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Manual of Traumatic Brain Injury
© Demos Medical Publishing
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Manual of Traumatic Brain Injury
Assessment and Management
Second Edition
Editor
Felise S. Zollman, MD, FAAN, FAAMAAssistant Professor
Department of Neurological Sciences Rush University Medical Center
Chicago, Illinois
New York
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Visit our website at www.demosmedical.com
ISBN: 9781620700938e-book ISBN: 9781617052699
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Medicine is an ever-changing science. Research and clinical experience are continually expanding our knowledge, in particular our understanding of proper treatment and drug therapy. The authors, editors, and publisher have made every effort to ensure that all information in this book is in accordance with the state of knowledge at the time of production of the book. Nevertheless, the authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the contents of the publication. Every reader should examine carefully the package inserts accompanying each drug and should carefully check whether the dosage schedules mentioned therein or the contraindications stated by the manufac-turer differ from the statements made in this book. Such examination is particularly important with drugs that are either rarely used or have been newly released on the market.
Library of Congress Cataloging-in-Publication Data
Names: Zollman, Felise S., editor.Title: Manual of traumatic brain injury : assessment and management / editor, Felise S. Zollman.Other titles: Manual of traumatic brain injury managementDescription: Second edition. | New York, NY : Demos Medical Publishing, [2016] | Preceded by: Manual of traumatic brain injury management / [edited by] Felise S. Zollman. c2011. | Includes bibliographical references and index.Identifiers: LCCN 2015051250| ISBN 9781620700938 | ISBN 9781617052699 (e-book)Subjects: | MESH: Brain Injuries—diagnosis | Brain Injuries—rehabilitation | Brain Injuries—complicationsClassification: LCC RC387.5 | NLM WL 354 | DDC 617.4/81044—dc23 LC record available at http://lccn.loc.gov/2015051250.
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v
Contents
Contributors xi
Preface xxi
Part I: Core Concepts
1. Traumatic Brain Injury: Definitions and Nomenclature 3Kristine O’Phelan
2. Essential Concepts in TBI Biomechanics and Neuropathology 10Michelle C. LaPlaca
3. Characterization of Traumatic Brain Injury Severity 18Lisa A. Lombard
4. Epidemiology of Traumatic Brain Injury 25Marie Crandall
5. Injury Prevention 30Arlene I. Greenspan, Matthew Breiding, and Joanne Klevens
Part II: Mild Traumatic Brain Injury
6. Concussion and Mild Traumatic Brain Injury: Definitions, Distinctions, and Diagnostic Criteria 43
Noah D. Silverberg, Rael T. Lange, and Grant L. Iverson
7. Mild Traumatic Brain Injury: Initial Medical Evaluation and Management 50
Micelle J. Haydel
8. The Natural History of Mild Traumatic Brain Injury 59Grant L. Iverson, Noah D. Silverberg, and Rael T. Lange
9. Sport-Related Concussion I: Injury Prevention and Initial Assessment 65
Philip H. Montenigro, Daniella C. Sisniega, and Robert C. Cantu
10. Sport-Related Concussion II: Managing the Injured Athlete and Return-to-Play Decision Making 71
Mary Alexis Iaccarino and Ross Zafonte
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vi Contents
11. Second Impact Syndrome 81Gary Goldberg and William A. Robbins
12. Structural and Functional Brain Imaging in Mild Traumatic Brain Injury 90
Jeffrey David Lewine
13. Selected Somatic Disorders Associated With Mild Traumatic Brain Injury: Fatigue, Dizziness and Balance Impairment, and Whiplash Injury 100
Michael Henrie and Elie P. Elovic
14. Cognition in Mild Traumatic Brain Injury: Neuropsychological Assessment 109
Theodore Tsaousides, Kristen Dams-O’Connor, and Wayne A. Gordon
15. Postconcussion Syndrome: Diagnostic Characteristics and Clinical Manifestations 116
Erica Bellamkonda, Blessen C. Eapen, and Felise S. Zollman
16. Postconcussion Syndrome: Symptom Management 123William C. Walker and Richard D. Kunz
17. Confounding Factors in Postconcussive Disorders 130Nathan D. Zasler
18. Recognizing Manifestations of Posttraumatic Stress Disorder in Patients With Traumatic Brain Injury 139
Eric B. Larson
Part III: Moderate to Severe Traumatic Brain Injury
19. Field Management: Prehospital Care 149Joshua B. Gaither
20. Emergency Department Management and Initial Trauma Care Considerations 155
Stephen V. Cantrill
21. Imaging in Moderate to Severe Traumatic Brain Injury 160David N. Alexander
22. Neurosurgical Management of Skull Fractures and Intracranial Hemorrhage 169
Joshua M. Rosenow
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Contents vii
23. The Neurointensive Care Unit: Intracranial Pressure and Cerebral Oxygenation 178
Brandon A. Francis and Matthew B. Maas
24. Anoxia Complicating TBI 189Caroline Sizer and Gary Goldberg
25. The Role of Neuroprotective Interventions in Traumatic Brain Injury 200
David M. Panczykowski and David O. Okonkwo
26. Nutritional Considerations 208Aaron M. Cook and Barbara Magnuson Woodward
27. Initial Rehabilitation Interventions in the Acute Hospital Setting and Transitioning to the Next Level of Care 214
Brian D. Greenwald and Christine Greiss
28. Disorders of Consciousness 221Brian D. Greenwald and Phalgun Nori
29. The Role of Specialized Brain Injury Units in the Rehabilitation Process 228
Billie Schultz and Allen W. Brown
30. Rehabilitation Nursing 234Ann S. Bines
31. Physical Therapy: Mobility, Transfers, and Ambulation; Vestibular Rehabilitation 242
Catherine Burress Kestner
32. Occupational Therapy: Activities of Daily Living, Driving, and Community Reintegration 249
Jennifer Fleming and Deirdre R. Dawson
33. Speech Therapy: Dysphagia and Cognitive Communication Impairments 256
Julie Fuith-Costa
34. Neuro-Visual Processing Rehabilitation for Visual Dysfunction 265
William V. Padula and Jonathan Jenness
35. Cognitive Impairment: Characterization and Management 271Eric B. Larson
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viii Contents
36. Behavioral Impairment: Recognition and Management 279Jennifer Bogner and Tracy Shannon
37. Rational Neuropharmacology in Traumatic Brain Injury 289Durga Roy and Vani Rao
38. Pain Management in Persons With Traumatic Brain Injury 299Nathan D. Zasler
39. Assistive Technology in Traumatic Brain Injury 308Kurt L. Johnson and Mark Harniss
40. Practical Guidelines for Prognostication After Traumatic Brain Injury 315
Sunil Kothari and Craig DiTommaso
41. Sexuality After Traumatic Brain Injury 321Angelle M. Sander
42. Assessment of Decision-Making Capacity 326Eric S. Swirsky
43. Community Integration 336James F. Malec
Part IV: Complications and Long-Term Sequelae
44. Cranial Nerve Palsies 345Flora Hammond and Todd Masel
45. Hydrocephalus 352David F. Long
46. Posttraumatic Seizures 359Kan Ding and Ramon Diaz-Arrastia
47. Heterotopic Ossification 369Nora Cullen, Christina Taggart, and Cassandra Cowie
48. The Management of Endocrine Dysfunction in Traumatic Brain Injury 376
Lucy-Ann Behan and Amar Agha
49. Autonomic Dysfunction 383Cherina Cyborski
50. Movement Disorders 391Sangeeta Patel Driver and Cindy Zadikoff
