A centric/non-centric impact protocol and finite element model methodology for the evaluation of American football helmets to evaluate risk of concussion

American football reports high incidences of head injuries, in particular, concussion. Research has described concussion as primarily a rotation dominant injury affecting the diffuse areas of brain tissue. Current standards do not measure how helmets manage rotational acceleration or how acceleration loading curves influence brain deformation from an impact and thus are missing important information in terms of how concussions occur. The purpose of this study was to investigate a proposed three-dimensional impact protocol for use in evaluating football helmets. The dynamic responses resulting from centric and non-centric impact conditions were examined to ascertain the influence they have on brain deformations in different functional regions of the brain that are linked to concussive symptoms. A centric and non-centric protocol was used to impact an American football helmet; the resulting dynamic response data was used in conjunction with a three-dimensional finite element analysis of the human brain to calculate brain tissue deformation. The direction of impact created unique loading conditions, resulting in peaks in different regions of the brain associated with concussive symptoms. The linear and rotational accelerations were not predictive of the brain deformation metrics used in this study. In conclusion, the test protocol used in this study revealed that impact conditions influences the region of loading in functional regions of brain tissue that are associated with the symptoms of concussion. The protocol also demonstrated that using brain deformation metrics may be more appropriate when evaluating risk of concussion than using dynamic response data alone.     

Finite element modeling of human brain response to football helmet impacts

The football helmet is used to help mitigate the occurrence of impact-related traumatic (TBI) and minor traumatic brain injuries (mTBI) in the game of American football. While the current helmet design methodology may be adequate for reducing linear acceleration of the head and minimizing TBI, it however has had less effect in minimizing mTBI. The objectives of this study are (a) to develop and validate a coupled finite element (FE) model of a football helmet and the human body, and (b) to assess responses of different regions of the brain to two different impact conditions – frontal oblique and crown impact conditions. The FE helmet model was validated using experimental results of drop tests. Subsequently, the integrated helmet–human body FE model was used to assess the responses of different regions of the brain to impact loads. Strain-rate, strain, and stress measures in the corpus callosum, midbrain, and brain stem were assessed. Results show that maximum strain-rates of 27 and 19 s^?1 are observed in the brain-stem and mid-brain, respectively. This could potentially lead to axonal injuries and neuronal cell death during crown impact conditions. The developed experimental-numerical framework can be used in the study of other helmet-related impact conditions.     

Evaluation of the protective capacity of baseball helmets for concussive impacts

The purpose of this research was to examine how four different types of baseball helmets perform for baseball impacts when performance was measured using variables associated with concussion. A helmeted Hybrid III headform was impacted by a baseball, and linear and rotational acceleration as well as maximum principal strain were measured for each impact condition. The method was successful in distinguishing differences in design characteristics between the baseball helmets. The results indicated that there is a high risk of concussive injury from being hit by a ball regardless of helmet worn.     

The influence of impact source on variables associated with strain for impacts in ice hockey

Concussion can occur from a variety of events (falls to ice, collisions etc) in ice hockey, and as a result it is important to identify how these different impact sources affect the relationship between impact kinematics and strain that has been found to be associated to this injury. The purpose of this research was to examine the relationship between kinematic variables and strain in the brain for impact sources that led to concussion in ice hockey. Video of professional ice hockey games was analyzed for impacts that resulted in reported clinically diagnosed concussions. The impacts were reconstructed using physical models/ATDs to determine the impact kinematics and then simulated using finite element modelling to determine maximum principal strain and cumulative strain damage measure. A stepwise linear regression was conducted between linear acceleration, change in linear velocity, rotational acceleration, rotational velocity, and strain response in the brain. The results for the entire dataset was that rotational acceleration had the highest r² value for MPS (r² = 0.581) and change in rotational velocity for cumulative strain damage measure (r² = 450). When the impact source (shoulder, elbow, boards, or ice impacts) was isolated the rotational velocity and acceleration r² value increased, indicating that when evaluating the relationships between kinematics and strain based metrics the characteristics of the impact is an important factor. These results suggest that rotational measures should be included in future standard methods and helmet innovation and design in ice hockey as they have the highest association with strain in the brain tissues.     

