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

features

4 Chairman’s Message 4 Editor’s Message 6 Publisher’s Message 6 Guest Editor’s Message 34 Professional Appointments 38 Conferences

contents

departments

vol. 1 issue 1, 2004

10 Biomechanics of Traumatic Brain Injury: A Review

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

16 The Biomechanics of Brain Injury: From Historical to Current Perspectives

by Albert I. King, Ph.D.

18 Biomechanics of Childhood Neurotrauma

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

22 Sports Concussion

by Christopher C. Giza, M.D.

26 The Biomechanical Assessment of Traumatic Brain Injury

by Mariusz Ziejewski, Ph.D.

32 Overview of Computer-Assisted Cognitive Function Diagnostic and Assessment Tools

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

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chairman’s message

executive editor’s message

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

As the executive editor of Brain Injury Professional, I am delighted to welcome you to this exciting premier issue of the publication. Brain Injury Professional is creating a novel venture specifically addressing your professional and scientific needs in an easy-to-read and highly informative format that will be very different from academic journals in the field.

Brain Injury Professional will be interdisciplinary in scope and designed to foster discussion and thinking about the key issues facing brain injury rehabilitation and research. Articles are designed to be lively and will often present reviews of state-of-the-art technologies and approaches to the treatment and rehabilitation of brain injury in its various forms.

NABIS is a multidisciplinary society which is comprised of professional members involved in the care and issues of brain injury. The principle mission of our organization is to move brain injury science forward, whether it is in the area of clinical care, research, policy, or litigation.

There are a number of scientific journals dedicated to traumatic brain injury including the IBIA's official journal, Brain Injury. However, this publication, Brain Injury Professional, seeks to provide an avenue to share information with professionals in a variety of disciplines. I am thrilled to have my friend and colleague, Dr. Donald Stein, as our executive editor. Brain injury needs a voice for the professionals within this ever changing field, and NABIS will be that voice. I encourage all of you to join us as we once again seek to enhance our professions through a collective effort.

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

In this issue we present current concepts in the biomechanics of brain injury written by leading experts in this field. In future issues we will cover topics such as the latest emerging pharmacological treatments for TBI, aging and brain injury, sports injuries, gender issues in CNS repair, and the uses of animals in research, just to name a few. Each quarterly issue of Brain Injury Professional will also contain professional career announcements, listings of upcoming conferences and news from the NABIS organization.

I would also like to share with you my excitement in launching this new publication. Working with me as editor in chief, to provide the excellent quality you expect in a professional publication, will be Dr. Nathan Zasler, one of the country's leading experts in rehabilitation from TBI. Together with an outstanding and dedicated editorial board and staff, Brain Injury Professional promises to be the publication you turn to when you want to know what is important to TBI research and rehabilitation.

Donald G. Stein, Ph.D. Asa G. Candler Professor Emory University School of Medicine Departments of Emergency Medicine and Neurology

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publisher’s message

guest editor’s message

Welcome to the premiere issue of Brain Injury Professional!

We are extremely excited about this new publication and its potential to communicate a wide range of brain injury information to professionals across North America.

This first issue of Brain Injury Professional highlights the contribution of biomechanics to the study of traumatic brain injury. The study of the biomechanics of injury began decades ago, long before the advent of modern day molecular biology research and imaging technology advances. The physical events surrounding an injury often occur in milliseconds and can be extremely variable from person to person.

These challenges are still faced by modern biomechanicians, although recent advances such as improved computer processing speed and the merge between engineering and biological sciences have elevated our understanding of the mechanical events surrounding an injury. This understanding will ultimately translate into improved injury prevention and treatment strategies.

HDI Publishers has been producing a variety of periodicals on the subject of brain injury for almost twenty years. A decade ago, we introduced i.e. Magazine, the first color magazine on the subject of brain injury. This year, we are pleased to begin publication of Brain Injury Professional, a publication we believe will become a leading voice and resource for the broader brain injury professional community.

Perhaps more than any other, brain injury is a multidisciplinary field. Our goal for Brain Injury Professional therefore, is to publish a resource that allows professionals to share their knowledge across a broad range of research, rehabilitation and treatment areas. In future editions of Brain Injury Professional, we will be covering both academic and clinical issues in an effort to increase the level of discourse and exchange between all professionals working in the field of brain injury.

Brain Injury Professional will be an important part of the North American Brain Injury Society’s mission of moving brain injury science into practice. Above all though, we want this publication to be a valuable resource for those who work to improve the lives of persons with brain injury and their families. We are always eager to receive feedback from our readers and members, so we encourage you to visit our website, www.nabis.org, and send in your comments.

J. Charles Haynes, J.D. Publisher Brain Injury Professional

The articles in this issue of Brain Injury Professional cover different aspects of brain injury taken from a biomechanical perspective. The first article (Biomechanics of Traumatic Brain Injury (TBI): A Review) is a synopsis of the biomechanics associated with traumatic brain injury and is intended as both a tutorial and a review article. The next article (The Biomechanics of Brain Injury: From Historical to Current Perspective) gives a historical perspective on the study of injury biomechanics and presents some of the current challenges with which researchers are faced. These are followed

by Biomechanics of Childhood Neurotrauma, which illustrates the differences between adults and children in injury situations, an important distinction in biomechanics research. The child cannot be modeled as a miniature adult and this article highlights the science behind these differences. The next article (Sports Concussion) gives a clinical perspective of this very important issue, summarizing the risk factors and need for biomechanical research into mild and repeat brain injury. The Biomechanical Assessment of Traumatic Brain Injury provides the reader with a glimpse into human occupant safety research studies and the application of biomechanics to injury prevention. And the last article in this series (Overview of Computer-Assisted Cognitive Function Diagnostic and Assessment Tools) demonstrates the use of technology that may assist the clinical sciences in both diagnostic and continued assessment of cognitive deficits using novel and sensitive tests.

We hope the reader finds this issue of Brain Injury Professional to be a reference for future use and contributes to your understanding of biomechanics.

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

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vol. 1 issue 1, 2004

north american brain injury society chairman Robert D. Voogt, PhD treasurer Bruce H. Stern, Esq. family liason Julian MacQueen executive vice president Michael P. Pietrzak, MD, FACEP executive director/administration Margaret J. Roberts executive director/operations J. Charles Haynes, JD communications manager Brandy Buzinski marketing manager Joyce Parker graphic designer Nikolai Alexeev administrative assistant Benjamin Morgan administrative assistant Bonnie Haynes

brain injury professional publisher Charles W. Haynes publisher J. Charles Haynes, JD executive editor Donald G. Stein, PhD editor in chief Nathan Zasler, MD managing editor Linda L. Thoi, DrPH design and layout Nikolai Alexeev advertising sales Joyce Parker data input Bonnie Haynes

editorial inquiries Managing Editor Brain Injury Professional PO Box 131401 Houston, TX 77219-1401 Tel 713.526.6900 Fax 713.526.7787 Website: www.nabis.org

advertising inquiries Joyce Parker Brain Injury Professional HDI Publishers PO Box 131401 Houston, TX 77219-1401 Tel 713.526.6900 Fax 713.526.7787

national office North American Brain Injury Society PO Box 1804 Alexandria, VA 22313 Tel 703.683.8400 Fax 703.683.8996 Website: www.nabis.org

Brain Injury Professional is a quarterly publication. Š 2004 NABIS/HDI Publishers. All rights reserved. No part of this publication may be reproduced in whole or in part in any way without the written permission from the publisher. 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 mail@hdipub.com

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Biomechanics of Traumatic Brain Injury: A Review

by Michelle C. LaPlaca, Ph.D. and Mariusz Ziejewski, Ph.D. SUMMARY Traumatic brain injury (TBI) is an acquired injury to the brain caused by an external physical force to the head (primary injury), resulting in total or partial functional disability and/or psychosocial impairment. Secondary, or prolonged, injuries are neurochemical and physiological events that occur in response to the primary injury and account for the ongoing and continual damage. Because of the biomechanical nature of TBI, researchers, clinicians, and therapists should understand the biomechanics surrounding the initial insult in order to utilize clinically relevant experimental models and to correlate insult parameters with clinical deficits. These efforts can, in turn, lead to the development of new treatments (both pharmacologic and rehabilitative) and tissue tolerances (useful for improvements to protective gear—both personal and automotive). This review article highlights the basic biomechanics that surround TBI, including the different types of insults. In addition, the importance of biomechanics in injury research is summarized.

INTRODUCTION The clinical definition of TBI is given as an occurrence of injury to the head that is documented in a medical record with one or more of the following conditions attributed to head injury: (a) observed or self-reported decreased level of consciousness including partial or complete loss of consciousness, stupor, or coma; (b) amnesia including the time preceding, during, and subsequent to the injury; (c) skull fracture; (d) objective neurological or neuropsychological abnormality; and (e) diagnosed intracranial lesion 10

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

Males are three times as likely as females to acquire TBI, with the highest risk in the 15-24 year age bracket. The next highest incidence of TBI occurs in individuals over 65 years old. The largest percentage of these injuries is due to motor vehicle accidents (43%), followed by firearm incidents (34%) and falls (9%).

Despite the high incidence and enormous health and socioeconomic consequences of TBI, few effective treatments exist. Biomechanics research is key to determining tolerances—the forces and deformations at which the tissues fail both structurally and functionally—and to provide clinically relevant models for determining mechanisms and testing new treatments.

BASIC BIOMECHANICS Biomechanics, first internationally recognized as a field in the early 1970s, is the study of forces and physical responses in stationary (static) and moving (dynamic) biological systems. How does a system (in the case of TBI—the human body, and more specifically, the head) react when a force, or load, is placed on it?

How do external loads result in initial damage? By what mechanism do external forces lead to delayed damage? What are the limits of these loads before a threshold is reached (in other words, what is the tolerance of the system)? And does the type of load matter? To answer these and other related questions, we must understand basic biomechanics. The basic terms, or descriptors, that biomechanicians use to describe applied loads are force and stress and the resulting responses are deformations and strains (Table 1).

Force is defined as the action of one body (a physical entity in the system, such as a windshield) on another (as a result of an impact) which will cause acceleration of the second body (in our Figure 1: Numbers of traumatic brain injuries in the United States.

Table 1: Concepts from Mechanics

Figure 2: Deformation and Strain

discussion this is usually the head) unless acted on by an equal and opposite action counteracting the effect of the first body.

The unit is a Newton (N); 1 N is the force that will give 1 kilogram an acceleration of 1 meter/second2 (English unit is pound-

force, lbf). When forces are generated in tissue, deformation may ensue depending on the material properties. Deformation is defined as the change in shape of a body undergoing a force. A rigid body, for example, would experience extremely small deformations, while biological tissue (usually referred to as deformable or nonrigid) can often undergo quite large deformations. Several biomechanical factors surround force analysis and ultimately predict whether damage occurs: ● Type of load: Loads are described as direct (physical contact between the head and another object) or indirect (as the result of motion of the head). In indirect loading, acceleration of the second body (i.e. the head) can act analogously to applied 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 resulting forces and deformations. ● Direction of force: The direction, or plane, of loading can be a determining factor (e.g., sagittal, lateral, etc.) since directional sensitivity of the brain has been shown, likely due to the irregular, or nonhomogeneous, shape of the brain and asymmetrical (not symmetrical) skull structures. ● Magnitude of force: The extent and severity of deformation increases with increasing force and this relationship is nonlinear. In other words, the proportional increase in brain tissue damage may be significantly greater than the proportional increase in force. ● Duration of force: The change in duration of acceleration will result in different types of internal forces and injuries to the brain tissue. For short durations of force, much of the effects of the force are reduced due to the material properties of brain tissue. As the duration of force increases, less reduction occurs and less force is needed to produce injuries within the brain. These injuries are often confined to the brain surface. As the force duration increases further, less of the effects of the force are reduced, resulting in brain deformations that are able to propagate deeper into the brain. ● Rate of force: While shorter duration forces may result in less damage, loads that are applied fast may incur more damage due to the material properties of the brain. The tissue cannot absorb (or reduce) the force fast enough and can fail both structurally and functionally. Slowly applied loads give the tissue “time” to reduce the force and generally result in less damage. This material property of brain (and of most soft biological tissues) is called viscoelasticity (see page 12). ● Region of the brain: Because different regions of the brain have different cellular orientations, structural and functional tolerances of the brain differ depending on the region affected. This consideration results in the directional sensitivities mentioned above.

