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Spinal Cord

Medicine

Principles
and Practice
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Spinal Cord
Medicine

Principles
and Practice

EDITOR-IN-CHIEF

VERNON W. LIN, M.D., PH.D.

ASSOCIATE EDITORS

DIANA D. CARDENAS, M.D., M.H.A.


NANCY C. CUTTER, M.D., P.T.
FREDERICK S. FROST, M.D.
MARGARET C. HAMMOND, M.D.
LAURIE B. LINDBLOM, M.D.
INDER PERKASH, M.D., F.A.C.S., F.R.C.S.
ROBERT WATERS, M.D.
ROBERT M. WOOLSEY, M.D.

New York
Demos Medical Publishing, Inc., 386 Park Avenue South, New York, New York 10016

2003 by Demos Medical Publishing, Inc. All rights reserved. This book is protected by copyright.
No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any
means, electronic, mechanical, photocopying, recording, or otherwise, without the prior written
permission of the publisher.

Library of Congress Cataloging-in-Publication Data

Spinal cord medicine : principles and practice / editor-in-chief, Vernon


W. Lin; associate editors, Diana D. Cardenas ... [et al.].
p. ; cm.
Includes bibliographical references and index.
ISBN 1-888799-61-7 (hardcover)
1. Spinal cordWounds and injuries.
[DNLM: 1. Spinal Cord Injuries. 2. Spinal Cord Diseases. WL 400
S757768 2002] I. Lin, Vernon W., 1959 II. Cardenas, Diana D.
RD594.3 .S6696 2002
617.4'2044dc21
2002004958

Made in the United States of America


Dedication

T his book is dedicated to our patients, who stimulate us to expand our


knowledge and skills for improving their health, function, independence, and
well being; to our interdisciplinary colleagues, who work with us side by side,
and stimulate us to be creative and diligent to provide the best care possible;
and to our families, who have demonstrated the love, support, and fore-
bearance necessary to make this text a reality.

v
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Contents

Preface xiii
Foreword xv
Contributors xvii

I INTRODUCTION

1. History of Spinal Cord Medicine


Ibrahim M. Eltorai, M.D. 3

2. Anatomy and Function of the Spinal Cord


Harry G. Goshgarian, Ph.D. 15

3. Imaging of the Spinal Cord


Roland R. Lee, M.D. and Blaine L. Hart, M.D. 35

4. Epidemiology of Spinal Cord Injury


Michael J. DeVivo, Dr.P.H. 79

5. Outcomes Following Spinal Cord Injury


Ien Sie, M.S., P.T. and Robert L. Waters, M.D. 87

II ACUTE SPINAL CORD INJURY MANAGEMENT


AND SURGICAL CONSIDERATIONS

6. Prehospital Management of Spinal Cord Injuried Patients


William Whetstone, M.D. 107

7. Acute Medical Management of Spinal Cord Injury


Cristina Barboi, M.D. and William T. Peruzzi, M.D. 113

vii
viii CONTENTS

8. Factors Afffecting Surgical Decision Making


Patrick J. Connolly, M.D. 125

9. Cervical Injuries: Indications and Options for Surgery


Christopher M. Bono, M.D., Michael J. Vives, M.D., and Christopher P. Kauffman, M.D. 131

10. Surgical Management for Thoracolumbar Spinal Injuries


Paul E. Savas, M.D. and Alexander R. Vaccaro, M.D. 143

III MEDICAL MANAGEMENT

11. Respiratory Dysfunction in Spinal Cord Disorders


Catherine S. H. Sassoon, M.D. and Ahmet Baydur, M.D., F.A.C.P., F.C.C.P. 155

12. Sleep Disorders in Spinal Cord Injury


Lawrence J. Epstein, M.D. and Robert Brown, M.D. 169

13. Cardiovascular Dysfunction in Spinal Cord Disorders


Sunil Sabharwal, M.D. 179

14. Thromboembolism in Spinal Cord Disorders


David Chen, M.D. 193

15. Infection and Spinal Cord Injury


Rabih O. Darouiche, M.D. 201

16. Thermoregulation in the SCI Patient


Thomas C. Cesario, M.D. and Rabih O. Darouiche, M.D. 209

17. The Immune System and Inflammatory Response in Persons with SCI
Fredrick S. Frost, M.D. and Lily C. Pien, M.D. 213

18. Endocrine and Metabolic Consequences of Spinal Cord Injuries


James K. Schmitt, M.D. and Diane L. Schroeder, M.D. 221

19. Primary Care for Persons with Spinal Cord Injury


James K. Schmitt, M.D., Jennifer James, M.D., Meena Midha, M.D.,
Brent Armstrong, M.D., and John McGurl, M.D. 237

20. Spinal Cord Injury: The Role of Pharmacokinetics in Optimizing Drug Therapy
J. Steve Richardson, Ph.D. and Jack L. Segal, M.D., F.A.C.P. 247

IV MANAGEMENT OF THE BLADDER, BOWEL, AND SEXUAL DYSFUNCTION

21. Normal and Abnormal Micturition


John Wheeler, M.D. 259

22. Renal Insufficiency in Patients with Spinal Cord Injury


Cyril H. Barton, M.D. and N.D. Vaziri, M.D., M.A.C.P. 263

23. Urologic Management in Spinal Cord Injury


Donald R. Bodner, M.D. and Inder Perkash, M.D. 299
CONTENTS ix

24. Urolithiasis in Spinal Cord Disorders


Daniel Culkin, M.D. and Michael V. Binins, M.D. 307

25. The Gastrointestinal System after Spinal Cord Injury


Steven Stiens, M.D., M.S., Noel R. Fajardo, M.D., and Mark A. Korsten, M.D. 321

26. Sexual Dysfunction and Infertility in Men with Spinal Cord Disorders
Stacy Elliot, M.D. 349

V NEUROLOGIC ASPECTS OF SPINAL CORD CARE

27. Neurologic Assessment of Spinal Cord Dysfunction


Ralph Marino, M.D., M.S. 369

28. The Electrodiagnostic Examination in Spinal Cord Disorders


Asa J. Wilbourn, M.D. 375

29. Electrophysiologic Evaluation of the Spinal Tracts


Mark A. Lissens, M.D., Ph.D. 399

30. Acute Nontraumatic Myelopathies


Robert M. Woolsey, M.D. and David S. Martin, M.D. 407

31. Chronic Nontraumatic Myelopathies


Robert M. Woolsey, M.D. and David S. Martin, M.D. 419

32. Multiple Sclerosis


Jack Burks, M.D., G. Kim Bigley, M.D., and Haydon Hill, M.D. 429

33. Pain Management in Persons with Spinal Cord Disorders


Thomas N. Bryce, M.D. and Kristjan T. Ragnarsson, M.D. 441

34. Management of Spasticity


Patricia W. Nance, M.D., F.R.C.P.C. 461

35. Autonomic Dysfunction in Spinal Cord Disease


Brenda Mallory, M.D. 477

36. Syringomyelia
James W. Little, M.D., Ph.D. 501

37. Dual Diagnosis: Spinal Cord Injury and Brain Injury


Ziyad Ayyoub, M.D., Fatima Badawi, M.A., C.C.C., S.L.P., Ann T. Vasile, M.D.,
Deborah Arzaga, R.N., Amy Cassedy, M.D., and Vance Shaw, R.N. 509

VI MUSCULOSKELETAL CARE

38. Musculoskeletal Pain and Overuse Injuries


Michael L. Boninger, M.D., Rory A. Cooper, Ph.D., Brian Fay, M.S., and Alicia Koontz, M.S. 527

39. Management of Long Bone Fractures


Douglas Garland, M.D. and Leslie Shokes, M.D. 535
x CONTENTS

40. Bone Loss and Osteoporosis Following Spinal Cord Injury


Beatrice Jenny Kiratli, Ph.D. 539
41. Functional Restoration of the Upper Extremity in Tetraplegia
Vincent R. Hentz, M.D. and Timothy R. McAdams, M.D. 549
42. The Medical Management of Pressure Ulcers
Michael M. Priebe, M.D., Melayne Martin, R.N., C.W.O.C.N., Lisa Ann Wuermser, M.D.,
Teodoro Castillo, M.D., and Jackie McFarlin, R.N., M.P.H. 567
43. The Surgical Management of Pressure Ulcers
Robert E. Montroy M.D., F.A.C.S. and Ibrahim Eltorai, M.D. 591
44. Heterotopic Ossification
Robert Montroy, M.D., F.A.C.S. 613
45. Cardiovascular Fitness after Spinal Cord Injury
Mark S. Nash, Ph.D., F.A.C.S.M. 623

VII REHABILITATION

46. Wheelchairs and Seating


Rory A. Cooper, Ph.D., Michael L. Boninger, M.D.,
Rosemarie Cooper, M.P.T., P.T., and Tricia Thorman, M.O.T., O.T.R. 635
47. Spinal Orthoses
Ed Ayyappa, M.S., C.P.O. and Kelly Downs, B.S. 655
48. Upper Limb Orthoses
Michael Atkins, M.A., O.T.R., Darrell Clark, C.O., and Robert L. Waters, M.D. 663
49. Lower Limb Orthoses and Rehabilitation
Ann Yamane 675
50. Activities of Daily Living
Catherine LeViseur, O.T.R. and Sherry Sonka-Maarek, M.D. 691

51. Recreation and Leisure Skills for People with Spinal Cord Disorders
Jo Lemons, T.R. and Nancy C. Cutter, M.D., P.T. 705

52. Vocational Rehabilitation


Kurt L. Johnson, Ph.D. 715

53. Driving with Spinal Cord Disorder


Norman F. Simoes, M.S.I.E. and Laurie Lindblom, M.D. 723

54. Functional Electrical Stimulation


Peter H. Gorman, M.D. 733

VIII RECENT ADVANCES IN SPINAL CORD RESEARCH

55. Functional Magnetic Stimulation


Vernon W. Lin, M.D., Ph.D. and Ian Hsiao, Ph.D. 749
CONTENTS xi

56. Mechanisms and Natural History of Spinal Cord Injury


Sandra K. Kostyk, M.D., Ph.D., Phillip G. Popovich, Ph.D., Bradford T. Stokes, Ph.D. 765

57. Acute Treatment Strategies for Spinal Cord Injury


Edward D. Hall, Ph.D. 777

58. Recent Advances in Neural Regeneration


Hans S. Keirstead, Ph.D. and Oswald Steward, Ph.D. 785

59. Spinal Cord Repair Strategies


Henrich Cheng, M.D., Ph.D. and Yu-Shang Lee, M.S. 801

60. Retraining the Human Spinal Cord


V. Reggie Edgerton, Ph.D., Susan J. Harkema, Ph.D., and Bruce H. Dobkin, M.D. 817

IX SPECIAL TOPICS IN SPINAL CORD MEDICINE

61. Spinal Cord Injury and Aging


Susan Charlifue, M.A. and Daniel Lammertse, M.A. 829

62. Womens Health Challenges after Spinal Cord Injury


Amie Jackson, M.D. 839

63. Spinal Cord Disorders in Children and Adolescents


Lawrence C. Vogel, M.D., Randal R. Betz, M.D., and Mary Jane Mulcahey, M.S., O.T.R./L. 851

64. The Prevention of Spinal Cord Injury


Russ Fine, Ph.D., M.S.P.H., Wendy Sykes-Horn, M.P.H., and Katherine Terry, M.P.H. 885

X PSYCHOSOCIAL ISSUES AND SUPPORT ENVIRONMENT

65. Psychosocial Factors in Spinal Cord Injury


Robert A. Moverman, Ph.D. 931

66. Social Issues in Spinal Cord Injury


Helen T. Bosshart, A.C.S.W./L.C.S.W. 941

67. The Costs of Spinal Cord Injury


Monroe Berkowitz, Ph.D. 949

68. Model Spinal Cord Injury Systems of Care


Michael J. DeVivo, Dr.P.H. 955

69. VA Spinal Cord Injury System of Care


Margaret C. Hammond, M.D. 959

70. Consortium for Spinal Cord Medicine Clinical Practice Guidelines


Dawn M. Sexton, Kenneth C. Parsons, M.D., and J. Paul Thomas 961

71. Subspecialty Certification in Spinal Cord Injury Medicine


Margaret C. Hammond, M.D. 967
xii CONTENTS

72. CARF: The Rehabilitation Accreditation Commission


Peggy S. Neale, M.A., M.B.A. 969

73. Architectural Considerations for Improving Access


Ian Hsiao, Ph.D. and Thomas Hodne, A.I.A. 975

74. Health Industry and Product Information


Pamela E. Wilson, M.D. and Gerald H. Clayton, Ph.D. 987

Index 993
Preface

S pinal cord medicine (SCM) is best described as the art sections that cover various aspects of medical manage-
and science underlying the diagnosis and treatment of ment, and the management of bladder, bowel, and sex-
patients with spinal cord injury (SCI) and spinal cord ual dysfunctions. A section on the neurologic aspects of
related disorders (SCD). The twentieth century was a spinal cord care considers topics that include the neuro-
landmark era in SCM, highlighted by the development of logic assessment of SCI, electrophysiologic evaluation of
emergency medical services, the establishment of the spe- the spinal tracts, myelopathies, multiple sclerosis, spas-
cialized spinal cord centers, and advances in antibiotic ticity and pain management, autonomic dysfunction, and
use, modern therapies, and technology breakthroughs. concomitant SCI and traumatic brain injury. The mus-
Many patients with SCI and SCD are now living healthy culoskeletal care section addresses overuse injuries, osteo-
lives, with life expectancies approaching that of the gen- porosis and long bone fractures, and interdisciplinary
eral population. Despite recent advances in SCM, con- approaches to upper extremity and pressure ulcer man-
siderable challenges remain and our patients suffer from agement. The rehabilitation section covers wheelchair and
multiorgan failures that require long-term and multidis- seating assessment, orthotics, activity of daily living train-
ciplinary care; and few residency training programs offer ing, vocational and driving training, and functional elec-
exposure or training in comprehensive SCI care. trical stimulation. This is followed by discussions of
This book had its origins in the first review course, recent advances in spinal cord research, including func-
Spinal Cord MedicineAn Intensive Review given at the tional magnetic stimulation, spinal cord regeneration and
annual meetings of the American Paraplegia Society, to repair strategies, and body weight supported ambulation.
prepare physicians to take the subspeciality board in Special topics on aging, womens issues, pediatric care,
spinal cord medicine. Our goal was to develop a com- and SCI prevention are also reviewed. The final section
prehensive text that would cover the breadth and depth considers psychosocial issues, cost of care, SCI systems of
of the field of SCM, covering topics from acute medical care, and various supportive environments for SCI and
and surgical management to cutting-edge research, reha- SCD care.
bilitation, and psychosocial care. This book was developed for all physicians, research
Spinal Cord Medicine consists of 74 chapters in 10 scientists, and other health care professionals involved
sections. It begins with a review of anatomy and physi- in the management of individuals with SCI, multiple scle-
ology, spinal cord imaging, and epidemiology, and is fol- rosis, and other spinal cord disorders. It is a practical
lowed by a comprehensive discussion of acute spinal cord guide, and has been developed to be the ultimate single
injury management that covers prehospital management, source of information on SCM. It will be especially use-
emergency room evaluation and intensive care, and con- ful for physicians who are preparing for the subspecialty
siderations relating to spine surgery. This is followed by certification examination on Spinal Cord Injury Medi-

xiii
xiv PREFACE

cine. We are honored to have chapter contributions from our colleagues in SCM and from all readers in the med-
over 130 authors, selected based upon their training, ical and scientific community.
experience, and clinical leadership, and representing over
20 medical specialties and subspecialties. We welcome Vernon W. Lin, M.D., Ph.D.
comments, suggestions, and constructive criticism from
Foreword

In early 1998, an organizing committee under the lead- In 74 chapters, written by 128 authors, this book
ership of Dr. Vernon Lin began the process of planning covers the normal and abnormal spinal cord from every
an annual review course on Spinal Cord Medicine. This conceivable perspective. Some of the chapters I have had
course has been presented on a yearly basis since. The the opportunity to read are the best I have seen in my 25
committee was unable to find a textbook that it could years of work as a spinal cord specialist (which
recommend to the course attendees that adequately cov- included editing two books on the subject). I have no
ered the course topics. Available texts were either too doubt that they will become the reference whenever
brief and superficial or too large with much content unre- future authors need to cite a review of the subject.
lated to the topic of Spinal Cord Medicine. The closest fit This book is truly a magnum opus. It is unlikely that
was a text by Dr. Robert Young and myself, Diagnosis anything like it will appear again for many years, if ever.
and Management of Disorder of the Spinal Cord, pub-
lished in 1995. However, this book did not cover all top-
ics included in the course. Also, much new information Robert M. Woolsey, M.D.
had become available since 1995 and a second edition Professor of Neurology
of that book was not planned. St. Louis University
Dr. Lin is a problem solver. If a satisfactory book is Director, Spinal Cord Injury Service
not available, he will produce one. In amazingly short St. Louis VA Medical Center
order he assembled the outstanding cadre of editors and
contributors who have created this book.
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Contributors

Brent Armstrong, M.D. Cristina Barboi, M.D.


Medical College of Virginia Assistant Professor of Anesthesiology
VA Medical Center Department of Anesthesiology and Critical Care
Richmond, Virginia Rush Medical College
Chicago, Illinois
Michael Atkins, M.A., O.T.R.
Clinical Specialist Cyril Barton, M.D.
Occupational Therapy Department Associate Professor
Spinal Cord Injury Service Department of Medicine
Rancho Los Amigos National Rehabilitation Center Division of Nephrology and Hypertension
Downey, California University of California, Irvine
Irvine, California
Deborah Arzaga, R.N.
Rancho Los Amigos National Rehabilitation Center Ahmet Baydur, M.D., F.A.C.P., F.C.C.P.
Downey, California University of Southern California
Los Angeles, California
Ed Ayyappa, M.S, C.P.O.
Prosthetic Clinical Manager Monroe Berkowitz, Ph.D.
Desert Pacific Veterans Integrated System Professor of Economics, Emeritus
Long Beach, California Rutgers University
Bureau of Economic Research
Ziyad Ayyoub, M.D. New Brunswick, New Jersey
Chief, Adult Brain Injury Rehabilitation Program
Rancho Los Amigos National Rehabilitation Center Randal R. Betz, M.D.
Assistant Clinical Professor of Medicine Professor of Orthopaedic Surgery
University of California at Los Angeles Temple University
School of Medicine Chief of Staff
Los Angeles, California Shriners Hospital for Children
Philadelphia, Pennsylvania
Fatima Badawi, M.A., C.C.C., S.L.P.
Rancho Los Amigos National Rehabilitation Center
Downey, California
xviii CONTRIBUTORS

G. Kim Bigley, M.D. Diana D. Cardenas, M.D., M.H.A.


Clinical Associate Professor Professor
University of Nevada School of Medicine Department of Rehabilitation Medicine
Medical Director, Multiple Sclerosis Center University of Washington School of Medicine
Washoe Institue for Neurosciences Project Director, Northwest Regional SCI System
Reno, Nevada Seattle, Washington

Michael V. Binins, M.D. Amy Cassedy, M.D.


University of Oklahoma Health Sciences Center University of California at Irvine
Department of Urology College of Medicine
Oklahoma City, Oklahoma Irvine, California

Donald R. Bodner, M.D. Teodoro Castillo, M.D.


Professor of Urology VA North Texas Health Care System
Case Western Reserve University VA Medical Center
University Urologists of Cleveland Dallas, Texas
VA Medical Center
Cleveland, Ohio Thomas C. Cesario, M.D.
Professor of Medicine
Michael L. Boninger, M.D. Dean, UCI College of Medicine
Associate Professor Orange, California
Department of Physical Medicine and Rehabilitation
University of Pittsburgh Susan Charlifue, M.A.
Medical Director of the Human Engineering Research Research Supervisor
Laboratories Craig Hospital
VA Pittsburgh Healthcare System Englewood, Colorado
Pittsburgh, Pennsylvania
David Chen, M.D.
Christopher M. Bono, M.D. Assistant Professor of Physical Medicine
Department of Orthopedic Surgery and Rehabilitation
New Jersey Medical School, UMDNJ-Newark Northwestern University Medical School
Newark, New Jersey George M. Eisenberg Chair in Spinal Cord Injury
Rehabilitation
Helen T. Bosshart, A.C.S.W./L.C.S.W. Medical Director, Spinal Cord Injury Program
SCI Homecare Coordinator Rehabilitation Institute of Chicago
VA Medical Center Chicago, Illinois
Augusta, Georgia
Henrich Cheng, M.D., Ph.D.
Robert Brown, M.D. Director
Director, Acute Ventilator Weaning Unit Neural Regeneration Laboratory
Pulmonary and Critical Care Division Neurological Institute
Massachusetts General Hospital Veterans General HospitalTaipei
Harvard Medical School Taipei, Taiwan
Boston, Massachusetts
Darrell Clark, C.O.
Thomas N. Bryce, M.D. Director, Orthotic Department
Assistant Professor Rancho Los Amigos National Rehabilitation Center
Department of Rehabilitation Medicine Downey, California
Mount Sinai School of Medicine
New York, New York Gerald H. Clayton, Ph.D.
University of Colorado Health Sciences Center
Jack Burks, M.D. Denver, Colorado
Clinical Professor
University of Nevada School of Medicine Patrick S. Connolly, M.D.
Medical Director Associate Professor of Orthopedic Surgery
Washoe Institute for Neurosciences State Universtiy of New York Upstate Medical University
Reno, Nevada Syracuse, New York
CONTRIBUTORS xix

Rory A. Cooper, Ph.D. Stacy Elliott, M.D.


Professor and Chairman Vancouver Hospital and Health Science Center
Department of Rehabilitation Science and Technology West Vancouver, B.C. Canada
Department of Physical Medicine and Rehabilitation
University of Pittsburgh Ibrahim M.Eltorai, M.D.
Director of the Human Engineering Research Laboratories Staff Surgeon
VA Pittsburgh Healthcare System Spinal Cord Injury/Disorder Health Care Group
Pittsburgh, Pennsylvania VA Long Beach Healthcare System
Long Beach, California
Rosemarie Cooper, MP.T., P.T.
Department of Rehabilitation Science and Technology Lawrence J. Epstein, M.D.
Department of Physical Medicine and Rehabilitation Medical Director
University of Pittsburgh Sleep Health Center
Human Engineering Research Laboratories Malden, Massachusetts
VA Pittsburgh Healthcare System
Pittsburgh, Pennsylvania Noel R. Fajardo, M.D.
Department in Internal Medicine
Daniel Culkin, M.D. Mount Sinai School of Medicine
Professor and Chairman VA Medical Center
Department of Urology Bronx, New York
University of Oklahoma Health Sciences Center
Oklahoma City, Oklahoma Brian Fay, M.S.
University of Pittsburgh Medical Center
Nancy C. Cutter, M.D., P.T. Department of PM&R
Director, SCI Department Pittsburgh, Pennsylvania
Barrow Neurology Instititute
Phoenix, Arizona Russ Fine, Ph.D., M.S.P.H.
University of Alabama at Birmingham
Rabih O. Darouiche, M.D. Birmingham, Alabama
Professor of PM&R and Medicine (Infectious Diseases)
Director, Center for Prostheses Infection Frederick S. Frost, M.D.
Baylor College of Medicine Cleveland Clinic Foundation
Houston, Texas Cleveland, Ohio
Michael J. DeVivo, Dr.P.H. Douglas Garland, M.D.
Professor Rancho Los Amigos Medical Center
Department of Physical Medicine and Rehabilitation Downey, California
University of Alabama at Birmingham
Director, National Spinal Cord Injury Statistical Center Peter H. Gorman, M.D.
Birmingham, Alabama Associate Professor
Department of Neurology and Rehabilitation
Bruce H. Dobkin, M.D. University of Maryland School of Medicine
Professor Director, Spinal Cord Injury Service
Department of Neurology Kernan Rehabilitation Hospital
University of California, Los Angeles Physical Medicine and Rehabilitation Service
Los Angeles, California VA Maryland Health Care System
Baltimore, Maryland
Kelly Downs, B.S.
Prosthetic Service Line Harry G. Goshgarian, Ph.D.
Desert Pacific Veterans Integrated System Professor of Anatomy/Cell Biology
Long Beach, California Wayne State University
School of Medicine
V. Reggie Edgerton, Ph.D. Detroit, Michigan
Professor
Brain Research Institute Edward D. Hall, Ph.D.
Physiological Science Department Senior Director
Neurobiology Department CNS Pharmacology
University of California, Los Angeles Pfizer Global Research and Development
Los Angeles, California
Ann Arbor, Michigan
xx CONTRIBUTORS

Margaret C. Hammond, M.D. Kurt L. Johnson, Ph.D.


Chief Consultant Associate Professor and Head
SCI Health Care Group Division of Rehabilitation Counseling
VA Puget Sound Health Care System Department of Rehabilitation Medicine
Professor of Rehabilitation Medicine University of Washington School of Medicine
University of Washington School of Medicine Seattle, Washington
Seattle, Washington
Christopher P. Kauffman, M.D.
Susan J. Harkema, Ph.D. Assistant Clinical Professor
Assistant Professor Department of Orthopedic Surgery
Brain Research Institute University of California at San Diego
Neurology Department San Diego, California
University of California, Los Angeles
Los Angeles, California Hans S. Keirstead, Ph.D.
Assistant Professor
Blain L. Hart, M.D. Department of Anatomy & Neurobiology
University of New Mexico Reeve-Irvine Research Center
VA Medical Center University of California at Irvine
Alburquerque, New Mexico College of Medicine
Irvine, California
Vincent R. Hentz, M.D.
Professor, Department of Surgery Beatrice Jenny Kiratli, Ph.D.
Stanford University School of Medicine Spinal Cord Injury Service
VA Palo Alto Health Care System VA Palo Alto Health Care System
Palo Alto, California Palo Alto, California

Haydon Hill, M.D. Alicia Koontz, M.S.


Clinical Associate Professor University of Pittsburgh Medical Center
University of Nevada School of Medicine Department of PM&R
Medical Director, Rehabilitation Services Pittsburgh, Pennsylvania
Washoe Institue for Neurosciences
Reno, Nevada Mark A. Korsten, M.D.
Professor of Medicine
Thomas Hodne, A.I.A. New York University
Chief Architect Chief of Gastroenterology
Eastern Paralyzed Veterans Association Department of Medicine
Jackson Heights, New York VA Medical Center
Bronx, New York
Ian Hsiao, Ph.D.
Department of Physical Medicine and Rehabilitation Sandra K. Kostyk, M.D., Ph.D.
University of California at Irvine Assistant Professor
Long Beach VA Healthcare System Department of Neurology & Neuroscience
Long Beach, California Ohio State University
Columbus, Ohio
Amie Jackson, M.D.
Medical Director and Chair Daniel Lammertse, M.D.
Department of Physical Medicine and Rehabilitation Craig Hospital
University of Alabama at Birmingham Englewood, Colorado
Birmingham, Alabama
Roland R. Lee, M.D.
Jennifer James, M.D. University of New Mexico
Staff Physician VA Medical Center
VA Puget Sound Health Care System Albuquerque, New Mexico
University of Washington School of Medicine
Seattle, Washington Yu-Shang Lee, M.S.
University of California, Irvine
Irvine, California
CONTRIBUTORS xxi

Jo Lemons, T.R. Melayne Martin, R.N., C.W.O.C.N.


Barrow Neurology Instititute Spinal Cord Injury Service
Phoenix, Arizona VA North Texas Health Care System
Dallas VA Medical Center
Catherine LeViseur, O.T.R. University of Texas Southwestern Medical Center
Department of Rehabilitation Medicine Department of Physical Medicine and Rehabilitation
University of Washington Medical Center Dallas, Texas
Seattle, Washington
Timothy R. McAdams, M.D.
Vernon W. Lin, M.D., Ph.D. Stanford University School of Medicine
Chief, Spinal Cord Injury/Disorder Health Care Group VA Palo Alto Health Care System
Long Beach VA Healthcare System Palo Alto, California
Associate Professor in Residence
Department of Physical Medicine and Rehabilitation Jackie McFarlin, R.N., M.P.H.
University of California, Irvine Spinal Cord Injury Service
Irvine, California VA North Texas Health Care System
Dallas VA Medical Center
Laurie Lindblom, M.D. University of Texas Southwestern Medical Center
Chief, Spinal Cord Injury Service Dallas, Texas
VA Medical Center
Associate Professor John McGurl, M.D.
Department of Physical Medicine and Rehabilitation Medical College of Virginia
Eastern Virginia Medical School VA Medical Center
Hampton, Virginia Richmond, Virginia

Mark A. Lissens, M.D., Ph.D. Meena Midha, M.D.


University Hospital of Ghent Chief, Spinal Cord Injury Service
Department of Physical Medicine and Rehabilitation VA Medical Center
Ghent, Belgium Medical College of Virginia
Richmond, Virginia
James W. Little, M.D.
VA Puget Sound Health Care System Robert E. Montroy, M.D., F.A.C.S.
Professor, Department of Rehabilitation Medicine Assistant Chief
University of Washington School of Medicine Spinal Cord Injury/Disorder Health Care Group
Seattle, Washington Long Beach VA Healthcare System
Long Beach, California
Brenda Mallory, M.D.
Department of Physical Medicine and Rehabilitation Robert A. Moverman, Ph.D.
Columbia University Director, Psychology Services
College of Physicians and Surgeons New England Neurological Associates
New York, New York North Andover, Massachusetts
Northeast Rehabilitation Hospital
Ralph Marino, M.D., M.S. Salem, New Hampshire
Clinical Associate Professor
Department of Rehabilitation Medicine Mary Jane Mulcahey, M.S., O.T.R./L.
Mt. Sinai School of Medicine School of Allied Health
New York, New York Temple University
Philadelphia, Pennsylvania
David S. Martin, M.D.
Associate Professor of Radiology Patricia W. Nance, M.D., F.R.C.P.C.
Saint Louis University Chief, Comprehensive Rehabilitation Health
School of Medicine Care Group
St. Louis, Missouri Long Beach VA Healthcare System
Clinical Professor
Department of Physical Medicine and Rehabilitation
University of California, Irvine
Irvine, California
xxii CONTRIBUTORS

Mark S. Nash, Ph.D., F.A.C.S.M. Kristjan T. Ragnarsson, M.D.


Assistant Professor Dr. Lucy G. Moses Professor
Department of Orthopedics & Rehabilitation Chairman
The Miami Project to Cure Paralysis Department of Rehabilitation Medicine
University of Miami School of Medicine Mt. Sinai School of Medicine
Miami, Florida New York, New York

Peggy S. Neale, M.A., M.B.A. J. Steve Richardson, Ph.D.


Former National Director Professor
Medical Rehabilitation Division Department of Pharmacology
CARFThe Rehabilitation Accreditation Commission University of Saskatchewan
Saskatoon, Saskatchewan, Canada
Kenneth C. Parsons, M.D.
Chairman Sunil Sabharwal, M.D.
Consortium for Spinal Cord Medicine Steering Chief, Spinal Cord Injury Service
Committee Clement J. Zablocki VA Medical Center
Director, Spinal Cord Injury Program Milwaukee, Wisconsin
Institute for Rehabilitation & Research
University of Texas Medical School Catherine S. H. Sassoon, M.D.
Houston, Texas Professor of Medicine
University of California at Irvine
Inder Perkash, M.D. Division of Pulmonary and Critical Care
Professor of Urology and Surgery Department of Medicine
Stanford University School of Medicine VA Long Beach Healthcare System
Chief, Spinal Cord Injury Service Long Beach, California
VA Palo Alto Healthcare System
Palo Alto, California Paul E. Savas, M.D.
Mid Atlantic Spine Specialists
William T. Peruzzi, M.D. Medical College of Virginia
Associate Professor of Anesthesiology Richmond, Virginia
Department of Anesthesiology
Northwestern University Medical School James K. Schmitt, M.D.
Chicago, Illinois Associate Professor of Medicine
Medical College of Virginia
Lily C. Pien, M.D. Chief, General Internal Medicine
Cleveland Clinic Foundation VA Medical Center
Cleveland, Ohio Richmond, Virginia

Phillip G. Popovich, Ph.D. Diane L. Schroeder, M.D.


Assistant Professor Medical College of Virginia
Department of Neurology & Neuroscience VA Medical Center
Department of Molecular Virology, Immunology and Richmond, Virginia
Medical Genetics
Department of Physiology and Cell Biology Jack L. Segal, M.D., F.A.C.P.
Ohio State University Professor of Medicine
Columbus, Ohio University of California at Los Angeles
Los Angeles County Harbor-UCLA Medical Center
Michael M. Priebe, M.D. Torrence, California
Chief, Spinal Cord Injury Service
VA North Texas Health Care System Dawn M. Sexton
Dallas VA Medical Center Project Administrator
Associate Professor Clinical Practice Guidelines
University of Texas Southwestern Medical Center Paralyzed Veterans of America
Department of Physical Medicine and Rehabilitation Washington, DC
Dallas, Texas
Vance Shaw, R.N.
Rancho Los Amigos National Rehabilitation Center
Downey, California
CONTRIBUTORS xxiii

Leslie Shokes, M.D. Tricia Thorman, M.O.T., O.T.R.


Rancho Los Amigos National Rehabilitation Center Department of Rehabilitation Science and Technology
Downey, California Department of Physical Medicine and Rehabilitation
University of Pittsburgh
Ien Sie, M.D., P.T. Human Engineering Research Laboratories
University of Southern California VA Pittsburgh Healthcare System
Rancho Los Amigos National Rehabilitation Center Pittsburgh, Pennsylvania
Downey, California
Alexander R. Vaccaro, M.D.
Norman F. Simoes, M.S.I.E. Professor of Orthopedic Surgery
Sr. Rehabilitation Engineering The Rothman Institute
California Department of Rehabilitation Jefferson Medical College
Rancho Los Amigos National Rehabilitation Center Thomas Jefferson University
Downey, California Philadelphia, Pennsylvania

Sherry Sonka-Maarek, M.D. Ann T. Vasile, M.D.


UCLA, School of Medicine Rehabilitation Associate Medical Group
Little Company of Mary Healthcare Service Long Beach, California
San Pedro, California
N. D. Vaziri, M.D., M A.C.P.
Oswald Steward, Ph.D. Professor
Professor Department of Medicine
Department of Anatomy and Neurobiology Division of Nephrology and Hypertension
Director University of California, Irvine
Reeve-Irvine Research Center Irvine, California
University of California, Irvine
College of Medicine Michael J. Vives, M.D.
Irvine, California Clinical Instructor
Department of Orthopedic Surgery
Steven A. Stiens, M.D., M.S. University of California at San Diego
Associate Professor of Rehabilitation San Diego, California
University of Washington School of Medicine
VA Puget Sound Health Care System Lawrence C. Vogel, M.D.
Seattle, Washington Associate Professor Pediatrics
Rush Medical College
Bradford T. Stokes, Ph.D. Chief of Pediatrics
Professor Shriners Hospital for Children
Department of Neurology & Neuroscience Chicago, Illinois
Department of Molecular Virology, Immunology and
Medical Genetics Robert L. Waters, M.D.
Department of Physiology and Cell Biology Ohio State Clinical Professor of Orthopedic Surgery
University University of Southern California
Columbus, Ohio Project Director, Southern California Regional
SCI System
Wendy Sykes-Horn, M.P.H. Chief Medical Officer
University of Alabama at Birmingham Rancho Los Amigos National Rehabilitation Center
Birmingham, Alabama Downey, California
Katherine Terry, M.P.H. John Wheeler, M.D.
University of Alabama at Birmingham Professor, Department of Urology
Birmingham, Alabama Loyola University Medical Center
Maywood, Illinois
J. Paul Thomas
Coordinator William Whetstone, M.D.
Consortium for Spinal Cord Medicine University of California
Consultant San Francisco, California
Research, Education and Clinical Practice Guideline
Program
Paralyzed Veterans of America
Washington, DC
xxiv CONTRIBUTORS

Asa J. Wilbourn, M.D. Lisa Ann Wuermser, M.D.


Director, EMG Laboratory Chief, Physical Medicine and Rehabilitation Service
Neurology Department Parkland Memorial Hospital
Cleveland Clinic Foundation Assistant Professor
Clinical Professor of Neurology University of Texas Southwestern Medical Center
Case Western Reserve University Department of Physical Medicine and Rehabilitation
Cleveland, Ohio Dallas, Texas

Pamela E. Wilson, M.D. Ann Yamane


University of Colorado Health Sciences Center University of Washington
Denver, Colorado Prosthetics and Orthotics, Rehabilitation Medicine
Seattle, Washington
Robert M. Woolsey, M.D.
Professor of Neurology
Saint Louis University
School of Medicine
St. Louis, Missouri
I

INTRODUCTION
This Page Intentionally Left Blank
1 History of Spinal Cord
Medicine

Ibrahim M. Eltorai, M.D.

he history of spinal cord injury is a of spinal cord injury are found in cases 2933 and 48 of

T long one, dating back to ancient


Egypt. Five thousand years of
recorded history reveal the chroni-
cles of those who labored to care for victims of this cat-
this ancient record. Case 31 states:

If thou examinest a man having a dislocation in a ver-


tebra of his neck, shouldst thou find him unconscious
astrophic injury. In this chapter, advances in the care of of his two arms and his two legs on account of it (and)
spinal cord injury are related in chronological order, from urine drips from his member without his knowing it, his
ancient times to the present. In addition, special attention flesh has received wind, his two eyes are bloodshot: it
is a dislocation of a vertebra of his neck extending to his
is paid to subjects such as surgery, rehabilitation, educa-
backbone, which cause him to be unconscious of his two
tion, and spinal cord regeneration. Although medical arms and his two legs. If, however, the middle vertebra
advances have benefited patients who suffer from spinal of the neck is dislocated, has an emissio seminis which
cord disorders, as well as those who have sustained spinal befalls his phallus, thou shouldst say concerning him,
cord injury, the history of spinal cord disorders is out- one having dislocation of vertebra of his neck while he
side of the scope of this chapter. is unconscious of his two legs and his two arms and his
urine dribbles, an ailment not to be treated [cured].

ANCIENT EGYPT Case 33 is very similar. These cases describe the car-
dinal symptoms of complete cervical cord injury sec-
The Edwin Smith papyrus, which dates to 3,000 to 2,500 ondary to fracture of the cervical spine: tetraplegia, com-
years B.C. is the most authentic document in ancient plete sensory loss, urinary incontinence, priapism,
Egypt. It was written by an Egyptian physician, most involuntary ejaculation, and conjunctival congestion
likely Imhotep (Figure 1.1), and later translated by the caused by the loss of vasomotor control.
famous Egyptologist, Dr. James Breasted of Chicago Uni- The Egyptians did not attempt surgical intervention
versity (1,2,3). It contains accurate descriptions of com- for spinal cord injury, although they did reduce fractures
plete injuries of the cervical spinal cord, as well as the and perform surgical decompression following skull frac-
observation that the best treatment for the injured verte- tures. They used bronze catheters for urinary drainage,
brae is rest and support (Figures 1.2, 1.3). Descriptions and described pressure ulcers.

3
4 INTRODUCTION

FIGURE 1.2
FIGURE 1.1
The Edwin Smith papyrus.
Imhotep.

ANCIENT INDIA His travels in Greece and Egypt greatly affected his med-
ical advancements. He created a method called succession
The Sushruta Samhita (4), written in India during the on a ladder, as well as other methods of traction, for the
third or fourth century A.D., describes the treatment of treatment of spinal cord injuries. He also described para-
spinal injury. The care of cervical dislocations involved plegia with bowel and bladder dysfunction, pressure
manipulative reduction, bandages, splints, and bed rest. ulcers, gibbosity at different levels, and paralysis accom-
Fractures of the lower spine were treated by immobiliza- panied by cold abscess (Potts disease). Indicating that
tion; the patient was placed on a board and tied down traumatic gibbosity is not correctable, he stated where-
by ropes to five pegs. The authors of the Sushruta did fore succession on a ladder has never straightened any-
not believe that spinal fractures were curable. body, as far as I know, it is principally practiced by those
Vaidya (400 B.C.) distinguished different types of physicians who seek to astonish the mob.... But the physi-
ulcers using clinical examination and auscultation (5). cians who follow such practice, as far as I have known
them, are all stupid. In Anatomy of the Spine, Hip-
pocrates mentioned details of articulation, nerves and ves-
ANCIENT GREECE sels, sheaths of the spinal marrow (cord), ligaments and
muscles. In regard to spinal injuries, he states:
Fragmentary records describe the contribution of the
In cases of displacement backward along the vertebrae,
ancient Greeks to spinal cord medicine. Aesculapius, god
it does not often happen, in fact, it is rare that one or
of medicine, was believed to be the son of Apollo, god of more vertebrae are torn from one another and dis-
the sun. The religious cult of Aesculapius took the place placed. For such injuries do not readily occur; as a
of scientific medicine. Hippocrates (460370 B.C.) (Fig- spine could not easily be displaced backward but by a
ure 1.4) disassociated medicine from religion, and severe injury on the fore part through the belly (which
brought Greek medicine to its highest achievement (6). would prove fatal) or if a person falls from height and
HISTORY OF SPINAL CORD MEDICINE 5

FIGURE 1.4

Hippocrates.

FIGURE 1.3
lotus, and many other topical applications on decubiti.
Translation of the Edwin Smith papyrus. He recommended wound irrigation with clean water or
boiled river water (7,8). Celsus advised cleaning with
vinegar and suturing small ulcers with womens hair.
should pitch on the nates or the shoulders (and even
Greek medicine, especially from the school of Alexandria,
in this case he would die, but not immediately). The
spinal marrow would suffer, if from displacement of
influenced and was succeeded by Roman medicine.
a vertebra it were to be bent, even to a small extent,
for the displaced vertebra would compress the spinal
marrow, producing insensitivity of many great and ANCIENT ROME
important organs and many other ill consequences of
a serious nature. In the first century A.D., Aulus Cornelius Celsus, in his
treatise De Medicina, included a brief discussion on spinal
He condemned the open reduction of such cases, and cord injuries, especially fractures of the spinous processes.
favored spontaneous callus formation. He mentioned that For incomplete spinal cord lesions, he recommended Hip-
displacement of vertebrae forward is mostly fatal. If it is pocrates method of traction for vertebral dislocations. In
not fatal, the patient loses the power of his legs and arms complete spinal cord lesions, death usually ensued.
(tetraplegia), and has torpor of the body and retention Galen (131201 A.D.) (9), who practiced in second-
of urine. He introduced the extension bench and other century Rome, was a physician to Marcus Aurelius. He
methods for the reduction of deformities, particularly gib- followed Hippocratic methods, adding very few new tech-
bous. Hippocrates did not distinguish between paralysis niques to medical treatments, but as a founder of exper-
caused by trauma or disease and considered treatment to imental physiology, he wrote over 400 separate treatises.
be the same for either of them. Not only did he describe the anatomy of the brain, but
Hippocrates recommended keeping ulcers dry and also that of the spinal cord and the brachial and lum-
exposed to the air, except when wine or a cataplasm is bosacral plexuses. In addition, he anticipated Brown
applied. He used juices, honey, vinegar, oil, lead, alum, Sequards hemisection. He described injuries of the first
6 INTRODUCTION

and second cervical vertebrae, stating that they are fatal, most comprehensive of which is the Canon of Medicine,
and that respiration stops with injuries at the third or in five volumes. This book was translated into Latin and
fourth vertebrae. He also described other lower-level was the main reference used in European schools for
injuries. Galen believed that evacuation of the bladder almost six centuries.
was accomplished by contraction of the abdominal mus- In relation to spinal injuries, Avicenna followed the
cles, and eminent scholars such as Vesalius and Albrecht method of Paul of Aegina. To reduce dislocations of the
von Haller promulgated this doctrine for centuries. thoracolumbar spine, the physician placed the patient in
Oribasius (10) was born in Greece in the fourth cen- the prone position and stood with his heels on the gib-
tury (324400). He later went to Rome at the invitation bosity. To reduce dislocations of the cervical spine, the
of the Emperor Julian, who requested that Oribasius com- patient was placed in the supine position and neck exten-
pile his knowledge of Greek medicine. While in Rome, he sion was followed by splint fixation. The Arab physician
modified the Hippocratic table to correct spinal deformity Moses Maimonides (Figure 1.6) wrote on diet, hygiene,
using forceful and brisk procedures. and toxicology (15). He practiced in Cairo and followed
Paul of Aegina (625690) (11), also a Greco- Avicennas system. His book, published in 1199, men-
Roman, compiled several books. Book VI described Hip- tioned paraplegia as well as some neurologic signs.
pocrates technique for treating spinal injuries and in Another Arab physician, Albucasis, recommended
addition advised postreduction spinal splinting for the removal of bone fragments from the spinal canal.
treatment of dislocations. He is considered the origina- Western medicine at this time was very primitive.
tor of laminectomy for spinal cord decompression and the Medicine was practiced not by physicians, but by monks
removal of the offending bony fragments. who used religious rites, herbs, salves, and brews to cure
These discoveries and advancements influenced later disease. Although there are many references to the med-
civilizations, just as Greek civilization had influenced that ical remedies of the time, there is nothing recorded about
of Rome. spinal cord medicine.

THE MIDDLE AGES (7001400 A.D.) THE EARLY RENAISSANCE

With the gradual infiltration of the Roman Empire by By the thirteenth century, the school of Salerno brought
barbarian tribes, science was replaced by superstition and European medicine out of the Dark Ages. Constantinus
intellectual stagnation. During this time, Jewish medicine Africanus (16) learned the Arabic language and practiced
may have been the only type of medicine practiced (12). Greco-Arabic medicine. Roland of Parma wrote his book,
In the seventh century, with the rise of Arabic and Islamic Chirurgia, (17) in Salerno in 1210. He discarded the use
civilizations, many works were translated from the Greek, of Hippocrates bench and used new methods for spinal
Latin, Persian, and Hindu languages into Arabic. Avi- cord injuries. For cervical dislocations, the patient was
cenna (9801037) (Figure 1.5), a Persian physician, trans- placed in the sitting position and reduction was effected by
lated and made contributions of his own (13,14). Dur- traction applied to the hair or by a cloth sling under the
ing his life, he compiled about one hundred books, the jaw. For thoracic and lumbar dislocations, the patient was
placed in the supine position and the physician exerted

FIGURE 1.5 FIGURE 1.6

Avicenna. Moses Maimonides.


HISTORY OF SPINAL CORD MEDICINE 7

traction on the legs, with countertraction applied to the ery. Almost a decade later in France, Louis removed a
upper half of the body by an assistant. During this time, metal fragment from a paraplegic officer who eventually
several famous authors in France and Italy published recovered. Trephining the lamina was suggested by
whole books on spinal cord medicine. A gradual transition Chopart (20) (17431795) and Desault (20) (17441795).
from the Latin and Greek languages to the French and The latter recommended trephining the laminae for
English languages paralleled the development of science, decompression even in the absence of visible fracture. In
mathematics, and philosophy in Western Europe. 1762 Antrine Louis (21) removed a bullet lodged in the
spine. In 1793, J. Soemmering wrote about dislocations
and fractures of the spine in his book, Bemerkungen ueber
THE LATER RENAISSANCE Verrenkung uns Bruch des Ruckgraths (20). In the second
half of the eighteenth century, Jean Louis Petit (21) wrote
Paul of Aeginas book (18), written in 1465, recom- his treatise, Les Maladies des Os (Diseases of the Bones),
mended a process for the reduction of a spinal fracture. and his method was used almost exclusively during that
While the physician exerts direct pressure at the fracture century. He reduced fractures by hyperflexion of the spine
site, traction is applied to the upper extremities by one in an attempt to disengage the spinous processes. Lorenz
assistant, and to the lower extremities by another. Heister (22) was a leading German surgeon who used
Ambroise Par was a progressive surgeon who wrote Petits method for thoracic and lumbar injuries, but used
the Ten Books of Surgery (Dix Livres de Chirurgie) 1564 extension for cervical injuries. Hunzovsky in Germany
(19). As a barber-surgeon, he joined the army, and hyperextended the neck for cervical injuries by suspend-
advanced to be the chief army surgeon to four successive ing the patient from the ceiling (23).
kings. He adopted and modified the Hippocratic tech-
nique of fracture reduction by placing the patient in the
prone position. However, he cautioned against causing NINETEENTH CENTURY
more damage through manipulation. The spine was
immobilized by lead splints, and the patient remained in The nineteenth century saw advances in anatomy, pathol-
bed in the supine position for a lengthy period of time. ogy, physiology, and surgery. Medicine became a more sci-
Par also went back to the work of Paul of Aegina, reviv- entific discipline. The history of spinal cord medicine in
ing laminectomy for fractures causing cord compression. the nineteenth century was reviewed by Ohry and Ohry-
For fractures of the spinous process, he only recom- Kossoy (24), and in Garrisons History of Neurology (25).
mended the removal of bony fragments if the patient was Sir Astley Cooper (26) described cauda equina lesions and
in pain. If the fragments were still attached by periosteum their management, as well as fractures and dislocations
and the patient was not in pain, he reduced the fracture of the spine resulting in paralysis. In 1860, BrownSequard
and splinted the back until full healing occurred. For cer- described different kinds of spinal paralysis based on vas-
vical dislocation, he had an attendant press hard on the cular changes (27,28,29). Injuries were divided into tho-
shoulders while he pulled up the head by two hands close racolumbar and cervical paraplegia until 1881, when Sir
to the ears. With some turning of the head, the disloca- William Gull coined the term quadriplegia.
tion was reduced and a stabilizing bandage was applied With the adoption of Joseph Listers (18271912)
around the shoulders. France followed Pars technique techniques of antisepsis, surgical morbidity and mortal-
for a long time; in fact, Jean-Franois Calot used the same ity decreased. Hence, surgeons were encouraged to inter-
techniques in the nineteenth century (20). Falicius Hildans vene more frequently, and progress was made in the field.
(15601634) used a clamp to reduce cervical dislocations, In 1815, H. Cline recommended a controversial new pro-
and in some cases, removed bone fragments and repaired cedure: The removal of the fractured spines and laminae
ligaments. (laminectomy) in fracture dislocations. Because laminec-
tomy weakens the spine, Burrell, in 1887, applied a plas-
ter jacket for postsurgical stabilization. This jacket was
SEVENTEENTH AND also used after manipulative reduction without surgery.
EIGHTEENTH CENTURIES In 1895, Sir Victor Horsley presented his results for treat-
ment of tuberculosis of the spine to the British Medical
By the seventeenth and eighteenth centuries, anatomic dis- Association (30).
section was permitted in Europe. Despite this advance- Two famous world leaders were the victims of spinal
ment, the management of spinal injuries was still primi- cord injuries caused by a gunshot wound, and both died.
tive. Pars technique, with some modification, was used Lord Nelson was injured at the battle of Trafalgar, and he
widely in Germany, Holland, Italy, and England. In France, died a few hours after the injury in 1805 (31,32). In 1881,
during the year 1753, Geraud removed a musket ball from James A. Garfield, the twentieth President of the United
the lumbar spine and the patient experienced partial recov- States, was shot, and died in less than three months (33).
8 INTRODUCTION

TWENTIETH CENTURY rehabilitation of SCI. Under his leadership, this unit


became a world-renowned center for teaching, research,
At the onset of the twentieth century, the prognosis for and clinical care. After the inception of these two units
victims of spinal cord injury remained poor, although it on either side of the Atlantic, many others followed. Drs.
had improved to some extent because of advances in bac- Ernest Bors and A. Estin Comarr in Long Beach, Cali-
teriology and disinfection by Pasteur and Lister, and fornia pioneered rehabilitation and urology protocols
Roentgens discovery of X-rays and ether anesthesia. In that were followed in all the other centers. In Boston H.
the Balkan wars, the mortality rate of spinal cord injury Talbot began an SCI clinic, as did B. Moeller in Mem-
was still 95 percent. Harvey Cushing (34) reported that phis, Tennessee. In the United Kingdom, a number of cen-
80 percent of the battlefield casualties with cervical spine ters developed: Lodgemoor in Sheffield; the Robert Jones
injuries died within the first two weeks. Those who sur- and Agnes Hunt Orthopedic Hospital at Oswestry,
vived had incomplete lower injuries. The British army Shropshire; the Pinderfield Hospital, Wakefield, York-
reported the same results. During the interwar period, the shire; the Liverpool Spinal Unit at Promenade Hospital;
prognosis was still poor, and those who survived led mis- the Edenhall Unit in Musselburgh, Scotland; Phillipshall
erable lives as cripples. Hospital near Glasgow; and Rookwood Hospital,
The scientific advances of the latter half of the twen- Cardiff, Wales. Centers of excellence in Europe included:
tieth century were very great. Advances in the fields of Tobelbad, Austria; Fontainebleau (Paris), Invalides
surgery, rehabilitation, education, urology, pharmacol- (Paris), and Mulhouse, France; Brugman, Belgium;
ogy, and special topics, and research in spinal cord regen- Koblenz, Bachum, Amsburg, Frankfurt, Murnau, Tub-
eration are described separately. ingen, Ludwigshafen, Heidelberg, Cologne, and Berlin in
Germany; Aardenburg, Amsterdam, Holland; and
Dublin, Ireland. A list of other centers in Europe, Canada,
SURGERY Australia, the Middle and Far East, and South America
can be obtained from The International Society of Para-
In 1902 Italy, Lorenzo Bonomo developed the technique plegia. At the present writing, the Department of Veter-
of hemilaminectomy, which was adopted and modified ans Affairs in the United States has twenty-three centers
by many surgeons. In 1905, Harvey Cushing described devoted to spinal cord injuries and disorders. The Depart-
the categories of spinal injuries, and the indications and ment of Health and Human Resources has established
contraindications for surgery in each case. Later advances regional centers in different states. In 1945, Lyndhurst
in surgery of the spinal cord included myelotomy, myelor- Lodge was established in Toronto, Canada, and the
raphy with or without interposition of nerves, and nerve Canadian Paraplegic Association was founded. The
cell transplantation (autologous or embryonic). Canadian Veterans Administration has also established
Numerous advances in orthopedic surgery can be wards for SCI care.
reviewed in the orthopedic and neurosurgical literature Many new diagnostic techniques were developed,
(35,36,37). Surgical orthopedic instrumentation such as such as positive contrast myelography, radionuclide mye-
rods, fixators, wires, screws, meshes, plates, clamps, hooks, lography, peridurography, discography, angiography,
and cements was developed. Different surgical approaches computerized axial tomography (CAT), magnetic reso-
to the spine came into use, including thoracoabdominal, nance imaging (MRI), digital subtraction angiography,
transoral, transthoracic, transabdominal, thorascopic, and ultrasonography, electrophysiological studies, evoked
laparoscopic. Laminotomy, laminectomy, foraminectomy, potentials (sensory and motor), and myelonoscopy.
arthrodesis, and bone grafting were introduced.
After World War I, German experiences in spinal
medicine were recorded by Foerster (38), Lhermitte and REHABILITATION
Roussy (34) did the same in France. In the United States,
dramatic changes began to occur in the early 1930s. Dr. In 1929, Alfred Taylor of New York used a traction hal-
Donald Munro (Figure 1.7), a neurosurgeon with a back- ter fitted to the occiput and the mandible for cervical
ground in general and urological surgery, developed an spinal injuries. In 1933, William A. Crutchfield devised
interest in the care of spinal cord injury (SCI) patients. cranial skeletal traction (45). Other traction devices were
He made great efforts to improve the rehabilitation of made by Barton (1938), Vinke (1948), and Gardner
SCI patients, as well as to meet their socioeconomic needs (1970s). In 1959, Perry and Nickel introduced halotrac-
(3944). Many view Dr. Munro as the true founder of tion, which is still in use.
modern SCI care. In England, on February 1, 1944, Sir The history of rehabilitation medicine is reviewed
Ludwig Guttmann (Figure 1.8) established a unit at Stoke in detail by DeLisa (46). In the three-volume work Prin-
Mandeville (44) in Aylesbury, and introduced multidis- ciples and Practice of Physical Therapy (48), published
ciplinary staffing for the comprehensive treatment and in 1939, there was no mention of SCI made under Phys-
HISTORY OF SPINAL CORD MEDICINE 9

FIGURE 1.8
FIGURE 1.7
Sir Ludwig Guttman.
Donald Munro, M.D.

EDUCATION
ical Therapy of the Nervous Diseases, probably because
the condition carried a mortality rate of 80 percent dur- The care of SCI was very briefly taught in medical schools
ing World War I. In the 1930s, Donald Munro, a neu- until Donald Munro introduced the concept of compre-
rosurgeon at Boston City Hospital, developed an inter- hensive care for SCI victims. His career heralded a turn-
est in and sympathy for the victims of SCI. He developed ing point in the history of SCI treatment. His ideas on neu-
a small center for the comprehensive care of SCI patients, rotraumatology and rehabilitation were first accepted in
and functioned not only as a neurosurgeon, but also as the military hospitals. For the next 40 years, the Veterans
a rehabilitation specialist, urologist, psychologist, Administration led SCI rehabilitation, and remarkable
socioeconomist, researcher, and teacher. He introduced achievements were produced. Annual conferences were
tidal drainage of the bladder (intermittent bladder irri- held, and the papers presented were recorded in the annual
gation), which reduced the risk of urinary tract infec- proceedings. In the 1970s, Erich Krueger, the national
tions. The U.S. Army initiated a SCI center in Oxford- director, initiated traineeships to prepare physicians qual-
Wingate, Massachusetts, where Munros methods were ified in the care of SCI. In the 1980s, Emanuele Manerino
adopted. Munro was a consultant to those Army hospi- initiated a two-year fellowship program, which graduated
tals having SCI sections in the Bronx, Long Beach, many physicians specialized in the comprehensive care of
Chicago, and elsewhere. Ernest Bors and A. Estin spinal cord injured patients. The Department of Health
Comarr carried the torch of care and research and and Human Services established eighteen SCI centers
opened the way for better care of SCI patients. Advances across the United States, leading to the development of SCI
in rehabilitation were carried out by neurosurgeons act- rehabilitation programs in many major universities. Joseph
ing as chiefs of paraplegia sections (Krueger in the Binard initiated annual courses in different regions and
Bronx, Cramer in Memphis, and Scarffond Pool in established educational courses for non-SCI centers.
Atlantic City). Howard Rusk, Arthur Abramson, and The American Paraplegia Society, founded in 1954
Harry Kessler were important figures in rehabilitation. by A. Estin Comarr, incorporated in 1977 and sponsored
Subspeciality areas began to develop, such as geni- annual educational meetings. The American Paraplegia
tourological rehabilitation, sex therapy, infertility ther- Society also established the Journal of Spinal Cord Med-
apy, drivers training, educational counseling, functional icine, which has become a leading journal in the field. In
independence, and development of assistive devices (47). 1978, the Society attempted to register as the American
10 INTRODUCTION

Board of Spinal Cord Injury, but was not approved by the sected cord (52). At this time, research into genetic engi-
American Board of Medical Specialties. Through the neering and stem cell studies also began (53,54).
efforts of Joel A. De Lisa and other leaders in the field,
in 1995 Spinal Cord Injury Medicine was approved as a
subspecialty under the American Board of Physical Med- SPINAL SHOCK
icine and Rehabilitation. Dr. Margaret Hammond, Chief
Consultant to the VA, headed the task of specifying the In 1874 Goltz and Freusberg in Strasbourg clearly
subject matter of the field. described spinal shock in the dog (55). Sherrington pro-
The American Spinal Injury Association (ASIA), duced spinal shock in the monkey, which he referred to
founded in 1971, has made great contributions to the as a neurogenic condition, by transection of the cervical
diagnosis and comprehensive management of SCI cord. Although he did not use the term autonomic dys-
through annual meetings, teaching sessions, workshops, reflexia, he described a rise in blood pressure elicited by
and research grants. ASIA has sponsored several pro- skin stimulation, which appears after the resolution of
grams overseas and thereby furthered the spread of spinal shock (56).
knowledge in many countries.
In 1961, Sir Ludwig Guttman founded The Inter-
national Medical Society of Paraplegia (IMSOP). This AUTONOMIC DYSREFLEXIA
was a major milestone in the care of SCI worldwide. The
Society holds annual meetings in Stoke Mandeville, U.K., Head and Riddoch first described autonomic dysreflexia
and is affiliated with national societies all over the world, in 1917 (57). Its significance and dangers were described
including the Association Francophone Internationale de by Whitteridge (58); Guttmann and Whitteridge (59),
Groupes dAnimation de la Paraplegie, the American Thompson and Witham (60), Pollock et al., Bors and
Paraplegia Society (APS), the American Spinal Injury French (61,62), Schreibert (63), and Arieff et al. (64).
Association (ASIA), the Australian Branch of IMSOP, the Many other reports followed from Europe, America, and
Deutschprachige Medizinische Gesellschaft fr Paralegie Australia.
(DMPG), the Japan Medical Society of Paraplegia
(JMSOP), the Dutch-Flemish Society of Paraplegia
(NVDP), the National Institute for Care of Paraplegia in HETEROTOPIC OSSIFICATION
Sri Lanka (NIP), the Nordic Medical Society of Paraple-
gia (NMSOP), the Southern African Spinal Cord Associ- Para-articular osteoarthropathy was first described by
ation (SASCA), the Spanish Society of Paraplegia (SEP), Riedel (1883) (65) and Eichart (1895). A detailed descrip-
and the Latin American Society of Paraplegia (SLAP). tion of the condition in paraplegics was elaborated by
IMSOP (now ISCOS) established Spinal Cord as their Madame Klumpke-Dejerine and Cellier (66) and Dejer-
official journal, previously known as Paraplegia. ine et al. (67). They were followed by many others, among
them Soule (68), Abramson (69), Abramson and Kam-
berg (70), Liberson (71), Damanski (72), Hardy and
SPINAL CORD REGENERATION Dickson (73), Paeslack (74) Freehafer and Yurick (75),
and Rossier et al. (76).
The work of Ramon y Cajal (19001920) showed that
although severed central nerve fibers in young and adult
mammals commenced to regenerate, the attempts proved URODYNAMICS
abortive and the process did not functionally benefit the
animal (49). During the next two decades, experiments The first measurement of intravesical pressure was made
on amphibia and reptiles showed that regeneration can by Rudolph Haidenhain (1837897) in Breslau. He and
follow cord injury. Colberg focused on sphincter tone; De Wittich and
From 1950 to 1970, Windle worked with DOCA, Rosenplanter (1867) recorded intravesical pressure, and
ACTH, Promin (bacterial polysaccharide), and millipore Julius Budge (18111888) discovered that the third and
tubules. He concluded that there is little evidence, as yet, fourth sacral anterior roots were the motor nerves of the
that true physiological recovery, either motor or sensory, bladder. Goltz experimentally transected the spinal cord
has been attained in mammals (50). From 1970 to 1980, at the thoracolumbar level in dogs and noted reflex blad-
Kao used microsurgery to transplant autogenous brain der evacuation, which disappeared by ablation of the
tissue, sciatic nerve, and nodose ganglion into the spinal lower cord below this level. Schatz (1841920) initiated
cord, and succeeded in demonstrating axonal growth the use of human subjects for spinal cord medicine
within the grafted tissue (51). Fetal neurons, as solid tis- research. Dubois (18481918) continued his work, mea-
sue and as suspension, were transplanted into the tran- suring bladder pressure and rectal pressure in normal con-
HISTORY OF SPINAL CORD MEDICINE 11

trols and paraplegics. Other names in this field are tified ulcers with five medicines. The bones were forti-
Quinke and Adler in Germany, Angelo Mosso and Paul fied with acid principle, the nerves with stinging princi-
Pellacani in Italy, Fritz Born in Switzerland, and Guyon ple, the pulse with salty principle, and respiration with
and Duchastelet in France (77). bitter principle (104). In ancient Egyptian practice, a wide
In Germany, Adler studied manometry in the neu- variety of topical remedies was offered for decubiti,
rogenic bladder and differentiated conal from supraconal including honey, moldy bread, meat, animal and plant
lesions. In Vienna, Schwartz studied cystometry in gun- extracts, copper sulfate, zinc oxide, and alum. Incanta-
shot wounds of the spinal cord. In the United States, tions and recitals were read before the dressings were
Walker, Dalton, Roussy, and Rossi also made advances. applied (105,106). In Persia, Avicenna applied a variety
In Baltimore, Walker proposed simple devices for cys- of topical treatments (107). Among the Arabs, Mai-
tometry. In St. Louis, Dalton coined the term cystome- monides made nutritional recommendations to promote
try, and described the different types of neurogenic blad- ulcer healing (108).
der. Roussy and Rossi studied cystometry in SCI at During the Renaissance there was no physician of
different levels. In England, Henry Head and George Rid- note until the time of Ambroise Par, who insisted on gen-
doch studied neurogenic bladders and described auto- tle handling and meticulous cleanliness of wounds, and
matic micturition as a part of the mass reflex in supra- made recommendations regarding diet and medication
conal lesions. Sir Gordon Holmes studied neurogenic (109).
bladders in soldiers in France (19151916). In 1933 in During the nineteenth century, the discovery of bac-
London, Denny-Brown and Robertson measured bladder teria by Pasteur and antisepsis by Lister improved the out-
pressure, urethral pressure at the bladder neck, external look of wounds in general. The discovery of X-rays by
sphincter pressure, and rectal pressure. In 1935, Kenneth Roentgen helped diagnose underlying bony pathology. In
Watkins described reflexic and areflexic bladders in cord the nineteenth century, Charcot believed in the trophic
injuries. Donald Munro, who in 1947 introduced tidal theory of pressure ulcers, which holds that ulcers are
drainage, described the atonic cord bladder early in injury, caused by the paralysis itself. However, BrownSequard
the autonomous cord bladder, the hypertonic cord blad- opposed this theory (110).
der, and the inhibited cord bladder. Many others con- The twentieth century brought in the antibiotic era.
tributed to the field in the early years, including Nesbit, Sulfonamide (Prontosil) was developed by Domag K in
Lapides, Tang, Ruch, Bors, Comarr, and Bradley. 1935. Penicillin was discovered by Alexander Fleming in
1929, and clinically applied by Florey and Chain in 1940.
Since then, a tremendous number of antibiotics have been
PHARMACOTHERAPY developed to control wound infection. The role of nutri-
tional factors, such as proteins, vitamins and minerals,
Numerous pharmacotherapeutic agents have been tried in ulcer healing, was recognized in the United States. The
in the treatment of SCI, including methylprednisolone, biomechanics of bedsores has also received a great deal
alone (78) or in combination with the antioxidants alpha- of attention (111).
tocopherol and selenium (79); lidocaine (80); alpha- It is impossible to enumerate the topical medications
methyltyrosine (81); aspirin; dipyridamole (82); naloxone and other forms of treatment that have been tried for pres-
(83); DMSO (84,85,86); immunosuppressive drugs (87); sure ulcers. They include antiseptics and antibiotics
nerve growth factor (88); enzyme therapy such as (112,113); antibacterials, which in some cases were cyto-
hyaluronidinase, trypsin, and elastase (89); calcium-chan- toxic (114,115); debriding agents such as enzymes, mag-
nel antagonists (90); gangliosides (91); thyrotropin releas- gots, and synthetic materials (116); electrostimulation (117);
ing hormone (TRH) (92); neurotrophic factors (53); preg- magnetic stimulation (118,119,120); low-intensity laser
nenolone combined with lipopolysaccarides and (121); ultraviolet light (heliotherapy) (122); topical oxygen
endothacin (93); and nitric acid inhibitors (94). Other therapy (123); hyperbaric oxygen therapy (124); ultrasound
approaches have included genetic strategies (53); cooling (125); ozone (126); dry air (127); carbon dioxide laser (128),
(hypothermia) (95); X-rays (96); electromagnetic stimu- occlusive dressing (129); placenta (130); aloe vera (131);
lation (97,98,99); hyperbaric oxygen therapy (100,101); xenografts (132,133); dermografts (134); growth factors
revascularization (102); and acupuncture (103). (135); topical hyperalimentation (136); and surgical closure
techniques such as flaps (137140) and grafts (141).