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Contents ix
51. Spasticity in Traumatic Brain Injury 400Mary Alexis Iaccarino, Saurabha Bhatnagar, and Ross Zafonte
52. Screening for Emotional Distress After Traumatic Brain Injury 408Angelle M. Sander
53. Chronic Neuropsychiatric Sequelae I: Mood Disorders 418Hazem Shahin and Ricardo E. Jorge
54. Sleep Disturbances 425Felise S. Zollman and Eric B. Larson
55. Chronic Neuropsychiatric Sequelae II: Behavioral Disturbances 432
Theodore Tsaousides and Jason Krellman
56. Cumulative Effects of Repeated Mild Traumatic Brain Injury and Chronic Traumatic Encephalopathy 438
Philip H. Montenigro, Daniella C. Sisniega, and Robert C. Cantu
57. Posttraumatic Headache 447Thomas K. Watanabe
58. Neurovascular Complications After Nonpenetrating Brain Injury 456
Sunil Kothari, Michael M. Green, and Ana Durand-Sanchez
Part V: Special Considerations and Traumatic Brain Injury Resources
59. Pediatric Considerations in Traumatic Brain Injury Care 465Christopher Giza, Daniel Shrey, and Sharief Taraman
60. Special Considerations in Caring for the Workers’ Compensation Patient 472
Felise S. Zollman
61. Developing a Life Care Plan 476Debra E. Berens and Roger O. Weed
62. Traumatic Brain Injury in a Forensic Context 485Jerry J. Sweet and Laura M. Benson
63. Alcohol Misuse and Traumatic Brain Injury 492John D. Corrigan
64. Ethical Considerations 499Teresa A. Savage
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x Contents
65. Special Considerations for Military Personnel: Unique Aspects of Blast Injury 507
Michael S. Jaffee
66. Treatment and Rehabilitation Services for Mild to Moderate Traumatic Brain Injury in the Military 515
Deep S. Garg, Jason Georgekutty, and Amy O. Bowles
67. Management of Traumatic Brain Injury in the Older Adult 529Blessen C. Eapen, Carlos A. Jaramillo, and David X. Cifu
68. Complementary and Alternative Medicine in Traumatic Brain Injury 537
Felise S. Zollman
69. Return to Work Following Traumatic Brain Injury 545Theodore Tsaousides
70. Resources for Traumatic Brain Injury Survivors and Caregivers 552
Lisa Rosen and Elizabeth Wojciechowski
71. Living With Traumatic Brain Injury: From a Survivor’s Perspective 559
Jennifer Field
Index 567
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xi
Contributors
Amar Agha, MDConsultant EndocrinologistDepartment of Endocrinology and
Diabetes MetabolismBeaumont Hospital and RCSI Medical
SchoolDublin, Ireland
David N. Alexander, MDProfessor, Department of NeurologyUniversity of California, Los Angeles; Medical DirectorCalifornia Rehabilitation Institute &
UCLA’s Neurological Rehabilitation and Research Unit
Reed Neurological Research Center Los Angeles, California
Lucy-Ann Behan, MDConsultant EndocrinologistDepartment of Endocrinology and
Diabetes MetabolismTallaght Hospital and Trinity College
Medical SchoolDublin, Ireland
Erica Bellamkonda, MDConsultant and Assistant ProfessorDepartment of Physical Medicine and
RehabilitationMayo ClinicRochester, Minnesota
Laura M. Benson, PhDNeuropsychology ServiceDepartment of Psychiatry and
Behavioral SciencesNorthShore University HealthSystemEvanston, Illinois
Debra E. Berens, PhDRehabilitation Consultant/Life Care
PlannerPrivate PracticeAtlanta, Georgia
Saurabha Bhatnagar, MDInstructorDepartment of Physical Medicine and
RehabilitationHarvard Medical School,
Massachusetts General Hospital, and Spaulding Rehabilitation Hospital
Boston, Massachusetts
Ann S. Bines, MS, RN, CCRNNurse ManagerBrain Injury Medicine and
Rehabilitation ProgramRehabilitation Institute of ChicagoChicago, Illinois
Jennifer Bogner, PhD, ABPPVice-Chair of Research and Academic
AffairsAssociate ProfessorDepartment of Physical Medicine and
RehabilitationThe Ohio State UniversityColumbus, Ohio
Amy O. Bowles, MDDeputy Chief, Department of
Rehabilitation MedicineChief, Brain Injury Rehabilitation
ServiceBrooke Army Medical Center (BAMC)San Antonio, Texas
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xii Contributors
Matthew Breiding, PhDTraumatic Brain Injury Team LeadDivision of Violence PreventionNational Center for Injury Prevention
and ControlCenters for Disease Control and
PreventionAtlanta, Georgia
Allen W. Brown, MDAssociate Professor of Physical
Medicine and RehabilitationMayo Clinic College of MedicineMayo ClinicRochester, Minnesota
Catherine Burress Kestner, PT, DPT, NCS
Physical TherapistOutpatient Allied HealthRehabilitation Institute of ChicagoChicago, Illinois
Stephen V. Cantrill, MD, FACEPDepartment of Emergency
MedicineDenver Health Medical CenterDenver, Colorado;Associate ProfessorDepartment of Emergency
MedicineUniversity of Colorado School of
MedicineAurora, Colorado
Robert C. Cantu, MD, MA, FACS, FACSM
Chief, Neurosurgery ServiceChairman, Department of SurgeryDirector, Service of Sports MedicineEmerson HospitalConcord, Massachusetts;Clinical ProfessorDepartment of NeurosurgeryCodirectorCenter for the Study of Traumatic
EncephalopathyBoston University School of
MedicineBoston, Massachusetts
David X. Cifu, MDChairman and Herman J. Flax, MD
ProfessorDepartment of Physical Medicine
and RehabilitationFounding Director, Center for
Rehabilitation Sciences and Engineering
Virginia Commonwealth University
Richmond, Virginia
Aaron M. Cook, PharmD, BCPSClinical Coordinator-Neuroscience-
Pulmonary/Critical CareAssociate Adjunct Professor,
PharmacyDirector, PGY1 Pharmacy Residency
ProgramUniversity of KentuckyLexington, Kentucky
John D. Corrigan, PhD, ABPPDirector, Division of Rehabilitation
PsychologyProfessor, Department of
Physical Medicine and Rehabilitation
The Ohio State UniversityColumbus, Ohio
Cassandra Cowie, BScDepartment of ResearchUniversity Health Network –
Toronto Rehabilitation Institute
Toronto, Ontario, Canada
Marie Crandall, MD, MPH, FACSProfessor of SurgeryDirector of Research, Department of
SurgeryUniversity of Florida College of
Medicine JacksonvilleJacksonville, Florida
Nora Cullen, MD, MScAssociate ProfessorUniversity of TorontoToronto Rehabilitation InstituteToronto, Ontario, Canada
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Contributors xiii
Cherina Cyborski, MDChief of Rehabilitation ServicesNICoE/National Intrepid Center of
ExcellenceBethesda, Maryland
Kristen Dams-O’Connor, PhDAssociate Professor, Rehabilitation
MedicineDepartment of RehabilitationMount Sinai HospitalNew York, New York
Deirdre R. Dawson, PhDAssociate ProfessorDepartment of Occupational
Science and Occupational Therapy, and Rehabilitation Sciences Institute
University of Toronto;Senior ScientistRotman Research Institute,
Baycrest;Adjunct ScientistToronto Rehabilitation InstituteToronto, Ontario, Canada
Ramon Diaz-Arrastia, MD, PhDDirector of Clinical Research Center
for Neuroscience and Regenerative Medicine
Professor of NeurologyUniformed Services University of the
Health SciencesRockville, Maryland
Kan Ding, MDAssistant ProfessorDepartment of Neurology and
NeurotherapeuticsUT Southwestern Medical Center
at DallasDallas, Texas
Craig DiTommaso, MDAssistant Professor and Director of
Inpatient RehabilitationDepartment of Physical Medicine and
RehabilitationBaylor College of MedicineHouston, Texas
Ana Durand-Sanchez, MDAssistant ProfessorDepartment of Physical Medicine and
RehabilitationIndiana UniversityIndianapolis, Indiana
Blessen C. Eapen, MDSection Chief, Polytrauma
