The Use of a Cellular Strain Injury Criterion and Diffusion Tensor Imaging in a Computational Model of Traumatic Brain Injury

Author(s):  
Rika M. Wright ◽  
K. T. Ramesh

With the increase in the number of soldiers sustaining traumatic brain injury from military incidents and the recent attention on sports related traumatic brain injury, there has been a focused effort to develop preventative and treatment methods for traumatic brain injury (TBI). Traumatic brain injury is caused by mechanical loading to the head, such as from impacts, sudden accelerations, or blast loading, and the pathology can range from focal damage in the brain to widespread diffuse injury [1]. In this study, we investigate the injury mechanisms of diffuse axonal injury (DAI), which accounts for the second largest percentage of deaths due to brain trauma [2]. DAI is caused by sudden inertial loads to the head, and it is characterized by damage to neural axons. Despite the extensive research on DAI, the coupling between the mechanical loading to the head and the damage at the cellular level is still poorly understood. Unlike previous computational models that use macroscopic stress and strain measures to determine injury, a cellular injury criterion is used in this work as numerous studies have shown that cellular strain can be related to the functional damage of neurons. The effectiveness of using this cellular injury criterion to predict damage in a finite element model of DAI is investigated.

Author(s):  
Rika M. Wright ◽  
K. T. Ramesh

There has been an ongoing effort to reduce the occurrence of sports-related traumatic brain injury. These injuries are caused by an impact to the head and often lead to the damage of neural axons in the brain. This type of damage is classified as diffuse axonal injury (DAI) or traumatic axonal injury (TAI) [1]. One of the difficulties in studying the progression of axonal injury is that the structural signature of DAI cannot be readily visualized with conventional medical imaging modalities since the damage occurs at the cellular level [2]. This also makes the injury difficult to diagnose. Many researchers have turned to finite element (FE) models to study the development of diffuse axonal injury. FE models provide a means for observing the mechanical process of injury development from the loads to the head at the macroscale to the damage that results at the cellular level. However, for a finite element model to be a viable tool for studying DAI, the model must be able to accurately represent the behavior of the brain tissue, and it must be able to accurately predict injury. In this work, we address both of these issues in an effort to improve the material models and injury criteria used in current FE models of TBI. We represent the white matter with an anisotropic, hyper-viscoelastic constitutive model, incorporate the microstructure of the white matter through the use of diffusion tensor imaging (DTI), and estimate injury using an axonal strain injury (ASI) criterion (Figure 1). We also develop a novel method to quantify the degree of axonal damage in the fiber tracts of the brain.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 886-887
Author(s):  
Andrei Irimia ◽  
Ammar Dharani ◽  
Van Ngo ◽  
David Robles ◽  
Kenneth Rostowsky

Abstract Mild traumatic brain injury (mTBI) affects white matter (WM) integrity and accelerates neurodegeneration. This study assesses the effects of age, sex, and cerebral microbleed (CMB) load as predictors of WM integrity in 70 subjects aged 18-77 imaged acutely and ~6 months after mTBI using diffusion tensor imaging (DTI). Two-tensor unscented Kalman tractography was used to segment and cluster 73 WM structures and to map changes in their mean fractional anisotropy (FA), a surrogate measure of WM integrity. Dimensionality reduction of mean FA feature vectors was implemented using principal component (PC) analysis, and two prominent PCs were used as responses in a multivariate analysis of covariance. Acutely and chronically, older age was significantly associated with lower FA (F2,65 = 8.7, p < .001, η2 = 0.2; F2,65 = 12.3, p < .001, η2 = 0.3, respectively), notably in the corpus callosum and in dorsolateral temporal structures, confirming older adults’ WM vulnerability to mTBI. Chronically, sex was associated with mean FA (F2,65 = 5.0, p = 0.01, η2 = 0.1), indicating males’ greater susceptibility to WM degradation. Acutely, a significant association was observed between CMB load and mean FA (F2,65 = 5.1, p = 0.009, η2 = 0.1), suggesting that CMBs reflect the acute severity of diffuse axonal injury. Together, these findings indicate that older age, male sex, and CMB load are risk factors for WM degeneration. Future research should examine how sex- and age-mediated WM degradation lead to cognitive decline and connectome degeneration after mTBI.


2018 ◽  
Vol 89 (10) ◽  
pp. A42.1-A42
Author(s):  
Graham Neil SN ◽  
Jolly Amy E ◽  
Bourke Niall J ◽  
Scott Gregory ◽  
Cole James H ◽  
...  

BackgroundDementia rates are elevated after traumatic brain injury (TBI) and a subgroup develops chronic traumatic encephalopathy. Post-traumatic neurodegeneration can be measured by brain atrophy rates derived from neuroimaging, but it is unclear how atrophy relates to the initial pattern of injury.ObjectivesTo investigate the relationship between baseline TBI patterns and subsequent neurodegeneration measured by progressive brain atrophy.Methods55 patients after moderate-severe TBI (mean 3 years post-injury) and 20 controls underwent longitudinal MRI. Brain atrophy was quantified using the Jacobian determinant defined from volumetric T1 scans approximately one year apart. Diffuse axonal injury was measured using diffusion tensor imaging and focal injuries defined from T1 and FLAIR. Neuropsychological assessment was performed.ResultsAbnormal progressive brain atrophy was seen after TBI (~1.8%/year in white matter). This was accompanied by widespread reductions in fractional anisotropy, in keeping with the presence of diffuse axonal injury. There was a strong negative correlation between FA and brain atrophy, whereby areas of greater white matter damage showed greater atrophy over time.ConclusionsThe results show a strong relationship between the location of diffuse axonal injury and subsequent neurodegeneration. This suggests that TBI triggers progressive neurodegeneration through the long-lasting effects of diffuse axonal injury.