Stress is another term frequently used in biomechanical analysis and refers to the distribution of forces relative to the areas on which they act. Normal stresses (designated by the Greek letter sigma (σ)) act perpendicular to the surface, while shear stresses (designated by the Greek letter tau (τ)) act tangential to the surface. The unit is the Pascal (Pa); 1 Pa = 1 N (Newton) / per meter2.

A given force acting on a small surface produces greater stress than the same force acting over a larger surface. In other words, the amount of mechanical stress created by a force is dependent on the size of the area over which the force is applied. The resulting strain that occurs relates the deformed state of the body to the undeformed state and is unitless. Biomechanicians refer to the type BRAIN INJURY PROFESSIONAL

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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 as being tension (positive strain) or compression (negative strain). Extensional strain results from stresses generated from linear (or translational) loads. ● Shear strain is also the change in length divided by the original length (γ = ∆l/lo), but is the strain resulting from shear stress, often a product of rotational loads. Brain tissue is thought to be more sensitive to shear strain than extensional strain and therefore loading that involves rotation of the head has been thought to result in more severe injuries, although this assumption has recently been questioned (see “The Biomechanics of Brain Injury” in this issue of Brain Injury Professional, page 16).

Figure 3: Constitutive Relations

Figure 4: General Concepts-Mechanical Characteristics of Brain Tissue

The relationships between stress and strain are referred to as constitutive relationships and the resulting equations are used to define behavior of the tissue (Figure 3). The response of a tissue to an applied load is dependent on the geometry and the material properties. The material properties of a tissue vary from individual to 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 responses generated within the various regions of the brain (see page 16).

VISCOELASTICITY Brain 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 the acceleration magnitude and duration, but also on the rate of straining, in addition to the amount of strain.

In a linearly viscoelastic material, energy is dissipated by plastic or viscous flow within the material as the material is stressed.

Because of this, stress and strain vary out of phase with one another so that the loading and unloading stress-strain curves show hysteresis (the stress-strain unloading relationship does not follow the loading relationship, even when the material is loaded within its elastic range) (Figure 4A). The area below each curve represents the strain energy stored during loading and subsequently recovered during unloading. The area between the two curves represents the energy dissipated due to viscous flow within the material.

Two additional behavior characteristics of viscoelastic materials should be considered: relaxation and creep. When the material instantly has a constant deformation, the corresponding forces induced decrease with time, which is called relaxation (Figure 4B).

As a material suddenly experiences a constant force, the corresponding deformation continues which is called creep (Figure 4C).

The importance of time dependent characteristics of the human brain becomes clear once we recognize that in a typical event human brain comes in contact with the interior of the skull numerous times. This signifies that after an initial brain contact with the skull there is a follow-up rebound phase causing the brain to strike the opposite side of the skull (see Figure 5A).

Since the brain exhibits high bulk modulus (high resistance to volume change) the initial impact and follow-up rebound impact will occur during a very short period of time. This time is sufficiently short that might not allow the brain to regain its initial shape after the initial deformation (see Figure 5B). This condition might lead to superposition of the brain deformation with significantly higher resulted deformation than one would expect from one brain/skull impact (see Figure 5C).

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

BIOMECHANICAL LOADS THAT LEAD TO TBI The basic biomechanics terms that we have defined are very useful in describing what mechanical conditions lead to injuries. We often refer to these mechanical conditions as the insult parameters and the result as the injury. We will focus on two categories of insults (static and dynamic loading of the head), two types of responses, or injuries (focal and diffuse) and two response phases (primary and secondary).

Types of Insults Static loading to the head is a very slowly applied direct load.

Usually there are no deficits until there is substantial brain deformation (see above discussion of duration of force). These loading conditions are relatively rare and often occur in human entrapment situations (e.g., earthquakes).

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

Figure 6: Types of Acceleration in TBI

are at a greater risk for more local and severe damage, perhaps in a penetrating manner. Impact loading can lead to either focal or diffuse injuries, or a combination of the two. Impulsive loading is due to inertial forces alone and leads to diffuse brain injuries (see Focal and Diffuse Injuries, below).

Types of Injuries

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

Focal injuries result from direct loading and can often occur without widespread, or diffuse, damage. Focal injuries include skull fracture (with or without brain damage), which can be linear, depressed, and quite complex (such as basilar skull fractures).

Epidural hematomas are often associated with focal injuries. Contact loading can also result in coup (at the site of impact) and contra-coup (away from the site of impact) contusions to the brain, involving both cellular and vascular components. Focal injuries account for one-half of all severe head injuries, but 2/3 of all deaths in this group. There is usually macroscopically visible damage at the site of impact. When there is osteal (referring to bone or specifically, skull) or dural (referring to the membranous encasement tissue of the brain) compromise this is often termed open head injury in the clinical setting. Often an object penetrates the skull as a result of a motor vehicle accident, gunshot wound, or a blow to the head. The clinical symptoms are often very specific to the area of the brain that is directly injured (e.g. the individual may experience difficulties with forming speech, but show no problem with writing words on paper).

Diffuse injuries are most often caused by inertial loading, which describe the motion of objects. The acceleration (velocity change divided by change in time) is an important parameter in determining response. The higher the acceleration of a body, the higher the force (force equals mass times acceleration, Newton’s second law). Thresholds for the acceleration that a human can undergo before tissue damage occurs has been, and continues to be, an active area of research. When the acceleration is translational, injuries tend to be localized to a smaller area. Rotational acceleration, on the other hand, can lead to large strains deep within the brain, resulting in diffuse axonal injury (DAI). Most injuries seen clinically are a combination of translational and rotational (referred to as angular acceleration) (Figure 6). Diffuse injuries are thought to occur as a result of not only the acceleration portion of loading, but from the deceleration portion of the insult, creating very fast moving, uneven load distributions. Diffuse strains can lead to differential movement of the skull relative to the brain, causing parasagittal bridging vein injury, as well as widespread intracerebral hemorrhage. Although cerebral contusion and brain edema can occur, damage is often only seen microscopically. Individuals with diffuse injury tend to have widespread dysfunction, making diffuse injury the most prevalent cause of persisting neurological disability. Clinically, diffuse injury is referred to as a type of closed head injury and arises most often from motor vehicle accidents. See Figure 7 for a summary of the relationships between input mechanical loading and resultant tissue deformations.

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

The initial damage that is a direct result from loading to the brain is the primary phase of injury (Figure 8). Biomechanicians study this phase in order to determine tissue tolerances to mechanical loading. Our understanding of human tolerance is still advancing from a cellular level to a human level and is vital to developing better safety equipment. It is believed that at the time of the insult there is a varying amount of primary damage, or damage that results from the physical force itself. This would include comproBRAIN INJURY PROFESSIONAL

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mised skin, bony fractures, tissue tearing, cellular rupture, and reorientation of the tissue components. If a deformation threshold is surpassed, these structural failures result and can severely compromise brain function. Tissue damage is more difficult to detect in cases of subtle physical insults. For example, cellular membranes may become compromised, leading to depolarization and abnormal ion movement across the membrane. Also, the vasculature may become “leaky” leading to influx of peripheral components into the brain tissue.

While there is no absolute time when primary damage evolves into delayed effects, the secondary phase of injury can be defined as any injury that occurs as a result of the primary insult. This may be in the acute (minutes to hours) period or in a more delayed fashion (days to months) and is dependent on the severity of the initial insult, as well as the health and age of the individual. There may be decreased blood flow to the brain, resulting in hypoxic conditions. This is exacerbated by decoupled cerebrovascular autoregulation and persistent cellular injury. In addition, the brain often enters a hypermetabolic phase, followed by a hypometabolic phase.

DAI is thought to be comprised mostly of a secondary effect, due to cellular dysfunction (e.g., reduced axonal transport and proteolytic activity), rather than a primary axotomy (severing of axons). There are also several deficits reported in neurotransmitter function as well as cellular energy production, that can lead to delayed cell death or persistent dysfunction. While a complete discussion of the cellular effects of TBI is beyond the scope of this article, it is easy to see that the secondary cascades can be quite complex and are therefore not completely understood. There is a role for biomechanics in determining injury mechanisms in both the primary and secondary phases of the injury response by utilizing laboratory models that best mimic the forces/stresses and deformations/strains that occur during a traumatic insult. The response (whether cellular or whole organism) can better represent the clinical setting and therefore potential treatments can be evaluated in a more relevant setting.

medical implications(Figure 9). The field of biomechanics has matured over the last three decades and researchers have learned a great deal about prevention and treatment. Biomechanics can play a role in improving preventative measures such as safety design in automobiles and sports equipment, as well as highway and road safety. Researchers can use their knowledge of mechanical engineering to determine thresholds to loading of the brain.

Clinicians and rehabilitative specialists can assist this effort by understanding the clinical variability and reporting injury circumstances. In addition to preventative strategies, biomechanics can play an important role in experimental modeling.

By applying clinically relevant mechanical parameters (e.g., shear strain applied at high rates) to isolated brain cells, the resulting knowledge can be used to develop mechanistically-inspired pharmaceutical agents. In addition to cellular level investigations, biomechanical models can be utilized at the animal level to achieve pre-clinical testing settings. To complement the physiological studies, researchers have also used computer simulations to better understand the complex response of brain tissue during traumatic loading con-

ditions. Taken together, these multilevel studies can be combined to improve the outcome of individuals with TBI. ABOUT THE AUTHORS Michelle C. LaPlaca, Ph.D.: Assistant Professor, Neural Injury Biomechanics and Repair Group Neuroengineering Laboratory, Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University. 313 Ferst Dr., Atlanta, GA 30332-0535, e-mail: michelle.laplaca@bme.gatech.edu.

Mariusz Ziejewski, Ph.D.: Associate Professor, Director of Impact Biomechanics Laboratory, College of Engineering, Director of Automotive Systems Laboratory, College of Engineering, North Dakota State University. 111 Dolve Hall, P.O. Box 5285, Fargo, ND 58105, e-mail: Mariusz.Ziejewski@ndsu.nodak.edu.

REFERENCES All epidemiological information obtained from the Centers for Disease Control and Prevention, National Center for Health 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: John Wiley and Sons, 2001.

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

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

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

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

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CONCLUSIONS Given the tremendous impact that TBI has on society, it is important to better understand the biomechanical circumstances of head injuries in addition to the 14

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THE BIOMECHANICS OF BRAIN INJURY: From Historical to Current Perspectives

by Albert I. King, Ph.D.

head has been a major bone of contention between the supporters of the angular acceleration theory of brain injury and the proponents of linear acceleration. For a period of about 20 years, this issue was strongly contested with researchers doing experiments that imparted purely linear or purely angular accelerations to the head. To date, the issue has not been resolved, even though the rhetoric has died down and there is general acceptance that no impact is purely linear or purely angular. What is more important is the fact that the schism in the brain injury research community did not help to advance the understanding of brain injury in terms of the mechanisms of injury as well as the level of tolerance. For example, to date, there is no accepted criterion for angular acceleration. It ranges from 1800 radians per second squared (rad/s2) to 16000 rad/s2. This commentary reports on some recent results of our research on brain injury using live human concussion data, brain motion data from cadaveric head impacts and an advanced computer model of brain response to blunt impact. However, before describing the results, I would like to report on the results of a series of dummy head impacts in which a Hybrid III head and neck system was placed on a mini-sled and made to impact different types of foam. Identical tests were done with the head bare or wearing a helmet used in American football. It was found that the helmet was able to reduce the head linear acceleration significantly but not its angular acceleration. We are thus forced to ask the inevitable question: If angular acceleration is the major cause of brain injury, then how does the helmet protect the brain?