PRESSURE ULCERS
CONCLUSION
Pressure ulcers have been recognized since antiquity, and
physicians of different civilizations have proposed vari- Throughout mans history, SCI has been a catastrophic
ous treatments. Chinese ulcer physicians (Young) (97) for- condition, and the prognosis a very gloomy one. Only
12 INTRODUCTION

after World War II did the labor of distinguished clini- 26. Cooper A. Lecture 181 of injuries of the spine. Lancet 1823;
1:303306.
cians and scientists improve the look of SCI victims. In 27. BrownSequard E. Possibility of repair and of return of function
universities all over the world, researchers are working to after a partial or a complete division of the spinal cord in man
erase Imhoteps dictum that spinal cord injury is an ail- and animals. Lancet 1859; 1:9697.
28. BrownSequard CE. Lecture III: Diagnosis and treatment of para-
ment not to be cured. As Professor Max Thoreck has plegia due to myelitis, meningitis or a simple congestion. Lancet
said, La science na pas de patrie (science has no home- 1860; 2:2728.
land). It is hoped that the efforts of researchers around 29. BrownSequard CE. Lecture III, part II. Lancet 1860; 2:7778.
30. Horsley Victor. Chronic spinal meningitis. Brit Med J 1909; 1:513
the world will soon fulfill mans wishes for a cure. 31. Trunkey D. The Admirals wounds. Amer Coll Surg Bull, Feb
1994; Vol 79, 2:1927.
32. Beatty W. Nelsons fatal wound. Lancet, 1906; 6:68.
References 33. Ridpath JC. The Life and Work of James A. Garfield, 20th Pres-
ident of the United States. Cinncinati: James Brothers, 1882.
1. Breasted JH. The Edwin Smith Surgical Papyrus. Chicago, IL. 34. Guttmann L. Spinal Cord Injuries: Comprehensive Management
1930; Vol I:316-342, 425428. & Research. Oxford: Blackwell Scientific, 1976; 5.
2. Elsberg C. The Edwin Smith Surgical Papyrus: The diagnosis and 35. Livshits AV. Surgery of the Spinal Cord. [Translated from Russ-
treatment of injuries to the skull and spine 5000 years ago. Annals ian by VE Tator-Chenko.] Madison, CT.: International Press, Inc.
of Med History, March 5, 1931; 271279. 1991.
3. Hughes JT. The Edwin Smith Surgical Papyrus: An analysis of the 36. Chapman MW, Madison M. Operative Orthopedics. Philadel-
first case reports of spinal cord injuries. Paraplegia 1988; (2) phia: JB Lippincott, 1993; Vol. 4.
7182. 37. Meyer Paul Jr. Surgery of Spinal Trauma. New York: Churchill
4. Kaviraj KLB. Sushutra Samhita. Calcutta: 1911; Vol II:100: Livingston, 1989.
284285. 38. Foerster O. Handbuch der Neurologie Ergangungsband. Berlin:
5. Majno A. The Healing HandMan and wound in the Ancient Springer, 1929.
World. Cambridge, MA.: Harvard University Press, 1975. 39. Munro D. The rehabilitation of patients totally paralyzed below
6. Adams F. The Genuine Works of Hippocrates [translated from the waist, with special reference to making them ambulatory and
the Greek]. Baltimore: Williams & Wilkins. 1939; 231242. capable of earning their own living. New Eng J Med: 233(16):
7. Ibid., 325336. 453461.
8. Ibid., 289306. 40. Munro D. The cord bladder: Its definition, treatment, and prog-
9. Galen. Omnia Opera [Carolus Kuhn Edition] Leipzig: 1821; nosis, when associated with spinal cord injury. New Eng J Med
170174, 237250. 1936; 215(17):766777.
10. Oribasius. Oeuvres dOribase [Daremberg Edition]. Paris: 1862; 41. Munro D. Tidal drainage of the urinary bladder. New Eng J Med
Vol IV: 242243, 394395, 449451. 1935; 212(6):229239.
11. Adams F. Paulus Aeginata. London: 1846; Vol II:455456, 42. Munro D. The treatment of the urinary bladder in cases with
493497. injury of the spinal cord. Am J Surg, 1937; 38(1):120-136
12. Ohry A, Ohry-Kossoy K. Spinal Cord Injuries in the nineteenth 43. Munro D. The Treatment of Injuries to the Nervous System.
century. A monograph published as a supplement to Paraplegia Philadelphia: WB Saunders, 1952.
1989; 12324. 44. Guttmann L. Spinal Cord Injuries: Comprehensive Management
13. Avicenna [Abu Ali Al Hussein]. Avicennae Operum de Rex Med- & Research. Oxford: Blackwell Scientific 1976.
ica. Venice, 1564; Vol II, Book IV, Chap XXIXXII. 45. Barnett GH, Hardy RW. Gardner tongs and cervical traction.
14. Avicenna [Ibn Sina]. Al Quanom FIT Tibb. Cairo: Government Medical Instrumentation 1982; 16:291292.
Press, Boulaque, 1877. 46. DeLisa J (ed.) Rehabilitation Medicine. Philadelphia: JP Lippin-
15. Rambam (Maimonides). Medical Aphorisms of Moses. Hebrew cott, 1993; 339.
translation by R. N Hameathi, 1283; 2nd edition edited by 47. Krueger Eric G. Birth of Holistic Spinal Neurotraumatology in
Bosner Fred, S Muntner. Jerusalem: Yeshiva Univ. Press 1982. America, Donald Munro Memorial Lecture J Am Parapl Soc
16. Howorth B, Petrie JG, Bennett G. Injuries of the Spine. Baltimore: (now Spinal Cord Med) 1984; 7:1012.
Williams and Wilkins, 1964; 113. 48. Mock HE, Pemberton R, Coulter JS. Principles and Practice of
17. Carbonelli G. La Chirurgia de M. Rolando da Parma. Rome: Physical Therapy. Hagerstown, MD: WF Prior, 1939.
1927. 49. Ramon y Cajal. Degeneration and Regeneration of the Nervous
18. Uenver AS. Serefeddin Subuncuoglus Album des Dessins de Cer- System, Vol 2, [RM May, translator and editor.] London: Oxford
rahiyei Ilhaniye. Istanbul: 1939; 3842, 58, 66. University Press, 1928; 397769.
19. Par A. Oeuvres. Paris: 1598; 528, 554, 559. 50. Windle WF. Regeneration of the central nervous system. In:
20. Guttmann L. Spinal Cord Injuries: Comprehensive Management French JD (ed.), Basic Research in Paraplegia. Springfield, IL.:
& Research. Oxford: Blackwell Scientific. 1976; 13. Charles C. Thomas, 1962; 38.
21. Louis A. Remarques et Observation sur la Fracture et la. Luxa- 51. Kao CC. Comparison of healing process in transected spinal
tion des Vertebras; Memoires lu a la sance publique de cords grated with autogenous brain tissue, sciatic nerve and
lAcadmie Royale de Chirurgie, le 18 avril 1774. Arch Gen Med nodose ganglion. Exp Neurol 1974; 44: 424439.
(2nd series) 11:397429, 1836. 52. Narnes H, Bjorklund A, Stenevi U. Transplantation strategies in
22. Petit JL. Trait des maladies chirurgicales et des oprations qui spinal cord regeneration. In: Sladek JR, Gash DM (eds.), Neural
leur conviennent, 3 vol. P Fr Didot. In: Greenblatt S, Dagi TF, Transplants; Development and Function. New York: Plenum
Epstein M (eds.), A History of Neurosurgery: in its scientific and Press, 1984; 407421.
professional contexts. Park Ridge IL: American Association of 53. Tator CH. Experimental and clinical studies of the pathophysi-
Neurological Surgeons, 1997; 75. ology and management of acute spinal cord injury. J Spinal Cord
23. Hunczovsky JH. Anweisung zu chirurgischen Operationen fr Med 1996; 19(4):206214.
seine Vorlesungen bestimmt. Wien R Graeffer, 1787; 249295, 54. DeLisa J (ed.). International Symposium on Spinal Cord Injury:
325326. Neurology and new therapeutic approaches. Spinal Cord Medi-
24. Ohry A, Ohry-Kossoy K. Spinal cord injuries in the nineteenth cine 1999; vol 22: 2530, Supplement.
century. A monograph published as a supplement in Paraplegia 55. Goltz P. Die Funktionen des Lendenmarkes des Hundes. Arch Ges
1989; 139. Physio 1874; 8:460.
25. McHenry L. Garrisons History of Neurology. Springfield, IL: 56. Denny-Brown D. Selected Writings of Sir Charles Sherrington.
Charles C. Thomas Publishers,1969; 421430. London: Hamish Hamilton, 1939; 120154.
HISTORY OF SPINAL CORD MEDICINE 13

57. Guttmann L. Spinal Cord Injuries: Comprehensive Management 89. Matinian LA, Windle WF. Functional structural restitution after
and Research. Oxford: Blackwell Scientific, 1976; 354363. transection of the spinal cord. Ann Res 1975; 181:423.
58. Silver JR. Historical review: The history of Guttmanns and Whit- 90. Faden A, Jacobs TP, Smith MT. Evaluation of calcium channel
teridges discovery of autonomic dysreflexia. Spinal Cord 2000; antagonist nimodepine in experimental spinal cord ischemia. J
38:581596. Neurol Surg 1984; 60:796799.
59. Guttmann L, Whitteridge D. Effects of bladder distention on 91. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor func-
autonomic mechanism after spnal cord injuries. Brain 1947; tion after spinal cord injury: A randomized placebo controlled
70:361404. trial with GM-1 ganglioside. New Eng J Med 1991;
60. Thompson CE, Witham AC. Paroxysmal hypertension in spinal 324:18291838.
cord injuries. N Engl J Med 1948; 239:2:291294. 92. Pitts LH, Ross A, Faden AP. Treatment with thyrotropin releas-
61. Pollock LJ. Defects in regulatory mechanism of autonomic func- ing hormone (TRH) in patients with traumatic spinal cord injury.
tion in injuries to the spinal cord. J Neurophysiol 1951; J Neurotrauma 1995; 12:235243.
14:8593. 93. Guth L, et al. Key role for pregnenolone in combination therapy
62. Bors E, French JD. Management of paroxysmal hypertension fol- that promotes recovery after spinal cord injury. Proc Natl Acad
lowing injury to cervical and upper thoracic segments of the Sci USA 1994; 91:1230812312.
spinal cord. Arch Surg 1952; 64:803812. 94. Hitchon PW, et al. Response of spinal cord blood flow to nitric
63. Schreibert CD. Studies on the sacral reflex arc in paraplegic sur- oxide inhibitor. Neurosurgery 1996; 39(4): 795803.
gical therapy of autonomic hyperreflexia in cervical and upper 95. Negrin J. Local hypothermia in spinal cord traumatic lesions.
thoracic myelopathy. J Neurosurg 1955; 12:468474. Third International Congress of Neurological Surgery, Copen-
64. Arieff AJ, Tigay EL, Ryzik, SW. Acute hypertension induced by hagen. Excerpta Med Int Con 1975; Series 110, 377381.
urinary bladder distention, headache and it correlates in quadri- 96. Turbes CC et al. X-radiation of experimental lesions of the spinal
plegic patients. Arch Neurol 1962; 6:8896. cord. Neurology 1960; 10:8489.
65. Riedel B, Verh. Dtsch. Ges. Chir, 1883; 12:93. 97. Young W, et al. Pulsed electromagnetic field (PEMF) and methyl-
66. Klumke-Dejerine C. Rev. neurol, 1918; 25:159, 207, 348. prednisolone (MP) alter calcium and functional recovery in spinal
67. Klumke-Dejerine C. & Cellier A. Para-osteo-arthropathies de cord injury. Paper 67, presented at Annual Meeting of American
paraplgiques par lsions mdullalaires, Am Med, 1919; 34:399. Association of Neurological Surgeons, San Francisco, April 812,
68. Soule AB. Neurogenic ossifying fibromyopathies. J Neurosurg 1984.
1945; 2:485. 98. Wilson DH, Jagadeesh P. Experimental regeneration in periph-
69. Abramson AS. Bone disturbances in injuries to spinal cord and eral nerves and spinal cord in laboratory animals exposed to a
cauda equina (paraplegia): their prevention by ambulation. J pulsed electromagnetic field. Paraplegia 1976; 14:1220.
Bone Joint Surg 1947; 30:982991. 99. Wilson DH. The use of peripheral nerve grafts in spinal cord
70. Abramson A, Kamberg G. J Bone Joint Surg 1949; 31A:982. repair: In: Glusta EDN, Frankel HL (eds.), Spinal Cord Medical
71. Liberson M. Am Med Ass. 1953; 152:1010. Engineering. Springfield, IL: Charles Thomas Publishers, 1986;
72. Damanski M. J Bone Joint Surg 1961; 43B:286. 115130.
73. Hardy A, Dickson JW. J Bone Joint Surg 1963; 4B:76. 100. Higgins Alfred et al. Effects of hypertonic oxygen therapy on long
74. Paeslack V. Inernistische Strungen bein Paraplegiker 1965; tract neural conduction in the acute phase of spinal cord injury.
5960. J Neurosurg 1981; 55:501510.
75. Freehafer A, Yurick R, Mast A. Para-articular ossification in 101. Asamoto S, et al. Hyperbaric oxygen (HBO) therapy for acute
spinal cord injury. Med Services J, Canada 1966; 22:471477. traumatic cervical spinal cord injury. Spinal Cord 2000;
76. Rossier, AB et al. Current facts on paraosteoarthropathy (POA). 38:538540.
Proceedings of the Annual Meeting of the International Medical 102. Goldsmith HS, De la Torre JC. Axonal regeneration after spinal
Society of Paraplegia, Heidelberg. Paraplegia, 1973; II:1:3678. cord injury and reconstruction. Brain Res 1991; 589:217224.
77. Ek Anders, Bradley William E, History of cystometry, Urol 1983; 103. Politis MJ, Korchinski MA. Beneficial effects of acupuncture
12:3:335350. treatment following experimental spinal cord injury: A behav-
78. Bracken MB, Collins WF, Freeman DF et al. Efficacy of methyl- ioral morphological and biochemical study. Acupuncture Elec-
prednisolone in acute spinal cord injury. JAMA 1984; 251:4552. trotherapeutics Res Int J 1990; Vol 15:3749.
79. Sanders RD, Dugan LL, Demedink P et al. Effect of methyl- 104. Constantian MB. Pressure Ulcers, Principles and Technique Man-
prednolone and combinations of alpha-tocopherol and selenium agement. Boston: Little Brown, 1980; 4.
on arachidonic acid metabolism and lipid peroxidation in trau- 105. Ebbell B. The Papyrus Ebers, The Greatest Egyptian Medical
matized spinal cord tissue. J Neurochem 1987; 49(1):2431. Document. London: Oxford University Press, 1937.
80. Siavash S et al. Effect of lidocaine treatment on acute spinal cord 106. Ebers A, Stern L. Papyrus Ebers: Das Hermetische Buch ber
injury. Neurosurgery, 1987; 20(4):536541. die Arzneimittel der alter Aegypten. Leipzig: JC Henriches, 1875;
81. Osterholm JL et al. A review of altered norepinephrine metab- 3 vols.
olism attending severe spinal injury. Results of alphamethylty- 107. Avicenna [Ibn Sina]. Al Knun Fil Tibb. Arabic text: Cairo Gov-
rosine treatment. Proceedings of the eighteenth Spinal Cord ernment Press, 1877; 168180.
Injury Conference, Oct. 1971; 1720. 108. Rosner F, Munter S. The Medical Aphorisms of Moses Mai-
82. Fujita Y et al. Evaluation of low dose aspirin, dipyridamole and monides. New York: Yeshiva University Press, 1971; Vol 2:28.
steroid therapeutic effects on motor function. Paraplegia 1985; 109. Par A. The works of Ambrose Parey translated out of Latin and
23:5657. compared with the French by Th. Johnson, London: Th. Coates
83. Black P et al. Naloxone and experimental spinal cord injury: Part & R Young, 1634.
I. Neurosurgery 1986; 19(6):905908. 110. Levine JM. Historical perspective: The neurotrophic theory of
84. Ruigrak TJC et al. The effect of dimethylsulfoxide on the calcium skin ulceration. J Amer Ger Soc 1991; 40: 12811283.
paradox. Am J Pathol 1981; 103:390403. 111. Kenedi RM, et al. Bedsore Biomechanics. Baltimore: University
85. De La Torre et al. Modification of experimental head and spinal Park Press, 1976.
cord injury using DMSO. Trans Amer Neurol Asoc 1972; 112. Morgan J. Topical therapy of pressure ulcers. Surg Gyn Obst
97:230233. 1975; 141:945947.
86. Kajihara K et al. Dimethylsulfoxide in the treatment of experi- 113. Michael J. Topical use of PVP (Betadine) preparations in patients
mental spinal cord injury. Surg Neurol 1973; 1:1622. with spinal cord injury. Drugs Explt Clin Res, 1985; XI(2):
87. Faringa R et al. Immunosuppressive treatment to enhance spinal 107109.
cord regeneration in rats. Neurology 1974; 24:287303. 114. Lineaweaver W, et al. Cellular and bacterial toxicities of topical
88. Scott D, Liu CN. Factors promoting regeneration of spinal neu- antimicrobials. Plastic and Recon Surg 1985; 75(3):394396.
rons. Positive influence of nerve growth factor. Prog Brain Res 115. Dakin HD. The antiseptic action of hypochlorites. Brit Med J
1964; 131:127150. 1915; 2:809810.
14 INTRODUCTION

116. Teich S et al. Maggot therapy for severe skin infections. S Med J 129. Ryan TJ. Beyond occlusive wound care. Royal Soc Med Intl Con-
1986; 79(1):153155. gress & Symposium #136; Royal Soc of Med Services, London,
117. Wolcott HE, et al. Accelerated healing of skin ulcers by elec- New York 1988.
trotherapy, South Med J 1969; 62:795. 130. Kumar N. Evaluation of the effect of placental extracts on bed-
118. Wood JM, et al. Multicenter study on the use of pulsed low inten- sores. Indian Med J 1994; 88(5):145.
sity direct current for healing of Stage II and Stage III decubitus 131. Wiseman DM et al. Wound dressing: design and use. In: Cohen
ulcers. Arch Dermatol 1993; 129:9991009. IK, Diegelmann RF, Lindblad EJ (eds), Wound Healing: Bio-
119. Cameron B. Experimental acceleration of wound healing. Amer hemical and Clinical Aspects. Philadelphia: W. B. Saunders, 1992.
J Orthop 1961; 336343. 132. Grotendorst AR. Chemattractants and growth factor. In: Cohen
120. Duma-Drzewinska A. Pulsed high frequency currents applied in IK, Diegelmann RF, Lindblad EJ (eds), Wound Healing: Bio-
treatment of bedsores (Polish with English translation) Polski hemical and Clinical Aspects. Philadelphia: W. B. Saunders, 1992.
Tygonik Lekarski 1978; 33(22):12. 133. Eresk RA, Lario J. The most indolent ulcers of the skin treated
121. Ceschino M, et al. Helium neon soft laser in the treatment of with porcine xenografts and silver ion. Surg Gyn & Ob 1984;
decubitus ulcer. Minerva Clinic 1988; 43(12):4956. 158:431436.
122. High S, High JP. Treatment of infected wounds using ultraviolet 134. Pham H, et al. Evaluation of human skin equivalent for treatment
radiation. J Physio Therap 1983; 69(10) 359360. of diabetic foot ulcers in a prospective randomized clinical trial.
123. Fischer BH. Topical hyperbaric oxygen treatment of pressure Wounds 1999; 11(4):79-86.
sores and skin ulcers. Lancet 1969; 2:405409. 135. Wiseman DM, et al. Wound dressings: design and use. In: Cohen
124. Eltorai I. Hyperbaric oxygen in the management of pressure sores IK, Diegelmann RF, Lindblad EJ (eds), Wound Healing: Bio-
in patients with injuries of the spinal cord. J Dermatol Surg Oncol hemical and Clinical Aspects. W. B. Saunders, 1992; 248325.
1981; 7:9:737740. 136. Niinikoski J, et al. Local hyperalimentation of experimental gran-
125. Paul BJ, Lafratte CW, et al. Use of ultrasound in the treatment ulation tissue. Current Surg 1978; 394418.
of pressure sores in patients with spinal cord injury. Arch Phys 137. Davis JS. The operative treatment of scars following bedsores.
Med Rehab 1960; 41:438. Surg 1938; 3:1.
126. Tahakova MA. Die ozonatherapie bei obliterierenden arteriellen 138. Conway H, et al. Plastic surgical closure of decubitus ulcers in
Gefaeserkrankungen und atomische Geschwuren. Med Heute patients with paraplegia. Surg Gyn Ob 1947; 85:321.
1967; 9:272274. 139. Constantian, MB. Pressure Ulcers, Principles and Technique Man-
127. Denholm DH. The hair dryer treatment for decubiti. Can Nurse agement. Boston: Little Brown, 1989; 149246.
1974; 10:33. 140. Mathes SJ, Nahai F. Clinical Atlas of Muscle and Myocutaneous
128. Stellar S, et al. Carbon dioxide laser debridement of decubitus Flaps. St Louis: CV Mosby, 1979.
ulcers followed by immediate rotation flap or skin graft closure. 141. Thiersch K. Orthopedic Operations of General Surgery. Philadel-
Ann Surg 1974; 179:230237. phia: WB Saunders, 1944:55.
2 Anatomy and Function
of the Spinal Cord

Harry G. Goshgarian, Ph.D.

his chapter is written for physicians GROSS ANATOMY

T and other practitioners who care for


patients with spinal cord injury
(SCI), and thus does not include all
of the macroscopic and microscopic details of human
Extent and Appearance
The spinal cord in man is roughly cylindrical in shape and
is slightly flattened anteriorly and posteriorly. It begins
spinal cord anatomy that may be included in standard
at the caudal end of the medulla oblongata and leaves
medical texts. Only major topics are discussed and, when-
the cranial vault by extending through the foramen mag-
ever possible, the issues are covered from a perspective
num into the vertebral canal. At birth, the spinal cord ter-
that is relevant to spinal cord medicine. For instance,
minates at the lower border of the third lumbar vertebra.
although the standard medical text description of the arte-
In adults, the spinal cord is between 42 and 45 cm in
rial blood supply to the spinal cord is included, there is a
length, weighs about 35 grams, and usually terminates
discussion of how an understanding of the distribution
at the level of the intervertebral disk between L1 and L2.
pattern of these arteries may lead to a diagnosis of ante-
However, the most inferior extent of the spinal cord, the
rior cord syndrome. In addition, although the function of
conus medullaris, may be found as high as T12 or as low
several ascending and descending spinal pathways is dis-
as L3. Thus, in adults, the spinal cord does not extend the
cussed, emphasis is placed only on those that are most rel-
entire length of the vertebral canal, but rather only occu-
evant to spinal cord injury. Details regarding the intrin-
pies its superior two-thirds (Figure 2.1). The basis for the
sic neuroanatomic organization of the gray and white
discrepancy in length between the vertebral column and
matter have been omitted, but references are included at
spinal cord is embryologic.
the end of the chapter so that a reader may pursue this
Briefly, during the first trimester of development the
information if it should become necessary. This chapter
spinal cord and vertebral column are approximately the
is organized into three major sections, which cover the
same length. During this time the spinal nerves establish
gross anatomy, neuroanatomic organization, and blood
connections with the periphery by passing through the
supply of the spinal cord.
appropriate intervertebral foramina at almost right angles
to the longitudinal axis of the developing cord. After the
body segments are innervated, the vertebral column elon-
gates caudally in subsequent stages of development, but
15
16 INTRODUCTION

spinal cord and vertebral column is a progressive increase


in the length of spinal nerve roots within the vertebral
canal, with the shortest extension found at lower cervi-
cal levels and the longest found at sacral levels. Thus, in
adults, upper and mid-cervical spinal nerves have the
shortest roots. From low cervical to sacral levels, the dis-
tance is progressively increased between the interverte-
bral foramen transmitting a nerve and the spinal cord seg-
mental level giving rise to the roots of that nerve, and
any particular spinal cord segment lies somewhat higher
than its corresponding numbered vertebra (Figure 2.1). It
is important to appreciate that during development spinal
nerves do not grow caudally in the vertebral canal to ulti-
mately find their way to the appropriate intervertebral
foramen and body segment. Rather, the connections are
made early in development, and then the nerve roots elon-
gate as the caudal half of the fetus grows in the later stages
of development.

Relation of Spinal Nerves and Segments


to the Vertebral Column
The thirty-one pairs of spinal nerves include eight cervi-
cal, twelve thoracic, five lumbar, five sacral, and one coc-
cygeal pair. Spinal nerves emerge from the vertebral canal
via the intervertebral foramina. The first seven cervical
nerves pass out of intervertebral foramina above the ver-
tebra having the corresponding number. For example, the
sixth cervical nerve passes out of the foramen above the
sixth cervical vertebra (Figure 2.1). Because there are eight
pairs of cervical nerves, but only seven cervical vertebrae,
it is best to remember that the eighth cervical nerve passes
out below the seventh cervical vertebra. This establishes
a pattern in which all remaining spinal nerves (thoracic,
lumbar, sacral and coccygeal) pass out below the verte-
bra with the corresponding number (Figure 2.1).
A knowledge of the anatomic relationship between
spinal cord segments and the vertebral column is impor-
tant for the diagnosis and treatment of certain spinal cord
disorders, such as compression injury caused by a tumor.
An appreciation of the relation of the spinal segment to
overlying vertebra and spinous process is necessary when
laminectomy is contemplated to relieve the spinal cord
compression. As a general rule, at the upper cervical lev-
els of the vertebral column (i.e., from C2C5) add 1 to
the number of the spinous process to indicate the number
FIGURE 2.1 of the underlying spinal segment at the tip of the process.
Thus, the tip of the fourth cervical spinous process over-
Diagram of the position of the spinal cord segments with ref-
erence to the bodies and spinous processes of the vertebrae.
lies the fifth cervical segment of the spinal cord. From
mid-cervical to mid-thoracic levels (i.e., C6T6), the
underlying spinal cord segment at the process tip is iden-
tified by adding 2 to the number of the spinous process;
the spinal cord does not match this caudal extension and and at mid-thoracic to low-thoracic levels (i.e., T7T10),
terminates superiorly in the vertebral canal, as mentioned by adding 3 to this number. The eleventh and twelfth tho-
earlier. The result of this disparate growth between the racic spinous processes overlie the five lumbar spinal cord
ANATOMY AND FUNCTION OF THE SPINAL CORD 17

segments, and the first lumbar spinous process overlies The spinal cord is not uniform in diameter; it con-
the five sacral segments. The part of the vertebral canal tains two enlargements associated with the innervation of
formed by the last four lumbar vertebrae and the sacrum the upper and lower limbs. The cervical enlargement is
contains a collection of long lumbar and sacral anterior the more prominent of the two and is found at the C5T1
and posterior roots known as the caudal equina (horses levels. These segmental levels are the same levels that give
tail) in addition to a specialization of the pia mater known rise to the nerve roots that form the brachial plexus and
as the filum terminale. thus provide innervation for the upper limb. The lumbar
enlargement gives rise to neurons and fibers that form the
lumbar plexus (L1L4) and the sacral plexus (L4S2),
Surface Anatomy and Enlargements
both of which are involved in the innervation of the lower
The surface of the spinal cord displays a number of lon- limbs. These enlargements are the natural result of the
gitudinally oriented grooves (Figure 2.2). On the poste- necessary increase in neurons and their processes at these
rior surface in the midline is the shallow posterior median levels for the innervation of limb musculature and skin.
sulcus. This sulcus is continuous with the posterior
median septum, a glial partition extending deeply to the
Terminal End of the Spinal Cord
gray matter. The posterolateral sulcus is a shallow groove
that demarcates the entrance of the dorsal roots into the As mentioned earlier, the tapered end of the spinal cord
spinal cord bilaterally. In the cervical and upper six tho- is usually found at the level of the intervertebral disk
racic spinal cord segments, the posterior intermediate sul- between L1 and L2 and is called the conus medullaris
cus and underlying posterior intermediate septum is (Figures 2.1 and 2.3). The conus medullaris consists of
found between the posterior median and posterolateral sacral spinal cord segments. It provides sensory innerva-
sulci on each side of the spinal cord. On the anterior sur- tion to the saddle area, motor innervation for the sphinc-
face, the prominent anterior median fissure penetrates the ters, and parasympathetic innervation for the bladder and
cord for a depth of approximately 3 mm and contains the lower bowel (i.e., from the left splenic flexure to the rec-
sulcal branches of the anterior spinal artery and vein (Fig- tum). Here again an appreciation of the anatomic rela-
ure 2.2). The anterolateral sulcus marks the site at which tionships between the spinal cord and vertebral column
the ventral root fibers exit the cord. However, because the is useful in the diagnosis of some spinal cord disorders
ventral roots exit at less regular intervals and are not as resulting from injury. Trauma in the lower back at the
numerous as dorsal roots, the anterolateral sulcus is not level of the L1 vertebra may result in conus medullaris
as easily seen as the posterolateral sulcus. syndrome, caused by a direct injury of the conus

FIGURE 2.2

Photomicrograph of spinal cord


showing division into gray and
white matter.
18 INTRODUCTION

medullaris at this level (Figures 2.1 and 2.3). The signs branch of the pudendal nerve (S2S4). As in the bowel,
and symptoms of this syndrome are permanent flaccid the bladder dysfunction of conus medullaris syndrome is
paralysis of the external anal sphincter and fecal inconti- caused by the destruction of neurons at the S24 levels
nence; bladder distension and incontinence; impotence; of the spinal cord. Generally, the bladder is permanently
and perianal or saddle anesthesia. areflexic in conus medullaris syndrome because of the loss
The flaccid paralysis of the external anal sphincter of the sacral spinal neurons that give rise to the bladder
is caused by the destruction of the somatic lower reflexes. Thus, a spastic or automatic bladder does
motoneurons that innervate this voluntary muscle at the not develop as it would when the cord is injured at more
S2S4 levels. These neurons normally project axons to the rostral levels; the sacral bladder reflex circuitry is spared,
muscle via the inferior rectal branch of the pudendal and these neurons become hyperactive after recovery
nerve. Bladder distension and incontinence is caused by from spinal shock.
paralysis of the detrusor muscle, the smooth muscle wall In conus medullaris syndrome, impotence is pri-
of the bladder innervated by the pelvic splanchnic nerves marily caused by a loss of parasympathetic neurons at
arising from preganglionic parasympathetic neurons at S2S4. Erection is achieved normally when parasympa-
S2S4, and also by paralysis of the urethral sphincter, the thetic stimulation causes the smooth muscle of the arter-
striated (voluntary) muscle innervated by the perineal ies associated with the erectile tissue of the penis to relax.
As a result, the arterial lumina enlarge and blood is
allowed to flow into and dilate the cavernous spaces in
the corpora of the penis. The bulbospongiosus and ischio-
cavernosus muscles are innervated by the deep branch of
the perineal nerve, a branch of the pudendal nerve
(S2S4). Normally, during erection, these muscles con-
tract and thus compress the venous plexuses at the periph-
ery of the corpora cavernosa, preventing the return of
venous blood. As a result, the penis becomes erect.
Because it is likely that neurons innervating the bul-
bospongiosus and ischiocavernosus muscles will also be
lost in conus medullaris syndrome, paralysis or paresis
of these muscles contributes to impotence.
Loss of sensory neurons in the dorsal horn at S4 and
S5 causes perianal anesthesia and saddle anesthesia (i.e.,
anesthesia of the posterior thigh). In conus medullaris
syndrome, this anesthesia is caused predominantly by a
loss of sensory neurons at the S2 level. In a pure conus
lesion, normal sensory and motor function is retained in
the lower limb (i.e., assuming only the conus medullaris
is injured and lumbar roots of the cauda equina are
spared). If the S1 level is spared, the ankle jerk is retained.
Finally, if the conus medullaris lesion is incomplete, some
of the signs and symptoms noted above may not occur.
Lesions of the cauda equina (Figure 2.3) below the
L1 vertebral level result in cauda equina syndrome. The
signs and symptoms of this syndrome are similar to those
following conus lesions. However, cauda equina lesions
usually affect not only peripheral nerve fibers from the
sacral segments of the cord, but also a varying number
of the lumbar dorsal and ventral nerve roots. The sensory
and motor losses are, as a rule, more extensive and reach
higher spinal levels (i.e., the lower limbs) following cauda
equina lesions when compared to lesions of the conus
medullaris. Furthermore, the distribution of motor and
sensory loss is usually more irregular because some of the
FIGURE 2.3 nerve roots will be damaged and others will be spared.
It is important to note that because of the anatom-
Posterior view of lower end of the dural sac. ical proximity of the conus medullaris and cauda equina,
ANATOMY AND FUNCTION OF THE SPINAL CORD 19

a single lesion is likely to affect both structures, thus mak-


ing the determination of the injury level and the specific
syndrome difficult on the basis of a neurologic examina-
tion alone. In fact, the International Standards for Neu-
rological and Functional Classification of Spinal Cord
Injury (1) define conus medullaris syndrome as an injury
of the sacral cord (conus) and lumbar nerve roots within
the spinal canal that usually results in areflexic bladder,
bowel, and lower limbs. Interestingly, cauda equina syn-
drome is defined as an injury to the lumbosacral nerve
roots within the neural canal resulting in the same deficits
noted under conus medullaris syndrome (1). In this chap-
ter we define the syndromes differently and present a sum-
mary of the signs and symptoms that would occur fol-
lowing injury to either structure, but not both, to
emphasize the anatomic and functional organization of
the spinal cord. It is noteworthy that conus medullaris
syndrome and cauda equina syndrome have been defined
in this same manner in other textbooks (2).
FIGURE 2.4
Meninges of the Spinal Cord Spinal cord in situ.
The three membranous investments of the spinal cord,
the dura mater, arachnoid, and pia mater, are continu-
ous with the meningeal investments of the brain. The under normal conditions. Several authors of anatomy
outermost covering, the dura mater forms a long tubu- have referred to a potential subdural space, which
lar sheath of dense, fibroelastic tissue around the spinal may be increased under pathologic conditions. For
cord and cauda equina that extends from the foramen instance, rupture of bridging veins between the dura and
magnum to the level of the second sacral vertebra (Fig- arachnoid may result in the accumulation of blood and
ure 2.3). In the cranial vault, the dura mater consists of the expansion of this space, a condition known as sub-
two layers: an outer periosteal layer adherent to the inner dural hematoma.
surface of the cranium, and an inner meningeal layer. The arachnoid is continuous with the same layer sur-
At various sites, the two layers of the cranial dura are rounding the brain. This delicate avascular membrane
separated by venous sinuses. In contrast, the spinal dura completely lines the dural sac and its dural root sleeves
mater is single layered, devoid of venous sinuses, and and thus covers the nerve roots and dorsal root ganglia.
continuous only with the meningeal layer of the cranial Like the dura, the arachnoid blends with the epineurium
dura. There is a separate periosteal lining against the of the spinal nerves. The arachnoid follows the dura infe-
bone of the vertebral canal. The small space between this riorly, where it ends as a sac at the level of the second
lining and the spinal dura mater is called the epidural sacral vertebra enclosing the cauda equina (Figure 2.3).
space. This space contains epidural fat, areolar tissue, The subarachnoid space, filled with CSF, surrounds the
and the internal vertebral venous plexus. The spinal dura spinal cord and pia mater including its specializations (the
forms dural root sleeves that follow the dorsal and ven- denticulate ligaments and filum terminale described later).
tral roots into each intervertebral foramen (Figure 2.3, The space is largest inferiorly between the level of the sec-
lower). At these sites, the sleeves end by blending with ond lumbar vertebra and the second sacral vertebra in a
the epineurium of each spinal nerve. The dura is adher- region known as the lumbar cistern (Figure 2.4). The lum-
ent to the periosteum lining the foramina at these sites. bar cistern contains the cauda equina and filum terminale,
At the level of the second sacral vertebra, the tubular which are free-floating within the CSF. Needles may be
dural sac tapers down to a slender covering for the filum inserted into the lumbar cistern at the intervertebral space
terminale (a specialization of the pia mater described between L3 and L4 or L4 and L5 to draw off CSF for sam-
later). This covering, referred to as the coccygeal liga- pling (a spinal tap) or to inject anesthetics (a spinal
ment, anchors the spinal cord with the vertebral canal block) without the risk of injuring the spinal cord, which
where it descends and attaches to the periosteum of the ends as the conus medullaris at the first lumbar vertebral
coccyx (Figure 2.4). Cerebrospinal fluid (CSF) pushes the level. The nerve roots of the cauda equina are generally
arachnoid directly up against the dura mater. Thus, there not injured by the procedure because, being suspended
actually is no space between the dura and arachnoid in fluid, they roll away from the needle point.
20 INTRODUCTION

The pia mater is the innermost of the three tively. The first cervical nerve lacks dorsal roots in 50 per-
meningeal investments and the only one that directly con- cent of people, and the coccygeal nerves may be absent
tacts the surface of the spinal cord (Figure 2.5). The pia entirely (3). It should be noted that the spinal nerves are
also directly covers the roots of the spinal nerves and the relatively short. Almost immediately after exiting the
spinal blood vessels. At the conus medullaris, the pia intervertebral foramen each nerve bifurcates into a dor-
mater continues inferiorly into the lumbar cistern as a sal and ventral ramus (Figure 2.5). The dorsal ramus pro-
slender filament called the filum terminale (Figure 2.3). vides the cutaneous innervation of the back and the motor
Surrounded by the nerve roots of the cauda equina, the innervation of the intrinsic or deep back muscles. All the
filum terminale pierces the arachnoid at the level of the appendicular and remaining trunk muscle innervation
second sacral vertebra and then becomes invested by dura and sensory innervation of the body (excluding the motor
mater to become the coccygeal ligament (Figure 2.4). By and sensory innervation provided by cranial nerves) is
attaching to the periosteum of the coccyx, the coccygeal provided by the ventral ramus of each spinal nerve. It is
ligament centers the spinal cord within the lumbar cistern important to appreciate that whereas the dorsal and ven-
and serves as an anchor to maintain that position to pre- tral roots convey pure sensory and motor fibers respec-
vent cord injury, especially under conditions of sudden tively, the dorsal and ventral rami are mixed nerves and
jarring that could force delicate spinal tissue up against each contains both sensory and motor fibers.
the bony walls of the vertebral canal.
Bilaterally thickened lateral extensions of the pia
mater give rise to the denticulate ligaments (Figure 2.5). NEUROANATOMIC ORGANIZATION OF THE
The two denticulate ligamentsone on the right and one SPINAL GRAY AND WHITE MATTER
on the leftare located between the dorsal and ventral
roots on each side of the spinal cord. From each ligament In cross section, the spinal cord is composed of a central
twenty to twenty-two toothlike triangular processes portion of butterfly-shaped gray matter and peripherally
extend further laterally, pierce the arachnoid, and fuse oriented white matter (Figure 2.5). The gray matter is
with the dura. The attachment of the processes of the lig- comprised predominantly of neurons, their processes, and
ament alternates with the passage of the nerve roots glial cells and has an enriched blood supply. The white
through the dura mater (Figure 2.5). The first attachment matter contains ascending and descending fiber tracts and
is at the level of the foramen magnum, whereas the most glial cells and appears white in unfixed tissue because of
caudal attachment is between the T12 and L1 nerve roots a predominance of myelin. The two halves of the gray
(Figure 2.3). As in the filum terminale and coccygeal lig- matter are connected across the midline by a dorsal and
aments, the attachments of the denticulate ligaments to ventral gray commissure, which is located above and
the dura mater provide an important fixation of the spinal below the central canal respectively (Figure 2.2). The gray
cord, protecting it from sudden displacements. matter is further subdivided into a posterior (dorsal) horn
(column) and an anterior (ventral) horn (column). The
thoracic and upper two lumbar spinal cord segments also
Organization of a Spinal Nerve
display a wedge-shaped, intermediate lateral horn (inter-
Sensory information (i.e., pain, temperature, touch, etc.) mediolateral cell column) (Figure 2.2).
is conveyed from the body into the spinal cord via the dor- The white matter on each side of the spinal cord is
sal roots, which enter the spinal cord posteriorly along organized into three large areas or funiculi (Figure 2.2).
the posterolateral sulcus (Figure 2.5). The neuron cell The posterior funiculus is the area of white matter
bodies responsible for conveying the sensory (afferent) between the posterior median sulcus and the posterolat-
information are located in a distal swelling of the dorsal eral sulcus. The lateral funiculus is defined as the white
root known as the spinal ganglion. The spinal ganglion matter between the posterolateral sulcus and an imagi-
is generally surrounded by bone and is found at the level nary line from the medial border of the anterior horn to
of the intervertebral foramen. The ventral roots of the the anterior surface of the spinal cord. The anterior
spinal cord convey motor (efferent) information from the funiculus is the remaining white matter medial to the
spinal cord to skeletal muscle. Ventral root fibers exit the imaginary line noted above and lateral to the anterior
spinal cord at the anterolateral sulcus and also contain median fissure (Figure 2.2). Each funiculus of the spinal
axons from pregangionic autonomic neurons (Figure 2.5). cord is comprised of bundles of fibers that run together
The dorsal and ventral roots that delineate a spinal cord and subserve the same function. Each bundle is referred
segmental level fuse at the level of the intervertebral fora- to as a tract or fasciculus. For instance, at cervical levels
men just distal to the spinal ganglion to form the spinal and the upper six thoracic levels of the spinal cord, the
nerve associated with that spinal cord segment. The spinal posterior funiculus is subdivided into two major fasci-
nerve is a mixed nerve, in that it contains both sensory culi (gracilis and cuneatus) by the posterior intermediate
and motor fibers from the dorsal and ventral roots respec- sulcus and septum (Figure 2.6). (The functional signifi-
ANATOMY AND FUNCTION OF THE SPINAL CORD 21

FIGURE 2.5

Spinal meninges and nerve roots.


22 INTRODUCTION

FIGURE 2.6 FIGURE 2.7

Diagram of the spinal cord showing the somatotopic organi- Diagram of the spinal cord showing the somatotopic organi-
zation of fibers in the posterior funiculus. zation of ventral horn motor neurons.

cance of these fiber tracts is discussed in the section laminae, each containing neurons with specific morpho-
White Matter). logic characteristics. Subsequently, the lamination pattern
was confirmed in several species, including man, and has
been referred to as Rexeds laminae (Figure 2.8). Briefly,
Gray Matter
the first six laminae are found in the posterior horn. Lam-
The posterior (dorsal) horn contains clusters of neurons ina I is equivalent to the nucleus posteromarginalis, lam-
concerned with sensory function. The central processes ina II to the substantia gelatinosa, and laminae III and
of spinal ganglion cells generally synapse on neurons in IV together comprise the nucleus proprius of the older lit-
the dorsal horn, where sensory information is relayed erature. Laminae V and VI comprise the neck and base
either to higher centers in the brain or segmentally within of the posterior horn respectively. Lamina VII is equiva-
the spinal cord. lent to the intermediate gray matter that includes the lat-
The lateral horn is limited to the thoracic and upper eral horn at T1L2 and Clarkes nucleus (nucleus dorsalis)
two lumbar spinal cord segments. It contains pregan- at C8L2 (see posterior spinocerebellar tract, later).
glionic sympathetic neurons whose axons exit the spinal Laminae VIII and IX are in the anterior horn. Lamina VIII
cord via the ventral roots. Preganglionic parasympathetic is composed of interneurons, whereas lamina IX is com-
neurons are located in a comparable region of the gray prised of individual clusters of alpha motoneurons.
matter at the S2S4 levels of the spinal cord. However, Finally, lamina X is comprised of small neurons sur-
well-defined lateral horn is not found at these sacral lev- rounding the central canal. For more detailed informa-
els. Axons of the preganglionic parasympathetic neurons tion regarding Rexeds laminae, consult Carpenter and
distribute to the descending colon, sigmoid colon, rectum, Sutin (4).
and all pelvic viscera via the pelvic splanchnic nerves.
The anterior (ventral) horn contains both interneu-
White Matter
rons and motoneurons. Motoneuron axons innervating
skeletal muscle comprise the major component of the ven- Heavily myelinated nerve fibers in the posterior funicu-
tral root. Alpha motoneurons of the anterior horn are lus are concerned primarily with two general modalities
somatotopically organized such that neurons supplying related to conscious proprioception. These are kinesthe-
flexor muscles are located dorsally in the anterior horn sia (sense of position and movement) and discrimative
and neurons supplying extensor muscles are located ven- touch (discriminating two points and localizing touch sen-
trally. In addition, neurons supplying the trunk muscula- sation). Injury to the spinal cord in the region of the pos-
ture are located medially, whereas neurons innervating terior funiculus may result clinically in a loss or diminu-
the limbs are located laterally within the anterior horn tion of vibratory sense, position sense, two-point tactile
(Figure 2.7). discrimination, and touch and weight perception in the
In 1952, the gray matter of the cat spinal cord was body ipsilateral and caudal to the spinal cord lesion. The
characterized as being comprised of ten distinct zones or central processes of neurons whose cell bodies are located
ANATOMY AND FUNCTION OF THE SPINAL CORD 23

spinothalamic pathways in the lateral funiculus. Thus,


painful stimuli are triggered by lower stimulation thresh-
olds and nonpainful stimuli are interpreted as being
painful. In both man and animals, there have been reports
of lesions in the posterior funiculus that result in no loss
of the sensory modalities presumably carried by this white
matter region: the presence of the spinocervical thalamic
tract in the lateral funiculus may compensate for some
posterior funiculus deficits.
Sensory stimuli transmitted via the posterior funi-
culi are of three types: those impressed passively on the
organism, those which have temporal or sequential com-
ponents added to a spatial cue, and those which are not
perceived without manipulation and active exploration
by the digits. The first type of stimulus is exemplified by
a vibrating tuning fork, two-point discrimination, or a
touch by a piece of cotton. These passive stimuli are trans-
mitted not only by the posterior funiculi, but also by a
number of parallel pathways, such as the spinocervical
thalamic tract. Thus, such passive sensations are often
preserved following lesions of the posterior funiculi. The
second type of stimulus is exemplified by a determination
of the direction of lines that are drawn on the skin or the
direction of movement of a digit or toe. This type of stim-
ulus, which contains temporal or sequential factors added
to a spatial cue, is transmitted exclusively by the poste-
FIGURE 2.8 rior funiculi. Thus, the information that concerns the rel-
ative changes in a stimulus over a period of time or the
Location of Rexeds laminae at the L5 level of the spinal cord.
direction of a stimulus is transmitted to higher CNS cen-
ters only by the posterior funiculi. This is also the case
with the third type of stimulus. Recognizing shapes and
in spinal ganglia form the fibers of the posterior funicu- patterns by active exploration with the digits (i.e., stere-
lus. The fibers that enter the spinal cord below the sixth ognosis) is mediated only by the posterior funiculi, and
thoracic segment form the fasciculus gracilis (gracile the ability to recognize these shapes is often lost with
tract), whereas fibers that enter the cord above the sixth lesions to this part of the spinal cord.
thoracic segment are located laterally and form the fas- Position and movement sense is severely affected fol-
ciculus cuneatus (cuneate tract). These two tracts are sep- lowing injury to the posterior funiculi, especially in the
arated by the posterior intermediate sulcus and septum, distal part of the extremities. Small passive movements
which is found at all cervical levels of the spinal cord and are not recognized as movements, but as touch or pres-
the upper six thoracic levels. Thus, the nerve fibers in the sure. The direction of movement is seldom perceived. This
posterior funiculus are somatotopically arranged with the loss of position sense greatly impairs motor function. The
greatest number of medial fibers arising from the sacral sensory loss causes movements to be clumsy, uncertain,
levels and the greatest number of lateral fibers coming and poorly coordinated, a condition referred to as pos-
from the cervical levels (Figure 2.6). Fibers in the gracile terior column or sensory ataxia.
and cuneate tract ascend ipsilaterally to the caudal
medulla where they synapse on neurons in the gracile and
cuneate nuclei respectively. Axons of these medullary neu- Ascending Tracts in the Lateral
rons cross the midline and ascend as the medial lemnis- and Anterior Funiculi
cus, which terminates on neurons in the thalamus (ven-
Posterior Spinocerebellar Tract
tral posterolateral nucleus). Thalamic neurons, in turn,
project to the cerebral cortex. This ascending tract is located in the dorsal aspect of the
A functional relationship exists between the poste- lateral funiculus (Figure 2.9). The tract conveys to the
rior funiculus and the tracts in the lateral funiculus of the cerebellum proprioceptive information from receptors
spinal cord. For example, injury to the posterior funicu- located in muscles, tendons, and joints. The central
lus augments all forms of sensation conveyed by the processes of spinal ganglion cells enter the spinal cord via
24 INTRODUCTION

FIGURE 2.9

Diagram of ascending (right)


and descending (left) path-
ways of the spinal cord.

the dorsal root and then ascend or descend in the fasci- some clinical cases involving preserved sensory function
culus gracilis for one or two segments before synapsing following SCI. In cats, the central processes of spinal gan-
on neurons in the nucleus dorsalis of Clarke (Clarkes glion cells conveying stimuli into the spinal cord from low-
nucleus), located within Rexeds lamina VII. Axons of threshold cutaneous receptors, pressure receptors, and
neurons in the nucleus dorsalis form the posterior spin- impulses following pinching of the skin, synapse on neu-
ocerebellar tract. Since Clarkes nucleus is found only rons in the ipsilateral dorsal horn. These neurons send their
between C8 and L2, the posterior spinocerebellar tract axons into the dorsal aspect of the lateral funiculus, where
is not found caudal to L2 in the spinal cord. The central they ascend to the upper two or three cervical segments
processes of those spinal ganglion cells conveying pro- and synapse on neurons of the lateral cervical nucleus. The
prioceptive information into the spinal cord below L2 lateral cervical nucleus is located lateral to the dorsal horn
ascend to the L2 level in the fasciculus gracilis before in the lateral funiculus of the upper three cervical segments
synapsing on cells in Clarkes nucleus. Similarly, incom- of the cat spinal cord (5). The lateral cervical nucleus gives
ing proprioceptive information entering the spinal cord rise to axons that cross the midline in the anterior white
rostral to C8 are carried by nerve fibers ascending in the commissure (Figure 2.2) at spinal levels C1 and C2 and
fasciculus cuneatus. The cuneate tract nerve fibers ascend with the medial lemniscus to terminate in the con-
synapse on neurons of the accessory cuneate nucleus in tralateral VPL of the thalamus. This spinocervical thala-
the medulla; this is homologous to the nucleus dorsalis. mic tract has a somatotopic organization similar to that of
Both pathways are uncrossed. the posterior funiculus pathways (i.e., sacral fibers are
The posterior spinocerebellar tract conveys to the medially located and cervical fibers are the most laterally
cerebellum information pertaining to muscle contraction, located, [6]). It is important to appreciate that there is evi-
including phase, rate, and strength of contraction. Clini- dence that the pathways in the posterior funiculus (dorsal
cal effects of posterior spinocerebellar tract destruction columnmedial lemniscal system) are functionally linked
in SCI are masked by the effects of destruction of the adja- with the spinocervical thalamic tract, because some spin-
cent lateral corticospinal tract. ocervical collaterals terminate in the dorsal column nuclei
and some cells in the dorsal column nuclei project to the
lateral cervical nucleus (7).
Spinocervical Thalamic Tract
The putative clinical relevance of this information is
Although the spinocervical thalamic tract has not been that the spinocervical thalamic tract accounts for the per-
demonstrated in man, a description of this tract is included sistance of kinesthesia and discriminative touch sensation
here because of its possible relevance to an explanation of following total interruption of the posterior funiculus in
ANATOMY AND FUNCTION OF THE SPINAL CORD 25

experimental animals. According to Afifi and Bergman loss of pain and temperature sensation in the dermatomes
(8), the presence of the spinocervical thalamic tract has corresponding to the affected spinal cord segments. This
been assumed in man because of the similar persistence last pattern of sensory loss is characteristic of
of posterior funiculus sensations after total posterior syringomyelia, a condition caused by a centrally located
funiculus lesions in patients. Thus, the old concept of the cavitation of the spinal cord that destroys the anterior
absolute necessity of the posterior funiculus for all dis- white commissure. Finally, in a BrownSequard lesion
criminatory sensation is evolving into a newer concept (hemisection of the spinal cord), the patient experiences
that attributes to the posterior funiculus a role in the dis- both a contralateral loss of pain and temperature in the
crimination of those sensations that an animal must body (caused by the destruction of the lateral spinothal-
explore actively and to the spinocervical thalamic path- amic pathway in the lateral funiculus) and a bilateral seg-
way a role in the perception of sensations that are mental loss of pain and temperature (caused by a destruc-
impressed passively on the organism (8). tion of the anterior white commissure) that will be slightly
higher than the contralateral loss of pain and temperature
sensation, but still below the level of the lesion.
Lateral Spinothalamic Tract
In the past, the lateral spinothalamic tract was sec-
One of the most clinically important pathways in the tioned surgically to relieve intractable pain. The proce-
spinal cord is the lateral spinothalamic tract, which is con- dure is referred to as cordotomy and may be carried out
cerned with the transmission of pain and temperature sen- unilaterally or bilaterally. If bilateral cordotomy is per-
sations (Figure 2.9). This tract is closely related to the formed, the lesions are made at slightly different levels
anterior spinothalamic tract, and authors often combine in the spinal cord. During surgery, the denticulate liga-
the two pathways and refer to them together as the ment is used as a landmark; lesions are made just ante-
anterolateral system (ALS). In this chapter the pathways rior to the denticulate ligament to locate and transect the
are discussed separately because of their clinical relevance. lateral spinothalamic tract. A unilateral lesion of the tract
Unmyelinated and thinly myelinated dorsal root results in anesthesia of the body wall and limbs, but not
fibers contributing to the lateral spinothalamic tract have the viscera, which are bilaterally represented (9). Fur-
their cell bodies in spinal ganglia. Incoming root fibers thermore, the anogenital region is not markedly affected
synapse on neurons in Rexeds laminae IIV of the dor- with unilateral lesions (9). Clinical results have indicated
sal horn. Neurons in these laminae in turn project axons that after variable periods of time following bilateral cor-
to neurons in laminae VVIII. The laminae VVIII neu- dotomies, there is often a return of pain and temperature
rons, as well as some neurons in lamina I, project axons sensation, thus suggesting that there may be other path-
across the midline in the anterior white commissure to the ways in the spinal cord to convey this modality. These
contralateral lateral funiculus and thus form the lateral pathways may be multisynaptic and pass through the
spinothalamic tract. The crossing fibers of the lateral reticular formation (i.e., spinoreticular, [10]) or involve
spinothalamic pathway ascend from one to two spinal shorter relays (i.e., spinospinal, [9]). In addition, Affifi
segments above their entry level before entering the tract and Bergman (10) have suggested that pain sensation may
in the contralateral lateral funiculus. The fibers of the be mediated through a spinotectal pathway and Carpen-
tract are somatotopically arranged with sacral fibers ter and Sutin (9) have suggested that uncrossed spinothal-
located laterally and cervical fibers located medially amic fibers may be responsible for the return of pain and
within the tract. Note that this arrangement is the reverse temperature sensation following unilateral lesion of the
of the posterior funiculus pathways, in which sacral fibers lateral spinothalamic pathway.
are located medially and cervical fibers are laterally
located. Once formed, the lateral spinothalamic tract
Anterior Spinothalamic Tract
ascends throughout the length of the spinal cord and
brainstem to ultimately terminate on neurons of the ven- The dorsal root fibers conveying light touch sensation and
tral posterolateral nucleus (VPL) of the thalamus. certain types of pain impulses synapse on dorsal horn neu-
Lesions of the lateral spinothalamic tract in the lat- rons in laminae VI to VIII. The axons of these dorsal horn
eral funiculus result in a loss of pain and temperature sen- neurons cross in the anterior white commissure over sev-
sation in the contralateral half of the body, beginning one eral segments and gather in the lateral and anterior funi-
or two segments below the level of the lesion. This pat- culi to form the anterior spinothalamic tract (Figure 2.9).
tern of sensory loss is in marked contrast to the loss that The course and termination of this tract in the spinal cord
occurs following injury to the dorsal roots, in which there and brainstem is similar to the lateral spinothalamic tract.
is segmental or dermatomal loss of sensation ipsilateral Functionally, light touch is defined as the sensa-
to the lesion. Moreover, if pain and temperature fibers are tion provoked by stroking an area of skin devoid of hair
injured as they cross the midline of the spinal cord in the (glabrous skin) with a feather or wisp of cotton (9). This
anterior white commissure, there is a bilateral segmental type of sensation is conveyed to higher CNS centers in
26 INTRODUCTION

addition to the pressure sense and discriminatory tactile lateral funiculus (Figure 2.9). The lateral corticospinal
sensations conveyed by the posterior funiculus. Because tract extends the entire length of the spinal cord and is
tactile sensation is transmitted centrally by the posterior somatotopically organized. As in the lateral spinothala-
funiculi, the anterior spinothalamic tract, and the spin- mic tract, cervical fibers are found medially. They are fol-
ocervical thalamic tract, clinically this particular sensory lowed laterally by thoracic, lumbar, and then sacral fibers.
modality is of little value in localizing injuries to the spinal Once again, it may be instructive to recall that the soma-
cord (9). If the anterior spinothalamic tract is lesioned, totopic organization of both the lateral corticospinal tract
there is little loss of tactile sensibility; however, the affec- and the lateral spinothalamic pathway in the lateral
tive aspect of sensation may be lost. Bilateral destruction funiculus is different from the somatotopic organization
of the anterolateral funiculi may cause a complete loss of the posterior funiculus in that in the latter, sacral fibers
of itching, tickling, and libidinous feeling (11), thus this are mostly medial and cervical fibers are located laterally.
region of the spinal cord has been associated with ones The uncrossed corticospinal fibers descend from the
ability to judge the pleasant or unpleasant character of medulla into the anterior funiculus of the spinal cord as
sensation. In addition to light touch stimuli, the anterior the anterior corticospinal tract (bundle of Trck) (Fig-
spinothalamic tract is thought to convey nondiscrimina- ure 2.9). The anterior corticospinal tract extends only to
tive pain sensations, in contrast to the lateral spinothal- the upper thoracic spinal cord and innervates neurons
amic tract, which is thought to convey the well-localized projecting to the muscles of the upper extremities and
discriminative pain sensations (12). neck. The fibers of this tract generally cross the midline
segmentally within the spinal cord before terminating on
contralateral neurons. In rare cases, fibers do not cross
Other Ascending Tracts
the midline at all and form extremely large anterior cor-
There are several other ascending tracts in the spinal cord ticospinal tracts (16).
lateral and anterior funiculi that are of little clinical sig- Corticospinal fibers terminate mostly on interneu-
nificance. These tracts include the spino-olivary, spino- rons in the spinal cord in laminae IVVII. Evidence also
tectal, spinoreticular, spinocortical, spinovestibular, and exists for a direct projection to alpha and gamma
anterior spinocerebellar. These multisynaptic pathways motoneurons in lamina IX. Because the corticospinal
do not have a well-delineated functional significance, but tracts innervate both alpha and gamma motoneurons,
may play a role in feedback control mechanisms or in the stimulation of corticospinal fibers leads to a co-contrac-
maintenance of the state of consciousness. For more tion of both intrafusal and extrafusal muscle fibers.
detailed information on these pathways consult Carpen- Because of the co-contraction of the two types of muscle
ter and Sutin (13). fibers, there is increased sensitivity of the muscle spindle
(intrafusal fiber) to changes in muscle length even when
the muscle is shortening.
Descending Tracts of the Lateral
It has been estimated that 55 percent of all corti-
and Anterior Funiculi
cospinal fibers end in the cervical cord, 20 percent in the
thoracic, and 25 percent in the lumbosacral segments
Corticospinal Tracts
(17). These data suggest that the corticospinal tracts have
As the name implies, neurons giving rise to the corti- a greater control and influence over the upper extremities
cospinal tracts are found in the cerebral cortex. The axon than over the lower. The corticospinal tracts are essen-
of these neurons projects through the brainstem and ter- tial for skill and precision in movement and also for the
minates in the spinal cord. The corticospinal tracts com- execution of precise movements of the fingers. Interest-
prise the largest, clinically important descending fiber sys- ingly, although the tracts are necessary for speed and
tem in the human neuraxis. The neurons that give rise to agility during precise movements, they are not necessary
the tracts are located in the primary motor cortex (i.e., for the initiation of voluntary movement. They also serve
the precentral gyrus or Brodmanns area 4), the premotor to regulate sensory relay processes and to determine
cortex (area 6), the primary sensory cortex (i.e., the post- which sensory modality reaches the cerebral cortex, as
central gyrus or areas 3, 1, and 2), and adjacent parietal evidenced by terminations on sensory neurons in laminae
cortex (14,15). Although both sensory and motor corti- IV to VII. The proper function of the corticospinal tracts
cal areas contribute to the tracts, the primary motor cor- is dependent on the extent of their myelination. Myeli-
tex and the premotor cortex give rise to 80 percent of the nation of corticospinal fibers begins near birth and is not
tracts. completed until the end of the second year of life.
At the caudal level of the medulla oblongata, the Neurons in the cerebral cortex and their axons that
majority of the corticospinal fibers cross the midline in form the corticospinal tracts have been referred to as
the pyramidal decussation to form the lateral corti- upper motor neurons. The alpha motoneurons in the
cospinal tract, which is located in the dorsal aspect of the spinal cord ventral horns and their axons that directly
ANATOMY AND FUNCTION OF THE SPINAL CORD 27

innervate skeletal muscle are referred to as lower motor Although the rubrospinal tract extends the length of
neurons. Lesion of the lateral corticospinal tract in the the spinal cord in most mammals, it only extends to the
spinal cord lateral funiculus results in an upper motor thoracic segments in man (20), is thinly myelinated, and
neuron syndrome which includes spasticity, hyperactive thought to be rudimentary. Any effect of injury to the
deep tendon reflexes, Babinski sign, clonus, and a loss or rubrospinal tract in patients will likely be masked by the
diminution of superficial reflexes, such as the abdominal severe motor deficits resulting from injury to the adjacent
or cremasteric reflex. In the acute phase of an SCI involv- lateral corticospinal tract.
ing bilateral lesion of the lateral corticospinal tracts, a
patient undergoes spinal shock, in which there is a
Lateral Vestibulospinal Tract
complete shutdown of neuronal activity in the spinal cord
below the level of the injury. The signs of spinal shock The neurons that give rise to this tract are found in the
include flaccid paralysis of muscles, hypotonia, and the lateral vestibular nucleus located at the junction between
absence of myotatic, bowel, and bladder reflexes. the medulla and pons. The axons of the lateral vestibu-
Depending on the level of injury, there may also be brady- lar nucleus descend uncrossed through the medulla and
cardia and significant lowering of blood pressure. Fol- form the lateral vestibulospinal tract in the anterior aspect
lowing a variable period (days to weeks) the patient of the lateral funiculus along the entire length of the spinal
recovers from spinal shock and the upper motor neuron cord (Figure 2.9). Fibers of the tract terminate mostly on
syndrome becomes apparent. The mechanisms underly- interneurons in laminae VII and VIII, but there are some
ing the induction and recovery from spinal shock are direct terminations on alpha motor neuron dendrites in
unknown. Lower motor neuron lesions result in signs the same laminae.
similar to those of a patient in spinal shock. In lower The primary function of the lateral vestibulospinal
motor neuron paralysis there is a loss of all movement, tract is to facilitate extensor muscle tone to maintain an
both reflex and voluntary, as well as a loss of muscle tone upright posture. With eyes closed and feet close together
and subsequent atrophy of the affected muscles. Unlike a normal individual sways slightly from side to side. Bal-
the transient deficits associated with spinal shock, lower ance is maintained because, for example, as the individ-
motor neuron deficits are permanent, assuming that there ual sways to the right impulses from the right semicircu-
is no reinnervation of the denervated structures. lar canals of the inner ear activate neurons in the
The signs associated with an upper motor neuron ipsilateral lateral vestibular nucleus. These neurons, in
syndrome are not always indicative of injury or disease turn, send impulses along the right vestibulospinal tract
of the spinal cord. In older individuals, there is a tendency to extensor muscles, which correct for the sway and move
for the superficial abdominal reflexes to be absent; this the body back to the midline center of gravity. When the
occurs more often in females than in males (18). Although individual sways to the left, the left lateral vestibulospinal
the Babinski sign is commonly associated with injury to tract is activated. Similarly, if a walking individual stum-
the corticospinal system, it can also be elicited in the new- bles, reflex extension of one of the lower extremities may
born infant, a sleeping or intoxicated adult, or following prevent a fall, but if a fall is imminent, extension of the
a generalized seizure. Interestingly, the Babinski sign may upper limbs often prevents severe injury to the face and
be absent in some patients with a known lesion of the cor- head. Under these circumstances, the reflex extension of
ticospinal tract (19). the limbs is also mediated by the lateral vestibulospinal
tracts. If the eighth cranial nerve (vestibulocochlear), lat-
eral vestibular nucleus, or the semicircular canals are
Rubrospinal Tract
injured on one side, a patient will often fall to that side
The neurons that give rise to the axons of the rubrospinal or veer to the side of the injury while walking. The effects
tract are located in the posterior two-thirds of the red of injury to the lateral vestibulospinal tract in the spinal
nucleus in the midbrain. The axons of the tract cross in cord, however, are generally masked by the more severe
the ventral tegmental decussation and descend to spinal deficits in motor capability that result from concomitant
levels, where the tract forms in the lateral funiculus mostly injury to the lateral corticospinal tract.
anterior to (partially overlapping) the lateral corticospinal
tract (Figure 2.9). The fibers of the rubrospinal tract ter-
Medial Vestibulospinal Tract
minate in the same laminae as the lateral corticospinal
tract and function to facilitate flexor motor neuron activ- The neurons that give rise to the medial vestibulospinal
ity. Because the red nucleus receives an input from the cor- tract are located in the medial vestibular nucleus of the
tex (corticorubral) and because of the similar termina- medulla. The fiber of these neurons descends through the
tions of both tracts in the spinal cord, the rubrospinal medulla bilaterally in a composite bundle of several dif-
tract is thought to be functionally related to the lateral ferent fiber systems known as the medial longitudinal fas-
corticospinal tract. ciculus (MLF). The MLF containing the medial vestibu-
28 INTRODUCTION

lospinal tract is located in the posterior aspect of the ante- turbances. If injury occurs at or above the T1 level,
rior funiculus of the cervical spinal cord (Figure 2.9). Horners Syndrome results because of injury to the sym-
Fibers of the medial vestibulospinal tract terminate on pathetic component of the descending autonomic path-
interneurons in laminae VII and VIII and play a role in ways. The signs of this syndrome are seen predominantly
the labyrinthine regulation of head positions. in the eye ipsilateral to injury and consist of miosis caused
by paralysis of the pupillary dilator muscle; slight ptosis
caused by paralysis of the smooth muscle (tarsal plate)
Reticulospinal Tracts
of the upper eyelid; and enophthalmos. The specific cause
The neurons that give rise to these tracts are located in of the enophthalmos is debated. Some suggest that the
the central core of the brainstem known as the reticular slight retraction of the eyeball into the orbit is caused by
formation, at the level of the pons and medulla. Because the paralysis of smooth muscles in the inferior orbital fis-
of the different origins and locations of these tracts in the sure, whereas others suggest that the enophthalmos is
spinal cord, they are often referred to separately as the caused by the interruption of sympathetic innervation to
pontine and medullary reticulospinal tracts. The pontine retro-orbital fat. Brodal (27) has argued that, because the
reticulospinal tract is mostly ipsilateral and descends in inferior orbital smooth muscles are so sparse, it is unlikely
the medial part of the anterior funiculus along the entire that they are responsible and that, because measurements
length of the spinal cord (Figure 2.9). The fibers termi- made with an exophthalmometer have indicated that the
nate in laminae VII and VIII. The medullary reticulospinal difference between the two sides is negligible, the enoph-
tract is also primarily ipsilateral and descends the length thalmos may simply be caused by the ptosis. In addition
of the spinal cord in the anterior part of the lateral funicu- to the signs in the eye, the patient may have anhydrosis
lus (Figure 2.9). The fibers of this pathway terminate in of the face because of the interruption of the sympathetic
laminae VII and VIII in close association with the termi- innervation of the sweat glands of the face ipsilateral to
nation of the fibers of the pontine reticulospinal tract, the the spinal cord injury.
rubrospinal tract, and the corticospinal tracts. When the descending autonomic pathways inner-
Animal studies have shown that stimulation of the vating preganglionic parasympathetic neurons are
brainstem reticular formation can facilitate or inhibit vol- lesioned bilaterally at any level of the spinal cord rostral
untary movement, cortically induced movement and to S2, the result is impotence and a loss of normal bowel
reflex activity; influence muscle tone; affect inspiratory and bladder function. However, after recovery from
phases of respiration; exert pressor or depressor affects spinal shock, spontaneous or reflex erection of the penis
on the circulatory system; and exert inhibitory effects on (or clitoris) may occur and bowel and bladder reflexes
sensory transmission (21). Those areas of the medullary may also return. This is in marked contrast to the deficits
reticular formation giving rise to the medullary reticu- associated with the conus medullaris and cauda equina
lospinal tract correspond closely with the regions from syndromes explained earlier in this chapter. In these lat-
which inspiratory, inhibitory, and depressor effects are ter cases, the preganglionic parasympathetic neurons at
obtained (2224). The areas of the reticular formation S2S4 are destroyed or their axons are severed; this usu-
related to facilitatory effects, expiration, and pressor ally results in a permanently areflexic bowel and bladder
vasomotor responses are rostral to the medulla and and the absence of spontaneous or reflex erections.
extend beyond the regions that give rise to reticulospinal In contrast to erection, ejaculation is controlled by
fibers (25). Thus, the reticulospinal tracts may not be the preganglionic sympathetic neurons located at the L1 and
mediators of some facilitatory effects originating from L2 levels of the spinal cord. During ejaculation, the sem-
neurons in the upper brainstem reticular formation. inal fluid from the seminal vesicles and prostate, as well
as sperm from each epididymis, flows into the prostatic
urethra and is ejected from the penis by rhythmic con-
Descending Autonomic Pathways
tractions of the bulbospongiosus muscle compressing the
Fibers belonging to this important descending system orig- urethra. This muscle is innervated by the somatic alpha
inate primarily from the hypothalamus. Although there is motor neurons located at the S2S4 levels of the spinal
evidence of direct projections from the hypothalamus to the cord via the pudendal nerves. Thus, erection is controlled
spinal cord (26), polysynaptic routes also pass through var- by parasympathetics and ejaculation is mediated by both
ious regions of the reticular formation before reaching the sympathetic and somatic neurons. During ejaculation,
spinal cord. The descending autonomic pathways are discharge of the semen into the bladder is prevented by
located predominantly in the lateral funiculi and terminate the contraction of the sphincter vesicae, which is inner-
on the preganglionic sympathetic and parasympathetic neu- vated by preganglionic sympathetics located at L1 and
rons located in lamina VII of T1L2 and S2S4 respectively. L2. When there is bilateral destruction of the descending
Lesion of the descending autonomic pathways in autonomic pathways in SCI, there is not only a loss of
spinal cord injury often leads to significant autonomic dis- erection, but also a loss of ejaculation. If the SCI is above
ANATOMY AND FUNCTION OF THE SPINAL CORD 29

FIGURE 2.10

Arteries of the spinal cord.


30 INTRODUCTION

FIGURE 2.11

Intrinsic distribution of spinal arteries.


ANATOMY AND FUNCTION OF THE SPINAL CORD 31

ented branches of the vertebral arteries and multiple


radicular arteries that arise from various segmental ves-
sels. The longitudinally oriented arteries are the anterior
spinal artery and a pair of posterior spinal arteries.

