Eva M Palacios1, Julia P Owen2, Esther L Yuh1,3, Mary Vassar3,4, Geoffrey T Manley3,4, and Pratik Mukherjee1,3,5
1Radiology & Biomedical Imaging, University of California San Francisco, San Francisco, CA, United States, 2Department of Radiology, University of Washington, Seattle, WA, United States, 3Brain and Spinal Cord Injury Center, San Francisco General Hospital and Trauma Center, San Francisco, CA, United States, 4Department of Neurological Surgery and Brain and Spinal Injury Center, University of California San Francisco, San Francisco, CA, United States, 5Department of Bioengineering & Therapeutic Sciences, University of California, San Francisco, San Francisco, CA, United States
Synopsis
Problem:
Mild traumatic brain
injury (mTBI) can result in long-term sequelae. Lack of sensitive biomarkers makes
diagnosis challenging.
Methods:
Cross-sectional and longitudinal study
of 40 mTBI patients at 2 weeks and 6 months after injury. Diffusion tensor
imaging and multishell neurite orientation dispersion and density imaging
(NODDI) parameters were assessed.
Results:
Cross-sectional analysis between
patients at 2-weeks and controls revealed a decrease of fractional anisotropy
and increase of mean diffusivity in the patient group together with elevated
free water values. Longitudinally, after mTBI, a decline in neurite density was
observed.
Conclusions: NODDI measurements are sensitive imaging
biomarkers for the subtle underlying white matter pathology after mTBI.
INTRODUCTION
Long term structural brain changes and cognitive
sequelae after mild traumatic brain
injury (mTBI) are understudied. The lack of sensitive imaging biomarkers to
detect subtle brain injury challenges the diagnosis and treatment of mTBI1. Diffusion tensor imaging (DTI) is the most widely
used technique worldwide to study the microstructural properties of white
matter in vivo2 despite some known limitations such as the
assumption of Gaussian diffusion3. Neurite orientation dispersion
and density imaging (NODDI), using multishell diffusion MRI, has been proposed
to capture additional information about the biophysical microarchitecture of
white mater4. Specifically, three measurements are calculated: a marker
of neurite density index (NDI); orientation dispersion index (ODI), and volume
fraction of the isotropic compartment (FISO) which represents free water. Comparing
DTI to NODDI serially after mTBI, we hypothesize that the early microstructural
white matter changes of mTBI are driven by increases of free water, such as
from neuroinflammation, whereas longer-term changes reflect decreases of
neurite density due to evolving white matter degeneration.METHODS
A cohort of 40 mTBI patients were enrolled at
the San Francisco General Hospital as part of the prospective multi center project
Transforming Research and Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI)5.
Patients were included within
24h after injury upon meeting the American Congress of Rehabilitation Medicine
(ACRM) criteria for mTBI6. Other inclusion criteria included: age 18-55yo, acute brain CT as part of
clinical care within the 24h of injury, and no previous psychiatric or
neurological disorder. Imaging acquisitions were acquired at 2 weeks and
6 months after injury. Images were acquired in a 3T GE MR750 scanner equipped
with an eight channel phased array head radiofrequency coil (GE Healthcare, Waukesha,
WI). Whole-brain DTI was performed with a multi-slice single-shot spin echo
echoplanar pulse sequence (echo time [TE] = 81 ms; repetition time [TR] = 9
sec) using 60 diffusion-encoding directions, isotropically distributed over the
surface of a sphere with electrostatic repulsion, acquired at b = 1300 sec/mm2
and b = 3000 sec/mm2, eight acquisitions at b = 0 sec/mm2, slices of 2.7-mm
thickness each with no gap between slices, a 128 x128 matrix, and a field of
view (FOV) of 350 x 350 mm. Fourteen control participants were matched to a
subsample of patients (n=25) to be
compared cross-sectionally in the acute
stage at 2 weeks post-injury with the same scanner and parameters of
acquisition. FSL tools were used to perform motion correction, brain
extraction, and DTIfit for DTI maps calculation7,8. NODDI metrics
were derived using the NODDI toolbox v0.9
(http://www.nitrc.org/projects/noddi_toolbox). Mean fractional anisotropy (FA), mean
diffusivity (MD), axial diffusivity (AD), radial diffusivity (RD), NDI, ODI, and FISO values were obtained
from each scan's FA skeleton map by using Tract-Based Spatial Statistics (TBSS)
pipeline. We used non-parametric
permutation testing voxel-wise analysis for group comparison among patients and
controls9.RESULTS
Cross-sectional
comparison at 2
weeks, patients and controls: patients showed decreased FA in the body of
the corpus callosum, anterior limb of internal capsule, anterior corona
radiata, external capsule and cingulum, and increases in MD and FISO
additionally in the genu and splenium of the corpus callosum, posterior limb of
internal capsule, superior longitudinal fasciculi and fronto-occipital tracts. See Figure1. Longitudinal comparison, patients at 2weeks
vs 6months: patients showed decreases over time in NDI mainly in posterior
brain tracts described and displayed in Figure2. No significant changes in DTI
metrics were observed.CONCLUSIONS
NODDI measurements are sensitive imaging
biomarkers for the subtle underlying white matter pathology after mTBI. Our
results show that the early decrease of FA and increase of MD after mTBI, which
are primarily anterior in the brain, correspond to white matter regions of
elevated FISO, possibly reflecting neuroinflammation. The longer-term changes from 2 weeks to 6
months after mTBI are marked by declining neurite density in predominantly
posterior white matter, suggesting neurodegeneration for which NODDI appears
more sensitive than any DTI metrics such as FA. Future research studies will
explore the prognostic significance of these white matter microstructural
changes for cognition and behavior after mTBI.Acknowledgements
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