Publications by Type: Journal Article

OBJECTIVE: The primary aim included explorations of: (1) the associations between the history of blast exposure (BE), close blast exposure (CBE), and blast-related traumatic brain injury (bTBI) and metabolic abnormality; and (2) the potential mediating effect of comorbid psychological and somatic conditions on these associations. The secondary aim explored the association of dose-response impact of BE, CBE, and bTBI and metabolic abnormality. SETTING: Data were collected by the Translational Research Center for TBI and Stress Disorders (TRACTS). PARTICIPANTS: Post-9/11 veterans from the TRACTS baseline sample who had conflict-zone deployment experience ( N = 734). DESIGN: Cross-sectional secondary data analysis. We computed relative risks (RRs) and 95% CI using modified Poisson regression. We quantified the impact of co-occurring psychological and somatic conditions on this association using mediation analyses. MAIN MEASURES: Exposures included BE (<100 m), CBE (<10 m), and bTBI. Metabolic abnormality outcomes included (1) overweight/obesity (defined by abnormal waist-hip ratio [WHR] and abnormal waist circumference [WC]); (2) glucose dysregulation; and (3) meeting criteria for cardiometabolic syndrome (defined by guidelines). RESULTS: The sample was majority male (91%) and White (68%), with a mean age of 34.6 years (SD = 8.99). Most participants had 1 or more BE (83%); 48% experienced 1 or more CBE. Overweight/obesity was highly prevalent in the sample (51% had abnormal WHR and 60% abnormal WC). There was no significant direct or indirect association between BE, CBE, and bTBI and metabolic abnormalities (RRs: 0.70-1.51; P 's > .05). CONCLUSION: Future research is needed to investigate the association of BE with metabolic abnormalities with larger, more targeted sample selection, and longer follow-up. Effective and sustainable weight management and metabolic health prevention interventions for this veteran cohort are needed.

Military service members disproportionately experience sexual violence (SV) and its related health concerns. Although recent work has shown physical activity to be an effective strategy for improving physical and mental health among trauma-exposed military populations, little of this work has focused specifically on military service members with a history of SV. To address these gaps in knowledge and practice, this study identified the most salient perceived benefits/barriers of exercise among men and women survivors of SV with military affiliations. Additionally, these analyses explore willingness to engage in exercise programs, and preferences for the structure/content of these programs, among men and women survivors of SV with military affiliations.An online, cross-sectional survey of women (n = 355) and men (n = 198) survivors of SV was completed using Amazon Mechanical Turk. Inclusion criteria were men and women, age between 18 and 65 years, self-reported history of SV, and located in the United States. Information on sociodemographics and post-traumatic stress disorder symptoms was collected alongside perceived barriers and benefits to exercise, willingness to engage in exercise programs, and preferences for the structure/content of these programs. Analyses were stratified by sex. Comparisons by history of military involvement (active duty military or veteran; no military involvement/civilian) were reported.Both military-involved men (n = 68) and women (n = 139) were more likely to prefer at-home and online exercise options when compared to civilians (Ps < .05; Cramer’s Vs 0.19–0.36). Additionally, both men and women with military involvement reported strongly favoring exercising with an instructor over no instructor and preferred that this instructor identifies with their same gender (Ps < .01; Cramer’s Vs 0.28–0.36). Women with military involvement also preferred shorter program durations and exercising alone or in a group online or in person, whereas men with military involvement were open to longer program durations, when compared to their civilian counterparts (Ps < .05; Cramer’s Vs 0.19–0.37). Women and men with military involvement were more likely than their civilian counterparts to perceive that exercise benefits their psychological outlook and social interactions. They were also more likely than civilians to indicate poor exercise environment, high time expenditure, and family discouragement as perceived barriers to exercise (Ps < .05; Cohen’s ds 0.21–0.97). Military-involved women were also more likely than civilian women to endorse the perceived barrier of hard physical exercise (P < .05; Cohen’s d = 0.25).This study identified perceived benefits and barriers to exercise, along with willingness to engage in exercise programs, and exercise preferences among men and women survivors of SV with military involvement. Targeting these factors in intervention planning will be important for physical activity promotion and program engagement among veterans to reduce the disproportionate impact of SV and disease burden among U.S. service members and veterans.