Anterior Spinal Artery


On the anterior surface of the medulla, two branches
from the vertebral arteries unite in the midline to form a
single anterior spinal artery that descends the length of
the spinal cord in the anterior median fissure (Figure
2.10). The sulcal arteries arising from the anterior spinal
artery enter the spinal cord through the anterior median
fissure. Successive sulcal arteries generally alternate in
their distribution to the left and right side of the spinal
cord (Figure 2.11), but occasionally a single sulcal artery
will distribute to both sides (Figure 2.12). The sulcal arter-
ies supply the anterior two-thirds of the spinal cord at any
cross-sectional level. This is anclinically important fea-
ture of the anatomy of the spinal cord, because occlusion
of the anterior spinal artery or its sulcal branches could
FIGURE 2.12
result in anterior cord (spinal artery) syndrome (Figure
Arterial supply and venous drainage of the spinal cord. 2.13). As in most vascular problems, the onset of signs
and symptoms is rapid. Figure 2.13 shows the zone of dis-
tribution of the anterior spinal artery in the cross-hatched
lumbar levels, reflex ejaculation may be possible in some area. The posterior funiculus and horns are spared
patients after recovery from spinal shock. Some patients because these areas are supplied by the posterior spinal
may have a normal ejaculation, but without external arteries. Initially, there is flaccid paralysis of the muscles
emission because of the paralysis of the sphincter vesicae. in the body below the level of infarct because of spinal
shock. In time, however, spastic paralysis and other upper
motor neuron signs develop because of bilateral destruc-
BLOOD SUPPLY OF THE SPINAL CORD tion of the corticospinal tracts. A variable degree of bowel
and bladder dysfunction exists because of the interrup-
The spinal cord is supplied by three longitudinally ori- tion of the descending autonomic pathways. Initially,

FIGURE 2.13

Diagram showing the extent of the lesion in anterior cord (spinal artery) syndrome and associated neurologic signs.
32 INTRODUCTION

FIGURE 2.14

Collateral circulation of the spinal cord. When posterior intercostals are tied off surgically, blood flows to the spinal cord via
internal thoracic and lateral thoracic (not shown) artery anastomoses with posterior intercostal arteries.

however, incontinence may be due to spinal shock. A car- Radicular Arteries


dinal sign of anterior cord syndrome is a dissociated sen-
The segmental vessels that pass through the intervertebral
sory loss characterized by a loss of pain and temperature
foramina divide into posterior and anterior radicular
sensations (bilateral lateral spinothalamic tract lesion)
arteries, which follow the posterior and anterior roots
with preservation of kinesthesia and discriminative touch
respectively (Figure 2.11). At variable levels the radicu-
sensations (sparing of posterior funiculi) in the body
lar arteries continue coursing medially until they anasto-
below the level of injury. Some patients develop painful
mose with either the anterior or posterior spinal arteries.
dysesthesias about 6 to 8 months after the onset of neu-
The anterior radicular arteries contribute to the anterior
rologic symptoms. The source of this pain is unknown,
spinal artery, and the posterior radicular arteries con-
but has been suggested to be attributed to the activation
tribute to the posterior spinal arteries. In the lumbar
of previously latent pathways that mediate pain sensa-
region, one anterior radicular artery is quite large and is
tion. The anterior spinal artery is dependent on segmen-
known as the artery of Adamkiewicz (Figure 2.10). This
tal contributions from anterior radicular arteries along
artery is usually found on the left and enters the verte-
the length of the spinal cord.
bral canal by following an anterior root at either a low
thoracic or upper lumbar level before anastomosing with
the anterior spinal artery. The artery of Adamkiewicz
Posterior Spinal Arteries
reinforces the circulation to two-thirds of the spinal cord,
The paired posterior spinal arteries derived from the ver- including the lumbosacral enlargement. Occlusion of this
tebral arteries descend on the posterior surface of the artery may seriously compromise spinal cord circulation,
spinal cord just medial to the posterior roots (Figure which could lead to infarct and paraplegia.
2.10). The arteries receive variable contributions from The greatest distance between radicular arteries that
the posterior radicular arteries. At points along the cord contributes significantly to the anterior and posterior
the posterior spinal arteries become so small that they spinal arteries is found at the thoracic level of the spinal
appear to be discontinuous. The arteries supply blood cord. At this level, occlusion of just one radicular artery
to the posterior one-third of the spinal cord. The periph- could lead to significant infarct of spinal tissue. The
eral portions of the lateral funiculi are supplied by the T1T4 levels of the thoracic cord are particularly vul-
arterial vasocorona, which is formed by an anastomosis nerable to infarct following occlusion of a radicular
between the anterior and posterior spinal arteries (Figure artery. Spinal cord segment L1 is another vulnerable
2.12). region.
ANATOMY AND FUNCTION OF THE SPINAL CORD 33

FIGURE 2.15

Veins of the spinal cord and the vertebral venous plexus.


34 INTRODUCTION

Collateral Circulation of the Spinal Cord


References
Severe trauma to the vertebral column on the left at the
1. Maynard FM Jr (Chair). International Standards for Neurologi-
thoracic level can fracture the bodies of one or more ver- cal and Functional Classification of Spinal Cord Injury, Revised
tebrae. A surgeon often must mobilize the descending 1996. Chicago: American Spinal Injury Association, 1996.
aorta to the right to expose the fractured vertebral bod- 2. Brodal A. Neurological Anatomy in Relation to Clinical Medicine,
3rd Edition. New York: Oxford University Press, 1981, 778780.
ies, remove the bony fragments, and stabilize the spine. 3. Moore KL and Dalley AF. Clinically Oriented Anatomy, 4th Edi-
The aorta is mobilized by first tying off several posterior tion. Philadelphia: Lippincott Williams and Wilkins, 1999, 477.
intercostal arteries close to their origin from the aorta, 4. Carpenter MB and Sutin J. Human Neuroanatomy, 8th Edition.
Baltimore: Williams and Wilkins, 1983, 241253.
severing the arteries in this region, and then moving the 5. Rexed B and Brodal A. The nucleus cervicalis lateralis: A spin-
aorta to the right (Figures 2.11, 2.14). The upper thoracic ocerebellar relay nucleus J Neurophysiol 1951; 14:399407.
spinal cord is particularly vulnerable to infarct if blood 6. Craig AD Jr, Burton H. The lateral cervical nucleus in the cat:
Anatomical organization of cervicothalamic neurons J Comp Neu-
flow into the cord from an important segmental vessel is rol 1979; 185:329346.
interrupted. The above surgical procedure, however, does 7. Craig AD Jr. Spinal and medullary input to the lateral cervical
not interrupt the flow of blood through the intervertebral nucleus J Comp Neurol 1978; 181:729743.
8. Afifi AK, Bergman RA. Functional Neuroanatomy. Text and Atlas.
foramen and thus to the spinal cord, because of collateral New York: McGraw-Hill, Health Professions Division, 1998;7677.
circulation. This collateral circulation results from the 9. Carpenter MB, and Sutin J. Human Neuroanatomy, 8th Edition.
anastomosis of the internal thoracic artery (a branch of Baltimore: Williams and Wilkins, 1983; 271273.
10. Afifi AK, Bergman RA. Functional Neuroanatomy. Text and Atlas.
the subclavian artery) with the posterior intercostal artery. New York: McGraw-Hill, Health Professions Divisions, 1998; 78.
As soon as blood flow from the aorta is interrupted, blood 11. Foerster O, Gagel O. Die Vorderseitenstrangdurchschneidung
begins retrograde flow from the internal thoracic artery beim Menschen. Eineklinischpathophysiologisch-Anatomische
Studie. Z Gesamte Neurol Psychiatry 1932; 138:192.
through the posterior intercostal artery and into the spinal 12. Afifi AK, Bergman RA. Functional Neuroanatomy. Text and Atlas.
cord (Figure 2.14). Although this is not shown in the fig- New York: McGraw-Hill, Health Professions Divisions, 1998;
ure, Hollinshead and Rosse (28) have suggested that the 8081.
13. Carpenter MB, Sutin J. Human Neuroanatomy, 8th Edition. Bal-
lateral thoracic artery (a branch of the axillary artery) also timore: Williams and Wilkins, 1983; 276282.
has anastomoses with the posterior intercostals and thus 14. Coulter JD, Ewing L, Carter C. Origin of primary sensorimotor
provides a second source of blood flow to the spinal cord cortical projections to lumbar spinal cord of cat and monkey.
Brain Res 1976; 103:366372.
under these conditions. 15. Jones EG, Wise SP. Size, laminar and columnar distribution of
efferent cells in the sensory-motor cortex of monkeys. J Comp
Neurol 1977; 175:391438.
16. Verhaart WJC, Kramer W. The uncrossed pyramidal tract. Acta
Veins of the Spinal Cord Psychiat Neurol Scand 1952; 27:181200.
17. Weil A, Lasser A. A quantitative distribution of the pyramidal tract
In general, the distribution pattern of the veins of the in man. Arch Neurol Psychiatry 1929; 22:495510.
spinal cord is similar to that of the spinal arteries (Figure 18. Madonick MJ. Statistical control studies in neurology. VII:
2.12). Three longitudinally oriented posterior spinal veins The cutaneous abdominal reflex. Neurology (Minneap) 1957;
7:459465.
and three anterior spinal veins communicate freely with 19. Nathan PW, Smith MC. Long descending tracts in man. I: Review
each other and are drained by anterior and posterior of present knowledge. Brain 1955; 78:248303.
radicular veins, which join the internal vertebral 20. Stern K. Note on the nucleus ruber magnocellularis and its effer-
ent pathway in man. Brain 1938; 61:284289.
(epidural) venous plexus lying in the epidural space (Fig- 21. Carpenter MB, Sutin J. Human Neuroanatomy, 8th Edition. Bal-
ure 2.12). This plexus of veins passes superiorly within timore: Williams and Wilkins, 1983; 297.
the vertebral canal through the foramen magnum to com- 22. Amoroso EC, Bell FR, Rosenberg H. The relationship of the vaso-
motor and respiratory regions of the medulla oblongata of the
municate with the dural sinuses and veins within the skull sheep. J Physiol (Lond) 1954; 126:8695.
(Figure 2.15). The internal vertebral venous plexus also 23. Pitts RF. The respiratory center and its descending pathways. J
communicates with the external vertebral venous plexus Comp Neurol 1940; 72:605625.
24. Torvik A, Brodal A. The origin of reticulbospinal fibers in the cat:
on the external surface of the vertebrae. An experimental study. Anat Rec 1957; 128:113137.
There are no valves in the spinous venous network. 25. Brodal A. The Reticular Formation of the Brain Stem. Anatomi-
Thus, blood flowing in these vessels could pass directly into cal Aspects and Functional Correlations Springfield IL: Charles
C Thomas, 1957.
the systemic venous system. For instance, when intra- 26. Saper CB, Loewry AD, Swanson LW, Cowan WM. Direct hypo-
abdominal pressure is increased, blood from the pelvic thalamo-autonomic connections. Brain Res 1976; 117:305312.
venous plexus passes superiorly via the internal vertebral 27. Brodal A. Neurological Anatomy in Relation to Clinical Medicine,
3rd Edition. New York: Oxford University Press, 1981; 763.
plexus. When the jugular veins are obstructed, blood leaves 28. Hollinshead WH, Rosse C. Text book of Anatomy, 4th Edition.
the skull by this same plexus. Because the prostatic plexus Philadelphia: Harper and Row, 1985; 182.
is continuous with the vertebral venous system, neoplasms 29. Batson OV. The function of the vertebral veins and their role in
the spread of metastases. Ann Surg 1940; 112:138149.
originating in the prostate gland may metastasize and
lodge in vertebrae, spinal cord, brain, or skull (29).
3 Imaging of the Spinal Cord

Roland R. Lee, M.D.


Blaine L. Hart, M.D.

magingin vivo visualizationof (CSF), allowing diagnosis of epidural, intradural-

I the spine and spinal cord is


extremely important in the evalua-
tion of patients with spinal cord
pathology. This chapter discusses the techniques used to
extramedullary, and intramedullary lesions. The contrast
between bone, spinal cord, and CSF is exquisite, but the
procedure is invasive.
Computed tomography (CT) gives good cross-
image the spine and spinal cord, concentrating on mag- sectional depiction of primarily the bony anatomy and
netic resonance imaging (MRI). The contribution of imag- the paraspinal soft tissues. However, the spinal cord itself,
ing to the diagnosis of major categories of spinal cord and the spinal nerve roots, are not well distinguished from
pathology is then discussed and illustrated. the surrounding intrathecal CSF. CT performed after
myelography, however, does give excellent visualization
of the spinal cord and nerve roots. However, it again relies
SPINAL IMAGING TECHNIQUES on the instillation of nonionic contrast into the spinal
canal. Also, images can only be obtained in the axial
For over a century, plain X-rays have been the imaging plane, although computer reconstructions in the sagittal
modality used to image the spine. The spinal vertebrae and coronal planes may be obtained, and may be of good
and their alignment are well evaluated, and the technique quality if the axial slices are thin (3 mm or thinner).
is simple and inexpensive, but the spinal cord proper can- Spinal angiography is the best way to image the
not be visualized on X-rays. arteries and veins of the spine and spinal cord, with good
Myelography, imaging of the spine by X-rays after depiction of vascular malformations and tumor vascu-
introduction of contrast material into the thecal sac, for larity. The diagnostic angiogram is a prerequisite en route
the first time enabled visualization of the silhouette of the to endovascular treatment of these lesions. However,
spinal cord within contrast-enhanced cerebrospinal fluid spinal angiography is invasive and technically difficult, so
that its use is generally limited to diagnosis and treatment
of spinal vascular malformations, and less commonly,
Portions of this chapter were previously published in Lee vascular tumors.
RR: Recent advances in MRI of the spine, and Lee RR: Spinal
tumors. In Lee RR (ed): Spinal Imaging (Spine: State of the Art Ultrasound is of limited utility in the diagnosis of
Reviews, vol 9). Philadelphia: Hanley & Belfus, 1995, 4560 spinal cord disease, because of the presence of the bony
and 261286. canal surrounding the theca and cord, which largely
35
36 INTRODUCTION

blocks transmission of sound waves. However, ultra- ter not only by its density (as does X-ray and CT), but
sound is a portable, noninvasive, and relatively inexpen- also by its different T1 and T2 relaxation parameters, is
sive modality that demonstrates good soft tissue contrast. of unparalleled value in differentiating between soft tis-
It is useful when the bony spinal elements are absent, such sues, such as gray and white matter, and normal vs. ede-
as during intraoperative visualization of the spinal cord matous tissue.
after the bony laminae have been surgically removed, or
in early infancy when spinal ossification is limited.
Imaging Speed
It has been little more than 15 years since the intro-
duction of MRI to spinal imaging. Although it is more Imaging speed is another important parameter, in addi-
expensive than some of the techniques listed above, tion to the three listed above. Unlike those prior three
because of its noninvasive nature (no ionizing radiation), parameters of image quality, which can be measured or
multiplanar imaging capabilities, superb soft tissue con- calculated directly from the image itself, the time required
spicuity, and ability to depict the spinal neural contents to produce the image cannot (although it is measurable
directly, MRI has established itself as the imaging modal- by other means). The imaging speed (i.e., the time
ity of choice for the spine and spinal cord (1). In certain required to obtain the image) is one of the most impor-
situations, however, one or more of the other modalities tant benchmarks of an imaging system, and this is where
discussed above may be more useful than MRI. many of the improvements in MRI (and indeed all med-
ical imaging) are being made.
Some portions of the human anatomy impose strin-
Basic Concepts of Imaging
gent requirements on imaging speed, most notably the
Three major parameters that characterize an imaging beating heart or respiratory motion of the thorax, but the
modality are spatial resolution, signal-to-noise (S/N), and spine in a supine patient is relatively motion-free and con-
contrast resolution (1). Any improvement in image qual- siderably less demanding in this regard. However, both in
ity represents some combination of improved spatial res- the interests of patient comfort and to avoid degradation
olution, increased S/N, and improved contrast resolution. by patient motion (especially in those patients with severe
Spatial resolution, essentially the smallest size back pain), it is desirable to minimize imaging time.
detectable by the technique, is determined by slice thick- Moreover, significant increases in imaging speed can yield
ness, field of view (FOV), and the size of the acquisition major improvements in signal-to-noise, as discussed in the
and display matrices. In a digital system such as MRI, section on fast spin-echo (FSE), also known as the rapid
the unit of in-plane spatial resolution (defined as a pixel) acquisition relaxation enhanced (RARE) sequence.
is the FOV divided by the matrix size. Thus, using a field As has historically occurred with all imaging modal-
of view of 48 cm (which is roughly the length of the spinal ities, including CT, improvements in image quality have
cord), and a 512  512 matrix size yields a nominal in- been accompanied by increases in imaging speed. Faster
plane spatial resolution of 0.94 mm, certainly adequate and more powerful computers, better reconstruction
for imaging spinal structures. Ideally, to achieve good spa- algorithms, and hardware improvements have all resulted
tial resolution, thin sections (3 mm) with a large matrix in these gains.
(256  256 or up to 512  512) should be used, but
unfortunately, as discussed in the following paragraph,
Phased-array Surface Coils
there is a trade-off between improving spatial resolution
and worsening signal-to-noise. Improved spatial resolution in spine imaging has long
Signal-to-noise (S/N), as the name implies, is the ratio been achieved with the use of surface coils, with their
of the desired signal to be measured, divided by the higher signal-to-noise ratio, but with a penalty of a
inevitable noise that degrades and contaminates the signal. smaller field of view and a limited penetration into the
Because the MRI signal is proportional to the number of body (2,3). Fortunately, though, the spinal structures lie
protons in the imaged volume element (voxel), increasing close to the posterior skin surface, so that virtually all
the volume sampled (i.e., increasing voxel and pixel size) modern spine MRI uses posterior surface coils to receive
increases the signal (more than the noise). However, the MR signals.
increasing pixel size means decreasing spatial resolution. The recent development of the phased-array surface
However, an intrinsic increase in S/N, such as from coil has solved the problem of limited longitudinal field-
increasing MRI magnet strength, or from improvements of-view by coupling many (4 to 6) such coils in a longi-
in coil technology, is extremely beneficial, not only tudinal array (4), mounted as a single long unit. This
because S/N is increased, but also because it allows for allows nearly the entire spine (48 cm) to be imaged in a
smaller pixel size and hence improved spatial resolution. single acquisition using a large field of view (FOV), with
Contrast resolution is the ability to discriminate good resolution (using a 512  512 or 512  384
between different tissues. MRI, which distinguishes mat- matrix), rather than requiring separate, time-consuming
IMAGING OF THE SPINAL CORD 37

imaging of the cervical, thoracic, and lumbar regions indi- through the levels of abnormality, rather than through the
vidually (Figure 3.1). Various combinations of the phased entire spine. A large FOV fast spin-echo (FSE) (discussed
coils may be electronically activated to view only the cer- below) T2-weighted sagittal image may be obtained in
vical, thoracic, or lumbar regions, or a combination about 3 to 6 minutes to clearly delineate regions of cord
thereof, without physically moving the coil or the patient. impingement (Figure 3.2.) The total imaging time for this
This allows screening studies of the entire spine to study is thus only about 20 minutes, which can generally
be made in one acquisition, rather than treating the spine be tolerated by almost any patient.
as three separate units (cervical, thoracic, and lumbar). Also, screening for intrathecal disease throughout the
It is particularly valuable in screening for metastatic dis- spine can be performed with a single postgadolinium sagit-
ease; a screening 3-mm series of T1-weighted sagittal
images of essentially the entire spine may be performed
in a single 3- to 7-minute sequence, and selected axial
images (T1 or fast spin-echo T2) should be obtained only

FIGURE 3.2

Fast spin-echo T2 (FSE-T2) used with phased-array spinal


FIGURE 3.1 coil. This screening FSE-T2 scan covered in only 6.5 minutes
48 cm (skull base through L3) in this kyphotic patient with
Sagittal T1 large field-of-view (48 cm, effective 512  512 metastatic thyroid carcinoma. Note the superb detail (0.9 mm
matrix using rectangular field-of-view) using a phased-array resolution) and uniformity of signal throughout the length of
coil, covers the entire spine of this normal 11-year-old girl the spine. T2-weighting yields an exquisite myelogram effect,
from pons through L4, in only 4.5 minutes. Spatial resolu- clearly delineating the retropulsed tumor mass at T2 that is
tion is 0.9 mm. Note the superb detail and uniform coverage posteriorly displacing and compressing the spinal cord, as
of all anatomy (1). well as the spondylotic changes in the cervical region (1).
38 INTRODUCTION

tal sequence in about 5 minutes, with a resolution of 0.9 al. (14), the RARE sequence and variations thereupon, have
mm (48 cm FOV / 512 matrix), using selected axial images been a major development in fast-scanning, particularly
only through the regions of abnormal enhancement. useful in spine MRI. This sequence, also known as fast-
spin-echo (FSE) or turbo-spin-echo, gives good T2-
weighted contrast in a fraction of the time required by true
FAST-SCANNING TECHNIQUES: RATIONALE (conventional) spin-echo, thus resulting in better resolution
and signal-to-noise than previously practically attainable
To improve the signal-to-noise ratio (S/N), one may (Figure 3.2). (FSE generally requires only a few minutes per
increase the signal by increasing the number of acquisitions sequence, rather than about 20 minutes for an equivalent
(i.e., the number of times the image data is acquired; in multiexcitation true T2-weighted acquisition.)
effect, scanning the patient multiple times), but this obvi- This sequence places several (from 3 to 16 or more)
ously significantly lengthens the exam and increases the different phase-encoding gradients followed by 180-
risk of image degradation from patient motion. However, degree radio frequency pulses after each 90-degree pulse,
if an imaging sequence is intrinsically very fast, doubling rather just one phase-encode and one or two 180-degree
or tripling the (very short) imaging time is a feasible option, pulses. This results in a much more efficient use of imag-
resulting in significant improvement in S/N and conse- ing time overall, cutting scanning time by a factor of 2
quently allowing smaller pixels (i.e., better spatial resolu- to 6 (or more).
tion). Hence, recent developments have focused on FSE images demonstrate less magnetic susceptibility
decreasing scan timea technique known as fast-scanning. artifact than true spin-echo images (15,16), which mini-
mizes artifacts from bone spurs, and (to a certain degree)
reduces artifact from surgical hardware (17) (See Figure
Gradient-echo Imaging
3.10). Possible disadvantages of FSE include bright signal
Many fast-scanning methods have been developed, of from fat and decreased sensitivity to hemosiderin (old blood
which gradient-echo imaging (GRE) was one of the first. products), as well as some blurring of images may occa-
This technique relies on gradients to refocus the spins, sionally be significant (14,15,16,18). One major artifact on
rather than 180-degree pulses, as are used in conventional FSE imaging is caused by CSF pulsation in the rostral
spin-echo imaging. Images are produced rapidly because regions of the spine, which yields signal voids that could
of small flip angles and short repetition times (TRs) (5,6). be misinterpreted as arteriovenous fistulas or AVMs in the
Its major advantage, besides speed, is the very thin slices CSF dorsal to the cord, especially on FSE images (15,17)
obtainable (less than 1mm thick), representing multiple
thin partitions of a large three-dimensional (3-D) imag-
ing volume, in contrast to the usual 3-mm minimum slice
thickness attainable with conventional 2-D spin-echo
slices. However, the signal characteristics of gradient-echo
images do not correspond directly to conventional T1- or
T2-weighted spin-echo imaging (7). In particular, GRE
images of the spine are inferior to conventional T2-
weighted or fast spin-echo images, because they consis-
tently overestimate the hydration of the disks, overesti-
mate the size of osteophytes because of susceptibility
artifact, and provide poor visualization of the neural
structures (7,8). Also, because of the lack of the 180-
degree refocusing pulse, gradient-echo scans are more
prone to susceptibility artifacts from tissue and magnetic
field inhomogeneity, and from motion (9).
In the spine, gradient-echo imaging currently has its
most widespread application in 3D-volumetric thin-sec-
tion axial images of the cervical spine, where the relatively
small size of the anatomic structures necessitates con-
tiguous thin-section images (10,11).
FIGURE 3.3

Fast Spin-echo (FSE or RARE) Imaging Consecutive sagittal FSE T2-weighted images of the thoracic
spine show multiple focal signal voids in the CSF posterior to the
Developed in 1990 by Melki and Mulkern et al. (12,13) spinal cord. These are common artifacts on this pulse sequence
as a refinement of a technique first proposed by Hennig et and must not be misinterpreted as a vascular malformation.
IMAGING OF THE SPINAL CORD 39

brain, because confounding bright CSF signal is sup-


pressed by the appropriate choice of inversion time (23).
However, its use in evaluating the spinal cord is contro-
versial, and some authors find that conspicuity of spinal
cord lesions with FLAIR is inferior to that with conven-
tional T2-weighted images (24).
Fast (short inversion-time inversion-recovery) STIR
images have an appearance similar to that of standard T2-
weighted images, with bright CSF and dark neural tis-
sue. However, normal fatty bone marrow also appears
dark on STIR images, compared with its relatively bright
appearance on FSE-T2 (Figure 3.6). A recent compara-
tive study concluded that fast-STIR images more sensi-
tively detected spinal cord lesions than FSE-T2 or fast-
FLAIR images (24).
All of these fast-imaging techniques will continue
to improve. There are a multitude of variables that may
be optimized (25). For example, in FSE, variables include
echo train length, partition of the various phase-encod-
ing steps in k-space, number of echoes obtained, and
interecho spacing, just to name a few.

Fast-imaging Techniques in the Spine


FIGURE 3.4
The myelographic effect on T2-weighted images, whereby
Axial FSE-T2 image through a lumbar disc shows a myelo- CSF is bright white, contrasting sharply with dark nerve
gram effect, with exquisite delineation of nerve roots in the roots, and dark vertebrae and discs, is very valuable in the
thecal sac. The disc, bones, and facet joints, as well as the diagnosis of spinal pathology. Even more important, T2-
paravertebral soft tissues, are well visualized (1). weighted images directly demonstrate edema or gliosis
within the spinal cord as bright T2-signal, contrasted with
T2-dark normal tissue.
(Figure 3.3). Cardiac gating, flow compensation, and other All the fast-imaging techniques discussed give a good
special pulse sequences may decrease artifacts from pul- myelographic effect except the fast-FLAIR sequence. The
satile CSF (19,20), but often some artifacts persist. best sequences for evaluating intrinsic spinal cord lesions
FSE sequences have dramatically improved spine are FSE-T2 and fast-STIR, but the former also gives the
imaging (17,21). Good T2 weighting (extremely useful in best depiction of the intervertebral disc and other soft
the axial as well as the sagittal plane) (Figure 3.4) can be tissues. In our experience, FSE proton-density images are
obtained in only a few (e.g., 3) minutes, as opposed to a useful adjunct to T2-weighted images in detecting spinal
about 10 minutes for a true single-excitation T2-weighted cord lesions, corroborating lesions suspected on FSE-T2,
sequence. As mentioned, this markedly faster sequence often with increased conspicuity (Figure 3.6).
permits higher resolution and more excitations (better One use of GRE images is in detecting small
S/N) to be achieved. T1- and T2-weighted images may amounts of hemosiderin (such as in spinal cord trauma)
be obtained in both sagittal and axial planes, with good or calcium, which could be missed on FSE images, and
resolution and S/N, in very short imaging times (about 30 may be missed on SE T2-weighted images.
minutes total examination time, or less). In summary, the screening MRI examination of the
Recent development of three-dimensional volumet- cervical spine should include a sagittal T1-weighted
ric FSE sequences (3D FSE-T2) provides thin-section, con- sequence; a sagittal flow-compensated, cardiac-gated con-
tiguous, high-resolution T2-weighted images that may be ventional, or preferably FSE T2-weighted sequence; and
reconstructed in any plane, from a single relatively rapid an axial 3-D gradient-echo sequence. Alternatively, a
acquisition (22) (Figure 3.5). sagittal 3-D FSE sequence, with axial reformation, may
replace the separate axial and sagittal T2-weighted
Other Fast-imaging Techniques sequences (Figure 3.5) (22).
Thoracic spine images should include sagittal T1-
Fast (fluid-attenuated inversion recovery) FLAIR is an weighted and FSE T2-weighted sequences, with axial
effective technique in evaluating T2-bright signal in the images obtained only through regions of abnormality.
40 INTRODUCTION

A B

FIGURE 3.5

Three-dimensional fast spin-echo (3D FSE-T2) of cervical spine. A. 1.2-mm-thick sagittal fast spin-echo T2-weighted image
was obtained as part of a 3-D volume acquisition, with forty-eight slices in 7.5 minutes. Note the clear delineation between the
vertebrae, CSF, and cord in this 36-year-old woman with prior C4-5 fusion. B. 0.9-mm-thick axial T2-weighted image was recon-
structed from the sagittal data acquired and shown in A. No axial images were directly acquired. Hence, both sagittal and axial
views can be obtained in a single 7.5-minute acquisition, with 1.2-mm resolution. Note the clear delineation of the spinal cord
and neural foramina on this reconstructed image (1).

In the lumbar spine, T1 and multiecho FSE T2- nerve roots in the neural foramina, and the surrounding
weighted images should be obtained in the sagittal plane, epidural fat. However, there are two major circumstances
followed by axial T1 and FSE T2-images. in which the presence of bright fat can mask pathology:
As discussed, the best technique for evaluating a) Enhancing structures on post-gadolinium T1-weighted
intrinsic spinal cord lesions includes sagittal FSE proton- sequences may be masked by surrounding T1-bright fat,
density and T2-weighted images, supplemented with and b) Intrinsically T2-bright lesions in the vertebral mar-
sagittal fast-STIR images. T1-weighted images after intra- row, such as metastases, may be masked by T2-bright fat
venous administration of Gd-DTPA are necessary to eval- on FSE images.
uate intradural-extramedullary or intramedullary lesions. In both these situations, suppression of the bright fat
signal by special pulse sequences enables the enhancement
or the T2-bright signal of lesions to be visualized; this may
Fat Saturation
provide better conspicuity of inflammatory and neoplas-
Fat is bright on T1-weighted images and fairly bright on tic lesions in the spine (18,26,27). Short inversiontime
FSE-T2 images. This can be advantageous, providing nat- inversion-recovery (STIR) is another method of fat sup-
ural contrast between the T1-dark CSF in the thecal sac, pression that may be especially useful in visualizing ver-
IMAGING OF THE SPINAL CORD 41

FIGURE 3.6

Sagittal MR images of a 58-year-old man with multiple sclerosis. Left. FSE proton-density image clearly demonstrates a small,
ovoid, bright plaque in the distal conus. Middle. FSE T2-weighted image only subtly demonstrates the lesion. Right. Fast-
STIR image subtly demonstrates the plaque slightly better than FSE-T2, but not as well as FSE proton-density. Note the dark
appearance of all the bony and soft tissue structures on the fast-STIR image, with only CSF and lesion hyperintense.

tebral metastases (28). Fat suppression may be applied


in combination with FSE sequences, as well as conven-
tional spin-echo images, to improve lesion conspicuity in
marrow (29), although T1-weighted images perhaps
remain most sensitive (29).
Another valuable application of spectroscopic fat
suppression is in the identification or diagnosis of fat-con-
taining lesions. Because subacute blood, proteinaceous
fluid, and occasionally calcium (30) can also be T1-bright,
the selective saturation of T1-bright fat can be diagnos-
tic in distinguishing among these possibilities (Figure 3.7).
(The presence of chemical shift artifact is also a clue to
the presence of fat, even without the use of fat saturation.)

CSF Flow: MRI Measurements


MRI can qualitatively and quantitatively measure CSF
flow because the phase of the precessing nuclei in the
magnetic field gradients is very sensitive to motion within
the field. In particular, the oscillatory motion of CSF in
the brain and spinal canal (especially in the more rostral FIGURE 3.7
spine), driven by brain expansion and contraction dur-
ing the cardiac cycle, and by motion of the brain and cord Use of fat saturation to diagnose intradural spinal lipoma.
Left. Sagittal T1 shows a very large well-circumscribed
itself, may be directly imaged by phase-contrast cine tech-
intradural-extramedullary T1-bright mass posterior to and
nique (18,3134). This technique can assess the degree of compressing the upper thoracic cord. Right. Fat-saturated
blockage of CSF flow within the spinal canalfor exam- postgadolinium T1 image shows complete suppression of the
ple, from congenital stenosis at the cervicomedullary junc- T1-bright signal, proving the presence of fat rather than T1-
tion, as seen in achondroplasia. Other possible uses bright blood. Hence, the diagnosis of lipoma rather than
include evaluating lack of normal cord motion in tethered hematoma was made and confirmed at surgery. A subtle thin
cords, and distinguishing between intradural subarach- rim of enhancement is noted around the tumor capsule (1).
42 INTRODUCTION

noid cyst versus a normally widened spinal canal,


A
although the interpretation of such studies has yet to be
perfected (18,32).

Titanium Spinal Hardware


Imaging the postoperative spine by CT or MRI after
implantation of fusion or stabilization metallic instru-
mentation is often frustrating and difficult because of
excessive beam-hardening artifacts in CT or very exten-
sive ferromagnetic susceptibility artifacts in MRI (Figure
3.8). Titanium is a strong metal that is less dense than
stainless steel and is nonferromagnetic when compared to
steel. Consequently, the imaging of titanium implants
both on CT and MRI, although far from perfect, is less
fraught with artifacts than imaging steel hardware. Often B
the relevant structures can be adequately evaluated by a
postoperative CT or MRI after titanium implants,
whereas steel implants would have resulted in a nondi-
agnostic study secondary to extensive artifact (Figures 3.9
and 3.10) (35).
As discussed in the section on FSE, this fast spin-echo
sequence should be used in concert with titanium instru-
mentation to minimize the metal susceptibility artifact.

Summary
There have been many recent developments in the fast-
growing field of spinal MRI. Some (fast imaging, espe-
cially FSE) result in faster intrinsic imaging times, with
the added benefit of improved signal-to-noise and spa-
tial resolution. Others (phased-array coil and variable
bandwidth) yield improved signal-to-noise and secon-
darily result in faster imaging and improved patient com-
fort. Still others (fat saturation, and use of titanium instru-
mentation) improve contrast resolution or otherwise
improve image quality.
All these developments are undergoing continual
refinement, and advances in the future will continue to
improve image quality, imaging speed, and ultimately, the
quality of patient care.

CONGENITAL ABNORMALITIES

With the exception of early infancy, when ultrasound of


the spine can be successfully performed because of the FIGURE 3.8
limited vertebral ossification at this age, MRI is the test
A. Axial CT image through a lumbar vertebra with stainless
of choice for imaging spinal malformations. In early
steel pedicle screws and vertebral body screw shows exten-
infancy, sonography can visualize the spinal cord between sive beam-hardening artifact from the hardware, completely
the areas of early ossification. Tethering of the spinal cord precluding evaluation of the spinal canal or the bony struc-
can be demonstrated not only by a low position of the tures at this level. B. Sagittal T1-weighted MR image of the
conus medullaris but by the failure of the spinal cord to same patient with stainless steel pedicle screws shows severe
move with positional changes and with cardiac and res- metallic susceptibility artifact, rendering this lumbar MRI
piratory movement. completely uninterpretable.
IMAGING OF THE SPINAL CORD 43

FIGURE 3.10
B Titanium hardware minimizes artifact on MRI. Axial fast spin-
echo (FSE) T2-weighted image of vertebra at level of bilat-
eral titanium pedicle screws shows only minimal suscepti-
bility artifact in the vicinity of the screws. The central canal
is still clearly visualized, as are the individual nerve roots.
Stainless steel hardware would have rendered this level unin-
terpretable. Use of fast spin-echo sequence also contributes
to minimizing artifact (1).

onal fusion of laminae of adjacent vertebrae, which, when


seen, is strongly associated with diastematomyelia, a mal-
formation resulting from a split notochord. CT can be
helpful to delineate bone abnormalities, identify bony or
cartilaginous septa, and identify fat within the spinal
canal. Myelography and postmyelography CT have a lim-
ited role in the evaluation of congenital abnormalities. For
almost all congenital spine malformations, MRI is by far
the best way to evaluate the spinal cord (36).
Myelomeningocele (Figure 3.11), which is an open
neural tube defect, is obvious at birth, and the role of
imaging is supplemental. Evaluation of the distal spinal
cord for tethering is a common problem at later ages.
FIGURE 3.9 Because a high percentage of patients with Chiari II mal-
formation and myelomeningocele have hydrocephalus,
Titanium hardware minimizes artifact on CT. A. Axial CT- CT or MRI of the head (or sonography in infancy) is com-
myelogram image at level of left-sided titanium laminar hook
monly used to help evaluate the need for shunt catheter
and right-sided rod shows only minimal artifact. Posterior ele-
ments and contents of the spinal canal, including cord and
placement and to monitor function of a shunt catheter
contrast-filled thecal sac, are clearly discernable. Steel hard- later. Syrinx can occur in Chiari II. Cervical spinal cord
ware would have rendered this level uninterpretable. B. Sagit- atrophy is occasionally seen, probably caused by com-
tal reconstruction from the axial CT data again clearly demon- pression from the downwardly displaced cerebellum in
strates the titanium hardware and the spine, with only the upper cervical spinal canal (Figure 3.12).
minimal beam-hardening artifact (1). Lipomyelomeningocele, despite its similar name, is a
quite different entity than myelomeningocele. It results
from the premature dysjunction of the skin from the neural
Plain radiographs are often very helpful to evaluate tube before complete closure, thus exposing mesoderm to
the bony structures of the spine. Spina bifida occulta is a the developing CNS and inducing the formation of fat.
common finding that may be seen with many different Thus, the spinal cord is intimately associated with fat that
types of congenital malformations, but it is not specific in is continuous with subcutaneous fat and therefore tethered.
predicting congenital abnormalities. A rare but fairly spe- Because the overlying skin is intact, the malformation may
cific plain-film finding is crossed laminar fusion, or diag- not present for years, or even for several decades. The
44 INTRODUCTION

FIGURE 3.11 FIGURE 3.12

Myelomeningocele. Sagittal T1-weighted MR image of 6-year- Chiari II and spinal cord atrophy. Sagittal T1-weighted MR
old child with symptoms of tethered cord and previous image of a 6-year-old child with myelomeningocele shows
surgery for myelomeningocele. The spinal cord extends infe- downward displacement of the cerebellum far down into the
riorly into the meningocele at the level of the sacrum. cervical spinal canal. The cervical spinal cord is atrophied.

lipoma can be demonstrated by CT but is especially well subpial collection of fat, nearly always along the dorsal
shown by MRI (Figure 3.13). Low attenuation on CT and surface of the spinal cord (Figure 3.15).
similar signal intensity to fat elsewhere on MRI are spe- A focal failure of disjunction of the spinal cord from
cific for lipomas in the spinal canal. The position of the dis- the overlying ectoderm leads to the formation of a dor-
tal spinal cord is best demonstrated by MRI. Spina bifida sal dermal sinus tract, lined by epithelial tissue. When a
occulta is seen at the site of communication with subcuta- dimple, patch of hair, or pigmented skin leads to suspi-
neous fat. Lipomyelomeningocele is not associated with the cion of such a tract, MRI can demonstrate the tract. Such
Chiari II malformation, and the incidence of hydrocephalus tracts often extend obliquely through the subcutaneous
in these patients is similar to that of the general population. tissue. They may terminate anywhere from subcutaneous
A lipoma of the filum terminale may be associated tissue to epidural space, to dura, to the spinal cord itself.
with a tethered cord (Figure 3.14). Very small amounts In about half of dorsal dermal sinus tracts, a dermoid or
of fat within the filum terminale are commonly seen and epidermoid cyst is present. MRI shows such tumors or
are of doubtful significance. The lipoma of the spinal cord cysts as round or oval masses in the spinal canal and can
is the least common of the spinal lipomas. It is actually a show their relationship to the spinal cord.
IMAGING OF THE SPINAL CORD 45

A B

FIGURE 3.13

Lipomyelomeningocele. Twelve-year-old boy with lifelong urinary incon-


tinence and no previous surgery. A. Sagittal T1-weighted MR image shows
large lipoma within the distal spinal canal. B. Axial T2-weighted MR
image discloses a syrinx (hydromyelia) of the distal spinal cord.

The spinal cord can be tethered from a variety of mentally divided in the sagittal plane, and the dural sac
causes. Myelomeningocele and lipomyelomeningocele may be intact or may also be divided. In about half of
both imply that the spinal cord is tethered. However, these cases there is a bony or cartilaginous septum
errors in a later stage of development relating to the cau- through the spinal canal. Such septa are best demon-
dal cell mass can lead to a tethered cord without the more strated by CT but may be shown by MRI, especially with
obvious abnormalities of the spinal cord and vertebra. gradient-echo techniques. The split spinal cord and the
The tip of the conus medullaris lies at the L2 level or length of the division are best shown by MRI.
above in 98 percent of people, and position of the conus
medullaris at or below the L23 level is generally con-
Trauma
sidered abnormally low (37). Sagittal MR images alone
can sometimes be confusing, because the nerve roots in Imaging plays a key role in the evaluation of spine
the cauda equina may simulate the conus medullaris; trauma, both in the acute situation and in the later imag-
additional coronal or axial images are often necessary to ing of complications. The complementary nature of var-
accurately image the distal spinal cord. T1-weighted ious imaging modalities is especially important in imag-
images are often most reliable to identify the conus ing spine trauma.
medullaris. As mentioned above, sonography is only pos- Plain radiographs are part of the routine evaluation
sible early in life but has the advantage of providing of patients in whom there is a strong suspicion of spine
dynamic information. injury. Radiographic evaluation of the cervical spine is
Diastematomyelia is a rare congenital malformation recommended for all patients with evidence of significant
resulting from a split notochord. The spinal cord is seg- injury above the clavicles. There is no consensus on which
46 INTRODUCTION

FIGURE 3.15

Intradural lipoma. Axial T1-weighted MR image of adult man


with scoliosis shows high signal intensity fat dorsal to the
spinal cord in the upper thoracic spine.

fractures, and adjacent soft tissue outlines (38). Focal


kyphosis or subluxation should suggest the possibility of
fracture or major ligamentous injury, although chronic
degenerative change can cause minor abnormalities of
alignment. In the cervical spine, anterior and posterior
margins of the vertebral bodies, the spinolaminar line
(along the posterior margin of the spinal canal and ante-
FIGURE 3.14 rior margin of the spinous processes), and the posterior
margin of the spinous processes should all demonstrate a
Tethered cord and filum lipoma. Sagittal T1-weighted MR regular, relatively smooth change. The prevertebral soft tis-
image of a young adult with back pain shows high signal sues in the cervical region can provide important clues to
intensity (arrow) in a lipoma of the filum terminale. injury, especially in the upper half of the cervical spine. The
presence of the esophagus adjacent to the lower cervical
spine normally widens the soft tissues in this region and
views should be obtained, and numerous different opin- makes it more difficult to identify swelling. At the C3 ver-
ions and protocols have been offered. A lateral view to tebral body, the prevertebral tissues should normally not
include the cervicothoracic junction should always be exceed 4 mm in thickness on a routine lateral view (72-
obtained, and a typical radiographic series for cervical inch [183-cm] distance); a portable technique using a
spine trauma includes AP and odontoid views as well. A shorter focal distance can cause magnification and slightly
swimmers view is often helpful if the cervicothoracic larger apparent thickness. In the thoracic spine, a
junction is obscured by the shoulders. Additional projec- paraspinous hematoma from a fracture is often visible on
tions such as oblique views or the pillar view may be the AP view. Fractures may be visualized directly or
obtained, but are often reserved for special cases. inferred from the loss of vertebral body height or from
Radiographic evaluation of the thoracic and lumbar increased density in the region of compressed bone. Frac-
spine includes at least lateral and often also AP views. tures of the posterior elements are particularly difficult to
Oblique views of the thoracolumbar spine are rarely indi- identify with plain films, and as many as half of all poste-
cated in the evaluation of acute trauma. rior element fractures identified on CT are missed on plain
In assessing spine radiographs, the interpreter should film. The odontoid process should be inspected carefully
look at alignment, the bones themselves for presence of for fractures.
IMAGING OF THE SPINAL CORD 47

CT is more sensitive than plain radiographs for the


A
detection of fractures (39,40). Fractures oriented in the
axial plane may be difficult to identify on CT. Such
injuries include fractures through the base of the odon-
toid process, some compression fractures, and Chance
fractures (which are discussed later in this chapter, under
thoracic and lumbar injury patterns). Sagittal and coro-
nal reformatted views can be particularly helpful in such
cases (Figure 3.16). 3-D reconstructions are sometimes
helpful in assessing alignment and displacement of frag-
ments. Such reconstructions, as well as routine CT scan-
ning of longer segments of the spine, are more readily per-
formed with spiral or helical techniques. CT of the spine
should be performed with a slice thickness small enough
to permit reformatted views and to identify fractures. In
the authors experience, slice thickness should not be
more than 3 mm; in areas such as the cervicocranial junc-
tion and odontoid process, thinner or overlapping slices
are often necessary.
MRI is particularly helpful for visualization of the
spinal cord and for identification of soft tissue injury.
Hematomas, disk herniation, and spinal cord contusion, B
hemorrhage, or compression can be directly demon-
strated by MRI, as can patency of the vertebral arteries
(41). Indications for MRI in the setting of acute spine
trauma include neurologic injury; evaluation of suspected
complicating factors, such as disk herniation when
surgery is being considered; and evaluation of soft tissue
injury, especially in patients in whom clinical assessment
is limited. Sagittal T1- and T2-weighted images can be
used to screen the spinal cord, with axial images used
through areas of particular concern. Because normal
paraspinal fat has high signal intensity on T2-weighted
fast-spin-echo (FSE), which could mask T2-bright edema
from injury to the soft tissues, it is important to use a fat-
suppression technique with FSE T2-weighted imaging.
Inversion-recovery techniques or chemical fat saturation
can be used with fast-spin-echo imaging.
Numerous types of cervical spine fractures can
occur, and a comprehensive review is beyond the scope of
this chapter. More extensive reviews are available, includ-
ing entire books (4244). However, it is useful to consider
cervical spine fractures in terms of the major mechanisms
of injury. Flexion injuries, resulting primarily from exces-
sive force in flexion, include compression or wedge frac-
ture, bilateral facet dislocation (Figure 3.17), spinous
process fracture (clay-shovelers), hyperflexion sprain,
and flexion-teardrop fracture. Injuries resulting primar- FIGURE 3.16
ily from excessive force in extension include hyperexten- Chance injury. Young adult woman in a motor vehicle acci-
sion dislocation, C1 anterior arch avulsion fracture, C1 dent had anterior loss of height seen on plain X-rays at the
posterior arch fracture, laminar fracture, extension T12 level. Axial CT scan (A) shows lucency and irregularity
teardrop fracture, hangmans fracture (traumatic spondy- at the anterior margin of T12 and subtle lucency through the
lolisthesis) (Figure 3.18), and hyperextension fracture-dis- right lamina, representing fractures. Sagittal 2D reconstruc-
location. A combination of rotation and flexion causes tion image (B) clarifies the anterior compression and poste-
unilateral facet dislocation (Figure 3.19). Rotation in rior widening between the lamina in this Chance-type injury.
48 INTRODUCTION

A C

FIGURE 3.17

Bilateral facet dislocation in a middle-aged man with quadri-


plegia after motor vehicle accident. Axial CT (A) shows dislo-
cation. Parasagittal 2-D reconstruction view (B) demonstrates
more directly the facet dislocation at C67 on the right. Simi-
lar findings were present on the left side. Sagittal T2-weighted
(inversion recovery) MR image (C) shows subluxation at C67,
spinal cord compression and edema, marrow edema in the
upper thoracic spine, and extensive posterior paraspinal soft
tissue edema.

combination with extension causes pillar or lateral mass Combined fractures of the pedicle and lamina result in a
fractures, which can be especially difficult to demonstrate separation of the lateral mass and risk of rotational insta-
on plain films. We have found that MRI can be helpful bility (Figure 3.20).
with these posterior-element fractures to demonstrate the Injuries resulting primarily from axial loading mech-
extent of accompanying ligamentous injury, which may anisms include the Jefferson burst fracture of C1, burst
be an important factor in determining instability (45). fractures of C3 through C7, burst fractures involving the
More extensive ligamentous injury probably indicates a thoracic or lumbar spine, and oblique sagittal fractures
greater risk of instability in these lateral mass fractures. (type 2) of the C2 body. The Jefferson fracture pattern
IMAGING OF THE SPINAL CORD 49

FIGURE 3.18

Hangmans fracture (traumatic spondylolisthesis). Axial CT B


at C2 shows bilateral fractures through the pars interarticu-
laris.

includes two or more fractures through the ring of C1.


CT is the best method for identifying this fracture (Figure
3.21). Plain film findings include lateral displacement of
the lateral masses of C1 on the AP odontoid view, lucency
through the posterior arch of C1 on the lateral view, and
upper cervical prevertebral soft tissue swelling.
Burst fractures occur from C3 through the lower cer-
vical and entire thoracic and lumbar spine. They result
when axially directed force transmitted through a disk is
transmitted to the centrum or body below, which then
fractures. A prominent sagittal component nearly always
occurs; more extensive comminution of the vertebral
body is variable. It is common for fragments to displace
posteriorly into the spinal canal, possibly compromising
the spinal cord.
The cervicocranial junction is complex, consisting
of the articulations of C1 and C2 and the occiput, as well
as multiple ligaments that contribute to stability and
motion in multiple directions. In addition to the fractures
of C1 and C2, the occipital condyles can fracture. Such
fractures are difficult to identify except with CT (46,47)
(Figure 3.22). Ligamentous injury can be inferred by soft
tissue swelling and can be more directly demonstrated
by MRI. The transverse ligament, responsible for main-
taining the relationship between C1 and the odontoid FIGURE 3.19
process, is very strong and is damaged only by major
Unilateral facet dislocation. Axial CT (A) shows reversal of
injuries. The ligament can be visualized directly by MRI, the usual relationship of the facets on the patients right
but injury is often identified on the lateral X-ray by abnor- (arrow). Note that unlike Figure 3.17 bilateral facet disloca-
mal widening of the anterior atlantodental interval. This tion, only one side is dislocated and there is less subluxa-
space should measure no more than 3 mm in adults. tion. Sagittal T2-weighted (inversion recovery) MR image (B)
Widening of this space can occur from traumatic injury shows subluxation at C56, spinal cord compression and
to the ligament, either rupture or avulsion from the tuber- edema, and dorsal soft tissue edema.
50 INTRODUCTION

FIGURE 3.20

Pedicolaminar fracture pattern. CT shows fractures of the


both the right pedicle and the right lamina.

cles on the lateral masses of C1, or from damage from


rheumatoid arthritis or other inflammatory conditions,
and some congenital conditions (Figure 3.23).
Atlanto-occipital dissociation (AOD) requires severe
forces to tear the ligaments attaching the occiput to the
atlas, especially the strong superior portion of the cruci-
ate ligament. Such injuries are often fatal (48). Severe
upper cervical prevertebral soft tissue swelling is present.
Some patients with less severe displacement can survive,
and plain film findings that indicate AOD can be subtle.

FIGURE 3.22

Occipital condyle fracture. Axial CT (A) shows subtle lucency


through the left occipital condyle. Coronal 2D reconstruction
(B) demonstrates the fracture more clearly (arrow).

A variety of measurements have been proposed to iden-


tify abnormalities of the relationship of C1, C2, and the
occiput. The most reliable appear to be those described
by Harris et al. (49). Two measurements are made from
FIGURE 3.21
the basion, or inferior tip of the clivus. The distance from
basion to the tip of the dens (basiondental interval or
Jefferson burst fracture of C1. CT shows four fractures in the BDI) should not exceed 12 mm in adults as measured on
anterior and posterior arches of C1. a lateral radiograph obtained at 40-inch (102 cm) tar-
IMAGING OF THE SPINAL CORD 51

FIGURE 3.23

Avulsion of the transverse ligament attachment.


Previous lateral cervical spine radiograph of a
young woman in a motor vehicle accident
showed widening of the anterior atlantodental
interval to 5 mm. CT shows fracture through the
tubercle where the transverse ligament attaches
on the patients left (arrow).

A B

FIGURE 3.24

Atlanto-occipital dissociation. MRI was performed on a patient who was in a high-speed motor vehicle accident. Midline sagit-
tal T2-weighted inversion recovery image (A) shows high signal intensity of severe anterior and posterior paraspinal soft tissue
edema at the cervicocranial junction. Heterogeneous signal intensity within the spinal canal reflects some blood present.
Parasagittal image (B) shows subluxation of the atlanto-occipital joint, with high signal intensity fluid between the occipital
condyle and lateral mass of C1 (arrow).
52 INTRODUCTION

get-film distance. The distance from basion perpendicu- very helpful for planning surgical intervention. MRI is the
larly to a line extended rostrally from the posterior cor- best imaging method to evaluate the spinal cord (Figure
tical margin of the body of C2 (basionaxial interval or 3.26). Finally, in any injury in which the surgical
BAI) measured on a lateral radiograph should not exceed approach may be affected by the location of the artery
12 mm in children or adults. MRI can more directly of Adamkiewicz, spinal angiography may be indicated.
demonstrate ligamentous disruption (Figure 3.24). A combination of flexion and distraction results in
Injury patterns in the thoracic and lumbar spine, in a distinctive type of injury, usually in the upper lumbar or
which motion is more restricted, are somewhat more lim- lower thoracic spine. The classic Chance fracture extends
ited than those in the cervical spine. Compression frac- horizontally through the vertebral body and through both
tures are common injuries that result in loss of height of pedicles, and may occur in automobile accidents when the
the vertebral body, anteriorly more so than posteriorly. In patient is wearing a lap belt but not a shoulder harness.
mild cases, radiographic findings include deformity of the It is often best demonstrated on plain radiographs,
cortical margins and end-plates. Axial loading can cause because axial CT is less well suited to identifying axially
a burst fracture, in which the force transmitted through oriented fractures (see Figure 3.16). However, other pat-
the intervertebral disk results in bursting of the centrum terns of flexion-distraction injuries can also occur, still
below. Posterior element fractures are usually present, with an axial orientation and posterior distraction. In
there is nearly always a prominent sagittal component of these injuries, shearing may occur through the disk space,
the vertebral body fractures, and displacement into the with posterior subluxation or dislocation of the facet
spinal canal is variable. CT is usually helpful to define the joints (50,51).
extent of fractures and posterior element involvement In addition to mechanical narrowing of the spinal
(Figure 3.25). Fracture-dislocations involve complex, canal by displaced bone, the spinal cord can be compro-
severe forces, variable amounts of dislocation of one ver-
tebra on another, and usually multiple fractures. Neuro-
logic deficits from spinal cord compression are common.
Multiple imaging modalities are often helpful in man-
agement. The dislocation is usually initially demonstrated
on plain radiographs, which are excellent for demon-
strating alignment. CT of the affected vertebrae can be

FIGURE 3.25 FIGURE 3.26

Burst fracture of T12 suffered in a parachuting accident. The Thoracic fracture-dislocation. Sagittal T2-weighted inversion
patient had incomplete paraplegia. Axial CT shows numer- recovery image of a young adult who suffered severe T1011
ous fractures in the body of T12, with posterior displacement fracture-dislocation in a logging accident shows dislocation
of fragments into the spinal canal. and spinal cord transection.
IMAGING OF THE SPINAL CORD 53

FIGURE 3.28

Stab injury of the spinal cord. Axial T2-weighted MR image


shows linear high signal intensity along the knife track
through the posterior soft tissues, left lamina of T10, and left
side of the spinal cord (arrows). The patient had left lower
FIGURE 3.27 extremity sensory loss, but intact strength.

Spinal cord contusion without fracture. Sagittal T2-weighted


inversion recovery MR image of a man who had upper
extremity weakness after a motor vehicle accident shows T1-weighted and T2-weighted images. MRI can demon-
stenosis of the cervical spinal canal, disc bulge or protrusion strate the size and extent of a posttraumatic syrinx and
at C45, and edema within the spinal cord at the same level can be used to follow the results of intervention. Post-
(arrow). traumatic myelomalacia appears as a thinning of the
spinal cord and often strandlike areas of soft tissue (Fig-
ure 3.29). Adhesions or cysts that may further limit spinal
mised by traumatic disk protrusion, hematoma, transient cord function can be visualized.
hyperextension, hyperflexion, distraction, or ischemia. In
all of these conditions, MRI is the best imaging test. Many
cases of injury that would otherwise be considered spinal DEGENERATIVE DISEASE AND
cord injury without radiographic abnormality (SCI- POSTOPERATIVE SPINAL IMAGING
WORA) have obvious abnormalities on MRI (52,53)
(Figure 3.27). Unexplained neurologic deficits should be Spinal degenerative disease is part of the normal aging
assessed with MRI when possible. In addition, MRI may process. Disc degeneration and associated endplate osteo-
aid in planning surgery by disclosing traumatic disc her- phyte formation, as well as facet hypertrophy and the
niations that can compromise the spinal cord after reduc- prominence of the ligamenta flava, may result in central
tion of fracture or dislocation (54). In the authors expe- or neural foraminal stenosis and spinal cord or nerve root
rience, MRI within the first 2 to 3 days after injury can compression. However, about 30 percent of all asymp-
exclude any major ligamentous injury that may threaten tomatic adults will have MRI findings of lumbar spinal
the stability of the cervical spine (55). degenerative disease, and 19 percent of asymptomatic
Penetrating trauma of the spine can also damage the people were found to have significant abnormalities on
spinal cord and may be more difficult to image if bony cervical spine MRI (56,57). Thus, it is essential for the
injuries are minor. MRI can sometimes demonstrate physician to carefully interpret the imaging findings in
spinal cord injury in these cases (Figure 3.28). light of the patients symptoms (56). Moreover, the nat-
The late sequelae of traumatic spinal cord injury are ural history of back pain is that about 80 percent of
best assessed by MRI. Syrinx appears as a region of fluid patients recover within 2 months without any treatment
within the spinal cord, with CSF-signal intensity on both (58); therefore, spinal imaging for back pain should not
54 INTRODUCTION

A B

FIGURE 3.29

Posttraumatic changes. The patient who previously had a


C56 dislocation and subsequent anterior instrumentation
returned after a new episode of more minor trauma. Sagittal
T2-weighted inversion recovery image (A) shows loss of spinal
cord contour at the level of the old injury. Myelomalacia is
corroborated on axial T2-weighted image (B); there are mul-
tiple strandlike areas of soft tissue, with a suggestion of pos-
sible septations and cystic change.

A B

FIGURE 3.30

Sixty-seven-year-old man with multiple thoracic disc protrusions. A. Axial image from postmyelogram CT shows a broadbased
central disc protrusion flattening the ventral thecal sac, compressing the spinal cord (black arrow), which is outlined by white
contrast-laden CSF. B. Sagittal reconstruction from the axial CT data shows two thoracic disc protrusions (white arrows) effac-
ing the ventral CSF; the lower protrusion corresponds to A.,, slightly compressing the spinal cord.
IMAGING OF THE SPINAL CORD 55

be obtained emergently except in cases of known or sus-


pected cancer, spinal infection, trauma, and the like.
Discogenic degeneration may be classified as disc
bulge, protrusion, extrusion, and sequestered fragment,
in order of increasing size and clinical symptomatology
(59). Bulges are extremely common (one study [59] found
disc bulges in 52 percent of asymptomatic normal adults)
and generally asymptomatic. These bulges are seen on
MRI as a diffuse, nonfocal bulging of the disc beyond
the normal contours of the disc and endplate. Bulges may
narrow the central spinal canal and inferior aspect of the
neural foramina, but unless very large, do not cause symp-
toms. Central canal stenosis and myelopathy may result
from advanced disease; these disorders present with very
large disc bulges and are commonly associated with mar-
FIGURE 3.31 ginal endplate bony osteophytes (Figure 3.30).
Disc protrusions are defined as focal posterior defor-
Axial FSE-T2 MR image shows a prominent disc protrusion mities of the anulus fibrosus caused by posterior hernia-
posterior to the L5 vertebra in the left lateral recess, com- tion of the nucleus pulposus with an intact posterior lig-
pressing and posteriorly displacing the traversing left L5 nerve amentous complex (Figure 3.31). Disc protrusions have
root. There is superb delineation between the CSF, disc, and
been incidentally found in 27 percent of asymptomatic
nerve roots (1).

A B

FIGURE 3.32

Cervical spinal cord compression and gliosis caused by large disc protrusions in a 62-year-old man. Sagittal (A) T1-weighted and (B)
T2-weighted MR images show large disc protrusions at essentially all cervical levels, with spinal cord compression and flattening at
C34 and C56. A small focus of T2-bright gliosis is present within the spinal cord (B) associated with the compression at C34.
56 INTRODUCTION

volunteers (59); however, protrusions may also be symp-


tomatic, causing spinal cord compression and resultant
edema or gliosis within the spinal cord, which is mani-
fested as T2-bright signal (Figure 3.32). Again, the physi-
cian must confirm the correlation between patient symp-
tomatology and the MRI findings before intervening
surgically.
Disc extrusions are generally larger than protru-
sions, and are generally associated with rupture of the
posterior anuloligamentous complex. Extrusions are
more likely to be symptomatic; only 1 percent of asymp-
tomatic adults had disc extrusions (59). Sequestered frag-
ments result when a disc extrusion becomes separated
from the parent disc.
Ossification of the posterior longitudinal ligament
(OPLL) is another less-common degenerative disorder,
most common in Japanese but also seen in others, which
can cause central stenosis and spinal cord compression
(58) (Figure 3.33).

Postoperative Complications
Postoperative complications include postoperative
hematomas, pseudomeningocele, infection, recurrent disc
herniation, and arachnoiditis (60). Recurrent disc herni-
ation can be distinguished from postoperative scar tissue
in that, unlike normal scar tissue, recurrent disc hernia-
tions do not enhance with IV gadolinium-DTPA (61).
Arachnoiditis has many causes, but may be associ-
ated with a history of pantopaque myelography or spinal
surgery. On MRI, the nerve roots are thickened and
clumped, and exhibit variable enhancement. They may
adhere to the periphery of the thecal sac. Intrathecal
arachnoid bands or cysts may be present (Figure 3.34).
Another postoperative complication is improperly
positioned spinal hardware. As discussed earlier, titanium
hardware is better visualized on CT and MRI than stain-
less steel (Figures 3.8, 3.9, 3.10). Occasionally, CT
demonstrates metal hardware directly impinging on
spinal nerve roots (Figure 3.35).

INFLAMMATION AND DEMYELINATION FIGURE 3.33

Ossification of posterior longitudinal ligament in a 60-year-


For purposes of evaluating demyelinating disease of the old man. Axial CT image through C4 (A) and (B) sagittal CT
spinal cord and other inflammatory, intramedullary reconstruction show a calcified, thickened posterior longitu-
processes, MRI stands essentially alone as an imaging dinal ligament (black arrow) compromising the spinal canal.
tool. Myelography and CT can show little more of the
spinal cord than change in contour, whereas MRI reveals
information about the contents of the spinal cord itself.
However, the findings on MRI are often nonspecific, espe- margin of the spinal cord but can be seen elsewhere in the
cially for a solitary lesion. spinal cord. As in the brain, enhancement sometimes
The plaques of multiple sclerosis (MS) appear as occurs in acute plaques, but lack of enhancement does not
areas of high-signal intensity within the spinal cord on exclude a plaque (62). In the presence of acute plaques,
T2-weighted images. They often occur at the dorsolateral the spinal cord can be enlarged, which can create concern
IMAGING OF THE SPINAL CORD 57

for a possible neoplasm. For this reason, when a lesion is


identified on MRI within the spinal cord, even if it
enhances, it is appropriate to consider MS in the differ-
ential diagnosis and obtain MRI of the brain to look for
additional evidence of MS. Finding multiple spinal cord
lesions increases the likelihood of MS and makes neo-
plasm much less likely (Figure 3.36).
Spinal cord lesions of Devics disease have an imag-
ing appearance similar to that of MS plaques, and the
additional findings of optic neuritis and the absence of
other brain lesions help establish the diagnosis.
Transverse myelitis is usually readily apparent on
MRI as a region of increased T2 signal intensity, often
having an elongated or spindle shape on sagittal images
(Figure 3.37). The term encompasses inflammation of the
spinal cord from a variety of causes, but the imaging
appearance is usually nonspecific (63).
Imaging plays an ancillary role in the evaluation of
the patient with suspected GuillainBarr syndrome.
However, if MRI of the spine is performed, the nerve
FIGURE 3.34 roots often appear thickened and enhance after intra-
venous contrast administration (Figure 3.38). Such
Pathologically proven arachnoiditis and central intradural enhancement is not specific and can also be seen with
arachnoid cyst in a 61-year-old man with prior lumbar drop metastases or with infection. In GuillainBarr syn-
surgery. Axial T2-weighted MR image at the L5-S1 level shows drome, enhancement of both ventral and dorsal nerve
a central arachnoid cyst, with nerve roots clumped together
roots or only ventral nerve roots can be seen; the latter is
and displaced lateral to the cyst. Old left hemilaminectomy
more specific (64,65).
defect noted.
The spinal canal and cord can also be compromised
by extradural inflammatory processes such as rheuma-
toid arthritis (RA). A variety of conditions can affect the
spinal cord, especially in the cervical spine. Erosions can
lead to subluxation. Pannus in the region of the synovial
space at the transverse ligament can lead to weakening or
destruction of the ligament, with subsequent instability
at C12. The softening of bone and ligament destruction
can result in basilar invagination, threatening the brain-
stem itself. Plain films and CT can demonstrate the ero-
sive changes and subluxation, and MRI can show the
pannus and the relationship of pannus and bone to the
spinal cord (Figure 3.39).
Patients with longstanding ankylosing spondylitis
may develop cauda equina syndrome. Their lumbar MRI
may demonstrate a classic appearance of intrathecal
arachnoiditis and a dilated thecal sac with erosion of the
posterior elements (66), obviating the need for myelog-
raphy (Figure 3.40).

FIGURE 3.35
SPINAL INFECTIONS
Sixty-four-year-old man with left S1 radiculopathy after spinal
surgery. Axial image from postmyelogram CT shows the left
pedicle screw incorrectly positioned, within the left S1 neural The incidence of central nervous system (CNS) infections,
canal, obliterating the left S1 nerve root and correlating with including spinal involvement, has increased in recent
the patients symptoms. The right pedicle screw is malposi- decades, largely because of AIDS (67). The most common
tioned medial to the right S1 neural canal. The black arrow site of spinal infection is the vertebral bodies and discs, which
points to the right S1 nerve root in its neural canal. can then exert mass effect on the thecal sac, spinal cord, and
58 INTRODUCTION

FIGURE 3.37

Transverse myelitis. Sagittal T2-weighted MR image of a


patient who developed urinary retention and spinal-cord level
3 weeks after a respiratory illness, shows a region of high sig-
nal-intensity in the cervical spinal cord. Abnormal signal con-
tinued into the thoracic spine.

nerve roots. Direct involvement of the epidural space is also


common. Spinal infections can also involve the intradural
space (Figure 3.41), being either extramedullary, involving
the meninges, as in arachnoiditis, or intramedullary, involv-
ing the spinal cord and cauda equina directly (as in parenchy-
mal myelitis, granuloma, or abscess).
FIGURE 3.36 Diagnostic imaging is essential in the diagnosis and
treatment of these patients. Conventional radiographs
Multiple sclerosis. This young adult had lower and then upper
extremity numbness. Sagittal T2-weighted image of the cer-
may be useful in initial evaluation of spinal infection
vical spine cord (A) shows two separate areas of high signal involving the vertebrae and discs, and can classically
intensity within the spinal cord (arrows). Sagittal T2-weighted demonstrate the loss of height of the disc, erosion of the
image of the brain (B) shows a plaque in the inferior margin adjacent endplates, and loss of vertebral body height. The
of the corpus callosum (arrow). most common bacterial organism is Staphylococcus; oth-
IMAGING OF THE SPINAL CORD 59

FIGURE 3.40

Cauda equina syndrome in 59-year-old man with longstand-


ing ankylosing spondylitis. Axial T2-weighted image through
the upper lumbar spine shows a patulous thecal sac with scal-
FIGURE 3.38 loped, eroded posterior elements. The inflamed, scarred nerve
roots adhere to the walls of the thecal sac.
GuillainBarr. Axial T1-weighted image through the lumbar
spine after intravenous gadolinium-DTPA administration
shows intense enhancement of the lumbar nerve roots. ers are Enterobacter, Salmonella, Pseudomonas, and Ser-
ratia species (68). However, although associated soft-tis-
sue masses may be demonstrated on plain films, only the
bony cortical structures are well demonstrated.
CT demonstrates both the bony anatomy and soft
tissue anatomy on cross-sectional images. However, the
spinal cord is not delineated unless intrathecal contrast
is introduced (myelography)an invasive procedure.
Computer-generated sagittal (and/or coronal) recon-
structions are necessary to appreciate abnormalities of
alignment and the 3-D anatomy of the infected spine.
MRI is the modality of choice in imaging spinal
infections, because it noninvasively and clearly demon-
strates soft tissue anatomy and pathology, including
spinal cord or nerve root involvement, in addition to the
bony anatomy demonstrated on plain X-rays. MRI can
directly image in the sagittal (or any other) plane, in addi-
tional to the axial plane.
Pyogenic infections generally involve the interver-
tebral disc and the adjacent portions of the vertebral bod-
ies, with loss of demarcation of the endplate cortex. The
disc and vertebrae demonstrate decreased signal on T1-
weighted images and increased signal on T2-weighted
images (69) (Figure 3.42). This study by Modic et al. (69)
reported that MRI has a sensitivity of 96 percent, speci-
FIGURE 3.39 ficity of 93 percent, and accuracy of 94 percent in the
Rheumatoid arthritis (RA) and basilar invagination. Sagittal
evaluation of osteomyelitis, equaling the results of com-
T2-weighted MR image of a woman with rheumatoid arthri- bined bone and gallium scanning, but with the added ben-
tis shows erosion of the dens and basilar invagination, with efits of superb anatomic resolution, as well as visualiza-
the dens nearly to the level of the pons. Subluxations at C23 tion of the soft tissues including the spinal cord, thecal
and C45 typical of RA, are noted. sac, and paraspinal tissues.
60 INTRODUCTION

A B

FIGURE 3.41

Fifty-seven-year-old woman with pyogenic spinal infection


and left psoas abscess, with intradural extension. A. Sagittal
postcontrast T1-weighted image shows diffuse thickening and
abnormal enhancement of the cauda equina and enhancing
intradural exudate around the distal spinal cord (small white
arrows). The anterior portion of the L4 vertebra is infected. B.
Axial postcontrast T1-weighted image again shows diffuse
thickening and abnormal enhancement of the cauda equina
(black arrows). White arrow points to pus in left psoas abscess.

