10


Linking Helmet Protection to Brain Injury

10.0 SUMMARY

The relationships between helmet deformation and brain injury are not well known. Most of the studies in biomechanical engineering and medicine are related to sports and vehicle collisions, and these investigations are based on a different range of stresses and stress rates from those encountered in the battlefield. The aim of this chapter is to present information on what is known, and the gaps, about the linkage between brain injury and current battlefield threats. The major finding is that helmet protection from penetration and backface deformation (BFD) greater than a particular value does not protect the brain from occurrence of many categories of tissue injury. Recommendations that can help focus research range from determination of the prevalence of reversible declines in hormonal function years after brain trauma to acceleration of research in computational modeling and simulation that can show shear stress fields associated with the known spectrum of threats and the protective capabilities of helmets.

10.1 INTRODUCTION

The transmission of stress to the brain from any substantial impact on the head can lead to traumatic brain injury (TBI). Acute brain injury, even mild injuries, may severely influence or restrict military operational capabilities, and long-term consequences will have an impact on individual quality of life.

The effects on brain function depend on the magnitude and direction of the force impacting the head. Therefore, it is important to understand linkages between blunt trauma and brain injury and how the helmet attenuates the effect of the impact (see Figure 10-1). For example, it is known that for lower severity ballistic or blunt inputs, the transfer of momentum and rate of change of momentum (force) from an impact can be sufficiently attenuated by the helmet to prevent brain tissue injuries. Thus, an understanding of brain tissue and brain physiological tolerance must be linked to the magnitude of the transfer of force or other mechanical parameters—from the impact to the helmet onto the head and into the brain.

For helmeted service personnel, nonpenetrating injuries may be caused by local contact of the deforming undefeated helmet onto the head/underlying skull or from more regional helmet/head contact with forces transmitted through the helmet webbing or padding to the skull (Bass et al., 2003). These forces may result in direct, local deformation of the skull and translation and/or rotation of the head, leading to brain injuries. Some mechanisms of brain injury, such as abrupt acceleration changes of the body due to an improvised explosive device (IED) blast or a paratrooper hard landing, are not necessarily attenuated by helmets, but the injury mechanisms are likely similar to injuries from blunt head trauma. Blast pressure stress from IEDs and artillery can directly or indirectly transmit pressure fields to the head that result in shear stresses in the brain (Panzer et al., 2012; Shridharani et al., 2012a).

The subject of this chapter is the right side of Figure 10-1. The committee presents what is known (and the gaps) about brain injury tolerances relative to current standards of helmet protection. This is an essential component in determining how much the helmet must attenuate the impact force to prevent brain trauma. Box 10-1 provides a glossary of terms used in this chapter.

10.2 BRAIN INJURIES

Types of Nonpenetrating Brain Injuries

Blunt trauma can lead to various types of brain injuries, ranging from concussion, hemorrhaging, hematoma (blood clots), skull fracture, anoxic injury (lack of oxygen), and diffuse axonal injury or DAI (damage to the brain neurons). Table 10-1 provides a listing of 13 major categories of brain injuries and potential causes.



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 70
10 Linking Helmet Protection to Brain Injury 10.0  SUMMARY injury and brain physiological tolerance must be linked to the magnitude of the transfer of force or other mechanical The relationships between helmet deformation and brain parameters—from the impact to the helmet onto the head injury are not well known. Most of the studies in biomechani- and into the brain. cal engineering and medicine are related to sports and vehicle For helmeted service personnel, nonpenetrating injuries collisions, and these investigations are based on a different may be caused by local contact of the deforming undefeated range of stresses and stress rates from those encountered in helmet onto the head/underlying skull or from more regional the battlefield. The aim of this chapter is to present infor- helmet/head contact with forces transmitted through the mation on what is known, and the gaps, about the linkage helmet webbing or padding to the skull (Bass et al., 2003). between brain injury and current battlefield threats. The These forces may result in direct, local deformation of the major finding is that helmet protection from penetration skull and translation and/or rotation of the head, leading to and backface deformation (BFD) greater than a particular brain injuries. Some mechanisms of brain injury, such as value does not protect the brain from occurrence of many abrupt acceleration changes of the body due to an impro- categories of tissue injury. Recommendations that can help vised explosive device (IED) blast or a paratrooper hard focus research range from determination of the prevalence landing, are not necessarily attenuated by helmets, but the of reversible declines in hormonal function years after brain injury mechanisms are likely similar to injuries from blunt trauma to acceleration of research in computational modeling head trauma. Blast pressure stress from IEDs and artillery and simulation that can show shear stress fields associated can directly or indirectly transmit pressure fields to the head with the known spectrum of threats and the protective capa- that result in shear stresses in the brain (Panzer et al., 2012; bilities of helmets. Shridharani et al., 2012a). The subject of this chapter is the right side of Figure 10-1. 10.1  INTRODUCTION The committee presents what is known (and the gaps) about brain injury tolerances relative to current standards of helmet The transmission of stress to the brain from any substan- protection. This is an essential component in determining tial impact on the head can lead to traumatic brain injury how much the helmet must attenuate the impact force to (TBI). Acute brain injury, even mild injuries, may severely prevent brain trauma. Box 10-1 provides a glossary of terms influence or restrict military operational capabilities, and used in this chapter. long-term consequences will have an impact on individual quality of life. The effects on brain function depend on the magnitude 10.2  BRAIN INJURIES and direction of the force impacting the head. Therefore, it is important to understand linkages between blunt trauma Types of Nonpenetrating Brain Injuries and brain injury and how the helmet attenuates the effect of Blunt trauma can lead to various types of brain injuries, the impact (see Figure 10-1). For example, it is known that ranging from concussion, hemorrhaging, hematoma (blood for lower severity ballistic or blunt inputs, the transfer of clots), skull fracture, anoxic injury (lack of oxygen), and momentum and rate of change of momentum (force) from an diffuse axonal injury or DAI (damage to the brain neurons). impact can be sufficiently attenuated by the helmet to prevent Table 10-1 provides a listing of 13 major categories of brain brain tissue injuries. Thus, an understanding of brain tissue injuries and potential causes. 70

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 71 Kinetic energy Helmet Pressure Deformation Momentum Acute Later Effects: Injuries: • Inflammation • Hemorrhage • Deposition of • Contusion protein • Diffuse aggregates (Tau, axonal amyloid) injury • Hypopituitarism • Intracranial • Behavioral pressure Issues FIGURE 10-1 Linkages between the force of the impact, how the helmet attenuates it, and resulting brain injuries. Many of these injuries are caused by differential motions/ Quasistatic compression as high as 50 MPa (7300 psi) or strains within the soft tissues of the brain. The motion of the more does not result in injury to mammalian cells (Grundfest, surface of the brain against the bony structures of the head 1936). Nerves and blood vessels are susceptible to stresses leads to tissue contusions, vascular tears, and hemorrhages. with strain tolerances usually less than 10 to 20 percent for Figure 10-1, editable These initiating injuries may degrade brain function through functional failure of neural tissues such as neurons/axons/ various mechanisms such as the restriction of blood supply or glia and probably less for some arterial networks (Margulies damage to cells. It is thought that compression (hydrostatic) and Thibault, 1992; Smith et al., 1999). alone is not an initiating cause of tissue injury unless it results The susceptibility of the brain to shearing forces, and in shear stress. (See Panzer et al., 2012, for results with high its very high incompressibility, may lead to contusions or rate blast impacts.) hemorrhaging at the surface of the brain. Rotational accel- eration and change in acceleration cause blood vessel rup- tures leading to bleeding between the brain covering (dura mater) and the skull with the result of increased intracranial pressure. Bleeding may also arise in the space between the TABLE 10-1 Categories of Brain Injuries dura mater and the brain (subdural hemorrhage). Injuries Categories associated with the rapid acceleration and deceleration of  1 Direct contusion of the brain from skull deformation or fracture the head result in forces that produce stretching and tearing  2 Brain contusion (including coup) from movement against interior of axons (causing DAI). Such strains and potentially large surfaces of the skull pressure or stress waves in small blood vessels can lead to  3 Indirect (countercoup) contusion from mechanical response of the small hemorrhages (petechial hemorrhages) deep within the brain opposite the side of the impact  4 Reduced blood flow due to infarction or pressure-based occlusion brain. Even when not life threatening, such injuries have the  5 Disruptive and non-disruptive diffuse axonal injury from shear potential for delayed injury, including local brain swelling, stresses as well as long-term consequences with symptoms persisting  6 Tissue stresses and strains produced by motion of the brain many years after the initial brain injury. hemispheres relative to the skull Important and frequently undiagnosed effects include  7 Subdural and epidural hematomas produced by rupture of bridging vessels between the brain and the dura mater alterations in microcirculation that can lead to hypoperfusion  8 Pressure-based rupture of small blood vessels leading to petechial or regional vasospasm with the result of inadequate delivery hemorrhages of vital metabolites to neural tissue. These mechanisms are  9 Strains beyond material tolerances of nerves and blood vessels believed to contribute to the short-term as well as long-term 10 Vasospasm resulting in diminished blood flow effects from ballistic helmet hits, head collisions, and expo- 11 Trauma induced hypopituitarism 12 Perturbations in brain biochemistry functioning with pathologic sures to high-intensity blasts. Other long-term effects from signs and symptoms long after the injury brain trauma may include declines in hormonal function 13 Temporary or permanent changes in visual, verbal, and motor related to disruption of the pituitary gland (e.g., growth hor- functioning