PRIMARY OBJECTIVE: Despite a high prevalence of intimate partner violence (IPV) and its lasting impacts on individuals, particularly women, very little is known about how IPV may impact the brain. IPV is known to frequently result in traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD). In this overview of literature, we examined literature related to neuroimaging in women with IPV experiences between the years 2010-2021. RESEARCH DESIGN: Literature overview. METHODS AND PROCEDURES: A total of 17 studies were included in the review, which is organized into each imaging modality, including magnetic resonance imaging (structural, diffusion, and functional MRI), Electroencephalography (EEG), proton magnetic resonance spectroscopy (pMRS), and multimodal imaging. MAIN OUTCOMES AND RESULTS: Research has identified changes in brain regions associated with cognition, emotion, and memory. Howeverto date, it is difficult to disentangle the unique contributions of TBI and PTSD effects of IPV on the brain. Furthermore, experimental design elements differ considerably among studies. CONCLUSIONS: The aim is to provide an overview of existing literature to determine commonalities across studies and to identify remaining knowledge gaps and recommendations for implementing future imaging studies with individuals who experience IPV.

After misinformation has been corrected, people initially update their belief extremely well. However, this change is rarely sustained over time, with belief returning towards pre-correction levels. This is called belief regression. The current study aimed to examine the association between memory for the correction and belief regression, and whether corrected misinformation suffers from belief regression more than affirmed facts. Participants from Prolific Academic (N = 612) rated the veracity of 16 misinformation and 16 factual items and were randomly assigned to a correction condition or test-retest control. Immediately after misinformation was corrected and facts affirmed, participants re-rated their belief and were asked whether they could remember the items' presented veracity. Participants repeated this post-test one month later. We found that belief and memory were highly associated, both immediately (⍴ = 0.51), and after one month (⍴ = 0.82), and that memory explained 66% of the variance in belief regression after correcting for measurement reliability. We found the rate of dissenting (accurately remembering that misinformation was presented as false but still believing it) remained stable between the immediate and delayed post-test, while the rate of forgetting quadrupled. After one month, 57% of participants who believed in the misinformation thought that the items were presented to them as true. Belief regression was more pronounced for misinformation than facts, but this was greatly attenuated once pre-test belief was equated. Together, these results clearly indicate that memory plays a fundamental role in belief regression, and that repeated corrections could be an effective method to counteract this phenomenon.

Sleep disturbances are strongly associated with mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD). PTSD and mTBI have been linked to alterations in white matter (WM) microstructure, but whether poor sleep quality has a compounding effect on WM remains largely unknown. We evaluated sleep and diffusion magnetic resonance imaging (dMRI) data from 180 male post-9/11 veterans diagnosed with (1) PTSD (n = 38), (2) mTBI (n = 25), (3) comorbid PTSD+mTBI (n = 94), and (4) a control group with neither PTSD nor mTBI (n = 23). We compared sleep quality (Pittsburgh Sleep Quality Index, PSQI) between groups using ANCOVAs and calculated regression and mediation models to assess associations between PTSD, mTBI, sleep quality, and WM. Veterans with PTSD and comorbid PTSD+mTBI reported poorer sleep quality than those with mTBI or no history of PTSD or mTBI (p = 0.012 to <0.001). Poor sleep quality was associated with abnormal WM microstructure in veterans with comorbid PTSD+mTBI (p < 0.001). Most importantly, poor sleep quality fully mediated the association between greater PTSD symptom severity and impaired WM microstructure (p < 0.001). Our findings highlight the significant impact of sleep disturbances on brain health in veterans with PTSD+mTBI, calling for sleep-targeted interventions.

