Archives of Physical Medicine and Rehabilitation

Archives of Physical Medicine and Rehabilitation

Volume 88, Issue 3, Supplement 1, Pages,1-99 (March 2007)

1. Masthead • MISCELLANEOUS Page A1

2. Editorial Board • EDITORIAL BOARD Page A2

3. Table of Contents • CONTENTS LIST Pages A3-A4

4. Guest Editors page • MISCELLANEOUS Page A5

5. The Sixth Edition: Self-Directed Physiatric Education Program (SDPEP) 2007 • EDITORIAL Page S1 Keith M. Robinson

6. Instructions for AAPM&R Self-Assessment Examinations • EDITORIAL Page S2

Industrial Medicine and Acute Musculoskeletal Rehabilitation

7. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 1. Diagnostic Testing in Industrial and Acute Musculoskeletal Injuries • ARTICLE Pages S3-S9 Andre Panagos, Aaron W. Sable, Joseph P. Zuhosky, Robert W. Irwin, William J. Sullivan and Patrick M. Foye

8. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 2. Medications for the Treatment of Acute Musculoskeletal Pain • ARTICLE Pages S10-S13 William J. Sullivan, Andre Panagos, Patrick M. Foye, Aaron W. Sable, Robert W. Irwin and Joseph P. Zuhosky

9. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 3. Work-Related Musculoskeletal Conditions: The Role for Physical Therapy, Occupational Therapy, Bracing, and Modalities • ARTICLE Pages S14-S17 Patrick M. Foye, William J. Sullivan, Aaron W. Sable, Andre Panagos, Joseph P. Zuhosky and Robert W. Irwin

10. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 4. Interventional Procedures for Work-Related Cervical Spine Conditions • ARTICLE Pages S18-S21 Robert W. Irwin, Joseph P. Zuhosky, William J. Sullivan, Andre Panagos, Patrick M. Foye and Aaron W. Sable

11. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 5. Interventional Procedures for Work-Related Lumbar Spine Conditions • ARTICLE Pages S22-S28 Robert W. Irwin, Joseph P. Zuhosky, William J. Sullivan, Patrick M. Foye, Aaron W. Sable and Andre Panagos

12. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 6. Upper- and Lower-Limb Injections for Acute Musculoskeletal Injuries and Injured Workers • ARTICLE Pages S29-S33 Patrick M. Foye, William J. Sullivan, Andre Panagos, Joseph P. Zuhosky, Aaron W. Sable and Robert W. Irwin

13. Industrial Medicine and Acute Musculoskeletal Rehabilitation. 7. Acute Industrial Musculoskeletal Injuries in the Aging Workforce • ARTICLE Pages S34-S39 Joseph P. Zuhosky, Robert W. Irwin, Aaron W. Sable, William J. Sullivan, Andre Panagos and Patrick M. Foye

14. 2007 SAE-P: Industrial Medicine and Acute Musculoskeletal Rehabilitation • MISCELLANEOUS Pages S40-S44 Amy H. Phelan, Venu Akuthota, Brian M. Kelly, Virginia S. Nelson and Vivian C. Shih

15. 2007 SAE-P: Industrial Medicine and Acute Musculoskeletal Rehabilitation: Answer Key and Commentary on Preferred Choice • MISCELLANEOUS Pages S45-S48

Spinal Cord Injury Medicine

16. Spinal Cord Injury Medicine. 1. Epidemiology and Classification • ARTICLE Pages S49-S54 Chester H. Ho, Lisa-Ann Wuermser, Michael M. Priebe, Anthony E. Chiodo, William M. Scelza and Steven C. Kirshblum

17. Spinal Cord Injury Medicine. 2. Acute Care Management of Traumatic and Nontraumatic Injury • ARTICLE Pages S55-S61 Lisa-Ann Wuermser, Chester H. Ho, Anthony E. Chiodo, Michael M. Priebe, Steven C. Kirshblum and William M. Scelza

18. Spinal Cord Injury Medicine. 3. Rehabilitation Phase After Acute Spinal Cord Injury • ARTICLE Pages S62-S70 Steven C. Kirshblum, Michael M. Priebe, Chester H. Ho, William M. Scelza, Anthony E. Chiodo and Lisa-Ann Wuermser

19. Spinal Cord Injury Medicine. 4. Community Reintegration After Spinal Cord Injury • ARTICLE Pages S71-S75 William M. Scelza, Steven C. Kirshblum, Lisa-Ann Wuermser, Chester H. Ho, Michael M. Priebe and Anthony E. Chiodo

20. Spinal Cord Injury Medicine. 5. Long-Term Medical Issues and Health Maintenance • ARTICLE Pages S76-S83 Anthony E. Chiodo, William M. Scelza, Steven C. Kirshblum, Lisa-Ann Wuermser, Chester H. Ho and Michael M. Priebe

21. Spinal Cord Injury Medicine. 6. Economic and Societal Issues in Spinal Cord Injury • ARTICLE Pages S84-S88 Michael M. Priebe, Anthony E. Chiodo, William M. Scelza, Steven C. Kirshblum, Lisa-Ann Wuermser and Chester H. Ho

22. 2007 SAE-P: Spinal Cord Injury Medicine • MISCELLANEOUS Pages S89-S92 Amy H. Phelan, Thomas S. Kiser, Theresa J. Lie-Nemeth, Virginia S. Nelson and Jeffrey Rosenbluth

23. 2007 SAE-P: Spinal Cord Injury Medicine Answer Key and Commentary on Preferred Choice • MISCELLANEOUS Pages S93-S95

24. Evaluation Forms and CME Application for Obtaining up to 30 CME Credits • MISCELLANEOUS Pages S97-S99

Copyright � 2007 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine andRehabilitation. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any meansnow or hereafter known, electronic or mechanical, including photocopy, recording, or any information storage and retrievalsystem, without permission in writing from the Publisher. Printed in the United States of America.

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The ideas and opinions expressed in Archives of Physical Medicine and Rehabilitation do not necessarily reflect those of theAmerican Academy of Physical Medicine and Rehabilitation, the American Congress of Rehabilitation Medicine, the Editor, orthe Publisher. Publication of an advertisement or other product mention in Archives of Physical Medicine and Rehabilitationshould not be construed as an endorsement of the product or the manufacturer’s claims. Readers are encouraged to contactthe manufacturer with any questions about the features or limitations of the products mentioned. The American Academy ofPhysical Medicine and Rehabilitation, the American Congress of Rehabilitation Medicine, and the Publisher do not assume anyresponsibility for any injury and/or damage to persons or property arising out of or related to any use of the material containedin this periodical. The reader is advised to check the appropriate medical literature and the product information currentlyprovided by the manufacturer of each drug to be administered to verify the dosage, the method and duration of administration,or contraindications. It is the responsibility of the treating physician or other health care professional, relying on independentexperience and knowledge of the patient, to determine drug dosages and the best treatment for the patient.

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Official Journal of the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

EDITOR-IN-CHIEFJeffrey R. Basford, MD, PhD (Academy)

Rochester, MNACADEMY EDITOR

Leighton Chan, MD, MPHBethesda, MD

Managing EditorMichael A. Vasko, MA

Editorial AssistantLissette Calderon

CONGRESS EDITORAllen W. Heinemann, PhD, ABPP

Chicago, IL

Editorial CoordinatorsCarol J. Manow

Lupe SotoEditorial Administrator

Karen K. ParksEditorial Board

Michael L. Boninger, MD (Academy)Pittsburgh, PA

Bruce Caplan, PhD, ABPP (Congress)Wynnewood, PA

Martin D. Hoffman, MD (Academy)Mather, CA

Kenneth M. Jaffe, MD (Congress)Seattle, WA

David D. Kilmer, MD (Academy)Sacramento, CA

David E. Krebs, DPT, PhD (Congress)Boston, MA

Jay M. Meythaler, MD, JD (Congress)Detroit, MI

Patrick K. Murray, MD (Academy)Cleveland, OH

Mary M. Rodgers, PhD, PT (Congress)Baltimore, MD

Elliot J. Roth, MD (Congress)Chicago, IL

Dale C. Strasser, MD (Academy)Atlanta, GA

Denise G. Tate, PhD, ABPP (Congress)Ann Arbor, MI

Robert A. Werner, MD (Academy)Ann Arbor, MI

Associate BoardJonathan F. Bean, MD, MS (Academy)

Boston, MABrenda J. Brouwer, PhD (Congress)

Kingston, ONJohn Chae, MD (Academy)

Cleveland, OHJohn DeLuca, PhD, ABPP (Congress)

West Orange, NJAlberto Esquenazi, MD (Academy)

Philadelphia, PARobert G. Frank, PhD, ABClinP (Congress)

Gainesville, FLLynn H. Gerber, MD (Academy)

Fairfax, VAHelen Hoenig, MD, MPH, OT (Congress)

Durham, NCMark P. Jensen, PhD (Congress)

Seattle, WA

Mark S. Kaplan, MD (Academy)Boston, MA

Christina M. Marciniak, MD (Academy)Chicago, IL

Julie D. Moreland, MSc (Congress)Hamilton, ON

Michael W. O’Dell, MD (Congress)New York, NY

Jeffrey B. Palmer, MD (Congress)Baltimore, MD

Thomas D. Rizzo Jr, MD (Academy CME Editor)Jacksonville, FL

Joan C. Rogers, PhD, OTR/L (Congress)Pittsburgh, PA

Bruce Shapiro, MD (Academy)Baltimore, MD

Robert W. Teasell, MD, FRCPC (Academy)London, ON

Richard D. Zorowitz, MD (Academy)Baltimore, MD

Editorial Office: Suite 2510, 330 North Wabash Avenue, Chicago, Illinois 60611-7617. Phone: (312) 464-9550. Fax: (312)464-9554. E-mail: [email protected] Internet Home Page: www.archives-pmr.org

Official Journal of the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and RehabilitationMISSION STATEMENT: The mission of the Archives of Physical Medicine and Rehabilitation is to disseminate information, with the ultimategoal of furthering the art and science of the practice of physical medicine and rehabilitation and interdisciplinary rehabilitation, and improvingthe health and welfare of persons with disabilities.

Self-Directed Physiatric Education ProgramStudy Guide and Self-Assessment Exam-Practitioners (SAE-P)

S1 ForewordKeith M. Robinson, MD

S2 Instructions for AAPM&R Self-Assessment Examinations

INDUSTRIAL MEDICINE AND ACUTE MUSCULOSKELETAL REHABILITATION

S3 1. Diagnostic Testing in Industrial and Acute Musculoskeletal InjuriesAndre Panagos, MD, Aaron W. Sable, MD, Joseph P. Zuhosky, MD, Robert W. Irwin, MD, William J. Sullivan, MD,Patrick M. Foye, MD

S10 2. Medications for the Treatment of Acute Musculoskeletal PainWilliam J. Sullivan, MD, Andre Panagos, MD, Patrick M. Foye, MD, Aaron W. Sable, MD, Robert W. Irwin, MD,Joseph P. Zuhosky, MD

S14 3. Work-Related Musculoskeletal Conditions: The Role for Physical Therapy, OccupationalTherapy, Bracing, and Modalities

Patrick M. Foye, MD, William J. Sullivan, MD, Aaron W. Sable, MD, Andre Panagos, MD, Joseph P. Zuhosky, MD,Robert W. Irwin, MD

S18 4. Interventional Procedures for Work-Related Cervical Spine ConditionsRobert W. Irwin, MD, Joseph P. Zuhosky, MD, William J. Sullivan, MD, Andre Panagos, MD, Patrick M. Foye, MD,Aaron W. Sable, MD

S22 5. Interventional Procedures for Work-Related Lumbar Spine ConditionsRobert W. Irwin, MD, Joseph P. Zuhosky, MD, William J. Sullivan, MD, Patrick M. Foye, MD, Aaron W. Sable, MD,Andre Panagos, MD

S29 6. Upper- and Lower-Limb Injections for Acute Musculoskeletal Injuries and Injured WorkersPatrick M. Foye, MD, William J. Sullivan, MD, Andre Panagos, MD, Joseph P. Zuhosky, MD, Aaron W. Sable, MD,Robert W. Irwin, MD

S34 7. Acute Industrial Musculoskeletal Injuries in the Aging WorkforceJoseph P. Zuhosky, MD, Robert W. Irwin, MD, Aaron W. Sable, MD, William J. Sullivan, MD, Andre Panagos, MD,Patrick M. Foye, MD

S40 2007 SAE-P: Industrial Medicine and Acute Musculoskeletal RehabilitationAmy H. Phelan, MD, DVM, Venu Akuthota, MD, Brian M. Kelly, DO, Virginia S. Nelson, MD, MPH, Vivian C. Shih, MD

S45 2007 SAE-P: Industrial Medicine and Acute Musculoskeletal Rehabilitation: Answer Key andCommentary on Preferred Choice

SPINAL CORD INJURY MEDICINE

S49 1. Epidemiology and ClassificationChester H. Ho, MD, Lisa-Ann Wuermser, MD, Michael M. Priebe, MD, Anthony E. Chiodo, MD, William M. Scelza, MD,Steven C. Kirshblum, MD

S55 2. Acute Care Management of Traumatic and Nontraumatic InjuryLisa-Ann Wuermser, MD, Chester H. Ho, MD, Anthony E. Chiodo, MD, Michael M. Priebe, MD, Steven C. Kirshblum, MD,William M. Scelza, MD

Volume 88 No 3, Suppl 1

March 2007

Table of Contents

S62 3. Rehabilitation Phase After Acute Spinal Cord InjurySteven C. Kirshblum, MD, Michael M. Priebe, MD, Chester H. Ho, MD, William M. Scelza, MD, Anthony E. Chiodo, MD,Lisa-Ann Wuermser, MD

S71 4. Community Reintegration After Spinal Cord InjuryWilliam M. Scelza, MD, Steven C. Kirshblum, MD, Lisa-Ann Wuermser, MD, Chester H. Ho, MD, Michael M. Priebe, MD,Anthony E. Chiodo, MD

S76 5. Long-Term Medical Issues and Health MaintenanceAnthony E. Chiodo, MD, William M. Scelza, MD, Steven C. Kirshblum, MD, Lisa-Ann Wuermser, MD, Chester H. Ho, MD,Michael M. Priebe, MD

S84 6. Economic and Societal Issues in Spinal Cord InjuryMichael M. Priebe, MD, Anthony E. Chiodo, MD, William M. Scelza, MD, Steven C. Kirshblum, MD,Lisa-Ann Wuermser, MD, Chester H. Ho, MD

S89 2007 SAE-P: Spinal Cord Injury MedicineAmy H. Phelan, MD, DVM, Thomas S. Kiser, MD, MPH, Theresa J. Lie-Nemeth, MD, Virginia S. Nelson, MD, MPH,Jeffrey Rosenbluth, MD

S93 2007 SAE-P: Spinal Cord Injury Medicine: Answer Key and Commentary on Preferred Choice

S97 Evaluation Forms and CME Application for Obtaining up to 30 CME Credits

The American Academy of Physical Medicine and Rehabilitation is accredited by the Accreditation Councilfor Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The2007 Study Guide and Self-Assessment Examination for Practitioners was planned and produced inaccordance with the ACCME Essentials for developing continuing medical education.

Peer Review Statement

The educational material in this Medical Education issue has been peer reviewed by special expertpanels of the AAPM&R through its Medical Education Committee with editorial supervision by guesteditors. It has not been peer reviewed by the Editorial Board of the Archives of Physical Medicine andRehabilitation. Correspondence commenting on the material in this issue should be directed to theChair of the Academy’s Study Guide Subcommittee.

March 2007, Volume 88, No. 3 Suppl 1

Sponsored byAMERICAN ACADEMY OF PHYSICAL MEDICINE AND REHABILITATION

Volume 88 No 3, Suppl 1

March 2007

Table of Contents (continued)

Medical Education IssueSelf-Directed Physiatric Education Program in Physical Medicine and Rehabilitation

Sponsored by the American Academy of Physical Medicine and Rehabilitation as a supplemental issue of the Archives of PhysicalMedicine and Rehabilitation.

GUEST EDITORSKeith M. Robinson, MD

Philadelphia, PA

Ira G. Rashbaum, MDNew York, NY

STUDY GUIDE FACULTIES

INDUSTRIAL MEDICINE AND ACUTEMUSCULOSKELETAL REHABILITATION

Patrick M. Foye, MD, ChairRobert W. Irwin, MDAndre Panagos, MDAaron W. Sable, MD

William J. Sullivan, MDJoseph P. Zuhosky, MD

Venu Akuthota, MD (SAES Liaison)Brian M. Kelly, DO (SAES Liaison)

Virginia S. Nelson MD, MPH, (SAES Liaison)Amy H. Phelan, MD, DVM (SAES Liaison)

Vivian C. Shih, MD (SAES Liaison)

SPINAL CORD INJURY MEDICINESteven C. Kirshblum, MD, Chair

Anthony E. Chiodo, MDChester H. Ho, MD

Michael M. Priebe, MDWilliam M. Scelza, MD

Lisa-Ann Wuermser, MDThomas S. Kiser, MD, MPH (SAES Liaison)Theresa J. Lie-Nemeth, MD (SAES Liaison)

Virginia S. Nelson MD, MPH, (SAES Liaison)Amy H. Phelan, MD, DVM (SAES Liaison)

Jeffrey Rosenbluth, MD (SAES Liaison)

MEDICAL EDUCATION COMMITTEE (MEC)Steve R. Geiringer, MD, Chair; Karen L. Andrews, MD(MOCS); James W. Atchison, DO (PPS); Diana D. Cardenas,MD (Member-at-Large); Nina E. Choi, MD, MPH (RPC);Bruce H. Hsu, MD (RPC); Michael F. Lupinacci, MD (BoardLiaison); Keith M. Robinson, MD (SGS); Charlotte H. Smith,MD (Member-at-Large); Joseph B. Webster, MD (SAES);Robert A. Werner, MD (Cyber Education); Robert P. Wilder,MD (PASSOR)

MAINTENANCE OF CERTIFICATIONSUBCOMMITTEE (MOCS)

Karen L. Andrews, MD, Chair; Diana D. Cardenas, MD; GaryS. Clark, MD, MMM, CPE; Steve R. Geiringer, MD (MEC);James T. McDeavitt, MD; Keith M. Robinson, MD (SGS)

PROGRAM PLANNING SUBCOMMITTEE (PPS)James W. Atchison, DO, Chair; Venu Akuthota, MD; JeffreyL. Cole, MD; Michael J. DePalma, MD; Elie P. Elovic, MD;Colleen M. Fitzgerald, MD; Michelle S. Gittler, MD; LawrenceJ. Horn, MD; Mary Anne McMahon, MD; Kevin M. Means,MD; Michael J. Meighen, MD; Andre Panagos, MD; SunilSabharwal, MD; Larry H. Chou, MD (PASSOR); SusanneSonik; Jeffrey A. Strakowski, MD; Heikki Uustal, MD;Thomas K. Watanabe, MD; David G. Welch, MD; Carolyn C.Zollar, MA, JD

SELF-ASSESSMENT EXAMINATIONSUBCOMMITTEE (SAES)

Joseph B. Webster, MD, Chair; Venu Akuthota, MD; John E.Begovich, DO; Michelle S. Gittler, MD; Joseph M. Ihm, MD;Brian M. Kelly, DO; Thomas S. Kiser, MD, MPH; Theresa J.Lie-Nemeth, MD; Virginia S. Nelson, MD, MPH; Atul T.Patel, MD; Amy H. Phelan, MD, DVM; Jeffrey Rosenbluth,MD; Vivian C. Shih, MD

STUDY GUIDE SUBCOMMITTEE (SGS)Keith M. Robinson, MD, Chair; Elie P. Elovic, MD; MitchellK. Freedman, DO; Steve R. Geiringer, MD; Stuart J. Glassman,MD; Steven Kirshblum, MD; Patrick M. Foye, MD; Ira G.Rashbaum, MD; William C. Walker, MD

DEPARTMENT OF EDUCATIONStephanie E. Mercado; Beth Arneson; Duane Kinoshita; AllisonPietrzak

2007 STUDY GUIDE SUPPORT STAFFJulie Chan

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he Sixth Edition: Self-Directed Physiatric Education Program
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HE SELF-DIRECTED PHYSIATRIC Education ProgramStudy Guide and Self-Assessment Examination for Practitio-

ers (SAE-P) contained in this supplemental issue of the Archivesre part of the Self-Directed Physiatric Education Program of themerican Academy of Physical Medicine and Rehabilitation

AAPM&R). On matters of physiatric practice, the opinions ex-ressed are those of the individual authors.

THE SIXTH EDITIONThis Medical Education Issue comprises the fifth and sixth

nstallments of the Sixth Edition Study Guide. The Sixth Edi-ion Study Guide continues the process of the previous editionsf presenting information on advances in the rehabilitationciences with particular focus on updated clinical consider-tions. Based on feedback from practicing physiatrists usinghe Study Guide, the faculty committees have expanded theseful text by formulating learning objectives that exemplifyany of the dilemmas faced in clinical physiatric practice. The

uthors have emphasized issues such as aging with disabilitynd functional outcome measures in recognition of the currentealities facing physiatric practitioners. Moreover, it is realizedhe Study Guides may be used as a mechanism to fulfill theifelong-Learning and Self-Assessment component for theaintenance of Certification program of the American Board

f Physical Medicine and Rehabilitation. If used to fulfill thisomponent, several competencies should be able to be metncluding medical knowledge, patient care, interpersonal andommunication skills, practice-based learning and improve-ent, and systems-based practice.Learners will find information on electrodiagnosis, therapeu-

ic modalities, orthotics and prosthetics, and age-related issueshroughout the topics presented in the Sixth Edition of thetudy Guide. The Sixth Edition reflects the scope of practice ofhysical medicine and rehabilitation, while maintaining a pub-ishing cycle that allows the learner to remain current. Theixth Edition will address the following topics:

© 2007 by the American Academy of Physical Medicine and Rehabilitation
0003-9993/07/8803S-1$32.00/0doi:10.1016/j.apmr.2006.12.041
2005 ● Neuromuscular Rehabilitation and Electrodiagnosis● Rehabilitation of Orthopedic and Rheumatologic

Disorders2006 ● Limb Deficiency and Prosthetic Management

● Cardiopulmonary Rehabilitation and CancerRehabilitation

2007 ● Industrial Medicine and Acute MusculoskeletalRehabilitation

● Spinal Cord Injury Medicine2008 ● Congenital and Acquired Brain Injury

● Interventions in Chronic Pain Management2009 ● Rehabilitation of Stroke and Neurodegenerative

Disorders● Sports and Performing Arts Medicine

Acknowledgments: The Study Guide Subcommittee wishes tocknowledge the commitment of the two faculty committees rep-esented in this issue. Chaired by Patrick M. Foye, MD (Industrial

edicine and Acute Musculoskeletal Rehabilitation), and Steven. Kirshblum, MD (Spinal Cord Injury Medicine), the facultyommittees approached this voluntary scholarly endeavor withnthusiasm and dedication to produce the best possible product forheir peers. Thanks also go to Venu Akuthota, MD, Brian M. Kelly,O, Thomas S. Kiser, MD, MPH, Theresa J. Lie-Nemeth, MD,irginia S. Nelson, MD, MPH, Amy H. Phelan, MD, DVM, Jeffreyosenbluth, MD, and Vivian C. Shih, MD, who served as Self-ssessment Examination Subcommittee liaisons and authored theAE-P questions associated with the study guide articles.The Study Guide Subcommittee would like to thank the members

f the AAPM&R Medical Education Committee, chaired by Steve. Geiringer, MD, for their ongoing interest in and support of thisnnual project. Thanks also to Cheryl L. Wilder, ELS, for herontinued editorial guidance.

I would personally like to thank the four other members of thetudy Guide Subcommittee, Stuart J. Glassman, MD, Robert J.aplan, MD, Ira G. Rashbaum, MD, and William C. Walker, MD,

or their hard work and dedication to this process.

Keith M. Robinson, MDChair

Study Guide Subcommittee of the
Medical Education Committee
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n examination component of the 2007 Study Guide enablesou to assess your need for continuing medical educationCME) in the topics presented: the Self-Assessment Exam-nation for Practitioners (SAE-P). An SAE-P with an ac-ompanying answer key for each Study Guide chapter isontained in this issue. Completion of the 2 Study Guideopics earns 30 hours of Category 1 CME credit. Credit maye obtained until March 31, 2010.The AAPM&R has designated each set of Study Guide

rticles and its corresponding SAE-P for a maximum of 15ategory 1 CME credits toward the AMA Physician’s Recog-ition Award. Each physician should claim only those hours ofredit that he/she actually spent in the educational activity.

Please complete the relevant program evaluation(s) andhe CME application enclosed in the back of this issue toeceive credit for these activities. Your participation in thetudy Guides will be documented to the American Board ofhysical Medicine and Rehabilitation (ABPMR). These ac-

ivities are an acceptable form of self-assessment requiredor Maintenance of Certification by the ABPMR. The Studyuide and the Self-Assessment Examination subcommitteeselcome your evaluation of these materials. Each year

© 2007 by the American Academy of Physical Medicine and Rehabilitation

V0003-9993/07/8803S-2$32.00/0doi:10.1016/j.apmr.2006.12.039

rch Phys Med Rehabil Vol 88, Suppl 1, March 2007

embers who have evaluated these materials have contrib-ted to the ongoing improvement of the Self-Directed Physi-tric Education Program.

Thank you for your cooperation and participation.

The AAPM&R Self-Assessment ExaminationSubcommittee

oseph B. Webster, MD, Chair, Professionalism, Practice-Based Learning, and Research

enu Akuthota, MD, Musculoskeletal Rehabilitation andSports Medicine

ohn E. Begovich, DO, Physiatric Therapeuticsichelle S. Gittler, MD, Prosthetics, Orthotics, and Assistive

Devicesoseph M. Ihm, MD, Industrial Rehabilitation and Systems-

Based Practicerian M. Kelly, DO, Neuromuscular Disordershomas S. Kiser, MD, MPH, Brain Disordersheresa J. Lie-Nemeth, MD, Medical Rehabilitationirginia S. Nelson, MD, MPH, Pediatric Rehabilitationtul T. Patel, MD, Electrodiagnosismy H. Phelan, MD, DVM, Physical Medicine and Rehabili-

tation Topicseffrey Rosenbluth, MD, Spinal Cord Disorders
ivian C. Shih, MD, Joint and Connective Tissue Disorders

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ABSTRACT. Panagos A, Sable AW, Zuhosky JP, IrwinW, Sullivan WJ, Foye PM. Industrial medicine and acuteusculoskeletal rehabilitation. 1. Diagnostic testing in in-

ustrial and acute musculoskeletal injuries. Arch Phys Medehabil 2007;88(3 Suppl 1):S3-9.

This self-directed learning module reviews the history andhysical examination of common acute musculoskeletal con-itions that occur in the occupational setting. It is part of thendustrial medicine and acute musculoskeletal rehabilitationtudy guide in the Self-Directed Physiatric Education Programor practitioners and trainees in physical medicine and rehabil-tation. This article presents case vignettes to review the diag-ostic evaluation of heel pain, whiplash, repetitive strain inju-ies, and low back pain.

Overall Article Objective: To understand the importantomponents of a history, physical examination, and conciseiagnostic testing when evaluating acute industrial and muscu-oskeletal injuries.

Key Words: Carpal tunnel syndrome; Cumulative traumaisorders; Low back pain; Rehabilitation; Sacroiliac joint; Te-osynovitis; Whiplash injuries.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Educational Activity: To discuss the diagnostic ap-proach in a 40-year-old home improvement ware-house worker who develops heel pain within severalweeks of starting a job that entails prolonged walkingand standing on concrete floors.

EEL PAIN IS THE MOST common presenting symptomin the foot, and plantar fasciitis is the most common

tiology of that pain.1 The diagnosis can be challenging tolinicians without a familiarity of midfoot and hindfoot anat-my. The midfoot is made up of the navicular, cuboid, and 3uneiform bones, and the hindfoot, or heel, is made up of the

From the Department of Rehabilitation Medicine, Weill Cornell Medical Center,ew York–Presbyterian Hospital, New York, NY (Panagos); St. John’s Macombospital, Warren, MI (Sable); Total Spine Specialists, Department of Physical Med-

cine and Rehabilitation, Carolinas Medical Center, Charlotte, NC (Zuhosky); De-artment of Rehabilitation Medicine, University of Miami, Miller School of Medi-ine, Miami, FL (Irwin); Department of Physical Medicine and Rehabilitation,niversity of Colorado at Denver and Health Sciences Center, Denver, CO (Sullivan);

nd Department of Physical Medicine and Rehabilitation, University of Medicine andentistry of New Jersey: New Jersey Medical School, Newark, NJ (Foye).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Andre Panagos MD, Dept of Rehab Med, Weill Cornelledical Center, New York-Presbyterian Hospital, 525 East 68th St, Box 142, Nework, NY, 10021, e-mail: [email protected]. Reprints are not available from

he author.

p0003-9993/07/8803S-11404$32.00/0doi:10.1016/j.apmr.2006.12.008

alus and calcaneus bones. Major soft-tissue regions include thealcaneal fat pad, the plantar fascia, and the Achilles’ tendonnsertion. The tendons that cross beneath the medial flexoretinaculum include the posterior tibialis, flexor digitorum lon-us (FDL), and flexor hallucis longus (FHL) tendons; theeroneal tendons pass beneath the lateral retinaculum.2

Any alteration of normal foot biomechanics can play a rolen the development of heel pain through increased plantarascia stress. The foot dissipates forces and adapts to a surfacey increasing flexibility through pronation at initial heel strike.ssociated movements include tibial internal rotation, subtalar

oint eversion, ankle dorsiflexion, and foot abduction. As theoot rolls forward to toe-off, it stabilizes itself by supinatinghrough the plantar fascia by means of a windlass mechanism.3

he longitudinal arch is then stabilized as the toe hyperextends.The plantar fascia is composed of fibrous connective

issues that are interwoven into multiple layers to form anponeurosis. This aponeurosis attaches to the 3 main weight-earing structures of the foot: the medial calcaneus and firstnd fifth metatarsal heads, which together form the longitudinalrch.2 It is composed of 3 parts, of which the central portion iseferred to as the plantar fascia.3 Underneath the plantar fascias the insertion of the flexor brevis muscle, where osteophytesan occur.3

Plantar fasciitis most commonly occurs in patients betweenhe ages of 40 and 70 years and in military recruits andunners.3-6 It affects men and women equally, and risk factorsnclude obesity.3,6 The clinical course is generally favorable,ith up to 90% of patients achieving complete resolution withnonsurgical approach within 11 months; the remaining 5%

equire surgery.7

The pain is located in the anteromedial or central part of theeel. It has a rapid onset if there has been a rupture of thelantar fascia; otherwise, it gradually worsens. It is exacerbatedith toe walking, significant changes in activity, or alterations

n footwear.3 The pain tends to be worse in the morning and ontanding after prolonged sitting.2 The history typically includes

recent increase in the amount or intensity of walking orunning. It may also include a change in footwear or annyielding walking or running surface.1 The cause is multifac-orial and poorly understood, but conditions that increase theension on the plantar fascia such as pes cavus, pes planus,ecreased subtalar motion, and a tight Achilles’ tendon mayontribute.2 The repetitive trauma associated with plantar fas-iitis is thought to cause a traction injury resulting in mi-rotears. This chronic situation can result in periostitis of thelantar fascia origin on the calcaneus.3

The physical examination routinely shows limited ankleorsiflexion with maximal tenderness at the anteromedial as-ect of the inferior heel.1 Examination should include assess-ent of the foot during weight bearing and non–weight bear-

ng, with these factors considered: altered arch height, such as
es planus or cavus; passive range of motion of the ankle,

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S4 DIAGNOSTIC TESTING IN INDUSTRIAL AND ACUTE MUSCULOSKELETAL INJURIES, Panagos

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ubtalar, and midfoot joints; and overall postural assessment. Aap noted with palpation of the plantar fascia may indicaterupture.3 The bony prominences and tendinous insertions

hould also be palpated near the heel and midfoot.2 The wind-ass test is positive if there is plantar fascia pain by forced greatoe dorsiflexion.3 Sensation should be evaluated to rule outeurogenic pathology.3

Imaging studies play a limited role. They are used to rule outther causes of heel pain including a calcaneal stress fracture orther bony lesion.1 Plain radiographs, ideally performed ineight bearing, can detect a fracture, dislocation, degenerative

oint disease, foreign bodies, tumors, and soft-tissue calcifica-ions.8 A calcaneal osteophyte (heel spur) is often noted, whichs often of no value in diagnosis or treatment.1 Wolff’s law ofone remodeling would suggest that the osteophyte is a re-ponse to plantar fascia tension rather than a primary etiologyf symptoms. A fluffy periostitis may suggest a spondyloar-hropathy.1 If a calcaneal stress fracture is suspected and plainadiographs are normal, a bone scan is recommended. A linearracture line or diffuse calcaneal uptake is consistent with aalcaneal stress fracture compared with increased activity at thealcaneal plantar fascia insertion site associated with plantarasciitis.1 Avascular necrosis (AVN) is often caused by trauma.

agnetic resonance imaging (MRI) is the most sensitive andpecific radiographic test for AVN, because plain radiographsre initially normal.8 MRI of normal plantar fascia is hypoin-ense on all pulse sequences, because the structure is composedainly of collagen.8 MRI of the foot with plantar fasciitis

hows increased tissue thickness and increased signal intensityn T2 and short tau inversion recovery sequences consistentith edema and structural microtears. There is also increased

ignal in the adjacent subcutaneous tissue and calcaneal inser-ion site.1 Diagnostic ultrasound is useful but uncommonlysed. Under ultrasound, the normal plantar fascia thickness is.4 to 4.3mm, whereas abnormal plantar fascia thickness is 4.3o 8.1mm. There is also a loss of definition at the interfaceetween the plantar fascia and surrounding tissue, as well asalcaneal origin edema.9

The differential diagnosis includes fracture, infection, malig-ancy, or rheumatologic disorders. The calcaneus is the secondost common site of stress fractures in the foot after the meta-

arsals.2 It occurs with excessive or repetitive weight bearingnd is associated with osteoporosis or an increase in occupa-ional or recreational activity.1 It presents with vague pain thats worsened with weight bearing and relieved with rest. Aediolateral calcaneal compression or squeeze may reproduce

ain.1 Plain radiographs may be normal initially, but, overime, show a sclerotic area directed inferiorly in an obliquengle from the superior calcaneous.1 A bone bruise mayresent with similar symptoms but is associated with directrauma without a cortical fracture on plain radiographs or

RI. The bone bruise is believed to be caused by trabecularicrofractures accompanied by hemorrhage, hyperemia, and

dema.10

Heel fat pad atrophy presents with symptoms similar tolantar fasciitis and is commonly found in elderly or obeseatients. The pain and tenderness is located in the central heelith associated atrophy and is more diffuse than with plantar

asciitis. Unlike plantar fasciitis, pain due to heel pad atrophyoes not radiate anteriorly or worsen with great toe dorsiflex-on, and it is not worse in the morning.1,2

Achilles tendinitis develops with overuse or abnormaltresses including jumping or running and may result in Achil-es’ insertion tenderness or swelling. The adult Achilles’ ten-on is approximately 10 to 15cm in length and is formed by the
nion of the gastrocnemius and soleus muscle tendons. U

t inserts on the posterior calcaneus and develops pathologylong a critical zone that is 2 to 6cm proximal to the calcanealnsertion.8 A chronic tendonopathy results in thickening asso-iated with microtears that may rupture with a characteristicop.11

Retrocalcaneal bursitis, also known as a pump bump, isharacterized by Achilles’ tendon insertion site pain. It isaused by abrasion and resulting inflammation of the bursaetween the Achilles’ tendon insertion site and the calcaneusy shoes with a stiff posterior edge.11 It is also associated withsystemic inflammatory arthritis.2 Haglund’s disease, a bony

rotuberance of the calcaneal tuberosity, may also result in aetrocalcaneal bursitis.8 A retroachilles’ bursitis presents withimilar findings but is caused by inflammation between thechilles’ tendon and the skin.2

Medial or lateral heel pain may result from a tendonopathyf the posterior tibialis, FDL, or FHL tendons in the medialompartment or a tendonopathy of the peroneus longus andrevis tendons in the lateral compartment. The peroneus brevisendon ruptures proximally to the insertion site at the base ofhe fifth metatarsal near or just distal to the lateral malleolus. Its associated with swelling and tenderness after recurrent in-ersion ankle sprains.11 A pes planus foot predisposes to aosterior tibial tendon rupture.11

Tarsal tunnel syndrome (TTS) is caused by posterior tibialerve irritation and/or compression as it dives beneath theedial retinaculum behind the medial malleolus.11 The poste-

ior tibial nerve separates into medial and lateral calcanealensory nerves and into the medial and lateral plantar nerves,hich have sensory and motor components. Increased tibialerve tension may be caused by increased forefoot abductionnd hindfoot valgus deviation.2 Nerve compression may beaused by trauma or degenerative bony conditions. It mayresent with numbness, tingling, or burning pain or tendernesslong the path of the nerve that may radiate along the plantarspect of the foot to the toes.1 It is worsened with prolongedeight bearing and ambulation on hard surfaces. A Tinel signay be found at the medial heel. Foot dorsiflexion and eversion

tretches the nerve and can reproduce symptoms.2 Nerve con-uction studies (NCS) for TTS should include the distal tibialotor, medial, and lateral plantar orthodromic sensory nerve

tudies and electromyography of the abductor hallucis longusnd abductor digiti quinti. The NCS results may be comparedith those of the asymptomatic side. Other causes of neuro-enic heel pain include a medial calcaneal neuroma, S1 radic-lopathy, or a neuropathy of the nerve to the abductor digitiuinti.1

.2 Clinical Activity: To review the etiology and diagnos-tic assessment in a Department of Transportationworker who presents with neck pain after a rear-endcollision while stopped at the side of the road.

The cervical spine is composed of 7 vertebrae that permitreater motion compared with the lumbar spine. The termhiplash describes the transfer of energy to the neck through

agittal acceleration–deceleration leading to bony and/or soft-issue injury. It is most commonly associated with rear-endotor vehicle collisions (MVCs). It has been associated with

hronic somatic and psychologic problems.A constellation of symptoms and signs has been named

hiplash-associated disorders. These disorders are associatedith disability, increased health care costs, and decreased in-

ome, social functioning, and overall well-being.12 In 1994, thestimated incidence of whiplash-associated disorders in the
nited States was 3.8 per 1000.13 Many people who are in-

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S5DIAGNOSTIC TESTING IN INDUSTRIAL AND ACUTE MUSCULOSKELETAL INJURIES, Panagos

olved in rear-end collisions do not suffer permanent injury,nd symptoms usually resolve within 4 to 6 weeks. However,p to 33% have chronic symptoms.14 Chronic pain does notepresent persistent acute pain but results from adaptations oferipheral and central pain modulation. Symptoms associatedith whiplash-associated disorder include neck pain and stiff-ess, arm pain, paresthesias, temporal mandibular joint dys-unction, headache, dizziness, visual disturbances, and diffi-ulty with memory and concentration.15

The Quebec Task Force on Whiplash-Associated Disorderseveloped a classification system grading severity from 0 to IVy stratifying patients on anatomic-clinical determinants (table).16 Not surprisingly, increased severity in the acute stageeads to increased risk of whiplash-associated disorders atollow-up.12

Whiplash was first identified in World War I pilots aftermergency ejection, but the prevalence decreased with theevelopment of the shoulder harness and headrest.12 Signifi-ant risk factors for whiplash after MVC include older age,igher acceleration and deceleration forces, seat belt use, pooreadrest positioning, poor car seat energy absorption, andmproper car design and construction.12,17

Cadavers exposed to rear-end collisions show tears in theigamentum flavum, disruption of the annulus of the interver-ebral disk and anterior longitudinal ligament, capsular strains,nd fractures of the zygapophyseal joints.18 These injuriesften do not show up on imaging studies.18 Lord et al19 usedontrolled diagnostic blocks to show zygapophyseal pain gen-rators in 60% of patients with chronic whiplash-associatedisorders.Two causes hypothesized for the cognitive impairment seen

ith these disorders are (1) disruption of the central homeo-tatic regulatory system resulting in neural, hormonal, andehavioral changes in response to stress12 and (2) a coup–ontrecoup traumatic brain injury.14

The center of the automobile headrest should be at ear levelo limit the amount of head and neck flexion and extension atmpact. The more reclined the car seat is during a rear-endollision, the larger the arc that the head and neck travel inelation to the chest.14 From the 1980s to mid-1990s, the properse of seat belts would have been expected to decrease therevalence of whiplash injuries, yet whiplash injuries increasedetween 1989 and 1995 although seat belt use remained sta-le.20

There is no specific historical or physical examination find-ng for the diagnosis of whiplash-associated disorders. Toauge the force of impact it is very important to review theetails, including speed at the time of the collision, possibleead injury with associated loss of consciousness, and condi-ion of the vehicle. Symptoms may be initially mild after theccident but may increase over the following 2 to 3 days.14

lthough the physical examination shows stiffness and de-

Table 1: Classification of W

Grade

0 A patient without subjective complaints or objective siI Neck complaints of pain, stiffness, or tenderness withoII Neck complaints with musculoskeletal signs including

dysfunctionIII Neck complaints with neurologic dysfunction including

sensationIV Patients with neck complaints associated with fracture

reased cervical spine range of motion, neurologic deficits are t

are. The mechanism of injury in combination with the pre-enting symptoms and signs on physical examination allowshe diagnosis of whiplash-associated disorders to be made.maging is useful to rule out bony or soft-tissue injury, includ-ng fractures and injuries to the disk and ligamentous struc-ures. Plain radiographs often show decreased lordosis andossible widening of adjacent soft tissues.14 Flexion and ex-ension films should be ordered to rule out instability. MRI andomputed tomography seldom show structural abnormalitieselated to the injury and are often unnecessary.

.3 Clinical Activity: To advise an executive secretarywho supervises a large secretarial pool about thepathogenesis of job-related wrist and elbow pain.

Work-related musculoskeletal disorders that result from re-etitive motions have had various names, including cumulativerauma disorders and repetitive strain injuries. Repetitiveovements in occupational and avocational settings may result

n these conditions21; however, debate exists concerning thectual existence of these injuries.22 The biomechanic risk fac-ors associated with tissue damage include the extent of tissueamage caused by repetitive or prolonged activities, forcefulxertion, awkward or static postures, vibration, localized me-hanical stress, and cold temperatures.23 Individual risk factorsnclude older age, obesity, diabetes, smoking, pregnancy, rheu-atoid arthritis, and psychologic stress.21 In 2002, there were

6,500 cases of repetitive strain injury reported in the Unitedtates, resulting in a median of 23 days lost from work.24

ausation is often difficult to identify.Repetitive strain injuries are often attributed to musculoten-

inous unit disorders.23 Tendons and ligaments require me-hanical stress to maintain function. When the load exceeds thebility to adapt, injury occurs, with resultant inflammation.his is associated with subsequent healing, scarring, and tissue

emodeling. If the injury is not allowed to heal completely,ontinued high–muscle-effort levels can result in further dis-bility.21 Several theories exist to explain such injuries, includ-ng (1) temporary lengthening of collagenous structures inesponse to prolonged loading,25 (2) intramuscular pressureise with resulting ischemia caused by prolonged loading,26 and3) inconsistent afferent information including visual and pro-rioceptive resulting motor responses.27 Some have termedepetitive strain injuries to be tendonopathy or tendonosis,ecause histopathology has not shown inflammatory media-ors.28

The history should include questions assessing occupationalnd avocational activities that include high repetition rates androlonged abnormal postures. The history may also identifybstacles to recovery such as “catastrophizing,” histrionic be-avior, job monotony, high work demands, and financial reli-nce on disability payments.29 The cardinal complaint is pain at

sh-Associated Disorders16

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hysical signseased range of motion and point tenderness without neurologic

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ess during palpation or resisted motion. Often there is asso-iated swelling and warmth. Evaluation for upper-extremityomplaints begins at the cervical spine and proceeds to theigits; it includes a screen of the unaffected contralateral side.he patient should be assured that there is no evidence thatontinued activity will increase the damage, although workctivities must be modified, with minimal time off from workaken.29 Treatment should include physical and/or occupationalherapy with work modifications.

De Quervain’s disease results in pain of the first dorsalompartment (fig 1) through which pass the tendons of thebductor pollicis longus and extensor pollicis brevis mus-les. Symptoms can also include tenderness and swellingver the radial styloid at the anatomic snuffbox.23 Theinkelstein’s test is accomplished by having the patientlace his/her thumb in the palm and closing the fingersround it, followed by ulnar deviation of the wrist. Increasedain on palpation of the site confirms the clinical diagnosis.ther tendinous disorders at the wrist may present as pain in

he region of the involved tendon reproduced with resistedotion.Carpal tunnel syndrome (CTS) can result in short- and/or

ong-term work absence, so early management and treatmentre essential. Classically, it causes pain, numbness, or tinglingt the thumb, index, and long fingers. It can cause wasting ofhe thenar muscles and significant loss of oppositional functionn advanced cases. It is caused by increased carpal tunnelressure impairing neurovascular flow and causing direct me-ian nerve compression. Repetitive or sustained flexed or ex-ended wrist positions, as well as finger flexion, can increasearpal tunnel pressure, leading to demyelination or Wallerianegeneration over months to years. The history should assessork factors associated with repetitive wrist motions.The Phalen test is accomplished by wrist flexion for about 1inute to reproduce dysesthesias and numbness in the median

erve distribution. The Tinel sign involves tapping over the

ig 1. Wrist extensor compartments (labeled 1 through 6), dorsaliew. Adapted from Jenkins.44(p187) Reprinted with permission.

rist crease to reproduce median nerve dysesthesias. However, t


he sensitivity of these tests is poor.30 Electrodiagnostic studiesave been found to provide a high degree of sensitivity�85%) and specificity (95%) for diagnosing CTS.31 At theeast, a 14-cm median sensory NCS across the wrist should beerformed and compared with a sensory NCS of an adjacenterve in the symptomatic limb followed by an 8-cm medianotor NCS to the abductor pollicis brevis (APB).31 Needle

lectromyography of the APB muscle can determine the sever-ty of the CTS and exclude other conditions. Ultrasound of thearpal tunnel is viewed as a new and promising diagnosticethod.32

.4 Clinical Activity: To formulate a diagnostic plan for aloading dock worker who has lower back pain.

Diagnosis and treatment of low back pain (LBP) in annjured worker can present formidable tasks for cliniciansecause of the interactive anatomic, functional, medical, andsychologic factors. The workers’ compensation system addsn additional layer of complexity, occasionally promoting ad-itional pain behaviors and disability. An early and accurateiagnosis is essential for the patient to return to work safely andffectively.

The peak prevalence of LBP is age 25 to 60 years, yet thege group that results in the highest costs is the 31- to 40-year-ld subgroup.33 LBP is associated with lifting, carrying, mate-ial handling, and lower job performance ratings.33 Accidentalnset has also been found to result in higher total treatmentosts.33

The objective of the history and physical examination is toirect the patient toward diagnostic tests of greatest yield, toormulate the most specific treatment, and to return the patiento the highest functional level. Failure to do this can lead toreatment failure and recurrence. It is important to recognizesychologic factors that may impede recovery yet be unbiasedo that one does not inadvertently attribute a treatment failureo psychologic factors when diagnostic errors may possiblyave occurred.34

The first step in assessing an occupational injury is to deter-ine whether it is indeed work related or is related to an

nderlying illness. This step consists of reviewing the mecha-ism of injury to clarify its association with work. Reviewinghe consistency of the injury report with witnesses may alsoelp complete the sequence of events. Occasionally, an asso-iation with a work injury remains elusive despite diligentnformation gathering. Possible litigation associated with thenjury either in the workplace or after an MVC can alert thehysician to possible counterproductive incentives.34 The phy-ician should not communicate a message of disbelief; other-ise, treatment of the patient may become more difficult.34

Pain localization often can be difficult for patients and phy-icians. Localized point tenderness that is easily identifiablend reproducible denotes localized injury. Dermatomal painatterns caused by nerve lesions are not as easy to localize butollow established distribution patterns. Sclerotomal and myo-omal referral patterns of non–nervous system tissues such asuscles and ligaments are not as well established. They can be

iffuse and overlap with dermatomal patterns. To further un-erstand a patient’s pain experience, additional informationbout intensity, frequency, quality, and aggravating and reliev-ng factors also must be articulated. A family history of spon-yloarthopathies and connective tissue disorders should belarified.

Fractures, infection, and cauda equina syndrome also muste excluded. Cauda equina syndrome can be a serious condi-
ion; therefore, inquiries regarding bowel or bladder function

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ust be made even in the absence of limb nerve root involv-ent.34 A patient with a cancer history must have malignancy

xcluded, especially if his/her pain has persisted longer thanmonth, is not relieved with bedrest, or is associated with

nplanned weight loss. Intravenous drug use, persistent fevers,nd/or night sweats suggest a spinal infection.

Detailed information on past treatments gives the physi-ian a unique view of the patient’s compliance and response.

review of medications, physical modalities, and exerciseegimens, as well as surgical and nonsurgical procedures, pro-ides a clue to previous diagnoses. Detailed inquiry needs to beade about medication names and doses, what nonsurgical

nvasive interventions were performed, and the responses tohese treatments.

The focused physical examination helps to confirm or ex-lude diagnoses suggested by the history. This examinationnvolves inspection, range of motion, flexibility, palpation,eurovascular testing, and performance of provocative maneu-ers.34 Inspection includes assessing for symmetry of thehoulders, iliac crests, and greater trochanteric areas and check-ng for muscle bulk symmetry and tone of the paraspinaluscles, for excessive or reduced kyphosis and lordosis, or forfixed or functional scoliosis. A functional scoliosis is reducedith forward flexion, whereas a fixed scoliosis does not

hange. Lumbar range of motion is checked in the 6 cardinallanes including forward flexion, extension, and right- andeft-side bending and rotation. Forward flexion involves a re-ersal of the normal lumbar lordosis and pelvic rotation. It cane measured with an inclinometer or the modified Schober test,n which a horizontal line is drawn between the posterioruperior iliac spines at approximately the S2 level. At theidline, a perpendicular line is drawn to 5cm below and 10cm

bove. An increase of more than 5cm is normal.34

Lower-limb joints are screened using the Quick test, inhich a patient squats 2 or 3 times and returns to standing. Thisrossly tests the sacrum, hips, knees, and ankles to rule outathology. This should not be performed by pregnant womennd should be used cautiously in elderly patients. Palpation issed to assess side-to-side differences in tenderness and tissueuality in the muscular, osseous, and ligamentous structures.rigger points are noted by their characteristic band-like qual-

ty and palpation-induced twitch response. Myotomal screen-ng should include strength assessments of the hip flexorsL1-3), knee extensors (L2-4), ankle dorsiflexors (L4-5), greatoe extension (L5), and ankle plantarflexors (S1). The anklelantarflexors should provocatively be tested with toe-walkingr 10 toe raises. Sensation should be tested at the knee (L3),edial malleolus (L4), dorsum of the foot (L5), and the lateralalleolus (S1). Muscle stretch reflexes are assessed at the

atella (L4), medial hamstring (L5), and the Achilles’ tendonS1). Because 98% of all lumbar disk herniations occur at the4-5 and L5-S1 levels affecting the L5 and S1 nerve roots, it

s important to screen the strength of the ankle dorsiflexors andreat toe extensors as well as the ankle reflexes and sensationt the medial, dorsal, and lateral foot.35 Peripheral vascularisease should be assessed by checking lower-extremity pulsesnd looking for signs of vascular insufficiency.

Hamstring and gluteus maximus inflexibility can cause aosterior pelvic tilt, decreasing lumbar lordosis, whereas a tightectus femoris and iliopsoas can increase anterior pelvic tilt,hereby increasing lumbar lordosis—both of which may in-rease forces across the lumbar spine.36 The Ely test, whichests for a tight rectus femoris, is accomplished by maximallyexing the knee toward the buttock while the patient is prone.levation of the buttocks constitutes a positive test. In the
homas test, which assesses the iliopsoas muscle, the contralat- p
ral leg is maximally flexed toward the chest while the patients supine. A positive sign is elevation of the nonflexed thigh offhe table. The straight-leg raise (SLR) test assesses hamstringexibility and is also a dural tension sign. A person testsositive if posterior leg pain occurs below the knee with atraight leg raise between 30° and 70° of hip flexion. Sac-oiliac dysfunction is uncovered at greater than 70°. Theositive crossed SLR suggests a large disk protrusion. Theemoral stretch test to assess pathology at the L4 nerve rootnd above is accomplished with the patient in the prone posi-ion by lifting the thigh off the table while flexing the knee to0°. Finally, it is also important to review the condition of theone and soft-tissue structures above and below the lumbarpine. These structures include the thoracic spine, the sacroiliacoint (SIJ), and the pelvic girdle muscles.34

The SIJ has been found to contribute to LBP. Several testsave been characterized, yet none are very sensitive or specif-c.37 The Patrick or FABER test is accomplished by flexing,bducting, and externally rotating the hip while applying pres-ure to the contralateral anterior superior iliac spine. Ipsilateralroin pain is of hip origin, whereas contralateral buttock painften originates from the SIJ.34 The Gaenslen test is performedith the patient supine by flexing the contralateral leg whileropping the ipsilateral leg off the table. A positive response isain in the region of the SIJ of the ipsilateral leg. The Gillet tests performed by palpating the posterior superior iliac spinehile the patient is standing and asking the patient to flex the

psilateral hip to 90°. A positive finding is the failure of theosterior superior iliac spine to descend. The 5 Waddell signsf nonorganic pathology include nonanatomic regional tender-ess, overreaction, nonanatomic regionalization, distractionusing a seated SLR), and stimulation (with axial loading). If 3f the 5 findings are positive, the Waddell signs suggest theeurotic triad of hysteria, depression, and hypochondriasis onhe Minnesota Multiphasic Personality Inventory.38

Diagnostic testing is based on history and physical exami-ation findings. If there are no red flags noted it is often prudento refrain from ordering imaging studies. The dogmatic reli-nce on plain radiographs predates the understanding of lumbarathology, recent surgical observations, and imaging tech-iques; therefore, minimal critical review has been done.39 Theoutine use of plain radiographs has been controversial, be-ause radiographic abnormalities are not necessarily related toymptoms. Criteria have been established for the early use oflain radiographs. They include age greater than 50 years,ignificant trauma, neurologic deficits, unplanned weight lossor longer than 6 months, and assessing for possible ankylosingpondylitis. Plain radiographs should also be considered ifhere is drug or alcohol abuse, a history of carcinoma, cortico-teroid use, fever, lack of improvement with conservative care,itigation, and no improvement after 7 weeks.39,40 They areptimal for checking spinal segment alignment during weightearing in the anteroposterior and lateral views to rule outpondylolisthesis and to assess for hypermobility using flexionnd extension films.39 Although oblique views significantlyncrease the radiation dose, they help assess the posteriorlements for fractures or other lesions. The presence of spon-ylolysis, spondylolisthesis, or posterior element hypertrophyan have a significant influence on the specific exercise pre-cription.

Computed tomography (CT) is an excellent means of assess-ng bony architecture—specifically, foraminal bony narrowingnd lateral recess stenosis. It is most often used to assessractures, especially stress fractures, or disk lesions in patientsho cannot have an MRI scan. CT myelography allows im-
roved visualization of compression by soft tissues or bone.

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he major limitation of CT is radiation exposure, restrictedeld of view, and poor delineation of intrathecal anatomy.41

MRI provides excellent osseous and soft-tissue detail. Diskegeneration is clearly shown through the state of hydration ofhe disk complex. High-intensity zones, which may representn annular tear as well as various stages of a herniated nucleusulposus, are clearly delineated. It is the study of choice toetect sequestered disk fragments and vertebral body endplatehanges,41 to assess for inflammatory processes and neoplasticonditions, and to assess structures in the retroperitoneal space.he addition of gadolinium contrast helps differentiate post-urgical granulation tissue from disk material and increases theensitivity of detecting pathologic fractures, neoplasms, andemyelinating conditions. MRI clearly delineates the zyg-pophyseal joints and eliminates the need for contrast in thevaluation of spinal stenosis. However, abnormal MRI findingsave been noted in asymptomatic people. Boden et al42 notedhat their 20- to 39-year-old subgroup had a 35% prevalence oft least 1 level of degenerative disk disease and that the chancef abnormal findings increased with age. Asymptomatic peoplelder than 60 years had a 36% prevalence of a herniated disknd a 21% prevalence of spinal stenosis in addition to a near00% prevalence of degenerative disk disease. Open MRIs arevailable for obese or claustrophobic patients but may com-romise image quality. Recently developed weight-bearingRIs allow assessment of loaded axial structures to identify

ccult nerve root compression.43

Bone scans assess function and tissue metabolism throughhe emission of absorbed technetium-99m. These scans canetect localized or systemic bony abnormalities caused byisturbances in the normally balanced activity of osteoblastsnd osteoclasts. Single photon emission computed tomographyncreases the sensitivity for bony abnormality detection andermits better lesion localization. This modality is useful forocalizing posterior element fractures or degenerative changesnd also helps identify neoplastic conditions and infections.

Electrodiagnostic studies are the only physiologic test of mus-le and nerve function and are useful in several ways: for differ-ntiating objective weakness from weakness resulting from pain,or ruling out a peripheral neuropathy or neuromuscular diseases,o localize the level of the lesion, to differentiate between neuro-raxic and axonal injuries, and to assist in prognosis.

References*1. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med

2004;350:2159-66.2. Aldridge T. Diagnosing heel pain in adults [published erratum in:

Am Fam Physician 2006;73:776]. Am Fam Physician 2004;70:332-8.

3. Brown C. A review of subcalcaneal heel pain and plantar fasci-itis. Aust Fam Physician 1996;25:875-81;884-5.

4. Sadat-Ali M. Plantar fasciitis/calcaneal spur among securityforces personnel. Mil Med 1998;163:56-7.

5. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospective case-control analysis of2002 running injuries. Br J Sports Med 2002;36:95-101.

6. Lapidus PW, Guidotti FP. Painful heel: report of 323 patientswith 364 painful heels. Clin Orthop Relat Res 1965;Mar-Apr(39):178-86.

7. Davis PF, Severud E, Baxter DE. Painful heel syndrome: resultsof nonoperative treatment. Foot Ankle Int 1994;15:531-5.

8. DiMarcangelo MT, Yu TC. Diagnostic imaging of heel pain andplantar fasciitis. Clin Podiatr Med Surg 1997;14:218-301.

*Key reference.


9. Gibbon WW, Long G. Ultrasound of the plantar aponeurosis(fascia). Skeletal Radiol 1999;28:21-6.

10. Kier R. MR imaging of plantar fasciitis and other causes of heelpain. MRI Clin North Am 1994;2:97-107.

11. McBryde AM, Hoffman JL. Injuries to the foot and ankle inathletes. South Med J 2004;97:738-41.

12. Sterner Y, Gerdle B. Acute and chronic whiplash disorders. Areview. J Rehabil Med 2004;36:193-210.

13. Barnsley L, Lord S, Bogduk N. Whiplash injury. Pain 1994;58:283-307.

14. Silber JS, Hayes VM, Lipetz J, Vaccaro AR. Whiplash: fact orfiction? Am J Orthop 2005;3423-8.

15. Rodriquez AA, Barr KP, Burns SP. Whiplash: pathology, diag-nosis, treatment, and prognosis. Muscle Nerve 2004;29:768-81.

16. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monographof the Quebec Task Force on Whiplash-Associated Disorders:redefining “whiplash” and its management [published erratum in:spine 1995;20:2372]. Spine 1995;20(8 Suppl):1S-73S.

17. Jones JA, Hart SF, Baskin DS, et al. Human and behavioralfactors contributing to spine-based neurological cockpit injuriesin pilots of high-performance aircraft: recommendations formanagement and prevention. Mil Med 2000;165:6-12.

18. Yoganandan N, Cusick JF, Pintar FA, Rao RD. Whiplash injurydetermination with conventional spine imaging and cryomic-rotomy. Spine 2001;26:2443-8.

19. Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chronic cervicalzygapophysial joint pain after whiplash. A placebo-controlledprevalence study. Spine 1996;21:1737-44.

20. Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ. Neck sprainafter motor vehicle accidents in drivers and passengers. EurSpine J 2000;9:547-52.

21. Mackinnon SE, Novak CB. Repetitive strain in the workplace.J Hand Surg [Am] 1997;22:2-18.

22. Hadler NM. Repetitive upper-extremity motions in the work-place are not hazardous. J Hand Surg [Am] 1997;22:19-29.

23. Piligian G, Herbert R, Hearns M, Dropkin J, Landsbergis P,Cherniack M. Evaluation and management of chronic work-related musculoskeletal disorders of the distal upper extremity.Am J Ind Med 2000;37:75-93.