OCR for page 70
72 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS BOX 10-1 Glossary Blast Detonation of liquid or solid explosive material results in the generation of gaseous products in the pressure range of 150,000 atmospheres or 1.5 billion Pascals (1.5 GPa) and temperature of 3000 Kelvin. DTI Diffusion tensor imaging—a MRI method that maps the magnitude of water diffusion in different directions. The method gives a value of diffusion anisotropy (DA), which will decline if the normal orientation of fiber in white matter is disrupted by edema or tears, for example. Epidural hematoma Collection of blood from rupture of vessels between the brain dura mater and the skull. FEM Finite element modeling—a computational system that provides the means to simulate the effects of forces on structures such as the skull and brain tissues. fMRI functional magnetic resonance imaging—fMRI is similar to MRI, but the image gives information regarding blood flow changes in the brain after some stimulation. G or g Symbol for the acceleration of gravity magnitude of 9.8 m s-2. Hypopituitarism Dysfunction of the pituitary organ manifested by low secretion of hormones such as ACTH, growth hormone, thyroid stimulating hormone, oxytocin, vasopressin, etc. J Joule is energy or force times the distance over which force acts. It is the unit for kinetic energy defined as mass times velocity squared/2. kPa (kiloPascal) is a unit of pressure equal to a 1000 Pascals (10 kPa is 1 atmosphere of pressure). Momentum Defined as the product of mass and velocity. The rate of change of momentum is force. MRI Magnetic resonance imaging N Newton is the unit of force or the product of mass times acceleration. NHTSA National Highway Traffic Safety Administration. National Institute This standard, designated “0101.04” stipulates the maximum deformation a soft armor vest can undergo without of Justice Standard penetration is 44-mm as measured in a clay substrate after a live fire test of the armor. PET Positron emission tomography—an imaging method that uses radioactive tracers that specifically target proteins and other functions of the body. It differs from SPECT in the types of tracers used and the characteristics of the instrumentation. Pituitary organ A 7-mm diameter organ suspended on a stalk from the base of the brain into a well at the floor of the skull. It secretes 9 hormones into the bloodstream in response to stimuli from the hypothalamus also at the base of the brain. These hormones include growth hormone and thyroid stimulating hormone. Shear modulus The ratio of the tangential force per unit area to the angular deformation in radians. Strain The fractional change in a physical dimension of matter in response to stress. It is frequently given as a percentage (e.g., 5 percent) and can be over 100 percent. Stress The force per area or volume with dimensions of newtons per meter squared or Pascal. Stress waves Compression waves in a material due to an impulse or sudden load change.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 73 mone and thyroid function deterioration) and the occurrence of abnormal proteins in the brain years after trauma. Some data on injury thresholds exist for low-rate skull fracture, concussion, and diffuse axonal injury. But these have been derived from animal and human studies using experiences from vehicle collisions and laboratory experi- ments with stresses and rate of change of stress (i.e., strain rate) much lower than those associated with projectile and blast threats in the battlefield. Thus, a translation of these low-stress-rate data from animals, physical models, and mathematical simulations to the ballistic blunt trauma case is not expected to be reliable. As a consequence, design of protection from typical military threats is compromised FIGURE 10-2  Incidence of traumatic brain injury classified by because we do not know the injury thresholds. severity for warfighters. SOURCE: DoD Worldwide Numbers for A study by the Institute of Medicine found evidence for Figure 10-2, fixed Traumatic Brain Injury, http://semanticommunity.info/­ inary_at_ B association between TBI and various disorders that included LandWarNet_2011/Defense_and_Veterans_Brain_­Injury_­Center_ adverse social-functions, endocrine dysfunction, depression, Site_Map/DoD_Worldwide_Numbers_for_­Traumatic_Brain_­ aggressive behavior, and dementias for moderate or severe Injury. TBI (Ishibe et al., 2009). Further, concussion is no longer accepted as a threshold for diagnosis of potential brain trauma. Modern diagnostic methods reviewed in Appendix F 2006). During this period, 220,430 service members had show signatures of mild TBI (mTBI) unrelated to presence sustained TBI, with 169,209 classified as concussion/mTBI of concussion. (Kelly et al., 2012). In a study of 3,973 soldiers who served Once the acute medical events are treated, current clini- in Iraq, 23 percent percent had a clinician-confirmed history cal practice is not capable of effectively enhancing natural of TBI (Terrio et al., 2009). In a separate study, mTBI in recovery or diminishing long-term effects after the blunt soldiers deployed in Iraq was found to be strongly associated trauma (Giza et al., 2013). Thus, the best approach is protec- with posttraumatic stress disorder and depression (Hoge et tion from blunt brain trauma. This chapter presents relevant al., 2008). The deployment of magnetic resonance imaging physiological and biomechanical aspects of blunt trauma, methods to the evaluation of brain injury related to blast the state of knowledge regarding injury tolerances, and per- exposure of warfighters (Mac Donald et al., 2011; Yeh et al., spectives on detection of mTBI through noninvasive imag- 2013) can potentially provide a refinement in diagnoses of ing. Current noninvasive methods of brain injury detection brain injury in warfighters exposed to non-concussive blast are in Appendix F. Aspects of helmet design and the threat and blunt trauma events. However, in one study white matter characteristics are given in Chapters 2 and 3. injuries were not revealed by magnetic resonance diffusion tensor imaging (DTI) on veterans with mTBI, despite their symptoms of compromised verbal memory (Levin et al., Historical Data 2010). TBI can result from a number of events: falls, motor vehi- cle accidents, bicycle accidents, collisions, blast exposure, 10.3  HEAD AND BRAIN INJURY TOLERANCES and blunt head trauma in the battlefield. More than 5 million Americans alive today have had a TBI, and the associated Brain response and brain injury tolerances are not well medical care cost is around $56 billion per year in the United established for high-rate impacts such as those from BFD or States. Cognitive, communicative disabilities and social blasts (Bass et al., 2003, 2012; Rafaels et al., 2012). behavior abnormalities as well as medical complications, such as hormonal deficiencies that affect functioning of the Head Injury Tolerance Standards for Vehicle Collisions brain, thyroid, and gonads, are prevalent in survivors of TBI. Figure 10-2 shows the annual incidence of TBIs in war- Early work on low-rate blunt trauma brain injury toler- fighters during the period 2000-2011.1 It is likely that the ance (Gurdjian et al., 1966; Ommaya and Hirsch, 1971; Ono increasing numbers of mild and moderate TBI relative to et al., 1980) emphasized that acceleration of the head and the severe TBI may be partly attributable to greater awareness time duration of the acceleration are important parameters of TBI risk among military clinicians (Okie, 2005; Warden, for assessing injury severity (Prasad and Mertz, 1985). Such criteria are in wide use in the automobile impact community 1Armed Forces Surveillance Program information available at http:// (FMVSS-208, EuroNCAP), but the injury risk functions semanticommunity.info/Binary_at_LandWarNet_2011/Defense_and_ using these parameters have not been universally accepted. Veterans_Brain_Injury_Center_Site_Map/DoD_Worldwide_Numbers_for_ The most widely used criterion is known as the Head Injury Traumatic_Brain_Injury. Last accessed on January 31, 2014.

OCR for page 70
74 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS Criterion (HIC) severity index. Although it is widely used, it levels specified in these standards range from 150 to 400 g, is recognized as inadequate to fully explain brain injury out- with more recent standards tending to the 150 g peak limit. come (Versace, 1971). For military helmets, HIC and similar Studies of football impacts suggest that an acceleration concepts incorporating global skull rotational parameters standard of approximately 80 g should be used to provide (e.g., Newman et al., 2000) assume rigid body motion of the protection below the threshold for changes in menta- head/brain system and do not incorporate local deformations tion (Duma, et al., 2005). Other relevant results include: that may be crucial for assessing the injury potential from the Advanced Combat Helmet standard (CO/PD-05-04), ballistic impacts (Bass et al., 2003). which is based on the motorcycle helmet Federal Motor Some measures based on internal stresses and/or strains Vehicle Safety Standard-218 (49 CFR Sec. 571.218); and have been proposed as the injury criteria for the brain (e.g., the National Operating Committee on Standards for Athletic Stalnaker et al., 1971; Takhounts et al., 2003). However, Equipment and standards incorporating the International there is still no universally acknowledged criterion, and Standards Organization headforms. Virginia Polytechnic the situation today is much the same as that articulated by Institute’s star rating system for helmets2 involves extensive Goldsmith (1981): impact tests and risk analysis to establish a rating for com- mercial football helmets. Thus, the state of knowledge concerning trauma of the hu- These criteria are based, in part, on underlying assump- man head is so scant that the community cannot agree on tions that are not realistic, especially for military use with new and improved injury criteria even though it is generally ballistic protective helmets. The first is that the head acts admitted that present designations are not satisfactory. Mini- as a rigid body so that acceleration or some derivative may mally, there is an urgent need to differentiate skull fracture be correlated with injury and that head injury of any type is and mechanical and/or physiological damage to the central nervous system, with a replacement of a critical acceleration associated with skull fracture (Hodgson and Thomas, 1973). level for the former by a limiting stress value. Previous studies show a poor correlation between skull fracture and brain injury (Viano, 1988). For ballistic BFD In the past 30 years, experimental data and models have injuries, local deformations invalidate the rigid body assump- been accumulating from animal, cadaver, physical models, tion, and injuries seen from BFD are not well correlated with and computational modeling and simulation studies (dis- acceleration-based measures. cussed later in this chapter). With further research, these data and models can lead to injury risk evaluations such as those 10.4  BRAIN TISSUE INJURY: EXPERIMENTAL done for the risk of a skull fracture for 9-mm bullet impacts RESULTS to the helmet as detailed below. A goal is to determine the injury risk function for the major brain tissue injuries of Over the past 70 years, researchers have attempted to Table 10-1 relevant to militarily relevant injuries such as understand the relationships between head, skull, and brain those associated with BFD and blunt and blast neurotrauma. injury mechanisms and blunt trauma using cadavers, physical models, animals, and computer simulations. This has been Recommendation 10-1. There is an urgent need to establish stimulated largely by the automobile industry in an effort to stress and stress rate or other parameters as metrics for cat- improve vehicle occupant safety. More recently, sports inju- egories of brain tissue injuries from ballistic and blast-based ries have triggered international efforts to improve helmet head exposures. protection and to make measurements on human subjects involved in collision sports. Currently, there is no satisfactory experimental model that can produce the complete spectrum Nonmilitary Helmet Protection Standards of brain injuries that are seen clinically while also being suf- There have been major advances in blunt head protection ficiently well controlled and quantifiable for defining brain over the past 30 years. Some of these advances are be due injury tolerances. Some data do exist for the stress associated to widespread use of helmets in athletics and the subsequent with skull fracture, but this is only part of the spectrum of reduction in both frequency and severity of head and neck short- and long-term consequences of ballistic impacts to the injuries. Many improvements in helmet technology have fol- helmeted soldier, and the low-rate tests generally available lowed from the development of standardized test methodolo- may not be applicable to ballistic impacts. gies based on mechanical blunt impact injury criteria. The Advisory Group for Aerospace Research and Development Early Investigations of Mechanisms (AGARD) Report AR-330 lists 29 blunt impact test standards (AGARD, 1996), and each of these standards has some form In the early 1940s, investigators proposed that brain injury of translational impact acceleration limiting criterion. Of from skull fractures was from intracranial pressure. However, these standards, 19 are based on acceleration or force peaks physical studies using photoelastic models of the head dem- alone, and 10 are based on acceleration/duration levels. The 2Additional information is available at http://www.sbes.vt.edu/nid.php.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 75 onstrated that the likely cause of diffuse brain injury is from tissue strains induced by rotational acceleration of the head a. (Holbourn, 1943). This was confirmed by Gurdjian et al. (1955). The investigation of the relative roles of translational and rotational accelerations using more elaborate experimen- tal models of the subhuman primate led to the conclusion that diffuse injuries to the brain occurred only in the presence of head rotational motion (Gennarelli et al., 1972; Gennarelli and Thibault, 1989; Ommaya and Gennarelli, 1974). Diffuse brain injuries occurred at lower angular deceleration levels as the pulse duration increased (Gennarelli and Thibault, 1989). In coronal plane rotational acceleration, the critical shear strain associated with the onset of diffuse axonal injury was about 10 percent, and the rotational acceleration threshold for severe diffuse axonal injury was about 16,000 rad/sec2 (Margulies et al., 1990). Inertial loading alone to the head can cause DAI, which is an important cause of fatality or late onset of disabilities due to head injury (Gennarelli et al., 1972). Modern Experimental Investigations of Injury Criteria To simulate the impact response of the human, the auto- motive industry developed the Hybrid III 50th Percentile Male anthropometric test device (ATD) in the early 1970s. Originally developed by General Motors, the ATD is now b. regulated by the National Highway Traffic Safety Admin- istration (NHTSA) in conjunction with the committees from the Society of Automotive Engineers. It has become a validated tool for the evaluation of automotive impacts Figure 10-3 fixed and can accommodate a wide range of instrumentation and transducers. It is also robust enough for repeated ballistic experiments (Bass et al., 2003). A collaborative effort between Natick laboratories, DRDC-Valcartier, and the University of Virginia (UVA) led to the development of a ballistic version of the Hybrid III head augmented with impact pressure sensors (Bass et al., 2003). The UVA headform is shown in Figure 10-3a. Instrumentation for the Hybrid III head and neck region consisted of three linear accelerometers and angular rate sensors at the center of the ATD headform and six-axis upper and lower neck load cells. Using the Hybrid III headform modified to accept surface pressure sensors, the pressure measurements at various locations were recorded, analyzed, and compared to human cadaver results (e.g., Bass et al., 2003). Injury metrics assessed using this head- form include force/pressure, the HIC injury criterion, and the National Institute of Justice Neck Injury Criteria. The force/pressure results correlated well with injury in the paired cadaver model, while HIC was poorly correlated with injury. This concept has been recently modified in a rigid headform with regional loadcell sensing under the FIGURE 10-3 (a) The University of Virginia’s Hybrid III head ballistic impact by Biokinetics (Figure 10-3b). model used for laboratory simulations and measurements. (b) Bio- kinetics headform variant of the Hybrid III headform for ballistic impact. SOURCE: Courtesy of Biokinetics and Associates, Ltd.

