scholarly journals Pathomorphological markers of blast-induced brain injury

Morphologia ◽  
2021 ◽  
Vol 15 (3) ◽  
pp. 96-100
Author(s):  
S.V. Kozlov ◽  
V.D. Mishalov ◽  
K.М. Sulojev ◽  
Yu.V. Kozlova
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Blast Wave ◽  
Age Distribution ◽  
Vascular Wall ◽  
Histopathological Analysis ◽  
Perivascular Spaces ◽  
Distribution Analysis ◽  
The Dead ◽  
The Brain

Background. Recently, interest in blast-induced brain injuries has been increasing due to military events and the use of explosive devices in eastern Ukraine. Considering the diagnostic uncertainty regarding the specific signs of brain injury after the distant action of an blast shock wave, the danger of prognostic consequences, the increase of the cases of explosive injury number, we consider that selected for study topic is relevant. Objective. Purpose – determination of pathomorphological changes of the brain after the action of the blast wave. Methods. To solving this purpose, a retrospective analysis of 280 cases of fatal military blast injuries was conducted. We selected 6 cases for microscopic examination of the brain. For histological examination, samples were taken from different parts of the brain. Results. Analysis of 280 deaths due to explosive trauma showed that 58.9% of the dead (165) had a traumatic brain injury, and in 131 cases it was accompanied by fractures of the bones of the vault and the base of the skull. Isolated traumatic brain injury was detected in only 33 cases (11.8%). Age distribution analysis of the dead people showed that 67.5% of the dead were between the ages of 21 and 40. Histopathological analysis of brain samples from the dead allowed to identify the characteristic signs of blast-induced brain injury in the form of diffuse formation of perivascular microhemorrhages with partial or complete separation of the vascular wall from the neuropil. Conclusion. The complex of microscopic signs in the brain, namely, the separation of vascular wall from neuroglia with the formation of perivascular space, fragmentation of these vessels walls, erythrocytes hemolysis, hemorrhage in the newly formed perivascular spaces, are direct evidences of the blast wave action.

Simulation of Blast Induced Traumatic Brain Injury using Finite Element Method

2021 ◽  
Vol 13 (2) ◽  
Author(s):  
G. Krishnaveni ◽  
D. Dominic Xavier ◽  
R. Sarathkumar ◽  
G. Kavitha ◽  
M. Senbagan
Keyword(s):  
Traumatic Brain Injury ◽  
Finite Element ◽  
Brain Injury ◽  
Blast Wave ◽  
Ambient Pressure ◽  
Memory Loss ◽  
Human Head ◽  
Head Model ◽  
Stress Concentrations ◽  
The Brain

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.

Computational Analysis for Validation of Blast Induced Traumatic Brain Injury and Protection of Combat Helmet

2018 ◽  
Author(s):  
X. Gary Tan ◽  
Amit Bagchi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Shock Tube ◽  
Blast Wave ◽  
High Fidelity ◽  
Blast Loads ◽  
Next Generation ◽  
Energy Transmission ◽  
The Brain

Current understanding of blast wave transmission and mechanism of primary traumatic brain injury (TBI) and the role of helmet is incomplete thus limiting the development of protection and therapeutic measures. Combat helmets are usually designed based on costly and time consuming laboratory tests, firing range, and forensic data. Until now advanced medical imaging and computational modeling tools have not been adequately utilized in the design and optimization of combat helmets. The goal of this work is to develop high fidelity computational tools, representative virtual human head and combat helmet models that could help in the design of next generation helmets with improved blast and ballistic protection. We explore different helmet configurations to investigate blast induced brain biomechanics and understand the protection role of helmet by utilizing an integrated experimental and computational method. By employing the coupled Eulerian-Lagrangian fluid structure interaction (FSI) approach we solved the dynamic problem of helmet and head under the blast exposure. Experimental shock tube tests of the head surrogate provide benchmark quality data and were used for the validation of computational models. The full-scale computational NRL head-neck model with a combat helmet provides physical quantities such as acceleration, pressure, strain, and energy to blast loads thus provides a more complete understanding of the conditions that may contribute to TBI. This paper discusses possible pathways of blast energy transmission to the brain and the effectiveness of helmet systems at blast loads. The existing high-fidelity image-based finite element (FE) head model was applied to investigate the influence of helmet configuration, suspension pads, and shell material stiffness. The two-phase flow model was developed to simulate the helium-air shock wave interaction with the helmeted head in the shock tube. The main contribution was the elucidation of blast wave brain injury pathways, including wave focusing in ocular cavities and the back of head under the helmet, the effect of neck, and the frequency spectrum entering the brain through the helmet and head. The suspension material was seen to significantly affect the ICP results and energy transmission. These findings can be used to design next generation helmets including helmet shape, suspension system, and eye protection.