Rehabilitation CenterTBI/Polytrauma Fellowship Program
DirectorSouth Texas Veterans Health Care
SystemSan Antonio, Texas
Elie P. Elovic, MDDirector, Traumatic Brain Injury
ProgramRenown Rehabilitation HospitalRenown HealthReno, Nevada
Jennifer FieldJ Field FoundationWhite Stone, Virginia
Jennifer Fleming, PhDConjoint Associate ProfessorSchool of Health and Rehabilitation
SciencesThe University of Queensland; Occupational Therapy
DepartmentPrincess Alexandra
HospitalBrisbane, Australia
Brandon A. Francis, MD, MPHFellow in Neurocritical CareDepartment of NeurologyNorthwestern University, Feinberg
School of MedicineChicago, Illinois
Julie Fuith-Costa, MS, CCC-SLPClinical ManagerDay RehabilitationThe Rehabilitation Institute of
ChicagoRiver Forest, Illinois
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Joshua B. Gaither, MDAssociate Professor, Department of
Emergency MedicineUniversity of Arizona College of
MedicineTucson, Arizona
Deep S. Garg, MDTraumatic Brain Injury/Polytrauma
FellowDepartment of Physical Medicine and
RehabilitationAudie L. Murphy VA Medical CenterSan Antonio, Texas
Jason Georgekutty, DOTraumatic Brain Injury/Polytrauma
FellowDepartment of Physical Medicine and
RehabilitationAudie L. Murphy VA Medical CenterSan Antonio, Texas
Christopher Giza, MDDepartments of Pediatrics and
Pediatric NeurologyRonald Reagan UCLA Medical CenterUCLA Medical CenterSanta Monica, California
Gary Goldberg, MDMedical Director, Polytrauma
Transitional Rehabilitation ProgramHunter Holmes McGuire VA Medical
Center;ProfessorDepartment of Physical Medicine and
RehabilitationMedical College of VirginiaVirginia Commonwealth University
Health SystemRichmond, Virginia
Wayne A. Gordon, PhDProfessor, Rehabilitation MedicineAssociate Professor, PsychiatryDepartment of RehabilitationMount Sinai HospitalNew York, New York
Michael M. Green, DOAssistant Professor, Physical Medicine
and RehabilitationDepartment of Pediatrics/Physical
Medicine and RehabilitationUniversity of Utah School of
MedicineSalt Lake City, Utah
Arlene I. Greenspan, DrPH, MPH, PT
Associate Director for ScienceNational Center for Injury Prevention
and ControlCenters for Disease Control and
PreventionAtlanta, Georgia
Brian D. Greenwald, MDMedical Director, JFK Johnson
Rehabilitation Center for Head Injuries
Associate Medical Director, JFK Johnson Rehabilitation Institute
Clinical Associate ProfessorRutgers Robert Wood Johnson Medical
SchoolEdison, New Jersey
Christine Greiss, DO, FAAPMRClinical Assistant ProfessorJFK Johnson Rehabilitation InstituteDepartment of Physical Medicine and
RehabilitationRutgers Robert Wood Johnson Medical
SchoolEdison, New Jersey
Flora Hammond, MDCovalt Professor of Physical Medicine
and RehabilitationChair, Indiana University Department
of Physical Medicine and Rehabilitation
Chief of Medical Affairs, Rehabilitation Hospital of Indiana
Indianapolis, Indiana
xiv Contributors
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Mark Harniss, PhDClinical Associate ProfessorDepartment of Rehabilitation
MedicineSchool of MedicineUniversity of WashingtonSeattle, Washington
Micelle J. Haydel, MDAlbert J. Lauro Endowed Professorship
in Emergency MedicineClinical Professor of Medicine/
Emergency MedicineDirector of Education, Emergency
MedicineLouisiana State University Health
Sciences CenterNew Orleans, Louisiana
Michael Henrie, DOAssistant ProfessorDepartment of Physical Medicine and
RehabilitationUniversity of UtahSalt Lake City, Utah
Mary Alexis Iaccarino, MDBrain Injury Medicine FellowDepartment of Physical Medicine and
RehabilitationHarvard Medical School,
Massachusetts General Hospital, and Spaulding Rehabilitation Hospital
Boston, Massachusetts
Grant L. Iverson, PhDProfessorDepartment of Physical Medicine and
RehabilitationHarvard Medical SchoolCharlestown, Massachusetts
Michael S. Jaffee, MDAssociate ProfessorDepartment of NeurologyUniversity of Virginia Health SystemCharlottesville, Virginia
Carlos A. Jaramillo, MD, PhDStaff PhysicianPolytrauma Rehabilitation CenterSouth Texas Veterans Health Care
SystemSan Antonio, Texas
Jonathan Jenness, ODSenior ResidentPadula Institute of Vision
RehabilitationGuilford, Connecticut
Kurt L. Johnson, PhDProfessorDepartment of Rehabilitation
MedicineNancy and Buster Alvord Endowed
Professor in Multiple Sclerosis Research
School of MedicineUniversity of WashingtonSeattle, Washington
Ricardo E. Jorge, MDProfessorMenninger Department of Psychiatry
and Behavioral SciencesBeth K. and Stuart C. Yudofsky
Division of NeuropsychiatryBaylor College of MedicineHouston, Texas
Joanne Klevens, MD, MPH, PhDEpidemiologist, Sexual Violence and
Child Maltreatment TeamResearch and Evaluation BranchDivision of Violence PreventionCenters for Disease Control and
PreventionAtlanta, Georgia
Sunil Kothari, MD, MAAssistant ProfessorDepartment of Physical Medicine and
RehabilitationBaylor College of MedicineHouston, Texas
Contributors xv
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Jason Krellman, PhDAssistant Professor, Rehabilitation
MedicineDepartment of Rehabilitation
MedicineMount Sinai HospitalNew York, New York
Richard D. Kunz, MDAssistant ProfessorDepartment of Physical Medicine
and RehabilitationVirginia Commonwealth UniversityRichmond, Virginia
Rael T. Lange, PhDSenior Scientist/Research DirectorDefense and Veterans Brain Injury
CenterWalter Reed National Military Medical
CenterBethesda, Maryland
Michelle C. LaPlaca, PhDAssociate ProfessorDepartment of Biomedical
EngineeringGeorgia Technical Institute and
Emory UniversityAtlanta, Georgia
Eric B. Larson, PhDAssistant ProfessorDepartment of Physical Medicine
and RehabilitationNorthwestern University,
Feinberg School of MedicineChicago, Illinois
Jeffrey David Lewine, PhDProfessor of Translational
NeuroscienceThe Mind Research NetworkAlbuquerque, New Mexico
Lisa A. Lombard, MD Medical Director, Rehabilitation
Hosptial of Indiana;Assistant ProfessorDepartment of Physical Medicine and
RehabilitationIndiana University School of
MedicineIndianapolis, Indiana
David F. Long, MDMedical DirectorBrain Injury ProgramBryn Mawr Rehabilitation
HospitalMalvern, Pennsylvania
Matthew B. Maas, MDAssistant Professor of Neurology and
AnesthesiologyNorthwestern University, Feinberg
School of MedicineChicago, Illinois
Barbara Magnuson Woodward, PharmD, CNSC
Nutrition Support Service, Coordinator
UK HealthCare – Pharmacy Services;Associate Professor (Adjunct Series)Department of Pharmacy Practice and
ScienceUniversity of KentuckyCollege of PharmacyLexington, Kentucky
James F. Malec, PhD, ABPP-Cn, RpProfessor and Research DirectorPhysical Medicine and
RehabilitationIndiana University School of Medicine
and Rehabilitation Hospital of Indiana
Indianapolis, Indiana
xvi Contributors
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Todd Masel, MDAssistant Professor, Department of
NeurologyResidency Program Director,
Department of NeurologyUniversity of Texas Medical Branch
at GalvestonGalveston, Texas
Philip H. Montenigro, PhDMD/PhD CandidateDepartment of Anatomy and
NeurobiologyAlzheimer’s Disease and Chronic
Traumatic Encephalopathy Center
Boston University School of MedicineBoston, Massachusetts
Phalgun Nori, MDStaff Physician and Clinical
InvestigatorSan Antonio Polytrauma
Rehabilitation CenterSouth Texas Veterans Health
