Experimental Study on Non-Exit Ballistic Induced Traumatic Brain Injury

Author(s):  
Jiangyue Zhang ◽  
Narayan Yoganandan ◽  
Frank A. Pintar ◽  
Yabo Guan ◽  
Thomas A. Gennarelli

Ballistic-induced traumatic brain injury remains the most severe type of injury with the highest rate of fatality. Yet, its injury biomechanics remains the least understood. Ballistic injury biomechanics studies have been mostly focused on the trunk and extremities using large gelatin blocks with unconstrained boundaries [1, 2]. Results from these investigations are not directly applicable to brain injuries studies because the human head is smaller and the soft brain is enclosed in a relatively rigid cranium. Thali et al. developed a “skin-skull-brain” model to reproduce gunshot wounds to the head for forensic purposes [3]. These studies focused on wound morphology to the skull rather than brain injury. Watkins et al. used human dry skulls filled with gelatin and investigated temporary cavities and pressure change [4]. However, the frame rate of the cine X-ray was too slow to describe the cavity dynamics, and pressures were only quantified at the center of skull. In addition, the ordnance gelatin used in these studies is not the most suitable simulant to model brain material because of differences in dynamic moduli [5]. Sylgard gel (Dow Corning Co., Midland, MI) demonstrates similar behavior as the brain and has been used as a brain surrogate to determine brain deformations under blunt impact loading [6, 7]. Zhang et al. used the simulant for ballistic brain injury and investigated the correlation between temporary cavity pulsation and pressure change [8, 9]. However, the skulls used in these models were not as rigid as the human cranium. The presence of a stronger cranial bone may significantly decrease the projectile velocity and change the kinematics of cavity and pressure distribution in the cranium. In addition, projectiles perforated through the models in these studies. Patients with through-and-through perforating gunshot wounds to the head have a greater fatality rate than patients with non-exit penetrating wounds [10]. Therefore, it is more clinically relevant to investigate non-exit ballistic traumatic brain injuries. Consequently, the current study is designed to investigate the brain injury biomechanics from non-exit penetrating projectile using an appropriately sized and shaped physical head model.

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Ligang Wang ◽  
Libo Wang ◽  
Zhibo Dai ◽  
Pei Wu ◽  
Huaizhang Shi ◽  
...  

Oxidative stress has been strongly implicated in the pathogenesis of traumatic brain injury (TBI). Mitochondrial ferritin (Ftmt) is reported to be closely related to oxidative stress. However, whether Ftmt is involved in TBI-induced oxidative stress and neurological deficits remains unknown. In the present study, the controlled cortical impact model was established in wild-type and Ftmt knockout mice as a TBI model. The Ftmt expression, oxidative stress, neurological deficits, and brain injury were measured. We found that Ftmt expression was gradually decreased from 3 to 14 days post-TBI, while oxidative stress was gradually increased, as evidenced by reduced GSH and superoxide dismutase levels and elevated malondialdehyde and nitric oxide levels. Interestingly, the extent of reduced Ftmt expression in the brain was linearly correlated with oxidative stress. Knockout of Ftmt significantly exacerbated TBI-induced oxidative stress, intracerebral hemorrhage, brain infarction, edema, neurological severity score, memory impairment, and neurological deficits. However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine. Taken together, these results reveal an important correlation between Ftmt and oxidative stress after TBI. Ftmt deficiency aggravates TBI-induced brain injuries and neurological deficits, which at least partially through increasing oxidative stress levels. Our data suggest that Ftmt may be a promising molecular target for the treatment of TBI.


2014 ◽  
Vol 80 (4) ◽  
pp. 335-338 ◽  
Author(s):  
Bellal Joseph ◽  
Hassan Aziz ◽  
Viraj Pandit ◽  
Daniel Hays ◽  
Narong Kulvatunyou ◽  
...  

Coagulopathy is a defined barrier for organ donation in patients with lethal traumatic brain injuries. The purpose of this study was to document our experience with the use of prothrombin complex concentrate (PCC) to facilitate organ donation in patients with lethal traumatic brain injuries. We performed a 4-year retrospective analysis of all patients with devastating gunshot wounds to the brain. The data were analyzed for demographics, change in international normalized ratio (INR), and subsequent organ donation. The primary end point was organ donation. Eighty-eight patients with lethal traumatic brain injury were identified from the trauma registry of whom 13 were coagulopathic at the time of admission (mean INR 2.2 ± 0.8). Of these 13 patients, 10 patients received PCC in an effort to reverse their coagulopathy. Mean INR before PCC administration was 2.01 ± 0.7 and 1.1 ± 0.7 after administration ( P < 0.006). Correction of coagulopathy was attained in 70 per cent (seven of 10) patients. Of these seven patients, consent for donation was obtained in six patients and resulted in 19 solid organs being procured. The cost of PCC per patient was $1022 ± 544. PCC effectively reveres coagulopathy associated with lethal traumatic brain injury and enabled patients to proceed to organ donation. Although various methodologies exist for the treatment of coagulopathy to facilitate organ donation, PCC provides a rapid and cost-effective therapy for reversal of coagulopathy in patients with lethal traumatic brain injuries.


