A Multi-Scale Finite Element Model for Shock Wave-Induced Axonal Brain Injury

2008 ◽  
Author(s):  
M. Sotudeh-Chafi ◽  
N. Abolfathi ◽  
A. Nick ◽  
V. Dirisala ◽  
G. Karami ◽  
...  
Keyword(s):  
Shock Wave ◽  
Brain Injury ◽  
Shock Waves ◽  
Brain Tissue ◽  
Scale Model ◽  
Micro Scale ◽  
Multi Scale ◽  
Injury Criteria ◽  
Wave Induced ◽  
The Brain

Traumatic brain injuries (TBIs) involve a significant portion of human injuries resulting from a wide range of civilian accidents as well as many military scenarios. Axonal damage is one of the most common and important pathologic features of traumatic brain injury. Axons become brittle when exposed to rapid deformations associated with brain trauma. Accordingly, rapid stretch of axons can damage the axonal cytoskeleton, resulting in a loss of elasticity and impairment of axoplasmic transport. Subsequent swelling of the axon occurs in discrete bulb formations or in elongated varicosities that accumulate organelles. Ultimately, swollen axons may become disconnected [1]. The shock waves generated by a blast, subject all the organs in the head to displacement, shearing and tearing forces. The brain is especially vulnerable to these forces — the fronts of compressed air waves cause rapid forward or backward movements of the head, so that the brain rattles against the inside of the skull. This can cause subdural hemorrhage and contusions. The forces exerted on the brain by shock waves are known to damage axons in the affected areas. This axonal damage begins within minutes of injury, and can continue for hours or days following the injury [2]. Shock waves are also known to damage the brain at the subcellular level, but exactly how remains unclear. Kato et al., [3] described the effects of a small controlled explosion on rats’ brain tissue. They found that high pressure shock waves led to contusions and hemorrhage in both cortical and subcortical brain regions. Based on their result, the threshold for shock wave-induced brain injury is speculated to be under 1 MPa. This is the first report to demonstrate the pressure-dependent effect of shock wave on the histological characteristics of brain tissue. An important step in understanding the primary blast injury mechanism due to explosion is to translate the global head loads to the loading conditions, and consequently damage, of the cells at the local level and to project cell level and tissue level injury criteria towards the level of the head. In order to reach this aim, we have developed a multi-scale non-linear finite element modeling to bridge the micro- and macroscopic scales and establish the connection between microstructure and effective behavior of brain tissue to develop acceptable injury threshold. Part of this effort has been focused on measuring the shock waves created from a blast, and studying the response of the brain model of a human head exposed to such an environment. The Arbitrary Lagrangian Eulerian (ALE) and Fluid/Solid Interactions (FSI) formulation have been used to model the brain-blast interactions. Another part has gone into developing a validated fiber-matrix based micro-scale model of a brain tissue to reproduce the effective response and to capturing local details of the tissue’s deformations causing axonal injury. The micro-model of the axon and matrix is characterized by a transversely isotropic viscoelastic material and the material model is formulated for numerical implementation. Model parameters are fit to experimental frequency response of the storage and loss modulus data obtained and determined using a genetic algorithm (GA) optimizing method. The results from macro-scale model are used in the micro-scale brain tissue to study the effective behavior of this tissue under injury-based loadings. The research involves the development of a tool providing a better understanding of the mechanical behavior of the brain tissue against blast loads and a rational multi-scale approach for driving injury criteria.

Pressure-dependent effect of shock waves on rat brain: induction of neuronal apoptosis mediated by a caspase-dependent pathway

2007 ◽  
Vol 106 (4) ◽  
pp. 667-676 ◽  
Author(s):  
Kaoruko Kato ◽  
Miki Fujimura ◽  
Atsuhiro Nakagawa ◽  
Atsushi Saito ◽  
Tomohiro Ohki ◽  
...  
Keyword(s):  
Shock Wave ◽  
Brain Injury ◽  
Shock Waves ◽  
Caspase 3 ◽  
Wave Exposure ◽  
Histological Changes ◽  
Dependent Effect ◽  
Wave Induced ◽  
Dependent Pathway ◽  
Active Caspase