It is well known that humans have a massive memory for pictures and scenes.(1)(,)(2)(,)(3)(,)(4) They show an ability to encode thousands of images with only a few seconds of exposure to each. In addition to this massive memory for "what" observers have seen, three experiments reported here show that observers have a "spatial massive memory" (SMM) for "where" stimuli have been seen and a "temporal massive memory" (TMM) for "when" stimuli have been seen. The positions in time and space for at least dozens of items can be reported with good, if not perfect accuracy. Previous work has suggested that there might be good memory for stimulus location,(5)(,)(6) but there do not seem to have been concerted efforts to measure the extent of this memory. Moreover, in our method, observers are recalling where items were located and not merely recognizing the correct location. This is interesting because massive memory is sometimes thought to be limited to recognition tasks based on sense of familiarity.

Veterans who deployed in support of Operation Enduring Freedom (OEF), Iraqi Freedom (OIF), and New Dawn (OND) commonly experience severe psychological trauma, often accompanied by physical brain trauma resulting in mild traumatic brain injury (mTBI). Prior studies of individuals with posttraumatic stress disorder (PTSD) have revealed alterations in brain structure, accelerated cellular aging, and impacts on cognition following exposure to severe psychological trauma and potential interactive effects of military-related mTBI. To date, however, little is known how such deployment-related trauma changes with time and age of injury of the affected veteran. In this study, we explored changes in cortical thickness, volume, and surface area after an average interval of approximately 2 years in a cohort of 254 OEF/OIF/OND Veterans ranging in age from 19 to 67 years. Whole-brain vertex-wise analyses revealed that veterans who met criteria for severe PTSD (Clinician-Administered PTSD Scale ≥60) at baseline showed greater negative longitudinal changes in cortical thickness, volume, and area over time. Analyses also revealed a significant severe-PTSD by age interaction on cortical measures with severe-PTSD individuals exhibiting accelerated cortical degeneration with increasing age. Interaction effects of comorbid military-related mTBI within the severe-PTSD group were also observed in several cortical regions. These results suggest that those exhibiting severe PTSD symptomatology have accelerated atrophy that is exacerbated with increasing age and history of mTBI.