Finite element modelling of equestrian helmet impacts exposes the need to address rotational kinematics in future helmet designs

Jockey head injuries, especially concussions, are common in horse racing. Current helmets do help to reduce the severity and incidences of head injury, but the high concussion incidence rates suggest that there may be scope to improve the performance of equestrian helmets. Finite element simulations in ABAQUS/Explicit were used to model a realistic helmet model during standard helmeted rigid headform impacts and helmeted head model University College Dublin Brain Trauma Model (UCDBTM) impacts.

Current helmet standards for impact determine helmet performance based solely on linear acceleration. Brain injury-related values (stress and strain) from the UCDBTM showed that a performance improvement based on linear acceleration does not imply the same improvement in head injury-related brain tissue loads. It is recommended that angular kinematics be considered in future equestrian helmet standards, as angular acceleration was seen to correlate with stress and strain in the brain.     

The use of accident reconstruction for the analysis of traumatic brain injury due to head impacts arising from falls

Brain injury is the leading cause of death in those aged under 45 years in both Europe and the USA. The objective of this research is to reconstruct and analyse real world cases of accidental head injury, thereby providing accurate data, which can be used subsequently to develop clinical tolerance levels associated with particular traumatic injuries and brain lesions. This paper looks at using numerical modelling techniques, namely multibody body dynamics and finite element methods, to reconstruct two real-life accident cases arising from falls. Preliminary results show the levels of acceleration of the head and deformation of brain tissue correspond well to those found by other researchers, suggesting that this method is suitable for modeling head-injury accidents.     

A fully nonlinear viscohyperelastic model for the brain tissue applicable to dynamic rates

Understanding the mechanical response of the brain to external loadings is of critical importance in investigating the pathological conditions of this tissue during injurious conditions. Such injurious loadings may occur at high rates, for example among others, during road traffic or sport accidents, falls, or due to explosions. Hence, investigating the injury mechanism and design of protective devices for the brain requires constitutive modeling of this tissue at such rates. Accordingly, this paper is aimed at critically investigating the physical background for viscohyperelastic modeling of the brain tissue with scrutinizing the elastic fields pertinent to large, time dependent deformations, and developing a fully nonlinear multimode Maxwell model that can mathematically explain such deformations. The proposed model can be calibrated using the simple monotonic uniaxial deformation of the sample extracted from the tissue, and does not require additional information from relaxation or creep experiments. The performance of the proposed model is examined using the experimental results of two different studies, which reveals a desirable agreement. The usefulness, limitations, and future developments of the proposed model are discussed in this paper.     

A computational study of the EN 1078 impact test for bicycle helmets using a realistic subject-specific finite element head model

Abstract

In the present study, the free fall impact test in accordance with the EN1078 standard for certification of bicycle helmets is replicated using numerical simulations. The impact scenario is simulated using an experimentally validated, patient-specific head model equipped with and without a bicycle helmet. Head accelerations and intracranial biomechanical injury metrics during the impacts are recorded. It is demonstrated that wearing the bicycle helmet during the impact reduces biomechanical injury metrics, with the biggest reduction seen in the metric for skull fracture.     

大鼠二次脑损伤后脑组织SOD及MDA的变化研究

目的:观察大鼠二次脑损伤后脑组织SOD及MDA的变化,进一步探讨过氧化反应在二次脑损伤机制中的作用。方法:90只雄性SD大鼠随机分为正常对照组(A组)、弥漫性脑损伤组(B组)和二次脑损伤组(C组),建模成功后,分别于伤后1 h、3 h、6h、12 h、24 h、48 h处死动物,取额叶组织匀浆,分别测定大鼠脑内SOD及MDA的含量。结果:伤后1h开始,B、C组中SOD含量呈现先上升后下降的趋势,并随时间呈持续下降趋势直至伤后24 h,C组较B组下降程度更加明显(P0.05);伤后3 h,B、C组中SOD含量均增高,B组增高程度和速率均高于C组(P0.05)。伤后1 h开始,B、C组MDA含量呈升高趋势,并于24小时达峰值,C组升高趋势较B组更显著,伤后6 h、24 h、48 h,C组与B组之间相比统计学差异显著(P0.05)。结论:创伤性脑损伤及二次脑损伤后,脑组织内过氧化反应明显加重,SOD及MDA均出现明显变化,二次脑损伤的过氧化反应较脑损伤组更加严重且持续时间更长,且MDA较SOD的变化具有滞后性。     

