Brain Injury Professional, vol. 1 issue 1

vol. 1 issue 1

Special Issue on Biomechanics

Biomechanics of Traumatic Brain Injury: A Review

The Biomechanics of Brain Injury

Sports Concussion

The Biomechanical Assessment of Traumatic

Brain Injury

Biomechanics of Childhood Neurotrauma

Overview of Computer-Assisted Cognitive

Function Diagnostic and Assessment Tools

Premiere Issue

conten

ts

BRAIN INJURY PROFESSIONAL 3

vol. 1 issue 1, 2004

Chairman’s Message

Editor’s Message

Publisher’s Message

Guest Editor’s Message

Professional Appointments

Conferences

Biomechanics of Traumatic Brain Injury: A Reviewby Michelle C. LaPlaca, Ph.D. and Mariusz Ziejewski, Ph.D.

The Biomechanics of Brain Injury: From Historical to CurrentPerspectivesby Albert I. King, Ph.D.

Biomechanics of Childhood Neurotraumaby Susan S. Margulies, Ph.D. and Betty Spivack M.D.

Sports Concussionby Christopher C. Giza, M.D.

The Biomechanical Assessment of Traumatic Brain Injuryby Mariusz Ziejewski, Ph.D.

Overview of Computer-Assisted Cognitive Function Diagnostic and Assessment Toolsby Corinna M. Wildermuth, David W. Wright, and Michelle C. LaPlaca

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4 BRAIN INJURY PROFESSIONAL

In May 2003, at the International Brain Injury Association’s(IBIA) World Congress in Stockholm, Sweden, many atten-dees commented on the lack of a North American organiza-tion dedicated to the brain injury profession such as IBIA,and indicated their desire for such a forum to discuss brainand brain injury research. Therefore, we established theNorth American Brain Injury Society (NABIS).

NABIS is a multidisciplinary society which is comprised ofprofessional members involved in the care and issues of braininjury. The principle mission of our organization is to movebrain injury science forward, whether it is in the area of clini-cal care, research, policy, or litigation.

There are a number of scientific journals dedicated to trau-matic brain injury including the IBIA's official journal, BrainInjury. However, this publication, Brain Injury Professional,seeks to provide an avenue to share information with profes-sionals in a variety of disciplines. I am thrilled to have myfriend and colleague, Dr. Donald Stein, as our executive edi-tor. Brain injury needs a voice for the professionals withinthis ever changing field, and NABIS will be that voice. Iencourage all of you to join us as we once again seek toenhance our professions through a collective effort.

Robert D. Voogt, Ph.D., C.R.C. Chairman North American Brain Injury Society

chairman’s message

As the executive editor of Brain Injury Professional, I amdelighted to welcome you to this exciting premier issue of thepublication. Brain Injury Professional is creating a novel ven-ture specifically addressing your professional and scientificneeds in an easy-to-read and highly informative format thatwill be very different from academic journals in the field.Brain Injury Professional will be interdisciplinary in scope anddesigned to foster discussion and thinking about the keyissues facing brain injury rehabilitation and research. Articlesare designed to be lively and will often present reviews ofstate-of-the-art technologies and approaches to the treatmentand rehabilitation of brain injury in its various forms.

In this issue we present current concepts in the biomechanicsof brain injury written by leading experts in this field. Infuture issues we will cover topics such as the latest emergingpharmacological treatments for TBI, aging and brain injury,sports injuries, gender issues in CNS repair, and the uses ofanimals in research, just to name a few. Each quarterly issueof Brain Injury Professional will also contain professionalcareer announcements, listings of upcoming conferences andnews from the NABIS organization.

I would also like to share with you my excitement in launch-ing this new publication. Working with me as editor in chief,to provide the excellent quality you expect in a professionalpublication, will be Dr. Nathan Zasler, one of the country'sleading experts in rehabilitation from TBI. Together with anoutstanding and dedicated editorial board and staff, BrainInjury Professional promises to be the publication you turn towhen you want to know what is important to TBI researchand rehabilitation.

Donald G. Stein, Ph.D.Asa G. Candler ProfessorEmory University School of MedicineDepartments of Emergency Medicine and Neurology

executive editor’s message


Welcome to the premiere issue of Brain Injury Professional!We are extremely excited about this new publication and itspotential to communicate a wide range of brain injury infor-mation to professionals across North America.

HDI Publishers has been producing a variety of periodicalson the subject of brain injury for almost twenty years. Adecade ago, we introduced i.e. Magazine, the first color mag-azine on the subject of brain injury. This year, we are pleasedto begin publication of Brain Injury Professional, a publica-tion we believe will become a leading voice and resource forthe broader brain injury professional community.

Perhaps more than any other, brain injury is a multidiscipli-nary field. Our goal for Brain Injury Professional therefore, isto publish a resource that allows professionals to share theirknowledge across a broad range of research, rehabilitationand treatment areas. In future editions of Brain Injury Profes-sional, we will be covering both academic and clinical issuesin an effort to increase the level of discourse and exchangebetween all professionals working in the field of brain injury.

Brain Injury Professional will be an important part of theNorth American Brain Injury Society’s mission of movingbrain injury science into practice. Above all though, we wantthis publication to be a valuable resource for those who workto improve the lives of persons with brain injury and theirfamilies. We are always eager to receive feedback from ourreaders and members, so we encourage you to visit our web-site, www.nabis.org, and send in your comments.

J. Charles Haynes, J.D.PublisherBrain Injury Professional

publisher’s message

This first issue of Brain Injury Professional highlights thecontribution of biomechanics to the study of traumatic braininjury. The study of the biomechanics of injury begandecades ago, long before the advent of modern day molecularbiology research and imaging technology advances. Thephysical events surrounding an injury often occur in millisec-onds and can be extremely variable from person to person.These challenges are still faced by modern biomechanicians,although recent advances such as improved computer pro-cessing speed and the merge between engineering and bio-logical sciences have elevated our understanding of themechanical events surrounding an injury. This understand-ing will ultimately translate into improved injury preventionand treatment strategies.

The articles in this issue of Brain Injury Professional coverdifferent aspects of brain injury taken from a biomechanicalperspective. The first article (Biomechanics of TraumaticBrain Injury (TBI): A Review) is a synopsis of the biomechan-ics associated with traumatic brain injury and is intended asboth a tutorial and a review article. The next article (TheBiomechanics of Brain Injury: From Historical to CurrentPerspective) gives a historical perspective on the study ofinjury biomechanics and presents some of the current chal-lenges with which researchers are faced. These are followedby Biomechanics of Childhood Neurotrauma, which illus-trates the differences between adults and children in injurysituations, an important distinction in biomechanicsresearch. The child cannot be modeled as a miniature adultand this article highlights the science behind these differ-ences. The next article (Sports Concussion) gives a clinicalperspective of this very important issue, summarizing the riskfactors and need for biomechanical research into mild andrepeat brain injury. The Biomechanical Assessment of Trau-matic Brain Injury provides the reader with a glimpse intohuman occupant safety research studies and the applicationof biomechanics to injury prevention. And the last article inthis series (Overview of Computer-Assisted Cognitive Func-tion Diagnostic and Assessment Tools) demonstrates the useof technology that may assist the clinical sciences in bothdiagnostic and continued assessment of cognitive deficitsusing novel and sensitive tests.

We hope the reader finds this issue of Brain Injury Profes-sional to be a reference for future use and contributes to yourunderstanding of biomechanics.

Michelle C. LaPlaca, Ph.D.Assistant Professor, Georgia Institute of Technology andEmory University

guest editor’s message

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north american brain injury societychairman Robert D. Voogt, PhDtreasurer Bruce H. Stern, Esq.family liason Julian MacQueenexecutive vice president Michael P. Pietrzak, MD, FACEPexecutive director/administration Margaret J. Robertsexecutive director/operations J. Charles Haynes, JDcommunications manager Brandy Buzinskimarketing manager Joyce Parkergraphic designer Nikolai Alexeevadministrative assistant Benjamin Morganadministrative assistant Bonnie Haynes

brain injury professional publisher Charles W. Haynes publisher J. Charles Haynes, JDexecutive editor Donald G. Stein, PhDeditor in chief Nathan Zasler, MDmanaging editor Linda L. Thoi, DrPHdesign and layout Nikolai Alexeevadvertising sales Joyce Parkerdata input Bonnie Haynes

editorial inquiriesManaging Editor Brain Injury ProfessionalPO Box 131401Houston, TX 77219-1401Tel 713.526.6900Fax 713.526.7787Website: www.nabis.org

advertising inquiriesJoyce ParkerBrain Injury ProfessionalHDI PublishersPO Box 131401Houston, TX 77219-1401Tel 713.526.6900Fax 713.526.7787

national officeNorth American Brain Injury SocietyPO Box 1804Alexandria, VA 22313Tel 703.683.8400Fax 703.683.8996Website: www.nabis.org

Brain Injury Professional is a quarterly publication. © 2004 NABIS/HDI Publishers. All rights reserved. No partof this publication may be reproduced in whole or in part in any way without the written permission from thepublisher. For reprint requests, please contact, Managing Editor, Brain Injury Professional, PO Box 131401,Houston, TX 77219-1400, Tel 713.526.6900, Fax 713.526.7787, e-mail [email protected]

vol. 1 issue 1, 2004

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SUMMARYTraumatic brain injury (TBI) is an acquired injury to the braincaused by an external physical force to the head (primaryinjury), resulting in total or partial functional disability and/orpsychosocial impairment. Secondary, or prolonged, injuries areneurochemical and physiological events that occur in response tothe primary injury and account for the ongoing and continualdamage. Because of the biomechanical nature of TBI, researchers,clinicians, and therapists should understand the biomechanicssurrounding the initial insult in order to utilize clinically relevantexperimental models and to correlate insult parameters withclinical deficits. These efforts can, in turn, lead to the develop-ment of new treatments (both pharmacologic and rehabilitative)and tissue tolerances (useful for improvements to protectivegear—both personal and automotive). This review article high-lights the basic biomechanics that surround TBI, including thedifferent types of insults. In addition, the importance of biome-chanics in injury research is summarized.

INTRODUCTIONThe clinical definition of TBI is given as an occurrence of injury tothe head that is documented in a medical record with one or moreof the following conditions attributed to head injury: (a) observedor self-reported decreased level of consciousness including partialor complete loss of consciousness, stupor, or coma; (b) amnesiaincluding the time preceding, during, and subsequent to theinjury; (c) skull fracture; (d) objective neurological or neuropsy-chological abnormality; and (e) diagnosed intracranial lesion

(Thurman 1995). There are an estimated 1.5 million cases of TBIin the US per year, including 51,600 deaths (Figure 1). Most ofthese cases are mild in nature and, in fact, the clinical and psy-chosocial impacts of mild TBIs are recently receiving attention atboth the research and clinical levels in order to improve outcome(Rees 2003). Symptoms associated with mild TBI include loss ofconsciousness, memory deficits, and concentration problems. Mostof these individuals do not seek medical attention and may be atrisk for future worsening of symptoms or vulnerability to moresevere repeat injuries (Cantu 1998). Of the 220,000 individualswith suspected or confirmed brain injury that are admitted to thehospital, there are 18,000 deaths following admission, pointing tothe need for acute diagnostics and improved treatment strategies(Sauaia et al 1995). Currently, there are few, if any, effective treat-ments for TBI, whether the injuries are mild or severe. In the U.S.in 1995, direct and indirect costs of TBI totaled an estimated $56.3billion (Thurman 2001).

Males are three times as likely as females to acquire TBI, withthe highest risk in the 15-24 year age bracket. The next highestincidence of TBI occurs in individuals over 65 years old. Thelargest percentage of these injuries is due to motor vehicle acci-dents (43%), followed by firearm incidents (34%) and falls (9%).Despite the high incidence and enormous health and socioeco-nomic consequences of TBI, few effective treatments exist. Bio-mechanics research is key to determining tolerances—the forcesand deformations at which the tissues fail both structurally andfunctionally—and to provide clinically relevant models for deter-mining mechanisms and testing new treatments.

BBiioommeecchhaanniiccss ooff TTrraauummaattiicc BBrraaiinn IInnjjuurryy:: AA RReevviieeww

by Michelle C. LaPlaca, Ph.D. and Mariusz Ziejewski, Ph.D.


BASIC BIOMECHANICSBiomechanics, first internationally recognized as a field in theearly 1970s, is the study of forces and physical responses in sta-tionary (static) and moving (dynamic) biological systems. Howdoes a system (in the case of TBI—the human body, and morespecifically, the head) react when a force, or load, is placed on it?How do external loads result in initial damage? By what mecha-nism do external forces lead to delayed damage? What are thelimits of these loads before a threshold is reached (in otherwords, what is the tolerance of the system)? And does the type ofload matter? To answer these and other related questions, wemust understand basic biomechanics. The basic terms, ordescriptors, that biomechanicians use to describe applied loadsare force and stress and the resulting responses are deforma-tions and strains (Table 1).