Military service members returning from theaters of war are at increased risk for mental illness, but despite high prevalence and substantial individual and societal burden, the underlying pathomechanisms remain largely unknown. Exposure to high levels of emotional stress in theaters of war and mild traumatic brain injury (mTBI) are presumed factors associated with risk for the development of mental disorders.To investigate (1) whether war zone–related stress is associated with microstructural alterations in limbic gray matter (GM) independent of mental disorders common in this population, (2) whether associations between war zone–related stress and limbic GM microstructure are modulated by a history of mTBI, and (3) whether alterations in limbic GM microstructure are associated with neuropsychological functioning.This cohort study was part of the TRACTS (Translational Research Center for TBI and Stress Disorders) study, which took place in 2010 to 2014 at the Veterans Affair Rehabilitation Research and Development TBI National Network Research Center. Participants included male veterans (aged 18-65 years) with available diffusion tensor imaging data enrolled in the TRACTS study. Data analysis was performed between December 2017 to September 2021.The Deployment Risk and Resilience Inventory (DRRI) was used to measure exposure to war zone–related stress. The Boston Assessment of TBI-Lifetime was used to assess history of mTBI. Stroop Inhibition (Stroop-IN) and Inhibition/Switching (Stroop-IS) Total Error Scaled Scores were used to assess executive or attentional control functions.Diffusion characteristics (fractional anisotropy of tissue [FAT]) of 16 limbic and paralimbic GM regions and measures of functional outcome.Among 384 male veterans recruited, 168 (mean [SD] age, 31.4 [7.4] years) were analyzed. Greater war zone–related stress was associated with lower FAT in the cingulate (DRRI-combat left: P = .002, partial r = −0.289; DRRI-combat right: P = .02, partial r = −0.216; DRRI-aftermath left: P = .004, partial r = −0.281; DRRI-aftermath right: P = .02, partial r = −0.219), orbitofrontal (DRRI-combat left medial orbitofrontal cortex: P = .02, partial r = −0.222; DRRI-combat right medial orbitofrontal cortex: P = .005, partial r = −0.256; DRRI-aftermath left medial orbitofrontal cortex: P = .02, partial r = −0.214; DRRI-aftermath right medial orbitofrontal cortex: P = .005, partial r = −0.260; DRRI-aftermath right lateral orbitofrontal cortex: P = .03, partial r = −0.196), and parahippocampal (DRRI-aftermath right: P = .03, partial r = −0.191) gyrus, as well as with higher FAT in the amygdala-hippocampus complex (DRRI-combat: P = .005, partial r = 0.254; DRRI-aftermath: P = .02, partial r = 0.223). Lower FAT in the cingulate-orbitofrontal gyri was associated with impaired response inhibition (Stroop-IS left cingulate: P < .001, partial r = −0.440; Stroop-IS right cingulate: P < .001, partial r = −0.372; Stroop-IS left medial orbitofrontal cortex: P < .001, partial r = −0.304; Stroop-IS right medial orbitofrontal cortex: P < .001, partial r = −0.340; Stroop-IN left cingulate: P < .001, partial r = −0.421; Stroop-IN right cingulate: P < .001, partial r = −0.300; Stroop-IN left medial orbitofrontal cortex: P = .01, partial r = −0.223; Stroop-IN right medial orbitofrontal cortex: P < .001, partial r = −0.343), whereas higher FAT in the mesial temporal regions was associated with improved short-term memory and processing speed (left amygdala-hippocampus complex: P < .001, partial r = −0.574; right amygdala-hippocampus complex: P < .001, partial r = 0.645; short-term memory left amygdala-hippocampus complex: P < .001, partial r = 0.570; short-term memory right amygdala-hippocampus complex: P < .001, partial r = 0.633). A history of mTBI did not modulate the ass ciation between war zone–related stress and GM diffusion.This study revealed an association between war zone–related stress and alteration of limbic GM microstructure, which was associated with cognitive functioning. These results suggest that altered limbic GM microstructure may underlie the deleterious outcomes of war zone–related stress on brain health. Military service members may benefit from early therapeutic interventions after deployment to a war zone.

Maladaptive anger and aggression are common in US military veterans and increase risk for impaired social relationships and functioning, justice-involvement and violence. Early life (before age 18) adversity predisposes veterans to later life psychopathology, though the link to increased later life anger is unclear. We analysed cross-sectional data of 158 post-9/11 veterans from the Translational Research Center for Traumatic Brain Injury and Stress Disorders study with and without a history of early life adversity (ns = 109 and 49, respectively). We explored the relationship among major clinical variables and current veteran anger (Dimensions of Anger Reactions) and whether the associations with these variables differed among participants with and without a history of retrospective self-reported early life adversity (Childhood Trauma Questionnaire). In the overall sample, posttraumatic stress disorder (PTSD) and depression severities had the strongest associations with current veteran anger (βs = 0.261 and 0.263; p-values = 0.0022 and 0.0103, respectively). In the subsample without early life adversity, only PTSD severity was significantly associated with anger (β = 0.577, p = 0.0004). In the early life adversity subsample, this strong association weakened and was no longer significant (β = 0.168, p = 0.1007); instead, anxiety and depression severities showed moderate associations with anger (βs = 0.243 and 0.287, p-values = 0.0274 and 0.0130, respectively). Findings suggest that clinicians should screen veterans with history of early life adversity for depression and anxiety when anger is present.

Cross-sectional work suggests that deployment-related posttraumatic sequelae are associated with increased disability in U.S. veterans deployed following the September 11, 2001 (9/11), terrorist attacks. However, few studies have examined the psychiatric and somatic variables associated with changes in functional disability over time. A total of 237 post-9/11 veterans completed comprehensive assessments of psychiatric and cognitive functioning, as well as a disability questionnaire, at baseline and 2-year follow-up. At baseline, higher levels of PTSD, depressive, and pain-related symptoms were associated with baseline global functional disability, semipartial r(2) = .036-.044. Changes in symptoms of PTSD, depression, pain, and sleep, but not anxiety or alcohol use, were independently associated with changes in functional disability, semipartial r(2) = .017-.068. Baseline symptoms of these conditions were unrelated to changes in disability, and cognitive performance was unrelated to disability at any assessment point. Together, this suggests that changes in psychiatric and somatic symptoms are tightly linked with changes in functional disability and should be frequently monitored, and even subclinical symptoms may be a target of intervention.

