2011
DOI: 10.1016/j.jmbbm.2011.06.007
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Computation of axonal elongation in head trauma finite element simulation

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Cited by 78 publications
(48 citation statements)
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“…These results were consistent with our previous DTI and tractography report in subacute TBI patients [Yeh et al, 2014] that revealed subcortical superior-inferiorly oriented tracts were particularly vulnerable to blast injury, as well as other reports of chronic changes in mTBI, either military personnel [Mac Donald et al, 2011] or civilian populations [Inglese et al, 2005;Kraus et al, 2007;Lipton et al, 2009]. The anatomical locations of low FA using tract specific analysis and tract profile analysis in this study are also consistent with the results from using mechanical simulation and finite element analysis of brain exposure to blasts, showing that the highest level of axonal shear/ strain effects developed in the regions of corpus callosum and corona radiata [Chatelin et al, 2011] in mTBI model. Secondary brain injury and repair mechanisms such as chronic inflammation and hypermetabolism may sensitize the brain to the subsequent injury [Calabrese et al, 2014], leading to axonal repair, reactive gliosis [Glushakova et al, 2014;Johnson et al, 2013;Kiraly and Kiraly, 2007] or irreversible axonal damage [Gupta and Przekwas, 2013].…”
Section: Group Analysissupporting
confidence: 88%
“…These results were consistent with our previous DTI and tractography report in subacute TBI patients [Yeh et al, 2014] that revealed subcortical superior-inferiorly oriented tracts were particularly vulnerable to blast injury, as well as other reports of chronic changes in mTBI, either military personnel [Mac Donald et al, 2011] or civilian populations [Inglese et al, 2005;Kraus et al, 2007;Lipton et al, 2009]. The anatomical locations of low FA using tract specific analysis and tract profile analysis in this study are also consistent with the results from using mechanical simulation and finite element analysis of brain exposure to blasts, showing that the highest level of axonal shear/ strain effects developed in the regions of corpus callosum and corona radiata [Chatelin et al, 2011] in mTBI model. Secondary brain injury and repair mechanisms such as chronic inflammation and hypermetabolism may sensitize the brain to the subsequent injury [Calabrese et al, 2014], leading to axonal repair, reactive gliosis [Glushakova et al, 2014;Johnson et al, 2013;Kiraly and Kiraly, 2007] or irreversible axonal damage [Gupta and Przekwas, 2013].…”
Section: Group Analysissupporting
confidence: 88%
“…25 Here, we extended previous work that used average orientations on coarse elements 18,20,21,27 or voxels 22 to analyze accumulated peak fiber strain, e p n , along the entire lengths of fibers using whole-brain tractography. Each fiber was represented by high resolution (1 mm) sampling points, improving on the native DTI voxel resolution (2 mm).…”
Section: Discussionmentioning
confidence: 98%
“…To address this inconsistency, recent studies have begun to use strains along WM fibers to characterize elongation of axonal bundles (termed ''axonal'' or ''fiber'' strain, e n ). 11,[16][17][18][19][20][21][22] Initial evidence suggests that fiber orientation-dependent e n improves injury prediction relative to its isotropic counterpart, e ep :…”
Section: Introductionmentioning
confidence: 99%
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“…A possible explanation is that in most of the currently used head models, anisotropic mechanical behavior of brain tissue is not included, even though experimental studies have concluded that neural tissue behaves clearly anisotropically in some regions of the brain (e.g., Margulies 1998, 1999;Prange and Margulies 2002;Nicolle et al 2005;Ning et al 2006;Hrapko et al 2008). In line with this, recent studies have been performed that take the axonal orientation into account leading to tissue strains in the axonal direction (Chatelin et al 2011;Wright and Ramesh 2012). Nevertheless, even if tissue strains could be predicted accurately by head models, the link to real injury is still not straightforward, as several studies concerning TBI have shown that tissue strains lead to injury at a cellular level (e.g., Bain et al 2001;Engel et al 2005;Floyd et al 2005;Morrison III et al 2006;Cater et al 2006;, whereby the microstructural heterogeneities at the cellular level are of influence.…”
Section: Introductionmentioning
confidence: 99%