2010 ◽  
Vol 3 (2) ◽  
pp. 111
Author(s):  
Hyung Jong Choi ◽  
Jong-Gu Kang ◽  
Seung Ho Ahn ◽  
Suk Hoon Ohn ◽  
Kwang-Ik Jung ◽  
...  

2018 ◽  
Vol 76 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Daphine Centola Grassi ◽  
David Macedo da Conceição ◽  
Claudia da Costa Leite ◽  
Celi Santos Andrade

ABSTRACT Traumatic brain injury (TBI) is the number one cause of death and morbidity among young adults. Moreover, survivors are frequently left with functional disabilities during the most productive years of their lives. One main aspect of TBI pathology is diffuse axonal injury, which is increasingly recognized due to its presence in 40% to 50% of all cases that require hospital admission. Diffuse axonal injury is defined as widespread axonal damage and is characterized by complete axotomy and secondary reactions due to overall axonopathy. These changes can be seen in neuroimaging studies as hemorrhagic focal areas and diffuse edema. However, the diffuse axonal injury findings are frequently under-recognized in conventional neuroimaging studies. In such scenarios, diffuse tensor imaging (DTI) plays an important role because it provides further information on white matter integrity that is not obtained with standard magnetic resonance imaging sequences. Extensive reviews concerning the physics of DTI and its use in the context of TBI patients have been published, but these issues are still hazy for many allied-health professionals. Herein, we aim to review the current contribution of diverse state-of-the-art DTI analytical methods to the understanding of diffuse axonal injury pathophysiology and prognosis, to serve as a quick reference for those interested in planning new studies and who are involved in the care of TBI victims. For this purpose, a comprehensive search in Pubmed was performed using the following keywords: “traumatic brain injury”, “diffuse axonal injury”, and “diffusion tensor imaging”.


2021 ◽  
pp. 0271678X2098515
Author(s):  
Margalit Haber ◽  
Franck Amyot ◽  
Cillian E Lynch ◽  
Danielle K Sandsmark ◽  
Kimbra Kenney ◽  
...  

Traumatic Brain Injury (TBI) is associated with both diffuse axonal injury (DAI) and diffuse vascular injury (DVI), which result from inertial shearing forces. These terms are often used interchangeably, but the spatial relationships between DAI and DVI have not been carefully studied. Multimodal magnetic resonance imaging (MRI) can help distinguish these injury mechanisms: diffusion tensor imaging (DTI) provides information about axonal integrity, while arterial spin labeling (ASL) can be used to measure cerebral blood flow (CBF), and the reactivity of the Blood Oxygen Level Dependent (BOLD) signal to a hypercapnia challenge reflects cerebrovascular reactivity (CVR). Subjects with chronic TBI (n = 27) and healthy controls (n = 14) were studied with multimodal MRI. Mean values of mean diffusivity (MD), fractional anisotropy (FA), CBF, and CVR were extracted for pre-determined regions of interest (ROIs). Normalized z-score maps were generated from the pool of healthy controls. Abnormal ROIs in one modality were not predictive of abnormalities in another. Approximately 9-10% of abnormal voxels for CVR and CBF also showed an abnormal voxel value for MD, while only 1% of abnormal CVR and CBF voxels show a concomitant abnormal FA value. These data indicate that DAI and DVI represent two distinct TBI endophenotypes that are spatially independent.


2020 ◽  
Vol 6 (32) ◽  
pp. eaaz6892 ◽  
Author(s):  
E. M. Palacios ◽  
J. P. Owen ◽  
E. L. Yuh ◽  
M. B. Wang ◽  
M. J. Vassar ◽  
...  

Neuroimaging biomarkers that can detect white matter (WM) pathology after mild traumatic brain injury (mTBI) and predict long-term outcome are needed to improve care and develop therapies. We used diffusion tensor imaging (DTI) and neurite orientation dispersion and density imaging (NODDI) to investigate WM microstructure cross-sectionally and longitudinally after mTBI and correlate these with neuropsychological performance. Cross-sectionally, early decreases of fractional anisotropy and increases of mean diffusivity corresponded to WM regions with elevated free water fraction on NODDI. This elevated free water was more extensive in the patient subgroup reporting more early postconcussive symptoms. The longer-term longitudinal WM changes consisted of declining neurite density on NODDI, suggesting axonal degeneration from diffuse axonal injury for which NODDI is more sensitive than DTI. Therefore, NODDI is a more sensitive and specific biomarker than DTI for WM microstructural changes due to mTBI that merits further study for mTBI diagnosis, prognosis, and treatment monitoring.


2009 ◽  
Vol 26 (4) ◽  
pp. 471-479 ◽  
Author(s):  
Gretchen M. Brophy ◽  
Jose A. Pineda ◽  
Linda Papa ◽  
Stephen B. Lewis ◽  
Alex B. Valadka ◽  
...  

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