Care SystemSan Antonio, Texas
David O. Okonkwo, MD, PhDProfessor of Neurological
SurgeryDepartment of Neurological
SurgeryUniversity of Pittsburgh Medical
CenterPittsburgh, Pennsylvania
Kristine O’Phelan, MDAssociate Professor of Clinical
NeurologyDirector, Neurocritical CareUniversity of Miami, Miller School
of MedicineMiami, Florida
William V. Padula, OD, SFNAP, FAAO, FNORA
Associate ProfessorDepartment of Neuro-OptometrySalus University of Health Sciences
College of OptometryElkins Park, Pennsylvania;DirectorPadula Institute of Vision
RehabilitationGuilford, Connecticut
David M. Panczykowski, MDResident PhysicianDepartment of Neurological SurgeryUniversity of Pittsburgh
Medical CenterPittsburgh, Pennsylvania
Sangeeta Patel Driver, MD, MPHAttending Physician, Rehabilitation
Institute of ChicagoAssistant Professor, Department of
Physical Medicine and RehabilitationNorthwestern University, Feinberg
School of MedicineChicago, Illinois
Vani Rao, MBBS, MDAssociate ProfessorDirector, Brain Injury ProgramDirector, Behavior Neurology and
Neuropsychiatry Fellowship ProgramDepartment of Psychiatry and
Behavioral ScienceJohns Hopkins Bayview Medical CenterBaltimore, Maryland
William A. Robbins, MDTBI Polytrauma FellowDepartment of Physical Medicine
and Rehabilitation Hunter Holmes McGuire VA
Medical CenterRichmond, Virginia
Contributors xvii
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Lisa Rosen, MSManager, LIFE CenterRehabilitation Institute of ChicagoChicago, Illinois
Joshua M. Rosenow, MD, FAANS, FACS
Director, Stereotactic and Functional Neurosurgery
Northwestern Memorial HealthcareNorthwestern Memorial Hospital;Associate Professor of
Neurosurgery, Neurology, and Physical Medicine and Rehabilitation
Northwestern University, Feinberg School of Medicine
Chicago, Illinois
Durga Roy, MDAssistant ProfessorDepartment of Psychiatry and
Behavioral ScienceJohns Hopkins University School
of MedicineBaltimore, Maryland
Angelle M. Sander, PhDAssociate Professor and
Director, Division of Clinical Neuropsychology and Rehabilitation Psychology
Department of Physical Medicine and Rehabilitation
Baylor College of MedicineHouston, Texas
Teresa A. Savage, PhD, RNClinical Assistant ProfessorDepartment of Women, Children,
and Family Health ScienceUniversity of Illinois at ChicagoChicago, Illinois
Billie Schultz, MDAssistant Professor of Physical
Medicine and RehabilitationMayo Clinic College of MedicineMayo ClinicRochester, Minnesota
Hazem Shahin, MDAttending Physician, Rehabilitation
Institute of ChicagoAssistant Professor, Department
of Physical Medicine and Rehabilitation
Northwestern University, Feinberg School of Medicine
Chicago, Illinois
Tracy Shannon, PsyDClinical Assistant ProfessorDivision of Rehabilitation PsychologyDepartment of Physical Medicine
and RehabilitationThe Ohio State University
Wexner Medical CenterColumbus, Ohio
Daniel Shrey, MDAssistant Clinical ProfessorDepartment of NeurologyChildren’s Hospital of Orange County;Department of PediatricsUniversity of California–Irvine,
School of MedicineIrvine, California
Noah D. Silverberg, PhDClinical Assistant ProfessorDivision of Physical Medicine
and RehabilitationUniversity of British Columbia
and GF Strong Rehab CentreVancouver, British ColumbiaCanada
Daniella C. Sisniega, BSMD StudentBoston University School of MedicineBoston, Massachusetts
Caroline Sizer, MDTraumatic Brain Injury/Polytrauma
Fellow PhysicianDepartment of Physical Medicine and
RehabilitationHunter Holmes McGuire VA
Medical CenterRichmond, Virginia
xviii Contributors
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Jerry J. Sweet, PhD, ABPPDirector, Neuropsychology
ServiceHead, Psychology DivisionVice Chair, Department of Psychiatry
and Behavioral SciencesNorthShore University
HealthSystemEvanston, Illinois
Eric S. Swirsky, JD, MADirector of Graduate StudiesClinical Assistant ProfessorCollege of Applied Health
SciencesDepartment of Biomedical and Health
Information SciencesUniversity of Illinois at
ChicagoChicago, Illinois
Christina Taggart, BA, MADepartment of ResearchUniversity Health Network – Toronto
Rehabilitation InstituteToronto, Ontario, Canada
Sharief Taraman, MDPediatric Neurology and Medical
InformaticsDirector, Multi-Disciplinary
Concussion ClinicAssistant Division Chief,
NeurologyCHOC Children’s SpecialistsHealth Sciences Assistant Clinical
ProfessorDepartment of PediatricsUniversity of California–Irvine, School
of MedicineIrvine, California
Theodore Tsaousides, PhDAssistant ProfessorDepartment of Rehabilitation
MedicineIcahn School of Medicine at
Mount SinaiNew York, New York
William C. Walker, MDErnst and Helga Prosser
ProfessorDepartment of Physical Medicine
and RehabilitationVirginia Commonwealth
UniversityRichmond, Virginia
Thomas K. Watanabe, MDClinical Director, Drucker Brain
Injury CenterDepartment of Physical Medicine
and RehabilitationMossRehab/Einstein Healthcare
NetworkElkins Park, Pennsylvania
Roger O. Weed, PhDProfessor EmeritusGeorgia State UniversityAtlanta, Georgia
Elizabeth Wojciechowski, PhD, PMH-CNS-BC
Education Program Manager, LIFE Center
Rehabilitation Institute of Chicago
Chicago, Illinois
Cindy Zadikoff, MD, MScAssociate ProfessorNorthwestern University,
Feinberg School of Medicine
Chicago, Illinois
Ross Zafonte, DOEarle P. and Ida S. Charlton Professor
and ChairmanDepartment of Physical Medicine and
RehabilitationHarvard Medical School,
Massachusetts General Hospital, and Spaulding Rehabilitation Hospital
Boston, Massachusetts
Contributors xix
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Nathan D. Zasler, MD, FAAPMR, FAADEP, DAAPM, CBIST
Professor, Department of Physical Medicine and Rehabilitation
Virginia Commonwealth UniversityRichmond, Virginia;Associate Professor, AdjunctDepartment of Physical Medicine and
RehabilitationUniversity of VirginiaCharlottesville, Virginia
Felise S. Zollman, MD, FAAN, FAAMA
Assistant ProfessorDepartment of Neurological SciencesRush University Medical CenterChicago, Illinois
xx Contributors
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Preface
The first edition of the Manual of Traumatic Brain Injury Management, published in 2011, was designed to fill a unique niche: to provide relevant clinical information about management of traumatic brain injury (TBI) in a succinct, readily accessible format while at the same time offering readers specific electronic and print recommendations on each topic for those who wished to delve deeper. This second edition serves to update chapter content on the basis of knowledge devel-oped in this rapidly growing field since publication of the first edition, and to further refine the approach to delivery of content. Every chapter has been revised to reflect our knowledge base as of 2016, from clinical content to additional read-ing recommendations. For many topics, content was comprehensively overhauled (e.g., expanded discussion of injury prevention and chronic traumatic encepha-lopathy). Several new chapters have also been added, including anoxia compli-cating TBI, screening for emotional distress in TBI patients, assistive technology in TBI, and management of chronic behavioral disturbances. Each chapter now includes a Key Points section, intended to focus the reader’s attention on the most critical content within.