FIGURE 3.42

Pyogenic spinal infection in an adult male with L5S1 diskitis, osteomyelitis, and epidural abscess. Left. Sagittal T2-weighted
image shows T2-bright pus within the L5S1 disc, extending posteriorly. T2-bright edema or infection is noted involving the
adjacent endplates. Middle. T1-weighted image better shows the associated epidural abscess compressing the distal thecal
sac. Right. Postcontrast T1-weighted image again shows enhancing phlegmonous tissue compressing the anterior aspect of the
thecal sac. T1-dark pus is noted centrally in the epidural abscess (arrows).
IMAGING OF THE SPINAL CORD 61

Epidural abscesses are often found in association Brucellosis presents with bony lytic lesions of the
with bony osteomyelitis and discitis (Figure 3.42), but vertebral body, usually in the lower lumbar spine (72,73).
also may be an isolated finding (Figure 3.43). Again, MRI Tuberculosis (74) differs from pyogenic bacterial
is the imaging modality of choice, especially with the use infections in that the intervertebral disc is often relatively
of intravenous gadolinium-DTPA. Staphylococcus aureus spared in early disease (possibly because mycobacteria
is the most common causative organism (in about 60 per- lack proteolytic enzymes). It appears without abnormal
cent of cases). Another 13 percent of cases are caused by T2-bright signal, more involvement of posterior aspects
other gram-positive cocci, and 15 percent are caused by of the vertebrae, involvement of more than two vertebral
gram-negative organisms (67,70,71). Most epidural bodies, and larger associated paraspinal masses. CT may
abscesses enhance homogeneously with IV Gd-DTPA, show the small soft-tissue calcifications suggestive of
suggesting that they are largely phlegmonous, but nonen- tuberculosis, which are not reliably shown on MRI (75).
hancing frank pus may also be recognized as a central col- Chronic tuberculosis infection may result in a classic
lection of fluidlike T1-dark, T2-bright signal surrounded kyphotic deformity, known as Potts disease, usually in
by an enhancing soft-tissue rim (Figures 3.42 and 3.43). the mid-thoracic region.
Patients with AIDS may often present with
polyradiculopathy caused by viruses, most commonly
cytomegalovirus (76). Gadolinium-enhanced MRI is by
far the best modality to visualize the enhancing nerve
roots of the cauda equina, which may appear normal on
standard T1- and T2-weighted images; occasionally
enhancement extends diffusely throughout the spinal sub-
arachnoid space (Figure 3.44). Infection of the spinal cord
by the HIV virus has been found to cause vacuolar
myelopathy in AIDS patients. Spinal MRI may be nor-
mal, but usually presents with spinal cord atrophy or
occasionally with T2-bright signal (77). Enhancement
with IV contrast is not generally seen in AIDS-associated
myelopathy (77).

VASCULAR LESIONS AND ISCHEMIA

Suspected vascular disease of the spine can be particularly


challenging to verify with imaging. The spinal cord itself
is best visualized with MRI, but angiography can have an
important role in some cases.
Spinal cord infarction appears on MRI as a region
of increased T2 signal-intensity (Figure 3.45). This
appearance is nonspecific, especially because the vascu-
lar territories are usually not as obvious in the spinal cord
as in the brain. Distinction of spinal cord infarction from
other entities, such as infectious or demyelinating
processes, is therefore often more dependent on clinical
information than on differences in imaging appearance.
Vascular malformations of the spine have been
divided into four types: intramedullary glomus-type arte-
riovenous malformation (AVM), juvenile AVM, dural
FIGURE 3.43 arteriovenous fistula, and perimedullary arteriovenous
Twenty-one-year-old woman with autoimmune hepatitis,
fistula (78). Patient age and the clinical presentations of
chronically on steroids, with diffuse posterior epidural cryp- these tend to differ. Symptoms can result from hemor-
tococcal abscess throughout her spine. Sequential postcon- rhage or from ischemia caused by venous hypertension or
trast sagittal T1-weighted images of the thoracolumbar spine steal.
show an abscess with thin enhancing rind, located posterior Hemorrhage within the spinal cord has an appear-
to the thoracic spinal cord and cauda equina and compress- ance similar to blood elsewhere in the CNS and depends
ing them. Note that the vertebrae and discs are normal. on the age of the hemorrhage. The details of MRI appear-
62 INTRODUCTION

FIGURE 3.44

Thirty-one-year-old man with AIDS, who presented with bilateral leg pain and weakness and loss of bowel and bladder control.
Left. Sagittal T1-weighted MR images of the cervical spine are normal, as are sagittal T2-weighted images, Right. (Patient is
angulated on the T2-weighted images; the lower spinal cord is out of view so that CSF, rather than cord, is imaged; note that
spinous processes are also out of field.) Middle. However, T1-weighted images after IV administration of gadolinium-DTPA
show diffuse marked enhancement of inflammatory tissue throughout the spinal subarachnoid space (white and black arrows).
Herpes simplex II virus was cultured from his CSF, and cytomegalovirus was cultured from his blood.

ance of hemorrhage are not reviewed here. It is important tral nidus in the case of AVMs, or the location of the direct
to consider the effect of MRI technique on the appear- fistulous connection in fistulas (Figure 3.47B); it also
ance of hemorrhage. Fast spin-echo techniques, which are shows the extent and direction of venous drainage.
widely used for spine imaging because of the advantages Depending on the nature and location of the malforma-
in acquisition time and artifact reduction, also reduce the tion, endovascular therapy, such as embolization, can be
susceptibility changes of blood. This can make blood less used either alone or in combination with surgery to treat
conspicuous with fast spin-echo techniques. Gradient- the condition. In some cases of suspected fistula, an
echo techniques, on the other hand, exaggerate magnetic exhaustive search of spinal arteries may be necessary,
susceptibility differences between blood and surrounding from the lowest lumbosacral branches up through the ver-
tissues. Although this can increase some artifacts, it has tebral, cervical, and external carotid arteries.
the potential advantage of making hemorrhage more con- Cavernous malformations can occur in the spinal
spicuous. cord as well in the brain, and the imaging characteristics
The differential diagnosis of hemorrhage within the are similar. Typically, blood products of varying age are
spinal cord includes trauma (which would usually be present with a surrounding rim of dark T2-signal inten-
obvious by history), vascular malformation, and neo- sity from hemosiderin. Larger lesions often have a retic-
plasm. The presence of multiple areas of flow void on ulated appearance because they contain pockets of methe-
MRI provides additional evidence of a high-flow vascu- moglobin, but small lesions may be seen only as
lar malformation. These may be present within the spinal hemosiderin scars. Acute hemorrhage within a cavernous
cord in the case of intramedullary AVMs (Figure 3.46), malformation has a less-specific appearance unless the
or on the surface of the spinal cord or more peripherally surrounding older blood products are visible.
in the case of AV fistulas (Figure 3.47). Tortuous drain-
ing veins are usually more conspicuous than the feeding
arteries. Superficial vessels, especially enlarged draining SPINAL TUMORS
veins, can be shown on myelography.
Angiography plays an important role in the diag- An estimated one in four or five central nervous system
nosis of spinal vascular malformations. It defines the loca- tumors are located in the spine (79,80,81). A study by
tion and number of feeding arteries, the size of the cen- Kurland (82) estimated the incidence of primary spine
IMAGING OF THE SPINAL CORD 63

FIGURE 3.46
FIGURE 3.45
Intramedullary spinal arteriovenous malformation (AVM) in
Spinal cord infarct in a 68-year-old man, sustained during sur- a 29-year-old man presenting with hemiparesis and difficulty
gical repair of abdominal aortic aneurysm. Sagittal T2-weighted breathing. Sagittal T2-weighted MRI image shows diffuse
image shows T2-bright edema (white arrows) within the distal swelling and edema throughout the cervical spinal cord. Ser-
thoracic spinal cord and conus, with small amount of dark piginous linear flow voids of the intramedullary AVM and
intramedullary hemorrhage (black arrowheads) distally. its draining vein extend from the C4 to C7 levels (small
white arrows). The AVM was successfully endovascularly
embolized via a right vertebral artery approach.

tumors to be 2.5 per 100,000 people per year. MRI is the


best single modality for imaging spine tumors (83). Its
unsurpassed soft tissue differentiation (including the abil- the disc spaces only, which could result in missing por-
ity to differentiate between CSF and neural tissue with- tions of the tumor. Slice thickness should be preferably
out the use of intrathecal contrast), absence of beam- 3 mm on the sagittal images, and 4 mm axially, with a
hardening artifact, and ability to image in multiple planes 1 mm gap to minimize partial-volume errors.
make it clearly superior to CT, myelography, plain films, T1-weighted gadolinium-enhanced images (in sagittal
and ultrasonography in evaluating epidural and and axial planes) are recommended to evaluate intradural
intradural disease. For bony disease and primary bone tumors (84). Generally, intradural extramedullary tumors
tumors, plain X-rays and CT are still essential. enhance significantly; enhancement of intramedullary
tumors is more variable. However, in imaging vertebral
metastases, gadolinium enhancement is not only not helpful,
TECHNIQUE but actually detrimental, because T1-dark marrow metas-
tases enhance and become isointense to normal T1-bright
The screening MRI technique we use for the spine is sagit- marrow.
tal TR 500-600, TE 11; and FSE sagittal TR 3000-4000, To minimize CSF pulsation and other motion arti-
TE 102 to obtain a quick myelogram in about 4 min- facts, flow compensation, cardiac gating, respiratory gat-
utes. Axial FSE T2-weighted images are obtained in a ing, and phase-frequency direction swapping are useful.
stacked fashion, rather than using oblique axials through However, in many systems, flow compensation is not yet
64 INTRODUCTION

A B

FIGURE 3.47

Spinal-dural arteriovenous fistula in a 42-year-old man presenting with paraplegia. A. Sagittal T2-weighted MRI image shows
swelling and edema (white arrows) within the mid-lower thoracic spinal cord and multiple serpiginous flow-voids of an abnor-
mal draining vein immediately dorsal to the spinal cord. B. Spinal angiogram with injection at the T7 level shows an abnormal
fistulous connection (black arrowhead) between the radicular artery (white arrow) and the abnormal tortuous, dilated draining
vein coursing superiorly. The patients symptoms resolved within 2 minutes of endovascular embolization with glue.

available with fast spin-echo, and motion artifacts can between soft tissue or tumor and CSF is poorer than on
be a problem for those inexperienced in reading FSE true-T2 or FSE-T2 images. GRE images are only useful
images. for detecting small amounts of hemosiderin or calcium,
The use of phased-array coils, if available, is which could be missed on FSE images and may be missed
extremely valuable in obtaining better signal-to-noise and on SE T2-weighted images.
obviating the need to move the coil or the patient when Spine tumors are generally classified according to
covering a large portion of the spine (as in screening for anatomic location as extradural; intradural, extramedullary;
epidural cord compression). or intramedullary.
In addition to T1-weighted images, inversion-recov-
ery (IR) (or preferably, FSE IR) sequences also demonstrate
Extradural Tumors
vertebral marrow metastases by nulling the neighboring
marrow fat (28, 29). Inversion-recovery images, like T2- These account for about a third of all spine neoplasms
weighted images, clearly demonstrate intramedullary and generally involve the vertebrae (79). The majority are
edema or tumors as bright signal. metastases to bone. Metastases to the epidural space are
Coronal imaging may be useful for example in imag- less common, and even less common are tumors (benign
ing cervicothoracic neurofibromas. or malignant) arising from the osseous or notochordal
Gradient-echo (GRE) images are generally not use- structures of the spine. A small fraction of neurofibromas
ful in the imaging of spinal tumors. The differentiation and meningiomas are completely extradural.
IMAGING OF THE SPINAL CORD 65

Primary bone lesions may have a more characteris-


A
tic appearance on plain X-rays than on MRI, because the
cortical pattern and calcification are not well-appreciated
on MR. However, MRI detects changes in marrow, rather
than the bony matrix, and so is the most sensitive detec-
tor of vertebral body tumors (85).

Extradural Malignancy
Metastases to bone are by far the most common malig-
nant tumors involving the spine encountered in every-
day practice. Often the site of disease cannot be accu-
rately localized clinically. Hence, it is important to be able
to quickly and efficiently screen the entire spine in these
patients. It is impractical and unnecessary to obtain sagit-
tal and axial T1- and T2-weighted images, as well as pre-
and postgadolinium images through all levels of the
spine. These patients often suffer excruciating pain and
are unable to lie motionless for even moderate lengths
of time.
Instead, the screening examination should consist of
first, a single T1-weighted sequence using a large field of
view (4850 cm) with a large matrix (512  512 or 512
 384) in the sagittal plane. This will cover essentially the
entire spine in a single acquisition of about 6 minutes or
less (Figure 3.48). A fast spin-echo T2-weighted (FSE-T2)
sagittal screening sequence can give a myelogram-effect
scan in another few minutes, pointing out regions of CSF
effacement by tumor. Then, 4-mm axial images (either
T1- or fast spin-echo T2) may be obtained only at the lev-
els of cord compression, to better delineate the degree of B
compression. Gadolinium is generally not needed to diag-
nose and evaluate cord compression from bony vertebral
metastases. Hence, a complete examination can be
obtained in about 20 minutes, which can be tolerated by
almost all patients.
Good analgesia, such as morphine, is important to
aid patient comfort and prevent image degradation by
motion. Anxiolytics such as diazepam (Valium) or mida-
zolam are less valuable; these patients move around in
the scanner more from pain than from claustrophobia
or anxiety.
Phased-array coils, if available, give superb signal-
to-noise and enable complete spinal coverage without
moving the patient or the coil. However, lacking a phased-
array coil, the body coil should be used to screen the entire FIGURE 3.48
spine using the single large FOV T1-weighted sagittal
sequence. Use of a conventional license-plate coil to ini- Metastatic bladder rhabdomyosarcoma in a 6-year-old girl.
A. Sagittal T1-weighted large field-of-view image of the entire
tially separately screen the cervical spine, the thoracic
spine obtained in only 5 minutes shows the regions of verte-
spine, and the lumbar spine, using both T1- and T2- bral tumor involvement (large arrows) and cord compression
weighted sequences in the axial and sagittal planes, fol- (arrowhead). B. Axial T1-image shows the large amount of
lowed by postgadolinium sagittal and axial images of the vertebral and paraspinal tumor, which anteriorly displaces the
cervical, thoracic, and lumbar regions will take hours, aorta and vena cava and extends medially through the neural
result in extreme patient discomfort, and reams of unnec- foramina into the spinal canal and compresses the cord (black
essary and motion-degraded images. arrow) from both sides (83).
66 INTRODUCTION

As mentioned, T1-weighted SE images are sensitive


to detecting these lesions, but their MRI appearance is not A
specific. They are dark on T1, bright on T2, and enhance
variably with contrast. Type I (fibrovascular) Modic degen-
erative changes and infection have similar signal charac-
teristics. An important distinguishing characteristic
between infection and tumor is that tumor generally spares
the disc space whereas infection (excepting tuberculosis)
characteristically involves it. An infected disc appears as
a very white T2-bright signal and shows erosion of the
adjacent endplates. Conversely, Modic degenerative
changes are associated with degenerated (i.e., T2-dark)
discs, whereas tumor should not affect the disc signal.
Although some authors have tried to find radi-
ographic signs distinguishing pathological from osteo-
porotic fractures, such as complete replacement of mar-
row by T1-dark signal, or posterior-convex vertebral
body border indicating tumor, it is often not possible to
make the distinction with certainty (86,87).

Multiple Myeloma
Plasma cell neoplasms commonly involve the spine, usu-
ally in the thoracic region and generally in patients
beyond middle age (88). The classic radiographic appear-
ance of small punched out lytic lesions may also be seen
as multiple small T1-dark foci in the vertebral body mar-
row on MRI. MRI is an efficient way to screen the entire

FIGURE 3.50
FIGURE 3.49
B-cell lymphoma in a 23-year-old man. A. Sagittal T1 MR-
Multiple myeloma in a 61-year-old woman. Left. Sagittal T1- image shows patchy increased and decreased signal within
weighted image shows diffuse abnormal low intensity in all the the vertebral marrow, indicating tumor involvement. A large
marrow because of multiple myeloma infiltration. Right. Sagit- posterior epidural tumor mass compresses the cord from
tal fast spin-echo T2-weighted image gives a myelogram effect behind. B. Axial T1-image at this level shows vertebral mar-
and shows good conspicuity between the posteriorly bulging row involvement, a large paravertebral tumor mass, and the
tumor-laden vertebrae and the CSF and neural structures (83). posterior epidural mass (arrow) compressing the cord (83).
IMAGING OF THE SPINAL CORD 67

spine for myeloma, and especially to evaluate for cord


compression (Figure 3.49).

Leukemia and Lymphoma


The spinal marrow is often involved by these tumors of
hematopoietic and lymphoid cells. Both may show vari-
able radiographic appearance on MRI, including diffuse
or patchy infiltration of marrow, sometimes causing cord
impingement by compression fracture or by focal tumor
deposits in bone. Extradural tumor may also present as
separate epidural foci (89) (Figure 3.50).

Hemangioma
These tumors are very common incidental findings on
MRI. They are found in 10 to 15 percent of patients at
autopsy (88), increasing in incidence with age. In our
experience, small bone hemangiomas are seen in almost
every older patient. The most common location is the tho-
racic spine, followed by the lumbar spine (89). Mottled
T1-bright signal caused by interspersed adipose tissue,
and a T2-bright signal of fluid and cells are characteris-
tic (Figure 3.51). They are usually round and small when
found incidentally, but may occupy the entire vertebral FIGURE 3.52
body, expanding it and causing neurologic symptoms.
The bony striations and spicules classically seen on plain Giant cell tumor, with vertebral collapse and posterior
films and CT may be seen on MRI. retropulsion into the spinal canal in a 28-year-old man, shown
on a sagittal T1-weighted MR image (83).

Other Primary Bone Tumors


(90). Their appearance on MRI is somewhat nonspecific,
Giant Cell Tumor as is their appearance on plain films (Figure 3.52).
Hemangiomas are the most common benign spinal bone
tumor; giant cell tumors are the second most common Aneurysmal Bone Cyst
These are expansile benign masses containing multiple
blood-filled cysts, well seen on MRI. Signal intensity is
somewhat variable depending on the state of the blood
contents. Only 20 percent of aneurysmal bone cysts
involve the spine (89).
Other bone tumors include eosinophilic granuloma
(histiocytosis X), osteoid osteoma, osteoblastoma, and
the chondral tumors such as osteochondromas and chon-
drosarcomas.

Intradural-Extramedullary Tumors

Nerve Sheath Tumors


These comprise schwannomas (Figure 3.53) and neuro-
FIGURE 3.51
fibromas (Figure 3.54) and occur most often in the tho-
Small hemangioma (arrows) in a 38-year-old woman. Left. T1- racic spine. Most are intradural-extramedullary, although
weighted sagittal image. Right. T2-weighted sagittal image (83). about 10 percent are both intradural and extradural;
68 INTRODUCTION

occasionally they are completely extradural (79). Schwan-


nomas are usually solitary unless the patient has neu-
rofibromatosis-2 (NF-2); these, along with meningiomas,
are the usual intradural-extramedullary spinal neoplasm
of NF-2 (Figure 3.55). (The typical intramedullary tumor
of NF-2 is the ependymoma [91].) Most cases are seen in
young to middle-aged adults (males slightly younger than
females); males and females are equally affected, unlike
meningiomas, which have a strong female predominance
(79). In a large series of intraspinal tumors cited in Slooff
et al. (92), schwannomas (29 percent) had a slightly
higher prevalence than meningiomas or gliomas.
Schwannomas and neurofibromas have a similar
radiographic appearance. They are fairly isointense on T1
and bright on T2, and enhance with contrast. Sometimes
schwannomas have a cystic component (Figure 3.53), FIGURE 3.54
unlike neurofibromas (93). On postgadolinium and T2-
Multiple cervical neurofibromas in NF-1 in a 15-year-old boy.
weighted images, neurofibromas may have a central, Consecutive postgadolinium coronal T1 MR images show
nonenhancing, T2-dark focus (94) (Figures 3.54 and multiple bilateral enhancing neurofibromas at nearly every
3.56). level. The cord is markedly compressed by the bilateral
tumors. Note the typical nonenhancing central core in these
neurofibromas (83).
Meningioma
These occur in middle-aged and older adults, at a female-
to-male ratio of greater than 4 to 1. Eighty percent are
located in the thoracic region (Figure 3.57). About 6 per-

FIGURE 3.53
FIGURE 3.55
Schwannoma in a 52-year-old man. Consecutive sagittal post-
gadolinium T1 images show an oval, well-circumscribed, Multiple cauda equina schwannomas in NF-2 in an 18-year-
intradural-extramedullary enhancing mass that contains old-woman. Sagittal postgadolinium T1-weighted MR image
darker cystic-appearing components and markedly com- shows multiple nodular enhancing masses adherent to the
presses the mid thoracic spinal cord (83). cauda (83).
IMAGING OF THE SPINAL CORD 69

based. Rarely, a meningioma may have an intramedullary


component.

Paraganglioma
Spinal paragangliomas have the same histology as their
more familiar counterparts elsewhere in the body, such as
the adrenal medulla and carotid body, and have similar
imaging characteristics, including prominent contrast
enhancement. They are found in adults and are generally
attached to the filum terminale or cauda equina (93) (Fig-
ure 3.58).
FIGURE 3.56

Multiple large sacral neurofibromas in NF-1, in an 8-year- Embryonal Tumors


old boy. Axial T2-weighted image shows multiple large bright Developmental tumors (e.g., epidermoids, lipomas, der-
neurofibromas involving all the sacral nerve roots within the moids, teratomas) have a variable appearance on MRI,
nerve root canals, and extending out along the sacral ala into
depending on the constituent components comprising the
the pelvis. Note the typical central core of darker signal in the
tumors (83).
tumor. Fat-saturation techniques in MRI are very help-
ful in making the diagnosis of fatty components (Figure

cent are intradural-extradural and an equivalent number


are completely extradural (79). These have similar sig-
nal characteristics to schwannomas, enhance brightly and
homogeneously (84), and characteristically are dural-

FIGURE 3.57

Meningioma in a 62-year-old woman, who presented with a sev- FIGURE 3.58


eral-month history of decreasing ability to walk. Postgadolinium
sagittal T1 MR image shows uniform enhancement of the well- Paraganglioma in a 47-year-old man. Sagittal postgadolinium
circumscribed intradural-extramedullary mass, which markedly T1 MR image shows a well-circumscribed enhancing mass
compresses the thoracic spinal cord at the T2 level. Note the adherent to the filum terminale at the L3 level. (Courtesy of
characteristic enhancing dural tail (arrow) (83). Dr. P. Burger) (83).
70 INTRODUCTION

3.59). The presence of fat is also definitively diagnosed Intramedullary Tumors


by CT (by fats very low attenuation of approximately
100 Hounsfield units). Glioma
In the spine, as in the brain, epidermoids may be dif-
These are the most common type of intramedullary
ficult to detect on MRI, because they may be isointense
tumor, particularly ependymomas (especially at the conus
to CSF on all pulse sequences (95) (Figure 3.60).
and filum terminale) in adults and astrocytomas in chil-
Abnormalities of spinal development, such as
dren. Sixty percent of primary cord tumors are ependy-
meningomyeloceles or tethered cord, are commonly
momas (93). These expand the cord and are slightly dark
accompanied by developmental tumors, especially lipo-
on T1 and bright on T2. Associated cysts or syrinx may
mas (Figure 3.61).
be seen either caudal or rostral to ependymomas, which
generally enhance with contrast. Hemorrhage is not
uncommonly associated with ependymomas, a fact
Metastases
stressed by Nemoto et al. in their study of cervical ependy-
Spinal subarachnoid metastases result from CSF seeding momas (96). They may also contain calcification. (Gra-
from intracranial primary tumors such as medulloblas- dient-echo sequence may be helpful in demonstrating
toma (Figure 3.62) or ependymoma, lung or breast can- hemosiderin, which may be missed on FSE imaging.)
cer (Figure 3.63), or lymphoma. These metastases are The myxopapillary subtype of ependymoma war-
often isointense or slightly hyperintense on T1, and some- rants special mention (93). These are well defined and
what hyperintense on T2, although this may be masked almost exclusively found at the conus or filum terminale
by T2-bright CSF. Gadolinium enhancement is extremely (Figure 3.64). They may become very large, filling and
helpful in increasing the conspicuity of these intradural- occasionally expanding the lower thecal sac with enhanc-
extramedullary lesions, which enhance brightly (84). ing soft tissue. As mentioned, the intramedullary ependy-

A B

FIGURE 3.59

Intradural extramedullary lipoma in a 20-year-old woman. A, Left. Sagittal T1 MR image shows a very large well-circumscribed
intradural-extramedullary T1-bright mass posterior to and compressing the upper thoracic cord. A, Right. Fat-saturated post-
gadolinium T1 image shows complete suppression of the T1-bright signal, proving the presence of fat rather than T1-bright blood.
A subtle thin rim of enhancement is noted around the tumor capsule. B. Axial T1 image shows the lipoma filling and expand-
ing the thecal sac and spinal canal, markedly flattening the cord (arrow) (83).
IMAGING OF THE SPINAL CORD 71

A A

FIGURE 3.60

Epidermoid in a 5-year-old boy. A. Consecutive sagittal T1-


images show a very subtle (almost undetectable) intradural
bipartite mass (small arrows) below the conus, at the levels
of L3 to L4. This lesion demonstrated no enhancement with
gadolinium. B, Left. Sagittal proton-density and Right, Sagit-
tal T2-weighted images again show the very subtle mass
which is almost isointense to CSF on all sequences, but is best
seen on the proton-density images. At surgery, this mass was
yellow-white in color. On being cut, it had the consistency and
flake-like texture of a bar of soap (83).

FIGURE 3.61
moma tumor is classically associated with neurofibro-
matosis-2. (91) (Figure 3.65). Tethered cord with conus lipomyelomeningocele in an 8-year-
Astrocytomas usually show a fusiform expansion of old girl. A. Sagittal T1 image shows a tethered cord with conus
(white arrow) at the L34 level, with posteriorly adherent T1-
the cord associated with T2-prolongation and (variable)
bright intradural lipoma. The posterior dura (small arrow) is
enhancement (89) (Figures 3.66 and 3.67). Cysts may be
well visualized, outlined by fat. Note the absence of normal
present, either intrinsic to tumor or at the edge of the posterior elements at this level and the wide spina bifida
tumor. defect (large arrow). B. Axial T1-image shows the C-shaped
Spinal cord oligodendrogliomas are rare, compris- T1-bright lipoma wrapped around the right side of the conus.
ing only 0.8 to 4.7 percent of intramedullary tumors of Note also the epidural lipoma posterior to the thecal sac and
the spinal cord and filum (97). They are found in the cer- the abnormal bony posterior elements (83).
72 INTRODUCTION

FIGURE 3.62

Intrathecal drop metastases from medulloblastoma in a 3-


year-old boy. Left. T2-weighted image shows expansion and FIGURE 3.63
edema of the cervical cord, extending up to the medulla. Note
that CSF occupies much of the midline posterior cranial fossa, Intrathecal metastases from lung cancer in a 25-year-old
because some cerebellum has been resected due to involve- woman. Consecutive sagittal postgadolinium T1-weighted
ment by medulloblastoma. Right. Postgadolinium sagittal T1 images show two small enhancing tumor nodules at the
image shows multiple enhancing subarachnoid metastases conus. There is also diffuse subtle enhancing tumor coating
coating the posterior aspect of the cord, with some larger the posterior spinal cord and cauda equina. Precontrast
deposits appearing to extend into the cord, thus accounting images showed no involvement of the vertebral body mar-
for the edema (83). row at any level (83).

A B

FIGURE 3.64

Conus myxopapillary ependymoma in a 43-year-old man. A, Left. Sagittal pre-contrast and Right, postgadolinium T1-weighted
images show a well-circumscribed enhancing mass at the conus. B. Consecutive sagittal T2-weighted images clearly demon-
strate the mass. The small T2-dark focus (arrow) suggests the presence of hemosiderin (blood products), a useful clue favoring
the diagnosis of ependymoma (83).
IMAGING OF THE SPINAL CORD 73

FIGURE 3.65

Recurrent cervical ependymoma in neurofibromatosis-2, in


a 22-year-old woman. Consecutive postgadolinium sagittal FIGURE 3.67
images show an extensive enhancing mass expanding the cer-
Astrocytoma in a 4-year-old boy. Sagittal T1-image shows
vical cord. Patient has had prior tumor resection, evidenced
marked fusiform expansion of the mid/lower thoracic cord (83).
by postsurgical changes posteriorly (83).

vicothoracic spine, usually in patients in their fourth


decade of life. One of the few published examples (97)
has an appearance similar to our surgically proven case
(Figure 3.68): an enhancing intramedullary expansile
mass in the cervicothoracic cord, with adjacent cystic
intramedullary component. Spinal oligodendrogliomas
are often associated with meningeal or intracranial oligo-
dendrogliomatosis (97,98).

Hemangioblastoma
These tumors may occur sporadically, but are often mul-
tiple and associated with the cerebellar hemangioblas-
tomas of von HippelLindau syndrome. They may exhibit
the typical cyst with associated mural nodule, which
enhances brightly with gadolinium (Figure 3.69). There
may be associated edema and, as in the brain, they may
have associated prominent vascularity (93).

FIGURE 3.66
Embryonal Tumor
Astrocytoma in a 4-year-old girl. Left. Sagittal postgadolin-
ium T1 MR image shows fusiform expansion of the upper cer- These were previously discussed in the section on
vical cord, with mild partial enhancement, and extensive T1- intradural-extramedullary tumors, but may also occur in
dark edema extending up to the medulla and down to C6. an intramedullary location. As mentioned, they may be
Right. Sagittal T2 image again shows the fusiform cord associated with spinal dysraphism, especially lipomas.
expansion. The T2-bright edema is well demonstrated (83). Dermoids and epidermoids have variable signal intensity,
74 INTRODUCTION

FIGURE 3.68 FIGURE 3.69

Oligodendroglioma. 64-year-old man presented with left leg Hemangioblastoma in von HippelLindau syndrome in a 28-
atrophy and weakness. Postcontrast sagittal T1-weighted MR year-old woman. Sagittal postgadolinium T1 image shows a
image shows an enhancing intramedullary mass (arrow- small enhancing nodule in the posterior upper cervical cord,
heads), with some cystic components. (Because of patients with an associated cyst that expands the cord slightly. Patient
scoliosis, normal neural foramina are noted between the has had cerebellar hemangiomas resected previously (83).
regions of tumor.)

5. Czervionke LF, Daniels DL, Ho PS, Yu S, Pech P, Strandt J, Williams


AL, Haughton VM. Cervical neural foramina: Correlative anatomic
depending on their composition. Cystic teratomas may be and MR imaging study. Radiology 1988; 169:753759.
found inside the cord substance (Figure 3.70). 6. Hedberg MC, Drayer BP, Flom RA, Hodak JA, Bird CR. Gradi-
ent echo (GRASS) MR imaging in cervical radiculopathy. AJR
1988; 150:683689.
Metastases 7. VanDyke C, Ross JS, Tkach J, Masaryk TJ, Modic MT. Gradi-
ent-echo MR imaging of the cervical spine: Evaluation of
Rarely, these present as intramedullary lesions with a pri- extradural disease. AJR 1989; 153:393398.
8. Enzmann DR, Rubin JB. Cervical spine: MR imaging with a par-
mary site in the brain or outside the CNS. Signal inten- tial flip angle, gradient-refocused pulse sequence: Part II. Spinal
sity is low on T1 and bright on T2; these usually enhance cord disease. Radiology 1988; 166:473478.
with gadolinium (Figure 3.71). 9. Tsuruda JS, Remley K. Effects of magnetic susceptibility artifacts
and motion in evaluating the cervical neural foramina on 3DFT
gradient-echo MR imaging. AJNR 1991; 12:237241.
References 10. Tsuruda JS, Norman D, Dillon W, Newton TH, Mills DG. Three-
dimensional gradient-recalled MR imaging as a screening tool for
1. Lee RR. Recent advances in spinal MRI. In: Lee RR (ed.), Spinal the diagnosis of cervical radiculopathy. AJNR 1989; 10:12631271.
Imaging (Spine: State of the Art Reviews, vol 9). Philadephia: Han- 11. Yousem DM, Atlas SW, Goldberg HI, Grossman RI. Degenerative
ley & Belfus, 1995, 4560. narrowing of the cervical spine neural foramina: Evaluation with
2. Kneeland JB, Hyde JS. High-resolution MR imaging with local high-resolution 3DFT gradient-echo MR imaging. AJNR 1991;
coils. Radiology 1989; 171:17. 12:229236.
3. Kulkarni MV, Patton JA, Price RR. Technical considerations for 12. Melki PS, Mulkern RV, Panych LP, Jolesz FA. Comparing the
the use of surface coils in MRI. AJR 1986; 147:373378. FAISE method with conventional dual-echo sequences. J Magn
4. Roemer PB, Edelstein WA, Hayes CE, Souza SP, Mueller OM. The Reson Imaging 1991:1:319326.
NMR phased array. Magn Reson Med 1990; 16:192223. 13. Mulkern RV, Wong STS, Winalski C, Jolesz FA. Contrast manip-
IMAGING OF THE SPINAL CORD 75

FIGURE 3.71

Metastatic prostate carcinoma invading sacral nerve roots in a


70-year-old man. Oblique-coronal postgadolinium T1-weighted
FIGURE 3.70 MR image shows diffuse enlargement and subtle enhancement
of the right-sided sacral nerve roots (arrows). At surgery, dif-
Recurrent intramedullary cystic teratoma in a 36-year-old fuse infiltration of the roots by prostate cancer was found. No
woman. Coronal T1-weighted MR image shows cystic expan- involvement of the vertebral marrow was present (83).
sion of the cord by proteinaceous fluid. There was essentially
no enhancement after IV contrast. At surgery this tumor con-
tained keratin, hair, and mucus (83).
fluid-attenuated inversion recovery (FLAIR) sequences. AJNR
1992; 13:15551564.
24. Hittmair K, Mallek R, Prayer D, et al. Spinal cord lesions in
ulation and artifact assessment of 2D and 3D RARE sequences. patients with multiple sclerosis: Comparison of MR pulse
Magn Reson Imaging 1990; 8:557566. sequences. AJNR 1996; 17:15551565.
14. Hennig J, Nauerth A, Friedburg H. RARE imaging: A fast imag- 25. Sze G, Kawamura Y, Negishi C, Constable RT, Merriam M, Oshio
ing method for clinical MR. Magn Reson Med 1986; K, Jolesz F. Fast spin-echo MR imaging of the cervical spine: Influ-
3:823833. ence of echo train length and echo spacing on image contrast and
15. Jones KM, Mulkern RV, Schwartz RB, Oshio K, Barnes PD, Jolesz quality. AJNR 14:12031213, 1993.
FA. Fast spin-echo MR imaging of the brain and spine: Current 26. Georgy BA, Hesselink JR. Evaluation of fat suppression in con-
concepts. AJR 1992; 158:13131320. trast-enhanced MR of neoplastic and inflammatory spine disease.
16. Mulkern RV, Wong STS, Winalski C, Jolesz FA. Contrast manip- AJNR 1994; 15:409417.
ulation and artifact assessment of 2D and 3D RARE sequences. 27. Tien RD, Olson EM, Zee CS. Diseases of the lumbar spine: Find-
Magn Reson Imaging 1990; 8:557566. ings on fat-suppression MR imaging. AJR 1992; 159:9599.
17. Sze G, Merriam M, Oshio K, Jolesz FA. Fast spin-echo imaging 28. Dwyer AJ, Frank JA, Sank VJ, Reinig JW, Hickey AM, Doppman
in the evaluation of intradural disease of the spine. AJNR 1992; JL. Short TI inversion-recovery sequence: Analysis and initial
13:13831392. experience in cancer imaging. Radiology 1988; 168:837841.
18. Georgy BA, Hesselink JR. MR imaging of the spine: Recent 29. Jones KM, Schwartz RB, Mantello MT, Ahn SS, Khorasani R,
advances in pulse sequences and special techniques. AJR 1994; Mukherji S, Oshio K, Mulkern RV. Fast spin-echo MR in the
162:923934. detection of vertebral metastases: Comparison of three sequences.
19. Rubin JB, Enzmann DR. Optimizing conventional MR imaging AJNR 1994; 15:401407.
of the spine. Radiology 1987; 163:777783. 30. Henkelman RM, Watts J, Kucharczyk W. High signal intensity in
20. Rubin JB, Enzmann DR, Wright A. CSF-gated MR imaging of MR images of calcified brain tissue. Radiology 1991;
the spine: Theory and clinical implementation. Radiology 1987; 179:199206.
163:784792. 31. Enzmann DR, Pelc NJ. Normal flow patterns of intracranial and
21. Ross JS, Ruggieri P, Tkach J, Obuchowski N, Dillinger J, Masaryk spinal cerebrospinal fluid defined with phase-contrast cine MR
TJ, Modic MT. Lumbar degenerative disk disease: Prospective imaging. Radiology 1991; 178:467474.
comparison of conventional T2-weighted spin-echo imaging and 32. Levy LM, Di Chiro G. MR phase imaging and CSF flow in the
T2-weighted rapid acquisition relaxation-enhanced imaging. head and spine. Neuroradiology 1990; 32:399406.
AJNR 1993; 14:12151223. 33. Nitz WR, Bradley WG, Watanabe AS, Lee RR, Burgoyne B,
22. Oshio K, Jolesz FA, Melki PS, Mulkern RV. T2 weighted thin slice OSullivan RM, Herbst MD. Flow dynamics of cerebrospinal
imaging with multi-slab 3D RARE. J Magn Reson Imaging 1991; fluid: Assessment with phase-contrast velocity MR imaging per-
1:695700. formed with retrospective cardiac gating. Radiology 1992;
23. De Coene B, Hajnal JV, Gatehouse P, et al. MR of the brain using 183:395405.
76 INTRODUCTION

34. Quencer RM, Donovan Post MJ, Hinks RS. Cine MR in the eval- Malkasian D, Ross JS. MRI of the lumbar spine in people with-
uation of normal and abnormal CSF flow: intracranial and out back pain. NEJM 1994; 331:6973.
intraspinal studies. Neuroradiology 1990; 32:371391. 60. Gundry CR, Heithoff KB, Pollei SR. Imaging of the postopera-
35. Rupp R, Ebraheim NA, Savolaine ER, Jackson WT. Magnetic res- tive lumbar spine. In: Lee RR (ed.), Spinal Imaging (Spine: State
onance imaging evaluation of the spine with metal implants. Spine of the Art Reviews, vol 9). Philadephia: Hanley & Belfus, 1995.
1993; 18:379385. 61. Bundschuh CV, Stein L, Slusser JH, et al. Distinguishing between
36. Barkovich AJ. Pediatric Neuroimaging (3rd ed.). Philadelphia: scar and recurrent herniated disk in postoperative patients: Value
Lippincott Williams & Wilkins, 2000. of contrast-enhanced CT and MR imaging. AJNR 1990;
37. Wilson DA, Prince JR. MR imaging determination of the loca- 11:949958.
tion of the normal conus medullaris throughout childhood. Am J 62. Larsson E-M, Holtas S, Nilsson O. GD-DTPA-enhancement of
Roentgenol 1989; 152:10291032. suspected spinal multiple sclerosis. Am J Neuroradiol 1989;
38. Daffner RH, Deeb ZL, Rothfus WE. Fingerprints of vertebral 10:10711076.
trauma: A unifying concept based on mechanism. Skeletal Radiol 63. Barakos JA, Mark AS, Dillon DW, Norman D. MR imaging of
1986; 15:815525. acute transverse myelitis and AIDS myelopathy. J Compt Assist
39. Acheson MD, Livingston RR, Richardson ML, Stimac GK. High- Tomogr 1990; 14:4550.
resolution CT in the evaluation of cervical spine fractures: Com- 64. Bryn WM, Park WK, Park BH, Ahn SH, Hwang MS, Chang JC.
parison with plain film examinations. Am J Roentgenol 187; GuillainBarr syndrome: MR imaging findings of the spine in
148:11791185. eight patients. Radiology 1998; 208:137141.
40. Woodring JH, Lee C. The role and limitations of computed tomo- 65. Gorson KC, Ropper AH, Muriello MA, Blair R. Prospective eval-
graphic scanning in the evaluation of cervical trauma. J Trauma uation of MRI lumbosacral nerve root enhancement in acute Guil-
1992; 33:698708. lainBarr syndrome. Neurology 1996; 47:813817.
41. Lee RR. MR imaging and cervical spine injury. Radiology 1996; 66. Kerslake RW, Mitchell LA, Worthington BS. Case report: CT and
201:617618. MRI of the cauda equina syndrome in ankylosing spondylitis. Clin
42. Hart BL, Butman JA, Benzel EC. Spine trauma. In: Orrison WW Radiol 1992; 45:134136.
(ed.), Philadelphia: W. B. Saunders, 2000, 14001439. 67. Reddy S, Leite CC, Jinkins JR. Imaging of infectious disease of the
43. Harris JH Jr, Mirvis SE. The Radiology of Acute Cervical Spine spine. In: Lee RR (ed.), Spinal Imaging (Spine: State of the Art
Trauma. Baltimore: Williams & Wilkins, 1996. Reviews, vol 9). Philadephia: Hanley & Belfus, 1995.
44. Daffner RH. Imaging of Vertebral Trauma. Philadelphia: Lippin- 68. Sklar EM, Post MJD, Lebwohl NH. Imaging of infection of the
cott-Raven, 1996. lumbosacral spine. Neuroimag Clin North Am 1993; 3:577590.
45. Halliday AL, Henderson BR, Hart BL, Benzel EC. The manage- 69. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis:
ment of unilateral lateral mass/facet fractures of the subaxial cer- Assessment using MR. Radiology 1985; 157:157166.
vical spine. Spine 1997; 22:26142621. 70. Hlavin ML, Kaminski HJ, Ross JS, Ganz E. Spinal epidural
46. Clayman DA, Sykes CH, Vines FS. Occipital condyle fractures: abscess: A ten-year perspective. Neurosurgery 1990; 27:177184.
Clinical presentation and radiologic adetection. Am J Neurora- 71. Angtuaco EJC, McConnell JR, Chadduck WM, et al. MR imag-
diology 1994; 15:13091315. ing of spinal epidural sepsis. AJNR 1987; 8:879883.
47. Bettini N, Malagutti MC, Sintinti M, et al. Fractures of the occip- 72. Sharif HS, Osarugue AA, Clark DC, et al. Brucellar and tubercu-
ital condyles: Report of four cases and review of the literature. lous spondylitis: Comparative imaging features. Radiology 1989;
Skeletal Radiol 1993; 22:187190. 171:419425.
48. Bucholz RW, Burkhead WZ. The pathological anatomy of fatal 73. Sharif HS, Clark DC, Aabed M, et al. Granulomatous spinal infec-
atlanto-occipital dislocations. J Bone Joint Surg Am 1979; tions: MR imaging. Radiology 1990; 177:101107.
61:248250. 74. Smith AS, Weinstein MA, Mizushima A, et al. MR imaging chara-
49. Harris JH Jr, Carson GC, Wagner LK, et al. Radiologic diagnosis cateristics of tuberculous spondylitis vs. vertebral osteomyelitis.
of traumatic occipitovertebral dissociation: 2. Comparison of three AJR 1989; 153:399405.
methods of detecting occcipitovertebral relationships on lateral radi- 75. Roos AD, van Meerten El, Bloem JL, et al. MRI of tuberculosis
ographs of supine subjects. Am J Roentgenol 1994; 162:887892. spondylitis. AJR 1987; 146:7982.
50. Smith WS, Kaufer H. Patterns and mechanisms of lumbar injuries 76. Talpos D, Tien RD, Hesselink JR. MRI of AIDS-related
associated with lap seat belts. J Bone Joint Surg Am 1969; polyradiculopathy. Neurology 1991; 41:19961997.
51:239254. 77. Chong J, Di Rocco A, Tagliati M, et al. MR findings in AIDS-asso-
51. Gertzbein SD, Court-Brown CM. Flexion-distraction injuries of ciated myelopathy. AJNR 1999; 20:14121416.
the lumbar spine: mechanisms of injury and classification. Clin 78. Anson JA, Spetzler RF. Interventional neuroradiology for spinal
Orthop 1988; 227:5260. pathology. Clin Neurosurg 1992; 39:388417.
52. Matsumura A, Meguro K, Tsurushima H, et al. Magnetic reso- 79. Nittner K. Spinal meningiomas, neurinomas and neurofibromas
nance imaging of SCI without radiologic abnormality. Surg Neuro and hourglass tumors. In: Vinken PJ, Bruyn GW (eds.), Handbook
1990; 33:281283. of Clinical Neurology. New York: Elsevier, 1976; 20:177322.
53. Davis JW, Phreaner DL, Hoyt DB, Mackersie RC. The etiology 80. Vinken PJ, Bruyn GW (eds.). Handbook of Clinical Neurology.
of missed cervical spine injuries. J Trauma 1993; 34:342346. Vol. 19: Spinal cord tumors: Part I. New York: Elsevier, 1975.
54. Robertson PA, Ryan MD. Neurological deterioration after reduc- 81. Vinken PJ, Bruyn GW (eds.). Handbook of Clinical Neurology.
tion of cervical subluxation: Mechanical compression by disk tis- Vol. 20: Spinal cord tumors: Part II. New York: Elsevier, 1976.
sue. J Bone Joint Surg Br 1992; 74:224227. 82. Kurland LT. The frequency of intraspinal neoplasms in the resi-
55. DAlise MD, Benzel EC, Hart BL. Magnetic resonance imaging dent population of Rochester, Minnesota. J Neurosurg 1958;
evaluation of the cervical spine in the comatose or obtunded 15:627641.
trauma patient. J Neurosurg 1999; 91(1 Suppl):5459. 83. Lee RR. Spinal tumors. In: Lee RR (ed.), Spinal Imaging (Spine:
56. Boden SD, Lee RR, Herzog RJ. MRI of the spine. In: Frymoyer J State of the Art Reviews, vol 9). Philadephia: Hanley & Belfus,
(ed.), The Adult Spine: Principles and Practice, 2nd ed. New York: 1995, 261286.
Raven Press, Ltd., 1996. 84. Sze G, Abramson A, Krol G, et al. Gadolinium-DTPA in the eval-
57. Boden SD, McCowin PR, Davis DO, et al. Abnormal magnetic uation of intradural extramedullary spinal disease. AJR 1988;
resonance scans of the cervical spine in asymptomatic subjects: 150:911921.
A prospective investigation. J Bone Joint Surg 1990; 72A: 85. Avrahami E, Tadmor R, Dally O, et al. Early MR demonstration
11781184. of spinal metastases in patients with normal radiographs and CT
58. Modic MT. Degenerative disorders of the spine. In: Modic MT, and radionuclide bone scans. J Comput Assist Tomogr 1989;
Masaryk TJ, Ross JS (eds.), MRI of the Spine, 2nd ed. St. Louis: 13:598602.
Mosby, 1994. 86. Baker LL, Goodman SB, Perkash I, Lane B, and Enzmann DR.
59. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Benign versus pathologic compression fractures of vertebral bod-
IMAGING OF THE SPINAL CORD 77

ies: Assessment with conventional spin-echo, chemical-shift, and 93. Burger PC, Scheithauer BW, Vogel FS. Surgical Pathology of the
STIR MR imaging. Radiology 1990; 174:495502. Nervous System and Its Coverings, 3rd ed. New York: Churchill
87. Yuh WT, Zachar CK, Barloon TJ, Sato Y, Sickels WJ, Hawes DR. Livingstone, 1991, Chapter 9: Spinal meninges, spinal nerve roots,
Vertebral compression fractures: Distinction between benign and and spinal cord, 605660.
malignant causes with MR imaging. Radiology 1989; 172:215218. 94. Burk DL Jr., Brumberg JA, Kanal E et al. Spinal and paraspinal
88. Burger PC, Scheithauer BW, Vogel FS. Surgical Pathology of the neurofibromatosis: Surface coil MR imaging at 1.5T. Radiology
Nervous System and Its Coverings, 3rd ed. New York: Churchill 1987; 162:797801.
Livingstone, 1991, Chapter 8: Spine and epidural space, 569603. 95. Barkovich AJ, Edwards MSB, Cogen PH. MR evaluation of spinal
89. Masaryk TJ. Spinal tumors. In: Modic MT, Masaryk TJ, Ross JS dermal sinus tracts in children. AJNR 1991; 12:123129.
(eds.), MRI of the Spine. St. Louis: Mosby, 1994; Chapter 7, 96. Nemoto Y, Inoue Y, Tashiro T, et al. Intramedullary spinal cord
249314. tumors: Significance of asssociated hemorrhage at MR imaging.
90. Dahlin DC, Unni KK. Bone Tumors: General Aspects and Data Radiology 1992; 82:793796.
on 8,542 Cases. Springfield: Charles C. Thomas, 1986, 6269. 97. Fortuna A, Celli P, Palma L. Oligodendrogliomas of the spinal
91. Egelhoff JC, Bates DJ, Ross JS, et al. Spinal MR findings in neu- cord. Acta Neurochir 1980; 52:305329.
rofibromatosis types 1 and 2. AJNR 1992; 13:10711077. 98. Gilmer-Hall HS, Ellis WG, Imbesi SG, Boggan JE. Spinal oligo-
92. Slooff JL, Kernohan JW, MacCarty CS. Primary Intramedullary dendroglioma with gliomatosis in a child: Case report. J Neuro-
Tumors of the Spinal Cord and Filum Terminale. Philadelphia: surg Spine 2000; 92:109113.
Saunders, 1964.
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4 Epidemiology of
Spinal Cord Injury

Michael J. DeVivo, Dr.P.H.

pinal cord injury (SCI) epidemiol- However, the NSCISC Database has several advantages,

S ogy has been studied extensively


over the past 30 years. Early popu-
lation-based epidemiologic investi-
gations of SCI include the studies of eighteen northern
including its large sample size, geographic diversity, the
range of information it contains, and its excellent data
quality.
Beginning in the 1980s, the Centers for Disease Con-
California counties conducted by Kraus et al., Olmsted trol and Prevention began funding population-based SCI
County Minnesota conducted by Griffin et al., and surveillance systems (registries) in many states (918).
national studies conducted by both Kalsbeek et al. and Data from these state registries have been used to demon-
Bracken et al.(14) These investigations were limited to strate slight biases in the NSCISC Database toward over-
descriptive epidemiology, including the documentation of representation of more severe injuries, non-whites, and
overall SCI incidence, age at time of injury, gender, racial injuries due to acts of violence (7). Given the comple-
or ethnic group, cause of injury, and mortality prior to mentary nature of the NSCISC Database and the popu-
either hospital admission or discharge. lation-based state registries, a relatively complete descrip-
In the early 1970s, the model SCI care system pro- tion of the epidemiology of SCI in the United States has
gram was initiated with funding from what is now the been obtained.
National Institute on Disability and Rehabilitation
Research in the United States Department of Education.
All funded model systems of care were required to sub- OVERALL INCIDENCE
mit data on patients they treated to a national database.
This database, the National Spinal Cord Injury Statisti- Published reports of the incidence of SCI vary from
cal Center (NSCISC) Database, began in Phoenix, Ari- twenty-five new cases per million population per year in
zona, and was moved to the University of Alabama at West Virginia to fifty-nine new cases per million popula-
Birmingham in 1983, where it remains today (5). tion per year in Mississippi (Table 4.1). Variation in SCI
Although this database has been used extensively to incidence rates among states is caused by differences in
develop a descriptive profile of new SCIs that occur in the population demographic characteristics, the definition of
United States each year, it is not population based (68). SCI, and the data collection methodology that is used in
Therefore, it cannot be used to calculate actual incidence each state. Overall, based on a combination of state reg-
rates or directly assess risk factors for obtaining a SCI. istry information, the incidence rate of SCI in the United
79
80 INTRODUCTION

States is approximately 40 cases per million population, several trends are apparent. SCI incidence rates are low-
or just over 10,000 new cases per year. Moreover, est for the pediatric age group, highest for persons in their
although there have been changes in the most common late teens and early twenties, and decline consistently there-
underlying causes of SCI during the past 20 years, the after (9,10,12,14,16). The state of Oklahoma is typical,
overall incidence of new cases each year has remained rel- where age-specific SCI incidence rates per million popu-
atively stable (19). lation for 19881990 were 6 for age 014 (3 percent of
This annual incidence rate of forty new cases per cases), 94 for age 1519 (18 percent of cases), 85 for age
million population does not include persons who die at 2024 (15 percent of cases), 71 for age 2529 (14 percent
the scene of the accident. Most population-based state of cases), 47 for age 3044 (27 percent of cases), 32 for
registries do not report deaths that occur prior to hospi- age 4559 (12 percent of cases), and 26 for persons who
tal admission. An exception is the state of Utah, where were at least 60 years of age (11 percent of cases) (10).
the incidence of prehospital SCI deaths from 19891991 A similar pattern emerges from the NSCISC Data-
was reported to be approximately 4 cases per million pop- base, where the mean age at time of injury is 32.7 years
ulation per year, or 9.3 percent of the incidence rate for ( 15.9 years), the median age at injury is 27 years, and
hospitalized cases (11). Nonetheless, incomplete report- the most common age at injury is 19 years (Table 4.2).
ing of these prehospital deaths is possible, and this esti- Overall, 52.7 percent of persons enrolled in the NSCISC
mate of fatal SCI incidence is probably conservative. Database since 1973 were between the ages of 16 and 30
Incidence of SCI elsewhere is consistently lower than at the time of their injury. However, these overall figures
in the United States, and usually does not exceed twenty mask a rather substantial trend toward increasing age at
new cases per million population per year (2026). The injury in recent years. From 19731977, the mean age at
increased incidence in the United States compared to injury for persons enrolled in the NSCISC Database was
other countries is caused in large part by the acts of vio- 28.2 years, whereas among persons injured between 1995
lence that are a common cause of SCI in the United States, and 1999, the mean age at injury was 36.5 years. These
but a rare cause of SCI elsewhere. However, even in the figures mirror the increasing average age of the general
absence of SCI caused by acts of violence, the incidence United States population, which was 28 years in 1970 and
rate is higher in the United States than in other countries. 34.9 years in 1997, although changes in underlying age-
specific incidence rates cannot be ruled out as also con-
tributing to this trend in age at time of SCI (8).
RISK FACTORS
Gender
Age at Injury
SCI occurs predominantly among men. Gender-specific
Comparisons of age-specific SCI incidence rates are diffi-
SCI annual incidence rates have been reported by several
cult among the state registries because of the lack of uni-
state registries, with men ranging from a 4.6 times higher
form categorization of reported age ranges. Nonetheless,
incidence rate in West Virginia (41 new cases per million
men vs. 9 new cases per million women), to only a 2.3
times higher incidence rate in Louisiana (67 new cases per
TABLE 4.1 million men vs. 29 new cases per million women) (12,16).
Annual SCI Incidence Rates Derived from The percentage of SCIs that occur among men is 81.5 per-
Population-based State Registries cent for persons enrolled in the NSCISC Database (Table
4.2); 80 percent for Oklahoma and Arkansas; 78 percent
ANNUAL for Virginia; 76 percent for Utah, Colorado, and Geor-
INCIDENCE gia; and 69 percent for Louisiana (811,14,1618). This
STATE DATES RATE/106 four-to-one ratio of male to female SCIs has remained
very consistent over time despite significant trends in age
Arkansas (9) 198089 27 at injury, ethnicity, and etiology of injury (Table 4.2).
New York (15) 198288 43
West Virginia (12) 198588 25
Oklahoma (10) 198890 40 Race and Ethnicity
Utah (11) 198991 43
Colorado (14) 198996 45 Fewer state registries have reported race and ethnicity
Virginia (17) 199092 30 data than information on age and gender. Nonetheless,
Louisiana (16) 1991 46 some clear patterns have emerged. SCI incidence rates are
Georgia (18) 199192 46 substantially and consistently higher for African Ameri-
Mississippi (13) 199295 59 cans than whites. In Oklahoma, the annual SCI incidence
rate for African Americans was 57 new cases per million
EPIDEMIOLOGY OF SPINAL CORD INJURY 81

TABLE 4.2
Trends in Demographic Characteristics of Persons Enrolled
in the NSCISC Database by Year of Injury

CHARACTERISTIC 197377 197894 199599 TOTAL

Age at Injury (percent)


115 7.7 3.6 3.0 3.8
1630 61.6 55.6 42.1 52.7
3145 17.7 23.5 28.1 24.2
4660 8.8 10.2 15.1 11.3
6175 3.6 5.5 8.5 6.1
76 0.7 1.6 3.2 1.9
Age at Injury (mean) 28.2 31.9 36.5 32.7
Male (percent) 82.7 82.1 79.5 81.5
Race/Ethnicity (percent)
White 76.8 65.1 62.2 65.3
African American 14.9 21.9 23.7 21.8
Hispanic Descent 6.2 10.2 0.3 0.8
Asian American 0.8 0.5 0.7 1.6
Native American 1.3 0.9 0.3 0.8
Other Race 0.0 0.5 0.7 0.5

population compared to 40 new cases per million popu- Interestingly, the average age at injury varies by
lation for whites and 29 new cases per million population racial and ethnic group. Among persons enrolled in the
for Native Americans (10). In Louisiana, the difference NSCISC Database, persons of Hispanic descent have the
is even more striking, with African Americans having an youngest average age at injury (27.8 years), followed by
annual SCI incidence rate of 72 new cases per million Native Americans (29.3 years), whites (32.5 years),
population compared to 36 new cases per million popu- African Americans (33.2 years), and Asian Americans
lation for whites (16). In fact, when race and gender were (35.6 years) (8). Moreover, since 1973, the average age at
considered together, the SCI annual incidence rate per mil- time of injury for persons enrolled in the NSCISC Data-
lion population in Louisiana in 1991 was 127 for African base has increased by about 10 years for whites while
American men, 41 for white men, 31 for white women, increasing only marginally for other racial groups (8).
and 26 for African American women (16). Unfortunately,
state registries have not yet published SCI incidence rates
for other racial and ethnic groups, such as Asian Ameri- ETIOLOGY OF INJURY
cans and persons of Hispanic descent.
Since 1995, 62.2 percent of newly injured persons
State Registries
enrolled in the NSCISC Database were white; 23.7 per-
cent were African American; 10.9 percent were Hispanic; Cause-specific incidence rates have been reported by gender
2.2 percent were Asian American; and 0.3 percent were for Arkansas, by race for Oklahoma, and by both gender
Native American (Table 4.2). However, between 1973 and race for Louisiana (9,10,16). Other states often report
and 1977, 76.8 percent of new persons enrolled in the data on causes of SCI only in percentage terms that are heav-
NSCISC Database were white; 14.9 percent were African ily influenced by the racial and ethnic composition of the
American; 6.2 percent were Hispanic; 0.8 percent were general population of each state (11,12,14). Overall, motor
Asian American; and 1.3 percent were Native American. vehicle crashes are the leading cause of SCI in all states. In
This trend toward an increasing percentage of new SCIs most states, such as Colorado, Oklahoma, Utah, West Vir-
occurring among minority populations may be caused by ginia, and Arkansas, falls rank second, followed by sports
periodic changes in the location of the model systems that and acts of violence (912,14). However, in states like
participate in the NSCISC Database and changes in refer- Louisiana and Mississippi, with greater proportions of
ral patterns to model systems. However, some changes African Americans and/or persons of Hispanic descent, acts
in underlying race-specific SCI incidence rates may also of violence are the second leading cause of SCI (13,16).
have occurred. Ultimately, data from the state registries In fact, Oklahoma data reveal that the higher annual
should be examined to address this question. incidence of SCI among African Americans is caused
82 INTRODUCTION

entirely by acts of violence (10). Overall in Oklahoma, participation rates, but have an annual incidence rate of
the annual incidence rate of SCI was 17 new cases per mil- only 1 case per 100,000 athletes (27).
lion population higher for African Americans than whites The overall pattern of causes of SCI varies substan-
(57 vs. 40), whereas the cause-specific annual incidence tially by racial group (Table 4.3). Among whites, auto-
rate of SCI caused by violence was 18 new cases per mil- mobile crashes rank first (38.9 percent), followed by falls
lion population higher for African Americans than whites (24.5 percent), diving mishaps (6.2 percent), motorcycle
(21 vs. 3). There were no other meaningful differences in crashes (5.8 percent), and gunshot wounds (4.6 percent).
cause-specific annual SCI incidence rates among the races Among African Americans, gunshot wounds rank first
in Oklahoma (10). (41.4 percent), followed by automobile crashes (25.2 per-
Although motor vehicle crashes are the overall lead- cent), falls (17.6 percent), person-to-person contact
ing cause of SCI, among African American men, violence (fights) (3.4 percent), and medical or surgical complica-
ranks first. In Louisiana during 1991, the annual cause- tions (2.6 percent). Among persons of Hispanic descent,
specific SCI incidence rate per million population caused the top five causes of SCI are gunshot wounds (37.0 per-
by acts of violence was 71 for African American men, but cent), automobile crashes (27.7 percent), falls (17.8 per-
only 10 for African American women, 5 for white cent), diving mishaps (3.2 percent), and being hit by
women, and 4 for white men (16). By comparison, annual falling or flying objects (2.9 percent). Among Asian Amer-
cause-specific SCI incidence rates per million population icans, the top five causes of SCI are automobile crashes
caused by motor vehicle crashes in Louisiana during 1991 (40.8 percent), gunshot wounds (21.1 percent), falls (16.2
were 26 for African American men, 22 for white men, percent), motorcycle crashes (4.9 percent), and medical
17 for white women, and 13 for African American or surgical complications (2.8 percent).
women (16). As reported by Nobunaga et al., causes of SCI
reported to the NSCISC Database between 1994 and
1998 also varied by gender and age (8). Automobile
NSCISC Database
crashes ranked first among both men and women, but
Specific causes of all new spinal cord injuries reported to caused a much greater share of SCIs among women than
the NSCISC Database between 1995 and 2000 by race men (49.1 vs. 29.7 percent). Gunshot wounds ranked sec-
and ethnicity appear in Table 4.3. Again, because Table ond among men (22.4 percent) but third among women
4.3 reflects percentages rather than actual incidence rates, (11.1 percent), whereas falls ranked third among men
the figures for all races combined are influenced by the (21.7 percent) but second among women (19.8 percent).
locations of the eighteen model systems that contributed Motor vehicle crashes are the leading cause of SCI among
data during this period. However, the race-specific per- persons younger than 45 years of age, whereas falls rank
centages should be reasonably representative of the typ- first among persons older than age 45. The occurrence
ical causes of SCI that occur within each racial group. of SCIs caused by recreational sports activities and acts
Overall, automobile crashes accounted for 34.5 per- of violence declines rapidly with advancing age (8).
cent of SCIs reported to the NSCISC Database, followed
by falls (22.0 percent), gunshot wounds (17.2 percent),
diving mishaps (4.5 percent), and motorcycle crashes (4.4 PREVALENCE
percent). Among recreational sports activities, diving
mishaps rank first, followed by snow skiing, other Although incidence reflects the number of new cases that
unspecified winter sports, and horseback riding. The occur each year, prevalence is defined as the number of per-
occurrence of SCIs while playing football, which once sons with a SCI who are currently alive. There are two ways
ranked second among recreational sporting activities, has to estimate prevalence. One approach is based on the epi-
declined dramatically in recent years because of rules demiologic relationship between prevalence, incidence, and
changes that have banned deliberate spearing and the the duration of the condition. When a condition occurs rel-
use of the top of the helmet as the initial point of contact atively rarely, as is the case with SCI, then the prevalence
in making tackles. rate can be estimated as the product of the incidence rate
Whereas diving mishaps are the most common and average duration. Using this mathematical formula and
recreational sporting activity leading to a SCI, that does the best available data at the time, the prevalence of SCI in
not mean that diving is the most risky of these activities. the United States in 1980 was estimated to be 906 persons
To assess risk, the underlying rate of exposure to that per million population, or just under 200,000 existing cases
activity must be known. For example, male gymnastics (28). However, an underlying assumption when making
causes few SCIs because of its low participation rates, but this calculation is that both incidence and duration (as mea-
has been reported to have an annual incidence rate of 14.3 sured in the case of SCI by life expectancy) have remained
per 100,000 athletes (27). By comparison, high school constant over time. Because life expectancy for persons with
and college football cause more SCIs because of higher SCI continues to increase, and a current estimate of life
EPIDEMIOLOGY OF SPINAL CORD INJURY 83

TABLE 4.3
Causes (%*) of New Spinal Cord Injuries Reported to the NSCISC Database
between 1995 and 2000, by Racial and Ethnic Group

RACE

AFRICAN HISPANIC ASIAN


ETIOLOGY WHITE AMERICAN DESCENT AMERICAN TOTAL

Vehicular
Automobile 38.9 25.2 27.7 40.8 34.5
Motorcycle 5.8 1.9 2.5 4.9 4.4
Bicycle 1.4 0.7 1.0 2.1 1.2
All Terrain Vehicle 1.1 0.1 0.3 0.7 0.8
Snowmobile 0.5 0.0 0.0 0.0 0.3
Fixed Wing Aircraft 0.3 0.0 0.1 0.0 0.2
Rotating Wing Aircraft 0.1 0.0 0.0 0.7 0.1
Boat 0.1 0.0 0.0 0.0 0.1
Other Vehicle 0.7 0.1 0.4 0.7 0.5
Violence
Gunshot 4.6 41.4 37.0 21.1 17.2
Personal Contact 0.5 3.4 0.7 0.7 1.2
Stab 0.3 0.7 0.6 0.7 0.4
Sports
Diving 6.2 1.1 3.2 1.4 4.5
Snow Skiing 1.0 0.0 0.3 0.7 0.7
Surfing 0.8 0.1 0.1 1.4 0.5
Horseback Riding 0.7 0.0 0.3 0.0 0.4
Wrestling 0.3 0.2 0.0 0.0 0.2
Track and Field 0.3 0.0 0.0 0.0 0.2
Football 0.2 0.5 0.1 0.0 0.2
Trampoline 0.3 0.0 0.1 0.0 0.2
Water Skiing 0.1 0.0 0.0 0.0 0.1
Gymnastics 0.1 0.1 0.0 0.7 0.1
Rodeo 0.2 0.0 0.0 0.0 0.1
Hang Gliding 0.1 0.0 0.0 0.0 0.1
Air Sports 0.2 0.0 0.0 0.0 0.1
Baseball 0.1 0.1 0.0 0.0 0.1
Other Winter Sports 0.7 0.0 0.0 0.0 0.5
All Other Sports 0.6 0.1 0.0 0.0 0.4
Falls 24.5 17.6 17.8 16.2 22.0
Falling Objects 3.0 1.5 2.9 0.7 2.6
Pedestrian 1.5 2.2 2.0 2.1 1.7
Medical/Surgical Complications 3.8 2.6 1.9 2.8 3.3
Other/Unclassified 1.1 0.3 0.9 1.4 0.9

*Percentages in each column do not sum to 100 because of rounding.

expectancy was used, prevalence was slightly overestimated Eventually, substantial funding was provided by the Par-
by using this formula (29). alyzed Veterans of America to use a sophisticated prob-
Of course, the more straightforward way to estimate ability sampling plan of small geographic areas and insti-
prevalence is simply to count people using standard sam- tutions to estimate conservatively the prevalence of SCI
pling and survey techniques. For many years, this was not in the United States at 721 persons per million popula-
attempted because of the large sample size, time, and tion, or approximately 176,965 persons in 1988 (30).
expense that would be required to produce an accurate More recently, current estimates of agesex-specific
estimate of prevalence for a condition as rare as SCI. incidence and mortality have been combined with the
84 INTRODUCTION

results of the 1988 survey to project the growth in preva- Traumatic SCI in Olmsted County, Minnesota, 19351981. Am
J Epidemiol 1985; 121:884895.
lence of SCI in the United States over time (31). Using new 3. Kalsbeek WD, McLaurin RL, Harris BSH, Miller JD. The national
mathematical models, the prevalence of SCI in the United head and spinal cord injury survey: Major findings. J Neurosurg
States was projected to increase to 246,882 persons by 1980; 53Suppl:1931.
4. Bracken MB, Freeman DH, Hellenbrand K. Incidence of acute
2004, and 276,281 persons by 2014 (31). This projected traumatic hospitalized spinal cord injury in the United States,
growth in prevalence results exclusively from improved 19701977. Am J Epidemiol 1981; 113:615622.
life expectancies rather than any anticipated change in 5. Stover SL, DeVivo MJ, Go BK. History, implementation, and cur-
rent status of the national spinal cord injury database. Arch Phys
SCI incidence rates. Med Rehabil 1999; 80:13651371.
Because of the lifetime duration of SCI as well as dif- 6. DeVivo MJ, Rutt RD, Black KJ, Go BK, Stover SL. Trends in
ferences in life expectancy for persons with different spinal cord injury demographics and treatment outcomes between
1973 and 1986. Arch Phys Med Rehabil 1992; 73:424430.
demographic characteristics and degrees of SCI impair- 7. Go BK, DeVivo MJ, Richards JS. The epidemiology of spinal cord
ment, the profile of persons with SCI who are alive today injury. In: Stover SL, DeLisa JA, Whiteneck GG, (eds.), Spinal
is different from the typical characteristics of persons who Cord Injury: Clinical Outcomes from the Model Systems.
Gaithersburg, MD.: Aspen Publishers, 1995, 2155.
incur these injuries each year. For example, the median 8. Nobunaga AI, Go BK, Karunas RB. Recent demographic and
current age of all persons with SCI who were alive in 1988 injury trends in people served by the model spinal care injury care
was estimated to be 41 years (15 years older than the systems. Arch Phys Med Rehabil 1999; 80:13721382.
9. Acton PA, Farley T, Freni LW, Ilegbodu VA, Sniezek JE, Wohlleb
median age of new cases occurring at that time) (30). JC. Traumatic spinal cord injury in Arkansas, 19801989. Arch Phys
Moreover, because that estimate of median age is now Med Rehabil 1993; 74:10351040.
12 years old, and because the median age of new cases 10. Price C, Makintubee S, Herndon W, Istre GR. Epidemiology of
traumatic spinal cord injury and acute hospitalization and reha-
that occur each year is increasing, the median age of all bilitation charges for spinal cord injuries in Oklahoma,
persons with SCI who are alive today would be somewhat 19881990. Am J Epidemiol 1994; 139:3747.
higher than it was in 1988 (but less than 12 years higher 11. Thurman DJ, Burnett CL, Jeppson L, Beaudoin DE, Sniezek JE.
Surveillance of spinal cord injuries in Utah, USA. Paraplegia 1994;
because of higher mortality rates among older persons). 32:665669.
Similarly, it was estimated in 1988 that only 71 per- 12. Woodruff BA, Baron RC. A description of nonfatal spinal cord
cent of persons with SCI who were alive at that time were injury using a hospital-based registry. Am J Prev Med 1994;
10:1014.
men, compared to 82 percent of new cases enrolled in 13. Surkin J. Spinal Cord Injury: Mississippis Facts and Figures. Jack-
the NSCISC Database (30). Again, the percentage of per- son, MS: Mississippi State Department of Health, 1995.
sons with SCI who are alive today and who are men will 14. Colorado Department of Public Health and Environment, Disease
Control and Environmental Epidemiology Division. 1996 Annual
be slightly lower than 71 percent, because men have Report of the Traumatic Spinal Cord Injury Early Notification
shorter life expectancies than women. However, there System. Denver, CO: Colorado Department of Transportation
have been no new attempts to develop a profile of preva- Printing Office, 1997.
15. Relethford JH, Standfast SJ, Morse DL. Trends in traumatic spinal
lence of persons with SCI since 1988, so one can only cord injuryNew York, 19821988. MMWR 1991; 40:535537,
speculate about current SCI population characteristics 543.
such as age, gender, race, neurologic level of injury, and 16. Bayakly AR, Lawrence DW. Spinal Cord Injury in Louisiana 1991
Annual Report. New Orleans, LA: Louisiana Office of Public
degree of injury completeness. Health, 1992.
17. Virginia Department of Rehabilitation Services. Spinal Cord
Injury in Virginia: A Statistical Fact Sheet. Fishersville, VA: Vir-
CONCLUSION ginia Spinal Cord Injury System, 1993.
18. Johnson SC. Georgia Central Registry: Spinal Cord Disabilities
and Traumatic Brain Injury. Warm Springs, GA: Roosevelt Warm
Thanks to the initiation of population-based SCI registries Springs Institute for Rehabilitation, 1992.
in several states, as well as the continued existence of the 19. Glick T. SCI surveillance: Is there a decrease in incidence?
[abstract] J Spinal Cord Med 2000; 23Suppl:61.
NSCISC Database, much is now known about the 20. Chen CF, Lien IN. Spinal cord injuries in Taipei, Taiwan,
descriptive epidemiology of SCI in the United States. 19781981. Paraplegia 1985; 23:364370.
Future epidemiologic efforts should focus on developing 21. Biering-Sorensen F, Pedersen V, Clausen S. Epidemiology of spinal
cord lesions in Denmark. Paraplegia 1990; 28:105118.
a more accurate profile of persons with SCI who are alive 22. Garcia-Reneses J, Herruzo-Cabrera R, Martinez-Moreno M. Epi-
today, as well as detailed investigations of the exact cir- demiological study of SCI in Spain 19841985. Paraplegia 1991;
cumstances surrounding how these injuries occur. Such 28:180190.
23. Karamehmetoglu SS, Unal S, Karacan I, Yilmaz H, Togay HS,
research might provide important clues to developing Ertekin M, Dosoglu M, Ziyal MI, Kassaroglu D, Hakan T. Trau-
cost-effective primary prevention programs. matic spinal cord injuries in Istanbul, Turkey: An epidemiologi-
cal study. Paraplegia 1995; 33:469471.
24. Schonherr MC, Groothoff JW, Mulder GA, Eisma WH. Rehabil-
References itation of patients with spinal cord lesions in The Netherlands: An
epidemiological study. Spinal Cord 1996; 34:679683.
1. Kraus JF, Franti CE, Riggins RS, Richards D, Borhani NO. Inci- 25. Otom AS, Doughan AM, Kawar JS, Hattar EZ. Traumatic spinal
dence of traumatic spinal cord lesions. J Chron Dis 1975; cord injuries in Jordanan epidemiological study. Spinal Cord
28:471492. 1997; 35:253255.
2. Griffin MR, Opitz JL, Kurland LT, Ebersold MJ, OFallon WM. 26. Martins F, Freitas F, Martins L, Dartigues JF, Barat M. Spinal cord
EPIDEMIOLOGY OF SPINAL CORD INJURY 85

injuriesepidemiology in Portugals central region. Spinal Cord and causes of death among persons with spinal cord injury. Arch
1998; 36:574578. Phys Med Rehabil 1999; 80:14111419.
27. Clark KS. Spinal cord injuries in organized sports. Model Sys- 30. Berkowitz M, Harvey C, Greene CG, Wilson SE. The Economic
tems SCI Digest 1980; 2:917. Consequences of Traumatic Spinal Cord Injury. New York:
28. DeVivo MJ, Fine PR, Maetz HM, Stover SL. Prevalence of spinal Demos Publishers, 1992.
cord injury: A reestimation employing life table techniques. Arch 31. Lasfargues JE, Custis D, Morrone F, Carswell J, Nguyen T. A
Neurol 1980; 37:707708. model for estimating spinal cord injury prevalence in the United
29. DeVivo MJ, Krause JS, Lammertse DP. Recent trends in mortality States. Paraplegia 1995; 33:6268.
This Page Intentionally Left Blank
5 Outcomes Following
Spinal Cord Injury

Ien Sie, M.S., P.T.