Brain Motion During Head Impact

The Inevitable Question Ever since the first steel ball was dropped from a height of 12 stories onto a dry skull by Professor Herbert Lissner, an engineer and Dr. Steve Gurdjian, a neurosurgeon, at Wayne State University, in 1939, laboratory research on head injury has continued at Wayne State and elsewhere for well over half a century. Looking back at the progress made, we can see that brain injury resulting from automotive crashes has been kept under control, using a rather primitive injury criterion, the Head Injury Criterion or HIC, as specified in Federal Motor Vehicle Safety Standard (FMVSS) 208. HIC is an integral function of the resultant linear acceleration of the head, maximized over a portion of the impact pulse and its value for the driver or front seat passenger must not exceed 1000 in a 48 km/hr barrier impact. The fact that it does not take into account the effect of angular acceleration of the 16

BRAIN INJURY PROFESSIONAL

Hardy et al., (2001) were the first to report quantitative data on the extent of brain motion during a blunt impact. A series of carefully orchestrated impacts on inverted and decapitated heads was conducted in conjunction with the use of a biplanar high-speed xray system that provided video pictures of the motion of neutral density targets in the brain at 1000 frames per second. It was found that linear acceleration caused very little brain motion, on the order of ±1 mm, while angular acceleration can result in target motions on the order of ±5 mm. However, even for angular accelerations in excess of 10000 rad/s2, the displacement is limited to ±5 mm. Thus, it is not entirely clear what the roles of linear and angular acceleration are in causing brain injury.

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

centile male head, including the scalp, skull with an outer table, diploĂŤ, and inner table, dura, falx cerebri, tentorium and falx cerebelli, pia, venous sinuses, CSF, lateral and third ventricles, cerebrum (white and gray matter), cerebellum, brain stem, and parasagittal bridging veins. The model was validated against all available cadaveric data at that time, including the brain displacement data collected by Hardy et al., (2001). In addition to displacement, the output of the model included normal and shear strain in all parts of the brain, intracranial pressure and stretch of the bridging veins. Strain rate was eventually computed because there is experimental evidence from tissue level experiments which show that strain rate is a significant factor in axonal dysfunction (LaPlaca et al., 1999). There is also evidence from animal experiments that the product of strain and strain rate is a good predictor of brain injury (Viano and Lovsund, 1999). Obviously such a model can use input parameters, such as linear and angular accelerations, to predict brain injury, based on the computed response of the brain. Logic also dictates that injury is directly dependent on the response of the brain and not on the input parameters.

Data from the National Football League During each football season, professional players are routinely concussed every Sunday.. They sustain what is termed a mild traumatic brain injury (MTBI) which is essentially reversible in the sense that there does not appear to be any permanent sequelae as a result of that single impact. A multi-center research effort, managed by Biokinetics, Inc., of Ottawa, Ontario and involving Duke University, the University of Pennsylvania and Wayne State University resulted in accurate estimates of the head accelerations of the two colliding players, one of whom has sustained a MTBI. The reconstruction process starts with a stereogrammetric analysis of the speed and location of impact of the two helmets, using video from at least two of the cameras on the field. A pair of instrumented and helmeted Hybrid III heads attached to their respective necks was used to reconstruct the impact so that the linear and angular acceleration of both heads could be measured (See Newman, et al., 1997). The data were then fed into the Wayne State model to compute the response parameters described in the previous section. There were a total of 53 cases of which there were 22 concussions and 31 non-concussions. Each case was simulated using the Wayne State University 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 probability of one and the non-concussed cases had a zero probability of injury. Chi square and p-values were calculated and it was found that the product of strain and strain rate was the best predictor, Table 1. Result of Logist Analysis for Reversible MTBI 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

followed by strain rate and HIC. Table 1 shows the top 5 predictors in the order of their Chi square values. It is seen that angular acceleration is fifth in that list and HIC is surprisingly high as a predictor of reversible MTBI.

Discussion The fact that the product of strain and strain rate is the leading predictor of MTBI is not surprising because there is experimental evidence from animal tests to support this. However, the low predictive power of angular acceleration is indeed a surprise. Both the cadaveric data and the model indicate that angular acceleration generates large displacements and principal strains in the brain and it was found that high values of strain rate occurred in regions where the strain was high. That is, the product of strain and strain rate can only be high in the presence of angular acceleration. On the other hand, linear acceleration does not bring about a lot of brain displacement and hence strain and it stands to reason that the strain rate is also low for this condition. The fact that HIC is rated as a good predictor of concussion must mean that in addition to the high strain rates generated by angular acceleration another injury mechanism is at work. It is important to consider the effect of shock or pressure waves passing through the brain tissue and perhaps concentrate on experimental animal studies that deliver shocks to the brain with very little head motion.

Conclusions By combining a series of different studies, some additional light has been shed on the parameters responsible for MTBI. The best predictors are response variables but the input variable linear acceleration is ranked quite high. These results suggested two different mechanisms at work, both of which can cause injury.

ABOUT THE AUTHOR Albert I. King, Ph.D.: Distinguished Professor and Chair, Department of Biomedical Engineering, Wayne State University. Contact information: Department of Biomedical Engineering, Wayne State University, 818 W. Hancock, Detroit, MI 48202.

Telephone: 313-577-1347 or 313-577-8333, e-mail: king@rrb.eng.wayne.edu.

REFERENCES Hardy WN, Foster CD, Mason MJ, Yang KH, King AI: Investigation of head injury mechanisms using neutral density technology and high-speed biplanar Xray. 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 neuronal injury: Loading rate dependent changes in acute cytosolic calcium and lactate dehydrogenase release. J. Neurotrauma. 14: 355-368.

Newman J, Beusenberg M, Fournier E, Shewchenko N, Withnall C, King A, Yang K, Zhang L, McElhaney J, Thibault L, McGinnis G (1999). A new biomechanical assessment of mild traumatic brain injury. Proc. 1999 IRCOBI Conference, pp.

17-36.

Viano DC, LĂśvsund P (1999). Biomechanics of brain and spinal cord injury: Analysis of neurophysiological experiments. Crash Prevention and Injury Control, 1:35-43 Zhang L, Yang KH, Dwarampudi R, Omori K, Li T, Chang K, Hardy WN, Khalil TB, King AI. Recent advances in brain injury research: A new human head model development and validation. Stapp Car Crash J., 45:369-394, Paper No. 200122-0017, 2001.

ACKNOWLEDGMENT The author wishes to acknowledge the contribution of Dr. King Yang, Dr. Liying Zhang, Mr. Warren Hardy, Dr. David Viano and Dr. Scott Tashman for their contribution to the work reported in this article. Funding for this work was provided by the Centers for Disease Control, the National Football League Charities and Honda R & D Co. Ltd.

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17

Biomechanics of Childhood Neurotrauma

by Susan S. Margulies, Ph.D. and Betty Spivack M.D. Over sixty years ago, Holbourn (1943) created specialized gelatin models of the human brain, and studied their response during rapid translational and rotational motions, and concluded that rotational or angular movements would create larger and more widespread brain distortions than translation or linear movements, and that the pattern of distortion would vary with the direction of head motion. In addition, he postulated that regional deformation (strain) would scale with brain mass, such that larger brains experiencing the same acceleration would deform more. Over the next 40 years, numerous experimental investigations not only confirmed these hypotheses, but created the foundation of critical data that we use today to understand mechanisms 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 et al., 1996; Ommaya 1995). Events are typically characterized as contact or inertial, the latter involving head motion. Contact events result in soft tissue injuries of the scalp, skull fracture or deformation, epidural or subdural hematomas, and cortical contusions. Inertial events are likely to produce concussion, subdural hematoma, subarachnoid hemorrhage, petechial hemorrhages, and/or widespread axonal injury.

Difficulty arises in applying the adult paradigm to pediatric head injury, because scaling by size alone is insufficient to include the role of changes in the stiffness of the braincase with maturation and the influence of neural development on the response of the brain to a specific deformation. Therefore, at this time we are unable to define a complete rubric for biomechanics of pediatric brain injury, but as additional experimental data regarding mechanical properties of pediatric neck, brain and skull are obtained, and injury thresholds are derived for the developing brain, we will be able to answer critical questions regarding mechanisms of injury that are unique to young children. The paucity of data for the child and immature animals has 18

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impeded our ability to understand if a specific event is likely to be associated with head injury in the child, to develop protective measures and treatments specifically for children and to distinguish with confidence between nonintentional head injuries and child abuse.

Identification of child abuse is particularly fraught with difficultly, because histories regarding the loading conditions (acceleration magnitude or direction, occurrence of impact, etc.) are unreliable. Despite objective information, a vigorous debate exists as to whether vigorous shaking, causing rapid movements of the head relative to the torso, may cause the subdural hematomas, axonal injury, and retinal hemorrhages documented in abused infants. Guthkelch (1971) and Caffey (1972, 1974) proposed that rotational acceleration-decelerations associated with shaking played a central role in generating brain injuries with greater morbidity and mortality than those in infants who had fallen short distances (Kravitz et al., 1969; Helfer et al., 1977; Nimityongskul and Anderson 1987; Lyons and Oates 1993). This proposed etiology was coined “whiplash-shaken infant syndrome” and also “shaken baby syndrome”; the latter name has continued in general use.

With the onset of computerized tomographic (CT) imaging in the late 1970’s, and the near-simultaneous increase in postmortem examination of infants who died suddenly or unexpectedly, there was a rapid increase in knowledge about the pathologic lesions seen in abused infants (Hahn et al., 1983, Ludwig and Warman 1984; Billmire and Myers 1985; Duhaime et al., 1987). Common findings included small or skim subdural hematomas, often parafalcine in location, frequent documentation of retinal hemorrhages, seizures, apnea and/or bradycardia at presentation, and poor outcome associated with high mortality. DAI (Diffuse Axonal Injury) and white matter injury were described in fatal cases (Calder et al., 1984; Vowles et al., 1987).

Bruises and skull fracture were frequent findings, especially in

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

To gain insight into the relative roles of shaking and inflicted impacts in generating these head injuries, Duhaime et al., (1987) and Prange et al., (2003) constructed doll models of infants and compared rotational accelerations and velocities experienced by the head during vigorous shaking, falls, and inflicted impacts against various surfaces. Inflicted impact onto hard surfaces produced peak accelerations significantly larger than falls from 5 feet onto concrete, and up to 30-50 times that produced by shaking alone. Large rotational accelerations occurred as the head rebounded after contact with firm surfaces, but was attenuated on soft surfaces that pocketed the head. It is important to note that actual neck properties of infants in flexion/extension are unknown, and the flexible neck representations used in the dolls may overestimate actual events. While these studies provide important objective biomechanical information regarding the comparative loading conditions across accidental and inflicted scenarios, there are several caveats. First, because of the paucity of injury threshold information for children, it is difficult to predict the occurrence of injury, but the higher rotational accelerations associated with impact increase the likelihood of injury. Second, little data is available to determine if a repeated motion causes more severe injury than a single movement of the same magnitude. Finally, if the soft skull of the young child deforms during contact, the deformation during the moment of contact event may cause additional brain damage, exacerbating the injury during the rotational rebound.

Over the last 30 years, mechanical properties of adult brain tissue have been measured in the laboratory (Ommaya 1968, McElhaney et al., 1969; Galford and McElhaney 1970; Miller et al., 1997, 2000, 2002; Mendis et al., 1995; Fallenstein et al., 1969; Metz et al., 1970, Thibault and Margulies 1998; Arbogast and Margulies 1997) and were found to vary over ten-fold, due to differing testing methods, species, interval after death, and region of the brain. More recently, mature and immature fresh porcine brain tissue was tested in a variety of orientations over a broad strain range, and results demonstrate that infant brain tissue is significantly stiffer than adult tissue (Prange and Margulies 2002), because of the lower levels of myelin in the young brain.

The stiffer brain offers resistance to deformation during contact or inertial loading conditions, but one cannot comment about the brain’s risk of injury until studies demonstrate if the infant brain tissue is injured more or less severely than the adult, if deformed in a similar manner. Raghupathi and Margulies (2002) recently compared axonal injuries in newborn piglets and adult piglets experiencing similar nonimpact rotational velocities. The neonatal porcine brain experienced more than 3 times more axonal injury than the mature brain. The marked differential is amplified further when one considers that intracranial strain levels would be expected to be lower in the younger animal with stiffer brain tissue and smaller brain size. Thus, we conclude that this study is consistent with the concept that pediatric brain tissue may have a lower injury threshold than adult. However, this conclusion must be confirmed in additional studies. Furthermore, it should be noted that this study was focused on singleimpulse events, rather than multiple-impulse episode.