24. US Department of Labor, Bureau of Labor Statistics. Table 3.Number and percent of nonfatal occupational injuries and ill-nesses involving days away from work resulting from repetitivemotion by selected worker and case characteristics, 2002. Avail-able at: http://www.stats.bls.gov/iif/oshwc/osh/case/ostb1258.pdf. Accessed June 12, 2006.

25. Solomonow M, Zhou BH, Baratta RV, Lu Y, Harris M. Biome-chanics of increased exposure to lumbar injury caused by cyclicloading. Part 1. Loss of reflexive muscular stabilization. Spine1999;24:2426-34.

26. McGill SM, Hughson RL, Parks K. Lumbar erector spinae ox-ygenation during prolonged contractions: implications for pro-longed work. Ergonomics 2000:43:486-93.

27. Harris AJ. Cortical origin of pathological pain. Lancet 1999;354:1464-6.

28. Almekinders LC, Temple JD. Etiology, diagnosis, and treatmentof tendonitis: an analysis of the literature. Med Sci Sports Exerc1998;30:1183-90.

29. Helliwell PS, Taylor WJ. Repetitive strain injuries. PostgradMed J 2004;80:438-43.

30. Herbert R, Gerr F, Dropkin J. Clinical evaluation and manage-ment of work-related carpal tunnel syndrome. Am J Ind Med2000;37:62-74.

31. American Association of Electrodiagnostic Medicine, AmericanAcademy of Neurology, and American Academy of Physical
Medicine and Rehabilitation. Practice parameter for electrodiag-
http://www.stats.bls.gov/iif/oshwc/osh/case/ostb1258.pdf

http://www.stats.bls.gov/iif/oshwc/osh/case/ostb1258.pdf

*

*

C

M


nostic studies in carpal tunnel syndrome: summary statement.Muscle Nerve 2002;25:918-22.

32. Keles I, Karagulle Kendi AT, Aydin G, Zog SG, Orkun S.Diagnostic precision of ultrasonography in patients with carpaltunnel syndrome. Am J Phys Med Rehabil 2005;84:443-50.

33. Bigos SJ, Spengler DM, Martin NA, Zeh J, Fisher L, NachemsonA. Back injuries in industry: a retrospective study. III. Employee-related factors. Spine 1986;11:252-6.

34. Nadler S, Stitik T. Occupational low back pain: history andphysical examination. Occup Med 1998;13:61-81.

35. Deyo RA, Rainville J, Kent DL. What can the history andphysical examination tell us about low back pain? JAMA 1992;268:760-5.

36. Esola MA, McClure PW, Fitzgerald GK, Siegler S. Analysis oflumbar spine and hip range of motion during forward bending insubjects with and without history of low back pain. Spine 1996;21:71-8.

37. Dreyfuss P, Michaelson M, Pauza K, McLarty J, Bogduk N. Thevalue of the medical history and physical examination in diag-nosing sacroiliac joint pain. Spine 1996;21:2594-602.

38. Waddell G, McCulloch JA, Kummel E, Venner RM. Nonorganic
physical signs in low-back pain. Spine 1980;5:117-25.
39. Simmons ED, Guyer RD, Graham-Smith A, Herzog R. Radio-graph assessment for patients with low back pain. Spine J 2003;3(3 Suppl):3S-5S.

40. Deyo RA, Diehl AK. Lumbar films in primary care: current useand effects of selective ordering criteria. J Gen Intern Med1986;1:20-5.

41. Herzog RJ, Ghanayem AJ, Guyer RD, Graham-Smith A, Sim-mons ED; NASS. Magnetic resonance imaging: use in patientswith low back pain or radicular pain. Spine J 2003;3(3 Suppl):6S-10S.

42. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Ab-normal magnetic-resonance scans of the lumbar spine in asymp-tomatic subjects. J Bone Joint Surg Am 1990;72:403-8.

43. Saifuddin A, Blease S, Macsweeney E. Axial loaded MRI of thelumbar spine. Clin Radiol 2003;58:661-71.

44. Jenkins DB. Hollinshead’s functional anatomy of the limbs andback. 7th ed. Philadelphia: WB Saunders; 1998.

Suggested Readingole AJ, Herring SA. The low back pain handbook: a guide for the

practicing clinician. 2nd ed. Philadelphia: Hanley & Belfus; 2003.alanga GA, Nadler SF. Musculoskeletal physical examination: an

evidence-based approach. Philadelphia: Elsevier Mosby; 2006.


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ndustrial Medicine and Acute Musculoskeletal Rehabilitation.. Medications for the Treatment of Acute Musculoskeletalainilliam J. Sullivan, MD, Andre Panagos, MD, Patrick M. Foye, MD, Aaron W. Sable, MD,
obert W. Irwin, MD, Joseph P. Zuhosky, MD
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ABSTRACT. Sullivan WJ, Panagos A, Foye PM, SableW, Irwin RW, Zuhosky JP. Industrial medicine and acuteusculoskeletal rehabilitation. 2. Medications for the treatment

f acute musculoskeletal pain. Arch Phys Med Rehabil 2007;8(3 Suppl 1):S10-3.

This self-directed learning module highlights medicationssed in the treatment of acute musculoskeletal pain in theontext of industrial rehabilitation. It is part of the study guiden industrial rehabilitation medicine and acute musculoskeletalehabilitation in the Self-Directed Physiatric Education Pro-ram for practitioners and trainees in physical medicine andehabilitation. This article compares various skeletal muscleelaxants, addresses issues related to nonsteroidal anti-inflam-atory medications, provides an algorithm for acute pain man-

gement in an injured worker, and discusses topical medica-ions for the treatment of pain.

Overall Article Objective: To summarize medication op-ions in the treatment of acute musculoskeletal pain in theetting of injured workers.

Key Words: Administration, topical; Analgesics; Anti-nflammatory agents; Muscle relaxants, central; Rehabilitation.

© 2007 by the American Academy of Physical Medicine andehabilitation

ase Presentation: A 45-year-old Department of Transpor-ation employee was working on a highway project whenhe vehicle she was driving was hit from behind. She expe-ienced neck pain immediately after the collision but hado focal neurologic problems. Since the collision, she hasad some difficulty with neck motions and is experiencing

ncreased pain on the job. Her duties include driving aickup truck loaded with barricades, setting up barricadesnd cones, and working as a flagperson. She was referred toou from her nurse case manager with a diagnosis ofwhiplash.”

From the Department of Physical Medicine and Rehabilitation, University ofolorado at Denver and Health Sciences Center, Denver, CO (Sullivan); Departmentf Rehabilitation Medicine, Weill Cornell Medical Center, New York–Presbyterianospital, New York, NY (Panagos); Department of Physical Medicine and Rehabil-

tation, University of Medicine and Dentistry of New Jersey: New Jersey Medicalchool, Newark, NJ (Foye); St. John’s Macomb Hospital, Warren, MI (Sable);epartment of Rehabilitation Medicine, University of Miami, Miller School ofedicine, Miami, FL (Irwin); and Total Spine Specialists, Department of Physicaledicine and Rehabilitation, Carolinas Medical Center, Charlotte, NC (Zuhosky).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to William J. Sullivan, MD, PO Box 6508, Mailstop F-493,

urora, CO 80045, e-mail: [email protected]. Reprints are not availablerom the author.

c0003-9993/07/8803S-11405$32.00/0doi:10.1016/j.apmr.2006.12.009


.1 Educational Activity: To differentiate the mechanismsof action and side effects of commonly prescribed“muscle relaxants” to consider in treating this work-er’s neck pain.

KELETAL MUSCLE RELAXANTS (SMRs) are oftenprescribed for the treatment of acute musculoskeletal pain.

he term “muscle relaxant” is a misnomer, because mostedications in this class have little or no direct action on the

ontractile mechanisms of striated skeletal muscle. Becauseany of these medications were initially used as treatment for

onspecific back pain typically labeled as a strain, sprain, orechanical back pain, these drugs were considered muscle

elaxants. It is unclear whether these medications actuallyecrease painful muscle spasm or if they exert other effects.1

his finding is in contrast to agents used to decrease spasticityssociated with upper motoneuron lesions. Agents used in thereatment of both neurogenic spasticity and local musclespasm,” such include medications as tizanidine (Zanaflex),aclofen (Lioresal), and diazepam (Valium).1 Antispasmodicgents, which are generally classified as muscle relaxants, areisted in table 1.

These medications have various primary sites of action, andonsequently they differ in their drug actions and side effects.owever, all can cause significant drowsiness. The drug man-facturers warn patients that activities such as driving or op-rating machinery may be impaired while they are taking theseedications. This is an important consideration in the case of

he injured Department of Transportation worker, who must beble to drive and/or function on the job in heavy, high-speedraffic. Also, these drugs are hepatically metabolized and re-ally excreted and must be used cautiously in patients withiver or kidney disease.

Three commonly prescribed agents used as SMRs includeetaxalone, cyclobenzaprine, and carisoprodol. Each SMR has

ifferent mechanisms of action and side-effect profiles, al-hough older studies have not shown any particular SMR toave superior efficacy. Medications that are approved for treat-ent of spasticity and are sometimes used to treat musculo-

keletal pain include baclofen and tizanidine.Metaxalone was initially introduced in 1962. Its exact mech-

nism of action is unknown; it is thought to act by depressingolysynaptic spinal reflexes. Studies2 have shown a low rate ofide effects with no reports of sedation. Double-blind placebotudies2 from the 1960s and 1970s showed positive effects ineducing back pain with no reports in the literature of danger-us side effects or safety concerns.Cyclobenzaprine is structurally similar to tricyclic antide-

ressants (TCAs) and was first studied as an antidepressantith regard to efficacy and safety.2 The exact mechanism of

ction is unknown, but it is presumed to work at the level of therainstem or higher with a generalized sedative effect.2 Studiesave repeatedly shown its superiority over placebo3 and effi-
acy at least comparable to diazepam.2 It is also more effective

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S11MEDICATIONS FOR THE TREATMENT OF ACUTE MUSCULOSKELETAL PAIN, Sullivan

hen used in combination with nonsteroidal anti-inflammatoryrugs (NSAIDs) than are NSAIDs alone.4 Its chemical simi-arity to TCAs explains its main side effects of sedation,ethargy, and other anticholinergic effects. There are case re-orts of adverse reaction of cyclobenzaprine in combinationith alcohol, tramadol, droperidol, and other multiple drug

nteractions.2

Carisoprodol has been in use for decades. Although its exactechanism is not clear, it may be related to its sedative effects.ome studies2 suggest blockage of interneuronal activity in theescending reticular formation and spinal cord. Although car-soprodol has been shown to be more effective than placebo,omparison with other SMRs has not shown any reproducibleifferences. More importantly, there are serious safety con-erns related to its active metabolite, meprobamate, which is achedule IV controlled substance. There are multiple reports2

f abuse and cases of impaired driving associated with cariso-rodol. Interestingly, a questionnaire probing prescribing prac-ices showed that a low percentage of physicians recognizedhe abuse potential and had an understanding of the activeetabolite, despite this being a heavily prescribed drug.2

Baclofen is a chemical analog of �-aminobutyric acid thatcts by inhibiting synaptic transmission in the spinal cord.1 It isainly used in the treatment of neurogenic spasticity with

fficacy similar to diazepam, dantrolene, and tizanidine. Itenerally causes less sedation but may lead to increased weak-ess. Baclofen is not generally used as therapy for acutearavertebral muscle spasm.1

Tizanidine is approved for the treatment of spasticity and islso used to treat pain and “spasm” from musculoskeletalonditions. It is an agonist at �2-adrenergic receptor sites and

Table 1: Antispasmotic Medications

Category Medication (Product) Manufacturer

Antihistamines Orphenadrine (Norflex) 3MCentral nervous system

depressantsChlorzoxazone (Parafon, Forte

DSC; Paraflex) Ortho-McNeilMetaxalone (Skelaxin) KingMethacarbamol (Robaxin) SchwarzCarisoprodol (Soma) Wallace

Central alpha2-adrenergicagonists

Tizanidine (Zanaflex) Elan

Tricyclic antidepressantagents

Cyclobenzaprine (Flexeril) McNeil

�-aminobutyric acid agonists Diazepam (Valium) RocheBaclofen (Lioresal) NovartisOther benzodiazepines

Table 2: Recent

Medication (trade name)

Ketorolac (Toradol) SyntexDiclofenac potassium (Cataflam) NovartisBromfenac (Duract) Wyeth-ACelecoxib (Celebrex) SearleRefecoxib (Vioxx) MerckMeloxicam (Mobic) BoehrinValdecoxib (Bextra) Searle

OTE. Data from Ridgway.14

resumably reduces spasticity by increased presynaptic inhibi-ion of motoneurons.1 Several studies1 have shown its efficacyor patients with musculoskeletal back pain with side effectsimilar to those of other SMRs and drowsiness as the primaryeason for discontinuing the medication. There is a case report1

f hypotension when used in combination with an antihyper-ensive medication, possibly due to its chemical similarity tolonidine.

In the case of the highway worker with presumed “musclepasm” and pain, the choice of SMR for pain relief is impor-ant. Side effects and abuse potential should be consideredefore prescribing this class of medication. Shorter duration ofreatment is generally recommended to limit potential of sideffects and/or abuse.1,2

.2 Educational Activity: To discuss the use of NSAIDs inthe treatment of neck pain in this highway worker.

NSAIDs are commonly prescribed medications. Since 1991,new NSAIDs have entered the U.S. market. These are listed

n table 2.Drug manufacturers are required to show analgesic efficacy

or each of the agents. The models most commonly used tobtain approval from the U.S. Food and Drug AdministrationFDA) are dental pain, postsurgical pain, dysmenorrheal, andostpartum cramps. Although some of these agents have FDApproval for the treatment of rheumatoid arthritis and osteoar-hritis, some are also approved for the treatment of acute pain.ote that several of these medications have been pulled from

he market because of the postmarketing identification of sideffects. Bromfenac was withdrawn because of liver toxicity.ofecoxib and valdecoxib were withdrawn because of cardio-ascular events. The FDA also recommended stronger warn-ngs for all NSAIDs because of gastrointestinal (GI) toxicitynd increased risk of cardiovascular events. This recommen-ation included conventional NSAIDs, because little informa-ion existed regarding their cardiovascular risks.5,6

Although there is no evidence to suggest superior efficacy ofne NSAID over another, individual patients may respondifferently to different medications. Conventional NSAIDs acty inhibiting cyclooxygenase (COX)–2 and the pathologicesponses to pain and inflammation. In the GI tract, they alsonhibit COX-1 activity, decrease prostaglandins, and increasehe risk of GI side effects such as life-threatening bleeding.onventional NSAIDs show dose-dependent side effects,hich may limit their use in elderly people or other patients atigh risk. Additional side effects include renal dysfunction andlatelet inhibition. The COX-2–specific agents (celecoxib)ave a decreased incidence of GI toxicity,7 but increased costsnd cardiovascular risks may limit their utility in the elderlynd in those with cardiovascular risk factors. COX-2–selectivegents (etodolac, meloxicam) have a decreased risk of clini-

proved NSAIDs

ufacturer Year FDA Approved

19911993

t 1997 (withdrawn 1998)1998

1999 (withdrawn 2004)gleheim/Abbott 2000

2001 (withdrawn 2005)

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S12 MEDICATIONS FOR THE TREATMENT OF ACUTE MUSCULOSKELETAL PAIN, Sullivan

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ally significant GI side effects compared with otherSAIDs.8,9 Etodolac has increased COX-2 selectivity com-ared with celecoxib and meloxicam, but the cardiovascularisks are unknown. Whether a patient is on a COX-2–selectiver –specific agent, those agents’ GI protectivity may be com-romised by concomitant use of even low-dose aspirin, andenal side effects are not decreased.10

A medication recently approved by the FDA for the treat-ent of osteoarthritis is flavocoxid (Limbrel). This product is a

lend of natural ingredients from phytochemical food sourceaterials. It is presumed to have action on COX and lipoxy-

enase pathways, limiting prostaglandins and leukotrienes. It isot a COX-2–specific or –selective agent, and its ingredientsre generally regarded as safe according to the FDA. To ournowledge, there is no literature available at the time of thisriting to suggest efficacy in the treatment of acute musculo-

keletal pain.

.3 Educational Activity: To outline a treatment algo-rithm for the medication management of acute pain ina 40-year-old home improvement warehouse storeworker who fell off a ladder, injuring his foot andankle.

Physicians most often recommend or prescribe oral medica-ions for the treatment of acute musculoskeletal pain. Acuteain generally does not require long-term use of analgesics.uch of the literature on oral analgesics defines the efficacy ofspecific medication as the proportion of patients who need to

ake that particular drug to experience a least a 50% reductionn pain when compared with placebo. The number needed toreat (NNT) is a concept that refers to the number of patientsho have to use the treatment for 1 patient to have a benefit. A

ower NNT is better. Other measures of pain relief include aisual analog scale, with a meaningful analgesia effect of3mm on a 100-mm scale.11

Acetaminophen is a unique medication without a clearlyefined mechanism of action related to analgesia. It has little oro anti-inflammatory effects. It also has an excellent safetyrofile with the exception of liver toxicity at doses exceeding000mg daily. An increased GI ulceration risk is not supportedy the current literature. Direct comparison studies betweencetaminophen (1000-mg dose) and NSAIDs show equivalentnalgesia in some settings (orthopedic surgery, tension head-che) and NSAID superiority in others (dental and menstrualain).11 Acetaminophen remains a good initial choice for mostild to moderate acute pain, with equivalent analgesia to

spirin but a better safety profile.NSAIDs remain excellent analgesics for the treatment of

cute pain. As noted above, some study models have shownSAIDs’ superiority to acetaminophen and equality to narcot-

cs for certain types of pain. Whether this means they areuperior for acute pain treatment in all people, such as theatient discussed, has yet to be proven. It is often the dose-ependent side effects that limit their usefulness. Epidemio-ogic studies support the use of ibuprofen at 400mg per dosehen first choosing NSAIDs.11 At 800 to 1200mg a day,

buprofen has an excellent safety profile that is not significantlyifferent from placebo. Higher doses are used for anti-inflam-atory effects and may provide better analgesia, but they are

ssociated with increased risk of side effects.11 Histamine2lockers, proton pump inhibitors, and misoprostol have beenhown to reduce the risk of duodenal ulcers with daily NSAIDse, but only misoprostol has been shown to reduce the risk ofI perforation and bleeding.11 However, because the NNT is

elatively high (264 patients), it is likely that misoprostol


ould only be necessary in high-risk patients.11 A meta-anal-sis of the COX-2 inhibitor celecoxib showed fair to goodfficacy for postsurgical pain but overall inconsistent evidenceo warrant its routine use in those without a history of GIleeding.11

Opioids are potent and appropriate analgesics for acute mod-rate to severe pain, although their use in chronic nonmalignantain conditions does not have universal consensus. There is noubstantial evidence to support the claim that any particularpioid has greater efficacy or fewer side effects than equipotentoses of morphine. The usual treatment of acute pain is withodeine, propoxyphene, hydrocodone, and oxycodone. Studiesave indicated that combination therapy with acetaminophen orbuprofen is highly effective for treatment of acute pain.11

odeine is a prodrug that depends on cytochrome P450 me-abolism to convert to morphine for its analgesic effect. Up to0% of the white population lacks this enzyme, and this mayxplain its poor efficacy in meta-analyses addressing acuteostsurgical and dental pain. Propoxyphene provides little ad-itional analgesia to acetaminophen alone and is associatedith significant adverse side effects.11 For this reason, it cannote recommended for routine use for the treatment of acute painuch as for the patient discussed.

Tramadol (Ultram) is a synthetic analog of codeine. It is aentral analgesic with a low affinity for opioid receptors; how-ver, its primary metabolite shows a higher affinity for opioideceptors than the parent drug. Moreover, the analgesic actionf tramadol is only partially inhibited by the opioid antagonistaloxone, which suggests the existence of another mechanismf action. This hypothesis was confirmed by the discovery ofonoaminergic activity that inhibits norepinephrine and sero-

onin reuptake, contributing to the analgesic action. Tramadolhould not be administered to patients receiving monoaminexidase inhibitors, and cotreatment with TCAs and selectiveerotonin reuptake inhibitors should be undertaken with cau-ion to avoid serotonin syndrome and increased risk of seizure.ramadol has pharmacologic properties that may make it less

ikely to lead to dependence. It may be of value in treating painonditions where treatment with stronger opioids is not re-uired. Others11 report side effects and a lack of efficacy, bothf which limit its usefulness. Additional preparations are25mg of acetaminophen with 37.5mg of tramadol (Ultracet)nd an extended-release preparation (Ultram ER).

Options for the treatment of acute ankle pain after a fall offladder thus can be summarized as shown in table 3.

.4 Educational Activity: To identify the rationale for theuse of topical analgesics in the treatment of lateralepicondylitis in a 50-year-old secretary.

Alternative delivery systems such as topical preparationsave been developed to try to minimize the adverse effects of

Table 3: Treatment Options for Acute Ankle Pain

Treatment Comment

Acetaminophen 1000mg up to 4 times dailyAcetaminophen plus

NSAIDIbuprofen 400mg every 4–6h

Combinationtherapy

Opioid or tramadol with acetaminophenand/or ibuprofen

Prescription NSAID For anti-inflammatory effects as neededGI protectant As needed for higher-risk patientsCOX-2 NSAID Reserved for elderly or high-risk

patients

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S13MEDICATIONS FOR THE TREATMENT OF ACUTE MUSCULOSKELETAL PAIN, Sullivan

SAIDs. When NSAIDs are applied topically, there is a highoncentration in the dermis and muscle levels at least equiva-ent to systemic administration. There is penetration into syno-ial fluid, but it is unclear if this is facilitated by systemicirculation. Several studies12 have addressed the efficacy ofopical analgesics, including a study on musculoskeletal andoft-tissue injuries. Each study reported efficacy of topicalSAIDs, whether it was by gel, spray, or patch. Most drug

eactions were local cutaneous reactions. GI effects were lessommon but were found to be more likely to occur in thoseho had GI side effects from oral NSAIDs.Topical opioid administration has recently been used for the

ocal treatment of painful ulcers and skin lesions. Factorsetermining bioavailability after application and the potentialor cutaneous side effects associated with histamine releaseeed to be evaluated.12 To our knowledge, there are no studiesddressing the use of topical opioids for acute musculoskeletalain. Delivery systems that minimize systemic uptake wouldlso be beneficial to minimize central nervous system sideffects.

Capsaicin—a natural constituent in red chili peppers—maynduce analgesia via desensitization from substance P andalcitonin gene–related peptide release. Capsaicin has beenound to activate a family of thermosensitive vanilloid recep-ors. Several studies have reported benefit in postherpetic neu-algia, postmastectomy pain, trigeminal neuralgia, clustereadache, osteoarthritis, and other conditions. Whereas painelief is widely observed, the degree is often modest, andapsaicin is usually reserved for use as an adjunct treatment.urther, side effects, such as burning pain in the initial treat-ent period, are often difficult for patients to tolerate; such

ain has been reported in clinical studies as a common reasonor patient drop-out.12 Compliance may also be an issue be-ause of the delay between onset of treatment and observationf therapeutic benefit. For acute musculoskeletal pain, capsa-cin likely is not a good treatment option.

Topical formulations of local anesthetics such as the 5%idocaine patch (Lidoderm) may be an effective alternative toystemic treatment, but most studies have focused on chronicain conditions. Studies12 on postherpetic neuralgia showedfficacy for treatment of pain with no systemic side effects.lthough the use of the 5% lidocaine patch in professional

thletes with soft-tissue pain has been reported,13 there is aaucity of published evidence regarding its use in the treatmentf acute musculoskeletal pain.Multiple other classes of medication have been developed,

ncluding topical doxepin, glutamate receptor antagonists,-adrenergic agonists, adenosine, cannabinoids, neostigmine

cholinesterase inhibitor), and gabapentin. These have beentudied in animal models and various chronic pain models12 but
ave not gained acceptance in the treatment of acute pain.
References1. Reeves RR, Algood TL, Wise PM. Skeletal muscle relaxants and

associated medications for nonspecific acute back pain. P&T2005;30:518-24.

*2. Harden RN, Argoff C. A review of three commonly prescribedskeletal muscle relaxants. J Back Musculoskeletal Rehabil 2000;15:63-6.

3. Browning R, Jackson JL, O’Malley PG. Cyclobenzaprine andback pain: a meta-analysis. Arch Int Med 2001;161:1613-20.

4. Borenstein DG, Lacks S, Wiesel SW. Cyclobenzaprine andnaproxen versus naproxen alone in the treatment of acute lowback pain and muscle spasm. Clin Ther 1990;12:125-31.

5. Kuehn BM. FDA panel: keep COX-2 drugs on market: black boxfor COX-2 labels, caution urged for all NSAIDs. JAMA 2005;293:1571-2.

6. US Food and Drug Administration. COX-2 selective (includes Bex-tra, Celebrex, and Vioxx) and non-selective non-steroidal anti-inflammatory drugs (NSAIDs). Available at: http://www.fda.gov/cder/drug/infopage/COX2/default.htm. Accessed June 12, 2006.

7. Oviedo JA, Wolfe MM. Gastroprotection by coxibs: what do theCelecoxib Long-Term Arthritis Safety Study and the VioxxGastrointestinal Outcomes Research Trial tell us? Rheum DisClin N Am 2003;29:769-88.

8. Hawkey C, Kahan A, Steinbruck K, et al. Gastrointestinal toler-ability of meloxicam compared to diclofenac in osteoarthritispatients. International MELISSA Study Group. MeloxicamLarge-scale International Study Safety Assessment [publishederratum in: Br J Rheumatol 1998;37:1142]. Br J Rheumatol1998;37:937-45.

9. Weideman RA, Kelly KC, Kazi S, et al. Risks of clinicallysignificant upper gastrointestinal events with etodolac andnaproxen: a historical cohort analysis. Gastroenterology 2004;127:1322-8.

10. Micklewright R, Lane S, Linley W, McQuade C, Thompson F,Maskrey N. Review article: NSAIDs, gastroprotections and cy-clo-oxygenase-II-selective inhibitors. Aliment Pharmacol Ther2003;17:321-32.

11. Sachs CJ. Oral analgesics for acute nonspecific pain. Am FamPhysician 2005;71:913-8.

12. Sawynok J. Topical and peripherally acting analgesics. Pharma-col Rev 2003;55:1-20.

13. Benoist JL, Gammaitoni AR. The 5% lidocaine patch reducespain intensity in professional athletes with sports injury painwithout significant systemic effects or cognitive and perfor-mance impairment [abstract]. Arch Phys Med Rehabil 2005;86:E34.

14. Ridgway D. Analgesics for acute pain: meeting the United StatesFood and Drug Administration’s requirements for proof of effi-cacy. Clin J Pain 2004;20:123-32.

*Key reference.


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ndustrial Medicine and Acute Musculoskeletalehabilitation. 3. Work-Related Musculoskeletal Conditions:he Role for Physical Therapy, Occupational Therapy,racing, and Modalities

atrick M. Foye, MD, William J. Sullivan, MD, Aaron W. Sable, MD, Andre Panagos, MD,
oseph P. Zuhosky, MD, Robert W. Irwin, MD
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ABSTRACT. Foye PM, Sullivan WJ, Sable AW, Panagos, Zuhosky JP, Irwin RW. Industrial medicine and acuteusculoskeletal rehabilitation. 3. Work-related musculoskele-

al conditions: the role for physical therapy, occupational ther-py, bracing, and modalities. Arch Phys Med Rehabil 2007;8(3 Suppl 1):S14-7.

This chapter focuses on the use of modalities, therapeuticxercise, and orthotic devices in the treatment of lateralpicondylitis, carpal tunnel syndrome, plantar fasciitis, neckain and low back pain. It is part of the study guide onndustrial rehabilitation medicine and acute musculoskeletalehabilitation in the Self-Directed Physiatric Education Pro-ram for practitioners and trainees in physical medicine andehabilitation.

Overall Article Objective: To review the medical literaturehat may help clinicians make treatment decisions regardingodalities, therapeutic exercise, and orthotic devices for treat-

ng common work-related conditions in the upper and lowerimbs.

Key Words: Carpal tunnel syndrome; Exercise therapy;ow back pain; Orthotic devices; Physical therapy techniques;ehabilitation; Tennis elbow.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Clinical Activity: To assess the efficacy of modalitiesand splinting to guide treatment of a 40-year-oldhome improvement warehouse worker with plantarheel pain.

2003 COCHRANE REVIEW1 examined the effectivenessof various treatments for plantar heel pain. Nineteen ran-

omized trials involving 1626 participants met the inclusionriteria for analysis. Trial quality was generally consideredoor and data from the various studies could not be pooled. All

From the Department of Physical Medicine and Rehabilitation, University ofedicine and Dentistry of New Jersey: New Jersey Medical School, Newark, NJ

Foye); Department of Physical Medicine and Rehabilitation, University of Coloradot Denver and Health Sciences Center, Denver, CO (Sullivan); St. John’s Macombospital, Warren, MI (Sable); Department of Rehabilitation Medicine, Weill Cornelledical Center, New York–Presbyterian Hospital, New York, NY (Panagos); Total

pine Specialists, Department of Physical Medicine and Rehabilitation, Carolinasedical Center, Charlotte, NC (Zuhosky); and Department of Rehabilitation Medi-

ine, University of Miami, Miller School of Medicine, Miami, FL (Irwin).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Patrick M. Foye, MD, Dept of PM&R, UMDNJ: New Jerseyedical School, 90 Bergen St., DOC-3100, Newark, NJ 07103, e-mail:

[email protected]. Reprints are not available from the author.

a0003-9993/07/8803S-11406$32.00/0doi:10.1016/j.apmr.2006.12.010


rials measured heel pain as the primary outcome. The review-rs found limited evidence that stretching exercises and heelads are associated with better outcomes than custom maderthoses in people who stand for more than 8 hours a day.here was some evidence that orthotic devices were not asffective as corticosteroid injections. Evidence for topical cor-icosteroids administered by iontophoresis was limited. Basedpon conflicting evidence for low energy extra corporeal shockave therapy (ECSWT) in reducing pain in the short term (6

nd 12wk), its effectiveness remains equivocal. No evidenceas found supporting the effectiveness of therapeutic ultra-

ound, low-intensity laser therapy, or insoles with magneticoil. In people with chronic (�6mo) plantar heel pain, thereas limited evidence that dorsiflexion night splints reduceain. Overall, the reviewers concluded that further researchtudies (eg, well-designed, randomized trials) are needed.

Since the 2003 Cochrane review, a more-recent, prospective,andomized study2 evaluated the effectiveness of 2 differentypes of stretching programs in 101 patients with chroniclantar fasciitis (at least 10mo). Researchers compared a pro-ram of non-weight-bearing stretching exercises specific to thelantar fascia versus a standard program of weight-bearingtretching exercises for the Achilles’ tendon. They concludedhat stretching the plantar fascia under non-weight-bearingonditions provides significantly better outcomes in terms ofain relief, activity limitations, and patient satisfaction. Theuthors also provided all patients with prefabricated soft in-oles and 3 weeks of nonsteroidal anti-inflammatory drugsNSAIDs), and concluded that these treatments (especiallyhen combined with non-weight-bearing stretching of thelantar fascia) can be very helpful nonsurgical treatments foratients with chronic, disabling plantar heel pain.2

.2 Clinical Activity: To evaluate the use of soft cervicalorthoses (“collars”) and modalities for a state Depart-ment of Transportation employee with neck pain fol-lowing a rear-end automobile collision.

Frequently, soft cervical orthoses are prescribed to patientsith whiplash, although recent studies question this approach.rawford et al3 prospectively studied 108 consecutive patientsith soft tissue cervical injuries from automobile collisions.atients were randomized to either early mobilization using anxercise regime or 3 weeks in a soft cervical orthosis followedy the same exercise regime. Results found no differencesetween the 2 groups for improvements in pain, range ofovement, or activities of daily living at any of the follow up

ntervals (3, 12, and 52wk). Patients treated with a collar tookignificantly longer to return to work after injury than thosereated with early mobilization (34d vs 17d, P�.05). Overall,reatment with a soft cervical orthosis had no obvious benefit
nd was adversely associated with prolonged time out of

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ork.3 Similarly, Gennis et al4 found that collars do not influ-nce the duration or degree of persistent pain.

In 2001, the Philadelphia Panel for Evidence Based Clinicalractice Guidelines on Selected Rehabilitation Interventionsor Neck Pain5 analyzed randomized controlled trials (RCTs)nd observational studies, regarding treatments for neck pain.he panel used methods defined by the Cochrane Collabora-

ion, using a systematic approach to literature search, studyelection, data extraction, and data synthesis. The panel con-luded that for patients with neck pain, therapeutic exercisesncluding both proprioceptive and traditional therapeutic exer-ises were the only intervention with clinically important ben-fits. Benefits included pain relief, functional improvement,nd improved patient global assessment compared with con-rols. There was a lack of evidence regarding whether tonclude or exclude the use of thermotherapy, massage, electro-

yographic biofeedback, mechanical cervical traction, ultra-ound, electric stimulation, and combined rehabilitation inter-entions for acute and chronic neck pain.5

.3 Clinical Activity: To review the use of counterforcebracing (forearm straps), modalities, and exercise inthe case of a secretary with lateral epicondylitis.

Counterforce bracing is frequently prescribed for patientsith lateral epicondylitis. The brace is a nonelastic strap that is

urved for better fit and support of the conical shape of theorearm. The orthosis decreases intrinsic muscular forces onensitive or vulnerable areas such as the wrist extensor originst the lateral epicondyle. Nirschl6 demonstrated improvementn wrist extension and grip strength with counterforce bracing.owever, some other investigators have not found benefit from

t. Wuori et al7 compared 50 patients who used 2 commerciallyvailable braces versus a placebo strap; that investigation foundo significant difference in pain-free grip.A nationwide occupational medicine network that cares for

pproximately 7% of U.S. workers’ compensation patientsecently retrospectively studied the efficacy of splinting forpicondylitis. Among 4000 patients, those given splints hadigher rates of limited-duty work, more medical visits, higherharges, and longer treatment durations than patients treatedithout splints. Logistic regression was used to minimize the

onfounding variable of whether more severe cases were moreikely to have been splinted. Other limitations of this studyncluded no standardization of the splinted site (forearm vsrist), type of splinting used, or site of epicondylitis (medial vs

ateral).8

Svernlov and Adolfson9 studied 38 patients with lateralpicondylitis who were randomly allocated to 2 treatmentroups: a contract-relax stretching program and an isotonicccentric exercise program. Reduced pain and increased griptrength were seen more frequently in the eccentric exerciseroup (71%), than in the stretching group (39%) (P�.09). Theccentric training regimen seemed more effective at reducingymptoms in a majority of the patients, regardless of symptomuration, and was superior to conventional stretching.9

In a systematic review and meta-analysis Bisset et al10

xamined 76 RCTs on physical modalities for lateral epicon-ylalgia. They found a lack of evidence for long-term benefit ofhysical interventions in general. Evidence suggested that EC-WT is not beneficial. Meanwhile, a Cochrane review ofCSWT included 2 trials that yielded conflicting results.11

Haahr and Andersen12 studied a cohort of 266 consecutiveew lateral epicondylitis cases and found that after 1 year, 83%f cases showed overall improvement. Poor overall improve-
ent was associated with employment in manual jobs, high f
evel of physical strain at work, and a high level of baselineain. Other studies13,14 had similar findings of poor prognosismong patients who reported neuropathic symptoms, key-oarding, or highly repetitive monotonous work. These find-ngs may imply that physiatrists should place a greater focus onorkplace modifications in order to reduce physical demandsuring recovery from lateral epicondylitis.

.4 Clinical Activity: To review the use of bracing, mo-dalities, and exercise in an assembly-line worker whohas carpal tunnel syndrome.

A Cochrane review15 of nonsurgical interventions for carpalunnel syndrome (CTS) found moderate evidence for short-erm benefit from oral steroids; limited evidence for short-termenefit from splinting, ultrasound, yoga, and carpal bone mo-ilization; and no clear evidence for other nonsurgical treat-ents. Among these, oral steroids are a simple, inexpensive

reatment, but side effects may be a concern.Werner et al16 found that autoworkers with symptoms con-

istent with CTS benefited from a 6-week nocturnal splintingrial and the benefits were still evident at the 1-year follow-up.he splinted group’s hand discomfort improved regardless ofegree of median nerve impairment, whereas the controlshowed improvement only among subjects with normal medianerve function. Results suggest that a short course of nocturnalplinting may reduce wrist, hand, and/or finger discomfortmong active workers with CTS symptoms.16

Walker et al17 found that CTS patients who were instructedo wear neutral splints full-time had superior motor and sensoryistal latency improvements compared to subjects instructed toear splints only at night. Function and symptom severity were

lso improved. Walker17 concluded that neutral wrist splintsre efficacious for CTS, particularly when worn as much asossible.

.5 Educational Activity: To educate a workers’ compen-sation nurse case manager regarding the use of lum-bosacral supports and directional-based exercises fora loading dock worker with low back pain.

A recent Cochrane back review18 systematically examined 5andomized and 2 nonrandomized preventative trials, and 6andomized therapeutic trials. Only 4 of 13 studies were ofigh quality. There was moderate evidence that lumbosacralupports are ineffective for primary low back pain (LBP)revention. No evidence supported the use of these supports forecondary LBP prevention. There was limited evidence thatumbosacral supports are more effective than no treatment, butas unclear whether they are more effective than other treat-ents for LBP. An essential issue to address in future trials is

ompliance with wearing the device.18

Petersen et al19 did an RCT with an 8-month follow-uperiod on 260 consecutive patients with LBP for longer than 8eeks. One subgroup was treated with the McKenzie method

nd another subgroup was treated with intensive dynamictrengthening training. The outpatient treatment period for bothroups was 8 weeks, followed by 2 months of self training atome. Petersen found no significant differences in pain reduc-ion at any time and no significant differences in disability.etersen19 concluded that the McKenzie method and intensiveynamic strength training were equally effective treatments forubacute or chronic LBP.

In a study of patient-specific exercises for LBP,20 312 pa-ients underwent a standardized mechanical assessment classi-
ying them by their pain responses, specifically eliciting a

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directional preference.” The patient’s directional preferenceas identified and thus defined by an immediate, lasting im-rovement in pain in a particular vector via repeated lumbarexion, extension, or side-glide or rotation tests. Subjects wereandomized to 10 directional exercises that either “matched”heir preferred direction, were “opposite” to it, or were “non-irectional” relative to their preferred direction. Outcome mea-ures included pain intensity, location, disability, medicationse, degree of recovery, depression, and work interference.esults showed that a directional preference was elicited in4% (230) of subjects. One third of the subjects treated withhe “opposite” exercises and one third of subjects treated withnd the “nondirectional” exercises withdrew within 2 weeksecause of no improvement or worsening symptoms. No sub-ects whose exercises matched their directional preferenceithdrew. Significantly greater improvements occurred in sub-

ects performing exercises that matched their directional pref-rence compared with both other treatment groups in everyutcome (P�.001), including a 3-fold decrease in medicationse. They concluded that standardized mechanical assessmentdentified a large subgroup of LBP patients with a directionalreference. Regardless of subjects’ direction of preference,xercise that matched their directional preference significantlynd rapidly decreased pain and medication use and improvedll other outcomes. Results suggest that patient-specific thera-eutic exercises are more effective than nonspecific exercises.his may explain the previously reported lack of efficacy ofxercise and physical therapy for LBP treatment.

.6 Educational Activity: To critique the literature re-garding modalities and exercise as treatment forAchilles’ tendinosis in a 45-year-old tree trimmer.

A Cochrane review for Achilles’ tendinosis found 9 trialsN�697) that met the inclusion criteria for review.21 Theyound weak evidence of benefit from oral NSAIDs, but weakvidence of no benefit for heel pads, topical laser therapy,eparin injection, or peritendinous steroid injections. Heat,old, and ultrasonography are anecdotally beneficial for Achil-es’ tendinosis, but well-designed research supporting their uses somewhat sparse.

Eccentrically loading the Achilles’ tendon via calf muscle train-ng is a well-supported treatment for Achilles’ tendinosis. It isavorably associated with reduction in abnormal Achilles’ tendonhickness, decreased pain, restoration of normal tendon architec-ure,22 and decreased abnormal neovascularization of the ten-on.23 A prospective study of 15 patients with chronic Achilles’endinosis showed that 12 weeks of this therapy, using eccentriceavy loading, resulted in full recovery to preinjury functionalevels, including running, while all patients in a control group hadersistent pain and underwent surgical treatment.24

References*1. Crawford F, Thomson C. Interventions for treating plantar heel

pain. Cochrane Database Syst Rev 2003;(3):CD000416.2. DiGiovanni BF, Nawoczenski DA, Lintal ME, et al. Tissue-

specific plantar fascia-stretching exercise enhances outcomes inpatients with chronic heel pain: a prospective, randomized study.J Bone Joint Surg Am 2003;85:1270-7.

3. Crawford JR, Khan RJ, Varley GW. Early management andoutcome following soft tissue injuries of the neck: a randomisedcontrolled trial. Injury 2004;35:891-5.

*Key Reference.


4. Gennis P, Miller L, Gallagher EJ, Giglio, Carter W, NathansonN. The effect of soft cervical collars on persistent neck pain inpatients with whiplash injury. Acad Emerg Med 1996;3:568-73.

*5. Philadelphia Panel. Evidence-based guidelines on selectedrehabilitation interventions for neck pain. Phys Ther 2001;81:1701-17.

6. Nirschl RP. Muscle and tendon trauma: tennis elbow. In: MorreyBF, editor. The elbow and its disorders. 3rd ed. Philadelphia: WBSaunders; 2000. p 523-35.

7. Wuori JL, Overend TJ, Kramer JF, MacDermind J. Strength andpain measures with lateral epicondylitis bracing. Arch Phys MedRehabil 1998;79:832-7.

8. Derebery VJ, Davenport JN, Giang GM, Fogarty WT. The ef-fects of splinting on outcomes for epicondylitis. Arch Phys MedRehabil 2005;86:1081-8.

9. Svernlov B, Adolfson L. Non-operative treatment regimen in-cluding eccentric training for lateral humeral epicondylalgia.Scan J Med Sci Sports 2001;6:328-34.

10. Bisset L, Paungmali A, Vicenzino B, Beller, E. A systemicreview and meta-analysis of clinical trials on physical interven-tions for lateral epicondylalgia. Br J Sports Med 2005;39:411-22.

11. Buchbinder R, Green S, White M, Barnsley L, Smidt N, Assen-delft WJ. Shock wave therapy for lateral elbow pain. CochraneDatabase Syst Rev 2002;(1):CD003524.

12. Haahr JP, Andersen JH. Prognostic factors in lateral epicondy-litis: a randomized trial with one-year follow-up in 266 newcases treated with minimal occupational intervention or the usualapproach in general practice. Rheumatology (Oxford) 2003;42:1216-25.

13. Waugh EJ, Jaglal SB, Davis AM, Tomilson G, Verrier MC.Factors associated with prognosis of lateral epicondylitis after8 weeks of physical therapy. Arch Phys Med Rehabil 2004;85:308-18.

14. Juul-Kristensen B, Jensen C. Self-reported workplace ergonomicconditions as prognostic factors for musculoskeletal symptoms:the “BIT” follow up study for office workers. Occup EnvironMed 2005;62:188-94.

15. O’Connor D, Marshall S, Massy-Westropp N. Non-surgicaltreatment (other than steroid injection) for carpal tunnel syn-drome. Cochrane Database Syst Rev 2003;(1):CD003219.

16. Werner RA, Franzblau A, Gell N. Randomized controlled trial ofnocturnal splinting for active workers with symptoms of carpaltunnel syndrome. Arch Phys Med Rehabil 2005;86:1-7.

17. Walker WC, Metzler M, Cifu DX, Swartz. Neutral wrist splint-ing in carpal tunnel syndrome: a comparison of night-only versusfull-time wear instructions. Arch Phys Med Rehabil 2000;81:424-9.

18. Jellema P, van Tulder MW, van Poppel MN, Nachemson AL,Bouter LM. Lumbar supports for prevention and treatment oflow back pain: a systematic review within the framework of theCochrane Back Review Group. Spine 2001;26:377-86.

19. Petersen T, Kryger P, Ekdahl C, Olsen S, Jacobsen S. The effectof McKenzie therapy as compared with that of intensivestrengthening training for the treatment of patients with subacuteor chronic low back pain: a randomized controlled trial. Spine2002;27:1702-9.

20. Long A, Donelson R, Fung T. Does it matter which exercise? Arandomized control trial of exercise for low back pain. Spine2004;29:2593-602.

21. McLauchlan GJ, Handoll HH. Interventions for treating acuteand chronic Achilles tendinitis. Cochrane Database Syst Rev2001;(2):CD000232.

22. Ohberg L, Lorentzon R, Alfredson H. Eccentric training inpatients with chronic Achilles tendinosis: normalised tendonstructure and decreased thickness at follow up. Br J Sports Med
2004;38:8-11.

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S17WORK-RELATED MUSCULOSKELETAL CONDITIONS, Foye

23. Ohberg L, Alfredson H. Effects on neovascularisation behind thegood results with eccentric training in chronic mid-portion Achillestendinosis? Knee Surg Sports Traumatol Arthrosc 2004;12:465-70.

24. Alfredson H, Pietila T, Jonsson P, Lorentzon R. Heavy-loadeccentric calf muscle training for the treatment of chronic Achil-
les tendinosis. Am J Sports Med 1998;26:360-6.
Suggested Readingorrey BF. The elbow and its disorders. 3rd ed. Philadelphia: WB

Saunders; 2000.ilson JJ, Best TM. Common overuse tendon problems: a review andrecommendations for treatment. Am Fam Physician 2005;72:
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ndustrial Medicine and Acute Musculoskeletal Rehabilitation.. Interventional Procedures for Work-Related Cervical Spineonditions

obert W. Irwin, MD, Joseph P. Zuhosky, MD, William J. Sullivan, MD, Andre Panagos, MD,
atrick M. Foye, MD, Aaron W. Sable, MD
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or work-related cervical spine conditions. Arch Phys Medehabil 2007;88(3 Suppl 1):S18-21.

This self-directed learning module outlines the use of interven-ional techniques in the treatment of neck pain with and withouteferred pain into the arm. It is part of the supplement on industrialehabilitation medicine and acute musculoskeletal rehabilitation inhe Self-Directed Physiatric Education Program for practitionersnd trainees in physical medicine and rehabilitation. This articlepecifically focuses on interventions used to diagnose or treat theonditions commonly seen in patients with neck pain or referredain into the upper limb. Techniques reviewed include the use ofotulinum toxin injections in the treatment of myofascial pain,ervical zygapophyseal joint injections and radiofrequency neu-oablation in the treatment of posterior column disorders, andpidural steroid injections in the treatment of cervical radicularnd referred upper-limb pain.

Overall Article Objective: To give an overview of theurrent state of the art regarding diagnostic and nonsurgicalnvasive treatment procedures for neck pain with and withouteferred upper-limb pain.

Key Words: Botulinum toxins; Facet joint; Disk, herniated;njections, epidural; Rehabilitation; Trigger points, myofascial.


.1 Educational Activity: To discuss the use of zygapophy-seal injections and the use of botulinum toxin to treat a45-year-old Department of Transportation worker withupper-thoracic and neck pain related to a “whiplash”injury for whom conservative treatment has failed.

PPER-THORACIC, PERISCAPULAR, and neck painfrom myofascial and/or whiplash-like injuries present a

otentially vexing challenge to the treating clinician. Prompt

From the Department of Rehabilitation Medicine, University of Miami, Millerchool of Medicine, Miami, FL (Irwin); Total Spine Specialists, Department ofhysical Medicine and Rehabilitation, Carolinas Medical Center, Charlotte, NCZuhosky); Department of Physical Medicine and Rehabilitation, University of Col-rado at Denver and Health Sciences Center, Denver, CO (Sullivan); Department ofehabilitation Medicine, Weill Cornell Medical Center, New York–Presbyterianospital, New York, NY (Panagos); Department of Physical Medicine and Rehabil-

tation, Department of Physical Medicine and Rehabilitation, University of Medicinend Dentistry of New Jersey: New Jersey Medical School, Newark, NJ (Foye); and St.ohn’s Macomb Hospital, Warren, MI (Sable).

No commercial party having a direct financial interest in the results of the researchupporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Robert W. Irwin, MD, Dept of Rehab Med, Univ of Miami, Miller Sch

f Med, PO Box 016960 (D-461), Miami, FL 33101, e-mail: [email protected] are not available from the author.

H0003-9993/07/8803S-11407$32.00/0doi:10.1016/j.apmr.2006.12.011


nd specific diagnosis coupled with early treatment generallyesults in better clinical outcomes. Much of the literature ad-ressing myofascial pain describes trigger points in the discus-ion of the pathogenesis of these disorders. Trigger-point in-ections are a commonly used therapeutic option for thisroblem. Variations of these injections include dry needling,ocal anesthetic injections only, and combined local anestheticsith corticosteroid injections. These variations appear to have

omparable efficacy. However, anecdotal experience and thevailable literature on trigger-point injections suggest that theenefits achieved may not be sustained if performed in isola-ion. In general, pain relief lasts 1 to 3 weeks when trigger-oint injections are given as stand-alone treatment. Adminis-ering trigger-point injections as 1 component of aomprehensive rehabilitation program may yield better results.

The pathogenesis of trigger points remains unknown. Elec-romyographic investigation1 has suggested that mini-endplateotentials found routinely in trigger points may be used toharacterize this phenomenon. These mini-endplate potentials,owever, are not pathognomonic and are not consistentlyound. Others1 have examined oxygen tension in trigger pointsnd note consistently lower oxygen levels in these musclebers. The mechanism that permits creation and maintenancef this lower level of muscle fiber oxygenation remains un-lear.

Another hypothesis of trigger points’ pathogenesis contendshat uncontrolled acetylcholine release results in chronic mus-le fiber contraction. In an attempt to address this possibleathogenesis in particular, clinicians have turned to botulinumoxin types A and B to break this cycle. A recent focusedeview2 has described the use of these agents in cervicalystonias, spasticity, headaches, myofascial pain, and chronicow back pain. Botulinum toxin’s mechanism of action is theeversible blockade of acetylcholine release at the neuromus-ular junction, generally lasting 3 to 4 months. Several smallrospective studies have yielded promising results; however,he variety of dosing schedules and the number, frequency, andattern of injections prove somewhat problematic in evaluatinghis research area.

Upper-thoracic, periscapular, and neck pain may emanaterom the cervical zygapophyseal joints, commonly referred tos facet joints. The patterns of pain provocation mapped out inygapophyseal-joint injections of symptomatic and asymptom-tic people have significant overlap with the patterns seen inyofascial and whiplash-associated disorders.3,4 The preva-

ence of cervical zygapophyseal-joint pain has been estimatedt greater than 25% in neck pain patients and, after whiplash-ike injuries, the prevalence is increased to greater than 50%,ost often affecting the C2-3 and C5-6 joints.5,6

On physical examination, neck pain reproduction with thepurling maneuver without referred pain into the arm and withervical extension or rotation, with reduced, painful range ofotion, may suggest a cervical zygapophyseal-joint disorder.
istory and physical examination alone, however, have proven

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o be unreliable predictors of zygapophyseal-joint pain. In-reased radioactive uptake in the zygapophyseal joint on bonecan may provide further diagnostic confirmation. Comparativeocal anesthetic blocks of the medial branches of the dorsalamus, commonly referred to as medial branch blocks, as aiagnostic tool have been established as a current criteriontandard.7 The dual innervation of the cervical zygapophysealoints is shown in figure 1. Many clinicians also use cervicalntra-articular zygapophyseal-joint blocks as part of a diagnos-ic regimen with or without medial branch blocks. Cervicalygapophyseal-joint intra-articular blocks can also providehort-term relief but may be less effective for chronic paintates.8,9

Studies3-8 for cervical zygapophyseal-joint pain initially fo-used on intra-articular blocks but more recently have includededial branch blocks not only for diagnostic benefits but also

or potentially therapeutic benefits. Medial branch blocks haveeveral advantages, including safety of the injection. There isess risk of a needle passing through the joint into the spinalord, compared with zygapophyseal-joint intra-articular injec-ions, because the articular pillars serve as an effective bonyackstop, preventing needle penetration into the spinal canal.hey may be technically easier to perform than intra-articular

njections, especially in older patients where osteophytes mayreclude needle entry into an arthritic joint.Analysis7 of dual comparative, local anesthetic, medial

ranch blocks shows variable duration of response, with someatients reporting pain relief longer than the duration of theocal anesthetic used. The injections have predictive validity,ith pain relief after medial branch blocks corresponding quite

avorably to pain relief after radiofrequency neuroablation.7

Radiofrequency neuroablation has proven to be safe andffective, with a greater than 70% response rate for cervicalygapophyseal-joint pain when performed after appropriatelyiagnostic, comparative, local anesthetic, medial branchlocks. Workers’ compensation patients did statistically as wells patients treated from the general population. Although theedial branch of the dorsal ramus nerve typically regenerates

n approximately 90 days, the relief achieved may last 7 to 9

ig 1. The midcervical spine and the medial branches, lateral view., articular branches; mb, medial branches; tb, terminal branches.

onths, or longer. If the pain returns, repeat radiofrequency u

euroablation can produce similar beneficial effects.10,11 It isnclear how many times the procedure may be repeated withchievement of the same results.

Pulsed radiofrequency neuroablation has been investigateds a treatment of zygapophyseal-joint pain partly in an effort toncrease the safety of these procedures. This procedure allowsower levels of heating (42°C vs 80°C), and the subsequent riskf deafferentation pain is theoretically decreased. Animal mod-ls show cellular changes and an increase of immunoreactiveells with the pulsed techniques when compared with a shamrocedure.12 Very few trials have looked critically at pulsedadiofrequency neuroablation. One suggested a positive re-ponse with greater than 50% relief sustained for 1 to 5 monthsn about 60% of patients.13 Further research is needed beforehis procedure can be widely recommended for clinical prac-ice.

.2 Educational Activity: The above Department ofTransportation worker has persistent pain in the neckand posterior shoulder and now has arm pain despitebotulinum toxin injections and facet injections. Dis-cuss other nonsurgical interventions that may be con-sidered, including their potential risks and benefits.

Upper-limb pain associated with spinal pathology is consid-red synonymous with cervical radiculopathy in some settings;owever, referred pain into the upper limb may in fact emanaterom other somatic sources (eg, cervical zygapophyseal joint,yofascial) and does not always represent irritation or injury of

he nerve root. Although pain related to a clear-cut radiculop-thy is generally perceived along the affected dermatome, painatterns from other causes often overlap dermatomes, scle-otomes, or myotomes, as well as peripheral nerve innervationatterns. Patients may also suffer with referred pain from anrritated nerve root without having associated neurologic defi-its. Some clinicians refer to this as radiculitis, but others usehe term radiculitis to denote inflammatory involvementwhether associated with neurologic deficits or not). Unfortu-ately, there is no consensus in differentiating the etiology ofadicular pain patterns in the upper limb. Hence, the literaturevaluating upper-limb referred pain remains confounded by aeterogeneous patient population with likely multiple underly-ng etiologies contributing to radicular pain. The distinctionetween truly radicular and referred upper-limb pain is impor-ant. A patient who has referred pain that is not clearly theesult of radiculopathy might not benefit from an epiduralteroid injection (ESI); however, treatments including zyg-pophyseal-joint injections and botulinum toxin injectionsight be more helpful. Conversely, if a physician fails to

ecognize a clear-cut radicular pain pattern, an inappropriateygapophyseal-joint injection or trigger-point injection mighte performed. A recent study suggests that tender points can bessociated with radiculopathies and/or with myofascial pain.arious shoulder pathologies may also create periscapular,

houlder, and upper-limb pain. The importance of a detailedistory, thorough physical examination, and correlation withppropriate advance imaging studies to arrive at a specificiagnosis cannot be overstated.In patients with a clear-cut cervical radiculopathy, direct

pplication of corticosteroids to the site of inflammation is aell-recognized treatment option. This can be achieved byeans of a cervical transforaminal or interlaminar ESI. No

rospective, randomized controlled trials have compared thesenjection techniques. A handful of prospective studies14,15 eval-
ating cervical transforaminal ESI have shown promising re-

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S20 INTERVENTIONAL PROCEDURES FOR WORK-RELATED CERVICAL SPINE CONDITIONS, Irwin

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ults in patients with cervical radiculopathy for whom conser-ative treatment protocols had failed. One theoretic advantagef this injection is the low volume of injectate yielding a highoncentration of corticosteroid directly to the site of inflam-ation. The cervical transforaminal ESI, in particular, is tech-

ically demanding because even small deviations in needlelacement may have profound deleterious effects. It is impor-ant that the physician performing this procedure know thenatomy of the cervical spine, be familiar with the use of liveuoroscopic images, and be well aware of the potential injec-

ion complications. Transforaminal ESI complications includenfection, nerve root injury, vertebral artery dissection, paral-sis, and stroke.16 It has been postulated that particulate steroideposition into an artery or arterial watershed zone has resultedn spinal cord and brain infarction, culminating in tetraplegiand death in some patients.17-22 There is also a risk of a highpinal block with respiratory compromise with inadvertentubarachnoid injection of anesthetic.

Compared with transforaminal ESI, the interlaminar ESIheoretically may have a disadvantage of less availability oforticosteroid anteriorly at the site of inflammation. Cervicalnterlaminar ESIs may present less risk of inadvertent arterialarticulate steroid deposition but are not without complica-ions.23,24 Risks of interlaminar ESI include delayed injury tohe spinal cord, which may occur because of mass effect fromither a hematoma or epidural abscess.24 One may also sustainirect spinal cord injury as a result of needle puncture of thepinal cord itself. High spinal block may occur with injectionf local anesthetic into the subarachnoid space, and for thiseason interlaminar ESIs with local anesthetic are typicallyerformed at C6-7 or below. To minimize complications, in-erlaminar ESI should not be performed at stenotic levels.

There exists a relative paucity of literature to support theoutine use of cervical ESI in the treatment of cervical radicularain. To our knowledge, no study exists to date directly com-aring the efficacy or safety of transforaminal ESI versusnterlaminar ESI, and thus this choice rests with the injectinghysician. The current debate as to which of the 2 injectionsay be more advantageous revolves more around the perceived

afety of each injection and the potential complication oferious central nervous system (CNS) injury. Several studiesave addressed the possible complications in retrospectivenalyses. In 1 study,23 the overall complication rate fromervical interlaminar ESI was 16.8%. Most of these complica-ions were characterized as minor and resolved within 24ours. However, there was 1 (0.3%) serious complication of aural puncture.23

A 2003 study of cervical transforaminal ESI found that9.4% of patients had intravascular injection on installation ofontrast medium under real time fluoroscopy.18 These intra-ascular injections did not always correlate with blood in theub of the needle on withdrawal of the syringe.There have been several case reports of CNS complications

esulting from cervical transforaminal ESI.19-22,25 Magnetic reso-ance imaging studies after these complications have shown in-ury or infarction to either the spinal cord or the brainstem. Onlystudy,22 which used computed tomography guidance during the

rocedure, showed evidence of arterial needle placement. In thistudy, the needle was placed in the vertebral artery before thenjection.22 The other studies did not have fluoroscopic guidancer image documentation of needle placement listed in their re-orts. The available literature and hypotheses of CNS injuriesuggests, at a minimum, that cervical transforaminal ESI proce-ures should always be performed with fluoroscopic guidanceith live fluoroscopic images during contrast installation to min-

mize the risk of inadvertent intravascular injection. Some clini-


ians have suggested a further safeguard of digital subtractionnalysis of the fluoroscopic images to further decrease this risk.

In summary, cervical ESI remains a treatment option forervical radicular pain; however, little literature exists to sup-ort the clinical efficacy of these injections. It is important toecognize and inform the patient of the potentially disablingnd life-threatening CNS complications that may occur withhese injections. Appropriate use of fluoroscopic guidance inhe performance of these injections may reduce, but certainlyo not eliminate, the risks associated with these injections.

References1. Borg-Stein J, Simons DG. Focused review: myofascial pain.

Arch Phys Med Rehabil 2002;83(3 Suppl 1):S40-7, S48-9.*2. Lang AM. Botulinum toxin type A therapy in chronic pain

disorders. Arch Phys Med Rehabil 2003;84(3 Suppl 1):S69-73.3. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint

pain patterns. I: A study in normal volunteers. Spine 1990;15:453-7.

4. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal jointpain patterns. II: A clinical evaluation. Spine 1990;15:458-61.

5. Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence ofchronic cervical zygapophysial joint pain after whiplash. Spine1995;20:20-5.