Force is defined as the action of one body (a physical entityin the system, such as a windshield) on another (as a result of animpact) which will cause acceleration of the second body (in our

discussion this is usually the head) unless acted on by an equaland opposite action counteracting the effect of the first body.The unit is a Newton (N); 1 N is the force that will give 1 kilo-gram an acceleration of 1 meter/second2 (English unit is pound-

force, lbf). When forces are generated in tissue, deformationmay ensue depending on the material properties. Deformation isdefined as the change in shape of a body undergoing a force. Arigid body, for example, would experience extremely smalldeformations, while biological tissue (usually referred to asdeformable or nonrigid) can often undergo quite large deforma-tions. Several biomechanical factors surround force analysis andultimately predict whether damage occurs:

● Type of load: Loads are described as direct (physical contactbetween the head and another object) or indirect (as theresult of motion of the head). In indirect loading, accelerationof the second body (i.e. the head) can act analogously toapplied forces.

● Type of force: Loads can be translational (linear), rotational,or angular (a combination of translational and rotational).We will see how the type of force can affect the resultingforces and deformations.

● Direction of force: The direction, or plane, of loading can bea determining factor (e.g., sagittal, lateral, etc.) since direc-tional sensitivity of the brain has been shown, likely due tothe irregular, or nonhomogeneous, shape of the brain andasymmetrical (not symmetrical) skull structures.

● Magnitude of force: The extent and severity of deformationincreases with increasing force and this relationship is nonlin-ear. In other words, the proportional increase in brain tissuedamage may be significantly greater than the proportionalincrease in force.

● Duration of force: The change in duration of accelerationwill result in different types of internal forces and injuries tothe brain tissue. For short durations of force, much of theeffects of the force are reduced due to the material propertiesof brain tissue. As the duration of force increases, less reduc-tion occurs and less force is needed to produce injuries with-in the brain. These injuries are often confined to the brainsurface. As the force duration increases further, less of theeffects of the force are reduced, resulting in brain deforma-tions that are able to propagate deeper into the brain.

● Rate of force: While shorter duration forces may result inless damage, loads that are applied fast may incur more dam-age due to the material properties of the brain. The tissuecannot absorb (or reduce) the force fast enough and can failboth structurally and functionally. Slowly applied loads givethe tissue “time” to reduce the force and generally result inless damage. This material property of brain (and of most softbiological tissues) is called viscoelasticity (see page 12).

● Region of the brain: Because different regions of the brainhave different cellular orientations, structural and functionaltolerances of the brain differ depending on the region affect-ed. This consideration results in the directional sensitivitiesmentioned above.

Stress is another term frequently used in biomechanical analy-sis and refers to the distribution of forces relative to the areas onwhich they act. Normal stresses (designated by the Greek lettersigma (σ)) act perpendicular to the surface, while shear stresses(designated by the Greek letter tau (τ)) act tangential to the sur-face. The unit is the Pascal (Pa); 1 Pa = 1 N (Newton) / per meter2.A given force acting on a small surface produces greater stress thanthe same force acting over a larger surface. In other words, theamount of mechanical stress created by a force is dependent onthe size of the area over which the force is applied. The resultingstrain that occurs relates the deformed state of the body to theundeformed state and is unitless. Biomechanicians refer to the type

Figure 1: Numbers of traumatic brain injuries in the United States.

Table 1: Concepts from Mechanics

Figure 2: Deformation and Strain


of strain generated in a tissue (Figure 2):● Extensional strain is the change in length divided by the

original length (ε = ∆l/lo) and can be further classified asbeing tension (positive strain) or compression (negativestrain). Extensional strain results from stresses generatedfrom linear (or translational) loads.

● Shear strain is also the change in length divided by the origi-nal length (γ = ∆l/lo), but is the strain resulting from shearstress, often a product of rotational loads. Brain tissue isthought to be more sensitive to shear strain than extensionalstrain and therefore loading that involves rotation of the headhas been thought to result in more severe injuries, althoughthis assumption has recently been questioned (see “The Bio-mechanics of Brain Injury” in this issue of Brain Injury Pro-fessional, page 16).

The relationships between stress and strain are referred to asconstitutive relationships and the resulting equations are used todefine behavior of the tissue (Figure 3). The response of a tissue toan applied load is dependent on the geometry and the materialproperties. The material properties of a tissue vary from individualto individual, as well as with age, previous injuries or disease.Many tissues, including brain, are very complex in composition,yet biomechanical analyses often approximate the tissue as uniform(or homogeneous). More complex and realistic computer models,however, have been developed to determine the different respons-es generated within the various regions of the brain (see page 16).

VISCOELASTICITYBrain materials show non-linear and time-dependent behavior(viscoelastic nature) when experiencing large deformations.Thus the extent of brain tissue damage depends not only in theacceleration magnitude and duration, but also on the rate ofstraining, in addition to the amount of strain.

In a linearly viscoelastic material, energy is dissipated by plasticor viscous flow within the material as the material is stressed.Because of this, stress and strain vary out of phase with one anoth-er so that the loading and unloading stress-strain curves show hys-teresis (the stress-strain unloading relationship does not follow theloading relationship, even when the material is loaded within itselastic range) (Figure 4A). The area below each curve representsthe strain energy stored during loading and subsequently recov-ered during unloading. The area between the two curves repre-sents the energy dissipated due to viscous flow within the material.Two additional behavior characteristics of viscoelastic materialsshould be considered: relaxation and creep. When the materialinstantly has a constant deformation, the corresponding forcesinduced decrease with time, which is called relaxation (Figure 4B).As a material suddenly experiences a constant force, the corre-sponding deformation continues which is called creep (Figure 4C).

The importance of time dependent characteristics of thehuman brain becomes clear once we recognize that in a typicalevent human brain comes in contact with the interior of the skullnumerous times. This signifies that after an initial brain contactwith the skull there is a follow-up rebound phase causing thebrain to strike the opposite side of the skull (see Figure 5A).Since the brain exhibits high bulk modulus (high resistance tovolume change) the initial impact and follow-up rebound impactwill occur during a very short period of time. This time is suffi-ciently short that might not allow the brain to regain its initialshape after the initial deformation (see Figure 5B). This condi-tion might lead to superposition of the brain deformation withsignificantly higher resulted deformation than one would expectfrom one brain/skull impact (see Figure 5C).

BIOMECHANICAL LOADS THAT LEAD TO TBIThe basic biomechanics terms that we have defined are very use-ful in describing what mechanical conditions lead to injuries. Weoften refer to these mechanical conditions as the insult parame-ters and the result as the injury. We will focus on two categoriesof insults (static and dynamic loading of the head), two types ofresponses, or injuries (focal and diffuse) and two responsephases (primary and secondary).

Types of InsultsStatic loading to the head is a very slowly applied direct load.Usually there are no deficits until there is substantial brain defor-mation (see above discussion of duration of force). These loadingconditions are relatively rare and often occur in human entrap-ment situations (e.g., earthquakes).

Dynamic loading, on the other hand, can occur quite rapidly(under 1 second, often <50 milliseconds) and is the most commoncause of TBI. Dynamic loading can further be broken down intoimpact loading (direct loading where an impact occurs with anobject hitting the head or the head hitting an object) or impulsiveloading (indirect loading where no contact occurs). Although pure

Figure 3: Constitutive Relations

Figure 4: General Concepts-Mechanical Characteristics of Brain Tissue

Figure 5: Cumulative Effect of Two Consecutive Impacts on the Level ofBrain Deformation


impact would involve contact with no head movement, impactloading is usually a combination of contact forces—from theimpact itself—and inertial forces—from the motion of the headand the brain within the skull. It is important to consider the size,mass, and hardness of the impacting object as well as the surfacearea and velocity at which contact occurs. Objects that are small incomparison to the head are more likely to concentrate stresses and

are at a greater risk for more local and severe damage, perhaps in apenetrating manner. Impact loading can lead to either focal or dif-fuse injuries, or a combination of the two. Impulsive loading isdue to inertial forces alone and leads to diffuse brain injuries (seeFocal and Diffuse Injuries, below).

Types of InjuriesFocal injuries result from direct loading and can often occurwithout widespread, or diffuse, damage. Focal injuries includeskull fracture (with or without brain damage), which can be lin-ear, depressed, and quite complex (such as basilar skull fractures).Epidural hematomas are often associated with focal injuries. Con-tact loading can also result in coup (at the site of impact) and con-tra-coup (away from the site of impact) contusions to the brain,involving both cellular and vascular components. Focal injuriesaccount for one-half of all severe head injuries, but 2/3 of alldeaths in this group. There is usually macroscopically visible dam-age at the site of impact. When there is osteal (referring to bone orspecifically, skull) or dural (referring to the membranous encase-ment tissue of the brain) compromise this is often termed openhead injury in the clinical setting. Often an object penetrates theskull as a result of a motor vehicle accident, gunshot wound, or ablow to the head. The clinical symptoms are often very specific tothe area of the brain that is directly injured (e.g. the individualmay experience difficulties with forming speech, but show noproblem with writing words on paper).

Diffuse injuries are most often caused by inertial loading,which describe the motion of objects. The acceleration (velocitychange divided by change in time) is an important parameter indetermining response. The higher the acceleration of a body, thehigher the force (force equals mass times acceleration, Newton’ssecond law). Thresholds for the acceleration that a human canundergo before tissue damage occurs has been, and continues tobe, an active area of research. When the acceleration is transla-tional, injuries tend to be localized to a smaller area. Rotationalacceleration, on the other hand, can lead to large strains deepwithin the brain, resulting in diffuse axonal injury (DAI). Mostinjuries seen clinically are a combination of translational androtational (referred to as angular acceleration) (Figure 6). Diffuseinjuries are thought to occur as a result of not only the accelera-tion portion of loading, but from the deceleration portion of theinsult, creating very fast moving, uneven load distributions. Dif-fuse strains can lead to differential movement of the skull relativeto the brain, causing parasagittal bridging vein injury, as well aswidespread intracerebral hemorrhage. Although cerebral contu-sion and brain edema can occur, damage is often only seenmicroscopically. Individuals with diffuse injury tend to havewidespread dysfunction, making diffuse injury the most preva-lent cause of persisting neurological disability. Clinically, diffuseinjury is referred to as a type of closed head injury and arisesmost often from motor vehicle accidents. See Figure 7 for a sum-mary of the relationships between input mechanical loading andresultant tissue deformations.

Response Phases The initial damage that is a direct result from loading to the brainis the primary phase of injury (Figure 8). Biomechanicians studythis phase in order to determine tissue tolerances to mechanicalloading. Our understanding of human tolerance is still advancingfrom a cellular level to a human level and is vital to developingbetter safety equipment. It is believed that at the time of the insultthere is a varying amount of primary damage, or damage thatresults from the physical force itself. This would include compro-

Figure 6: Types of Acceleration in TBI

Figure 7: Summary of Biomechanics in Tissue Deformation

Figure 8: Cause and Effect of Traumatic Brain Injury

Figure 9: Improving the Outcome of Brain Injury: Industry to Research Laboratory to Clinic


mised skin, bony fractures, tissue tearing,cellular rupture, and reorientation of thetissue components. If a deformationthreshold is surpassed, these structural fail-ures result and can severely compromisebrain function. Tissue damage is more dif-ficult to detect in cases of subtle physicalinsults. For example, cellular membranesmay become compromised, leading todepolarization and abnormal ion move-ment across the membrane. Also, the vas-culature may become “leaky” leading toinflux of peripheral components into thebrain tissue.

While there is no absolute time whenprimary damage evolves into delayedeffects, the secondary phase of injury canbe defined as any injury that occurs as aresult of the primary insult. This may be inthe acute (minutes to hours) period or in amore delayed fashion (days to months)and is dependent on the severity of the ini-tial insult, as well as the health and age ofthe individual. There may be decreasedblood flow to the brain, resulting in hypox-ic conditions. This is exacerbated bydecoupled cerebrovascular autoregulationand persistent cellular injury. In addition,the brain often enters a hypermetabolicphase, followed by a hypometabolic phase.DAI is thought to be comprised mostly of asecondary effect, due to cellular dysfunc-tion (e.g., reduced axonal transport andproteolytic activity), rather than a primaryaxotomy (severing of axons). There are alsoseveral deficits reported in neurotransmit-ter function as well as cellular energy pro-duction, that can lead to delayed cell deathor persistent dysfunction. While a com-plete discussion of the cellular effects ofTBI is beyond the scope of this article, it iseasy to see that the secondary cascades canbe quite complex and are therefore notcompletely understood. There is a role forbiomechanics in determining injury mech-anisms in both the primary and secondaryphases of the injury response by utilizinglaboratory models that best mimic theforces/stresses and deformations/strainsthat occur during a traumatic insult. Theresponse (whether cellular or whole organ-ism) can better represent the clinical set-ting and therefore potential treatments canbe evaluated in a more relevant setting.