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

multiple of the natural frequency of the skull and intracranial contents. Willinger et al. demonstrated that the first resonance frequency of the adult head ranges between 67 and 100 Hz (Willinger et al., 1994, 1996, 1999), and the pediatric head would have a higher natural frequency due to its smaller size. In contrast, Ommaya identified the natural frequency of skull and intracranial contents as 5-10 Hz in subhuman primates, and proposed that the natural frequency in the adult human would scale to be 4-5 Hz(Ommaya et al., 1971, 1993). It is clear that additional studies are needed to define more narrowly the natural frequency in children, to evaluate if this mechanism may give rise to substantial intracranial deformations, and associated brain injuries.

Despite these inherent limitations of the instrumented doll studies, it has become clear that a high proportion of infants with inflicted head trauma have evidence of impact to the head, and that the proportion is even higher in children who die of their injuries (Hahn et al., 1983; Duhaime et al., 1987; Hadley et al., 1989). Because the infant skull has 1/8 the strength of adult skull but can deform more than six times as much before fracture (Margulies and Thibault 2000), impact may deform the infant skull significantly, causing diffuse brain injuries. These data correlate well with the rarity of documented skull fracture in observed infant falls from low heights (Helfer et al., 1977; Nimityongskul and Anderson 1987) but is not consistent with reported data of near-universal skull fractures obtained by dropping infant cadavers on a variety of surfaces from 32 inches (Weber 1984, 1985). These latter studies do not describe methods for cadaver preservation, handling or postmortem duration prior to the impact testing. Routine storage in a morgue refrigerator, with some passage of time, may be expected to produce dehydration of the bone resulting in a more brittle skull (Sasaju and Enyo 1995). In contrast, Margulies and Thibault (2000) used recommended techniques of rewarming and rehydrating bone samples prior to biomechanical testing.

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

Given that the infant neck is so flexible, attention has extended to biomechanical events at the cervicomedullary junction during trauma as a potential precipitating event leading to changes in respiratory and cerebrovascular control centers, causing brain injury secondary to hypoxia and ischemia. Hadley (1989) demonstrated pathology at the cervico-medullary junction in five of six fatal cases of abusive head trauma where no evidence of impact injury was present. Accompanying pathologic lesions included spinal cord subdural and epidural hematomas, and spinal cord contusions. More recently, Geddes has found traumatic axonal injury at the cervico-medullary junction, and raises concern that this region may be vulnerable during shaking events (Geddes et al., 2000, 2001a, 2001b). Vertebral artery compression in the neck by periadventitial hemorrhage has also been reported (Gleckman et al., 2000). Injury at the cervicomedullary junction may be the mechanism for the high incidence of apnea seen in infants with abusive head trauma (Ludwig and Warman 1984), and thereby contribute to the encephalopathy seen in children dying of abusive head trauma (Geddes et al., 2000, 2001a, 2001b; Johnson et al., 1995). The BRAIN INJURY PROFESSIONAL

19

paucity of data regarding the mechanical properties of the neck in infants and young children is an obstacle to engineering efforts to investigate the relative influence of shaking, falls, and inflicted impact on injuries to the cervico-medullary junction.

Recently, Ommaya et al., (2002) proposed that neck or spinal cord injury would be present in all cases, if whiplash injury has caused SDH or other intracranial pathology. However, previous studies do not consistently support this hypothesis.

Data from primates (Ommaya et al., 1968) experiencing a whiplash nonimpact type of event and infants (Geddes et al., 2001a, 2001b) who died of abusive head trauma suggest that only 30-50% of cases with intracranial pathology may have accompanying brainstem or spinal cord injuries visible on the surface or on histologic examination. No data is available on the frequency of muscular, ligamentous, or bony injury in this setting. The presence of acute episodes of apnea or cerebral blood flow alterations can precipitate secondary brain injuries. Geddes (2000, 2001a, 2001b) has noted frequent appearance of hypoxic-ischemic encephalopathy in the brains of infants who have died of abusive head trauma and Gleckman (2000) has reported similar findings. Levels of quinolinic acid, inflammatory mediators and excitatory amines including glutamine (Whalen et al., 1998, 2000; Bell et al., 1999; Ruppel et al., 2001) have been reported to be high in all types of pediatric traumatic brain injury, but were much higher in children suffering from abusive head trauma. The neurotoxicity of many of these substances, and secondary injuries due to hypoxia and altered CNS metabolism may contribute to the high mortality rate and severe morbidity of children with abusive head trauma, compared with survivors of accidental head trauma (Bonnier et al., 1995; Haviland and Russell 1997; Ewing-Cobbs., 1998).

Retinal hemorrhages also appear to have a much stronger correlation with abusive head trauma than with accidental head trauma, 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 documented accidental head trauma requiring hospitalization (nearly all were falls and motor vehicle accidents) had dilated retinal examinations performed by a pediatric ophthalmologist. Only 3 children had retinal hemorrhages (1.0%); all three were victims of motor vehicle accidents. There have been isolated reports of retinal hemorrhages incurred in household accidents (Christian et al., 1999). In all cases, the retinal hemorrhages consisted of a few, small unilateral hemorrhages isolated to the posterior pole.

In contrast, retinal hemorrhages extending to the far periphery of the retina, traumatic retinoschisis, optic nerve sheath hemorrhage and axonal injury of the optic nerve have been reported as a common occurrence in infants with abusive head trauma (Levin 2000). Use of beta-amyloid precursor protein staining can facilitate identification of traumatic axonal injury of the optic nerve (Gleckman et al., 2000). Proposed injury mechanisms include orbital shaking and vitreous traction during a shaking event, but experimental data to support these hypotheses are needed.

CONCLUSIONS While the general paradigm of adult traumatic brain injury has a solid research basis, the applicability of this paradigm to children still presents significant gaps and challenges. Basic biomechanical properties have not been well established for infant skull or brain tissues, nor has the infant neck been well characterized. Early evidence indicates that simple brain mass scaling 20

BRAIN INJURY PROFESSIONAL

does not accurately predict thresholds for traumatic axonal injury in immature brains. Little or no experimental work has been performed using oscillatory loads, such as shaking, to derive injury thresholds in either mature or immature animals.

It is unknown at present whether thresholds for intracranial injury with such repetitive loading patterns will be higher, lower or identical to thresholds for single impact or impulsive loads.

The relative contribution of secondary neural injuries in the observed pathology in victims of abusive head trauma remains unclear, but emerging data indicates that hypoxic-ischemic injury may be a significant and complicating factor. Research in the biomechanics of different patterns of retinal hemorrhage is only at an early stage.

Head injury is a leading cause of death and acquired disability in childhood. However the biomechanics of pediatric head injury is poorly understood, primarily due to the paucity of age-specific data regarding mechanical properties of immature tissue and its response to specific loads. Research is needed to understand the unique biomechanics associated with pediatric neurotrauma.

ABOUT THE AUTHORS Susan S. Margulies, Ph.D., is an Associate Professor in the Departments of Bioengineering and Neurosurgery at the University of Pennsylvania. Her research emphasis is biomechanics associated with pediatric brain injury, with the goal of enhancing avenues for injury prevention, intervention and treatment.

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

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Ommaya AK. Head injury mechanisms and the concept of preventive management: a review and critical synthesis. J Neurotrauma 1995, 12:527-546.

Ommaya AK, Faas F and Yarnell P. Whiplash injury and brain damage. JAMA 1968, 204:285-289.

Ommaya AK, Fisch FJ, Mahone RM, Corrao P and Letcher F. Comparative tolerances for cerebral concussion by head impact and whiplash injury in primates. SAE 1970, reprinted in Biomechanics of Impact Injury and Injury Tolerances of the Head Neck Complex, Backaitis S (editor), Society of Automotive Engineers 1993, pp 265 â&#x20AC;&#x201C; 274.

Ommaya AK and Hirsch AE. Tolerances for cerebral concussion from head impact and whiplash in primates. J Biomechanics 1971, 4:13-21.

Ommaya AK, Goldsmith W, Thibault L. Biomechanics and neuropathology of adult and paediatric head injury. Br J Neurosurg. 2002, Jun;16(3):220-42.

Prange MT, Coats B, Duhaime AC and Margulies SS. Anthropomorphic simulations of falls shakes, and inflicted impacts for infants. J Neurosurg. 2003, 99: 143-150.

Prange MT, Margulies SS. Regional, directional, and agedependent properties of the brain undergoing large defor-

mation. ASME J Biomech Eng. 2002, Apr; 124(2):244-52.

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2002, Jul; 19(7):843-53.

Ruppel RA, Kochanek PM, Adelson PD, Rose ME, Wisniewski SR, Bell MJ et al., Excitatory amino acid concentrations in ventricular cerebrospinal fluid after severe traumatic brain injury in infants and children: the role of abuse. J Pediatr 2001, 138:18-25.

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SPORTS CONCUSSION

by Christopher C. Giza, M.D. Introduction A high profile athlete sustains a head injury and we read about it in the sports pages. But for every professional athlete who experiences a sports concussion, there are many more amateur athletes, both adults and children, who don’t make the papers. Still, head injury in sports is an important and timely medical topic, and this review will briefly cover aspects of sports concussion, including epidemiology, biomechanics, sports-related recurrent head injuries, and basic clinical management.

Epidemiology of Sports-Related Brain Injury The majority of head injury in sports falls into the category of mild traumatic brain injury, also referred to as concussion. A concussion is defined as any biomechanically-induced impairment of neurological function, with or without loss of consciousness (American Academy of Neurology, 1997). Because of its mild nature, many sports concussions go unreported. In fact, a desire of the athlete with brain injury to quickly return to play often results in minimizing or ignoring the symptoms of concussion. The Centers for Disease Control estimate that 300,000 sports-related brain injuries occur annually in the United States, the vast majority of them concussions (Centers for Disease Control and Prevention, 1999). Of all traumatic brain injuries, 1 in 5 is incurred during sports participation.

Perhaps more compelling are the estimated rates of concussion among athletes in particular sports. Concussive head injuries account for a significant proportion of total injuries in contact sports. Collegiate ice hockey (12.2%), football (8%) and soccer (4.8%) all showed a significant percentage of concussions out of total injuries sustained during the 2002-2003 season, as reported 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 from 235 U.S. high schools, where 5.5% of total injuries were mild traumatic brain injuries (Powell and Barber-Foss, 1999). This 22

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percentage was highest for football (7.3%), wrestling (4.4%), and soccer (3.9%) in boys’ sports. In girls’ sports, the percentage of concussions out of total reported sports injuries was highest in soccer (4.3%). Ice hockey was not assessed in the latter study.

Among the 10 high school sports analyzed, however, it was estimated that over 60,000 mild head injuries occur annually in varsity high school athletes. This underlines the fact that many sports-related head injuries occur in children and adolescents, whose brain development is ongoing and where the effects of injury may be distinct from those seen in adults.

Most persons are able to recover completely from concussions. While a single mild injury may not result in lasting cognitive or behavioral deficits, an accumulation of injuries over time, or repeated injury with incomplete recovery between concussions, 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 concussion is the likelihood for repeated mild injuries and potential for lasting problems. This is anecdotally demonstrated by professional athletes whose careers have been cut short by multiple concussions. Furthermore, several published studies exist that quantify the risk of recurrence (Guskiewicz, Weaver, Padua et al., 2000; Zemper, 2003). Guskiewicz reported that high school and college football players who sustained a concussion were three times more likely to suffer a second concussion during the same season. More recently, Zemper showed that a previous concussion is associated with an almost overall 5.86-fold increased relative risk of another concussion (not necessarily limited to the same season). Several possibilities exist to explain this increased risk. One is that athletes with a more aggressive style of play are more likely to sustain repeated head injuries. A second explanation may be that certain individuals are somehow predisposed to concussions. A third possibility is that concussion results in cerebral dysfunction that makes the injured brain more vulnerable to subsequent biomechanical insults. While the existing studies

cannot determine which of these is more likely, these explanations are not mutually exclusive. Moreover, there is increasing laboratory evidence that recurrent traumatic brain injuries can exacerbate 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).

an important role in traumatically-induced loss of consciousness.

Furthermore, the pathology of these diffuse rotational injuries can be subtle, and is generally not well detected by conventional CT scanning. Thus, the vast majority of CT scans performed on athletes after concussion appear normal, despite the fact that microscopic damage may be present..

Pathophysiology of Concussion Biomechanics of Sports Concussion Traumatic or concussive injury represents a unique type of brain injury, whereby pathophysiological changes are initiated by mechanical forces imparted to the brain-mechanical forces imparted to the brain initiate pathophysiological changes.