This edition is divided into five parts. Part I, Core Concepts, acquaints the reader with the basic essentials needed to provide a context for clinical decision-making. Part II, Mild Traumatic Brain Injury, offers a comprehensive treatment of this topic, including natural history, initial management, postconcussion syn-drome, and sport concussion. Part III, Moderate to Severe Traumatic Brain Injury, covers prehospital and intensive care management, rehabilitation care, commu-nity reintegration, and management of selected associated impairments, including cognitive and behavioral impairments, challenges with sexuality, and decision-making capacity. A chapter on prognosis in TBI provides an evidence-based, concise approach to understanding postinjury outcomes. Part IV, Complications and Long-Term Sequelae, covers a variety of topics from posttraumatic epilepsy and hydrocephalus to chronic cognitive, behavioral, and motor impairments, including spasticity and movement disorders. Part V, Special Considerations and Traumatic Brain Injury Resources, addresses selected populations based on age (pediatrics and geriatrics) or injury environment (military, workers’ compensa-tion), as well as return to work, complementary and alternative treatment modali-ties, and ethical and medicolegal issues associated with TBI, and offers a unique perspective on life after TBI from a patient’s perspective.
The content of this book can be digested at several levels of complexity: as a succinct introduction to TBI, reliant on the Key Points provided in each chapter; as a concise but thorough chapter by chapter treatment of each topic relevant to TBI; or as a springboard to more comprehensive learning based on the directed addi-tional resource recommendations of each chapter author. There is truly something meaningful in the pages which follow for everyone interested in understanding the management of traumatic brain injury.
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PART I
Core Concepts
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1
Traumatic Brain Injury: Definitions and Nomenclature
Kristine O’Phelan
Traumatic brain injury (TBI) has a broad spectrum of severity, pathology, physiology, and sequela. This chapter will present pertinent definitions, nomen-clature, and concepts relevant to the discussion of TBI.
PRIMARY VERSUS SECONDARY INJURY
The distinction is somewhat arbitrary and the specific combination and magnitude of secondary injury is to a great extent determined by the nature of the primary injury. This description is useful, however, in order to aid clinicians in identifying potential preventable or reversible causes of secondary brain injury. (See Chapter 2 for further details.)
• Primary injury—the physiological or anatomical insult, often but not exclusively the result of direct trauma to head. The primary injury may be associated with structural changes resulting from mechanical forces initially applied during injury. These forces may cause tissue distortion, shearing, and vascular injury as well as destabilization of cell membranes and frank mem-brane destruction.
• Secondary injury—systemic or local changes, which increase tissue damage. Many secondary insults result directly from the primary injury and some are caused by discreet systemic or local phenomena. Secondary injury mechanisms include generation of free radicals, excitotoxicity, disturbance of ionic homeo-stasis, disruption of the blood–brain barrier, generation of nitric oxide, lipid peroxidation, mitochondrial dysfunction and energy failure, inflammation, secondary hemorrhage, axonal disruption, apoptotic cell death, and ischemia. Ischemia may be due to microvascular changes, systemic hypotension or hypoxia, or elevated intracranial pressure.
CLASSIFICATION OF TBI BY MECHANISM
This classification is useful because injuries produced by different mechanisms are distinct in their pathophysiologies and natural courses.
• Closed/blunt force—injury caused by direct force to head, acceleration– deceleration, or rotational forces. Common causes include falls, assaults, and motor vehicle collisions.
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4 I. Core Concepts
• Blast injury—injury caused by overpressure waves generated from high-grade explosives. A large amount of thermal, mechanical, and electromagnetic energy is transferred to the brain. Energy can come directly through the cranium or be transmitted indirectly through oscillating pressures in fluid-filled large blood vessels. This may cause damage to the blood–brain barrier or gray–white matter junction, and can cause cerebral edema, axonal injury, apoptosis, and tissue degeneration.
• Penetrating injury—injury induced by an object that penetrates the cranial vault. Common causes include gunshot wounds, shrapnel, and knife wounds.
TABLE 1.1 Glasgow Coma Scale
Eye Opening Best Verbal Response Best Motor ResponseSpontaneous 4 Oriented 5 Obeys commands 6To speech 3 Confused conversation 4 Localizes pain 5To pain 2 Inappropriate words 3 Withdrawal 4None 1 Incomprehensible sounds 2
None 1Abnormal flexion
(decorticate) 3Extension (decerebrate) 2None 1
STRUCTURALLY BASED DESCRIPTIONS OF TBI
Structural descriptions incorporate information from imaging studies. They often aide in selection of patients who may benefit from a specific therapy such as surgi-cal evacuation of a hematoma.
CLINICAL CLASSIFICATION OF TBI
The Glasgow Coma Scale (GCS) [1] (Table 1.1) is central to clinical classification of TBI. Clinical/injury severity classification is the most com-monly used classification system in the clinical care of patients with TBI as well as in clinical neurotrauma research. (See Chapter 3 for further discussion of this topic.)
• Mild TBI (MTBI)—GCS 13 to 15, the majority of patients with cranial trauma fall in this group. Patients are awake, and may be confused but can communi-cate and follow commands.
• Moderate TBI—GCS 9 to 12, these patients are generally drowsy to obtunded but not comatose. They can open their eyes and localize painful stimuli. They are at high risk of clinical deterioration and must be monitored carefully.
• Severe TBI—GCS 3 to 8, these patients are obtunded to comatose, they do not follow commands and may exhibit decerebrate or decorticate posturing. They have significant structural and metabolic brain dysfunction and are at high risk of secondary brain injury and deterioration.
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1. Traumatic Brain Injury: Definitions and Nomenclature 5
• Epidural hematoma (EDH) (Figure 1.1)—an extradural collection of blood. It is often associated with a skull fracture and typically has an arterial origin. Margins of the hematoma do not cross the skull suture lines and often appear convex on imaging studies. If an EDH is evacuated in a timely fashion to reverse mass effect or if the hematoma is small in size, patient outcomes are usually good.
• Subdural hematoma (SDH) (Figure 1.2)—a collection of blood in the subdural space. SDHs may be chronic or acute, and are caused by venous bleeding from cortical bridging veins. Bleeding may extend over the entire hemisphere. Acute SDHs are significantly associated with seizures. Acute SDHs are also associated with significant alteration of cerebral blood flow and metabolism of the under-lying hemisphere and generally have a worse outcome than EDHs.
FIGURE 1.1 Epidural hematoma.
FIGURE 1.2 Subdural hematoma.
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6 I. Core Concepts
• Traumatic axonal injury (TAI, also referred to as diffuse axonal injury [DAI])—injury to axonal connections triggered by inertial forces, predominantly acceleration–deceleration, with subsequent structural and metabolic conse-quences of mechanical deformation.
• Traumatic subarachnoid hemorrhage (TSAH or SAH) (Figure 1.3)— hemorrhage in the subarachnoid space that is not associated with significant mass effect. It often accompanies other types of traumatic hemorrhage. The presence of TSAH has been associated with an increased risk of an unfavorable 6-month outcome in patients with moderate to severe TBI [2].
• Intraventricular hemorrhage (IVH)—bleeding into the ventricular system after trauma. It may be associated with acute hydrocephalous and is a risk fac-tor for development of delayed hydrocephalous. IVH is typically seen in con-junction with TSAH.
• Contusion (Figure 1.4)—parenchymal hemorrhage, typically in frontal or tem-poral lobes. Contusions may be “coup” or “contre coup.” ° Coup injury—results from direct transmission of force to brain tissue under-
lying the region of impact. ° Contre coup injury—results from the indirect forces acting in a region con-
tralateral to the region of impact.• Skull fractures—skull fractures may occur after trauma because of blunt
or penetrating injury. They may involve the convexity or the skull base and may be open or closed depending on the presence of an overlying scalp laceration. Large depressed skull fractures may need to be surgically elevated. Depressed skull fractures are associated with an increased risk of seizures [3].