Object Shock waves have been experimentally applied to various neurosurgical treatments including fragmentation of cerebral emboli, perforation of cyst walls or tissue, and delivery of drugs into cells. Nevertheless, the application of shock waves to clinical neurosurgery remains challenging because the threshold for shock wave–induced brain injury has not been determined. The authors investigated the pressure-dependent effect of shock waves on histological changes of rat brain, focusing especially on apoptosis. Methods Adult male rats were exposed to a single shot of shock waves (produced by silver azide explosion) at over-pressures of 1 or 10 MPa after craniotomy. Histological changes were evaluated sequentially by H & E staining and terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL). The expression of active caspase-3 and the effect of the nonselective caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK) were examined to evaluate the contribution of a caspase-dependent pathway to shock wave–induced brain injury. High-overpressure (> 10 MPa) shock wave exposure resulted in contusional hemorrhage associated with a significant increase in TUNEL-positive neurons exhibiting chromatin condensation, nuclear segmentation, and apoptotic bodies. The maximum increase was seen at 24 hours after shock wave application. Low-overpressure (1 MPa) shock wave exposure resulted in spindle-shaped changes in neurons and elongation of nuclei without marked neuronal injury. The administration of Z-VAD-FMK significantly reduced the number of TUNEL-positive cells observed 24 hours after high-overpressure shock wave exposure (p < 0.01). A significant increase in the cytosolic expression of active caspase-3 was evident 24 hours after high-overpressure shock wave application; this increase was prevented by Z-VAD-FMK administration. Double immunofluorescence staining showed that TUNEL-positive cells were exclusively neurons. Conclusions The threshold for shock wave–induced brain injury is speculated to be under 1 MPa, a level that is lower than the threshold for other organs. High-overpressure shock wave exposure results in brain injury, including neuronal apoptosis mediated by a caspase-dependent pathway. This is the first report in which the pressure-dependent effect of shock wave on the histological characteristics of brain tissue is demonstrated.

Nanobubbles, cavitation, shock waves and traumatic brain injury

2016 ◽  
Vol 18 (48) ◽  
pp. 32638-32652 ◽  
Author(s):  
Upendra Adhikari ◽  
Ardeshir Goliaei ◽  
Max L. Berkowitz
Keyword(s):  
Shock Wave ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Shock Waves ◽  
Tight Junction ◽  
Blood Brain Barrier ◽  
Neurological Complications ◽  
Tight Junction Proteins ◽  
Wave Induced ◽  
Junction Proteins

Shock wave induced cavitation denaturates blood–brain barrier tight junction proteins; this may result in various neurological complications.

scholarly journals Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Target Genes ◽  
Neural Function ◽  
Stress Genes ◽  
Expression Of Genes ◽  
Delayed Recovery ◽  
The Brain ◽  
Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

scholarly journals Fangchinoline ameliorates the expressions of angiogenic molecule in cerebral ischemia induced neuronal degeneration in neonatal rats

2018 ◽  
Vol 9 (1) ◽  
pp. 117-122
Author(s):  
Han Daicheng ◽  
Xia Shiwen ◽  
Zhu Huaping ◽  
Liu Yong ◽  
Zhou Qianqian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Neuronal Degeneration ◽  
Neuronal Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neonatal Rats ◽  
Markers Of Oxidative Stress ◽  
The Brain

AbstractBackgroundPresent investigation evaluates the beneficial effect of fangchinoline on cerebral ischemia induced neuronal degeneration in neonatal rats and also postulates the possible mechanism of its action.MethodologyCerebral ischemia was produced by the ligation of right common carotid artery in neonatal rats on postnatal day 5 (P5) and further pups were treated with fangchinoline 3, 10 and 30 mg/kg, i.p. for the period of 3 days. Effect of fangchinoline was estimated by determining the brain injury and enzyme linked immunosorbent assay (ELISA) method was used for the estimation of pro-inflammatory mediators and markers of oxidative stress in the cerebral tissues of neonatal rats. Moreover western blot assay and histopathology study was also performed on the brain tissue.ResultsResult of this investigation reveals that the percentage of brain injury significantly reduces and enhancement of myelin basic protein in the cerebral tissues of fangchinoline than ischemic group. Treatment with fangchinoline attenuates the altered level of proinflammatory mediators and markers of oxidative stress in the cerebral tissue of cerebral ischemia induced neuronal injury neonatal rats. Moreover expressions of inducible nitric oxide synthtase (iNOS), vascular endothelial growth factor (VEGF), p53 and nuclear receptor factor-2 (Nrf2) in the brain tissue attenuated by fangchinoline treated group.ConclusionIn conclusion, fangchinoline ameliorates the cerebral ischemia induced neuronal injury in neonatal rats by enhancing angiogenesis molecules.

A Micro-Scale Model for Fiber Tow Characterization under Nondeterministic Assumption: Longitudinal and Transverse Permeability

2013 ◽  
Vol 554-557 ◽  
pp. 2348-2354 ◽  
Author(s):  
Pierpaolo Carlone ◽  
Gaetano S. Palazzo
Keyword(s):  
Scale Model ◽  
Liquid Composite Molding ◽  
Trial And Error ◽  
Flow Simulations ◽  
Micro Scale ◽  
Multi Scale ◽  
Representative Cell ◽  
Transverse Permeability ◽  
Composite Molding ◽  
Cure Models