CONCLUSIONSGiven the tremendous impact that TBI

has on society, it is important to betterunderstand the biomechanical circum-stances of head injuries in addition to the

medical implications(Figure 9). The fieldof biomechanics has matured over the lastthree decades and researchers havelearned a great deal about prevention andtreatment. Biomechanics can play a role inimproving preventative measures such assafety design in automobiles and sportsequipment, as well as highway and roadsafety. Researchers can use their knowl-edge of mechanical engineering to deter-mine thresholds to loading of the brain.Clinicians and rehabilitative specialists canassist this effort by understanding the clin-ical variability and reporting injury cir-cumstances. In addition to preventativestrategies, biomechanics can play animportant role in experimental modeling.By applying clinically relevant mechanicalparameters (e.g., shear strain applied athigh rates) to isolated brain cells, theresulting knowledge can be used to devel-op mechanistically-inspired pharmaceuti-cal agents. In addition to cellular levelinvestigations, biomechanical models canbe utilized at the animal level to achievepre-clinical testing settings. To comple-ment the physiological studies, researchershave also used computer simulations tobetter understand the complex response ofbrain tissue during traumatic loading con-

ditions. Taken together, these multilevelstudies can be combined to improve theoutcome of individuals with TBI.

ABOUT THE AUTHORSMichelle C. LaPlaca, Ph.D.: Assistant Professor, NeuralInjury Biomechanics and Repair Group NeuroengineeringLaboratory, Coulter Department of Biomedical Engineering,Georgia Institute of Technology and Emory University. 313Ferst Dr., Atlanta, GA 30332-0535, e-mail: [email protected].

Mariusz Ziejewski, Ph.D.: Associate Professor, Director ofImpact Biomechanics Laboratory, College of Engineering,Director of Automotive Systems Laboratory, College ofEngineering, North Dakota State University. 111 Dolve Hall,P.O. Box 5285, Fargo, ND 58105, e-mail: [email protected].

REFERENCESAll epidemiological information obtained from the Centersfor Disease Control and Prevention, National Center forHealth Statistics. See: www.cdc.gov.

Thurman DJ. Epidemiology and economics of head trauma.In: Miller L and Hayes R, eds. Head trauma therapeutics:basic, preclinical and clinical aspects. New York, NY: JohnWiley and Sons, 2001.

Sauaia A, Moore FA, Moore EE, Moser KS, Brennan R, ReadRA, Pons PT. Epidemiology of trauma deaths: a reassess-ment. J. Trauma, 38(a) 185-43, 1995.

Thurman DJ, Sniezek JE, Johnson D, et al. Guidelines forSurveillance of Central Nervous System Injury, Atlanta,Centers for Disease Control and Prevention, 1995.

Cantu RC. Second-impact syndrome. Clinics in Sports Med-icine, 17(1) 37-44, 1998.

Rees PM. Contemporary issues in mild traumatic braininjury. Arch Phys Med Rehabil., 84(12) 1885-94, 2003.

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The Inevitable QuestionEver since the first steel ball was dropped from a height of 12stories onto a dry skull by Professor Herbert Lissner, an engineerand Dr. Steve Gurdjian, a neurosurgeon, at Wayne State Univer-sity, in 1939, laboratory research on head injury has continuedat Wayne State and elsewhere for well over half a century. Look-ing back at the progress made, we can see that brain injuryresulting from automotive crashes has been kept under control,using a rather primitive injury criterion, the Head Injury Criteri-on or HIC, as specified in Federal Motor Vehicle Safety Standard(FMVSS) 208. HIC is an integral function of the resultant linearacceleration of the head, maximized over a portion of the impactpulse and its value for the driver or front seat passenger must notexceed 1000 in a 48 km/hr barrier impact. The fact that it doesnot take into account the effect of angular acceleration of the

head has been a major bone of contention between the support-ers of the angular acceleration theory of brain injury and the pro-ponents of linear acceleration. For a period of about 20 years,this issue was strongly contested with researchers doing experi-ments that imparted purely linear or purely angular accelerationsto the head. To date, the issue has not been resolved, eventhough the rhetoric has died down and there is general accep-tance that no impact is purely linear or purely angular. What ismore important is the fact that the schism in the brain injuryresearch community did not help to advance the understandingof brain injury in terms of the mechanisms of injury as well asthe level of tolerance. For example, to date, there is no acceptedcriterion for angular acceleration. It ranges from 1800 radiansper second squared (rad/s2) to 16000 rad/s2. This commentaryreports on some recent results of our research on brain injuryusing live human concussion data, brain motion data fromcadaveric head impacts and an advanced computer model ofbrain response to blunt impact. However, before describing theresults, I would like to report on the results of a series of dummyhead impacts in which a Hybrid III head and neck system wasplaced on a mini-sled and made to impact different types offoam. Identical tests were done with the head bare or wearing ahelmet used in American football. It was found that the helmetwas able to reduce the head linear acceleration significantly butnot its angular acceleration. We are thus forced to ask theinevitable question: If angular acceleration is the major cause ofbrain injury, then how does the helmet protect the brain?

Brain Motion During Head ImpactHardy et al., (2001) were the first to report quantitative data onthe extent of brain motion during a blunt impact. A series of care-fully orchestrated impacts on inverted and decapitated heads wasconducted in conjunction with the use of a biplanar high-speed x-ray system that provided video pictures of the motion of neutraldensity targets in the brain at 1000 frames per second. It wasfound that linear acceleration caused very little brain motion, onthe order of ±1 mm, while angular acceleration can result in targetmotions on the order of ±5 mm. However, even for angular accel-erations in excess of 10000 rad/s2, the displacement is limited to±5 mm. Thus, it is not entirely clear what the roles of linear andangular acceleration are in causing brain injury.

A Computer Model of Human Brain ImpactAn advanced model of human brain response to head impactwas developed by Zhang et al (2001). It is a finite element modelconsisting of over 314,000 elements, as shown in Figure 1. Itsimulates in detail all essential anatomical features of a 50th per-

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by Albert I. King, Ph.D.

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centile male head, including the scalp, skull with an outer table,diploë, and inner table, dura, falx cerebri, tentorium and falxcerebelli, pia, venous sinuses, CSF, lateral and third ventricles,cerebrum (white and gray matter), cerebellum, brain stem, andparasagittal bridging veins. The model was validated against allavailable cadaveric data at that time, including the brain dis-placement data collected by Hardy et al., (2001). In addition todisplacement, the output of the model included normal andshear strain in all parts of the brain, intracranial pressure andstretch of the bridging veins. Strain rate was eventually comput-ed because there is experimental evidence from tissue levelexperiments which show that strain rate is a significant factor inaxonal dysfunction (LaPlaca et al., 1999). There is also evidencefrom animal experiments that the product of strain and strainrate is a good predictor of brain injury (Viano and Lovsund,1999). Obviously such a model can use input parameters, suchas linear and angular accelerations, to predict brain injury, basedon the computed response of the brain. Logic also dictates thatinjury is directly dependent on the response of the brain and noton the input parameters.

Data from the National Football LeagueDuring each football season, professional players are routinelyconcussed every Sunday.. They sustain what is termed a mildtraumatic brain injury (MTBI) which is essentially reversible inthe sense that there does not appear to be any permanent seque-lae as a result of that single impact. A multi-center researcheffort, managed by Biokinetics, Inc., of Ottawa, Ontario andinvolving Duke University, the University of Pennsylvania andWayne State University resulted in accurate estimates of the headaccelerations of the two colliding players, one of whom has sus-tained a MTBI. The reconstruction process starts with a stere-ogrammetric analysis of the speed and location of impact of thetwo helmets, using video from at least two of the cameras on thefield. A pair of instrumented and helmeted Hybrid III headsattached to their respective necks was used to reconstruct theimpact so that the linear and angular acceleration of both headscould be measured (See Newman, et al., 1997). The data werethen fed into the Wayne State model to compute the responseparameters described in the previous section. There were a totalof 53 cases of which there were 22 concussions and 31 non-con-cussions. Each case was simulated using the Wayne State Univer-sity brain injury model and response parameters were computed.A Logist analysis was performed with many of these parameters.The concussed cases were assumed to have an injury probabilityof one and the non-concussed cases had a zero probability ofinjury. Chi square and p-values were calculated and it was foundthat the product of strain and strain rate was the best predictor,

followed by strain rate and HIC. Table 1 shows the top 5 predic-tors in the order of their Chi square values. It is seen that angularacceleration is fifth in that list and HIC is surprisingly high as apredictor of reversible MTBI.

DiscussionThe fact that the product of strain and strain rate is the leadingpredictor of MTBI is not surprising because there is experimentalevidence from animal tests to support this. However, the low pre-dictive power of angular acceleration is indeed a surprise. Both thecadaveric data and the model indicate that angular accelerationgenerates large displacements and principal strains in the brainand it was found that high values of strain rate occurred in regionswhere the strain was high. That is, the product of strain and strainrate can only be high in the presence of angular acceleration. Onthe other hand, linear acceleration does not bring about a lot ofbrain displacement and hence strain and it stands to reason thatthe strain rate is also low for this condition. The fact that HIC israted as a good predictor of concussion must mean that in addi-tion to the high strain rates generated by angular accelerationanother injury mechanism is at work. It is important to considerthe effect of shock or pressure waves passing through the brain tis-sue and perhaps concentrate on experimental animal studies thatdeliver shocks to the brain with very little head motion.

ConclusionsBy combining a series of different studies, some additional lighthas been shed on the parameters responsible for MTBI. The bestpredictors are response variables but the input variable linearacceleration is ranked quite high. These results suggested twodifferent mechanisms at work, both of which can cause injury.

ABOUT THE AUTHORAlbert I. King, Ph.D.: Distinguished Professor and Chair, Department of BiomedicalEngineering, Wayne State University. Contact information: Department of Biomed-ical Engineering, Wayne State University, 818 W. Hancock, Detroit, MI 48202.Telephone: 313-577-1347 or 313-577-8333, e-mail: [email protected].

REFERENCESHardy WN, Foster CD, Mason MJ, Yang KH, King AI: Investigation of headinjury mechanisms using neutral density technology and high-speed biplanar X-ray. Stapp Car Crash J., 45:337-368, Paper no. 2001-22-0016, 2001.

LaPlaca MC, Lee VM, Thibault LE (1997). An in vitro model of traumatic neu-ronal injury: Loading rate dependent changes in acute cytosolic calcium and lac-tate dehydrogenase release. J. Neurotrauma. 14: 355-368.

Newman J, Beusenberg M, Fournier E, Shewchenko N, Withnall C, King A, YangK, Zhang L, McElhaney J, Thibault L, McGinnis G (1999). A new biomechanicalassessment of mild traumatic brain injury. Proc. 1999 IRCOBI Conference, pp.17-36.

Viano DC, Lövsund P (1999). Biomechanics of brain and spinal cord injury:Analysis of neurophysiological experiments. Crash Prevention and InjuryControl, 1:35-43

Zhang L, Yang KH, Dwarampudi R, Omori K, Li T, Chang K, Hardy WN, KhalilTB, King AI. Recent advances in brain injury research: A new human head modeldevelopment and validation. Stapp Car Crash J., 45:369-394, Paper No. 2001-22-0017, 2001.

ACKNOWLEDGMENTThe author wishes to acknowledge the contribution of Dr. King Yang, Dr. LiyingZhang, Mr. Warren Hardy, Dr. David Viano and Dr. Scott Tashman for their con-tribution to the work reported in this article. Funding for this work was providedby the Centers for Disease Control, the National Football League Charities andHonda R & D Co. Ltd.

Parameter Model p Rank

Chi-Square

Product of strain and strain rate (s-1) 34.1 0.0000 1

Strain rate (s-1) 30.1 0.0000 2

HIC 26.3 0.0000 3

Linear acceleration 20.9 0.0000 4

Angular acceleration 20.7 0.0000 5

Table 1. Result of Logist Analysis for Reversible MTBI


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Over sixty years ago, Holbourn (1943) created specialized gelatinmodels of the human brain, and studied their response duringrapid translational and rotational motions, and concluded thatrotational or angular movements would create larger and morewidespread brain distortions than translation or linear move-ments, and that the pattern of distortion would vary with thedirection of head motion. In addition, he postulated that regionaldeformation (strain) would scale with brain mass, such that larg-er brains experiencing the same acceleration would deformmore. Over the next 40 years, numerous experimental investiga-tions not only confirmed these hypotheses, but created the foun-dation of critical data that we use today to understand mecha-nisms of head injury in the adult (Ommaya et al., 1968,1993,1971; Hirsch and Ommaya 1973; Gennarelli et al., 1972,1982a,1982b, 1987; Gennarelli 1993; Bandak 1995; McIntosh etal., 1996; Ommaya 1995). Events are typically characterized ascontact or inertial, the latter involving head motion. Contactevents result in soft tissue injuries of the scalp, skull fracture ordeformation, epidural or subdural hematomas, and cortical con-tusions. Inertial events are likely to produce concussion, sub-dural hematoma, subarachnoid hemorrhage, petechial hemor-rhages, and/or widespread axonal injury.