6. Bogduk N, Marsland A. The cervical zygapophysial joints as asource of neck pain. Spine 1988;13:610-7.

*7. Lord SM, Barnsley L, Bogduk N. The utility of comparativelocal anesthetic blocks versus placebo-controlled blocks for thediagnosis of cervical zygapophysial joint pain. Clin J Pain 1995;11:208-13.

8. Barnsley L, Lord SM, Wallis BJ, Bogduk N. Lack of effect ofintraarticular corticosteroids for chronic pain in the cervicalzygapophyseal joints. N Engl J Med 1994;330:1047-50.

*9. Manchikanti L, Staats PS, Singh V, et al. Evidence-Based Prac-tice Guidelines for interventional techniques in the managementof chronic spinal pain. Pain Physician 2003;6:3-81.

10. Lord SM, Barnsley L, Wallis BJ, McDonald GJ, Bogduk N.Percutaneous radio-frequency neurotomy for chronic cervicalzygapophyseal-joint pain. N Engl J Med 1996;335:1721-6.

11. McDonald GJ, Lord SM, Bogduk N. Long-term follow-up ofpatients treated with cervical radiofrequency neurotomy forchronic neck pain. Neurosurgery 1999;45:61-7.

12. Van Zundert J, de Louw AJ, Joosten EA, et al. Pulsed andcontinuous radiofrequency current adjacent to the cervical dorsalroot ganglion of the rat induces late cellular activity in the dorsalhorn. Anesthesiology 2005;102:125-31.

13. Mikeladze G, Espinal R, Finnegan R, Routon J, Martin D. Pulsedradiofrequency application in treatment of chronic zygapophy-seal joint pain. Spine J 2003;3:360-2.

14. Rathmell JP, Aprill C, Bogduk N. Cervical transforaminal injec-tion of steroids. Anesthesiology 2004;100:1595-600.

15. Bush K, Hillier S. Outcome of cervical radiculopathy treated withperiradicular/epidural corticosteroid injections: a prospective studywith independent clinical review. Eur Spine J 1996;5:319-25.

16. Ma DJ, Gilula LA, Riew KD. Complications of fluoroscopicallyguided extraforaminal cervical nerve blocks. An analysis of 1036injections. J Bone Joint Surg Am 2005;87:1025-30.

17. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse centralnervous system sequelae after selective transforaminal block: therole of corticosteroids. Spine J 2004;4:468-74.

*Key reference.

*

S21INTERVENTIONAL PROCEDURES FOR WORK-RELATED CERVICAL SPINE CONDITIONS, Irwin

18. Furman MB, Giovanniello MT, O’Brien EM. Incidence of intra-vascular penetration in transforaminal cervical epidural steroidinjections. Spine 2003;28:21-5.

19. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforami-nal injection of corticosteroids into a radicular artery: a possiblemechanism for spinal cord injury. Pain 2003;103:211-5.

20. Hodges SD, Castleberg RL, Miller T, Ward R, Thornburg C.Cervical epidural steroid injection with intrinsic spinal corddamage. Two case reports. Spine 1998;23:2137-42.

21. Rozin L, Rozin R, Koehler SA, et al. Death during transforaminalepidural steroid nerve root block (C7) due to perforation of the left
vertebral artery. Am J Forensic Med Pathol 2003;24:351-5.
22. Rosenkranz M, Grzyska U, Niesen W, et al. Anterior spinalartery syndrome following periradicular cervical nerve root ther-apy. J Neurol 2004;251:229-31.

23. Botwin KP, Castellanos R, Rao S, et al. Complications of fluo-roscopically guided interlaminar cervical epidural injections.Arch Phys Med Rehabil 2003;84:627-33.

24. Huang RC, Shapiro GS, Lim M, Sandhu HS, Lutz GE, HerzogRJ. Cervical epidural abscess after epidural steroid injection.Spine 2004;29:E7-9.

25. Brouwers PJ, Kottink EJ, Simon MA, Prevo RL. A cervicalanterior spinal artery syndrome after diagnostic blockade of the
right C6-nerve root. Pain 2001;91:397-9.

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ndustrial Medicine and Acute Musculoskeletalehabilitation. 5. Interventional Procedures forork-Related Lumbar Spine Conditions

obert W. Irwin, MD, Joseph P. Zuhosky, MD, William J. Sullivan, MD, Patrick M. Foye, MD,
aron W. Sable, MD, Andre Panagos, MD
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ABSTRACT. Irwin RW, Zuhosky JP, Sullivan WJ, FoyeM, Sable AW, Panagos A. Industrial medicine and acuteusculoskeletal rehabilitation. 5. Interventional procedures forork-related lumbar spine conditions. Arch Phys Med Rehabil007;88(3 Suppl 1):S22-8.

This chapter emphasizes the importance of establishing aifferential diagnosis for low back pain (LBP) with and withouteferred lower-limb pain and outlines potential interventionalreatments appropriate for each diagnosis. It is part of the studyuide on industrial rehabilitation and acute musculoskeletalehabilitation in the Self-Directed Physiatric Education Pro-ram for practitioners and trainees in physical medicine andehabilitation. The article specifically focuses on the variousnterventions used to diagnose or treat those conditions com-only seen in patients with work-related LBP or referred pain

n the lower limb. Current criterion treatments for lumbar diskain, including surgical options, are reviewed.Overall Article Objective: To give an overview of the

urrent state of diagnosis and treatment options for low backain with or without referred leg pain focusing on interven-ional procedures.

Key Words: Arthroplasty; Biochemical markers; Disk, her-iated; Facet joint; Injections, epidural; Low back pain; Lum-ar region; Rehabilitation; Sacroiliac joint.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Clinical Activity: To discuss the differential diagnosisand procedural management of a 40-year-old dock-worker with low back pain and leg pain for whomconservative treatment has failed.

O ESTABLISH AN APPROPRIATE treatment plan for aninjured worker with low back pain (LBP) and referred leg

ain, it is imperative to develop a proper differential diagnosis.learly, this process is guided by the history, physical exami-ation and laboratory and imaging studies. The clinician must

From the Department of Rehabilitation Medicine, University of Miami, Millerchool of Medicine, Miami, FL (Irwin); Total Spine Specialists, Department ofhysical Medicine and Rehabilitation, Carolinas Medical Center, Charlotte, NCZuhosky); Department of Physical Medicine and Rehabilitation, University of Col-rado at Denver and Health Sciences Center, Denver, CO (Sullivan); Department ofhysical Medicine and Rehabilitation, University of Medicine and Dentistry of Newersey: New Jersey Medical School, Newark, NJ (Foye); St. John’s Macomb Hospital,

arren, MI (Sable); and Department of Rehabilitation Medicine, Weill Cornelledical Center, New York–Presbyterian Hospital, New York, NY (Panagos).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Robert W. Irwin, MD, Dept of Rehab Med, Univ of Miami,iller Sch of Med, PO Box 016960 (D-461), Miami, FL 33101, e-mail:


p0003-9993/07/8803S-11408$32.00/0doi:10.1016/j.apmr.2006.12.012


valuate and rule out systemic diseases including cancer andheumatologic disease, which may have been exacerbated byctivity at work or home. Obtaining a detailed medical history,eview of systems (including constitutional symptoms), andsychosocial background are critical in determining an appro-riate differential diagnosis. After systemic diseases have beenuled out, the differential diagnosis then dictates the treatmentlgorithm and appropriate diagnostic and therapeutic interven-ions.

In this patient with both LBP and referred leg symptoms, theifferential diagnosis should include but not be limited toumbar disk herniation, sacroiliac joint pain, zygapophysealoint pain, diskogenic pain, piriformis syndrome, spondylolis-hesis, lumbosacral plexopathy, and in today’s aging workorce, exacerbation of lumbar spinal stenosis. To determinehich spinal intervention is most appropriate in these cases,ne must consider the goal of the intervention. Some spinalnterventions can be useful diagnostically, whereas others areherapeutic. For persistent pain presumed to emanate from theygapophyseal joint or the sacroiliac joint, intra-articular in-ections are appropriate treatment options.

The prevalence of zygapophyseal joint�mediated pain,ommonly referred to as a facet syndrome, varies between 15%nd 40% of chronic LBP patients.1,2 Intra-articular zygapophy-eal-joint injections can be used therapeutically and may alsoe diagnostic if pain relief is achieved. For a more purelyiagnostic approach, performing anesthetic blocks of the me-ial branches of the dorsal rami supplying the zygapophysealoint in question may help ascertain the exact level of involve-ent and may also help correlate the patient’s history, physical

xamination, and imaging study results. In the double-blockpproach, injections targeting the medial branches of the dorsalami, commonly referred to as medial branch blocks, are per-ormed at 2 separate occasions. Different anesthetics withifferent durations of action are administered at the 2 occa-ions. Pain relief lasting at least the minimum length of effec-iveness of the local anesthetic constitutes a positive response.his technique is considered superior to single anestheticlocks in the diagnosis of zygapophyseal joint�mediated painnd is the criterion standard for making the diagnosis. Based onbeneficial response to these injections, one might consider

adiofrequency ablation of the appropriate medial branches.The prevalence of sacroiliac joint pain ranges from 18% to

0% of chronic LBP patients. Intra-articular sacroiliac jointorticosteroid injections remain the only interventional optionroven useful in this condition.3-5 However, these injectionsave been controversial. Diagnostic injections using the com-arative local anesthetic block approach may also help confirmhe role of the sacroiliac joint as a pain generator.

There are 3 approaches for performing epidural injections:audal, interlaminar, and transforaminal. Lumbar spinal steno-is, lumbar disk herniation, and lumbar diskogenic pain may all
resent as LBP with or without a radicular component and are

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S23INTERVENTIONAL PROCEDURES FOR WORK-RELATED LUMBAR SPINE CONDITIONS, Irwin

ommon diagnoses for which an epidural steroid injectionESI) is routinely performed. To date, prospective, blinded, andontrolled scientific studies supporting the efficacy of lumbarSIs for the treatment of these disorders have been lacking.ertain patient populations warrant specific mention. For pa-

ients with lumbar stenosis, interlaminar ESI should be per-ormed below the level of stenosis to minimize the risk ofntrathecal injection. Interlaminar ESI may not be helpful in thereatment of neuroforaminal stenosis, whereas a transforaminalSI may be more appropriate.

.2 Educational Activity: To discuss the biomechanicchanges and treatment recommendations for this 40-year-old dockworker diagnosed with a lumbar diskherniation.

Various treatment options exist for lumbar herniated nucleusulposus (HNP), including medications, therapies, injections,urgical diskectomy, and fusion. Although there have beenultiple treatments proposed for a lumbar HNP, the natural

istory is favorable for spontaneous improvement. In a con-rolled, matched cohort of patients with lumbar HNP, the groupreated conservatively had similar pain improvement at the0-year follow-up. Further evaluation showed that the surgicalroup had a slightly better result for complete relief of painhan did the conservatively treated patients.6 No specific treat-

ent has had a clear advantage over another. After an appro-riate trial of more conservative treatments including medica-ions, physical therapy, and activity modifications (but not bedest), one may consider interventional procedures if pain per-ists. To understand the rationale behind these treatments, onehould have a basic understanding of the biochemistry andathophysiology associated with a lumbar HNP.Radicular pain as a result of lumbar HNP has been de-

cribed.6 Although initial studies focused on mass effect andressure on the nerve root created by HNP, more recent re-earch7-13 has focused on the subsequent inflammatory milieu.tudies7-14 showed that neural compression can cause painlesseakness, and many studies7-13 have confirmed that the nu-

leus pulposus contains a multitude of inflammatory mediators.he combination of mechanical compression of the nerve rootnd presence of inflammatory mediators seems to be more thanust additive.7 Researchers have searched for the inflammatory

arkers associated with a lumbar HNP. Phospholipase A2 wasound within the extravasated nucleus pulposus,8 validating theheory that nuclear material can cause inflammation. Severalther inflammatory markers have been associated with theucleus pulposus including nitric oxide, interleukin-6, prosta-landin E2, and matrix metalloproteinases. These markers maylso be tied to increases in interleukin-1.9,10 The isolation ofumor necrosis factor alpha (TNF-�) has been inconsistent inhe setting of disk herniation. The presence of both leukotriene

4 and thromboxane B2 has also been associated with theNP.11

In various animal studies of lumbar HNP, changes in nerveunction and structure, cellular matrix, and inflammatory mark-rs have been observed.7-17 These studies examined both ex-erimentally induced disk disruption in vivo and exposure toucleus pulposus materials in tissue culture. Leukotaxis andncreased vascular permeability have been noted in vitro as aesult of exposure to nucleus pulposus material.12 Differentesearchers have noted an increase in macrophages and aossible increase in mast cells in the inflammatory milieu.13 Ofote, in nerve tissue surrounded by nucleus pulposus, myelinhanges occur in the local area of exposure. Other changes
nclude an increase in Schwann cell cytoplasmic and intracel- b
ular edema.15 Decreases in nerve conduction velocity (NCV)nd amplitude of the compound muscle action potential arelso seen.7 The presence of TNF-� has been correlated with aecrease in NCV in nerve roots that have been exposed toucleus pulposus. One animal study16 has shown that applica-ion of the nucleus pulposus decreases the blood flow to theorsal root ganglion, with increased edema of the dorsal rootanglion and interneural space. This may be a result of in-reased vascular permeability mentioned earlier. Other re-earchers have found a direct relation between blood flow tohe nerve and NCV. There is a time lag between the exposurend the measured decrease in NCV.17

In accordance with the described pathophysiology, cortico-teroids and anesthetics have been used for injection into thepidural space in the setting of lumbar HNP. Studies havehown that corticosteroids may have more than anti-inflamma-ory effects. Corticosteroids may have some anesthetic affectsn small unmyelinated C fibers in irritated neural tissue.18 Inorcine models, high doses of methylprednisolone given earlyfter an exposure to nucleus pulposus material showed a pro-ective effect on NCV in the exposed nerves.19 Lidocaine haslso shown a mild protective effect in nerves exposed toucleus pulposus when evaluating the NCV. It seems to havets greatest effect when administered early. Studies have alsouggested that lidocaine may exhibit anti-inflammatory prop-rties such as decreasing phagocytosis, polymorpholeucocyteysosomal enzyme release, and superoxide anion produc-ion.18,20,21

ESIs are used to deliver anti-inflammatory medications andocal anesthetics in concentrated amounts to the epidural spaceurrounding areas of presumed pathology and inflammation.audal and interlaminar approaches were the initial routes ofdministration of medication in epidural injections pioneeredefore the advent of fluoroscopy. The advantage of thesepproaches is easy access to the epidural space. Without fluo-oscopy, however, no approach allowed confirmation of suc-essful deposition of medication into the epidural space. Flu-roscopic studies of interlaminar injections performed withoutmaging (blind) have shown that, even in experienced hands,early one third of blind injections do not truly access thepidural space.22 The efficacy of blind interlaminar injectionsas subsequently been questioned. Lack of fluoroscopic con-rmation of epidural flow on injection of contrast medium also

ikely increases the risk of dural puncture. Fluoroscopicallyuided ESI with contrast confirmation improves the accuracynd—by supposition—the efficacy of these injections. Retro-pective and limited prospective trials have shown generallyhort-term pain relief in heterogeneous patient populations withuestionable long-term benefits.23 The lack of well-controlled,rospective trials assessing the efficacy of interlaminar ESI,ith or without fluoroscopic guidance, leaves the true efficacyf these injections open to debate. Further, this literature rarelyncludes functional outcome measures beyond pain relief.

Compared with interlaminar ESI, transforaminal ESI has aheoretic advantage of delivering medication to the anteriorpidural space where the nerve root traverses. By necessity,hese injections are performed with fluoroscopic guidance and,deally, with contrast medium to confirm needle placementithin the epidural space and to prevent injection inadvertently

nto vascular structures. Several studies24-26 evaluated the ef-ectiveness of these injections for a lumbar HNP. In particular,ecent prospective, controlled studies show that transforaminalSI may help patients avoid surgery and reduce pain in theetting of lumbar HNP.24,25

Given these studies and the evolving evidence regarding the
iomolecular effects and pathophysiology of lumbar HNP, it is

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S24 INTERVENTIONAL PROCEDURES FOR WORK-RELATED LUMBAR SPINE CONDITIONS, Irwin

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easonable to recommend ESIs performed with fluoroscopicuidance and contrast confirmation as appropriate treatmentsor HNP. The literature suggests potential advantages with aransforaminal approach; however, currently no well-con-rolled comparative study evaluates the various epidural ap-roaches for delivering medications.

.3 Educational Activity: To describe, in a 35-year-oldhome improvement warehouse worker with predom-inantly LBP, the use of interventional procedures inthe diagnosis and treatment of posterior element pain.

The posterior elements of the lumbar spine include theygapophyseal joints and the sacroiliac joints. The use ofnterventional techniques to confirm the diagnosis of zyg-pophyseal joint� or sacroiliac joint�mediated pain and in-erventional treatment options for these conditions are outlineds follows.

Revel et al27 described a set of criteria increasing the like-ihood of a diagnosis of zygapophyseal-joint pain in the lumbarpine, including age greater than 65 years; pain well relievedy recumbency; and no pain exacerbation with coughing,neezing, forward flexion, lumbar extension, rising from aexed lumbar spine, or extension combined with rotation.ther investigators28 have challenged these criteria, claiming

hat these screening tests yield a low sensitivity and a highpecificity for the diagnosis of zygapophyseal-joint pain. Aingle physical examination maneuver or combination of ma-euvers correctly identifying the zygapophyseal joints as therimary source of pain remains to be elucidated.1,29 Otherethods are often used to confirm the clinical suspicion of

ygapophyseal-joint pain. The zygapophyseal-joint pain refer-al patterns, based on provocative injections, may include theower back and ipsilateral hip.2 Clinicians often use controlledomparative local anesthetic blocks. These are a more objec-ive way to confirm the diagnosis of zygapophyseal-joint pain.he dual innervation of the lumbar zygapophyseal joints (fig 1)ust be considered when contemplating medial branch blocks.Although generally considered diagnostic, medial branch

locks may also be therapeutic, with long-term pain reliefchieved in some patients. Therapeutic benefit may result fromisruption of the central feedback loop that forms in chronicain states or by inadvertent neurotomy of the medial branchy the needle tip. Adding steroid to the local anesthetic in thesenjections may potentiate the anesthetic blockade effects, buto literature supports its use.The interventional treatment options commonly used to al-

eviate zygapophyseal-joint pain include intra-articular injec-ions and radiofrequency ablation of the medial branches. Intra-rticular zygapophyseal-joint injections with corticosteroidsnd local anesthetic have been validated as an effective treat-ent for zygapophyseal-joint pain.2 Drawbacks of zygapophy-

eal-joint intra-articular corticosteroid injections include lim-ted long-term efficacy. Because of potential deleterious effectsf steroids on the synovial lining and ligamentous supports forhese joints, as well as potential local osteoporotic effects,linicians should limit the number of injections a patient re-eives.

Several studies have confirmed the efficacy and long-term painelief of radiofrequency ablation of neural structures. In this pro-edure, the nerve and tissues surrounding the electrode are heatedo 80°C, thus causing destruction of the medial branch of theorsal ramus itself. When it is administered after diagnostic,omparative, local-anesthetic, medial branch blocks, this ther-py relieves pain in up to 85% of these patients, providing
ong-term (median, 263d) relief sometimes lasting longer than u

year. Workers’ compensation patient outcomes for this ther-py rival those of the general population.22 The nerve typicallyegenerates in 90 days. If the pain returns, a repeat of theadiofrequency ablation generally affords the same long-termelief obtained by the initial treatment. Although the medialranch also innervates a small portion of the lumbar multifidususcle, no functional weakness has been associated with this

rocedure. One study30 validated good relief of pain withadiofrequency neuroablation after a single anesthetic block;owever, the efficacy is diminished compared with the use ofiagnostic, controlled, comparative, local anesthetic medicalranch blocks.31

The sacroiliac joint is a true diarthrodial joint containingpproximately 2 to 3mL of synovial fluid. Joint pain may resultrom trauma, cumulative sheer forces (eg, lifting, running,ltered gait mechanics), a rheumatologic process such as an-ylosing spondylitis or pregnancy, or it may be idiopathic.32

hysical examination maneuvers, particularly in isolation, haveimited diagnostic utility. Use of combination maneuvers mayncrease diagnostic yield.33 Pain maps of the sacroiliac jointhow significant overlap with those generated for the lower-umbar zygapophyseal joints and pain patterns from radiculop-thies or diskogenic pain but do not typically include painbove the L5 level. One study suggests pain may refer distallyo the feet.34 The double-block procedure has become theiagnostic standard.Intra-articular injection of local anesthetic and corticosteroid

ig 1. Left posterior view of the midlumbar spine showing the dualnnervation of the zygapophyseal joints by paired articular branchesrom the medial branches of the dorsal rami. Legend: a, articularranch; DR, dorsal ramus; ib, intermediate branch; mb, medialranch; tb, terminal branches; VR, ventral ramus.

nder fluoroscopic guidance is a common interventional treat-

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ent for sacroiliac joint pain. Given the technical difficulty ofhe injection even under fluoroscopic guidance, successful in-ection of the sacroiliac joint occurs rarely when performedlindly. Injections for sacroiliitis due to ankylosing spondylitisenerally last 6 months or less. Patients who had a singlenesthetic block that provided pain relief responded well tontra-articular corticosteroid injections.5 These injections af-orded long-term relief of up to 12 months, with patientsrequently requiring multiple injections (average, 2.1) tochieve results. Intra-articular injections of the sacroiliac jointre best used as part of an integrated rehabilitation program.ewer studies have applied the zygapophyseal-joint doublelock procedure to select patients for radiofrequency neuroab-ation to denervate the sacroiliac joint. This treatment may onlyddress the extra-articular pain sensations and not the intra-rticular pain associated with sacroiliac joint disorders. A com-lex and variable innervation of the sacroiliac joint existsompared with that of the zygapophyseal joints. Given thisariability and the limited anatomic landmarks for the nervesnnervating the sacroiliac joint, consistent denervation of theoint is difficult to achieve. Although radiofrequency neuroab-ation to treat sacroiliac joint pain had favorable results in aecent, small cohort study,35 further research is needed.

.4 Educational Activity: To discuss further diagnosticinvestigation and treatment for the above 40-year-olddockworker with disk degeneration, LBP, and re-ferred leg pain for whom conservative managementhas failed.

The diagnosis of true diskogenic pain emanating from thentervertebral disk is difficult to definitively establish. In pa-ients with chronic LBP, the prevalence of diskogenic pain isstimated at 40%.36 In an attempt to establish the diagnosis ofiskogenic pain, researchers have evaluated several tests. Aigh-intensity zone on magnetic resonance imaging within thentervertebral disk is presumed to reflect a potentially painfulnnular tear. These tears may be partial-thickness or completeears without frank herniation. Because of morphologichanges, increased nociception may occur in a disk with annnular tear. Also, leakage of inflammatory mediators presentn the nucleus pulposus may increase nociception. This phe-omenon may result from an ingrowth of sinuvertebral nervebers as the body attempts to heal the tear. However, theigh-intensity zone exists in both symptomatic and asymptom-tic subjects, thus clouding its role in the diagnosis of disko-enic pain.Diskography has been promoted as the de facto criterion

tandard in the evaluation of diskogenic pain in the absence oftrue standard. Diskography is typically performed at 3 levels

n the lumbar spine to provide at least 1 theoretic control, oronpainful, disk level. The procedure is painful, and risksnclude nerve injury, diskitis, and epidural abscess. Its routinese should be avoided. However, it may have a role in patientsith chronic back and/or referred leg pain to spare nonpainful

djacent disks from an intervention, to narrow or establishreatment options, and to serve as yet another correlate tomaging studies. Diskography has limited value for predictinguccess with surgical fusion.37 Several researchers have notedbnormal results with diskography in asymptomatic pa-ients.38-40 Other chronic pain states such as fibromyalgia mayffect diskography interpretation.41

New interventions, including intradiskal electrothermal annu-oplasty, nucleoplasty, percutaneous disk decompression, intradis-al restorative injections, and disk replacement have fueled the
iskography debate. Because the validity of diskography in t
iagnosing true diskogenic pain has been called into question,esearchers have focused on isolating variables that may createalse positive studies. A recent study with manometric pressureeasurements suggests that asymptomatic patients with painful

iskograms report only a lower intensity of pain occurring onlyt very high pressures.40 More recent studies suggest thatainful disks at low pressures and with smaller injectate vol-mes on diskography more likely identify “true diskogenic”ain generators.40 Pressure manometry may also improve in-erexaminer reliability.

Intradiskal electrothermal annuloplasty was developed basedn the theory that annular tear is a cause for diskogenic pain. Itas potential advantages over fusion in that it is less invasive,ess costly, and it preserves motion of the lumbar segment.

There are 3 proposed mechanisms by which this electrother-al approach may reduce pain and treat the annular tear.hermal injury applied to the annulus via the heating elementatheter may produce collagen remodeling with potential fi-rous contraction of the tear. Some researchers questionhether the target temperature of 90°C would result in collagen

emodeling. A second proposed mechanism is thermal ablationf nerve endings in the outer third of the annulus fibrosus. Theisk receives its innervation from the sinuvertebral nerves,hich contain A-delta and C fibers. These nerve fibers haveeen shown to penetrate into the annulus of degenerative disks.his suggests that thermal ablation of these nerves shouldchieve immediate relief of pain emanating from the disk itself.lthough some patients experience immediate relief after in-

radiskal electrothermal annuloplasty, it may take up to severaleeks or longer for the full effects to be realized. The thirdechanism is the proposed shrinkage of the nucleus pulposus

y the thermal energy.The indications for intradiskal electrothermal annuloplasty

nclude axial pain with sitting intolerance, lasting longer than 6onths with or without referred lower-limb pain, 50% preser-

ation of the height of the disk when compared with normalisks, and an absence of significant spinal stenosis. Provocationiskography with follow-up computed tomography beforereatment may further define the anatomy and may confirm theresence of an annular tear without significant disk protrusion.he symptomatic disk, when provoked, should produce con-ordant pain at low pressures with control disks exhibitingiscordant or no pain.Contraindications for intradiskal electrothermal annuloplastyay include bleeding diatheses, previous surgery at the poten-

ial site of intervention, disk protrusion beyond the posteriorongitudinal ligament in proximity to the nerve root origins,nd stenosis at the level of interest. Smoking and obesityepresent risk factors for a poor outcome after this therapy.

Complication rates are estimated at between 0.7% and6%36 and are generally self-limited. There have been severaleports of avascular necrosis of the vertebral body after in-radiskal electrothermal annuloplasty. The mechanism of thisnjury is unknown. A report42 of a frank disk herniation alsoxist, as does a report43 of cauda equina syndrome after it. Theauda equina syndrome was attributed to inadvertent catheterlacement and heating in the spinal canal. Although infectionnd thermal injury of the nerve root origins are theoretic risks,here have been no cases reported to date.

In prospective case series of intradiskal electrothermal an-uloplasty for chronic LBP, 50% to 81% of patients had goodr excellent results. The variable outcomes may result from these of different outcome scales and inconsistent definitions ofgood” or “excellent” results.42-45 Versus a sham treatment, thelectrothermally treated patients in a randomized placebo con-
rolled trial had a statistically significant decrease in pain,

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lthough 50% of the annuloplasty group had no relief.45 Basedn the Oswestry Disability Index, only 13.5% of the treatmentroup received more than 75% pain relief. Further analysisuggests greater benefit from intradiskal electrothermal annu-oplasty for patients with either very high pain scores or lowerevels of function before treatment. Patients with more moder-te or mild symptoms benefit less.46 Results in all favorabletudies suggest better outcomes with single as opposed toultiple disk levels of treatment. A subsequent study reported

o benefit from intradiskal electrothermal annuloplasty whenompared with placebo.47

Percutaneous nucleoplasty uses radiofrequency energy toreak down molecular structures in a nucleus pulposus. Ca-aver studies suggest that nucleoplasty may decrease diskressures and allow the disk to shrink, thus relieving intradiskalnd intraspinal pressure.48

Indications for nucleoplasty may include axial back painith or without referred leg pain, 50% preservation of diskeight, and imaging confirmation of disk protrusion. Contrain-ications include infection and bleeding diathesis. This proce-ure is approved for no more than 2 disk levels per treatment.nly a few prospective cohort studies have investigateducleoplasty. These studies have shown that up to 80% of theatients undergoing nucleoplasty have good to excellent relieff their symptoms.49,50 Another prospective study48 evaluatedatients who underwent nucleoplasty with or without concur-ent intradiskal electrothermal annuloplasty. The patients werencluded if they had referred leg pain with or without backain. Only 1 in 16 patients had greater than 50% relief. Someatients who had not been using opioid pain medications beganuch treatment after nucleoplasty. The researchers suggestedhat different patient selection criteria might have explained theoor outcome in this study. There is a paucity of literature toupport nucleoplasty, with numerous critics questioninghether denaturation of central nucleus pulposus material af-

ects in vivo disk pressure or the inflammatory milieu in theuter annulus and spinal canal.Intradiskal injections of steroids were performed previously

nd recently reexamined, but no studies to date have shown aositive treatment effect.51 Intradiskal injection of a mixture oflucosamine, chondroitin sulfate, hypertonic dextrose, and dis-ethylsulfoxide resulted in improved pain based on the Ro-

and-Morris Disability Questionnaire and visual analog painating scales.52

Limited study of percutaneous lumbar disk decompressionuggests that patients for whom conservative management hasailed, have 50% disk height preserved, and experience radic-lar pain associated with a contained herniation less than orqual to 6mm may benefit. Disk material is removed throughhe introducer needle after a drill-like bit is threaded throughhe needle, removing up to 1 to 2mL of nuclear material. Theest study to date showed a 65% decrease in pain.53 However,his procedure is relatively new and needs further investigation.

Based on research54 that suggested a role for TNF-� in theathogenesis of pain from an HNP, intravenous infliximab (aonoclonal antibody inhibiting TNF-�) has been used to treatNP. An initial open label study55 of a small number ofatients with sciatica from HNP had promising results; how-ver, the results of a randomized controlled study56 did notorroborate the initial study findings.

Disk arthroplasty (complete replacement of the disk) wasrst approved in the United States in 2004. The first-ever diskeplacement was performed in Europe in 1984. Disk arthro-lasty theoretically preserves physiologic and functional mo-ion of the spinal segment. Since its inception, over 100 pros-
hetic disk types have been designed and manufactured;

owever, only 10 have been implanted into human subjects toate.57 In general, disk replacements are composed of a slidingolyethylene core affixed to the vertebra bodies by 2 metalmplants. Some designs have a metallic core. Outcomes ofnitial studies suggest that lumbar disk arthroplasty was at leasts efficacious as lumbar fusion. Approximately 80% of theatients reported excellent results in these studies. Some haveorrelated this favorable clinical outcome with preservation ofotion of the spinal segment.58

The clinical indications for lumbar disk arthroplasty areairly broad and include back pain, with or without leg pain,solated to no more than 2 symptomatic disks. Provocationiskography may help determine the appropriate disk levelsor treatment but has the aforementioned diagnostic limita-ions. Several factors predict possible failure of this treat-ent, including osteoporosis, structural deformities, and

ain localized to the zygapophyseal joints.59 Reported com-lications are uncommon, with rates ranging from 1.5% to%. Most complications are device related, including im-roper sizing, seating, and location of the prosthesis.60

ong-term clinical data are currently lacking, with impor-ant questions remaining regarding patient selection, in vivourability, and revision options.

References1. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N.

Clinical features of patients with pain stemming from the lumbarzygapophyseal joints. Is the lumbar facet syndrome a clinicalentity? Spine 1994;19:1132-7.

2. Saal JS. General principles of diagnostic testing as related topainful lumbar spine disorders: a critical appraisal of currentdiagnostic techniques. Spine 2002;27:2538-45; discussion 2546.

3. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint inchronic low back pain. Spine 1995;20:31-7.

4. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac jointdouble block and value of sacroiliac pain provocation tests in 54patients with low back pain. Spine 1996;21:1889-92.

5. Slipman CW, Lipetz JS, Plastaras CT, et al. Fluoroscopicallyguided therapeutic sacroiliac joint injections for sacroiliac jointsyndrome. Am J Phys Med Rehabil 2001;80:425-32.

*6. Atlas SJ, Keller RB, Wu YA, Deyo RA, Singer DE. Long-termoutcomes of surgical and nonsurgical management of sciaticasecondary to a lumbar disc herniation: 10 year results from theMaine Lumbar Spine Study. Spine 2005;30:927-35.

7. Takahashi N, Yabuki S, Aoki Y, Kikuchi S. Pathomechanisms ofnerve root injury caused by disc herniation: an experimentalstudy of mechanical compression and chemical irritation. Spine2003;28:435-41.

8. Saal JS, Franson RC, Dobrow R, Saal JA, White AH, Gold-thwaite N. High levels of inflammatory phospholipase A2 activ-ity in lumbar disc herniations. Spine 1990;15:674-8.

9. Kang JD, Georgescu HI, McIntyre-Larkin L, Stefanovic-RacicM, Donaldson WF 3rd, Evans CH. Herniated lumbar interverte-bral discs spontaneously produce matrix metalloproteinases, ni-tric oxide, interleukin-6, and prostaglandin E2. Spine 1996;21:271-7.

10. Kang JD, Stefanovic-Racic M, McIntyre LA, Georgescu HI,Evans CH. Toward a biochemical understanding of human in-tervertebral disc degeneration and herniation. Contributions ofnitric oxide, interleukins, prostaglandin E2, and matrix metallo-proteinases. Spine 1997;22:1065-73.

*Key reference.

*

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*

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11. Nygaard OP, Mellgren SI, Osterud B. The inflammatory prop-erties of contained and noncontained lumbar disc herniation.Spine 1997;22:2484-8.

12. Olmarker K, Blomquist J, Stromberg J, Nannmark U, ThomsenP, Rydevik B. Inflammatogenic properties of nucleus pulposus.Spine 1995;20:665-9.

13. Brisby H, Olmarker K, Larsson K, Nutu M, Rydevik B. Proin-flammatory cytokines in cerebrospinal fluid and serum in patientswith disc herniation and sciatica. Eur Spine J 2002;11:62-6.

14. Halperin N, M Agasi, D Hendel. Painless root compressionfollowing disc extrusion: a report of three cases. Arch OrthopTrauma Surg 1982;101:63-6.

15. Olmarker K, Nordborg C, Larsson K, Rydevik B. Ultrastructuralchanges in spinal nerve roots induced by autologous nucleuspulposus. Spine 1996;21:411-4.

16. Yabuki S, Igarashi T, Kikuchi S. Application of nucleus pulpo-sus to the nerve root simultaneously reduces blood flow in dorsalroot ganglion and corresponding hindpaw in the rat. Spine 2000;25:1471-6.

17. Otani K, Arai I, Mao GP, Konno S, Olmarker K, Kikuchi S.Nucleus pulposus-induced nerve root injury: relationship be-tween blood flow and motor nerve conduction velocity. Neuro-surgery 1999;45:614-9; discussion 619-20.

18. Slipman CW, Chow DW. Therapeutic spinal corticosteroid in-jections for the management of radiculopathies. Phys Med Re-habil Clin N Am 2002;13:697-711.

19. Olmarker K, Byrod G, Cornefjord M, Nordborg C, Rydevik B.Effects of methylprednisolone on nucleus pulposus-inducednerve root injury. Spine 1994;9:1803-8.

20. Onda A, Yabuki S, Kikuchi S, Satoh K, Myers RR. Effects oflidocaine on blood flow and endoneurial fluid pressure in a ratmodel of herniated nucleus pulposus. Spine 2001;26:2186-91;discussion 2191-2.

21. Yabuki S, Kawaguchi Y, Nordborg C, Kikuchi S, Rydevik B,Olmarker K. Effects of lidocaine on nucleus pulposus-inducednerve root injury. A neurophysiologic and histologic study of thepig cauda equina. Spine 1998;23:2383-9; discussion 2389-90.

22. White AH, Derby R, Wynne G. Epidural injections for thediagnosis and treatment of low-back pain. Spine 1980;5:78-86.

23. Manchikanti L, Staats PS, Singh V, et al. Evidence-Based Prac-tice Guidelines for interventional techniques in the managementof chronic spinal pain. Pain Physician 2003;6:3-81.

24. Vad VB, Bhat AL, Lutz GE, Cammisa F. Transforaminal epi-dural steroid injections in lumbosacral radiculopathy: a prospec-tive randomized study. Spine 2002;27:11-6.

25. Riew KD, Yin Y, Gilula L, et al. The effect of nerve-rootinjections on the need for operative treatment of lumbar radicularpain. A prospective, randomized, controlled, double-blind study.J Bone Joint Surg Am 2000;82:1589-93.

26. Depalma MJ, Bhargava A, Slipman CW. A critical appraisal ofthe evidence for selective nerve root injection in the treatment oflumbosacral radiculopathy. Arch Phys Med Rehabil 2005;86:1477-83.

27. Revel M, Poiraudeau S, Auleley GR, et al. Capacity of theclinical picture to characterize low back pain relieved by facetjoint anesthesia. Proposed criteria to identify patients with pain-ful facet joints. Spine 1998;23:1972-6; discussion 1977.

28. Laslett M, Öberg B, Aprill CN, McDonald B. Zygapophysialjoint blocks in chronic low back pain: a test of Revel’s model asa screening test. BMC Musculoskelet Disord 2004;5:43.

29. Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R.Prevalence and clinical features of lumbar zygapophysial jointpain: a study in an Australian population with chronic low back
pain. Ann Rheum Dis 1995;54:100-6.
30. van Kleef M, Barendse GA, Kessels A, Voets HM, Weber WE,de Lange S. Randomized trial of radiofrequency lumbar facetdenervation for chronic low back pain. Spine 1999;24:1937-42.

31. Dreyfuss P, Halbrook B, Pauza K, Joshi A, McLarty J, BogdukN. Efficacy and validity of radiofrequency neurotomy for chroniclumbar zygapophysial joint pain. Spine 2000;25:1270-7.

32. Chou LH, Slipman CW, Bhagia SM, et al. Inciting events initi-ating injection-proven sacroiliac joint syndrome. Pain Med 2004;5:26-32.

33. Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis ofsacroiliac joint pain: validity of individual provocation tests andcomposites of tests. Man Ther 2005;10:207-18.

34. Slipman CW, Jackson HB, Lipetz JS, Chan KT, Lenrow D,Vresilovic EJ. Sacroiliac joint pain referral zones. Arch PhysMed Rehabil 2000;81:334-8.

35. Yin W, Willard F, Carreiro J, Dreyfuss P. Sensory stimulation-guided sacroiliac joint radiofrequency neurotomy: techniquebased on neuroanatomy of the dorsal sacral plexus. Spine 2003;28:2419-25.

36. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N.The prevalence and clinical features of internal disc disruption inpatients with chronic low back pain. Spine 1995;20:1878-83.

37. Cohen SP, Larkin TM, Barna SA, Palmer WE, Hecht AC,Stojanovic MP. Lumbar discography: a comprehensive review ofoutcome studies, diagnostic accuracy, and principles. RegAnesth Pain Med 2005;30:163-83.

38. Carragee EJ, Alamin TF, Miller J, Grafe M. False-positive find-ings on lumbar discography. Reliability of subjective concor-dance assessment during provocative disc injection. Spine 1999;24:2542-7.

39. Derby R, Kim BJ, Lee SH, Chen Y, Seo KS, Aprill C. Compar-ison of discographic findings in asymptomatic subject discs andthe negative discs of chronic LBP patients: can discographydistinguish asymptomatic discs among morphologically abnor-mal discs? Spine J 2005;5:389-94.

40. Derby R, Lee SH, Kim BJ, Chen Y, Aprill C, Bogduk N.Pressure-controlled lumbar discography in volunteers withoutlow back symptoms. Pain Med 2005;6:213-21.

41. Carragee EJ, Alamin TF, Miller J, Grafe M. Provocative discog-raphy in volunteer subjects with mild persistent low back pain.Spine J 2002;2:25-34.

42. Lutz C, Lutz GE, Cooke PM. Treatment of chronic lumbardiskogenic pain with intradiskal electrothermal therapy: a pro-spective outcome study. Arch Phys Med Rehabil 2003;84:23-8.

43. Chou LH, Lew HL, Coelho PC, Slipman CW. Intradiscalelectrothermal annuloplasty. Am J Phys Med Rehabil 2005;84:538-49.

44. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronicdiscogenic low back pain: a prospective outcome study withminimum 1-year follow-up. Spine 2000;25:2622-7.

45. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronicdiscogenic low back pain: prospective outcome study with aminimum 2-year follow-up. Spine 2002;27:966-73; discussion973-4.

46. Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K, BogdukN. A randomized, placebo-controlled trial of intradiscal electro-thermal therapy for the treatment of discogenic low back pain.Spine J 2004;4:27-35.

47. Freeman BJ, Fraser RD, Cain CM, Hall DJ, Chapple DC. Arandomized, double-blind, controlled trial: intradiscal electro-thermal therapy versus placebo for the treatment of chronicdiscogenic low back pain. Spine 2005;30:2369-77; discussion2378.

48. Cohen SP, Williams S, Kurihara C, Griffith S, Larkin TM.
Nucleoplasty with or without intradiscal electrothermal therapy

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(IDET) as a treatment for lumbar herniated disc. J Spinal DisordTech 2005;18(Suppl):S119-24.

49. Alexandre A, Coro L, Azuelos A, Pellone M. Percutaneousnucleoplasty for discoradicular conflict. Acta Neurochir Suppl2005;92:83-6.

50. Marin F. CAM versus nucleoplasty. Acta Neurochir Suppl 2005;92:111-4.

51. Khot A, Bowditch M, Powell J, Sharp D. The use of intradiscalsteroid therapy for lumbar spinal discogenic pain: a randomizedcontrolled trial. Spine 2004;29:833-6; discussion 837.

52. Klein RG, Eek BC, O’Neill CW, Elin C, Mooney V, Derby RR.Biochemical injection treatment for discogenic low back pain: apilot study. Spine J 2003;3:220-6.

53. Alo KM, Wright RE, Sutcliffe J, Scott A, Brandt SA. Percuta-neous lumbar discectomy: one year follow-up in an initial cohortof fifty consecutive patients with chronic radicular pain. PainPractice 2005;5:116-24.

54. Olmarker K, Larsson K. Tumor necrosis factor alpha and nucle-
us-pulposus-induced nerve root injury. Spine 1998;23:2538-44.

55. Karppinen J, Korhonen T, Malmivaara A, et al. Tumor necro-sis factor-alpha monoclonal antibody, infliximab, used tomanage severe sciatica. Spine 2003;28:750-3; discussion753-4.

56. Korhonen T, Karppinen J, Paimela L, et al. The treatment of discherniation-induced sciatica with infliximab: results of a random-ized, controlled, 3-month follow-up study. Spine 2005;30:2724-8.

57. Regan JJ. Clinical results of charite lumbar total disc replace-ment. Orthop Clin North Am 2005;36:323-40.

58. Huang RC, Girardi FP, Cammisa FP Jr, Lim MR, Tropiano P,Marnay T. Correlation between range of motion and outcomeafter lumbar total disc replacement: 8.6-year follow-up. Spine2005;30:1407-11.

59. McAfee PC. The indications for lumbar and cervical disc re-placement. Spine J 2004;4(6 Suppl):177S-81S.

60. Bertagnoli R, Zigler J, Karg A, Voigt S. Complications andstrategies for revision surgery in total disc replacement. Orthop
Clin North Am 2005;36:389-95.

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ndustrial Medicine and Acute Musculoskeletal Rehabilitation.. Upper- and Lower-Limb Injections for Acuteusculoskeletal Injuries and Injured Workers

atrick M. Foye, MD, William J. Sullivan, MD, Andre Panagos, MD, Joseph P. Zuhosky, MD,
aron W. Sable, MD, Robert W. Irwin, MD
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ABSTRACT.. Foye PM, Sullivan WJ, Sable AW, Panagos A,uhosky JP, Irwin RW. Industrial medicine and acute musculo-keletal rehabilitation. 6. Upper- and lower-limb injections forcute musculoskeletal injuries and injured workers. Arch Physed Rehabil 2007;88(3 Suppl 1):S29-33.

This self-directed study module focuses on the use of corti-osteroids and other injections in the treatment of lateral epi-ondylitis, de Quervain’s tenosynovitis, carpal tunnel syn-rome, Achilles’ tendinitis, and plantar fasciitis. It is part of thetudy guide on industrial rehabilitation medicine and acuteusculoskeletal rehabilitation in the Self-Directed Physiatricducation Program for practitioners and trainees in physicaledicine and rehabilitation.Overall Article Objective: To review the medical literature

o help clinicians make treatment decisions regarding cortico-teroid and other injections in the upper and lower limbs innjured workers.

Key Words: Achilles tendon; Carpal tunnel syndrome; Cor-icosteroids; Injections; Fasciitis; Rehabilitation; Tendinitis;ennis elbow; Tenosynovitis; Tendon injuries.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Clinical Activity: To analyze the risks and benefits ofcorticosteroid injections for a 40-year-old right-handed carpenter with lateral epicondylitis.

RECENT LITERATURE REVIEW1 of complications ofcorticosteroid injections for musculoskeletal conditions in-

luding lateral epicondylitis concluded that, among dozens ofandomized controlled trials (RCTs), only minor complicationsere reported. Overall, approximately 15% of patients reported

ide effects, with 10% reporting postinjection pain (the mostommon side effect), about 2% reporting skin atrophy, and lesshan 1% reporting either skin depigmentation, localized erythemaith warmth, or facial flushing.

From the Department of Physical Medicine and Rehabilitation, University ofedicine and Dentistry of New Jersey: New Jersey Medical School, Newark, NJ

Foye); Department of Physical Medicine and Rehabilitation, University of Coloradot Denver and Health Sciences Center, Denver, CO (Sullivan); Department of Reha-ilitation Medicine, Weill Cornell Medical Center, New York–Presbyterian Hospital,ew York, NY (Panagos); Total Spine Specialists, Department of Physical Medicine

nd Rehabilitation, Carolinas Medical Center, Charlotte, NC (Zuhosky); St. John’sacomb Hospital, Warren, MI (Sable); and Department of Rehabilitation Medicine,niversity of Miami, Miller School of Medicine, Miami, FL (Irwin).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Patrick M. Foye, MD, Dept of PM&R, UMDNJ: New Jerseyedical School, 90 Bergen St, DOC-3100, Newark, NJ 07103, e-mail:


w0003-9993/07/8803S-11409$32.00/0doi:10.1016/j.apmr.2006.12.013

Postinjection exacerbations seem to be of short duration. Aecent RCT2 of patients with lateral epicondylitis compared 3reatments: corticosteroid injection, naproxen, and oral placebo.he study showed that although 62% of patients may initiallyave increased pain after the injection, by day 4 their pain scoresere significantly lower and they were less likely to be taking

cetaminophen than patients who received either naproxen or orallacebo. The researchers concluded that patients would perceivehe “modest” increased pain postinjection “to be acceptable, givenhe clear benefits of localized corticosteroid injection treatmentver the following few weeks.”2(p333)

Although serious complications were not reported within theecently reviewed RCTs, published case reports have describedoncerning side effects such as tendon rupture, including rup-ure at the lateral epicondyle tendon origin.1 However, theiterature review1 concluded that the case reports could notrove that corticosteroid injections actually cause tendon rup-ure, because the underlying tendon pathology that promptsnjection may also be the underlying cause (or at least aontributing factor) to subsequent tendon rupture. Even thease reports of tendon rupture after multiple injections at aarticular site could possibly reflect cases with more severereinjection pathology (and thus the failure to respond ade-uately to a single injection). It still may be prudent, however,o consider multiple injections as a source of increased risk forupture. Overall, the literature does not provide clear evidenceo confirm what constitutes a safe maximal number of cortico-teroid injections, although various investigators have opinedn this.Different corticosteroid agents have had varying impacts on

osttreatment tendon strength. Mechanical structural defectsnd tendon rupture occurred more commonly in tendons treatedith triamcinolone acetonide than in those treated with meth-lprednisolone, betamethasone, or hydrocortisone.1

A recent literature review3 concluded that these injections weressociated with statistically significant and clinically relevant im-rovements in pain, global improvement, and grip strength com-ared with placebo, local anesthetic injections (without steroid),nd noninjection treatments. In fact, among the published studieshat met the criteria for that review, almost all studies concludedhat corticosteroid injections provided more favorable outcomesor all measured parameters (eg, pain, grip strength) in the shorterm (�6wk). Longer-term benefit (�6wk) was more difficult tossess because of variable study designs and the lack of high-uality studies. Thus, the researchers concluded that the currentiterature does not provide a basis for firm conclusions regardingenefit beyond 6 weeks.3

In the context of workers’ compensation injuries, the initialaster onset of improvement clearly provided by the injectionsay presumably translate into quicker return to work and/or

etter tolerance for work-related activities during those initial
eeks.

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S30 UPPER- AND LOWER-LIMB INJECTIONS FOR ACUTE MUSCULOSKELETAL INJURIES AND INJURED WORKERS, Foye

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Thus, the literature indicates that corticosteroid injectionsre very effective in the treatment of lateral epicondylitisparticularly during the initial months after injection) and thaterious complications of injections are uncommon.

Substances other than corticosteroids have also been injected toreat lateral epicondylitis. There are a few published studies4,5 onhe potential role of botulinum toxin in treating chronic lateralpicondylitis, with mixed results. There is a single, modest-sizedtudy6 with impressive outcomes after autologous blood injectiont the lateral epicondyle region. Of 28 patients with refractoryateral epicondylitis despite various nonsurgical treatments whoere injected with 2mL of autologous blood at the lateral elbow,2 (79%) had complete pain relief even with strenuous activity.6

he researchers speculated that the local injection of blood maynduce inflammatory changes that improve recovery, althoughverall the mechanism remains unclear. Further research is neededefore any definitive consensus can be reached on these treatmentpproaches.

.2 Clinical Activity: To assess the advantages and disad-vantages of administering focal corticosteroid injec-tions in a right-handed male secretary with de Quer-vain’s tenosynovitis at the right wrist. His symptomsfailed to resolve after ergonomic modifications of hiscomputer workstation, use of nonsteroidal anti-in-flammatory drugs, and use of a thumb spica splint.

A recently published, pooled, quantitative evaluation7 assessedhe medical literature for treatment outcomes for de Quervain’senosynovitis. The researchers excluded from review any articleshat did not meet their diagnostic criteria (documentation of paint the radial wrist, tenderness at the first dorsal wrist extensorompartment, a positive Finkelstein test) and also excluded arti-les that did not re-evaluate these same 3 findings after treatment.nly 7 studies met the criteria to be included in this review. Thesestudies included 459 wrists subjected to 1 or several therapeuticodalities. The results were pooled for analysis. The most com-on intervention was corticosteroid injection alone. Analysis

howed that a symptomatic cure was achieved in 83% of the 226rists that received injection alone, 61% of the 101 wrists that

eceived injection and splint immobilization, and 14% of the 76rists that received splinting alone. Conversely, no such symp-

omatic cure was achieved in any of the 17 wrists treated with restlone or in any of the 39 wrists treated with nonsteroidal anti-nflammatory drugs (NSAIDs) alone. Thus, the pooled resultseem to indicate that corticosteroid injection alone (without splint-ng or other treatment) is by far the most effective. The investi-ators concluded that such injections are a simple, cost-effective,nd definitive treatment.7

The complication rate of corticosteroid injection to treat deuervain’s tenosynovitis is very low. A literature review byichie and Briner7 of 327 wrists that received 1 or multiple

njections (either alone or in combination with splinting) re-orted no cases of tendon rupture. The reported side effects ofnjections were 18 cases of skin color changes (eg, hypopig-entation), 16 cases of subcutaneous fat atrophy (all of whichere among those same 18 cases of skin color changes), 5

ases of flare, 2 nontender nodules, and a single case ofuperficial thrombophlebitis.7 Because that article was not ex-licit on the total number of injections given among the subsetf patients receiving multiple injections, it is unfortunately notossible to calculate the exact complication rate per injection.owever, there were at least 357 injections, and thus the

alculated complication rate would be, at most, 5% for skinolor changes, 1.4% for flare, 0.6% for nontender nodules, and
.3% for superficial thrombophlebitis. The literature contains s

nly 1 case report8 of corticosteroid injection into a first dorsalompartment causing persistent cheiralgia paresthetica (painfulysesthesias in the distribution of the superficial radial nerve).Thus, overall, the literature strongly supports the use of first

orsal compartment corticosteroid injection for de Quervain’senosynovitis, with very favorable outcomes (ie, most patientschieved a symptomatic cure) and very low rates of complica-ions.

.3 Clinical Activity: To discuss the use of corticosteroidinjection into the carpal tunnel for an assemblyworker with carpal tunnel syndrome in whom the useof a wrist splint has given inadequate relief.

Injecting corticosteroids into the carpal tunnel can be doney injecting just ulnar to the palmaris longus tendon at the wristnto the ulnar bursa (tenosynovium surrounding the deep anduperficial flexors of digits 2–5).

There are some discrepancies in the medical literature abouthe effectiveness of corticosteroid injection to treat carpal tun-el syndrome (CTS). A recent meta-analysis9 of RCTs con-luded that compared with placebo injection, local injection oforticosteroids provided symptomatic improvement of CTS 1onth after injection. Further, the same meta-analysis con-

luded that compared with oral steroids, local injection oforticosteroids provides significantly greater clinical improve-ent up to 3 months after treatment.9

Even more recently, a 1-year, prospective RCT in 163 wristsith CTS compared surgical decompression versus local injectionf corticosteroids into the carpal tunnel. All clinical diagnosesf CTS were electrodiagnostically confirmed. Subjects withlinically visible thenar atrophy were excluded. The studyoncluded that over the short term (3mo), local injection oforticosteroids is better than surgical decompression for theymptomatic relief of CTS. At 1 year, local injection is asffective as surgical decompression for the symptomatic relieff CTS.10

Thus, the literature suggests that corticosteroid injectionrovides at least short-term (1–3mo) symptomatic relief forTS patients, and may rival surgical treatment even at 1 year.hese studies may suggest that, at least for patients with justild or moderate CTS, corticosteroid injection may be theost appropriate initial treatment (eg, combined with wrist

plinting), with surgery reserved for patients with severe oronresponsive CTS. The caveat may be to provide close med-cal monitoring to make sure that patients being treated non-urgically do not progress to the point of irreversible nerveamage and muscle atrophy.The literature has also indicated that injecting corticosteroids

nto the carpal tunnel can improve median nerve function, aseasured by motor and sensory nerve conduction studies. A

ecent study11 of CTS treatments showed that corticosteroid in-ection is superior to iontophoresis and phonophoresis and foundhat that the most sensitive neurophysiologic parameters in fol-ow-up were the difference between the median and ulnar distalensory latencies to the fourth digit and also the difference be-ween median distal sensory latency to second digit and ulnaristal sensory latency to the fifth digit.

Other studies have also shown electrodiagnostic improvementsn objective median nerve conduction parameters after injectionnto the carpal tunnel. For example, 1 prospective study12 evalu-ted clinically mild CTS (defined as intermittent symptoms with-ut thenar atrophy, thenar weakness, or absence of sensations).hese 48 clinically mild CTS cases included electrodiagnosticallyild, moderate, and severe CTS but excluded the electrically most

evere cases (needle electromyography showing abnormal spon-

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aneous activity in the thenar muscles and/or a median nerve distalotor latency greater than 7.5ms). The study showed that at 3onths after the injection, 93.7% of the patients reported marked

mprovement in their symptoms, with significant improvement inistal motor latencies, distal sensory latencies, symptom severity,nd functional scores. Improvements were seen among patientsith electrically mild, moderate, and severe CTS. Significant

mprovement was still present for median distal motor latency at2 months. Almost 50% of patients achieved normalization in thelectrophysiologic study. At an average follow-up of 16 months,9% of patients continued to have improvement in symptoms. Ofatients studied, 16.6% relapsed clinically after an initial responsehat lasted 7 to 15 months. The researchers concluded that localnjection of corticosteroid results in long-term improvement inerve conduction parameters, symptom severity, and functionalcores in patients whose CTS is clinically mild and electrodiag-ostically mild, moderate, or somewhat severe.12

One RCT13 examined intracarpal insulin injection to treatTS. In patients with non–insulin-dependent diabetes mellitusnd mild to moderate CTS, 20mg of methylprednisolone wasnjected into the carpal tunnel. A week after receiving a corti-osteroid injection, patients were randomized to receive addi-ional injections into the carpal tunnel, with placebo orsophane insulin (12U), weekly for 7 weeks. Those patientsho received insulin injections showed a more significant

mprovement in mean median nerve distal motor latency, me-ian nerve sensory velocity, and global symptom score. Thensulin injections did not appreciably change the overall glu-ose control, and the mechanism of CTS improvement wasnclear. Further research is needed to establish what rolensulin injections into the carpal tunnel may have in the non-urgical treatment of CTS.

.4 Clinical Activity: To critique the risks and benefits offocal corticosteroid injections in the treatment ofAchilles’ tendinitis in a heavy laborer.

The medical literature currently provides no definitive con-ensus regarding the benefits and risks of focal corticosteroidnjections for Achilles’ tendinitis.

Regarding risks, a 1% overall incidence of side effectsincluding subcutaneous atrophy and depigmentation) was re-orted by a systematic review14 of 145 published articleselated to Achilles’ tendinitis and corticosteroid injections. Theeviewers noted that animal studies of intratendinous injectionshowed decreased tendon strength, thus suggesting increased riskf tendon rupture. Although they found multiple published in-tances of Achilles’ tendon rupture after injection, most of theseere isolated case reports or small case series. One inherentroblem with case reports of complications is that they generallyail to have any control group for comparison, thus making itmpossible statistically to conclude that the risk of that complica-ion was increased. The reviewers concluded that no publishedigorous studies existed evaluating the risk of Achilles’ tendonupture. Finally, they concluded that insufficient published dataxist to determine the comparative risks and benefits of cortico-teroid injections for Achilles’ tendinitis.14

Another study15 looked retrospectively at 64 consecutiveatients with Achilles’ tendon pain (excluding, eg, rupturesnd excluding patients with concomitant peroneal tendon-tis) who specifically had Achilles’ pain at rest that im-roved with activity. Of these 64 patients, 35 chose tondergo corticosteroid injection and 29 chose not to have itot randomized. Subsequently, 2 patients in each groupeveloped tendon rupture, representing 6% of patients who
ad undergone injection and 8% of those who had not s
ndergone injection. The researchers concluded that injec-ions did not increase the rupture rate.

A recent review article analyzed 9 randomized or quasi-andomized trials involving 697 patients with Achilles’ ten-initis.16 There was weak evidence of a modest benefit ofSAIDs for alleviation of acute symptoms. There was weak

vidence of no difference (compared with no treatment) ofow-dose heparin, heel pads, topical laser therapy, and peri-endinous injection of corticosteroids. The reviewers con-luded that evidence from RCTs was insufficient to deter-ine the most appropriate treatment of acute or chronicchilles’ tendinitis.A number of recent studies have examined the potential

ole of ultrasound (eg, Doppler) or fluoroscopy for imageuidance during injections for Achilles’ tendon pathology.heoretically, better outcomes (improved benefits and/orecreased side effects) could be obtained by more preciseeritendinous placement of the corticosteroid along the ten-on sheath, rather than inadvertent injection into the sub-tance of the tendon itself. A recent retrospective cohorttudy17 examined fluoroscopically guided injections alonghe anterior aspect of the Achilles’ tendon for Achilles’endinopathy: 43 patients had undergone injections, with aollective total of more than 80 injections (including 1atient having 14), and all subjects had at least 2 years ofollow-up after injection. There was 1 minor complicationpersistent purplish skin discoloration after 2 injections), buto tendon ruptures or other major complications were re-orted. Of the patients, 17 (40%) reported improvementfter the procedure(s), 23 (53%) thought that their conditionas unchanged, and 3 (7%) thought that their condition wasorse than it had been before the injection.Although the literature is increasingly reporting the use of

uch image guidance for Achilles’-related injections, the liter-ture currently lacks any substantial studies comparing theutcomes with and without it, thus leaving it to each individuallinician to decide whether to use such imaging techniques.

Other published articles have examined treating Achilles’endinitis with injections of agents other than corticoste-oids. These potential alternatives include injection of scle-osing agents into newly proliferated blood vessels (neoves-els),18 injection of viscosupplementation agents (eg, Hylan-F 20),19 and a variety of other biologic substances. Fur-

her research is needed to determine what role these agentsave in the management of Achilles’ tendinitis.

.5 Clinical Activity: To evaluate the role of corticoste-roid injections in the management of persistent plan-tar fasciitis in a salesperson working at a home im-provement warehouse. The proximal plantar pain hasprogressed to the point where it is painful not onlywith the first steps in the morning but also throughoutthe workday, which involves prolonged standing andwalking on concrete floors.