Robert L. Waters, M.D.

pinal cord injury (SCI) is one of the resources that will only minimally improve a patients

S most devastating injuries an indi-


vidual can sustain. In the United
States, the incidence of SCI is
approximately 10,000 cases per year with a prevalence of
overall function. Accurate prognostication following SCI
will determine the treatment plan and minimize unnec-
essary interventions while justifying needed care and
resources.
approximately 200,000 cases (1). Victims are typically Patients and their families also must know what to
relatively young, male, and are often injured because of expect in regard to functional outcomes so that they can
violence or high-speed trauma. Following injury, the plan ahead for the modifications or additional assistance
potential for maximal function is one of the primary con- which may be needed at discharge. For patients, the abil-
cerns for patients, their families, and clinicians. The ity to walk is the primary functional outcome of interest.
dilemma for care providers is to encourage individuals However, personal care abilities, sexuality, and occupa-
to attain the highest functional level possible without tional and recreational handicaps are also concerns.
offering false hope for performance of activities that may Motor function is the primary determinant of over-
be impossible or impractical to achieve. all function following SCI. Therefore, an accurate diag-
It is important for both clinicians and patients to nosis of the level and completeness of SCI and a detailed
have a reasonable expectation of functional outcomes fol- assessment of neurologic function is essential for prog-
lowing SCI. Clinicians must be able to prognosticate out- nostication. A carefully performed neurologic examina-
comes to plan a realistic, effective rehabilitation program. tion performed immediately after injury not only is essen-
Knowledge of expected outcomes also helps to determine tial to plan treatment interventions but to provide a
the effectiveness of various treatment interventions (phar- baseline to measure the rate of recovery over the days
macologic and rehabilitation protocols). Finally, in the immediately following injury. Following an incomplete
current healthcare system, with declining resources and injury, rapid early recovery will likely be sustained over
a shift to managed care, it is essential to know expected subsequent weeks and months, and the prognosis for
outcomes so that the most cost-effective protocols to long-term functional recovery is excellent. Various inves-
attain optimal function can be implemented. Just as it is tigators have determined that a detailed neurologic exam-
inappropriate to deny or fail to provide essential and ination performed at least 72 hours following traumatic
appropriate rehabilitation services, it is also inappropri- SCI is a better prognostic tool for determining outcomes
ate to provide valuable rehabilitation services and than an examination performed immediately following
87
88 INTRODUCTION

injury, because the results of an early examination may ery (or deterioration) that has occurred in the intervening
be compromised by pain, confusion, and associated period. By dividing the difference between scores by the
injuries (24). number of days in the interval, the change per day can
The accuracy of predicting recovery based on neu- be calculated. Finally, by multiplying the change per day
rologic examination improves with a longer interval by 365 days, the annualized rate of change can be deter-
between onset of injury and the most recent neurologic mined. The annualized rate of change represents the rate
examination. Whereas Waters and associates studied of change during a particular interval that could be
neurologic recovery in over 500 patients and found long- expected if it were to continue for one year.
term motor recovery could be reliably predicted using the Once completeness of injury and level of injury
1-month neurologic examination to predict recovery (tetraplegia or paraplegia) have been determined, rate of
(58), Marino and colleagues found that a neurologic recovery and individual muscle recovery data can be
examination performed 1 week following injury had reviewed to predict recovery in a specific patient group. For
prognostic value for determining recovery (9). These the following discussion, patients are categorized into one
investigators used the ASIA Impairment Scale (AIS) and of four groups: complete tetraplegia, incomplete tetraple-
the Frankel scale to predict neurologic recovery. Clearly, gia, complete paraplegia, and incomplete paraplegia.
it is the responsibility of the rehabilitation practitioner
to perform serial examinations on a frequent basis dur-
ing the rehabilitation process so that functional goals can MOTOR RECOVERY
be updated and modified appropriately. The authors rec-
Complete Paraplegia (5)
ommend such examinations be performed on a weekly
basis. In the overwhelming majority (96 percent) of patients with
The International Standards for Neurologic and complete paraplegia 1 month following injury, the injury
Functional Classification of SCI have been accepted as the will remain complete. For the few patients, 4 percent, who
most accurate and reliable instrument for documenting undergo late conversion to incomplete status, motor
neurologic status following SCI (10). These standards recovery is small. Late conversion is significant, however,
require determination of both motor and sensory levels for recovery of sacral functions. Approximately half of
bilaterally, as well as determination of completeness of patients who undergo late conversions will regain voli-
injury. Impairment is graded on a five-point scale, which tional bowel and bladder function.
is a modified version of the Frankel scale. Activities of Recovery of motor function is related to level of
daily living are assessed by use of the Functional Inde- injury. No patients with a neurologic level of injury (NLI)
pendence Measure (FIM). above T9 regained motor function 1 year following
To determine motor level of injury, ten key muscles injury. At the more caudal levels of injury, there is a
representing specific spinal levels are tested bilaterally greater recovery of motor functions.
using the standard six-point (zero to five) manual mus- Recovery of functional strength (3/5 or greater) is
cle testing (MMT) scale. An individual with no neurologic minimal in muscles with a grade of 0/5 at 1 month (Table
deficit has an ASIA Motor Score (AMS) of 100 points (50 5.1). Only about 5 percent of these muscles will regain
points each for left and right sides of the body or 50 points functional strength 1 year following injury. In contrast,
each for the bilateral upper extremities and the bilateral 64 percent of muscles with either 1/5 or 2/5 strength at
lower extremities). Sensory level is determined by testing one month will have grade 3/5 strength at 1 year.
key points in each of twenty-eight dermatomes on both Only 5 percent of individuals with complete para-
the right and left sides of the body. Both pinprick and plegia will become community ambulators 1 year after
light-touch sensation are tested in each dermatome. Sen- injury. By definition, community ambulators are able to
sory function is scored on a three-point scale (zero to walk for more than 250 meters (the distance needed to
three). The total possible score for each of the sensory perform routine community activities). Paraplegics lack-
modalities is 112 points. Details of neurological assess- ing sufficient hip flexion to achieve a reciprocal gait pat-
ment of SCI is covered in Chapter 27. tern must utilize an energy intensive swing-through,
Determining completeness of injury by the sacral crutch-assisted gait pattern to walk. This type of gait pat-
sparing definition is the most important factor in deter- tern is generally impractical and unsuitable for routine
mining recovery at neurologic levels distal to the lesion. mobility because of the required severe arm exertion and
A complete injury is one without any sensory or motor high rates of energy expenditure.
function in the lowest sacral segments. In an incomplete
injury, there is partial preservation of motor and/or sen-
Incomplete Paraplegia (6)
sory function in the lowest sacral segments.
The differences in motor and sensory scores between In patients with incomplete paraplegia, motor recovery is
successive neurologic examinations represent the recov- independent of level of injury. The average increase in
OUTCOMES FOLLOWING SPINAL CORD INJURY 89

TABLE 5.1 TABLE 5.2


Prediction of Lower Extremity Prediction of Upper Extremity Motor Recovery
Motor Recovery (23) (23)

PERCENT WITH FUNCTIONAL  3/5 PERCENT WITH FUNCTIONAL  3/5


STRENGTH AT 1 YEAR STRENGTH AT 1 YEAR

MANUAL MANUAL MUSCLE


MUSCLE STRENGTH COMPLETE INCOMPLETE
STRENGTH AT COMPLETE INCOMPLETE INCOMPLETE AT ONE MONTH* TETRAPLEGIA TETRAPLEGIA
ONE MONTH* PARAPLEGIA PARAPLEGIA TETRAPLEGIA
0/5 20% 24%
0/5 5% 26% 24% 1/5 90% 73%
1/5, 2/5 64% 85% 97% 2/5 100% 100%

*ASIA key muscles *ASIA key muscles

motor scores was 12 points at 1 year after injury. Among sequentially. As with other categories of injury, the rate
patients with incomplete paraplegia, 76 percent will of motor recovery declines rapidly in the first 6 months
attain community ambulation status at 1 year. Thus, just following injury. Recovery of functional strength in indi-
knowing only whether a paraplegic is complete or incom- vidual muscles is very good for those patients with incom-
plete after injury is a very powerful predictor of future plete tetraplegia. All upper extremity muscles and 97 per-
ambulatory function. cent of lower extremity muscles with initial strength
Recovery of functional strength is also improved in grades of 1/5 or 2/5 will recover to at least 3/5 by 1 year.
incomplete paraplegia in comparison to complete para- In the upper extremity, 20 percent of muscles with an ini-
plegia. For muscles with 0/5 strength at 1 month, 26 per- tial grade of 0/5 will recover functional strength (Tables
cent will recover functional strength at 1 year. Eighty-five 5.1 and 5.2). In the lower extremity, 24 percent of those
percent of muscles with an initial strength of 1/5 or 2/5 with absent strength initially will recover to at least 3/5
will recover to 3/5 strength at 1 year (Table 5.1). by 1 year (Table 5.2).
Forty-six percent of those with incomplete tetraple-
gia become community ambulators at 1 year. The percent
Complete Tetraplegia (7)
of incomplete tetraplegics who attain community ambu-
Only 10 percent of those with complete tetraplegia at lation status is lower than for patients with incomplete
1 month following injury will convert to incomplete sta- paraplegia who have equivalent lower extremity function.
tus. As in patients with complete paraplegia, motor recov- Because the upper extremities may be severely impaired
ery is minimal in those with conversion to incomplete sta- in patients with incomplete tetraplegia, these individuals
tus, but recovery of sacral function is enhanced. may be unable to use their upper extremities for the
Recovery of motor strength is again independent of crutch-assisted gait that may be necessary to compensate
level of injury. Prediction of individual muscle recovery for lower extremity weakness.
to functional strength will help in determining indepen-
dent functioning. For example, 97 percent of wrist exten-
Timing of Motor Recovery
sors with an initial strength of 1/5 will recover to at least
3/5 at 1 year following injury. Therefore, an individual Graphing the annualized rates of change against time
who is initially dependent or needs assistance with table- since injury reveals the course of motor recovery. Regard-
top activities and transfers can anticipate independence less of level or completeness of injury, the majority of
in these activities at 1 year following injury. With the recovery occurs in the first 6 months following injury. The
exception of the triceps, all upper extremity muscles with rate-of-change plateaus at approximately 9 months but it
an initial strength grade of at least 1/5 recovered to at least does not equal zero (Figure 5.1). Although some motor
3/5 by 1 year (Table 5.2). recovery may continue 2 or more years after injury, the
amount is generally small and not likely to significantly
improve function.
Incomplete Tetraplegia (8)
Mange and associates examined motor recovery in
For patients with incomplete tetraplegia, recovery in the the zone of injury and compared recovery of motor com-
upper and lower extremities occurs concurrently, not plete and motor incomplete subjects. Their results suggest
90 INTRODUCTION

motor and sensory function is fairly consistent within a


given NLI. Guidelines for expected outcomes have been
developed for these patients.
An expert panel of SCI professionals has developed
a table of expected functional outcomes for various lev-
els of motor complete SCI (Table 5.3). The panel empha-
sized that the outcomes are only generalizations of
expected function under optimal conditions. They further
stressed the importance of a careful evaluation of the
unique circumstances and abilities of each patient in
establishing goals for functional outcomes (12).
Outcomes are categorized into seven groups, repre-
senting activities of daily living (ADL), mobility concerns,
and communication issues. Expected levels of assistance,
based on FIM scores, and possible adaptations or spe-
FIGURE 5.1
cialized equipment needs are also presented.
The seven groups are as follows:

1. Respiratory, bowel, and bladder function. For res-


that patients with motor incomplete injuries recover ear- piratory function, this category includes the ability
lier (11). to breathe with or without mechanical assistance
and the ability to clear secretions. For bowel and
bladder function, the ability to adjust clothing, man-
FUNCTIONAL RECOVERY age elimination, and maintain hygiene are necessary
components for successful performance.
Marino and colleagues have determined that the 1-week 2. Bed mobility, bed and wheelchair transfers, wheel-
Frankel and AIS scales have prognostic value for func- chair propulsion and positioning, and pressure
tional motor recovery (9). Individuals with AIS grade D relief. Neurologic deficits resulting from SCI can
have the best outcome and those with AIS grade A have severely affect the ability to perform these activities
the poorest outcome. Furthermore, Functional Indepen- safely. Modifications or specialized equipment may
dence Measures (FIM) scores at discharge are also depen- be needed to attain expected outcomes.
dent on level and completeness of injury (12). Discharge 3. Standing and ambulation. Standing and ambulation
FIM scores are strongly related to neurologic level for activities may be for psychologic or physiologic ben-
ASIA Impairment grades A (motor complete), B (sensory efit as well as for functional mobility.
incomplete), and C (motor incomplete with the majority 4. Eating, grooming, dressing, and bathing.
of muscles below the NLI having muscle grades less than 5. Communication (keyboard use, handwriting, and
3/5). However, individuals with motor-incomplete lesions telephone use).
with the majority of muscles below the NLI having 6. Transportation (driving, attendant-operated vehicle,
strength 3/5 or greater (ASIA grade D) had relatively high and public transportation). The ability to utilize one
FIM scores regardless of the neurologic level (12). or more transportation options is essential for inde-
Graves and associates studied the effects of various pendence within the community.
rehabilitation indices, as well as neurologic measures on 7. Homemaking (meal planning and preparation, and
functional gains, and concluded that the ASIA Motor home management). Equipment and modifications,
Score (AMS) was the most powerful predictor of gains as well as hours of weekly assistance for homemak-
in self-care activities and mobility (13). Furthermore, they ing activities, are presented.
determined that separating the AMS into upper extrem-
ity and lower extremity motor scores added to the pre- Patients with injuries at the upper cervical levels
dictive power. (C13) are typically dependent for all activities includ-
Levels of function are dependent on patient moti- ing respiration. Using a power wheelchair with head,
vation and training as well as on neurologic status. chin, or breath control and a powered reclining chair-
Because individuals with incomplete injuries can have back, they may become independent in pressure relief and
vastly different motor and sensory function even at the positioning, and in wheelchair propulsion. These indi-
same neurologic level of injury, it is not possible to pre- viduals may be independent in communication if spe-
dict functional outcomes based on NLI in incomplete cialized adaptive equipment is available (e.g., mouthstick,
patients. In patients with complete injuries, however, the high-tech computers, environmental control units).
OUTCOMES FOLLOWING SPINAL CORD INJURY 91

TABLE 5.3
Expected Functional Outcomes, LEVEL C1-3

Functionally relevant muscles innervated: Sternocleidomastoid, cervical paraspinal, neck accessories


Movement possible: Neck flexion, extension, rotation
Patterns of weakness: Total paralysis of trunk, upper extremities, lower extremities; dependent on ventilator
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12
FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Ventilator dependent Two ventilators


Inability to clear secretions (bedside, portable)
Suction equipment or other suction
management device
Generator/battery backup
Bowel Total assist Padded reclining shower/commode 1 1
chair (if roll-in shower available)
Bladder Total assist 1 1
Bed Mobility Total assist Full electric hospital bed with
Trendelenburg feature and side rails
Bed/Wheelchair Total assist Transfer board 1 1
Transfers Power or mechanical lift with sling
Pressure Relief/ Total assist; may be independent Power recline and/or tilt wheelchair
Positioning with equipment Wheelchair pressure-relief cushion
Postural support and head control
devices as indicated
Hand splints may be indicated
Specialty bed or pressure-relief
mattress may be indicated
Eating Total assist 1 1
Dressing Total assist 1 1
Grooming Total assist 1 1
Bathing Total assist Handheld shower 1 1
Shampoo tray
Padded reclining shower/commode
chair (if roll-in shower available)
Wheelchair Manual: Total assist Power recline and/or tilt wheelchair 6 1
Propulsion Power: Independent with equipment with head, chin, or breath control
and manual recliner
Vent tray
Standing/ Standing: Total assist
Ambulation Ambulation: Not indicated
Communication Total assist to independent, depending Mouth stick, high-tech computer
on work station setup and access, environmental control unit
equipment availability Adaptive devices everywhere as
indicated
Transportation Total assist Attendant-operated van (e.g., lift,
tie-downs) or accessible public
transportation
continued on next page
92 INTRODUCTION

TABLE 5.3
Expected Functional Outcomes, LEVEL C1-3 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Homemaking Total assist


Assist Required 24-hour attendant care to 24* 24*
include homemaking
Able to instruct in all aspects of care

LEVEL C4

Functionally relevant muscles innervated: Upper trapezius, diaphragm, cervical paraspinal muscles
Movement possible: Neck flexion, extension, rotation, scapular elevation, inspiration
Patterns of Weakness: Paralysis of trunk, upper extremities, lower extremities; inability to cough, endurance and
respiratory reserve low secondary to paralysis of intercostals
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory May be able to breathe without If not ventilator free, see C1-3 for
a ventilator equipment requirements
Bowel Total assist Reclining shower/commode chair 1 1
(if roll-in shower available)
Bladder Total assist 1 1
Bed Mobility Total assist Full electric hospital bed with
Trendelenburg feature and side rails
Bed/Wheelchair Total assist Transfer board 1 1
Transfers Power or mechanical lift with sling
Pressure Relief/ Total assist; may be independent Power recline and/or tilt wheelchair
Positioning with equipment Wheelchair pressure-relief cushion
Postural support and head control
devices as indicated
Hand splints may be indicated
Specialty bed or pressure-relief
mattress may be indicated
Eating Total assist 1 1
Dressing Total assist 1 1
Grooming Total assist 1 1
Bathing Total assist Shampoo tray 1 1
Handheld shower
Padded reclining shower/commode
chair (if roll-in shower available)
Wheelchair Power: Independent Power recline and/or tilt wheelchair 6 1
Propulsion Manual: Total assist with head, chin, or breath control and
manual recliner
Vent tray
OUTCOMES FOLLOWING SPINAL CORD INJURY 93

TABLE 5.3
Expected Functional Outcomes, LEVEL C4 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Standing/ Standing: Total assist Tilt table


Ambulation Ambulation: Not usually indicated Hydraulic standing table
Communication Total assist to independent, depending Mouth stick, high-tech computer
on work station setup and equipment access, environmental control unit
availability
Transportation Total assist Attendant-operated van (e.g., lift,
tie-downs) or accessible public
transportation
Homemaking Total assist
Assist Required 24-hour care to include homemaking 24* 24*
Able to instruct in all aspects of care

LEVEL C5

Functionally relevant muscles innervated: Deltoid, biceps, brachialis, brachioradialis, rhomboids, serratus anterior
(partially innervated)
Movement possible: Shoulder flexion, abduction, and extension; elbow flexion and supination, scapular adduction and
abduction
Patterns of Weakness: Absence of elbow extension, pronation, all wrist and hand movement. Total paralysis of trunk
and lower extremities
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Low endurance and vital capacity


secondary to paralysis of intercostals;
may require assist to clear secretions
Bowel Total assist Padded shower/commode chair or 1 1
padded tub transfer bench with
commode cutout
Bladder Total assist Adaptive devices may be indicated 1 1
(electric leg bag emptier)
Bed Mobility Some assist Full electric hospital bed with
Trendelenburg feature with
patients control
Side rails
Bed/Wheelchair Total assist Transfer board 1 1
Transfers Power or mechanical lift

continued on next page


94 INTRODUCTION

TABLE 5.3
Expected Functional Outcomes, LEVEL C5 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Pressure Relief/ Independent with equipment Power recline and/or tilt wheelchair
Positioning Wheelchair pressure-relief cushion
Hand splints
Specialty bed or pressure-relief mattress
may be indicated
Postural support devices
Eating Total assist for setup, then independent Long opponens splint 5 5
eating with equipment Adaptive devices ad indicated
Dressing Lower extremity: Total assist Long opponens splint 1 1
Upper extremity: Some assist Adaptive devices as indicated
Grooming Some to total assist Long opponens splints 13 1
Adaptive devices as indicated
Bathing Total assist Padded tub transfer bench or 1 1
shower/commode chair
Handheld shower
Wheelchair Power: Independent Power: Power recline and/or tilt with 6 6
Propulsion Manual: Independent to some assist arm drive control
indoors on noncarpet, level surface; Manual: Lightweight rigid or folding
some to total assist outdoors frame with handrim modifications
Standing/ Total assist Hydraulic standing frame
Ambulation
Communication Independent to some assist after Long opponens splint
setup with equipment Adaptive devices as needed for page
turning, writing, button pushing
Transportation Independent with highly specialized Highly specialized modified van
equipment; some assist with accessible with lift
public transportation; total assist for
attendant-operated vehicle
Homemaking Total assist
Assist Required Personal care: 10 hours/day 16* 23*
Homecare: 6 hours/day
Able to instruct in all aspects of care
OUTCOMES FOLLOWING SPINAL CORD INJURY 95

TABLE 5.3
Expected Functional Outcomes, LEVEL C6

Functionally relevant muscles innervated: Clavicular pectoralis supinator; extensor carpi radialis longus and brevis,
serratus anterior, latissimus dorsi
Movement possible: Scapular protractor, some horizontal adduction, forearm supination, radial wrist extension
Patterns of Weakness: Absence of wrist flexion, elbow extension, hand movement. Total paralysis of trunk and lower
extremities
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Low endurance and vital capacity


secondary to paralysis of intercostals;
may require assist to clear secretions
Bowel Some to total assist Padded tub bench with commode 12 1
cutout or padded shower/commode
chair
Other adaptive devices as indicated
Bladder Some to total assist with equipment; Adaptive devices as indicated 12 1
may be independent with leg bag
emptying
Bed Mobility Some assist Full electric hospital bed
Side rails
Full to king standard bed may
be indicated
Bed/Wheelchair Level: Some assist to independent Transfer board 3 1
Transfers Uneven: Some to total assist Mechanical lift
Pressure Relief/ Independent with equipment and/or Power recline wheelchair
Positioning adapted techniques Wheelchair pressure-relief cushion
Postural support devices
Pressure-relief mattress or overlay
may be indicated
Eating Independent with or without Adaptive devices as indicated 56 5
equipment; except cutting, which (e.g., U-cuff, tenodesis splint, adapted
is total assist utensils, plate guard)
Dressing Independent upper extremity; some Adaptive devices as indicated 13 2
assist to total assist for lower extremities (e.g., button, hook, loops on zippers,
pants, socks, Velcro on shoes)
Grooming Some assist to independent Adaptive devices as indicated 36 4
with equipment (e.g., U-cuff, adapted handles)
Bathing Upper body: Independent Padded tub transfer bench or 13 1
Lower body: Some to total assist shower/commode chair
Adaptive devices as needed
Handheld shower
Wheelchair Power: Independent with standard Power: May require power recline or 6 6
Propulsion arm drive on all surfaces standard upright power wheelchair
Manual: Independent indoors; Manual: Lightweight rigid or folding
some to total assist outdoors frame with modified rims
continued on next page
96 INTRODUCTION

TABLE 5.3
Expected Functional Outcomes, LEVEL C6 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Standing/ Standing: Total assist Hydraulic standing frame


Ambulation Ambulation: Not indicated
Communication Independent with or without equipment Adaptive devices as indicated
(e.g., tenodesis splint, writing splint
for keyboard use, button pushing,
page turning, object manipulation)
Transportation Independent driving from wheelchair Modified van with lift
Sensitized hand controls
Tie-downs
Homemaking Some assist with light meal preparation; Adaptive devices as indicated
total assist for all other homemaking
Assist Required Personal care: 6 hours/day 10* 17*
Homecare: 4 hours/day

LEVEL C78

Functionally relevant muscles innervated: Latissimus dorsi, sternal pectoralis, triceps, pronator quadratus, extensor
carpi ulnaris, flexor carpi radialis, flexor digitorum profundus and superficialis, extensor communis, pronator/flexor/
extensor/abductor pollicis, lumbricals [partially innervated]
Movement possible: Elbow extension; ulnar/wrist extension, wrist flexion, finger flexions and extensions, thumb flexion/
extension/abduction
Patterns of Weakness: Paralysis of trunk and lower extremities, limited grasp release and dexterity secondary to partial
intrinsic muscles of the hand
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12
FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Low endurance and vital capacity


secondary to paralysis of intercostals;
may require assist to clear secretions
Bowel Some to total assist Padded tub bench with commode 14 1
cutout or shower commode chair
Adaptive devices as needed
Bladder Independent to some assist Adaptive devices as indicated 26 3
Bed Mobility Independent to some assist Full electric hospital bed or full to
king standard bed
Bed/Wheelchair Level: Independent With or without transfer board 37 4
Transfers Uneven: Independent to some assist

Pressure Relief/ Independent Wheelchair pressure-relief cushion


Positioning Postural support devices as indicated
Pressure-relief mattress or overlay
may be indicated
OUTCOMES FOLLOWING SPINAL CORD INJURY 97

TABLE 5.3
Expected Functional Outcomes, LEVEL C78 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Eating Independent Adaptive devices as indicated 67 6


Dressing Independent upper extremities; Adaptive devices as indicated 47 6
independent to some assist lower
extremities
Grooming Independent Adaptive devices as indicated 67 6
Bathing Upper body: Independent Padded tub transfer bench or 36 4
Lower extremity: Some assist to shower/commode chair
independent Handheld shower
Adaptive devices as needed
Wheelchair Manual: Independent all indoor Manual: Rigid or folding lightweight or 6 6
Propulsion surfaces and level outdoor terrain; folding wheelchair with modified rims
some assist with uneven terrain
Standing/ Standing: Independent to some assist Hydraulic or standard standing frame
Ambulation Ambulation: Not indicated
Communication Independent Adaptive devices as indicated
Transportation Independent car if independent with Modified vehicle
transfer and wheelchair loading/ Transfer board
unloading; independent driving
modified van from captains seat
Homemaking Independent light meal preparation Adaptive devices as indicated
and homemaking; some to total
assist for complex meal prep and
heavy housecleaning
Assist Required Personal care: 6 hours/day 8* 12*
Homecare: 2 hours/day

LEVEL T19

Functionally relevant muscles innervated: Intrinsics of the hand including thumbs, internal and external intercostals,
erector spinae, lumbricals, flexor/extensor/abductor pollicis
Movement possible: Upper extremities fully intact, limited upper trunk stability. Endurance increased secondary inner-
vation of intercostals.
Patterns of Weakness: Lower trunk paralysis. Total paralysis lower extremities
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Compromised vital capacity


and endurance
Bowel Independent Elevated padded toilet seat or padded 67 6
tub bench with commode cutout
continued on next page
98 INTRODUCTION

TABLE 5.3
Expected Functional Outcomes, LEVEL T19 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Bladder Independent 6 6
Bed Mobility Independent Full to king standard bed
Bed/Wheelchair Independent May or may not require transfer board 67 6
Transfers
Pressure Relief/ Independent Wheelchair pressure-relief cushion
Positioning Postural support devices as indicated
Pressure-relief mattress or overlay may
be indicated
Eating Independent 7 7
Dressing Independent 7 7
Grooming Independent 7 7
Bathing Independent Padded tub transfer bench or 67 6
shower/commode chair
Handheld shower
Wheelchair Independent Manual rigid or folding lightweight 6 6
Propulsion wheelchair
Standing/ Standing: Independent Standing frame
Ambulation Ambulation: Typically not functional
Communication Independent
Transportation Independent in car, including loading Hand controls
and unloading wheelchair
Homemaking Independent with complex meal prep
and light housecleaning; total to
some assist with heavy housekeeping
Assist Required Homemaking: 3 hours/day 3* 3*

LEVEL T10L1

Functionally relevant muscles innervated: Fully intact intercostals, external obliques, rectus abdominis
Movement possible: Good trunk stability
Patterns of Weakness: Paralysis of lower extremities
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Intact respiratory function


Bowel Independent Padded standard or raised padded 67 6
toilet seat
Bladder Independent 6 6
Bed Mobility Independent Full to king standard bed 7
OUTCOMES FOLLOWING SPINAL CORD INJURY 99

TABLE 5.3
Expected Functional Outcomes, LEVEL T10L1 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Bed/Wheelchair Independent 7
Transfers
Pressure Relief/ Independent Wheelchair pressure-relief cushion
Positioning Postural support devices as indicated
Pressure-relief mattress or overlay
may be indicated
Eating Independent 7 7
Dressing Independent 7 7
Grooming Independent 7 7
Bathing Independent Padded tub transfer bench 67 6
Handheld shower
Wheelchair Independent all indoor and Manual rigid or folding lightweight 6 6
Propulsion outdoor surfaces wheelchair
Standing/ Standing: Independent Standing frame
Ambulation Ambulation: Functional, some assist Forearm crutches or walker
to independent Knee, ankle, foot orthosis (KAFO)
Communication Independent
Transportation Independent in car, including loading Hand controls
and unloading wheelchair
Homemaking Independent with complex meal
prep and light housecleaning; some
assist with heavy housekeeping
Assist Required Homemaking: 2 hours/day 2* 2*

LEVEL L2S5

Functionally relevant muscles innervated: Fully intact abdominals and all other trunk muscles; depending on level,
some degree of hip flexors, extensors, abductors, adductors; knee flexors, extensors; ankle dorsi flexors, plantar flexors
Movement possible: Good trunk stability. Partial to full control lower extremities
Patterns of Weakness: Partial paralysis lower extremities, hips, knees, ankle, foot
FIM/Assistance Data: Exp  Expected FIM Score
Med  NSCISC Median
NSCISC Sample Size: FIM  15 Assist  12
FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Respiratory Intact function


Bowel Independent Padded toilet seat 67 6
Bladder Independent 6 6
Bed Mobility Independent
Bed/Wheelchair Independent Full to king standard bed 7 7
Transfers
continued on next page
100 INTRODUCTION

TABLE 5.3
Expected Functional Outcomes, LEVEL L2S5 (continued)

FIM/ASSISTANCE
DATA
EXPECTED FUNCTIONAL OUTCOMES EQUIPMENT EXP MED

Pressure Relief/ Independent Wheelchair pressure-relief cushion


Positioning Postural support devices as indicated
Eating Independent 7 7
Dressing Independent 7 7
Grooming Independent 7 7
Bathing Independent Padded tub bench 7 7
Handheld shower
Wheelchair Independent all indoor and Manual rigid or folding lightweight 6 6
Propulsion outdoor surfaces wheelchair
Standing/ Standing: Independent Standing frame
Ambulation Ambulation: Functional, independent Knee, ankle, foot orthosis or ankle-foot
to some assist orthosis
Forearm crutches or cane as indicated
Communication Independent
Transportation Independent in car, including loading Hand controls
and unloading wheelchair
Homemaking Independent: complex cooking and
light housekeeping; some assist with
heavy housekeeping
Assist Required Homemaking: 01 hour/day 01* 0*

*Hours per day


Adapted from Outcomes Following Traumatic SCI: Clinical Practice Guidelines for Health-Care Professionals (12).

Patients with a C4 NLI may be able to breathe without munity mobility, at the C78 levels, a manual chair is typ-
a ventilator. They are generally dependent for all other ically used.
functional activities. Individuals with paraplegia have the potential to be
At the C5 NLI, individuals need less assistance for independent in all self-care activities, as well as with
activities of daily living. For some activities, such as eat- bowel and bladder management. The amount of assis-
ing and upper-extremity dressing, they may require assis- tance required for housekeeping declines with a more cau-
tance with setup but then are able to complete tasks. At dal NLI. Finally, ambulation is dependent on the level of
this level, the use of specialized adaptive devices becomes NLI. Patients with NLI above T10 typically do not ambu-
critical in determining the level of assistance required to late in a functional manner. At the T10L2 levels, func-
perform various dressing, eating, and grooming activities. tional ambulation is possible but will probably entail a
The use of a manual chair with handrim projections is a high energy cost if a swing-through gait pattern is
possibility at this level, although some assistance will required. Thus, at these levels, even an individual capa-
likely be required for propulsion outdoors, up inclines, or ble of walking may still elect to use a wheelchair as a more
on a rough surface. efficient means of mobility.
At the lower cervical levels, C6 and C78, individ- Because expected functional outcomes are general-
uals will still likely need assistance with bowel and blad- ized, it is important for providers and patients to be alert
der management, but they have the capability to be inde- to individual circumstances that may limit the realization
pendent with nearly all other functional activities (with of the stated outcomes. Patient motivation and training
appropriate adaptive equipment). Although patients with play a large role in the ability to attain a certain functional
a C6 level may still need a power wheelchair for com- level. Additionally, physical limitations or concomitant
OUTCOMES FOLLOWING SPINAL CORD INJURY 101

conditions may limit function. For example, patients with A reciprocal gait pattern can be utilized when there
a NLI of C6 can typically attain independence in sliding is pelvic control with at least 3/5 strength in the hip flex-
board transfers. If, however, there is an elbow flexion con- ors and in one quadriceps (16). This gait allows for knee
tracture, independence will be delayed until full elbow stability without the use of a knee-ankle-foot orthosis
extension is achieved. Similarly, whereas patients with (KAFO). Although a reciprocal gait pattern requires less
paraplegia can become independent in dressing activities, energy than a swing-through pattern, the rate of energy
they will be limited if they do not have adequate range of expenditure is still higher than that demonstrated by able-
motion in the hamstrings. In addition to conditions that bodied subjects.
may limit range of motion (i.e., contractures, joint defor- When the population of individuals with SCI is stud-
mities, heterotopic bone), other factors that can affect ied as a whole, experts generally agree that a minority of
achievement of optimal function include patient age, level individuals are able to ambulate following SCI. The pro-
of physical conditioning and potential for conditioning, portion of patients who are able to ambulate following a
length of time since injury, family support, spasticity, obe- SCI does, however, vary with the level and completeness
sity, and other medical complications. of injury. Daverat and co-workers reported that 28 per-
cent of 157 patients with SCI were functional walkers
1 year following injury (17). Of those with cervical lesions,
Ambulation
24 percent were functional walkers compared to 38 per-
A primary concern of SCI patients (and their families) is cent in the individuals with paraplegia. Maynard and asso-
whether they will be able to walk following an injury. ciates reported that among patients with tetraplegia, 47
Ambulation, like other functional outcomes, is dependent percent of those with incomplete sensory deficit and 87
on many factors in addition to neurologic function. In percent of those with incomplete motor deficit were able
addition to the basic question of whether a patient will to walk (18). Burns and colleagues studied 105 patients
be able to ambulate or will rely solely on a wheelchair, with ASIA C or D tetraplegia and found that all patients
there is the complicating factor of the degree of ambula- with ASIA D tetraplegia were able to ambulate at discharge
tory function that can be attained. from inpatient rehabilitation. Among individuals with
Stauffer divided ambulatory status into four cate- ASIA C-type injuries, those younger than 50 years had a
gories: community ambulatory, household ambulatory, better prognosis for ambulation than those older than 50
exercise ambulatory, and nonambulatory (14). Commu- years (91 percent versus 42 percent, respectively) (19).
nity ambulators are able to transfer themselves out of bed Crozier estimated that 20 percent of patients who are
or a wheelchair and walk reasonable distances in and out motor complete and sensory incomplete are ambulatory
of the home without assistance from another person. (20). Waters and colleagues determined that only 5 per-
Household ambulators may or may not require assistance cent of patients with complete paraplegia, 76 percent of
with transfers from bed or wheelchair; they are able to those with incomplete paraplegia, and 46 percent of those
ambulate in the home with relative independence, but are with incomplete tetraplegia were able to attain community
unable to ambulate outside of the home for any signifi- ambulation at 1 year following injury (5,6,8). No patients
cant distance. These individuals frequently use a wheel- with complete tetraplegia were able to ambulate.
chair for mobility outside the home. The exercise ambu- Hussey and Stauffer determined that there is a direct
lator attains functional mobility with a wheelchair and relationship between lower extremity strength and the
can ambulate only under closely controlled conditions. ability to ambulate (16). They reported that pelvic con-
Considerable physical assistance is also required to ambu- trol with at least fair hip extensor strength and at least
late. Individuals who are nonambulators rely exclusively fair strength in one knee extensor is required for com-
on a wheelchair. Both community and household ambu- munity ambulation with a reciprocal gait pattern.
lation are considered functional ambulation, whereas Crozier and colleagues reported on two measures
exercise ambulation is considered nonfunctional. that they found to be predictive of ability to ambulate
The type of gait pattern utilized depends on the (20). These investigators performed initial neurologic
degree of neurologic loss. A swing-through gait pattern examinations 72 hours following injury and found that
requires arm and shoulder girdle strength sufficient to lift among individuals with motor complete injuries, those
the weight of the entire body and swing it forward. This who had preserved pinprick as well as light touch sensa-
type of gait pattern requires a much higher rate of energy tion had an excellent prognosis for ambulation com-
expenditure and results in a substantially slower walk- pared to those with preservation of only light touch.
ing velocity (15). Thus, although an individual may uti- In another study, Crozier and coworkers studied
lize a swing-through gait pattern to negotiate architec- individuals with Frankel C (motor useless) injuries
tural barriers or to walk for exercise or psychologic (21). They studied recovery of the quadriceps muscle and
reasons, few employ this manner of ambulation as their reported that all patients who had achieved a quadriceps
primary mode of mobility. strength of at least 3/5 at 2 months following injury pro-
102 INTRODUCTION

gressed to become functional ambulators, whereas only Social Outcomes


2 of 8 patients who had not attained at least 3/5 by 2
Whereas rehabilitation has traditionally focused on sta-
months became functional ambulators. Thus, they con-
bilizing impairments and maximizing the ability to per-
cluded that the quadriceps strength 2 months following
form functional activities, there is a gaining recognition
injury was predictive of ambulatory status.
of the importance of quality-of-life issues. Community
Waters and colleagues measured energy expenditure
integration and societal participation are important com-
during walking with instrumented crutches that measured
ponents of a subjective sense of well-being. The Craig
axial loading. They found that the motor scoring system
Handicap Assessment and Reporting Technique
utilized by the American Spinal Injury Association (ASIA)
(CHART) is one measure of the degree of patient partic-
was a simple clinical measure that also correlated strongly
ipation in the community (24). Whiteneck and associates
with walking ability (22). Individuals with ASIA lower
have established normative data for four groups of
extremity motor scores (LEMS) less than or equal to 20
patients: high tetraplegia with ASIA A, B, or C grades;
were limited ambulators. These patients had slower aver-
low tetraplegia with ASIA A, B, or C grades; paraplegia
age velocities, higher heart rates, subsequent greater energy
with ASIA A, B, or C grades; and all patients with ASIA
expenditure, and greater axial loading exerted on assistive
D grades. As expected, the physical and mobility com-
devices when compared to patients with LEMS of  30
ponents of the CHART are lowest for those with tetraple-
who attained community ambulation status. Individuals
gia compared to paraplegia and patients with D grade
with LEMS of  30 ambulated with physiologic parame-
injuries. However, in the social component of the
ters close to those demonstrated by able-bodied subjects.
CHART, even individuals with high tetraplegia demon-
Early determination of LEMS was also found to be
strated a score of 89 points out of a total of 100 points.
predictive of ambulatory function 1 year following injury.
Dijkers found no statistically significant relationship
Waters et al. determined the LEMS on admission to the
between quality of life and impairment (25). This inves-
rehabilitation setting and found that when patients were
tigator determined that the effect of social role barriers
categorized by level and completeness of injury, the pro-
on quality of life was stronger than the influence of activ-
portion of those who were ambulatory 1 year following
ity limitations. Quality of life has also been associated
injury increased as the initial LEMS increased (23) (see
with social support, social integration, and family roles
Table 5.4). For example, among incomplete paraplegics,
as well as with mobility and occupation (25).
33 percent of those with an initial LEMS of 0 ambulated,
Tate and colleagues found that improvements in
compared to 70 percent of those with LEMS between 1
subjective well-being could result in fewer secondary com-
and 9, and 100 percent for those with LEMS above 10.
plications, activity limitations, and social role barriers.
Because the LEMS represents strength in some of the key
This was attributed to increased involvement in self-care
muscles involved in ambulation, it follows that a higher
and health maintenance behaviors (26).
initial LEMS is predictive of successful ambulation.
The Diener Satisfaction of Life Scale is an instrument
that can be used to describe well-being. This scale rates
5 items on a 1 to 7 point scale, with higher scores repre-
senting greater life satisfaction. When individuals with
SCI are grouped into four groups (as with the CHART
data), Diener scale scores range from 17.6 for those with
high tetraplegia to 21.1 for individuals with ASIA D
TABLE 5.4
injuries. These results again imply that impairment may
1-Year Follow-up Ambulation Status (23)
not be a significant prognosticator of well-being.
COMMUNITY AMBULATION
STATUS (1 YEAR)
CONCLUSION
LOWER EXTREMITY
ASIA MOTOR Detailed neurologic examinations performed approxi-
SCORE COMPLETE INCOMPLETE INCOMPLETE
mately 1 month following injury can provide data that
(1 MONTH) PARAPLEGIA PARAPLEGIA TETRAPLEGIA
can be used to reliably predict neurologic recovery at 1
year. Using data on motor function in complete patients,
0 1% 33% 0%
110 45% 70% 21% expected functional outcomes have been determined.
1120 100% 63% When considering expected functional outcomes, it is cru-
 20 100% 100% cial that individual patient characteristics are carefully
Total 5% 76% 47% evaluated, because they will affect the actual level of func-
tion that a patient can attain.
OUTCOMES FOLLOWING SPINAL CORD INJURY 103

Finally, although motor function affects functional plete cervical spinal cord injured patients. Arch Phys Med Reha-
bil 1990; 71:562565.
outcomes following SCI, self-reported quality of life is not 12. Outcomes Following Traumatic Spinal Cord Injury: Clinical Prac-
necessarily affected. Therefore, although prognosis of tice Guidelines for Health-Care Professionals. Consortium for
functional outcomes is a key factor in setting realistic Spinal Cord Medicine. Paralyzed Veterans of America, 1999.
13. Graves DE, Frankiewicz RG, Carter E. Gain in functional ability
goals and implementing effective rehabilitation programs, during medical rehabilitation as related to rehabilitation process
psychosocial needs and expected outcomes must also be indices and neurologic measures. Arch Phys Med Rehabil 1999;
considered to plan any needed interventions to maximize 80:14641470.
14. Stauffer ES. Study of 100 Paraplegics. Rancho Los Amigos Papers,
a patients life satisfaction. 1968.
15. Waters RL, Lunsford BR. The energy cost of paraplegic locomo-
tion. JBJS 1985; 67A:12451250.
References 16. Hussey RW, Stauffer ES. Spinal Cord Injury: Requirements for
ambulation. Arch Phys Med Rehabil 1973; 54:544547.
1. The National SCI Statistical Center. Spinal Cord Injury: Facts and 17. Daverat P, Sibrac MC, Dartigues JF, Mazaux JM, Marit E,
Figures at a Glance. Birmingham: University of Alabama at Birm- Debelleix X, Barat M. Early prognostic factors for walking in
ingham National SCI Center, April 1999. spinal cord injuries. Paraplegia 1988; 26: 255261.
2. Brown PJ, Marino RJ, Herbison GJ, et al. The 72-hour examina- 18. Maynard FM, Reynolds GG, Fountain S, et al. Neurologic prog-
tion as a predictor of recovery in motor complete quadriplgia. nosis after traumatic quadriplegia. J Neurosurg 1979;
Arch Phys Med Rehabil 1991; 2:546548. 50:611616.
3. Herbison GJ, Zerby SA, Cohen ME, et al. Motor power difference 19. Burns SP, Golding DG, Rolle WA, Graziani V, Dittuno JF. Recov-
within the first two weeks post-SCI in cervical spinal cord quad- ery of ambulation in motor incomplete tetraplegia. Arch Phys Med
riplegic subjects, J Neurotrauma 1991; 9:373380. Rehabil 1997; 78:11691172.
4. Mange KC, Ditunno JF, Herbison GJ, et al. Recovery of strength 20. Crozier KS, Graziani V, Ditunno JF, Herbison GJ. Spinal cord
at the zone of injury in motor complete and motor incomplete cer- injury: Prognosis for ambulation based on sensory examination
vical spinal cord injured patients. Arch Phys Med Rehabil 1990; in patients who are initially motor complete. Arch Phys Med
71:562565. Rehabil 1991; 72:119121.
5. Waters RL, Yakura JS, Adkins RH, Sie I. Recovery following com- 21. Crozier, KS. Cheng LL, Graziani V, Zorn G, Herbison G, Ditunno
plete paraplegia. Arch Phys Med Rehabil 1992; 73:784-789. JF. Spinal cord injury: Prognosis for ambulation based on quadri-
6. Waters RL, Yakura JS, Adkins RH, Sie I. Motor and sensory recov- ceps recovery. Paraplegia 1992; 30:762767.
ery following incomplete paraplegia. Arch Phys Med Rehabil 22. Waters RL, Adkins R, Yakura J, Vigil D. Prediction of ambulatory
1994; 75:67-72. performance based on motor scores derived from standards of the
7. Waters RL, Yakura JS, Adkins RH, Sie I. Motor and sensory recov- American Spinal Injury Association. Arch Phys Med Rehabil
ery following complete tetraplegia. Arch Phys Med Rehabil 1993; 1994; 75:756760.
4:242247. 23. Waters RL, Yoshida GM. Prognosis of spinal cord injuries. In:
8. Waters RL, Yakura JS, Adkins RH, Sie I. Motor and sensory recov- Levine AM (ed.), Orthopaedic Knowledge Update, Trauma.
ery following incomplete tetraplegia. Arch Phys Med Rehabil American Academy of Orthopaedic Surgeons, 303310, 1996.
1994; 75:306311. 24. Whiteneck GG, Charlifue SW, Gerhart KA et al. Quantifying
9. Marino RJ, Dittuno JF, Donovan WH, Maynard F. Neurologic handicap: A new measure of long-term rehabilitation outcomes.
recovery after traumatic spinal cord injury: Data from the model Arch Phys Med Rehabil 1992; 73:519526.
spinal cord injury systems. Arch Phys Med Rehabil 1999; 25. Dijkers M. Quality of life after spinal cord injury: A meta-analy-
80:13911396. sis of the effects of diablement components. Spinal Cord 1997;
10. American Spinal Injury Association/International Medical Society 35:829840.
of Paraplegia (ASIA/IMSOP). International Standards for Neu- 26. Tate DG, Stiers W, Daugherty J et al. The effects of insurance ben-
rologic and Functional Classification of Spinal Cord Injury, efits coverage on functional and psychosocial outcomes after
Revised 1996. Chicago, IL: ASIA. spinal cord injury. Arch Phys Med Rehabil 1994; 75:407414.
11. Mange KC, Dittuno JF, Herbison GJ, Jaweed MM. Recovery of 27. Diener E, Emmons RA, Larson RJ, et al. The satisfaction with life
strength at the zone of injury in motor complete and motor incom- scale. J Personality Assessment 1985; 49:7174.
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II

ACUTE SPINAL CORD


INJURY MANAGEMENT
AND SURGICAL
CONSIDERATIONS
This Page Intentionally Left Blank
6
Prehospital Management
of Spinal Cord Injured
Patients

William Whetstone, M.D.

anagement of the spinal cord Evaluation

M injured (SCI) patient begins imme-


diately post-injury with the first
providers at the accident scene.
Many studies have demonstrated the critical role of the
The evaluation phase consists of the Advanced Trauma
Life Support (ATLS) emphasized primary and secondary
survey (4). The ABCDEs of the trauma primary survey
are: Airway maintenance with cervical spine control;
prehospital provider in both preventing extension of SCI
Breathing and ventilation; Circulation with hemorrhage
and in maximizing oxygenation and circulation to
control; Disability (neurologic status); and Exposure/
improve the chances of neurologic recovery. It has been
Environmental control (completely undressing the patient
previously estimated that 3 to 25 percent of SCIs occur
while preventing hyper- or hypothermia).
after the initial traumatic insult, either during transit or
After completing the primary survey, the prehospi-
early in the course of treatment (1). Over the last 20 years,
tal provider should perform an abbreviated secondary
there has been a dramatic improvement in prehospital
survey, which consists of a more detailed head to toe eval-
management and thus an improvement in the neurologic
uation of the injured patient. During this evaluation, it is
status of SCI patients arriving in the emergency depart-
of utmost importance to assume the patient has not only
ment. During the 1970s, the majority of SCI patients
an SCI, but also a potentially unstable spinal fracture.
arrived with complete cord lesions. This statistic, how-
Thus, all evaluation must take place with full spinal
ever, changed during the 1980s, when the majority of
immobilization. The prehospital spinal cord evaluation
patients were found to have incomplete lesions (2). Most
attempts to quickly identify injured areas. Obviously, it is
of this improvement lies in the development of the Emer-
important to note if the patient is complaining of neck
gency Medical Systems (EMS), which trains providers in
or back pain or has tenderness on palpation in those
proper extrication techniques and coordinates transfer to
areas. To evaluate the spine, the patient should be log-
a trauma center. In this chapter, the five responsibilities
rolled by three providers and the spine checked for bony
of prehospital care (evaluation, resuscitation, immobi-
tenderness or gross signs of trauma (Figure 6.1 and 6.2).
lization, extrication, and transportation) (3) are defined
A quick motor examination of grip strength and a foot
and discussed.
dorsiflexion evaluation, in addition to a gross sensory
examination should alert the prehospital provider to a
complete or partial cord injury. Signs of incontinence, uri-
107
108 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

FIGURE 6.1 FIGURE 6.2

Log-roll technique. One provider (designated log-roll leader) Log-roll technique. On leaders command, all three providers
at the head of the patient controls the head and cervical spine. roll patient in a single, fluid motion (carefully avoiding any
Meanwhile, two assistants with interlinked arms control trunk twisting motion). The fourth provider evaluates the thoracic
and lower body. and lumbar/sacral spine for tenderness.

nary retention, priapism, or loss of anal sphincter tone stabilization. Many authors have demonstrated that oro-
should be noted. Skin temperature and appearance should tracheal intubation with in-line stabilization (Figure 6.3)
also be evaluated. Warm, flushed skin suggests loss of is a safe method if performed by experienced personnel
sympathetic vascular tone below the injury. Even in the (57). In a cadaver model, Gerling et al. showed that intu-
absence of any of the above findings, the multi-trauma or bation with in-line stabilization did not cause any signif-
major trauma mechanism patient must be placed in a rigid icant vertebral body movement. Intubation attempts with
collar and backboard to be immobilized for transport. cervical collar immobilization, however, did produce a
significant amount of vertebral distraction. Thus, the cer-
vical collar should always be opened prior to attempted
RESUSCITATION intubation. If the airway cannot be secured following
three intubation attempts, the prehospital provider should
Resuscitation begins during the evaluation and primary be prepared to perform a surgical airway.
survey. Airway control is of the highest priority and Prehospital circulation resuscitation consists of
should start with the immediate application of oxygen aggressive intravenous access and proper fluid resuscita-
while the cervical spine is being immobilized. Initial air- tion. The cervical SCI patient may present with either neu-
way management includes the basic maneuvers of chin- rogenic or hemorrhagic shock. Neurogenic shock is the
lift, jaw thrust, and the placement of a nasal or oral air- result of an SCI at or above the fourth thoracic vertebra.
way. Suction should be available to remove blood, These injuries cause a loss of sympathetic peripheral vas-
secretions, and possible foreign bodies. If adequate oxy- cular tone and thus reduce central venous return. There
genation cannot be maintained and the paramedic crew is also an associated bradycardia caused by loss of sym-
is properly trained, the patient should be prepared for pathetic innervation to the heart and unopposed
intubation. Both blind nasotracheal intubation (assum- parasympathetic tone. This clinical picture is in contrast
ing the patient has no evidence of midface trauma) or oro- to the tachycardia associated with hemorrhagic hypoten-
tracheal intubation are considered appropriate, assuming sion. Both hemorrhagic and neurogenic shock may be ini-
that they are performed with proper in-line cervical spine tially treated by placing the patient in a spine-immobi-
PREHOSPITAL MANAGEMENT OF SPINAL CORD INJURED PATIENTS 109

findings must be validated in further randomized investi-


gations. Because there appears to be excellent agreement
between paramedics and physicians regarding clinical cer-
vical spine examinations, there may soon be new proto-
cols developed to clinically clear patients in the field. At
the present time, however, liberal use of prehospital spinal
immobilization is still considered the standard.

Preparation for Immobilization


At the scene of the injury, the provider should place the
patient in a neutral supine position. Using only gentle trac-
tion, and while locking hands under the jaw and neck, the
patients head should be moved into vertical alignment
with the body. This neutral position is critical to prevent
any further damage to the cord. When removing a patient
from a seated position, a cervical collar is first placed on
the patient. One provider is responsible for the head and
neck, while the other personnel help move the patients
body in a coordinated movement that keeps the head and
FIGURE 6.3 body in a neutral position. The patient is then immediately
placed on a backboard, while the person responsible for
In-line stabilization: With rigid collar open, assistant prevents the head continues to maintain in-line stabilization.
motion of head and neck while the patient is intubated.

Helmet Removal
lized Trendelenburg position (8). This maneuver helps to The on-site management of a neck-injured patient with
decrease the lower extremity pooling of blood and a helmet is different from that of other traumatic cervi-
increases central return. Bleeding from the neck or spinal cal spine injuries. Although the helmet causes the patients
area should be controlled by direct pressure. Large-bore neck to be slightly flexed (especially in the absence of
peripheral intravenous lines should be placed in antici- shoulder pads) and may be concealing life threatening
pation of saline and blood infusion. hemorrhage, its removal is not required in the field unless
airway problems exist. If the helmet must be removed for
airway access, the two-person technique recommended
IMMOBILIZATION by the American College of Surgeons should be used. One
provider maintains in-line immobilization, while the other
To prevent further SCI, all prehospital personnel must be provider gently removes the helmet (12).
well trained in the techniques of immobilization. All major
trauma victims, patients complaining of neck pain or neu-
Immobilizing the Injured Athlete
rologic symptoms, and any patient with altered mental sta-
tus of uncertain cause must be immobilized. Within these Unique management issues can arise when caring for the
liberal guidelines, cervical spine immobilization has injured athlete. They include on-field evaluation, immo-
become one of the most frequently performed prehospital bilization techniques, and removal of protective equip-
procedures (9). It is estimated that nearly 5 million patients ment. The first step in evaluating the athlete with a poten-
receive spinal immobilization annually, at a cost of $15 per tial cervical spine injury is the on-field evaluation. The
person (10). In addition to the cost, immobilization causes unconscious athlete should be carefully log-rolled into a
patient discomfort and increased paramedic scene time. supine position. The mouthpiece should be removed while
Recently Hauswald et al. (11) examined the effect of emer- the airway, breathing, and circulation are assessed. Pro-
gency out-of-hospital spinal immobilization on neurologic tective equipment (e.g., helmet and shoulder pads) should
injury by comparing trauma patients in Malaysia (no pre- be left in place until adequate immobilization of the head
hospital emergency medical services) with a group of and neck has occurred (13). Multiple studies have demon-
trauma patients in New Mexico (with prehospital spinal strated that immobilizing the neck-injured football player
immobilization.) Suprisingly, the unimmobilized with only the helmet or only the shoulder pads in place
Malaysian patients were found to have a lower rate of neu- causes significant cervical spine malalignment (1416). If
rologic disability. Although this study is intriguing, the protective equipment must be removed in the prehospital
110 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

setting, the American College of Surgeons recommends


using a team of three to four members. The helmet should
first be removed using a two-person technique (12). Shoul-
der pads also must be removed in an orderly manner, while
the head and neck are stabilized at the level of the torso.
The anterior and axillary straps should be cut first. The
head and thorax should then be elevated as a unit as the
shoulder pads are slid from under the athlete. Finally, the
patient should be lowered back down to the spinal board
with a cervical collar applied (15).

Technique of Immobilization
Because SCIs are likely to involve multiple levels, it is
imperative to immobilize the entire spine. The best FIGURE 6.5
method is to use a rigid board. The neck is first secured
with a rigid collar and sandbags are placed on each side Properly immobilized patient.
of the head. Alternatively, some paramedics prefer to use
a prefabricated immobilization kit with its own cushions
and sandbag equivalents (Figure 6.4). Tape and Velcro and transportation. The scene commander must take into
straps are placed over the patients forehead to prevent account geography, weather, man-made obstacles (pow-
flexion of the neck. It important to note that cervical col- erlines), distance to the designated trauma center, and other
lars alone are relatively ineffective in minimizing neck unique aspects of the accident scene. Some individual acci-
motion (17). Collars must be combined with taping to dent scenes will be easily accessible by EMS flight crews,
limit both flexion and extension (18,19). Following whereas other sites will be more rapidly accessed by
proper neck immobilization, the chest and abdomen are ground transport. As in all trauma situations, the com-
immobilized with seatbelts tightly fastened, yet allowing mander must aim to quickly stabilize the SCI patient, while
for inspiration (Figure 6.5). arranging for the most rapid transport to a trauma center.
Proper prehospital immobilization, resuscitation, and
transportation not only prevents further SCI, but maxi-
EXTRICATION AND TRANSPORTATION mizes the possibility of neurologic recovery.

Once the patient has been properly immobilized, the pre- References
hospital accident scene commander must make the deci-
1. Podolsky S, Baraff LJ, Simon RR. Efficacy of cervical spine immo-
sion regarding the safest and fastest method of extrication bilization methods. J Trauma 1983; 23: 461465.
2. Green B, Eismont F, and OHeir J. Spinal cord injury as systems
approach: Prevention, emergency medical services and emergency
room management. Crit Care Clin 1987: 3(3): 471493.
3. Soderstrom CA, Brumback RJ. Early care of the patient with cer-
vical spine injury. Orthop Clin North Am 1986; 17(1): 313.
4. American College of Surgeons. Advanced Trauma Life Support.
Chicago: American College of Surgeons, 1993.
5. Suderman VS, Crosby ET. Occasional review: Elective oral tra-
cheal intubation in cervical spine-injured adults. Can J Anesth
1991; 38:785791.
6. Shatney CH, Brunner RD, Nguyen TQ. The safety of orotrachael
intubatoin in patients with unstable cervical spine fracture or high
spinal cord injury. Am J Surg 1995; 170:676680.
7. Criswell JC, Parr MJA, Nolan JP. Emergency airway management
in patients with cervical spine injuries. Anaesthesia 1994; 49:
900903.
8. Hockberger RS, Kirshenbaum KJ, Doris PE. Spinal injuries. In:
Rosen P, (ed.), Emergency Medicine: Concepts and Clinical Prac-
tice, Vol. 1. St. Louis: Mosby, 1998: 462505.
9. DeLorenzo RA. A review of spinal immobilization techniques. J
Emerg Med 1996; 14: 603613.
10. Orledge JD, Pepe PE. Out of hospital immobilization: Is it really
FIGURE 6.4 necessary? Acad Emerg Med 1998; 5:203204.
11. Hauswald M, Ong G, Tandberg D. Out-of-hospital spinal immo-
Immobilization equipment: Rigid board, rigid collar, prefab- bilization: Its effect on neurologic injury. Acad Emerg Med 1998;
ricated immobilization kit with cushions and Velcro straps. 5: 214219.
PREHOSPITAL MANAGEMENT OF SPINAL CORD INJURED PATIENTS 111

12. McSwain N, Camelli R. Helmet removal from injured patients. 16. Donaldson W, Lauerman W, Heil B. Helmet and shoulder pad
In: American College of Surgeons Committee on Trauma. removal from a player with suspected cervical spine injury: A
Chicago: American College of Surgeons, 1997. cadaveric model. Spine 1998; 23: 17291733.
13. Warren W, Bailes J. On the field evaluation of athletic neck injury. 17. Rosen P, McSwain N, Arata M. Comparison of two new immo-
Clin Sports Med 1998; 17:99110. bilization collars. Ann Emerg Med 1992; 21:11891195.
14. Palumbo M, Hulstyn M, Fadale P. The effect of protective foot- 18. McGuire R, et al. Spinal instability and the log-rolling maneuver.
ball equipment on alignment of the injured cervical spine: Radi- H Trauma 1987; 27:525531.
ographic analysis in a cadaveric model. Am J Sports Med 1996; 19. Graziano A, Scheidel E, Cline J. A radiographic comparison of
24:446453. prehospital cervical immobilization methods. Ann Emerg Med
15. Gastel J, Palumbo M, Hulstyn M. Emergency removal of foot- 1987; 16:11271131.
ball equipment: A cadaveric cervical spine injury model. Ann
Emerg Med 1998; 32:411417.
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7
Acute Medical
Management of Spinal
Cord Injury

Cristina Barboi, M.D.