Difficulty arises in applying the adult paradigm to pediatrichead injury, because scaling by size alone is insufficient toinclude the role of changes in the stiffness of the braincase withmaturation and the influence of neural development on theresponse of the brain to a specific deformation. Therefore, at thistime we are unable to define a complete rubric for biomechanicsof pediatric brain injury, but as additional experimental dataregarding mechanical properties of pediatric neck, brain andskull are obtained, and injury thresholds are derived for thedeveloping brain, we will be able to answer critical questionsregarding mechanisms of injury that are unique to young chil-dren. The paucity of data for the child and immature animals has

impeded our ability to understand if a specific event is likely tobe associated with head injury in the child, to develop protectivemeasures and treatments specifically for children and to distin-guish with confidence between nonintentional head injuries andchild abuse.

Identification of child abuse is particularly fraught with diffi-cultly, because histories regarding the loading conditions (accel-eration magnitude or direction, occurrence of impact, etc.) areunreliable. Despite objective information, a vigorous debateexists as to whether vigorous shaking, causing rapid movementsof the head relative to the torso, may cause the subduralhematomas, axonal injury, and retinal hemorrhages documentedin abused infants. Guthkelch (1971) and Caffey (1972, 1974)proposed that rotational acceleration-decelerations associatedwith shaking played a central role in generating brain injurieswith greater morbidity and mortality than those in infants whohad fallen short distances (Kravitz et al., 1969; Helfer et al.,1977; Nimityongskul and Anderson 1987; Lyons and Oates1993). This proposed etiology was coined “whiplash-shakeninfant syndrome” and also “shaken baby syndrome”; the lattername has continued in general use.

With the onset of computerized tomographic (CT) imagingin the late 1970’s, and the near-simultaneous increase in post-mortem examination of infants who died suddenly or unexpect-edly, there was a rapid increase in knowledge about the patho-logic lesions seen in abused infants (Hahn et al., 1983, Ludwigand Warman 1984; Billmire and Myers 1985; Duhaime et al.,1987). Common findings included small or skim subduralhematomas, often parafalcine in location, frequent documenta-tion of retinal hemorrhages, seizures, apnea and/or bradycardiaat presentation, and poor outcome associated with high mortali-ty. DAI (Diffuse Axonal Injury) and white matter injury weredescribed in fatal cases (Calder et al., 1984; Vowles et al., 1987).Bruises and skull fracture were frequent findings, especially in

by Susan S. Margulies, Ph.D. and Betty Spivack M.D.


fatal cases, although in a high proportion of such cases, evidenceof impact was not found until postmortem examination (Hahn etal., 1983; Duhaime et al., 1987).

To gain insight into the relative roles of shaking and inflictedimpacts in generating these head injuries, Duhaime et al., (1987)and Prange et al., (2003) constructed doll models of infants andcompared rotational accelerations and velocities experienced bythe head during vigorous shaking, falls, and inflicted impactsagainst various surfaces. Inflicted impact onto hard surfaces pro-duced peak accelerations significantly larger than falls from 5feet onto concrete, and up to 30-50 times that produced byshaking alone. Large rotational accelerations occurred as thehead rebounded after contact with firm surfaces, but was attenu-ated on soft surfaces that pocketed the head. It is important tonote that actual neck properties of infants in flexion/extensionare unknown, and the flexible neck representations used in thedolls may overestimate actual events. While these studies pro-vide important objective biomechanical information regardingthe comparative loading conditions across accidental and inflict-ed scenarios, there are several caveats. First, because of thepaucity of injury threshold information for children, it is difficultto predict the occurrence of injury, but the higher rotationalaccelerations associated with impact increase the likelihood ofinjury. Second, little data is available to determine if a repeatedmotion causes more severe injury than a single movement of thesame magnitude. Finally, if the soft skull of the young childdeforms during contact, the deformation during the moment ofcontact event may cause additional brain damage, exacerbatingthe injury during the rotational rebound.

Over the last 30 years, mechanical properties of adult braintissue have been measured in the laboratory (Ommaya 1968,McElhaney et al., 1969; Galford and McElhaney 1970; Miller etal., 1997, 2000, 2002; Mendis et al., 1995; Fallenstein et al.,1969; Metz et al., 1970, Thibault and Margulies 1998; Arbogastand Margulies 1997) and were found to vary over ten-fold, dueto differing testing methods, species, interval after death, andregion of the brain. More recently, mature and immature freshporcine brain tissue was tested in a variety of orientations over abroad strain range, and results demonstrate that infant brain tis-sue is significantly stiffer than adult tissue (Prange and Margulies2002), because of the lower levels of myelin in the young brain.The stiffer brain offers resistance to deformation during contactor inertial loading conditions, but one cannot comment aboutthe brain’s risk of injury until studies demonstrate if the infantbrain tissue is injured more or less severely than the adult, ifdeformed in a similar manner. Raghupathi and Margulies (2002)recently compared axonal injuries in newborn piglets and adultpiglets experiencing similar nonimpact rotational velocities. Theneonatal porcine brain experienced more than 3 times moreaxonal injury than the mature brain. The marked differential isamplified further when one considers that intracranial strain lev-els would be expected to be lower in the younger animal withstiffer brain tissue and smaller brain size. Thus, we conclude thatthis study is consistent with the concept that pediatric brain tis-sue may have a lower injury threshold than adult. However, thisconclusion must be confirmed in additional studies. Further-more, it should be noted that this study was focused on single-impulse events, rather than multiple-impulse episode.

Shaking produces an oscillatory motion due to the repeatedapplication of the impulse in a periodic fashion, typically at a fre-quency of 4-10 Hz (Duhaime et al., 1987). Therefore, harmonicamplification of the energy, force and stresses experienced by thebrain may occur if the frequency of shaking is a small integer

multiple of the natural frequency of the skull and intracranialcontents. Willinger et al. demonstrated that the first resonancefrequency of the adult head ranges between 67 and 100 Hz(Willinger et al., 1994, 1996, 1999), and the pediatric headwould have a higher natural frequency due to its smaller size. Incontrast, Ommaya identified the natural frequency of skull andintracranial contents as 5-10 Hz in subhuman primates, and pro-posed that the natural frequency in the adult human would scaleto be 4-5 Hz(Ommaya et al., 1971, 1993). It is clear that addi-tional studies are needed to define more narrowly the natural fre-quency in children, to evaluate if this mechanism may give riseto substantial intracranial deformations, and associated braininjuries.

Despite these inherent limitations of the instrumented dollstudies, it has become clear that a high proportion of infantswith inflicted head trauma have evidence of impact to the head,and that the proportion is even higher in children who die oftheir injuries (Hahn et al., 1983; Duhaime et al., 1987; Hadley etal., 1989). Because the infant skull has 1/8 the strength of adultskull but can deform more than six times as much before frac-ture (Margulies and Thibault 2000), impact may deform theinfant skull significantly, causing diffuse brain injuries. Thesedata correlate well with the rarity of documented skull fracturein observed infant falls from low heights (Helfer et al., 1977;Nimityongskul and Anderson 1987) but is not consistent withreported data of near-universal skull fractures obtained by drop-ping infant cadavers on a variety of surfaces from 32 inches(Weber 1984, 1985). These latter studies do not describe meth-ods for cadaver preservation, handling or postmortem durationprior to the impact testing. Routine storage in a morgue refriger-ator, with some passage of time, may be expected to producedehydration of the bone resulting in a more brittle skull (Sasajuand Enyo 1995). In contrast, Margulies and Thibault (2000)used recommended techniques of rewarming and rehydratingbone samples prior to biomechanical testing.

Children with milder degrees of neurologic injury, who stillmay have SDH and retinal hemorrhages, are less likely to haveevidence of head impact (Jenny et al., 1999), but are more likelyto be misdiagnosed initially. It must be noted, that nine percent(5/54) of these children with “missed” abusive head trauma diedafter recurrent abuse. This finding also underscores the lack ofdata regarding injury thresholds for repeated events – occurringhours, days, or weeks apart.

Given that the infant neck is so flexible, attention has extend-ed to biomechanical events at the cervicomedullary junction dur-ing trauma as a potential precipitating event leading to changesin respiratory and cerebrovascular control centers, causing braininjury secondary to hypoxia and ischemia. Hadley (1989)demonstrated pathology at the cervico-medullary junction in fiveof six fatal cases of abusive head trauma where no evidence ofimpact injury was present. Accompanying pathologic lesionsincluded spinal cord subdural and epidural hematomas, andspinal cord contusions. More recently, Geddes has found trau-matic axonal injury at the cervico-medullary junction, and raisesconcern that this region may be vulnerable during shakingevents (Geddes et al., 2000, 2001a, 2001b). Vertebral arterycompression in the neck by periadventitial hemorrhage has alsobeen reported (Gleckman et al., 2000). Injury at the cervico-medullary junction may be the mechanism for the high inci-dence of apnea seen in infants with abusive head trauma (Lud-wig and Warman 1984), and thereby contribute to theencephalopathy seen in children dying of abusive head trauma(Geddes et al., 2000, 2001a, 2001b; Johnson et al., 1995). The


paucity of data regarding the mechanical properties of the neckin infants and young children is an obstacle to engineeringefforts to investigate the relative influence of shaking, falls, andinflicted impact on injuries to the cervico-medullary junction.

Recently, Ommaya et al., (2002) proposed that neck orspinal cord injury would be present in all cases, if whiplashinjury has caused SDH or other intracranial pathology. However,previous studies do not consistently support this hypothesis.Data from primates (Ommaya et al., 1968) experiencing awhiplash nonimpact type of event and infants (Geddes et al.,2001a, 2001b) who died of abusive head trauma suggest thatonly 30-50% of cases with intracranial pathology may haveaccompanying brainstem or spinal cord injuries visible on thesurface or on histologic examination. No data is available on thefrequency of muscular, ligamentous, or bony injury in this set-ting. The presence of acute episodes of apnea or cerebral bloodflow alterations can precipitate secondary brain injuries. Geddes(2000, 2001a, 2001b) has noted frequent appearance of hypox-ic-ischemic encephalopathy in the brains of infants who havedied of abusive head trauma and Gleckman (2000) has reportedsimilar findings. Levels of quinolinic acid, inflammatory media-tors and excitatory amines including glutamine (Whalen et al.,1998, 2000; Bell et al., 1999; Ruppel et al., 2001) have beenreported to be high in all types of pediatric traumatic braininjury, but were much higher in children suffering from abusivehead trauma. The neurotoxicity of many of these substances, andsecondary injuries due to hypoxia and altered CNS metabolismmay contribute to the high mortality rate and severe morbidity ofchildren with abusive head trauma, compared with survivors ofaccidental head trauma (Bonnier et al., 1995; Haviland and Rus-sell 1997; Ewing-Cobbs., 1998).

Retinal hemorrhages also appear to have a much strongercorrelation with abusive head trauma than with accidental headtrauma, even when the accidental injury is severe (Elder et al.,1991; Duhaime et al., 1992; Johnson et al., 1993; Dashti et al.,1999). Combining the cited studies, 287 children with docu-mented accidental head trauma requiring hospitalization (nearlyall were falls and motor vehicle accidents) had dilated retinalexaminations performed by a pediatric ophthalmologist. Only 3children had retinal hemorrhages (1.0%); all three were victimsof motor vehicle accidents. There have been isolated reports ofretinal hemorrhages incurred in household accidents (Christianet al., 1999). In all cases, the retinal hemorrhages consisted of afew, small unilateral hemorrhages isolated to the posterior pole.In contrast, retinal hemorrhages extending to the far periphery ofthe retina, traumatic retinoschisis, optic nerve sheath hemor-rhage and axonal injury of the optic nerve have been reported asa common occurrence in infants with abusive head trauma(Levin 2000). Use of beta-amyloid precursor protein staining canfacilitate identification of traumatic axonal injury of the opticnerve (Gleckman et al., 2000). Proposed injury mechanismsinclude orbital shaking and vitreous traction during a shakingevent, but experimental data to support these hypotheses areneeded.

CONCLUSIONSWhile the general paradigm of adult traumatic brain injury

has a solid research basis, the applicability of this paradigm tochildren still presents significant gaps and challenges. Basic bio-mechanical properties have not been well established for infantskull or brain tissues, nor has the infant neck been well charac-terized. Early evidence indicates that simple brain mass scaling

does not accurately predict thresholds for traumatic axonalinjury in immature brains. Little or no experimental work hasbeen performed using oscillatory loads, such as shaking, toderive injury thresholds in either mature or immature animals.It is unknown at present whether thresholds for intracranialinjury with such repetitive loading patterns will be higher, loweror identical to thresholds for single impact or impulsive loads.The relative contribution of secondary neural injuries in theobserved pathology in victims of abusive head trauma remainsunclear, but emerging data indicates that hypoxic-ischemicinjury may be a significant and complicating factor. Research inthe biomechanics of different patterns of retinal hemorrhage isonly at an early stage.