Overuse and microtears of the plantar fascia may contributeo plantar fasciitis, because histologic studies show collagenegeneration and necrosis.20 Because the histologic findings doot universally show inflammatory changes, some cliniciansrefer the term plantar fasciopathy or fasciosis rather thanlantar fasciitis.20 The possible lack of inflammation is ger-ane to the discussion of injecting anti-inflammatory agents

uch as corticosteroids. Still, corticosteroid injections are com-only used as part of the nonsurgical treatment for plantar

asciitis. More than 80% to 90% of patients respond to non-
urgical care, including corticosteroid injections.20 It has been

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S32 UPPER- AND LOWER-LIMB INJECTIONS FOR ACUTE MUSCULOSKELETAL INJURIES AND INJURED WORKERS, Foye

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uggested that corticosteroids may be beneficial because ofheir antinociceptive and membrane-stabilizing propertiesather than just their anti-inflammatory properties.21

A recent RCT of plantar fasciopathy treatment comparedxtracorporeal shockwave therapy (ECSWT) with cortico-teroid injection, with 3- and 12-month follow-ups. Thenvestigators concluded that the injections were more effi-acious (significantly lower pain scores, per visual analogcale) and were much more cost effective than ECSWT.22

One potential drawback to corticosteroid injection forlantar fasciitis is the pain of the injection. A recent RCT ofuoroscopically guided corticosteroid injection for plantarasciitis compared performing the injection with versusithout an antecedent posterior tibial nerve block with 5mLf 1% lidocaine.23 Except for a mild burning sensation, painuring posterior tibial block was negligible in all cases.mong patients who had undergone the posterior tibialerve block, the plantar injection was considered painless in0% (9/10) and just mildly painful in 10% (1/10). Amongatients who had not received the nerve block, the plantarnjection was considered severely painful in 70% (7/10) andoderately painful in 30% (3/10). Among those who re-

eived the nerve block, no patients had complications (de-pite an increased number of injections per patient, becauseatients receiving nerve blocks were more likely to allowhe injection to be repeated). Among those who did noteceive the nerve block, 10% (1/10) of patients developedat necrosis and 10% (1/10) developed pressure periostitis.

Plantar fascia rupture has been reported as a possibleomplication of corticosteroid injections. In a retrospective,onrandomized study of 122 patients who received 1 orore injections, 12 (10%) patients developed plantar fascia

uptures.20 An overlapping patient population in that studyhowed that of 51 patients with plantar fascia rupture, 4384%) had received 1 or more injections into the calcanealrigin of the fascia.20 The retrospective, nonrandomizedature of this and similar studies makes it impossible toonclude that the corticosteroid injection actually causeslantar fascia rupture, because perhaps patients with moreevere pathology (and hence a higher likelihood for rupture)ere more likely to receive injections in the first place. Still,ased on the number of case reports of plantar fascia rupturefter injection, it seems prudent during informed consent todvise patients of this possible risk.

Plantar fat pad necrosis has been reported as another possibleerious complication of corticosteroid injection for plantar fas-iitis.22

Until further research clarifies the role of image guidanceeg, via fluoroscopy or ultrasound) in the performance oflantar fascia injections, clinicians must use their own discre-ion in deciding whether to use such guidance in a givennjection.

References*1. Nichols AW. Complications associated with the use of cortico-

steroids in the treatment of athletic injuries. Clin J Sport Med2005;15:370-5.

2. Lewis M, Hay EM, Paterson SM, Croft P. Local steroid injec-tions for tennis elbow: does the pain get worse before it getsbetter? Results from a randomized controlled trial. Clin J Pain2005;21:330-4.

*Key reference.


3. Smidt N, Assendelft WJ, van der Windt DA, Hay EM, Buch-binder R, Bouter LM. Corticosteroid injections for lateral epi-condylitis: a systematic review. Pain 2002;96:23-40.

4. Hayton MJ, Santini AJ, Hughes PJ, Frostick SP, Trail IA, Stan-ley JK. Botulinum toxin injection in the treatment of tenniselbow. A double-blind, randomized, controlled, pilot study.J Bone Joint Surg Am 2005;87:503-7.

5. Keizer SB, Rutten HP, Pilot P, Morre HH, v Os JJ, Verburg AD.Botulinum toxin injection versus surgical treatment for tenniselbow: a randomized pilot study. Clin Orthop Relat Res 2002;Aug(401):125-31.

6. Edwards SG, Calandruccio JH. Autologous blood injections forrefractory lateral epicondylitis. J Hand Surg [Am] 2003;28:272-8.

*7. Richie CA 3rd, Briner WW Jr. Corticosteroid injection for treat-ment of de Quervain’s tenosynovitis: a pooled quantitative liter-ature evaluation. J Am Board Fam Pract 2003;16:102-6.

8. Chodoroff G, Honet JC. Cheiralgia paresthetica and linear atro-phy as a complication of local steroid injection. Arch Phys MedRehabil 1985;66:637-9.

9. Marshall S, Tardif G, Ashworth N. Local corticosteroid injectionfor carpal tunnel syndrome. Cochrane Database Syst Rev 2002;(4):CD001554.

10. Ly-Pen D, Andreu JL, de Blas G, Sanchez-Olaso A, Millan I.Surgical decompression versus local steroid injection in car-pal tunnel syndrome: a one-year, prospective, randomized,open, controlled clinical trial. Arthritis Rheum 2005;52:612-9.

11. Aygul R, Ulvi H, Karatay S, Deniz O, Varoglu AO. Determina-tion of sensitive electrophysiologic parameters at follow-up ofdifferent steroid treatments of carpal tunnel syndrome. J ClinNeurophysiol 2005;22:222-30.

12. Agarwal V, Singh R, Sachdev A, Wiclaff, Shekhar S, Goel D. Aprospective study of the long-term efficacy of local methylpred-nisolone acetate injection in the management of mild carpaltunnel syndrome. Rheumatology (Oxford) 2005;44:647-50.

13. Ozkul Y, Sabuncu T, Yazgan P, Nazligul Y. Local insulininjection improves median nerve regeneration in NIDDMpatients with carpal tunnel syndrome. Eur J Neurol 2001;8:329-34.

14. Shrier I, Matheson GO, Kohl HW 3rd. Achilles tendonitis: arecorticosteroid injections useful or harmful? Clin J Sport Med1996;6:245-50.

15. Read MT. Safe relief of rest pain that eases with activity inachillodynia by intrabursal or peritendinous steroid injection: therupture rate was not increased by these steroid injections. Br JSports Med 1999;33:134-5.

16. McLauchlan GJ, Handoll HH. Interventions for treating acuteand chronic Achilles tendinitis. Cochrane Database Syst Rev2001;(2):CD000232.

17. Gill SS, Gelbke MK, Mattson SL, Anderson MW, Hurwitz SR.Fluoroscopically guided low-volume peritendinous corticoste-roid injection for Achilles tendinopathy. A safety study. J BoneJoint Surg Am 2004;86:802-6.

18. Ohberg L, Alfredson H. Ultrasound guided sclerosis of neoves-sels in painful chronic Achilles tendinosis: pilot study of a newtreatment. Br J Sports Med 2002;36:173-5; discussion 176-7.

19. Tatari H, Skiak E, Destan H, Ulukus C, Ozer E, Satoglu S. Effectof hylan G-F 20 in Achilles’ tendonitis: an experimental study inrats. Arch Phys Med Rehabil 2004;85:1470-4.

20. Acevedo JI, Beskin JL. Complications of plantar fascia rup-ture associated with corticosteroid injection. Foot Ankle Int1998;19:91-7.

21. Akuthota V, Chou LH, Drake DF, Nadler SF, Toledo SD. Sports
and performing arts medicine. 2. Shoulder and elbow overuse

*S

S33UPPER- AND LOWER-LIMB INJECTIONS FOR ACUTE MUSCULOSKELETAL INJURIES AND INJURED WORKERS, Foye

injuries in sports. Arch Phys Med Rehabil 2004;85(3 Suppl1):S52-8.

22. Porter MD, Shadbolt B. Intralesional corticosteroid injectionversus extracorporeal shock wave therapy for plantar fasciopa-thy. Clin J Sport Med 2005;15:119-24.

23. Govindarajan R, Bakalova T, Doss NW, Splain SH, Michael R,
Abadir AR. Posterior tibial nerve block in the therapeutic man-
agement of painful calcaneal spur (plantar fasciitis): a prelimi-nary experience. Can J Anaesth 2003;50:862-3.

Suggested Readingtitik TP, Foye PM, Chen B, Nadler SF, Joint and soft tissue cortico-

steroid injections: a practical approach. Consultant 2000;40:
1469-75.

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ndustrial Medicine and Acute Musculoskeletal Rehabilitation.. Acute Industrial Musculoskeletal Injuries in the Agingorkforce

oseph P. Zuhosky, MD, Robert W. Irwin, MD, Aaron W. Sable, MD, William J. Sullivan, MD,
ndre Panagos, MD, Patrick M. Foye, MD
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ABSTRACT. Zuhosky JP, Irwin RW, Sable AW, SullivanJ, Panagos A, Foye PM. Industrial medicine and acute mus-

uloskeletal rehabilitation. 7. Acute industrial musculoskeletalnjuries in the aging workforce. Arch Phys Med Rehabil 2007;8(3 Suppl 1):S34-9.

This learning module highlights the unique challenges facedy physicians treating the aging workforce. It is part of thendustrial medicine and acute musculoskeletal rehabilitationtudy guide in the Self-Directed Physiatric Education Programor practitioners and trainees in physical medicine and rehabil-tation. Factors intrinsic and extrinsic to the patient that in-rease the risk of injury with aging are outlined. Low backnjuries are the most common musculoskeletal complaint in theging workforce. A conceptual framework for low back painith aging, a differential diagnosis, and appropriate laboratory

nd radiographic investigations are also presented. Determina-ion of causation in the setting of comorbid medical conditionsnd rehabilitation strategies are reviewed.

Overall Article Objective: To recognize diagnosis andreatment issues that are unique to the aging worker.

Key Words: Aging; Cumulative trauma disorders; Industrialedicine; Low back pain; Rehabilitation.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Educational Activity: To explain the current and fu-ture demographic trends in the aging population ofworkers in the United States.

HE AGING OF THE U.S. population has been well chron-icled in both the medical literature and the general media.

greater proportion of U.S. citizens is over age 65 currentlyhan at any other time in history, with projections for continuedrowth in this segment of the population over the next 30 years.ccording to the 2000 census, there was a 49% increase in the5-to-54–year age group over the previous 10 years, the mostapid increase in any demographic group.1 This rise reflects the

From the Total Spine Specialists, Department of Physical Medicine and Rehabil-tation, Carolinas Medical Center, Charlotte, NC (Zuhosky); Department of Rehabil-tation Medicine, University of Miami, Miller School of Medicine, Miami, FLIrwin); St. John’s Macomb Hospital, Warren, MI (Sable); Department of Physical

edicine and Rehabilitation, University of Colorado at Denver and Health Sciencesenter, Denver, CO (Sullivan); Department of Rehabilitation Medicine, Weill Cornelledical Center, New York–Presbyterian Hospital, New York, NY (Panagos); andepartment of Physical Medicine and Rehabilitation, University of Medicine andentistry of New Jersey: New Jersey Medical School, Newark, NJ (Foye).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Joseph P. Zuhosky, MD, Total Spine Specialists, 9611 Sherrill

states Rd, Ste B, Huntersville, NC 28078, e-mail: [email protected]. Re-rints are not available from the author.

m0003-9993/07/8803S-11410$32.00/0doi:10.1016/j.apmr.2006.12.014


ging of the “baby boomer” generation, those born between946 and 1964. This generation remains quite active, and whenolled, the American Association of Retired Persons reportedhat up to 79% of seniors (age �50y) plan to work part time orull time after “retirement.”2 With an “older worker” definedrbitrarily in the literature as age 40 years and older, this groupill soon become a majority of the workforce in the very near

uture. Injuries in this “graying workforce” will present newhallenges to the medical community, employers, and workers’ompensation insurance carriers.

.2 Clinical Activity: To identify the factors intrinsic andextrinsic to a 65-year-old industrial worker that maypredispose her to a workplace injury.

Many factors increase the risk of occupational injuries inlder workers. Those commonly cited in the literature includegeneral decline in vision and hearing with increasing age.

indings from the Health and Retirement Study,3 validatedy the National Health Interview Survey,4 and other studies5

ffirm that diminished vision and hearing are independent riskactors for occupational injury. Diminished sensory inputlaces older workers at risk for falls and is 1 of the leadingauses of injury among all older adults, regardless of worktatus. Much of the literature, however, focuses on extrinsic,nvironmental sources of falls such as surface traction, con-aminant control, and footwear.6 Among those workers pre-enting to an emergency department with an industrial muscu-oskeletal injury, workers over age 65 years are most likely toresent with a fracture or dislocation, an injury resulting from

fall to the ground from the same level, and to requireospitalization.7 Besides diminished vision and hearing, olderdults also experience depressed autonomic reflexes, whichredisposes them to postural hypotension, syncopal episodes,nd, hence, to falls. Concomitant medication usage, particu-arly antihypertensive medications, may compound this risk.lder workers also may have aging-related decreases in sen-

ory and motor nerve conduction. Although the prevalence ofhese decreases in nerve function in older workers has not beenstablished, affected workers may have clinically impairedibratory sensation, reduced cutaneous pressure sensation, androlonged sensory and motor latencies.8 Although the mostommon diagnosable cause of peripheral neuropathy in thenited States remains diabetes mellitus, other etiologies occur-

ing with increasing frequencies in older adults include periph-ral neuropathies associated with herpes zoster, vitamin B12eficiency, and carcinoma. Identifying these impairments androviding modifications in work requirements and work envi-onment are crucial for successful rehabilitation and re-entry tohe workforce.

Less commonly considered factors in older workers maylso contribute to work-related injuries. The prevalence ofepression tends to increase with age. Somatic manifestations
ay mimic acute musculoskeletal injury and should be sought

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ut, especially in those patients not responding to treatment. Inatients on cholesterol-lowering medications, side effects ofuscle pains and myopathy9 may also mimic acute musculo-

keletal injury and confound the etiology of these symptoms.Older workers have long been considered predisposed tousculoskeletal injuries. The vicious cycle of musculotendi-

ous overload presents a schematic and conceptual frameworkor this inherent risk (fig 1).10

The biomechanic deficits enumerated in figure 1 all occur, toarying degrees, with aging and cumulative trauma.11 Muscu-ar weakness occurs after age 30 years in association witheneralized muscle fiber atrophy, decreased muscle density,nd increased intramuscular fat.12,13 The resultant diminisheduscle mass and strength may be further compounded by

nactivity and aerobic deconditioning. This reduction in muscleass, strength, and endurance appears to accelerate after age

0 years. The observed reductions in strength are 15% perecade between ages 50 to 70 years and 30% per decadehereafter.11,12

Inflexibility results from shortening of muscle fiber lengthnd diminished extensibility of tendons and connective tissuesurrounding joints. With age, the tensile strength of tendonsecreases.14 Coupled with the loss of strength is a decrease inoth insoluble and total collagen.15 This combination results inecreased flexibility, which increases the likelihood of tissuerauma. Cumulative microtrauma from repetitive activities pro-uces inflammation, or even “scarring,” and thickening of theendinous sheath.16 In conjunction with the weakening muscu-ature associated with aging, the resultant inflexibility andicrotrauma further exacerbate muscle imbalances resulting

rom improper or compensatory strategies, improper body me-hanics, and poor posture accumulating over years.15 Over-tressing of these soft tissues leads to muscle strain, ligamentprain, tendon strain, or rupture as described by in the viciousycle of musculotendinous overload.

.3 Clinical Activity: To identify specific occupationsand work-related activities that predispose an olderworker to potential work-related injury.

The literature exploring this observation of an increased riskf musculoskeletal injury in older workers varies depending onhe industry. In certain populations, such as workers in the coalining17 and construction industries,18 age is clearly a risk

actor for industrial musculoskeletal injury. Types of injuriesithin these groups may also differ when stratified for age.lder union carpenters are more likely to sustain fractures of

he foot but less likely to sustain contusions of the hand oroot.19 Older workers in the service industries, agriculture,

ig 1. Vicious cycle of musculotendinous overload. From Kibler etl.10 Reprinted with permission.

orestry, and fishing industries7 mechanics, repairers, and those c

erforming heavy lifting3 have been observed by some inves-igators to be particularly at risk for musculoskeletal injury.owever, another investigation20 suggested a lower injury rate

mong older workers than younger (age �25y) workers. In atudy of poultry workers and data-entry personnel (groupsnown to have high rates of cumulative trauma disordersCTDs]), there was no statistical increased susceptibility toTDs such as nerve compression syndromes, tenosynovitis,picondylitis, or tendinitis in older workers when comparedith their younger counterparts.8 In a study21 of materialandlers in a home improvement retail chain, musculoskeletalnjury rates in workers over age 55 years were similar to thosen younger workers, even when length of employment andifting intensity were taken into consideration.

.4 Educational Activity: To discuss the available litera-ture addressing the impact of older age on functionaloutcomes in work-related injuries.

When observing outcome studies of injured workers, there isclearer trend of longer periods of disability resulting from

ccupational injuries in older workers. In the study of materialandlers cited earlier,21 although the prevalence of injury waso greater in the older cohort (age �55y), the amount of lostork time because of injury was significantly greater in thisroup. Among construction workers, a retrospective assess-ent determined that the risk of development of chronic symp-

oms after a musculoskeletal soft-tissue injury was significantlyreater in older workers.22 Prospective trials affirm the sig-ificant correlation among lost work time in older workers,heir decreased likelihood of return to work, and a higherrobability of future disability.23 Considering the subset oforkers with spine injuries, age was linearly associated withoth pretreatment duration of disability and frequency of sur-eries.24 Further, older workers have a higher level of post-reatment disability, and they have a higher likelihood of re-urrent injury.23 A review25(p162) of the international literatureuggests that older workers “sustain more serious injuries, takeonger to recover, and are less likely to return to work thanounger workers.” The risk of fatality associated with injury inhe workplace clearly increases with age as well,20,26 with deathesulting from falls of lesser heights and lower energies ofmpact.27

.5 Clinical Activity: To summarize how increasing ageaffects the differential diagnosis of low back pain.

Medical comorbidities in older workers present further con-ounding variables in their diagnosis and treatment. For exam-le, low back injuries are the most common musculoskeletalnjuries in the aging workforce and present unique diagnostichallenges. The maximal frequency of low back pain (LBP)ccurs between the ages of 35 and 55 years, and the duration ofymptoms increases with increasing age.28 The differentialiagnosis for these symptoms should extend well beyond theolloquial lumbosacral sprain or strain. Spinal etiologiesay include a lumbar annular tear or disk protrusion, a

umbar or lower-thoracic compression fracture, zygapophy-eal joint mediated pain, or segmental injury and dysfunctionith myofascial pain, that is, the sprain alluded to earlier. Theegenerative cascade model of Kirkaldy-Willis provides aramework in which to conceptualize the dynamic changes thatccur during aging of the lumbar spine.29 In this model, the-joint complex of the intervertebral disk and paired zyg-pophyseal joints undergo characteristic and somewhat predict-ble changes with aging. Initially, in stage I (dysfunction), the
umulative trauma of aging is manifest at the zygapophyseal

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S36 ACUTE INDUSTRIAL MUSCULOSKELETAL INJURIES IN THE AGING WORKFORCE, Zuhosky

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oints by cartilage degeneration, joint synovitis, and subluxa-ion. The intervertebral disk experiences tears within the annu-us with breakdown of the nucleus pulposus matrix and, po-entially, even disk herniation. This may explain the peakncidence of lumbar disk herniations that occurs in the third andourth decades of life. Stage II (instability) is characterized byurther collagen degradation within the zygapophyseal joint,ssociated with capsular laxity and increased rotational move-ent. Within the intervertebral disk, further annular tears with

r without herniation and coalescence also increase annularaxity, with further increased translational forces. Stage IIIstabilization) is marked by typical changes of osteoarthritisithin the zygapophyseal joints. There is loss of joint surface

artilage and joint space narrowing, with fibrosis and osteo-hyte formation. The intervertebral disk undergoes further de-erioration of the nucleus pulposus, with changes in collagenype, disk resorption, fibrosis, and loss of disk height. Thesedvanced changes may account for the peak in lumbar spinaltenosis in the sixth and seventh decades of life. In olderatients presenting with back and referred leg pain, the asso-iated findings also include both central and foraminal stenosis.

.6 Clinical Activity: To explain the various nonspinediagnoses that may present with back pain in theaging worker and delineate their specific diagnosticconsiderations.

Vascular etiologies for LBP are a potentially fatal cause thatay be overlooked. Abdominal aortic aneurysms may occur in

p to 4% of the population over the age of 50.30 Smoking is theisk factor most strongly associated with abdominal aorticneurysms, followed by age, hypertension, hyperlipidemia, andtherosclerosis.31 Men are 10 times more likely than women toave a clinically significant abdominal aortic aneurysm (ie,cm or larger). There is also a genetic predilection, with a 30%ncreased risk in patients with a family history. On physicalxamination in slender people, a pulsatile mass may beppreciated. Plain film radiographs may show a widenedortic silhouette with a curvilinear calcification if there isignificant atherosclerosis. Contrast-enhanced computed to-ography (CT) and magnetic resonance angiography are the

referred studies to define aortic aneurysms in both the thoracicnd abdominal regions.

Genitourinary causes of LBP also may occur with increasingrequency after the age of 40 years. Prostatitis can cause LBP,acral pain, and pelvic pain.32 It generally is characterized ascute or chronic, bacterial, or abacterial. An acute bacterialrostatitis may be easily confirmed on prostate examinationtenderness, bogginess) and with a positive urine culture andensitivity, indicating the need for an appropriate course ofntibiotics. It may otherwise present as a chronic, ill-definedelvic pain known as chronic pelvic pain syndrome.33 Becausef the extensive overlap of symptoms among benign prostaticypertrophy, chronic bacterial, and abacterial prostatitis, con-ultation with a urologist is recommended. Nephrolithiasisypically presents acutely with severe flank, low back, and, atimes, pelvic pain. In a study of machinists exposed to highemperatures, there was a significantly increased prevalence ofric acid stones compared with the control group of machinistsorking in normal temperatures.34 Older employees working

n occupations exposed to high heat appear particularly at riskor uric acid stones. Counseling regarding adequate fluid intakend avoidance of beverages that contain oxaloacetic acid (eg,lack tea) are critical components to minimize this risk.Gastrointestinal disorders can also present with low back and
usculoskeletal-type symptoms. Gastric and duodenal ulcers i

ypically present with boring abdominal pain associated witheferred pain in the lumbar spine or sometimes with midbackain only. Risk factors include cigarette smoking, intake ofspirin and nonsteroidal anti-inflammatory medications, in-reased dietary salt, and excessive alcohol use.35 The risk ofastric and duodenal ulcer increases with age, fairly precipi-ously after age 60 years. This risk should be consideredspecially when prescribing nonsteroidal anti-inflammatoryedications in the older worker. Workers performing rotating

hift and night work and immigrant workers appear to be atignificantly increased risk for the development of gastric anduodenal ulcers,36-38 which are presumed to be related to sleepisturbance and disruption of circadian rhythm in these work-rs. Pancreatitis is also a potentially overlooked cause of backain in older workers. Pancreatitis should be especially con-idered in workers with significant alcohol and tobacco use. Inhe Health and Retirement Study, older male workers wereore likely to answer 3 out of 4 CAGE alcoholism screening

uestions positively and consume 4� drinks per day.39 TheAGE acronym stands for trying to cut down alcohol use (C),ngry when discussing alcohol use (A), feeling guilty aboutlcohol use (G), and taking an eye opener (E).

Rheumatologic disorders may also present with acute mus-uloskeletal pain including LBP. Polymyalgia rheumatica typ-cally presents with shoulder girdle pain and stiffness, but aubset of these patients present with hip girdle symptoms. Aget onset is invariably greater than 50 years, with most over thege of 60 years. It affects women twice as often as men.rythrocyte sedimentation rates (ESR) of 80 to 100mm perour (or greater) are highly suggestive of this diagnosis, al-hough elevated C-reactive protein levels may be a more sen-itive indicator of disease presence.40 Dramatic response toow-dose prednisone (10–20mg/d) provides both confirmationnd treatment. The potential development of temporal arteritisnd its inherent risk of blindness must be given careful con-ideration in this population. Diffuse idiopathic skeletal hyper-stosis (DISH) presents generally after the age of 50 years.lowing syndesmophytes in the thoracic and potentially the

umbar spine give the appearance of a “bamboo spine” in theseatients. In addition to causing a gradual decrease in spineexibility and range of motion, even trivial trauma may result

n fractures in DISH patients. Whenever there is a history ofISH in the setting of trauma, the clinician must maintain aigh index of suspicion for underlying fracture and thus pursuearly and aggressive radiologic investigation.

Osteoporosis is 1 of the more common underlying comor-idities increasing the risk of injury in older workers. Riskactors for osteoporosis include being postmenopausal, partic-larly in a woman of eastern European descent, hyperthyroid-sm, previous steroid treatments, excessive alcohol intake, cal-ium deficiency, eating disorders, and smoking. The singlereatest risk factor for injury from fall in older patients issteoporosis, with vertebral compression fracture a likely re-ult.41 Despite this, there is a paucity of research on the effectsf osteoporosis on work-related injuries and their prevention.or working women in Canada older than 60 years, there is aignificantly increased risk of hand fractures in the workplaceompared with younger cohorts and men, likely associatedith the increased prevalence of osteoporosis in this popula-

ion.42 In addition, research43 shows predictable fracture pat-erns in older women compared with men, with women moreikely than older men to sustain forearm and wrist fractures,resumably from osteoporosis. Recognition of these injuryatterns and identification of osteoporosis in this patient pop-lation is critical. Within the workers’ compensation system,
nstructions on weight-bearing exercise and fall prevention in

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he workplace are appropriate and important for the preventionf future injury. Involvement of the primary care physicianutside the workers’ compensation system for medical inves-igation and treatment of the osteoporosis is vital as well.

A higher index of suspicion for malignancy in older workersust also be maintained, especially in workers over the age of

0 years. Malignancies creating back and spine pain mayepresent a primary malignancy, most commonly multiple my-loma, or metastatic disease. The most common malignancieshat metastasize to the spine are those of the prostate, lung,hyroid, breast, and renal cell. Red flags that signal the possi-ility of malignancy in the history and presentation of theseatients44 are outlined in appendix 1.

The presence of weight loss greater than 4.5kg (10lb) in 6onths and ESR higher than 50mm per hour, especially in

ombination, are reasonably sensitive and specific indicators ofalignancy in the setting of LBP.45 Serologic studies should

nclude a complete blood count with differential, because theresence of anemia rivals elevated ESR in sensitivity for ma-ignancy. Serum calcium and alkaline phosphatase levels mayndicate states of rapid bone turnover seen with some malig-ancies. Serum and urine immunoelectrophoresis studies toxclude a monoclonal protein spike, as seen in multiple my-loma, may also be helpful. Anteroposterior (AP) and lateralumbosacral plain film radiographs are the initial radiologiccreen and may show compression fracture or more subtlesteolytic or osteoblastic lesions. Because of the predilection ofetastatic tumor to be harbored in more highly vascular sites,

articular attention should be paid to the pedicle region wheneviewing these images. A triple-phase bone scan can be aensitive indicator of metastatic disease in the spine but mayppear normal in the setting of multiple myeloma. CT of thepine has proven both sensitive and specific in differentiatingenign and malignant lesions46 and in detecting metastaticesions in the spine.47 Magnetic resonance imaging (MRI) withadolinium remains the criterion standard for identification ofpinal malignancies because of its superior soft-tissue resolu-ion and staging of malignant spinal cord compression.48

.7 Clinical Activity: To discuss appropriate historicaland diagnostic considerations in a 62-year-old dockworker presenting with LBP after a fall.

Given the complexities noted above, the investigation forlder workers must be tailored to their symptoms. For instance,ounger workers with back and leg pain most likely have aiskogenic source for their radicular symptoms. In older work-rs, spinal stenosis, whether central or foraminal, can causeeurogenic claudication, with bilateral leg pain that mimicsascular claudication. Differentiating these conditions is im-ortant. Walking uphill tends to improve the symptoms ofeurogenic claudication but worsen those of vascular claudi-ation. After symptom onset, standing still tends to improve theymptoms of vascular claudication, whereas the prolongedrect posture would typically cause persistence or worsening ofhe leg symptoms of neurogenic claudication. Neurogenic clau-ication symptoms may improve with walking behind andeaning forward on a shopping cart (the “shopping cart sign”),hich generally results in no benefit for patients with vascular

laudication. Noninvasive arterial studies including arterial ul-rasound and ankle-brachial indices may further help differen-iate neurogenic versus vascular claudication. The radiographicnvestigation has special considerations as well. It is generallyccepted that AP and lateral films of the lumbar spine representn adequate screening study, with the possible exception of
linical suspicion of a pars interarticularis fracture (spondylo- w
ysis), which may be missed with these studies alone.49-51

dditional oblique radiographs may increase the diagnosticield in this clinical setting. Indications for plain film radio-raphs in the setting of acute LBP44 are outlined in appendix 2.When a bone scan is ordered to evaluate for spinal fracture52

r malignancy,53 requesting single-photon emission computedomography (SPECT) significantly increases the diagnosticield, sensitivity, and specificity of this diagnostic modality.hen malignancy or fracture is suspected, routine inclusion of

PECT imaging is recommended. When ordering CT or MRI,linicians should be mindful that these yield increasing rates ofalse-positive results with advancing age.54-56 The history,hysical examination, and imaging studies should all be cor-elated to arrive at an appropriate working diagnosis.

.8 Clinical Activity: To analyze the effect of advancingage on the determination of causation in the workers’compensation system.

The establishment of causation of injury in older workersresents yet another challenge to clinicians. The Americanedical Association Guides to the Evaluation of Permanent

mpairment, 5th Edition, define causation as “an identifiableactor (eg, accident or exposure to hazards or disease) thatesults in a medically identifiable condition.”57(p11) Inherent inhis definition is the general concept of a sentinel event or setf conditions—that is, environmental exposure or cumulativerauma—that either results in clear injury or exacerbates annderlying condition. For an older worker, underlying condi-ions such as spondylosis can significantly affect this determi-ation. By age 60 years, 100% of the population will haveistologic changes of osteoarthritis.58 Employers and workers’ompensation insurance carriers have an economic interest inelating symptoms to preexisting conditions. Thus, sentinelvents that bring an otherwise quiescent condition to a symp-omatic state become crucial to document. Ultimate compen-ability of an injury or symptom complex relies on the partic-lar policy of each individual state’s workers’ compensationystem.

.9 Educational Activity: To summarize factors specific tothe employee or employer that affect the functionaloutcomes of older workers.

In the rehabilitation of older workers, goals should includeesolution of symptoms, reduction of the risk of further injury,nd successful return to the workplace. An injury at workrecipitates an earlier-than-planned retirement in up to 11% oforkers and correlates with preinjury dissatisfaction with their

ob or medical care and poor physical and mental health sta-us.59 Successful return to work is enhanced by rehabilitationhat emphasizes improved flexibility, increased aerobic fitness,trengthening, education on fall prevention and lifting tech-iques, and early return to the worksite.60 Older workers ineneral may be more likely to return to their previous employ-ents because of their longer workplace attachment.61 Mean-hile, various return-to-work factors are under the control of

mployers. Employers who are deemed rigid, inflexible, andonsupportive are less likely to see their older workers return.62

mployer policies that promote shared governance betweennions and management with emphasis on joint safety pro-rams and appropriate workplace modifications will provideore accommodating environments for worker return.63 Em-

loyers who value experience and transition workers to moreupervisory roles may also realize greater retention of older
orkers.

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S38 ACUTE INDUSTRIAL MUSCULOSKELETAL INJURIES IN THE AGING WORKFORCE, Zuhosky

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APPENDIX 1: “RED FLAGS” SIGNALING POSSIBLESPINAL MALIGNANCY

ight painPain at restNo position of reliefFeverWeight lossPrior history of malignancy

APPENDIX 2: INDICATIONS FOR PLAIN FILMRADIOGRAPHS TO INVESTIGATE ACUTE LBP

Age greater than 50 yearsEven trivial trauma in older patientsNeurologic deficitUnexplained weight loss of more than 4.5kg (10lb) in 6

monthsDrug or alcohol abuse history predisposing to infectionSuspicion of ankylosing spondylitisHistory of malignancyUse of corticosteroidsRecent visit within the month for same symptoms without

improvementPatient seeking compensation for back painFever

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31. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Cir-culation 2005;111:816-28.

32. Rask MR. Low back pain due to neisseria prostatitis: report ofthree cases. Clin Orthop Relat Res 1977;(127):120-2.

33. Hua VN, Schaeffer AJ. Acute and chronic prostatitis. Med ClinN Am 2004;88:483-94.

34. Borghi L, Meschi T, Amato F, Novarini A, Romanelli A, Cigala F.
Hot occupation and nephrolithiasis. J Urol 1993;150:1757-60.
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35. Sonnenberg A. Factors which influence the incidence and courseof peptic ulcer. Scand J Gastroenterol 1998;155(Suppl):119-40.

36. Costa G. The impact of shift and night work on health. ApplErgon 1996;27:9-16.

37. Knutsson A. Health disorders of shift workers. Occup Med2003;53:103-8.

38. Segawa K, Nakazawa S, Tsukamoto Y, et al. Peptic ulcer isprevalent among shift workers. Digest Dis Sci 1987; 32:449-53.

39. Zwerling C, Sprince NL, Wallace RB, Davis CS, Whitten PS,Heeringa SG. Alcohol and occupational injuries among olderworkers. Accid Analysis Prev 1996;28:371-6.

40. Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymyalgiarheumatica. Best Pract Res Clin Rheum 2004;18:705-22.

41. Melton LJ, Riggs BL. Risk factors for injury after fall. ClinGeriatr Med 1985;1:525-39.

42. Schofield MM. Work-related hand injuries in Ontario: an histor-ical perspective. Clin Plastic Surg 2005;32:485-93.

43. Tornetta P, Hirsch EF, Howard R, McConnell T, Ross E. Skel-etal injury patterns in older females. Clin Orthop Rel Res 2004;May(422):55-6.

44. Mazanec DJ. Differential diagnosis of low back pain and sciat-ica. Semin Spine Surg 1994;6:180-5.

45. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency,clinical presentation, and diagnostic strategies. J Gen Intern Med1988;3:230-8.

46. Kubota T, Yamada K, Ito H, Kizu O, Nishimura T. High-resolutionimaging of the spine using multidetector-row computed tomogra-phy: differentiation between benign and malignant vertebral com-pression fractures. J Comput Assist Tomogr 2005;29:712-9.

47. Rafii M, Firooznia H, Kramer E, Golimbu C, Sanger J. The roleof computed tomography in evaluation of skeletal metastases.J Comput Tomogr 1988;12:19-24.

48. Abrahm JL. Assessment and treatment of patients with malignantspinal cord compression. J Support Oncol 2004;2:377-88, 391.

49. Scavone JC, Latshaw RF, Roharar GV. Use of lumbar spinefilms: statistical evaluation at a university teaching hospital.JAMA 1982;246:1105-8.

50. Scavone JC, Latshaw RF, Widener WA. Anteroposterior andlateral radiographs: an adequate lumbar spine examination. Am J
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51. Simmons ED Jr, Guyer RD, Graham-Smith A, Herzog R. Ra-diographic assessment for patients with low back pain. Spine1995;20:1839-41.

52. Read MT. Single photon emission computed tomography(SPECT) scanning for adolescent back pain. A sine qua non?Br J Sport Med 1994;28:56-7.

53. Savelli G, Maffioli L, Maccauro M, De Deckere E, BombardieriE. Bone scintigraphy and the added value of SPECT (singlephoton emission tomography) in detecting skeletal lesions. QJ Nucl Med 2001;45:27-37.

54. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N. Astudy of computer-assisted tomography. I. The incidence ofpositive CAT scans in an asymptomatic group of patients. Spine1984;9:549-51.

55. Jensen MC, Brant-Zawadzki MN, Obuchowski N. Magneticresonance imaging of the lumbar spine in people without lowback pain. N Engl J Med 1994;331:69-73.

56. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Ab-normal magnetic resonance scans of the lumbar spine in asymp-tomatic patients: a prospective investigation. J Bone Joint SurgAm 1990;72:403-8.

57. Cocchiarelli L, Andersson GB, editors. Guides to the evaluationof permanent impairment, 5th ed. Chicago: AMA Pr; 2001.

58. Loeser RF Jr. Aging and the etiopathogenesis and treatment ofosteoarthritis. Rheum Dis Clin North Am 2000;26:547-67.

59. Pransky GS, Benjamin KL, Savageau JA. Early retirement due tooccupational injury: who is at risk? Am J Ind Med 2005;47:285-95.

60. Nadler SF, Stitik TP, Malanga GA. Optimizing outcome in theinjured worker with low back pain. Crit Rev Phys Med RehabilMed 1999;11:139-69.

61. Pransky GS, Benjamin KL, Savageau JA, Currivan D, FletcherK. Outcomes in work-related injuries: a comparison of older andyounger workers. Am J Ind Med 2005;47:104-12.

62. Stikeleather J. An older worker’s decision to “push or protectself” following a work-related injury. Work 2004;22:139-44.

63. Freeman EJ. Union-management solutions for preventing work-
place injury of older workers. Work 2004;22:145-51.

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007 SAE-P: Industrial Medicine and Acute Musculoskeletalehabilitation

my H. Phelan, MD, DVM, Venu Akuthota, MD, Brian M. Kelly, DO, Virginia S. Nelson, MD, MPH,
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Educational Activity 1.11. Which is a risk factor for plantar fasciitis?

(a) Obesity(b) Female gender(c) Age younger than 40 years(d) Increased subtalar motion

Ref: (a) Aldridge T. Diagnosing heel pain in adults [pub-ished erratum in: Am Fam Physician 2006;73:776]. Am Famhysician 2004;70:332-8.(b) Brown C. A review of subcalcaneal heel pain and plantar

asciitis. Aust Fam Physician 1996;25:875-81, 884-5.(c) Sadat-Ali M. Plantar fasciitis/calcaneal spur among se-

urity forces personnel. Mil Med 1998;163:56-7.(d) Taunton JE, Ryan MB, Clement DB, McKenzie DC,

loyd-Smith DR, Zumbo BD. A retrospective case-controlnalysis of 2002 running injuries. Br J Sports Med 2002;36:5-101.(e) Lapidus PW, Guidotti FP. Painful heel: report of 323

atients with 364 painful heels. Clin Orthop Relat Res 1965;ar-Apr(39):178-86.

Clinical Activity 1.22. The best position for the center of the automobile head-

rest to limit the amount of head and neck flexion andextension during rear-end collisions is at(a) eye level.(b) ear level.(c) chin level.(d) comfortable resting level.

Ref: Silber JS, Hayes VM, Lipetz J, Vaccaro AR. Whiplash:act or fiction? Am J Orthop 2005;3423-8.

Clinical Activity 1.33. De Quervain’s disease includes the tendons of which 2

muscles?(a) Extensor pollicis longus and extensor pollicis brevis(b) Abductor pollicis brevis and extensor indicis(c) Abductor pollicis longus and extensor pollicis brevis(d) Extensor digitorum and extensor carpi radialis brevis

Ref: Piligian G, Herbert R, Hearns M, Dropkin J, Lands-ergis P, Cherniack M. Evaluation and management of chronicork-related musculoskeletal disorders of the distal upperxtremity. Am J Ind Med 2000;37:75-93.

Clinical Activity 1.44. Which factor is NOT a criterion for early use of plain

radiographs in the assessment of low-back pain?(a) Age less than 50 years(b) Unplanned weight loss for more than 6 months(c) Evaluation for ankylosing spondylitis(d) Significant trauma

Ref: (a) Simmons ED, Guyer RD, Graham-Smith A, Herzog. Radiograph assessment for patients with low back pain.
pine J 2003;3(3 Suppl):3S-5S.

(b) Deyo RA, Diehl AK. Lumbar films in primary care:urrent use and effects of selective ordering criteria. J Genntern Med 1986;1:20-5.

Clinical Activity 1.45. Which diagnostic study best detects sequestered disk

fragments and vertebral body end plate changes?(a) Plain radiographs(b) Computed tomography(c) Magnetic resonance imaging(d) Bone scans

Ref: Herzog RJ, Ghanayem AJ, Guyer RD, Graham-Smith A,immons ED; NASS. Magnetic resonance imaging: use inatients with low back pain or radicular pain. Spine J003;3(3 Suppl):6S-10S.

Educational Activity 2.16. Which muscle relaxant has the greatest abuse potential?

(a) Carisoprodol (Soma)(b) Cyclobenzaprine (Flexeril)(c) Tizanidine (Zanaflex)(d) Metaxalone (Skelaxin)

Ref: Harden RN, Argoff C. A review of three commonlyrescribed skeletal muscle relaxants. J Back Musculoskeletalehabil 2000;15:63-6.

Educational Activity 2.27. Advantages of cyclooxygenase-2 specific agents (cele-

coxib) include(a) low cost.(b) cardioprotection.(c) decreased gastrointestinal toxicity.(d) low potential for liver toxicity.

Ref: Micklewright R, Lane S, Linley W, et al. Review article:SAIDs, gastroprotections and cyclo-oxygenase-II-selective

nhibitors. Aliment Pharmacol Ther 2003;17:321-32.

Educational Activity 2.38. Tramadol (Ultram) should be used with caution with

which of the following medications?(a) diazepam (Valium)(b) acetaminophen (Tylenol)(c) fluoxetine (Prozac)(d) propoxyphene (Darvocet, Darvon)

Ref: Sachs CJ. Oral analgesics for acute nonspecific pain.m Fam Physician 2005;71:913-8.

Educational Activity 2.39. Which statement is TRUE regarding the metabolism of

oral codeine?(a) It converts to morphine through the cytochrome

P-450 system.(b) It exclusively blocks kappa opioid receptors.(c) It does not undergo first pass metabolism.
(d) It blocks N-methyl-D-aspartate receptors.

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Ref: Sachs CJ. Oral analgesics for acute nonspecific pain.m Fam Physician 2005;71:913-8.

Educational Activity 2.410. What is a mechanism of action of capsaicin?

(a) Increasing substance P over time(b) Blocking mu opioid receptors(c) Increasing calcitonin gene–related peptide(d) Activating vanilloid receptors

Ref: Sawynok J. Topical and peripherally acting analgesics.harmacol Rev 2003;55:1-20.

Clinical Activity 3.111. According to a 2003 Cochrane Review of articles relat-

ing to the treatment of plantar heel pain, which factor isTRUE?(a) There was strong evidence that therapeutic ultra-

sound effectively reduced chronic heel pain.(b) Randomized trials showed surgery to be more ef-

fective in decreasing heel pain than no treatment.(c) There was limited evidence for the superiority of

corticosteroid injections over orthotic devices inreducing heel pain.

(d) Several articles showed that custom-made orthoseswere superior to heel pads and stretching exercisesin reducing heel pain.

Ref: Crawford F, Thomson C. Interventions for treatinglantar heel pain. Cochrane Database Syst Rev 2003;(3):D000416.

Clinical Activity 3.212. After soft-tissue injury to the neck from an automobile

accident (“whiplash”), which factor has statisticallybeen found to delay return to work?(a) Full-time use of a soft cervical collar for 3 weeks(b) Referral to physical therapy(c) Instruction in a home exercise program(d) Use of nonsteroidal anti-inflammatory drugs

Ref: Crawford JR, Khan RJ, Varley GW. Early managementnd outcome following soft tissue injuries of the neck: a ran-omised controlled trial. Injury 2004;35:891-5.

Clinical Activity 3.313. In patients with lateral epicondylitis, which treatment

has been found to decrease pain significantly?(a) Counterforce bracing (forearm strap)(b) Isotonic eccentric exercise program(c) Extracorporeal shock wave therapy(d) Laser therapy

Ref: (a) Wuori JL, Overend TJ, Kramer JF, MacDermind J.trength and pain measures with lateral epicondylitis bracing.rch Phys Med Rehabil 1998;79:832-7.(b) Buchbinder R, Green S, White M, Barnsley L, Smidt N,

ssendelft WJ. Shock wave therapy for lateral elbow pain.ochrane Database Syst Rev 2002;(1):CD003524.(c) Svernlov B, Adolfson L. Non-operative treatment regimen

ncluding eccentric training for lateral humeral epicondylal-ia. Scan J Med Sci Sports 2001;6:328-34.

Clinical Activity 3.414. In published studies, which intervention for carpal tun-

nel syndrome was shown to improve symptoms?(a) Ultrasound treatment for 2 weeks
(b) Nonsteroidal anti-inflammatory drugs
(c) Use of ergonomic keyboards(d) Nocturnal splinting for 6 weeks

Ref: O’Connor D, Marshall S, Massy-Westropp N. Non-surgi-al treatment (other than steroid injection) for carpal tunnelyndrome. Cochrane Database Syst Rev 2003;(1):CD003219.

Educational Activity 3.515. The medical literature supports which statement regard-

ing low-back pain (LBP)?(a) Lumbar supports prevent LBP.(b) Lumbar supports are more effective than other types

of prevention for LBP.(c) Lumbar supports plus back school reduce days ab-

sent from work because of back injury.(d) Lumbar supports are more effective in reducing

back pain than other types of treatment.

Ref: Jellema P, van Tulder MW, van Poppel MN, NachemsonL, Bouter LM. Lumbar supports for prevention and treatment of

ow back pain: a systematic review within the framework of theochrane Back Review Group. Spine 2001;26:377-86.

Educational Activity 4.116. The pathogenesis of trigger points includes

(a) muscle fiber inflammation.(b) lower tissue oxygen levels.(c) focal muscle spasm.(d) endplate denervation.

Ref: (a) Borg-Stein J, Simons DG. Focused review: myofas-ial pain. Arch Phys Med Rehabil 2002;83(3 Suppl 1):S40-7.

(b) Simons D, Travell J, Simons L, Cummings B. Travell &imons’ myofascial pain and dysfunction: the trigger pointanual. Philadelphia: Lippincott Williams & Wilkins; 1999.(c) Lang AM. Botulinum toxin type A therapy in chronic pain

isorders. Arch Phys Med Rehabil 2003;84(3 Suppl 1):S69-73.

Educational Activity 4.117. Pain associated with cervical zygapophyseal joints can

be most reliably diagnosed by(a) physical examination.(b) plain radiographs.(c) medial branch blocks.(d) bone scan.

Ref: Bogduk N, A Marsland. The cervical zygapophysialoints as a source of neck pain. Spine 1988;13:610-7.

Educational Activity 4.118. Once cervical zygapophyseal joint pain has been con-

firmed by selective medial branch blocks, the mosteffective treatment is(a) radiofrequency neuroablation.(b) cervical fusion surgery.(c) trigger point injections.(d) intra-articular corticosteroid injection.

Ref: Lord SM, Barnsley L, Wallis BJ, McDonald GJ, Bogduk N.ercutaneous radio-frequency neurotomy for chronic cervicalygapophyseal-joint pain. N Engl J Med 1996;335:1721-6.

Educational Activity 4.219. For which type of cervical pain are epidural steroid

injections indicated?(a) Axial(b) Facet joint(c) Radicular
(d) Diskogenic

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Ref: (a) Ma DJ, Gilula LA, Riew KD. Complications ofuoroscopically guided extraforaminal cervical nerve blocks.n analysis of 1036 injections. J Bone Joint Surg Am 2005;7:1025-30.(b) Rathmell JP, Aprill C, Bogduk N. Cervical transforami-

al injection of steroids. Anesthesiology 2004;100:1595-600.

Educational Activity 4.220. Although there are risks associated with all injection

procedures, which cervical injection technique has beenassociated with acute catastrophic neurologic injury?(a) Facet joint injection(b) Transforaminal epidural steroid injection(c) Paraspinal trigger point injection(d) Interlaminar epidural steroid injection

Ref: (a) Tiso RL, Cutler T, Catania JA, Whalen K. Adverseentral nervous system sequelae after selective transforaminallock: the role of corticosteroids. Spine J 2004;4:468-74.(b) Rathmell JP, Aprill C, Bogduk N. Cervical transforami-

al injection of steroids. Anesthesiology 2004;100:1595-600.(c) Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical

ransforaminal injection of corticosteroids into a radicularrtery: a possible mechanism for spinal cord injury. Pain003;103:211-5.(d) Furman MB, Giovanniello MT, O’Brien EM. Incidence

f intravascular penetration in transforaminal cervical epi-ural steroid injections. Spine 2003;28:21-5.(e) Rozin L, Rozin R, Koehler SA, et al. Death during

ransforaminal epidural steroid nerve root block (C7) due toerforation of the left vertebral artery. Am J Forensic Medathol 2003;24:351-5.(f) Rosenkranz M, Grzyska U, Niesen W, et al. Anterior

pinal artery syndrome following periradicular cervical nerveoot therapy. J Neurol 2004;251:229-31.

Clinical Activity 5.121. Sacroiliac pain and dysfunction can most reliably be

diagnosed by(a) physical examination.(b) imaging studies.(c) anesthetic block.(d) bone scan.

Ref: (a) Schwarzer AC, Aprill CN, Bogduk N. The sacroiliacoint in chronic low back pain. Spine 1995;20:31-7.

(b) Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliacoint double block and value of sacroiliac pain provocationests in 54 patients with low back pain. Spine 1996;21:1889-92.

(c) Slipman CW, Lipetz JS, Plastaras CT, et al. Fluoroscop-cally guided therapeutic sacroiliac joint injections for sacro-liac joint syndrome. Am J Phys Med Rehabil 2001;80:425-32.

(d) Slipman CW, Jackson HB, Lipetz JS, Chan KT, Lenrow, Vresilovic EJ. Sacroiliac joint pain referral zones. Archhys Med Rehabil 2000;81:334-8.

Educational Activity 5.222. Which inflammatory marker is most commonly present

in cases of lumbar disk herniation?(a) Histamine(b) Phospholipase A2(c) Prostaglandin C(d) C-reactive protein

Ref: (a) Saal JS, Franson RC, Dobrow R, Saal JA, WhiteH, Goldthwaite N. High levels of inflammatory phospholipase
2 activity in lumbar disc herniations. Spine 1990;15:674-8.

(b) Olmarker K, Blomquist J, Stromberg J, Nannmark U,homsen P, Rydevik B. Inflammatogenic properties of nucleusulposus. Spine 1995;20:665-9.(c) Nygaard OP, Mellgren SI, Osterud B. The inflammatory

roperties of contained and noncontained lumbar disc herni-tion. Spine 1997;22:2484-8.(d) Kang JD, Stefanovic-Racic M, McIntyre LA, Georgescu

I, Evans CH. Toward a biochemical understanding of humanntervertebral disc degeneration and herniation. Contributionsf nitric oxide, interleukins, prostaglandin E2, and matrixetalloproteinases. Spine 1997;22:1065-73.(e) Kang JD, Georgescu HI, McIntyre-Larkin L, Stefanovic-

acic M, Donaldson WF 3rd, Evans CH. Herniated lumbarntervertebral discs spontaneously produce matrix metallopro-einases, nitric oxide, interleukin-6, and prostaglandin E2.pine 1996;21:271-7.

Educational Activity 5.323. Once the diagnosis of zygapophyseal joint pain has been

established, options for long-term relief of pain include(a) phenol medial branch blocks.(b) intra-articular corticosteroid injection.(c) cage fusion.(d) radiofrequency ablation.

Ref: (a) Dreyfuss P, Halbrook B, Pauza K, Joshi A, McLarty, Bogduk N. Efficacy and validity of radiofrequency neurot-my for chronic lumbar zygapophysial joint pain. Spine 2000;5:1270-7.(b) van Kleef M, Barendse GA, Kessels A, Voets HM, WeberE, de Lange S. Randomized trial of radiofrequency lumbar

acet denervation for chronic low back pain. Spine 1999;24:937-42.(c) Schofferman J. A narrative review of intra-articular

orticosteroid injections for low back pain: Nikolai Bogduk.ain Med 2005;6:297-8.

Educational Activity 5.424. Findings on magnetic resonance imaging suggestive of

acute annular tear include(a) loss of disk height.(b) high-intensity zone.(c) vertebral endplate edema.(d) Schmorl’s nodes.

Ref: (a) Aprill C, Bogduk N. High-intensity zone: a diagnos-ic sign of painful lumbar disc on magnetic resonance imaging.r J Radiol 1992;65:361-9.(b) Schellhas KP, Pollei SR, Gundry CR, Heithoff KB. Lum-

ar disc high-intensity zone. Correlation of magnetic reso-ance imaging and discography. Spine 1996;21:79-86.(c) Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo

ward winner in clinical studies: lumbar high-intensity zonend discography in subjects without low back problems. Spine000;25:2987-92.

Educational Activity 5.425. Options for nonsurgical treatment of annular tears in-

clude intradiskal electrothermy annuloplasty, which in-volves heating of the annular collagen. Candidates forthis treatment should have(a) axial pain of less than 6 months in duration.(b) disk protrusion beyond the posterior longitudinal

ligament.(c) 50% or greater preservation of disk height.(d) low to moderate pain ratings and good levels of

function.

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Ref: (a) Chou LH, Lew HL, Coelho PC, Slipman CW. Intra-iscal electrothermal annuloplasty. Am J Phys Med Rehabil005;84:538-49.(b) Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K,

ogduk N. A randomized, placebo-controlled trial of intradis-al electrothermal therapy for the treatment of discogenic lowack pain. Spine J 2004;4:27-35.(c) Lutz C, Lutz GE, Cooke PM. Treatment of chronic

umbar diskogenic pain with intradiskal electrothermal ther-py: a prospective outcome study. Arch Phys Med Rehabil003;84:23-8.(d) Saal JA, Saal JS. Intradiscal electrothermal treatment for

hronic discogenic low back pain: prospective outcome studyith a minimum 2-year follow-up. Spine 2002;27:966-73.

Educational Activity 5.426. Which nonsurgical treatment option for diskogenic low-

back pain is conclusively determined NOT to be effec-tive?(a) Intradiscal electrothermal annuloplasty(b) Intradiskal steroid injection(c) Percutaneous nucleoplasty(d) Percutaneous lumbar disk decompression

Ref: (a) Khot A, Bowditch M, Powell J, Sharp D. The use ofntradiscal steroid therapy for lumbar spinal discogenic pain:

randomized controlled trial. Spine 2004;2:833-6.(b) Aoki M, Kato F, Mimatsu K, Iwata H. Histologic changes

n the intervertebral disc after intradiscal injections of meth-lprednisolone acetate in rabbits. Spine 1997;22:127-31.

(c) Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K,ogduk N. A randomized, placebo-controlled trial of intradis-al electrothermal therapy for the treatment of discogenic lowack pain. Spine J 2004;4:27-35.(d) Chou LH, Lew HL, Coelho PC, Slipman CW. Intradiscal

lectrothermal annuloplasty. Am J Phys Med Rehabil 2005;84:38-49.(e) Alo KM, Wright RE, Sutcliffe J, Scott A. Brandt SA.

ercutaneous lumbar discectomy: one year follow-up in annitial cohort of fifty consecutive patients with chronic radicu-ar pain. Pain Practice 2005;5:116-24.

(f) Cohen SP, Williams S, Kurihara C, Griffith S, Larkin TM.ucleoplasty with or without intradiscal electrothermal ther-py (IDET) as a treatment for lumbar herniated disc. J Spinalisord Tech 2005;18(Suppl):S119-24.

Clinical Activity 6.227. The most effective nonsurgical treatment for de Quer-

vain’s tenosynovitis is(a) relative rest and anti-inflammatories.(b) splinting and ice packs 4 times a day.(c) corticosteroid injection and splinting.(d) corticosteroid injection alone.

Ref: Richie CA, Briner WW Jr. Corticosteroid injection forreatment of de Quervain’s tenosynovitis: a pooled quantitativeiterature evaluation. J Am Board Fam Pract 2003;16:102-6.

Clinical Activity 6.328. Injection of corticosteroid into the carpal tunnel pro-

duces clinical improvement(a) better than surgical decompression at 1 year.(b) equal to iontophoresis or phonophoresis.(c) in nerve conduction studies.(d) that is augmented by insulin in non–insulin-depen-

dent diabetes mellitus patients. s

Ref: (a) Ozkul Y, Sabuncu T, Yazgan P, Nazligul Y. Localnsulin injection improves median nerve regeneration inIDDM patients with carpal tunnel syndrome. Eur J Neurol001;8:329-34.(b) Ly-Pen D, Andreu JL, de Blas G, Sanchez-Olaso A,illan I. Surgical decompression versus local steroid injection

n carpal tunnel syndrome: a one-year, prospective, random-zed, open, controlled clinical trial. Arthritis Rheum 2005;52:12-9.(c) Aygul R, Ulvi H, Karatay S, Deniz O, Varoglu AO.

etermination of sensitive electrophysiologic parameters atollow-up of different steroid treatments of carpal tunnel syn-rome. J Clin Neurophysiol 2005;22:222-30.

Clinical Activity 6.429. The clinical practice of avoiding local corticosteroid

injection into the Achilles’ tendon because of the risk oftendon rupture is based on(a) randomized controlled trials.(b) prospective studies.(c) retrospective studies.(d) case reports and case series.

Ref: (a) Shrier I, Matheson GO, Kohl HW 3rd. Achillesendonitis: are corticosteroid injections useful or harmful?lin J Sport Med 1996;6:245-50.(b) McLauchlan GJ, Handoll HH. Interventions for treating

cute and chronic Achilles tendinitis. Cochrane Database Systev 2001;(2):CD000232.(c) Read MT. Safe relief of rest pain that eases with activity

n achillodynia by intrabursal or peritendinous steroid injec-ion: the rupture rate was not increased by these steroidnjections. Br J Sports Med 1999;33:134-5.

(d) Gill SS, Gelbke MK, Mattson SL, Anderson MW, HurwitzR. Fluoroscopically guided low-volume peritendinous corti-osteroid injection for Achilles tendinopathy. A safety study.Bone Joint Surg Am 2004;86:802-6.

Clinical Activity: 6.530. The pain associated with corticosteroid injection of the

plantar fascia can be successfully reduced by(a) applying topical capsaicin cream before injection.(b) mixing lidocaine with corticosteroid solution.(c) using ultrasound guidance to avoid the calcaneus.(d) administering a posterior tibial nerve block before

injection.

Ref: Govindarajan R, Bakalova T, Doss NW, Splain SH,ichael R, Abadir AR. Posterior tibial nerve block in the

herapeutic management of painful calcaneal spur (plantarasciitis): a preliminary experience. Can J Anaesth 2003;50:62-3.

Clinical Activity 7.231. Which factor places the aging worker at the greatest risk

of occupational injury?(a) Cumulative trauma disorders(b) Vision impairment(c) Cardiac disease(d) Osteoarthritis

Ref: Zwerling C, Sprince NL, Wallace RB, Davis CS, Whit-en PS, Heeringa SG. Risk factors for occupational injuriesmong older workers: an analysis of the health retirement
tudy. Am J Public Health 1996;86:1306-9.

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Educational Activity 7.432. How do aging workers differ from younger workers in

injury outcome studies?(a) Their risk of developing chronic symptoms after

injury is lower.(b) They have a lower return-to-work rate after serious

injury.(c) Their incidence of fatality at the workplace is lower.(d) They have a lower rate of recurrent injury.

Ref: (a) Salminen S. Have young workers more injuries thanlder ones? An international literature review. J Safety Res004;35:513-21.(b) Peek-Asa C, McArthur DL, Kraus JF. Incidence of

ow-back injury among older workers in a cohort of materialandlers. J Occup Environ Hyg 2004;1:551-7.(c) Welsch LS, Hunting KL, Nessel-Stephens L. Chronic

ymptoms in construction workers treated for musculoskeletalnjuries. Am J Ind Med 1999;36:532-40.

(d) Crook J, Moldofsky H. The probability of recovery andeturn to work from work disability as a function of time. Qualife Res 1994;3:S97-109.

Clinical Activity 7.533. What is the most common musculoskeletal injury in the

aging worker?(a) Rotator cuff tear(b) Low back pain(c) Hip fracture(d) Osteoporotic compression fracture

Ref: Andersson GB. Epidemiologic aspects on low-back pain
n industry. Spine 1981;6:53-60. R

Educational Activity 7.934. Which factor has NO direct influence on the decision for

premature retirement in an elderly worker?(a) Preinjury job satisfaction(b) Good physical health status(c) Quality of work environment(d) Difficulty of employer accommodating light-duty

work

Ref: (a) Pransky G, Benjamin K, Hill-Fotouhi C, et al.utcomes in work-related upper extremity and low back inju-

ies: results of a retrospective study. Am J Ind Med 2000;37:00-9.(b) Pransky GS, Benjamin KL, Savageau JA. Early retire-

ent due to occupational injury: who is at risk? Am J Ind Med005;47:285-95.(c) Stikeleather J. An older worker’s decision to “push or

rotect self” following a work-related injury. Work 2004;22:39-44.