FIGURE 1.3 Traumatic subarachnoid hemorrhage.
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1. Traumatic Brain Injury: Definitions and Nomenclature 7
TABLE 1.2 Commonly Used Tools to Identify Those Individuals With Concussion After Sport-Related Head Trauma
PCS: Post concussive symptom scaleGSC: Graded symptom checklistSAC: Standardized assessment of concussionNeuropsychological testingBESS: Balance error scoring systemSOT: Sensory organization test
Source: From Ref. [4]. Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports. Neurology. 2013;80:2250–2257.
FIGURE 1.4 Cerebral contusion.
CONCUSSION
This term is generally used to refer to an altered mental state occurring after trauma, which may or may not include brief loss of consciousness. Symptoms reflect a functional disturbance rather than structural injury. There are several diagnostic tools that can be used to aid in identifying those with concussion after head injury. Several of these are listed in Table 1.2; however, they are not meant to be used to “rule out” concussion. Please refer to the AAN 2013 guideline on the management of concussion in sports [4]. (See also Chapter 6 for a more detailed discussion of concussion vs. MTBI.)
POSTTRAUMATIC AMNESIA
Posttraumatic amnesia (PTA) is the impaired recall of events surrounding the injury. Retrograde PTA involves impaired recollection of events immediately pre-ceding the injury and anterograde PTA is a deficit in forming new memories after the injury [5].
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8 I. Core Concepts
POSTCONCUSSION DISORDER
Also known as postconcussion syndrome, this term refers to postconcussive symptoms that persist for 3 or more months postinjury. Symptoms are quite vari-able and are not unique to this diagnosis [6]. (See Table 1.3.) (See Chapters 15–17 for further discussion of this topic.)
SECOND-IMPACT SYNDROME
A second MTBI occurring while an individual remains symptomatic from the first MTBI may cause the “second-impact syndrome.” This rare phenomenon involves acute cerebrovascular congestion and loss of cerebrovascular autoregulation resulting in malignant brain swelling, which is life threatening [7]. (See Chapter 11 for further discussion of this topic.)
RECOVERY AND SEQUELAE
Definitions
• Diaschisis—dysfunction in an area of the brain that is remote from an area with structural damage but is connected to the damaged area via neuronal pathways.
• Neuroprotection—therapies or management strategies that prevent or limit secondary injury and lead to improved survival of neurons, microglia, or the supporting microvasculature.
• Neuroplasticity—changes in brain structure (neuronal and glial connectivity) and function due to experience. This is a major mechanism for recovery of func-tion after traumatic injury.
• Gliosis—formation of a dense network of glial cells in areas of brain injury that do not contribute to functional recovery. This can occur after trauma, stroke, or demyelination.
• Atrophy—loss of neurons and glia and their connections. This can occur after TBI and is usually related to the severity of the initial injury.
TABLE 1.3 Symptoms of Postconcussion Disorder
Depression, dizziness, drowsinessExcess sleep, fatigue, feel “in a fog”Feel “slowed down,” headache, irritabilityMemory problems, nausea, nervousnessNumbness/tingling, poor balance, poor concentrationRinging in ears, sadness, sensitivity to lightSensitivity to noise, trouble falling asleep, vomiting
Source: From Ref. [5]. Cantu RC. Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl Train. 2001;36(3):244–248.
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1. Traumatic Brain Injury: Definitions and Nomenclature 9
ADDITIONAL READING
Electronic ReferenceBrain Trauma Foundation Website. http://www.braintrauma.org
Textbook/ChapterReilly P, Bullock MR. Head Injury: Pathophysiology and Management. 2nd ed. London: Hodder
Arnold; 2005.
Journal ArticlesAarabi B, Simard JM. Traumatic brain injury. Curr Opin Crit Care. 2009;15:548–553.Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HF. Cerebral circulation and
metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg. 1991;75(5):685–693.
Buki A, Povlishock JT. All roads lead to disconnection?—traumatic axonal injury revisited. Acta Neurochirugica. 2006;148:181–194.
Cernak I, Noble-Haeusslein LJ. Traumatic brain injury: an overview of pathobiology with emphasis on military populations. J Cereb Blood Flow Metab. 2010;30(2):255–266.
Garga N, Lowenstein DH. Posttraumatic epilepsy: a major problem in desperate need of major advances. Epilepsy Currents. 2006;6(1):1–5.
Verweij BH, Amelink GJ, Muizelaar JP. Current concepts of cerebral oxygen transport and energy metabolism after severe traumatic brain injury. Prog Brain Res. 2007;161:111–124.
REFERENCES
1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2:81–84.
2. Steyerberg EW, Mushkudiani N, Perel P, et al. Predicting outcome after traumatic brain injury: development and international validation of prognostic scores based on admis-sion characteristics. PLoS Med. 2008;5(8):e165; discussion e165.
3. Temkin NR. Antiepileptogenesis and seizure prevention trials with antiepileptic drugs: meta-analysis of controlled trials. Epilepsia. 2001;42(4):515–524.
4. Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports. Neurology. 2013;80:2250–2257.
5. Cantu RC. Posttraumatic retrograde and anterograde amnesia: pathophysiology and implications in grading and safe return to play. J Athl Train. 2001;36(3):244–248.
6. McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med. 2005;39(4):196–204.
7. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology. 1997;48:575–580.
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10
2
Essential Concepts in TBI Biomechanics and Neuropathology
Michelle C. LaPlaca
GENERAL PRINCIPLES
Traumatic Brain Injury as a Continuum
Traumatic brain injury (TBI) can be defined as transient or persistent brain dysfunction, occurring as the result of head movement and/or collision between the head and an object or surface that causes suprathreshold loading to the brain. TBI occurs as a continuum of events, from the traumatic insult to the primary injury to secondary injury to the clinical outcome. Biomechanics plays a critical role in understanding the TBI continuum.
• Traumatic insult: The external cause is categorized by the mechanism (e.g., motor vehicle collision) and the intent (e.g., unintentional) [1]. Traumatic loading typi-cally occurs on the order of milliseconds to seconds.
• Primary injury: The immediate (milliseconds to seconds) result of the associated traumatic event. This is the mechanical response to the insult.
• Secondary injury: The cascade of changing biochemical and molecular events (seconds to weeks) that results from the primary injury.
• Injury outcome (weeks to years): Consequences of the primary and secondary injury, combined with recovery and repair of the brain. The ability to heal will depend on many factors, including metabolic state and endogenous repair capacity of the brain. The cell and tissue level events in the brain can manifest as sensory, motor, cognitive, behavioral, affective, systemic, and/or somatic conditions.
Confounding Factors in the TBI Response
The TBI response is the result of numerous interrelated processes that have inher-ent heterogeneity and complexity across time scales (the continuum) and system levels (subcellular [nano], cellular [micro], tissue/organ [meso], and systemic/organism [macro]).
Secondary injury mechanisms that mediate TBI pathologies are variable due to:
• Heterogeneity in traumatic insults and individual responses• Complexity of interactions among cellular signaling pathways• Constantly changing cellular activities and systemic adaptations [2]• Periods of hyperactivity and hypoactivity
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2. Essential Concepts in TBI Biomechanics and Neuropathology 11
Types and Sources of Heterogeneity
TBI is extremely heterogeneous due to its nature [3]. Heterogeneity stems from the variation in the inherent nature of a system and/or in the response to a changing state.