Understanding the basic biomechanics of concussion, then, is important not only to understand the clinical injury itself, but also to design appropriate research models with which to study concussion.

Brain tissue is a gelatinous substance with a consistency likened to that of firm oatmeal. The brain is wrapped in a thick covering (the dura) that both protects and segments the brain.

Within this covering, the brain essentially floats in a bath of cerebrospinal fluid. All of these components are then housed within the bony skull. When mechanical forces are applied to the head, the brain moves within the fluid-filled skull, and injury can result from the brain striking the skull at the point of impact (coup injury), forces applied to the brain on the side opposite from impact (contrecoup injury), or by shearing/twisting of brain

Figure 1: Biomechanics of Concussion

It is important to realize that significant cerebral dysfunction can exist, even when brain anatomy appears normal, such as usually occurs in the setting of a concussed athlete. Animal models of diffuse concussive injury have shown profound cellular and physiological alterations that can last minutes to days after impact. In general, experimental concussive injury results in an indiscriminate depolarization of neurons, widespread release of glutamate, efflux of potassium, alteration and impairment of cerebral glucose metabolism, and derangements of cerebral blood flow (Giza and Hovda, 2001; Katayama, Becker, Tamura et al., 1990; Yoshino, Hovda, Kawamata et al., 1991). Many of these findings have been confirmed in humans with severe traumatic brain injury (Bergsneider, Hovda, Shalmon et al., 1997; Reinert, Hoelper, Doppenberg et al., 2000). Moreover, a profound reduction in brain glucose metabolism was reported in a football player who experienced a concussion, demonstrating that brain physiology can be affected even after milder injuries (Bergsneider, Hovda, Lee et al., 2000). One recent study demonstrated impaired cerebral blood flow activation in response to a working memory task in mildly head-injured patients with persistent symptoms (Chen, Kareken, Fastenau et al., 2003).

Another showed abnormal patterns of fMRI activation during a similar task in patients that had experienced mild TBI (McAllister, Saykin, Flashman et al., 1999). There is now substantial experimental and clinical data to confirm that concussive brain injury can result in physiological dysfunction in the absence of structural damage.

Recurrent Brain Injury tissue around an axis of injuryimpact force. Forces causing concussion can thus be simplistically categorized as either linear or rotational (Figure 1).

Generally, linear forces, sometimes referred to as translational forces, can result either from the head being struck by a moving object (fist, ball, etc.) or by the head being driven against an unmoving object (ground, wall, etc.). At the point of impact, there is transient deformation of the skull that can result in compression of the brain. With very high forces, permanent skull deformation can occur in the form of a fracture; however, this is very unusual in the setting of sports concussions. Opposite the point of impact, negative or tensile forces can exert their injurious effects on the pliable brain tissue. It has been hypothesized that the cause of contrecoup injuries is due to this negative pressure, or alternatively, to rebounding of the â&#x20AC;&#x2DC;floatingâ&#x20AC;&#x2122; brain against the inside of the bony skull.

It is rare for translational forces to occur in isolation, particularly in a sports setting. More often, linear forces are combined with rotational or angular or rotational forces that can result in twisting of the brain within the skull. These types of more diffuse forces are particularly damaging to white matter fiber tracts that interconnect brain regions. Rotational forces also appear to play

One 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 distinct problems. First, there appears to be some cumulative effect of total concussions sustained over a longer period of time, even if an adequate period of recuperation is permitted after each individual concussion. In animal models of repeated mild traumatic brain injury, rats demonstrate enduring difficulties in cognitive and behavioral tasks, even in the absence of significant anatomical injury (DeFord, Wilson, Rice et al., 2002; Laurer, Bareyre, Lee et al., 2001). There are also multiple studies in humans that demonstrate worse neurological symptoms and cognitive function 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 have all been performed in athletes and are thus directly relevant to the problem of sports concussion.

Second, there is the risk of a second concussion occurring in a brain that has not yet physiologically recovered from a first concussion. This brain may then be more vulnerable to the effects of a mild injury. Second impact syndrome is a rare but catastrophic phenomenon characterized by fulminant cerebral edema and neurological collapse, occurring when a second (often mild) head injury is superimposed upon an earlier injury BRAIN INJURY PROFESSIONAL

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

Table 1: Concussion Severity: Grading

Clinical Management of Sports Concussion Current guidelines for the classification and management of concussion, including return-to-play guidelines, are based primarily upon expert opinion and consensus (American Academy of Neurology, 1997; Cantu, 2000b; Colorado Medical Society, 1990) (Table 1). Some data regarding the timing of physiological recovery are available from animal models, but extrapolating these time intervals to the human condition is problematic. The proper clinical management of sports concussion involves accurately describing the injury, early assessment, further diagnostic investigation for unusual or persistent symptoms, follow up until symptoms resolve, and finally, instruction regarding returning to play and prevention of future head injuries.

There are a myriad of guidelines for classification of concussion severity consensus (American Academy of Neurology, 1997; Cantu, 2000b; Colorado Medical Society, 1990). To accurately describe the injury, the initial medical evaluation should include the following: 1) some mention of the biomechanics of the accident (i.e. helmet-to-helmet collision, back of head striking the ground), 2) presence of protective headgear, 3) initial neurological symptoms, 4) presence and duration of any loss of consciousness, 5) presence and duration of post-traumatic amnesia and 6) history of prior concussions â&#x20AC;&#x201C; both recent and distant. It is important to be aware of the fact that a concussion can occur even if the player does not lose consciousness.

Early assessment can be done by the team trainer or physician on the sidelines. The standardized assessment of concussion (SAC) is a simple, validated tool that can be performed quickly and reproducibly (McCrea, Kelly, Kluge et al., 1997) (Table 2).

The SAC has been shown to be sensitive to detect subtle impairment resulting from a concussion, and can even be administered at the beginning of the season so that a baseline score may be recorded for each athlete. (editor note: see page 32 for more details about assessment technology for mild TBI).

Any loss of consciousness merits closer evaluation. The decision to obtain a head CT scan is largely based on the severity and persistence of symptoms. Prolonged unconsciousness, suspicion of skull fracture, seizures and/or focal neurological deficits suggest more than a simple concussion and indicate a need for neuroimaging. Other worrisome signs include persistent/worsening headache, altered mental status, and/or nausea/vomiting. In cases of simple concussion, initial observation is a reasonable clinical plan, with the possibility left open to re-evaluate the player if problems worsen or fail to resolve.

After the acute period, any athletes with persistent symptoms may require follow up evaluation. Post-concussive symptoms can span a wide range, but most commonly include some combination of the following: headache, poor attention, memory impairment, fatigue, dizziness, ringing in the ears, mood changes and sleep disturbances. Current guidelines take persistent neurocognitive symptoms as a sign of ongoing cerebral dysfunction and presumed increased risk of a second injury. Therefore, it is recommended that no athlete with a concussion return to play if symptoms persist. In fact, current guidelines for time intervals until return-to-play are based upon resolution of all neurological 24

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Table 2: Standardized Assessment of Concussion (SAC)

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

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

Other important interactions with the athlete at the follow up evaluation include education as to the risks of repeated concussion and proper use of head protective gear. While many think of sports concussion as occurring only in team sports, it should be remembered that many mild and severe head injuries also occur as a result of bicycle, scooter and rollerblade accidents. Many studies have documented the efficacy of bicycle helmet laws in reducing the number of head injuries (Cook and Sheikh, 2000).

Currently, there are no effective brain-specific therapies for head injury, and thus, the best management of sports-related concussion must include preventive and protective measures.

Conclusions Concussion is defined as any transient neurological dysfunction resulting from biomechanical forces imparted to the brain, with or without loss of consciousness. Concussion is by far the most common type of head injury, and is frequently associated with sports participation. Concussive brain injury is mediated by both linear and rotational forces. Linear forces are associated with impact, and can result in both focal and diffuse injury.

Rotational forces result in twisting or shearing of neural tissue, even in the absence of impact. Most sports concussions result from a combination of these types of forces. Concussion results in a complex pathophysiological cascade in the injured brain, rendering it dysfunctional even in the absence of clear anatomic damage. During this time, the injured brain is particularly vulnerable to further injury. Current return-to-play guidelines treat persistent neurological symptoms as evidence of ongoing neural dysfunction and limit return-to-play only until after a variable symptom-free observation period. Appropriate clinical management of sports-related head injury includes an accurate injury description, a rapid sideline assessment, careful monitoring of symptoms, and education of the athlete with regards to return-to-play and prevention of future injuries.

letic Head and Spine Injuries. RC Cantu, (Ed.) W.B. Saunders Company, St. Louis. Pages 76-79, 2000b.

Centers for Disease Control and Prevention, Traumatic Brain Injury in the United States: A Report to Congress.

1999.

Chen SH, Kareken DA, Fastenau PS et al. A study of persistent post-concussion symptoms in mild head trauma using positron emission tomography. J.Neurol.Neurosurg.Psychiatry. 74:326-332, 2003.

Collins MW, Grindel SH, Lovell MR et al. Relationship between concussion and neuropsychological performance in college football players. JAMA: The Journal of the American Medical Association. 282:964-970, 1999.

Collins MW, Lovell MR, Iverson GL et al. Cumulative Effects of Concussion in High School Athletes. Neurosurgery. 51:1175-1181, 2002.

Colorado Medical Society, Guidelines for the Management of Concussion in Sports. Report of the Sports Medicine Committee. 1990.

Cook A and Sheikh A, Trends in serious head injuries among cyclists in England: analysis of routinely collected data. BMJ. 321:1055-1055, 2000.

DeFord SM, Wilson MS, Rice AC et al. Repeated mild brain injuries result in cognitive impairment in B6C3F1 mice. Journal of Neurotrauma. 19:427-438, 2002.

DeRoss AL, Adams JE, Vane DW et al. Multiple head injuries in rats: effects on behavior. J.Trauma. 52:708714, 2002.

Giza CC and Hovda DA, The Neurometabolic Cascade of Concussion. J.Athl.Train. 36:228-235, 2001.

Guskiewicz KM, McCrea M, Marshall SW et al. Cumulative Effects Associated With Recurrent Concussion in Collegiate Football Players: The NCAA Concussion Study. JAMA: The Journal of the American Medical Association. 290:2549-2555, 2003.

Guskiewicz KM, Weaver NL, Padua DA et al. Epidemiology of concussion in collegiate and high school football players. Am.J.Sports Med. 28:643-650, 2000.

Kanayama G, Takeda M, Niigawa H et al. The effects of repetitive mild brain injury on cytoskeletal protein and behavior. Meth.Find.Exp.Clin.Pharmacol. 18:105-115, 1996.

Katayama Y, Becker DP, Tamura T et al. Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.

Journal of Neurosurgery. 73:889-900, 1990.

Laurer HL, Bareyre FM, Lee VM et al. Mild head injury increasing the brain’s vulnerability to a second concussive impact. Journal of Neurosurgery. 95:859-870, 2001.

McAllister TW, Saykin AJ, Flashman LA et al. Brain activation during working memory one month after mild traumatic brain injury: a functional MRI study. Neurology. 53:1300-1308, 1999.

McCrea M, Kelly JP, Kluge J et al. Standardized assessment of concussion in football players. Neurology.

48:586-588, 1997.

McCrea M, Guskiewicz KM, Marshall SW et al. Acute Effects and Recovery Time Following Concussion in Collegiate Football Players: The NCAA Concussion Study.

JAMA: The Journal of the American Medical Association.

290:2556-2563, 2003.

Powell JW and Barber-Foss KD, Traumatic Brain Injury in High School Athletes. JAMA: The Journal of the American Medical Association. 282:958-963, 1999.

Reinert M, Hoelper B, Doppenberg E et al. Substrate delivery and ionic balance disturbance after severe human head injury. Acta Neurochir.Suppl. 76:439-444, 2000.

Yoshino A, Hovda DA, Kawamata T et al. Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state. Brain Research. 561:106119, 1991.

Zemper ED, Two-Year Prospective Study of Relative Risk of a Second Cerebral Concussion. Am.J.Phys.Med.Rehabil. 82:653-659, 2003.

ABOUT THE AUTHOR Christopher C. Giza, M.D.: UCLA Brain Injury Research Center, Division of Neurosurgery/Department of Surgery, Division of Neurology/Department of Pediatrics, Brain Research Institute, David Geffen School of Medicine at UCLA. Email: cgiza@mednet.ucla.edu.