Educational Activity 7.935. After injury, an older worker’s successful return to work

is NOT enhanced by which aspect in the rehabilitationprogram?(a) Exercise to improve flexibility(b) A program to increase aerobic fitness(c) Fall prevention education(d) Return to worksite after symptoms resolve

Ref: Nader SF, Stitik TP, Malanga GA. Optimizing outcomesn injured workers with low back pain. Crit Rev Phys Med
ehabil Med 1999;11:139-69.

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S45


007 SAE-P: Industrial Medicine and Acute Musculoskeletalehabilitationnswer Key and Commentary on Preferred Choice

QUESTION ANSWER COMMENTARY1. (a) Obesity is a risk factor for plantar fasciitis. Plantar fasciitis affects both men and women

equally. It also most commonly occurs in people between the ages of 40 and 70 years.Factors that increase the tension on the plantar fascia, such as decreased subtalarmotion, pes cavus, pes planus, and a tight Achilles’ tendon, may contribute to plantarfasciitis.

2. (b) The center of the automobile headrest should be at ear level.3. (c) De Quervain’s disease results in pain in the abductor pollicis longus and extensor pollicis

brevis tendons, which pass through the first dorsal compartment.4. (a) Criteria for the early use of plain radiographs include age greater than 50 years, unplanned

weight loss for longer than 6 months, the need to assess for ankylosing spondylitis,significant trauma, and neurologic deficits.

5. (c) Magnetic resonance imaging is the study of choice to detect sequestered disk fragments andvertebral body endplate changes, because it provides excellent osseous and soft-tissuedetail that are not seen with the other diagnostic studies.

6. (a) Carisoprodol (Soma) is an older muscle relaxant that breaks down to meprobamate, whichhas been classified as a schedule 4 controlled substance. There are reports of abuse andimpaired driving with carisoprodol.

7. (c) Cyclooxygenase-2 (COX-2)–specific agents, when used alone, have less serious gastroin-testinal complications than traditional nonsteroidal anti-inflammatories. Whether one is ona COX-2–selective or –specific agent, the gastrointestinal protection may be compromisedby concomitant use of even low-dose aspirin, and renal side effects are not decreased.

8. (c) Tramadol should not be administered to patients receiving monoamine oxidase inhibitors,and cotreatments with tricyclic antidepressants and serotonin selective reuptake inhibitorsshould be undertaken with caution to avoid serotonin syndrome and an increased risk ofseizures.

9. (a) Codeine is a prodrug converted to morphine through cytochrome P-450 metabolism. Up to10% of whites lack this enzyme, and this may be a reason why codeine is not effectivein all patients.

10. (d) Capsaicin is a topical agent derived from red chili peppers. Topical capsaicin depletessubstance P and calcitonin gene–related peptide, leading to a pharmacologic desensitiza-tion of nociceptors. Capsaicin activates vanilloid receptors, a newly found family ofthermosensitive receptors.

11. (c) Nineteen randomized trials of treatment of plantar heel pain were reviewed. Trial qualitywas noted to be generally poor. There was no evidence to support effectiveness oftherapeutic ultrasound. There were no randomized trials evaluating surgery. There waslimited evidence for the superiority of corticosteroid injections over orthotic devices.There is limited evidence that stretching exercises and heel pads were associated withbetter outcomes than custom-made orthoses in people who stand more than 8 hours a day.

12. (a) A study in the United Kingdom randomized 108 consecutive patients after a “whiplash”injury into either an exercise group or a group that was immobilized in a soft cervicalcollar for 3 weeks followed by the same exercise program. No differences were foundbetween the 2 groups for pain, range of motion, or activities of daily living at follow-upsat 3, 12, and 52 weeks postinjury. The collar-treatment group took significantly longer toreturn to work (34d) than did the early-exercise group (17d).

13. (b) In a randomized trial no significant differences in pain were found with counterforcebracing. A Cochrane review of the literature showed no significant benefit of extracor-poreal shock wave treatment over placebo. One study of 39 patients with lateral epicon-dylitis showed significantly better reduction of pain in the group treated with an isotoniceccentric exercise program versus a contract-relax stretching program.

14. (d) Both nocturnal and full-time splinting have been found to alleviate symptoms in carpaltunnel syndrome. Use of nonsteriodal anti-inflammatory drugs, ergonomic keyboards, andshort-term ultrasound have not been found helpful in controlled trials.


S46 SAE-P ANSWER KEY, Phelan

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15. (c) Studies have generally found that lumbar supports have little to no effect in preventing ortreating back injury, but 1 study showed fewer days of absence from work because of backinjury in workers who used lumbar supports and attended back school compared withthose who only attended back school.

16. (b) The exact pathogenesis of trigger points remains unknown; however, researchers have notedconsistently lower oxygen levels in these muscle fibers. Inflammation has not been shownin trigger point muscle tissue biopsy. Electromyographic evaluation of trigger points hassometimes shown an increase in miniendplate potentials, but this finding is not consistentor considered pathognomonic for trigger points. Electromyographic evaluation does notshow evidence of spasm or denervation potentials associated with trigger points.

17. (c) Cervical zygapophyseal-joint pain can most reliably be diagnosed by selective block of thenerves that innervate the joint, the medial branches of the cervical dorsal rami. Imagingstudies can detect abnormal joint morphology but not whether or not the joint is a sourceof pain. Bone scans may also help identify abnormal joints, but they, too, do not indicatewhether or not the joint is a source of pain. Mechanism of injury and physical examinationfindings may be suggestive of zygapophyseal-joint dysfunction as a cause of axial neckpain but are considered nonspecific.

18. (a) Radiofrequency neurotomy/neuroablation is an effective treatment for primary zygapophy-seal joint pain and dysfunction, with pain relief reported for 7 to 9 months or longer. Incontrast, intra-articular injection of corticosteroid provides only short-term relief of 1 to4 weeks. This finding was not statistically different from injection of local anestheticalone. Trigger point injections are of limited, transient benefit and do not address the jointitself. Cervical fusion is not indicated for primary zygapophyseal joint pain.

19. (c) A small number of prospective studies has shown beneficial effects of epidural corticoste-roid injections for treatment of cervical radiculopathy/radiculitis. No studies have beenperformed comparing the transforaminal and interlaminar approaches. Epidural steroidinjections are not indicated for the treatment of axial neck pain from either the facet jointsor intervertebral disks.

20. (b) Recent reports of acute catastrophic neurologic injury have been associated with thetransforaminal approach for epidural injection of corticosteroids. These injuries werehypothesized to be secondary to intra-arterial injection of particulate solutions andsubsequent infarction of the central nervous system. The vessels most likely involved arethe vertebral artery and radicular arteries of the spinal cord. Techniques used to help avoidsuch events include the use of fluoroscopic guidance during injection of contrast to assessfor vascular flow. Digital subtraction analysis may also be used to assess for vascular flowduring injection. Intralaminar epidural steroid injection is also associated with complica-tions and neurologic injury due to epidural hematoma, abscess, or direct puncture of thespinal cord; however, these injuries are usually subacute and rarely result in death ifproperly treated. The possibility of neurologic injury exists with cervical facet injections,but such injury is easily avoided with good technique, and there are no published reportsof such injury. Paraspinal trigger point injections, if properly performed, are not likely tobe associated with neurologic injury.

21. (c) Intra-articular injection of local anesthetic, with subsequent pain relief, is the only reliablemeans of diagnosing primary sacroiliac joint (SIJ) pain. Physical examination findings,imaging studies, and nuclear medicine studies may suggest SIJ abnormalities but do notestablish the SIJ as a cause of pain. Referral patterns of SIJ pain overlap with othersources of lumbar and lower-limb pain, and differentiation is important to determineeffective treatment.

22. (b) Phospholipase A2 has been shown as an enzymatic marker for inflammation associated withlumbar disk herniations. It is the enzyme responsible for the release of arachidonic acidand subsequent production of prostaglandins and leukotrienes. Prostaglandin E2 andleukotriene B4 are also associated with disc herniations, as are interleukin-1, tumornecrosis factor-�, nitric oxide, and thromboxane.

23. (d) In the patients whose low-back pain is caused by the zygapophyseal joints, radiofrequencyablation of the medial branches has been shown to provide a 90% reduction in pain in atleast 60% of selected patients, with 87% of patients obtaining at least 60% reduction inpain. Pain relief lasted at least 12 months in these patients. It is possible to repeat theprocedure if and when pain recurs. Intra-articular injection of corticosteroid may providesome relief of zygapophyseal joint pain but is usually short-lived, lasting only a few daysto a few weeks. Phenol blocks of the medial branches are not an established treatment forzygapophyseal joint pain and have not been studied. Cage fusion addresses anteriorcolumn/diskogenic pain and would not relieve posterior column/zygapophyseal joint pain.


S47SAE-P ANSWER KEY, Phelan

24. (b) A high-intensity zone is a focal area in the outer annulus that appears bright on T2-weightedmagnetic resonance images. It was originally described by Aprill and Bogduk and thoughtto be associated with painful annular tears. The presumption of symptoms associated withimaging has been questioned and refuted by Carragee. A high-intensity zone may befound in 24% of asymptomatic people and 59% of symptomatic people. When a high-intensity zone is present, diskography is positive approximately 70% of the time in bothsymptomatic and asymptomatic people. It is currently thought that the high-intensity zoneis associated with acute or subacute tears of the outer annulus; however, the clinicalsignificance of the high-intensity zone remains questionable. The other options listed areabnormalities that may be seen on magnetic resonance imaging but are not specific to thedisk annulus.

25. (c) Intradiskal electrothermy annuloplasty is used to address annular tears not associated withdisc herniations that are less than 4mm and do not protrude past the posterior longitudinalligament. Further, the disk should have less than 50% loss of disk height on magneticresonance imaging compared with normal disks. Patient selection for this interventionalso includes a lack of response to conservative care with pain persisting for at least 6months. The patient should have no symptoms of nerve root compression or significantspinal stenosis. Patients with high pain ratings and lower levels of function pretreatmentshow greater benefit than those with low to medium pain ratings and high functionallevels.

26. (b) Some evidence exists to support the use of intradiskal electrothermal annuloplasty, nucleo-plasty, and percutaneous disk decompression in the treatment of painful lumbar disks.There is no evidence to support the use of intradiskal steroids. Not only have intradiskalsteroids failed to show benefit, they may actually be harmful. Animal studies show diskdegeneration in response to intradiskal steroid injections.

27. (d) Local corticosteroid injection is proven effective as a treatment for de Quervain’s tenosyn-ovitis, both with and without splinting. Injection alone produced an 83% cure rate, withinjection plus splinting producing a 61% cure rate. Splinting alone produced a 14% curerate, and rest and anti-inflammatories were of no benefit.

28. (d) Insulin has been hypothesized to stimulate nerve regeneration, similar to nerve growthfactor. Injection of corticosteroid into the carpal tunnel followed by similar injections ofinsulin produced more significant improvement than did corticosteroid alone in patientswith non–insulin-dependent diabetes mellitus. This improvement was measured by globalsymptom score and median nerve motor/sensory distal latency improvement. Corticoste-roid injection produced clinical improvement superior to surgical decompression at 3months and equal to surgical decompression at 1 year. Results of corticosteroid injectionwere superior to iontophoresis and phonophoresis. Corticosteroid injection results inimproved nerve conduction parameters and symptom severity in patients with mild tomoderate carpal tunnel syndrome.

29. (d) Review of the medical literature does not show a clear association between local cortico-steroid injection and Achilles’ tendon rupture. Animal studies indicate decreased tendonstrength associated with intratendinous injection of corticosteroid, with presumed increasein tendon rupture. Clinical studies of peritendinous injections did not show an increase inrupture rate. Some clinicians advocate for injection under fluoroscopic or ultrasoundguidance to avoid intratendinous injection. Evidence is inadequate to support the use oflocal corticosteroid injections as a treatment for Achilles’ tendonitis.

30. (d) Corticosteroid injections are an effective treatment for plantar fasciitis; however, patientsmay be reluctant to undergo the procedure because of the significant pain that isassociated with injection. This pain can be significantly reduced or eliminated by blockingthe posterior tibial nerve before performing the injection. This procedure also significantlyincreased the willingness of patients to undergo repeat injections. Mixing lidocaine withthe corticosteroid would not decrease the pain associated with the injection, it mightactually increase the pain. Topical capsaicin would not affect pain at the deeper levels.Although contact with the calcaneus may increase the pain associated with injection fromcontact with the periosteum, avoidance of the calcaneus would not eliminate the painassociated with injection.

31. (b) A multitude of factors place the aging worker at an increased risk for injury. Riskscommonly cited in the literature include a decrease in vision and hearing with increasingage. Findings from the Health Retirement Study affirm that decreased hearing and visionare independent risk factors for occupational injury.



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32. (b) Outcome studies of injured workers show a clear trend of older workers having longerperiods of disability from their occupational injuries than do younger workers. Prospec-tive trials affirm that older workers are less likely to return to work after injury, withlonger periods of disability after injury when compared with younger workers. Theincidence of injury-associated fatality advances with age. Development of chronic symp-toms after injury is higher for workers aged 50 years and older, and they are at greater riskfor recurrent injury.

33. (b) Low back pain injuries are the most common musculoskeletal injury in the aging workforce.34. (d) Earlier-than-planned retirement correlates with preinjury job dissatisfaction, poor medical

care, and poor physical and mental health status. Difficulty keeping up with job-relatedtasks and poor quality of the work environment has led to earlier retirement. Difficultyarranging alternative duty is associated with prolongation of work disability and thus mayindirectly influence retirement decisions. Employers who are deemed rigid, inflexible, andnonsupportive are less likely to see their older workers return.

35. (d) Successful return to work is enhanced by a rehabilitation program that emphasizes improvedflexibility, increased aerobic fitness, strengthening, education on fall prevention andlifting techniques, and early return to the worksite. Early return to the worksite has ahigher success rate for return to work but may not be compatible with complete symptomresolution.


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PINAL CORD INJURY MEDICINE

pinal Cord Injury Medicine. 1. Epidemiology andlassification

hester H. Ho, MD, Lisa-Ann Wuermser, MD, Michael M. Priebe, MD, Anthony E. Chiodo, MD,
illiam M. Scelza, MD, Steven C. Kirshblum, MD
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ABSTRACT. Ho CH, Wuermser LA, Priebe MM, ChiodoE, Scelza WM, Kirshblum SC. Spinal cord injury medicine.. Epidemiology and classification. Arch Phys Med Rehabil007;88(3 Suppl 1):S49-54.

This self-directed learning module reviews the demographics ofraumatic and nontraumatic spinal cord injuries (SCIs). It is part ofhe study guide on SCI medicine in the Self-Directed Physiatricducational Program for practitioners and trainees in physicaledicine and rehabilitation. This article specifically focuses on the

hanging demographics of traumatic SCI, the classification ofCI, the common causes of nontraumatic SCI, and the incidencend prevalence of myelomeningocele.

Overall Article Objective: To summarize the demographicsnd classification of traumatic and nontraumatic spinal cordnjuries in adults and children.

Key Words: Classification; Meningomyelocele; Multipleclerosis; Rehabilitation; Spinal cord injuries; Spinal cord neo-lasms; Spinal stenosis.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Educational Activity: To discuss the epidemiologicfactors relevant to a 70-year-old man who fell andsustained a neurologically incomplete C4 injury.

INCE 1973, THE NATIONAL Spinal Cord Injury Data-base (NSCID) has been collecting data on people with new

pinal cord injuries (SCIs) from the facilities participating inhe Model Spinal Cord Injury System (MSCIS). Analyses ofhese data have shown changing trends in traumatic SCI. Suchpidemiologic data can guide us on the use of resources forreventing and treating SCI.The case of this 70-year-old man who fell illustrates several

ignificant trends in traumatic SCI: the increasing average agef onset, the increasing incidence of falls as one of the leadingauses of SCI, the increasing incidence of cervical injuries, andhe continuing trend of people with incomplete tetraplegia ashe largest group by neurologic classification.1

From the Louis Stokes Cleveland Department of Veterans Affairs Medical Centernd Department of Physical Medicine and Rehabilitation, Case Western Reserveniversity, Cleveland, OH (Ho); Department of Physical Medicine and Rehabilita-

ion, Mayo Clinic, Rochester, MN (Wuermser, Priebe); Department of Physicaledicine and Rehabilitation, University of Michigan Hospital, Ann Arbor, MI

Chiodo); Department of Physical Medicine and Rehabilitation, Carolinas Rehabili-ation, Charlotte, NC (Scelza); Spinal Cord Injury Services, Kessler Institute forehabilitation, West Orange, NJ (Kirshblum); and Department of Physical Medicinend Rehabilitation, University of Medicine and Dentistry–New Jersey Medicalchool, Newark, NJ (Kirshblum).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Chester Ho, MD, Louis Stokes Cleveland Dept of VAMC, SCI

28W, 10701 E. Blvd, Cleveland, OH 44106, e-mail: [email protected]. Reprintsre not available from the author.

fi0003-9993/07/8803S-11415$32.00/0doi:10.1016/j.apmr.2006.12.001

ncreasing Age at Onset of SCIBetween 1973 and 1979, the average age at injury was 28.7

ears, with most of the injuries occurring between the ages of6 and 30 years. The average age has since been increasingteadily to an average age of 37.6 years between 2000 and003.2 With the exception of violence as a cause of injury, thisncrease in the average age at injury has been found in all othertiology groups (motor vehicle crashes, falls, sports). A closerook at the data showed that, although the relative order ofrevalence of SCI in the various age groups (0–15, 16–30,1–45, 46–60, 65�y) has remained unchanged, the absoluteercentage for each group has significantly changed over theast 3 decades. The prevalence in older adults above the age of5 years has increased from 4.7% between 1973 and 1979 to0.9% since 2000, whereas the prevalence among childrenetween the ages of 0 and 15 years has decreased from 6.4% to.0% in the same periods2 (table 1). This trend of increasingverage age of injury is significant; the larger percentage oflderly people with SCI has implications on the need to con-ider specific aging-related and geriatric needs in the rehabili-ation of these people.

hanges in EtiologyThe most common cause of SCI between 2000 and 2003

ontinued to be motor vehicle crashes (table 2). They accountor 50.4% of all the causes for all age groups during the timeeriod, compared with a similar rate of 48.7% between 1973nd 1979.2 However, the rates for falls have progressivelyncreased over the last 3 decades, from 16.5% in the 1970s to3.8% between 2000 and 2003.2 Even though falls were stillhe second most common cause of SCI across all age groups, itas the only cause with a rate that has steadily increased over

he last 3 decades. When data were stratified by age group, itas apparent that falls were by far the most common cause ofCI in people over age 60 years. Successful fall preventionducation for the elderly may mitigate the prevalence of SCI inhis population.

Examination of the other causes of SCI shows that the ratesssociated with sports have decreased over the decades, from4.4% between 1973 and 1979 to 9% between 2000 and 2003.iolence as an etiology as reported by the NSCID initially

ncreased from 13.3% between 1973 and 1979 to a peak of1.8% in the 1990s. However, it has since declined to 11.2%etween 2000 and 2003. When compared with internationaltatistics, with the exception of acts of violence as causes ofCI, the etiologies of SCI were similar in other countries,

ncluding Denmark, Taiwan, and Spain.2

he Increasing Incidence of Cervical InjuriesThroughout all the time periods observed, cervical injuries

ccurred more often than thoracic and lumbar injuries. Further-ore, there was an increasing percentage of cervical injuries

rom 53.5% between 1973 and 1979 to 56.5% between 2000nd 2003. This increase was statistically significant but also has
nancial implications, because the lifetime costs for the care of

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eople with tetraplegia were much higher than for those witharaplegia. For all age groups since 2000, people with incom-lete tetraplegia made up the highest number (34.5%), fol-owed by complete paraplegia (23.1%), complete tetraplegia18.4%), and incomplete paraplegia (17.5%).1

ther TrendsNSCID data show that from the 1970s to the 1990s, the

ercentage of whites with SCI decreased from 76.8% between973 and 1979 to 59.9% between 1990 and 1999. However, theercentage has risen to 67.4% between 2000 and 2003. At theame time, the increase in percentage among African Ameri-ans and Hispanics from the 1970s to the 1990s was reversedetween 2000 and 2003.2 During the periods when the percent-ge of ethnic minorities with SCI rose, there was a strikingorrelation with an increase in acts of violence as causes forCI.The percentage of females with SCI has increased since the

970s, from 18.2% between 1973 and 1979 to 21.8% between000 and 2003. When the data from the Shriners Hospitals forhildren SCI database were combined with the NSCID from973 to 2002, analysts noted that males were a consistentlyecreasing proportion of new SCI patients.3 Therefore, thisnding appeared to reflect a trend observed across different ageroups.The NSCID has provided the most comprehensive and help-

ul epidemiologic data on SCI in the United States, noting thehanging trends of traumatic SCI over the last 3 decades.owever, the data represent only the facilities participating in

he MSCIS. Furthermore, over the decades, the profile of thearticipating facilities has changed. Therefore, it is not clearow generalizable these data are to the general U.S. population.uch factors should be taken into account when interpreting

hese data.

.2 Clinical Activity: To classify the injury for a 70-year-old man with diabetes mellitus who fell from a ladder.

ensationExamining the patient at 72 hours after injury, you note the

ollowing: sensation is normal to pin prick and light touch overhe face and neck, in the supraclavicular region anteriorly, andver the acromioclavicular joints bilaterally. Sensation to pin-rick is diminished, but present, at the lateral antecubital fossailaterally and in all dermatomal segments below. Light touchs intact throughout except at midcalf and below bilaterally.roprioception is absent at the toes bilaterally.

otor FunctionMotor examination results are in table 3.

eflexesAreflexia is observed in biceps, brachioradialis, and tricep

eflexes bilaterally; hyperreflexic without clonus at the patellaendons; and areflexic at the Achilles’ tendon. There is an

Table 1: Changes in Age at Onset of SCI

Characteristic 1973–1979 2000–Present

Average age at injury (y) 28.7 37.6Percentage of people �60y at injury 4.7 10.9

OTE. Data from the National Spinal Cord Injury Statistical Center.1,2

xtensor response to plantar stimulation bilaterally.NI


ectal ExaminationThe patient’s sensation to light touch is present at the anocuta-

eous junction with absent voluntary anal contraction. There isncreased sphincter tone and a present bulbocavernosus reflex.

Based on these examination findings, this patient’s neurologiclassification according to the American Spinal Injury AssociationASIA) International Standards for Neurological Classification ofpinal Cord Injury4 is as follows: sensory level of injury, C4ilaterally; motor level of injury, C4 bilaterally; and degree ofompleteness, ASIA Impairment Scale (AIS) grade C. This com-ination of findings follows a pattern of central cord syndromeith an underlying peripheral neuropathy.In 1982, ASIA published its first edition of the Standards for

eurological Classification of Spinal Injured Patients.5 Thisocument arose from a need to more precisely define neuro-ogic levels and the extent of incomplete injuries. The ASIAtandards focused on key muscles and key sensory points to beested during the neurologic assessment. Ten key muscles wereelected, 5 in the upper limb and 5 in the lower limb (table 4).ach muscle represents a single myotome from C5 through T1nd L2 through S1. The muscles were chosen to be testableith the patient supine and with minimal movement of the

pinal column. Likewise, key sensory points were selected toepresent each sensory dermatome from C2 through S4-5. Atandardized form to be used as a flow chart for classifyingpinal injuries was also developed by ASIA (fig 1).

Over the next 10 years, refinements were made to definitionsf neurologic levels, key muscles and key sensory points, theone of partial preservation, and the Frankel Scale. In 1992 theourth edition of the Standards was published. In this edition,he most important change incorporated was the definition ofomplete versus incomplete injuries using the sacral sparingasis for definition of completeness. An injury was defined aseurologically incomplete if there was any sparing present athe lowest sacral segments. This edition also included recom-endations for use of the FIM instrument for assessment of

isability. The Frankel Scale was further modified and wasermed the ASIA Impairment Scale (AIS). Also in 1992, thenternational Medical Society of Paraplegia (now the Interna-ional Spinal Cord Society) endorsed these standards, creatinghe International Standards for Neurological and Functionallassification of Spinal Cord Injury.6

The International Standards document has evolved and im-roved over the past 20 years. These standards have becomeccepted as the appropriate method for describing the neurologicmpairment of SCI for clinical and research use. The standardsave been used in numerous clinical trials and have been incor-orated into the International Core SCI Data Set.7 Although not allatients fit the International Standards matrix perfectly, mostatients can be adequately classified using this approach.

Appendix 1 also lists the most common terms used in SCIedicine. Appendix 2 describes the steps to classify the SCI,

nd appendix 3 outlines the AIS. An ASIA Standards Teachingackage8 and Additional Teaching Manuals (2003, Revised)8

Table 2: Changes in Etiology of SCI

Etiology of SCI 1973–1979 2000–Present

Motor vehicle crashes 48.7 50.4Falls 16.5 23.8Sports 14.4 9Violence 13.3 11.2

OTE. Values are percentages. Data from National Spinal Cordnjury Statistical Center.1,2

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S51EPIDEMIOLOGY AND CLASSIFICATION, Ho

ave been developed as a companion volume to the currenttandards. The teaching package provides a detailed explana-ion of the examination elements, rationale for inclusion, scor-ng instructions, and background references. It is availablenline from the ASIA Website.8

In the sample case the stocking-glove loss of sensation isost likely caused by the history of diabetes mellitus and is

nrelated to the patient’s SCI. Although reflexes are an impor-ant part of the neurologic examination they are not used forlassification in the International Standards.

.3 Educational Activity: To identify the common causesof nontraumatic SCI pertinent to a 30-year-oldwoman who presents with subacute onset of paraple-gia associated with a T6 sensory level.

Nontraumatic SCI affects a vast number of people and is arowing population for admission to inpatient rehabilitation.he percentage of inpatient rehabilitation admissions for SCI

or nontraumatic injuries has been growing. In a comparison ofraumatic and nontraumatic SCI, Chapman9 found that non-raumatic SCI was more likely to present with a neurologicallyncomplete lesion and was associated with a lower frequency ofecondary conditions such as spasticity, deep vein thrombosis,nd autonomic dysreflexia. However, among an older popula-ion, other comorbidities and generalized deconditioning moreignificantly affected functional outcome. In patients with non-raumatic SCI, there tended to be a longer period betweeniagnosis and rehabilitation than in traumatic SCI. Nontrau-atic SCI patients had a lower rate of discharge home (73%),ith favorable discharge seen in patients who had incomplete

njury, were married, and had an established bowel and bladderanagement program and intact skin.Excluding multiple sclerosis (MS) and degenerative central

ervous system (CNS) diseases, causes for nontraumatic SCIave included neoplasms (25%), vascular disease (25%), in-

Table 3: The Patient’s Muscle Gr

Side Elbow Flexion Wrist Extension Elb

Right 1/5 1/5Left 0/5 0/5

Hip Flexion Knee Extension Ank

Right 3/5 4/5Left 2/5 2/5

Table 4: The 10 Key Muscles Tested to Determine an ASIASCI Classification

Muscle Group Root Level

Upper limbElbow flexors C5Wrist extensors C6Elbow extensors C7Long finger flexors C8Small finger abductors T1

Lower limbHip flexors L2Knee extensors L3Ankle dorsiflexors L4Long toe extensor L5

sAnkle plantarflexors S1

ammatory disease (19.5%), and spinal stenosis (18.6%).10 Innother study,11 spinal stenosis (21%) and spinal cord tumors14%) were the most common causes of nontraumatic SCI.pinal stenosis patients with cord compression were moreommonly paraplegic (73%) and neurologically incomplete90%) than their traumatic SCI counterparts.12

Inflammatory disorders of the spinal cord were commonlyepresented among SCI patients who participate in rehabilita-ion. MS was most commonly seen in young adults, althoughediatric and elderly presentations are common and may affecthe spinal cord. Pediatric disease was usually relapsing-remit-ing and with a longer time course to disability, althoughisability occurs at an earlier age. Negative prognostic indica-ors among children were a short interattack interval, a highelapse rate, a relapsing-progressive course, a shift to the sec-ndary progressive phase, and early accumulation of disabil-ty.13 Elderly presentation, representing 4% to 10% of cases,as often primary progressive with pyramidal or cerebellar

nvolvement seen in more than half. Progression to disability isaster in elderly patients than younger patients. Differentialiagnoses included cerebrovascular disease, hypertension-re-ated encephalopathy, cerebellar degenerative diseases, othereurodegenerative diseases, and nutritional disorders. Diseaseshat mimic MS included Devic’s neuromyelitis optica andcute disseminated encephalomyelitis. Devic’s neuromyelitisptica was diagnosed clinically and by magnetic resonancemaging (MRI), with evidence of myelitis and optic neuritis.oorer prognosis was seen clinically in people with relapses in

he first 2 years of the disease, with older age, and in women.14

ntiphospholipid syndrome can clinically mimic MS. In MS,RI is an accepted tool for monitoring disease progression,ith the number of new lesions seen on T2 images and degreef brain atrophy being predictive of subsequent disease inrimary progressive patients.Transverse myelitis (TM) is another common inflammatory

isorder of the spinal cord. It can be primary or may beecondary to vasculitis or rheumatologic disorders such asystemic lupus erythematosis or Sjögren’s syndrome. TM has aemale-to-male ratio of 4:1, with peaks in the second and fourthecades. The time course of progression is longer than 48 hoursnd less than 6 weeks. At nadir, half have paraplegia, all haveeurogenic bladder, and 80% to 94% have sensory symptoms.ver time, one third recovered, one third had neurologic def-

cits, and one third had paraplegia. Poor recovery was predictedy rapid progression, back pain, and spinal shock.15

SCI from epidural abscess in immunocompromised and dia-etic patients is not rare. Epidural hematoma can be associatedith anticoagulation, vascular malformations, or myelodysplasticiseases. Arterial disease associated with thrombosis or embolismo spinal arteries may cause spinal cord ischemia and injury.

Infarction of the spinal cord can occur in many other vas-ular diseases, including vasculitis and diabetes. Idiopathic

by Location 72 Hours Postinjury

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SCI in patients after thoracoabdominal aneurysm repair waseported in 9% to 18% of cases. Increased occurrence wasssociated with rupture, dissection, or prolonged surgery.16

mproved outcome has occurred with preoperative planningith spinal angiography, reattachment of intercostal arteries,ood distal aortic perfusion, spinal cord hypothermia, intraop-rative cerebrospinal fluid drainage, and intraoperative neuro-hysiologic monitoring.17

Radiation myelopathy may occur months after treatment.his myelopathy involves an injury to the white matter thatredominates in the lateral spinal cord. Etiology remains elu-ive, with injury to glial cells and vascular injury remaining ashe most likely mechanisms.18

Spinal cord tumors can be primary or metastatic, intradural, orxtradural. In patients with intramedullary tumors, favorable func-ional outcome was observed in 94.1% of patients with vascularumors, in 61.3% of patients with low-grade neuroepithelial tu-ors, and in 53.3% of patients with malignant tumors.19 The

trongest predictors of functional outcome were the tumor typend the preoperative neurologic status.19 In patients with meta-tatic spine disease, quality-of-life measurements have been gen-rally favorable except for those patients who have high emotional

ig 1. The standard ASIA method for classifying SCI by neurologermission.

istress.20 a


Comprehensive inpatient rehabilitation that included mobil-ty, activities of daily living, bowel and bladder care, andatient and family training and equipment prescription wasmportant for nontraumatic injuries. The prognosis of the un-erlying disease process will guide the rehabilitation goals.npatient rehabilitation lengths of stay were shorter, but FIMfficiency and home discharge rates were comparable withhose of traumatic spinal cord patients.11

.4 Educational Activity: To discuss the epidemiologicfactors related to a girl born with spina bifida at theL2 level with a lower motoneuron injury.

Embryonic development of the CNS starts with the forma-ion of the neural tube at approximately day 18. Neural tubeefects or, as they are most accurately termed, spinal dysra-hism, result in failure of the ectodermal, mesodermal, andeuroectodermal tissues to develop properly. In the Unitedtates, spinal dysraphism incidence has dramatically decreased

o about 3.2 per 10,000 live births.21 Recent trends show aniform incidence in all ethnic groups with no geographicariation. The reduction in incidence is largely believed to be

vel. Source: American Spinal Injury Association.4 Reprinted with

ssociated with better national nutritional habits. Folic acid

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S53EPIDEMIOLOGY AND CLASSIFICATION, Ho

upplementation of 0.4mg a day is recommended for allomen of childbearing age to reduce the risk.22 The risk to

iblings of those with spinal dysraphism increases to 2% to 5%ith 1 affected sibling and to 10% to 15% with 2 affected

iblings. In those with spina bifida, allergy to latex has arevalence of up to 40%. It is immunoglobulin E mediated anday be mild with urticaria or more severe with laryngeal

dema and bronchospasm; it is recommended that latex expo-ure be minimized as much as possible.23 Cognitive dysfunc-ion, obesity, and precocious puberty are also commonly seenn people with myelomeningocele.24

In spinal dysraphism’s most common form, myelomeningo-ele, neural elements are exposed, causing complete neurologiceficits. They can present anywhere throughout the spine butre most commonly seen in the thoracolumbar regions, result-ng in paraplegia. After birth, in the presence of a myelomen-ngocele, immediate surgical closure is usually undertakenithin 24 hours. Goals of the operation are to preserve neuro-

ogic function and to prevent infection. In a meningocele, theural sac is exposed and the neural elements may be intactithout neurologic deficits. Prompt closure is suggested for the

ame reasons as with myelomeningocele.25

Occult spinal dysraphism refers to closed spinal deficitsncluding spinal lipomas, diastematomyelia, and a tetheredpinal cord. These conditions are suspected when a cutaneousarker such as a dimple with a pinhole tract, a hairy patch, or

evus is discovered. Neurologic deficits at the time of birthay or may not be present, but further investigation should

nsue. Spinal lipomas may present with a subcutaneous fattyass without any neurologic deficits but may gradually change

ver the first years of life and should be closely monitored.urgical treatment is usually focused on untethering of the spinalord. The lipomas are not typically removed, because neural tissues usually enmeshed within them and removal would potentiallyreate a more severe deficit.24 Spina bifida occulta is strictly aefect in bony closure of the posterior elements without neuro-ogic deficit and is usually an incidental finding.

In people with myelomeningocele, hydrocephalus is seen inpproximately 90% of patients and usually manifests itselffter surgical closure. Most of these people will also requireentriculoperitoneal (VP) shunting, which is placed at the sameime as the surgical closure. Classic symptoms of elevatedntracranial pressure such as headache, nausea, vomiting, andethargy may be present in shunt malfunctions and must beeviewed with the patient and his/her caregivers. Adolescents,owever, may have a more subtle presentation, which may berritability, worsening performance at school, and generalizedeakness. Chiari II malformations are usually the underlying

tiology of hydrocephalus, because they are present in almostll cases. Dysphagia, stridor, vocal cord paralysis, cranial nervealsies, and central respiratory dysfunction may occur in about0% of cases, and symptoms will primarily occur in the firsteveral months of life.26 These symptoms are usually treatedith VP shunting but sometimes will need a posterior fossaecompression to relieve pressure exerted on the brainstem.ognitive dysfunction is also prevalent, with approximately0% of people having below-normal intelligence.Hydrosyringomyelia (syrinx) or cystic fluid–filled cavities

ithin the spinal cord are common in myelomeningocele, buthe precise prevalence is not known. The syrinx cavity canresent in any portion of the spinal cord but is most commonn the cervical segments. Classic presentation of syrinx forma-ion includes cervical pain, new weakness, spasticity, and sco-iosis. A syrinx may be asymptomatic and may not presentlinically until adulthood. Possible etiologies could exist from
tethered spinal cord, which will place traction on the spinal t
ord over time and contribute to syrinx formation. Tethering ofhe spinal cord is usually from scar formation or traction ofeural tissue attached to the dura. Symptoms of tethered cordre very similar to syrinx. If severe, surgical procedures can beerformed to release the tethered area, but scar tissue will oftenllow them to recur in 15% to 20% of cases.27

Scoliosis affects most people with myelomeningocele asell, especially when at the thoracic levels. Neuromusculareakness, lower-extremity contractures, and primary vertebral

bnormalities all contribute to the formation of scoliosis. Syr-nx formation, uncompensated hydrocephalus, or tethered cordyndrome, as mentioned before, should be considered when acoliosis abruptly worsens, especially in someone who is skel-tally mature. Curvature generally less than 25° should beonitored closely. Greater curvature may require a thoraco-

umbosacral orthosis brace to prevent further curvature. Severeurves will occasionally require surgery.

APPENDIX 1: GLOSSARY OF KEY TERMS USEDIN SCI

ey muscle groups: The 10 muscle groups that are tested inhe standardized spinal cord examination.

Motor level: The most caudal key muscle group that israded 3/5 or greater with the segments cephalad to that levelraded normal (5/5) strength.Sensory level: The most caudal dermatome to have normal

ensation for both pinprick and light touch on both sides.Neurologic level of injury: The most caudal level at which

oth motor and sensory modalities are intact.Complete injury: The absence of sensory and motor func-

ion in the lowest sacral segments.Incomplete injury: Preservation of motor or sensory func-

ion below the neurologic level of injury that includes theowest sacral segments.

Sacral sparing: Presence of motor function (voluntary ex-ernal anal sphincter contraction) or sensory function (lightouch, pinprick at S4/5 dermatome, or anal sensation on rectalxamination) in the lowest sacral segments.

Zone of partial preservation: All segments below the neu-ologic level of injury that have preserved motor or sensoryndings; used only in complete SCI.

APPENDIX 2: STEPS TO CLASSIFYING INJURYSEVERITY IN A PATIENT WITH SCI28

1. Perform sensory examination in 28 dermatomes bilat-erally for pinprick and light touch, including S4/5 der-matome, and test for anal sensation.

2. Determine sensory level (right and left).3. Perform motor examination in the 10 key muscle

groups, including anal contraction.4. Determine motor level (right and left).5. Determine neurologic level of injury.6. Classify injury as complete or incomplete.7. Categorize ASIA Impairment Scale (A–E).8. Determine zone of partial preservation if ASIA A.

APPENDIX 3: THE AIS4

A � Complete: No sensory or motor function preserved inhe lowest sacral segments (S4/5).

B � Sensory incomplete: Sensory but no motor functionreserved below the neurologic level including the sacral seg-ents S4/5.C � Motor incomplete: Motor function is preserved below

he neurologic level, and more than half of the key muscles


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APPENDIX 3: THE AIS4 (cont’d)elow the neurologic level have a muscle grade less than 3.here must be some sparing of sensory and/or motor function

n the segments S4/5.D � Motor incomplete: Motor function is preserved below

he neurologic level, and more than half the key muscles belowhe neurologic level have a muscle grade greater than or equalo 3. There must be some sparing of sensory and/or motorunction in the segments S4/5.

E � Normal: Sensory and motor functions are normal.atient may have abnormalities on reflex examination.

References1. National Spinal Cord Injury Statistical Center. Spinal cord in-

jury: facts and figures at a glance. J Spinal Cord Med 2005;28:379-80.

*2. Jackson AB, Dijkers M, DeVivo MJ, Paczatek RB. A demo-graphic profile of new traumatic spinal cord injuries: change andstability over 30 years. Arch Phys Med Rehabil 2004;85:1740-8.

3. DeVivo MJ. Epidemiology of traumatic spinal cord injury. In: Kirsh-blum S, Campagnolo DI, DeLisa JA, editors. Spinal cord medicine.Philadelphia: Lippincott Williams & Wilkins; 2002. p 69-81.

4. American Spinal Injury Association. International standards forneurological classification of spinal cord injury (revised 2000).Chicago: ASIA; 2002.

5. American Spinal Injury Association. Standards for neurologicalclassification of spinal injured patients. Chicago: ASIA; 1982.

6. American Spinal Injury Association, International Medical So-ciety of Paraplegia (ASIA/IMSOP). International standards forneurological and functional classification of spinal cord injury(revised 1992). Chicago: ASIA; 1992.

7. International Spinal Cord Society (ISCoS). Available at: http://www.iscos.org.uk. Accessed October 31, 2006.

8. American Spinal Injury Association. Available at: http://www.asia-spinalinjury.org. Accessed October 31, 2006.

9. Chapman J. Comparing medical complications from nontrau-matic and traumatic spinal cord injury [abstract]. Arch Phys MedRehabil 2000;81:1264.

10. Citterio A, Franceschini M, Spizzichino L, Reggio A, Rossi B,Stampacchia G. Nontraumatic spinal cord injury: an Italian sur-vey. Arch Phys Med Rehabil 2004;85:1483-7.

11. McKinley WO, Huang ME, Tewksbury MA. Neoplastic vs.traumatic SCI: an inpatient rehabilitation comparison. Am J PhysMed Rehabil 2000;79:138-44.

*Key reference.


12. McKinley WO, Tellis AA, Cifu DX, et al. Rehabilitation out-come of individuals with nontraumatic myelopathy resultingfrom spinal stenosis. J Spinal Cord Med 1998;21:131-6.

13. Ghezzi A. Clinical characteristics of multiple sclerosis with earlyonset. Neurol Sci 2004;25(Suppl 4):S336-9.

14. Bergamaschi R, Ghezzi A. Devic’s neuromyelitis optica: clinicalfeatures and prognostic factors. Neurol Sci 2004;25(Suppl 4):S364-7.

15. Transverse Myelitis Consortium Working Group. Proposed di-agnostic criteria and nosology of acute transverse myelitis. Neu-rology 2002;59:499-505.

16. Rectenwald JE, Huber TS, Martin TD, Ozaki CK, Devidas M,Welborn MB, Seeger JM. Functional outcome after thoraco-abdominal aortic aneurysm repair. J Vascular Surg 2002;35:640-7.

17. Tabayashi K. Spinal cord protection during thoracoabdominalaneurysm repair. Surg Today 2005;35:1-6.

18. Okada S, Okeda R. Pathology of radiation myelopathy. Neuro-pathology 2001;21:247-65.

19. Sandalcioglu IE, Gasser T, Asgari S, et al. Functional outcomeafter surgical treatment of intramedullary spinal cord tumors:experience with 78 patients. Spinal Cord 2005;43:34-41.

20. Levack P, Graham J, Kidd J. Listen to the patient: quality of lifeof patients with recently diagnosed malignant cord compressionin relation to their disability. Palliat Med 2004;7:594-601.

21. Centers for Disease Control (CDC). Spina bifida incidence atbirth—United States, 1983-1990. MMWR Morb Mortal WklyRep 1992;41:447-500.

22. From the Centers for Disease Control and Prevention. Recom-mendations for folic acid to reduce the number of spina bifidacases and other neural tube defects. JAMA 1993;269:1233-8.

23. Tosi LL, Slater JE, Shaer C, Mostello LA. Latex allergy in spinabifida patients: prevalence and surgical implications. J PediatrOrthop 1993;13:709-12.

24. Molnar GE. Spina bifida. In: Molnar GE, Alexander MA, editors.Pediatric rehabilitation. 3rd ed. Philadelphia: Hanley & Belfus;1999. p 219-44.

25. Kaufman BA. Neural tube defects. Pediatr Clin North Am 2004;51:389-419.

26. Charney EB, Rorke LB, Sutton LN, Schut L. Management ofChiari II complications in infants with myelomeningocele. J Pe-diatr 1987;111:364-71.

27. Tamaki N, Shirataki K, Kojima N, Shouse Y, Matsumoto S.Tethered cord syndrome of delayed onset following repair ofmyelomeningocele. J Neurosurg 1988;69:393-8.

28. Kirshblum SC, Donovan WH. Neurologic assessment and clas-sification of traumatic spinal cord injury. In: Kirshblum S, Cam-pagnolo DI, DeLisa JA. Spinal cord medicine. Philadelphia:
Lippincott Williams & Wilkins; 2002. p 82-95.
http://www.iscos.org.uk.

http://www.iscos.org.uk.

http://www.asia-spinalinjury.org.

http://www.asia-spinalinjury.org.

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pinal Cord Injury Medicine. 2. Acute Care Management ofraumatic and Nontraumatic Injury

isa-Ann Wuermser, MD, Chester H. Ho, MD, Anthony E. Chiodo, MD, Michael M. Priebe, MD,
teven C. Kirshblum, MD, William M. Scelza, MD
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ABSTRACT. Wuermser LA, Ho CH, Chiodo AE, PriebeM, Kirshblum SC, Scelza WM. Spinal cord injury medicine.

. Acute care management of traumatic and nontraumatic in-ury. Arch Phys Med Rehabil 2007;88(3 Suppl 1):S55-61.

This self-directed learning module highlights the basiccute care management of traumatic and nontraumatic spinalord injury (SCI). It is part of the chapter on SCI medicinen the Self-Directed Physiatric Education Program for prac-itioners and trainees in physical medicine and rehabilita-ion. Acute traumatic SCI is optimally managed in a level 1rauma center. Decompression of the neural elements, sta-ilization of the spine, and maintenance of tissue perfusionre fundamental to optimizing outcomes. SCI patients are atigh risk of pressure ulcers, venous thromboembolism,tress ulceration, bowel impaction, dysphagia, and pulmo-ary complications. Physiatric interventions are needed torevent these complications. Prognostication of neurologicutcome based on early examination is an important skill toid in creating a rehabilitation plan and to test for efficacy ofarly interventions. Nontraumatic SCI is an increasing pop-lation in rehabilitation centers. Establishing a diagnosisnd treatment plan is essential, in conjunction with preven-ion of complications and early physiatric intervention.

Overall Article Objectives: (a) To describe the diagnosticvaluation of traumatic and nontraumatic spinal cord inju-ies and (b) to summarize the medical, surgical, and physi-tric interventions during acute hospitalization for thesenjuries.

Key Words: Acute care; Prognosis; Rehabilitation; Spinalord injuries.


From the Department of Physical Medicine and Rehabilitation, Mayo Clinic,ochester, MN (Wuermser, Priebe); Louis Stokes Cleveland Department ofeterans Affairs Medical Center and Department of Physical Medicine andehabilitation, Case Western Reserve University, Cleveland, OH (Ho); Depart-ent of Physical Medicine and Rehabilitation, University of Michigan Hospital,nn Arbor, MI (Chiodo); Spinal Cord Injury Services, Kessler Institute forehabilitation, West Orange, NJ (Kirshblum); Department of Physical Medicinend Rehabilitation, University of Medicine and Dentistry–New Jersey Medicalchool, Newark, NJ, (Kirshblum); and Department of Physical Medicine andehabilitation, Carolinas Rehabilitation, Charlotte, NC (Scelza).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Lisa-Ann Wuermser, MD, Dept of PM&R, Mayo Clinic,

00 First St SW, Rochester, MN 55905. e-mail: [email protected] are not available from the author.

b0003-9993/07/8803S-11411$32.00/0doi:10.1016/j.apmr.2006.12.002

.1 Clinical Activity: To discuss the acute care manage-ment of a 20-year-old man admitted to the traumacenter with a C4 American Spinal Injury Associationgrade A spinal cord injury after a snowboardingaccident.

ATIENTS WITH ACUTE TRAUMATIC spinal cord in-jury (SCI) should be managed at a trauma center with SCI

xperience, particularly patients with concomitant injuries.evel 1 trauma centers have been shown to have better out-omes in acute SCI than lower-level trauma centers or nondes-gnated hospitals, although the differences between level 1 andevel 2 were small in isolated SCI.1 Transfer to such a center isdvocated as soon as the patient is stable, with the suggestionhat emergency medical services in urban areas should considerypassing the nearest hospital to take SCI patients to level 1rauma centers directly.2 Level 1 trauma centers are required toave in-house neurosurgical consultation and can thereforeore rapidly assess patients and intervene. These centers also

ften have well-defined, evidence-based protocols for SCI carend staff well-trained in SCI because of a higher volume of antherwise low-incidence injury.Principles of spine stabilization are well established and

ave changed little in recent years. Timing of decompression ofhe neural elements, however, is controversial. Animal dataave consistently suggested increased neuronal loss from pro-onged compression.3,4 Human studies have been conflicting,ut comparisons are marred by differences in time pointshosen, types of injuries included, and surgical procedureserformed. It is likely that little difference exists in outcomeetween patients undergoing surgical decompression later than8 hours and those treated even later than that.5 However,ecompression within 24 hours may improve neurologic re-overy, particularly in patients with incomplete injuries, but toate, data are inadequate to mandate such a standard.6 Thesetudies agree that there is not an increased risk of neurologiceterioration from early surgery, as was previously thought.urther, early surgery is associated with fewer complicationsnd shorter acute care lengths of stay.7,8

Although adopted as a standard of care more than a decadego,9,10 the use of high-dose methylprednisolone as a neuro-rotective agent in acute SCI has now been called into ques-ion, based on methodologic concerns of the primary studies.11

n light of the enrollment of a high number of patients withinimal deficit into the National Acute Spinal Cord Injurytudy (NASCIS) trials, it is particularly difficult to determine

he benefit of the protocol in people with complete SCI and ineople who have incomplete SCI with a significant deficit.oth the neurosurgical guidelines12 and the Consortium forpinal Cord Medicine clinical practice guideline2 consider these of high-dose methylprednisolone to be a treatment optionather than a standard. Concerns have been expressed about thencreased risk of infection and gastrointestinal bleeding asso-iated with the 48-hour–long infusion. Steroid myopathy has
een shown to be associated with both the 24-hour–long and

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he 48-hour–long infusions.13 The prevalence and functionalmplications of this myopathy are presently unknown. Despitehese caveats, the use of the NASCIS protocol remains high inhe United States.14

Spinal cord perfusion has been a recent area of explorationor neuroprotection. Hypotension has been recognized as aontributor to secondary neurologic injury and should bevoided.15 However, clear data on optimal blood pressure tonsure adequate perfusion, as well as any other intervention tomprove spinal cord perfusion in traumatic SCI, are lacking.outine use of a lumbar drain to reduce cerebrospinal fluid

CSF) pressure has reduced the prevalence of ischemic SCIssociated with abdominal aortic aneurysm repair.16 The effectf this intervention in traumatic SCI is currently in clinicalrial. Although human data are limited, the neurosurgicaluideline has recommended that the mean arterial pressure beaintained at 85 to 90mmHg for the first 7 days after injury.17

owever, a randomized controlled trial is needed to confirmhe safety and efficacy of this intervention. Physiatrists mayacilitate transfer of patients receiving this care out of thentensive care unit (ICU) by advocating for the use of abdom-nal binders, lower-limb compression, and oral vasopressorsuch as midodrine as other options to maintain adequate corderfusion.Autonomic dysfunction is common in acute SCI and is

articularly noticeable in cervical level injuries. Bradycardiand neurogenic shock18 are commonly seen in the acute careetting, but autonomic dysreflexia may also occur in this earlyeriod19 and will certainly be a concern in hospitalized chronicCI patients. Spinal shock and neurogenic shock, althoughelated, are separate entities. Spinal shock refers to the loss ofeflex neurologic activity in the spinal cord, and is defined byoss of all spinal reflexes. Neurogenic shock is loss of adequateissue perfusion associated with hypotension of neurologicrigin. However, acute SCI patients may have multiple causesf shock. Sepsis, hypovolemia, and cardiogenic shock must alle considered in the early period of SCI.2 Volume resuscitations an appropriate initial measure, but vasopressors are oftenecessary. Patients using antihypertensive medications beforenjury may be particularly difficult to control until the medi-ation effects are inactive. Bradycardia occurs because of un-pposed vagal tone, with a greater effect seen in higher levelsf injury. Stimulation of vagally innervated tissue may furtherower heart rate, as is seen commonly during deep trachealuctioning. Although the bradycardia is often self-limited, at-opine may be used either as treatment or as pretreatment in thease of identifiable triggers.18 External pacing may be of ben-fit as well. Autonomic dysreflexia requires intact spinal cordeflexes19 and so will not be seen until emergence from spinalhock. Although hypertensive emergencies are uncommon inhe early period, the instability of blood pressure as low-levelysreflexia occurs and resolves can be confounding to the acuteare team. The physiatrist can be helpful not only with man-gement but in identifying the source of dysreflexia. Hyper-hermia is not a component of autonomic dysreflexia but mayndicate the source of dysreflexia. However, heat dispersion ismpaired in SCI,20 such that fever from a typical source mayesult in higher temperatures and longer periods of fever com-ared with a neurologically intact population. Strictly speaking,nvironmental fevers are unlikely in the ICU setting, consid-ring its constant environmental control. However, a fever inhe early weeks after tetraplegia without any identified source,r “quad fever,” can occur.21 This is a diagnosis of exclusionnd may be related to a heightened febrile response to atelec-
asis. d

Preventing complications remains vital in acute SCI. Pro-hylaxis of venous thromboembolism should begin no laterhan 72 hours after the onset of SCI and should include anti-oagulation for most injuries.2,22 Low–molecular-weight hep-rin has been compared with unfractionated heparin, at 5000Utimes daily, with similar rates of deep vein thrombosis but

igher rates of pulmonary embolism (PE) and bleeding in thenfractionated heparin group found.23 In light of the high ratef PE, an inferior vena cava (IVC) filter should be used in SCIatients who have contraindications to anticoagulation.24 If theontraindication is temporary, a temporary filter can be placedntil pharmacologic prophylaxis can be instituted. There is novidence to support routine placement of IVC filters.25

SCI confers a substantially higher risk of stress ulcerationhan all other kinds of trauma.26 Those with cervical injuriesppear to be at particularly high risk. Either H2-blockers orroton pump inhibitors are indicated, to be started at admissionnd continued for 4 weeks.2 The use of acid-reducing agentseyond 4 weeks is not indicated unless other risk factors foreptic ulceration are present, such as a bleeding disorder,echanical ventilation, or history of ulcer disease. Ongoing use

f acid reducing agents may increase the risk of Clostridiumifficile bowel infection.27

.2 Clinical Activity: To summarize the physiatric inter-ventions (in acute care) for the prevention of compli-cations in this young man with an acute SCI.

The physiatrist is an important member of the team caringor the person with SCI in the acute care setting, both duringhe period immediately after injury and during any subsequentospitalization. Although prevention of complications commono SCI is a fundamental role, balancing the standard practicessed in acute care with the unique physiology of SCI is equallymportant.

Interventions that may be considered routine in any rehabil-tation setting must not be overlooked during an acute hospitaltay. Range of motion (ROM) should be started as soon ashere are no medical or orthopedic contraindications to do so.oss of shoulder ROM in the early period has been associatedith increased shoulder pain during the rehabilitation phase.28

here may be reluctance to provide full range out of concernor spine stability, but there is no evidence that shoulder ROMn a supine patient wearing a hard cervical collar alters spinallignment (with the exception of patients with ankylosingpondylitis). The swimmer’s radiographic view, which pro-ides full range of the shoulder, is used routinely in emergencyepartments to evaluate for cervical spine injury, without con-ern that it might induce neurologic deterioration, even in anntact patient. Depending on the likely length of stay, splintingnd orthoses may also be appropriate to preserve joint ROM inhe highly susceptible areas of the hands and feet.

Bowel and bladder management are also fundamental needsn the acute care setting. The initiation of a bowel programhould begin soon after enteral feeding is initiated.2 After aew injury, patients must be assessed for the presence orbsence of the bulbocavernosus reflex to ascertain whether anpper motoneuron or lower motoneuron bowel program isppropriate.29 Established guidelines for bowel managementeed minimal adaptation for the acute care setting, althoughraining of personnel may be necessary. In those with chronicCI, the physiatrist should assist the acute care team in imple-enting the patient’s usual program so far as feasible. See

ection activity 3.330 for further discussion. A bladder programay also be initiated during the acute period, although this

oes not have the same urgency as the bowel program. The

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S57ACUTE CARE MANAGEMENT OF TRAUMATIC AND NONTRAUMATIC INJURY, Wuermser

emoval of an indwelling urinary catheter and initiation ofntermittent catheterization can be recommended as soon as theatient no longer requires intravenous fluids and the medicaltatus does not require strict monitoring of urinary outputs.2

owever, physiatrists should be aware of the diuresis of thirdpaced fluid associated with mobilizing the patient and warngainst volumes higher than 500mL per catheterization. Theoutine use of prophylactic antibiotics to prevent urinary tractnfections is not recommended.31

Pulmonary complications are the leading cause of mortalityn the first year after SCI.32 Pulmonary complication ratesuring the acute hospitalization have been reported to be 84%or C1-4 levels of injury, 60% for C5-8, and 65% for thoracicevels, indicating that all neurologic levels of injury are atisk.33 The primary contributors to pulmonary dysfunction afterCI are difficulty handling secretions, atelectasis, and hy-oventilation.Clearance of secretions is primarily achieved by abdominaluscle contraction producing a forced expiration or cough.eak or paralyzed abdominal muscles preclude an effective

ough. Techniques of manually assisted cough have beenhown to be more effective in clearing secretions than standarductioning, which is limited to effective clearance of only theight mainstem bronchus.34 This is significant because pneu-onia is most common in SCI in the left lower lobe.35 In

ddition, larger and firmer mucus plugs can be mobilized thatannot be accommodated by the suction catheter. The “quadough,” or abdominal thrust, and the tussive squeeze or costo-hrenic technique, in which the hands are placed over the lowerib cage instead of the epigastrium, are both easily applied inhe acute care setting.36 Contraindications to the abdominalhrust are abdominal injuries or recent surgery. A recentlylaced IVC filter is a relative contraindication because ofotential migration of the filter. Contraindications to the tussivequeeze include lower-rib fractures and thoracic injury or sur-ery. Neither should be performed within 1 hour of a meal. Theechanical insufflator–exsufflator (M-IE) is extremely effec-

ive and can be administered via tracheostomy or mouth piece.ontraindications to use of the M-IE include a history ofneumothorax, barotrauma, or emphysema. There is also risk,s with traditional suctioning, of excessive vagal stimulationnd bradycardia in those with tetraplegia.

After SCI, a restrictive ventilatory deficit occurs and there isresultant decrease in all lung volumes. Vital capacity (VC)

eclines in tetraplegia and high paraplegia from respiratoryuscle weakness. Prompt mechanical assistance (either intu-

ation or noninvasive means) should be performed in peopleith severe respiratory distress or in patients whose VC iselow 15mL/kg.37 Atelectasis has been estimated to be presentn 60% of SCI patients on admission to rehabilitation facili-ies.38 The Consortium for Spinal Cord Medicine clinicaluidelines for Respiratory Management Following Spinal Cordnjury37 supports the use of higher tidal volumes than thosesually used in intensive care settings in patients requiringechanical ventilatory assistance. The tidal volume is titrated

pward while monitoring the airway pressure, until the atelec-asis resolves on chest radiograph and the patient is afebrile.37

n a retrospective review, this protocol was shown to speedesolution of atelectasis and decrease ventilator weaningime.38 However, it is well established that low-volume venti-ation improves outcomes in the general trauma setting, pri-arily because of the high frequency of acute lung injury and

dult respiratory distress syndrome in this population. There-ore, these 2 disorders should be resolved or ruled out before
nitiation of a high-volume weaning protocol.2 p
Dysphagia is also a contributor to respiratory deteriorationfter SCI. Although up to 30% of patients with tetraplegia haveysphagia at admission to inpatient rehabilitation,39 up to twohirds of patients undergoing elective cervical spine surgeryave postoperative dysphagia, which has been shown in bothnterior and posterior cervical spine approaches.40 It is likely,hen, that the rate of dysphagia in acute SCI is higher than thatocumented later in the course in the rehabilitation setting.eople with cervical spine surgery, tracheostomy, prolongedrotracheal intubation, halo stabilization, and concomitantrain injury should be evaluated for dysphagia.2 A dysphagiavaluation in this early phase should be considered in all peopleith cervical SCI. Older age is also associated with increased

isk of dysphagia in both the acute and rehabilitation settings.n the presence of a rigid cervical orthosis or halo, it is difficulto compensate for dysphagia using a typical chin-tuck position.se of nasogastric access for short-term enteral feeding can besed until the risk of aspiration diminishes.An understanding of acute SCI physiology is needed to

ptimize early nutrition as well. Nutrition is a key parameter inutcomes of trauma patients. However, estimates of nutritionaleeds after SCI are difficult. Nitrogen loss is obligatory afterCI and cannot be prevented by increased protein feeding.herefore, measuring urine urea nitrogen is an unreliable way

o estimate nutritional needs. Even commonly used caloricstimates for people with SCI have been shown to causeverfeeding in the acute period. Whenever possible, a meta-olic cart should be used to determine actual needs.41 Althought is now common practice to initiate nutritional support within2 hours in all trauma patients, 1 study has suggested that earlyeeding of people with acute traumatic SCI confers no benefitnd may increase risk of pneumonia.42 Further data are neededn this area.

