Abstract

White matter (WM) disruption is an important determinant of cognitive impairment after mild traumatic brain injury (mTBI), but traditional diffusion tensor imaging (DTI) shows some limitations in assessing WM damage. Diffusion kurtosis imaging (DKI) and neurite orientation dispersion and density imaging (NODDI) show advantages over DTI in this respect. Therefore, we used these three diffusion models to investigate complex WM changes in the acute stage after mTBI. From 32 mTBI patients and 31 age-, sex-, and education-matched healthy controls, we calculated eight diffusion metrics based on DTI (fractional anisotropy, axial diffusivity, radial diffusivity, and mean diffusivity), DKI (mean kurtosis), and NODDI (orientation dispersion index, volume fraction of intracellular water (Vic), and volume fraction of the isotropic diffusion compartment). We used tract-based spatial statistics to identify group differences at the voxel level, and we then assessed the correlation between diffusion metrics and cognitive function. We also performed subgroup comparisons based on loss of consciousness. Patients showed WM abnormalities and cognitive deficit. And these two changes showed positive correlation. The correlation between Vic of the splenium of the corpus callosum and Digit Symbol Substitution Test scores showed the smallest p-value (p = 0.000, r = 0.481). We concluded that WM changes, especially in the splenium of the corpus callosum, correlate to cognitive deficit in this study. Furthermore, the high voxel count of NODDI results and the consistency of mean kurtosis and the volume fraction of intracellular water in previous studies and our study showed the functional complementarity of DKI and NODDI to DTI.

Highlights

  • The considerable rate of mild traumatic brain injury [1] and the high incidence of postconcussion symptoms such as cognitive deficits and behavioral and emotional changes [2, 3] impose a burden on society

  • Trail Making Test (TMT)-A data were unavailable in 5 mild traumatic brain injury (mTBI) patients because three patients had hand fractures and two patients needed to stay in a reclining position

  • TMT-B data were unavailable in 10 mTBI patients and seven healthy controls for the same reasons as TMTA, and five patients and seven controls forgot the order of the alphabet, resulting in an unusually long test time

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Summary

Introduction

The considerable rate of mild traumatic brain injury (mTBI) [1] and the high incidence of postconcussion symptoms such as cognitive deficits and behavioral and emotional changes [2, 3] impose a burden on society. Diffuse axonal injury is thought to be the predominant pathological mechanism underlying mTBI [4–7], and increasing evidence has shown that abnormalities in white matter (WM) caused by mTBI can affect post-concussion symptoms [8, 9]. Visualization of WM integrity has become a key part of clinical research. There has been controversy over both the direction and the magnitude of diffusion abnormalities in prior studies on WM tracts [11]. Injury type, time since injury, and sample type may cause inconsistencies between studies, the lack of consensus suggests fundamental limitations of DTI for detecting specific damage in mTBI

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