scholarly journals Effects of traumatic brain injury on sleep and enlarged perivascular spaces

2018 ◽  
Vol 39 (11) ◽  
pp. 2258-2267 ◽  
Author(s):  
Ryan A Opel ◽  
Alison Christy ◽  
Erin L Boespflug ◽  
Kristianna B Weymann ◽  
Brendan Case ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Total Sleep Time ◽  
Brain Mri ◽  
Sleep Time ◽  
Perivascular Spaces ◽  
History Of ◽  
The Relationship ◽  
The Brain

Clearance of perivascular wastes in the brain may be critical to the pathogenesis of amyloidopathies. Enlarged perivascular spaces (ePVS) on MRI have also been associated with amyloidopathies, suggesting that there may be a mechanistic link between ePVS and impaired clearance. Sleep and traumatic brain injury (TBI) both modulate clearance of amyloid-beta through glymphatic function. Therefore, we sought to evaluate the relationship between sleep, TBI, and ePVS on brain MRI. A retrospective study was performed in individuals with overnight polysomnography and 3T brain MRI consented from a single site ( n = 38). Thirteen of these individuals had a medically confirmed history of TBI. ePVS were visually assessed by blinded experimenters and analyzed in conjunction with sleep metrics and TBI status. Overall, individuals with shorter total sleep time had significantly higher ePVS burden. Furthermore, individuals with TBI showed a stronger relationship between sleep and ePVS compared to the non-TBI group. These results support the hypothesis that ePVS may be modulated by sleep and TBI, and may have implications for the role of the glymphatic system in ePVS.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

Providing Care of Mild Traumatic Brain Injury by the Family Practice/Primary Care Optometrist

2018 ◽  
pp. 110-119
Keyword(s):  
Primary Care ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Family Practice ◽  
Advanced Training ◽  
Entry Level ◽  
The Family ◽  
Basic Understanding ◽  
The Brain

Primary Objectives: By extending the scope of knowledge of the primary care optometrist, the brain injury population will have expanded access to entry level neurooptometric care by optometric providers who have a basic understanding of their neurovisual problems, be able to provide some treatment and know when to refer to their colleagues who have advanced training in neuro-optometric rehabilitation.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

scholarly journals Engineered glycomaterial implants orchestrate large-scale functional repair of brain tissue chronically after severe traumatic brain injury

2021 ◽  
Vol 7 (10) ◽  
pp. eabe0207
Author(s):  
Charles-Francois V. Latchoumane ◽  
Martha I. Betancur ◽  
Gregory A. Simchick ◽  
Min Kyoung Sun ◽  
Rameen Forghani ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Large Scale ◽  
Growth Factor Signaling ◽  
Neuronal Circuit ◽  
Reach To Grasp ◽  
Function Recovery ◽  
Cellular Repair ◽  
The Brain

Severe traumatic brain injury (sTBI) survivors experience permanent functional disabilities due to significant volume loss and the brain’s poor capacity to regenerate. Chondroitin sulfate glycosaminoglycans (CS-GAGs) are key regulators of growth factor signaling and neural stem cell homeostasis in the brain. However, the efficacy of engineered CS (eCS) matrices in mediating structural and functional recovery chronically after sTBI has not been investigated. We report that neurotrophic factor functionalized acellular eCS matrices implanted into the rat M1 region acutely after sTBI significantly enhanced cellular repair and gross motor function recovery when compared to controls 20 weeks after sTBI. Animals subjected to M2 region injuries followed by eCS matrix implantations demonstrated the significant recovery of “reach-to-grasp” function. This was attributed to enhanced volumetric vascularization, activity-regulated cytoskeleton (Arc) protein expression, and perilesional sensorimotor connectivity. These findings indicate that eCS matrices implanted acutely after sTBI can support complex cellular, vascular, and neuronal circuit repair chronically after sTBI.

scholarly journals The Challenge of Managing Patients Suffering from TBI: The Utility of Multiparametric MRI

CNS Spectrums ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 178-179
Author(s):  
John L. Sherman ◽  
Laurence J. Adams ◽  
Christen F. Kutz ◽  
Deborah York ◽  
Mitchell S. Szymczak
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Family History ◽  
Diffusion Tensor ◽  
Multiparametric Mri ◽  
Psychiatric History ◽  
Post Injury ◽  
Negative Family History ◽  
Imaging Result ◽  
The Brain

AbstractTraumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.We have selected two TBI patients with diffuse traumatic brain injury.The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.

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