Pressure ulcers are a leading cause of failure to makerogress in acute inpatient rehabilitation and so should be arimary concern for the physiatrist during the acute stage.ressure ulcers are largely preventable, and prevention strate-ies should start as soon as possible after an injury and con-inue throughout hospitalization. During acute hospitalizations,hen patients are most often supine, the sacrum, heels, andcciput are the most common sites of injury. Time on theackboard should be minimized, because this is a predictor ofacral breakdown. Rather, flat supine positioning should besed during the immediate diagnostic and resuscitativeeriod.43 Once complete, concerns of spine stability may stillroduce reluctance among staff to appropriately turn the patientnd offload pressure areas. Rotating beds designed for thenstable spine are indicated in this case. Patient positioningust be monitored, however, to ensure that the patient is not

liding laterally in the bed with each turn, creating sacral shearnd increasing the risk of skin breakdown. Once the spine istable, routine turning every 2 hours should be implemented.2

Although the choice of surgery and spine orthosis are pri-arily the purview of the surgeon, physiatrists are expert in the

unctional implications of these choices. Case discussions withurgical teams may facilitate optimal decisions for both short-nd long-term rehabilitation goals. The physiatrist and thera-eutic team also have a role in preparing the patient and his/heramily for the rehabilitation process. Education about the in-ury, about the rehabilitation process in general, about specificspects of the intended rehabilitation location, and about livingith SCI may all be started during the acute period as the
atient and the family begin to ask those questions.

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.3 Clinical Activity: To prognosticate the extent of neu-rologic recovery for this newly injured person withSCI discussed above.

It is important to be able to prognosticate neurologic recov-ry of people who have sustained an SCI to provide accuratenformation to patients and their families, to guide each pa-ient’s rehabilitation, and to help determine if new treatmentethods are effective. Prognosis for neurologic recovery afterCI is best predicted by the neurologic physical examination,sing the International Standards for Neurological Classifica-ion of Spinal Cord Injury.44,45 The examination at 72 hoursostinjury is superior to that at 24 hours postinjury for predict-ng recovery.

The major factors in predicting recovery in the first year afterraumatic SCI include the initial neurologic level of injury, theatient’s initial motor strength, and, most importantly, whethery examination the injury is classified as neurologically com-lete or incomplete.46

omplete TetraplegiaMost upper-extremity (UE) recovery occurs during the firstmonths, with the greatest rate of change during the first 3onths. Motor recovery can continue, however, especially for

atients with initial 0/5 strength, with lesser gains seen in theecond year. Most patients with complete cervical lesions willecover 1 root level of function. The initial strength of thisuscle is a significant predictor of achieving antigravity

trength by 1 year postinjury. If the first level below theeurologic level of injury has 0/5 strength at 72 hours to 1eek, only 30% to 40% of patients will recover to 3/5 strength

n that muscle. However, if 1/5 or 2/5 strength is present, 70%o 80% of patients will regain antigravity strength at 1 year.resence of sensation at that level increases chances of recov-ry. Also, the faster an initial 0/5 muscle starts to recover sometrength, the better the prognosis for recovery. Only a smallercentage of subjects have motor recovery below the firstevel caudal to the neurologic level of injury. Muscles 2 levelselow the neurologic level of injury have only a 10% ofecovering any strength at 1 year if they are still 0/5 at 1 monthnd less than a 1% chance of achieving antigravity strength.46

ncomplete TetraplegiaUE motor recovery is approximately twice as great in in-

omplete tetraplegia as in complete tetraplegia, with the poten-ial for varying degrees of lower-extremity (LE) motor recov-ry and functional ambulation. For patients who are sensoryncomplete initially, the prognosis for motor recovery is moreavorable in those with sparing of pin sensation rather thanhose with light-touch sensation alone. The basis of a moreavorable outcome for pinprick sparing may be explained byhe close anatomic relation of the motor tracts (lateral cortico-pinal tract) to the sensory tracts carrying pain and temperaturebers (lateral spinothalamic tract).47 Functional and neurologicecovery is even more favorable for patients with an initialotor incomplete injury.Most motor recovery occurs within the first 6 months after

njury, and the early return of motor function suggests a betterunctional outcome. Motor recovery in the UEs and LEs occursoncurrently rather than sequentially.

omplete ParaplegiaThe potential for LE motor recovery improves with lower

nitial neurologic levels of injury: 15% of patients with a
eurologic level of injury between T9-11 and 55% of those a

ith an initial neurologic level of injury below T12 recoverome strength in the lower limbs. Most movement gained is inhe proximal LE musculature and may represent recovery ofartially injured lumbar roots or “root escape.”46 There are noecent studies that report the likelihood of conversion fromomplete to incomplete neurologic status in thoracic SCI.

ncomplete ParaplegiaPeople with incomplete paraplegia have the best prognosis

or LE motor recovery and ambulation. Eighty percent ofeople with incomplete paraplegia regain antigravity hip flex-rs and knee extensors at 1 year. People with no LE motorontrol at 1 month may still show significant return by 1 year.

ate RecoveryThe Model Spinal Cord Injury Systems (MSCIS) data report

hat up to 16% of patients classified initially as neurologicallyomplete improve at least 1 classification grade from initialarly examination to the 1-year follow-up, with 5.8% improv-ng to grade C and 3% to grade D.48 Burns et al49 recentlyeported that at year 1 or later, 6.7% (2/30) of American Spinalnjury Association (ASIA) grade A subjects initially testedithin 2 days without factors affecting examination reliability

onverted to ASIA grade B status, and none developed voli-ional motor function below the zone of injury. Between 4%nd 10% of patients may convert from neurologically completeo incomplete after 30 days. Late conversion has been reportedo occur even years after injury, although usually only to ASIArade B or C. In a retrospective review of MSCIS data,50 lateonversion (improvement of ASIA Impairment Scale) after 1ear occurred in up to 5.6% of cases, but only up to 2.1% ofases improved to a motor incomplete injury at the 5-yearxamination. There was greater potential for conversion ineople with tetraplegia than in those with paraplegia. Approx-mately 20% of subjects improved their motor level and theireurologic level of injury from the first to fifth year postinjury.unctional changes were not studied.

ther Predictors of Neurologic RecoveryThe presence of spinal shock may play a role in prognosis:

or the same degree of SCI, the presence of spinal shockmplies a more rapid evolution of injury and a poorer progno-is. The order that reflexes return in the postinjury period mayelp prognosticate outcome.51 The delayed plantar response,hich may be the first reflex to return, usually occurs withinours or days after SCI, and its persistence shows a highorrelation with complete injuries and a poor prognosis for LEotor recovery and function (ambulation).52 The presence of

he crossed adductor response to patellar tendon taps in thecute stage is highly predictive of functional motor recovery.53

f absent, motor recovery does not usually take place.For similar severity of the injury, older people may have a

ess favorable outcome with regard to neurologic recovery,alking, and bowel and bladder independence than youngeratients, and they have more associated medical problems.54

his decreased recovery may be caused by a decrease in neurallasticity as one ages. Estrogen may have neuroprotectiveroperties relative to central nervous system disorders. Only aew studies have looked at gender in relation to neurologicecovery in SCI, and these show either no difference or only alight improvement in neurologic recovery for women.55,56

Radiologic and electrodiagnostic results early after injuryelp confirm the prognosis obtained from the clinical evalua-ion. The type of fracture may correlate with whether one has

neurologically complete or incomplete injury. Normal cord

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ignal intensity on magnetic resonance imaging (MRI) is con-idered a positive predictor for neurologic recovery. Thereater the extent of cord signal abnormality on MRI, thereater the chance of having a complete injury. An in-ramedullary hemorrhage correlates with a more severe initialeurologic deficit and carries a poorer prognosis. The locationf the hemorrhage corresponds anatomically to the level of theeurologic injury. In the chronic stage after SCI, people withersistent cord signal changes on MRI show little improvementn ASIA grades compared with the improvements made byatients whose signal abnormalities resolve.Electrophysiologic techniques include nerve conduction

tudies, late responses (H-reflex and F-wave responses), so-atosensory evoked potentials, motor evoked potentials, and

ympathetic skin responses that can supplement clinical andeuroradiologic findings. These tests, however, are most usefuln differentiating lesions between the central and peripheralervous system. They may also help differentiate between aeurologically complete versus incomplete injury in uncoop-rative or unconscious patients or rule out a conversion disor-er, because they do not require the cooperation of the patient.hey are not a routine part of the acute investigation of a newly

njured person to offer prognosis for neurologic or functionalutcome.Cortical stimulation examines the corticospinal tract by re-

ording from different peripheral muscles. Motor evoked po-entials can document the level of injury in the UE and mayelp predict mobility and activities of daily living. They are noturrently part of the routine evaluation for people with SCI.

.4 Clinical Activity: To describe the acute evaluation of a30-year-old woman who presents with a profound andrapid onset incomplete tetraplegia categorized as anontraumatic SCI.

The initial evaluation includes a comprehensive history andhysical examination, electrodiagnostic studies, and radiologicvaluation. The importance of the history and physical exam-nation cannot be underestimated. Classic examples illustratinghis need include people with spinal stenosis with myelopathy,otoneuron disease, and presumed multiple sclerosis (MS).or people presenting with neck or back pain, symptoms origns, including a history of bowel and bladder disturbances,ait disorder, weakness, clumsiness, sensory loss, and changesn reflexes, will lead one to suspect myelopathy. Specific find-ngs will lead the clinician to the appropriate diagnostic inves-igation. To illustrate the importance of the examination, in 1tudy57 performed at an academic center, the history and ex-mination identified an alternative diagnosis for 70% of pa-ients who presented with abnormal MRI findings and pre-umed MS.

MRI has revolutionized the anatomic evaluation of the spinalord. MRI can identify cord changes associated with cervicalnd lumbar stenosis and is the study of choice in evaluatingontraumatic SCI. Contrast enhancement is essential for eval-ating inflammatory and neoplastic lesions of the spinal cord.RI with gadolinium enhancement and T2-weighted imaging

n diagnosing MS is highly sensitive, yet the specificity isimited because other diseases can mimic it by MRI criteria.58

fter a diagnosis of presumed MS, disease progression de-ends on the identification of new lesions. A characteristicnding in transverse myelitis is T2 hyperintensity centrally

nvolving more than two thirds of the volume of the spinalord.59 Intramedullary tumors are typically hyperintense on
1-weighted images.
Vascular abnormalities can be identified by MRI and mag-etic resonance angiography.60 Spinal angiography is the cri-erion standard for the diagnosis of spinal cord arteriovenousalformations and their characterization for treatment. When

xtradural spinal lesions are suspected, computed tomographycan is most helpful to evaluate for primary bone metastasesnd bony metastases of the vertebral column.

CSF evaluation is important in diagnosing inflammatoryisorders of the spinal cord. In MS, the common tests includeyelin basic protein antibodies, oligoclonal bands, and a host

f other immunologic assays. Despite the utility of CSF anti-odies in the diagnosis and prognosis of MS, some contentionemains that MS is a metabolically dependent degenerativeisease rather than an autoimmune disorder.61 The presencend persistence of CSF oligoclonal bands almost universallyllows the distinction between MS and Devic’s neuromyelitisptica.62,63 Further CSF evaluation includes the evaluation ofiral titers, especially in cases of suspected transverse myelitis.Serum laboratory investigation is directed at diseases that

ause spinal cord pathology. Serology tests for Lyme disease,yphilis, human immunodeficiency virus, and other viral agentshould be ordered. Rheumatologic studies should be investi-ated for causes of spinal vasculitis that could mimic MS andransverse myelitis. Glucose tolerance testing and serum he-oglobin A1C should be ordered for evidence of diabetesellitus. Antiphospholipid antibodies should be tested, al-

hough with up to 32% of MS patients being positive, antibod-es to �2 glycoprotein I should be included in this investigationo make the diagnosis.64

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28. Waring WP, Maynard FM. Shoulder pain in acute traumaticquadriplegia. Paraplegia 1991;29:37-42.

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31. Morton SC, Shekelle PG, Adams JL, et al. Antimicrobial pro-phylaxis for urinary tract infection in persons with spinal corddysfunction. Arch Phys Med Rehabil 2002;83:129-38.

32. DeVivo M, Stover S. Long-term survival and causes of death. In:Stover S, DeLisa J, Whiteneck GG, editors. Spinal cord injury:clinical outcomes from the model systems. Gaithersburg: Aspen;1995. p 289-316.

33. Jackson AB, Groomes TE. Incidence of respiratory complica-tions following spinal cord injury. Arch Phys Med Rehabil1994;75:270-5.

34. Bach JR. Mechanical insufflation-exsufflation: comparison ofpeak expiratory flows with manually assisted and unassistedcoughing techniques. Chest 1993;104:1553-62.

35. Fishburn MJ, Marino RJ, Ditunno JF Jr. Atelectasis and pneu-monia in acute spinal cord injury. Arch Phys Med Rehabil1990;71:197-200.

36. Massery M. Manual breathing and coughing aids. Phys MedRehabil Clinic N Am 1996;7:407-22.

37. Consortium for Spinal Cord Medicine. Respiratory managementfollowing spinal cord injury: a clinical guideline for health-careprofessionals. Washington (DC): Paralyzed Veterans of Amer-ica; 2005.

38. Peterson WP, Barbalata L, Brooks CA, Gerhart KA, Mellick DC,Whiteneck GG. The effects of tidal volumes on the time to weanpersons with high tetraplegia from ventilators. Spinal Cord 1999;37:284-8.

39. Kirshblum S, Johnston M, Brown J, O’Connor KC, Jarosz P.Predictors of dysphagia after spinal cord injury. Arch Phys MedRehabil 1999;80:1101-5.

40. Smith-Hammond CA, New KC, Pietrobon R, Curtis DJ, Schar-ver CH, Turner DA. Prospective analysis of incidence and riskfactors of dysphagia in spine surgery patients: comparison ofanterior cervical, posterior cervical, and lumbar procedures.Spine 2004;29:1441-6.

41. Rodriguez DJ, Benzel EC, Clevenger FW. The metabolic re-sponse to spinal cord injury. Spinal Cord 1997;35:599-604.

42. Dvorak MF, Noonan VK, Belanger L, et al. Early versus lateenteral feeding in patients with acute cervical spinal cord injury:a pilot study. Spine 2004;29:E175-80.

43. Consortium for Spinal Cord Medicine. Pressure ulcer preventionand treatment following spinal cord injury: a clinical practiceguideline for health-care professionals. Washington (DC): Para-lyzed Veterans of America; 2000.

44. Marino RJ, Barros T, Biering-Sorenson F, et al; ASIA Neuro-logical Standards Committee. International standards for neuro-logical classification of spinal cord injury. J Spinal Cord Med2003;26:S50-6.

45. Marino R. Neurological and functional outcomes in spinal cordinjury: review and recommendations. Top Spinal Cord Inj Re-habil 2005:10:51-64.

46. Ditunno JF, Flanders A, Kirshblum SC, Graziani V, Tessler A.Predicting outcome in traumatic SCI. In: Kirshblum S, Campag-nolo DI, DeLisa JA, editors. Spinal cord medicine. Philadelphia:Lippincott Williams & Wilkins; 2002. p 108-22.

47. Oleson CV, Burns AS, Ditunno JF, Geisler FH, Coleman WP.Prognostic value of pinprick preservation in motor complete,sensory incomplete spinal cord injury. Arch Phys Med Rehabil2005;86:988-92.

48. Marino RJ, Ditunno JF, Donovan WF, Maynard F. Neurologicrecovery after traumatic spinal cord injury: data from the ModelSpinal Cord Injury Systems. Arch Phys Med Rehabil 1999;80:1391-6.

49. Burns AS, Lee BS, Ditunno JF, Tessler A. Patient selection forclinical trials: the reliability of the early spinal cord injury
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50. Kirshblum S, Millis S, McKinley W, Tulsky D. Late recoveryafter traumatic spinal cord injury. Arch Phys Med Rehabil 2004;85:1811-7.

51. Ditunno JF, Little LW, Tessler A, Burns AS. Spinal shockrevisited: a four phase model. Spinal Cord 2004;42:383-95.

52. Ko HY. The pattern of reflex recovery during spinal shock.Spinal Cord 1999;37:402-9.

53. Calancie B, Molano MR, Broton JG. Tendon reflexes for pre-dicting movement recovery after SCI in humans. Clin Neuro-physiol 2004;115:2350-63.

54. Scivoletto G, Morganti B, Ditunno P, Ditunno JF, Molinari M.Effects of age on spinal cord lesion in patients’ rehabilitation.Spinal Cord 2003;41:457-46.

55. Sipski ML, Jackson AB, Gomez-Marin O, Estores I, Stein A.Effects of gender on neurologic and functional recovery afterspinal cord injury. Arch Phys Med Rehabil 2004;85:1826-36.

56. Furlan JC, Krassioukov AV, Fehlings MG. The effects of genderon clinical and neurological outcomes after acute cervical spinalcord injury. J Neurotrauma 2003;20:368-81.

57. Carmosino MJ, Brousseau KM, Arciniegas DB, Corboy JR.
Initial evaluations for multiple sclerosis in a university multiple
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58. Bastianello S, Pichiecchio A, Spadaro M, et al. Atypical multiplesclerosis: MRI findings and differential diagnosis. Neurol Sci2004;25(Suppl 4):S356-60.

59. Transverse Myelitis Consortium Working Group. Proposed di-agnostic criteria and nosology of acute transverse myelitis. Neu-rology 2002;59:499-505.

60. White ML, El-Khoury GY. Neurovascular injuries of the spinalcord. Eur J Radiol 2002;42:117-26.

61. Chaudhuri A, Behan PO. Multiple sclerosis is not an autoim-mune disease. Arch Neurol 2004;61:1610-2.

62. Bergamaschi R, Tonietti S, Franciotta D, et al. Oligoclonal bandsin Devic’s neuromyelitis optica and multiple sclerosis: differ-ences in repeated cerebrospinal fluid examinations. Mult Scler2004;10:2-4.

63. de Seze J, Lebrun C, Stojkovic T, Ferriby D, Chatel M, Verm-ersch P. Is Devic’s neuromyelitis optica a separate disease? Acomparative study with multiple sclerosis. Mult Scler 2003;9:521-5.

64. Chapman J. The interface of multiple sclerosis and antiphospho-
lipid antibodies. Thrombosis Res 2004;114:477-81.

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pinal Cord Injury Medicine. 3. Rehabilitation Phase Aftercute Spinal Cord Injury

teven C. Kirshblum, MD, Michael M. Priebe, MD, Chester H. Ho, MD, William M. Scelza, MD,
nthony E. Chiodo, MD, Lisa-Ann Wuermser, MD
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ABSTRACT. Kirshblum SC, Priebe MM, Ho CH, ScelzaM, Chiodo AE, Wuermser LA. Spinal cord injury medicine.

. Rehabilitation phase after acute spinal cord injury. Archhys Med Rehabil 2007;88(3 Suppl 1):S62-70.

This self-directed learning module highlights the rehabilita-ion aspects of care for people with traumatic spinal cord injurySCI). It is part of the chapter on SCI medicine in the Self-irected Physiatric Education Program for practitioners and

rainees in physical medicine and rehabilitation. This articlepecifically focuses on the formulation of a rehabilitation planased on functional goals by level of injury. Such a planncludes mobility, activities of daily living, equipment needs,nd adjustment issues after injury. The effect of a concomitantrain injury on rehabilitation is discussed. Medical complica-ions seen in the rehabilitation stage such as autonomic dysre-exia, heterotopic ossification, neurogenic bowel, and orthos-

asis are addressed. Preparation for discharge is crucial to allowor a smooth transition to home. There have been advances inCI rehabilitation research including in wheelchair technology,unctional electric stimulation, and partial body weight�upported ambulation.

Overall Article Objective: To describe outcomes and issueshat may arise during the rehabilitation phase after spinal cordnjury.

Key Words: Electric stimulation; Gait; Rehabilitation; Spi-al cord injuries.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Clinical Activity: To formulate functional goals span-ning the first 6 months after onset of spinal cordinjury for the 20-year-old patient discussed in chapter2 and admitted to your inpatient rehabilitationprogram.

ETERMINING THE POTENTIAL functional outcome ofa person after spinal cord injury (SCI) is essential to

ormulating a rehabilitation plan. Functional outcomes are de-

From the Spinal Cord Injury Services, Kessler Institute for Rehabilitation, Westrange, NJ (Kirshblum); Department of Physical Medicine and Rehabilitation, Uni-ersity of Medicine and Dentistry–New Jersey Medical School, Newark, NJ, (Kirsh-lum); Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester,N (Priebe, Wuermser); Louis Stokes Cleveland Department of Veterans Affairsedical Center and Department of Physical Medicine and Rehabilitation, Caseestern Reserve University, Cleveland, OH (Ho); Department of Physical Medicine

nd Rehabilitation, Carolinas Rehabilitation, Charlotte, NC (Scelza); and Departmentf Physical Medicine and Rehabilitation, University of Michigan Hospital, Annrbor, MI (Chiodo).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Steven C. Kirshblum, MD, Spinal Cord Injury Services, Kessler

nstitute for Rehab, 1199 Pleasant Valley Way, West Orange, NJ 07052, e-mail:[email protected]. Reprints are not available from the author.

f0003-9993/07/8803S-11412$32.00/0doi:10.1016/j.apmr.2006.12.003


ermined based on the level of SCI and the American Spinalnjury Association (ASIA) Impairment Scale (AIS) classifica-ion, in conjunction with knowledge of the age, medical status,edical comorbidities, motivation, and family support of the

atient. Generalized projected outcomes have been publishedo document the optimal functional potential of people withCI.1,2

Rehabilitation begins in the intensive care setting and in-ludes addressing the SCI-specific needs to help each personeet his/her potential in terms of medical, physical, social,

motional, recreational, vocational, and functional recovery. Ifarly medical complications can be prevented, the inpatientehabilitation course is facilitated, and the total cost of care isessened. Early initiation of SCI-specific rehabilitation is ex-remely important. A delay in starting these interventions mayegatively influence a patient’s ultimate functional capabilitynd increase his/her length of rehabilitation stay.3,4 A special-zed unit is preferred to provide for comprehensive manage-ent of a person with SCI.5 One of the primary goals of

ehabilitation during the early recovery period is to convey thatife with an SCI can be fulfilling.

The interdisciplinary approach of the rehabilitation team,ncluding the patient and family, is important for the optimalare of a person with SCI. Each team member plays a vital rolen the rehabilitation process providing care and patient andamily education. As the lengths of stay shorten in acuteehabilitation, coordination of the entire team becomes evenore important if a person is to have a timely and safe

ischarge back to the community. Frequent team conferencesith an early home evaluation should be performed.Once a patient’s motor level of injury, AIS grade, and

rognosis for neurologic recovery are determined at the onsetf rehabilitation, short- and long-term functional goals can beormulated and a therapy prescription established. Tables 1 andlist the functional goals by injury level expected for a personith a motor complete injury to achieve at 1 year. The idealutcome may not always be achieved for each patient, becausendividual outcomes vary, despite similar levels of injury.hese variations are related to age, sex, and comorbidities.

utcomes by Motor Level of InjuryC1-4 level. People with motor levels at or above C3 will

sually require long-term ventilator assistance, whereas mosteople with lesions at C4 will be able to wean off the ventila-or. The benefit of specialized acute rehabilitation for theseeople is justifiable, despite their inability initially to tolerate 3ours a day of therapy and having what may seem to be limitedoals. The SCI medical and nursing care given during the firstew months after injury are crucial for monitoring, treating, andreventing medical complications that can lead to future mor-idity and mortality. Patient and family education, training sohat the patient can direct his/her own care, emotional andocial support, and exposure to advanced technology that mayllow independence in the proper environment make the dif-
erence between returning to the family/community or living in

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S63REHABILITATION PHASE AFTER ACUTE SPINAL CORD INJURY, Kirshblum

long-term care facility. Appropriate equipment evaluationnd prescription is an integral aspect of the rehabilitation.

C5 level. The C5 motor level adds the key muscle group ofhe elbow flexors (biceps), the deltoids and rhomboids, andartial innervation of the brachialis, brachioradialis, supraspi-atus, infraspinatus, and serratus anterior. It is important duringhe acute period after SCI to prevent elbow flexion and forearm

Table 1: Projected Functional Outcomes for Mot

Measure C1-4 C5

Feeding Dependent Independent with adapequipment after setu

Grooming Dependent Minimal assistance witequipment after setu

UE dressing Dependent Requires assistanceLE dressing Dependent Dependent

Bathing Dependent Dependent

Bed mobility Dependent Requires assistance

Weightshifts

Independent in powerchair with power tiltor recline mechanism

Requires assistance unin power chair

Transfers Dependent Requires maximumassistance

Wheelchairpropulsion

Independent with powerchair; dependent inmanual wheelchair

Independent with powechair; independent tosome assist in manuwheelchair withadaptations on levelsurfaces

Driving Unable Independent withadaptations

OTE. Adapted from Kirshblum et al.2 Adapted with permission.bbreviations: LE, lower extremity; UE, upper extremity.

Table 2: Potential Functional Outcomes at 1 Yea

Measure T2-9

ADLs (grooming, feeding,dressing, bathing)

Independent

Bowel/bladder IndependentTransfers IndependentAmbulation Standing in frame, tilt table,

or standing wheelchair;exercise only

Braces Bilateral KAFOs withforearm crutches orwalker

2
OTE. Adapted from Kirshblum et al. Adapted with permission.bbreviations: AFOs, ankle-foot orthoses; KAFO, knee-ankle-foot orthose
upination contractures caused by unopposed biceps activity.ew advances in power-assist and power wheelchairs shoulde introduced. Driving a specially modified van is possible athis level, with a lift for wheelchair access enabling a patient toe fully independent.C6 level. The C6 level adds the key muscle group that

erforms wrist extension (extensor carpi radialis), as well as

mplete SCI at 1 Year Postinjury, by Injury Level

C6 C7 C8-T1

Independent with orwithout adaptiveequipment

Independent Independent

Some assistance toindependent withadaptiveequipment

Independent withadaptiveequipment

Independent

Independent Independent IndependentRequires assistance Some assistance

to independentwith adaptiveequipment

Usuallyindependent

Some assistance toindependent withequipment

Some assistanceto independentwith equipment

Independent withequipment

Requires assistance Independent tosome assistance

Independent

Independent Independent Independent

Some assistance toindependent onlevel surfaces

Independent withor withoutboard for levelsurfaces

Independent

Independent withmanualwheelchair withcoated rims onlevel surfaces

Independent,except for curbsand uneventerrain

Independent

Independent withadaptations

Independent in carwith handcontrols oradapted van

Independent in carhand controls oradapted van

tinjury for Complete Paraplegia, by Injury Level

T10-L2 L3-S5

dependent Independent

dependent Independentdependent Independentousehold ambulation withorthoses; can trialambulation outdoors

Community ambulation ispossible

AFOs with forearmcrutches

Possibly KAFO or AFOs, withcanes or crutches

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artially innervating the supinator, pronator teres, and latissi-us dorsi. Active wrist extension can permit tenodesis to

ccur: the opposition of the thumb and index finger withexion as these tendons are stretched with wrist extension. Onehould avoid overly stretching the finger flexors initially afternjury (“selective tightening”) in patients injured at the C5 and6 motor levels. Stretching these flexors prematurely may

esult in a loss of the tenodesis action. Tenodesis may allowome people with this level of injury to perform an intermittentatheterization program (ICP).

C7 and C8 levels. The C7 motor level adds the elbowxtensors (triceps) as the key muscle group, and C8 adds theong finger flexors. The C7 level is considered the key level forecoming independent in most activities at the wheelchairevel, including weight shifts, transfers between level surfaces,nd light meal preparation. Bowel care on a padded commodeeat, especially suppository insertion, may still require assis-ance or the use of adaptive devices (ie, suppository inserter).

T1-12 levels. For most people with higher levels of tho-acic injury, community ambulation is not a functional long-erm goal. The lower the level of injury, the greater the trunkontrol associated with abdominal and paraspinal muscle in-ervation. Although people with injuries at the high-thoracicnd midthoracic levels may be interested in gait training andhould undergo this if there are no medical contraindications, its usually not an inpatient goal. The improved trunk controlssociated with lower levels of thoracic injuries facilitatesmbulation training with bilateral lower-extremity orthoses.uch training permits exercise and short-distance householdmbulation once the patient has mastered basic wheelchairkills.

L1-2 levels. Muscles gained at these levels include the hipexors and part of the quadriceps. Although the person may beble to ambulate for short distances, a wheelchair will still beequired for functional mobility. Bladder care is usually byCP.

L3-4 levels. The knee extensors are fully innervated withome strength of ankle dorsiflexion. Ambulation usually re-uires ankle-foot orthoses with assistive devices (ie, canes,rutches). Bowel and bladder management should be indepen-ent. These injuries are typically lower motoneuron in nature,nd bowel management is usually by contraction of abdominaluscles and manual disimpaction. Suppositories will not be

ffective because of the loss of sacral reflexes. Bladder man-gement is usually performed by ICP or Valsalva’s maneuverf postvoid residuals are within normative limits and urologicnvestigation shows no contraindication to this method. Absor-ent pads can be used.L5 level and below. These people should be independent in

ll activities unless there are associated problems such asevere pain or cardiac conditions.

mbulationAmbulation after SCI is often 1 of the first goals that many

eople with SCI set for themselves. It is important that patientsith SCI understand their prognosis in terms of achieving thisoal and when it should be initiated. There are 4 generalategories of ambulation: community ambulation, householdmbulation, ambulation for exercise, and nonambulatory.ommunity ambulation requires independence in performing

ransfers, the ability to go from the sit-to-stand positions, andmbulating unassisted in and outside the home for reasonableistances (�45m [�150ft]) with or without braces and assis-ive devices. Household ambulation is the ability to ambulatenly within the home with relative independence, but the
erson may require assistance for transfers. Ambulation for d

xercise is appropriate for a person who requires significantssistance for ambulation.

Although there is no one definite level at which patientshould not perform training with braces, there are factors thatill contribute to difficulty in ambulation, including older age,reater weight, lack of motivation, poor agility and coordina-ion, and greater spasticity. All patients with the potential formbulation should be given a trial if they want to pursue it. Foreople with thoracic-level injuries, training should usually note initiated until transfer training and wheelchair activities areastered.Community ambulation requires bilateral hip flexors

trength to be graded stronger than 3/5 and 1 knee extensor toe graded at least 3/5, with a maximum amount of bracing oflong leg brace and 1 short leg brace. Prognosis for ambula-

ion can be determined early after injury by the initial injuryevel and the AIS classification. Of people with incompleteetraplegia, 46% advance to community ambulation at 1 year,ith an additional 14% performing household ambulation. This

s compared with 5% of complete paraplegics and 76% ofncomplete paraplegics regaining community ambulation. Theercentage of people with incomplete tetraplegia able tochieve community ambulation is lower than for incompletearaplegia with equivalent lower-extremity motor strength, be-ause the upper-extremity strength may be compromised andnsufficient to enable assistive device ambulation if required.

.2 Clinical Activity: To describe the potential impact onthe rehabilitation program that a concomitant braininjury has on a 70-year-old patient with a C4 ASIAgrade C SCI.

The presence of concomitant traumatic brain injury (TBI) ineople with SCI (“dual diagnosis”) is common and presents ahallenge to the rehabilitation staff because of the associatedognitive and behavioral difficulties. There are only a fewtudies that quantify these cognitive deficits and define thempact that these deficits have on functional outcome anduality of life. Approximately 25% to 64% of people withcute SCI sustain a concomitant TBI.6-10 In these studies, theresence of TBI was determined retrospectively using medicalecords documenting a loss of consciousness and coma and byecreased performance on neuropsychologic testing whenvailable. It is likely that many mild to moderate brain injuriesustained at the time of acute SCI may be undiagnosed andherefore untreated.11

Variables that put people with SCI at higher risk for sustain-ng a concomitant TBI include (1) tetraplegia resulting from aigh-energy deceleration crash, (2) loss of consciousness atime of injury, (3) evidence of cortical or brainstem neurologicamage, and (4) respiratory support required at time of injury.6

In a retrospective review of 41 pairs of subjects with SCIatched with subjects with SCI and TBI after rehabilitation,

ubjects with both injuries had significantly lower cognitiveubscale scores on the FIM instrument both at admission andischarge and lower overall motor FIM change scores.7 Thereas no significant effect on length of stay or discharge place-ent. However, length of time before rehabilitation admission

veraged 24 days in the dual-diagnosis group compared with2 days for those with SCI only.7

Specific issues that require attention in patients with dualiagnosis include the effect of TBI on new learning and onnitiation of self-care in the prevention of secondary conditions.inding ways to break down the sequence of the tasks is often

mportant in training these people. Of key importance is un-
erstanding how to manage the behavioral changes, such as

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gitation, often seen in TBI. Behavioral and pharmacologicnterventions for the cognitive changes after brain injury aremportant to implement.12 One should be familiar with the inter-ction of medications often used in SCI that should be prescribedith caution in people with brain injury. These include centrally

cting medications that interfere with new learning, that is, neu-oleptic agents, benzodiazepines, and other centrally acting anti-pasticity medications.

Dowler et al13 evaluated long-term cognitive outcome inubjects who sustained SCI in acceleration–deceleration acci-ents. Approximately 60% of subjects with chronic SCI hadong-term cognitive impairment, although it is unclear if theseatients suffered a TBI initially. In this era of medical costontainment, early identification of people with dual diagnosisf SCI and TBI is important for the appropriate delivery ofehabilitation services. A need exists for research to elucidatehe true impact of a dual diagnosis on functional outcomes anduality of life.

.3 Clinical Activity: To formulate a plan to prevent andtreat common medical complications in the first 6months postinjury for a 20-year-old man with trau-matic SCI (C6 ASIA grade A).

People with injury levels at T6 and above are at risk foreveloping autonomic dysreflexia (AD). AD is a symptomomplex that arises from a noxious or intense stimulus belowhe level of injury that leads to an unopposed discharge of theympathetic nervous system. This sympathetic discharge isnable to be modulated from higher cerebral centers and oftenesults in hypertension. Many people with SCI have a baselineystolic blood pressure in the 90- to 110-mmHg range, and anncrease of the baseline blood pressure of 20 to 40mmHg maye a sign of AD. A reflex bradycardia is classically observed inany cases as a compensatory response because the carotid

aroreceptors stimulate an increase in vagal tone14; however,achycardia may also be seen. If left undetected and untreated,ypertension associated with AD can lead to stroke, intracra-ial or retinal hemorrhages, seizures, myocardial infarction,nd death. AD will generally not appear within the first monthfter an injury or while the patient is in spinal shock. It isstimated that 92% of people who develop AD will have theirrst episode of it within the first year after their injury.15 Latenset of AD should alert the clinician of other etiologies, thats, syrinx or cervical cord compression.

Signs and symptoms of AD include hypertension, bradycar-ia, and a severe headache. Above the level of injury, flushing,weating, and nasal congestion can occur because of a com-ensatory increase in parasympathetic tone. Below the level ofnjury, increased and unmodulated sympathetic tone predomi-ates and will lead to piloerection, pallor, and cool extremities.ccasionally, patients will also have silent AD, when they willot have any obvious symptoms but blood pressure will beignificantly elevated.16

The most common cause of AD is related to bladder dys-unction such as an overdistended bladder, detrusor sphincteryssynergia, and kidney and bladder stones. Other causes in-lude ingrown toenails, menstrual cramps, infections, bowelmpaction, pressure ulcers, or undetected musculoskeletal con-itions. The primary treatment for AD includes sitting theatient upright, removal of any constricting garments, anddentifying and eliminating the underlying cause.17 When eval-ating the urinary system, the first priority is to empty aistended bladder by intermittent catheterization or correctionf a kinked or clogged indwelling catheter. If this initial survey
oes not identify the cause, the patient should undergo a c
omplete head-to-toe evaluation including a rectal examinationo identify fecal impaction. Acute abdominal pathology shouldlso be considered, because typical signs of abdominal pain oristress may not be obvious because the affected areas arensensate. Control of hypertension may require rapidly actingntihypertensive agents and close monitoring of the patient forersistent hypertension and rebound hypotension.17

Neurogenic bowel is ubiquitous among people with SCI.onstipation and incontinence may lead to social isolation.ome bowel programs can take 2 hours or more to take effect,

eading to frustration. It is, therefore, quite important to educateatients regarding appropriate techniques for effective bowelare.

People with upper motoneuron bowel dysfunction can takedvantage of the intrinsic reflex activity of the bowel. Bowelrograms are ideally performed on a daily to every third dayasis depending on each person desired or preinjury patterns.itting upright on a padded commode can facilitate a moreatural position and is preferred to a side lying position. Keyomponents of bowel management include the use of digitaltimulation, high-fiber dietary intake, use of oral medications,nd rectal evacuants. Fluid intake should be adequate to main-ain soft stools and is recommended at 2 to 3L a day. Caffeineay act as a stimulant and is sometimes used strategically

efore a bowel program to help facilitate fecal evacuation.ietary or supplemental fiber acts as a bulking agent and can

nhance colonic transit time. It is suggested that the dailyntake of fiber be at least 30g a day. It is also advisable to haveregular pattern of food intake.The use of oral agents should be individualized to the pa-

ient. Chronic use of these agents is not necessarily required. Ifhanges are made in the bowel program regimen, they shoulde done one at a time, and at least 3 to 4 bowel cycles shoulde completed to realize the effects of the change. The use ofarge-volume enemas may be indicated for episodes of consti-ation but are not recommended for chronic use. Bisacodyl isn active ingredient in most suppository preparations. Thoseuppositories with a water-soluble base (Magic Bulleta) haveeen shown to dissolve more quickly and to significantlyhorten the time to complete a bowel program compared withtandard preparations with a vegetable oil base.18

People with a lower motoneuron injury often have a muchore difficult time with bowel programs. They are not able to

se the reflexes of the bowel, and digital stimulation andtimulant preparations are usually not effective. There also isecreased anal sphincter tone, which can lead to incontinenceith any type of the Valsalva’s maneuver. These people willften have to perform rectal checks and manual removal oftool sometimes as frequently as 3 times a day.19,20

Colostomy is used by some people for bowel management inases where a consistent program is difficult to establish.tudies show that subjects who have undergone a colostomyre generally happy with the procedure and wish they hadursued it sooner.21

Orthostatic hypotension (OH) is a common problem initiallyncountered in the inpatient SCI rehabilitation unit. It mayccur acutely after a spinal injury, that is, spinal shock, whichs the absence of all spinal cord�mediated reflexes below theevel of injury including sympathetic responses. As a conse-uence, once a person starts to sit up, orthostasis may occur.ack of muscle tone in the lower extremities also contributes toH. Initial compensatory measures should include using grad-al positional changes, and blood pressure will usually normal-ze. Ace wraps or compression stockings can also be initiallysed to enhance venous return. Abdominal binders also help
ompress the abdominal contents to combat venous pooling

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hat occurs. Over time, as the spinal reflexes return, OH willsually resolve. If treatment is necessary, the use of salt tabletsan increase circulating blood volume. In addition, �-adrener-ic agonists (ie, midodrine) may be used. If symptoms persist,ineralocorticoid supplements (fludrocortisone) may also be

sed to enhance intravascular blood volume, but one mustatch closely for the subsequent development of edema. The

linician should monitor the patient closely for the develop-ent of AD and taper the medications when able.Immobilization hypercalcemia can present during an acute

ehabilitation phase. It is most common in young men with aeurologically complete injury. Common clinical signs includeausea, vomiting, decreased appetite, lethargy, and polyuria.nitial resorption of bone mass will occur within the first weeknd usually present itself clinically within 1 to 2 monthsostinjury. Hypercalcuria will occur first, and when the cal-ium burden becomes too great for the kidneys to compensate,ypercalcemia will occur and the constellation of clinicalymptoms may become apparent. Initial treatment includesydration with intravenous fluids. The use of intravenous pam-dronate, a bisphosphonate used to treat hypercalcemia in can-er patients, is an effective way to manage elevated calciumevels.22

Heterotopic ossification (HO) also usually presents duringhe acute rehabilitation phase after SCI. Its incidence is be-ween 16% and 53% in SCI, with 10% to 20% clinicallyignificant and 3% to 5% developing into ankylosis. Swellingf the extremities may be present with a decrease in range ofotion of a joint. Most commonly, HO presents in the hips,

ollowed by the knees, elbows, and shoulders. Deep venoushrombosis must also be ruled out, because there is an associ-tion between the 2 conditions. HO is more common in peopleith a neurologically complete injury who present with spas-

icity. The diagnosis is confirmed initially with a triple-phaseone scan, because plain films may take a few weeks to showeriarticular bone formation radiographically. Serum alkalinehosphatase can be elevated but may be nonspecific. C-reactiverotein and creatine phosphokinase are markers of inflamma-ory activity related to HO.23,24 The treatment of HO consists oftidronate at 20mg/kg orally for 3 to 6 months. Nonsteroidalnti-inflammatory drugs (NSAIDs) may be used if there are noontraindications. Surgery is usually performed in cases ofignificant HO that causes functional limitations; surgery iselayed until there are signs of HO maturity. It is often fol-owed by use of radiation, NSAIDs, and etidronate.25

After the period of spinal shock, spasticity may develop ineople with upper motoneuron injuries. Spasticity may or mayot be detrimental for the patient. At times, spasticity may beeneficial; that is, a patient may use extensor muscle tone toerform stand pivot transfers. Initial management of spasticityncludes range-of-motion activities. Modalities may also besed but tend to be less effective and are not sustained. Anyoxious stimulus below the level of injury may worsen spas-icity and should be sought as a cause of increasing symptoms.

urinary tract infection, for example, may cause an abruptncrease in muscle tone. Identifying and treating the infectionhould bring the spasticity back to its baseline level. If thepasticity is painful, interfering with positioning, transfers, orygiene, pharmacologic treatment may be indicated. Com-only used agents during the acute rehabilitation process in-

lude baclofen, benzodiazepines, dantrolene sodium, and �2gonists (tizanidine, clonidine). One must use caution, becausehe primary side-effect profile of these medications includesedation. Other treatments for localized spasticity include these of chemical neurolysis with botulinum toxin or phenol.
urgery or intrathecal baclofen also may be considered should b

here be inadequate or intolerable side effects with oral drugherapies, but these treatments are not commonly used during thecute rehabilitation phase.

Difficulty with emotional adjustment after SCI is extremelyommon. Complications include depression, drug addiction,nd, if married, divorce. Depressive disorders are the mostommon form of psychologic distress after SCI, estimated toffect 20% to 45% of those injured and usually occurringithin the first month. Depression should be viewed as a

omplication that is amenable to treatment rather than as atage through which the patient must pass. The suicide ratefter SCI is 2 to 6 times greater than that of the able-bodiedopulation. Suicide is the leading cause of death in people whoave SCI and are younger than 55 years, with 75% of theuicides occurring within 5 years of injury. The suicide rate isigher for those with paraplegia and for those “marginally”njured (incomplete grade D or E) who have a near-completeecovery. Treatment includes psychologic counseling for theatient and his/her family and pharmacologic intervention.26

he rehabilitation staff can help to reduce depression, anxiety,nd self-neglect behaviors by promoting self-directed behav-ors and engaging patients in problem-solving to find person-lly acceptable solutions. Peer support is extremely helpful fordjustment issues. Substance abuse prevention and treatmentrograms should be included as part of SCI rehabilitation.

.4 Clinical Activity: To assist with the discharge plan-ning of a 20-year-old man with C4 ASIA grade A whois ready for discharge to an accessible home.

Rehabilitation goals for people with high cervical SCI pri-arily include prevention of secondary medical complications,

ducation and training of the patient and family members, andrescription of appropriate durable medical equipment andnvironmental modification. The Outcomes Following Trau-atic Spinal Cord Injury: Clinical Practice Guidelines forealth-Care Professionals1 delineates expected functional out-

omes and equipment needs based on the level of injury foreople with SCI. Anticipated equipment based on level ofnjury is included in table 3.

It is important to recognize the unique support that patientsith higher levels of injury require if they are to return to theirome environments safely. Lifestyle adaptations include a lifto assist in transfers and a padded commode or shower chair. Aower wheelchair with head, chin, or breath control mechanismhould be prescribed for independent mobility. The wheelchairhould be equipped with a pressure-relief cushion and reclinend/or tilt features for independent pressure relief. A manualheelchair with a high back that tilts or reclines should berescribed to use as a back-up wheelchair for assisted mobilityn the home and in the community as needed.

To facilitate independence in their interpersonal communi-ations and in control of their local environment, patientshould be evaluated for a mouth stick, computer access, annvironmental control unit, and other technologies. An atten-ant-operated van with a lift and tie-down or accessible publicransportation is necessary for community mobility.

Housing evaluation and modifications should ensure thatafe wheelchair access and egress and space to maneuver aheelchair in the home are available. Access to bathing and

oileting areas and adequate heating, cooling, and ventilationystems should also be in place. The home should be free fromre, health, and safety hazards, and an adequate electricalupply to meet the needs of additional medical equipment must
e present. The local power company and emergency services

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hould be alerted to the patient’s status and condition beforeischarge.Determining the appropriate equipment and support services

s made more complex by variations unique to each person’social support and discharge location. A trained SCI rehabili-ation team is required to fully assess each case. Family andocial support; financial resources; personal preferences; edu-ational, vocational, and avocational goals; and living arrange-ents after discharge must be fully considered during the

valuation. Support throughout the day is needed for morningnd evening activities of daily living (ADLs), bowel and blad-er care, nighttime turning, and meal preparation and feeding.ostacute medical, psychosocial, and rehabilitation care shoulde prescribed in the home or outpatient setting. Although thevaluation process requires input from many specialist teamembers, the physiatrist is ultimately responsible for medical

ustification of all equipment decisions and should be directlynvolved in the durable medical equipment evaluation and

Table 3: Suggested Equipm

Measure

OrthoticsBFO (mobile arm support)Resting hand splintLong opponens splintSpiral splintWrist-driven tenodesis splintRachet tenodesis splintShort opponens splintUniversal cuffLumbrical barMouthstick

Transfers/mobilityPower/mechanical liftTransfer boardPower wheelchair with tilt/reclinePower wheelchairManual wheelchairPower-assist wheelchair

FeedingAdapted equipment (eg, plate)Utensils with built-up handles

Grooming and dressingADL splints (eg, wash mitt, razor holders)Dressing equipment (pant loops, sock aide, dressing stick, lonGooseneck mirror

CommunicationEnvironmental control unitComputerBook holder

BathingGrab barsReclining shower/commode chairTub seat/shower chair (padded)Hand-held spray attachment

BedsFull electric hospital bedFull specialized mattressOverlay mattress

OTE. Adapted from Kirshblum et al.2 Adapted with permission.bbreviations: BFO, balance forearm orthosis; X, yes; —, no; ?, pos

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.5 Educational Activity: To identify the advances in re-habilitation research to improve functional outcomesafter SCI.

Rehabilitation research in SCI has brought advances in theunctional outcomes of people with SCI.27 The key areas ofehabilitation research in SCI include functional electric stim-lation (FES), wheelchair technologies and designs, partialody weight�supported ambulation, the use of robotics, andhe potential use of brain control for assistive technology,obots, and neuroprostheses.

unctional Electric StimulationThe use of FES has evolved to support functional gains in

eople with SCI across multiple body systems. FES can bepplied through surface stimulation, percutaneous fine wires, ormplanted electrodes. Advances in electrode designs have ledo the development of microelectrodes, which are potentially

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nvasive than surface stimulation, it has 2 advantages: precisetimulation of target muscles and elimination of the need to donnd doff the electrodes. With the advances in implantation pre-autions and techniques, the risk of infection has been minimized.or FES to be effective, no significant lower motoneuron injuryhould be present. The use of FES is shown to improve theollowing functions: upper-extremity use (in particular handrasp), lower-extremity use, bladder control, respiration, and car-iovascular and tissue health.28-31

The upper-extremity FES system is an implanted system thatllows people with C5 and C6 tetraplegia to achieve a handrasp. If necessary, it can be implanted in conjunction withendon transfer surgery; this intervention can dramatically im-rove the person’s ability to perform ADLs and can restoreunctional use of the upper extremities. The principle of tendonransfer surgery is to use the functional proximal muscles toontrol the paralyzed distal parts. For instance, someone with5 motor level is not able to extend his/her arm or to useis/her hand. This person may have functioning deltoid mus-les and brachioradialis muscles (both with primarily C5 in-ervation) but not wrist extensors (primarily C6 innervation) orriceps (primarily C7 innervation). With posterior deltoid-to-riceps tendon transfer surgery, this person may now achievelbow extension, which significantly increases functionaleach. It may also allow the person to assist with transfers,ressure relief, and wheelchair propulsion. Therefore, this per-on with C5 injury may now perform some activities as some-ne with a C7 motor level. With brachioradialis-to-wrist ex-ensor (extensor carpi radialis brevis) tendon surgery, thiserson may now achieve wrist extension, which allows teno-esis for hand grasp. He/she may now function as someoneith a C6 motor level injury. Together with an FES system that

nables hand grasp, the functional activity level of this personay be noticeably improved. Currently, research on the use of

uch an FES system, as well as the use of different controlwitches, is underway on people with C4 tetraplegia.28

Lower-extremity FES is an implanted system that allowseople with appropriate paraplegia and tetraplegia withoutignificant lower motoneuron damage to stand up, to transfer,nd to ambulate with necessary assistive devices, for instance,walker. Initially, this system was designed for people with

omplete injuries, but now appropriate candidates with incom-lete injuries can also benefit from this system. A hybridystem combining lower-extremity FES and bracing is beingtudied. The implantation of electrodes in the lumbar paraspi-al muscles and the lower extremities may potentially improverunk control.28

Bladder FES has been widely adopted around the world. It isn implanted system that controls bladder contraction by stim-lation of the sacral nerve roots. The current system is usuallyombined with posterior sacral rhizotomy to improve conti-ence and bladder capacity. Benefits of this FES system in-lude supporting effective voiding, bladder continence, and theeduction of urinary tract infections.28 This sacral nerve stim-lation system can also be used for erectile dysfunction, aommon problem after SCI. Despite the effectiveness of thisystem, some eligible people with SCI would prefer to avoidosterior sacral rhizotomy, thus eliminating the possibility ofts implantation. Current research on a new generation ofladder FES is exploring the use of such a system withoutosterior rhizotomy.28

The restoration of respiratory function has been achieved byhe use of various FES methods. Phrenic nerve pacing was theriginal method, and diaphragmatic pacing is now being stud-ed.29 Phrenic nerve pacing is a more involved procedure, and
he nerve may become fatigued with prolonged stimulation. a

iaphragmatic pacing is performed by laparoscopic implanta-ion of FES electrodes at motor points of the diaphragm with-ut any denervation. People with high tetraplegia and respira-ory failure who require mechanical ventilation may be weanedff of the ventilator through the use of this FES system, whichas also shown significant improvements in the physiologiceasures of respiration.30 These changes also enhance speech

roduction and the quality of life.Cardiovascular fitness can be improved by the use of FES

ycling, through surface stimulation of the lower extremities.his approach is significant because aerobic exercises are oth-rwise difficult for people with SCI to perform. Several sys-ems are commercially available, but they all share the samerinciple—the generation of a cycling motion of the lowerxtremities by computer-coordinated surface stimulation of theip and knee muscles. Other beneficial effects of such anxercise regimen have been reported, including muscle bulkreservation and spasticity control.Another innovative use of FES is the management of tissue

ealth. Pressure ulcers are a common complication after SCI,ffecting the rehabilitation progress of SCI patients. Healthroviders have used surface electrode stimulation for woundare for many years, although its effects on the underlyinguscles and vasculature are largely unknown. More recently,

he development of an FES system implanted in the glutealuscles has shown hypertrophy of the gluteus maximus mus-

les and dynamic pressure relief of the sacral seating surface byhe alternating stimulation of bilateral gluteal muscles.31 Thisreatment modality warrants further investigations.

heelchair Designs and TechnologiesAdvances in wheelchair technologies have generated new

heelchairs that further increase functional independence.ushrim-activated power-assist wheelchairs are such an exam-le. These manual wheelchairs have a motor linked to each rearub. With each manual propulsion by the user, supplementaryower is provided by the motor. Therefore, the force requiredf the user for propulsion over the same distance is decreasedhen compared with a regular manual wheelchair withoutower-assist. This feature is particularly useful for people withetraplegia and hence weakness in the upper extremities orhose with paraplegia and overuse injury causing shoulder pain.n a research study,32 investigators noted that pushrim-acti-ated power-assist wheelchairs can help improve the ADLs ineople with tetraplegia compared with the use of regular man-al wheelchairs.Another recent significant wheelchair development is the

ndependence iBOT 4000 Mobility System.b One of its uniqueunctions is the ability to negotiate curbs and stairs. The di-ensions of the stairs should meet the recommended guide-

ines, and there must be at least 1 sturdy handrail. The userust also ascend the stairs backward, that is, facing down. The

BOT device is not necessarily appropriate for all power-heelchair users, because users must meet certain prerequi-

ites. To climb the stairs, upper-extremity function adequate torab the handrail and to stabilize the iBOT device while initi-ting the climbing movement is necessary. Otherwise, stairegotiation can be performed with the assistance of a caregiver.here are only a few training and evaluation centers in thenited States at the current time.Advances in wheelchair research have provided useful data

n appropriate manual wheelchair propulsion methods that willreserve the upper extremities of people with SCI. A multi-enter trial33 with paraplegic people found that during manualheelchair propulsion, lower peak forces, slower cadence, and
circular propulsive stroke in which the hand falls below the

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ocomotor TrainingPartial body weight�support treadmill training (PBWSTT) has

enerated much interest in the field of rehabilitation. PBWSTT isased on the principle of generating normative, locomotor-likeensory input to promote the recovery of the spinal cord neuralircuitry.34,35 With PBWSTT, the weight of the person is partiallyupported by an overhead harness while the therapists guide theips and legs, enabling the person to walk on the treadmill.

Studies36,37 performed in subjects with neurologically in-omplete lesions (mostly chronic injuries) have shown im-rovement in ambulatory capacity. However, a multicenter trialf 146 subjects with acute, neurologically incomplete injuriesndergoing conventional gait training versus PBWSTT did notnd a significant difference in subjects regaining the ability tombulate.38 Gait training with conventional PBWSTT is laborntensive, and PBWSTT with automated robotic systems isvailable (eg, Lokomatc). To date, however, there is no evi-ence that robotic PBWSTT produces superior outcomes toherapist-assisted PBWSTT.39

rain-Based Command SignalsThe use of brain-based command signals for controlling

ssistive technology, robotics, or neuroprostheses is a newerrea of rehabilitation engineering research. It may prove usefulor people with tetraplegia and upper-extremity impairments.rain signals are collected and processed through electrodes

hat may be placed or implanted at various levels. Intracorticalignals can be collected directly from microelectrodes in therain, or electroencephalogram (EEG)/field potentials can beetected through electrodes placed at any level between theurface of the brain and the scalp. The detection of EEG/fieldotentials is less invasive, but the signal will also have loweresolution and provide potentially less useful information,hereas intracortical microelectrode placement is more inva-

ive but will acquire higher resolution and probably deliverore useful information. Once the signal has been processed,

t can potentially be used to control various devices, fromomputers and environmental control units to neuroprostheseseg, through an FES system) or robotic devices for assistanceith ADLs. Therefore, the ability to use brain signals may bebreakthrough in the design of control units for assistive

evices. Currently, the BrainGate system is being developed byhe Cyberkinetics Neurotechnology Systems.d It involves themplantation of electrodes in the brain, with the detected sig-als being transmitted to a computer system. A pilot study ofhe BrainGate system on subjects with SCI, muscular dystro-hy, and stroke is underway at 3 rehabilitation centers in thenited States. The goal of this investigational medical device

tudy is to show the system’s ability to record subjects’ brainctivity and translate their thoughts directly into a computerontrol signal. At present no clinical product is available forrain-based command signals, and much more research isecessary for its application.

References1. Consortium for Spinal Cord Medicine. Outcomes following trau-

matic spinal cord injury: clinical practice guidelines for health-care professionals. Washington (DC): Paralyzed Veterans ofAmerica; 1999.

2. Kirshblum S, Ho CH, House JG, Druin E, Nead C, Drastal S.
Rehabilitation of spinal cord injury. In: Kirshblum SC, Campagnolo
DI, DeLisa JA, editors. Spinal cord medicine. Philadelphia:Lippincott Williams & Wilkins; 2002. p 275-98.

3. Scivoletto G, Morganti B, Molinari M. Early versus delayedinpatient spinal cord injury rehabilitation: an Italian study. ArchPhys Med Rehabil 2005;86:512-6.

4. Sumida M, Fujimoto M, Tokuhiro A, Tominaga A, Uchida R.Early rehabilitation effect for traumatic spinal cord injury. ArchPhys Med Rehabil 2001;82:391-5.

5. Smith M. Efficacy of specialist versus non-specialist manage-ment of spinal cord injury within the UK. Spinal Cord 2002;40:11-6.

6. Wilmot CB, Cope DN, Hall KM, Acker M. Occult head injury:its incidence in spinal cord injury. Arch Phys Med Rehabil1985;66:227-31.

7. Macciocchi SN, Bowman B, Coker J, Apple D, Leslie D. Effectof co-morbid traumatic brain injury on functional outcome ofpersons with spinal cord injuries. Am J Phys Med Rehabil2004;83:22-6.

8. Davidoff GN, Roth EJ, Richards JS. Cognitive deficits in spinalcord injury: epidemiology and outcome. Arch Phys Med Rehabil1992;73:275-84.

9. Davidoff G, Thomas P, Johnson M, Berent S, Dijkers M, DoljanacR. Closed head injury in acute traumatic spinal cord injury: inci-dence and risk factors. Arch Phys Med Rehabil 1988;69:869-72.

10. Strubreither W, Hackbusch B, Hermann-Gruber M, Stahr G,Jonas HP. Neuropsychological aspects of the rehabilitation ofpatients with paralysis from a spinal injury who also have a braininjury. Spinal Cord 1997;35:487-92.

11. Sommer JL, Witkiewicz PM. The therapeutic challenges of dualdiagnosis: TBI/SCI. Brain Inj 2004;18:1297-308.

12. Lombard LA, Zafonte RD. Agitation after traumatic brain injury:considerations and treatment options. Am J Phys Med Rehabil2005;84:797-812.

13. Dowler RN, Harrington DL, Haaland KY, Swanda RM, Fee F,Fiedler K. Profiles of cognitive functioning in chronic spinal cordinjury and the role of moderating variables. J Int NeuropsycholSoc 1997;3:464-72.

14. Teasell R, Arnold J, Krassioukov A. Cardiovascular conse-quences of loss of supraspinal control of the sympathetic nervoussystem after spinal cord injury. Arch Phys Med Rehabil 2000;81:506-16.

15. Lindan R, Joiner E, Freehafer AA, Hazel C. Incidence andclinical features of autonomic dysreflexia in patients with spinalcord injury. Paraplegia 1980;18:285-92.

16. Kirshblum SC, House JG, O’Connor KC. Silent autonomic dys-reflexia during a routine bowel program in persons with spinalcord injury: a preliminary study. Arch Phys Med Rehabil 2002;83:1774-6.

17. Consortium for Spinal Cord Medicine. Acute management ofautonomic dysreflexia: adults with spinal cord injury presentingto health-care facilities. Washington (DC): Paralyzed Veterans ofAmerica; 1997.

18. Stiens SA, Lutrel W, Binard JE. Polyethylene glycol versusvegetable oil based bisacodyl suppositories to initiate side-lyingbowel care: a clinical trial in persons with spinal cord injury.Spinal Cord 1998;36:777-81.

19. Stiens SA, Bergman SB, Goetz LL. Neurogenic bowel dysfunc-tion after spinal cord injury: clinical evaluation and rehabilitativemanagement. Arch Phys Med Rehabil 1997;78(3 Suppl 1):S86-102.

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20. Consortium for Spinal Cord Medicine. Neurogenic bowel man-agement in adults with spinal cord injury. Washington (DC):Paralyzed Veterans of America; 1998.

21. Rosito O, Nino-Murcia M, Wolfe VA, Kiralti J, Perkash I. Theeffects of colostomy on the quality of life in patients with spinalcord injury: a retrospective analysis. J Spinal Cord Med 2002;25:174-83.

22. Massagli TL, Cardenas DD. Immobilization hypercalcemia treat-ment with pamidronate disodium after spinal cord injury. ArchPhys Med Rehabil 1999;80:998-100.

23. Estores I, Harrington A, Banovac K. C-reactive protein and ESRrate in patients with HO. J Spinal Cord Med 2004;27:434-7.

24. Singh RS, Craig MC, Katholi CR, Jackson AB, Mountz JM. Thepredictive value of creatine phosphokinase and alkaline phos-phatase in identification of heterotopic ossification in patientsafter spinal cord injury. Arch Phys Med Rehabil 2003;84:1584-8.