A. Preinjury heterogeneity (innate, premorbid):1. Innate heterogeneity (nonchangeable): individual characteristics such as
sex, age, stature, genetic variation, and neuroanatomic and musculoskel-etal variations
2. Premorbid factors (potentially changeable): individual preexisting medi-cal conditions or disease (e.g., previous head injury exposure, cardiovas-cular disease); health state at time of injury (e.g., hydration, nutritional status, recent sleep pattern, stress state)
B. Event heterogeneity (biomechanics, environmental):1. Biomechanics of the causative event: magnitude and direction of force
and acceleration, surface area of impact (i.e., force distribution), loading duration
2. Environmental heterogeneity at the time of the event: temperature, humid-ity, head protection, impact surface, degree of anticipation
C. Peri-injury heterogeneity (early injury response, clinical intervention):1. Primary injury or biomechanical response: dependent on tissue mechani-
cal properties, tissue orientation, loading direction2. Early secondary injury: complex cell signaling cascades dependent on
type and number of cells affected, intrinsic cellular characteristics3. Clinical intervention: variations in the time window to care and prehos-
pital protocolsD. Postinjury heterogeneity (secondary injury, repair capacity, clinical
management):1. Secondary injury: overlapping signaling cascades, systemic influence2. Repair capacity: innate and premorbid factors superimposed with the
injury response and ability to stably repair (i.e., neuroplasticity)3. Clinical management: variable stabilization protocols, treatment options,
and rehabilitation strategies [4]
BIOMECHANICS AND PRIMARY INJURY
The event biomechanics (traumatic insult and resulting head movement) and the mechanical response (primary injury to the brain) are linked. For a TBI to occur, the traumatic load to the head must be transduced to the brain tissue. Force trans-duction to the tissue and cells is not well understood because each loading event and individual is unique. Details of the biomechanical conditions around a trau-matic insult are typically not known.
Event Biomechanics: Load → Dynamic Head Response → Transduction to Brain → Brain Response
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12 I. Core Concepts
• Loading conditions: The forces, rates, and other parameters of the traumatic insult. Load is usually a combination of impact and inertial forces: ° Impact load: Force resulting from a moving person striking a mass or
obstruction, or a moving object or obstruction striking a person. The colli-sion transfers energy and produces contact phenomenon (focal injury).
° Inertial or impulsive load: Load resulting when a person is put in motion by an applied force. Unless there is rigid support, the head will rotate, with the neck as a pivot. Diffuse injury may result from the inertial load (especially high angular acceleration) and from the brain movement upon deceleration.
° Penetrating load (e.g., bullet): It has high velocity and energy transfer over a small impact area.
° Loading rate is important: Slowly applied force will result in lower stress than rapidly applied force.
The force produced by loading and subsequent head movement (accelera-tion pattern) will be transduced to the brain tissue and the cell components.
• Acceleration = velocity/time of the head can be angular or linear (usually a com-bination). An impact will cause the head to accelerate, then decelerate.
• Force = mass × acceleration. The lower the mass, the higher the acceleration must be to keep the force constant.
• Protective gear and safety measures aim to distribute and dissipate force.
The biomechanical response is a function of material properties and cell ori-entation and will dictate the primary injury.
• Material properties across brain regions vary [5]. The brain is a relatively soft tissue. Cell orientation and tissue composition (e.g., blood vessels, white matter tracts) contribute to differences in properties and overall tissue response.
• More force + softer tissue = more strain; suprathreshold force will deform tissue to the point of damage. Deformation (or strain) can be tensile (stretch), com-pressive, and/or shear (note: the brain is especially vulnerable to shear strain).
• Higher strain rate is more damaging than lower strain rate.• Structural failure of the brain includes microtears, macrotears, compression,
tension and/or shearing within and between brain regions, damage of vascular structures (resulting in bleeding) (meso and macroscale).
• Insults to the neural cells will, in turn, depend on mechanical response of the cells (strain and strain rate). Primary damage may manifest in neurons, glial cells, and vascular cells as axonal stretching, membrane disruption, ion imbal-ance, interruption in normal conduction and synaptic transmission, and glial damage (nano and microscale).
Injury threshold: The insult level at which structural and functional compro-mise or failure takes place; described using injury tolerance criteria. Development of tolerance criteria requires understanding of the relationship among traumatic insult, mechanical response of the brain tissue, and the resulting injury cascades and neuropathology.
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2. Essential Concepts in TBI Biomechanics and Neuropathology 13
SECONDARY INJURY
Primary structural damage (membranes and cell processes, intercellular connections) initiates and exacerbates secondary injury. The following general cat-egories of secondary injury processes are interrelated:
A. Neurochemical and electrochemical imbalances (ions, neurotransmitters, cell signaling)1. Disruption of ion homeostasis (Ca2+/Na+ influx) [6], ion channel dysfunc-
tion [7], leading to membrane potential changes, high energy demand, and mitochondrial overload.
2. Excess excitatory neurotransmitter release (e.g., glutamate); overactiva-tion of glutamate receptors, leading to excitotoxicity [8].
3. Aberrant cell signaling: ion channel dysfunction, abnormal G-protein acti-vation, and subsequent second messenger pathways, leading to abnormal action at downstream targets [9].
4. Electrophysiological abnormalities such as hyperexcitability, leading to network disturbances [10].
B. Impaired brain metabolism (oxygen and glucose availability and use)1. Changes in cerebral perfusion result in hypoxia, exacerbating secondary
injury [11].2. Fluctuation in metabolic demand and glucose metabolism [12,13].3. Impaired mitochondrial function, diminished glucose substrates, leading
to reduced cellular respiration and less adenosine triphosphate (ATP) pro-duction, increases in CO2 (hypercapnia), H+ (acidosis).
C. Biomolecular degradation (enzyme activation, free radical attack)1. Proteases attack cytoskeleton (e.g., calpain [14]), lipases upset lipid metab-
olism (e.g., phospholipase A2), endonucleases initiate nucleic acid damage.2. Free radical production (reactive oxygen species [ROS]; reactive nitrogen
species [RNS]). Increase in hydroxyl radicals causes lipid peroxidation and compounds degradative processes [15].
3. Secondary membrane damage (e.g., lipid peroxidation) impairs transport and signaling, as well as stability of membrane phospholipids [16].
D. Axonal damage and diffuse axonal injury (DAI) [17,18]1. Axons are stretched during the traumatic insult, causing transient axolem-
mal permeability.2. Both unmyelinated and myelinated axons are affected.3. Cytoskeletal damage impairs axonal transport, leading to axonal swelling.4. Oligodendrocyte damage may contribute to myelin degradation, further
affecting white matter tracts and network function.E. Vascular dysfunction (permeability, hemorrhage, reactivity) [19]
1. Blood–brain barrier (BBB) disruption causes infiltration of blood-borne proteins, cells [20].
2. Vascular leakage and microbleeding cause brain toxicity, hypoxia, coagu-lation, and hematoma formation.
3. Uncoupling of cerebral blood flow and metabolism, hyperemia, uncon-trolled cerebral perfusion pressure, vasospasm, contribute to edema, and raised intracranial pressure.
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14 I. Core Concepts
F. Inflammation (central and peripheral contribution) [21,22]1. Acute inflammatory response (release of cytokines, histamines, arachi-
donic acid, bradykinin, nitric oxide) can become chronic/degenerative.2. Activation of microglia (increase in pro-inflammatory cytokines: e.g.,
IL-1-β, IL-6, TNF-α) [23].3. Pro-inflammatory and anti-inflammatory processes both contribute to the
overall response [24].G. Cerebral edema [25]
1. Cerebral edema can occur when osmolality changes, resulting in fluid movement from one compartment to another.
2. Underlying causes are increased intravascular hydrostatic pressure (vasogenic edema), increased interstitial fluid pressure due to blood pressure and protein leakage/abnormal oncotic pressures (interstitial edema), and cellular swelling due to ionic imbalance and osmosis (cyto-toxic edema).
H. Cell death and cytotoxicity [26]1. Apoptosis: unscheduled “programmed” cell death; portions of cell death
pathways are activated by the insult.2. Necrosis: traditionally distinct from apoptosis; likely one of many death
pathways; features are end stage; enzymatically driven; exacerbated by inflammation.