Head injury is a leading cause of death and acquired disabilityin childhood. However the biomechanics of pediatric head injuryis poorly understood, primarily due to the paucity of age-specificdata regarding mechanical properties of immature tissue and itsresponse to specific loads. Research is needed to understand theunique biomechanics associated with pediatric neurotrauma.

ABOUT THE AUTHORSSusan S. Margulies, Ph.D., is an Associate Professor in the Departments of Bioengineeringand Neurosurgery at the University of Pennsylvania. Her research emphasis is biomechanicsassociated with pediatric brain injury, with the goal of enhancing avenues for injury preven-tion, intervention and treatment.

Betty Spivack, M.D., is a Clinical Assistant Professor in Pediatrics and Pathology at KosairChildren's Hospital and the University of Louisville School of Medicine, and Forensic Pedia-trician at the Kentucky Medical Examiner's Office. She has received national recognition forher activities on behalf of abused children. Her current research includes shortfall mortalityand the biomechanics of swing accidents.

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IntroductionA high profile athlete sustains a head injury and we read

about it in the sports pages. But for every professional athletewho experiences a sports concussion, there are many more ama-teur athletes, both adults and children, who don’t make thepapers. Still, head injury in sports is an important and timelymedical topic, and this review will briefly cover aspects of sportsconcussion, including epidemiology, biomechanics, sports-relat-ed recurrent head injuries, and basic clinical management.

Epidemiology of Sports-Related Brain InjuryThe majority of head injury in sports falls into the category

of mild traumatic brain injury, also referred to as concussion. Aconcussion is defined as any biomechanically-induced impair-ment of neurological function, with or without loss of conscious-ness (American Academy of Neurology, 1997). Because of itsmild nature, many sports concussions go unreported. In fact, adesire of the athlete with brain injury to quickly return to playoften results in minimizing or ignoring the symptoms of concus-sion. The Centers for Disease Control estimate that 300,000sports-related brain injuries occur annually in the United States,the vast majority of them concussions (Centers for Disease Con-trol and Prevention, 1999). Of all traumatic brain injuries, 1 in 5is incurred during sports participation.

Perhaps more compelling are the estimated rates of concus-sion among athletes in particular sports. Concussive headinjuries account for a significant proportion of total injuries incontact sports. Collegiate ice hockey (12.2%), football (8%) andsoccer (4.8%) all showed a significant percentage of concussionsout of total injuries sustained during the 2002-2003 season, asreported by the National Collegiate Athletic Association (NCAA)Injury Surveillance System (McCrea, Guskiewicz, Marshall et al.,2003). Similar results were reported in a study of athletes from235 U.S. high schools, where 5.5% of total injuries were mildtraumatic brain injuries (Powell and Barber-Foss, 1999). This

percentage was highest for football (7.3%), wrestling (4.4%), andsoccer (3.9%) in boys’ sports. In girls’ sports, the percentage ofconcussions out of total reported sports injuries was highest insoccer (4.3%). Ice hockey was not assessed in the latter study.Among the 10 high school sports analyzed, however, it was esti-mated that over 60,000 mild head injuries occur annually in var-sity high school athletes. This underlines the fact that manysports-related head injuries occur in children and adolescents,whose brain development is ongoing and where the effects ofinjury may be distinct from those seen in adults.

Most persons are able to recover completely from concus-sions. While a single mild injury may not result in lasting cogni-tive or behavioral deficits, an accumulation of injuries over time,or repeated injury with incomplete recovery between concus-sions, can have lasting effects (Collins, Lovell, Iverson et al.,2002; DeFord, Wilson, Rice et al., 2002; Guskiewicz, McCrea,Marshall et al., 2003). Thus, a unique aspect of sports concus-sion is the likelihood for repeated mild injuries and potential forlasting problems. This is anecdotally demonstrated by profes-sional athletes whose careers have been cut short by multipleconcussions. Furthermore, several published studies exist thatquantify the risk of recurrence (Guskiewicz, Weaver, Padua etal., 2000; Zemper, 2003). Guskiewicz reported that high schooland college football players who sustained a concussion werethree times more likely to suffer a second concussion during thesame season. More recently, Zemper showed that a previous con-cussion is associated with an almost overall 5.86-fold increasedrelative risk of another concussion (not necessarily limited to thesame season). Several possibilities exist to explain this increasedrisk. One is that athletes with a more aggressive style of play aremore likely to sustain repeated head injuries. A second explana-tion may be that certain individuals are somehow predisposed toconcussions. A third possibility is that concussion results in cere-bral dysfunction that makes the injured brain more vulnerable tosubsequent biomechanical insults. While the existing studies

SSPPOORRTTSS CCOONNCCUUSSSSIIOONNby Christopher C. Giza, M.D.


cannot determine which of these is more likely, these explana-tions are not mutually exclusive. Moreover, there is increasinglaboratory evidence that recurrent traumatic brain injuries canexacerbate injury pathophysiology and result in lasting deficits(DeFord, Wilson, Rice et al., 2002; DeRoss, Adams, Vane et al.,2002; Kanayama, Takeda, Niigawa et al., 1996; Laurer, Bareyre,Lee et al., 2001).

Biomechanics of Sports ConcussionTraumatic or concussive injury represents a unique type of

brain injury, whereby pathophysiological changes are initiatedby mechanical forces imparted to the brain-mechanical forcesimparted to the brain initiate pathophysiological changes.Understanding the basic biomechanics of concussion, then, isimportant not only to understand the clinical injury itself, butalso to design appropriate research models with which to studyconcussion.

Brain tissue is a gelatinous substance with a consistencylikened to that of firm oatmeal. The brain is wrapped in a thickcovering (the dura) that both protects and segments the brain.Within this covering, the brain essentially floats in a bath of cere-brospinal fluid. All of these components are then housed withinthe bony skull. When mechanical forces are applied to the head,the brain moves within the fluid-filled skull, and injury canresult from the brain striking the skull at the point of impact(coup injury), forces applied to the brain on the side oppositefrom impact (contrecoup injury), or by shearing/twisting of brain

tissue around an axis of injuryimpact force. Forces causing con-cussion can thus be simplistically categorized as either linear orrotational (Figure 1).

Generally, linear forces, sometimes referred to as translation-al forces, can result either from the head being struck by a mov-ing object (fist, ball, etc.) or by the head being driven against anunmoving object (ground, wall, etc.). At the point of impact,there is transient deformation of the skull that can result in com-pression of the brain. With very high forces, permanent skulldeformation can occur in the form of a fracture; however, this isvery unusual in the setting of sports concussions. Opposite thepoint of impact, negative or tensile forces can exert their injuri-ous effects on the pliable brain tissue. It has been hypothesizedthat the cause of contrecoup injuries is due to this negative pres-sure, or alternatively, to rebounding of the ‘floating’ brain againstthe inside of the bony skull.

It is rare for translational forces to occur in isolation, partic-ularly in a sports setting. More often, linear forces are combinedwith rotational or angular or rotational forces that can result intwisting of the brain within the skull. These types of more diffuseforces are particularly damaging to white matter fiber tracts thatinterconnect brain regions. Rotational forces also appear to play

an important role in traumatically-induced loss of consciousness.Furthermore, the pathology of these diffuse rotational injuriescan be subtle, and is generally not well detected by conventionalCT scanning. Thus, the vast majority of CT scans performed onathletes after concussion appear normal, despite the fact thatmicroscopic damage may be present..

Pathophysiology of ConcussionIt is important to realize that significant cerebral dysfunction

can exist, even when brain anatomy appears normal, such asusually occurs in the setting of a concussed athlete. Animal mod-els of diffuse concussive injury have shown profound cellularand physiological alterations that can last minutes to days afterimpact. In general, experimental concussive injury results in anindiscriminate depolarization of neurons, widespread release ofglutamate, efflux of potassium, alteration and impairment ofcerebral glucose metabolism, and derangements of cerebralblood flow (Giza and Hovda, 2001; Katayama, Becker, Tamura etal., 1990; Yoshino, Hovda, Kawamata et al., 1991). Many ofthese findings have been confirmed in humans with severe trau-matic brain injury (Bergsneider, Hovda, Shalmon et al., 1997;Reinert, Hoelper, Doppenberg et al., 2000). Moreover, a pro-found reduction in brain glucose metabolism was reported in afootball player who experienced a concussion, demonstratingthat brain physiology can be affected even after milder injuries(Bergsneider, Hovda, Lee et al., 2000). One recent study demon-strated impaired cerebral blood flow activation in response to aworking memory task in mildly head-injured patients with per-sistent symptoms (Chen, Kareken, Fastenau et al., 2003).Another showed abnormal patterns of fMRI activation during asimilar task in patients that had experienced mild TBI (McAllis-ter, Saykin, Flashman et al., 1999). There is now substantialexperimental and clinical data to confirm that concussive braininjury can result in physiological dysfunction in the absence ofstructural damage.

Recurrent Brain InjuryOne of the characteristics of sport-related concussion is the

possibility, and indeed, likelihood, of repeated mild injuries.The effects of repeated injury are best considered as two distinctproblems. First, there appears to be some cumulative effect oftotal concussions sustained over a longer period of time, even ifan adequate period of recuperation is permitted after each indi-vidual concussion. In animal models of repeated mild traumaticbrain injury, rats demonstrate enduring difficulties in cognitiveand behavioral tasks, even in the absence of significant anatomi-cal injury (DeFord, Wilson, Rice et al., 2002; Laurer, Bareyre,Lee et al., 2001). There are also multiple studies in humans thatdemonstrate worse neurological symptoms and cognitive func-tion with increasing number of concussions (Collins, Grindel,Lovell et al., 1999; Collins, Lovell, Iverson et al., 2002;Guskiewicz, McCrea, Marshall et al., 2003). These studies haveall been performed in athletes and are thus directly relevant tothe problem of sports concussion.

Second, there is the risk of a second concussion occurring ina brain that has not yet physiologically recovered from a firstconcussion. This brain may then be more vulnerable to theeffects of a mild injury. Second impact syndrome is a rare butcatastrophic phenomenon characterized by fulminant cerebraledema and neurological collapse, occurring when a second(often mild) head injury is superimposed upon an earlier injury

Figure 1: Biomechanics of Concussion


from which the athlete has not completely recovered (Cantu,2000a). Children appear to be more vulnerable than adults tomalignant brain swelling after mild head trauma, sometimes evenafter only a single injury (Bruce, Alavi, Bilaniuk et al., 1981).

Clinical Management of Sports ConcussionCurrent guidelines for the classification and management of

concussion, including return-to-play guidelines, are based pri-marily upon expert opinion and consensus (American Academyof Neurology, 1997; Cantu, 2000b; Colorado Medical Society,1990) (Table 1). Some data regarding the timing of physiologicalrecovery are available from animal models, but extrapolatingthese time intervals to the human condition is problematic. Theproper clinical management of sports concussion involves accu-rately describing the injury, early assessment, further diagnosticinvestigation for unusual or persistent symptoms, follow up untilsymptoms resolve, and finally, instruction regarding returning toplay and prevention of future head injuries.

There are a myriad of guidelines for classification of concus-sion severity consensus (American Academy of Neurology, 1997;Cantu, 2000b; Colorado Medical Society, 1990). To accuratelydescribe the injury, the initial medical evaluation should includethe following: 1) some mention of the biomechanics of the acci-dent (i.e. helmet-to-helmet collision, back of head striking theground), 2) presence of protective headgear, 3) initial neurologi-cal symptoms, 4) presence and duration of any loss of conscious-ness, 5) presence and duration of post-traumatic amnesia and 6)history of prior concussions – both recent and distant. It isimportant to be aware of the fact that a concussion can occureven if the player does not lose consciousness.

Early assessment can be done by the team trainer or physi-cian on the sidelines. The standardized assessment of concussion(SAC) is a simple, validated tool that can be performed quicklyand reproducibly (McCrea, Kelly, Kluge et al., 1997) (Table 2).The SAC has been shown to be sensitive to detect subtle impair-ment resulting from a concussion, and can even be administeredat the beginning of the season so that a baseline score may berecorded for each athlete. (editor note: see page 32 for moredetails about assessment technology for mild TBI).

Any loss of consciousness merits closer evaluation. The deci-sion to obtain a head CT scan is largely based on the severity andpersistence of symptoms. Prolonged unconsciousness, suspicionof skull fracture, seizures and/or focal neurological deficits sug-gest more than a simple concussion and indicate a need for neu-roimaging. Other worrisome signs include persistent/worseningheadache, altered mental status, and/or nausea/vomiting. In casesof simple concussion, initial observation is a reasonable clinicalplan, with the possibility left open to re-evaluate the player ifproblems worsen or fail to resolve.