Liquid Composite Molding processes are characterized by the impregnation of a dry fibrous perform by means of injection or infusion of a catalyzed resin. In recent years computational flow and cure models allowed for a remarkable time and cost compression in process planning with respect to trial and error procedures. In this contest multi-scale simulative approaches are gaining considerable attention and intriguing results have been recently presented. Most of the proposed models, however, rely on deterministic hypothesis, assuming perfect fiber packing and neglecting dimensional variations between fibers, in strong contrast with experimental observations. In this paper the influence of the stochastic variability of the fiber packing on tow permeability has been investigated by means of a CFD micro scale model. The variability of the microstructure defining the Representative Volume Element has been considered introducing random perturbations of the fiber packing. The components of the permeability tensor, in each case, have then been derived applying the Darcy model to flow simulations through the representative cell.

scholarly journals Multi-scale, multi-modal analysis uncovers complex relationship at the brain tissue-implant neural interface: new emphasis on the biological interface

2018 ◽  
Vol 15 (3) ◽  
pp. 033001 ◽  
Author(s):  
Nicholas J Michelson ◽  
Alberto L Vazquez ◽  
James R Eles ◽  
Joseph W Salatino ◽  
Erin K Purcell ◽  
...  
Keyword(s):  
Modal Analysis ◽  
Brain Tissue ◽  
Neural Interface ◽  
Complex Relationship ◽  
Multi Scale ◽  
Biological Interface ◽  
The Brain

scholarly journals Ultrafast ignition with relativistic shock waves induced by high power lasers

2014 ◽  
Vol 2 ◽  
Author(s):  
Shalom Eliezer ◽  
Noaz Nissim ◽  
Shirly Vinikman Pinhasi ◽  
Erez Raicher ◽  
José Maria Martinez Val
Keyword(s):  
Shock Wave ◽  
Shock Waves ◽  
Radiation Pressure ◽  
Ponderomotive Force ◽  
Relativistic Hydrodynamics ◽  
Pressure Shock ◽  
Compression Pressure ◽  
High Power Lasers ◽  
Relativistic Shock ◽  
Wave Induced

Abstract In this paper we consider laser intensities greater than $\def \xmlpi #1{}\def \mathsfbi #1{\boldsymbol {\mathsf {#1}}}\let \le =\leqslant \let \leq =\leqslant \let \ge =\geqslant \let \geq =\geqslant \def \Pr {\mathit {Pr}}\def \Fr {\mathit {Fr}}\def \Rey {\mathit {Re}}10^{16}\ \mathrm{W\ cm}^{-2}$ where the ablation pressure is negligible in comparison with the radiation pressure. The radiation pressure is caused by the ponderomotive force acting mainly on the electrons that are separated from the ions to create a double layer (DL). This DL is accelerated into the target, like a piston that pushes the matter in such a way that a shock wave is created. Here we discuss two novel ideas. Firstly, the transition domain between the relativistic and non-relativistic laser-induced shock waves. Our solution is based on relativistic hydrodynamics also for the above transition domain. The relativistic shock wave parameters, such as compression, pressure, shock wave and particle flow velocities, sound velocity and rarefaction wave velocity in the compressed target, and temperature are calculated. Secondly, we would like to use this transition domain for shock-wave-induced ultrafast ignition of a pre-compressed target. The laser parameters for these purposes are calculated and the main advantages of this scheme are described. If this scheme is successful a new source of energy in large quantities may become feasible.

scholarly journals NEUROSONOGRAPHIC STUDY OF CHILDREN WITH HYPOXIC-ISCHEMIC BRAIN IJURY

2020 ◽  
pp. 7-11
Author(s):  
Volotko L. O.
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Brain Tissue ◽  
Ischemic Injury ◽  
Ischemic Brain ◽  
Destructive Processes ◽  
The Brain ◽  
Hypoxic Ischemic Injury

The study is aimed at neurosonographic characteristics of brain injury in newborn patients with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process (meningitis, ventriculitis). It is settled that brain immaturity, hydrocephalic syndrome, ischemia of the brain tissue and intraventricular hemorrhages are found 2 times more often in infants with perinatal hypoxic-ischemic injury of central nervous system, complicated with inflectional process. This fact generally characterizes disorders of the hemato-encephalic barrier and the development of destructive processes in the tissue of the brain.

scholarly journals Does Blast Exposure to the Torso Cause a Blood Surge to the Brain?