OCR for page 70
76 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS Brain Injury/Concussion Risk/Thresholds Modern Football Helmet Instrument Data versus Concussion Symptoms Concussion is a symptom of the state of awareness or consciousness and is not a category of pathological brain In the early 1970s, head-bands of suspension-style foot- tissue injury. The linkage between a diagnosis of concussion ball helmets were instrumented with an accelerometer and and a specific brain injury has been the subject of controversy electroencephalogram system (Moon et al., 1971; Reid et al., among neurologists and neurosurgeons since the mid-1920s 1974) that allowed records from a single player at a time. (Saucier, 1955). For example, one cannot say to what extent Around 2000, hockey and football helmets were instru- structural damage, such as vascular ruptures or neuronal mented with three-dimensional accelerometers, and these strains, cause loss of consciousness. What have been defined measurements gave an average of 29 g from 158 impacts experimentally are the relations between stress and animal from high school athletes with no observed symptoms of consciousness over a limited range of stress rates that have TBI. Addition of video analysis and dummy reenactments not included the rates associated with a high-velocity, ballis- allowed laboratory simulations and measurements of head tic, nonpenetrating hit to a helmet. The threshold for concus- acceleration, although there are substantial limitations in sion increases as the duration of impact decreases (Guardjian inferring accelerations directly from video (Newman et al., et al., 1955). See Table 10-2 for the median concussion levels 2005; Pellman et al., 2003). Velocities and changes in veloci- trauma given in dimensions of energy, power, and pressure. ties were interpreted from video recordings, and threshold The criteria for concussion in the animal laboratory stud- values for concussion were given based on analyses simulat- ies reflected in most of the studies of Table 10-2 are much ing the video impacts with the Hybrid III dummy headform. different from concussions diagnosed in sports, vehicle col- These studies did not clear up potential distinction between lisions, falls, and battlefield events. The majority of concus- injuries from rotational and translational accelerations sions do not result in a loss of consciousness. In particular, (Genarelli and Thibault, 1989; King et al., 2003). But it is for sports injuries, a concussion is diagnosed if the athlete is important to note that: (1) purely translational or rotational confused, complains of dizziness, headaches, blurred vision, accelerations of the head are not likely for a head tethered or sensitivity to light, sound, or odors or by the physical signs to the inertial mass of the body (King et al., 2003); and (2) of motor coordination dysfunction (cf. Appendix F). Ninety- even purely translational acceleration of the head produces five percent of high school football concussions did not rotational behavior in the brain tissue, and purely rotational involve loss of consciousness (Meehan et al., 2010). In the excitation of the brain produces local translational behavior battlefield, a diagnosis of mTBI or equivalently “concussion” in the brain tissue. Thus, the debate regarding the severity involves a protocol called Military Acute Concussion Evalu- of rotational acceleration versus translational acceleration ation (MACE). This examination is given as soon as possible brain trauma is largely artificial and is based on a rigid body after a warfighter has been exposed to blast, projectile blunt view of the head. trauma, or vehicle collision. It measures orientation, recent Actual measurements of direction and magnitude of memory, concentration, and memory recall. head accelerations football players receive became avail- able when sensors and telemetry units were provided to multiple players using an in-helmet 6-accelerometer system TABLE 10-2 Brain Injury Criteria and Median Values for that transmits data via radio frequency to a sideline receiver Concussion for Low-Rate Blunt Impact and laptop computer system (Duma et al., 2005). Using this Brain Injury Median Values commercial system, a risk of sustaining a concussion for a Criteria for Concussion Source given impact was derived from data collected from 63,011 impacts including 244 concussions (Rowson and Duma, Energy 22-24 J Denny-Brown and Russell (1941) 2013). Both linear and rotational accelerations as well as the combination of linear and rotational accelerations were used Power 13 kW Newman et al. (2000) in the derivation of a concussion risk function. The predictive Strain 0.2 Bain and Meaney capability of linear acceleration was about the same as that (2000); Morrison et al. for the combined probability. (2003)a A study of the linkage of impact severity was done on high Strain x strain rate 30 s-1 Viano and Lövsund school football players using cognitive tests and magnetic (1999) resonance imaging (MRI) before and after two seasons of Stress (von Mises) 6-11 kPa Shreiber et al. (1997) football while wearing accelerometer instrumented helmets Cumulative strain 0.55 Takhounts et al. (2003) (Breedlove et al., 2012). A relationship was found between damage measure the number of impacts and cognitive tests and the number Strain energy density 0.8-1.9 kJ/m3 Shreiber et al. (1997) of hits and functional MRI changes (see also Talavage et Pressure 173 kPa Ward et al. (1980) al., 2013). It is expected that an expansion of these types of study will improve the development of head injury criteria a Strains less than 0.15 can cause diffuse axonal injury.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 77 and clinical evaluation techniques as well as enhance return- Skull to-play decision making. Strain Sensors Force/Strain Military helmet sensor instrumentation programs in the Sensors at Impact Site Intracranial United States were initiated in 2008 in order to collect battle- Strain Sensors field data that could then be used by medical epidemiologists as well as design and manufacturing communities to improve Acoustic design. These data should help significantly in the quest to Crack Sensor Neck Potting understand the linkages between stresses on the helmet and Cup Oral Head brain injuries. Accelerometers Neck Load Cell Neck Load Cell Skull Fracture Intracranial Pressure Sensors Modern ballistic protective helmet materials (McManus et al., 1976; Carey et al., 2000) can deform sufficiently so FIGURE 10-4 Instrumented cadaver head. SOURCE: NRC (2012). that the backface of the helmet contacts the head, potentially causing head injuries (Bass et al., 2002). Potential injuries fracture tests, the calculated injury assessment value was include both depressed and long-linear skull fractures and well below the usual low-rate blunt trauma injury reference closed-head brain injuries. Substantial work has been done value. Further, there was no obvious association of accelera- on skull fracture injury, especially at low rates, but most of tion-based responses to the occurrence of BFD and fracture. it is not directly applicable to military helmet injury criteria. This study developed injury criteria for both test round Skull fracture is a measure of head injury that can be velocity and cadaver peak-impact pressure. For this injury related to the forces applied and thus can provide one of risk function, there is a 50 percent risk of skull fracture for the needed links between level of protection and threats. a peak impact pressure of 51 MPa as measured by the force/ But most of the existing measurements are restricted to low strain instrumentation (Figure 10-4). Using a simple velocity velocities and large impact areas (Yoganandan et al., 1995; correlation between the dummy and cadaver, a dummy injury Bass and Yoganandan, 2013) and have limited relevance to risk function is developed that has a 50 percent risk of skull the goal of linking battlefield threats to required protection fracture for dummy peak impact pressure of 15,220 kPa. for head and brain injury protection. This injury risk function may be used with a general helmet Whatever is known is based on cadaver measurements and the Hybrid III dummy discussed earlier in this section. of skull fracture and recordings from internally placed pres- Automobile injury criteria, including the HIC, were not sure sensors and accelerometers. The mechanical properties found to be a good predictor of cadaveric injury. Skull frac- of stiffness, force deflection, and energies to fracture were ture from ballistic BFD is an intrinsically high rate event. measured on 12 unembalmed cadaver skulls (Yoganandan et Energy is deposited locally, and local skull deformations al., 1995) at low rates typical of blunt trauma from conven- are significant. Use of HIC requires essentially rigid body tional falls and vehicle crashes. Impact loading at 7 to 8 m/s motion of the head at relatively low rate compared to bal- revealed failure loads of 6.4 kN (±1.1) and energies averag- listic events. ing 33.5 J (±8.5). Quasistatic loading at 2.5mm/s showed failure at 12 mm (±1.6). Variability was great in all param- Finding 10-1. Most of the experimental work that links eters with, for example, a range of stiffness of 467 to 5,867 brain injury to blunt trauma is related to vehicle collisions N/mm. Delye et al. (2007) found skull fracture energy level and football collisions. The data from these studies are not in the range of 22 to 24 J for dynamic loading of the cadaver directly relevant to BFD and blast TBI because the rate of head having one degree of freedom. A human cadaver study momentum change is higher and contact times shorter for of fracture thresholds for 37-mm diameter projectiles of 25 military TBI situations. to 35 g gave force values of 6 kN for the forehead, 1.9 kN for the mandible, and 1.6 kN for the zygoma (Viano et al., 2004). Impact stress values for the adult skull are given as Brain Intracranial Pressure and Edema 43 MPa (Ommaya et al., 2002) and are age and size related. Symptoms from intracranial pressure (ICP) increases can Two series of ballistic impact tests used human cadaver be acute and an immediate consequence of the stress wave heads with protective helmets (Bass et al., 2003). These tests from blunt trauma to the brain or transmitted pressures from used UHMWPE helmets with 9-mm full-metal-jacket test trauma delivered to remote parts of the body. The experimen- rounds under various impact velocities to 460 m/s (1,510 tal data that link ICP elevations to blunt trauma to the surface ft/s). Measurements taken from cadavers with and without of a helmet or surrogate protective material come from a skull fracture show no correlation with existing blunt trauma limited number of experiments that used live animal models, injury models based on the Wayne State Concussive Toler- cadavers, and physical models (Engelborghs et al., 1998; ance Curve or similar concepts, including HIC. For the skull

