Document Type

Dissertation

Degree

Doctor of Philosophy

Major

Psychology

Date of Defense

4-18-2025

Graduate Advisor

Carissa Philippi

Committee

Sandra Langeslag

Michael Griffin

David Tate

Elisabeth Wilde

Abstract

The conflicts in Afghanistan and Iraq led to a significant surge in blast-related traumatic brain injuries (bTBIs). However, our understanding of their lasting neurological impacts remains incomplete. To our knowledge, this is the first longitudinal study of its size to explore whether increasing levels of blast exposure predict neural atrophy or cognitive decline over time. We analyzed 149 baseline and follow-up data sets from service members categorized by blast exposure: blast naïve (n = 57), single blast (n = 70), and multiple blasts (n = 22). Participants underwent structural magnetic resonance imaging (MRI) and neuropsychological assessment.

All data were drawn from the Long-term Impact of Military-relevant Brain Injury Consortium–Chronic Effects of Neurotrauma Consortium (LIMBIC-CENC). Blast exposure group was determined using self-reported data in combination with a structured clinical interview. Regional brain volume was calculated using FreeSurfer version 7.4.1 on T1-weighted structural scans. Cognitive and psychiatric assessments were collected at the initial visit and repeated at each follow-up timepoint.

We hypothesized that regional and overall brain volume would show the most atrophy in those with the highest blast exposure and greatest time since index injury. We also hypothesized that cognitive outcomes would decline most steeply in the highest blast exposure group over time. Further, we expected that brain volume would predict cognitive decline, even when controlling for blast group. However, no significant effects were found for group, time, or Time × Group interactions in any of our primary analyses.

Several exploratory findings emerged, outside of the scope of our hypotheses. These included caudate volume as a predictor of processing speed; depressive symptom influence on the amygdala; the combined influence of depressive and PTSD symptoms on working memory; and time-since-injury interactions in the thalamus and caudate.

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