Brain response to traumatic brain injury in wild-type and interleukin-6 knockout mice: a microarray analysis

Traumatic injury to the brain is one of the leading causes of injury-related death or disability. Brain response to injury is orchestrated by cytokines, such as interleukin (IL)-6, but the full repertoire of responses involved is not well known. We here report the results obtained with microarrays in wild-type and IL-6 knockout mice subjected to a cryolesion of the somatosensorial cortex and killed at 0, 1, 4, 8 and 16 days post-lesion. Overall gene expression was analyzed by using Affymetrix genechips/oligonucleotide arrays with approximately 12,400 probe sets corresponding to approximately 10,000 different murine genes (MG_U74Av2). A robust, conventional statistical method (two-way anova) was employed to select the genes significantly affected. An orderly pattern of gene responses was clearly detected, with genes being up- or down-regulated at specific timings consistent with the processes involved in the initial tissue injury and later regeneration of the parenchyma. IL-6 deficiency showed a dramatic effect in the expression of many genes, especially in the 1 day post-lesion timing, which presumably underlies the poor capacity of IL-6 knockout mice to cope with brain damage. The results highlight the importance of IL-6 controlling the response of the brain to injury as well as the suitability of microarrays for identifying specific targets worthy of further study.     

Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

Due to the high mortality incident brought about by traumatic brain injury (TBI), methods that would enable one to better understand the underlying mechanisms involved in it are useful for treatment. There are both in vivo and in vitro methods available for this purpose. In vivo models can mimic actual head injury as it occurs during TBI. However, in vivo techniques may not be exploited for studies at the cell physiology level. Hence, in vitro methods are more advantageous for this purpose since they provide easier access to the cells and the extracellular environment for manipulation.Our protocol presents an in vitro model of TBI using stretch injury in brain microvascular endothelial cells. It utilizes pressure applied to the cells cultured in flexible-bottomed wells. The pressure applied may easily be controlled and can produce injury that ranges from low to severe. The murine brain microvascular endothelial cells (cEND) generated in our laboratory is a well-suited model for the blood brain barrier (BBB) thus providing an advantage to other systems that employ a similar technique. In addition, due to the simplicity of the method, experimental set-ups are easily duplicated. Thus, this model can be used in studying the cellular and molecular mechanisms involved in TBI at the BBB.     

Influence of rapidly successive head impacts on brain strain in the vicinity of bridging veins

Acute subdural hematoma due to a bridging vein rupture is a devastating but rare injury. There has to date been no satisfactory biomechanical explanation for this infrequent but costly injury. We surmise that it may be associated with multiple head impacts. Though numerical models have been used to estimate vein strains in single impact events, none to date have examined the influence on localized brain strain of rapidly consecutive impacts. Using the Simulated Injury Monitor, we investigated the hypothesis that such double impacts can increase strain beyond that created by any single impact. Input to our parametric study comprised hypothetical biphasic rotational head accelerations producing a maximum angular velocity of 40 rad./s. In each of 19 simulations, two identical angular inputs are applied at right angles to each other but with time separations varying from 0 to 40 ms. For these double impacts, it has been generally found that strain in the region of the bridging veins is different, than what would be associated with any corresponding single impact. In some cases, the effect is to actually reduce the tissue strain. In others, the strain in the region of the bridging veins is increased markedly. The mechanistic explanation for the strain increase is that the tissue strain from the first impact has not diminished fully when strain from the second impact is initiated. Rapidly consecutive impacts could be a potential mechanism leading to vein rupture that warrants further investigation.     