REFERENCES American Academy of Neurology, Practice parameter: the management of concussion in sports (summary statement). Neurology. 48:1997.

Bergsneider M, Hovda DA, Lee SM et al. Dissociation of cerebral glucose metabolism and level of consciousness during the period of metabolic depression following human traumatic brain injury. Journal of Neurotrauma.

17:389-401, 2000.

Bergsneider M, Hovda DA, Shalmon E et al. Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study [see comments]. Journal of Neurosurgery. 86:241-251, 1997.

Bruce DA, Alavi A, Bilaniuk L et al. Diffuse cerebral swelling following head injuries in children: the syndrome of “malignant brain edema”. Journal of Neurosurgery. 54:170-178, 1981.

Cantu RC, Malignant brain edema and second impact syndrome. In: Neurologic Athletic Head and Spine Injuries.

RC Cantu, (Eds.) W.B. Saunders Company, St.Louis.

Pages 132-137, 2000a.

Cantu RC, Overview of Concussion. In: Neurologic AthBRAIN INJURY PROFESSIONAL

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The Biomechanical Assessment Of Traumatic Brain Injury

by Mariusz Ziejewski, Ph.D. Introduction Traumatic Brain Injury (TBI) is a serious disease that has been overlooked for many decades. The Center for Disease Control reported 1.5 million people diagnosed with TBI in 2001 (National Center for Injury Prevention and Control, 2003). One of the major problems with TBI is a lack of sufficiently reliable diagnostic tools to assist the Emergency Medicine (EM) physician when he or she sees a person involved in an automobile collision. A correct diagnosis of TBI is difficult because the presence of a head injury may be masked, among other things, by serious injury to another body part, subtle and changeable symptoms, or a delayed onset of symptoms. Various studies indicate a significant percentage of undiagnosed TBI in Emergency Room (ER) settings, in some cases over 50% (Zhang, Yang, King, 2001; Edberg, Rieker, Angrist, 1963; Gurdjian, et al., 1967; Pudenz, Sheldon, 1946). New developments in neurodiagnostics, the use of biological markers such as the S-100 serum can, to some extent, improve the unfortunate statistics of undiagnosed TBI. Further gains can be achieved by utilizing the knowledge from trauma biomechanics.

At an injury assessment stage the information regarding the impact scenario is highly desirable. When ER physicians encounter patients with possible TBI, they typically are hindered by a lack of knowledge about the collision. Many EM physicians already employ a basic understanding of trauma biomechanics in the course of their career. They look at photos of the damaged vehicle or talk to the persons involved in the collision in order to determine what happened during an accident and how those events may 26

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

The best-known general knowledge vehicle collision database is the Crashworthiness Data System (CDS), part of the National Accident Sampling System (NASS) (National Center for Statistics and Analysis, 2003). The results from the studies are very useful for the intended purposes, one of which is to understand the mechanics of serious automotive collisions to improve crashworthiness strategies in automotive design. Although this type of analysis is useful in crashworthiness strategy setup, it is not conducive to an ER setting.

Reconstruction of the biomechanical forces in vehicle crashes for a specific collision is feasible, and enables quantitative stratification of TBI severity. Application of biomechanical methodologies for in-depth reconstruction of vehicle crashes has been applied for several decades. The majority of the relevant literature is published in governmental reports and journals in the field of engineering and biomechanics. Multi-diciplinary teams including physicians, scientists, and engineers in relevant areas have developed many of these reports (Jamison, Tait, 1996; Guenther, 1993; Robbins, Melvin, Huelke, 1993; Simpson, Ryan, Paix, 1991; Ashton, 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).

Overall Approach in the Biomechanical Evaluation of TBI The biomechanical assessment of TBI directly relates to the extent of understanding of the brain injury mechanism. Although the majority of the concepts regarding the cause of TBI are merely hypotheses, in general it is accepted that brain injury can result from the sudden change in velocity. This can occur due to trauma such as head impact or inertia loading of the head when torso is accelerated or stopped rapidly.

An engineering parameter that by definition represents the change in the velocity as a function of time is acceleration. Therefore the head acceleration has been used in characterization of the severity of an insult to the brain. The complete global representation of the head motion in terms of acceleration can only be achieved if and only if the complex input of linear and angular acceleration is known. This includes the three components for linear acceleration and three components for angular acceleration (see Figure 1).

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

Biomechanical engineers do not assess TBI based on acceleration alone; they “look inside the box” – i.e., the skull – and try to assess what’s happening inside. Based on that analysis, additional parameters that deal with local brain deformation were developed.

They are an extension of the evaluation based on head acceleration. It has been suggested that brain surface contusions, Diffuse Axonal Injury (DAI), and acute subdural hematoma can be predicted using, among other things, brain motion (Meany, 1991; Gennarelli, Thibault, 1982; Abel, Gennarelli, Segawa, 1978; Edberg, Rieker, Angrist, 1963; Gurdjian, et al., 1967; Unterharnscheidt, Higgins, 1969; Pudenz, Sheldon, 1946), sudden change in the intercranial pressure which is largely due to the linear acceleration (Zhang, Yang, King, 2001), sheer strain, stress/strain concentration (Ross et al., 1994; Holbourn, 1943), the product of stress and strain rate (Viano, Lovsine, 1999).

Evaluation Process When performing a biomechanical analysis, there are many factors about a collision that must be taken into account. Significant parameters of a collision that must be considered in these analyses include, 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 in a collision combine to form a singular, unique scenario. The per-

son performing the analysis must consider all of these factors together to determine what cumulative effect they had during the collision.

The overall procedure to perform the biomechanical assessment includes three separate steps – vehicle dynamics analysis, human body dynamics analysis, and human body tolerance analysis.

Less force transmitted to the occupant compartment of the vehicle means less potential for occupant injury. The transmission of forces throughout the vehicle is influenced by the physical deformation of its structural components and their energy absorption capabilities (Ziejewski , Anderson, 1996; Ziejewski, Goettler, 1996; Grosh, Hochgeschwender, 1989; Scharnhorst, 1988; Mahmood, Paluszny, Tang, 1988). Extensive experimental data is available in different databases (www.nhtsa.dot.gov, www.hwysafety.org, www.maceng.com).

Vehicle Dynamics Analysis When performing a specific vehicle dynamics analysis, one must first gather all necessary engineering data about the vehicles involved in the collision. Severity of the collision in engineering is typically assessed based on the extent of the physical damage to the structure of the vehicle. In a specific evaluation, automotive analyses have turned to numerical techniques to approximate the severity of the crash (EDCRASH). It is also important to look at the laboratory collision experiments that have been done on the vehicle type that was involved in the accident. While this kind of test is not available for all vehicles, it is important that the person conducting the analysis is familiar with the results of the available tests. From an engineering perspective a complete representation of the severity of vehicular structure includes parameters such as change in velocity, direction of impact, and duration of impact.

The results from this phase of the analysis are based entirely on engineering knowledge, engineering experience, and structural mechanics.

Once the severity of the impact is understood, one can move on to the next step, which is called human body dynamics analysis. This portion of the analysis relies entirely on biomechanical knowledge and experience.

Human Body Dynamics Analysis The most recognized parameters influencing the nature and the extent of human body response include: body position, gender, height, weight, and others. Body position at the time of impact has been identified as being very significant in assessing the likelihood of an injury (Yliniemi, Ziejewski, Perry, 2000; Ziejewski, et al., 1999; Ziejewski, Anderson, 1997). In medical literature it has been documented that “trivial trauma” sustained in an accident can result in an acute subdural hematoma. It has been speculated that bridging veins in the brain normally stretch 30%-35% before they tear; however, in the pre-loading state (i.e., abnormal body position), the veins may rupture with little force applied (Ommaya, 1995; Ommaya et al., 1994; Schneider, Reifel, Schneider, 1973; Chrisler, 1961). Another example is gender effect. It has been shown that for the same external force a female’s head exhibited significantly higher acceleration in comparison to males.

Head acceleration for a female in comparison to male has been reported up to 2 ½ times higher in a collision (van den Kroonenberg et al., 2002; Hell et al., 2002). Additionally, body proportion can affect how a seatbelt fits a person, or how a person fits into their vehicle. Height can affect how far a person’s head is from the BRAIN INJURY PROFESSIONAL

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headrest or how far a personâ&#x20AC;&#x2122;s knees are from the dashboard. A single anomalous factor can cause different injuries in an otherwise identical situation. For example, a difference in speed and/or the direction of impact can cause an increase or decrease in the severity of the injuries, as can a few inches difference in height or a few degrees 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 evaluate trauma. 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 that allow the user to include all relevant factors simultaneously.

It is impossible to experiment with human beings fitted with instrumentation under injury producing conditions. Human beings are only used on low-severity tests; that is, tests that are below human pain thresholds. These tests, limited by rigid regulations and guidelines, contribute to general knowledge on the human body non-injurious response. The human subjects are mostly young, well-trained, military volunteers (see Figure 2).

Their pain tolerance is usually much higher than that of the general population. Therefore, the test results are not representative of groups such as females, children, and elderly people. An advantage of the use of human volunteers is that the effect of muscle tone and prebracing on the dynamical response can be studied.

But this influence, which might be relatively large at low impact levels, simply cannot be extrapolated to higher impact levels.

A useful research tool to evaluate injurious biomechanical response is a human cadaver (also referred to as a PMHS: postmortem human subject). Disadvantages of the human cadavers are the absence of muscle tone and undeterminable physiologic responses. The age of cadavers is often high, and since the mechanical strength of most tissues in the human body tends to decrease with age, the data obtained are not necessarily representative of the general population.

Research using anaesthetized animals as human surrogates is vital to obtain information on physiologic responses in injury-producing loading conditions, especially for specific body areas like the brain. Furthermore, tests with animals can provide insight in the differences between dead and living surrogates and as such provide information for correct interpretation of human cadaver testing. However, due to differences between humans and animals, quantitative scaling and extrapolation of the results of animal testing to a human scale is difficult.

Mechanical models or crash dummies (also referred to as anthropomorphic test devices, or ATD) normally consist of a metal or plastic skeleton, including joints, covered by a flesh-simulating plastic or foam. They are constructed to be biofidelic; that is, the dimensions, masses, mass-distribution, and, therefore, the kinematics in a crash are as human-like as possible. An ATD is fitted with instrumentation to measure accelerations, forces, and deflections that correlate with the injury criteria for human beings. ATDs are often used in approval tests on vehicles or safety devices in which the measured values should remain below certain injury tolerance levels. An important objective during these tests is a repeatable response of the dummy in identical tests. The ATDs have been specifically designed for high-severity frontal impacts.

Therefore, its application to low severity impacts can result in significant inaccuracies. The comparison between human response and ATDs (such as the Hybrid III model) show a difference as high as five times for low severity frontal impact (see Figure 3).

Mathematical models can also simulate the behavior of human 28

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beings in a variety of impacts (Ziejewski, et al., 1999; Cheng, Rizer, 1998). Together with a mathematical description of the environment (e.g., the dimensions of the steering-wheel, dashboard, seat, and belts) and the impact conditions (e.g., vehicle deceleration), the model provides a numerical description of the crash event.

The advanced approach to trauma biomechanical requires an analysis based on brain deformation. The usefulness of this data is based on our understanding of the relation between the deformation of the brain and its physiological effects. Biomechanical brain modeling results are a case specific evaluation of the forces on the patient’s brain. The case specific components include gender, height, weight, body position, change in velocity, direction and duration of impact, and geometry of the brain that can be based on the MRI data of the person’s brain. The results from a biomechanical analysis indicating the location and the extent of the brain damage for case specific analysis can be compared to the results from the MRI, the PET scan and neuropsychological testing, thus providing the link between the medical diagnosis and the event of interest.

Additionally, biomechanical brain mapping can provide information about the time history at different intervals of a specific event that MRI and PET scans cannot. The ability to understand the time history of the brain deformation is important due to the viscoelastic nature of the brain tissue. For example, the time dependent characteristics of the brain tissue may indicate a significantly larger brain deformation due to the cumulative effect of consecutive multiple impacts (initial contact of the brain with the skull with a follow-up rebound effect) that one would expect from the analysis based on human head motion alone.