OCR for page 70
78 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS Shridharani et al., 2012b; Rafaels et al., 2012; Sarron et al., 2004). The models differ in characteristics, and the ballistic trauma mechanism varies from dropping masses from vary- ing heights in order to vary the velocities of projectiles (e.g., 9-mm rounds from 300 to 800 m/s). These types of data can be used to extrapolate a threshold for ICP elevation versus armor characteristics and threat velocity. Although there are limitations in animal model biofidelity with human skulls, these types of experimental data are needed to better assess brain injury tolerances and risk levels for defined threats. Some models, although illustrative of the sequence of events after brain trauma (e.g., occurrence of edema, blood brain barrier changes, ion concentration variations), are difficult to interpret relative to the ballistic threats and even collision impacts as they use impactors systems of low velocity (3m/s) and poorly or undefined energy or force metrics (e.g., Cernak et al., 2004). FIGURE 10-5 Thresholds for diffuse axonal injury based on non- Brain Shear Stress and Diffuse Axonal Injury human primate rotational acceleration experiments and scaling through computational modeling to human brain masses of 500 g Diffuse brain injury from low-rate traumatic impacts to (thick solid curve), 1,067 g (solid curve), and 1,400 g (dotted curve). Figure 10-5, fixed the head results in both destructive and nondestructive axo- Regions to the upper and right of each curve are regions of diffuse nal injury. Destructive axonal injury was first described for axonal injury. SOURCE: Reprinted from Margulies and Thibault cases of collision-based injuries leading to limited periods (1992) with permission from Elsevier. of survival with autopsy findings of disrupted white mat- ter tracks and normal grey matter (Strich, 1956, 1961). It is unknown whether such injuries can arise from ballistic BFD. Morphological studies of axonal injuries using non- human primates subjected to head acceleration have shown that shear forces create varying degrees of axonal damage, occurs when neuronal axons are stretched by more than including fragmentation. Nondisruptive or reactive axonal about 20 percent. The results from simulations presented injuries manifest over long time periods and are ascribed to in the discussion of modeling and simulations later in this axonal membrane damage. It is now recognized that animal chapter show maximum strain levels of 14 percent and lower models do not reflect the spatial and temporal patterns of (from 9-mm rounds) at 360 m/s striking helmets (Aare and axonal injury in human brains (Maxwell et al., 1997; Bain Kleiven, 2007). However, it is not clear if these thresholds and Meaney, 2000). are safe for injury effects that might manifest years after Margulies and Thibault (1992) is one of the most detailed the injury. experimental and modeling studies relative to thresholds of The threshold for nondisruptive axonal damage of 15 brain injury, and it showed that a combination of a peak rota- percent has been suggested by Maxwell and associates tional acceleration of more than 10 krad/s2 and a peak change (Maxwell et al., 1997). But it is not clear that the 15 percent in rotational velocity of more than 100 rad/s causes diffuse strain criterion should be an important benchmark, because axonal injury. These criteria are proposed to be valid only tissue tolerance of the hippocampus and brainstem might be for pure rotational accelerations, but the experimental model much lower, and the strain criteria are expected to be stress- incorporates translational accelerations about the brain center rate dependent. Computational models and simulations of gravity and the effect of these accelerations is uncertain. can explore the structural strains of simulated brain tissues Lower injurious risk levels for rotational acceleration were related to physical variables of a ballistic or blast impact proposed by others (Ueno and Melvin, 1995; Meaney et al., (e.g., acceleration, stress rate, stress duration, etc.). But an 1995). Thresholds for human brain injuries from Margulies important point is the understanding that nondestructive and Thibault (1992) are shown in Figure 10-5. axonal damage can be the major cause of the high prevalence Animal studies, physical model experiments, and analyti- of posttraumatic stress syndrome months and years after cal model simulations have been employed to determine the brain trauma. critical tolerances in terms of strain (relative elongation) and A summary of the current status of mechanisms, symp- deterioration in function (Gennarelli et al., 1972; Lewis et toms, and possible treatments of DAI is now available from al., 1996; Bain et al., 2001). Based on animal studies, the the May 2011 workshop hosted by the National Institute of strain tolerance for frank axonal injury that may lead to DAI Neurological Disorders and Stroke (Smith et al., 2013).

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 79 Biological Response of Cells Exposed to Mechanical linear and angular accelerations of 1.5 g and 120-140 rad s–2, Forces respectively. These accelerations are orders of magnitude less than those associated with concussions. Small displace- A key aspect of defining tissue tolerances is to describe ments were found in regions having brain-skull connections. the pathophysiological activation of cellular biochemical Strain fields seen in this study exhibited significant areas with cascades that produce delayed cell damage and death. This maximal principal strains of 5 percent or greater at these can be accomplished by measurements of the consequences low experimental accelerations. Simple head flexion causes of mechanical injuries on living brain tissue through observa- cerebellum rotation of a few degrees and a downward motion tions of cell viability and tissue biochemical changes using a of up to 1.6 mm of the brain stem (Ji et al., 2004). tissue culture model of rapid stretch induced injury (Ahmed et al., 2000) or pulse pressure pulse exposure TBI (Morrison et al., 2003). Stretch-induced injuries associated with about Hemorrhage: Petechial Disruption, Subdural Hematoma, 30 percent strains alter mitochondrial membrane potential and Epidural Hemorrhage and cellular bioenergetic molecules, as shown by chemical There are three principal types of internal vascular dis- assay methods applied at various times after injury (Ahmed ruptions from shear stresses and rotational accelerations et al., 2000). Strains and strain rates can be precisely applied that cause shear strain on small and large blood vessels and and responses measured by fluorescent imaging and immu- lymphatics: petechial, subdural, and epidural hemorrhages. nostaining, including cell death quantification (Morrison et Petechial hemorrhages can occur throughout the brain al., 2003). Cellular energy metabolism perturbations have and give evidence of shear strain as well as a pressure-based been shown through standard molecular biology studies disruption of capillaries and arterioles. The pressure can be using in vitro and in vivo shock tube models of blast-induced from a remote stress such as a blunt trauma to any part of TBI (Peethambaran et al., 2013). Blast exposures resulted the body and possibly from blast stresses of high intensities in significant decreases in neuronal adenosine triphosphate (NRC, 2012). These hemorrhages appear as blood extrusions levels at 6  post-blast that returned towards normal levels h of a millimeter or less in diameter in the midbrain, but they by 24 h. can be extensive throughout the brain. They are not recog- nized as a clinical entity unless they disrupt sensory or motor Finding 10-2. There are no data on axonal injuries from functions of the brain. But they can cause some compromise backface deformation. Also, currently there is no method to of brain function and perhaps play a role in progressive brain detect if diffuse axonal injury has occurred from head trauma deterioration. They can be detected by high-field MRI if the in the battlefield. proper MRI pulse sequence is used. Subdural hemorrhages leading to subdural hematomas occur in the space between Recommendation 10-2. Methods including blood sampling the dura (the outer cover over the brain) and the arachnoid and brain imaging should be explored for feasibility of early space. detection of diffuse axonal injuries. Epidural hemorrhages are bleedings from ruptured vessels between the skull and the outer layer of dura. The build-up Evidence for Differential Motion of the Brain and Skull of blood causes an increase in pressure within the intracra- nial space, with subsequent compression of brain tissue and A mechanism for many consequences of rapid accelera- obstruction of the flow of blood and cerebral spinal fluid. tions and decelerations is the shearing caused by differential This is associated with particularly serious brain injury motion between the skull and local brain tissue. Typical because 15 to 31 percent of patients die of the injury (Leitgeb injuries include contusions and meningeal hematomas seen et al., 2013). in automobile accidents. The first definitive study of brain motion after a traumatic skull impact was done on live sub- human primates using a Lucite cover over the skull vertex. Pituitary/Hypothalamus Damage Blunt trauma was applied by a pneumatic impactor, and The pituitary gland is a pea-sized gland suspended from observations were made with cinephotography (Pudenz et a pedicle at the base of the brain. It is surrounded by a skull al., 1946). These authors also provided a detailed review of base bone structure whose saddle-shaped structure is known theories and observations from the late 1800s regarding brain as the sella turcica (Figure 10-6). This gland secretes nine motion as well as contusion and hemorrhage mechanisms. hormones, some of which control the secretion of other hor- Although experimental studies demonstrate motion mones that are vital to growth and metabolism and whose between brain and skull, little data exist regarding the base of dysfunctions have been related to disorders beyond metabo- the skull. Experiments on human subjects used MRI tagging lism, including behavioral and affective disorders. Pituitary techniques to show that the brain rotates relative to the skull gland dysfunction has been inferred from the occurrence (Kleiven and Hardy, 2002). Relative brain-skull displace- of hypopituitarism in victims of head injury from low-rate ments of 2 to 3 mm in some areas of the brain for induced impact.

OCR for page 70
80 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS FIGURE 10-6 Left: The base of the human skull supports the bottom of the brain and the brain stem that descends through the large orifice in the center known as the foramen magnum. Right: Positron tomography of the uptake of ammonia- 13N in the normal pituitary. SOURCE: (Left) Im- age provided courtesy of member Tom Budinger. (Right) This research was originally published in JNM. Xiangsong, Z., Y. Dianchao, and T. Anwu. Dynamic 13N-Ammonia PET: A new imaging method to diagnose Hypopituitarism. Journal of Nuclear Medicine. 2005;46:44-47. Copyright by the Society of Nuclear Medicine and Molecular Imaging, Inc. Chronic hypopituitarism, defined as deficient produc- Recommendation 10-3. Modeling and simulation studies tion of one or more pituitary hormones at least 1year after should incorporate the biomechanics of blunt brain trauma injury, occurs in 40 percent of subjects who have sustained that affects the pituitary organ in the base of the brain in Figure 10-6, fixed blunt brain trauma (Bondanelli et al., 2005). In contrast, the order to determine injury thresholds and tolerances for blunt prevalence of hypopituitarism in the general population is trauma and for ballistic backface injuries. estimated at 0.03 percent. As the hormones released from the pituitary are triggered by events in the hypothalamus, one Recommendation 10-4. The medical community should cannot be certain of which tissue has been damaged. Growth institute a data collection program to determine the preva- hormone decreases develop in 15 to 20 percent of patients lence of hypopituitarism in warfighters relevant to ballistic with complicated mild, moderate, or severe TBI and are and blast blunt trauma with appropriate warfighter controls. associated with symptoms of posttraumatic stress disorder (Kelly et al., 2006; Powner et al., 2006). About 15 percent of There is high prevalence of pituitary hypofunction in TBI patients develop gonadal hormone deficiencies, and 10 brain trauma from all causes. The recent discovery of low to 30 percent of them develop hypothyroidism. After brain levels of pituitary hormones in TBI soldiers, coupled with trauma, the short-term decline in hormones can recover in the known replacement treatments for this disorder, mean some cases, but there is a high prevalence of long-term defi- that the medical community should launch a broad program ciencies after severe TBI (Leal-Cerro et al., 2005; Agha et of long-term periodic tests for veterans of head and blast al., 2004). Chronic adrenal failure can occur because of low injuries. adrenocorticotropic hormone secretion from the pituitary in TBI patients. Neurobehavioral Effects from Traumatic Brain Injury Most studies found the occurrence of posttraumatic hypopituitarism to be unrelated to injury severity. In the The linkages between the severity and frequency of blunt past 2 years, researchers have found that about 42 percent brain trauma to various physical injury classifications listed of veterans with blast injuries showed abnormally low levels in Table 10-1 are the topics emphasized in this chapter. But of at least one of the pituitary hormones (Wilkinson et al., there is another classification associated with brain trauma 2012). Some veterans had abnormal levels of vasopressin and that has an association with TBI from all causes. Neu- oxytocin, and these hormones are linked to psychological robehavioral changes include the specific neuropsychiatric or behavioral abnormalities. It is not clear if this applies to syndromes of depression, mania, psychoses (e.g., paranoia ballistic BFD impacts. and obsessive compulsive disease), aggressive behavior, and Blood tests, some of which are complicated, can assess personality changes as well as cognitive decline. The causal pituitary function. Positron emission tomography (PET) associations have been debated for 100 years since the early (Figure 10-6) and MRI, discussed in Appendix F, can papers on shell shock and also more recently because of the noninvasively image metabolic function and structural prevalence of psychiatric symptoms in veterans from wars of abnormalities of the pituitary. MRI and PET can visualize the past 70 years. Clear evidence of a causative relationship anatomical and metabolic changes, respectively, as presented between negative neurobehavior and brain trauma has arisen in Appendix F. in the past few years from pathological studies on athletes who have sustained TBI. Yet, despite some continuing skepti-

