A randomized trial of a cognitive-behavior intervention and two forms of information for patients with spinal pain. Spine 25:2825-2831, 2000. Loisel P, Abenhaim L, Durand P, et al: A population-based, randomized clinical trial on back pain management. Spine 22:2911-2918, 1997. Loisel P, Gosselin L, Durand P, et al: Implementation of a participatory ergonomics program in the rehabilitation of workers suffering from subacute back pain. Appl Ergon 32:53-60, 2001. Loisel P, Lemaire J, Poitras S, et al: Cost-benefit and cost-effectiveness analysis of a disability prevention model for back pain management: a six year follow up study. Occup Environ Med 59:807-815, 2002. Main C, Glozier N, Wright I: Validity of the HSE stress tool: an investigation within four organizations by the Corporate Health and Performance Group. Occup Med (Lond) 55:208-214, 2005. Main CJ: Early psychosocial interventions for LBP in primary care. BMJ 331:88, 2005. Malmivaara A, Hakkinen U, Aro T, et al: The treatment of acute LBP—bed rest, exercises, or ordinary activity? N Engl J Med 332:351-355, 1995. McAfee PC, Fedder IL, Saiedy S, Shucosky EM, Cunningham BW: Experimental design of total disk replacement-experience with a prospective randomized study of the SB Charite. Spine 28:S153-S162, 2003. McGuirk B, King W, Govind J, Lowry J, Bogduk N: Safety, efficacy, and cost effectiveness of evidence-based guidelines for the management of acute LBP in primary care. Spine 26:2615-2622, 2001. Nachemson A, Jonsson E: Neck and back pain: the scientific evidence of causes, diagnosis and treatment. Philadelphia, 2000, Lippincott Williams & Wilkins. Nordin M, Skovron ML, Hiebert R, et al: Early predictors of delayed return to work in patients with LBP. J Musculoskel Pain 5:5-27, 1999. Nordin M, Weiser S, Campello MA, Pietrek M: Self care techniques for acute episodes of LBP. Best Pract Res Clin Rheumatol 16:89-104, 2002. Oleske DM, Neelakantan J, Andersson GB, et al: Factors affecting recovery from workrelated, low back disorders in autoworkers. Arch Phys Med Rehabil 85:1362-1364, 2004. Proper KI, Staal BJ, Hildebrandt VH, van der Beek AJ, van Mechelen W: Effectiveness of physical activity programs at worksites with respect to work-related outcomes. Scand J Work Environ Health 28:75-84, 2002. Roberts L, Little P, Chapman J, et al: The back home trial: general practitioner-supported leaflets may change back pain behavior. Spine 27:1821-1828, 2002. 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. Roland M, Morris R: A study of the natural history of low-back pain. Part II. Development of guidelines for trials of treatment in primary care. Spine 8:145-150, 1983. Roland M, Fairbank J: The Roland-Morris Disability Questionnaire and the Oswestry Disability Questionnaire. Spine 25:3115-3124, 2000. Spitzer WO, Leblanc FE, DuPuis M: Scientific approach to the assessment management of activity-related spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 12(7 Suppl):S1-S59, 1987. Staal JB, Hlobil H, Twisk JW, et al: Graded activity for LBP in occupational health care: a randomized, controlled trial. Ann Intern Med 140:77-84, 2004. Staal JB, Hlobil H, van Tulder MW, et al: Return-to-work interventions for LBP: a descriptive review of contents and concepts of working mechanisms. Sports Med 32:251-267, 2002. Staiger TO, Gaster B, Sullivan MD, Deyo RA: Systematic review of antidepressants in the treatment of chronic LBP. 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CHAPTER
4e
Workplace Adaptation for the Low Back Region Shrawan Kumar and Steve Konz
THE NATURE OF LOW BACK PAIN The nature of low back pain (LBP) and even its broad categorization into acute, subacute, and chronic categories defy scientific precision. In many cases, its insidious onset, relief without medical intervention, recurrence despite all precautions, and eventual chronicity have not only perplexed medical practitioners but also posed an intellectual challenge even for a scientific conception of the phenomenon. Although many risk factors have been associated with LBP, its etiology remains obscure. Kumar14 categorized all known risk factors into four broad categories: (1) morphologic, (2) genetic, (3) biomechanical, and (4) psychosocial. He stated that whereas morphologic and genetic factors are hardly manipulable, the biomechanical and psychosocial factors lend themselves to manipulation. It was, however, conceded that all strategies must take into account the genetic and morphologic data for optimal results. Many studies have been conducted to examine the possible impact of different risk factors, but the human back is like a multilink chain that is only as strong as its weakest link. Unfortunately, the weakest link is most elusive, being different in different people and also at different times in the same individual because of varying internal and external circumstances.