2020 ◽  
Vol 8 ◽  
Author(s):  
Jose E. Rubio ◽  
Maciej Skotak ◽  
Eren Alay ◽  
Aravind Sundaramurthy ◽  
Dhananjay Radhakrishnan Subramaniam ◽  
...  
Keyword(s):  
Brain Injury ◽  
Carotid Artery ◽  
Brain Tissue ◽  
Shear Stresses ◽  
Fe Model ◽  
Cerebral Vasculature ◽  
Blast Exposure ◽  
Indirect Mechanism ◽  
Wall Shear ◽  
The Brain

The interaction of explosion-induced blast waves with the torso is suspected to contribute to brain injury. In this indirect mechanism, the wave-torso interaction is assumed to generate a blood surge, which ultimately reaches and damages the brain. However, this hypothesis has not been comprehensively and systematically investigated, and the potential role, if any, of the indirect mechanism in causing brain injury remains unclear. In this interdisciplinary study, we performed experiments and developed mathematical models to address this knowledge gap. First, we conducted blast-wave exposures of Sprague-Dawley rats in a shock tube at incident overpressures of 70 and 130 kPa, where we measured carotid-artery and brain pressures while limiting exposure to the torso. Then, we developed three-dimensional (3-D) fluid-structure interaction (FSI) models of the neck and cerebral vasculature and, using the measured carotid-artery pressures, performed simulations to predict mass flow rates and wall shear stresses in the cerebral vasculature. Finally, we developed a 3-D finite element (FE) model of the brain and used the FSI-computed vasculature pressures to drive the FE model to quantify the blast-exposure effects in the brain tissue. The measurements from the torso-only exposure experiments revealed marginal increases in the peak carotid-artery overpressures (from 13.1 to 28.9 kPa). Yet, relative to the blast-free, normotensive condition, the FSI simulations for the blast exposures predicted increases in the peak mass flow rate of up to 255% at the base of the brain and increases in the wall shear stress of up to 289% on the cerebral vasculature. In contrast, our simulations suggest that the effect of the indirect mechanism on the brain-tissue-strain response is negligible (&lt;1%). In summary, our analyses show that the indirect mechanism causes a sudden and abundant stream of blood to rapidly propagate from the torso through the neck to the cerebral vasculature. This blood surge causes a considerable increase in the wall shear stresses in the brain vasculature network, which may lead to functional and structural effects on the cerebral veins and arteries, ultimately leading to vascular pathology. In contrast, our findings do not support the notion of strain-induced brain-tissue damage due to the indirect mechanism.

scholarly journals CX3CL1 Recruits NK Cells Into the Central Nervous System and Aggravates Brain Injury of Mice Caused by Angiostrongylus cantonensis Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Rong Zhang ◽  
Tingting Miao ◽  
Min Qin ◽  
Chengsi Zhao ◽  
Wei Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Flow Cytometry ◽  
Nervous System ◽  
Brain Injury ◽  
Nk Cells ◽  
Brain Tissue ◽  
Brain Damage ◽  
Adoptive Transfer ◽  
Angiostrongylus Cantonensis ◽  
The Brain

BackgroundAngiostrongylus cantonensis (A. cantonensis), is a food-borne zoonotic parasite that can cause central nervous system (CNS) injury characterized by eosinophilic meningitis. However, the pathogenesis of angiostrongylosis remains elusive. Natural killer cells (NK cells) are unique innate lymphocytes important in early defense against pathogens. The aim of this study was to investigate the role of NK cells in A. cantonensis infection and to elucidate the key factors that recruit NK cells into the CNS.MethodsMouse model of A. cantonensis infection was established by intragastric administration of third-stage larvae. The expression of cytokines and chemokines at gene and protein levels was analyzed by qRT-PCR and ELISA. Distribution of NK cells was observed by immunohistochemistry and flow cytometry. NK cell-mediated cytotoxicity against YAC-1 cells was detected by LDH release assay. The ability of NK cells to secrete cytokines was determined by intracellular flow cytometry and ELISA. Depletion and adoptive transfer of NK cells in vivo was induced by tail vein injection of anti-asialo GM1 rabbit serum and purified splenic NK cells, respectively. CX3CL1 neutralization experiment was performed by intraperitoneal injection of anti-CX3CL1 rat IgG.ResultsThe infiltration of NK cells in the CNS of A. cantonensis-infected mice was observed from 14 dpi and reached the peak on 18 and 22 dpi. Compared with uninfected splenic NK cells, the CNS-infiltrated NK cells of infected mice showed enhanced cytotoxicity and increased IFN-γ and TNF-α production ability. Depletion of NK cells alleviated brain injury, whereas adoptive transfer of NK cells exacerbated brain damage in A. cantonensis-infected mice. The expression of CX3CL1 in the brain tissue and its receptor CX3CR1 on the CNS-infiltrated NK cells were both elevated after A. cantonensis infection. CX3CL1 neutralization reduced the percentage and absolute number of the CNS-infiltrated NK cells and relieved brain damage caused by A. cantonensis infection.ConclusionsOur results demonstrate that the up-regulated CX3CL1 in the brain tissue recruits NK cells into the CNS and aggravates brain damage caused by A. cantonensis infection. The findings improve the understanding of the pathogenesis of angiostrongyliasis and expand the therapeutic intervention in CNS disease.

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