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 81 cism about the lack of objective studies, there is compelling This section of the chapter, on linkages between a bal- evidence for associations between both behavioral and cog- listic or blast threat and brain injury, is directed toward the nitive disorders and TBI. From the vast literature of reports important role of computational models, as it is through this of psychiatric and cognitive evaluations of TBI subjects, two tool that one can equate needed protection from brain injury cited below have measures of the prevalence. to helmet design. One principal value of M&S in human Depression, anxiety, and low self-esteem were the prin- injury biomechanics is its ability to obtain information in cipal disabilities in half of 360 head-injured individuals situations in which it is fundamentally impossible to conduct evaluated from the group who had survived for 7 years after in vivo tests on the actual system (the human), although an initial head injury (Whitnall et al., 2006). Another study postmortem testing is possible using human cadaver tests. showed the prevalence of depression is 6 to 39 percent with This approach may be supplemented by in vivo testing in mTBIs (Schoenhuber and Gentilini, 1988). animal surrogates to understand force effects on the human Cognitive impairments 10 years following TBI were body and possible ways to mitigate them. There are cases in found to be associated with injury severity using tests of which this approach has provided useful insights into injury attention, processing speed, memory, and executive func- biomechanics such as blast lung injury criteria (Bass et al., tion (Draper and Ponsford, 2008). Even mTBI patients may 2008) and to develop test equipment for vehicle collision perform worse than controls on some tests of reasoning tests against tissue injury criteria. However, as discussed in (Borgaro et al., 2003). Long-term effects of mild head injury this report, in the particular case of military helmets, evalu- approximately 8 years post injury included complex atten- ation and acceptance protocols are based exclusively on tests tion and working memory defects (Vanderploeg et al., 2005). that use head surrogates with poor biofidelity. Early-onset dementia in particular is frequently associated It is therefore clear that M&S can play a significant role with head injury history (McMurtray et al., 2006). Repeated both in improving understanding of injury biomechanics and concussions have been linked to dementia (Guskiewicz et in guiding the design of protective systems with enhanced al., 2005) and chronic traumatic encephalopathy (McKee injury mitigation performance. Analytical approaches et al., 2009). include mathematical modeling and computer simulations using advanced constitutive models and coupled fluid-solid Finding 10-3. An increased prevalence of neurobehavioral mechanics. In the past, these approaches have been chal- abnormalities has been confirmed from many scientific lenged as inadequate because of limitations in the fidelity evaluations of individuals involved in TBI incidents. of the computer simulations, realism of the tissue material properties, and the lack of validation. 10.5  COMPUTATIONAL MODELING AND SIMULATION Computational Simulations of Brain Injuries from Blunt Computational modeling and simulation (M&S) has long Trauma been considered an invaluable tool for analyzing engineering systems in a wide range of technology areas. Recently, M&S Ten years ago NHTSA developed a Simulated Injury has also been used effectively in the broad field of injury Monitor (SIMon), based on a finite-element head model. biomechanics and to a limited extent in the evaluation and This tool uses vehicle-dummy-head kinematics as an input design of force protection systems. and estimates the probability of three types of injuries: dif- M&S can provide a quantitative description of the rel- fuse axonal injury, contusions, and subdural hematomas evant physical system response that can be used to assess (Takhounts et al., 2003). This system is intended for vehicle system performance and inform potential improvements. crashes, and it is unclear how the results might apply to bal- Significant effort has been devoted in the past several decades listic BFD injuries. to developing the basic science, algorithms, simulation soft- SIMon has been upgraded and recently did evaluations ware, and hardware infrastructure to meet this goal. How- using input from instrumented helmets on professional ever, owing to the unique complexities associated with the football players (Takhounts et al., 2008) and vehicle col- interplay between the physics and biology of injury, the full lisions (von Holst and Li, 2013). A finite element model potential of M&S in understanding of injury biomechanics of the human head described the dynamic response of the and the design of protection systems is yet to be realized. brain during the first milliseconds after the impact with Analytical and computational modeling of ballistic perfo- velocities of 10, 6, and 2 m/s, respectively. Their simula- ration of materials has been exhaustively reviewed up to 1978 tions show what is called a dynamic triple maxima sequence: (Backman and Goldsmith, 1978) with an update 10 years (1) strain energy density, (2) intracranial pressure, (3) the later (Anderson and Bodner, 1988). More recent reviews first principal strain. Limitations of the NHTSA simulation are provided by King et al. (1995). But the biomechanics system include limited spatial fidelity, uncertainty in brain of blunt trauma to tissues is a major added complexity to material properties, and limited incorporation of potentially M&S because of the need to incorporate biophysical and important brain structures such as the hippocampus and the biomedical parameters. amygdala. For example, the relative motion of the brain and

OCR for page 70
82 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS skull is not modeled well with current computational model injury dating from World War I when soldiers with neurologi- mesh sizes that do not provide the opportunity for insertion cal and neuropsychological symptoms were labeled “shell of the anatomy and material properties of vessels and tether shocked” (cf. Bass et al., 2012). The linkage between symp- points between the brain and the inner table of the skull. For toms and blast exposures is not the subject for this chapter, example, the tensile strength of the dura material is much but the role of the helmet and face shield in mitigating the larger than brain tissues. strain field is of great importance. Several papers (including Moore et al., 2009; Chafi et al., 2010; Panzer et al., 2011; Przekwas et al., 2011; Nyein et al., Simulations of Brain Strains from Ballistic Impacts on 2010; and Sharma and Zhang, 2011) developed human head Helmeted Head models from medical imaging data to study the interaction Finite element simulations to determine expected skull of blast waves with the head, including various anatomical and brain tissue injuries from ballistic BFD trauma were structures resolved to various scales. Work still remains to performed in Sweden (Aare and Kleiven, 2007). These were be done on material properties, especially at blast-different performed using a validated human head and brain model as stress rates (Panzer et al., 2012), but the body of this work well as a model of the coupling between helmets of various suggests that blasts are a plausible cause of TBI, including stiffnesses and the head, so that tissue trauma parameters the potential for axonal injury at various locations within could be assessed based on the ballistic kinetic energy (ca. the brain. 518 J) of an 8 g, 9-mm bullet impact and angle of impact. It has been clearly demonstrated that blasts can lead to The trauma parameters measured were stress in the cranial the development of significant levels of pressure, volumetric bone, strain in brain tissue, pressure in the brain, change in tension, and shear stress in focal areas on a short time scale rotational velocity, and translational and rotational accelera- and that stress patterns are dependent on the orientation of tion, as shown in Figure 10-7. the blast wave and the complex geometry of the skull, brain, and tissue interfaces (Taylor and Ford, 2009; Moore et al., 2009; Panzer et al., 2012). Computational Simulations of Brain Injury from Blast A numerical and experimental investigation into the Recent efforts in computational modeling of traumatic effects of low-level blast exposure on pigs used a two- physical effects on the central nervous system have focused dimensional pig head model that consisted of a skull model on blast-induced TBI. A reason for this effort is the need to (Teland et al., 2010). They found that the blast wave propa- resolve the controversy regarding the mechanism for brain gates directly through the skull and that the orientation of FIGURE 10-7 Principal strains in simulated brain material from projectile-induced kinetic energy striking a helmet at two angles. Blue is 0 percent, green is 2 percent, and red is >4 percent. SOURCE: Reprinted from Aare and Kleiven (2008), with permission from Elsevier.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 83 the head is important. Another study constructed a better to conduct simulations of the stress and strain distributions computational pig model consisting of skull, brain, cerebro- after a frontal force of 7 kN impulse of 2.75 ms (Kraft et al., spinal fluid, dura, and pia using computed tomography and 2012). They then used a damage model based on data from MRI data (Zhu et al., 2013). The researchers found high rat experiments to predict cellular death based on axonal pressures in the frontal and occipital regions, possibly due to strain and strain rate. The temporal and occipital regions wave reflection at the skull/brain interface. Examining strain, had the largest values of axonal strain and thus the highest they found that the highest strains of 1.7 percent were in the amount of cellular death. Four days after injury, 19.7 percent brainstem, and the lowest strains of 0.2 percent were in the of the network edges were fully degraded, but the network of center of the brain. They also found that strains within the axons remained intact. This type of analysis is new to blast- skull were two orders of magnitude lower than the strains induced injury research and offers a promising route to con- within the brain and that the maximum deflection of the skull nect biomechanical response to neurophysiological insight. was less than 0.5 mm. It is unclear, however, what the brain material properties Very-high-resolution anisotropic models have been and detailed network behavior are in this basis, because the developed MRI T1 relaxation weighting and DTI with a underlying experimental work has not been done. three-dimensional, biofidelic finite-element volume mesh FIGURE 10-8 Computational simulations of the protective effect of the Advanced Combat Helmet (center column) and face shield (right column) show a significant attenuation of the transmitted pressure field when compared to the unprotected head (left column). SOURCE: Nyein et al. (2010). Figure 10-8 fixed

OCR for page 70
84 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS Figure 10-8 shows results from large-scale computational simulations to compare the stress fields for blast exposures involving the head alone, head with helmet, and head with helmet and face shield (Nyein et al., 2010). Computer-aided design models of the actual ACH, including foam pads as well as a conceptual model of a mask protecting the face, were added to the detailed MRI-based model of the human head. For front blast conditions, the propagation of stress waves into the brain tissue is somewhat attenuated by the existing ACH and significantly attenuated by the addition of a face cover. This suggests a possible strategy to improve protection against blast-induced mTBI. Other recent studies have considered the blast-mitigating effect of helmets (Panzer et al., 2010; Zhang et al., 2011; Shridharani et al., 2012a; Przekwas et al., 2011). These FIGURE 10-9 Experimental determination of brain shear modulus models and measurements have consistently shown strong (magnitude of the complex shear modulus) showing wide variance mitigation of blast pressure behind the ACH. Figure 10-9 fixed of experimental results from different researchers. Finding 10-4. Computational simulations of the protective effect of helmet and face shield show a significant attenuation of the transmitted pressure field. In conclusion, M&S can prove a valuable tool in the anal- ysis of the effects of mechanical threats (blast, impact) on brain tissue. Its main usefulness is in explaining mechanisms of momentum transfer from the external threat to the internal tissues, including the identification of areas of the brain that can be most vulnerable for particular threats. Simulations can also guide the design of protective gear and the assessment of the comparative effectiveness in mitigating the effect of the external threat on brain tissue. There is a clear opportunity to extend the existing use of M&S in the area of brain injury biomechanics and protective gear design, as in many other areas of science and engineering. 10.6  MECHANICAL AND CONSTITUTIVE PROPERTIES OF TISSUES FIGURE 10-10 Dependence of shear strain on stress rate shows Characterization of the dynamic mechanical properties the importance offixed Figure 10-10, correct simulation of the shear stress rate in of brain tissue is important for developing a comprehensive simulations. SOURCE: Adapted from Donelly and Medige (1997). knowledge of the mechanisms underlying brain injury and for developing computational models of potential ballistic and blunt neurotrauma. There are regional, directional, and Figure 10-10. For a given shear stress, the strain on brain age-dependent changes in the properties of the brain when it tissues is inversely related to the stress rate. undergoes large deformations (Prange and Margulies, 2002). There has recently been significant progress in the The frequency dependence of elastic properties must be experimental characterization and constitutive modeling of included in comprehensive models, along with the frequency the mechanical response of brain tissue (Pervin and Chen, characteristics of the changing pressure field (Figure 10-9). 2009; Prevost et al., 2011a, b). Tissue response exhibits Previous brain material characterizations at various stress moderate compressibility, substantial nonlinearity, hys- rates suffer from wide experimental dispersion (Figure 10-9), teresis, conditioning, and rate dependence. A large-strain nearly three orders of magnitude in the complex modulus. nonlinear viscoelastic model has been described that suc- This has made comparison of computational results using cessfully captures the observed complexities of the material these disparate data difficult (Panzer et al., 2012). Strain is response in loading, unloading, and relaxation (Prevost et al., dependent on the shear stress and stress rate, as shown in 2011a). This model covers strain rates—from quasistatic to