BACKGROUND: Post-9/11 veterans exhibit high prevalence of deployment stress, psychological conditions, and traumatic brain injury (TBI) which impact reintegration, especially among those with a history of interpersonal early life trauma (I-ELT). The relative importance of each risk factor is unclear. PURPOSE: We examined major deployment and clinical exposures of reintegration challenges among veterans with and without I-ELT. METHOD: We analyzed cross-sectional data of 155 post-9/11 veterans from the Translational Research Center for TBI and Stress Disorders study. FINDINGS: Depression severity had the strongest association with reintegration challenges, followed by posttraumatic stress disorder (PTSD) severity, post-deployment stress, and deployment safety concerns. Deployment safety concerns had a stronger, significant association among veterans with I-ELT. In nearly every model, PTSD and depression severities were weaker for veterans with I-ELT, compared to those without. DISCUSSION: Clinicians should consider the relative risk of concurrent clinical conditions and trauma histories when considering veterans' reintegration needs.

INTRODUCTION: Since 2006, efforts have been made to increase the accurate identification of traumatic brain injuries (TBIs) in post-9/11 military personnel. The Boston Assessment of TBI-Lifetime (BAT-L) is the first validated instrument designed specifically to diagnose TBIs throughout the life span in post-9/11 Veterans. The objective was to compare the diagnostic accuracy of the BAT-L with medical records from the Department of Defense (DoD). MATERIAL AND METHODS: Traumatic brain injury diagnosis for 153 Veterans deployed in 2011 enrolled in the Translational Research Center for TBI and Stress Disorder longitudinal cohort study from the BAT-L clinical interview was compared to DoD online medical records to determine diagnostic prevalence and injury severity for all head injury cases during deployment. Sensitivity, specificity, Cohen's kappa, and Kendall's tau-b were calculated for TBI diagnosis and severity. Concordant TBI cases and discordant TBI cases were compared using chi-square and t-test analyses. This study has been approved by VA Boston by Institutional Review Boards for human participants' protection. RESULTS: Correspondence of TBI diagnoses from the BAT-L with DoD records was fair (κ = 0.42; sensitivity = 72.7%; specificity = 82.8%). Comparison of injury severity also showed fair correspondence (κ = 0.41). Missing TBI diagnostic data from DoD records were frequent; 43% of TBIs reported on the BAT-L did not have any documentation of assessment or diagnoses in DoD records. CONCLUSION: This study addresses a critical gap in research by comparing the diagnostic accuracy of a validated, semi-structured clinical interview with available medical records. Diagnosis of TBIs via the BAT-L was both sensitive and specific when compared to DoD records, supporting the validity of the BAT-L for retrospective assessment of military TBI. However, diagnostic correspondence was only fair. This lack of diagnostic agreement was related to multiple factors including lack of documentation at the time of injury by DoD, differences in assessment and goals, and other combat-related motivational factors associated with failure to report injuries while deployed. Several policies have been implemented to address underreporting and under-documentation of TBIs, yet challenges remain. Recommendations for evaluating TBI are presented. Accurate diagnosis of TBI is necessary for appropriate treatment planning, as well as service-related compensation.