Author(s):  
Jiangyue Zhang ◽  
Narayan Yoganandan ◽  
Frank A. Pintar ◽  
Steven F. Son ◽  
Thomas A. Gennarelli

Traumatic brain injury from explosive devices has become the signature wound of the U.S. armed forces in Iraq and Afghanistan [1–4]. However, due to the complicated nature of this specific form of brain injury, little is known about the injury mechanisms. Physical head models have been used in blunt and penetrating head trauma studies to obtain biomechanical data and correlate to mechanisms of injury [5–8]. The current study is designed to investigate intracranial head/brain injury biomechanics under blast loading using a physical head model.


2017 ◽  
Vol 36 (4) ◽  
pp. 314-321 ◽  
Author(s):  
Branislava Stefanović ◽  
Olivera Đurić ◽  
Sanja Stanković ◽  
Srđan Mijatović ◽  
Krstina Doklestić ◽  
...  

SummaryBackground: The objective of our study was to determine the serum concentrations of protein S100B and neuron specific enolase (NSE) as well as their ability and accuracy in the prediction of early neurological outcome after a traumatic brain injury. Methods: A total of 130 polytraumatized patients with the associated traumatic brain injuries were included in this prospective cohort study. Serum protein S100B and NSE levels were measured at 6, 24, 48 and 72 hours after the injury. Early neurological outcome was scored by Glasgow Outcome Scale (GOS) on day 14 after the brain injury. Results: The protein S100B concentrations were maximal at 6 hours after the injury, which was followed by an abrupt fall, and subsequently slower release in the following two days with continual and significantly increased values (p<0.0001) in patients with poor outcome. Secondary increase in protein S100B at 72 hours was recorded in patients with lethal outcome (GOS 1). Dynamics of NSE changes was characterized by a secondary increase in concentrations at 72 hours after the injury in patients with poor outcome. Conclusion: Both markers have good predictive ability for poor neurological outcome, although NSE provides better discriminative potential at 72 hours after the brain injury, while protein S100B has better discriminative potential for mortality prediction.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Juliane Schiweck ◽  
Kai Murk ◽  
Julia Ledderose ◽  
Agnieszka Münster-Wandowski ◽  
Marta Ornaghi ◽  
...  

AbstractThe brain of mammals lacks a significant ability to regenerate neurons and is thus particularly vulnerable. To protect the brain from injury and disease, damage control by astrocytes through astrogliosis and scar formation is vital. Here, we show that brain injury in mice triggers an immediate upregulation of the actin-binding protein Drebrin (DBN) in astrocytes, which is essential for scar formation and maintenance of astrocyte reactivity. In turn, DBN loss leads to defective astrocyte scar formation and excessive neurodegeneration following brain injuries. At the cellular level, we show that DBN switches actin homeostasis from ARP2/3-dependent arrays to microtubule-compatible scaffolds, facilitating the formation of RAB8-positive membrane tubules. This injury-specific RAB8 membrane compartment serves as hub for the trafficking of surface proteins involved in astrogliosis and adhesion mediators, such as β1-integrin. Our work shows that DBN-mediated membrane trafficking in astrocytes is an important neuroprotective mechanism following traumatic brain injury in mice.


2021 ◽  
Vol 5 (4) ◽  
pp. 1218-1222
Author(s):  
Yuliarni Syafrita ◽  
Nora Fitri

Background : Traumatic brain injury is still the main cause of death and disability in productive age. Assessment the level of consciousness and imaging examinations after a brain injury can not always describe the severity of damage in the brain, this is because the pathological process is still ongoing due to secondary brain injury. Therefore, it is necessary to examine biomarkers that can describe the severity of the pathological process that occurs. The purpose of this study was to assess serum neuron-specific enolase (NSE) levels and their relationship to the severity and outcome of a traumatic brain injury. Methods : A cross sectional design was conducted in the emergency department of DR M Djamil Hospital, Padang. There were 72 patients who met the inclusion criteria. A Glasgow Coma Scale examination was performed to assess the severity of brain injury and examination of NSE serum levels at 48 hours post- injury using ELISA technique and assess the Glasgow outcome scale (GOS) at 6 weeks post-injury. Data analysis using SPSS 22 program, the results are significance if the p value <0.05  Results : The average NSE level was higher in severe brain injuries than moderate and mild brain injuries and this difference was statistically significant (p<0.05).  The NSE serum levels were higher in poor outcomes than in good outcomes and this difference was statistically significant (p<0.05).  Conclusion : High NSE serum levels in the acute phase were associated with the severity of the brain injury and poor outcome 6 weeks after the brain injury. 