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 85 dynamic rates—comparable or exceeding those in blast and lations of dynamic transients (impact from ballistic BFD/ ballistic events with stress rates from 0.01 to 3000 s-1. But blunt trauma, blast/shock wave propagation) leading to TBI. the low-strain-level behavior of brain tissue at high stress rates is not well known, and currently available results are Finding 10-5. For models and simulations of brain trauma not reliable because of the experimental methods employed to be meaningful for injury assessments, they should include to date. The results gathered to date on bovine and porcine constitutive models of brain tissue response that account for tissue properties have been obtained mostly in vitro (Pervin nonlinear and rate-dependent viscoelastic effects. Viscoelas- and Chen, 2009; Prevost et al., 2011a). Previous studies on tic brain properties for high rate, low strain levels necessary brain properties of note were on the juvenile pig (Gefen and for ballistic BFD calculations are not established. Margulies, 2004). These results might differ quantitatively from those encountered in vivo, and this knowledge is criti- 10.7  CONCLUSION cal for the development of biofidelic brain models. Further, different regions of the brain respond differently to identical The protection of the warfighter afforded by helmets from mechanical stimuli, as shown in culture studies of the rat threats ranging from bullets, shrapnel, blasts, vehicle colli- cortex and rat hippocampus. The cortex was less vulnerable sions, and parachute landings has improved with improved to stretch-induced injury than the hippocampus (Elkin and helmet design and materials. However, the level of protec- Morrison, 2007). tion from nonfatal brain tissue injuries, which may have Recently, Prevost et al. (2011b) measured the nonlinear health consequences beyond the acute phase, is not known. dynamic response of the cerebral cortex to indentation of the This chapter and Chapter 3 give information regarding what exposed frontal and parietal lobes of anesthetized porcine is known about brain injury from blunt trauma and what subjects. Measurements included nonlinear, rate-dependent, is known about injury tolerances. In addition, this chapter hysteretic, and conditioning white and gray matter response defines the types of injuries that occur and most of the meth- in vivo, in situ, and in vitro. Results showed similar responses ods for diagnosis of both near- and long-term-onset medical between in vivo and in vitro studies with respect to load conditions. versus indent and a “stiffening” with increase rate of stress. The principal finding is that there is not a known rela- The data raise concerns regarding doing measurements in tionship between brain injury to the ballistic parameters of situ, wherein central circulation and cerebral spinal fluid momentum, rate of change of momentum, acceleration, and pressures are much less than in vivo. Without the intact dura time duration of the impact force. Findings in Chapter 3 mater, whose tensile strength is much greater than other emphasize that there is no known relationship between the brain membranes, in vivo or in vitro measurements can be measure of BFD by helmet evaluation protocols and skull questioned, thus characterization of brain material proper- fracture and brain trauma. This finding is known to the U.S. ties might best be done by elastography using magnetic Army Medical Research and Materiel Command. Research resonance techniques in vivo. But elastography does not is already underway on skull fracture injury criteria.3 Link- have the spatial resolution to give region specific elastic age of the ballistic threats whose physical parameters are properties and published values might be too low for stud- known to brain injury must include knowledge of the pro- ies of brain-surface-to-cortex relative motion or strains (cf. tective attenuation of the helmet. The degree to which the Coats et al., 2012). listed types of brain-injury parameters are moderated by the Magnetic resonance elastography enables the visalization helmet is not known. and measurement of mechanical waves propagating in three Vehicle and sports collisions have been studied and mod- dimensions throughout a sample (Muthupillai et al., 1995; eled with attendant animal experiments. But parameters for Manduca et al., 2001). From this information, the shear stiff- the rate of change of momentum (i.e., force) and duration ness of the sample can be inferred. In MRE, oscillating shear of contact are orders of magnitude different from those for displacements are generated by harmonic vibrations induced ballistic injuries. Therefore, considerations in the design of mechanically or acoustically on the skull or brain surface. sports and vehicle head protective devices as well as the The displacements are measured from phase images obtained parameters of injury tolerance are not the same as those by modulating the gradient field of the magnetic resonance encountered by the warfighter. The committee notes a broad scanner at the vibration frequency. These measurements have effort to define mechanisms, develop diagnostic methods already shown the skull acts as a low-pass filter for frequen- for evaluating organic damage to the brain, and methods for cies of 45, 60, and 80 Hz. Skull transmission decreases, and treatment. But the current principal approach is protection shear-wave attenuation in the brain increases with increasing from transfer of injurious forces afforded by the helmet. frequency (Clayton et al., 2012). Further work is required to continue to improve and validate constitutive models—not just for brain but also for 3Karin Rafaels, Army Research Laboratory, Survivability/Lethality bone and other tissues. These models are essential for simu- Analysis Directorate, “Joint Live Fire Test Program Behind Helmet Blunt Trauma Skull Injury,” presentation to the committee on January 24, 2013.

