Biomechanical Analysis of Blast-induced Traumatic Brain Injury Using Multiscale Brain Modeling PDF Download

Author: Mahdi Sotudeh Chafi
Publisher:
ISBN:
Category : Brain
Languages : en
Pages : 408

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Author:
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ISBN:
Category :
Languages : en
Pages :

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Author: Soroush Assari
Publisher:
ISBN:
Category :
Languages : en
Pages : 91

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The focus of this dissertation was the biomechanics of blast-induced traumatic brain injury (bTBI). This study had three specific aims. One of the specific aims was to investigate the thoracic mechanism of bTBI by characterizing the cerebral blood pressure change during local blast exposure to head or chest in a rat model. This model utilized a shock tube to simulate the blast wave. The results showed that there is a blood pressure rise with high amplitude and short duration during both Head-Only and Chest-Only exposure conditions. It was shown that cerebral blood pressure rise was significantly higher in Chest-Only exposure, and resulted in astrocyte reactivation, and infiltration of blood-borne macrophages into the brain. It was concluded that due to chest exposure to a blast wave, high amplitude pressure waves that transfer from thoracic large vessels to cerebrovasculature can lead to blood-brain barrier disruption or perivascular injury and consequently trigger secondary neuronal damage. The second and third aims were related to the viscoelasticity and heterogeneity of brain tissue respectively for blast rate loading conditions. For the second specific aim, a novel test method was developed to apply shear deformation to samples of brain tissue with strain rates in the range of 300 to 1000 s-1. The results of shear tests on cylindrical samples of bovine brain showed that the instantaneous shear modulus (about 6 kPa) increased about 3 times compared to the values reported in the literature. For the third specific aim, local viscoelastic behavior of rat brain was characterized using a micro-indentation setup with the spatial resolution of 350 mm. The results of micro-indentation tests showed that the heterogeneity of brain tissue was more pronounced in long-term shear moduli. Moreover, the inner anatomical regions were generally more compliant than the outer regions and the gray matter generally exhibited a stiffer response than the white matter. The results of this study can enhance the prediction of brain injury in finite element models of TBI in general and models of bTBI in particular. These results contribute to development of more biofidelic models that can determine the extent and severity of injury in blast loadings. Such predictions are essential for designing better injury mitigation devices for soldiers and also for improving neurosurgical procedures among other applications.

Author: Mark F. Horstemeyer
Publisher: Academic Press
ISBN: 0128181451
Category : Technology & Engineering
Languages : en
Pages : 278

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Multiscale Biomechanical Modeling of the Brain discusses the constitutive modeling of the brain at various length scales (nanoscale, microscale, mesoscale, macroscale and structural scale). In each scale, the book describes the state-of-the- experimental and computational tools used to quantify critical deformational information at each length scale. Then, at the structural scale, several user-based constitutive material models are presented, along with real-world boundary value problems. Lastly, design and optimization concepts are presented for use in occupant-centric design frameworks. This book is useful for both academia and industry applications that cover basic science aspects or applied research in head and brain protection.The multiscale approach to this topic is unique, and not found in other books. It includes meticulously selected materials that aim to connect the mechanistic analysis of the brain tissue at size scales ranging from subcellular to organ levels. - Presents concepts in a theoretical and thermodynamic framework for each length scale - Teaches readers not only how to use an existing multiscale model for each brain but also how to develop a new multiscale model - Takes an integrated experimental-computational approach and gives structured multiscale coverage of the problems

Author: Sowmya N. Sundaresh
Publisher:
ISBN:
Category :
Languages : en
Pages : 0

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Together, this illustrated the ability of these two enzymes to regulate the response to exposure of bTBI-induced pathogenic forms of tau. This study indicates the potential of targeting PP2A activity as a viable strategy for therapeutic intervention. In conclusion, this research expands our understanding of the complexity of brain tissue injury mechanics to inform computational models of TBI, illustrates the deleterious effect of pathogenic forms of tau induced by blast injury on cognitive function, and presents a potential target mechanism for the investigation of therapeutic strategies.

Author: Ke Feng
Publisher:
ISBN:
Category : Biomechanics
Languages : en
Pages : 198

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Comparisons between brains with varies ICP readings demonstrate differences of the numbers of neuronal degeneration and apoptosis within the imaged volume. Additionally, comparisons between sections at different locations of the head did not show spatial changes for cellular responses. These metrics provide a pathway for direct connection between the cellular damage and the measured biomechanical responses of the brain within the same experimental model, and could be critical in understanding the mechanisms of bTBI. This experimental data can be used to validate computer models of bTBI.