William T. Peruzzi, M.D.

he medical treatment of spinal cord normal rotation, and 65 percent of normal lateral bend-

T injury (SCI) patients starts from the


moment of initial evaluation.
Emphasis must be placed on assur-
ance of a clear airway, provision of adequate oxygenation
ing (2). Because of this, alternate forms of spinal immo-
bilization for patients judged to have marked spinal insta-
bility must be employed soon after intensive care unit
admission. Cervical spine immobilization is best achieved
and ventilation, and maintenance of appropriate spinal with a halo or tongs that are affixed to the skull and to
cord perfusion. Goals in the management of SCI patients a weight system that applies traction to the cervical ver-
include minimizing the neurologic damage caused during tebrae. The halo device allows less than 5 percent of nor-
the primary injury and preventing further cord injury sec- mal cervical spine motion. Although the halo device offers
ondary to hypoperfusion, ischemia, and biochemical and superior immobilization for many cervical injuries, its use
inflammatory changes. is not without risk, especially in elderly patients. Patients
may experience neck extension, and pulmonary function
and treatment may be compromised in the acute setting
VERTEBRAL COLUMN STABILIZATION (3). Patients with thoracic and lumbar injuries should be
kept supine and carefully moved, using a log-rolling tech-
Most injuries of the vertebral column do not result in nique, to avoid flexion or extension of the spine. They can
spinal cord damage, but traumatic spinal instability places be immobilized in standard beds, rotating beds, or turn-
the patient at risk for neurologic injury if the injured ing frames. Turning frames require considerable nursing
spinal segments are not protected. All trauma victims, expertise for safe and effective use. The use of turning
especially those complaining of neck or back pain, should frames by inexperienced personnel is likely to result in
be properly immobilized as quickly as possible. The cer- inadequate spinal stabilization. Respiratory status must
vical spine can be immobilized on a short-term basis with be carefully monitored, because many patients will not
a hard cervical collar, and sandbags should be placed on readily tolerate the prone position (4).
each side of the head. The most commonly used collars If the initial neurologic examination is suggestive of
are the Philadelphia or Miami J collars. These devices are SCI, or if the traumatic injury renders the patient uncon-
adequate for emergency use but may not be appropriate scious, the stability of the spine is determined with radi-
for long-term stabilization (1). Cervical collars allow 30 ologic studies. Throughout radiologic assessments,
percent of normal flexion and extension, 45 percent of patients should have their spine immobilized and extreme
113
114 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

care should be taken to avoid vertebral column move- necrotic tissue. These two phases of the cellular inflam-
ment. When there is radiologic evidence of vertebral col- matory response are implicated in the axonal demyeli-
umn bony or ligamentous displacement, the goal of man- nation that starts within 24 hours after injury and
agement is the realignment and fixation of the involved increases for several weeks (13).
segments. Indications for surgery include an unstable frac-
ture, a fracture that will not reduce with spinal traction,
gross spinal misalignment, evidence of cord compression CORTICOSTEROID THERAPY
in the presence of an incomplete injury, deteriorating neu-
rologic status, and persistent instability following con- Corticosteroids have been used in neurotrauma based on
servative management (57). in-vitro and animal studies that demonstrated their the-
The timing of surgical stabilization is controversial. oretical ability to stabilize membranes, inhibit lipid per-
Some favor early surgical stabilization because it has been oxydation, suppress vasogenic edema by restoring the
demonstrated that systemic complications in patients with blood-central nervous system (CNS) barrier, enhance the
SCI decrease if surgery is performed within 24 hours of spinal cord blood flow, inhibit pituitary endorphin
injury (8). Advocates of delayed surgery prefer to perform release, and attenuate the inflammatory response
a well-planned procedure on patients who are medically sta- (23,2528). Steroid therapy was chosen for clinical inves-
ble and whose neurologic status has reached a plateau (9). tigation in humans based on the extensive preclinical data
supporting its use (29). Methylprednisolone sodium suc-
cinate (MPSS) has been used in three randomized,
PHARMACOLOGIC MANAGEMENT prospective double-blinded multicenter clinical trials in
OF SPINE INJURIES patients with acute SCI. This agent is less likely to pro-
duce neutropenia and crosses cell membranes more
Aside from the mechanical factors that compromise spinal rapidly and completely than other steroids (26,30).
cord function, local tissue perfusion and oxygenation can In 1979, the first National Acute Spinal Cord Injury
profoundly modulate the extent of injury resulting from Study (NASCIS I) was begun and results were reported in
any given mechanical stress (10). Other processes that 1984. This study compared the efficacy of administering
take place at the site of injury such as edema, hemorrhage, 100 mg versus 1,000 mg of MPSS each day for a total of
axonal degeneration, or demyelination ultimately alter 10 days to patients with any motor or sensory deficit
the cellular bioenergetic mechanisms. Damage of the cord below the level of injury. The study found no difference
vessels produces leakage of plasma protein and leads to in the recovery of motor or sensory function between the
cord edema (11, 12) that will further diminish local spinal two groups at 6 weeks, 6 months, and 1 year after injury
cord blood flow (13). Mechanical injury or systemic coag- (31). However the beneficial or detrimental effects of
ulation abnormalities may lead to petechial hemorrhages steroid therapy could not be determined because of the
in the cord and thus impair spinal perfusion (11). Focal lack of a placebo group in the study protocol. Addition-
ischemia is compounded by systemic hypoxia or hypoten- ally, a trend towards a higher risk of complications was
sion, because autoregulation is lost in the region of injury noted in the high-dose steroid group.
and blood flow changes more directly with alterations in Between 1985 and 1988, the NASCIS II trial was
systemic hemodynamics (1012,14,15). At the cellular conducted, with the final year follow-up examination per-
level, the initial ischemic process is followed by the devel- formed in 1990. In this study, patients were randomized
opment of toxic levels of excitatory amino-acids (EAA) to receive MPSS (30 mg /kg bolus, then 5.4 mg/kg/h infu-
(16,17) an eight-time increase in the glutamate levels sion for 23 hours), naloxone (5.4 mg/kg bolus, then
(18,19), depletion of ATP stores (1820), and sustained 4mg/kg/h infusion for 23 hours), or placebo. Patients who
elevation of cytosolic calcium concentration, the final received a high-dose MPSS infusion within 8 hours of
pathway mediating cell death (16,21,22). Other processes spinal cord injury had better neurologic recovery at 6
that potentiate cell damage include an alteration of the weeks, 6 months, and after 1 year following injury when
ratio between thromboxane and prostacycline produc- compared with placebo or naloxone treated patients (32).
tion, lipid peroxydation and free radical production Those who received MPSS after 8 hours had worse neu-
(23,24), and the production of endogenous opioids and rologic function than the placebo group. This study has
pro-inflammatory cytokines. been criticized for deficiencies in experimental design and
Histopathologically, the region of injury demon- incomplete data reporting. The number of subgroups of
strates signs of inflammation caused by an early neu- patients treated within 8 hours could produce a statisti-
trophil invasion. These neutrophils release lytic enzymes cally significant result by chance alone (33). The initial
that further damage vascular, neuronal, and glial cells resuscitation protocols varied with each center, no func-
(25). This is followed by macrophage penetration, thus tional assessment scale was used as an outcome measure,
precipitating the phagocytosis of hemorrhagic and and no analysis of individual muscle group function to
ACUTE MEDICAL MANAGEMENT OF SPINAL CORD INJURY 115

determine the region of drug-induced improvement was ing wound infections, pneumonia, and gastrointestinal
performed (34). In 1995, two retrospective studies were bleeding. Careful observation for the development of
published and both failed to demonstrate improvement these complications and prompt initiation of treatment
in neurologic function after administration of MPSS in is essential.
SCI patients (35,36). Although all patients involved in
NASCIS II had blunt SCIs, the study results were inap-
21-Aminosteroids (Lazeroids)
propriately extrapolated by practicing clinicians to pen-
etrating injury, radicular, and cauda equina lesions. In The best-studied compound from this group of medica-
1997, a retrospective review of patients with gunshot tion is tirilazad mesylate, a 21-aminosteroid with potent
wounds to the spine treated with intravenous steroids antioxidant effects. In the NASCIS III trial, patients
demonstrated no neurologic benefit (37). The conse- receiving a 48-hour infusion of tirilazad had patterns of
quences of high-dose steroid therapy, particularly the rate motor recovery similar to those receiving MPSS infusion
of infectious complications, were analyzed and the inci- for 24 hours, but with fewer side effects (41). However,
dence of pneumonia was demonstrated to be 4 times because an initial bolus of MPSS was administered in
higher during the acute phase of spinal cord injury and patients who received TM, the role of TM in SCI is not
2.6 times higher overall, although this finding did not well defined (41).The 21-aminosteroids lack mineralo-
reach statistical significance (38). corticoid or glucocorticoid activity, but are more potent
In 1997, the third NASCIS was reported. This study inhibitors of iron-dependent lipid peroxydation than
analyzed the effects of the duration of MPSS therapy. All methylprednosolone (44). Tirilazad mesylate was well tol-
patients received MPSS 30 mg/kg via intravenous bolus, erated during NASCIS III trial. The observed secondary
and then patients were randomized to receive an infu- effects were nausea, abdominal pain, back ache, muscle
sion of MPSS at 5.4 mg/kg/h for 24 hours or 48 hours, twitching, and cramps (43). At present, MPSS and TM
or an infusion of tirilazad mesylate (48 TM), a lipid per- could be considered a reasonable alternative to conven-
oxydase inhibitor, for 48 hours. This trial was prompted tional MPSS treatment.
by the information that tirilazad offered superior free rad-
ical scavenger efficacy with little glucocorticoid activity
GM1 Ganglioside
(39). High doses of glucocorticoids might interfere with
neuronal protection by inhibiting immune cellular activ- Gangliosides are sialic acidcontaining glycolipids in cell
ity, thus exacerbating acute postischemic neuronal necro- membranes. These glycolipids promote neuronal sprout-
sis, and inhibiting axonal sprouting. The investigators ing, outgrowth, and synaptic transmission (13,42). A
acknowledged the fact that the timing of steroid therapy prospective, randomized, placebo-controlled, double-
may be a critical element in its ultimate efficacy. The blinded trial of GM-1 use in eighteen SCI patients showed
mechanism of lipid peroxydation inhibition may be lost that GM-1 enhances recovery of neurologic function at
if MPSS is administered more than 8 hours after the spine 1 year following injury when compared to patients receiv-
injury (29,30). ing placebo. The drug was administered within 48 hours
NASCIS III found that patients who were treated after injury and was continued for approximately 26
within 3 hours of injury had similar recovery at 6 weeks, days. The dose used in this trial was the highest approved
6 months, and after 1 year, whether they were treated for by the FDA for investigation in the United States. The sec-
24 or 48 hours. Patients whose treatment with MPSS ond multicenter GM-1 trial, enrolling hundreds of
started between 3 and 8 hours of injury had better motor patients, has yet to be published (34). Gangliosides can
and functional recovery if the infusion was continued for block some of the neuroprotective effects of MPSS by
48 hours. Patients started on MPSS more than 8 hours modulating the protein-kinase activity that inhibits
after injury did worse, in terms of neurologic outcome, lipocortins. Lipocortins are known for mediating the anti-
than the placebo group in NASCIS II trial, perhaps inflammatory effects of methylprednisolone (27). During
because of the lack of protective effect against lipid per- the early European use of this drug, a link with the devel-
oxidation (40). The conclusions of the NASCIS III trial opment of GuillainBarr syndrome was implicated, but
were that MPSS therapy, when started within 3 hours of further study failed to determine a clear association
spine injury, should be continued for 24 hours, and when (44,45). Other secondary effects include rash and pain
initiated between 3 and 8 hours should be continued for at the injection site (45).
48 hours unless there are complicating medical factors.
This protocol has gained widespread acceptance in clin-
Opiate Antagonists
ical practice, in part from medico-legal reasons and also
because steroids are a reasonable therapeutic idea with It is well documented that the local release of endogenous
treatable adverse effects. It must be appreciated that opioid peptides occurs after spine trauma, and there are
steroid therapy is associated with systemic effects includ- theoretical concerns regarding their contribution to sec-
116 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

ondary injury through an opioid receptormediated should have adequate volume resuscitation, as reflected
mechanism (42). The  and opioid receptors have been by their filling pressures and, if needed, vasopressor ther-
found to be the mediators of the pathophysiologic mech- apy. The ideal MAP necessary to maximize spinal cord
anisms implicated in cord injury, but precisely which opi- perfusion after acute injury is not known, but a high nor-
oids and which receptors are involved remains the sub- mal MAP range of 80 to 100 mmHg has been selected
ject of debate (42). Endogenous opioids released in based on clinical experience with patients suffering cere-
response to shock alter the autonomic tone by inhibiting bral ischemia. Intensive care unit monitoring is a priority,
the dopaminergic system and produce depression of the because pulmonary edema from aggressive volume reple-
cardiovascular system. Opioid antagonists, therefore, tion must be avoided.
may prevent this systemic hypotension, thus improving
spinal cord microcirculation (48,49). In the NASCIS II
trial, naloxone initially failed to demonstrate any clini- AIRWAY MANAGEMENT
cal benefit compared with placebo, but subsequent
reanalysis of the data indicated that naloxone improved Airway management in patients with cervical spine (c-
functional recovery when administered within 8 hours spine) injury requires skill and expertise. Alert trauma
of injury (26,30). Further studies are needed to define the patients who report neck pain or tenderness may be eval-
appropriate drug dosing schedule and the optimal tim- uated for SCI. Those who are alert and do not complain
ing of opiate antagonist therapy. of neck pain or tenderness should not have cervical injury
Other pharmacologic agents have been used in and should not require further c-spine evaluation, neck
experimental SCI, but their clinical efficacy is still to be immobilization, or special precautions during airway
proved. Excitatory amino acid receptor antagonists, management. These are very stringent criteria; and if there
specifically n-methyl-d-aspartate (NMDA) GK 11, are is the slightest neck discomfort, depressed consciousness,
currently under evaluation (40). The administration of or other painful injuries, c-spine precautions must be
calcium channel antagonists after SCI is controversial maintained until the absence of injury is demonstrated.
(21). Thyrotropine-releasing hormone (TRH), platelet- SCI patients require establishment of a definitive
activating factor antagonists, free radical scavengers, and endotracheal airway in the following circumstances: a)
4-aminopyridine continue to be investigated as potential diminished or absent airway protective mechanisms
treatments of acute SCI (40,42,45). because of coexistent intracranial injury or other pathol-
ogy; b) evidence of airway obstruction in the context of
multiple trauma; c) acute respiratory failure in patients
AXONAL REGENERATION with injuries at or above C4 who lack diaphragmatic
function and in patients with coexistent thoracoabdom-
Experimental studies in neurobiology are exploring the inal trauma; d) inability to cough, clear secretions, and
potential of an injured spinal cord for regrowth. Embry- participate in bronchial hygiene maneuvers secondary to
onic spinal cord transplantation (50), transplantation of the reductions in forced expiratory volume and forced
Schwann cells (51), monoclonal antibodies against myelin vital capacity that develop with loss of intercostal and
(52), and gene therapy that promotes axonal regenera- abdominal muscle activity. Once a cervical injury is sus-
tion (53) are promising studies that open a new chapter pected, the vertebral column should be immobilized.
in the management of SCI. Options for relieving upper airway obstruction
include chin lift, jaw thrust continuous positive airway
pressure, or nasal or oral airway insertion. The use of chin
MINIMIZING THE SECONDARY INJURY lift and jaw thrust is discouraged in the setting of poten-
tial spinal instability, because this maneuver may cause a
The inciting events that lead to SCI are followed by a more than 5 mm widening of the disk space and C56
series of detrimental hemodynamic and biochemical instability (54). This instability is not diminished by a
processes that can be mitigated by early and aggressive rigid collar. On the other hand, oral or nasopharyngeal
medical management. Below the level of injury, the spinal airway insertion produces minimal cervical spine move-
cord is often hypoperfused because of the associated neu- ment. Bag and mask ventilation provides oxygenation but
rogenic shock, hemorrhage, vasospasm, or thrombosis. is not a long-term airway control method.
The posttraumatic hemorrhage and edema is followed by Endotracheal intubation should be performed while
axonal and neuronal necrosis (14). The goal in treating maintaining an immobile spine. One method to immobi-
post SCI hypotension is to restore the mean arterial pres- lize the neck during laryngoscopy and oral tracheal intu-
sure (MAP) to normal levels. Hypertension should be bation is manual in-line axial stabilization (MIAS). Dur-
avoided because of the theoretic risk of enhancing ing direct laryngoscopy, the cervical movement is
intramedullary hemorrhage and edema (14). All patients concentrated at the occipitoatlantoaxial complex and, in
ACUTE MEDICAL MANAGEMENT OF SPINAL CORD INJURY 117

normal patients and volunteers, there is minimal move- ization, more commonly using the fiberoptic technique,
ment below C3 (5557). Thus, patients with unstable C1 or after administering intravenous anesthetics and mus-
or C2 injuries might be the most vulnerable to neurologic cle relaxants. Before administering intravenous medica-
damage from atlanto-occipital extension. MIAS reduces tions, the physician must make sure that ventilation by
by 60 percent atlanto-occipital extension and flexion in the mask can be adequately performed. If mask ventilation
lower cervical spine. Sudden worsening of the neurologic and direct laryngoscopy are expected to be difficult or
deficits has been reported when traction is applied for spine there is coexistent facial trauma, the practitioner must
stabilization or to expose C7 on radiographs (58). Over be prepared to secure the airway using a surgical tech-
the past decade, there have been five reports of SCI fol- nique (e.g., cricothyroidotomy) (62).
lowing direct laryngoscopy and tracheal intubation (59). When manipulating the airway of an SCI patient,
Difficult or failed tracheal intubation is another dan- the practitioners goal must be to maintain adequate
ger of direct laryngoscopy in patients with potential SCI. spinal cord blood flow and spinal cord perfusion pressure
MIAS prevents complete alignment of the mouth and (SCPP). SCPP depends on MAP, cerebrospinal fluid (CSF)
glottis, and the person stabilizing the neck is in the way pressure, and the pressure in the spinal canal or dural sac.
of the laryngoscopist. Therefore, spine immobilization is The clinician should also remember that the autoregula-
associated with a high incidence of poor glottic visual- tion of blood flow to damaged neurologic tissue might be
ization during conventional laryngoscopy. Facial and absent (63), so SCPP becomes dependent on MAP. All the
neck trauma and the prevertebral swelling associated with intravenous anesthetic agents that are administered before
cervical spine injury can increase the difficulty of laryn- intubation have the potential to decrease the MAP to lev-
goscopy. Rigid fiberoptic devices (e.g., Bullard laryngo- els that compromise the SCPP; thus, judicious dosages
scope) have been successfully used to intubate the trachea adjusted to a patients specific hemodynamic profile
in patients with cervical spine injury; these devices require should be utilized. The CSF pressure can increase with
less neck movement than direct laryngoscopy using the alterations of the spinal cord curvature, thus decreasing
McIntosh or Miller laryngoscope blades (60). The inci- the SCPP by as much as 20 mmHg (64).
dence of grade 3 and 4 laryngeal views ranges from 22 In conclusion, maintaining the head and neck in neu-
to 34 percent, when using MIAS in paralyzed, anes- tral position; performing the intubation technique with
thetized patients and a McIntosh blade, to 64 percent which the practitioner is most comfortable; and assuring
when the patients cervical spine is immobilized using a adequate spinal cord perfusion pressure, proper oxy-
rigid collar, tape, and sand bags. genation, and ventilation are the primary goals to be
Another alternative to direct, rigid laryngoscopy is achieved while managing the airway of a SCI patient.
fiberoptic endoscopy using either the flexible or the rigid
scope. The fiberoptic method provides better views and
is associated with a lower degree of difficulty when com- RESPIRATORY MANAGEMENT
pared with direct rigid laryngoscopy; the rate of success-
ful intubation and the time to intubation is similar Spinal cord disease has a most profound impact on pul-
between groups (61). Fiberoptic tracheal intubation per- monary function. Pulmonary complications are the sin-
formed in an awake patient requires cooperation, a secre- gle most common cause of morbidity and mortality after
tion- and blood-free airway, a pharyngeal space unre- SCI and currently constitute the leading primary cause
stricted by edema, and adequate supra- and infraglottic of death (i.e., pneumonia ) (65). The level of cord injury,
anesthesia. Although this technique does not depend on the age of the patient, and the presence of pre-existing
atlanto-occipital extension, there is no documentation to medical problems all contribute to the mortality associ-
show that it minimizes neck movement. ated with SCI and pulmonary dysfunction.
Cricothyroidotomy is a rapid but invasive method Lumbar cord lesions have little or no effect on ven-
of controlling the airway. The procedure may be more dif- tilation or cough. Lesions of the thoracic cord can impair
ficult when the cervical spine is immobile. There are no cough, but have little effect on normal breathing. Cord
studies of neurologic outcome after cricothyroidotomy in injury at or above C5 can affect diaphragmatic function;
patients with cervical spine injuries (62). Transtracheal complete lesions at C3 or higher produce bilateral
ventilation is a temporary mode of ventilation and oxy- diaphragm paralysis. Obviously, this is incompatible with
genation; it does not protect against aspiration and does life in the absence of artificial ventilation. C45 lesions
not allow adequate hyperventilation. It may be difficult are associated with variable degrees of diaphragmatic dys-
to perform if the neck cannot be extended. Other tech- function. Lesions from C6 to T12 are typically charac-
niques available are blind nasotracheal intubation, light terized by an intact diaphragm, which can provide up to
wands, and retrograde intubation. 90 percent of tidal volume, but nonfunctional intercostals
Securing the airway in SCI patients can be per- that cannot stabilize the rib cage. When the accessory
formed with an awake patient after appropriate topical- muscles are used, the increase in the anteroposterior
118 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

diameter of the upper rib cage pulls the diaphragm cepha- pressure breathing, and therapy with beta agonists may
lad, and induces negative intra-abdominal pressure and be helpful, depending on the clinical situation. SCI
paradoxical breathing. The spontaneously breathing patients with cervical lesions have abnormal pulmonary
tetraplegic patient develops acute restrictive disease with dynamics during cough in the supine position. The most
a drop in total lung capacity (TLC), vital capacity (VC), effective method of producing a cough in this patient pop-
tidal volume (TV), functional residual capacity (FRC), ulation is a combination of positive pressure and assisted
mean inspiratory pressure (MIP), and mean expiratory cough (70,71).
pressure (MEP). There is an accompanying rise in resid- In summary, conscientious pulmonary assessment
ual volume (RV). and aggressive bronchial hygiene are paramount in pre-
The loss of FRC and the decrease in static lung com- venting and detecting pulmonary complications follow-
pliance is followed by the retention of pulmonary secre- ing acute SCI.
tions, increased ventilation perfusion (V/Q) mismatch,
and a poor ability to sigh and cough. Following the acute
SCI, while the patient is in spinal shock, oxygen diffusion CARDIOVASCULAR RESUSCITATION
capacity is impaired. This process can be accentuated by
the aggressive volume resuscitation that is often necessary, The physiologic and anatomic transection of the spinal
and it can result in impaired gas exchange and hypoxemia cord, followed by loss or depression of all or most spinal
(66). reflex activity below the level of the injury, is known as
Patients with lesions above C5 must usually be intu- spinal shock. This term usually implies temporary loss
bated and placed on mechanical ventilation. Even in the or depression of all spinal reflex activity below the level
absence of high cervical injury, the presence of respiratory of injury. Hypotension may be an accompanying sign,
difficulty requires intubation and full ventilatory support. depending on the level of injury, and is caused by a with-
Ventilation with TV of 15 to 20 cc/kg, rather than 5 to drawal of sympathetic tone. With the loss of the sympa-
10 cc/kg has been found to decrease complication rates thetic innervation, the unopposed parasympathetic tone
and shorten the time on the ventilator (66,67). Patients predominates (72). The vasodilatation, hypotension,
who retain diaphragmatic function can use some acces- decreased peripheral vascular resistance (PVR), decreased
sory respiratory muscles to augment respiration, but res- preload, and bradycardia are part of the clinical syndrome
piratory deterioration frequently develops gradually, of neurogenic shock (73,74). Because the sympathetic ner-
often between day 4 and 7 post injury (68). Pulmonary vous system (SNS) extends from T1 to L1, any SCI above
function must be closely monitored through serial VC, L1 is at risk for some degree of neurogenic shock. Patients
negative inspiratory force (NIF), and serial blood gas with injuries above the most cephalad sympathetic out-
analysis, as well. If the VC decreases to less than 15 ml/kg flow at T6 are most likely to exhibit profound autonomic
(in a 70 kg adult
1,000 ml) or the NIF falls below 20 changes. In this setting, a lack of activity in the T1T4
cm H2O, the patient will require intubation for bronchial cardioacceleratory fibers is responsible for bradycardia
hygiene needs. Acute respiratory failure development is (75). Although patients with blunt SCI are at risk for a
indicated by rising PCO2 and falling pH; these patients concomitant hemorrhagic injury, 70 percent of those with
will require intubation for mechanical ventilatory support hypotension have neurogenic shock. The hypotension
(66). Monitoring patients exclusively by pulse oximetry seen in neurogenic shock is rapidly responsive to cate-
is not adequate and capnography or frequent arterial cholamine infusion; in the clinical context of trauma this
blood gas analyses are generally required. Hypoxemia, hypotension should be differentiated from that of hem-
caused by retained bronchial secretions, or atelectasis can orrhagic shock. Compounding this scenario is the poten-
lead to pneumonia and may necessitate intubation for tial risk for the development of pulmonary edema sec-
both bronchial hygiene and mechanical ventilatory sup- ondary to the unopposed catecholamine surge triggered
port. The unopposed vagal tone of the submucosal glands by the spinal cord trauma. The initial sympathetic dis-
in the respiratory tract results in mucus hypersecretion. charge associated with trauma often lasts several minutes
Many patients will require suctioning several times an and produces hypertension; increase in the afterload;
hour. Comprehensive respiratory management has been tachycardia and arrhythmia followed by left ventricular
shown to considerably reduce mortality from respiratory strain; or failure and disruption of the pulmonary capil-
failure (15). The goal is to achieve 60 percent of predicted lary endothelium. Soon after trauma, neurogenic pul-
VC with various therapeutic procedures (66). monary edema may become clinically manifest as left ven-
The greatest incidence of atelectasis and pneumo- tricular failure with a pulmonary artery occlusion
nia occurs in the first 5 to 7 days, and is often focused pri- pressure (PCOP) above 18 mmHg or capillary leak syn-
marily in the left lower lobe (69). Atelectasis is managed drome (PCOP less than 18 mmHg).
primarily with incentive spirometry, but percussion and After trauma the spinal cord suffers a secondary
vibration, frequent position changes, intermittent positive ischemic injury and the autoregulation of the blood flow
ACUTE MEDICAL MANAGEMENT OF SPINAL CORD INJURY 119

is known to be impaired. The degree of post-traumatic sumptiondelivery curve reaches a plateau (82). The bal-
ischemia correlates with the severity of the injury, is pro- ance between volume, pressors, and inotropic agents is
gressive during the first few hours, and persists for at least based on changes in the SVR, PCOP, and stroke index.
24 hours. It should be aggressively treated to prevent If the persistent bradycardia associated with
post-traumatic infarction. In the face of systemic hypoten- hypotension does not respond to anticholinergic therapy
sion, spinal cord blood flow (SCBF) declines even more, (atropine, glycopyrolate, etc.) transcutaneous pacing may
and the severely injured cord cannot maintain its perfu- be required as a temporary step before permanent pace-
sion. Animal studies have shown that elevation of post- maker placement. The actual occurrence of bradycardia
traumatic MAP to more than 160 mmHg did not improve in cervical SCI is > 50 percent, on average occurs 2.4 +
SCBF at the injury site and caused hyperemia at adjacent 4.1 days after injury, and has a first occurrence ranging
sites (14). from day 0 to day 18 after initial injury (Peruzzi, unpub-
The treatment of secondary vascular injury should lished data). The bradycardia noted in SCI can be signif-
be directed toward local circulatory effects in the cord and icant, but serious episodes usually resolve after approxi-
systemic neurogenic shock (14). The treatment goals dur- mately 6 weeks, and permanent cardiac pacemakers are
ing the acute phase of SCI are restoration of cardiac out- rarely required (83).
put (CO) and tissue perfusion. The relative hypovolemia, The degree and extent of organ failure that develops
in relation to the expanded vascular bed, is corrected with from the sudden loss of a functioning nervous system
intravenous crystalloid solutions. An ongoing controversy below the level of injury depends on the severity of neu-
exists over the use crystalloid as opposed to colloid flu- rologic injury and its location. Therefore, clinicians man-
ids. If hypotension persists after reasonable volume resus- aging patients with neurogenic shock require exceptional
citation has occurred, invasive hemodynamic monitoring vigilance and management skills to limit the extent of tis-
should be instituted to assess the adequacy of fluid sue damage from original trauma as well as developing
replacement and to measure the PAOP, CO, and SVR. complications.
The PAOP should not be allowed to rise above 18 mmHg,
because these patients are at risk for developing pul-
monary edema (76). The ideal MAP necessary to maxi- ACUTE FLUID AND ELECTROLYTE
mize spinal cord perfusion after injury is not known with DISTURBANCES
certainty; thus, the practitioner should aim toward nor-
motension (MAP8090mmHg) (77,78). Peripheral per- In the acute SCI patient, fluid and electrolyte balance can
fusion, rather than pressure, should be used as a measure be affected by the respiratory acidosis that results from
of oxygen delivery at the site of SCI (79). The SCPP alveolar hypoventilation; metabolic alkalosis because of
depends on MAP, spinal fluid pressure (SFP), spinal vomiting or gastric suction;and hypochloremia caused by
venous pressure (SVP), and spinal cord interstitial pres- vomiting, gastric suction, or loss into a dilated gut (84).
sure (SCIP). A reduction in the SCPP to less than 40 Within the first week post injury, patients with acute SCI
mmHg in an otherwise normal spinal cord is associated are at risk for developing hyponatremia, especially if
with diminished dorsal cord evoked potentials (80). In the hypotonic fluids are administered. Patients with more
absence of function, it is suggested to maintain the SCPP severe neurologic injuries, as described by the Frankel A
in the 60 to 70 mmHg range. Only if fluid therapy fails classification, are at higher risk of becoming hypona-
should pressor agents be utilized, because increasing cir- tremic than those with less severe neurologic damage (85).
culating volume rather than vascular resistance is of most The mechanisms implicated include excessive antidiuretic
benefit to SCBF (81). hormone (ADH, vasopressin) secretion and a disruption
The vasopressors used are direct the alpha agonists in the normal sodium excretion rhythms post injury (86).
phenylephrine, dopamine, norepinephrine, and phento- Because patients with complete or incomplete injuries
lamine. In addition to raising the SVR, these agents also appear to have the reduced ability to excrete free water
increase the pulmonary vascular resistance (PVR). After and retain sodium, they should be primarily resuscitated
acute SCI; patients exhibit a reduced pressor response to with 0.9 percent NaCl or other balanced electrolyte solu-
conventional volume challenge within the pulmonary vas- tions. Close observation of electrolyte balance is neces-
cular bed. This returns to normal after dopamine infusion sary to avoid serious imbalances during the acute phase
(77). The cardiac index (CI) may drop because of the of SCI.
direct cardiac effect of SCI and may be related to an Numerous experimental and clinical studies indicate
increase in the level of circulating catecholamine (77). The that high plasma glucose adversely influences recovery
administration of inotropic agents is indicated in this cir- from ischemic neurologic injury. Therefore, it is reason-
cumstance and is aimed at improving blood flow and per- able to be concerned about hyperglycemia in the setting
fusion. Although controversial, this intervention is of a traumatized spinal cord. Plasma glucose levels as lit-
believed by some to be adequate when the oxygen con- tle as 40 mg /dL above normal may worsen the injury pro-
120 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

duced by spinal cord ischemia. Thus, glucose-containing the risk of bacterial infections. If the Foley catheter is
fluids should be used judiciously or not at all in victims removed too early, high bladder-filling pressures can
of spinal cord trauma, and efforts should be made to result in detrusor damage and reflux (90).
maintain a normal plasma glucose level (87). The most frequent secondary medical complication
reported during the acute care of SCI patients is urinary
tract infection (UTI). Between 1986 and 1992, 80.4 per-
GASTROINTESTINAL CARE cent of all patients reported by the Model Spinal Cord
Injury System had UTI or bacteriuria. Symptomatic UTI
During spinal shock, gastric dilatation and paralytic ileus with fever, leukocytosis, and pyuria should be treated
may develop. This can worsen the patients already com- with appropriate antibiotics for 7 to 14 days. Asympto-
promised respiratory status by restricting diaphragmatic matic bacteriuria does not need to be treated routinely,
movements. A distended stomach also predisposes to and prophylactic antibiotics, urinary antiseptics, and uri-
vomiting and aspiration. To avoid this complication, the nary acidification drugs have little role in the acute set-
stomach must be decompressed with a nasogastric tube ting. In some instances the presence of urease-producing
(88). In some instances, percutaneous gastrostomy is nec- organisms (i.e., Proteus, Klebsiella, Serratia) that are asso-
essary for protracted management. ciated with stone formation may warrant antibiotic treat-
Stress ulcers may occur in the acute phase follow- ment (91). Prevention of UTI requires meticulous
ing SCI. The incidence of gastrointestinal hemorrhage catheterization technique and the understanding that no
increases with the level and the severity of neurologic artificial drainage method guarantees the maintenance
injury. Another factor contributing to the occurrence of of sterile urine.
gastrointestinal hemorrhage after SCI is the use of steroids
(32). Prophylactic therapy with H2 blockers should be
instituted as soon as possible to decrease the incidence SKIN CARE
of gastrointestinal bleeding. Other acute gastrointestinal
complications after SCI include superior mesenteric artery Pressure ulcers continue to be a frequent complication of
syndrome and pancreatitis (89). Obviously, one must be SCI; therefore, prevention should start from the acute care
alert to the potential for such problems, because symp- phase. The NASCIS III study found a 12.3 percent inci-
toms are often masked by the loss of neurologic function. dence of pressure ulcers in SCI patients. Immediately fol-
Even though altered bowel elimination is a late com- lowing the SCI, patients must be turned every 2 hours to
plication of SCI patients, it should be addressed early, and avoid the development of ulcers (92). The time spent in each
an aggressive bowel management program should be position can be increased gradually as skin tolerance allows.
established once normal bowel sounds and motility are Specially designed foam, water, or air mattresses can reduce
restored. Rectal emptying methods, most commonly a the pressure over bony prominences, but will not obviate
combination of suppository use and finger anorectal stim- the need for turning. Patients with unstable spines may be
ulation, promotes a physiologic pattern of evacuation in placed on rotating beds that rock continuously. The beds
the distal colon. Although gentle oral cathartics may be should be adjusted so that no sliding or shear forces are
used, the use of strong cathartic medications precludes exerted, especially over the sacral prominence.
the development of a normal column of stool in the colon
and interferes with the re-establishment of normal elec-
trolyte levels. Strong cathartics also increase gaseous dis- DEEP VENOUS THROMBOSIS:
tension, which may restrict pulmonary expansions; thus, PREVENTION AND TREATMENT
such agents should be used sparingly.
The Model SCI System reported an incidence of 13.6 per-
cent of deep venous thrombosis (DVT) during acute inpa-
BLADDER CARE tient stay. The incidence of DVT was found to be similar
in patients between ages 16 and 75 years, occurred more
During the period of spinal shock, the urinary bladder commonly in male patients with paraplegia rather than
will not empty spontaneously. If not drained by catheter- tetraplegia, and more often in patients with complete
ization, bladder distension, urinary reflux, and kidney injuries. The factors implicated in the pathogenesis of
failure can result. Upon admission to the hospital, a Foley DVT are immobility, vascular dilatation and stasis,
catheter should be inserted. The return of the micturi- endothelial damage, and an increase in the level of fac-
tion reflex is variable and sometimes the reflex may never tor VIII and fibrinogen (93). The risk of DVT drops
be recovered. Intermittent bladder catheterization is approximately 20 days after the initial SCI (94).
started during the subacute phase of injury, when fluid When there is clinical suspicion, DVT can be diag-
intake and output have stabilized, in an effort to decrease nosed with a venogram. Venograms have high sensitiv-
ACUTE MEDICAL MANAGEMENT OF SPINAL CORD INJURY 121

ity and specificity, and can be performed as the initial 3. Chandler DR, Nemejc C, Adkins RH, Waters RL. Emergency cer-
vical-spine immobilization. Ann Emerg Med 1992;21:11851188.
diagnostic procedure. However, the venogram is an inva- 4. McGuire RA, Green BA, Eismont FJ, Watts C. Comparison of sta-
sive test that is not risk free. Real-time ultrasound and bility provided to the unstable spine by the kinetic therapy table
color Doppler are very sensitive methods of diagnosing and the Stryker frame. Neurosurgery 1988; 22:842845.
5. Meyer P, Lamour O. The performance of scoring systems in pre-
DVT. In 1997, the Consortium for Spinal Cord Medicine dicting outcome of head trauma patients [letter; comment]. J
recommended guidelines for the prevention of DVT based Trauma 1989; 29:1454.
on the level of risk. Among the recommendations were: 6. Aebi M, Mohler J, Zach GA, Morscher E. Indication, surgical
technique, and results of 100 surgically treated fractures and frac-
ture-dislocations of the cervical spine. Clin Orthop1986:244257.
Compression hose or pneumatic devices should be 7. Meyer P, Heim S. Surgical stabilization of the cervical spine. In:
applied to the lower extremities for the first 2 weeks Meyer P, (ed.), Surgery of Spine Trauma. New York: Churchill Liv-
ingstone, 1989:397523.
after the injury; 8. Wilberger JE. Diagnosis and management of spinal cord trauma.
In the event that thromboprophylaxis is delayed for J Neurotrauma 1991; 8 Suppl 1:S218; discussion S2930.
more than 72 hours, the extremities should be tested 9. Bohlman HH, Anderson PA. Anterior decompression and arthrode-
sis of the cervical spine: Long-term motor improvement. Part I
with either noninvasive ultrasound studies or venog- Improvement in incomplete traumatic quadriparesis. J Bone Joint
raphy for thrombi formation prior to application Surg [Am] 1992; 74:671682.
of compression boots; 10. Dolan EJ, Tator CH. The effect of blood transfusion, dopamine,
and gamma hydroxybutyrate on posttraumatic ischemia of the
Anticoagulant prophylaxis with unfractionated spinal cord. J Neurosurg 1982; 56:350358.
heparin or low molecular weight heparin (LMWH) 11. Sandler AN, Tator CH. Effect of acute spinal cord compression
should be initiated within 72 hours and continued injury on regional spinal cord blood flow in primates. J Neuro-
surg 1976; 45:660676.
until discharge in patients with incomplete motor 12. Sandler AN, Tator CH. Review of the effect of spinal cord trauma
injuries and for 8 weeks in patients with uncompli- on the vessels and blood flow in the spinal cord. J Neurosurg 1976;
cated complete motor injuries; 45:638646.
13. Schwab ME, Bartholdi D. Degeneration and regeneration of axons
Patients with complete injuries or other risk factors in the lesioned spinal cord. Physiol Rev 1996; 76:319370.
should receive LMWH for 12 weeks or until dis- 14. Tator CH, Fehlings MG. Review of the secondary injury theory
charge from rehabilitation (95). of acute spinal cord trauma with emphasis on vascular mecha-
nisms [see comments]. J Neurosurg 1991; 75:1526.
15. Chapman JR, Anderson PA. Thoracolumbar spine fractures with
Careful assessment should be done every 8 hours to neurologic deficit. Orthop Clin North Am 1994; 25:595612.
properly assess the lower extremities for swelling or 16. Tymianski M, Tator CH. Normal and abnormal calcium home-
ostasis in neurons: A basis for the pathophysiology of traumatic
edema formation and to ensure proper placement of and ischemic central nervous system injury. Neurosurgery 1996;
pneumatic devices. If the diagnosis of DVT is made, full 38:11761195.
anticoagulation is recommended either with intravenous 17. Wrathall JR, Teng YD, Choiniere D. Amelioration of functional
deficits from spinal cord trauma with systemically administered
heparin or with subcutaneous LMWH. NBQX, an antagonist of non-N-methyl-D- aspartate receptors.
Exp Neurol 1996; 137:119126.
18. Choi DW. Calcium-mediated neurotoxicity: Relationship to spe-
cific channel types and role in ischemic damage. Trends Neurosci
CONCLUSION 1988; 11:465469.
19. Rothman SM, Olney JW. Glutamate and the pathophysiology of
Acute SCI presents a unique and serious challenge to the hypoxicischemic brain damage. Ann Neurol 1986; 19:105111.
20. Greenamyre JT, Porter RH. Anatomy and physiology of glutamate
acute care/critical care medicine practitioner. Physical in the CNS. Neurology 1994; 44:S713.
examination is compromised, ancillary injuries and clin- 21. Siesjo BK. Historical overview. Calcium, ischemia, and death of brain
ical conditions frequently complicate the medical man- cells. Ann N Y Acad Sci 1988; 522:638661.
22. Lipton SA, Rosenberg PA. Excitatory amino acids as a final com-
agement, and the physiologic perturbations associated mon pathway for neurologic disorders [see comments]. N Engl J
with SCI present unique difficulties that make the resus- Med 1994; 330:613622.
citation and care of these patients more challenging. 23. Hall ED. The role of oxygen radicals in traumatic injury: Clinical
implications. J Emerg Med 1993; 11:3136.
Careful and recurrent assessments are necessary to fully 24. Hall ED, Wolf DL. A pharmacological analysis of the patho-
define the pattern and extent of injury. Constant adjust- physiological mechanisms of posttraumatic spinal cord ischemia.
ments of supportive and therapeutic interventions are J Neurosurg 1986; 64:951961.
25. Anderson DK, Means ED, Waters TR, Green ES. Microvascular
necessary for successful and positive outcomes in this perfusion and metabolism in injured spinal cord after methyl-
patient population. prednisolone treatment. J Neurosurg 1982; 56:106113.
26. Bracken MB et al. Methylprednisolone or naloxone treatment
after acute spinal cord injury: 1-year follow-up data. Results of
References the second National Acute Spinal Cord Injury Study [see com-
ments]. J Neurosurg 1992; 76:2331.
1. Przybylski G, Marion, DW. Injury to the vertebrae and spinal cord. 27. Constantini S, Young W. The effects of methylprednisolone and
In: Moore E, Matt KL, Feliciano DV., (eds.), Trauma. Engelwood the ganglioside GM1 on acute spinal cord injury in rats. J Neu-
Cliff: Appleton and Lange, 1996. rosurg 1994; 80:97111.
2. Pringle RG. Early management of the severely injured patient [let- 28. Janssen L, Hansebout RR. Pathogenesis of spinal cord injury and
ter; comment]. J R Soc Med 1998; 91:233. newer treatments. A review. Spine 1989; 14:2332.
122 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

29. Hall ED. The neuroprotective pharmacology of methylpred- growth of supraspinal and segmental projections after cervical
nisolone. J Neurosurg 1992; 76:1322. spinal cord hemisection in the neonatal rat. J Neurosci 1998;
30. Bracken MB, Holford TR. Effects of timing of methylprednisolone 18:779793.
or naloxone administration on recovery of segmental and long- 51. Guest JD, Rao A, Olson L, Bunge MB, Bunge RP. The ability of
tract neurological function in NASCIS 2 [see comments]. J Neu- human Schwann cell grafts to promote regeneration in the tran-
rosurg 1993; 79:500507. sected nude rat spinal cord. Exp Neurol 1997; 148:502522.
31. Bracken MB et al. Efficacy of methylprednisolone in acute spinal 52. Bregman BS, Kunkel-Bagden E, Schnell L, Dai HN, Gao D,
cord injury. JAMA 1984; 251:4552. Schwab ME. Recovery from spinal cord injury mediated by anti-
32. Bracken MB et al. A randomized, controlled trial of methylpred- bodies to neurite growth inhibitors [see comments]. Nature 1995;
nisolone or naloxone in the treatment of acute spinal-cord injury. 378:498501.
Results of the Second National Acute Spinal Cord Injury Study 53. Holtmaat AJ, Oestreicher AB, Gispen WH, Verhaagen J. Manip-
[see comments]. N Engl J Med 1990; 322:14051411. ulation of gene expression in the mammalian nervous system:
33. Nesathurai S. Steroids and spinal cord injury: Revisiting the Application in the study of neurite outgrowth and neuroregener-
NASCIS 2 and NASCIS 3 trials [see comments]. J Trauma 1998; ation-related proteins. Brain Res Rev 1998; 26:4371.
45:10881093. 54. Aprahamian C, Thompson BM, Finger WA, Darin JC. Experi-
34. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor function mental cervical spine injury model: Evaluation of airway man-
after spinal-cord injurya randomized, placebo-controlled trial agement and splinting techniques. Ann Emerg Med 1984;
with GM-1 ganglioside [published erratum appears in N Engl J 13:584587.
Med 1991 Dec 5;325(23):16591660] [see comments]. N Engl J 55. Sawin PD, Todd MM, Traynelis VC, Farrell SB, Nader A, Sato Y,
Med 1991; 324:18291838. Clausen JD, Goel VK. Cervical spine motion with direct laryn-
35. George ER, Scholten DJ, Buechler CM, Jordan-Tibbs J, Mattice goscopy and orotracheal intubation. An in vivo cinefluoroscopic
C, Albrecht RM. Failure of methylprednisolone to improve the study of subjects without cervical abnormality. Anesthesiology
outcome of spinal cord injuries. Am Surg 1995; 61:659663; dis- 1996; 85:2636.
cussion 663664. 56. Horton WA, Fahy L, Charters P. Disposition of cervical verte-
36. Gerhart KA, Johnson RL, Menconi J, Hoffman RE, Lammertse brae, atlanto-axial joint, hyoid and mandible during X-ray laryn-
DP. Utilization and effectiveness of methylprednisolone in a pop- goscopy. Br J Anaesth 1989; 63:435438.
ulation- based sample of spinal cord injured persons. Paraplegia 57. Calder I, Calder J, Crockard HA. Difficult direct laryngoscopy in
1995; 33:316321. patients with cervical spine disease [see comments]. Anaesthesia
37. Heary RF, Vaccaro AR, Mesa JJ, Northrup BE, Albert TJ, Balder- 1995; 50:756763.
ston RA, Cotler JM. Steroids and gunshot wounds to the spine 58. Kaufman HH, Harris JH, Jr., Spencer JA, Kopanisky DR. Dan-
[see comments]. Neurosurgery 1997; 41:576-83; discussion ger of traction during radiography for cervical trauma [letter].
583584. JAMA 1982; 247:2369.
38. Gerndt SJ, Rodriguez JL, Pawlik JW, Taheri PA, Wahl WL, 59. McLeod A. Spinal cord injury and direct laryngoscopy- the leg-
Micheals AJ, Papadopoulos SM. Consequences of high-dose end lives on. Brit J Anesthesia 2000; 84:705708.
steroid therapy for acute spinal cord injury. J Trauma 1997; 60. Hastings RH, Vigil AC, Hanna R, Yang BY, Sartoris DJ. Cervical
42:279284. spine movement during laryngoscopy with the Bullard, Macin-
39. Hall ED, Yonkers PA, Andrus PK, Cox JW, Anderson DK. Bio- tosh, and Miller laryngoscopes. Anesthesiology 1995;
chemistry and pharmacology of lipid antioxidants in acute brain 82:859869.
and spinal cord injury. J Neurotrauma 1992; 9 Suppl 2:S425442. 61. Smith CE, Pinchak AB, Sidhu TS, Radesic BP, Pinchak AC, Hagen
40. Amar AP, Levy ML. Pathogenesis and pharmacological strategies JF. Evaluation of tracheal intubation difficulty in patients with cer-
for mitigating secondary damage in acute spinal cord injury. Neu- vical spine immobilization: Fiberoptic (WuScope) versus conven-
rosurgery 1999; 44:10271039; discussion 10391040. tional laryngoscopy. Anesthesiology 1999; 91:12531259.
41. Bracken MB et al. Administration of methylprednisolone for 24 62. Hastings RH, Marks JD. Airway management for trauma patients
or 48 hours or tirilazad mesylate for 48 hours in the treatment of with potential cervical spine injuries [see comments]. Anesth Analg
acute spinal cord injury. Results of the Third National Acute 1991; 73:471482.
Spinal Cord Injury Randomized Controlled Trial. National Acute 63. Guha A, Tator CH, Rochon J. Spinal cord blood flow and sys-
Spinal Cord Injury Study. JAMA 1997; 277:15971604. temic blood pressure after experimental spinal cord injury in rats.
42. Faden AI, Salzman S. Pharmacological strategies in CNS trauma. Stroke 1989; 20:372377.
Trends Pharmacol Sci 1992; 13:293. 64. Dinsmore J, Bacon RC, Hollway TE. The effect of increasing
43. Landi G, DAlessandro R, Dossi BC, Ricci S, Simone IL, Ciccone degrees of spinal flexion on cerebrospinal fluid pressure [see com-
A. GuillainBarr syndrome after exogenous gangliosides in Italy. ments] [published erratum appears in Anaesthesia 1998
BMJ 1993; 307:14631464. Oct;53(10):1032]. Anaesthesia 1998; 53:431434.
44. Quarles RH, Ilyas AA, Willison HJ. Antibodies to gangliosides 65. DeVivo MJ, Black KJ, Stover SL. Causes of death during the first
and myelin proteins in GuillainBarr syndrome. Ann Neurol 12 years after spinal cord injury. Arch Phys Med Rehabil 1993;
1990; 27:S4852. 74:248254.
45. Seidl EC. Promising pharmacological agents in the management 66. Peterson P. Pulmonary physiology and medical management. In:
of acute spinal cord injury. Crit Care Nurs Q 1999; 22:4450. Whiteneck Gea, (ed.), The Management of High Quadriplegia.
46. Regan RF, Panter SS, Witz A, Tilly JL, Giffard RG. Ultrastruc- New York: Demos, 1989:3550.
ture of excitotoxic neuronal death in murine cortical culture. Brain 67. Massaro GD, Massaro D. Morphologic evidence that large infla-
Res 1995; 705:188198. tions of the lung stimulate secretion of surfactant. Am Rev Respir
47. Fleishaker JC, Peters GR, Cathcart KS. Evaluation of the phar- Dis 1983; 127:235236.
macokinetics and tolerability of tirilazad mesylate, a 21-aminos- 68. Jackson AB, Groomes TE. Incidence of respiratory complications
teroid free radical scavenger: I. Single-dose administration. J Clin following spinal cord injury. Arch Phys Med Rehabil 1994;
Pharmacol 1993; 33:175181. 75:270275.
48. Faden AI, Jacobs TP, Smith MT, Holaday JW. Comparison of thy- 69. Carter RE. Respiratory aspects of spinal cord injury management.
rotropin-releasing hormone (TRH), naloxone, and dexametha- Paraplegia 1987; 25:262266.
sone treatments in experimental spinal injury. Neurology 1983; 70. Braun SR, Giovannoni R, OConnor M. Improving the cough in
33:673678. patients with spinal cord injury. Am J Phys Med 1984; 63:110.
49. Faden AI, Jacobs TP, Smith MT, Holaday JW. Comparison of thy- 71. Lucke KT. Pulmonary management following acute SCI. J Neu-
rotropin-releasing hormone (TRH), naloxone, and dexametha- rosci Nurs 1998; 30:91104.
sone treatments in experimental spinal injury. Neurology 1983; 72. Piepmeier JM, Lehmann KB, Lane JG. Cardiovascular instability
33:673678. following acute cervical spinal cord trauma. Cent Nerv Syst
50. Diener PS, Bregman BS. Fetal spinal cord transplants support Trauma 1985; 2:153160.
ACUTE MEDICAL MANAGEMENT OF SPINAL CORD INJURY 123

73. Atkinson PP, Atkinson JL. Spinal shock. Mayo Clin Proc 1996; 85. Peruzzi WT, Shapiro BA, Meyer PR, Jr., Krumlovsky F, Seo BW.
71:384389. Hyponatremia in acute spinal cord injury. Crit Care Med 1994;
74. White RJ, Likavec MJ. Spinal shockspinal man [editorial; com- 22:252258.
ment]. J Trauma 1999; 46:979980. 86. Claus-Walker J, Campos RJ, Carter RE, Lipscomb HS, Vallbona
75. Malliani A, Peterson DF, Bishop VS, Brown AM. Spinal sympathetic C. Longitudinal analyses of daily excretory rhythms in men with
cardiocardiac reflexes. Circ Res 1972; 30:158. tetraplegia due to cervical spinal cord transection. Paraplegia
76. Chiles BW 3rd, Cooper PR. Acute spinal injury [see comments]. 1972; 10:142152.
N Engl J Med 1996; 334:514520. 87. Goto T, Crosby, G. Anesthesia and the spinal cord. Anesthesiol
77. Levi L, Wolf A, Belzberg H. Hemodynamic parameters in patients Clin N Am 1992; 10:493511.
with acute cervical cord trauma: Description, intervention, and 88. Nikas DL. Resuscitation of patients with central nervous system
prediction of outcome. Neurosurgery 1993; 33:10071016; dis- trauma. Nurs Clin N Am 1986; 21:693704.
cussion 10161017. 89. Gore RM, Mintzer RA, Calenoff L. Gastrointestinal complica-
78. Vale FL, Burns J, Jackson AB, Hadley MN. Combined medical tions of spinal cord injury. Spine 1981; 6:538544.
and surgical treatment after acute spinal cord injury: Results of a 90. Lloyd LK, Kuhlemeier KV, Fine PR, Stover SL. Initial bladder man-
prospective pilot study to assess the merits of aggressive medical agement in spinal cord injury: Does it make a difference? J Urol
resuscitation and blood pressure management. J Neurosurg 1997; 1986; 135:523527.
87:239246. 91. The prevention and management of urinary tract infections among
79. Fraser A, Edmonds-Seal J. Spinal cord injuries. A review of the prob- people with spinal cord injuries. National Institute on Disability
lems facing the anaesthetist. Anaesthesia 1982; 37:10841098. and Rehabilitation Research Consensus Statement. January
80. Griffiths IR, Trench JG, Crawford RA. Spinal cord blood flow and 2729, 1992. J Am Paraplegia Soc 1992; 15:194204.
conduction during experimental cord compression in normoten- 92. McCagg C. Postoperative management and acute rehabilitation
sive and hypotensive dogs. J Neurosurg 1979; 50:353360. of patients with spinal cord injuries. Orthop Clin North Am 1986;
81. Gilbert J. Critical care management of the patient with acute spinal 17:171182.
cord injury. Crit Care Clin 1987; 3:549567. 93. Petaja J, Myllynen P, Rokkanen P, Nokelainen M. Fibrinolysis and
82. Shoemaker WC, Appel PL, Kram HB. Oxygen transport mea- spinal injury. Relationship to post-traumatic deep vein thrombo-
surements to evaluate tissue perfusion and titrate therapy: Dobu- sis. Acta Chir Scand 1989; 155:241246.
tamine and dopamine effects. Crit Care Med 1991; 19:672688. 94. Green D, Lee MY, Lim AC, Chmiel JS, Vetter M, Pang T, Chen
83. Winslow EB, Lesch M, Talano JV, Meyer PR. Spinal cord injuries D, Fenton L, Yarkony GM, Meyer PR, Jr. Prevention of throm-
associated with cardiopulmonary complications. Spine 1986, 11 boembolism after spinal cord injury using low-molecular-weight
(8); 809812. heparin [see comments]. Ann Intern Med 1990; 113:571574.
84. Babinski MF. Anesthetic considerations in the patient with acute 95. Prevention of thromboembolism in spinal cord injury. Consortium
spinal cord injury. Crit Care Clin 1987; 3:619636. for Spinal Cord Medicine. J Spinal Cord Med 1997; 20:259283.
This Page Intentionally Left Blank
8 Factors Affecting Surgical
Decision Making

Patrick J. Connolly, M.D.

pine injuries in the United States PATIENT EVALUATION

S number more than a million cases


per year. The vast majority of these
injuries are soft tissue injuries that
do not require surgical treatment or prolonged immobi-
Patients with spine injuries may present as victims of mul-
tiple trauma or with an isolated injury to the spine. At the
time of admission to the hospital, EMT personnel are
lization. In the United States, there are approximately invaluable in relaying information concerning the scene
50,000 spine fractures each year, 10,000 of which involve of the accident.
injury to the spinal cord with associated neurologic deficit The physician should initially survey the vital signs,
(1). Although spine fractures are most often secondary airway, breathing, and circulation. Following this, a brief
to motor vehicle accidents, falls, or diving accidents, examination of the patients level of consciousness and
recent reports indicate a disturbing increase in the inci- neurologic status should be obtained. At completion of
dence of spine injuries related to gunshot (2). the initial resuscitation efforts and primary survey for life-
Typically, the patient who has sustained a spinal col- threatening injuries, the spine trauma evaluation may pro-
umn injury is a young male between the ages of 15 and ceed. In a multitrauma setting, a patient should be con-
35. The injury to the spinal column frequently occurs at sidered to have cervical spine injury until completion of
either the thoracolumbar or cervicothoracic junctions. the secondary physical examination and thorough radi-
An increased awareness by emergency personnel has ographic assessment. Noncontiguous spinal injuries occur
allowed earlier spine stabilization both at the scene of the in 5 to 20 percent of those with spine fractures. As many
accident and in the emergency room. Rapid stabilization as 15 percent of patients have associated major visceral
of the spine contributes to a reduction in the progression involvement (4).
of an incomplete spinal cord injury (SCI) to a complete A complete examination first involves inspection for
SCI. Despite this heightened awareness of cervical spine evidence of head injury, abdominal contusion, or skin lac-
injuries, a number of cervical spine fractures are still erations. Severe facial and scalp injuries can be associated
missed early in the evaluation process. Evaluation for with cervical spine injury and may help the examiner
spine injury requires taking a complete history from the deduce the mechanism of injury. Abdominal contusion is
patient or EMTs, as well as a comprehensive orthopaedic a diagnostic clue for flexiondistraction (lap belt) injuries
and neurologic examination (3). to the spine. In a cooperative patient, palpation of the spine

125
126 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

from the skull to the coccyx for areas of localized tender- ographs are an essential part of the evaluation. Although
ness is extremely helpful to localize a spinal injury. Root- 85 percent of significant injuries will be detected with a lat-
specific muscle strength testing of the upper and lower eral cervical spine radiographs that allows visualization
extremities and rectal examination for tone and sensation of C 7, an injury at the cervical thoracic junction may
are extremely important in determining the anatomic level escape detection. Consequently, current spine trauma pro-
of injury. Cranial nerve examination, sensory response to tocol should require complete cervical spine radiographs
pin and light touch, deep tendon, and plantar reflexes com- with full visualization of the body of T1. If this is not pos-
plete the spine injury assessment. Finally, careful docu- sible a swimmers view or CT scan is required.
mentation of the initial examination is essential. MRI is extremely helpful in the evaluation of
patients with SCI or neurologic deficit. It may comple-
ment, but does not replace CT. A thin-section CT scan
GENERAL PRINCIPLES OF TREATMENT of the spine provides greater bone detail and remains the
gold standard for demonstrating fracture pattern and
The important steps of treating patients who have sus- canal compromise in spinal injuries.
tained a spine injury are immobilization, medical stabi- Technetium bone scanning is occasionally helpful in
lization, restoration of spinal alignment, neural decom- ruling out occult injuries of the spine in patients with pro-
pression, and spinal stabilization. longed symptoms and a negative radiographic evaluation.
Immobilization should be performed in the field
using a rigid cervical collar as well as a spinal board and
sandbags. Immobilization should be maintained until the MECHANISM OF INJURY AND
patient has been evaluated and cleared by the treating STABILITY OF THE FRACTURE
physician. If the patient has not been stabilized in the field,
cervical spinal stabilization should be one of the first steps Spine fractures can be classified on the basis of the mech-
taken by the evaluating physician in the emergency room. anism of injury (59). Injuries to the spine may occur sec-
Medical stabilization follows the basic principles of ondary to the forces of flexion, extension, lateral rota-
trauma care. This requires continuous monitoring of the tion, axial loading, or a combination of these forces. The
patients respiratory and cardiovascular status and is gen- forces that most often cause injury to the spinal cord are
erally conducted in the emergency room or intensive care a combination of flexion and axial loading. The specific
unit setting. Patients with spinal cord injuries and neuro- fracture that these forces produce varies according to the
genic shock present with hypotension and bradycardia as age of the patient, pre-existing medical conditions (i.e.,
a result of the traumatic sympathectomy. Spinal shock is osteoporosis, ankylosing spondylolitis, etc.), as well as
different from neurogenic shock and is defined as the the level of injury.
absence of spinal reflex activity below an SCI. The sig- Spine fractures classification, along with personal
nificance of spinal shock is that it limits the ability to both experience and training, enable the surgeon to develop a
classify the extent of paralysis and predict recovery of treatment plan. The degree of stability or instability of an
cord function. Spinal shock should be considered resolved SCI will change with time as the osseous elements heal.
with the return of the bulbocavernosus reflex (BCR) Therefore, an injury that might initially be considered unsta-
within 48 hours after injury. In a small percentage of ble may well be stable 12 weeks after injury. Conversely,
patients, the BCR never returns. an injury that involves primarily ligamentous structures may
Realignment of the injured cervical spine is usually become more unstable with time. Most spine fracture clas-
accomplished with skeletal traction via halo ring or Gard- sification systems are designed to evaluate acute injuries.
ner Wells tongs. Although recently there has been some Holdsworth (8) is credited with developing the first
concern about the necessity of MRI or myelography spine fracture classification that included specific recom-
before the reduction of a cervical spine dislocation, this mendations for treatment. Denis (6) modified this system
is generally not necessary in a setting where the patient by adding the concept of the three columns of the thoracic
is being placed in traction while awake and is subjected and lumbar spine. Allen and Ferguson (5) developed a
to repeat neurologic and radiographic evaluation. mechanistic classification of closed, indirect, fractures and
dislocations of the lower cervical spine. In each system, the
goal of fracture classification is to determine whether the
IMAGING fracture is stable or unstable. The locations of most spine
fractures are most often the transitional zones of the spine,
The open-mouth anteroposterior view of the spine is essen- specifically the cervicothoracic junction and the thora-
tial for evaluation of the upper cervical spine. The stan- columbar junction. The explanation of this phenomenon
dard AP view of the spine allows evaluation of lateral mass is twofold: a change in rigidity associated with the rib cage
and sagittal plane fractures. Lateral cervical spine radi- and thoracic spine, and the change in the saggital align-
FACTORS AFFECTING SURGICAL DECISION MAKING 127

ment that occurs at the thoracic spine (cervical lordosis, in an older patient with a pre-existing cervical spondylo-
thoracic kyphosis, lumbar lordosis). The location of a frac- sis. Clinically, the patient has a greater loss of function
ture can be just as important as the fracture pattern in in the upper extremities than in the lower extremities.
regard to stability. Specifically, fractures in the mid-tho- Perianal sensation is often preserved. Historically, this has
racic region are inherentally more stable in the presence been ascribed to the somatotopic organization of the cor-
of an intact rib cage than similar fractures at the thora- ticospinal tract (CST), because the arm fibers are centrally
columbar junction. Although the specifics of spinal stabi- located. However, more recent investigations show that
lization are beyond the scope of this chapter, in general, a the CST in higher primates is not somatotopically orga-
patient who has been realigned with traction or postural nized and that the clinical syndrome may be secondary to
reduction, and do not have significant canal compromise the disproportionate influence of the CST to hand and
are often treated with posterior stabilization and fusion upper extremity motor function.
alone. In injuries that are treated with an anterior decom- BrownSequard syndrome is produced by a pre-
pressive procedure, anterior bone grafting alone does not dominant injury to the lateral half of the spinal cord.
provide immediate internal fixation and an anterior plate Motor paralysis and proprioception are greater on the
or posterior stabilization is required. side of the injury. Pain and temperature sensory loss are
Fractures producing SCI are, by definition, unsta- greater contralateral to the side of the SCI. This syndrome
ble and are usually best treated with surgical stabilization. has a fair prognosis for functional recovery.
Immediate stabilization allows for early mobilization and In the clinical setting, there often arises some con-
rehabilitation. These benefits must be weighed against the fusion in the labeling of cord injury syndromes. In a
potential risks of surgeryspecifically, infection and inad- partial SCI, the caudal segments of the spinal cord are
equate fracture stabilization. Each fracture has a per- either stronger, weaker, or the same. Caudal loss is con-
sonality of its own, and the method of spinal stabiliza- sistent with an anterior cord syndrome. A patient with
tion depends on the personality of the fracture, as well better caudal motor strength than cranial motor strength
as the ability of the surgeon. If surgery will not provide has a central cord-type lesion. Patients with isolated nerve
immediate improved spinal stability, it should probably root injuries should be classified as having neurologic loss
not be performed. without SCI.