OCR for page 70
86 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS 10.8  REFERENCES Cernak, I., R. Vink, D.N. Zapple, M.I. Cruz, F. Ahmed, T. Chang, S.T. Fricke, and A.I. Faden. 2004. The pathobiology of moderate diffuse Aare, M., and S. Kleiven. 2007. Evaluation of head response to ballistic traumatic brain injury as identified using a new experimental model of helmet impacts using the finite element method. International Journal injury in rats. Neurobiology of Disease 17(1):29-43. of Impact Engineering 34(3):596-608. Chafi, M.S., G. Karami, and M. Ziejewski. 2010. Biomechanical assess- AGARD (Advisory Group for Aerospace Research and Development). ment of brain dynamic responses due to blast pressure waves. Annals 1996. Anthropomorphic Dummies for Crash and Escape System Testing. of Biomedical Engineering 38(2):490-504. AGARD AR-330. Neuilly-Sur-Seine, France. Clayton, E.H., G.M. Genin, and P.V. Bayly. 2012. Transmission, attenuation Agha, A., B. Rogers, M. Sherlock, P. O’Kelly, W. Tormey, J. Phillips, and and reflection of shear waves in the human brain. Journal of the Royal C.J. Thompson. 2004. Anterior pituitary dysfunction in survivors of Society Interface 9(76):2899-2910. traumatic brain injury. Journal of Clinical Endocrinology and Metabo- Coats, B., S.A. Eucker, S. Sullivan, and S.S. Margulies. 2012. Finite element lism 89(10):4929-4936. model predictions of intracranial hemorrhage from non-impact rapid Ahmed, S.M., B.A. Rzigalinski, K.A. Willoughby, H.A. Sitterding, and head rotations in the piglet. International Journal of Developmental E.A. Ellis. 2000. Stretch-induced injury alters mitochondrial membrane Neuroscience 30(3):191-200. potential and cellular ATP in cultured astrocytes and neurons. Journal Delye, H., P. Verschureen, I. Verpoest, D. Berckmans, J. Vander-Sloten, of Neurochemistry 74(5):1951-1960. G. Van Der Perre, and J. Goggin. 2007. Biomechanics of frontal skull Anderson, Jr., C.E., and S.R. Bodner. 1988. Ballistic impact: The status fracture. Journal of Neurotrauma 24(10):1576-1586. of analytical and numerical modeling. International Journal of Impact Denny-Brown, D., and W.R. Russell. 1941. Experimental cerebral concus- Engineering 7(1):9-35. sion. Brain 64(2-3):93-164. Backman, M.E., and W. Goldsmith. 1978. The mechanics of penetration Donnelly, B.R., and J. Medige. 1997. Shear  properties of human brain tis- of projectiles into targets. International Journal of Engineering Science sue. Journal of Biomechanical Engineering 119(4):423-432. 16(1):1-99. Draper, K., and J. Ponsford. 2008. Cognitive functioning ten years fol- Bain, A.C., and D.F. Meaney. 2000. Tissue-level thresholds of axonal dam- lowing traumatic brain injury and rehabilitation. Neuropsychology age in an experimental model of central nervous system white matter 22(5):618-625. injury. Journal of Biomechanical Engineering 122(6):615-622. Duma, S.M., and S.J. Manoogian, W.R. Bussone, P.G. Brolinson, M.W. Bain, A.C., R. Raghupathi, and D.F. Meaney. 2001. Dynamic stretch cor- Goforth, J.J. Donnenwerth, R.M. Greenwald, J.J. Chu, and J.J. Crisco. relates to both morphological abnormalities and electrophysiological 2005. Analysis of real-time head accelerations in collegiate football impairment in a model of traumatic axonal Injury. Journal of Neu- players. Clinical Journal of Sport Medicine 15(1):3-8. rotrauma 18(5):499-511. Elkin, B.S., and B. Morrison. 2007. Region-specific tolerance criteria for Bass, C.R., and N. Yoganandan. 2013. Skull and facial bone injury biome- the living brain. Stapp Car Crash Journal 51:127-138. chanics. In Accidental Injury (N. Yoganandan, ed.). Springer Verlag, Engelborghs, K., J. Verlooy, J. Van Reempts, B. Van Deuren, M. Mies Van London, U.K. de Ven, and M. Borgers. 1998. Temporal changes in intracranial pres- Bass, C.R., M. Bolduc, and S. Waclawik. 2002. Development of a nonpen- sure in a modified experimental model of closed head injury. Journal of etrating, 9-mm, ballistic trauma test method. Pp. 18-22 in Proceedings Neurosurgery 89(5):796-806. of the Personal Armor Systems Symposium (PASS 2002), The Hague, Gefen, A., and S.S. Margulies. 2004. Are in vivo and in situ brain tissues Netherlands, November 18-22, 2002. Prins Maurits Laboratorium, Rose mechanically similar? Journal of Biomechanics 37(9):1339-1352. International Exhibition Management and Congress Consultancy, The Gennarelli, T., and L. Thibault. 1989. Clinical rationale for a head injury an- Hague, Netherlands. gular acceleration criterion. In Proceedings of Head Injury Mechanisms: Bass, C.R., B. Boggess, B. Bush, M. Davis, R. Harris, M.R. Rountree, The Need for an Angular Acceleration Criterion. Washington D.C. Avail- S. Campman, J. Ecklund, W. Monacci, G. Ling, G. Holborow, E. able at http://www-nrd.nhtsa.dot.gov/pdf/esv/esv16/98S8O07.PDF. Sanderson, and S. Waclawik. 2003. “Helmet Behind Armor Blunt Gennarelli, T.A., L.E. Thibault, and A.K. Ommaya. 1972. Pathophysiologi- Trauma.” Paper presented at the RTO Applied Vehicle Technology Panel/ cal responses to rotational and translational accelerations of the head. Human Factors and Medicine Panel Joint Specialists’ Meeting held in Stapp Car Crash Journal 16:296-308. Koblenz, Germany, May 19-23, 2003. NATO Science and Technology Giza, C.C., J.S. Kutcher, J. Barth, T.S.D. Getchius, G.A. Gioia, G.S. Organization, Neuilly-Sur-Seine, France. Grpnsethj, K. Guskiewicz, S. Mandel, G. Manley, D.B. McKeag, D.J. Bass, C.R., K. Rafaels, and R. Salzar. 2008. Pulmonary injury risk assess- Thurman, and R. Zaafonte. 2013. Summary of evidence-based guideline ment for short duration blasts. Journal of Trauma 65(3):604-615. update: Evaluation and management of concussion in sports. Neurology Bass, C.R., M.B. Panzer, K.A. Rafaels, G. Wood, and B. Capehart. 2012. 80(24):2250-2257. Brain injuries from blast. Annals of Biomedical Engineering 40(1):185- Goldsmith, W. 1981. Current controversies in the stipulation of head injury 202. criteria. Journal of Biomechanics 14(12):883-884. Bondanelli, M., M.R. Ambrosio, M.C. Zatelli, and L. De Marinis. 2005. Grundfest, H. 1936. Effects of hydrostatic pressures upon the excitability, Hypopituitarism after traumatic brain injury. European Journal of En- the recovery, and the potential sequence of frog nerve. Cold Spring docrinology 152(5):679-691. Harbor Symposia on Quantitative Biology 4:179-187. Borgaro, S.R., G.P. Prigatano, C. Kwasnica, and J.L. Rexer. 2003. Cognitive Gurdjian, E.S., J.E. Webster, and H.R. Lissner. 1955. Observations on the and affective sequelae in complicated and uncomplicated mild traumatic mechanism of brain concussion, contusion, and laceration. Surgery, brain injury. Brain Injury 17(3):189-198. Gynecology and Obstetrics 101(6):680-690. Breedlove, E.L., Robinson, M., Talavage , T.M., Morigaki.K.E., Yoruk, K., Gurdjian, E.S., V.L. Roberts, and L.M. Thomas. 1966. Tolerance curves of O’Keefe, U., King, J. Leverenz, L J., Gilger, J.W., and Nauman, E.A. acceleration and intracranial pressure and protective index in experimen- 2012. Biomechanical correlates of symptomatic and asymptomatic tal head injury. Journal of Trauma and Acute Care Surgery 6(5):600-604. neurophysiological impairment in high school football. Journal of Bio- Guskiewicz, K.M., S.W. Marshall, J. Bailes, M. McCrea, R.C. Cantu, mechanics 45(7):1265-1272. C. Randolph, and B.D. Jordan. 2005. Association between recurrent Carey, M.E., M. Herz, B. Corner, J. McEntire, D. Malabarba, S. Paquette, concussion and late-life cognitive impairment in retired professional and J.B. Sampson. 2000. Ballistic helmets and aspects of their design. football players. Neurosurgery 57(4):719-724. Neurosurgery 47(3):678-689. Hodgson, V.R., L.M. Thomas, and J. Brinn. 1973. Concussion levels deter- mined by HPR windshield impacts. SAE Technical Papers.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 87 Hoge, C., D. McGurk, J. Thomas, A. Cox, C. Engel, and C. Castro. 2008. McKee, A.C., R.C. Cantu, C.J. Nowinski, E.T. Hedley-Whyte, B.E. Gavett, Mild traumatic brain injury in US soldiers returning from Iraq. New A.E. Budson, V.E. Santini, H.-S. Lee, C.A. Kubilus, R.A. Stern. 2009. England Journal of Medicine 358(5):453-463. Chronic traumatic encephalopathy in athletes: Progressive tauopathy Holbourn, A.H.S. 1943. Mechanics of head injuries. Lancet 2:438-441. following repetitive head injury. Journal of Neuropatholology and Ex- Ishibe, N., R.C. Wlordarczyk, and C. Fulco. 2009. Overview of the Institute perimental Neurology 68(7):709-735. of Medicine’s Committee search strategy and review process for Gulf McManus, L.R., P.E. Durand, and W.D. Claus. 1976. Development of a War and Health: Long-term consequences of traumatic brain injury. One Piece Infantry Helmet. Report 76-30-CEMEL. U.S. Army Natick Journal of Head Trauma Rehabilitation 24(6):424-429. Research and Development Command, Natick, Mass. Ji, S., Q. Zhu, L. Dougherty, and S.S. Margulies. 2004. In vivo measure- McMurtray, A., D.G. Clark, D. Christine, and M.F. 2006. Early-onset ments of human brain displacement. Stapp Car Crash Journal 48:227- dementia: Frequency and causes compared to late-onset dementia. 237. Dementia and Geriatric Cognitive Disorders 21(2):59-64. Kelly, D.F., D.L. McArthur, H. Levin, S. Swimmer, J.R. Dusick, P. Cohan, Meaney, D.F., D.H. Smith, D.L. Schreiber, A.C. Bain, R.T. Miller, D.T. C. Wang, and R. Swerdloff. 2006. Neurobehavioral and quality of life Ross, and T.A. Gennarelli. 1995. Biomechanical analysis of experi- changes associated with growth hormone insufficiency after com- mental diffuse axonal injury. Journal of Neurotrauma 12(4):689-694. plicated, mild, moderate or severe traumatic brain injury. Journal of Meehan, W., P. d’Hemecourt, D. Comstock. 2010. High school concussions Neurotrauma 23(6):928-942. in the 2008-2009 academic year: Mechanism, symptoms, and manage- Kelly, M.P., R.L. Coldren, R.V. Parish, M.N. Dretsch, and M.L. Russell. ment. American Journal of Sports Medicine 38(12):2405-2409. 2012. Assessment of acute concussion in the combat environment. Moon, D.W., C.W. Beedle, and C.R. Kovacic. 1971. Peak head accel- Archives of Clinical Neuropsychology 27(4):375-388. eration of athletes during competition. Medicine and Science in Sports King, A.I., J.S. Ruan, C. Zhou, W.N. Hardy, and T.B. Khalil. 1995. Recent 3(1):44-50. advances in biomechanics of brain injury research: A review. Journal of Moore, D.F., A. Jerusalem, M. Nyein, L. Noels, M.S. Jaffee, and R. Neurotrauma 12(4):651-658. Radovitzky. 2009. Computational biology, modeling of primary blast ef- King, A.I., K.H. Yang, L. Zhang, W. Hardy, D.C. Viano. 2003. Is head injury fect on the central nervous system. NeuroImage 47(Suppl. 2):T10-T20. caused by linear or angular acceleration. Pp. 1-12 in Proceedings of the Morrison III, B., H.L. Cater, C.C.-B. Wang, F.C. Thomas, C.T. Hung, G.A. 2003 International IRCOBI Conference on the Biomechanics of Impact. Ateshian, and L.E. Sundstrom. 2003. A tissue level tolerance criterion IRCOBI, Lisbon, Portugal. for living brain developed with an in vitro model of traumatic mechani- Kleiven, S., and W.N. Hardy. 2002. Correlation of a FE model of the human cal loading. Stapp Car Crash Journal 47:93-105. head with experiments on localized motion of the brain- consequences Muthupillai, R., D.J. Lomas, P.J. Rossman, J.F. Greenleaf, A. Manduca, and for injury prediction. Stapp Car Crash Journal 46:123-144. R.L. Ehman. 1995. Magnetic resonance elastography by direct visual- Kraft, R.H., P.J. McKee, A.M. Dagro, and S.T. Grafton. 2012. Combining ization of propagating acoustic strain waves. Science 269(5232):1854- the finite element method with structural connectome-based analysis 1857. for modeling neurotrauma: Connectome neurotrauma mechanics. PLoS Newman, J.A., N. Shewchenko, and E. Welbourne. 2000. A proposed new Computational Biology 8(8):pcbi.1002619. biomechanical head injury assessment function—The maximum power Leal-Cerro, A., J.M. Flores, M. Rincon, F. Murillo, M. Pujol, F. Garcia- index. Stapp Car Crash Journal 44:215-246. Pesquera, C. Dieguez, and F.F. Casanueva. 2005. Prevalence of hypo- Newman, J.A., M.C. Beusenberg, N. Shewchenko, C. Withnall, and E. pituitarism and growth hormone deficiency in adults long-term after Fournier. 2005. Verification of biomechanical methods employed severe traumatic brain injury. Clinical Endocrinology 62(5):525-532. in a comprehensive study of mild traumatic brain injury and the ef- Leitgeb, J., W. Mauritz, A. Brazinov, M. Majdan, and I. Wilbacher. 2013. fectiveness of American football helmets. Journal of Biomechanics Outcome after severe brain trauma associated with epidural hematoma. 38(7):1469-1481. Archives of Orthopaedic and Trauma Surgery 133(2):199-207. NRC (National Research Council). 2012. Testing of Body Armor Materials: Levin, H.S., E. Wilde, M. Troyanskaya, N.J. Petersen, R. Scheibel, M. Phase III. The National Academies Press, Washington, D.C. Newsome, M. Radaideh, T. Wu, R. Yallampalli, Z. Chu, and X. Li. 2010. Nyein, M., A.M. Jason, L. Yua, C.M. Pita, J.D. Joannopoulos, D.F. Moore, Diffusion tensor imaging of mild to moderate blast-related traumatic R.A. Radovitzky. 2010. In silico investigation of intracranial blast miti- brain injury and its sequelae. Journal of Neurotrauma 27(4):683-694. gation with relevance to military traumatic brain injury. Proceedings of Lewis, S.B., J.W. Finnic, P.C. Blumbergs, G. Scott, J. Manavis, C. Brown, the National Academy of Sciences U.S.A. 107:20703-20708. P.L. Reilly, N.R. Jones, and A.J. McLean. 1996. A head impact model of Okie, S. 2005. Traumatic brain injury in the war zone. New England Journal early axonal injury in the sheep. Journal of Neurotrauma 13(9):505-514. of Medicine 352:2043-2047. Mac Donald, C.L., A.M. Johnson, D. Cooper, E.C. Nelson, N.J. Werner, Ommaya, A.K., and R.A. Gennarelli. 1974. Cerebral concussion and J.S. Shimony, A.Z. Snyder, M.E. Raichle, J.R. Witherow, R. Fang, S.F. traumatic unconsciousness: Correlation of experimental and clinical Flaherty, and D.L. Brody. 2011. Detection of blast-related traumatic observations on blunt head injuries. Brain 97(4):633-654. brain injury in U.S. military personnel. New England Journal of Medi- Ommaya, A.K., and A.E. Hirsch. 1971. Tolerances for cerebral concussion cine 64(22):2091-2100. from head impact and whiplash in primates. Journal of Biomechanics Manduca, A., T.E. Oliphant, M.A. Dresner, J.L Mahowald, S.A. Kruse, E. 4(1):13-21. Amromin, J.P. Felmlee, J.F. Greenleaf, and R.L. Ehman. 2001. Mag- Ommaya, A.K., W. Goldsmith, L.E. Thibault. 2002. Biomechanics and netic resonance elastography: Non-invasive mapping of tissue elasticity. neuropathology of adult and paediatric head injury. British Journal of Medical Image Analysis 5(4):237-254. Neurosurgery 16(3):220-242. Margulies, S.S., and L. Thibault. 1992. A proposed tolerance criteria for Ono, K., Kikuchi, A., Nakamura, M., Kobayashi, H., and N. Nakamura. diffuse axonal injury in man. Journal of Biomechanics 25(8):917-923. 1980. Human head tolerance to sagittal impact reliable estimation de- Margulies, S.S., L. Thibault, and T. Gennarelli. 1990. Physical model duced from experimental head injury using subhuman primates and hu- simulation of brain injury in the primate. Journal of Biomechanics man cadaver skulls. SAE Technical Paper 801303, doi:10.4271/801303. 23(8):823-836. SAE International, Warrendale, Pa. Maxwell, W.L., J.T. Povlishock, and D.L. Graham. 1997. A mechanistic Panzer, M.B., C.R. Bass, and B.S. Myers. 2010. Numerical study on the role analysis of nondisruptive axonal injury: A review. Journal of Neu- of helmet protection in blast brain injury. Presented at Personal Armor rotrauma 14(7):419-440. Systems Symposium (PASS 2010), Quebec City, Calif.