Author(s):  
Ermias G. Koricho ◽  
Elizabeth Dimsdale

Traumatic Brain Injuries (TBI) occur approximately 1.7 million times each year in the U.S., with motor vehicle crashes as the second leading cause of TBI-related hospitalizations, and the first leading cause of TBI-related deaths among specific age groups. Several studies have been conducted to better understand the impact on the brain in vehicle crash scenarios. However, the complexity of the head is challenging to replicate numerically the head response during vehicle crash and the resulting traumatic Brain Injury. Hence, this study aims to investigate the effect of vehicle structural padding and head form modeling representation on the head response and the resulting causation and Traumatic Brain Injury (TBI). In this study, a simplified and complex head forms with various geometries and materials including the skull, cerebrospinal fluid (CSF), neck, and muscle were considered to better understand and predict the behavior of each part and their effect on the response of the brain during an impact scenario. The effect of padding thickness was also considered to further analyze the interaction of vehicle structure and the head response. The numeral results revealed that the responses of the head skull and the brain under impact load were highly influenced by the padding thickness, head skull material modeling and assumptions, and neck compliance. Generally, the current work could be considered an alternative insight to understand the correlation between vehicle structural padding, head forms, and materials modeling techniques, and TBI resulted from a vehicle crash.


Author(s):  
G. Krishnaveni ◽  
D. Dominic Xavier ◽  
R. Sarathkumar ◽  
G. Kavitha ◽  
M. Senbagan

Because of increase in threat from militant groups and during war exposure to blast wave from improvised explosive devices, Traumatic Brain Injury (TBI), a signature injury is on rise worldwide. During blast, the biological system is exposed to a sudden blast over pressure which is several times higher than the ambient pressure causing the damage in the brain. The severity of TBI due to air blast may vary from brief change in mental status or consciousness (termed as mild) to extended period of unconsciousness or memory loss after injuries (termed as severe). The blast wave induced impact on head propagates as shock wave with the broad spectrum of frequencies and stress concentrations in the brain. The primary blast TBI is directly induced by pressure differentials across the skull/fluid/soft tissue interfaces and is further reinforced by the reflected stress waves within the cranial cavity, leading to stress concentrations in certain regions of the brain. In this paper, an attempt has been made to study the behaviour of a human brain model subjected to blast wave based on finite element model using LSDYNA code. The parts of a typical human head such as skull, scalp, CSF, brain are modelled using finite element with properties assumed based on available literature. The model is subjected to blast from frontal lobe, occipital lobe, temporal lobe of the brain. The interaction of the blast wave with the head and subsequent transformation of various forms of shock energy internally have been demonstrated in the human head model. The brain internal pressure levels and the shear stress distribution in the various lobes of the brain such as frontal, parietal, temporal and occipital are determined and presented.


2013 ◽  
Vol 4 (4) ◽  
pp. 56-60 ◽  
Author(s):  
Mariy Lazarevna Chukhlovina

The review article concerns some issues of improved diagnostics and main neuro-radiological criteria of traumatic brain injuries in childhood. Special attention is given to anatomic and physiological features of brain in children, aiming for proper evaluation of severity in traumatic brain injury. We provide a summary of data concerning modern echniques of brain trauma diagnostics, and its consequences in children. Utility of neurovisualization, electrophysiological techniques, biochemical approaches for detecting the brain damage biomarkers, demonstrated in order to determine severity of brain trauma in childhood.


Author(s):  
Valerie Gray Hardcastle

The Centers for Disease Control and Prevention estimates that the lifetime traumatic brain injury (TBI) rates for prisoners are higher than for the general population. The impulsive and aggressive behaviors resulting from TBI also parallel incarceration rates. But how scientific communities understand the origins of behavior clashes with how our justice system does. Medicine, psychiatry, neuropsychology, and neurology all hold that deformities in the brain can influence or even determine a person’s thoughts, desires, impulses, and ability to control behavior. In contrast, U.S. law assumes that adults are rational beings who act for specific reasons and that, in each instance, an individual could have done otherwise. Yet, the American court system is beginning to differentiate returning combat vets with brain disorders from other offenders, creating diversion courts for veterans accused of a variety of crimes. These courts allow military offenders to enter a mental health treatment program instead of being jailed. Several questions arise from this practice. Should vets be treated differently than other noncombatant defendants with similar brain injuries? Should brain disorders affect how we assign or understand legal notions of punishment and responsibility? How do we connect data regarding neural interventions with punishment and remediation? And how do we distinguish “mad” from “bad”? This chapter attempts to answer these questions.


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