Dissertations, Theses, and Capstone Projects

Date of Degree

6-2026

Document Type

Master's Thesis

Degree Name

Master of Science

Program

Cognitive Neuroscience

Advisor

Junghoon Kim

Committee Members

David Johnson

Subject Categories

Cognitive Neuroscience

Abstract

Moderate-severe traumatic brain injury (TBI) is associated with a range of persistent neuropsychiatric consequences that significantly affect long-term recovery and quality of life. Among these, apathy — a persistent reduction in motivation and goal-directed behavior — is one of the most prevalent, affecting up to 71% of patients and remaining elevated for years post-injury. Prior neuroimaging work has implicated the anterior cingulate cortex and nucleus accumbens in post-traumatic apathy, but whether a broader motivational circuit undergoes progressive structural change following TBI, and whether such change predicts apathy severity, has not been examined. The present study extends this prior work by characterizing longitudinal changes across an eight-region motivational circuit composite and examining its relationship with apathy during the first year post-injury.

Thirty-nine patients with moderate-severe TBI were assessed at 3, 6, and 12 months post-injury, alongside 34 healthy volunteers assessed at a single timepoint. Structural MRI data were processed using FastSurfer, a deep learning-based segmentation pipeline chosen for its improved robustness to lesion-related artifacts compared to traditional atlas-based methods, and HypVINN for hypothalamic subregion volumes. A composite volume score was derived from eight bilateral regions selected for their established roles in motivated behavior and their known vulnerability to TBI-related neurodegeneration: the anterior cingulate cortex, nucleus accumbens, caudate, thalamus, amygdala, medial orbitofrontal cortex, hippocampus, and lateral hypothalamus. Together these structures form the motivational circuit examined throughout this study. Each region was z-scored and averaged to form the composite. Apathy was assessed using the Frontal Systems Behavior Scale (FrSBe) in both self-rated and family-rated formats. Brain-behavior relationships were examined using partial Spearman correlations controlling for intracranial volume, age, and sex.

TBI patients showed significantly lower composite motivational circuit volumes than controls at all three timepoints (all p_FDR = .024), with TBI means of −0.08, −0.09, and −0.13 z-score units at 3, 6, and 12 months respectively, compared to the control mean of 0.29 (medium-to-large effect sizes: d = −0.55 to −0.72). Within the TBI group, composite volume declined significantly from 3 to 12 months (p_FDR < .001) and from 6 to 12 months (p_FDR = .001), driven primarily by progressive atrophy in the thalamus, nucleus accumbens, hippocampus, and amygdala. Apathy T-scores were significantly elevated in TBI patients relative to controls at all three timepoints (all p ≤ .004) and showed no significant recovery over the year. Despite these parallel findings, the composite motivational circuit trajectory did not predict apathy severity at 12 months (composite: self ρ = .130, p = .485; family ρ = −.067, p = .746), though two individual ROIs reached nominal uncorrected significance for self-rated apathy.

These findings suggest that motivational circuit atrophy and apathy are both sustained features of the first year following moderate-severe TBI, but that they unfold along largely independent trajectories. The structural substrate for apathy may be established by the acute injury rather than by progressive neurodegeneration, pointing toward white matter connectivity disruption as a more plausible proximal mechanism. Future studies combining volumetry with diffusion tensor imaging and functional connectivity measures are needed to fully characterize the neural basis of post-traumatic apathy.

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