1028 Self-Reported Sleep Quality is Associated with Reductions in White-Matter Integrity Following Recent Mild Traumatic Brain Injury

Abstract

Introduction: Individuals with a history of mild traumatic brain injury (mTBI) often report post-injury sleep disruption that may persist for months up to years after the initial injury. These disruptions include insomnia, hypersomnia, pleiosomnia, as well as subjectively reported poor sleep quality. While the associations between mTBI and sleep disruption are known, there is little research supporting these observations from a neurophysiological perspective. The purpose of this study was to examine white-matter correlates of sleep quality in mTBI. Methods: As part of a larger Department of Defense funded study, 34 individuals with a recent mTBI (<12 months post-injury) completed a comprehensive neuropsychological battery, including the Pittsburgh Sleep Quality Index (PSQI), and neuroimaging protocol, including diffusion-weighted imaging (DWI). Diffusion-weighted images were analyzed using a standardized processing pipeline, yielding four diffusion- related metrics: fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD). Whole-brain correlations were computed between the DWI metrics and PSQI total scores, controlling for age, sex, and days post-injury. Post-hoc correlation values were computed as the mean DWI-metric value over all significant voxels. Results: PSQI total scores were significantly negatively correlated with FA (r=-0.805, p<0.001) and positively correlated with RD (r=0.793, p<0.001). Correlations were primarily observed in the bilateral internal capsules, corona radiata, and superior fronto-occipital fasciculi. Conclusion: Increasingly poor sleep quality, evidenced by increasing PSQI total scores, in post-mTBI individuals was linearly associated with lower white-matter fiber coherence (lower FA) and potentially reduced myelination and/or axonal density (higher RD). These findings are consistent with the hypothesis that the clinical presentation and pathophysiology following mTBI result from diffuse axonal injuries, affecting both projection and association white-matter tracts. Furthermore, the identified tracts are integrally involved in sleep regulation, information processing, attention, and executive function. Damage to these white-matter tracts may explain often comorbid presentations of both sleep-related and cognitive complaints following mTBI. These findings extend the current evidence for mTBI-related changes in white-matter integrity and pathways associated with clinically-relevant outcomes.