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Abstract Details

Verbal Retrieval Deficits Due to Traumatic Brain Injury Are Linked to White Matter Changes Mediated by Altered Oscillatory Brain Activity
Aging, Dementia, and Behavioral Neurology
P4 - Poster Session 4 (5:00 PM-6:00 PM)
3-012

This study investigated associations between verbal retrieval (VR) deficits and changes in electrophysiological activity and white matter structure in veterans with chronic traumatic brain injury (TBI).

VR deficits are a common sequela of TBI with unclear neural mechanisms and limited treatment options.

Sixty veterans (42 ± 10.6 years, 4 women) with TBI histories (>1 year) underwent neuropsychological testing and an EEG-based Go-NoGo task. Regional skeletonized white matter tract fractional anisotropy (FA) was quantified using diffusion-weighted imaging obtained in 41 subjects. Participants were categorized into those with impaired VR (VR-, n =27; 20 with FA; < -1.5 Z in letter/category fluency, picture naming, or total verbal learning) versus intact VR (VR+, n = 33; 21 with FA). We analyzed group differences in (1) frontal theta/alpha activity during Go/NoGo trials, (2) relationships between theta/alpha activity and executive function [EF]/processing speed [PS], and (3) correlations between FA in specific tracts and theta/alpha activity, using General Linear Modeling adjusting for age and education. We examined direct and indirect (via theta/alpha) effects of FA on cognition using mediation analyses.
The VR- group exhibited significantly lower frontal NoGo theta power (p = 0.015). Higher Go/NoGo frontal theta power predicted better PS in the VR- but not VR+ group (p = 0.002). In the VR- compared to VR+ group, greater frontal Go theta power correlated with higher FA values in the right superior longitudinal fasciculus (SLF), left perforant pathway (PP), bilateral frontal occipital fasciculi (FOF), and forceps minor (FMin) (ps = 0.006 – 0.049). The right SLF, bilateral FOFs, and FMin showed significant indirect effects on PS via frontal theta activity.
VR deficits may be influenced by structural changes in specific white matter tracts following TBI, mediated by altered frontal theta activity. These findings offer biological insights for designing novel assessment and intervention strategies for TBI.
Authors/Disclosures
Hsueh-Sheng Chiang, MD, PhD (Beth Israel Deaconess Medical Center)
PRESENTER
The institution of Dr. Chiang has received research support from NIH/NIDCD. The institution of Dr. Chiang has received research support from Texas Alzheimer's Research and Care Consortium.
Jeremy Strain, PhD Dr. Strain has nothing to disclose.
Ashna Adhikari Ms. Adhikari has nothing to disclose.
Jeffrey Spence (UT Dallas) Jeffrey Spence has nothing to disclose.
Kyle B. Womack, MD (Washington University School of Medicine) The institution of Dr. Womack has received research support from NIH. The institution of Dr. Womack has received research support from Janssen.
Munro Cullum, PhD (Univ of Texas Southwestern Medical Center) The institution of Dr. Cullum has received research support from NIH. Dr. Cullum has received intellectual property interests from a discovery or technology relating to health care. Dr. Cullum has received personal compensation in the range of $10,000-$49,999 for serving as a Scientific Director with Texas Alzheimers Research and Care Consortium.
John Hart, MD (The University of Texas At Dallas) The institution of Dr. Hart has received research support from Department of Defense.