TERESA GERHALTER1, Martijn Cloos2, Seena Dehkharghani1, Anna M. Chen1, Rosermary Peralta1, Fatemeh Adlparvar1, James S. Babb1, Tamara Bushnik3, Jonathan M. Silver4, Brian S. Im3, Stephen P. Wall5, Guillaume Madelin1, and Ivan Kirov1
1Center for Biomedical Imaging, Department of Radiology, New York University Grossman School of Medicine, NEW YORK, NY, United States, 2Centre for Advanced Imaging, The University of Queensland, Brisbane, Australia, 3Department of Rehabilitation Medicine, New York University Grossman School of Medicine, NEW YORK, NY, United States, 4Department of Psychiatry, New York University Grossman School of Medicine, NEW YORK, NY, United States, 5Ronald O. Perelman Department of Emergency Medicine, New York University Grossman School of Medicine, NEW YORK, NY, United States
Synopsis
We analyzed
brain MRI data including clinical
imaging and MR fingerprinting (MRF) of 22 mild traumatic brain
injury (mTBI) patients measured ~1 month after injury and 18 healthy controls. T1 and T2 values in mTBI were not significantly
different from controls’. However, increased T1
of three brain regions enabled the identification of non-recovered patients at 3-months
(AUC=0.80-0.88). This suggests that T1 quantification is more sensitive
to mTBI damage than T2, and is a potential candidate to predict patient outcome.
Introduction
Traumatic brain injury (TBI) is one of the main causes
of neurological disabilities worldwide.1 Despite its low severity, individuals with mild TBI (mTBI)
often present physical, psychiatric, emotional and cognitive disorders.2 However, reliable quantitative MRI biomarkers to
predict the risk of persistent symptoms in these individuals are lacking. Since T1 and T2 of water are sensitive to their
local molecular environment, quantitative T1 and T2 assessment could capture
pathological changes following TBI. In animal models of TBI, an increase in T2
has been linked to vasogenic edema and correlated with histologically-quantified
neurodegeneration and neurological outcome.3–5 We therefore assessed the prognostic
performance of T1 and T2 measured with MR fingerprinting (MRF) in gray matter
(GM) and white matter (WM) for symptomatic
and cognitive outcome after human mTBI.Materials & Methods
We analyzed
brain MRI data including clinical
imaging and MRF of 22 mTBI
patients (17 female, 38±12 years) within two months after injury (time 1, 22.1±10.2 days) and 18 healthy
controls (12 female, 31.6±7.6
years). MRI data were acquired
on a 3T scanner (Magnetom Prisma, Siemens Healthineers) with a 20-channel
quadrature head coil (Siemens Healthineers). Standard imaging included 3D MPRAGE
(TR/TE/TI=2400/2.24/1060 ms; flip angle=8°; in-plane FOV=256×256 mm2;
208 slices, slab thickness=0.8 mm; voxel size=0.8×0.8×0.8 mm³; TA=6:38 min),
FLAIR (TR/TE/TI=9000/81/2500 ms; 30 slices, in-plane FOV=220×220 mm2;
voxel size=0.7×0.7×5.0 mm³; TA=2:44 min) and SWI (TR/TE=28/20 ms;
flip angle=15°; in-plane FOV=220×220 mm2; voxel size=0.7×0.7×3.0 mm³;
TA=3:46 min). A radiologist examined qualitative 1H images
for
areas with possible hematoma, haemorrhage, diffuse or traumatic axonal injury, which were
excluded for T1 and T2 quantification. For
multiparametric mapping, we applied a multi-slice 2D radial MRF method to
simultaneously measure T1 and T2, which is described in detail in reference6 (resolution=1.25×1.25×5 mm3, TA=7:49 min). A dictionary with simulated fingerprints was
created using extended phase graphs with T1 and T2 entries in the ranges
150-4642 ms and 10-350 ms, respectively (step size of 2.5%). The MRF data was reconstructed offline with an
in-house MATLAB script. Visual quality control ensured that only artifact-free
slices were included in the analysis.7 Twelve ROI
masks were extracted from the MPRAGE image and used to obtain ROI
voxel-averaged values of T1, T2, FA, and ADC (Fig. 1). All TBI
patients also underwent clinical and neurocognitive testing at baseline (time 1)
and at a three-month follow-up (time 2), including the Rivermead post-concussion
symptoms questionnaire (RPQ)8, the Glasgow Outcome Scale – Extended (GOSE)9, and the Brief Test of Adult Cognition by Telephone
(BTACT).10 Data
from mTBI versus controls were compared using Mann-Whitney (MW) test omitting the
three oldest non-age-matched patients, since the association between age and T1 and T2 is
unknown. Comparisons with all patients were made with respect to MRI and
clinical recovery (GOSE=8 is recovered and GOSE<8 is non-recovered),
with (ANCOVA) and without (MW) an adjustment for the elapsed time from injury,
respectively. Spearman
rank correlation was used to assess the association between TSC and BTACT and
RPQ. Statistical significance was defined as p<0.05.Results
The
demographics and injury characteristics of the TBI and control cohort are
compiled in Table 1. Fig. 2A shows T1 and T2 maps next to qualitative 1H
images from one TBI patient. GM exhibited generally higher T1 and T2 values
than WM regions, producing high gray-white matter contrast. In a
cross-sectional analysis, no
statistically significant difference in T1 and T2 was observed between mTBI
patients and controls (Fig. 2B). Several
correlations were found between MRI measures and clinical presentations (Fig. 3). The strongest association of
T1 at time 1 with clinical outcome at time 2 was observed for the T1 in corona
radiata and the word list recall from the BTACT (r=0.85 with p<0.001),
followed by the T1 in genu of corpus callosum and the BTACT composite z-score (r=0.79 with p<0.001). The mTBI
patients were dichotomized according to the GOSE at time 2 in recovered (n=8)
or non-recovered (n=11). Statistical
testing using the receiver-operating-characteristic
curve showed that increased
T1 of three brain regions enabled the identification of non-recovered patients
at follow-up with AUCs between 0.80
and 0.88 (Table 2).Discussion & Conclusion
We evaluated for the first time, to the best of
our knowledge, the potential of T1 and T2 measurements from MRF to predict patient
outcome after mild TBI. T1 showed stronger predictive value, particularly in brain regions which have been identified as common
sites of DTI abnormalities.11,12 In conclusion, we show that MRF-based
relaxometry, especially T1, was linked to clinical and neurocognitive
impairments in mTBI, and identified non-recovered patients 3 months after
injury with AUC>0.80.Acknowledgements
This work was supported by grants R01NS097494 and
R01EB026456 from the National Institutes of Health (NIH).References
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