CAUSAL MECHANISMS AND CONTROL Humans have evolved over millions of years into what they are today. Evolutionary pressures and consequent speciation resulted in an upright biped creature with dextrous upper limbs and a highly evolved brain. For a large duration of its existence, the species relied on hunting and gathering as its primary means of sustenance.5 With the advancement of science, technology, and industrialization, the physical occupational stresses have changed dramatically in an evolutionary “flash” so that none of the body systems that one uses today was either designed or evolved for the current purpose. As a result, demand for force exertion, activity repetition, or posture assumption for prolonged periods places stress on human physical systems that is inherently unnatural. This is further aggravated by many psychologic stresses emanating from financial or interpersonal factors. In addition, most human occupations have become complex, requiring significant organization and thereby enhancing the chances of errors. As a function of a multivariate complex system (in many cases under multiple partial controllers), significant
chances emerge for unplanned events. These then result in various kinds of accidents with property damage and/or personal injuries. A meaningful attempt to control such injuries makes it imperative to understand them. Most cases compensated by the Workers’ Compensation Board are regional musculoskeletal problems. Workers in different economic sectors generally have injuries characteristic of those sectors. People in forestry, construction, and manufacturing have a higher proportion of back injuries. Those working in office jobs involving keyboarding have cumulative trauma disorders (also called musculoskeletal disorders and repetitive strain injuries). Because heavy physical workers do not develop repetitive strain or injury of the upper extremity and office workers do not injure their backs, the argument can be made that the nature of the physical stress and the region enduring the load largely determine the affected area and probably the nature of injury. If therefore one could delineate the mechanisms of injuries and the quantitative details of the relevant variables, one might develop a more effective intervention. An effective intervention would result in better control of injuries, which clearly has a significant payoff. Thus, the long-term success in controlling these injuries depends on understanding their causality. Because for ethical reasons human beings cannot be subjected to controlled experiments exposing them to risk of injury, Kumar et al16 performed an integrative synthesis of information in the scientific literature to formulate biologically plausible theories as to the mechanisms of injury causality. Through this exercise they proposed four theories of musculoskeletal injury causality described briefly below. 1. The Cumulative Load Theory16: Because biologic tissues are composed of both solid and liquid, their combined mechanical behavior or viscoelasticity is determined largely by the proportion of these components. Biologic tissues therefore deform partially like solids and partially like liquids in a blended manner. Such properties are time dependent: a longer exposure to the same load will produce larger deformation and vice versa. As a result, recovery from deformation takes time also. If the succeeding load does not allow sufficient recovery time, the tissue begins to deform further from its compromised stage. As demonstrated by Kumar13 in an epidemiologic study, repeated loading results in a cumulative effect of reduced threshold to failure. 2. The Differential Fatigue Theory16: Occupational tasks are kinesiologically complex and hardly ever performed in one plane. Asymmetric activities requiring the use of many body parts of the bilaterally symmetric human organism result in differential unequal loads on various muscles, joints, and connective tissue. One task may stress one tissue element to 80% of its capacity, whereas another one is stressed only 10%. Additionally, this distribution is not determined by the tolerance of the tissue concerned. Such diverse distribution of stress results in one muscle becoming more fatigued than others.15,16 This differential fatigue causes loss of coordination resulting in sudden and significant stress concentration that precipitates an injury. 3. The Overexertion Theory16: The basic tenet of this theory is that even a rested and normal tissue can, and probably will, fail when the stress/load exceeds its tolerance time. Although stressed and fatigued tissues cannot withstand stress concentration, it is not necessary for tissues to reach that stage to fail.