Author: Amirhamed Bakhtiarydavijani
Publisher:
ISBN:
Category :
Languages : en
Pages : 118

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n the current study, mechanoporation-related neuronal injury as a result of mechanical loading has been studied using a multiscale approach. Injurious mechanical loads to the head induce strains in the brain tissue at the macroscale. As each length scale has its own unique morphology and heterogeneities, the strains have been scaled down from the macroscale brain tissue to the nanoscale neuronal components that result in mechanoporation of the neuronal membrane, while relevant neuronal membrane mechanoporation-related damage criteria have been scaled up to the macroscale. To achieve this, first, damage evolution equations has been developed and calibrated to molecular dynamics simulations of a representative neuronal membrane at the nanoscale. These damage evolution equations are strain rate and strain state dependent. The resulting damage evolution model has been combined with Nernst-Planck diffusion equations to analytically compare to intracellular ion concentration disruption through mechanical loading of in vitro neuron cell culture and found to agree well. Then, these damage evolution equations have been scaled up to the microscale for dynamic simulations of 3-dimensional reconstructed neurons of similar mechanical loads. It was found that the neuronal orientation significantly affects average damage accumulation on the neuron, while the morphology of neurons, for a given neuron type, had little effect on the average damage accumulation. At the mesoscale, finite element simulations of geometrical complexities of sulci and gyri, and the structural complexities of the gray and white matter and CSF on stress localization were studied. It was found that the brain convolutions, sulci, and gyri, along with the effects of impedance mismatch between the cerebrospinal fluid (CSF) and brain tissue localized shear stresses, at the depths of the sulcus end (near field effects) and in-between sulci (far field effects), that correlated well with the regions of tau protein accumulation that is observed in chronic traumatic encephalopathy (CTE). Further, sulcus length and orientation, with respect to impending stress waves, had a significant impact on the magnitude of stress localization in the brain tissue. Lastly, gray-white matter differentiation, pia matter, and brain-CSF interface interaction properties had minimal impact of the shear stress localization trends observed in these simulations.

Author: Eyitejumade A. Sogbesan
Publisher:
ISBN:
Category :
Languages : en
Pages :

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Author: Michelle Kyaw Nyein
Publisher:
ISBN:
Category :
Languages : en
Pages : 113

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Blast-induced TBI has gained prominence in recent years due to the conflicts in Iraq and Afghanistan, yet little is known about the mechanical effects of blasts on the human head; no injury thresholds have been established for blast effects on the head, and even direct transmission of the shock wave to the intracranial cavity is disputed. Still less is known about how personal protective equipment such as the Advanced Combat Helmet (ACH) affect the brain's response to blasts. The goal of this thesis is to investigate the mechanical response of the human brain to blasts and to study the effect of the ACH on the blast response of the head. To that end, a biofidelic computational model of the human head consisting of 11 distinct structures was developed from high-resolution medical imaging data. The model, known as the DVBIC/MIT Full Head Model (FHM), was subjected to blasts with incident overpressures of 6 atm and 30 atm and to a 5 m/s lateral impact. Results from the simulations demonstrate that blasts can penetrate the intracranial cavity and generate intracranial pressures that exceed the pressures produced during impact; the results suggest that blasts can plausibly directly cause traumatic brain injury. Subsequent investigation of the effect of the ACH on the blast response of the head found that the ACH provided minimal mitigation of blast effects. Results from the simulations conducted with the FHM extended to include the ACH suggest that the ACH can slightly reduce peak pressure magnitudes and delay peak pressure arrival times, but the benefits are minimal because the ACH does not protect the main pathways of load transmission from the blast to brain tissue. A more effective blast mitigation strategy might involve altering the helmet design to more completely surround the head in order to protect it from direct exposure to blast waves.

Author: Daniel Laskowitz
Publisher: CRC Press
ISBN: 1498766579
Category : Medical
Languages : en
Pages : 388

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Traumatic brain injury (TBI) remains a significant source of death and permanent disability, contributing to nearly one-third of all injury related deaths in the United States and exacting a profound personal and economic toll. Despite the increased resources that have recently been brought to bear to improve our understanding of TBI, the developme