After the acute period, any athletes with persistent symp-toms may require follow up evaluation. Post-concussive symp-toms can span a wide range, but most commonly include somecombination of the following: headache, poor attention, memoryimpairment, fatigue, dizziness, ringing in the ears, mood changesand sleep disturbances. Current guidelines take persistent neu-rocognitive symptoms as a sign of ongoing cerebral dysfunctionand presumed increased risk of a second injury. Therefore, it isrecommended that no athlete with a concussion return to play ifsymptoms persist. In fact, current guidelines for time intervalsuntil return-to-play are based upon resolution of all neurological

symptoms at rest and with exertion (American Academy of Neu-rology, 1997) (Table 3).

Other important interactions with the athlete at the follow upevaluation include education as to the risks of repeated concus-sion and proper use of head protective gear. While many think ofsports concussion as occurring only in team sports, it should beremembered that many mild and severe head injuries also occuras a result of bicycle, scooter and rollerblade accidents. Manystudies have documented the efficacy of bicycle helmet laws inreducing the number of head injuries (Cook and Sheikh, 2000).Currently, there are no effective brain-specific therapies for headinjury, and thus, the best management of sports-related concus-sion must include preventive and protective measures.

Table 1: Concussion Severity: Grading

Table 2: Standardized Assessment of Concussion (SAC)

Table 3: Repeated Concussion in Sports: Return to Play Guidelines


Conclusions Concussion is defined as any tran-

sient neurological dysfunction resultingfrom biomechanical forces imparted tothe brain, with or without loss of con-sciousness. Concussion is by far the mostcommon type of head injury, and is fre-quently associated with sports participa-tion. Concussive brain injury is mediatedby both linear and rotational forces. Lin-ear forces are associated with impact, andcan result in both focal and diffuse injury.Rotational forces result in twisting orshearing of neural tissue, even in theabsence of impact. Most sports concus-sions result from a combination of thesetypes of forces. Concussion results in acomplex pathophysiological cascade inthe injured brain, rendering it dysfunc-tional even in the absence of clearanatomic damage. During this time, theinjured brain is particularly vulnerable tofurther injury. Current return-to-playguidelines treat persistent neurologicalsymptoms as evidence of ongoing neuraldysfunction and limit return-to-play onlyuntil after a variable symptom-free obser-vation period. Appropriate clinical man-agement of sports-related head injuryincludes an accurate injury description, arapid sideline assessment, careful moni-toring of symptoms, and education of theathlete with regards to return-to-play andprevention of future injuries.

ABOUT THE AUTHORChristopher C. Giza, M.D.: UCLA Brain Injury ResearchCenter, Division of Neurosurgery/Department ofSurgery, Division of Neurology/Department of Pediatrics,Brain Research Institute, David Geffen School of Medi-cine at UCLA. Email: [email protected].

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IntroductionTraumatic Brain Injury (TBI) is a serious disease that has beenoverlooked for many decades. The Center for Disease Controlreported 1.5 million people diagnosed with TBI in 2001 (NationalCenter for Injury Prevention and Control, 2003). One of the majorproblems with TBI is a lack of sufficiently reliable diagnostic toolsto assist the Emergency Medicine (EM) physician when he or shesees a person involved in an automobile collision. A correct diag-nosis of TBI is difficult because the presence of a head injury maybe masked, among other things, by serious injury to another bodypart, subtle and changeable symptoms, or a delayed onset ofsymptoms. Various studies indicate a significant percentage ofundiagnosed TBI in Emergency Room (ER) settings, in some casesover 50% (Zhang, Yang, King, 2001; Edberg, Rieker, Angrist,1963; Gurdjian, et al., 1967; Pudenz, Sheldon, 1946). New devel-opments in neurodiagnostics, the use of biological markers such asthe S-100 serum can, to some extent, improve the unfortunate sta-tistics of undiagnosed TBI. Further gains can be achieved by utiliz-ing the knowledge from trauma biomechanics.

At an injury assessment stage the information regarding theimpact scenario is highly desirable. When ER physicians encounterpatients with possible TBI, they typically are hindered by a lack ofknowledge about the collision. Many EM physicians alreadyemploy a basic understanding of trauma biomechanics in thecourse of their career. They look at photos of the damaged vehicleor talk to the persons involved in the collision in order to deter-mine what happened during an accident and how those events may

affect the person’s injuries. However, these EM physicians use a“common sense” approach to trauma biomechanics; this approachis not scientifically based but rather uses deductive reasoning andpast experiences as opposed to formal training and research.

The best-known general knowledge vehicle collision databaseis the Crashworthiness Data System (CDS), part of the NationalAccident Sampling System (NASS) (National Center for Statisticsand Analysis, 2003). The results from the studies are very usefulfor the intended purposes, one of which is to understand themechanics of serious automotive collisions to improve crashwor-thiness strategies in automotive design. Although this type ofanalysis is useful in crashworthiness strategy setup, it is not con-ducive to an ER setting.

Reconstruction of the biomechanical forces in vehicle crashesfor a specific collision is feasible, and enables quantitative stratifi-cation of TBI severity. Application of biomechanical methodolo-gies for in-depth reconstruction of vehicle crashes has beenapplied for several decades. The majority of the relevant literatureis published in governmental reports and journals in the field ofengineering and biomechanics. Multi-diciplinary teams includingphysicians, scientists, and engineers in relevant areas have devel-oped many of these reports (Jamison, Tait, 1996; Guenther, 1993;Robbins, Melvin, Huelke, 1993; Simpson, Ryan, Paix, 1991; Ash-ton, Cesari, Wijk, 1989; Hoyt, MacLaughin, Kessler, 1988;MacLennon, Ommaya, 1986; McLaughlin et al., 1985; Manavis,Blumberg, Scott, 1984; McGrath, Segal, 1984; Mackay, 1984;Langwieder, Backitis, Ommaya, 1981).

by Mariusz Ziejewski, Ph.D.

TThhee BBiioommeecchhaanniiccaall AAsssseessssmmeennttOOff TTrraauummaattiicc BBrraaiinn IInnjjuurryy


Overall Approach in the Biomechanical Evaluationof TBIThe biomechanical assessment of TBI directly relates to the extentof understanding of the brain injury mechanism. Although themajority of the concepts regarding the cause of TBI are merelyhypotheses, in general it is accepted that brain injury can resultfrom the sudden change in velocity. This can occur due to traumasuch as head impact or inertia loading of the head when torso isaccelerated or stopped rapidly.

An engineering parameter that by definition represents thechange in the velocity as a function of time is acceleration. There-fore the head acceleration has been used in characterization of theseverity of an insult to the brain. The complete global representa-tion of the head motion in terms of acceleration can only beachieved if and only if the complex input of linear and angularacceleration is known. This includes the three components for lin-ear acceleration and three components for angular acceleration(see Figure 1).

The head acceleration data can be used directly to assess theprobability of TBI by extracting the resultant maximum values andthe rate of change of acceleration or by calculating head injuryassessment functions such as the Head Injury Criteria (HIC)(NHTSA 49), Head Impact Power (HIP), Power Index (PI) (New-man, Shewchenko, Welbourne, 2000), and others.

Biomechanical engineers do not assess TBI based on accelera-tion alone; they “look inside the box” – i.e., the skull – and try toassess what’s happening inside. Based on that analysis, additionalparameters that deal with local brain deformation were developed.They are an extension of the evaluation based on head accelera-tion. It has been suggested that brain surface contusions, DiffuseAxonal Injury (DAI), and acute subdural hematoma can be pre-dicted using, among other things, brain motion (Meany, 1991;Gennarelli, Thibault, 1982; Abel, Gennarelli, Segawa, 1978;Edberg, Rieker, Angrist, 1963; Gurdjian, et al., 1967; Unterharn-scheidt, Higgins, 1969; Pudenz, Sheldon, 1946), sudden changein the intercranial pressure which is largely due to the linear accel-eration (Zhang, Yang, King, 2001), sheer strain, stress/strain con-centration (Ross et al., 1994; Holbourn, 1943), the product ofstress and strain rate (Viano, Lovsine, 1999).

Evaluation ProcessWhen performing a biomechanical analysis, there are many factorsabout a collision that must be taken into account. Significant para-meters of a collision that must be considered in these analysesinclude, but are not limited to, the following: change in velocity,direction and duration of impact, body position, gender, height,weight, and vehicle interior design factors. All of the parameters ina collision combine to form a singular, unique scenario. The per-

son performing the analysis must consider all of these factorstogether to determine what cumulative effect they had during thecollision.

The overall procedure to perform the biomechanical assess-ment includes three separate steps – vehicle dynamics analysis,human body dynamics analysis, and human body toleranceanalysis.

Less force transmitted to the occupant compartment of thevehicle means less potential for occupant injury. The transmissionof forces throughout the vehicle is influenced by the physicaldeformation of its structural components and their energy absorp-tion capabilities (Ziejewski , Anderson, 1996; Ziejewski, Goettler,1996; Grosh, Hochgeschwender, 1989; Scharnhorst, 1988; Mah-mood, Paluszny, Tang, 1988). Extensive experimental data isavailable in different databases (www.nhtsa.dot.gov,www.hwysafety.org, www.maceng.com).

Vehicle Dynamics AnalysisWhen performing a specific vehicle dynamics analysis, one mustfirst gather all necessary engineering data about the vehiclesinvolved in the collision. Severity of the collision in engineering istypically assessed based on the extent of the physical damage tothe structure of the vehicle. In a specific evaluation, automotiveanalyses have turned to numerical techniques to approximate theseverity of the crash (EDCRASH). It is also important to look at thelaboratory collision experiments that have been done on the vehi-cle type that was involved in the accident. While this kind of test isnot available for all vehicles, it is important that the person con-ducting the analysis is familiar with the results of the availabletests. From an engineering perspective a complete representationof the severity of vehicular structure includes parameters such aschange in velocity, direction of impact, and duration of impact.The results from this phase of the analysis are based entirely onengineering knowledge, engineering experience, and structuralmechanics.

Once the severity of the impact is understood, one can moveon to the next step, which is called human body dynamics analy-sis. This portion of the analysis relies entirely on biomechanicalknowledge and experience.

Human Body Dynamics AnalysisThe most recognized parameters influencing the nature and theextent of human body response include: body position, gender,height, weight, and others. Body position at the time of impact hasbeen identified as being very significant in assessing the likelihoodof an injury (Yliniemi, Ziejewski, Perry, 2000; Ziejewski, et al.,1999; Ziejewski, Anderson, 1997). In medical literature it hasbeen documented that “trivial trauma” sustained in an accidentcan result in an acute subdural hematoma. It has been speculatedthat bridging veins in the brain normally stretch 30%-35% beforethey tear; however, in the pre-loading state (i.e., abnormal bodyposition), the veins may rupture with little force applied(Ommaya, 1995; Ommaya et al., 1994; Schneider, Reifel, Schnei-der, 1973; Chrisler, 1961). Another example is gender effect. Ithas been shown that for the same external force a female’s headexhibited significantly higher acceleration in comparison to males.Head acceleration for a female in comparison to male has beenreported up to 2 ½ times higher in a collision (van den Kroonen-berg et al., 2002; Hell et al., 2002). Additionally, body proportioncan affect how a seatbelt fits a person, or how a person fits intotheir vehicle. Height can affect how far a person’s head is from the


headrest or how far a person’s knees are from the dashboard. Asingle anomalous factor can cause different injuries in an otherwiseidentical situation. For example, a difference in speed and/or thedirection of impact can cause an increase or decrease in the severi-ty of the injuries, as can a few inches difference in height or a fewdegrees of body rotation.

To evaluate the effect of relevant factors on the human body,there are five types of human models that can be used to evaluatetrauma. They are human volunteers, human cadavers, animals,mechanical models, and mathematical models. Out of all five,mathematical models of the human body are the only models thatallow the user to include all relevant factors simultaneously.

It is impossible to experiment with human beings fitted withinstrumentation under injury producing conditions. Humanbeings are only used on low-severity tests; that is, tests that arebelow human pain thresholds. These tests, limited by rigid regula-tions and guidelines, contribute to general knowledge on thehuman body non-injurious response. The human subjects aremostly young, well-trained, military volunteers (see Figure 2).Their pain tolerance is usually much higher than that of the gener-al population. Therefore, the test results are not representative ofgroups such as females, children, and elderly people. An advan-tage of the use of human volunteers is that the effect of muscletone and prebracing on the dynamical response can be studied.But this influence, which might be relatively large at low impactlevels, simply cannot be extrapolated to higher impact levels.

A useful research tool to evaluate injurious biomechanicalresponse is a human cadaver (also referred to as a PMHS: post-mortem human subject). Disadvantages of the human cadavers arethe absence of muscle tone and undeterminable physiologicresponses. The age of cadavers is often high, and since themechanical strength of most tissues in the human body tends todecrease with age, the data obtained are not necessarily representa-tive of the general population.

Research using anaesthetized animals as human surrogates isvital to obtain information on physiologic responses in injury-pro-ducing loading conditions, especially for specific body areas likethe brain. Furthermore, tests with animals can provide insight inthe differences between dead and living surrogates and as suchprovide information for correct interpretation of human cadavertesting. However, due to differences between humans and animals,quantitative scaling and extrapolation of the results of animal test-ing to a human scale is difficult.