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4. The Multivariate Interaction Theory16: Over and above the three previous theories, the variability in the individual threshold indicates also that a precipitation of musculoskeletal injury may be modulated by the interaction of genetic, morphologic, psychosocial, and biomechanical factors. Within each of these categories are many variables that may potentiate an injury. Interaction between the relative weights of the variables and the extent to which these have been stressed in any given individual determines the final outcome. Although these four theories have been presented as distinct, all four are simultaneously operative but to a different degree depending on the circumstances and individuals. As pointed out above, humans have not evolved over the past 250 million years to be industrial workers. Humans will therefore always find themselves in the middle of a conflict between their nature and an industrial requirement. Such a backdrop clearly makes occupational injury prevention not only a daunting and lofty goal but an unachievable objective. Control of injuries to reduce their incidence and severity, however, remains a goal that may be achieved to varying degrees. With this in mind, Kumar12 presented a strategy to quantify the risk based on the discrete physical elements of the task in question.
THE EXTENT OF THE PROBLEM As a medical condition LBP has only one redeeming feature—it is not fatal. In spite of the obscurities associated with its etiology, classification, and treatment, human and economic impacts have been approximately quantifiable. Chapter 4a on the epidemiology of LBP offers a comprehensive picture of the problem; suffice it to say here that it is a large social and economic one. Although it occurs in less developed countries also, the impact of LBP is much more recognized in Western and industrialized countries. To put the extent of the problem in perspective, a brief description follows. Andersson1 stated that national statistics from the European countries reveal 10% to 15% of all sickness absence to be due to back pain, with the number of work days lost per worker increasing steadily. An annual prevalence of 25% to 45% was reported, and chronic back pain was present in 3% to 7% of the adult population. The lifetime prevalence of LBP has been variously reported as between 70% and 80%. In Canada, LBP has steadily constituted approximately 27% of all industrial injuries; these have been reported to cost disproportionately higher amounts than all other injuries. In the United States, the annual prevalence has been reported to be in the 15% to 20% range. Khalil8 reported that on any given day, roughly 75 million Americans have back pain, 6.5 million of whom are in bed. Webster and Snook23 reported the cost of LBP in 1989 incurred by Liberty Mutual, the largest insurer in the United States; it constituted 16% of the claims and accounted for 33% of the total expense. They reported also that the mean cost per case of LBP was $8300 compared with $4100 for all other claims combined, whereas the median cost was $396 ($168 for other claims). In these claim settlements, 34% of the total cost for LBP was medical, whereas 66% was indemnity cost for lost time and wages.23 No matter which way one looks, LBP is prevalent and expensive. Some of the socioeconomic aspects of our society may accentuate
the problem because of the alleged secondary gain. We have been able to reduce neither the incidence nor the severity of LBP; a cure neither exists nor is likely to emerge in the foreseeable future. No difference in long-term outcome between aggressive and conservative treatments has been identified, and we seem unable to control the problem in a significant or meaningful way. LBP is clearly here to stay. It is therefore of utmost importance to focus on workplace adaptations to reduce human suffering and economic cost. Our endeavor to identify these adaptations must try to reduce the magnitude of identified risk factors and the exposure of workers to them, decrease the incidence of LBP in healthy people, and reduce stress in patients who already have the condition. Such adaptations will be helpful in returning workers to work after injury.