25. Banovac K, Sherman AL, Estores IM, Banovac F. Preventionand treatment of heterotopic ossification after spinal cord injury.J Spinal Cord Med 2004;27:376-82.

26. Consortium for Spinal Cord Medicine. Depression followingspinal cord injury: a clinical practice guideline for primary carephysicians. Washington (DC): Paralyzed Veterans of America;1998.

27. Kirshblum S. New rehabilitation interventions in spinal cordinjury. J Spinal Cord Med 2004;27;342-50.

28. Peckham PH, Gorman PH. Functional electrical stimulation inthe 21st century. Top Spinal Cord Inj Rehabil 2005;10:126-50.

29. DiMarco AF, Onders RP, Ignagni A, Kowalski KE. Inspiratorymuscle pacing in spinal cord injury: case report and clinicalcommentary. J Spinal Cord Med 2006;29:95-108.

30. DiMarco AF, Kowalski KE, Geertman RT, Hromyal DR. Spinalcord stimulation: a new method to produce an effective cough inpatients with spinal cord injury. Am J Respir Crit Care Med2006:173:1386-9.

31. Bogie KM, Wang X, Triolo RJ. Long-term prevention of pres-sure ulcers in high-risk patients: a single case study of the use ofgluteal neuromuscular electric stimulation. Arch Phys Med Re-
habil 2006;87:585-91.

32. Algood SD, Cooper RA, Fitzgerald SG, Cooper R, BoningerML. Effect of a pushrim-activated power-assist wheelchair onthe functional capabilities of persons with tetraplegia. Arch PhysMed Rehabil 2005;86:380-6.

33. Boninger ML, Koontz AM, Sisto SA, et al. Pushrim biomechan-ics and injury prevention in spinal cord injury: recommendationsbased on CULP-SCI investigations. J Rehabil Res Dev 2005;42:9-19.

34. Dobkin B. Overview of treadmill locomotor training with partialbody weight support: a neurophysiologically sound approachwhose time has come for randomized clinical trials. NeuroRe-habil Neural Repair 1999;13:157-65.

35. Barbeau H. Locomotor training in neurorehabilitation: emergingrehabilitation concepts. NeuroRehabil Neurol Repair 2003;17:3-11.

36. Protas EJ, Holmes SA, Qureshy H, Johnson A, Lee D, SherwoodAM. Supported treadmill ambulation training after spinal cordinjury: a pilot study. Arch Phys Med Rehabil 2001;82:825-31.

37. Wernig A, Nanassy A, Muller S. Maintenance of locomotorabilities following Laufband (treadmill) therapy in para- andtetraplegic persons: follow-up studies. Spinal Cord 1998;36:744-9.

38. Dobkin B, Apple D, Barbeau H, et al; Spinal Cord InjuryLocomotor Trial Group. Weight-supported treadmill vs over-ground training for walking after acute incomplete SCI. Neurol-ogy 2006;66:484-93.

39. Field-Fote EC, Lindley SD, Sherman AL. Locomotor trainingapproaches for individuals with spinal cord injury: a preliminaryreport of walking-related outcomes. J Neurol Phys Ther 2005;29:127-37.

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pinal Cord Injury Medicine. 4. Community Reintegrationfter Spinal Cord Injury

illiam M. Scelza, MD, Steven C. Kirshblum, MD, Lisa-Ann Wuermser, MD, Chester H. Ho, MD,
ichael M. Priebe, MD, Anthony E. Chiodo, MD
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ABSTRACT. Scelza WM, Kirshblum SC, Wuermser LA,o CH, Priebe MM, Chiodo AE. Spinal cord injury medicine.. Community reintegration after spinal cord injury. Arch Physed Rehabil 2007;88(3 Suppl 1):S71-5.

This self-directed learning module highlights communityeintegration after spinal cord injury (SCI). It is part of thetudy guide on spinal cord injury medicine in the Self-Directedhysiatric Education Program for practitioners and trainees inhysical medicine and rehabilitation. This article specificallyocuses on physical, social, psychologic, and environmentalarriers that affect people with SCI and on how these issuesffect relations with others. Recreational and exercise optionsre also discussed.

Overall Article Objective: To summarize the barriers andpportunities of community reintegration for people with spi-al cord injury.Key Words: Exercise; Interpersonal relations; Recreation;

ehabilitation; Spinal cord injuries.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Educational Activity: To describe barriers and oppor-tunities that may be encountered by the 20-year-oldman described in chapter 3 who has spinal cord injuryand who is planning his return to school and work.

HE GOAL OF REHABILITATION is to promote theassumption or resumption of culturally and developmen-

ally appropriate social roles after injury or illness.1 Rehabili-ation should promote the full inclusion and participation ofeople with disabilities in the physical and psychosocial envi-onment.2 Participation in community activities correlatestrongly with subjective quality of life.3 However, most ofhat occurs in spinal cord injury (SCI) rehabilitation today isirected toward minimizing functional limitations. Specific in-erventions to maximize community participation are limited.4

s a result, the potential for full reintegration of a person into

From the Department of Physical Medicine and Rehabilitation, Carolinas Rehabil-tation, Charlotte, NC (Scelza); Spinal Cord Injury Services, Kessler Institute forehabilitation, West Orange, NJ (Kirshblum); Department of Physical Medicine andehabilitation, University of Medicine and Dentistry–New Jersey Medical School,ewark, NJ, (Kirshblum); Department of Physical Medicine and Rehabilitation,ayo Clinic, Rochester, MN (Wuermser, Priebe); Louis Stokes Cleveland Depart-ent of Veterans Affairs Medical Center and Department of Physical Medicine andehabilitation, Case Western Reserve University, Cleveland, OH (Ho); and Depart-ent of Physical Medicine and Rehabilitation, University of Michigan Hospital, Annrbor, MI (Chiodo).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to William M. Scelza, MD, Carolinas Rehab, 1100 Blythe Blvd,

harlotte, NC 28203, e-mail: [email protected]. Reprints areot available from the author.

g0003-9993/07/8803S-11413$32.00/0doi:10.1016/j.apmr.2006.12.004

is/her community is often incompletely met. Community in-egration is a complex issue, with obvious and not-so-obviousarriers and opportunities that affect its success. Advocacy forccessibility, both physical and societal, has had a major im-act on the ability of people with SCI to resume many of theirreinjury roles. However, much remains to be done to enableeople with disabilities to participate in their communities tohe fullest extent desired.

Demographic variables, including level and severity of neu-ologic injury, are not generally good predictors of manyong-term psychologic and productivity outcomes in SCI.hese outcomes are more strongly affected by factors such as

amily support, emotional adjustment, and coping style. How-ver, in 1 study, people with less severe neurologic injury,onger duration of injury, and younger age at injury had betterommunity participation outcomes.5

The physical environment has traditionally been viewed asn important but modifiable barrier for people with mobilitympairments. Changes in public policy that resulted in theresence of curb cuts, elevators, and accessible public trans-ortation systems, to name a few, have greatly improved thebility of people in wheelchairs to participate in society. Recenttudies have reported that environmental factors have only amall effect on community integration. Factors including fam-ly support, self-esteem, informational support, and copingtyle had a much greater impact.6,7 Physical accessibility inany communities has improved dramatically in the past 20

ears and therefore, it is conceivable that the environment inhose communities no longer acts a major barrier. However, inommunities where the physical environment remains inacces-ible, people with disabilities continue to be faced with majorarriers.An important barrier to full community participation is lim-

ted community resources—that is, those medical and socialervices needed by people with disabilities to live in the com-unity.8 Independent living services (ILS) are designed toinimize barriers to physical independence, mobility, occupa-

ion, social integration, and economic self-sufficiency, but ac-ess to these services may not be ideal. The transition fromcute rehabilitation to home is especially critical, because peo-le are confronted with many obstacles as they attempt toesume participation in the community. If services are madevailable to assist with this transition, successful reintegrations more likely. Unfortunately, many people with SCI do noteceive adequate ILS, resulting in many unmet needs (table 1).

Centers for independent living (CILs) can play an importantole in facilitating successful reintegration by providing peerentoring and role modeling, access to transportation, acces-

ible housing, attendant care personnel, and general knowledgebout independent living, advocacy, and other community re-ources. However, communication between the CIL and theedical rehabilitation community is often inadequate.4

Maintaining community participation is a separate, butqually important, consideration for people with SCI as they
row older. A longitudinal study of people with longstanding

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S72 COMMUNITY REINTEGRATION AFTER SPINAL CORD INJURY, Scelza

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CI found a general decline in community integration overime, specifically in physical independence, mobility, occupa-ion, and social integration. However, economic self-suffi-iency appeared to improve over time. Measures of emotionalistress—that is, of stress, life satisfaction, depression, psycho-ogic well-being, and perceived quality of life—were not re-ated to changes in community integration.8 Changes in healthtatus and social support systems, as well as changes in culturalxpectations and personal preferences for participation, occurs a person ages, resulting in different patterns of communityarticipation over time. More research is needed to determineow to meet the changing needs of the SCI population to allowhem to continue to be active throughout their lives.

.2 Clinical Activity: To outline recreational and fitnessoptions available for a 30-year-old woman with trans-verse myelitis with a T6 neurologic–level injury whohas successfully completed postacute care rehabilitation.

People with SCI are on the lowest end of the fitness spec-rum, and people with paraplegia, despite having more abilitynd opportunity for physical fitness, are only marginally moret than those with tetraplegia.9 Sedentary lifestyles in thoseith SCI are thought to contribute to a number of abnormaletabolic and fitness parameters. After SCI, the decreased base-

ine energy expenditure can contribute to weight gain and obesityf physical activity is not adequately increased.10 Twenty-twoercent of people with SCI were found to have diabetes com-ared with 6% of able-bodied controls; 34% had glucose in-olerance compared with 12% in a control group.11 High-ensity lipoproteins, which are believed to have a protectiveffect on cardiovascular health, have been found to be lower inhe SCI population.

Numerous barriers confront people with SCI as they con-ider becoming more physically active. Only 8% of fitnessacilities were found to provide adequate accessibility to peopleith disabilities.12 People with SCI have also expressed con-

erns about lack of experience of staff at fitness facilities, lackf privacy, and fear of injury as barriers to activity. Moreover,hysicians have recommended physical activity to less thanalf of those with SCI.13 These items leave a tremendouspportunity for health professionals involved in the care ofeople with SCI to intervene to improve participation in rec-eation and fitness activities.

The need for exercise in the SCI population has been well

Table 1: ILS: Unmet Needs

Attendant Care ServicesPeople With SCI Reporting

Unmet Needs (%)

Recruiting 17Supervising 14Conflict resolution 14Housing 27Transportation 17Vocational 16Legal rights and advocacy 37Government benefits 28Insurance benefits 22Counseling and education 28Recreation 30Support group 14

OTE. From Forchheimer and Tate.4 Reprinted with permission.

ecognized and does not vary dramatically from the general c


opulation. Generally, it is suggested that 3 to 5 exerciseessions occur on a weekly basis. Sessions should be 20 to 60inutes in duration with an intensity of 50% to 80% of each

erson’s peak heart rate. The American College of Sportsedicine has published recommended exercise programming

or people with SCI.14 Recommendations for an exercise pro-ram include various modes of cardiopulmonary training con-isting of arm-crank ergometry, wheelchair propulsion, swim-ing, vigorous wheelchair sports, ambulation with crutches or

races, seated aerobic exercise, and the use of electricallytimulated leg cycle activities. Considerations in the preventionf overuse injuries are important components of any exerciseegimen. It is suggested to try to vary activities as much asossible to avoid overuse injuries to the upper extremities ando provide strengthening activities to all major muscle groups.mphasis on precautions to minimize the risk of secondaryonditions to which people with SCI are susceptible are alsomphasized. It is suggested that consultation with a physicianhould occur to prevent potential secondary conditions. Use ofppropriate pressure relief cushions and proper positioning andalancing to avoid falls and risk of fractures are outlined. Smallut progressive improvements in strength and endurance shoulde the goal. Expectations should be based on the amount of theuscle mass being exercised (ie, the larger the muscle mass

eing exercised, the greater the improvements in fitness thatould be expected).Options for recreation and exercise continue to expand.

ecreational and sporting activities include a number of com-etitive and individual sports. In 1960, the first Paralympicames were held in Rome, with 400 athletes from 23 countriesarticipating; the 2004 games in Athens expanded to nearly000 participants from 136 countries. Sports-n-Spokes maga-ine, a publication from the Paralyzed Veterans of America,utlines numerous recreational options for people with SCI andther disabilities. Sporting associations and recreational eventsrom all over the world are listed, and there are contacts forver 40 disabled sporting organizations in every issue. Otherrganizations such as Wheelchair Sports, USA (http://www.susa.org) boast membership representing thousands of peopleith disabilities. The 2005�2008 mission of this organization

s “to provide sports and recreation for people with physicalisabilities by facilitating and developing a national commu-ity-based outreach program, providing resources and educa-ion, conducting regional and national competitions, and pro-iding access to international competitions.” Their guidingrinciples are to “promote the opportunity to experience com-etitive sport, increase self esteem, develop social and lifekills, improve health and fitness, and raise society’s expecta-ions of people with disabilities.”

Other types of recreational activities are also available.heelchair dance and theater also have representative groups

or those interested in the arts. People with tetraplegia andther high-level injuries have a range of adapted sports andctivities to choose from as well. In July 2005, the film Mur-erball introduced the sport of wheelchair rugby and the livesf its participants. Handcycling has opened the opportunity foreople to ride with their families as well as to compete andaintain fitness. Other publications such as Spinal Network15

ffer personal stories of people with SCI and their recreationalursuits.Travel and transportation are other ways for people with SCI

o expand their recreational options and endeavors. The 1986ir Carrier Access Act prohibits discrimination against peopleith physical or mental impairments; boarding assistance and

ircraft accessibility features are required in newly built air-
raft.16 It is recommended that people with power wheelchairs
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S73COMMUNITY REINTEGRATION AFTER SPINAL CORD INJURY, Scelza

r other special equipment contact the airlines before travel andhat they arrive early at the airport. Despite the provisionsequired by law, however, people should make provisions forheir own personal needs. Seat cushions for pressure reliefhould be brought into the aircraft if needed; those usingir-filled cushions should be aware of the possibility of expan-ion with altitude changes. Plans for bladder management (eg,atheterization, emptying of drainage appliance, medications)hould be addressed in case there is a delay. It is also wise forhe person to have all necessary medication and equipment atll times and not checked into baggage.

Driving is an option that most people with SCI can pursue.predriving assessment needs to be completed by a certified

ccupational therapist during which a person’s medical history,unctional capacity, vision, reaction time, and necessary mo-ility equipment are assessed. Many automobile manufacturersill often allow up to $1000 for adaptive equipment. Peopleith C5 injuries are thought to have the highest level of injury

ompatible with independent driving. A van with adapted driv-ng technologies and a remote-control ramp or lift system wille required for high-level injuries; an adapted vehicle can costbout $60,000.

.3 Educational Activity: To discuss the adjustment issuesthat influence the health and community reintegrationof a 30-year-old woman with a T6 neurologic level ofinjury.

Psychologic issues affect outcome after SCI. Premorbid is-ues such as alcohol and other substance abuse, depression,sychosis or behavioral or learning disorders will affect reha-ilitation and long-term outcome. Psychosocial issues such aselationship outcome, peer group acceptance, and family re-ources have a greater impact on functional outcome andecondary conditions than does the neurologic level of injury.17

igher education, better physical health, and lack of negativeood states improve overall level of functional indepen-

ence.18 Cognitive-behavioral therapy results in fewer hospitaldmissions, less medication use, and improved subjective ad-ustment when conducted during the inpatient phase of reha-ilitation. Decreases in anxiety and improved mood were sus-ained for at least 2 years after postinjury rehabilitation.19 FIMfficiency and length of stay are adversely affected by premor-id alcohol problems.20

In a large study of people with SCI at least 1 year postinjury,4% had alcohol abuse issues; 11% had used illegal drugs orisused prescription medications.21 Substance abuse was more

ommonly seen in younger single men and those who were lessducated. Substance abuse is associated with more pain andess satisfaction with life. Pressure ulcers are associated withubstance abuse, although their relation to other secondaryonditions is unknown.21

In a study 1 year postinjury, 11.5% of patients had probableajor depression.22 This finding was not related to neurologicmerican Spinal Injury Association classifications but was

een more frequently in middle-aged people and less in peopleho were single. Depression was associated with poor subjec-

ive health, decreased satisfaction with life, and more difficultyith daily role functioning. It also was not related to demo-raphic or injury variables.22 Minorities and women are atarticularly high risk of depression. Education and incomeorrelate negatively with depression.23

Suicide is seen in 7.3% of patients who have sustained aajor acute illness and 25% who have a concomitant major

epressive disorder; this finding holds true for patients with
CI.24 The suicide rate in a paraplegic cohort was 10 times the 2
ate in an able-bodied control group.25 Functional status, sex,nd socioeconomic status at the time of injury did not predictuicide risk, although premorbid psychiatric disorder did.26

The Consortium for Spinal Cord Injury Medicine guidelinesn depression after SCI27 provide a very comprehensive toolor assessment, diagnosis, and treatment of depression after anCI. A treatment plan for depression will depend on previousistory of psychologic disorders, suicidal ideation, complexsychiatric diagnoses, and substance abuse, and these factorshould be assessed so appropriate referral to qualified mentalealth professionals can be undertaken. Treatment of underly-ng medical disorders and pain also must be addressed. Psy-hologic counseling should also be a core component of thereatment plan. Referral to social workers, peer and familyupport groups, and rehabilitation counselors are other toolshat can help newly injured patients cope with the recent loss.aving such resources available facilitates transition into the

ommunity. The use of pharmacologic agents should be tai-ored to each person, and education about side effects of thepecific agents being used is a key component to antidepressantherapy. A comprehensive list of the different classes andide-effect profiles of individual classes and agents can beeviewed in the Consortium Guidelines.27

.4 Educational Activity: To summarize, while speakingto a patient/family support group, the challenges ofinterpersonal relationships after SCI.

Among many sources of uncertainty after SCI, there isoncern about potential and existing relationships, most partic-larly romantic relationships. Historically, a bias has existedgainst the desirability of a romantic partner with a disability,o such an extent that social scientists sought to determine thesychopathology of people who chose to enter into such rela-ionships.28 Advances in social and vocational integration ofeople with disabilities have helped to dispel such myths, butegative personal biases and assumptions sometimes pervadehese discussions.

Studies have shown that the rate of divorce after SCI isigher among preinjury marriages than in the general popula-ion, with a higher risk of divorce among women who sustainCI, childless couples, those with prior divorce, and Africanmericans. These divorces most commonly occur within 3ears of injury. Postinjury marriages have similar emotionaluality to marriages among able-bodied peers, and these cou-les show better marital adjustment than do couples in prein-ury marriages.28 However, variability exists in findings aboutarriage among different cultures and countries.Single people with SCI are less likely to become married

ompared with age- and sex-matched controls. However, overheir lifespans up to 80% of single people with SCI eventuallyarry. People with SCI who are socially and vocationally

ctive are more likely to establish stable relationships andarry. Their partners are noted to be similar in personality

raits to the general population, except for a lower tendency toespond according to rules and convention and more likely tossert themselves in social situations.29 Models of courtship arelso similar to those of nondisabled peers.

Recent data on marriage in people with spina bifida are notvailable, with previous studies reporting few marriages in thisopulation. Sexual activity may serve as proxy data for datingnd future marriage. Among young adults (age range, 16–25y)ith spina bifida, nearly half had been sexually active, and 25%ad a partner at the time of a cross-sectional study.30 However,
0% of women in this study reported unwanted sexual activity.

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S74 COMMUNITY REINTEGRATION AFTER SPINAL CORD INJURY, Scelza

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Rates of sexual and physical abuse are similar betweeneople with disabilities and the general population, althougheople with disabilities tend to experience abuse for longereriods of time. As with the general population, abusers areost likely to be intimate partners. However, people with

isabilities experience higher rates of physical and sexualbuse at the hands of nonintimate caregivers, including paidttendants and health care providers.31 Most data are based ontandard instruments to screen for abuse and fail to ask forisability-specific forms of abuse. The Abuse Assessmentcreen–Disability31 was developed to remedy this by expand-

ng the standard screening tool to include questions on whethernecessary assistive device was withheld or necessary assis-

ance from a usual caregiver was denied. Compared with thispecific tool, standard tools have been shown to miss up to 20%f abuse.32

Perceived burden of care is a key concern among manyeople with SCI, with newly injured patients often expressingistress over the demands on spouses, parents, or other rela-ives. Spouses who serve as caregivers report higher levels oftress, burnout, fatigue, resentment, and depression comparedith spouses who are not caregivers. Greater levels of stress inartners were associated with increased burden of care ofatients. Interestingly, two thirds of partners reported no needor further assistance. Additional predictors of higher perceivedurden of care were greater psychologic problems of the pa-ient, older age of the partner, female partner of a male patient,nd proximity to onset of injury.33

Studies on parenting have failed to show substantial dif-erences in parental satisfaction and outcomes of childrenetween parents with SCI and able-bodied parents, regardlessf whether the parent with SCI is the mother or father. Al-hough differences exist in how parents with SCI and theirartners perceive their children and their own lives34 and inarenting technique,35 these differences have not been showno result in differences in behavioral or social outcomes of thehildren nor in parental satisfaction of either parent.

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17. Holicky R, Charlifue S. Aging with spinal cord injury: the impactof spousal support. Disabil Rehabil 1999;21:250-7.

18. Putzke JD, Richards JS, Hicken BL, DeVivo MJ. Predictors oflife satisfaction: a spinal cord injury cohort study. Arch PhysMed Rehabil 2002;83:555-61.

19. Craig A, Hancock K, Dickson H. Improving the long-term ad-justment of spinal cord injured persons. Spinal Cord 1999;37:345-50.

20. Bombardier CH, Stroud MW, Esselman PC, Rimmele CT. Dopreinjury alcohol problems predict poorer rehabilitation progressin persons with spinal cord injury? Arch Phys Med Rehabil2004:85:1488-92.

21. Tate DG, Forchheimer MB, Krause JS, Meade MA, BombardierCH. Patterns of alcohol and substance use and abuse in personswith spinal cord injury: risk factors and correlates. Arch PhysMed Rehabil 2004:85:1837-47.

22. Bombardier CH, Richards JS, Krause JS, Tulsky D, Tate DG.Symptoms of major depression in people with spinal cord injury:implications for screening. Arch Phys Med Rehabil 2004;85:1749-56.

23. Krause JS, Kemp B, Coker J. Depression after spinal cord injury:relation to gender, ethnicity, aging and socioeconomic indicators.Arch Phys Med Rehabil 2000:81:1099-109.

24. Kishi Y, Robinson RG, Kosier JT. Suicidal ideation amongpatients with acute life-threatening physical illness: patients withstroke, traumatic brain injury, myocardial infarction, and spinalcord injury. Psychosomatics 2001;42:382-90.

25. Rish BL, Dilustro JF, Salazar AM, Schwab KA, Brown HR.Spinal cord injury: a 25-year morbidity and mortality study. MilMed 1997;162:141-8.

26. Hartkopp A, Bronnum-Hansen H, Seidenschnur AM, Biering-Sorensen F. Suicide in a spinal cord injured population: itsrelation to functional status. Arch Phys Med Rehabil 1998:79;1356-61.

27. Consortium for Spinal Cord Injury Medicine. Depression follow-ing spinal cord injury: a clinical practice guideline for primarycare physicians. Washington (DC): Paralyzed Veterans of Amer-ica; 1998.

28. Kreuter M. Spinal cord injury and partner relationships. Spinal
Cord 2000;38:2-6.
http://www.dotcr.ost.dot.gov/asp/airacc.asp

S75COMMUNITY REINTEGRATION AFTER SPINAL CORD INJURY, Scelza

29. Crewe NM, Krause JS. Marital status and adjustment to spinalcord injury. J Am Paraplegia Soc 1992;15:14-8.

30. Verhoef M, Barf H, Vroege J, et al. Sex education, relationshipsand sexuality among young adults with spina bifida. Arch PhysMed Rehabil 2005;86:979-87.

31. Young ME, Nosek MA, Howland C, Chanpong G, Rintala DH.Prevalence of abuse of women with disabilities. Arch Phys MedRehabil 1997;78(12 Suppl 5):S34-8.

32. McFarlane J, Hughes RB, Nosek MA, Groff JY, Swedlend N,Dolan Mullen P. Abuse Assessment Screen–Disability (AAS-D):
measuring frequency, type, and perpetrator of abuse toward
women with physical disabilities. J Women Health Gen BasedMed 2001;10:861-6.

33. Post MW, Bloemen J, deWitte LP. Burden of support for partners ofpersons with spinal cord injuries. Spinal Cord 2005;43:311-9.

34. Alexander CJ, Hwang K, Sipksi ML. Mothers with spinal cordinjuries: impact on marital, family and children’s adjustment.Arch Phys Med Rehabil 2002;83:24-30.

35. Rintala DH, Herson L, Hudler-Hull T. Comparison of parentingstyles of persons with and without spinal cord injury and theirchildren’s social competence and behavior problems. J Spinal
Cord Med 2000;23:244-56.

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pinal Cord Injury Medicine. 5. Long-Term Medical Issuesnd Health Maintenancenthony E. Chiodo, MD, William M. Scelza, MD, Steven C. Kirshblum, MD, Lisa-Ann Wuermser, MD,
hester H. Ho, MD, Michael M. Priebe, MD
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ABSTRACT. Chiodo AE, Scelza WM, Kirshblum SC,uermser LA, Ho CH, Priebe MM. Spinal cord injury medicine.

. Long-term medical issues and health maintenance. Arch Physed Rehabil 2007;88(3 Suppl 1):S76-83.

This self-directed learning module highlights long-term caressues in patients with spinal cord injury (SCI). It is part of thetudy guide on SCI in the Self-Directed Physiatric Educationrogram for practitioners and trainees in physical medicine andehabilitation. The most common secondary medical compli-ations include pressure ulcers, pneumonia, and genitourinaryssues. Health care maintenance is important to prevent medi-al complications, for general health as well as for issuespecific to SCI. Women with SCI have gender-specific issuesegarding amenorrhea, sexuality, fertility, and menopause. Op-ions exist to assist disabled men with sexuality and fertilityomplications. Pain is a common complication after SCI. Manyew areas of research in the field of SCI are discussed.Overall Article Objective: To discuss long-term care issues

n patients with spinal cord injury, including health mainte-ance, secondary conditions, women’s health, sexual function,ain, and spinal cord regeneration and recovery.Key Words: Pain; Rehabilitation; Sexual disorders; Spinal

ord injuries; Women’s health.© 2007 by the American Academy of Physical Medicine and

ehabilitation

.1 Educational Activity: To formulate a list of secondarymedical conditions that commonly occur in a 20-year-old man with a C4 American Spinal Injury Associa-tion grade A spinal cord injury who is 1 yearpostinjury.

ECONDARY MEDICAL COMPLICATIONS are ex-tremely common in patients with chronic spinal cord injury

SCI). The Model Spinal Cord Injury Systems data indicatehat the incidence of secondary conditions changes based onhe number of years that a person has had an SCI. Pressurelcers are the most common secondary condition, with the

From the Department of Physical Medicine and Rehabilitation, University ofichigan Hospital, Ann Arbor, MI (Chiodo); Department of Physical Medicine andehabilitation, Carolinas Rehabilitation, Charlotte, NC (Scelza); Spinal Cord Injuryervices, Kessler Institute for Rehabilitation, West Orange, NJ (Kirshblum); Depart-ent of Physical Medicine and Rehabilitation, University of Medicine and Dentistry–ew Jersey Medical School, Newark, NJ, (Kirshblum); Department of Physicaledicine and Rehabilitation, Mayo Clinic, Rochester, MN (Wuermser, Priebe); and

ouis Stokes Cleveland Department of Veterans Affairs Medical Center and Depart-ent of Physical Medicine and Rehabilitation, Case Western Reserve University,leveland, OH (Ho).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Anthony E. Chiodo, MD, Dept of PM&R, Univ of Michigan

ospital, 325 E Eisenhower, Ann Arbor, MI, e-mail: [email protected]. Reprintsre not available from the author.

s0003-9993/07/8803S-11416$32.00/0doi:10.1016/j.apmr.2006.12.015


ncidence increasing with time postinjury.1 Pneumonia ratesre highest in tetraplegia and in older patients.1 Rehospitaliza-ion rates have remained static over the last 10 years.2 The mostommon reasons for rehospitalization include genitourinaryomplications, pressure ulcers, and respiratory complications.rinary complications and pressure ulcers are more frequently

eported in people with complete injuries. Pneumonia is moreommon in people with tetraplegia, whereas pressure ulcers areore common in people with paraplegia. Patients from skilled

ursing facilities, those with lower motor scores on the FIMnstrument, or who are using state or federal health insurancelans have a higher rehospitalization rate.2

Pressure ulcers are common but tend to cluster in a selectopulation of patients. In 1 study 75% of participants failed toeport recurrent pressure ulcers (never had any or had themnly immediately after SCI onset), whereas 13% reported alear pattern of recurring pressure ulcers of 1 or more per year.nly pressure ulcer history, cigarette use, and use of sleepedication predicted future recurrent pressure ulcers.3 Treat-ent options outlined in the Consortium Guidelines4 are pre-

ented in abbreviated form in appendix 1.Urologic issues are detailed in the Consortium Guidelines, and

ladder management strategies are abbreviated in appendix 2.5

he use of prophylactic antibiotics to prevent urinary tract infec-ions (UTIs) after SCI continues to be unsupported by prospectivetudies.6 Intradetrussor botulinum toxin type A is effective inreating spastic bladder in SCI.7 Intravesical resinofiritoxin is alsoffective but is not currently approved by the U.S. Food and Drugdministration (FDA).8 Major risk factors for the development ofrolithiasis among patients with SCI include recurrent UTIs, in-welling catheters, vesicoureteral reflux, prior kidney stones, andmmobilization hypercalciuria.9 Shock wave lithotripsy success is0% to 90%, and percutaneous nephrolithostomy is as successfuls in the able-bodied population.10 Chronic indwelling catheters,moking, and kidney stones are risks factors for bladder cancer.ross hematuria should be aggressively evaluated as the most

ommon sign of bladder cancer. False-negative rates for cystos-opy approach 20%. Fifty percent survival is seen at 17 monthsrom the time of diagnosis.10 Although renal failure rates haveeclined dramatically over the last 50 years, the best test toonitor renal function has not been experimentally determined.Diseases of the respiratory system are the leading cause of

eath after SCI. Of deaths from respiratory diseases, 72.3% arepecifically due to pneumonia.2 Pneumonia is the leading causef death for each age group and all time periods postinjury ands highest in tetraplegia. Mortality rates because of respiratoryiseases have been increasing in people with SCI. Pulmonaryanagement issues are detailed in the Consortium Guide-

ines.11 Sleep disordered breathing is seen in as many as 60%f people with tetraplegia within 4 weeks of injury.12 Sleeppnea in patients with SCI is as responsive to continuous orilevel positive airway pressure treatment as the general pop-lation.13

Musculoskeletal issues including loss of bone mineral den-
ity (BMD), fractures, and overuse injuries are other important

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S77LONG-TERM MEDICAL ISSUES AND HEALTH MAINTENANCE, Chiodo

econdary conditions. In a study of men with SCI, 61% met theorld Health Organization criteria for osteoporosis, 19.5%ere osteopenic, and 19.5% had normal BMD.14 Fracture afterCI occurred in 34%. Considered simultaneously with age,uration of SCI, and level of SCI, BMD was the only signifi-ant predictor of the number of fractures.14 Ten milligrams oflendronate daily has been shown to have some limited positiveffect on osteoporosis in chronic SCI patients measured byual-energy x-ray absorptiometry,15 but there is no strongvidence for routine use in this population to decrease risk ofracture. Functional electric stimulation cycling applied shortlyfter SCI does not significantly attenuate bone loss.16

.2 Educational Activity: To detail the recommendationsfor health maintenance after SCI for this 20-year-oldman with SCI.

People with SCI require regular and comprehensive healthare throughout their lifetimes. This care includes routineealth monitoring and treatment for non-SCI problems as wells for SCI-specific problems. The altered physiology and thebsence of many typical symptoms for common problems afterCI pose a unique problem for health care providers.The Canadian Task Force on Preventive Health Care and the

.S. Preventive Services Task Force for Periodic Health Ex-minations have provided guidelines for routine screening andreventive health care.17 These guidelines are, for the mostart, appropriate to use as a starting point for people with SCI.very periodic health examination should include the follow-

ng components: current concerns and medications, review ofystems (ROS), social history, medical history, family history,hysical examination, counseling, and a plan for age-appropri-te screening, immunizations, and treatment for problems iden-ified. Areas of focus should also include the unique issues ofCI and aging with a disability.Some of the important aspects to record include screening

or gingivitis, decreased vision, hearing, flexibility, and cogni-ive slowing, as well as a screen for depression and suicide risk.uestions of smoking and counseling for smoking cessation,

lcohol and drug use, exercise, risks for sexually transmittediseases, and current employment status also should be in-luded.

An expanded ROS is needed to address the specific problemsommon in SCI. Questions about bladder and bowel control,lood pressure control, skin integrity, pain, spasticity, sexualunction, equipment needs, and changes in strength, sensation,nd functional ability are important SCI-specific problems toddress. In 1 study,18 subjects with SCI reported that 1 of theost important components of the comprehensive annual phys-

cal examination was the ability to talk to their physician aboutroblems, especially muscle strength and weakness, bladderssues, pain, bowel and digestion problems, and equipmenteeds.In addition to a general physical examination, a skin exam-

nation for abnormal moles and an examination of the oralavity in smokers, ex-smokers, and alcoholics are recom-ended. A digital rectal examination for men over age 50

ears, clinical breast examination for women aged 50 to 69ears, pelvic examination with Papanicolaou smear, gonorrheand chlamydia swab if at high risk, and examination for ovar-an masses are gender-specific, evidence-based recommenda-ions. The general physical examination for people with SCIhould be expanded to include an SCI-specific neurologicxamination to document changes in motor or sensory func-
ion, a skin examination to assess for risk and/or presence of S
ressure ulcers, and a musculoskeletal examination to identifyroblems related to aging with SCI and pain.Counseling for smoking cessation, advice for daily personal

nd annual professional dental care, sun exposure, and safetyssues including use of safety belts, drinking and driving,icycle helmet use, and hearing protection if exposed to loudachinery is recommended. Counseling is recommended for

ifestyle issues including diet and nutrition, physical activity,nd advice against alcohol abuse and prevention of sexuallyransmitted diseases if earlier screening identifies a problem.ounseling regarding wheelchair and other equipment mainte-ance and safety, pressure ulcer prevention, and complianceith the person’s bladder management program are issues that

hould be included for people with SCI.Recommendations for the general periodic health examina-

ions include screening for colon cancer with either fecal occultlood testing or flexible sigmoidoscopy for those over age 50ears and colonoscopy if at high risk. Mammography is rec-mmended for women every 1 to 2 years between ages 50 and9 years. A tuberculosis skin test, human immunodeficiencyirus testing if at high risk, fasting glucose every 3 years forhose over age 40 years or annually for people with risk factorsor type 2 diabetes, screening for nutritional deficiencies withomplete blood count, B12, albumin and iron levels if at risk,asting lipid profile for men over 40 years and for women over0 years, and prostate-specific antigen testing in men betweenges 50 and 70 years or after age 45 years if at increased riskre also recommended. These screening interventions appear toe appropriate for people with SCI who will fall into high-riskategories for many of the diseases being screened, includingiabetes, lipid abnormalities, and osteoporosis. However, fewtudies have formally evaluated these recommendations in theCI population. Routine laboratory screening in a populationf people with chronic SCI resulted in low diagnostic andherapeutic yield (�1.5%) except for serum glucose and lipidests.19 In 1 study20 of 100 non-SCI outpatients, ROS andhysical examination had a higher therapeutic yield than chestadiography, electrocardiography, and routine laboratory tests,xcept for the lipid profile. Further research is needed to definehich screening tests are appropriate for the SCI population.Because people with SCI are at significant risk for renal

omplications, regular screening of the urinary tract is impor-ant. Eighty-five percent of urologists in the United Statesurveyed recommended annual renal ultrasound, and 20% rec-mmended renal scintigraphy as the preferred screening exam-nation for the upper urinary tract. For surveillance of the lowerrinary tract (LUT), 65% used annual video-urodynamics and5% recommended cystoscopy, whereas 35% performed nooutine surveillance and only examined the LUT when patientsad recurrent UTIs or abnormalities were found on renal ul-rasound or scintigraphy.21 However, routine screening withenal ultrasound was found to be cost effective only if used inCI patients with genitourinary symptoms or signs.22,23 Theddition of abdominal radiography did not increase the sensi-ivity or specificity of renal ultrasound for identifying renaltones in people with SCI.24 Creatinine clearance is unreliables a monitor for renal function because of its poor repeatability,rimarily because of the difficulty of obtaining correctly col-ected 24-hour urine specimens.25

Rubella vaccination is recommended for women with noistory of previous immunization who become pregnant. Im-unization for pneumonia and influenza are especially impor-

ant for people with SCI who are considered to be a high-riskopulation.26

Communication among medical providers for a person with
CI is critical to prevent duplication of some services while

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verlooking others. In 1 study,27 93% of people with SCI hadfamily doctor, 63% were followed up by an SCI specialist,

nd 56% were followed up by both. There was significantuplication in general medical and preventive services, al-hough lifestyle and emotional issues were not addressed inore than 75% of the sample.

.3 Educational Activity: To address the health issues fora tetraplegic 30-year-old woman with traumatic SCI.

With the exception of a relatively brief period of amenorrhean the acute and subacute periods after injury, the hypothala-ic–pituitary axis returns to normal. Management of menstru-

tion is a common concern after SCI, because erratic onset isarticularly problematic with an insensate perineum. Althoughomen report lower rates of menstrual cramping after SCI,early 25% report increased spasticity, bladder spasm, andysautonomia during menstruation.28 Advances in hormone-ased contraceptives, particularly those producing quarterlyenstrual periods rather than monthly, may prove helpful.There are no data to suggest a decline in fertility among

omen after SCI. Issues of contraceptive choice, however,emain clouded by insufficient data regarding additional risksn the presence of SCI. Although the risk of oral contraceptive–ssociated thromboembolism increases with age and smokingn nondisabled people, few data exist to determine if chronicaralysis increases risk as well. Concerns that an insensateterus would result in failure to detect problems with an intra-terine device in the early stages have led to little use of thisevice in SCI. Compared with their nondisabled peers, womenith disabilities are more likely to use surgical methods, in-

luding hysterectomy, or a natural method, and are less likelyo use hormonal or barrier methods.29

Pregnancy in women with SCI is generally categorized asigh risk, primarily from a high rate of complications specifico SCI, including UTI, autonomic dysreflexia (AD), and func-ional deficits.30 The SCI physician should work in collabora-ion with the obstetrician to manage these issues. Women withCI may be more likely to have low–birth-weight infants butre no more likely to have a preterm infant or an infant withongenital abnormality.28 They are more likely to have a for-eps delivery or Cesarean section, but no more likely to expe-ience a miscarriage or stillbirth. Surprisingly, despite recom-endations that labor and delivery in women with SCI,

pecifically those prone to AD, be managed with epidural/pinal anesthesia,30 50% of labors among women with SCIere managed without any anesthetic.28

Women with SCI experience menopause at similar ages andith most symptoms similar to women without SCI. As withenstruation, women with SCI report increased spasticity,

ladder spasm, and dysautonomia during menopause. How-ver, women with SCI also report a higher rate of psychologicymptoms and sleep disturbances compared with women with-ut SCI.Physiologic parameters of sexual function in women with

CI have been described in recent years. Libido is generallyreserved after injury.31 Genital vasocongestion creates theubrication and engorgement necessary for intercourse. Preser-ation of psychogenic genital vasocongestion is associatedith the preservation of sensation in the T11-L2 dermatomes.32

eflexogenic vasocongestion can be induced via manual gen-tal stimulation in women with upper motoneuron injuries.pproximately 50% of all women with SCI are able to achievergasm, although time to orgasm is prolonged compared withomen without SCI.33 Functional magnetic resonance imaging

tudies suggest that the vagus nerve, which bypasses the spinal n


ord, carries genital sensory afferents to the brain, mediatinghe orgasm response.34 However, lower motor neuron injuryffecting the S2-5 levels greatly reduces the ability to achievergasm. Sildenafil has been shown to improve subjectiverousal when used with manual stimulation and may improveenital vasocongestion as well.33

There are no data to suggest that women with SCI haveifferent rates of disease affected by estrogen, such as breast orterine cancer. Although rates of screening for these cancersas consistently been shown to be lower among women withisabilities than among nondisabled women,35 more recent datahow less disparity based on disability alone, with differencesccounted for by race and socioeconomic status.36 Heart dis-ase is now the leading cause of death among women with SCIho have survived the first year of injury, as it is with men andomen without SCI.Premenopausal women with SCI do not appear to have any

reater risk of osteoporosis than men with SCI. It is unclear tohat degree women with chronic SCI experience subsequentenopause-related bone loss. One cross-sectional study37 has

uggested that postmenopausal women with SCI have lowerone mass below the level of injury than premenopausalomen with SCI, but there are no longitudinal data to confirm

hese findings. Whether women with osteoporosis who sustainn SCI have further bone loss from immobilization is alsonclear. Little evidence exists to guide treatment of SCI-relatedone loss, regardless of sex or menopausal status, and studiesn the use of bisphosphonates in both acute and chronic SCIre conflicting.15 Although these studies include women, theumbers have been too small to draw conclusions in thisubpopulation.

.4 Clinical Activity: To counsel a 20-year-old man withC4 American Spinal Injury Association grade A SCIon options regarding sexual function and fertility.

As a person assimilates into the community after an injury,ssues relating to his/her sexuality and fertility are crucialomponents to a healthy transformation. For men, SCI signif-cantly impacts erectile and ejaculatory dysfunction. It is re-orted that although 92% of men with SCI are able to achieven erection, only 44% with complete injuries and 56% withncomplete injuries are successful with intercourse and lesshan 5% of men can have an unassisted ejaculation.38

Treatment options for erectile dysfunction (ED) include de-ices, implants, intracavernosal injections, and pharmacologicgents. Vacuum suction draws blood into the erectile tissue andconstrictor ring is placed at the base of the penis. This device

an be used only for less than 30 minutes, and the potential forkin breakdown limits its use. Penile implants can be in theorm of a malleable metal rod or an inflatable implant activatedy a pump implanted into the abdomen or scrotum. The po-ential for penile erosions caused by decreased or absent sen-ation and the high risk of infection make implantable devicesnfavorable, especially with the advancements in pharmaco-ogic options. Phosphodiesterase type 5 inhibitors (sildenafil,adalafil, vardenafil) are now the most commonly used agentso treat ED. These agents enhance the nitrous oxide–mediatedasodilatation of the erectile tissue. Stimulation is required toctivate the erectile response, and these agents are more effi-acious in men who have reflexogenic erections. In reviewingandomized control trials, it is estimated that up to 94% ofubjects with SCI reported their erections were improved withidenafil.39 Side-effect profiles include hypotension, headache,acial flushing, and visual disturbances. Simultaneous use of
itrate-based medications or alpha receptor blockers should be

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voided because of a potentiated hypotensive event. Side-effectrofiles of the phosphodiesterase type 5 inhibitors can closelyimic symptoms of AD (ie, headache, facial flushing). Patients

aking these medications should advise their clinicians andvoid the use of nitrates to treat AD, should pharmacologiceans be necessary. Intracavernosal injections with alprostidil,prostaglandin derivative, are an effective means to treat ED

fter SCI. Injections can cause priapism and are not routinelyecommended to use more than 3 times a week to preventenile fibrosis. An intraurethral form of the prostaglandin didot prove to be effective. ED treatments have little effect onne’s ability to have an ejaculation.Newer technologies and advances in fertility care now make

t increasingly possible for men with SCI to father children,ith success rates as high as 40%.40 Barriers to fatherhood

nclude anejaculation, poor semen quality, and the need forssistive reproductive technologies to achieve a pregnancy.hus, interventions directed by urologists and reproductivendocrinologists must be used. Penile vibratory stimulation hasong been known to produce ejaculation and is the first line ofreatment if a person is unable to ejaculate on his own. Theibrator is held over the frenulum of the penis until ejaculationccurs. Recent research shows that parameters of 2.5mm am-litude and frequency of 100Hz are optimal.41 For injuries at10 and above, intact bulbocavernosus reflex and a tripleexion response to plantar stimulation are good prognosticactors for success with this stimulation method. If unsuccess-ul, electroejaculation can be attempted. Rectal probes willirectly stimulate deep pelvic nerves to stimulate ejaculation.or men with intact sensation, and those with injuries at T6 andbove susceptible to AD, this procedure must be performed inmonitored setting. Electroejaculation is generally more reli-

ble, with success rates of 80% to 90%. As a last resort, directesticular extraction of sperm can be performed.

Poor sperm quality is a routine finding in men with SCI.perm counts may be normal, but their quality and motility cane poor. The precise etiology of the abnormal semen charac-eristics is not known and likely multifactorial. Time sincenjury has not been shown to influence sperm quality. As aesult, assistive reproductive technologies are generally re-uired to achieve pregnancy. The simplest is intrauterine in-emination, a direct injection of a sperm into the uterus. Aome technique can also be performed with the semen beingirectly inserted into the vagina with a syringe. In-vitro fertil-zation (IVF) requires the use of fertility drugs and invasiverocedures to obtain eggs that will be fertilized outside theomb and reimplanted into the uterus 48 to 72 hours later.

ntracytoplasmic sperm injection (ICSI) requires only a fewealthy motile sperm that are directly injected into an eggnder microscopic guidance for fertilization and are then re-mplanted as with IVF. Given the poor semen quality in menith SCI, ICSI has greatly improved the chances of a couple

chieving pregnancy.42 The cost of these technologies is ex-ensive.

.5 Clinical Activity: To assess a 20-year-old tetraplegicman who presents with diffuse pain.

Subjective pain in the SCI population varies from 64% to0%. Forty-seven percent of SCI patients reported onset ofhronic pain within the first year after their SCI.43 Chronic painffects mood, function, and quality of life. Most patients areypically dissatisfied with current treatment efforts, and at least9% in 1 study and 39% in another study reported experiencing
evere pain.44 Pain severity is associated with completeness of a
njury, depression, and unemployment and is not associatedith level of injury.45

Two common classifications for pain are currently used inCI. The International Association for the Study of PainIASP) taxonomy has 3 tiers based on pain type. The Bryce andagnarsson Classification46 (table 1) is similar to the IASP butas a greater number of pain categories, which are based onocation and etiology.

Nociceptive pain is caused by injury at a specific site, withhe nerve activation occurring at the site of injury at local nervendings. Visceral pain is not well defined but arises fromamage to, or irritation or distention of, internal organs (ie,owel, bladder) or supporting ligaments. It is reported in 15%f patients with chronic SCI, with 38% characterizing it asevere. In contrast, neuropathic pain is caused by injury of aerve; that is, pain at the level of the injured spinal cord, at theerve root, or at the site of a local nerve injury (eg, carpalunnel syndrome). Sympathetic pain is a type of neuropathicain caused by activation of the autonomic nervous system inesponse to a noxious stimulus.

Neuropathic pain is reported below the level of injury in9% to 24% of patients with SCI, with 27% of them rating its severe. At the level of injury, 11% to 36% of SCI patientsad neuropathic pain, with 39% reporting the pain as severe.43

europathic pain is more common in patients older than 40ears and in patients whose injuries are motor and sensoryomplete.47 Neuropathic pain is more commonly seen in pa-ients injured by gunshot wounds. Studies point to neuropathicain as being the most difficult to treat; this is especially truef neuropathic pain at or below the level of injury.48

Approximately 42% of SCI patients reported musculoskel-tal pain, with 22% rating it as severe. Upper-extremity painfter SCI is most likely associated with repetitive overuseuring transfers, pressure relief, and wheelchair mobility; 65%f the time, it interferes with a patient’s ability to transfer.49

he most common upper-extremity pain problems occur in thehoulders (75%), wrists (53%), hands (43%), and elbows35%). Shoulder pain is associated with time since injury,imitations in shoulder range of motion, lower overall health,

Table 1: The Bryce and Ragnarsson SCI PainClassification System

Location Type Etiologic Subtype

Above levelNociceptive 1 Mechanical/musculoskeletal

2 AD headache3 Other

Neuropathic 4 Compressive neuropathy5 Other

At levelNociceptive 6 Mechanical/musculoskeletal

7 VisceralNeuropathic 8 Central

9 Radicular10 Compressive neuropathy11 Complex regional pain syndrome

Below levelNociceptive 12 Mechanical/musculoskeletal

13 VisceralNeuropathic 14 General

15 Other

OTE. From Bryce and Ragnarsson.46 Reprinted with permission.

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icular joint narrowing, rotator cuff muscle imbalances, anddductor weakness in the general and elite athlete SCI popu-ations. It is suspected that imbalances lead to glenohumeralotion abnormalities that trigger impingement, inflammation,

nd pain. Anterior muscular tightness with posterior musculareakness is also a common association.The diagnostic investigation of pain in SCI must be specific

o the symptoms being evaluated. A thorough history, physicalxamination, radiologic studies, and electrodiagnostic evalua-ion may help delineate the exact diagnosis. Identifying thetiology of the pain is crucial to determining appropriate treat-ent.Treatment of neuropathic pain in SCI can be complex and

hould have a multifaceted approach. This approach includeshe use of modalities, medications, psychotherapy, and surgicalnterventions. The clinical use of anticonvulsants, antidepres-ants, antispasticity, and other adjunct medications is common,ith some benefit shown in the SCI population. Althoughpioids were historically rated as an effective treatment, moreecent studies show that they have little effect on neuropathicain and are associated with decreased leisure activity andncreased affective complaints.52 Surgical procedures includepinal cord stimulators, intrathecal medications, and the dorsaloot entry zone procedure with intramedullary electric guid-nce.

Treatment of musculoskeletal shoulder pain includes shoul-er stretching and strengthening, which specifically improvesuscle balance, biomechanics, and endurance training. These

ctivities are associated with a decrease in the severity andrequency of shoulder pain and improvement in function.53

ocal injections and systemic medications such as nonsteroidalnti-inflammatories and opiates are used. Activity restriction isecommended but may be difficult because of functional needs.

any already limit their activities because of pain, which hassignificant impact on functional skills and independence.

.6 Educational Activity: To discuss the current researchn interventions for neurologic recovery in SCI for a 30-ear-old tetraplegic woman after traumatic SCI.Numerous changes occur within the spinal cord after initial

njury that hinder return of function. Many of these changesave been elucidated in this last decade. According to recentndings, potential treatments fall into 1 or more of 5 catego-ies54: (1) protection, to prevent death of neuronal cells un-amaged by the initial injury; (2) stimulating axonal growth, tonhance the intrinsic regenerative capacity of spinal and su-raspinal neurons or to block or remove endogenous inhibitors;3) bridging, to provide a permissive substrate for elongatingxons and replacing lost tissue; (4) enhancing axonal trans-ission, to alleviate conduction block in spared or regenerated

xons; and (5) rehabilitation, to enhance functional plasticityn surviving tissue or to promote repair.

Many animal studies have focused on these experimentalspects of treatment. Appendix 3 lists some of the areas ofesearch in each of the categories of treatment after SCI. Theext below summarizes recently completed trials, current orngoing trials, or trials planned for human clinical investiga-ion in the near future.

EXPERIMENTAL TREATMENTS

rotectionMethylprednisolone was previously discussed in Activity

.1.55 Although the initial report of the second National Acute
pinal Cord Injury Study indicated no beneficial effects of c

aloxone, a subsequent report found that patients with incom-lete lesions treated with naloxone within 8 hours had signif-cantly greater recovery than patients treated with placebo.56

n initial small study treating patients with monosialoganglio-ide (Sygen) within 48 hours of injury for an average of 26ays found greater mean recovery at 1 year, including somemproved recovery in muscles that had no strength at entry ofhe study.57 A subsequent large multicenter study reported arend toward improvement in neurologic recovery in peopleith American Spinal Injury Association (ASIA) grade B at 26eeks after being treated for 8 weeks, as well as a significant

ffect in people who received Sygen who did not have surgery.o significant effect was noted at the principle endpoint of 26eeks in the total group of patients studied.58

Improving perfusion to the cord in the acute phase afternjury includes the use of a lumbar drain to decrease intraspinalesistance to perfusion, elevation of mean arterial pressure, andalcium channel blockers. Calcium channel blockers decreaseasospasm and improve blood flow with improved axonalunction; however, they also cause systemic hypotension thatay compound the ischemic deficit. In animal models, mino-

ycline, a semisynthetic tetracycline antibiotic, showed im-roved hindlimb function and strength59; human trials mayegin soon.The ProCord (Activated Macrophage) study60 was an inter-

ational multicenter trial for people with an acute, neurologi-ally complete SCI. Macrophages isolated from the patient’slood were activated through a process proprietary to Proneu-on and then injected directly into the patient’s injured spinalord by day 14 after injury. In a phase 1 trial initiated in 2000,greater number of a small group of those subjects improved

rom neurologically complete to incomplete status by 1 year.60

n the phase 2 trial, subjects with a neurologically completeCI between C5 and T11 were randomized in a 2:1 ratio of

reatment to control subjects. Control subjects did not receivehe procedure, but all subjects received standard SCI rehabili-ation and follow-up testing for 1 year. After two thirds of theubjects were recruited, the trial was halted because of financialonstraints.

timulating Axonal GrowthA phase 1 clinical trial61 was performed on 10 subjects with

eurologically complete injury (AISA Impairment Scale [AIS]rade A) between the levels of C5 and T10, using oscillatingeld electric stimulation (OFS). The OFS device was im-lanted within 18 days of the injury and was removed at 15eeks. At 1 year, the degree of pain as measured by the visual

nalog scale pain score was decreased, with improvementoted in light touch and pinprick sensation as well as someuscle strength improvement. The FDA has given permission

o extend the study.Cethrin (BA-210), a Rho pathway antagonist that may pro-ote neuroregeneration and neuroprotection in the central ner-

ous system, is currently in clinical trial.62 Cethrin is applied tohe surface of the dura mater of the spinal cord together withissel, a fibrin sealant normally used to repair small dural tears,ithin 7 days of injury. The study is being performed in centers

n the United States and Canada for people with a neurologi-ally complete SCI.

ridgingPeripheral nerves have been implanted at the site of the

njury with mixed results.63 Olfactory ensheathing glial (OEG)ell grafting in humans is being performed in a number of
enters around the world. Preliminary results of a study64

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nvestigating OEG in Australia were published, with no reportsf neurologic improvement at 1 year in 3 subjects but withoutny noted adverse events. Lima reported on the first 7 patientsho underwent autologous OEG transplantation at the site of

he lesion. These patients with neurologically complete injuriesad some sensory and motor function recovery.65,66 Results ofetal stem cell implants in China were published (not a con-rolled study),67 with reports of almost immediate and dramaticmprovement in some cases. Clinical follow-up was limitednd the results have been questioned.68

nhancing Axonal TransmissionPreliminary work with 4-aminopyridine (Fampridine), a po-

assium (K�) channel blocker, in subjects with chronic incom-lete SCI (phase 1 and 2 studies) showed trends toward im-rovement in pain and spasticity. Phase 3 multicenter trialsere completed and did not show significant results, although

here were improvements in multiple sclerosis (MS) trials andurther study is currently underway in MS subjects.69

A phase 2 trial has been completed using HP-184, a K� andodium channel blocker, although data have not yet beenublished. The phase 1 trial in 48 subjects with chronic incom-lete SCI resulted in increased motor index scores.70 The phasetrial has recruited 240 subjects with chronic incomplete SCI

AIS grades C and D), with injury levels C4-T10. Outcomeeasures include changes in motor index score and gait.A number of the above-mentioned surgical procedures may

nhance axonal regeneration as well as serve as a bridge forxonal recovery. Some of the animal work listed in Appendix

has shown promise, and human-based studies are beinglanned.

ehabilitationNew rehabilitation techniques and research are covered in

ducational Activity 3.5.Research to discover therapies for SCI has made steady

rogress, and a number of clinical trials are being proposed forubjects with SCI. Recommended guidelines have been pro-osed for the planning, initiation, and conduct of these trials.71

hese guidelines include the following: the proposed clinicalrial should be based on supportive preclinical animal efficacyata that would be considered predictive of lasting clinicalenefits; there should be a high benefit-to-risk ratio, especiallyith invasive studies; outcome measures should be objective

nd should include safety, pain issues, and maintenance ofunction both above and below the lesion; and placebo controlroups should be included when possible.Great excitement exists in the field of SCI medicine over

esearch that has moved from the laboratory to human clinicalrials. Despite the excitement with respect to cure and theptimism regarding the development of therapies, at present noharmacologic, surgical, or rehabilitative therapy exists thatan cure all of the impairments caused by the injury. Mostikely, a combination of the treatments discussed above will beequired to address the complex issues of SCI. Further study isequired, not only to find treatments to enhance neurologic andunctional recovery but also to decrease medical complicationsnd optimize the quality of life of people with SCI.

APPENDIX 1: WOUND CARE MANAGEMENTISSUES IN SCI

. Prevention considerationsa. Inspectionb. Pressure relief
c. Seating and positioning (including pressure mapping) p
APPENDIX 1: WOUND CARE MANAGEMENTISSUES IN SCI (cont’d)

d. Cushion and support surface prescriptione. Psychologic and social factors

. Correction of underlying factorsa. Nutritionb. Incontinencec. Spasms and contracturesd. Smokinge. Heterotopic ossificationf. Wound infectiong. Bowel and bladder management

. Débridement optionsa. Autolyticb. Enzymaticc. Mechanicald. Sharpe. Surgical

. Wound carea. Moist dressingsb. Débridementc. Infection controld. Vacuum-assisted closure systeme. Growth factorsf. Impact of caregiver time

APPENDIX 2: BLADDER MANAGEMENT IN SCIPharmacologic interventions

Anticholinergic medications�-blockersBotulinum toxin

Intermittent catheterizationCredé and Valsalva maneuversIndwelling catheterizationReflex voidingUrethral stentsTransurethral sphincterotomyElectric stimulation and posterior sacral rhizotomyBladder augmentationContinent urinary diversionCutaneous ileovesicostomy

APPENDIX 3: RESEARCH CATEGORIES IN THETREATMENT OF SCI

Protection against SCIPreviously studied methods

Methylprednisolone, naloxone, calcium channel blockers,M-1Present and future studies

Minocycline, erythropoetin, riluzole, sulfonylureas, hy-erdynamic therapy, and cerebral spinal fluid drainageStimulating axonal growth

Electric stimulation (oscillating field stimulator), Nogo-locking antibody, myelin associated glycoprotein, oligoden-rocyte myelin glycoprotein, Rho inhibitors (eg, Cethrin), ac-ivated macrophages, chondroitin sulfate proteoglycans,nosine, heparan sulfate proteoglycans, keratan sulfate proteo-lycans, nerve growth factors, estrogen, and serotonin selectiveeuptake inhibitors

BridgingPeripheral nerve grafts, Schwann cells, olfactory en-

heathing glial cells, and nanotubesEnhancing axonal transmission

Schwann cells, olfactory ensheathing glial cells, 4-amino-
yridine, HP-184, neuroprogenitor cell transplants (stem cells)


A

APPENDIX 3: RESEARCH CATEGORIES IN THETREATMENT OF SCI (cont’d)

RehabilitationElectric stimulation, weight-supported ambulation

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29. Nosek MA, Wuermser L, Walter LJ. Difference in contraceptivemethods used by women with physical disabilities compared towomen without disabilities. Prim Care Update Ob Gyns 1998;5:172-3.

30. ACOG Committee Opinion: Number 275, September 2002. Ob-stetric management of patients with spinal cord injuries. ObstetGynecol 2002;100:625-7.

31. Matzarogluo C, Assimakopoulos K, Panagiotopoulos E, Kasima-tis G, Dimakopoulos P, Lambiris E. Sexual function in femaleswith severe cervical spinal cord injuries: a controlled study withthe Female Sexual Function Index. Int J Rehabil Res 2005;28:375-7.

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51. Dyson-Hudson TA, Kirshblum SC. Shoulder pain in chronicspinal cord injury, part I: epidemiology, etiology, and pathome-chanics. J Spinal Cord Med 2004;27:4-17.

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57. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor func-tion after spinal cord injury: a randomized, placebo controlledtrial with GM-1 ganglioside [published erratum in: N Engl J Med1991;325:1659-60]. N Engl J Med 1991;324:1829-38.

58. Fehlings MG, Bracken MB. Summary statement: the Sygen(GM-1 ganglioside) clinical trial in acute spinal cord injury.Spine 2001;26(24 Suppl):S99-100.