Mechanical models or crash dummies (also referred to asanthropomorphic test devices, or ATD) normally consist of a metalor plastic skeleton, including joints, covered by a flesh-simulatingplastic or foam. They are constructed to be biofidelic; that is, thedimensions, masses, mass-distribution, and, therefore, the kine-matics in a crash are as human-like as possible. An ATD is fittedwith instrumentation to measure accelerations, forces, and deflec-tions that correlate with the injury criteria for human beings. ATDsare often used in approval tests on vehicles or safety devices inwhich the measured values should remain below certain injurytolerance levels. An important objective during these tests is arepeatable response of the dummy in identical tests. The ATDshave been specifically designed for high-severity frontal impacts.Therefore, its application to low severity impacts can result in sig-nificant inaccuracies. The comparison between human responseand ATDs (such as the Hybrid III model) show a difference as highas five times for low severity frontal impact (see Figure 3).

Mathematical models can also simulate the behavior of human

beings in a variety of impacts (Ziejewski, et al., 1999; Cheng,Rizer, 1998). Together with a mathematical description of theenvironment (e.g., the dimensions of the steering-wheel, dash-board, seat, and belts) and the impact conditions (e.g., vehicledeceleration), the model provides a numerical description of thecrash event.


The advanced approach to trauma biomechanical requires ananalysis based on brain deformation. The usefulness of this data isbased on our understanding of the relation between the deforma-tion of the brain and its physiological effects. Biomechanical brainmodeling results are a case specific evaluation of the forces on thepatient’s brain. The case specific components include gender,height, weight, body position, change in velocity, direction andduration of impact, and geometry of the brain that can be basedon the MRI data of the person’s brain. The results from a biome-chanical analysis indicating the location and the extent of thebrain damage for case specific analysis can be compared to theresults from the MRI, the PET scan and neuropsychological test-ing, thus providing the link between the medical diagnosis andthe event of interest.

Additionally, biomechanical brain mapping can provide infor-mation about the time history at different intervals of a specificevent that MRI and PET scans cannot. The ability to understandthe time history of the brain deformation is important due to theviscoelastic nature of the brain tissue. For example, the timedependent characteristics of the brain tissue may indicate a signifi-cantly larger brain deformation due to the cumulative effect ofconsecutive multiple impacts (initial contact of the brain with theskull with a follow-up rebound effect) that one would expect fromthe analysis based on human head motion alone.

One can find an extensive amount of research work on theexperimental as well as computational modeling of the brain tissueand skull. On the experimental part, efforts are being continued tofind suitable mathematical models and material parameters. Gal-ford and McElhaney (1970) attempted a series of relaxation testsperformed in tension on monkey scalp specimens. As a result, theviscoelastic stress relation behavior for the monkey scalp was seen.Low velocity animal experiments have been simulated using 3-Danimal FE (Finite Element) model by Miller et al., (2000). On thecomputational side, the latest efforts on FEM nonlinear modelingthe works of Brands et al., (2000 a, b) and Kleiven (2002) are ref-erenced. An integrated experimental work to simulate the materialand to determine the associated parameters in conjunction withthe development of the computational schemes to employ and ver-ify these experimental data into a mechanized FEM model shouldbe pursued.

Finite elements computational methodology can be employedto determine this mechanical response during the impact providedone can solve the complications in material and geometry of thebrain and also to express the proper nature of the impact loading.Digital imaging has facilitated to a great extent the geometricalmodeling, but lack of accurate material properties description bymathematical formulation is a big pursuit in this multidisciplinaryresearch field. The interaction of the skull and the brain tissues isanother subject to be explored more accurately. Without propermaterial modeling and the compatibility of interactions, the resultswould be still far from reality in many circumstances. Thus, theaim should still be focused on how to improve the constitutivemodeling to accurately predict the dynamic behavior of brain tis-sues and skull during an impact.

Experimental research has shown that the brain tissues exhibita type of viscoelastic behavior. It should be mentioned, thatalthough nonlinear theoretical and computational modeling is adifficult task by itself, efforts should also be spent toward deter-mining the associated physical and material parameters. Theobjective here is to focus on a highly nonlinear material modelingfor brain tissue by assuming an incompressible, non-linear vis-

coelastic behavior. The constitutive modeling will be incorporatedin a FE modeling under impact loading.

An example of case specific biomechanical modeling of braininjury as a result of head impact is given in Figure 4. The humanbrain model is based on MRI data, which is considered to be themost reliable geometrical representation of an injured person’sbrain. The model is homogenous with typical brain materialproperties.

The acceleration components of the patient’s head acquired asa result of a case-specific computer simulation using the Articulat-ed Total Body (ATB) program is shown in the upper right cornerof Figure 4 (Cheng, Rizer, 1998). Different time frames wereselected for different orientations to depict the maximum level ofbrain tissue deformation. The color-coding on the brain modelindicates the force levels that correspond to the brain deformationscale. The corresponding stress distribution for several selectedtime frames at the specified elevation is shown in Figure 5.

Injury severity, criteria, and tolerancesThe severity of the resulting injury is indicated by the expressioninjury severity. It is defined as the magnitude of changes, in termsof physiological alterations and/or structural failure, which occurin a living body as a consequence of mechanical violence (Aldman,Mellander, Mackay, 1983). Various methods to assess the injuryseverity level are available, including the widely used AbbreviatedInjury Scale (AIS) (AAAM, 1998).

Injury criterion is defined as a physical parameter or a func-tion of several physical parameters that correlate well with theinjury severity of the body region under consideration. Frequentlyused parameters are those quantities that relatively easily can bedetermined in tests with human substitutes such as the linearacceleration.

In conjunction with the injury criterion, the term tolerancelevel (or injury criterion level) is defined as the magnitude of load-ing indicated by the threshold of the injury criterion that producesa specific type of injury severity. It should be noted that there arelarge variations in tolerance levels between individuals. Tolerancelevels for populations can therefore only be determined statistically.

The discussion of the specific numerical values for tolerancelevels is beyond the scope of this article; however, there arenumerous resources available for more information on the topic(see references Zhang et al., 2001; Newman, Shewchenko, Wel-bourne, 2000; Ziejewski, 1997).

ConclusionTrauma biomechanics can be an eminently useful tool for ER doc-tors and other medical professionals. By utilizing the results of abiomechanical assessment, medical professionals can gain a betterunderstanding of impact conditions; thus, they have an increasedability to diagnose TBI at an early stage. However, the trauma bio-mechanics scientific community still does not know why somehumans end up with brain injury from low-level accelerationwhile others can sustain high acceleration with no ill effects. Thelethal combinations are not yet known (Zhang et al., 2001).

ABOUT THE AUTHORDr. Ziejewski is a professor in the Mechanical Engineering department at North Dakota StateUniversity, where he received his Ph.D. in Mechanical Engineering in 1985. Dr. Ziejewski isalso an Adjunct Professor in the Department of Neuroscience at the University of NorthDakota School of Medicine. He is a member of many professional organizations and is onthe International Brain Injury Association Board of Governors.

Address correspondence to: 111 Dolve Hall, P.O. Box 5285, Fargo, ND 58105, e-mail:[email protected].


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In the United States, approximately 750,000 mild traumaticbrain injuries (mTBI) occur every year.1 mTBI remains a seriouspublic health and socioeconomic problem, resulting in long-termdisability and death from secondary complications when notproperly diagnosed.2,3,4 Diagnosing mTBI is difficult even in thebest setting. The signs and symptoms of mTBI are often verysubtle and difficult to detect. Undiagnosed or underdiagnosedmTBI leads to poor clinical management and can often causecognitive deficits, psychosocial problems, and secondary compli-cations such as depression.5 -14 Further complicating diagnosis isthat in many cases mTBI is overshadowed by other injuries or bythe events surrounding the injury.

Presently, cognitive deficits are determined using test batter-ies consisting of paper and pencil tests. These tests are consid-ered the gold standard.15,16 However, conventional neuropsycho-logical testing requires a quiet room void of distractions and thepresence of trained personnel to administer, score, and interpretthe results. In addition, these tests may require several hours toperform. In many situations, such as sideline assessment of con-cussion in sports, these requirements make standard neuropsy-chological testing difficult or impossible. Several efforts areunderway to translate and transition these paper and pencil tocomputer-based tools. We briefly summarize products from vari-ous companies that have developed computer-based solutions,which are at various stages of development.

These computer-based solutions offer a wide range of advan-tages over the conventional pen and paper neuropsychologicaltests, including various components of the following: 1) ease ofuse and administration; 2) portability; 3) dramatically reducedtesting duration; 4) potentially increased sensitivity for monitor-ing and detection of subtle cognitive changes; 5) minimized“learning effects” from repeat testing; and, 6) automated dataanalysis and testing results.

Based on our research, we discovered a variety of differentcomputerized assessment tools in varying stages of development.All of these assessment tools are based on computerized neuropsy-chological testing. We focus our discussion on the following prod-ucts: CogState, Ltd. (AUS), Headminder, Inc. (USA), CambridgeCognition Ltd. (UK), ImPACT Applications, Inc. (USA),CogScreen LLC (USA), Neuroscience Solutions Corporation (US),NuCog (AUS) and DETECT (USA). These assessment tools differprimarily on the comprehensiveness of the offered solution, thetechnology platform chosen, and the market segment targeted.

CogStateThe CogState17 solution offers four distinct cognitive assess-

ment tools. The first tool, called Cogstate, offers diagnostic prod-ucts and engages in the development of therapeutics for earlyAlzheimer’s Disease (AD), mild cognitive impairment, and con-cussions from all causes. CogSport is designed to specifically

evaluate and manage sports-related concussions. The third andfourth tools detect the direct or indirect effect of drugs or deviceson the brain, monitors elderly patients’ cognitive health(CogHealth), and assists with decisions about when an employeeshould return to duty following a work-related injury (CogSafe).

CogState is a software package that has been developed byresearchers from Australian universities for the measurement ofcognitive impairment. It can be used for the identification andongoing management of an injury or illness of the brain. As such,it probes a variety of cognitive domains: alertness, attention, work-ing memory, spatial awareness, memory, and executive functions.

The test is available for download from the Internet and isadministered on a computer, which can be a desktop or laptop.Once the test is completed, an Internet connection has to beestablished and an encrypted data file is transmitted to theCogState server located at CogState Ltd., in Australia for theautomated analysis of the test. The results are then returned tothe test computer in the form of a pdf-report. The novelty andinherent benefits of this solution are: portability, it can be takenlocation-independent provided a computer and Internet connec-tion are available; the remote testing can occur in close to realtime (the actual testing is done offline and then requires an inter-net connect to transmit and obtain a test result) and allow forrapid and accurate assessment based on instant central compari-son with prior baseline performance data; it is language and cul-ture-independent through the use of familiar and universallyknown visual forms (playing cards) and; it does not require askilled administrator.

HeadminderThe Headminder18 solution consists of web-based neurocognitiveand neurobehavioral tests. The solutions are primarily offered intwo tracks: one is a customized research tool targeted at pharma-ceutical and other research organizations and the other is aninjury or illness-specific protocol. We focus here on the injuryand illness-specific protocol that is available for four specificcases: screening and management for central nervous system dis-eases, cognitive-vocational management of at-risk populations,ADD/ADHD screening and medication management, and con-cussion management in sports settings.

An individual taking the computerized test registers itsresponses via the keyboard. The solution provided by Headmin-der combines on-line assessment and wireless technology withcomprehensive reporting and records management.

The Headminder solution provides the following functionali-ty: administration of on-line tests, availability of test taker infor-mation, generation of reports, administration of follow-up testsfor longitudinal assessment of cognitive change, access to profes-sional support documents. Tests have to be administered byqualified personnel and access to the internet is required.

Overview of Computer-Assisted CognitiveFunction Diagnostic and Assessment Tools

by Corinna M. Wildermuth, David W. Wright, M.D. and Michelle C. LaPlaca, Ph.D.


ImPactImPACT19 is, an assessment tool primarily focused on the man-agement of sports-related concussions and brain injuries. How-ever, efforts to broaden the scope from sports-related braininjuries to all causes of traumatic brain injury are underway.

The assessment tool consists out of five primary modules:demographic and background information, symptoms, neu-ropsychological testing, injury description, graphic display ofdata. The neuropsychological testing module contains tests per-taining to word discrimination, design memory, X’s and O’s,symbol as well as color matching and three letters. This toolevaluates and documents multiple aspects of neuro-cognitivefunctioning including memory, brain processing speed, reactiontime and post-concussive symptoms. According to claims by thedevelopers the system has the capability to measure the reactiontime to 1/100th of a second.

ImPact is currently used by a variety of users: professionalsports leagues such as the National Football League, MajorLeague Baseball, the Ontario Hockey League, professional racingteams amongst others, colleges and high schools sports pro-grams, sports medicine centers, and neuropsychology clinics inseveral US states.