DISABILITY CAUSED BY LBP LBP is associated with considerable disability that results in work loss, its most important social and economic consequence despite the influence by many other factors. A direct correlative scale between LBP, disability, and work loss has not been established. A simple clinical and subjective assessment of disability, however, has been claimed to have considerable relevance to quality of life as well as industrial performance. This assessment is focused on loss of function rather than pain. The emphasis is on whether an activity can be performed by an individual or is restricted because of LBP. Implicit in this assumption is that the restriction must have its onset coincident with that of the back pain and must therefore be the functional limitation. The specific criteria used by Waddell et al21 are as follows: 1. Bending and lifting 2. Sitting 3. Standing 4. Walking 5. Traveling 6. Social life 7. Sleep 8. Sex life 9. Dressing/undressing The aforementioned criteria combine postural, strength, metabolic, and everyday living activities that are involved also in occupational activities. LBP and loss of function through disability are results of biomechanical (kinematic and kinetic) perturbation of the human system. These demands are covered in Chapter 4b, but we note here that the functional activities accentuating these demands are divided into two main categories: static load (sitting, holding) and dynamic load (pushing/pulling, carrying, and lifting/ lowering). The concentration must therefore be on those activities that reduce hazards for initial injury and subsequent recurrences.
ADAPTATIONS Static work Spitzer et al20 report the LBP incidence in Quebec, Canada of individuals required to do heavy work but also include sedentary
Chapter 4e
work areas such as “government, wholesale and retail, and finance and insurance.” Magora17 reported on LBP for bank tellers and for those who perform heavy work.
Seated work Problem Because intervertebral disks are avascular, their nutrition depends entirely on diffusion. Intervertebral disks also are viscoelastic. While an individual is sitting, the load on the intervertebral disk is 140% of that imposed by standing. This static load progressively decreases the water content of a disk; an increased load accelerates this process. Loss of water from a disk makes the diffusion process more difficult and results in reduced oxygen tension and lack of nourishment, leading to disk degeneration. Sedentary occupations involve prolonged exposure to static loads, hastening this process and making the disk more vulnerable to injuries. A constant static load also deforms the viscoelastic disk and causes compression creep. Because creep is time dependent, elimination of a load does not immediately restore either the preload disk configuration or the water content. The reduction in water and oxygen is therefore prolonged, interfering with disk metabolism by decreasing the amount of glycosaminoglycans (which have a strong affinity for water) and increasing the content of keratan sulfate (which is amorphous with far less capacity to imbibe water). In the short term, the viscoelastic deformation may lead also to laxity of the ligament and lack of coordination, potentiating injury through biomechanical perturbations. Over the long term, it leads to degenerative and permanent changes that are a hazard to the back. The problem of seated sedentary work worsens considerably when prolonged sitting is combined with whole-body vibration, such as with truck driving. The frequencies of many vehicles are close to the natural frequency (4 to 8 Hz) of the human spine, causing resonance and thus amplification of the motion amplitude. Truck drivers must contend not only with this vibration but also with the static loading of the disk while driving. In addition, often they have periodic acute loading of the back when they load or unload their vehicles.
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stools; both conventional and sit/stand chairs should have backrests. Sit/stand chairs should have a forward tilt of 15-30 degrees and a fabric seat.4 Another technique to encourage movement is job rotation. A chair is the key component of seated work, but because not all seated work is the same, chairs should be matched to specific jobs. Of course, people vary in height and weight, and many of them often sit in the same chair because of multiple shifts, parttime workers sharing a shift, and holiday or vacation replacements. Thus chairs should be easily adjustable in terms of seat pan height, back rest height and forward/back location, and armrest width and height. The seat should be padded with a breathable fabric; avoid plastic and leather. It should not be contoured, because this reduces micropostural changes. A curved front edge (waterfall front) maximizes contact with the underside of the thigh; avoid upholstered beading on the front edge. Normally, the seat should tilt backward 1-5 degrees and permit swiveling. For seat width, the wider the better; for depth, the most common problem is a seat that is too deep. A deep seat forces the sitter forward (losing support of the backrest) or back (with the legs dangling). The ideal backrest is a