OCR for page 70
88 REVIEW OF DEPARTMENT OF DEFENSE TEST PROTOCOLS FOR COMBAT HELMETS Panzer, M.B., B.S. Myers, and C.R. Bass. 2011. Mesh considerations for Shridharani, J.K., G.W. Wood, M.B. Panzer, K.A. Matthews, C. Perritt, K. finite element blast modeling in biomechanics. Computer Methods in Masters, and C.R. Bass. 2012a. Blast effects behind ballistic protective Biomechanics and Biomedical Engineering 16(6):612-621. helmets. Presented at the Personal Armor Systems Symposium (PASS Panzer, M.P., B.S. Myers, B.P. Capehart, and C.R. Bass. 2012. Development 2012), Nuremburg, Germany. of a finite element model for blast brain injury and the effects of CSF Shridharani, J.K., G.W.Wood, M.B. Panzer, B.P. Capehart, M.K. Nyein, cavitation. Annals of Biomedical Engineering 40(7):1530-1544 R.A. Radovitzky, and C.R. Bass. 2012b. Porcine head response to blast. Peethambaran, A., R. Abu-Taleb, S. Oguntayo, Y. Wang, M. Valiyaveettil, Frontiers in Neurology, Article 70, May. J.B. Long, and M.P. Nambiar. 2013. Acute mitochondrial dysfunction Smith, D.H., J.A. Wolf, T.A. Lusardi, V.M.Y. Lee, and D.F. Meaney. 1999. after blast exposure: Potential role of mitochondrial glutamate oxaloac- High tolerance and delayed elastic response of cultured axons to dy- etate transaminase. Journal of Neurotrauma 30(19):1645-1651. namic stretch injury. Journal of Neuroscience 19(11):4263-4269. Pellman, E.J., D.C. Viano, A.M. Tucker, I.R. Casson, and J.F. Waeckerle. Smith, D.H., R. Hicks, and J.T. Povlishock. 2013. Therapy development for 2003. Concussion in professional football: Reconstruction of game diffuse axonal injury. Journal of Neurotrauma 30(5):307-323. impacts and injuries. Neurosurgery 53:799-814. Stalnaker, R.L., J.H. McElhaney, and V.L. Roberts. 1971. MSC tolerance Pervin, F., and W. Chen. 2009. Dynamic mechanical response of bovine curve for human heads to impact. ASME Paper No. 71WA/BHF-10. gray matter and white matter brain tissues under compression. Journal American Society of Mechanical Engineers, New York. of Biomechanics 42(6):731-735. Strich, S.J. 1956. Diffuse degeneration of the cerebral white matter in severe Powner, D.J., C. Boccalandro, M.S. Alp, and D.G. Vollmer. 2006. Endo- dementia following head injury. Journal of Neurology Neurosurgery and crine failure after traumatic brain injury in adults. Neurocritical Care Psychiatry 19(3):163-185. 5(1):61-70. Strich, S.J. 1961. Shearing of nerve fibres as a cause of brain damage due Prange, M.T., and S.S. Margulies. 2002. Regional, directional, and age- to head injury. The Lancet 278(7200):443-448. dependent properties of the brain undergoing large deformation. Journal Takhounts, E.G., R.H. Eppinger, J.Q. Campbell, R.E. Tannous, E.D. Power, of Biomechanical Engineering 124(2):244-252. and L.S. Shook. 2003. On the development of the SIMon Finite Element Prasad, P., and H.J. Mertz. 1985. The position of the United States delegation Head Model. Stapp Car Crash Journal 47:107-133. to the ISO working group on the use of HIC in the automotive environ- Takhounts, E.G., S.A. Ridella, V. Hasija, E. Rabih, R.E. Tannous, J.Q. ment. SAE Transactions 94(5):106-116. Campbell, D. Malone, K. Danelson, J. Stitzel, S. Rowson, S. Duma. Prevost, T.P., A. Balakrishnan, S. Suresh, and S. Socrate. 2011a. Biomechan- 2008. Investigation of traumatic brain injuries using the next generation ics of brain tissue. Acta Biomaterialia 7(1):83-95. of simulated injury monitor (SIMon) Finite Element Head Model. Stapp Prevost, T.P., G. Jin, M.A. de Moya, H.B. Alam, S. Suresh, and S. Socrate. Car Crash Journal 52:1-31. 2011b. Dynamic mechanical response of brain tissue in indentation in Talavage, T.M., E.A. Nauman, E.L. Breedlove, U. Yoruk, A.E. Dye, K. vivo, in situ, and in vitro. Acta Biomaterialia 7(12):4090-4101. Morigaki, H. Feuer, and L.J. Leverenz. 2013. Functionally-detected Przekwas, A., X.G. Tan, V. Harrand, D. Reeves, Z.J. Chen, and K. Sedberry. cognitive impairment in high school football players without clinically- 2011. Integrated experimental and computational framework for the de- diagnosed concussion. Journal of Neurotrauma. April 11. E-pub ahead velopment and validation of blast wave brain biomechanics and helmet of print, doi:10.1089/neu.2010.1512. protection. Pp. 34-1–34-20 in HFM-207—A Survey of Blast Injury Taylor, P.A., and C.C. Ford. 2009. Simulation of blast-induced early-time Across the Full Landscape of Military Science. RTO Human Factors intracranial wave physics leading to traumatic brain injury. Journal of and Medicine Panel (HFM) Symposium, Halifax, Canada. Biomechanical Engineering 131(6):061007. Pudenz, R.H., and C.H. Sheldon. 1946. The Lucite calvarium—A method Teland, T., A. Hamberger, M. Huseby, A. Säljö, and E. Svinsås. 2010. for direct observation of the brain. II. Cranial trauma and brain move- Numerical simulation of mechanisms of blast-induced traumatic brain ment. Journal of Neurosurgery 3(6):487-505. injury. Journal of the Acoustical Society of America 127(3):1790. Rafaels, K.A., C.R. Bass, M.B. Panzer, R.S. Salzar, W.W. Woods, S. Terrio, H., L. Brenner, B. Ivins, J. Cho, K. Helmick, K. Schwab, K. Scally, Feldman, T. Walilko, R. Kent, B. Capehart, J. Foster, B. Derkunt, and A. R. Bretthauer, D. Warden, and L. French. 2009. Traumatic brain injury Toman. 2012. Brain injury risk from primary blast. Journal of Trauma screening: Preliminary findings in a U.S. army brigade combat team. and Acute Care Surgery 73(4):895-901. Journal of Head Trauma Rehabilitation 24(1):14-23. Reid, S.E., H.M. Epstein, T.J. O’Dea, and M.W. Louis. 1974. Head protec- Ueno, K., and J. Melvin. 1995. Finite element model study of head im- tion in football. Journal of Sports Medicine 2(2):86-92. pact based on hybrid III Head acceleration: The effects of rotational Rowson, S., and S.M. Duma. 2011.  Development of the STAR Evaluation and translational acceleration. Journal of Biomechanical Engineering System for football helmets: Integrating player head impact exposure 117(3):319-328. and risk of concussion. Annals of Biomedical Engineering 39(8):2130- Vanderploeg, R.D., G. Curtiss, and H.G. Belanger. 2005. Long-term neuro- 2140. psychological outcomes following mild traumatic brain injury. Journal Sarron, J.C., M. Dannawi, A. Faure, J.-P. Caillou, J. Da Cunha, and R. of the International Neuropsychological Society 11(3):228-236. Robert. 2004. Dynamic effects of a 9 mm missile on cadaveric skull Versace, J. 1971. A Review of the Severity index. Pp. 771-796 in Proceed- protected by aramid, polyethylene or aluminum plate: An experimental ings of the Fifteenth Stapp Car Crash Conference. Stapp Car Crash study. Journal of Trauma—Injury, Infection and Critical Care 57(2):236- Conference, Atlanta, Ga. 242. Viano, D.C. 1988. Cause and control of automotive trauma. Bulletin of the Saucier, J. 1955. Concussion: A misnomer. Canadian Medical Association New York Academy of Medicine: Journal of Urban Health 64(5):367. Journal 72(11):816-820. Viano, D.C., and P. Lövsund. 1999. Biomechanics of brain and spinal-cord Schoenhuber, R., and M. Gentilini.1988. Anxiety and depression after mild injury: Analysis of neuropathologic and neurophysiologic experiments. head injury: A case controlled study. Journal of Neurology Neurosurgery Journal of Crash Prevention and Injury Control 1(1):35-43. and Psychiatry 51(5):722-724. Viano, D.C., C. Bir, T. Walilko, and D. Sherman. 2004. Ballistic impact to Schreiber, D.I., A.C. Bain, and D.F. Meaney. 1997. In vivo thresholds for the forehead, zygoma, and mandible: Comparison of human and fran- mechanical injury to the blood brain barrier. SAE Technical Paper gible dummy face biomechanics. Journal of Trauma—Injury, Infection 973335. SAE International, Warrendale, Pa. and Critical Care 56(6):1305-1311. Sharma, S., and L. Zhang. 2011. “Prediction of Intracranial Responses from von Holst, H., and X. Li. 2013. Consequences of the dynamic triple peak Blast Induced Neurotrauma Using a Validated Finite Element Model impact factor in traumatic brain injury as measured with numerical of Human Head.” Bioengineering Centre, Wayne State University, simulation. Frontiers in Neurology 4:1-8. Detroit, Mich.

OCR for page 70
LINKING HELMET PROTECTION TO BRAIN INJURY 89 Ward, C.C., M. Chan, and A.M. Nahum. 1980. Intracranial pressure—A Yeh, P.-H., B. Wang, T.R. Oakes, L.M. French, P. Hai, J. Graner, W. Liu, brain injury criterion. SAE Technical Paper 801304. SAE International, and G. Riedy. 2013. Postconcussional disorder and PTSD symptoms Warrendale, Pa. of military-related traumatic brain injury associated with compromised Warden, D. 2006. Military TBI during the Iraq and Afghanistan wars. Jour- neurocircuitry. Human Brain Mapping, doi:10.1002/hbm.22358. nal of Head Trauma Rehabilitation 21(5):398-402. Yoganandan, N., F.A. Pintar, A. Sances, Jr, P.R. Walsh, C.L. Ewing, D.J. Whitnall, L., T.M. McMillan, G.D. Murray, and G.M. Teasdale. 2006. Dis- Thomas, and R.G. Snyder. 1995. Biometrics of skull fracture. Journal ability in young people and adults after head injury: 5-7 year follow up of Neurotrauma 12(4):659-668. of a prospective cohort study. Journal of Neurology, Neurosurgery and Zhang, L., R. Makwana, and S. Sharma. 2011. Comparison of the head Psychiatry 77(5):640-645. response in blast insult with and without combat helmet. Pp. 33-1–33- Wilkinson, C.W., Pagulayan, K.F., petrie, E.C., Mayer, C.L., Colasurdo, 18 in HFM-207—A Survey of Blast Injury Across the Full Landscape E.A., Shofer, J.B., Hart, K.L., Hoff, D., Tarabochia, M.A., and Peskind, of Military Science. RTO Human Factors and Medicine Panel (HFM) E.R. 2012. High prevalence of chronic pituitary and target-organ Symposium, Halifax, Canada. hormone abnormalities after blast-related mild traumatic brain injury. Zhu, F., P. Skelton, C.C. Chou, H. Mao, K.H. Yang, and A.I. King. 2013. Frontiers in Neurology, February, Article 11. Biomechanical responses of a pig head under blast loading: A compu- Xiangsong, Z., Y. Dianchao, and T. Anwu. 2005. Dynamic 13N-Ammonia tational simulation. International Journal for Numerical Methods in PET: A new imaging method to diagnose Hypopituitarism. Journal of Biomedical Engineering 29(3):392-407. Nuclear Medicine 46(1):44-47.

OCR for page 70