Multimodal Longitudinal Neuroimaging after TBI - a PET, diffusion MRI, and functional MRI Study
Poster No:
1251
Submission Type:
Abstract Submission
Authors:
Ana Radanovic1, Keith Jamison2, Yeona Kang3, Sudhin Shah1, Amy Kuceyeski4
Institutions:
1Weill Cornell Graduate School of Medical Sciences, New York, NY, 2Weill Cornell Medicine, New York, NY, 3Howard University, Washington, DC, 4Cornell, Ithaca, NY
First Author:
Co-Author(s):
Introduction:
Traumatic brain injury (TBI) is a leading cause of disability globally (Ahsman et al., 2006), and is associated with several multi-scale changes in brain anatomy and physiology. These include neuronal dysfunction and axonal shearing, imaged as alterations in diffusion (d)MRI measures, changes in resting-state functional (f)MRI connectivity patterns, and alterations in Binding Potential (BPnd) measured by Flumazenil PET (FMZ-PET). It is not understood how microscale neurobiological changes relate to macroscale connectivity, knowledge that is crucial for gaining insights into recovery mechanisms. Here we relate dMRI, fMRI and PET after TBI to garner a more comprehensive understanding of recovery mechanisms.
Methods:
FMZ-PET, dMRI, and resting-state fMRI were collected in individuals with TBI and non-injured healthy controls (HCs). TBI subjects were imaged at 4-6 months (T1) and 12 months (T2) after injury. HC's were imaged once to serve as a baseline for comparison. FMZ-PET data was collected from 7 TBI patients (3 male, aged 33–58, avg 48) and 19 HCs (12 male, aged 22–65, avg 44). dMRI and fMRI data were collected from 16 TBI patients (12 male, aged 19–73, avg 48) and 14 HCs (9 male, aged 23–86, avg 56). 7 TBI PET subjects are a subset of the 16 TBI MRI subjects. BPnd to GABAA receptors was extracted as a proxy for neuronal integrity via PMOD software (Kang et al., 2022). DMRI and fMRI were processed using standard pipelines. Functional connectivity (FC) and structural connectivity (SC) networks were extracted by taking the average across the edges of a region or mean node strength. Only values >0 were used for FC. Fractional amplitude of low frequency fluctuations (fALFF) was calculated from fMRI as the ratio of power in the low-frequency band to the power of the entire frequency range. Regional BPnd, fALFF, FC node strength, and SC node strength were compared across TBI and HC at T1 and T2 via ANCOVA, with age and sex as covariates. Longitudinal change within TBI subjects was analyzed via a paired t-test. Modality's test statistics (TBI vs HC contrast, t-test) were correlated via Spearman rank and p-values calculated using 1000 permutations.
Results:
Fig 1. Group-level comparisons revealed BPnd was generally lower in TBI subjects than HCs at both time points with increases in TBI subjects over time. fALFF was generally higher in TBI across the cortex at both timepoints, with increases in parietal and occipital regions and decreases in frontal and subcortical regions over time. FC was higher in TBI subjects at both timepoints, with some decrease over time, although still higher than HC at T2. SC was generally decreased in the cortex in TBI at both timepoints, with significant increases in temporal lobe SC over time.
Fig 2. Correlations revealed TBI-related differences in BPnd are positively significantly correlated with TBI-related differences in fALFF and SC at T2. Longitudinal changes in BPnd and FC are positively correlated. Longitudinal changes in regional fALFF and FC and SC are negatively correlated in the cortex. TBI-related differences in FC and SC in the cortex are positively correlated at T1 and T2.
Fig 2. Correlations revealed TBI-related differences in BPnd are positively significantly correlated with TBI-related differences in fALFF and SC at T2. Longitudinal changes in BPnd and FC are positively correlated. Longitudinal changes in regional fALFF and FC and SC are negatively correlated in the cortex. TBI-related differences in FC and SC in the cortex are positively correlated at T1 and T2.
·Figure 1
·Figure 2
Conclusions:
We found increased FC and fALFF in TBI that gradually decreases over time but remains elevated, possibly reflecting a pathological or a compensatory mechanism that begins to exhaust at 1 year. Regions with pathologically higher FC had higher SC in TBI compared to HCs, possibly reflecting structural changes driven by this functional compensation. Also, decreased BPnd had increased towards HC levels, possibly reflecting neural recovery. Regions with lower BPnd also had lower SC, possibly reflecting damage to neurons and their connections. BPnd and FC tended towards being anticorrelated at 1 year, perhaps indicating regions with pathologically elevated FC had more neuronal damage. This is novel work using multi-modal longitudinal imaging to shed light on multi-scale structural and functional changes that occur during recovery post-TBI.
Modeling and Analysis Methods:
Connectivity (eg. functional, effective, structural) 1
PET Modeling and Analysis
Novel Imaging Acquisition Methods:
BOLD fMRI
Diffusion MRI
PET 2
Keywords:
Cortex
FUNCTIONAL MRI
GABA
MRI
Positron Emission Tomography (PET)
STRUCTURAL MRI
Trauma
WHITE MATTER IMAGING - DTI, HARDI, DSI, ETC
Other - Multimodal
1|2Indicates the priority used for review
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Provide references using APA citation style.
Y Kang, K Jamison, A Jaywant, K Dams-O’Connor, N Kim, N A Karakatsanis, T Butler, N D Schiff, A Kuceyeski, S A Shah, Longitudinal alterations in gamma-aminobutyric acid (GABAA) receptor availability over ∼ 1 year following traumatic brain injury, Brain Communications, Volume 4, Issue 4, 2022, fcac159.