Cross-sectional and longitudinal studies in active duty and veteran cohorts have both demonstrated that deployment-acquired traumatic brain injury (TBI) is an independent risk factor for developing post-traumatic stress disorder (PTSD), beyond confounds such as combat exposure, physical injury, predeployment TBI, and pre-deployment psychiatric symptoms. This study investigated how resting-state brain networks differ between individuals who developed PTSD and those who did not following deployment-acquired TBI. Participants included postdeployment veterans with deployment-acquired TBI history both with and without current PTSD diagnosis. Graph metrics, including small-worldness, clustering coefficient, and modularity, were calculated from individually constructed whole-brain networks based on 5-min eyes-open resting-state magnetoencephalography (MEG) recordings. Analyses were adjusted for age and premorbid IQ. Results demonstrated that participants with current PTSD displayed higher levels of small-worldness, F(1,12) = 5.364, p < 0.039, partial eta squared = 0.309, and Cohen's d = 0.972, and clustering coefficient, F(1, 12) = 12.204, p < 0.004, partial eta squared = 0.504, and Cohen's d = 0.905, than participants without current PTSD. There were no between-group differences in modularity or the number of modules present. These findings are consistent with a hyperconnectivity hypothesis of the effect of TBI history on functional networks rather than a disconnection hypothesis, demonstrating increased levels of clustering coefficient rather than a decrease as might be expected; however, these results do not account for potential changes in brain structure. These results demonstrate the potential pathological sequelae of changes in functional brain networks following deployment-acquired TBI and represent potential neurobiological changes associated with deployment-acquired TBI that may increase the risk of subsequently developing PTSD.
Objective: To identify differential effects of mild traumatic brain injury (TBI) occurring in a deployment or nondeployment setting on the functional brain connectome. Setting: Veterans Affairs Medical Center. Participants: In total, 181 combat-exposed veterans of the wars in Iraq and Afghanistan (n = 74 with deployment-related mild TBI, average time since injury = 11.0 years, SD = 4.1). Design: Cross-sectional observational study. Main Measures: Mid-Atlantic MIRECC (Mid-Atlantic Mental Illness Research, Education, and Clinical Center) Assessment of TBI, Clinician-Administered PTSD Scale, connectome metrics. Results: Linear regression adjusting for relevant covariates demonstrates a significant (P < .05 corrected) association between deployment mild TBI with reduced global efficiency (nonstandardized β = −.011) and degree of the K-core (nonstandardized β = −.79). Nondeployment mild TBI was significantly associated with a reduced number of modules within the connectome (nonstandardized β = −2.32). Finally, the interaction between deployment and nondeployment mild TBIs was significantly (P < .05 corrected) associated with increased mean (nonstandardized β = 9.92) and mode (nonstandardized β = 14.02) frequency at which connections occur. Conclusions: These results demonstrate distinct effects of mild TBI on the functional brain connectome when sustained in a deployment versus nondeployment context. This is consistent with findings demonstrating differential effects in other areas such as psychiatric diagnoses and severity, pain, sleep, and cognitive function. Furthermore, participants were an average of 11 years postinjury, suggesting these represent chronic effects of the injury. Overall, these findings add to the growing body of evidence, suggesting the effects of mild TBI acquired during deployment are different and potentially longer lasting than those of mild TBI acquired in a nondeployment context.
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