急诊绿色通道提高颅脑外伤患者救治效果的体会

目的:评价建立急诊绿色通道对救治颅脑外伤患者的价值.方法:采用回顾性分析方法,收集我院2007年1月～2012年1月救治的颅脑外伤患者199例,其中急诊绿色通道组111例(A组)和非急诊绿色通道组88例(B组)的救治情况进行比较,分析两组救治的疗效、死亡率及预后.结果:199例颅脑外伤患者中,绿色通道组(A组)111例(55.78％),死亡26例(23.42％),对照组88例(44.22％),死亡30例(34.09％).A组的有效治疗时间较B组明显缩短,差异有统计学意义(0.01＜P＜0.05);A组硬膜外血肿(33例)的术前血肿量少于B组(30例),预后较B组好,差异有统计学意义(0.01＜P＜0.05);A组的中重型颅脑外伤的死亡率明显低于B组,差异有统计学意义(0.01＜P＜0.05),两组特重性颅脑外伤的死亡率仍较高,差异无统计学意义(P＞0.05).结论:急诊绿色通道可缩短颅脑外伤患者救治等待时间,改善中重型颅脑外伤患者的预后.     

Towards reducing impact-induced brain injury: lessons from a computational study of army and football helmet pads

We use computational simulations to compare the impact response of different football and U.S. Army helmet pad materials. We conduct experiments to characterise the material response of different helmet pads. We simulate experimental helmet impact tests performed by the U.S. Army to validate our methods. We then simulate a cylindrical impactor striking different pads. The acceleration history of the impactor is used to calculate the head injury criterion for each pad. We conduct sensitivity studies exploring the effects of pad composition, geometry and material stiffness. We find that (1) the football pad materials do not outperform the currently used military pad material in militarily relevant impact scenarios; (2) optimal material properties for a pad depend on impact energy and (3) thicker pads perform better at all velocities. Although we considered only the isolated response of pad materials, not entire helmet systems, our analysis suggests that by using larger helmet shells with correspondingly thicker pads, impact-induced traumatic brain injury may be reduced.     

Foxj1 在脑外伤后的表达变化

目的:探讨脑外伤后Foxj1在脑组织中的表达变化及其意义。方法:建立大鼠脑外伤模型,利用Western blot和免疫组织化学方法检测脑外伤后Foxj1在脑组织中表达的变化。结果:Western blot显示大鼠脑外伤后,Foxj1的表达逐步增高,伤后3 d升至最高点,之后逐渐降低;免疫组织化学的结果与Western blot一致。结论:脑外伤后Foxj1在脑组织中的表达增高,这种增高的表达参与了脑外伤后脑组织的病理生理和生化变化。     

N-Terminal Arginylation of Sciatic Nerve and Brain Proteins Following Injury

N-terminal protein arginylation has been demonstrated in vitro and in situ and has been reported to increase following injury to sciatic nerves of rats. The present study attempts to demonstrate these reactions in vivo by applying [³H]Arg to the cut end of sciatic nerves in anesthetized rats and assaying for N-terminal arginylation using Edman chemistry and acid precipitation of labeled proteins in the proximal nerve segment. No evidence was found for arginylation in an aqueous soluble fraction. However, N-terminal arginylation was detected in a urea soluble fraction at 2 hours after nerve crush. The data show that arginylation of rat sciatic nerve proteins occurs in vivo and suggest that the arginylated proteins formed an aqueous insoluble/urea soluble aggregate after arginylation. In other experiments, rat brains were injured and assayed for arginylation in vitro to test the hypothesis that injury causes an up-regulation of these reactions. Results showed an activation of the reaction at 2 hours post crush and indicate that increases in N-terminal arginylation are likely to be a general response to injury in nervous tissue.     

液压脑损伤大鼠大脑皮质突触素的动态变化

目的:探讨液压脑损伤后突触素在皮质区表达的动态变化.方法:应用液压脑损伤复制脑损伤动物模型,应用免疫组织化学和计算机图像分析技术定量分析皮质受损区突触素表达的动态变化.结果:突触素在皮质受伤区表达呈现两次高峰:分别为3～12h和15～30d,90d表达接近正常.结论:突触素在皮质受伤区第2次表达增高可能与脑的结构和功能恢复有关.急性期表达增高则可能与脑的直接损伤有关.     

