Analysis of Diffuse Axonal Injury Using Diffusion Tensor Imaging in Traumatic Brain Injury Patients

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”.


2019 ◽  
Vol 13 ◽  
pp. 117906951985862 ◽  
Author(s):  
Wouter S Hoogenboom ◽  
Todd G Rubin ◽  
Kenny Ye ◽  
Min-Hui Cui ◽  
Kelsey C Branch ◽  
...  

Mild traumatic brain injury (mTBI), also known as concussion, is a serious public health challenge. Although most patients recover, a substantial minority suffers chronic disability. The mechanisms underlying mTBI-related detrimental effects remain poorly understood. Although animal models contribute valuable preclinical information and improve our understanding of the underlying mechanisms following mTBI, only few studies have used diffusion tensor imaging (DTI) to study the evolution of axonal injury following mTBI in rodents. It is known that DTI shows changes after human concussion and the role of delineating imaging findings in animals is therefore to facilitate understanding of related mechanisms. In this work, we used a rodent model of mTBI to investigate longitudinal indices of axonal injury. We present the results of 45 animals that received magnetic resonance imaging (MRI) at multiple time points over a 2-week period following concussive or sham injury yielding 109 serial observations. Overall, the evolution of DTI metrics following concussive or sham injury differed by group. Diffusion tensor imaging changes within the white matter were most noticeable 1 week following injury and returned to baseline values after 2 weeks. More specifically, we observed increased fractional anisotropy in combination with decreased radial diffusivity and mean diffusivity, in the absence of changes in axial diffusivity, within the white matter of the genu corpus callosum at 1 week post-injury. Our study shows that DTI can detect microstructural white matter changes in the absence of gross abnormalities as indicated by visual screening of anatomical MRI and hematoxylin and eosin (H&E)-stained sections in a clinically relevant animal model of mTBI. Whereas additional histopathologic characterization is required to better understand the neurobiological correlates of DTI measures, our findings highlight the evolving nature of the brain’s response to injury following concussion.


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.


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.


2017 ◽  
Vol 24 (3) ◽  
pp. 237-246 ◽  
Author(s):  
Amanda R. Rabinowitz ◽  
Tessa Hart ◽  
John Whyte ◽  
Junghoon Kim

AbstractObjectives: The goal of the present study was to elucidate the influence of demographic and neuropathological moderators on the longitudinal trajectory neuropsychological functions during the first year after moderate to severe traumatic brain injury (TBI). In addition to examining demographic moderators such as age and education, we included a measure of whole-brain diffuse axonal injury (DAI), and examined measures of processing speed (PS), executive function (EF), and verbal learning (VL) separately. Methods: Forty-six adults with moderate to severe TBI were examined at 3, 6, and 12 months post-injury. Participants underwent neuropsychological evaluation and neuroimaging including diffusion tensor imaging. Using linear mixed effects modeling, we examined longitudinal trajectories and moderating factors of cognitive outcomes separately for three domains: PS, VL, and EF. Results: VL and EF showed linear improvements, whereas PS exhibited a curvilinear trend characterized by initial improvements that plateaued or declined, depending on age. Age moderated the recovery trajectories of EF and PS. Education and DAI did not influence trajectory but were related to initial level of functioning for PS and EF in the case of DAI, and all three cognitive domains in the case of education. Conclusions: We found disparate recovery trajectories across cognitive domains. Younger age was associated with more favorable recovery of EF and PS. These findings have both clinical and theoretical implications. Future research with a larger sample followed over a longer time period is needed to further elucidate the factors that may influence cognitive change over the acute to chronic period after TBI. (JINS, 2018, 24, 237–246)


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