CLASSIFICATION OF SPINAL CORD INJURY SPINAL CORD INJURY

SCI can be broadly classified as complete or incomplete Most spinal cord deficit is attributed to contusion and/or
(3). The diagnosis of complete SCI cannot be made until compression, rather than to complete transection. The ini-
spinal cord shock resolves. If the BCR is present and there tial blunt injury leads to a secondary sequence of molecu-
is no motor or sensory function below the injury, by def- lar and cellular events that results in ischemia, tissue
inition the injury is complete. If, following the return of hypoxia, and secondary tissue degeneration. The extent of
the BCR, the patient has some sensation below the level tissue damage and the resulting neural injury can be related
of injury, he is considered to be sensory incomplete. If to the magnitude of the initial force. Whether the initial
the BCR has returned and the patient has some motor blunt insult or the effect of continued pressure on the dam-
function and sensation below the level of injury, he is con- aged neural elements is greater in causing persistence of
sidered to be sensory and motor incomplete. neural deficit remains a topic of controversy. The microvas-
There are four incomplete SCI syndromes. The ante- culature can be disrupted by mechanical deformation and
rior cord syndrome is characterized by injury to the ante- propagated by edema, thrombosis, or further vasconstric-
rior cord opposite the area of spinal injury, with relative tion induced by local and circulating factors. Although the
sparing of dorsal column sensory pathways. The mecha- initial insult to the spinal cord is currently irreversible,
nism of injury is usually a compression or flexion type maintenance of perfusion at the cellular level of the spinal
injury. Clinically, there is paralysis in portions of the cord, if possible, is important to protect the remaining liv-
upper limbs. In the lower extremities, deep pressure and ing, healthy tissue and to possibly improve recovery.
position sense are preserved, with no motor function
below the area of injury. The prognosis for anterior cord
syndrome is the worst of all the incomplete syndromes. PHARMACOLOGIC TREATMENT OF
Posterior cord syndrome is rare. In this injury, there SPINAL CORD INJURY
is preservation of motor function with loss of sensory
function below the level of injury. The goal of pharmacologic intervention is to decrease sec-
The central cord syndrome is common. The mech- ondary neurologic damage rationale following the initial
anism of injury is usually an extension injury that occurs mechanical injury (1,10,11). To understand the rationale
128 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

of pharmacologic treatment of SCI, a brief discussion of shown a significant benefit for patients with both complete
secondary SCI is necessary. and incomplete quadriplegia. Although the exact timing
Numerous theories exist regarding secondary SCI. of anterior decompressive procedures is not entirely clear,
Overall, the SCI site becomes an area of ischemia, animal studies indicate that the effect of spinal cord com-
hypoxia, and edema. The free-radical theory suggests pression is inversely related to the duration of compres-
that, because of depletion of antioxidants, free radicals sion. It appears that patients with SCI, both complete and
accumulate and attack membrane lipids. Lipid peroxides incomplete, should undergo imaging assessment following
are produced, and the cell membranes fail. In the calcium their initial stabilization and realignment. If significant
theory, there is an influx of extracellular calcium into the anterior cord compression remains following realignment
nerve cell. This, in turn, activates phospholipases, caus- with traction, then an anterior decompressive procedure
ing a resultant interruption of mitochondrial activity and should be considered in both the incomplete and complete
a disruption of the cell membrane. SCI patient to maximize the recovery of cord injury and
The explanation for the observed effects of methyl- root return, respectively.
prednisolone is that it suppresses the breakdown of cell In general, because of the relative size of the upper
membranes by inhibiting lipid peroxidation and hydrol- cervical spine, a decompressive procedure of the upper
ysis at the site of injury. The high doses required are those cervical spine is rarely, if ever, indicated. In the lower cer-
shown to be most effective in inhibiting lipid peroxida- vical spine, the vast majority of patients can be success-
tion and the breakdown of neurofilaments in laboratory- fully stabilized by a posterior procedure alone. If signifi-
induced SCI. cant canal compromise by disc or bony fragments occurs
Because the beneficial effects of methylprednisolone following reduction, an anterior decompression along
on SCI are believed to be unrelated to its glucocorticoid with surgical stabilization is usually performed. The ben-
effects, interest has developed in the utilization of 21- efits of anterior cervical decompression with residual
aminosteroids for SCI. Tirilazad is a lazeroid (synthetic canal compromise are twofold; it provides a biomechan-
21-aminosteroid). It is a potent antioxidant without the ically sound fusion environment and provides an opti-
glucocorticoid effects of methylprednisolone. GM 1 gan- mal environment for neurologic recovery and root return.
gliosides are complex glycolipids of an acid nature that In thoracic and lumbar injuries, realignment and pos-
are present in high concentrations in central nervous sys- terior stabilization provides an indirect decompression of
tem (CNS) cells. Although their functions are not entirely the spinal canal that often eliminates the requirement for
clear, there is experimental evidence that suggests they anterior decompression. If significant canal compromise
augment neurite outgrowth, induce regeneration and (often defined as greater than 50 percent canal compromise)
sprouting of neurons, and restore neurologic function remains following posterior reduction and stabilization, an
after injury. GM-1 may be effective in treating SCI even anterior decompression may be necessary. In most clinical
if administration is delayed for 48 hours. Unfortunately, situations, an anterior thoracic or lumbar decompression
the one major drawback of GM-1 is that it may have an is not urgently or emergently required. The decision to per-
antagonistic effect on the neuroprotective role of methyl- form an anterior decompression in the acute setting, via a
prednisolone. This may become quite cumbersome in the thoracotomy or a thoracolumbar approach, requires care-
design of further clinical trials. ful consideration. The potential benefit of anterior decom-
Current recommendations are a result of the third pression is often outweighed by the deleterious effect that a
National Acute Spinal Cord Injury Study (NASCIS-III). thoracotomy may have on a multitrauma patient.
The recommended guideline for patients who receive
treatment within three hours of injury is the administra-
tion of methylprednisolone as a bolus (30 mg/kg-body TIMING OF SURGERY
weight) followed by an infusion (5.4 mg/kg/hr) for 23
hours. For those patients in which methylprednisolone When a progressive neurologic deficit exists in the pres-
is initiated within three to eight hours of injury, the infu- ence of malalignment and spinal canal compromise, emer-
sion should continue for 48 hours. gency decompression is indicated. In all others with SCI,
the timing of surgery is controversial (1,12,13). Some
authors recommend treatment as soon as the patient is
ROLE OF ANATERIOR DECOMPRESSION medically stable, whereas others advocate a delay of 4 or
more days to allow for posttraumatic swelling to resolve.
Direct anterior spinal cord decompression (12,13) should Delamarter evaluated the effect of the timing of spinal
be considered when there is significant residual anterior cord decompression in a canine SCI model. In his study, a
compression of the spinal cord following realignment. In constriction band was utilized to create a controlled para-
the past, concern existed about further injury and desta- plegia. In the group that was decompressed at 1 hour fol-
bilization by anterior procedures, but recent work has lowing injury, the animals recovered neurologic function.
FACTORS AFFECTING SURGICAL DECISION MAKING 129

In the group that was decompressed at 6 hours following metastatic disease, and ankylosing spondylitis are asso-
injury, there was no neurologic recovery. The results of ciated with spine fractures. Each disease presents its own
his study suggested that not all injury to the spinal cord challenges in the treatment of spine fractures (1418).
occurred at the initial trauma and that early decompres- Osteoporosis is the most prevalent metabolic bone
sion had a significant role in neurologic recovery. disease. Osteoporotic compression fractures often occur
Whether early decompression and reduction of neural in the elderly. Most often, these fractures are stable in
structures enhances neurologic recovery continues to be nature and do not require surgical intervention. Unsta-
debated. Although animal studies suggest a benefit with ble fractures associated with SCI, when they do occur,
early decompression, this hypothesis has not been clinically require careful surgical planning. The usual methods of
proven. Indeed, significant functional recovery has been surgical stabilization often fail to provide adequate sur-
observed following anterior decompression of the spinal gical stabilization in light of this soft bone. The judi-
cord in patients whose initial injury was up to 20 years old. cious use of polymethylmethocroylate is often necessary.
Currently, a reasonable approach would be to treat non- Metastatic spinal lesions are an important consid-
progressive neurologic deficits on a semiurgent basis, when eration in the evaluation of low-impact spine fractures.
the patients systemic condition is medically stable. Metastatic lesions are identified at autopsy in 40 to 80
percent of patients who die of cancer. Spinal cord com-
pression occurs in 20 percent of patients with spinal
GUNSHOT WOUNDS metastases. In treating patients with metastatic spine frac-
tures, the surgeon must consider the overall health of the
Over the last 10 years, a significant increase in the inci- patient, the degree of pain, and the biology of the primary
dence of spinal cord injury is related to gunshot wounds. tumor, as well as the integrity and stability of the spinal
The most recent data is that 25 percent of SCI is related column.
to gunshot wounds. There data, from 1991, reported that Patients with ankylosing spondylitis have a 3.5 times
52 percent of total admissions for SCI at one regional SCI greater incidence of cervical spine injury than the nor-
center were related to gunshot wound trauma. mal population. Seventy-five percent of the spine fractures
These injuries rarely cause sufficient bone or liga- sustained by patients with ankylosing spondylitis occur
mentous injury to warrant surgical treatment. Immobi- in the cervical spine. The diagnosis is often delayed.
lization with a halo vest or rigid cervical orthosis usually Patients typically present with complaints of neck pain
provides adequate stability for healing. The issue of following minimal trauma. The mechanism of injury is
removing a bullet from the spinal canal remains contro- most often a hyperextension injury. Because of the disease
versial. The argument for bullet removal revolves around process, the spine breaks like a solid long bone. These
diminishing the risk of CSF leak, meningitis, lead toxic- fractures are highly unstable. Patients are at a high risk
ity, pain, neurologic decline, and bullet fragment migra- for neurologic complications.
tion. The argument for the nonoperative approach is that Traditional treatment for this type of fracture is rigid
retention of bullet fragments does not routinely lead to immobilization with a halo cast or a vest, paying careful
complications and that the risks of surgical intervention attention to align and maintain the patients preinjury
outweigh the potential benefits of fragment removal. alignment. Recent development in spinal instrumentation
Overall, these cases are never straightforward. They has allowed for rigid internal fixation; in the hands of
must be evaluated on a case-by-case basis. If the bullet some experienced spine surgeons, early stabilization with
fragment is creating compressive pathology, its removal a combined anterior and posterior procedure is now the
may benefit the patient. Likewise, bullet migrations in the treatment of choice for fractures in patients with anky-
spinal canal or progression of neurologic deficit are indi- losing spondylitis.
cations for surgical intervention. Recent studies evaluated
the impact of bullet removal in SCI patients. The con-
clusion of the studies was that removal of the bullet did CONCLUSION
not affect the incidence of pain. Bullet removal from the
canal between T1T11 had no significant affect on motor When treating patients with SCI, the physician must look
recovery, but when bullets were removed from the cauda at the individual needs of the patient. Age, level of injury,
equina region, patients did receive some benefit. fracture pattern, preexisting medical conditions, and asso-
ciated traumatic injuries are factors that influence the
treatment plan. If early mobilization of the patient
PATHOLOGIC BONE through surgical stabilization is realistic, then early sur-
gical intervention should be performed.
Fractures associated with minimal trauma are most
often associated with pathologic bone. Osteoporosis,
130 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

References fractures. Reliability of Frankel and Sunnybrook scales. Spine


1993; 18:257263.
CA Dickman, MA Yahiro, HT Lu, MN Melkerson. Surgical treatment
1. Delamarter RB, Coyle J. Acute management of spinal cord injury. alternatives for fixation of unstable fractures of the thoracic and
J Am Acad Orthop Surg 1999, 7:166175. lumbar spine. A meta-analysis. Spine 1994; 19:2266S2273S.
2. Waters RL, Adkins RH. The effects of removal of bullet fragments TA Duff. Management of cervical spine fractures. J Neurosurg 1990;
retained in the spinal canal. Spine 1991; 16, 934939. 73:478479.
3. Connolly PJ, Yuan HA. Cervical Trauma. Orthopaedic Knowledge DK Ebelke, MA Asher, JR Neff, DP Kraker. Survivorship analysis of
Update V (OKU-V). AAOS Publications. 1996. VSP spine instrumentation in the treatment of thoracolumbar and
4. Vaccaro AR, An HA, Lin SS. J Spinal Disorders 1992; 5:320329. lumbar burst fractures. Spine 1991; 16:S428432.
5. Allen BL, Ferguson RL, Lehmann TR, OBrien RP. Mechanistic FJ Eismont, MJ Arena, BA Green. Extrusion of an intravertebral disc
classification of closed indirect fractures and dislocations of the associated with traumatic subluxation or dislocation of cervical
lower cervical spine. Spine 1982; 7:127. facets. J Bone Joint Surg 1991; 73A:15551560.
6. Denis F. The three column spine and its significance in the classi- TA Garvey, FJ Eismont, LJ Roberti. Anterior decompression, structural
fication of acute thoracolumbar spinal injuries. Spine 1983; bone grafting, and Caspar plate stabilization for unstable cervi-
8:817831. cal spine fractures and/or dislocations. Spine 1992; 17:S431435.
7. Gertzbein SD. Spine update. Classification of thoracic and lum- KI Ha, SH Han, M Chung, BK Yang, GH Youn. A clinical study of the
bar fractures. Spine 1994; 19:626628. natural remodeling of burst fractures of the lumbar spine. Clin
8. Holdsworth FW. Fractures, fislocations, and fracture-dislocations Orthop 1996; 210-214.
of the spine. JBJS 1963; 45B:620. RJ Huler, S. I. Esses, and D. J. Botsford. Work status after posterior fix-
9. McCormack T, Karaikovic E, Gaines RW. The load sharing clas- ation of unstable but neurologically intact burst fractures of tho-
sification of spine fractures. Spine 1994; 19:17411744. racolumbar spine. Paraplegia 1991; 29:600606.
10. Bracken MD, et al. A randomized controlled trial of methylpred- H Kinoshita, Y Nagata, H Ueda, K Kishi. Conservative treatment of
nisolone or naloxone in the treatment of acute spinal cord injury. burst fractures of the thoracolumbar and lumbar spine. Paraple-
N Engl J Med 1990; 322:14051411. gia 1993; 31:5867.
11. Geisler FH, Dorsey FC, ColemanWP. Recovery of motor function GR Klein, AR Vaccaro, TJ Albert, M Schweitzer, D Deely, D Karasick,
after spinal cord injury: A randomized placebo-controlled trial with JM Cotler. Efficacy of magnetic resonance imaging in the evalua-
GM-1 ganglioside. N Engl J Med 1991; 324:18291838. tion of posterior cervical spine fractures. Spine 1999; 24:771774.
12. Anderson PA, Bohlman, HH. Anterior decompression and RW Lindsey, W Dick. The fixateur interne in the reduction and stabi-
arthrodesis of the cervical spine: Long-term motor improvement. lization of thoracolumbar spine fractures in patients with neuro-
Improvement in complete traumatic quadriplegia. JBJS 1991; logic deficit. Spine 1991; 16:S140145.
74A:683692. RW Lindsey, W Dick, S Nunchuck, and G Zach. Residual interseg-
13. Bohlman, HH, Anderson PA. Anterior decompression and mental spinal mobility following limited pedicle fixation of tho-
arthrodesis of the cervical spine: Long-term motor improvement. racolumbar spine fractures with the fixateur interne. Spine 1993;
Improvement in incomplete traumatic quadriparesis. JBJS 1992; 18:474478.
74A:671682. DC Mann, BW Bruner, JS Keene, AB Levin. Anterior plating of unsta-
14. Lane JM, Sandhu HA. Osteoporosis of the Spine. Orthopaedic ble cervical spine fractures. Paraplegia 1990; 28:564572.
Knowledge Update. Spine 1997, 227234 C Olerud, S Andersson, B Svensson, J Bring. Cervical spine fractures
15. Heller JG, Pedlow FX.Tumors of the Spine, Orthopaedic Knowl- in the elderly: factors influencing survival in 65 cases. Acta Orthop
edge Update. Spine 1997, 235256. Scand 1999; 70:509513.
16. Broom MJ, Raycroft JF. Complications of fractures of the cervi- DR Ripa, MG Kowall, PR Myer, JJ. Russin. Series of 92 Traumatic Cer-
cal spine in ankylosing spondylitis. Spine 1988; 13:763766. vical Spine Injuries Stabilized with Anterior ASIF Plate Fusion
17. Foo D, Sarkarati M, Marcelino V. Cervical spinal cord injury com- Technique. Spine 1991; 16 (Suppl): 4655.
plicating ankylosing spondylitis. Paraplegia 1985; 23:358363. RC Sasso, HB Cotler, JD Reuben. Posterior fixation of thoracic and
18. Taggard DA, Traynelis VC. Management of cervical spinal frac- lumbar spine fractures using DC plates and pedicle screws. Spine
tures in ankylosing spondylitis with posterior fixation. Spine 2000; 1991; 16:S134139.
25:20352039. RC Sasso, HB Cotler. Posterior instrumentation and fusion for unsta-
ble fractures and fracture-dislocations of the thoracic and lum-
Bibliography bar spine. A comparative study of three fixation devices in 70
patients. Spine 1993; 18:450460.
E Sim, PM Stergar. The fixateur interne for stabilising fractures of the
LD Anderson, RT DAlonzo. Fractures of the odontoid process of the thoracolumbar and lumbar spine. Int Orthop 1992; 16:322329.
axis. J Bone Joint Surg 1974; 56A:16631674. AM Star, AA Jones, JM Cotler, RA Balderson, R Sinha. Immediate
HH Bohlman. Acute fractures and dislocations of the cervical spine. J Closed Reduction of Cervical Spine dislocations using traction.
Bone Joint Surg 1979; 61A:11191142. Spine 1990; 15:10681072.
HH Bohlman, J S Kirkpatrick, R B Delamarter, M Leventhal. Anterior JS Torg, H Pavlov, SE Genuraio, B Sennett, RJ Wisniewski, BH Robi,
decompression for late pain and paralysis after fractures of the C Jahre. Neuropraxia of the cervical spinal cord with transient
thoracolumbar spine. Clin Orthop 1994; 2429. quadraplegia. J Bone Joint Surg 1986; 68A:13541370
DP Chan, NK Seng, K T Kaan. Nonoperative treatment in burst frac- JS Torg, SG Glasgow. Criteria for return to contact activities after cer-
tures of the lumbar spine (L2-L5) without neurologic deficits. vical spine injury. Athletic Injuries to the Head, Neck, and Face.
Spine 1993; 18:320325. 2nd edition New York: Mosby 1991; 589608.
JR Chapman, PA Anderson. Thoracolumbar spine fractures with neu- AR Vaccaro. Combined anterior and posterior surgery for fractures of
rologic deficit. Orthop Clin North Am 1994; 25:595612. the thoracolumbar spine. Instr Course Lect 1999; 48:443449.
JC Clohisy, BA Akbarnia, RD Bucholz, JK Burkus, RJ Backer. Neuro- JN Weinstein. Differential diagnosis and surgical treatment of patho-
logic recovery associated with anterior decompression of spine logic spine fractures. Instr Course Lect 1992; 41:301315.
fractures at the thoracolumbar junction (T12-L1). Spine 1992; M Yazici, B Atilla, S Tepe, A Calisir. Spinal canal remodeling in burst
17:S325330. fractures of the thoracolumbar spine: A computerized tomo-
LA Davis, SA Warren, DC Reid, K Oberle, LA Saboe, MG Grace. graphic comparison between operative and nonoperative treat-
Incomplete neural deficits in thoracolumbar and lumbar spine ment. J Spinal Disord 1996; 9:409-413.
9
Cervical Injuries:
Indications and
Options for Surgery

Christopher M. Bono, M.D.


Michael J. Vives, M.D.
Christopher P. Kauffman, M.D.

ervical spine injuries frequently unstable injury (9), and this chapter focuses on the for-

C require surgical intervention (17).


The choice of procedure depends on
a number of factors. Conceptually,
the two main objectives in surgery are decompression and
mer. Blunt trauma can arise from a variety of mechanisms
(10). In general, fracture or dislocation can be secondary
to flexion, extension, or axial load. These are produced
in a number of ways. Most commonly, the body under-
stabilization. In both instances, the optimal approach may goes a sudden acceleration and deceleration force, which
be anterior, posterior, or both. In some situations, cervi- causes the head to be propelled either backwards or for-
cal traction and halo immobilization are useful preoper- wards, respectively. Abrupt acceleration causes extension-
ative adjuncts. In all cases, the goal of surgery is to pro- type injuries. Deceleration causes flexion-type injuries.
vide a stable spine to minimize further neural damage. Less frequently, the head or neck itself sustains a direct
Stabilization can be effected by both internal and exter- force. Although pure flexion and extension injuries may
nal methods. Instrumentation, including wiring, plating, occur from such a mechanism, axial loading is more
and screw techniques are effective frequently-used tech- likely. An illustrative example is a diving injury, caused
niques (4,6,8). These techniques have been used in both by a direct load through the head and cervical spine.
anterior and posterior surgery. Instrumentation can aug- Lastly, rotational forces can also produce cervical spinal
ment or protect spinal fusion (1,4). In some cases, such as injury. In reality, cervical trauma is produced by a com-
odontoid injuries, screws can be placed to fix the frac- bination of these mechanisms (10).
tured segment without fusing motion segments. The goals Recognizing the mechanism of injury is an impor-
of orthopaedic intervention are to allow the patient to tant component of preoperative evaluation. For instance,
be mobilized early and allow for rehabilitation. flexion-type injuries of the subaxial spine (below C2) can
produce anterior vertebral body fractures. These can
appear as tear-drop fractures (11). In many cases, flex-
PREOPERATIVE EVALUATION ion-type injuries are associated with a disruption of the
posterior spinal ligamentous complex, which may not be
readily apparent on plain radiographs. Further evaluation
Injury Mechanism
using magnetic resonance imaging (MRI) can reveal the
Cervical injury can occur from both blunt and penetrat- injury or frank disruption that indicates a highly unsta-
ing trauma (9,10). Penetrating trauma rarely produces ble lesion (12). In the upper cervical segments, as in C2
131
132 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

traumatic spondylolisthesis (the hangmans fracture), is caused. Mechanical stability refers to the relative
recognition of the mechanism also plays a key role. The motion of vertebral segments under the physiologic loads
majority of these injuries arise from an extension force, of everyday activity. An illustrative case is a ventilator-
although some are the result of flexion-type mechanism dependent patient who sustained a cervical fracture dis-
(7). In contrast to other patterns, flexion-type fracture is location along with a massive nonfatal head injury and
exaggerated by cervical traction and thus necessitates pulmonary contusion. At bed rest, he is undergoing strict
axial compression for adequate reduction. log-roll precautions. The spine injury was reduced with
longitudinal traction at the time of presentation, and the
patient has since been placed on 15 pounds of mainte-
Imaging
nance weight. MRI and CT scans indicated no herniated
High-quality radiographs are crucial to effective preop- disc or significant canal compromise. Neurologically, the
erative planning. Films should include anteroposterior danger of further cord compression is unlikely, given that
and lateral views of the entire cervical spine. Failure to the patient is not being mobilized or seated upright, this
adequately image each spinal segment can lead to missed despite the fact that the vertebral fracture-dislocation is
injuries, especially because the rate of concomitant mechanically unstable. Before further mobilization can be
injuries in the cervical spine is high (7). Open-mouth and contemplated, surgical stabilization must be accom-
swimmers views are helpful in imaging the atlantoaxial plished. This will require both initial intensive care and
and cervicothoracic junctions, respectively. In some further rehabilitative efforts once the patients medical
patients, especially obese individuals, plain film visual- condition has stabilized. Stabilization of the spine facili-
ization is difficult and more advanced imaging modalities tates nursing care, and respiratory, physical, and occu-
must be pursued. pational therapy for these patients.
Computerized tomography (CT) provides highly To assess mechanical stability, the subaxial cervical
detailed axial images of each vertebral segment and is supe- vertebral elements have been divided into three columns
rior to MRI for delineating fractures. CT can demonstrate (13). Effectively, the columns can be considered longi-
nondisplaced fractures not discernible on plain roentgen- tudinal members that span the length of the spine. The
ograms. In addition, CT is an excellent method for evalu- anterior column consists of the ALL, the anterior aspect
ating and quantifying the degree of spinal canal compro- of the intervertebral disc, and the anterior half of the ver-
mise. Although these advantages are clear, CT alone is not tebral body. Likewise, the middle column is made up of
a substitute for plain radiographs, because the latter are the PLL and the respective posterior aspects of the disc
better for determining overall spinal alignment and coro- and vertebral body. The posterior column refers to all
nal or sagittal deformity. Pure dislocations can be easily remaining structures, including the pedicles, laminae,
missed with CT alone and are best diagnosed by plain radi- transverse processes, facet joint, and the PLC (inter-
ograph. CT machines also allow for reconstructed three- spinous, supraspinous ligaments). The junction of the
dimensional (3D) images, which may provide further middle and posterior columns forms the spinal canal.
information. However, these are computer generated and Normally, the spine rotates around an axis within the
limited by the number of axial images obtained and the spinal canal, ensuring as little motion as possible in the
computer program used for reformatting. region of the neural elements (14).
MRI is the modality of choice for evaluating the A column can be disrupted by either fracture or lig-
spinal cord and neural elements. In addition, MRI can amentous disruption. By definition, disruption of two or
reveal edematous soft tissues, in either the anterior or pos- more columns imparts instability (13). Gunshot wounds
terior cervical spine. MRI is especially important in trau- to the cervical spine are an exception to this rule. Because
matic spine injuries because it visualizes the cord. Often, of the mechanism of injury, gunshot wounds can be sta-
diffuse cord edema represents the degree and extent of ble even with two- or three-column injury (9). By collat-
injury. MRI offers information regarding the integrity of ing information from plain radiography, CT scans, and
the ligamentous structures, including the anterior longi- MRI imaging, the integrity of each column can be deduced.
tudinal ligament (ALL) and the posterior ligamentous In some situations, spinal injury occurs without
complex (PLC), and the presence of herniated disc mate- obvious radiographic findings. Spinal cord injury (SCI)
rial in the spinal canal or foramina (11,12). may or may not be present. In the awake, neurologically
intact, cooperative patient, dynamic flexion-extension lat-
eral radiographs can reveal abnormal motion between
SPINAL STABILITY vertebral segments. This is best judged by drawing a lon-
gitudinal line along the anterior and posterior aspects of
Stability can refer to both mechanical and neurologic fac- the vertebral bodies. An abrupt break in the line should
tors. Neurologic stability denotes a state in which, under be measured. If the break is more than 3.5 millimeters,
the stresses that are imposed, no further neural damage or 11 degrees of motion is present, the spine is unstable
CERVICAL INJURIES: INDICATIONS AND OPTIONS AND SURGERY 133

and likely requires operative intervention (15). Some ditionally, this is filled with a tricortical bone graft (3,17).
advocate deferring flexion-extension lateral radiographs The purpose of the graft is two-fold. First, it acts as a strut
until 2 weeks after acute injury, because of the risk of to maintain the height of the anterior column. For this rea-
false-negative studies from motion limitations caused by son, cortical bone must be used. Softer cancellous
pain and muscle spasm (16). (medullary) bone cannot sustain these large forces. Most
commonly, tricortical autograft from the patients anterior
iliac crest is used, although allograft can also be utilized.
SURGICAL TREATMENT OPTIONS The second purpose of the graft is to fuse the vertebrae.
The bone graft is wedged between the endplates.
Goals of Surgery High compressive forces help to maintain its position.
With neck extension, however, these compressive forces
As stated previously, the main objectives in the operative may be diminished. Normally, the ALL acts as a check
treatment of cervical spine injuries are to decompress the rein to these distraction forces. Although postoperative
spinal canal and achieve mechanical stability. Decom- neck extension can be controlled to some extent with a
pression can be effected by anterior or posterior hard cervical collar, many surgeons opt to place anterior
approaches. Anterior decompression consists of the instrumentation (1). Fixed to the uninjured vertebral bod-
removal of the vertebral body and/or intervertebral disc. ies with screws, anterior plates span the fused vertebral
Posterior decompression is accomplished by removing the segments and act as an artificial ALL. In some circum-
posterior neural arch, namely the spinous processes, lam- stances, anterior instrumentation can obviate the need for
inae, and PLC. Stabilization usually consists of a fusion external postoperative orthoses, shorten the length of
procedure. Anteriorly, this is achieved by implanting time they are worn postoperatively, or allow for less rigid
structural bone graft material between adjacent vertebrae. immobilization.
Posteriorly, this is accomplished by on-lay bone grafting Rarely, the C12 junction is approached anteriorly
over decorticated posterior elements. The use of instru- (2). Because the mandible and its associated structures
mentation can protect the fusion mass until healing create an obstruction, a transoral approach has been
occurs, thus preventing graft dislodgment, and obviating developed. By incising the posterior pharyngeal mucosa
the need for postoperative orthoses in some cases. at the approximate level of the hard palate, the surgeon
gains access to the anterior atlantoaxial joint. The bony
elements can then be removed as necessary. Stabilization
Anterior Decompression and Stabilization
procedures are difficult and dangerous to perform
The anterior approach to the cervical spine can be used through this approach, but have been described (2). If sta-
for decompression of C3 to C7 (3,11,17). Palpable sur- bility is compromised, posterior fusion and/or instru-
face landmarks include the cricoid cartilage (C6), thyroid mentation is recommended (2).
cartilage (C4), the hyoid bone (C6), and the carotid tuber-
cle (C6). Dissection is carried medial to the carotid sheath.
Posterior Decompression
In its deepest layers, the interval between the longus colli
and Stabilization
muscle and the anterolateral aspects of the vertebral body
is utilized. Anatomic dangers are the recurrent laryngeal The cervical spine can be approached posteriorly at any
nerve, more at risk on the right side than the left, and the level. Utilizing a midline incision, the paraspinal muscles
sympathetic chain, which is at risk with lateral dissec- are elevated off the bony elements to expose the spinous
tion on top of the longus colli. With retractors in place, processes, laminae, and tiny transverse processes. At the
the vertebral body and anterior disc are easily visualized. C1 level, lateral dissection is limited by the vertebral
The injured disc(s) are incised and removed piece- artery nerve, which lies 1.5 centimeters from the midline.
meal. The posterior limit to discectomy is the PLL. After In the subaxial spine, the medial aspect of the transverse
disc removal, the vertebral body is removed in a similar processes form the vertebral artery foramen; this is the
fashion. With the corpectomy complete, the PLL is lateral border of the safe zone.
inspected. If free fragments of bone or disc were noted Posterior decompressive procedures are used less fre-
on preoperative imaging, the canal must be visualized. If quently after cervical spinal trauma. Following anterior
not already disrupted from the initial injury, the PLL can column injury, a posterior approach is often contraindi-
be carefully incised. At all times, clear visualization of the cated and will cause worsening of stability in an already
neural elements must be maintained when working in the compromised spine. Canal compromise is approached
spinal canal. At each disc level, the exiting nerve roots are from the direction of the offending elements. Retropulsed
inspected and decompressed. fragments of vertebral body or disc are the usual culprit.
Anterior decompression leaves a void between the cra- In some situations, a laminectomy is indicated to retrieve
nial and caudal endplates of the uninjured segments. Tra- posterior fragments of bone or intervertebral disc. Lam-
134 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

inal fractures are associated with dural tears, which SPECIFIC INJURIES
require requiring repair in 50 percent of cases. Decom-
pressive laminectomy begins with removal of the spin- Bony Anatomy
ous processes down to the junction with the laminae.
Briefly, the atlas is a bony ring that rotates around the
Next, the laminae are carefully removed piecemeal until
dens of the axis (C2). Broad inferior articular surfaces
the dural sac is visualized.
enhance the stability of the atlantoaxial relationship. The
In certain cases, the stability of the posterior mid-
atlas articulates with the occiput through two broad artic-
line structures can be preserved with more limited
ular lateral surfaces. The posterior ligaments are loose, to
decompression laminotomies and foraminotomies.
allow greater range of motion. The dens is an upward
However, after traumatic injury, a stabilization or fusion
projection of the C2 body. Transverse and apical liga-
procedure should be performed regardless of limited pos-
ments stabilize the atlantodens articulation. Transverse
terior bone removal, to prevent progressive deformity in
ligaments extend from the posterior aspect of the dens
most situations.
(odontoid process) to the posterior aspect of the anterior
In cases of dislocation or fracture-dislocation,
arch of C1. The apical ligament spans from the tip of the
closed reduction with longitudinal tong traction is usu-
odontoid process (C2) to the anterior aspect of the fora-
ally effective. In some cases, however, the dislocation
men magnum (C0). The axis (C2) intimates with C3
may be irreducible. The most common scenario is of
through lateral articular masses (the lateral masses) and
locked facets in which the inferior articular process of
marks the transition to the lower cervical spine. Because
the cranial vertebra (which normally lies posterior to the
of this unique function, the cranial and caudal articula-
superior articular process of the caudal vertebra) is
tions of the axis are substantially offset anterior and pos-
trapped in front of the superior articular process of the
terior, respectively. This offset puts the region between the
caudal segment (11,18). Using the posterior approach,
upper and lower articular processes at particular risk for
the offending superior articular process is carefully
fracture (hangmans fracture). The subaxial spine is sim-
removed, thus allowing the cranial segment to return to
ilar to vertebral segments at other levels. The anterior ver-
its antomic position. In this case, laminectomy is not nec-
tebral body is connected to the posterior arch through
essary, because reduction and restoration of alignment
two pedicles. At the pediclelamina junction, superior and
has decompressed the canal. If the patient was not
inferior processes project to articulate with adjacent
awake and alert for a full neurologic exam prior to
motion segments.
surgery, a preoperative MRI is necessary (12). Postop-
erative MRI is useful to detect a herniated disc after
reduction, which may necessitate subsequent anterior Atlas (C1)
decompression if further neurologic deficit develops. The majority of atlas injuries can be treated nonsurgically
Postoperative studies can be difficult to interpret fol- using either a halo vest or cervical collar. With a spacious
lowing any type of instrumentation. spinal canal, cord injury is less likely in the C1C2 region
After laminectomy or reduction of facet disloca- than with subaxial trauma. Injuries can be divided into
tions, posterior fusion is advised. In both cases, the PLC two groups: a) posterior ring fractures and lateral mass
has been disrupted either by the injury or iatrogenically. fractures (Jefferson fractures), and b) transverse ligament
Various techniques of fusion exist. Functionally, they disruptions.
consist of on-lay bone graft across vertebral segments
following decortication to stimulate bone formation. In
Posterior Ring Fractures
the upper cervical spine, a bone graft can be wedged
between the C1 and C2 arches, if they are intact. Occip- Most posterior ring fractures of the atlas are stable and
itoatlantal fusion can be achieved by securing large struts heal well using a hard collar. The mechanism of injury is
of cortical graft to the posterior ring of C1 and the occip- usually axial load with hyperextension. These fractures
ital protuberance. are associated with concomitant cervical spinal injuries
As in the anterior spine, methods of posterior instru- in 50 percent of cases (7). The most frequently encoun-
mentation have been developed (4,6). Interspinous tered concomitant lesion is a type II dens fracture, which
wiring, lateral mass plates, and vertebral screw-rod sys- may be displaced or nondisplaced. In this situation, the
tems have all been used successfully. Conceptually, the dens fracture should be stabilized. It is the authors pref-
constructs act to partially replace the missing or injured erence to place an odontoid screw to stabilize the frac-
posterior ligaments and protect the fusion mass until heal- ture. This can preserve motion of the atlantoaxial joint
ing occurs. Again, these techniques may obviate external and obviates a larger fusion procedure posteriorly. With
postsurgical immobilization, although this depends on the odontoid fixed, a halo vest or hard collar can be used
surgeon preference, the quality of fixation, and the pres- postoperatively to protect the fixation in light of a dis-
ence of concomitant injuries. rupted posterior ring.
CERVICAL INJURIES: INDICATIONS AND OPTIONS AND SURGERY 135

Lateral Mass Fractures until healed. If the condition is irreducible, open reduction
through a posterior approach, followed by posterior
The term lateral mass denotes the articular complex
fusion, is indicated.
of the atlas and its supporting structures. The superior
and inferior joint surfaces are situated directly on top of
one another. They act as the communication between the Axis (C2)
anterior and posterior rings. Fractures can develop ante-
riorly, across, or posteriorly to the articular surfaces. The Odontoid (Dens) Fracture
mechanism of injury is usually axial load with varying
Odontoid fractures occur from flexion or extension
degrees of flexion or extension.
mechanisms. Injuries are classified according to anatomic
Fractures can be unilateral or bilateral. Bilateral frac-
location. Type I fractures arise at the tip or apex of the
tures are colloquially referred to as Jefferson fractures.
process and most probably represent a bony avulsion of
Unique to injury at this level, stability is assessed by the
the apical ligament. These can be treated with good
amount of lateral displacement. On an open-mouth
results using a rigid collar.
anteroposterior radiograph, this can be measured as the
Type II fractures are the most problematic. Because
bilateral total millimeters of lateral overhang of the atlanto
the dens embryologically arises from the C1 level and the
articular processes in relation to the occiptal articular
base (i.e., vertebral body) from the C2 level, there is a water-
processes. A total displacement of greater than 7 to 10 mil-
shed area of blood supply at this junction. With greater than
limeters implies disruption of the transverse ligaments and
4 to 5 millimeters of displacement, nonunion is likely (7).
instability (7,20). Stable lateral mass fractures can be
Closed reduction with flexion or extension maneuvers
treated using a hard cervical orthosis. Unstable fractures
using halo stabilization is effective in most cases. However,
are reduced with an initial period of traction followed by
if fracture reduction cannot be maintained, open reduc-
halo vest immobilization. Because the transverse ligament
tion and stabilization must be entertained.
may not heal, flexion-extension views should be obtained
In the absence of an associated posterior ring frac-
after radiographic bony union. If atlantoaxial instability is
ture, a simple posterior C1C2 fusion using wiring is
present, then posterior C1C2 fusion is indicated.
effective in preventing late atlantoaxial instability. As in
all C1C2 fusions, this sacrifices 50 percent of the rota-
Atlantoaxial Dissociation tion of the head. With ring discontinuity, lateral mass plat-
ing or transarticular screw and fusion can be utilized.
Transverse Ligament Disruption Alternatively, an anterior odontoid screw can be inserted
across the fracture site (19). However, this can only be
Pure, isolated transverse ligament injury can occur with- used when anatomic alignment can be achieved. The
out fracture. Clinically, it can result in C1C2 instability. advantage of this method is that it preserves the rotatory
In the awake, neurologically intact patient, careful motion of the atlantodens articulation. In regards to
dynamic lateral radiographs can demonstrate instability. patient mobilization, the transfacet or Magerl technique
Normally, the atlantodens interval is less than 3 millime- provides the greatest immediate and long-term stability.
ters . Greater intervals imply discontinuity of the trans- Type III dens fractures occur through the body of the
verse ligament. Instability is best treated with a posterior ring. Blood supply is good and healing is reliable. Immo-
C1C2 fusion, with or without instrumentation. Spin- bilization in a rigid cervical collar is usually sufficient.
ous process wiring with on-lay autograft is an effective
method of stabilization.
Traumatic Spondylolisthesis (Hangmans Fracture)
This injury is a subluxation of the axis on the C3 verte-
Rotatory Subluxation or Dislocation
bra in association with a fracture. The fracture occurs in
Rotatory subluxation or dislocation occurs most com- the region between the more anterior cranial articular
monly in children and is often the sequela of nontraumatic process and the posteriorly situated caudal articular
processes, such as retropharyngeal infection (i.e., Grisels surface.
syndrome). After trauma, it can occur from abrupt rota- Type I fractures are nondisplaced. This is a stable
tional forces in both adults and children. Presentation can injury and can be treated in a collar. Type II injuries are
be of a cock-robin posture of the neck, in which the head displaced more than 3 millimeters. Reduction is through
is rotated away and tilted toward the side of the injury. the use of cervical tong traction with slight hyperexten-
Dynamic CT scans can be diagnostic, with comparison of sion of the neck. Alignment is maintained in a halo vest
axial images obtained with the head turned fully to the left for 8 to 12 weeks. If greater than 6 millimeters of dis-
and the right. In most cases, gentle traction leads to a com- placement is present, and it cannot be further reduced,
plete reduction, and the patient can be placed in a halo vest then posterior fusion of C2 to C3 is performed.
136 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

A subcategory of type II is the type IIa injury. This


is characterized by marked angulation of the anterior
fragment with little forward translation. These injuries
are reduced with axial load and extension of the neck. A
halo vest maintains compression on the fracture for 8 to
12 weeks until bony union occurs.
Type III fractures display severe angulation and dis-
placement. Characteristically, there is a unilateral or bilat-
eral facet subluxation or dislocation of the inferior articu-
lar process on C3. They are associated with a higher rate
of SCI and are highly unstable. They represent disruption
of the ring of C2 along with injury to the PLC. In most cases,
they require open reduction and posterior fusion. Instru-
mentation is advantageous in achieving adequate stability
and should be protected with a halo vest postoperatively.

Subaxial Spine (C3 to C7)


In a smaller spinal canal, subaxial cervical spine injuries
are associated with a much higher rate of neurologic dam-
age than C1 and C2 trauma (3,11,17). As such, they often
require decompressive procedures, usually to remove
retropulsed bony or disc fragments through an anterior
approach. In addition, disruption of the posterior liga-
ments necessitates a posterior fusion in many cases.
Injuries can be divided into three groups: dislocations FIGURE 9.1
(subluxation), vertebral body compression fractures, and
pedicle fractures (fracture-dislocations). Lateral c-spine C67 unilateral facet fracture. Note that this
is not well visualized on regular lateral view.

Dislocations and Subluxation


With abrupt deceleration moments, the head is projected
forward in relation to the body. Hyperflexion of the spine
creates tension forces along the posterior ligaments of the
cervical spine and compressive forces in the anterior ver-
tebral body and disc. Variations of this mechanism are
responsible for the majority of injuries to the subaxial
spine. Although dislocation and subluxation can arise
from extension moments, it is in this position that the
facet joints are most stable and less likely to dissociate.
The facet joint, which is comprised of the inferior
and superior articular processes of adjacent vertebrae, can
be disrupted. The two opposing articular surfaces can be
subluxed, indicating that part of the two surfaces are still
in contact, or frankly dislocated, indicating that the sur-
faces are not touching at all. The superior articular
process is pulled up and over its inferior counterpart.
Facet dislocations can be unilateral or bilateral. Bilateral
variants are associated with higher energy mechanism and
imply greater posterior ligamentous injury.
Unilateral injury can occur with or without disrup-
tion of the PLC. If it is intact, the injury is stable and will
heal (Figures 9.1 through 9.4). Reduction by closed means FIGURE 9.2
with traction is difficult. Persistent unilateral dislocation
can limit motion, cause chronic pain, and may lead to Same patient; swimmers view visualizing C67 subluxation.
CERVICAL INJURIES: INDICATIONS AND OPTIONS AND SURGERY 137

radiculopathy (11). To minimize these complications, a


posterior reduction and fusion is usually recommended.
Bilateral facet dislocations are usually associated
with disruption of the PLC, facet capsule, posterior lon-
gitudinal ligament, and posterior intervertebral disc.
Thus, they represent a two-column injury, indicating
instability. Reduction is readily achieved by closed means,
using cervical traction with weights of up to 100 pounds.
Because of the massive soft injury, reduction alone does
not impart sufficient stability. Posterior fusion and/or
instrumentation is indicated to maintain alignment. Bar-
ring anterior pathology, realignment is effective in decom-
pressing the spinal canal.
A unique situation is a bilateral facet dislocation
with a herniated disc detected on preoperative MRI.
Because of the possible risk of further disc herniation and
cord compromise, anterior discectomy and fusion are rec-
ommended prior to reduction (12). Postoperatively, a
halo vest is fitted to protect the construct until bony heal-
ing is evident. Alternatively, a staged posterior fusion pro-
cedure can provide further stability and obviate the need
for prolonged external immobilization.

FIGURE 9.3 Vertebral Body Fractures


Same patient; CT scan showing fracture dislocation. Unsta- Compression forces on the vertebral body can lead to frac-
ble injury. ture. The bone usually fails at the superior endplate first,
leading to the classic tear-drop fracture pattern. With
higher energy, the bone can be comminuted into more than
two fragments. If the fracture is contained within the ante-
rior half of the vertebral body (one column disruption) and
there is less than 3.5-millimeter translation or 11 degrees
of angulation, then the injury may be considered stable
(15). Often, this determination must be made after an ini-
tial period (1 week) of cervical collar immobilization,
because spasm can mask occult instability.
Burst fractures arise with greater compression forces
(see Figures 9.5 through 9.7). By definition, vertebral body
fracture lines extend into the middle column (posterior
half). With at least two-column disruption, burst fractures
are unstable and require operative intervention (13).
Often, the posterior vertebral fragments are pushed pos-
teriorly and can compress the spinal cord. Although exact
numbers are not clear, a canal compromise of greater than
40 to 50 percent is considered unacceptable and must be
decompressed. Prior to operative decompression, each
patient should be immediately aligned with either halo or
Gardner-Wells tongs. Aligning the canal helps to decom-
press the spinal cord, because the retropulsed fragments
are often attached to the annulus of the disc above or
below. These attachments allow for reduction by liga-
FIGURE 9.4 mentotaxis (Fredrickson). Anterior corpectomy is indi-
cated if any neurologic deficit is present. The use of instru-
Same patient; following reduction and anterior instrumented mentation after anterior column reconstruction can
fusion. shorten the period of postoperative hard collar or halo use.
138 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

FIGURE 9.5

Nineteen-year-old male s/p MVA. C4 and C5 burst fractures


with incomplete cord injury.

Pedicle Fractures
FIGURE 9.7
Pedicle fractures represent very unstable, high-energy
lesions (see Figures 9.8 through 9.12). In essence, they are Same patient; following staged anteriorposterior fixation, the
a posterior fracture-dislocation, where the upper spine is patient could be mobilized and rehabilitated with almost full
displaced anteriorly and the lower spine posteriorly. The return of function.

intervertebral disc and anterior half of the pedicle follow


the upper segment. The posterior pedicle and facet com-
plex follow the inferior segment. In this injury, the facet
complex at the level of injury is, by necessity, disrupted
and dislocated. The disc space is often disrupted as well.
Emergent cervical tong traction should be initiated as
soon as possible, because it is effective in restoring align-
ment. Operative fixation consists of combined anterior
and/or posterior stabilization and fusion. A halo vest or
orthosis supplements the surgical construct.

Disc Injuries
Traumatic injury to the intervertebral disc usually requires
surgical stabilization. A traumatic injury may represent
part of a complete ligamentous disruption, known as a
Chance fracture. These are persistently unstable injuries
(because of poor healing of the ligamentous structures),
FIGURE 9.6 and thus require anterior discectomy and fusion. In these
settings, anterior instrumentation allows for a more rigid
Same patient; CT scan showing injury to all three columns construct, higher fusion rates, and faster mobilization
of the spine. from the orthosis.
CERVICAL INJURIES: INDICATIONS AND OPTIONS AND SURGERY 139

FIGURE 9.10
FIGURE 9.8
Same patient; CT scan showing C5 pedicle and facet fracture.
Twenty-year-old female s/p MVA vs. pedestrian. AP with C5
facet and pedicle fracture.

FIGURE 9.11
FIGURE 9.9
Same patient; AP c-spine following anterior C56 anterior
Same patient; 2 weeks following injury with progressive sub- instrumentation and fusion. Surgery performed anteriorly
luxation of C5 on C6. because the disc is disrupted as well.
140 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

the patients pain and apprehension level are tolerable.


Halo immobilization is employed to protect particularly
unstable injuries or in cases where poor bone quality pre-
cludes adequate purchase of internal fixation. The halo
should be maintained until there is radiographic evidence
of fracture or fusion healing, usually in 10 to 12 weeks.
Cervical orthoses should be used until the soft tissues
have healed. Full-time orthotic use can be associated with
skin breakdown and patient discomfort. Unfortunately, no
hard and fast rules exist when it comes to the early removal
of orthoses. Most surgeons agree that removal is all right
once the fusion is solid. Prior to this, treating physicians
and other health care professionals should address any
concerns with each individual surgeon.

COMPLICATIONS

Despite the effectiveness of surgical treatment of cervical


spine injuries, complications are not infrequent. In addi-
tion to the morbidity associated with SCI, complications
may involve the cervical wound, the bone graft site, or the
postoperative orthosis.
FIGURE 9.12 Anterior cervical procedures have a low incidence of
wound infections. Posterior cervical procedures, however,
Same patient; lateral c-spine following anterior reduction and may be associated with a higher rate of postoperative
instrumented fusion. wound drainage. The investing fascia of the trapezius is
directly attached to the subdermal skin layer. As a result,
upper-extemity motion causes tension across the closure.
Miscellaneous
Postoperative wound infection is usually accompanied by
Fractures can arise in the subaxial posterior ring, trans- prolonged drainage, pyrexia, and erythema. Definitive
verse processes, and spinous processes. By themselves, they treatment usually involves surgical debridement and the
are inherently stable and typically can be managed with a taking of intraoperative cultures to identify the offend-
hard collar. Most importantly, they should alert the prac- ing pathogen. Depending on the extent of infection, clo-
titioner to other possible cervical spine injuries. If stabil- sure can be done primarily, on a delayed basis, or with
ity is questionable, a collar should be left in place until flap coverage after a period of granulation. Instrumenta-
spasm has subsided, at about 1 week. Flexionextension tion is generally left in situ to provide stability for fusion,
views can reveal occult ligamentous instability, but should and removed only after solid arthrodesis is achieved (21).
only be done in the awake, alert, nonintoxicated patient. Wound healing problems can also plague the iliac
crest bone graft donor site (22). Anteriorly, meralgia
paresthetica is a painful neuropathy from stretch or sharp
POSTOPERATIVE CARE injury to the lateral femoral cutaneous nerve. This can
lead to severe pain and numbness in the proximal ante-
Instrumentation for cervical trauma has the added benefit rior thigh. Even without injury to nerves about the inci-
of reducing the need for external means of postoperative sion, patients may report substantial discomfort at the
immobilization, although this depends on surgeon prefer- graft harvest site (23).
ence and the security of fixation. Using anterior corpectomy Although halo skeletal fixation offers the advantage
and fusion alone, a halo fixator or hard collar should be of rigid immobilization, complications are frequently
maintained for 8 to 12 weeks until there is radiographic evi- encountered (24). Pin loosening may occur in 36 to 60
dence of healing. If instrumentation is used, and there is percent of patients. If no infection is present, the pin can
no associated posterior ligament injury, then the halo can be retightened if resistance is met upon the first few rota-
be removed and a collar can be used for a short period. tions (25). If no resistance is met, the pin should be
Today, most surgeons prefer instrumentation to sup- removed after a new pin is placed at an adjacent location.
plement posterior fusion. With stable fixation and no Pin site infection occurs in approximately 20 percent of
associated anterior injury, a hard collar can be used until patients. Drainage or erythema should be treated with
CERVICAL INJURIES: INDICATIONS AND OPTIONS AND SURGERY 141

local pin care and oral antibiotics. If the drainage does 8. Hamilton A, Webb JK. The role of anterior surgery for vertebral
fractures with and without cord compression. Clin Orthop 1994;
not resolve, or if cellulitis or an abscess develops, the pin 300:7989.
should be removed after a new pin is inserted at a differ- 9. Kupcha PC, An HS, Cotler JM. Gunshot wounds to the cervical
ent site. Incision and drainage may be required, followed spine. Spine 1990; 15:10581063.
10. Allen BL, Ferguson RL, Lehmann TR, OBrient RP. A mechanis-
by intravenous antibiotic therapy. tic classification of closed, indirect fractures and dislocations of
Pressure sores can develop under the halo vest (26). the lower cervical spine. Spine 1982; 7:1982.
This may be the result of insufficient padding, inappro- 11. Stauffer ES. Managment of Spine Fractures: C3 to C7. Orthop
Clin N America 1986; 17:4553.
priate sizing, or poor cast application (for those in halo 12. Eismont FJ, Arena MJ, Green BA. Extrusion of an intervertebral
casts). Even padded two- and four-poster collars can cause disc associated with traumatic subluxation or dislocation of cer-
decubiti on the occiput. Frequent, careful skin inspection vical facets: Case report. J Bone Joint Surg 1991; 73-A:15551560.
13. Cybulski GR, Douglas RA, Meyer PR, Rovin RA. Complications
beneath any orthotic is essential, especially in patients with in three-column cervical spine injuries requiring anterior-posterior
paralysis or poor protective sensibility (24,25). stabilization. Spine 1992; 17:253256.
14. Haher TR, OBrien M, Felmly WT, Welin D, Perrier G, Choueka
J, Devlin V, Vassiliou A, Chow G. Instantaneous axis of rotation
as a function of the three columns of the spine. Spine 1992;
CONCLUSION 17:S149154.
15. White AA, Panjabi MM. Clinical Biomechanics of the Spine, 2nd
edition. Philadephia: Lippincott-Raven, 1990.
The goals of operative cervical fracture care are to decom- 16. Wang JC, Hatch JD, Sandhu HS, Delamarter RB. Cervical flex-
press the canal, stabilize the cervical spine, restore align- ion and extension radiographs in acutely injured patients. Clin
ment, and prevent late deformity. When spinal stability Orthop 1999; 365:111116.
17. Anderson PA, Bohlman HH. Anterior decompression and
is achieved through internal fixation and/or well-fitting arthrodesis of the cervical spine: Long-term motor improvement.
orthoses, early mobilization can help avoid the morbid- J Bone Joint Surg 1992; 74-A:683692.
ity of prolonged recumbence. 18. Rizzolo SJ, Vaccaro AR, Cotler JM. Cervical Spine Trauma. Spine
1994; 19:22882298.
19. Henry AD, Bohly J, Grosse A. Fixation of odontoid fractures by
References an anterior screw. J Bone Joint Surg 1999; 81-B:472477.
20. Spence KF, Decker S, Sell KW. Bursting atlantal fracture associ-
1. Apfelbaum RI. The use of anterior Caspar plate fixation in acute ated with rupture of the transverse ligament. J Bone Joint Surg
cervical spine injury. Surg Neurol 1992; 38:162163. 1970; 52-A:543549.
2. Bohler J. Anterior stabilization for acute fractures and non-unions 21. Weinstein MA, McCabe JP, Cammisa FP. Postoperative spinal
of the dens. J Bone Joint Surg 1982; 64-A:1826. wound infection: A review of 2,391 consecutive index procedures.
3. Bohlman HH, Anderson PA. Anterior decompression and J Spinal Disord 2000; 13:422426.
arthrodesis of the cervical spine: Long-term motor improvement 22. Younger EM, Chapman MW. Morbidity at the bone graft donor
(Part I-improvement in incomplete traumatic quadriparesis). J sites. J Orthop Trauma 1989; 3:192195.
Bone Joint Surg 1992; 74-A:671682. 23. Schnee LL, Freese A, Weil RJ, Marcotte PJ. Analysis of harvest
4. Ebraheim NA, Rupp RE, Savolaine ER, Brown JA. Posterior plat- morbidity and radiographic outcome using autograft for anterior
ing of the cervical spine. J Spinal Disord 1995; 8:111115. cervical fusion. Spine 1997; 22: 22222227.
5. Osti OL, Fraser RD, Griffiths ER. Reduction and stabilization of 24. Garfin SR, Botte MJ, Waters RL, et al. Complications in the use
cervical dislocations. J Bone Joint Surg 1989; 71-B:275282. of the halo fixation device. J Bone Joint Surg 1986; 68-A:320325.
6. Murphy MJ, Daniaux H, Southwick WO. Posterior cervical fusion 25. Lind B, Sihlbom H, Hordwall A. Halo-vest treatment of unstable
with rigid internal fixation. Orthop Clin N America 1986; traumatic cervical spine injuries. Spine 1988; 13:425432.
17:5565. 26. Botte MJ, Byren TP, Abrams RA, Garfin SR. Halo skeletal fixa-
7. Levine AM, Edwards CC. Treatment of injuries in the C1C2 tion: Techniques of application and prevention of complications.
complex. Orthop Clin N America 1986; 17: 3144. J Am Acad Orthop Surg 1996; 4:4453.
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10
Surgical Management
for Thoracolumbar
Spinal Injuries

Paul E. Savas, M.D.


Alexander R. Vaccaro, M.D.

he thoracolumbar region of the or more organ systems (3). Intra-abdominal injury can

T spine is a common site for vertebral


injuries. The majority of thora-
columbar injuries are caused by
high-energy trauma. Almost half of these injuries result
occur in almost 50 percent of patients with a distraction-
type spine fracture (4). In approximately 5 to 20 percent
of patients with traumatic spine injuries, concomitant,
noncontiguous spine fractures may occur (5).
from motor vehicle accidents. the remaining from falls, The patient history should investigate the circum-
sports-related activities, violence, and other causes (1). stances of the accident. The physical examination should
Thoracolumbar fractures from low-energy injuries and include careful visual inspection and systematic palpation.
metabolic causes occur less frequently. These injuries are An abdominal contusion caused by a lap belt may be a
more often encountered in the elderly and may cause diagnostic clue for a flexion-distraction type injury of the
chronic severe pain and progressive neurologic deficit. spine and associated intra-abdominal injuries (6,7).
The indications for treatment and strategies of man- A complete systematic neurological examination can
agement for thoracolumbar injuries should be guided by help determine the anatomic level of spinal injury. The
a thorough understanding of spinal anatomy and biome- examination of reflex function can determine the extent
chanics, and injury mechanisms. of spinal cord injury (SC I) and spinal shock. The bulbo-
cavernosus reflex and the presence of sacral sensory spar-
ing can prognostically indicate functional recovery and
CLINICAL EVALUATION the presence of a complete or incomplete neurologic
deficit (8).
A careful patient history and physical examination are
essential in the evaluation of a patient with a spine injury.
Spine injuries may be missed during the initial emergency RADIOGRAPHIC EVALUATION
room evaluation because of diverting factors (2). In
patients with traumatic thoracolumbar injuries, associ- Anteroposterior and lateral radiographs of the entire
ated injuries are not uncommon. Up to 50 percent of these spine are the initial radiographic method for determin-
patients may have multisystem trauma: 30 percent hav- ing the level of spinal abnormality. Greater detail of the
ing trauma to one other organ system, 10 percent to 20 injury pattern can be revealed by computed tomography
percent to two other organ systems, and 5 percent to three (CT) scans and magnetic resonance imaging (MRI) scans.
143
144 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

CT is indicated for further evaluation of thora- protection. This may explain the increased incidence of
columbar injuries. Approximately 25 percent of burst catastrophic neurologic injury associated with thoracic
fractures may be misdiagnosed as stable wedge fractures spine fractures (18).
by plain radiographs (911). The lateral CT scout views The thoracolumbar region is a transitional junction
should not be overlooked; they may indicate vertebral between the stable, less mobile thoracic spine and the
fractures, particularly in the lumbar spine (12). more flexible lumbar spine. In this junctional region, the
MRI can provide prognostic information that may rib cage no longer provides protection and support, thus
help in the treatment of SCI. MRI is indicated in all cases rendering the thoracolumbar spine more vulnerable to
of acute neurologic deficit and in cases of progressive neu- injury and making it the most common location for burst
rological deterioration. fractures (19).
A classification of MRI spinal cord signal patterns
has been developed for T2 weighted images in acute
spinal injury (13). In Type I lesions a central hypo-dense SPINAL STABILITY
signal of hemorrhage surrounded by a hyper-dense sig-
nal of edema is observed. This lesion has the poorest prog- The definitions and classifications of spinal stability are
nosis for functional neurologic recovery. Type II lesions, various and are based on the integrity of both the skele-
are characterized by spinal cord enlargement and an area tal and neural structures of the spinal column.
of hyper-intensity or edema extending superiorly or infe- The evaluation of radiographs and biomechanical
riorly. Type II lesions have the best prognosis for neuro- studies of thoracolumbar injuries has demonstrated that
logic recovery. Type III lesions contain a small central area the spine functionally consists of load-bearing columns
of hypo-intense hemorrhage surrounded by an area of (2028). The anterior spinal column contains the ante-
hyper-intensity or edema, and can indicate the potential rior longitudinal ligament (ALL) and the anterior half of
for intermediate recovery. For the evaluation of late spine the vertebral body and annulus fibrosus. The middle col-
trauma, MRI can detect posttraumatic syringomyelia and umn contains the posterior half of the vertebral body and
myelomalacia. In the evaluation of SCI without radi- annulus fibrosus and the posterior longitudinal ligament
ographic abnormalities, MRI may be useful. This type of (PLL). The posterior column contains all structures pos-
SCI more commonly occurs in children less than 8 years terior to the PLL.
of age, and may be attributable to the characteristic fea- The anterior and middle vertebral columns provide
tures of the spine in this age group (14). the majority of the axial load-bearing capacity of the
spine. The posterior column resists tension and stabilizes
the load shared by the anterior column (22,29,30).
SPINAL ANATOMY Instability may occur after disruption of the middle
column, in addition to disruption of either the anterior or
The anatomic characteristics of the thoracic and lumbar posterior columns. Each column, however, does not con-
spine may contribute to the pattern of spinal injury. tribute equally to spinal stability (26).
The thoracic spinal cord is shielded from injury by The Dennis classification (24,25) of acute thora-
the regional paraspinal musculature and by the rigid tho- columbar injury is probably the most widely accepted.
racic rib cage. The sternum and rib cage significantly In this classification system, thoracolumbar injuries are
restrict thoracic spine motion and stabilize this region grouped into minor and major injuries. Minor injuries
(15). Increased stability of the thoracic spine is also a include fractures of the spinous and transverse processes,
function of facet joint orientation. The more coronal tho- the pars inter-articularis, and the facet joints. Major spinal
racic facets resist flexion and extension and provide min- injuries include compression wedge fractures, burst frac-
imal resistance to torsional loads. The more sagittal lum- tures, shear fractures, and fracture-dislocations.
bar facets permit significant flexion and extension and The criteria for spinal stability (24,25) have been
limit rotation (16). expanded to also include neurologic deficit, degree of
The physiologic kyphosis of the thoracic spine is deformity, and canal compromise (31).
related to the anterior wedging of the vertebral bodies. A mechanistic classification system, based on the
This kyphosis may predispose the thoracic spine to flex- column concept of spinal stability and associated deform-
ion instability, particularly after surgical laminectomy or ing forces, provides insight into the pathogenesis of tho-
traumatic posterior element destruction (17). racolumbar injuries (32).
Although the increased stability of the supporting In compression-flexion injuries, loading of the flexed
structures in the thoracic spine provides relative protec- spine creates compressive stress through the anterior col-
tion for the spinal cord, the narrower thoracic spinal umn and tension strain through the middle and posterior
canal diameter, as compared with the larger lumbar canal columns. Three major patterns of failure in this type of
diameter, leaves little room to spare for neural element mechanism can occur. In one pattern, only the anterior
SURGICAL MANAGEMENT FOR THORACOLUMBAR SPINAL INJURIES 145

column fails in compression: an anterior wedge com- the involved vertebra (37). These fractures are usually asso-
pression fracture results and the middle and posterior ciated with paraplegia. Neurologic decline occurs most
columns remain intact. In a second pattern, the posterior often with this injury mechanism (36,38). If there is no sur-
column is disrupted by tensile forces: an anterior wedge gically stabilization, progressive deformity can occur (39).
fracture develops and the middle column remains intact.
In a third pattern, the middle column fails in conjunction
with the other columns and elements of the middle col- NONOPERATIVE TREATMENT
umn are retropulsed into the spinal canal. Compression-
flexion injuries represent the most common mechanism Medical Management
of injury in thoracolumbar fractures.
Distraction injuries are less common and may occur Early medical management may play a critical role in the
in conjunction with flexion, extension, and lateral bend- treatment of acute thoracolumbar injuries with neuro-
ing deforming forces. Approximately 50 percent of logic deficit. Maintaining optimal spinal profusion
patients with distraction-type injuries have associated through aggressive medical resuscitation can favorably
intra-abdominal injuries and an increased incidence of influence neurologic recovery (40).
concomitant, noncontiguous spine fractures (4,6). Neurologic deficit following traumatic SCI is related
In flexion-distraction injuries, the fracture pattern is to structural damage of the neural elements and to com-
determined by the location of the axis of rotation at the plex molecular and cellular mechanisms. Local edema,
time of injury. When the axis of rotation is in the verte- microvascular disruption, and thrombotic events propa-
bral body, a compression fracture of the anterior verte- gate the release of various neurotoxic and inflammatory
bral body occurs in combination with posterior ligament mediators that may damage the blood-brain barrier and
disruption and facet joint dislocation. All the spinal neural elements (13,41,42).
columns fail under tension when the axis of rotation is Pharmacologic agents can protect the neural tissues
anterior to the vertebral column. from the deleterious effects of neurotoxic mediators
Chance-type fractures (33), or variations thereof, released at the time of spinal cord injury. Although vari-
occur primarily as a result of tensile failure. Tension fail- ous pharmacologic therapies have been suggested, none
ure can propagate through the bony spine only, through has unequivocally demonstrated reversal of SCI.
the ligamentous structures only, or through a combina- Intravenous steroids can contribute to cellular mem-
tion of these two patterns. brane stabilization, reduce edema, and buffer electrolyte
Distraction-extension injuries result from tension imbalances (13,43,44). The use of steroids, however, may
failure of the anterior column and compression failure increase the likelihood of pneumonia and sepsis in
of the posterior column: they are relatively rare (34). patients receiving a 48-hour steroid regimen (43,65).
These injuries may be difficult to detect by plain radi- Other pharmalogic agents and protocols are being
ographs, because they may spontaneously reduce shortly investigated (46), but none has unequivocally demon-
after injury (32,35). strated the reversal of SCI.
Lateral-flexion injuries develop when lateral bend-
ing of the spine causes an asymmetric compression of the
Closed Reduction and Immobilization
vertebral body and of the posterior elements. In one pat-
tern, the anterior and middle vertebral columns fail uni- Most mechanically stable thoracolumbar injuries with-
laterally. In another pattern, failure of the posterior ele- out neurologic deficit can be treated nonoperatively (46).
ments occurs from compression on one side and tension Nonoperative treatment should be considered in stable
on the other. On the side of tension failure, a unilateral injury patterns with limited potential for progressive
facet dislocation may occur. deformity and neurologic compromise.
Translational injuries develop when shear forces dis- Minor spine fractures are considered stable and may
place the vertebral body anteriorly, posteriorly, or later- be treated symptomatically, with or without bracing (48).
ally. With displacements greater than 25 percent, the facet These fractures should not be ignored and may signal
joints and all ligamentous structures, including the ALL, more significant associated injuries. Major spine frac-
are often disrupted. Because few or no stabilizing struc- tures, such as flexion-compression type fractures, with a
tures remain, this injury pattern has the highest risk of loss of vertebral body height of less than 50 percent, and
associated neurologic injury and can result in disabling initial kyphosis of less than 30 degrees, may be treated
chronic deformity (21,36). with closed reduction and immobilization by casting or
In torsion-flexion injuries, the anterior column fails bracing (49,50).
in compression and rotation while the posterior column Nonoperative treatment of mechanically unstable
fails in tension and rotation. The facet joints are usually thoracolumbar injuries without neurologic deficit remains
fractured and dislocated and the ALL may be stripped off controversial. The initial degree of mechanical instability,
146 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

kyphosis, and canal occlusion that can be managed non- can facilitate early rehabilitation and prevent late post-
operatively is not clear. Complication rates appear simi- traumatic deformity.
lar in both nonoperative and operative cases, with the
exception of surgical wound infections. The length of hos-
pital stay is longer in patients treated nonoperatively (51). OPERATIVE TREATMENT
Burst fractures with less than 30 degrees of kypho-
sis, less than 50 percent loss of vertebral body height, and Indications for Surgery
less than 50 percent canal compromise are considered sta-
The indications for surgical intervention of thoracolum-
ble (52,53). For stable thoracolumbar burst fractures
bar injuries depend on the pattern of injury, alignment
without neurologic deficit, no significant difference in
and stability of the vertebral fracture, neurologic status
functional outcome was observed in patients treated non-
of the patient, and overall medical condition of the
operatively when compared with those patients treated
patient.
operatively (54). Of forty-one patients treated nonoper-
atively, 66 percent had good or excellent results and 90
percent returned to full-time work (55). Similar results Timing of Surgery
have been observed by others (56,57). In patients with spinal injury and neurologic deficit, the
In some unstable thoracolumbar burst fractures optimal timing for medical and/or surgical intervention is
without neurologic deficit, functional outcomes appear debated.
favorable when treated nonoperatively (58,59). Although not conclusively demonstrated in human
Nonoperative treatment is less commonly used for clinical studies, a critical window of opportunity may
thoracolumbar flexion-distraction injuries and fracture- exist in which decompression of the spinal elements may
dislocations. Nonoperative treatment may be considered enhance functional neurologic outcome. In animal mod-
for purely bony flexion-distraction injuries. The results of els, early decompression influenced the potential for neu-
nonoperative treatment, however, are relatively poor. In rologic recovery. Decompression performed within 1 to
twenty-eight patients with a flexion-distraction injury, 3 hours of spinal injury led to recovery of electrophysio-
only one of thirteen patients treated surgically had a poor logic function (69). Some clinical studies suggest that early
outcome when compared to four of seven patients who decompression occurring less than 24 hours post injury,
were treated nonoperatively (60). Results were poor if may be optimal (70). In other cases, early surgical inter-
there was facet joint involvement or an initial kyphosis vention has led to an increase in neurologic deterioration
greater than 17 degrees (61). (71). In the only controlled prospective randomized study
Neurologic recovery can occur in patients with tho- to date, no significant difference in functional neural
racolumbar injuries treated nonoperatively. In patients recovery was demonstrated with surgical intervention,
with an incomplete neurologic deficit, improvement of early or late (72).
at least one Frankel grade was observed in as many as
95 percent of patients (62). When treated nonoperatively,
Surgical Decompression
eight of thirteen patients with thoracolumbar fractures
with neurologic deficit demonstrated complete neuro- In thoracolumbar injuries with neurologic deficit, the ben-
logical recovery. Neurologic recovery may in part be efit of surgical decompression is still undetermined
attributed to spontaneous remodeling of impinging bony (36,73,74). In patients with an incomplete neurologic
fragments within the spinal canal (58). deficit, improvement in neurologic function has been
Neurologic decline has been observed in 2 to 21 per- observed after surgical reduction and stabilization
cent of patients with thoracolumbar injuries treated non- (75,76). In patients with a complete neurologic deficit
operatively (6264). This may be related to late kyphotic and/or unstable thoracolumbar fracture, surgical stabi-
deformity and/or late spinal stenosis. Segmental kypho- lization has decreased hospitalization and rehabilitation
sis increased by an average of 6 to 10 degrees in 10 to 36 times and the rate of complication (77,78). Although
percent of patients managed nonoperatively (65,66). approximately 60 percent of patients with neurologic
Canal stenosis and kyphosis may additively cause neural injury below T12 will gain some return of neurologic
compression. Approximately 20 degrees of kyphosis function with nonoperative treatment, neurologic recov-
appears acceptable with less than 35 percent spinal canal ery is more predictable after anterior decompression in
occlusion, whereas 30 degrees of kyphosis, combined certain cases (73,79,80). Late decompression, even years
with more than 70 percent canal occlusion, increases the following injury, may enhance neurologic recovery at the
risk of neurologic symptoms (67). cord level, the conus medullaris, and the cauda equina
In patients with complete neurologic injury, nonop- (8183).
erative treatment with 4 to 6 weeks of bed rest yielded Despite varied opinions, there is no direct correla-
satisfactory results (68). Surgical stabilization, however, tion between the percentage of canal occlusion demon-
SURGICAL MANAGEMENT FOR THORACOLUMBAR SPINAL INJURIES 147

strated radiographically and the severity of neurologic terior instrumentation (91). A laminectomy may be per-
deficit following burst fractures (8486). The initial max- formed in selective cases of thoracolumbar injuries: the
imal amount of contusion of the spinal cord or cauda repair of dural tears caused by posterior-element fractures,
equina may be an underlying cause of neurologic injury. the evacuation of an epidural hematoma, and when direct
In patients with burst fractures, an increased risk of neu- neural compression from displaced posterior vertebral
rologic injury may be observed with spinal canal occlu- fracture fragments occurs (84). Posterolateral approaches
sion greater than 35 percent at T11 and T12, 45 percent for spinal decompression include costotransversectomy,
at L1, and 55 percent at L2 (87). In 148 patients with posterolateral transpedicular decompression, lateral extra-
burst fractures of the thoracolumbar spine, the average cavitary decompression, and lateral extrapleural paras-
percentage of canal compromise was higher in those with capular decompression (9296). Where there is signifi-
neurologic deficit (52 percent) than in those without neu- cantly lateralized or asymmetric anterior canal occlusion,
rologic deficit (35 percent). The degree of neurologic the posterolateral transpedicular and the lateral extra-cav-
impairment was greater in those patients with disruption itary approaches may be useful. These approaches are
of the posterior elements (69.2 percent) than in those with more advantageous in the lower lumbar regions, where
intact posterior elements (29.8 percent). However, the anterior instrumentation and reconstructive techniques
extent of neurologic recovery was greater in the patients pose risks to the neighboring great vessels. The lateral
with disruption of the posterior elements (60.7 percent) extrapleural parascapular decompression, a modification
than in those with no disruption of the posterior elements of the lateral extracavitary approach, may simplify access
(88). to the upper thoracic spine.
The outcomes of anterior versus posterior spinal The anterior approach is the most direct and reliable
surgery for the management of thoracolumbar injuries method for visualizing and decompressing the affected
have been compared. neural elements (83,97).
In a retrospective review of eighty-seven patients
with incomplete neurologic injuries, neurologic recovery
was greater with anterior decompression as compared INDICATIONS AND OPERATIVE TECHNIQUES
with posterior decompression, 88 versus 64 percent FOR THORACOLUMBAR INJURIES
respectively. This was more evident with regard to blad-
der and bowel control, 65 versus 33 percent respectively. Compression Fractures
Patients with inadequate posterior decompression and Surgical stabilization is indicated in compression wedge
residual neurologic deficit improved after a subsequent fractures if there is greater than 30 degrees of initial
anterior decompression (83). kyphosis, and/or greater than 50 percent loss of anterior
In sixty consecutive patients with SCI and greater vertebral body height with posterior element disruption.
than 20 percent encroachment of the spinal canal, no sig- Posterior spinal surgery is the most common method of
nificant change in neurologic improvement was detected the operative management of this injury. It relies on reduc-
if posterior or anterior surgery was performed (85 and 88 tion and stabilization of the fracture with distraction
percent respectively) (85). instrumentation (98).
In a prospective randomized study of forty patients Lateral flexion-compression fractures at risk for pro-
with burst fractures, treated either with indirect posterior gression can be stabilized with a distraction construct on
spinal decompression and stabilization with the AO fix- the injury side and a compression construct on the unin-
ateur, or with anterior decompression and fixation with jured side.
the Kostuik-Harrington device, it was found that anterior
decompression resulted in more effective canal clearance.
Burst Fractures
Correction of kyphosis was similar in both groups. Blood
loss was greater with the anterior surgery (79). The management of thoracolumbar burst fractures is con-
troversial. If surgery is elected, stabilization techniques
should be constructed for the specific fracture pattern. For
Surgical Approaches for Spinal Decompression
unstable burst fractures at the thoracolumbar junction
Decompression procedures may be performed posteriorly, with neurologic deficit, direct anterior decompression of
posterolaterally, or anteriorly. the neural elements followed by spinal stabilization
In thoracolumbar injuries, decompression by a should be considered (79).
laminectomy is usually destabilizing and should be avoided If decompression is elected, an anterior surgical
(89). A laminectomy, in these cases, may lead to post- approach provides more direct, predictable spinal canal
laminectomy kyphosis and progressive neurologic deficit decompression when compared to indirect decompres-
(37,90). The risk of progressive deformity from a laminec- sion by posterior ligamentotaxis (97). In one series, ante-
tomy may be reduced by the application of stabilizing pos- rior decompression improved spinal canal occlusion from
148 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

58 percent preoperatively to 4 percent postoperatively. By struct, spanning one level above and one level below the
posterior indirect reduction, spinal canal occlusion injured level, usually provides adequate stability. If the
improved from 45 percent preoperatively to 16.5 percent middle vertebral column is disrupted, caution should be
postoperatively (79). exercised to avoid retropulsion of bony fragments into
Following decompression, the type of reconstruc- the spinal canal. If the axis of rotation is within the ver-
tive technique selected should be based on the type of tebral body, and anterior column compression failure
fracture pattern and the extent of vertebral deficiency and develops, a distraction construct may be used. The ALL
deformity. serves as a stabilizing tension band in this situation.
If the posterior element tension band remains intact,
anterior and middle column insufficiency at the thora-
Fracture-Dislocations
columbar junction should be reconstructed with an inter-
body implant and reinforced with stand-alone anterior Fracture-dislocations are rotationally and/or translation-
instrumentation (99105). In 150 patients with thora- ally unstable and require surgical stabilization. Postural
columbar burst fractures with associated neurologic reduction is ineffective in bilateral facet dislocations
deficit managed with a one-stage anterior decompression, (122). Standard techniques of hyperextension position-
strut grafting, and anterior instrumentation, 95 percent ing are counterproductive in the reduction of fracture-dis-
of the patients demonstrated functional neurologic locations and may make the reduction more difficult. If
improvement of at least one Frankel grade, and 72 per- posterior reduction is not adequate, or residual neural
cent of the patients experienced complete neurologic compression is detected, additional anterior decompres-
recovery (106). In unstable fractures with posterior col- sion and stabilization may be performed following the
umn disruption, additional posterior stabilization should posterior approach (123).
be considered.
Despite the increased rigidity of posterior pedicle
Distraction-Extension Injuries
screw systems (107110), stand-alone posterior short-seg-
ment pedicle screw fixation of unstable thoracolumbar Distraction-extension injuries are uncommon, unstable
fractures has resulted in high failure rates (111,112). injuries that often are associated with neurologic injury.
These failures appear to be related to the fracture pat- Supine positioning may exacerbate the deformity and
tern and to the inability of the injured vertebral bodies may contribute to neurologic decline. After postural
to load-share. reduction, spinal stability and alignment can be main-
The best burst-fracture candidates for stand-alone tained by posterior segmental fixation. Anterior proce-
posterior short-segment fixation are those with less than dures are reserved for injuries with a significant anterior
30 percent vertebral body comminution on sagittal CT fish-mouth type deformity, which may lead to late spinal
images, less than 2 mm displacement between fracture instability.
fragments, and less than 10 degrees of kyphosis correc-
tion required (113).
In cases with significant anterior column deficiency CONCLUSION
not requiring decompression, stand-alone posterior short-
segment fusion and instrumentation should be avoided The appropriate treatment of thoracolumbar spinal
(111,114,115). A circumferential surgical approach injuries should be guided by a thorough understanding of
should be considered (116118). The sequence of surgi- the interrelationships of spinal anatomy, spinal biome-
cal technique depends on the fracture pattern. Anterior chanics, injury mechanisms, and fracture patterns. Early
decompression, and/or reconstruction, is usually per- medical management and early surgical decompression
formed first. Anterior column reconstruction improves may be beneficial in preserving and improving neurologic
the load-sharing and load-transferring ability of the ante- function. Nonoperative treatment can provide satisfac-
rior spinal column (119,120). If posterior instability is tory outcomes in most stable thoracolumbar injuries. For
present following the anterior procedure, posterior sta- unstable thoracolumbar injuries, with or without neuro-
bilization is recommended (121). logic deficit, surgical treatment should be considered.