59. Lee SM, Yune TY, Kim SJ, et al. Minocycline reduces cell deathand improves functional recovery after traumatic spinal cordinjury in the rat. J Neurotrauma 2003;20:1017-27.

60. Knoller N, Auerbach G, Fulga V, et al. Clinical experience usingincubated autologous macrophages as a treatment for completespinal cord injury: phase I study results. J Neurosurg Spine2005;3:173-81.

61. Shapiro S, Borgens R, Pascuzzi R, et al. Oscillating field stim-ulation for complete spinal cord injury in humans: a phase 1 trial.J Neurosurg Spine 2005;2:3-10.

62. McKerracher L, Higuchi H. Targeting Rho to stimulate repairafter spinal cord injury. J Neurotrauma 2006;23:309-17.

63. Tadie M, Liu S, Robert R, et al. Partial return of motor functionin paralyzed legs after surgical bypass of the lesion site by nerveautografts three years after spinal cord injury. J Neurotrauma2002;19:909-16.

64. Feron F, Perry C, Cochrane J. Autologous olfactory ensheathingcell transplantation in human spinal cord injury. Brain 2005;128:2951-60.

65. Lima C, Pratas-Vital J, Escada P, Hasse-Ferreira A, Capucho C,Peduzzi JD. Olfactory mucosa autografts in human spinal cordinjury: a pilot trial. J Spinal Cord Med 2006;29:191-203; discus-sion 204-6.

66. Kirshblum S. “A start”. Olfactory mucosa autografts in humanspinal cord injury. J Spinal Cord Med 2006;29:204-6.

67. Huang H, Wang H, Chen L, et al. Influence of patients’ age onfunctional recovery after transplantation of olfactory ensheathingcells into injured spinal cord injury. Chin Med J 2003;116:1488-91.

68. Dobkin BH, Curt A, Guest J. Cellular transplants in China:observational study from the largest human experiment inchronic spinal cord injury. Neurorehabil Neural Repair 2006;20:5-13.

69. Schwid SR, Petrie MD, McDermott MP, Tierney DS, MasonDH, Goodman AD. Quantitative assessment of sustained-release4-aminopyridine for symptomatic treatment of multiple sclerosis.Neurology 1997;48:817-21.

70. Gorman P, Mody V, Jariwala N, et al. Safety and tolerability ofHP 184, an oral sodium and potassium channel blocker, inchronic incomplete SCI: a phase II study. Am J Phys MedRehabil 2005;84:167-76; quiz, 177-9, 198.

71. Anderson DK, Beattie M, Blesch A, et al. Editorial. Recom-mended guidelines for studies of human subjects with spinal cord
injury. Spinal Cord 2005;43:453-8.

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pinal Cord Injury Medicine. 6. Economic and Societal Issuesn Spinal Cord Injury

ichael M. Priebe, MD, Anthony E. Chiodo, MD, William M. Scelza, MD, Steven C. Kirshblum, MD,
isa-Ann Wuermser, MD, Chester H. Ho, MD
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ABSTRACT. Priebe MM, Chiodo AE, Scelza WM, Kirsh-lum SC, Wuermser LA, Ho CH. Spinal cord injury medicine.. Economic and societal issues in spinal cord injury. Archhys Med Rehabil 2007;88(3 Suppl 1):S84-8.

This self-directed learning module presents a variety ofocial and economic issues facing people with spinal cordnjury (SCI). It is part of the study guide on SCI medicine in theelf-Directed Physiatric Education Program for practitionersnd trainees in physical medicine and rehabilitation. This arti-le focuses on the economic consequences of SCI, ethicalssues in SCI, and the legislative efforts that have improvedccess and quality of life for people with disabilities. Costs ofCI include direct health care expenditures and lost earnings asresult of unemployment after SCI. Lifelong costs can be

nticipated with the development of a comprehensive life carelan. Barriers to vocational reintegration continue to limit fullarticipation for most people with SCI. Ethical issues central toCI are related to the principles of autonomy and justice. Asure research becomes clinically applicable, the SCI commu-ity must work together to develop appropriate procedures toespect moral decision-making by all parties. Key legislation inhe past century has resulted in important advances in the rightsf people with disabilities.Overall Article Objectives: (a) To review the economic

onsequences of spinal cord injury, including lifelong directosts, life care planning, and factors affecting employment andb) to identify current ethical issues facing the spinal cordnjury community and review the advances made in the rightsf people with disabilities in the United States throughegislation.

Key Words: Economics; Ethics; Legislation; Rehabilitation;pinal cord injuries.© 2007 by the American Academy of Physical Medicine and

ehabilitation

From the Department of Physical Medicine and Rehabilitation, Mayo Clinic,ochester, MN (Priebe, Wuermser); Department of Physical Medicine and Rehabil-

tation, University of Michigan Hospital, Ann Arbor, MI (Chiodo); Department ofhysical Medicine and Rehabilitation, Carolinas Rehabilitation, Charlotte, NCScelza); Spinal Cord Injury Services, Kessler Institute for Rehabilitation, Westrange, NJ (Kirshblum); Department of Physical Medicine and Rehabilitation, Uni-ersity of Medicine and Dentistry–New Jersey Medical School, Newark, NJ, (Kirsh-lum); and Louis Stokes Cleveland Department of Veterans Affairs Medical Centernd Department of Physical Medicine and Rehabilitation, Case Western Reserveniversity, Cleveland, OH (Ho).No commercial party having a direct financial interest in the results of the research

upporting this article has or will confer a benefit upon the author(s) or upon anyrganization with which the author(s) is/are associated.Correspondence to Michael M. Priebe, MD, Dept of PM&R, Mayo Clinic, 200 First

t SW, Rochester, MN 55905, e-mail: [email protected]. Reprints are notvailable from the author.

j0003-9993/07/8803S-11414$32.00/0doi:10.1016/j.apmr.2006.12.005


.1 Educational Activity: To predict the life-long eco-nomic costs of a 22-year-old man with complete tet-raplegia after a traumatic spinal cord injury.

PINAL CORD INJURY (SCI) is expensive. Significantcosts are incurred throughout the life of a person with

CI, including initial hospitalization and acute rehabilita-ion, home and vehicle modifications, and recurring costs forurable medical equipment, medications, supplies, and per-onal assistance.

The average hospital charges for initial hospitalization andehabilitation were reported to be $282,245 in 2003, the mostecent year the Model Spinal Cord Injury System (MSCIS) hasomplete data for analysis of hospital charges.1 Mean length oftay in acute care and rehabilitation has been relatively stable forhe past decade at approximately 18 days and 45 days, respec-ively.1,2 The level and extent of injury are important factorsontributing to first-year costs. People with high tetraplegia in-urred over 3 times the charges that people with incomplete,otor functional SCI incurred.3 The estimated first-year and an-

ual recurring costs for medical care, medications, supplies, du-able medical equipment, and personal assistance, as well asstimated lifetime costs adjusted for age at injury, are shown inable 1.

Home and vehicle modifications can be expensive and aremportant for community reintegration. However, they are notonsistently included in the estimated expenses of people withCI. Home modifications averaged $21,000 (in 1996 dollars)or people with SCI who required them.2 The most commonodifications were building ramps (83%), widening doors

57%), and remodeling bathrooms (46%) or other rooms in theouse (43%). Because over 88% of people with acute SCI areischarged to home,3 housing accessibility is vital to successfulischarge planning and social reintegration. Vehicle modifica-ion costs—whether to allow the person with SCI to drive or forransportation with an attendant driving—range greatly, fromess than $1000 to over $65,000. Costs depend on the modifi-ations needed and the type of vehicle being modified; mini-ans are the most expensive to modify and cars least expen-ive.2

One study found that for people who required assistanceith activities of daily living (ADLs), the average estimated

nnual costs for attendant care exceeded $21,000 (in 1996ollars). Approximately 61% of this was paid assistance, withhe remainder provided by family members or others withoutirect payment.2

In addition to the direct costs described above, there is theoss of wages, fringe benefits, and productivity related to un-mployment or underemployment after SCI. These costs arestimated to be more than $57,000 annually but vary widelyepending on education, severity of injury, and type of prein-
ury employment.3

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S85ECONOMIC AND SOCIETAL ISSUES IN SPINAL CORD INJURY, Priebe

.2 Clinical Activity: To analyze the components of a lifecare plan for a 54-year-old man with T6 paraplegia.

A life care plan is a comprehensive interdisciplinary docu-ent that delineates the future medical and rehabilitative needs

f the person who has sustained a catastrophic injury or illness.t is an extension of the rehabilitation process and has evolvednto a valuable tool for rehabilitation planning and long-termanagement.4-7

The life care plan should not be undertaken until the patientith SCI has stabilized medically and functionally. Compo-ents of the life care plan (appendix 1) are the medical problemist (eg, bowel and bladder functions, skin integrity, spasticity);sychologic, vocational, recreational, and social issues; reha-ilitative goals (eg, for mobility, ADLs); prognosis for im-rovement; and the short- and long-term equipment needs andources for them (ie, equipment, therapy, architectural, homeare). Complications of the aging process are estimated; pre-entive measures are recommended to minimize complicationsnd maximize functional independence, with the goal being toeduce complications and hospitalizations. Last, the projectedosts of needed equipment and services over the person’sstimated life span is estimated.4,5

The life care plan is based on patient need rather than onnancial situation or insurance benefit. If a life care planner isompleting the document, the SCI physician should be in-olved to offer the medical and rehabilitative needs and thereventive measures required. The costs cited should representhe ranges of the local market rate where the patient resides andstimated inflation.

Problems with life care planning include unexpected com-lications and the cost of new technology not available at theime of the initial life care planning. These cannot be reliablyalculated in the final cost analyses, and all parties should benformed of the potential for these. Recommendations of costsre determined on recommendations based on a reasonableegree of medical necessity and probability.The life care plan often serves as an educational tool on

hich patients and families may rely to make informed deci-ions, anticipate changes throughout the life span of the patient,nd plan for future care. By defining a patient’s long-termeeds, identifying costs of care and rehabilitation, and decreas-ng complications by recommending proactive preventive in-erventions, a life care plan can enhance the quality of lifeQOL) of a person with SCI.5

.3 Educational Activity: To describe the determinants ofreturn to work for this 54-year-old man with T6paraplegia after SCI.

Overall rates of employment for people after SCI range from3% to 58%.8,9 Berkowitz et al2 reported that although 44% ofheir sample had been employed at some time since their injury

Table 1: Expenses Related to SCI

Severity of Injury

Average Year

First Year

High tetraplegia (C1–4) 741,425Low tetraplegia (C5–8) 478,782Paraplegia 270,913Incomplete motor functional at any level 218,504

OTE. Values in dollars. Data from the National Spinal Cord Injury

nly 27% were employed at the time of the survey. The MSCIS d

ata indicate that in the first year after injury only 14% returno work; by year 10, 27% are working, and by 20 years afternjury nearly 40% are employed.1 Berkowitz2 reported a ratheroncerning finding: 66% of people with SCI have stoppedorking and/or are no longer looking for work. Because they

re “out of the labor force,” these people are not counted inational unemployment statistics. The most common reason foro longer looking for a job was being “physically unable”64%), followed by “retired” (13%), and “in school” (8.5%).2

Whether a person returns to work after SCI is greatly influ-nced by that person’s educational level. Although this is trueor the general public, it is especially important for the SCIopulation. The more education a person has at the time ofnjury, the more likely it is that he/she will return to work. Over4% of people with a bachelor’s degree and 77% of those withmaster’s degree have been employed after SCI, whereas only4% of people with a high school diploma and 9% of thoseho did not graduate from high school were employed.2

The rates of employment also depend on functional status.eople with paraplegia are employed more frequently (32.8%)

han those with tetraplegia (24.7%).1 More specifically, thoseeople who require assistance with ADLs are less than half asikely (18.2% employed) to return to work than those who doot require ADL assistance (42% employed).2 The presence ofvehicle modified to allow the person with SCI to drive

orrelated highly with employment after SCI. The employmentate for people who could drive and had a vehicle adapted forndependent driving was 40%, compared with 12% for thoseho did not.2 Another study reported similar findings—thoseho could use transportation independently and had a higher

evel of functional independence were more likely to be em-loyed after injury.8

Being employed at the time of injury is not consistently aignificant factor predicting return to work. However, beingmployed in a white-collar job before injury increased aerson’s likelihood of postinjury employment. Possiblyore important was the finding that those who had computer

xperience in their preinjury jobs increased the likelihood ofostinjury employment by nearly the same degree. Of peo-le with SCI who are employed, 67% use a computer atork compared with 47% in the general population.2 Before

njury, two thirds of the people with SCI were working inlue-collar jobs. However, of those who had returned toork since injury, 86% were working in white-collar jobs,

specially managerial, administrative support, and profes-ional positions. There was also an interesting shift awayrom private sector jobs to not-for-profit or government jobsnd to self-employment.2

The above findings were replicated in a study of adults withCI who were injured before the age of 18 years, 51% of whomere employed. Four factors were found to predict employ-ent—education, community mobility, functional indepen-

verity of Injury and Age at Injury

enses (in May 2006lars)

Estimated Lifetime Costs by Age atInjury (discounted at 2%)

ach Subsequent Year 25 Years Old 50 Years Old

132,807 2,924,513 1,721,67754,400 1,653,607 1,047,18927,568 977,142 666,47315,313 651,827 472,392

tical Center.3 Reprinted with permission.

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S86 ECONOMIC AND SOCIETAL ISSUES IN SPINAL CORD INJURY, Priebe

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mize a person’s likelihood of returning to work after SCI,btaining a college degree; maximizing functional indepen-ence (including learning to use a computer for work pur-oses); optimizing access to community transportation, whichay include having access to a vehicle adapted for independent

riving; and maintaining a higher level of health appear to bemportant factors.

.4 Clinical Activity: To educate your 22-year-old patientwith complete tetraplegia regarding basic principlesof medical ethics, in an effort to encourage an optimalself-direction during his lifespan.

In the United States, 4 principles are considered fundamentalo biomedical ethics: autonomy, benevolence, nonmalevolence,nd justice. The principle of autonomy has evolved in the lastew decades, in particular, and has coincided with the advance-ent of the independent living movement, such that autonomy

f people with disabilities is sometimes used an example ofounteracting paternalism. Advocates of patient autonomy sup-ort a model of joint decision-making, with health care pro-iders educating patients and then assisting them in makingreatment decisions based on their own preferences andeeds.11 This approach is ideal in SCI, where education is aital part of patient care and patients seek information fromany sources, including peers, the Internet, and consumer

roups.A more complex aspect of autonomous decision-making

egards life-sustaining treatment. Although patients and/oramily members are the primary decision makers, health carerofessionals frame the discussion based on their own biasesegarding QOL. According to Kohari, “It is difficult to imaginehealthcare professional providing hope to patients and fam-

lies when the professional actually believes the quality of lifefter such an injury is poor.”12(p306) Unfortunately, there is aast discrepancy between perceived and actual QOL of peopleith SCI. In 1 study, most emergency care providers presumed

hat people with SCI have a poor QOL, with only 18% pre-icting that a person with tetraplegia would be “glad to belive,” compared with an actual rate of 92%.13 This study alsoeported that 41% of emergency care providers thought thatesuscitation after SCI was too aggressive, and 22% wouldant no treatment whatsoever if they sustained an SCI them-

elves.13 Bringing information about actual QOL among thoseith SCI to the treatment discussions in acute care is a key rolef SCI professionals.Advance directives are also flawed. For example, although

hese documents and the discussions that accompany themoutinely include prolonged mechanical ventilation, rarely haveamilies considered chronic ambulatory ventilation or nonin-asive ventilatory support. The use of a proxy decision maker,r health care power of attorney, permits exploration of situa-ions that are not covered by an advance directive. However, inypothetic situations, surrogate decision makers and patientsnly agree about 70% of the time, even when the surrogate ispecifically instructed to answer according to what the patientould say, not what the surrogate thinks is “best.”14 Uncer-

ainty about potential for recovery reduces accuracy.“Optimizing informed consent” has been advocated in cases

f requests for withdrawal of care after SCI. In this paradigm,uch a request is not honored until the patient has had anpportunity to fully understand the potential for life with dis-bility.15 Depression remains a concerning factor in requests toerminate treatment.

In chronic SCI, the use of advance directives is low. Al-
hough only 8% of people with SCI had completed an advance r

irective in 1 survey, most were interested in doing so afteraving learned about them.16 Contrary to those advance direc-ives executed before SCI, those initialized after SCI are basedn a more realistic understanding of life with SCI and futureeeds. SCI professionals play an important role in initiatingiscussions of advance directives and designation of healthare power of attorney and in assisting in discussions regardingptions.An increasing area of moral concern for rehabilitation pro-

iders is resource utilization, embedded within the ethicalrinciple of justice. Payers frequently deny expensive assistiveechnology and skilled caregiver needs. SCI, in particular, as aow-incidence event, lacks influence on insurance plan devel-pment. The absence of evidence to prove the utility of manyustomary interventions adds to the difficulty of obtainingoverage for services. Private payers also assume that mosteople with SCI will not return to work and so will move to theublic system in the first years after injury. Arguments ofong-term cost effectiveness and prevention therefore fail.anja17 reminds us that insurance plans are contracts, so thatenial of a noncovered item is not unethical at an individualevel. At a broader level, however, consumer groups and reha-ilitation professionals should advocate parity in care for dis-bility-related needs, including equipment and rehabilitationervices.

Advances in neuroprotective and neuroregenerative inter-entions will also raise moral dilemmas for the SCI physician.ews coverage of amazing benefits in animal models raisesope among those with SCI and their loved ones. Although theuture does hold promise, the press rarely comments on theany years and studies needed to determine if humans would

enefit as well. People with disability have historically beenalled the “incurable.” That people with SCI are so desperate tond a “cure” has created an environment suggesting tolerancef significant risk for unclear benefit. To combat this, theommunity of SCI researchers has to set standards for conduct-ng clinical trials in SCI, including ethical standards. These areiscussed in greater detail in activity 5.6.18

Embryonic stem cell transplants for SCI are on the horizon.pproaching patients, particularly in the very early period after

njury, will be delicate. Some health care providers may them-elves be reluctant to participate in such trials on moralrounds. The SCI community must work together to developppropriate procedures to respect moral decision-making by allarties.

.5 Clinical Activity: To educate your 22-year-old patientwith tetraplegia by describing key legislation that hasadvanced rights of people with SCI.

The 20th century saw many important advances in the rightsf people with disabilities, including those with SCI. Theoldier’s Rehabilitation Act of 1918 established federallyunded vocational rehabilitation services for veterans. This wasxpanded in 1920 to include civilians, with block grants totates to establish services, but the Act was not made a perma-ent program until the Social Security Act of 1935. Medicalervices and income replacement were added to serve the needsf disabled veterans of World War II. The enormous expansionf vocational rehabilitation over these 2 decades supporteddvances in the emerging field of rehabilitation medicine, withncreasing professionalism and legitimacy as an academic dis-ipline. Unfortunately, people with disabilities themselvesere not among the vocational professionals, and the commu-ities of people with disabilities became alienated. In an envi-
onment of civil rights struggles and social activism, the Inde-

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S87ECONOMIC AND SOCIETAL ISSUES IN SPINAL CORD INJURY, Priebe

endent Living Movement was born. Centers for independentiving (CIL) began as the Physically Disabled Students Pro-ram, which was established by a group of disabled students athe University of California–Berkeley in the early 1960s tomprove accessibility on campus. These former students for-ally incorporated as the CIL in 1972, with a goal of creating

ommunities accessible to all people. Later that year, Congressassed the Rehabilitation Act, only to be vetoed by Presidentichard Nixon. It was reintroduced in 1973 and again vetoed,ut nationwide protests and letter-writing campaigns garnerednough support to override the veto, and the bill became law.he Rehabilitation Act guaranteed the civil rights of peopleith disabilities within federal programs and also established

he concept that the person with a disability was a “consumer”ather than a patient or client. In 1975, the Education of Allandicapped Children Act (now called the Individuals withisabilities Education Act) was passed, establishing public

ducation for children with disabilities in the least restrictivenvironment possible.

By 1990, an entire generation had grown up seeing peopleith disabilities as peers in their own classrooms and membersf their communities in public places. The civil rights move-ent of the sixties and seventies laid the groundwork for auch broader nondiscrimination law: The Americans withisabilities Act (ADA). Signed into law in 1990 by Presidenteorge H. Bush, it has proved both landmark and controver-

ial. In the 2 decades since its passage, it has been challengedt the U.S. Supreme Court level over 20 times, resulting in aerceived weakening of the legislation. Yet for people withCI, the ADA remains a key protection, because even incom-lete SCI continues to meet the definitions of disability estab-ished through case law. To date, 2 cases have involved plain-iffs with SCI. In Barrios v Dupont, the plaintiff was awardedack pay and punitive damages for over $1 million, establish-ng that functional capacity evaluations to establish eligibilityor employment must be related to individual job functions. Inpecter v Norwegian Cruise Line, the plaintiffs asserted thathe cruise line was ill-equipped to accommodate people withisabilities. The district court, ruling in favor of the plaintiffs,as upheld by the Supreme Court, establishing that foreign-agged ships that operate in U.S. waters and ports are required

o meet the provisions of the ADA.The effect of the ADA is difficult to measure by case law,

ecause many of the more important adaptations in the publicector and workplaces have occurred without dispute. Thesedaptations include curb cuts, accessible bathrooms, and low-red retail and service counters. However, employment dis-rimination remains a key concern. People with SCI are nowncluded among the ranks of graduate and professional schoolsn nearly every field. However, employment of people with SCIho were not planning on pursuing undergraduate and gradu-

te degrees remains low. The potential loss of access to publicealth insurance was identified as a barrier to work, resulting inhe passage of the Ticket to Work and Work Incentive Im-rovement Act in 1999. In addition to creating a ticket that aisabled consumer could use to purchase needed services, itxpanded the earning guidelines for Medicare and Medicaid tollow more people with disabilities to be employed whileaintaining medical coverage.

APPENDIX 1: COMPONENTS OF A LIFECARE PLAN

atient data (eg, individual medical, social, and functionaltatus obtained from the patient, family, and medical record)orm the basis of a life care plan, with the following specific
omponents:
APPENDIX 1: COMPONENTS OF A LIFECARE PLAN (cont’d)

1. Medical rehabilitation problem list and current status.2. Recommendations/interventions, including projected

evaluations by physicians, therapists, psychology ser-vices, vocational and recreational therapies, and casemanagement. Projected therapeutic interventions (fre-quency, duration, and type) and diagnostic testing re-quirements should be included.

3. Ongoing medical needs, including medications, homecare assistance, projected medical and surgical needs,and disposable medical supplies.

4. Housing and architectural adaptations for accessibility.5. Equipment needs, including home equipment, exercise

equipment, driving and transportation needs, orthotics,wheelchair needs, and recreational equipment.

6. Recommendations for preventive actions and interven-tions to decrease the frequency, severity, and duration ofcomplications.

7. Estimated length of each required service.8. Estimated costs for each required service.9. Estimated life expectancy.

References1. The 2005 annual statistical report for the Model Spinal Cord

Injury Care Systems. Birmingham: National SCI Statistical Cen-ter; June 2005.

*2. Berkowitz M, O’Leary PK, Kruse DL, Harvey C. Spinal cordinjury: an analysis of medical and social costs. New York:Demos; 1998.

3. National Spinal Cord Injury Statistical Center. Spinal cord injuryfacts and figures at a glance. Birmingham: Univ Alabama; June2006.

4. Stiens SA, Kirshblum SC, Groah SL, McKinley WO, Gittler MS.Spinal cord injury medicine. 4. Optimal participation in life afterspinal cord injury: physical, psychosocial, and economic reinte-gration into the environment. Arch Phys Med Rehabil 2002;83(3 Suppl 1):S72-81.

*5. Deutch PM, Allison L, Cimino-Ferguson S. Life care planningassessments and their impact on quality of life in spinal cordinjury. Top Spinal Cord Inj Rehabil 2005;10:135-45.

6. Blackwell TL. Spinal cord injury desk reference: guidelinesfor life care planning and case management. New York:Demos; 2001.

7. Katz RT, Delaney GA. Life care planning. Phys Med RehabilClin N Am 2002;13:287-308, ix.

8. Jang Y, Wang YH, Wang JD. Return to work after spinal cordinjury: the contribution of functional independence. Arch PhysMed Rehabil 2005;86:681-6.

9. Valtonen K, Karlsson AK, Alaranta H, Viikari-Juntura E. Workparticipation among persons with spinal cord injury and menin-gomyelocele. J Rehabil Med 2006;38:192-200.

10. Anderson CJ, Vogel LC. Employment outcomes of adults whosustain spinal cord injury as children or adolescents. Arch PhysMed Rehabil 2002;83:791-801.

11. Struhkamp RS. Patient autonomy: a view from the kitchen. MedHealth Care Philos 2005;8:105-14.

12. Kothari S. Clinical (mis)judgments of quality of life after dis-ability. J Clin Ethics 2004;15:300-7.

13. Gerhart K, Kozial-McLain J, Lowenstein SR, Whiteneck GC. Qual-ity of life following spinal cord injury: knowledge and attitudes ofemergency care providers. Ann Emerg Med 1994;23:807-12.

*Key reference.


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14. Shalowitz DI, Garrett-Mayer E, Wendler D. The accuracy ofsurrogate decision makers: a systematic review. Arch Intern Med2006;166:493-7.

15. Trevor-Deutsch B, Nelson RF. Refusal of treatment, leading todeath: towards optimization of informed consent. Ann R CollPhysicians Surg Can 1996;29:487-9.

16. Blackmer J, Ross L. Awareness and use of advance directives in thespinal cord injured population. Spinal Cord 2002;40:581-94.

17. Banja JD. When the payer says “no!” Ethical considerations inpatient advocacy. J Spinal Cord Med 2001;24:230-4.

18. Chiodo AE, Scelza WM, Kirshblum SC, Wuermser LA, Ho CH,Priebe MM. Spinal cord injury medicine. 5. Long-term medicalissues and health maintenance. Arch Phys Med Rehabil 2007;88
(3 Suppl 1):S76-83.

Selected Readingisability Rights and Independent Living Movement Project. Avail-

able at: http://bancroft.berkeley.edu/collections/drilm. AccessedSeptember 22, 2006.

enter for Independent Living. Available at: www.cilberkeley.org/history.htm. Accessed September 22, 2006.

cDonald G, Oxford M. History of independent living. Available at:www.acils.com/acil/ilhistory.html. Accessed September 22, 2006.

ate DG, Kalpakjian CZ, Paasuke L, Homa D. Vocational rehabilita-tion, independent living and consumerism. In: DeLisa JA, GansBM, Walsh NE, editors. Physical medicine and rehabilitation:principles and practice. Philadelphia: Lippincott Williams &
Wilkins; 2005. p 1073-84.
http://bancroft.berkeley.edu/collections/drilm

http://www.cilberkeley.org/history.htm.

http://www.cilberkeley.org/history.htm.

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Educational Activity 1.11. According to the Standards for Neurological Classifica-

tion of Spinal Cord Injury published by the AmericanSpinal Injury Association (ASIA)(a) shoulder abductors are 1 of the 5 key upper-extremity

muscle groups.(b) the zone of partial preservation is only pertinent in

complete spinal cord injury.(c) if half the key muscles below the neurologic level of

injury have a muscle grade less than 3, the ASIAgrade is D.

(d) the patient should be examined in a seated position.

Ref: American Spinal Injury Association. International stan-ards for neurological classifications of spinal cord injuryrevised 2000). Chicago: ASIA; 2002.

Educational Activity 1.12. The only cause of spinal cord injury that has steadily

increased over the last 3 decades is(a) violence.(b) falls.(c) motor vehicle crashes.(d) sports.

Ref: Jackson AB, Dijkers M, DeVivo MJ, Paczatek RB. Aemographic profile of new traumatic spinal cord injuries:hange and stability over 30 years. Arch Phys Med Rehabil004;85:1740-8.

Educational Activity 1.33. Compared with traumatic spinal cord injury (SCI), non-

traumatic SCI is more likely to be associated with(a) an incomplete lesion.(b) a higher incidence of spasticity.(c) a higher rate of home discharge.(d) a shorter time between diagnosis and rehabilitation.

Ref: Chapman J. Comparing medical complications fromontraumatic and traumatic spinal cord injury [abstract]. Archhys Med Rehabil 2000;81:1264.

Educational Activity 1.34. Transverse myelitis

(a) results in paraplegia 70% of the time.(b) progresses in more than 1 week and less than 4

weeks.(c) is associated with a poor recovery if there is a rapid

progression.(d) is rarely associated with sensory symptoms.

Ref: Transverse Myelitis Consortium Working Group. Pro-osed diagnostic criteria and nosology of acute transverseyelitis. Neurology 2002;59:499-505.

Educational Activity 1.45. In people with myelomeningocele,

(a) the majority have below-normal intelligence.(b) posterior fossa decompression is frequently required.
(c) hydrosyringomyelia (syrinx) is uncommon.
(d) hydrocephalus is seen in approximately 90% ofpatients.

Ref: (a) Molnar GE MK. Spina bifida. In: Molnar GE,lexander MA, editors. Pediatric rehabilitation. 3rd ed. Phil-delphia: Hanley & Belfus; 1999. p 219-44.(b) Charney EB RL, Sutton LN, Schut L. management of

hiari II complications in infants with myelomeningocele.Pediatr 1987;111:364-71.

Clinical Activity 2.16. Which treatment is NOT standard management for acute

care of spinal cord injury?(a) Prophylaxis for venous thromboembolism within 72

hours(b) Volume resuscitation to optimize spinal cord perfu-

sion(c) High-dose methylprednisolone as a neuroprotective

agent(d) Assessment and treatment of spinal and neurogenic

shock

Ref: (a) Consortium for Spinal Cord Medicine. Early acuteanagement in adults with spinal cord injury: a clinical prac-

ice guideline for health-care providers. Washington (DC):aralyzed Veterans of America; 2007.(b) Qian T, Guo X, Levi AD, Vanni S, Shebert RT, Sipski MS.

igh-dose methylprednisolone may cause myopathy in acutepinal cord injury patients. Spinal Cord 2004;43:199-203.

Clinical Activity 2.17. Which statement is TRUE concerning autonomic dys-

function?(a) It is associated with injury below T9.(b) It is common in the acute period.(c) Bradycardia occurs in response to blood pressure

elevations.(d) Hypothermia is common because of poor thermo-

regulation.

Ref: (a) Bilello JF, Davis JW, Cunningham MA, Groom TF,emaster D, Sue LP. Cervical spinal cord injury and the need

or cardiovascular intervention. Arch Surg 2003;138:1127-9.(b) Krassioukov AV, Furlan JC, Fehlings MG. Autonomic

ysreflexia in acute spinal cord injury: an underrecognizedlinical entity. J Neurotrauma 2003;20:707-16.

(c) Price MJ, Campbell IG. Effects of spinal cord lesion levelpon thermoregulation during exercise in the heat. Med Sciports Exerc 2003;35:1100-7.(d) Sugarman B. Fever in recently injured quadriplegic

ersons. Arch Phys Med Rehabil 1982;63:639-40.

Clinical Activity 2.28. Which statement is TRUE concerning bladder manage-

ment considerations in acute spinal cord injury?(a) Increased urine volumes occur with immobilization.(b) Intermittent catheterization may begin once intrave-

nous fluids are discontinued and strict urine outputs
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(c) Intermittent catheterization volumes should begreater than 250mL.

(d) Prophylactic antibiotics for prevention of urinarytract infections are recommended.

Ref: (a) Morton SC, Shekelle PG, Adams JL, et al. Antimi-robial prophylaxis for urinary tract infection in persons withpinal cord dysfunction. Arch Phys Med Rehabil 2002;83:129-8.(b) Consortium for Spinal Cord Medicine. Early acute man-

gement in adults with spinal cord injury: a clinical practiceuideline for health-care providers. Washington (DC): Para-yzed Veterans of America; 2007.

Clinical Activity 2.39. Which statement is TRUE about neurologic recovery in

tetraplegia?(a) Recovery occurs sequentially in the upper, then

lower extremities.(b) Most complete cervical lesions will recover 1 root

level of function.(c) Neurologic examination at 24 hours is superior to 72

hours postinjury for predicting recovery.(d) The presence of the crossed adductor response in the

acute stage indicates a poor prognosis for lower-extremity motor recovery and function.

Ref: (a) Marino RJ, Ditunno JF, Donovan WF, Maynard F.eurologic recovery after traumatic spinal cord injury: data

rom the Model Spinal Cord Injury Systems. Arch Phys Medehabil 1999;80:1391-6.(b) Ditunno JF, Flanders A, Kirshblum SC, Graziana V,

essler A. Predicting outcome in traumatic SCI. In: KirshblumC, Campagnolo D, DeLisa JD, editors. Spinal cord medicine.hiladelphia: Lippincott Williams & Wilkins; 2002. p 108-22.(c) Ko HY. The pattern of reflex recovery during spinal

hock. Spinal Cord 1999;37:402-9.

Clinical Activity 2.410. In a magnetic resonance imaging evaluation of the spinal

cord, contrast enhancement is most useful in the evalua-tion of(a) spinal stenosis.(b) arteriovenous malformation.(c) intramedullary tumor.(d) primary or metastatic bone lesion.

Ref: (a) White ML, El-Khoury GY. Neurovascular injuries ofhe spinal cord. Eur J Radiol 2002;42:117-26.

(b) Bastianello S, Pichiecchio A, Spadaro M, et al. Atypicalultiple sclerosis: MRI findings and differential diagnosis.eurol Sci 2004;(25 Suppl 4):S356-60.

Clinical Activity 3.111. A patient with a C6 spinal cord injury would typically

have partial innervation to which muscle group?(a) Anconeus(b) Supinator(c) Extensor carpi ulnaris(d) Flexor digitorum profundus

Ref: Clinical Activity 3.1.

Clinical Activity 3.212. Compared with people with the single diagnosis of spinal

cord injury (SCI), people with a dual diagnosis of SCI
and traumatic brain injury have a

(a) longer length of stay (LOS) in an acute care hospitalbefore admission to a rehabilitation hospital.

(b) longer LOS in a rehabilitation hospital.(c) higher likelihood of being discharged to an institu-

tional setting.(d) lower cognitive FIM score at admission but not at

discharge from a rehabilitation hospital.

Ref: Macciocchi SN, Bowman B, Coker J, Apple D, Leslie D.ffect of co-morbid traumatic brain injury on functional out-ome of persons with spinal cord injuries. Am J Phys Medehabil 2004;83:22-6.

Clinical Activity 3.313. In spinal cord injury, heterotopic ossification presents

most commonly in the(a) shoulders.(b) elbows.(c) knees.(d) hips.


Educational Activity 3.514. The biggest barrier to the acceptance and use of the

functional electric stimulation system implanted to im-prove bladder function has been(a) the need for a posterior sacral rhizotomy.(b) the potential loss of penile erectile function.(c) the need for a sacral laminectomy.(d) the increased risk of urinary tract infections.

Ref: Educational Activity 3.5.

Educational Activity 3.515. Which wheelchair propulsion method decreases injury to

the upper extremities?(a) Circular propulsive stroke in which the hand falls

below the pushrim during the recovery phase(b) Figure-of-eight motion in which the hand rises above

the pushrim at the midpoint of the recovery phase(c) Faster cadence and an attempt to limit the time the

hand is on the pushrim during the stroke phase(d) Maximum peak force and an attempt to increase the

duration of the recovery phase

Ref: Boninger ML, Koontz AM, Sisto SA, et al. Pushrimiomechanics and injury prevention in spinal cord injury:ecommendations based on CULP-SCI investigations. J Reha-il Res Dev 2005;42:9-19.

Educational Activity 4.116. Which factor is the LEAST important for successful

community reintegration of people with disabilities?(a) Self-esteem(b) Family support(c) Physical environment(d) Informational support

Ref: (a) Whiteneck G, Meade MA, Dijkers M, Tate DG,ushnik T, Forchheimer MB. Environmental factors and theirole in participation and life satisfaction after spinal cordnjury. Arch Phys Med Rehabil 2004;85:1793-803.

(b) Song HY. Modeling social reintegration in persons withpinal cord injury. Disabil Rehabil 2005;27:131-41.

Educational Activity 4.117. People with SCI exhibit a decline over time in all of the

following EXCEPT

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(a) mobility.(b) economic self-sufficiency.(c) occupation.(d) social integration.

Ref: Charlifue S, Gerhart K. Community integration in spi-al cord injury of long duration. NeuroRehabilitation 2004;9:91-101.

Clinical Activity 4.218. Which factor limits the participation of people with spinal

cord injury in physical exercise?(a) Lack of accessibility(b) Lack of privacy(c) Fear of injury(d) All of the above

Ref: Scelza WM, Kalpakjian CZ, Zemper ED, Tate DG.erceived barriers to exercise in people with spinal cord

njury. Am J Phys Med Rehabil 2005;84:576-83.

Educational Activity 4.319. How does the suicide rate in paraplegics compare with

the rate in an able-bodied control group?(a) Equal rate(b) Twice as high(c) Five times as high(d) Ten times as high

Ref: Rish BL, Dilustro JF, Salazar AM, Schwab KA, BrownR. Spinal cord injury: a 25-year morbidity and mortality

tudy. Mil Med 1997;162:141-8.

Educational Activity 4.420. Which subgroup of patients with spinal cord injury (SCI)

has a higher rate of divorce than the general population?(a) African Americans(b) Couples with children(c) Male partners with SCI(d) Couples in postinjury marriages

Ref: Kreuter M. Spinal cord injury and partner relation-hips. Spinal Cord 2000;38:2-6.

Educational Activity 5.121. Which statement is TRUE about the incidence of com-

plications after the first year of a spinal cord injury?(a) Pressure ulcer frequency increases from year 1 to

year 10 postinjury.(b) The frequency of pulmonary embolus increases from

year 1 to year 10 postinjury.(c) Pneumonias are more frequent in year 1 postinjury

than in year 10.(d) The incidence of deep venous thrombosis increases

from year 1 to year 10.

Ref: McKinley WO, Jackson AB, Cardenas DD, DeVivo MJ.ong-term medical complications after traumatic spinal cord

njury: a multicenter analysis. Arch Phys Med Rehabil 2004;5:1257-64.

Educational Activity 5.122. The most common reason for rehospitalization for med-

ical complications after spinal cord injury is disease ofthe(a) skin and subcutaneous system.(b) respiratory system.(c) genitourinary system.
(d) musculoskeletal system. R
Ref: Cardenas DD, Hoffman JM, Kirshblum S, McKinley W.tiology and incidence of rehospitalization after traumaticpinal cord injury: a multicenter analysis. Arch Phys Medehabil 2004;85:1757-63.

Educational Activity 5.123. Which statement was found to be TRUE in a meta-

analysis of studies of antimicrobial prophylaxis in peoplewith spinal cord dysfunction?(a) Antimicrobial prophylaxis is associated with a re-

duced number of symptomatic urinary tract infec-tions.

(b) Antimicrobial prophylaxis is associated with a reduc-tion in bacteriuria in the first 90 days after spinal cordinjury.

(c) Antimicrobial prophylaxis results in a 4-fold increasein the proportion of antimicrobial-resistant bacteria.

(d) Antimicrobial prophylaxis is more effective in pre-venting symptomatic urinary tract infections inwomen than in men.

Ref: Morton SC, Shekelle PG, Adams JL, et al. Antimicrobialrophylaxis for urinary tract infection in persons with spinalord dysfunction. Arch Phys Med Rehabil 2002;83:129-38.

Clinical Activity 5.524. What is the most common type of pain experienced by

people with spinal cord injuries more than 6 monthspreviously?(a) Visceral(b) Below-level neuropathic(c) Sympathetic(d) Musculoskeletal

Ref: Barrett H, McClelland JM, Rutkowski SB, Siddall PJ.ain characteristics in patients admitted to hospital with com-lications after spinal cord injury. Arch Phys Med Rehabil003;84:789-95.

Educational Activity 6.125. Which expense is NOT considered a direct cost of spinal

cord injury?(a) Initial hospitalization(b) Rehabilitation(c) Loss of wages(d) Home modification

Ref: Berkowitz M, O’Leary PK, Druse DL, Harvey C. Spinalord injury: an analysis of medical and social costs. New York:emos; 1998.

Clinical Activity 6.226. A life care plan does NOT address

(a) complications of the aging process.(b) costs of new technology.(c) prognosis for improvement.(d) rehabilitative goals.

Ref: (a) Deutch PM, Allison L, Cimino-Ferguson S. Life carelanning assessments and their impact on quality of life inpinal cord injury. Top Spinal Cord Injury Rehabil 2005;10:35-45.(b) Blackwell TL. Spinal cord injury desk reference: guide-

ines for life care planning and case management. New York:emos; 2001.(c) Katz RT, Delaney GA. Life care planning. Phys Med

ehabil Clin N Am 2002;13:287-308, ix.


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Educational Activity 6.327. Factors found to predict employment after spinal cord

injury include(a) unemployment at time of injury.(b) community mobility.(c) functional dependence.(d) greater medical complications.

Ref: (a) Anderson CJ, Vogel LC. Employment outcomes ofdults who sustain spinal cord injury as children or adoles-ents. Arch Phys Med Rehabil 2002;83:791-801.

(b) Jang Y, Wang YH, Wang JD Return to work after spinalord injury: the contribution of functional independence. Archhys Med Rehabil 2005;86:681-6.(c) Valtonen K, Karlsson AK, Alaranta H, Biikari-Juntura E.ork participation among persons with spinal cord injury andeningomyelocele. J Rehabil Med 2006;38:192-200.

Clinical Activity 6.428. Which statement is TRUE regarding autonomy and ad-

vance directives in people with a spinal cord injury(SCI)?(a) Surrogate decision makers are able to decide what is

“best” for the patient.(b) Quality-of-life biases are not a factor in the determi-

nation of life-sustaining treatment.


(c) Health care providers are better able to make treat-ment decisions in cases of SCI.

(d) There is minimal use of advance directives in chronicSCI.

Ref: (a) Blackmer J, Ross L. Awareness and use of advanceirectives in the spinal cord injured population. Spinal Cord002;40:581-94.(b) Shalowitz DI, Garrett-Mayer E, Wendler D. The accu-

acy of surrogate decision makers: a systematic review. Archntern Med 2006;166:493-7.

(c) Gerhart K, Kozial-McLain J, Lowenstein SR, WhiteneckC. Quality of life following spinal cord injury: knowledge andttitudes of emergency care providers. Ann Emerg Med 1994;3:807-12.(d) Struhkamp RX. Patient autonomy: a view from the

itchen. Med Health Care Philos 2005;8:105-14.

Clinical Activity 6.529. The landmark law passed in the 1990s to advance the

rights of all people with disabilities was the(a) Rehabilitation Act.(b) Americans with Disabilities Act.(c) Social Security Act.(d) Individuals with Disabilities Education Act.


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007 SAE-P: Spinal Cord Injury Medicinenswer Key and Commentary on Preferred Choice

QUESTION ANSWER COMMENTARY1. (b) The 5 key upper-extremity muscle groups are elbow flexion, wrist extension, triceps, finger

flexors, and intrinsics. The examination as described in the Standards was designed to beperformed in a supine position.

2. (b) The most common cause of spinal cord injury (SCI) over the last 30 years continues to bemotor vehicle crashes. Falls remain the second most common cause of SCI and are theonly cause that has steadily increased over the last 3 decades. Falls are the most commoncause of SCI in people over the age of 60 years. Sports-related SCI has decreased over thedecades. Violence, although a rising cause of SCI through the 1990s, declined to a 30-yearlow between 2000 and 2003.

3. (a) Nontraumatic spinal cord injury (SCI) is a growing population for admission to inpatientrehabilitation. The nontraumatic SCI population is more likely to present with a neuro-logically incomplete lesion and was associated with a lower frequency of secondarycomplications such as spasticity, deep vein thrombosis, and autonomic dysreflexia.Patients with nontraumatic SCI had a lower rate of discharge to home (73%), withfavorable discharge seen in patients whose injuries were incomplete, who were married,and who had an established bowel and bladder management program and intact skin.

4. (c) Transverse myelitis has a female-to-male ratio of 4:1, with peaks in the second and fourthdecades. The time course of progression is more than 48 hours and less than 6 weeks. Atnadir, half have paraplegia, all have neurogenic bladder, and 80% to 94% have sensorysymptoms. Over time, one third recovered, one third had neurologic deficits, and one thirdhad paraplegia.

5. (d) Hydrocephalus is seen in approximately 90% of patients with myelomeningocele andusually manifests itself after surgical closure. Most of these people will also requireventriculoperitoneal (VP) shunting. Symptomatic hydrocephalus is usually treated withVP shunting but sometimes will need a posterior fossa decompression to relieve pressureexerted on the brainstem. Hydrosyringomyelia (syrinx) is commonly seen in myelome-ningocele.

6. (c) The Consortium for Spinal Cord Injury Medicine Clinical Practice Guidelines consider theuse of high-dose methylprednisolone to be a treatment option rather than a standard. Theeffectiveness of high-dose methylprednisolone as a neuroprotective agent has beenquestioned, and it has been associated with increased risk of infection, gastrointestinalbleeding, and steroid myopathy.

7. (c) Autonomic dysfunction is more common in cervical and high-thoracic (above T6) injuries.Autonomic dysreflexia may be seen in the early period but requires intact spinal reflexesand, therefore, will not be seen until spinal shock has resolved. Bradycardia occurs inresponse to initial hypertension, but later heart rate may increase. There is impaired heatdissipation in spinal cord injury, resulting in hyperthermia or “quad fever” in the earlyweeks after tetraplegia.

8. (b) Intermittent catheterization may begin once intravenous fluids are discontinued and moni-toring of strict urine outputs is no longer necessary. Mobilization of the patient will causea diuresis of third space fluids and an increase in urine output. Intermittent catheterizationvolumes should not exceed 500mL. Prophylactic antibiotics are not recommended.

9. (b) Most upper-extremity recovery occurs in the first 6 months, with the greatest rate of changeduring the first 3 months. Motor recovery in the upper and lower extremities occursconcurrently rather than sequentially. The neurologic examination at 72 hours has greaterpredictive value for recovery than the 24-hour examination. The crossed adductor re-sponse to patellar tendon taps is highly predictive of functional motor recovery.

10. (c) Magnetic resonance imaging with gadolinium enhancement is useful in evaluating inflam-matory and neoplastic lesions of the spinal cord. Spinal angiography is the criterionstandard for the diagnosis of spinal cord arteriovenous malformations. Computed tomog-raphy scan is most helpful in evaluating primary or metastatic bone lesions. Contrast is notroutinely used for evaluation of spinal stenosis with myelopathy.

11. (b) A patient with a C6-level spinal cord injury has the extensor carpi radialis as the key musclegroup and partially innervates the supinator, pronator teres, and latissimus dorsi. Theanconeus is usually innervated by C7-T1; flexor digitorum profundus C8, T1; andextensor carpi ulnaris C7, C8.



A

12. (a) Patients with a dual diagnosis had significantly lower cognitive FIM scores both atadmission and at discharge, but no significant effect has been reported on the rehabilita-tion hospital length of stay or discharge placement. However, length of time in the acutecare hospital was 24 days compared with 12 days for people with a spinal cord injuryonly.

13. (d) Most commonly, heterotopic ossification presents in the hips, followed by the knees,elbows, and shoulders.

14. (a) The current bladder functional electric stimulation (FES) is an implanted system thatstimulates the sacral nerves and is combined with a posterior sacral rhizotomy to improvecontinence and bladder capacity. Research studies have shown the benefits of the bladderFES to be improved voiding, bladder continence, and reduced urinary tract infections.However, eligible people with spinal cord injury did not choose it because they want toavoid a posterior sacral rhizotomy.

15. (a) It has been found that lower peak forces, slower cadence, and a circular propulsive strokemay help prevent injury of the upper extremities.

16. (c) Modifying the physical environment to make it more accessible helps people with mobilityimpairments to participate in society, but recent studies have shown that environmentalfactors have only a small effect on community integration.

17. (b) Economic self-sufficiency actually improved over time in a longitudinal study of peoplewith long-standing spinal cord injury.

18. (d) Barriers to physical activity in people with spinal cord injury include lack of accessibilityand lack of staff experience at fitness facilities, lack of privacy, and fear of injury.

19. (d) Depression and suicide are significant problems in people with spinal cord injury. Thesuicide rate in paraplegics was found to be 10 times the rate of that for an able-bodiedcontrol group.

20. (a) The divorce rate is higher for couples married before the injury than for those in postinjurymarriages. The rates are also higher in women spinal cord injury, childless couples,persons with prior divorce, and African Americans.

21. (a) The frequency of pressure ulcers increases from 15% to 23% in the 10 years after a spinalcord injury. Pulmonary embolus and pneumonia incidence is unchanged during this timeperiod. Deep venous thrombosis is more common at year 1 (2.1%) than at year 10 (0.7%).

22. (c) Diseases of the genitourinary system are the most common reason for rehospitalizationaccording to a multicenter analysis of 3978 patients with SCI, which found that genito-urinary cases (n�284) were most common, followed by diseases of the skin (n�230),respiratory system (n�117), and musculoskeletal system (n�99).

23. (b) In a meta-analysis article, antimicrobial prophylaxis was found to be only associated witha reduction in bacteriuria (asymptomatic urinary tract infection). Antimicrobial prophy-laxis results in a 2-fold increase in bacterial resistance.

24. (d) Musculoskeletal is the most common type of pain experienced by people with chronic spinalcord injury (44%). It is followed in incidence by below-level neuropathic pain (24%),visceral pain (15%), and sympathetic pain (6%).

25. (c) Loss of wages is an indirect cost of spinal cord injury (SCI). The other choices are all directcosts of SCI.

26. (b) A life care plan is a comprehensive document that delineates the future medical andrehabilitative needs of the person who has sustained a catastrophic injury or illness. Itincludes the medical problem list; psychologic, vocational, recreational, and social issues;rehabilitative goals; prognosis for improvement; short- and long-term equipment needs;complications of the aging process estimates; preventive measure recommendations; andprojected costs over the person’s estimated life span. It does not include unexpectedcomplications and cost of new technology, although the potential for these is understood.

27. (b) Four factors found to predict employment after spinal cord injury are education, communitymobility, functional independence, and fewer medical complications. Employment at thetime of injury is not consistently a significant factor predicting return to work.

28. (d) As determined by a survey, only 8% of people with spinal cord injury (SCI) had completedan advance directive, although most were interested in doing so after having learned aboutthem. Surrogate decision makers are supposed to make decisions based on what thepatient would want and not on their own personal judgment as to what they think is “best.”Health care providers’ perceptions of quality of life after SCI may introduce bias intotreatment decisions. A vast discrepancy continues to exist between perceived and actualquality of life in people with SCI. The concept of autonomy supports a joint decision-making model, with health care providers educating patients and then assisting them inmaking treatment decisions, instead of making decisions for the patient.


S95SAE-P ANSWER KEY, Phelan

29. (b) The Americans with Disabilities Act was the landmark legislation passed in 1990 thatadvanced the civil rights of all people with disabilities. The Rehabilitation Act was passedin 1973 and guaranteed the civil rights of people with disabilities within federal programsand established the concept of the person with disability as a consumer. The SocialSecurity Act of 1935 established federally funded vocational rehabilitation services forcivilians. The Individuals with Disabilities Education Act passed in 1975 and establishedpublic education for children with disabilities in the least restrictive environment.


AAPM&R 2007 STUDY GUIDE AND SELF ASSESSMENT EXAMINATION FOR PRACTITIONERS (SAE-P)

** INDUSTRIAL MEDICINE AND ACUTE MUSCULOSKELETAL REHABILITATION**PROGRAM EVALUATION

CME CERTIFICATES WILL NOT BE PROCESSED WITHOUT THE COMPLETION OF THE RELEVANT PROGRAM

EVALUATION(S)OVERALL ARTICLE OBJECTIVES:Objective 1: To understand the important components of a history, physical examination, and concise diagnostic

testing when evaluating acute industrial and musculoskeletal injuries. Objective 2: To summarize medication options in the treatment of acute musculoskeletal pain in the setting of injured

workers. Objective 3: To review the medical literature that may help clinicians make treatment decisions regarding modalities,

therapeutic exercise, and orthotic devices for treating common work-related conditions in the upper and lower limbs.

Objective 4: To give an overview of current state of the art regarding diagnostic and nonsurgical invasive treatment procedures for neck pain with and without referred upper-limb pain.

Objective 5: To give an overview of the current state of diagnosis and treatment options for low back pain with or without referred leg pain focusing on interventional procedures.

Objective 6: To review the medical literature to help clinicians make treatment decisions regarding corticosteroid and other injections in the upper and lower limbs, in injured workers.

Objective 7: To recognize diagnosis and treatment issues that are unique to the aging worker.

INDICATE THE DEGREE TO WHICH YOU AGREE OR DISAGREE WITH EACH STATEMENT ABOUT THE

** INDUSTRIAL MEDICINE AND ACUTE MUSCULOSKELETAL REHABILITATION ** STUDY GUIDE AND SAE-P. Strongly Disagree

Disagree Not Certain Agree Strongly Agree

1. Objective 1 was met. ...................... SD...............D ................ NC ................A................SA 2. Objective 2 was met. ...................... SD...............D ................ NC ................A................SA 3. Objective 3 was met. ...................... SD...............D ................ NC ................A................SA 4. Objective 4 was met. ...................... SD...............D ................ NC ................A................SA 5. Objective 5 was met. ...................... SD...............D ................ NC ................A................SA 6. Objective 6 was met. ...................... SD...............D ................ NC ................A................SA 7. Objective 7 was met. ...................... SD...............D ................ NC ................A................SA 8. The material was fair, objective,

and unbiased toward any product or program. ............................................ Yes...............No 9. I learned a new skill or

patient management approach. ....... SD...............D ................ NC ................A................SA 10. This material will enhance

my professional effectiveness......... SD...............D ................ NC ................A................SA 11. I plan to implement a change(s)

to my practice as a result of this material........................................... SD...............D ................ NC ................A................SA

If you circled “Agree” or “Strongly Agree,” please give one example: ____________________________________________________________________________________________________________________________________________________________

12. In what ways did/will you utilize the ** INDUSTRIAL MEDICINE AND ACUTE MUSCULOSKELETAL REHABILITATION

** Study Guide and SAE-P in your medical practice? I have used/will use it to: (Check all that apply.) Confirm previous knowledge and reinforce clinical practice Study for recertification examination Serve as initial resource for clinical problems Apply new techniques/procedures to the care of my patients Use the information to train staff Share the information with colleagues Help develop new policy and procedures Other (please specify): ______________________________________________________________

Too Basic Just Right Too Advanced 13. The content was:................................................................. TB.................... JR.....................TA14. Please share any general comments, recommendations, or an elaboration of any item on this form: __________________________________________________________________________________________________________________________________________________________________________

Evaluation data collected from this form will be processed confidentially by a third party and will only be reviewed by Academy staff in the aggregate.

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AAPM&R 2007 STUDY GUIDE AND SELF ASSESSMENT EXAMINATION FOR PRACTITIONERS (SAE-P)

** SPINAL CORD INJURY MEDICINE ** PROGRAM EVALUATION

CME CERTIFICATES WILL NOT BE PROCESSED WITHOUT THE COMPLETION OF THE RELEVANT PROGRAM

EVALUATION(S)

OVERALL ARTICLE OBJECTIVES:Objective 1: To summarize the demographics and classification of traumatic and nontraumatic spinal cord injuries in

adults and children. Objective 2a: To describe the diagnostic evaluation of traumatic and nontraumatic spinal cord injuries. Objective 2b: To summarize the medical, surgical and physiatric interventions during acute hospitalization for these

injuries. Objective 3: To describe outcomes and issues that may arise during the rehabilitation phase after spinal cord injury. Objective 4: To summarize the barriers and opportunities of community reintegration for individuals with spinal cord

injury. Objective 5: To discuss long-term care issues in patients with spinal cord injury, including health maintenance, secondary

conditions, women’s health, sexual function, pain, and spinal cord regeneration and recovery. Objective 6a: To review the economic consequences of spinal cord injury, including lifelong direct costs, life care planning,

and factors affecting employment. Objective 6b: To identify current ethical issues facing the spinal cord injury community and review the advances made in

the rights of people with disabilities in the United States through legislation.

INDICATE THE DEGREE TO WHICH YOU AGREE OR DISAGREE WITH EACH STATEMENT ABOUT THE

** SPINAL CORD INJURY MEDICINE ** STUDY GUIDE AND SAE-P. Strongly Disagree

Disagree Not Certain Agree Strongly Agree

1. Objective 1 was met.............................. SD.................D ...................NC.................. A..................SA2. Objective 2a was met. ........................... SD.................D ...................NC.................. A..................SA3. Objective 2b was met............................ SD.................D ...................NC.................. A..................SA4. Objective 3 was met.............................. SD.................D ...................NC.................. A..................SA5. Objective 4 was met.............................. SD.................D ...................NC.................. A..................SA6. Objective 5 was met.............................. SD.................D ...................NC.................. A..................SA7. Objective 6a was met. ........................... SD.................D ...................NC.................. A..................SA8. Objective 6b was met............................ SD.................D ...................NC.................. A..................SA9. The material was fair, objective,

and unbiased toward any product or program. ......................................................... Yes.................. No 10. I learned a new skill or

patient management approach............... SD.................D ...................NC.................. A..................SA 11. This material will enhance

my professional effectiveness. .............. SD.................D ...................NC.................. A..................SA 12. I plan to implement a change(s)

to my practice as a result of this material. ................................................ SD.................D ...................NC.................. A..................SA

If you circled “Agree” or “Strongly Agree,” please give one example: ________________________________________________________________________________________________________________________________________________________________________________

13. In what ways did/will you utilize the ** SPINAL CORD INJURY MEDICINE ** Study Guide and SAE-P in your medical practice? I have used/will use it to: (Check all that apply.)

Confirm previous knowledge and reinforce clinical practice Study for recertification examination Serve as initial resource for clinical problems Apply new techniques/procedures to the care of my patients Use the information to train staff Share the information with colleagues Help develop new policy and procedures Other (please specify):________________________________________________________________________

Too Basic Just Right Too Advanced 14. The content was:…………………………………………………….….TB….. ........ JR........................TA

15. Please share any general comments, recommendations, or an elaboration of any item on this form: ________________________________________________________________________________________________________________________________________________________________________________________________

Evaluation data collected from this form will be processed confidentially by a third party and will only be reviewed by Academystaff in the aggregate.

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AAPM&R2007 STUDY GUIDE AND SELF ASSESSMENT EXAMINATION FOR PRACTITIONERS (SAE-P)

CONTINUING MEDICAL EDUCATION (CME) CREDIT APPLICATION

CME PROCESSING FEES

TO RECEIVE CME CREDIT AND MOC SELF-ASSESSMENT PARTICIPATION: YOU MUST COMPLETE THE FOLLOWING 4 ITEMS.

1. Check one: AAPM&R Member Membership/ID Number: Non-Member

2. The relevant Program Evaluation(s).

3. Number of hours: The AAPM&R has designated each set of Study Guide articles and corresponding SAE-P for a maximum of 15 Category 1 CME credits toward the AMA Physician’s Recognition Award. Each physician should claim only those hours of credit that he/she actually spent on the educational activity. Credit may be obtained until March 31, 2010.

By checking this box I confirm that I studied the Industrial Medicine and Acute Musculoskeletal Rehabilitationarticles, consulted the reference materials as needed, and completed the SAE-P.

Therefore, I claim (fill in blank) CME Category 1 credit hours (up to 15 hours).

By checking this box I confirm that I studied the Spinal Cord Injury Medicine articles consulted the reference materials as needed, and completed the SAE-P.

Therefore, I claim (fill in blank) CME Category 1 credit hours (up to 15 hours).

4. To ensure that we accurately process your CME certificate, please print/type your full name, degree(s), and address as they should appear on your certificate.

Name and Degrees: ___________________________________________________________ Address: ___________________________________________________________________ ___________________________________________________________________________ ___________________________________________________________________________

E-mail: _____________________________________________________________________

Signature: __________________________________ Date:

Completing Study Guide activities is an acceptable form of the self assessment required for Maintenance of Certification by the American Board of Physical Medicine and Rehabilitation (ABPMR).

PLEASE COMPLETE AND RETURN THIS APPLICATION, EVALUATION(S) AND CHECK PAYMENT TO:AAPM&R

PO Box 95528 Chicago, IL 60694-5528

Your CME certificate will be mailed to you following receipt of your application, evaluation(s), and check payment to the AAPM&R. The AAPM&R will document your participation in Study Guide activities to the ABPMR.

Before June 15, 2007 After June 15, 2007 AAPM&R member $100.00 AAPM&R member $125.00 Non-member $190.00 Non-member $215.00

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