One can find an extensive amount of research work on the experimental as well as computational modeling of the brain tissue and skull. On the experimental part, efforts are being continued to find suitable mathematical models and material parameters. Galford and McElhaney (1970) attempted a series of relaxation tests performed in tension on monkey scalp specimens. As a result, the viscoelastic stress relation behavior for the monkey scalp was seen.

Low velocity animal experiments have been simulated using 3-D animal FE (Finite Element) model by Miller et al., (2000). On the computational side, the latest efforts on FEM nonlinear modeling the works of Brands et al., (2000 a, b) and Kleiven (2002) are referenced. An integrated experimental work to simulate the material and to determine the associated parameters in conjunction with the development of the computational schemes to employ and verify these experimental data into a mechanized FEM model should be pursued.

Finite elements computational methodology can be employed to determine this mechanical response during the impact provided one can solve the complications in material and geometry of the brain and also to express the proper nature of the impact loading.

Digital imaging has facilitated to a great extent the geometrical modeling, but lack of accurate material properties description by mathematical formulation is a big pursuit in this multidisciplinary research field. The interaction of the skull and the brain tissues is another subject to be explored more accurately. Without proper material modeling and the compatibility of interactions, the results would be still far from reality in many circumstances. Thus, the aim should still be focused on how to improve the constitutive modeling to accurately predict the dynamic behavior of brain tissues and skull during an impact.

Experimental research has shown that the brain tissues exhibit a type of viscoelastic behavior. It should be mentioned, that although nonlinear theoretical and computational modeling is a difficult task by itself, efforts should also be spent toward determining the associated physical and material parameters. The objective here is to focus on a highly nonlinear material modeling for brain tissue by assuming an incompressible, non-linear vis-

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

An example of case specific biomechanical modeling of brain injury as a result of head impact is given in Figure 4. The human brain model is based on MRI data, which is considered to be the most reliable geometrical representation of an injured person’s brain. The model is homogenous with typical brain material properties.

The acceleration components of the patient’s head acquired as a result of a case-specific computer simulation using the Articulated Total Body (ATB) program is shown in the upper right corner of Figure 4 (Cheng, Rizer, 1998). Different time frames were selected for different orientations to depict the maximum level of brain tissue deformation. The color-coding on the brain model indicates the force levels that correspond to the brain deformation scale. The corresponding stress distribution for several selected time frames at the specified elevation is shown in Figure 5.

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

Injury criterion is defined as a physical parameter or a function of several physical parameters that correlate well with the injury severity of the body region under consideration. Frequently used parameters are those quantities that relatively easily can be determined in tests with human substitutes such as the linear acceleration.

In conjunction with the injury criterion, the term tolerance level (or injury criterion level) is defined as the magnitude of loading indicated by the threshold of the injury criterion that produces a specific type of injury severity. It should be noted that there are large variations in tolerance levels between individuals. Tolerance levels for populations can therefore only be determined statistically.

The discussion of the specific numerical values for tolerance levels is beyond the scope of this article; however, there are numerous resources available for more information on the topic (see references Zhang et al., 2001; Newman, Shewchenko, Welbourne, 2000; Ziejewski, 1997).

Conclusion Trauma biomechanics can be an eminently useful tool for ER doctors and other medical professionals. By utilizing the results of a biomechanical assessment, medical professionals can gain a better understanding of impact conditions; thus, they have an increased ability to diagnose TBI at an early stage. However, the trauma biomechanics scientific community still does not know why some humans end up with brain injury from low-level acceleration while others can sustain high acceleration with no ill effects. The lethal combinations are not yet known (Zhang et al., 2001).

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

Address correspondence to: 111 Dolve Hall, P.O. Box 5285, Fargo, ND 58105, e-mail: Mariusz.Ziejewski@ndsu.nodak.edu.

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Overview of Computer-Assisted Cognitive Function Diagnostic and Assessment Tools

by Corinna M. Wildermuth, David W. Wright, M.D. and Michelle C. LaPlaca, Ph.D. In the United States, approximately 750,000 mild traumatic brain injuries (mTBI) occur every year.1 mTBI remains a serious public health and socioeconomic problem, resulting in long-term disability and death from secondary complications when not properly diagnosed.2,3,4 Diagnosing mTBI is difficult even in the best setting. The signs and symptoms of mTBI are often very subtle and difficult to detect. Undiagnosed or underdiagnosed mTBI leads to poor clinical management and can often cause cognitive deficits, psychosocial problems, and secondary complications such as depression.5 -14 Further complicating diagnosis is that in many cases mTBI is overshadowed by other injuries or by the events surrounding the injury.

Presently, cognitive deficits are determined using test batteries consisting of paper and pencil tests. These tests are considered the gold standard.15,16 However, conventional neuropsychological testing requires a quiet room void of distractions and the presence of trained personnel to administer, score, and interpret the results. In addition, these tests may require several hours to perform. In many situations, such as sideline assessment of concussion in sports, these requirements make standard neuropsychological testing difficult or impossible. Several efforts are underway to translate and transition these paper and pencil to computer-based tools. We briefly summarize products from various companies that have developed computer-based solutions, which are at various stages of development.

These computer-based solutions offer a wide range of advantages over the conventional pen and paper neuropsychological tests, including various components of the following: 1) ease of use and administration; 2) portability; 3) dramatically reduced testing duration; 4) potentially increased sensitivity for monitoring and detection of subtle cognitive changes; 5) minimized “learning effects” from repeat testing; and, 6) automated data analysis and testing results.

Based on our research, we discovered a variety of different computerized assessment tools in varying stages of development.

All of these assessment tools are based on computerized neuropsychological testing. We focus our discussion on the following products: CogState, Ltd. (AUS), Headminder, Inc. (USA), Cambridge Cognition Ltd. (UK), ImPACT Applications, Inc. (USA), CogScreen LLC (USA), Neuroscience Solutions Corporation (US), NuCog (AUS) and DETECT (USA). These assessment tools differ primarily on the comprehensiveness of the offered solution, the technology platform chosen, and the market segment targeted.

CogState

The CogState17 solution offers four distinct cognitive assessment tools. The first tool, called Cogstate, offers diagnostic products and engages in the development of therapeutics for early Alzheimer’s Disease (AD), mild cognitive impairment, and concussions from all causes. CogSport is designed to specifically 32

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

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

The test is available for download from the Internet and is administered on a computer, which can be a desktop or laptop.

Once the test is completed, an Internet connection has to be established and an encrypted data file is transmitted to the CogState server located at CogState Ltd., in Australia for the automated analysis of the test. The results are then returned to the test computer in the form of a pdf-report. The novelty and inherent benefits of this solution are: portability, it can be taken location-independent provided a computer and Internet connection are available; the remote testing can occur in close to real time (the actual testing is done offline and then requires an internet connect to transmit and obtain a test result) and allow for rapid and accurate assessment based on instant central comparison with prior baseline performance data; it is language and culture-independent through the use of familiar and universally known visual forms (playing cards) and; it does not require a skilled administrator.

Headminder

The Headminder18 solution consists of web-based neurocognitive and neurobehavioral tests. The solutions are primarily offered in two tracks: one is a customized research tool targeted at pharmaceutical and other research organizations and the other is an injury or illness-specific protocol. We focus here on the injury and illness-specific protocol that is available for four specific cases: screening and management for central nervous system diseases, cognitive-vocational management of at-risk populations, ADD/ADHD screening and medication management, and concussion management in sports settings.

An individual taking the computerized test registers its responses via the keyboard. The solution provided by Headminder combines on-line assessment and wireless technology with comprehensive reporting and records management.

The Headminder solution provides the following functionality: administration of on-line tests, availability of test taker information, generation of reports, administration of follow-up tests for longitudinal assessment of cognitive change, access to professional support documents. Tests have to be administered by qualified personnel and access to the internet is required.

ImPact

ImPACT19 is, an assessment tool primarily focused on the management of sports-related concussions and brain injuries. However, efforts to broaden the scope from sports-related brain injuries to all causes of traumatic brain injury are underway.

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

ImPact is currently used by a variety of users: professional sports leagues such as the National Football League, Major League Baseball, the Ontario Hockey League, professional racing teams amongst others, colleges and high schools sports programs, sports medicine centers, and neuropsychology clinics in several US states.

The benefits provided by ImPact are as follows. It can be administered by an athletic trainer or physician with minimal training. The test battery is set up in such a way that the stimulus array can be randomly varied in a near infinite number of ways to minimize the adverse effects of “practice”. The output of the ImPact test are individual scores for each test module as well as composite scores for Verbal and Visual Memory, Reaction Time, Processing Speed and Total Symptom Composite Score. A six-page clinical report presents these scores graphically and

Focus Areas

summarizes the other data points that were entered into the system for the individual case studies. The comprehensive reporting functionality allows for user-friendly extraction of the data.

Cantab

Similar to the other solutions reviewed, Cantab20 offers a computerized system for the assessment of different cognitive functions. The system is available for use in academic and commercial settings and currently boasts its use in over 400 universities and institutions in 26 countries.

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

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

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

Cogstate

Headminder

Impact

Cantab

Cogscreen

USC Virtual Office

Australia

USA

USA

UK

Australia

USA

pharmaceutical and medical device companies

pharmaceutical and other research organizations

sensitive to many central nervous system disorders

concussion management in sports settings (mTBI)

central nervous disease screening and management

cognitive screening with focus on aviation / aeromedical applications

Cognitive and functional impairments in adults (mTBI, Alzheimer's Disease)

Detection of early Alzheimers Disease

cognitive-vocational management of atrisk populations

Occupational Health and Safety environment

concussion management in sports settings (mTBI)

pharmaceutical clinical trials

DETECT USA concussion management in sports settings early detection of Alzheimer's Disease

early detection of Alzheimer's disease

ADD/ADHD screening and medication management concussion management in sports settings (mTBI)

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Reduced Learning Effects

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Increased Sensitivity to subtle Changes

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CogScreen

CogScreen is a scored cognitive-screening instrument administered using a computer. It is designed to rapidly assess the following functions: immediate and short-term memory, visual perceptual, sequencing, reaction time, simultaneous information processing and executive functions. At its origination, it was designed to meet the Federal Aviation Administration’s (FAA) need for an instrument that could detect subtle changes in cognitive functioning. As such, the applications offered by CogScreen are targeted predominantly at the aviation industry. This focus has been expanded to pharmaceutical research to assess the effects of pharmaceuticals on brain function.

The screening tools consist of a series of computerized cognitive tasks. Each of them is self-contained and presented with instructions and a practice segment. The aeromedical edition of CogScreen has the capability to produce a results report.

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USC Virtual Office

At the Integrated Media Systems Center (IMSC) at the University of Southern California (USC) researchers have developed an application in the field of user-centered sciences. The application consists of a head-mounted-device (HMD) delivered virtual reality (VR) system for the assessment and rehabilitation of cognitive and functional impairments in adults.

The scenes that make up the “virtual office” are HMD-delivered. Additionally, various performance challenges can be delivered via the computer screen (visual mode) and the phone (auditory mode). Utilizing these immersive 3D environments allows users 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 fully adjustable delivery of cognitive challenges and distractions, as well as the recording and storage of cognitive, motor behavior within a naturalistic, ecologically valid environment. Like all the other solutions mentioned in this article, it is fully laptop-deliverable, but adds the advantage of an immersive environment.

The USC Virtual Office22 application is currently used in initial clinical trials in the U.S. to test memory performance in individuals with brain injury, and an International Consortium of test sites is currently beginning clinical trials using the virtual office environment.

DETECT

DETECTTM23 is a cognitive assessment tool currently under development at Emory University and the Georgia Institute of Technology. Similar to the USC system, DECTECT incorporates one aspect that the other aforementioned solutions lack – immersiveness. The cognitive functions tested are information processing speed, working memory, work list learning and recall, as well as several variations of these tasks. The testing is designed to be completed in less than 15 minutes. The DETECT device is an integrated solution that is comprised of the software application, a portable computer, and a virtual reality headgear that totally immerses the individual within the test environment. In a usability study, it was found that there was no difference in test results obtained from DETECT in a quiet room versus a simulated noisy environment. The advantage of total immersion allows the device to be used on site, even in a noisy environment such as a sporting event. Therefore, this system has great potential for use as a side-line assessment tool for mTBI as well as application that require portability and ease-of-use.