Flexion-Distraction Injuries
References
1. Gertzbein SD. Scoliosis Research Society. Multicenter spine frac-
Flexion-distraction injuries involving predominantly soft ture study. Spine 1992; 17:528539.
tissue disruption should be surgically stabilized, because 2. Stansias MJ, Latham JM, Porter KM. A high-risk group for tho-
the disrupted interspinous ligaments, PLL and disc heal racolumbar fractures. Injury 1998; 29(1):1518.
3. Savitsky E, Votey S. Emergency department approach to acute
slowly and unpredictably in the adult (6). If the middle thoracolumbar spine injury J Emergency Med 1997; 15(1):4960.
column fulcrum is intact, a posterior compression con- 4. Gumley G, Taylor TKF, Ryan MD. Distraction fractures of the
SURGICAL MANAGEMENT FOR THORACOLUMBAR SPINAL INJURIES 149

lumbar spine. J Bone Surg Br 1982; 64(5):520525. columbar spine fractures. Clin Orthop Rel Res 1984; 189:7788.
5. Albert TJ, et al. Concomitant noncontiguous thoracolumbar and 33. Chance GQ. Note on a type of flexion fracture of the spine. Br
sacral fractures. Spine 1993; 18(10): 12851291. J Radiol 1948; 21:452.
6. Gertzbein S, Count-Brown C. Flexion-distraction injuries of the 34. Mabeshima Y, Iguchi T, Mastubara N. Extension injury of the tho-
lumbar spine. Clin Orthop 1988;227: 5052. racolumbar spine. Spine 1997; 22(13):15221525.
7. Ball, ST, Vaccaro, AR, Albert, TJ. Injuries of the thoracolumbar 35. Denis F, Burkus JK. Shear fracture-dislocations of the thoracic
spine associated with restraint use in head-on motor vehicle acci- and lumbar spine associated with forceful hyperextension (lum-
dents. J Spinal Disord 2000; 13(4): 297304. berjack paraplegia). Spine 1992; 17(2):156161.
8. Stauffer ES. Spinal cord injury syndromes. Semin Spine Surg 36. Gertzbein SD. Neurologic deterioration in patients with thoracic
1991; 3:8791. and lumbar fractures after admission to the hospital. Spine 1994;
9. Saboe LA, Reid DC, Davis LA. Spine trauma and associated 19(15):17231725.
injuries. J Trauma 1991; 31(1):4348. 37. An HS, Vaccaro AR, Cotler JM. Low lumbar burst fractures:
10. Keene JS. Radiographic evaluation of thoracolumbar fractures. Comparison among body cast, Harrington rod, Luque rod, and
Clin Orthop 1984; 189:58. Steffe plate. Spine 1991; 16:440444.
11. McAfee PC, Yaun HA, Fredrickson BE. The value of computed 38. Dorr LD, Harvey JP, Nickel VL. Clinical review of the early sta-
tomography in thoracolumbar fractures: An analysis of one hun- bility of spine injuries. Spine 1998; 7:545.
dred consecutive cases and a new classification. J Bone Joint Surg 39. Roberts J, Custiss P. Stability of the thoracic and lumbar spine
Am 1983; 65:461. in traumatic paraplegia following fracture or fracture-disloca-
12. Takada M, Wu CY, Lang TF. Vertebral fracture assessment using tion. J Bone Joint Surg Am 1970; 52(6): 11151130.
the lateral scoutview of computed tomography in comparison 40. Vale FL, Burns J, Jackson AB. Combined medical and surgical
with radiographs. Osteoporos Int 1998; 8(3):197-03. treatment after acute spinal cord injury: Results of a prospective
13. Bracken MB, Shephard MJ, Collins WF. A randomized, con- pilot study to assess the merits of aggressive medical resuscita-
trolled trial of methyl-prednisolone or naloxone in the treatment tion and blood pressure management. J Neurosug 1997;
of acute spinal-cord injury: Results of the Second National Acute 87(2):239246.
Spinal Cord Study. N Engl J Med 1990; 322:14051411. 41. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal
14. Pang D, Wilberger JE Jr. Spinal cord injury without radiographic cord injury: Recovery after immediate and delayed decompres-
abnormalities in children. J Neurosurg 1982; 57:11419. sion. J Bone Joint Surg Am 1995; 77:10421049.
15. Andriacchi TP, Schultz AB, Belytscko TB. A model for studies of 42. Salzman SK, Betz RR. Experimental treatment of spinal cord
mechanical interactions between the human spine and rib cage. injuries. In: Betz RR, Mulcaheny MJ (eds.), The Child with a
J Biomech 1974; 7:497. Spinal Cord Injury. Rosemont, IL: American Academy of
16. Markolf KL. Deformation of the thoracolumbar intervetebral Orthopaedic Surgeons, 1996; 63.
joints in response to external loads: A biomechanical study using 43. Bracken MB, Shephard MJ, Holford TR. Administration of
autopsy material. J Bone Joint Surg 1972; 54A:511533. methylprednisolone for 24 or 48 hours of tirilazad mesylate for
17. Denis F. Spinal stability as defined by the three-column spine con- 48 hours in the treatment of acute spinal cord injury. Results of
cept in acute spinal trauma. Clin Orthop 1984; 189:6576. the Third National Acute Spinal Cord Injury Randomized Con-
18. Harris JH Jr, Harris WM. The Radiology of Emergency Medi- trolled Trial. National Acute Spinal Cord Injury Study. JAMA
cine. Baltimore: Wilkins & Wilkins, 1975; 96. 1997; 277(20): 15971604.
19. Benzel EC, Larson SJ. Functional recovery after decompressive 44. Bracken MB, Holford TR. Effects of timing of methylpred-
operation for thoracic and lumbar spine fractures. Neurosurgery nisolone or naloxone administration on recovery of segmented
1986; 19:772777. and long-tract neurological function in NASCIS II. J Neurosurg
20. Holdsworth FW. Fractures, dislocations, and fracture-disloca- 1993; 79:500507.
tions of the spine. J Bone Joint Surg Br 1963; 45:6. 45. Bohlman HH, Ducker TB. Spine and spinal cord injuries. In:
21. Holdsworth FW. Fractures, dislocations, and fracture-disloca- Herkowitz HN, Garfin SR, Balderston FJ (eds.), The Spine, 3rd
tions of the spine. J Bone Joint Surg Am 1970; 52(8);15341551. ed. Philadelphia: W. B. Saunders, 1992; 9731103.
22. Kelly RP, Whitesides TE Jr. Treatment of lumbrosacral fracture- 46. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor func-
dislocations. Ann Surg 1968; 167:705. tion after spinal-cord injury: A randomized, placebo-controlled
23. Panjabi MM, Hausfeld JN, White AA. A biomechanical study trial with GM-1 ganglioside. New Engl J Med 1991; 324
of the ligamentous stability of the thoracic spine in man. Acta (26):18291838.
Orthop Scand 1981; 52:315326. 47. Vanichkachorn JS, Vaccaro AR. Nonoperative treatment of tho-
24. Denis F. The three-column spine and its significance in the clas- racolumbar fractures. Orthopedics 1997; 20:948953.
sification of acute thoracolumbar spinal injuries. Spine 1983; 48. Argenson C, Boileau. Specific injuries and management. In: Flo-
8(8):817831. man Y, Farcy JP, Argenson C (eds.), Thoracolumbar Spine Frac-
25. Denis F. Spinal instability as defined by the three-column spine tures. New York: Raven Press Ltd., 1993; 195214.
concept in acute spinal trauma. Clin Orthop Rel Res 1984; 49. Patwardhan AG, Li S, Gavin T. Orthotic stabilization of thora-
189:6576. columbar injuries. Spine 1990; 15:654661.
26. James KS, Wenger KH, Schlegel JA. Biomechanical evaluation 50. Hitchon PW, Turner JC, Haddad SF. Management options in tho-
of the stability of thoracolumbar burst fractures. Spine 1994; racolumbar burst fractures. Surg Neurol 1998; 49(6):619626.
19(15):17311740. 51. Rechtine GR, Cahill D, Chrin AM. Treatment of thoracolumbar
27. Oxland TR, Panjabi MM, Southern EP. An anatomic basis for trauma: Comparison of complications of operative versus non-
spinal instability: A porcine trauma model. J Orthop Res 1991; operative treatment. J Spinal Disord 1999; 12(5):406409.
9:452462. 52. Fredrickson BE, Yuan HA, Bayley JC. The nonsurgical treatment
28. Panjabi MM, Kifune M, Liu W. Graded thoracolumbar spinal of thoracolumbar injuries. Semin Spine Surg 1990; 2:7078.
injuries: Development of multidirectional instability. Eur Spine 53. Reid DC, Hu R, Davis LA. The nonsurgical treatment of burst
J 1998; 7(4):332339. fractures in the thoracolumbar spine. J Trauma 1988;
29. Haher TR, Bergman M, OBrien M. The effect of the three 28:11881194.
columns of the spine on the instantaneous axis of rotation on flex- 54. Kraemer WJ, Schemitsch EH, Lever J, et al. Functional outcome
ion and extension. Spine 1991; 16(Suppl 8):S312S318. of thoracolumbar burst fractures without neurological deficit. J
30. Haher TR, OBrien M, Felmy WT. Instantaneous axis of rotation Orthop Trauma 1996; 10:541544.
as a function of the three columns of the spine. Spine 1992; 55. Mumford JE, Weinstein JN. Conservative management of burst
17(Suppl 6):S149S154. fractures. In: Floman Y, Farcy JP, Argenson C (eds.), Thora-
31. McAfee PC, Yuan HA, Lasda NA. The unstable burst fracture. columbar Spine Fractures. New York: Raven Press Ltd., 1993;
Spine 1982; 7:365. 215222.
32. Ferguson RL, Allen BL. A mechanistic classification of thora- 56. Cantor JB, Lebwohl NH, Garvey T. Non-operative treatment of
150 ACUTE SPINAL CORD INJURY MANAGEMENT AND SURGICAL CONSIDERATIONS

stable thoracolumbar burst fractures with early ambulation and 83. Bradford DS, McBride GG. Surgical management of thora-
bracing. Spine 1993; 18:971976. columbar spine fractures with incomplete neurologic deficits. Clin
57. Weinstein JN, Collalto P, Lehmann TR. Thoracolumbar fractures Orthop Rel Res 1987; 218:201216.
treated conservatively: a long term follow up. Spine 1988; 84. Cammisa FP, Eismont FJ, Green BA. Dural laceration occurring
13:3338. with burst fractures and associated laminar fractures. J Bone Joint
58. de Klerk LW, Fontijne WP, Stijnen T. Spontaneous remodeling Surg Am 1989; 71:10441052.
of the spinal canal after conservative management of thora- 85. Gertzbein SD, Court-Brown CM, Marks P. The neurological out-
columbar burst fractures. Spine 1998; 23(9):10571060. come following surgery for spinal fractures. Spine 1988;
59. Shen WJ, Shen YS. Nonsurgical treatment of three-column tho- 13:641644.
racolumbar junction fractures without neurologic deficit. Spine 86. Johnson R, Herrlin K, Hagglund G. Spinal canal remodeling after
1999; 24(4):412415. thoracolumbar fractures with trauma spinal bone fragments: 17
60. Anderson PA, Henley MB, Rivara FP. Flexion-distraction injuries cases followed 14 years. Acta Orthop Scand 1991; 62:125127.
to the thoracolumbar spine. J Orthop Trauma 1991; 5:153160. 87. Hashimoto T, Kaneda K, Abumi K. Relationship between traumatic
61. Le Gay DA, Petrie DP, Alexander DL. Flexion-distraction injuries spinal canal stenosis and neurologic deficits in thoracolumbar burst
of the lumbar spine and associated abdominal trauma. J Trauma fractures. Spine 1988; 13:12681272.
1990; 30:436444. 88. Kim NH, Lee HM, Chun IM. Neurologic injury and recovery in
62. Fredrickson BE, Yuan HA, Miller HM. Burst fractures of the fifth patients with burst fracture of the thoracolumbar spine. Spine
lumbar vertebra. J Bone Joint Surg Am 1982; 64(7):10881093. 1999; 24(3):290294.
63. Denis F, Armstrong GW, Searls K. Acute thoracolumbar burst 89. Garfin SR, Mowery CA, Guerra J. Confirmation of the posterolat-
fractures in the absence of neurologic deficit. Clin Orthop Rel eral technique to decompress and fuse thoracolumbar spine burst
Res 1984; 189:142149. fractures. Spine 1985; 10(3):218223.
64. Mumford J, Weinstein JN, Spratt KF. Thoracolumbar burst frac- 90. Whitesides TE. Traumatic kyphosis of the thoracolumbar spine.
tures, the clinical efficacy, and outcome of nonoperative man- Clin Orthop Rel Res 1977; 128:7892.
agement. Spine 1993; 18:955970. 91. Cotler JM, Vernace JV, Michalski JA. The use of Harrington rods
65. Willen J, Lindahl S, Nordwall A. Unstable thoracolumbar frac- in thoracolumbar fractures. Orthop Clin North Am 1986;
tures. Spine 1985; 10(2):111122. 17(1):87103.
66. Spivak JM, Vaccaro AR, Cotler JM. Thoracolumbar spine 92. Hardaker WT, Cook WA, Friedman AH. Bilateral transpedicu-
trauma: II. Principles of management. J Am Acad Orthop Surg lar decompression and Harrington rod stabilization in the man-
1995; 3(6):353360. agement of severe thoracolumbar burst fractures. Spine 1992;
67. Tencer AF, Ferguson RL, Allen BL. A biomechanical study of tho- 17(2):162171.
racolumbar spinal fractures with bone in the canal: Part II. The 93. Ahlgren BD, Herkowitz HN. A Modified posterolateral approach
effect of flexion angulation. Spine 1985; 10:586589. to the thoracic spine. J Spinal Disord 1995; 8(1):6975.
68. Bohlman HH, Freehafer A, Dejak J. The results of treatment of 94. Maiman DJ, Larson SJ. Lateral extracavitary approach to the
acute injuries of the upper thoracic spine with paralysis. J Bone thoracic and lumbar spine. In: Rengachary SS, Wilkins RH (eds.),
Joint Surg Am 1985; 67:360369. Neurosurgical Operative Atlas. Philadelphia: Williams and
69. Carlson GD, Minato Y, Okada A. Early time-dependent decom- Wilkins, 1992; 153161.
pression for spinal cord injury: Vascular mechanisms of recov- 95. Graham AW, MacMillan M, Fessler RG. Lateral extracavitary
ery. J Neurotrauma 1997; 14(12):951962. approach to the thoracic and thoracolumbar spine. Orthopedics
70. Gaebler C, Maier R, Kutscha-Lissberg F. Results of spinal cord 1997; 20(7):605610.
decompression and thoracolumbar pedicle stabilization in rela- 96. Fessler RG, Dietz DD, MacMillan. Lateral parascapular
tion to the time of operation. Spinal Cord 1999; 37(1):3339. extrapleural approach to the upper thoracic spine. J Neurosurg
71. Sonntag VK, Francis PM. Patient selection and timing of surgery. 1991; 75:349355.
In: Benzel EC, Tator CH (eds.), Contemporary Management of 97. Crutcher JP, Anderson PA, King HA. Indirect spinal canal decom-
Spinal Cord Injury. Park Ridge, IL: American Association of pression in patients with thoracolumbar burst fractures treated
Neurologic Surgeons, 1995; 97108. by posterior distraction rods. J Spinal Disord 1991; 4:3948.
72. Vaccaro AR, Daugherty RJ, Sheehan TP. Neurologic outcome of 98. Harrington PR. Treatment of scoliosis: Correction and internal fix-
early versus late surgery for cervical spinal cord injury. Spine ation by spine instrumentation. J Bone Joint Surg Am 1962; 44:591.
1997; 22(22):26092613. 99. White AA, Panjabi M, Thomas CL. The clinical biomechanics
73. Kostuik JP. Anterior fixation for burst fractures of the thoracic of kyphotic deformities. Clin Orthop 1977; 128:817.
and lumbar spine with or without neurologic involvement. Spine 100. Marguiles JY, Caruso SA, Group J. Mechanical characterization
1988; 13:286293. of spinal fusion implant assemblies using a vertebrectomy model.
74. Boeger TO, Limb D, Dickson RA. Does canal clearance affect Spine State Art Rev 1996; 10:379396.
neurological outcome after thoracolumbar burst fractures? J 101. Caruso SA, Haher TR, Merola AA. The inverse effects of load
Bone Joint Surg Br 2000; 82(5):629635. transfer and load sharing on axial compression spinal stiffness:
75. Jacobs RR, Asher MA, Snider RK. Thoracolumbar spinal A mechanical model. Presented at the 64th Annual Meeting of
injuries. Spine 1980; 5(5):463477. the Academy of Orthopaedic Surgeons, San Francisco, 1997.
76. McEvoy RD, Bradford DS. The management of burst fractures 102. An HS, Lim TH, You JW. Biomechanical evaluation of anterior
of the thoracic and lumbar spine: Experience in 53 patients. Spine thoracolumbar spinal instrumentation. Spine 1995;20:19791983.
1985; 10:631. 103. Yuan HA, Mann KA, Found EM. Early clinical experience with
77. Schlegel J, Yuan H, Fredrickson B. Timing of surgical decom- the Syracuse I-plate: An anterior spinal fixation device. Spine
pression and fixation of acute spinal fractures. Ortho Trans 1992; 1988; 13:278285.
16:688. 104. Haas N, Blauth M, Tscherne H. Anterior plating in thoracolum-
78. Wilmont CB, Hall KM. Evaluation of acute surgical interven- bar spine injuries. Spine 1991; 16(3S):S100S111.
tion in traumatic paraplegia. Paraplegia 1986; 24:7176. 105. Kaneda K, Taneichi H, Abumi K. Anterior decompression and sta-
79. Esses SI, Botsford DJ, Kostuick JP. Evaluation of surgical treat- bilization with the Kaneda device for thoracolumbar burst frac-
ment of burst fractures. Spine 1990; 15:667673. tures associated with neurological deficits. J Bone Joint Surg Am
80. Dunn HK. Anterior stabilization of thoracolumbar injuries. Clin 1997; 79(1):6983.
Orthop Rel Res 1984; 189:116124. 106. Parker JW, Lane JR, Karaikovic EE. Successful short-segment
81. Bohlman HH, Kirkpatrick JS, Delamarter RB. Anterior decom- instrumentation and fusion for thoracolumbar spine fractures:
pression for late pain and paralysis after fractures of the thora- A consecutive 412-year series. Spine 2000; 25(9):11571170.
columbar spine. Clin Orthop Rel Res 1994; 300:2429. 107. Roy-Camille R, Saillant G, Mazel C. Plating of thoracic, thora-
82. Cooper PR. Management of posttraumatic spinal instability. columbar, and lumbar injuries with pedicle screw plates. Orthop
Amer Assoc Neurol Surg Publications Comm 1990; 135167. Clin North Am 1986; 17:147.
SURGICAL MANAGEMENT FOR THORACOLUMBAR SPINAL INJURIES 151

108. Dick W. The Fixateur Interne as a versitile implant for spine 116. Acaraglu ER, Schwab FJ, Farcy JP. Simultaneous anterior and
surgery. Spine 1987; 12(9):882889. posterior approaches for correction of late deformity due to tho-
109. Wiltse LL. A review of Stabilization of the lower thoracic and racolumbar fractures. Eur Spine J 1996; 5:5562.
lumbar spine with external skeletal fixation by Friedrich P. 117. Vaccaro AR. Combined anterior and posterior surgery for fractures
Magerl, MD. Clin Orthop Rel Res 1986; 203:6366. of the thoracolumbar spine. Instr Course Lect 1999; 48:443449.
110. Sasso RC, Cotler HB. Posterior instrumentation and fusion for 118. Been HD, Bouma GJ. Comparison of two types of surgery for
unstable fractures and fracture-dislocations of the thoracic and lum- thoracolumbar burst fractures: Combined anterior and posterior
bar spine. Spine 1993; 18(4):450460. stabilization vs. posterior instrumentation only. Acta Neurochir
111. McClain RF, Sparling E, Benson DR. Early failure of short-seg- 1999; 141(4):349357.
ment pedicle instrumentation for thoracolumbar fractures. J Bone 119. Thalgott JS, Kabins MB, Timlin M. Four-year experience with
Joint Surg Am 1993; 75(2): 162167. the AO anterior thoracolumbar locking plate. Spinal Cord 1997;
112. Ebelke DK, Asher MA, Neff JR. Survivorship analysis of VSP 35:286291.
spine instrumentation in the treatment of thoracolumbar and 120. Ghanayem AJ, Zdeblick TA. Anterior instrumentation in the
lumbar burst fractures. Spine 1991; 16:428. management of thoracolumbar burst fractures. Clin Orthop
113. McCormack T, Karaikovic E, Gaines RW. The load-sharing clas- 1997; 335:89100.
sification of spine fractures. Spine 1994; 19(15): 17411744. 121. Shiba K. Transpedicular fixation with Zielke instrumentation in
114. Gertzbein SD, Court-Brown CM, Jacobs RR. Decompression and the treatment of thoracolumbar and lumbar injuries. Spine 1994;
circumferential stabilization of unstable spinal fractures. Spine 19:19401949.
1988; 13:89213895. 122. Levine AM, Bosse M, Edwards CC. Bilateral facet dislocations
115. Allardyce TJ, Ramsey M, Cotler JM, Vaccaro AR. Early outcome in the thoracolumbar spine. Spine 1988; 13(6):630640.
of short segment pedicle fixation for thoracolumbar and lumbar 123. Edwards CC, Levine Am. Early rod-sleeve stabilization of the
burst fractures. Presented at the American Academy of injured thoracic and lumbar spine. Orthop Clin North Am 1986;
Orthopaedic Surgeons, Atlanta, GA, February, 1996. 17:121.
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III

MEDICAL MANAGEMENT
This Page Intentionally Left Blank
11 Respiratory Dysfunction in
Spinal Cord Disorders

Catherine S. H. Sassoon, M.D.


Ahmet Baydur, M.D., F.A.C.P., F.C.C.P.

ata from the U.S. National Spinal PATHOPHYSIOLOGY

D Cord Injury Statistical Center


reveal that the mortality rates for
individuals with neurologically
incomplete and complete cervical cord lesions are 9 and
Respiratory Muscles
The degree of respiratory impairment in patients with SCI
depends on the level of the injury, although partially func-
18 times higher, respectively, than for those of the same
tioning segments may contribute to improved function.
age in the general population (1). Life expectancy for
High cervical cord lesions (C1C4) are associated with the
complete tetraplegic patients who survive at least 24
greatest respiratory muscle dysfunction. Patients with
hours after injury is 22 years for 20-year-olds, 10 years
lesions at C1 and C2 cannot maintain effective sponta-
for 40-year-olds, and only 2 to 3 years for 60-year-old
neous ventilation. Low cervical cord lesions (C5C8) affect
patients. Diseases of the respiratory system are the lead-
the intercostal, parasternal, scalene, and abdominal mus-
ing cause of death in patients with cervical spinal cord
cles but leave the diaphragm, trapezii, sternocleidomas-
injuries (SCIs). Overall, 20 percent of deaths during the
toid, and the clavicular portion of the pectoralis major
first 15 years after injury are caused by respiratory ill-
muscles intact. Lesions at the thoracic level affect the inter-
nesses. Several factors adversely affect mortality, includ-
costal and abdominal muscles, whereas lesions at lumbar
ing the level of cord injury, age, pre-existing cardiopul-
levels cause little, if any, respiratory compromise.
monary disease, concomitant injuries, and delayed
Most studies on respiratory muscle function have
recognition of and attention to pulmonary problems
been performed, in the seated position, in patients with
(2,3). The level and the duration of cord injury have a
chronic injury (defined as an injury of 1 year duration or
significant impact on the function of the respiratory sys-
longer) (4). Recently Hopman and coworkers (5) showed
tem and its defenses. To understand the extent of respi-
that in patients with cord lesion at C4-C7, global respi-
ratory dysfunction in these patients, it is necessary to
ratory muscle strength decreased when compared to that
review the pathophysiology of respiratory dysfunction
of control subjects matched for age and body mass. Res-
that causes alterations in the respiratory pump and res-
piratory muscle strength was measured as maximum
piratory system control mechanisms.
inspiratory (PImax) and expiratory (PEmax) airway pres-
sures. PImax in the cord injury patients was 60 cm H2O

155
156 MEDICAL MANAGEMENT

versus 86 cm H2O in the control subjects. The PEmax was major for 6 weeks improves the expiratory function in
57 cm H2O versus 126 cm H2O, respectively. these patients (16). Estenne and coworkers (17) demon-
In the study by Sinderby and coworkers (6), approx- strated that the abdominal muscles retain their force-gen-
imately 80 percent of patients with low cervical cord erating ability if they are stimulated by an external source.
injury (C5C8) had diaphragm muscle strength within the The application of paired magnetic stimulation to the
range of that of normal subjects (mean, 120 cm H2O). abdominal muscles achieves an increased intrathoracic
Diaphragm muscle strength was measured as the maxi- pressure that exceeds the pressure required to cause
mum transdiaphragmatic pressure (PDImax). Subjects dynamic airway compression, thus providing the poten-
achieved this maximum pressure using a visual-feedback tial to improve cough and airway clearance. There was a
method in which the subject was encouraged to generate positive correlation between the change in gastric pres-
a target transdiaphragmatic pressure displayed on an sure (Pga) obtained during magnetic stimulation of the
oscilloscope (7). Despite the maintenance of inspiratory abdominal muscles at total lung capacity (TLC) and
muscle and diaphragm muscle strength, both global inspi- abdominal muscle thickness. This confirmed the associ-
ratory and diaphragm muscle endurance is limited in ation between atrophy of the abdominal muscles and the
these patients. When they breathed against an incremen- reduction in abdominal muscle strength. In these patients,
tal threshold load, the ratio of the pressure generated at abdominal muscle strength is 60 percent less than in
the maximum load to the PImax was significantly lower healthy control subjects (14). Abdominal muscles also
than that of the control subjects (49 versus 82 percent), demonstrate phasic electrical activity when ventilatory
suggesting that the inspiratory muscles have limited demand increases; such activity is absent during tidal
capacity to generate pressure against the load (5). These breathing (18). This phasic electromyographic activity is
findings indicate early development of inspiratory mus- believed to be triggered by stretching of the abdominal
cle fatigue (5). During resting breathing, the tensiontime wall on inspiration. Its effect decreases the compliance
index of the diaphragm (TTDI), defined as the product of of the abdominal wall, allowing the diaphragm to gener-
the ratio of mean transdiaphragmatic pressure (PDI) and ate a greater intra-abdominal pressure during inspiration,
PDImax, and the duty cycle (TI/Ttot; the ratio of inspira- and causing improved inflation of the lower rib cage.
tory time to total breath cycle duration, respectively) is With paralysis of both the major inspiratory and
higher than that of normal subjects (0.07 versus 0.04, expiratory muscles, as in patients with high spinal cord
respectively). This provides further evidence of diaphragm injury (C1C2), De Troyer and coworkers (19) demon-
muscle fatigue (6,8). In fact, during arm or leg ergome- strated that these patients can use the sternocleidomas-
ter exercises, seven of the ten patients with low cervical toid muscles, as well as other neck muscles (trapezeii,
cord injury were observed to develop diaphragm muscle platysma, sterno, and mylohyoid) to sustain brief periods
fatigue at low workloads, preceding the development of of spontaneous breathing. Contraction of these muscles
task failure (9). Despite the development of diaphragm expands the upper rib cage anteriorly, decreases pleural
muscle fatigue, those patients were still capable of increas- pressure, and is accompanied by a fall in intra-abdomi-
ing the PDI associated with increasing tidal volume (VT) nal pressure, thus causing inward displacement of the lat-
and respiratory frequency (fr) until task failure. Further- eral walls of the lower rib cage. Thus, the benefit of
more, conditioning of the diaphragm with inspiratory recruiting the accessory muscles to augment spontaneous
resistive training (10) or phrenic nerve stimulations breathing can be negated by the paradoxical movement
appear to improve strength and endurance of the of the lower rib cage.
diaphragm (11) and lung function (12).
In patients with low cervical cord injury, the
Respiratory Mechanics
diaphragm not only functions as the major inspiratory
muscle, but also as a trunk extensor muscle (13). When
Lung Mechanics
performing forward trunk flexion, these patients exhibit
continuous and augmented diaphragm electrical activity During acute injury, the forced vital capacity (FVC) of
and abdominal pressures (14). During posture imbalance, patients with tetraplegia is markedly reduced, with no
the postural needs temporarily override the respiratory expiratory reserve volume detectable (20). The level of
function, but this postural loading to the diaphragm risks injury, however, does not correlate with the FVC (21).
the development of diaphragm muscle fatigue (13). Ledsome and Sharp (20) showed that 1 week after injury,
Paralysis of the abdominal muscles in patients with the FVC of patients with tetraplegia (C5C6) was 30 per-
SCI results in ineffective cough and impaired clearance of cent and the forced expiratory volume in 1 sec (FEV1)
airway secretions. To assist in cough, during forced expi- was 27 percent of predicted normal value (20). Both FVC
ration patients with tetraplegia can recruit the clavicular and FEV1 improve significantly at 5 weeks (45 and 42
portion of the pectorals major to deflate the rib cage (15). percent of predicted, respectively) and continue to
Repetitive isometric contraction training of the pectoralis improve at 5 months after the injury (58 and 59 percent
RESPIRATORY DYSFUNCTION IN SPINAL CORD DISORDERS 157

of predicted, respectively) (20). Gains in ventilatory para- tion of changes in total lung capacity (TLC) and functional
meters are small thereafter (4,22). In the Ledsome and residual capacity (FRC) is similar to that of healthy sub-
Sharp (20) study, five patients with injury to the lowest jects: that is, both TLC and FRC decrease in the supine
functional segment of C4 showed a mean FVC 24 percent posture when compared to the seated posture (26,27). In
of predicted, and all of these patients required mechani- healthy subjects, VC decreases when changing from the
cal ventilatory support for 2 to 3 weeks. Three months upright to the supine posture (28). In contrast, patients
postinjury, their FVC increased to 44 percent of predicted with tetraplegia and high paraplegia exhibit VC increases
(range 18 to 62 percent). when changing from the upright to the supine posture (27)
The impaired function of the diaphragm in the acute (Figure 11.1). Estenne and De Troyer (27) described supine
stage of injury is attributable to the mechanical ineffi- position increases of 16 percent in tetraplegic subjects and
ciencies associated with paradoxical rib cage movement 11 percent in paraplegic subjects. This increase in VC in
and unfavorable changes in thoracoabdominal compli- the supine posture results primarily from the reduction in
ance as a result of inspiratory muscle paralysis. The residual volume (RV) caused by the effect of gravity on the
improvement of lung function over time could be related abdominal contents (Figure 11.2). The application of an
to improved neurologic function in the cord segments at abdominal binder helps to maintain the RV in the seated
and above the injury level. The development of spastic- posture by compressing the abdominal contents into the
ity and reflex contraction of the intercostal and abdomi- diaphragm, thus improving thoracoabdominal compliance
nal muscles may cause the rib cage to become more sta- and placing the diaphragm at a more efficient, stretched,
ble (23). In the acute stage, the degree of lung function resting posture. This effect appears to be independent of
impairment and the level of the injury are not predictive changes in intrathoracic blood volume (27).
of the recovery of lung function (22). The lung compliance (CstL) of patients with acute
In the chronic stage of injury, the level and com- and chronic tetraplegia is markedly reduced, approxi-
pleteness of injury, combined with tobacco smoking his- mately 52 percent of that of control healthy subjects (29).
tory, serve as predictors of lung function impairment This reduction in CstL plateaus 1 month after the injury
(24,25). Almenoff and coworkers (24) studied 165 and does not change significantly over time. When CstL
patients with SCI. Patients with high complete cervical is corrected for lung volume, the mean value falls to near
tetraplegia had lower FVC, FEV1, and peak expiratory 70 percent of predicted value for healthy subjects (29).
flow (PEF) than those with incomplete lesions of the same This suggests that the decrease in CstL is partly attribut-
and lower levels of injury. In the patients with low able to reduced lung volume and partly to the altered
tetraplegia or high and low paraplegia, the extent of the mechanical properties of the lung. De Troyer and Heil-
motor lesion did not affect the degree of lung function porn (30) demonstrated similar findings in their patients
impairment. Tobacco smoking played a significant role. with chronic tetraplegia (CstL of 60 percent of predicted
The FEV1 and PEF in current smokers were markedly value for healthy subjects) in whom intercostal muscle
reduced compared with ex-smokers and those who never activity was completely absent. Conversely, in the two
smoked. patients in whom intercostal muscle electrical activity was
Posture affects lung function in patients with SCI detected, CstL was within normal limits (93 percent of
(25). With the exception of vital capacity (VC), the direc- predicted). The authors concluded that the intercostal

5.0 7.0 FIGURE 11.1


Spinal Cord Injury Normal
The effect of the supine and
6.0 seated posture on vital capacity
4.0
VC - S upine (L)

(VC) in patients with SCI and


healthy subjects. In contrast to
3.0 5.0 healthy subjects, the VC of
patients with SCI (C4T7) is
higher in the supine than in the
2.0 4.0 seated posture. The dashed line is
line of identity. (From reference 27
with permission.)
1.0 3.0

1.0 2.0 3.0 4.0 5.0 3.0 4.0 5.0 6.0 7.0
VC - Seated (L) VC - Seated (L)
158 MEDICAL MANAGEMENT

4.0 FIGURE 11.2


Spinal Cord Injury Normal
3.0 The effect of the supine and
seated posture on residual vol-
3.0 ume (RV) in patients with SCI
RV - S upine (L)

and healthy subjects. The


2.0 markedly reduced residual vol-
ume (RV) in the supine posture is
2.0 responsible for the elevated vital
capacity (see Figure 11.1) and is
1.0 caused by the effect of gravity on
the abdominal contents in those
1.0 patients with paralyzed abdomi-
nal muscles. The dashed line is
line of identity. (From reference
1.0 2.0 3.0 4.0 1.0 2.0 3.0
27 with permission.)
RV - Seated (L) RV - Seated (L)

muscles help to stabilize the chest wall and prevent lung compared to healthy subjects (33). In addition, when
collapse. abdominal contents fall toward the pelvis as an upright
posture is achieved, the diaphragm lacks a fulcrum;
diaphragm contraction results in reduced lower rib cage
Chest Wall Mechanics
expansion and further reduces tidal volume. The use of
The chest wall compliance of patients with tetraplegia is binders while the patient is supine is not recommended,
also reduced. Estenne and De Troyer (31) studied thora- because restriction of the lower rib cage by this practice
coabdominal compliance in twenty patients with chronic reduces tidal volumes.
tetraplegia. The thoracic compliance decreased to an aver-
age of 55 percent of normal, whereas the abdominal com-
Airway Mechanics
pliance increased to 170 percent of normal. Thus, the
decreased chest wall compliance is primarily caused by During cough, healthy subjects develop peak pleural pres-
the abnormally stiff rib cage in the chronic stage of injury sures of greater than 100 cm H2O (34). This induces
(Table 11.1). The stiffened rib cage in these patients is dynamic compression of the intrathoracic airways, which
likely caused by alterations in the elastic properties of the causes the linear velocity and kinetic energy of the flow-
rib cage itself. With decreased physical activity, fewer ing gas to increase markedly (35), thus accelerating mucus
sighs (32), and paralysis of the intercostal muscles, rib secretions mouthward. Because of paralysis of the
cage excursion is diminished. With reduced load on rib abdominal muscles, the cough effort is impaired in
cage structures, a gradual stiffening of rib cage tendons patients with SCI, particularly in patients with tetraple-
and ligaments occurs, which can lead to ankylosis in the gia. Despite paralysis of the expiratory muscles, Estenne
rib cage joints (31). These compliance changes result in and coworkers (36) recently demonstrated evidence of
greater abdominal contribution to tidal volume, when dynamic airway compression in six of the twelve patients

TABLE 11.1
Static Lung and Chest Wall Compliance and its Rib Cage and
Abdominal Components in Patients with Quadriplegia

STATIC LUNG COMPLIANCE STATIC CHEST WALL COMPLIANCE RIB CAGE COMPLIANCE ABDOMINAL COMPLIANCE

LITER/CM LITER/CM LITER/CM LITER/CM


H2O PERCENT PRED H2O PERCENT PRED H2O PERCENT PRED H2O PERCENT PRED

0.215  0.010 73.4  3.4 0.132  0.009 72.1  4.5 0.085  0.005 55.1  3.4 0.047  0.004 170.7  15.0

Values are mean  SE; n  20. (From reference 31 with permission.)


RESPIRATORY DYSFUNCTION IN SPINAL CORD DISORDERS 159

studied. Patients who demonstrated dynamic airway com- larly, the metacholine hyperresponsiveness is also blocked
pression show an obvious flow plateau at lower lung vol- by baclofen, a -aminobutyric acid (GABA) agonist.
umes on the isovolume esophageal pressure flow curves Through interaction with GABA receptors, baclofen
(Figure 11.3). Direct observation with videoendoscopy inhibits the release of acetylcholine from the postgan-
confirms the dynamic compression of the airways in those glionic cholinergic neurons that innervate airway smooth
patients. The results of this study suggest that contraction muscle (41).
of the clavicular portion of the pectoralis major is capa-
ble of producing dynamic compression of the airways.
Control of Breathing
For this reason, strength-training of the pectoralis major
to enhance its pressure generating capacity will poten-
Pattern of Breathing
tially enhance cough effort, particularly when combined
with the application of an abdominal binder (36). The resting breathing pattern in patients with tetraple-
Although patients with tetraplegia demonstrate gia is characterized by a small VT, increased respiratory
dynamic airway collapse, one study of patients with rate, and a VE similar to that of age-matched healthy con-
chronic tetraplegia demonstrated a significant bron- trols (42). The inspiratory time (TI) is the same as in con-
chodilation effect with the administration of inhaled trols, whereas expiratory time (TE) is significantly short-
bronchodilator (37) and airway hyperreactivity to inhaled ened, thus accounting for the increase in respiratory
metacholine (38). The mechanism of this airway hyper- frequency. Mean inspiratory flow rate (VT/Ti) is smaller
responsiveness is thought to be caused by the unopposed than in controls. In the seated position, when VT is par-
cholinergic tone, since the inhaled anticholinergic agent, titioned between the rib cage and abdominal compart-
ipatropium bromide, blocks the response (3840). Simi- ments, expansion of the abdomen is associated with
expansion of the lower rib cage. However, rib cage expan-
sion is greater in the transverse than in the anteroposte-
8 A 70% VC
rior diameter. In addition, many of these patients have a
50% VC reduced anteroposterior diameter of the upper rib cage
30% VC (paradoxical rib cage motion) (43,44) (Figure 11.4). This
Ve xp (L/s )

paradoxical rib cage motion is predominantly seen in the


supine rather than in the seated posture, and is caused
4
by a paralysis of the rib cage inspiratory muscles, partic-
ularly the parasternal intercostals and the scalenes. This
.

paradoxical rib cage motion is less frequently seen in SCI


patients with injury at or below C7, because of the per-
0 sistent activity of the scalene muscles (43).
8 B
Ventilatory Drive
Ve xp (L/s )

Studies on the control of breathing in patients with


tetraplegia have shown conflicting results (4548). The
4 drive to breathe can be assessed as the ventilatory or
occlusion pressure response to hypercapnia during CO2
.

rebreathing. The occlusion pressure is the airway or


mouth pressure measured at 0.1 msec when the subject
0 breathes against an occlusion; this is commonly called
-20 0 20 40 P0.1. P0.1 reflects the neuromuscular drive, unaffected
Pes (cm H2O) by alterations in respiratory system mechanics. One study
in patients with chronic tetraplegia (C4C7) noted that
FIGURE 11.3 the slope of the ventilatory and P0.1 responses to hyper-
capnia were similar to those of the control subjects (45).
Isovolume esophageal pressure-flow curves computed at 70
This finding was attributed to the incomplete nature of
percent (closed circles), 50 percent (open circles), and 30 per-
cent (closed triangles) of vital capacity in representative
the spinal injury and the relatively low ventilatory
patients with quadriplegia. A. Patient without dynamic com- response in the control subjects. In other studies, depres-
pression of the airways. B. Patient with dynamic compression sion of the ventilatory and P0.1 responses to hypercapnia
of the airways, as indicated by the flow plateau at 50 percent was found after SCI. This was attributed to respiratory
and 30 percent of vital capacity. (From reference 36 with per- muscle weakness (46), decreased compliance (46), and/or
mission.) altered geometry of the chest wall (49). Recently, Man-
160 MEDICAL MANAGEMENT

A ness alone does not explain the blunted hypercapnic


Abdomen AP response and that these patients have an impairment in
chemoreceptor function.
Lower rib cage AP Information regarding the respiratory center
Lower rib cage response to hypoxia after tetraplegic injury is limited and
transverse inconclusive (45).
Upper rib cage AP
I 2 sec Load Compensation
B Despite the blunted response to hypercapnia, tetraplegic
Abdomen AP
patients free of hypoxemia have the ability to compensate
for an increased mechanical load, such as breathing
Lower rib cage AP against added inspiratory resistance (45). An added inspi-
Lower rib cage ratory resistive load results in an increase in the P0.1
transverse response to hypercapnia when compared to that of the
Upper rib cage AP
I unloaded condition (45). Neural inspiratory drive, esti-
2 sec
mated as the rate of rise of the moving average of the
FIGURE 11.4 diaphragmatic electromyogram (EMG), also increased
with an added load (47). These responses were similar
The pattern of breathing in a healthy control subject (A) and
to those seen in normal subjects. Likewise, the ventilatory
a patient with C5 SCI (B) partitioned into the abdominal and
and P0.1 responses to hypercapnia remain unchanged
rib cage compartments. The figure shows the respiratory
changes in anteroposterior (AP) diameter of the abdomen, with change in posture from the supine position to a 60-
lower rib cage (at fifth costal cartilage), and upper rib cage (at degree tilted position (48) or seated position (51) (which
manubrium sterni). Changes in the transverse diameter of the foreshortens the diaphragm and places it at a mechani-
lower rib cage are shown with an upward deflection indicat- cal disadvantage). Sassoon et al. (51) noted that the rate
ing an increase, and a downward deflection indicating a of rise of the diaphragmatic electromyogram response to
decrease in diameter. I indicates the duration of inspiration. hypercapnia was significantly higher in the seated than in
In the healthy subject, the abdomen and the rib cage diame- the supine position, a change that was not observed in a
ters increase uniformly and synchronously. In the patient with control group. Hence, the compensatory increase in
quadriplegia, the lower ribcage expands more in the transverse diaphragmatic activation with ventilatory loading or
than in the AP diameter, and the upper rib cage AP diameter
change in posture remains intact, despite disrupted affer-
decreases rather than increases (paradoxical motion of the
ent feedback from rib cage mechanoreceptors.
upper rib cage). (From reference 44 with permission.)
When tetraplegic patients are challenged with an
inspiratory resistive load, VT is preserved through the use
of defenses similar to those employed by healthy controls
ning and coworkers (50) demonstrated that tetraplegic (52). However, the inspiratory duration is significantly
patients (C5C8) having complete cord injury for at least less than in controls (53). In control subjects, the pro-
1 year had blunting of the ventilatory and P0.1 responses longed inspiratory duration during breathing against
to hypercapnia. The slope of the ventilatory response to inspiratory resistive load serves to minimize peak pres-
hypercapnia was significantly less than in control sub- sure, a variable directly proportional to the sensation of
jects, and the P0.1 response to CO2 was lower in the dyspnea (52,54). This is achieved at the expense of the
patients than in the control group. Even after normaliz- increased energy requirements of the inspiratory muscles
ing the above values with indices of respiratory muscle (52). Thus, the intensity of central neural output in
functionthat is, maximal voluntary ventilation and vital patients with SCI is maintained under loaded condition
capacity (VC)the responses remained low (Figure 11.5). to achieve adequate VT, but the respiratory timing com-
The blunting of the hypercapnic response does not seem ponent is altered, partly as a result of chest wall receptor
to be mediated by endogenous opioids, because the activity, perhaps in an attempt to minimize energy
administration of naloxone did not improve the response requirements (55).
(50). The authors also studied two subjects with acute
cord injury in whom sequential measurements were
obtained over 7 to 8 months. The blunted hypercapnic Sensation of Dyspnea
response persisted despite a 50 percent increase in VC, a In healthy subjects, the sensation of dyspnea that is per-
67 percent increase in PImax, and marked increase in expi- ceived as air hunger can be distinguished from dysp-
ratory reserve volume (ERV) (Figure 11.6). This suggests nea perceived as increased work and effort (56). Per-
that in patients with tetraplegia, respiratory muscle weak- ceived air hunger is consistently associated with
RESPIRATORY DYSFUNCTION IN SPINAL CORD DISORDERS 161

VE/ P CO2 / MVV [(mm Hg .102)-1]

VE/ P CO2 / VC [(min.mm Hg)-1]


4.0 2.0 0.8

VE/ P CO2 (L.min-1.mm Hg -1)


3.0 1.5 0.6

2.0 1.0 0.4

1.0 0.5 0.2

0.0 0.0 0.0


N Q N Q N Q

FIGURE 11.5

Left panel: Ventilatory response to hypercapnia (D E/ D PCO2) in nine patients with quadriplegia (Q) and eight normal (N)
subjects. Middle panel: The ventilatory response to hypercapnia normalized for maximum voluntary ventilation (MVV). Right
panel: The ventilatory response to hypercapnia normalized for vital capacity (VC), respectively. The ventilatory response to
hypercapnia in patients with Q is significantly less than in N subjects (p  0.001), even when normalized for indices of respi-
ratory muscle performance. Closed circles are mean values, bars are standard deviation. (From reference 50 with permission.)

changes in PCO2, whereas perceived work and effort ning and coworkers (58) studied the sensation of air
is associated with changes in ventilation. The sensation hunger in ventilator-dependent patients with C23
of air hunger arises as a result of chemoreceptor affer- quadriplegia. In this study, first VT and the respiratory
ent activity or medullary corollary discharge (56,57). frequency of the ventilator were maintained constant at
Conversely, the sensation of work and effort arises baseline ventilator settings while end-tidal CO2 (PETCO2)
from respiratory muscle mechanoreceptors, awareness of was increased. Then, VT was reduced 40 to 70 percent of
cortical motor drive to respiratory muscles, or both (56). baseline VT, while PETCO2 was maintained constant. The
In patients with SCI, the perception of air hunger to sensation of air hunger correlated significantly with the
increased PCO2 or reduced tidal volume is intact. Man- mean PETCO2. Similarly, there was a correlation between

2.0 FIGURE 11.6


0.4
P 0.1/ P CO2
VE/ P CO2

Upper panel: Sequential mea-


(cm H2O/torr)

1.6
(L/min/torr)

0.3
surements of the ventilatory
1.2
0.2 ( VE/ PCO2) and occlusion pres-
. 0.8 sure ( P0.1/ PCO2) responses to
0.1 hypercapnia, and respiratory
0.4
muscle function in two patients
0.0 0.0 with acute quadriplegia. Lower
0 100 200 300 0 100 200 300 panel: Improvement in respira-
Time from injury (days) tory muscle function, vital capac-
ity (VC), and maximum inspira-
tory pressure (MIP) was not
5 90 0.75 associated with an increase in the
ventilatory or occlusion pressure
MIP (cm H20)

4
response to hypercapnia. (From
ERV (L)

60 0.50
3
VC (L)

reference 50 with permission.)


2
30 0.25
1

0 0 0.00
0 100 200 300 0 100 200 300 0 100 200 300

Time from injury (days)


162 MEDICAL MANAGEMENT

VT and the sensation of air hunger, although the sen- amounts of secretions are produced because of unop-
sation of work or effort was not evaluated. Neverthe- posed vagal tone (64). This leads to acute respiratory dis-
less, these findings suggest that the sensation of air tress, hypoxemia, worsening hypercapnia (which may be
hunger in patients with tetraplegia is intact, and its mod- superimposed on chronic alveolar hypoventilation), and
ification is independent of afferent information from the the need for intubation for ventilatory support and air-
chest wall. way suctioning. When the expiratory muscles are assisted
to help eliminate secretions, these events can often be
avoided.
MANAGEMENT OF RESPIRATORY Cough flows will be diminished when a) the patient
COMPLICATIONS cannot inhale at least 1.5 L because of weak inspiratory
muscles; b) inadequate thoracic abdominal pressures can-
Respiratory Complications not be generated because of weak abdominal muscles or
loss of glottic control; c) weakened bulbar muscles or tra-
Respiratory failure following acute SCI may occur cheostomy preclude firm glottic closure or upper airway
because of partial or complete respiratory muscle paral- stability during the cough; or d) irreversible airway
ysis, fatigue of remaining intact muscles, or in association obstruction occurs, such as with tracheal stenosis or
with pleuropulmonary pathology. Jackson and Groomes chronic obstructive pulmonary disease. To prevent pneu-
(59), in their study of 205 patients with high quadriple- monia and respiratory failure, these patients more often
gia (C14), found the most common complications were receive supplemental oxygen and physical therapy to clear
atelectasis in 40 percent and pneumonia in 63 percent of airway secretions, rather than therapies to assist their res-
the patients. These findings are similar to those in Fish- piratory muscles.
burns study (60), which showed a 50 percent incidence
of atelectasis or pneumonia in spinal cord-injured patients
with injury level from C3 to T11. Assisted Cough Techniques
Many patients with high cervical cord injury will As a rule, anyone with a VC below 1.5 L should receive
recover substantial respiratory function following the a maximal insufflation delivered by a manual resuscita-
acute insult. Ledsome and Sharp (20) measured the vital tor or portable volume ventilator to achieve adequate
capacity (VC) sequentially in patients still breathing spon- cough flows. This action alone can more than double
taneously after cervical spinal damage and demonstrated peak cough flows (65). Once an optimal volume is
a progressive improvement from 31 percent to 58 percent reached, the expiratory muscles can either be self-assisted
of predicted VC between the 1st and 20th week. In a ret- or manually assisted by one of several methods that
rospective study, Carter et al. (61) showed that of the require care-provider assistance (66). Manually assisted
twenty-two patients with injury level at and below C4 coughing techniques include the costophrenic assist, the
with unilateral diaphragmatic paralysis, sixteen (73 per- Heimlich-type or abdominal thrust assist, anterior chest
cent) had improvement of VC after a mean interval of compression assist, and the counterrotation assist (65,66).
76 days, the longest duration for recovery being 14 Most individuals with inadequate vital capacities but
months. Even patients with a C2C3 level of injury can good bulbar muscle function can also be taught glos-
expect a significant recovery of diaphragmatic function. sopharyngeal breathing to obtain optimal volume (67).
Oo et al. (62) found that 25 percent of patients with a VC
of 15 ml/kg could be weaned off ventilatory support
between 93 and 430 (mean 246) days after injury; those Mechanically Assisted Coughing
with a VC of 10 ml/kg weaned later, on the average of Mechanical insufflationexsufflation involves the deliv-
290 days. The weaning time is likely to be influenced by ery of a maximal insufflation followed immediately by a
the duration of paralysis, because those recovering after decrease in pressure of about 80 cm H2O. It is indicated
prolonged paralysis have to regain diaphragm bulk. if the individual cannot maintain a spontaneous VC of
at least 1.5 L because of weak oropharyngeal muscles.
Mechanical insufflationexsufflation can generate as
Cough Effort and Secretion Clearance
much as 600 L/min of expiratory flow that exsufflates
Patients with neuromuscular disorders have diminished (sucks out) both the left and right airways. Insuffla-
cough capacity, primarily because of expiratory muscle tionexsufflation can be applied through a full-face mask,
weakness (63). When these patients, including those who a simple mouthpiece, or a translaryngeal or tracheostomy
have SCI, contract an upper respiratory infection, they tube. It is most effective when bulbar muscle function and
often produce airway secretions that they cannot clear airway patency are adequate to permit manually assisted
because of an ineffective cough. The most difficult prob- peak cough flows of 160 L/min or greater. The ability to
lem is in the acute phase of the cord injury, when large generate adequate peak cough flows is more important
RESPIRATORY DYSFUNCTION IN SPINAL CORD DISORDERS 163

than the ability to breathe in, because it permits the long-


TABLE 11.2
term management of individuals with high cervical cord
Indications for Assisted Ventilation in Individuals
injuries (68). Mechanical insufflationexsufflation can be
with Quadriplegia and Respiratory Failure
simpler and easier than manually assisted coughing,
which requires a cooperative patient, good coordination A. Signs and Symptoms:
between the patient and caregiver, and adequate physi- Clinical evidence of inspiratory muscle fatigue:
cal effort and frequent application. Dyspnea, tachypnea  30 breaths/min, paradoxi-
A weaning approach, emphasizing noninvasive cal breathing (chest-abdomen asynchrony)
inspiratory and expiratory muscle aids, can eliminate the Sleep dysfunction [frequent nocturnal awakenings
need for indwelling tracheostomy tubes and tracheal suc- (3), difficult arousals, morning or continuous
tioning in appropriate SCI individuals. In addition to the headaches]
cost reduction, ventilator users who are converted from Hypersomnolence
tracheostomy to predominantly noninvasive positive Difficulty with concentration
pressure ventilation (NPPV) for long-term ventilatory Irritability, anxiety
Impaired intellectual function
support prefer it for safety, convenience, comfort, speech,
Cor pulmonale
swallowing, sleep, and appearance (69). Evidence also Polycythemia
suggests that noninvasively supported 24-hour ventilator B. Physiologic Criteria:
users with functional bulbar musculature have signifi- FVC  10 ml/kg or 25 percent predicted
cantly fewer respiratory complications than tra- MVV  25 percent predicted (40 L/min in
cheostomy-supported patients (68). males,  25 L/min in females)
Fiberoptic bronchoscopy (FOB) should be reserved PImax 50 cm H2O
for atelectasis resulting from large mucus plugs, which Daytime PaCO2  50 mm Hg
cannot be removed by manual or mechanical coughing
Abbreviations: FVC, forced vital capacity; MVV, maximum
measures. Because FOB may cause tracheobronchial irri- voluntary ventilation; PImax, maximal inspiratory mouth pressure.
tation, edema, hypoxemia, and aspiration, this technique
is usually reserved for patients who have not responded
to more conservative measures, such as use of curved-tip
suction catheters for left lower lobe atelectasis (70), prone 37 percent mortality in 3 years for 26 traumatic SCI
positioning, bronchodilators, and careful hydration to patients on T-IPPV, including 20 patients with C13
ensure liquid secretions. quadriplegia. Carter et al. (74) reported a 49 percent mor-
tality rate in 35 respirator-dependent tetraplegic patients
on T-IPPV or electrophrenic respiration at a mean of 1.5
Ventilatory Assistance
years post-injury or 4 years after pacemaker placement,
respectively. Late ventilator weaning can occur months to
TRACHEOSTOMYINTERMITTENT POSITIVE PRESSURE years post-injury (75,76).
VENTILATION (T-IPPV). Tracheostomy and trach- Continuous ventilation at high volumes can help
eostomy-IPPV have been the mainstay in the long-term prevent the development of atelectasis, a common prob-
management of the high-level SCI patient. The lem in the acute setting. When it is used judiciously, the
tracheostomy is also maintained in patients using risks of complications from bronchopleural air leak, alve-
electrophrenic stimulation because of the tendency of these olar damage (volutrauma, pulmonary edema), and altered
patients to experience upper airway collapse during sleep hemodynamics can be minimized. Peterson and col-
(71) and as a safety measure in the event of phrenic pacer leagues (77) compared the weaning ability of twenty-three
failure. Indications for assisted ventilation in the SCI individuals with C34 quadriplegia receiving low VT ven-
individual are listed in Table 11.2. Because of an increased tilation (20 ml/kg body weight) with nineteen individ-
incidence of sleep-disordered breathing in SCI individuals, uals who received high VT ventilation (20 ml/kg body
periodic evaluation of lung function and nocturnal weight). Although the two groups were equivalent in neu-
monitoring of oxyhemoglobin saturation and end-tidal rologic level and completeness, muscular function, ini-
PCO2 should be done to determine the need for assisted tial spontaneous VC, the weaning method used (T-piece),
ventilation (67). and final spontaneous VC, those in the large VT group
Morbidity and mortality are high with T-IPPV. successfully weaned an average 21 days faster than the
Whiteneck et al. (72) reported that 55 percent of venti- lower VT group (38 days versus 59 days, p  0.02). Com-
lator-dependent SCI patients experienced yearly pul- plications (mostly pneumonia) were few and occurred at
monary problems with an average hospital stay of 22 days about the same rate in both groups.
per year. The survival rate in this study was 40 percent With the widespread use of endotracheal methods,
at 5 to 9 years post-injury (72). Splaingaard (73) reported complications related to tracheostomy and long-term
164 MEDICAL MANAGEMENT

T-IPPV are numerous. These include nosocomial pneu- tages as an option for interim or permanent ventilation of
monia, mucus plugging, cardiac arrhythmias, accidental high SCI individuals without severe bulbar dysfunction.
disconnection, chronic purulent bronchitis, granulation Miller et al. (82) described their experience using the pneu-
tissue formation, stomal infections, sinusitis, tracheoma- mobelt in high tetraplegic patients. Twelve subjects were
lacia, tracheal perforation, hemorrhage, stenosis, fistula, able to progress within days to up to 4 hours of continu-
vocal cord paralysis, and hypopharyngeal muscle dys- ous use, and thereafter to 12-hour or all-day use. The
function (2). The tracheostomy tube requires special major advantages included improved appearance (no tra-
attention, including regular bronchial suctioning, site cheostomy), speech, and mobility. Disadvantages included
care, and cannula changes. Swallowing difficulties may pump noise, promotion of stomach gas, and positioning
occur as a result of impediment to the strap muscles, glot- difficulties. By placing the corsets horizontal upper bor-
tic closure and cricopharyngeal sphincter function, and der approximately two finger breadths below the
compression of the esophagus. Tracheal suctioning may costophrenic junction, one can avoid the paradoxical
cause irritation, bleeding, the formation of granulation expansion of the chest caused by enclosure of the lower
tissues, increased secretions, and hypoxia. Suctioning thorax, as described by Hill (83). The pneumobelts major
often misses the left main bronchus (60). limitation is that individuals must be sitting upright to use
it. This device employs the same principle as the rocking
(oscillating) bed in displacing abdominal contents.
Noninvasive Ventilation
Noninvasive (i.e., nontracheostomy assisted) positive pres-
Electrophrenic Pacing
sure ventilation (NPPV) is increasingly used as an alterna-
tive for patients with chronic respiratory insufficiency. Such The main indications for electrophrenic stimulation are ven-
techniques have been described mostly in the management tilatory insufficiency caused by disruption of central control
of patients with muscular dystrophy and poliomyelitis over phrenic nerve motoneurons and malfunction of the res-
(67,78,79). Until the early 1980s, the literature concern- piratory control center (71). Diaphragmatic pacemakers
ing these methods was mostly limited to the application of cannot be used in patients with respiratory muscle paraly-
body (negative pressure, iron lung) ventilators (67). sis resulting from phrenic nerve (cell body) damage,
Upper airway collapse and aspiration are potential com- parenchymal lung disease, or acute respiratory failure. High
plications, and many patients are unable to tolerate this cervical cord injuries are treatable by diaphragmatic pacing,
method of ventilation over an extended period. provided that the lower motoneurons of the phrenic nerves
Respiratory support by intermittent positive pres- (C3C5) are intact (84). In addition, SCI individuals should
sure via a variety of nasal or oral interfaces has been used be neurologically stable for at least 3 months, and long-term
to support individuals with various neuromuscular and access to technological and clinical support services must be
chest wall disorders (67,76,80). Bach and Alba (76) present. Full time ventilatory support can often be achieved
showed that twenty-three of twenty-five ventilated with progressive conditioning of the diaphragm, usually
patients with traumatic tetraplegia could be converted after 3 to 4 months of bilateral pacing (84).
from tracheostomies to noninvasive ventilation through Fodstadt (85) reported the outcomes in forty
a carefully monitored sequence of manual and mechani- patients using diaphragm pacing unilaterally, on alternate
cal coughing techniques, progressive tracheostomy cuff sides, or both sides simultaneously, 8 to 24 hours daily.
deflation, and adjustment of delivered ventilator volumes Five tetraplegics used their pacers at different time inter-
for adequate insufflation and speech. Some patients can vals during sleep and intermittently during wakefulness.
master the use of mouth IPPV, or learn glossopharyngeal Six tetraplegics stopped pacing after intermittent phrenic
breathing to supplement tidal volumes. nerve stimulation for 1 month to 3 years. By lengthening
The biphasic positive airway pressure system the pulse duration, adjusting the threshold ramp, and
(BiPAP) is a simple, mechanical system that provides non- changing the inspiratory time, it was possible to increase
invasive respiratory pressure support via nasal mask. tidal volumes, decrease upper airway resistance, and
Unlike continuous positive airway pressure, it has the achieve smoother diaphragmatic contractions.
ability to provide different levels of inspiratory and expi- A permanent tracheostomy is usually a necessity
ratory positive airway pressure. The latter also provides with full-time pacing to keep the upper airway unob-
positive end-expiratory pressure. Tromans et al. (81) were structed. There is a lack of coordination between the
able to apply BiPAP successfully in twenty-eight patients. paced diaphragm, the upper airway muscles, and the
This technique was shown to be useful in preventing res- accessory respiratory muscles in these patients. Upper air-
piratory failure and as a means of facilitating weaning way resistance is augmented by diaphragmatic contrac-
from full-time ventilation. tion or diminished inspiratory upper airway muscular
Of the ventilator devices available for home use, the activity and may be induced by diaphragmatic pacing
pneumobelt (a cyclically inflated corset) may have advan- during sleep in patients with SCI (86).
RESPIRATORY DYSFUNCTION IN SPINAL CORD DISORDERS 165

Quality-of-Life Issues decrease in the ratio of high to low amplitude of the


diaphragmatic electromyogram) did not develop.
The incidence of traumatic SCI in the U.S. varies between
Other training programs have been described in
7,000 and 10,000 cases annually. Although 41 percent
tetraplegia. Huldtgren et al. (91) assessed lung volumes
of all SCI individuals require mechanical ventilation at
and PImax in patients who were treated 15 minutes a day
some time during the initial hospitalization, far fewer
for 6 weeks by lung insufflation using a manually oper-
patients require ventilatory support at discharge. Despite
ated pump and performing forced voluntary expirations
this, more patients with ventilator-dependent tetraplegia
and inspirations against a resistance. TLC, ERV, and VC
are surviving; 2 percent of patients were discharged uti-
all improved significantly upon treatment. PEmax and
lizing ventilators in 1973, compared to 6 percent through
PImax more than doubled after 6 weeks of treatment.
1986 (87). Although substantial personal care needs are
Interestingly, however, Huldtgren et al. (91) found that
required for all individuals with tetraplegia, there is a
while lung volumes remained well preserved in five
widely held belief that being dependent on a ventilator is
patients who were reassessed 5 years after treatment,
inconsistent with a high quality of life. Most of the liter-
PImax values had deteriorated towards pretreatment val-
ature on the quality of life in this population has focused
ues. These findings are consistent with the spontaneous
on the mentally incompetent or terminally ill individuals
improvement (without muscle training) in VC and other
for whom ventilator use does not prolong meaningful life
lung volumes seen several weeks following injury in SCI
(88). Recently, Bach and Tilton (89) evaluated the effects
individuals, but also the near return to baseline of mus-
of complete traumatic tetraplegia on the life satisfaction
cle force generation after cessation of nonresistive venti-
and well-being of eighty-seven persons, forty-two of
latory muscle endurance training in subjects with cystic
whom were ventilator supported 2 or more years after
fibrosis (92). Similar improvements in respiratory func-
injury. The ventilator-assisted individuals with tetraple-
tion were found by Rutchik et al. (93), who employed
gia were significantly more satisfied with their housing,
inspiratory resistive training over 8 weeks. By contrast,
family life, and employment (when applicable) than were
however, these authors found that in seven subjects in
the spontaneously breathing tetraplegics. Only 24 percent
whom measurements were obtained 6 months later, both
of the ventilator-assisted tetraplegic patients expressed
FVC and PImax remained preserved.
general dissatisfaction with their lives compared with 36
The endurance-type challenge offered by inspiratory
percent of the spontaneously breathing individuals.
resistive breathing is compatible with the predominant
Another longitudinal study by Krause (90) found
recruitment of Type I (slow) fibers (94). Endurance train-
that an SCI individuals life satisfaction continued to
ing has previously been shown to reprogram the genetic
improve over a 15-year period, which started at least 2
expression pattern of skeletal muscle, transforming its
years after injury. The ventilator-dependent individuals,
components to make it more resistant (95). Recently Gea
with more limited functional abilities than spontaneously
et al. (96) showed that breathing against moderate levels
breathing SCI patients, seem to place more importance
of inspiratory resistance quickly induces an increase in
on their family lives and personal relationships in evalu-
expression of the genes encoding the slow isoform of
ating their quality of life.
myosin-heavy chain (MHC) in canine respiratory mus-
cles. Thus, even transient respiratory overloads affect the
phenotypic characteristics of muscles. The type of MHC
Ventilatory Muscle Training in Quadriplegia
is the main factor that determines the velocity of muscle
One of the first clinical applications of respiratory mus- contraction, ATPase activity, and hence, the rate of mus-
cle training was diaphragm training in tetraplegic patients cle fatigue. Fibers consisting of slow MHC isoforms pro-
(10). Some patients are dyspneic in the upright position duce slow, economic contractions, whereas fast MHC iso-
(while performing daily activities). This is caused by the forms are adapted to producing rapid, powerful
caudal displacement of the diaphragm, which results in movements. An interesting implication of the study of
a shortening of its resting length. In these patients, respi- Gea et al. (96) is the possibility of inducing a phenotypic
ratory infections can increase respiratory load and reduce adaptation of respiratory muscles in humans through the
breathing reserves. Gross et al. (10) thought it reasonable use of a training protocol designed to increase endurance.
to train the diaphragm for increased strength and De Troyer et al. (15) demonstrated the expiratory
endurance under heavy loads at near-normal ventilations. activity generated by the clavicular portion of the pec-
The method chosen was voluntary eupneic inspiratory toralis major during voluntary expiratory efforts in
resistive training in tetraplegic patients. These authors tetraplegic subjects (see above). This was demonstrated
demonstrated a significant and progressive increase in by an expiratory reserve volume that averaged 0.5 L in
PImax at FRC and in the critical inspiratory mouth pres- the seated position. Because the pectoralis major has a
sure that developed in each inspiration below which elec- motor innervation from C5 to C7, its function is at least
tromyographic changes of diaphragmatic fatigue (i.e., a partly preserved after transection of the lower cervical
166 MEDICAL MANAGEMENT

cord, and its insertion on the medial half of the clavicle traumatic quadriplegia. J Neurosurg 1973; 39:596600.
3. Hachen HJ. Idealized care of the acutely injured spinal cord in
enables it to pull down the manubrium and upper ribs. Switzerland. J Trauma 1977; 17:931936.
This action results in the compression of the upper por- 4. Haas F, Axen K, Pineda H, Gandino D, Haas A. Temporal pul-
tion of the rib cage and partial deflation of the lungs. monary function changes in cervical cord injury. Arch Phys Med
Rehabil 1985; 66:139144.
Thus, cough in tetraplegic patients results from more than 5. Hopman MTE, Van der Woude LVH, Dallmeijer AJ, Snock G,
just passive elastic recoil of the respiratory system (97). Folgering HTM. Respiratory muscle strength and endurance in
By binding the abdomen with a nonelastic strap and individuals with tetraplegia. Spinal Cord 1997; 35:104108.
6. Sinderby C, Weinberg J, Sullivan L, Borg J, Lindstrom L, Grassino
strengthening the clavicular portion of the pectoralis A. Diaphragm function in patients with cervical cord injury or
major through appropriate training program (16), prior poliomyelitis infection. Spinal Cord 1996; 34:204213.
patients with SCI can increase their cough effort and clear 7. Laporta D, Grassino A. Assessment of transdiaphragmatic pres-
sure in humans. J Appl Physiol 1985; 58:14691471.
bronchial secretions. They might also be able to gener- 8. Bellemare F, A Grassino. Effect of pressure and timing of con-
ate higher intrathoracic pressures and the expiratory traction on human diaphragm fatigue assessed by phrenic nerve
flows described by Bach (65). stimulation. J Appl Physiol 1982; 53:11901195.