3. Autophagy: cell death through phagocytic processes [27].
IMPLICATIONS FOR THE FUTURE: DIAGNOSIS AND TREATMENT
Improved understanding of TBI requires both experimental and clinical data col-lection across the continuum. Complex data analytics and systems approaches are required for successful bidirectional translation. TBI heterogeneity may necessi-tate personalized diagnostic and treatment strategies.
Mechanistic Diagnostics
• Blood and cerebrospinal fluid (CSF) biomarkers are promising diagnostic aids, will likely require use of a panel of biomarkers [28,29].
• Biomarkers can unveil cellular injury mechanisms and be correlated with symptoms to increase understanding of TBI pathology.
Secondary Injury Mitigation
• Clinical symptoms are caused by numerous changing secondary injury cascades, necessitating frequent evaluation of clinical management strategies.
• It is difficult to narrow down dominant secondary injury pathways at the cell level as they relate to clinically significant features and injury mitigation.
• Combination therapeutics: Neuroprotection strategies will likely need to target multiple pathways [30–32], for example, glucose metabolism, inflammation, antioxidant protection, and axonal stabilization.
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2. Essential Concepts in TBI Biomechanics and Neuropathology 15
KEY POINTS
• The full spectrum of TBI (from biomechanics to outcome) is complex and heterogeneous across both time scales and system levels.
• Biomechanics can provide important information about human tolerance to TBI, improving preventative and safety interventions.
• The traumatic insult initiates the propagation of secondary injury cas-cades, which manifest as physiologic and neurologic symptoms.
• Clinical outcome is a function of primary and secondary injury responses, as well as endogenous repair capability and intervention measures.
ADDITIONAL READING
Websiteshttp://www.neuroskills.com/brain-injury/biomechanics-of-brain-injury.phphttp://www.nhtsa.gov/Research/Biomechanics+&+Trauma/Brain+Injury+Researchhttp://www.cdc.gov/TraumaticBrainInjury/index.html
Textbooks/ChaptersGrafman J, Salazar AM, eds. Handbook of Clinical Neurology. Traumatic Brain Injury, Part I.
Vol. 127. Amsterdam, the Netherlands, Kidlington, Oxford, UK, Waltham, MA: Elsevier; 2015.
Grafman J, Salazar AM, eds. Handbook of Clinical Neurology. Traumatic Brain Injury, Part II. Vol. 128. Amsterdam, the Netherlands, Kidlington, Oxford, UK, Waltham, MA: Elsevier; 2015.
Journal ArticlesAgoston DV. Bench-to-bedside and bedside back to the bench; seeking a better under-
standing of the acute pathophysiological process in severe traumatic brain injury. Front Neurol. 2015;6(47):1–6.
Goriely A, Geers MG, Holzapfel GA, et al. Mechanics of the brain: perspectives, challenges, and opportunities. Biomech Model Mechanobiol. 2015;14(5):931–965.
McAllister TW. Neurobiological consequences of traumatic brain injury. Dialogues Clin Neurosci. 2011;13(3):287–300.
Meaney DF, Morrison B, Dale Bass C. The mechanics of traumatic brain injury: a review of what we know and what we need to know for reducing its societal burden. J Biomech Eng. 2014;136(2):1–14.
REFERENCES
1. CDC. ICD Injury Matrices. 2009; Available from http://www.cdc.gov/nchs/injury/injury_matrices.htm
2. Wijayatilake DS, Sherren PB, Jigajinni SV. Systemic complications of traumatic brain injury. Curr Opin Anaesthesiol. 2015;28(5):525–531.
3. Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted therapies. J Neurotrauma. 2008;25(7):719–738.
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16 I. Core Concepts
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7. von Reyn CR, Mott RE, Siman R, et al. Mechanisms of calpain mediated proteolysis of voltage gated sodium channel alpha-subunits following in vitro dynamic stretch injury. J Neurochem. 2012;121(5):793–805.
8. Lau A, Tymianski M. Glutamate receptors, neurotoxicity and neurodegeneration. Pflugers Arch. 2010;460(2):525–542.
9. Chico LK, Van Eldik LJ, Watterson DM. Targeting protein kinases in central nervous system disorders. Nat Rev Drug Discov. 2009;8(11):892–909.
10. Greer JE, Povlishock JT, Jacobs KM. Electrophysiological abnormalities in both axoto-mized and nonaxotomized pyramidal neurons following mild traumatic brain injury. J Neurosci. 2012;32(19):6682–6687.
11. Yan EB, Satgunaseelan L, Paul E, et al. Post-traumatic hypoxia is associated with pro-longed cerebral cytokine production, higher serum biomarker levels, and poor out-come in patients with severe traumatic brain injury. J Neurotrauma. 2014;31(7):618–629.
12. Prins M, Greco T, Alexander D, Giza CC. The pathophysiology of traumatic brain injury at a glance. Dis Model Mech. 2013;6(6):1307–1315.
13. Foley N, Marshall S, Pikul J, et al. Hypermetabolism following moderate to severe trau-matic acute brain injury: a systematic review. J Neurotrauma. 2008;25(12):1415–1431.
14. Saatman KE, Creed J, Raghupathi R. Calpain as a therapeutic target in traumatic brain injury. Neurotherapeutics. 2010;7(1):31–42.
15. Hall ED, Vaishnav RA, Mustafa AG. Antioxidant therapies for traumatic brain injury. Neurotherapeutics. 2010;7(1):51–61.
16. Adibhatla RM, Hatcher JF. Role of lipids in brain injury and diseases. Future Lipidol. 2007;2(4):403–422.
17. Siedler DG, Chuah MI, Kirkcaldie MT, et al. Diffuse axonal injury in brain trauma: insights from alterations in neurofilaments. Front Cell Neurosci. 2014;8:429.
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19. Hovda DA, Glenn TC. Human cerebral blood flow and traumatic brain injury. In: Lo EH, Lok J, Ning M, Whalen MJ, eds. Vascular Mechanisms in CNS Trauma. New York, NY: Springer; 2013;47–54.
20. Chodobski A, Zink BJ, Szmydynger-Chodobska J. Blood–brain barrier pathophysiol-ogy in traumatic brain injury. Transl Stroke Res. 2011;2(4):492–516.
21. Corps KN, Roth TL, McGavern DB. Inflammation and neuroprotection in traumatic brain injury. JAMA Neurol. 2015;72(3):355–362.
22. Hinson HE, Rowell S, Schreiber M. Clinical evidence of inflammation driving second-ary brain injury: a systematic review. J Trauma Acute Care Surg. 2015;78(1):184–191.
23. Hernandez-Ontiveros DG, Tajiri N, Acosta S, et al. Microglia activation as a biomarker for traumatic brain injury. Front Neurol. 2013;4:30.
24. Ziebell JM, Morganti-Kossmann MC. Involvement of pro- and anti-inflammatory cytokines and chemokines in the pathophysiology of traumatic brain injury. Neurotherapeutics. 2010;7(1):22–30.
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This is a sample from MANUAL OF TRAUMATIC BRAIN INJURY:ASSESSMENT AND MANAGEMENT, SECOND EDITION
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2. Essential Concepts in TBI Biomechanics and Neuropathology 17
26. Stoica BA, Faden AI. Cell death mechanisms and modulation in traumatic brain injury. Neurotherapeutics. 2010;7(1):3–12.
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29. Zetterberg H, Smith DH, Blennow K. Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood. Nat Rev Neurol. 2013;9(4):201–210.
30. Smith DH, Hicks R, Povlishock JT. Therapy development for diffuse axonal injury. J Neurotrauma. 2013;30(5):307–323.
31. Loane DJ, Stoica BA, Faden AI. Neuroprotection for traumatic brain injury. Handb Clin Neurol. 2015;127:343–366.
32. Margulies S, Anderson G, Atif F, et al. Combination therapies for traumatic brain injury: retrospective considerations. J Neurotrauma. 2016;33(1):101–112.
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