There are a variety of other efforts under way to devise a neuropsychological assessment tool. Like the aforementioned ones, most of these solutions are software-based and aim to 34

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assess the cognitive functioning or impairment of the brain. For example, Neuroscience Solutions uses proprietary technology, sublicensed from Scientific Learning Corporation, based on established principles of “brain plasticity” to address neuropsychological disorders. NuCog is a cognitive assessment tool, developed by researchers in Australia, and is only available for limited use in research and clinical settings. We have tried to be complete in our briefing of cognitive assessment technology and look forward to the completion of these and related products.

In summary, mild cognitive decline that results from mTBI or degenerative diseases are often very subtle and difficult to detect. Frequently the mTBI is overshadowed by other injuries or by the events surrounding the injury. The need for rapid and simple diagnostic testing for early detection is immense. The gold standard for evaluating mTBI is neuropsychological testing.

However, neuropsychological testing requires a quiet room void of distractions and the presence of trained personnel to administer, score, and interpret the measures. In addition, these tests may require several hours to perform. In many situations such as sideline assessment of concussion in sports, these requirements make standard neuropsychological testing impractical. Several computer-based solutions are in development or in clinical testing and address many of the needs for fast, reproducible testing.

We feel that many of these solutions are feasible and the eventual point-of-care and application may vary depending on the type of deficit or setting. For sports assessment of mTBI, length of test, ease-of-administration, and immersiveness are the top three criteria. Based on this application, DETECT may offer a solution that combines many attributes of other systems, including ImPact and IMSC. It is important that the training and clinical teams associated with diagnosis and assessment of individuals with mild injuries recognize the need for improved tools and will utilize technology to ultimately choose the best course of therapy and improve functional outcome.

REFERENCES 1 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 insured population: 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 disability 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 impairment and 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, in Mild Head Injury, H.S. Levin, Eisenberg, Howard M., Editor, Oxford University Press; New York. p. 153-162, 1989.

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

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

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

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

13 Stambrook M, Moore AD, Peters LC, Deviaene C and Hawryluk GA. Effects of mild, moderate 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 in mild to moderate head injury: the predictive value of acute injury characteristics related to 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 of minor head injury. J Neurol Neurosurg Psychiatry, 1986. 49(11): p. 1227-32.

16 Leininger BE, et al., Neuropsychological deficits in symptomatic minor head injury patients after concussion and mild concussion. J Neurol Neurosurg Psychiatry, 1990.

53(4): p. 293-6.

17 Cogstate website www.cogstate.com accessed in December 2003.

18 Headminder website, www.headminder.com accessed in January 2004.

19 Impact website www.impacttest.com accessed in November 2003.

20 Cantab website www.bioportfolio.com/cantab accessed in November 2003.

21 CogScreen website www.cogscreen.com accessed in December 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 of DETECT.

ABOUT THE AUTHORS Michelle C. LaPlaca, Ph.D. is an Assistant Professor, Neural Injury Biomechanics and Repair Laboratory, Coulter Department of Biomedical Engineering, at Georgia Institute of Technology and Emory University. 313 Ferst Dr., Atlanta, GA 30332-0535, e-mail: michelle.laplaca@bme.gatech.edu.

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David W. Wright, M.D., F.A.C.E.P., is an Assistant Professor and Assistant Director of the Emergency Medicine Research Center, Department of Emergency Medicine, Emory University. He is a board ceritifed practicing Emergency Physician. He completed his residency at the University of Cinicinnati in 1997. He is a translational researcher, conducting NeuroInjury and Neurorepair research in both the basic and clinical sciences for 7 years. He is currently the Project Leader for a major NIH sponsered clinical trial in TBI. Corinna M. Wildermuth is currently working on MBA at the DuPree College of Management at the Georgia Institute of Technology from where she will graduate in May 2004. Since August 2002, Graduate Research Assistant with the Advanced Technology Development Center (ATDC), a high-technology business incubator at the Georgia Institute of Technology. In this role, she supports entrepreneurs with research pertaining to the business aspects of building a venture in the life sciences space. Her prior work experience has been with financial institutions and in the aviation industry with roles in marketing, operations and quality management.

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professional appointments

Occupational Therapist - Tree of Life Services, a nationally known program directed by Nathan Zasler, MD, is expanding and looking for an occupational therapist with experience in neurorehabilitation (especially acquired brain injury). Position is in an outpatient/community based setting including assisted living and transitional rehab programs.

Great opportunity for professional growth including diverse patient mix and speaking/publishing. Salary commensurate with experience.

Hours negotiable.Please e-mail resume to: abrown@cccv-ltd.com or fax to (804)346-1956 to the attention of Andrea Brown.

Physical Therapist - Tree of Life Services, a nationally known transitional/residential rehabilitation program directed by Nathan Zasler, MD, is seeking a full-time physical therapist due to program expansion. Experience in neurorehabilitation highly preferred. Must exhibit good interpersonal skills, great initiative and flexibility. Excellent opportunity to shine and grow as an active part of a comprehensive rehabilitation team. Highly competitive salary. Please e-mail resume to: abrown@cccv-ltd.com or fax to (804)346-1803 to the attention of Andrea Brown.

National Marketing Director - Learning Services seeks a marketing professional responsible for collecting/analyzing market data, employing resulting analysis to create individualized marketing strategies/marketing tools for Sales Reps. Compare/contrast Programs with competitors, identify/understand/articulate customer base, oversee marketing staff, assess new markets, assist Sales with identifying/evaluating contracting with national payers, insure Sales Staff armed with marketing tools/information. Travel required. E-mail resumes to: ltoomey@learningservices.com Vocational Specialist/Case Manager - needed immediately.Virginia NeuroCare, Inc. is a residential and outpatient facility for persons with acquired brain injuries. We serve the military and the general public.

We are located in historic Charlottesville, VA under the backdrop of

the beautiful Blue Ridge Mountains. Quality of life is excellent in this medium sized progressive and outdoor-oriented city. We are seeking a license eligible vocational counselor with case management experience and experience working with persons who have neurological injuries.

The qualified applicant should be positive, dynamic, flexible, and comfortable in a leadership position. The prospective employee will be responsible for counseling, job analysis and coaching, updating families and external case managers on a weekly basis, and coordinating discharge/disposition plans with patients, families, and external case managers. Caseload is low due to heavy demands for multitasking. The employee will work closely with a fun interdisciplinary team under the supervision of the Clinical Director, Dr. Babin. Excellent benefits.

Salary will be commensurate with experience AND demonstration of leadership ability, attitude, organization skills, and initiation. Send resume and 3-4 letters of recommendation (2 from supervisors or faculty) to Dr. Babin, Clinical Director, Virginia NeuroCare, Inc., 401 E. High Street, Charlottesville, VA 22902. Fax: (434) 293.2041, ph: (434) 984.5218, e-mail: Dr.Babin@vanc.org.

RNs and LPN's - Lakeview is a Specialty Hospital and Rehabilitation Center located in Waterford, Wisconsin. All shifts open with highly competitive salaries plus quarterly retention bonuses. A few of the benefits Lakeview offers: 17 days paid time off, 6 paid holidays, loan forgiveness program, health, dental, life and disability insurance, and a 401K retirement plan. For more information or to apply, contact: Lakeview Rehabilitation Center, 1701 Sharp Road, Waterford, WI 53185, (262) 534-7297, www.lakeviewsystem.com. EOE - JCAHO Accredited.

To list your professional appointments on this page, please contact Joyce Parker, (713) 526-6900, or by e-mail: jparker@hdipub.com.

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conferences

2004 MAY 6-8 – Traumatic Brain Injuries sponsored by Contemporary Forums in Tampa, Florida. Contact: (800) 377-7707, ext. 0, email: info@cforums.com, web: www.contemporaryforums.com.

20-23 – American Occupational Therapy Association 84th Annu al Conference & Expo. Minneapolis, Minnesota. Contact: (301) 652-2682, TDD: (800) 377-8555, web: www.aota.org.

JUNE 15-19 – Case Management Society of America’s 14 th Annual Conference and Expo. Gaylord Opryland Resort and Convention Center, Nashville, Tennessee. Contact: (501) 225-2229, e-mail: cmsa@cmsa.org, web: www.cmsa.org.

18-20 – The North American Brain Injury Society’s 1st Annual Professional Assembly, Ritz Carlton, Pentagon City, Virginia.

Contact: (703) 683-8400, e-mail: conference@nabis.org, web: www.nabis.org.

30-July 3 – Physical Therapy 2004: Annual Conference & Expo sition of the American Physical Therapy Association. Chicago, Illinois. Contact: (703)684-APTA, e-mail:svcctr@apta.org, web: www.apta.org.

23-25 – The Pacific Coast Brain Injury Conference. Vancouver, BC, Canada. Contact: (604) 944-2652, e-mail: info@pcbic.org, web: www.pcbic.org.

OCTOBER 6-9 – The Human Brain, Modeling and Remodeling, Fondazione IRCCSA Santa Lucie, Rome, Italy. Contact by e-mail: secretariat@thehumanbrain.org, or visit: www.thehumanbrain.org.

8 – The 5th Annual Conference on Brain Injury Managing Challenging Situations in Brain Injury Care. Bethesda Rehabilitation Hospital, Bethesda, Maryland. Contact: Lia Christiansen, (651) 232-2725, e-mail: lchristiansen@healtheast.org.

NOVEMBER 18-20 – Toronto ABI Network Conference, Exploring the Spectrum of Brain Injury: Sharing the Tools of the Trade. Toronto Hilton, Toronto, Ontario. Contact: Cora Moncada, (416) 5973422 ext. 3961, e-mail: conference@abinetwork.ca, web: www.abinetwork.ca.

17-20 – 24 th Annual Conference of the National Academy of Neuropsychology. Seattle, Washington. Contact: (303) 6913694, e-mail: office@nanonline.org, web: www.nanonline.org.

2005 SEPTEMBER 13-14 – 25th Annual Neurorehabilitation Conference on Trau matic Brain Injury and Stroke. Boston Marriott, Cambridge, Massachusetts. Contact: Donna Carr: (781) 348-2113, e-mail: donna.carr@ healthsouth.com, web: www.braintreehospital.org.

18-20 – The Annual Conference on Legal Issues in Brain Injury.

Ritz Carlton, Bachelor Gulch, Colorado. Contact: (703) 6838400, e-mail: conference@nabis.org, web: www.nabis.org.

MAY 5-8 – IBIA’s 6th World Congress on Brain Injury, Melbourne Exhibition and Convention Centre, Melbourne, Australia. Contact: +61 3 9682 0244, e-mail: braininjury@icms.com.au, web: www.icms.com.au/braininjury.

To list your professional event on this page, e-mail: conference@nabis.org

north american brain injury society supporters (through 1st quarter, 2004) Chairman's Council Julian and Kim MacQueen, Robert and Karen Voogt

Sustaining Member Thomas Keefe, Carlton Bennett Gordon Johnson, Joel D. Bieber, Dale K. Perdue, Bruce Stern, Mariusz Ziejewski

Conference, Corporate and General Supporters Law Office of Timothy Titolo, Brain Injury Law Center, Harrell & Johnson, P.A., Creative Capital, Vocational Economics, Charles Haynes, Michael Peitrzak, Margaret Roberts.

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Innovative options in supported living for persons with ABI Learning Services’ case managed community- • Supported community living integrated Supported Living Programs provide compassionate, specialized care for • Supported campus-based living persons with acquired brain injury and • Supervised independent living other neurological disorders.

• Behavior management

With program locations in nine states, Learning Services is one of the most trusted providers of brain injury care in America.

• Rehabilitation interventions • Day activity programming • Respite care

To learn more about our brain injury care programs nationwide, call 888.419.9955 ext. 12 or visit us on the web at learningservices.com Learning Services is the first brain injury care company in the nation to have Supported Living Programs accredited under CARF’s newly-developed Assisted Living Standards.

Several Learning Services’ Supported Living programs are accredited by CARF.

Learning Services Specialists in

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Acquired Brain Injury Care

At lanta, GA • Baltimore, MD • Charlottesville, VA • Cr eedmoo Atlanta, Creedmoo eedmoor,r, NC • Denver, CO Detroit, MI • Durham, NC • Madison, WI • Salt Lake City, U UTT • San Diego, CA • San Jose, CA

Titolo Law Office see Titolo Law Office CD

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