The benefits provided by ImPact are as follows. It can beadministered by an athletic trainer or physician with minimaltraining. The test battery is set up in such a way that the stimu-lus array can be randomly varied in a near infinite number ofways to minimize the adverse effects of “practice”. The output ofthe ImPact test are individual scores for each test module as wellas composite scores for Verbal and Visual Memory, ReactionTime, Processing Speed and Total Symptom Composite Score. Asix-page clinical report presents these scores graphically and

summarizes the other data points that were entered into the sys-tem for the individual case studies. The comprehensive reportingfunctionality allows for user-friendly extraction of the data.

CantabSimilar to the other solutions reviewed, Cantab20 offers a

computerized system for the assessment of different cognitivefunctions. The system is available for use in academic and com-mercial settings and currently boasts its use in over 400 universi-ties and institutions in 26 countries.

The assessment tool, CANTAB, is based on the CambridgeNeuropsychological Test Automated Battery (CANTAB) andoffers a cognitive assessment tool with the following attributes:affordability, flexibility, sensitivity, ease of administration, andspeed. In addition, it is suitable for multinational studies due tothe language-independence of its tests. At the foundation of it all,is a well standardized and validated, large normative databasethat is based on data gathered through the testing of over 2,000individuals. These normative data are available for people fromthe ages of 4 to 90 years, in four IQ bands.

The CANTAB tool is software-based and requires a touchscreen response from the patient for the administration of thetests. The test battery allows for flexible testing according to testschedules that meet the users’ needs, i.e. they can be groupedtogether to be performed in an order of the clinicians’ choice.

Overall 13 tests are available which assess different aspectsof mental functioning including learning, memory, attention,and problem solving, as well as tests of “executive” function andvigilance. The CANTAB results manager is a tool that allows youto organize and analyze the data collected. For the output of thedata, three different reports are available: a summary report, asummary datasheet and a detailed report.

Cogstate Headminder Impact Cantab Cogscreen USC Virtual Office DETECT

Australia USA USA UK Australia USA USA

Focus Areas

pharmaceutical andmedical device com-panies

concussion man-agement in sportssettings (mTBI)

Detection of earlyAlzheimers Disease

Occupational Healthand Safety environ-ment

pharmaceutical andother research orga-nizations

central nervous dis-ease screening andmanagement

cognitive-vocationalmanagement of at-risk populations

ADD/ADHD screen-ing and medicationmanagement



sensitive to manycentral nervous sys-tem disorders

pharmaceutical clin-ical trials

early detection ofAlzheimer's disease

cognitive screeningwith focus on avia-tion / aeromedicalapplications

Cognitive and func-tional impairmentsin adults (mTBI,Alzheimer's Dis-ease)

concussion man-agement in sportssettings

early detection ofAlzheimer's Disease

Reduced TestingDuration ✔ ✔ ✔ ✔ ✔ ✔ ✔

Laptop portable ✔ ✔ ✔ ✔ ✔ ✔ ✔

Reduced Learn-ing Effects ✔ ✔ ✔ ✔ - ✔ ✔

Increased Sensi-tivity to subtle

Changes

✔ ✔ ✔ ✔ ✔ ✔ ✔

Automated DataAnalysis ✔ ✔ ✔ ✔ ✔ - -

Reporting Func-tionality ✔ ✔ ✔ ✔ ✔ - -

Immersiveness - - - - - ✔ ✔


CogScreenCogScreen21 is a scored cognitive-screening instrument adminis-tered using a computer. It is designed to rapidly assess the fol-lowing functions: immediate and short-term memory, visual per-ceptual, sequencing, reaction time, simultaneous informationprocessing and executive functions. At its origination, it wasdesigned to meet the Federal Aviation Administration’s (FAA)need for an instrument that could detect subtle changes in cogni-tive functioning. As such, the applications offered by CogScreenare targeted predominantly at the aviation industry. This focushas been expanded to pharmaceutical research to assess theeffects of pharmaceuticals on brain function.

The screening tools consist of a series of computerized cog-nitive tasks. Each of them is self-contained and presented withinstructions and a practice segment. The aeromedical edition ofCogScreen has the capability to produce a results report.

USC Virtual OfficeAt the Integrated Media Systems Center (IMSC) at the Universityof Southern California (USC) researchers have developed anapplication in the field of user-centered sciences. The applicationconsists of a head-mounted-device (HMD) delivered virtual reali-ty (VR) system for the assessment and rehabilitation of cognitiveand functional impairments in adults.

The scenes that make up the “virtual office” are HMD-deliv-ered. Additionally, various performance challenges can be deliv-ered via the computer screen (visual mode) and the phone (audi-tory mode). Utilizing these immersive 3D environments allowsusers to focus on the assessment and rehabilitation of attention,memory and executive processes as well as visuospatial abilities.The benefits provided through this application lie in the fullyadjustable delivery of cognitive challenges and distractions, aswell as the recording and storage of cognitive, motor behaviorwithin a naturalistic, ecologically valid environment. Like all theother solutions mentioned in this article, it is fully laptop-deliv-erable, but adds the advantage of an immersive environment.

The USC Virtual Office22 application is currently used in ini-tial clinical trials in the U.S. to test memory performance in indi-viduals with brain injury, and an International Consortium oftest sites is currently beginning clinical trials using the virtualoffice environment.

DETECTDETECTTM23 is a cognitive assessment tool currently under devel-opment at Emory University and the Georgia Institute of Tech-nology. Similar to the USC system, DECTECT incorporates oneaspect that the other aforementioned solutions lack – immersive-ness. The cognitive functions tested are information processingspeed, working memory, work list learning and recall, as well asseveral variations of these tasks. The testing is designed to becompleted in less than 15 minutes. The DETECT device is anintegrated solution that is comprised of the software application,a portable computer, and a virtual reality headgear that totallyimmerses the individual within the test environment. In a usabil-ity study, it was found that there was no difference in test resultsobtained from DETECT in a quiet room versus a simulated noisyenvironment. The advantage of total immersion allows the deviceto be used on site, even in a noisy environment such as a sport-ing event. Therefore, this system has great potential for use as aside-line assessment tool for mTBI as well as application thatrequire portability and ease-of-use.

There are a variety of other efforts under way to devise aneuropsychological assessment tool. Like the aforementionedones, most of these solutions are software-based and aim to

assess the cognitive functioning or impairment of the brain. Forexample, Neuroscience Solutions uses proprietary technology,sublicensed from Scientific Learning Corporation, based onestablished principles of “brain plasticity” to address neuropsy-chological disorders. NuCog is a cognitive assessment tool,developed by researchers in Australia, and is only available forlimited use in research and clinical settings. We have tried to becomplete in our briefing of cognitive assessment technology andlook forward to the completion of these and related products.

In summary, mild cognitive decline that results from mTBIor degenerative diseases are often very subtle and difficult todetect. Frequently the mTBI is overshadowed by other injuries orby the events surrounding the injury. The need for rapid andsimple diagnostic testing for early detection is immense. Thegold standard for evaluating mTBI is neuropsychological testing.However, neuropsychological testing requires a quiet room voidof distractions and the presence of trained personnel to adminis-ter, score, and interpret the measures. In addition, these testsmay require several hours to perform. In many situations such assideline assessment of concussion in sports, these requirementsmake standard neuropsychological testing impractical. Severalcomputer-based solutions are in development or in clinical test-ing and address many of the needs for fast, reproducible testing.We feel that many of these solutions are feasible and the eventualpoint-of-care and application may vary depending on the type ofdeficit or setting. For sports assessment of mTBI, length of test,ease-of-administration, and immersiveness are the top three cri-teria. Based on this application, DETECT may offer a solutionthat combines many attributes of other systems, includingImPact and IMSC. It is important that the training and clinicalteams associated with diagnosis and assessment of individualswith mild injuries recognize the need for improved tools and willutilize technology to ultimately choose the best course of therapyand improve functional outcome.

REFERENCES1 Anonymous. Injury Fact Book, National Center for Injury Prevention and Control: Atlanta,

2002.2 Cantu R C. Second-impact syndrome. Clinics in Sports Medicine. 17(1):37-44, 1998.3 Cantu RC and Voy R. Second-impact syndrome - a risk in any contact sport. Physician and

Sports Medicine. 23(6):27, 1995.4 Kelly JP, Nichols JS, Filley CM, Lillehei KO, Rubinstein D and Kleinschmidt-DeMasters BK.

Concussion in sports. Guidelines for the prevention of catastrophic outcome. JAMA.266(20):2867-9, 1991.

5 Englander J, Hall K, Stimpson T and Chaffin S. Mild traumatic brain injury in an insuredpopulation: subjective complaints and return to employment. Brain Inj. 6(2):161-6., 1992.

6 Fann JR, Katon WJ, Uomoto JM and Esselman PC. Psychiatric disorders and functional dis-ability in outpatients with traumatic brain injuries. Am J Psychiatry. 152(10):1493-9.,1995.

7 Gomez-Hernandez R, Max JE, Kosier T, Paradiso S and Robinson RG. Social impairmentand depression after traumatic brain injury. Arch Phys Med Rehabil. 78(12):1321-6., 1997.

8 Gronwall D. Cumulative and persisting effects of concussion on attention and cognition, inMild Head Injury, H.S. Levin, Eisenberg, Howard M., Editor, Oxford University Press; NewYork. p. 153-162, 1989.

9 Gronwall D. Performance changes during recovery from closed head injury. Proc AustAssoc Neurol. 13:143-7, 1976.

10 Gronwall D and Wrightson P. Delayed recovery of intellectual function after minor headinjury. Lancet. 2(7881):605-9., 1974.

11 Gronwall D and Wrightson P. Memory and information processing capacity after closedhead injury. J Neurol Neurosurg Psychiatry. 44(10):889-95., 1981.

12 Jorge RE, Robinson RG, Arndt SV, Forrester AW, Geisler F and Starkstein SE. Comparisonbetween acute- and delayed-onset depression following traumatic brain injury. J Neuropsy-chiatry Clin Neurosci. 5(1):43-9., 1993.

13 Stambrook M, Moore AD, Peters LC, Deviaene C and Hawryluk GA. Effects of mild, mod-erate and severe closed head injury on long-term vocational status. Brain Inj. 4(2):183-90.,1990.

14 van der Naalt J, van Zomeren AH, Sluiter WJ and Minderhoud JM. One year outcome inmild to moderate head injury: the predictive value of acute injury characteristics relatedto complaints and return to work. J Neurol Neurosurg Psychiatry. 66(2):207-13., 1999.

15 Dikmen S, McLean A and Temkin. Neuropsychological and psychosocial consequences ofminor head injury. J Neurol Neurosurg Psychiatry, 1986. 49(11): p. 1227-32.

16 Leininger BE, et al., Neuropsychological deficits in symptomatic minor head injurypatients after concussion and mild concussion. J Neurol Neurosurg Psychiatry, 1990.53(4): p. 293-6.


17 Cogstate website www.cogstate.com accessed in Decem-ber 2003.

18 Headminder website, www.headminder.com accessed inJanuary 2004.

19 Impact website www.impacttest.com accessed in Novem-ber 2003.

20 Cantab website www.bioportfolio.com/cantab accessed inNovember 2003.

21 CogScreen website www.cogscreen.com accessed inDecember 2003.

22 www.imsc.usc.edu accessed in December 2003.23 Detect personal communications with developers. Note:

two of the authors of this article are developers ofDETECT.

ABOUT THE AUTHORSMichelle C. LaPlaca, Ph.D. is an Assistant Professor, NeuralInjury Biomechanics and Repair Laboratory, Coulter Depart-ment of Biomedical Engineering, at Georgia Institute of Tech-nology and Emory University. 313 Ferst Dr., Atlanta, GA30332-0535, e-mail: [email protected].

David W. Wright, M.D., F.A.C.E.P., is an Assistant Professorand Assistant Director of the Emergency Medicine ResearchCenter, Department of Emergency Medicine, Emory Universi-ty. He is a board ceritifed practicing Emergency Physician. Hecompleted his residency at the University of Cinicinnati in1997. He is a translational researcher, conducting NeuroInjuryand Neurorepair research in both the basic and clinical sci-ences for 7 years. He is currently the Project Leader for a majorNIH sponsered clinical trial in TBI.

Corinna M. Wildermuth is currently working on MBA at theDuPree College of Management at the Georgia Institute ofTechnology from where she will graduate in May 2004. SinceAugust 2002, Graduate Research Assistant with the AdvancedTechnology Development Center (ATDC), a high-technologybusiness incubator at the Georgia Institute of Technology. Inthis role, she supports entrepreneurs with research pertainingto the business aspects of building a venture in the life sci-ences space. Her prior work experience has been withfinancial institutions and in the aviation industry with rolesin marketing, operations and quality management.

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Vocational Specialist/Case Manager - needed immediately.VirginiaNeuroCare, Inc. is a residential and outpatient facility for persons withacquired brain injuries. We serve the military and the general public.We are located in historic Charlottesville, VA under the backdrop of

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