丙泊酚镇静对颅脑损伤患者脑氧供需平衡的影响

目的:探讨丙泊酚实施不同程度镇静对颅脑损伤患者脑氧供需平衡的影响。方法:选择急性闭合性颅脑损伤需行机械通气患者46例,随机分为轻度镇静组(A组),设定目标脑电双频谱指数(BIS)值75%;中度镇静组(B组),设定目标BIS值65%。主要观察达设定目标BIS值时丙泊酚靶控输注(TCI)浓度、Ramsay镇静评分、脑氧供需平衡指标颈内静脉血氧饱和度(SjvO_2)和脑氧摄取率(CERO_2)以及心率(HR)、平均动脉压(MAP)。结果:两组设定镇静目标需丙泊酚TCI浓度有明显差异(P0.05),但Ramsay评分比较差异无统计学意义;中度镇静组SjvO_2较基础值增加约12%(P0.05),CERO_2较基础值下降约15%(P0.05);而轻度镇静组对SjvO_2和CERO_2基础值没有影响。两组HR均较基础值减慢(P0.05),但对MAP均没有影响。结论:颅脑损伤患者维持目标镇静BIS值65%,调控丙泊酚靶浓度1.5-1.6μg/mL,更有利于改善脑氧供需平衡。     

脑外伤所致精神障碍的危险因素分析

目的：探究脑外伤所致精神障碍的的危险因素,以探究各类因素与脑外伤患者预后的关联,为今后的临床治疗及干预措施提供理论依据。方法：对我院2009年6月-2012年9月收治的217例脑外伤患者进行回顾分析,按照其是否出现精神障碍分为精神障碍组及非精神障碍组,对比其临床资料,将存在统计学意义的指标纳入Logistic多因素回归分析,探讨脑外伤所致精神障碍的的危险因素。结果：217例脑外伤患者共出现162例精神障碍,精神障碍发病率74．7％;两组患者一般资料对比可见,颅内血肿、脑干损伤、脑叶损伤范围、GCS评分及EPQ评分存在统计学意义（p〈0．05）;多因素回归分析发现,GCS评分s8分及EPQ评分≥30分存在统计学差异（p〈0．05）,是影响脑外伤所致精神障碍的独立危险因素。结论：GCS评分s8分及EPQ评分≥30分存在统计学差异（p〈0．05）,是影响脑外伤所致精神障碍的独立危险因素,应在患者接受常规脑外伤治疗后进行环境护理、日常生活护理及心理护理,改善其不稳定情绪,并对其意识状态进行密切监测,必要时可预防性使用抗精神病药物,以降低患者精神障碍患病率,改善其生活质量。     

Directed cellular self-assembly to fabricate cell-derived tissue rings for biomechanical analysis and tissue engineering

Each year, hundreds of thousands of patients undergo coronary artery bypass surgery in the United States.(1) Approximately one third of these patients do not have suitable autologous donor vessels due to disease progression or previous harvest. The aim of vascular tissue engineering is to develop a suitable alternative source for these bypass grafts. In addition, engineered vascular tissue may prove valuable as living vascular models to study cardiovascular diseases. Several promising approaches to engineering blood vessels have been explored, with many recent studies focusing on development and analysis of cell-based methods.(2-5) Herein, we present a method to rapidly self-assemble cells into 3D tissue rings that can be used in vitro to model vascular tissues. To do this, suspensions of smooth muscle cells are seeded into round-bottomed annular agarose wells. The non-adhesive properties of the agarose allow the cells to settle, aggregate and contract around a post at the center of the well to form a cohesive tissue ring.(6,7) These rings can be cultured for several days prior to harvesting for mechanical, physiological, biochemical, or histological analysis. We have shown that these cell-derived tissue rings yield at 100-500 kPa ultimate tensile strength(8) which exceeds the value reported for other tissue engineered vascular constructs cultured for similar durations (<30 kPa).(9,10) Our results demonstrate that robust cell-derived vascular tissue ring generation can be achieved within a short time period, and offers the opportunity for direct and quantitative assessment of the contributions of cells and cell-derived matrix (CDM) to vascular tissue structure and function.