BACKGROUND: Posttraumatic stress disorder (PTSD) is heritable and a potential consequence of exposure to traumatic stress. Evidence suggests that a quantitative approach to PTSD phenotype measurement and incorporation of lifetime trauma exposure (LTE) information could enhance the discovery power of PTSD genome-wide association studies (GWASs). METHODS: A GWAS on PTSD symptoms was performed in 51 cohorts followed by a fixed-effects meta-analysis (N = 182,199 European ancestry participants). A GWAS of LTE burden was performed in the UK Biobank cohort (N = 132,988). Genetic correlations were evaluated with linkage disequilibrium score regression. Multivariate analysis was performed using Multi-Trait Analysis of GWAS. Functional mapping and annotation of leading loci was performed with FUMA. Replication was evaluated using the Million Veteran Program GWAS of PTSD total symptoms. RESULTS: GWASs of PTSD symptoms and LTE burden identified 5 and 6 independent genome-wide significant loci, respectively. There was a 72% genetic correlation between PTSD and LTE. PTSD and LTE showed largely similar patterns of genetic correlation with other traits, albeit with some distinctions. Adjusting PTSD for LTE reduced PTSD heritability by 31%. Multivariate analysis of PTSD and LTE increased the effective sample size of the PTSD GWAS by 20% and identified 4 additional loci. Four of these 9 PTSD loci were independently replicated in the Million Veteran Program. CONCLUSIONS: Through using a quantitative trait measure of PTSD, we identified novel risk loci not previously identified using prior case-control analyses. PTSD and LTE have a high genetic overlap that can be leveraged to increase discovery power through multivariate methods.

Previous work identified a cognitive subtype of PTSD with impaired executive function (i.e., impaired EF-PTSD subtype) and aberrant resting-state functional connectivity between frontal parietal control (FPCN) and limbic (LN) networks. To better characterize this cognitive subtype of PTSD, this study investigated (1) alterations in specific FPCN and LN subnetworks and (2) chronicity of PTSD symptoms. In a post-9/11 veteran sample (N = 368, 89% male), we identified EF subgroups using a standardized neuropsychological battery and a priori cutoffs for impaired, average, and above-average EF performance. Functional connectivity between two subnetworks of the FPCN and three subnetworks of the LN was assessed using resting-state fMRI (n = 314). PTSD chronicity over a 1–2-year period was assessed using a reliable change index (n = 175). The impaired EF-PTSD subtype had significantly reduced negative functional connectivity between the FPCN subnetwork involved in top-down control of emotion and two LN subnetworks involved in learning/memory and social/emotional processing. This impaired EF-PTSD subtype had relatively chronic PTSD, while those with above-average EF and PTSD displayed greater symptom reduction. Lastly, FPCN-LN subnetworks partially mediated the relationship between EF and PTSD chronicity (n = 121). This study reveals (1) that an impaired EF-PTSD subtype has a specific pattern of FPCN-LN subnetwork connectivity, (2) a novel above-average EF-PTSD subtype displays reduced PTSD chronicity, and (3) both cognitive and neural functioning predict PTSD chronicity. The results indicate a need to investigate how individuals with this impaired EF-PTSD subtype respond to treatment, and how they might benefit from personalized and novel approaches that target these neurocognitive systems.

BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with inflammation and various forms of chronic disease. The Absent in Melanoma 2 (AIM2) gene has been implicated in mechanisms of inflammation and anxiety, and methylation at a particular locus in this gene (cg10636246) has previously been shown to influence the association between PTSD and elevated C-reactive protein levels in blood. METHOD: We tested if this association might extend to other indicators of inflammation and to plasma-based measures of neuropathology in a cohort of post-9/11 US military veterans. Using a Bayesian approach, mediation models were tested cross-sectionally (n = 478) and longitudinally (n = 298). Peripheral markers of inflammation and neuropathology were measured with ultra-sensitive Single Molecule Array (Simoa®) technology. RESULTS: Analyses revealed indirect effects of PTSD symptom severity on peripheral indices of both inflammation (interleukin [IL]6, IL-10, tumor necrosis factor-α; indirect standardized [std.] ß range = 0.018-0.023, all p-values adjusted for multiple testing [p(adj) ] < 0.05) and neuropathology (neurofilament light [NFL]; indirect std. ß = -0.018, p(adj)  = 0.02) via AIM2 methylation. This indirect effect was also evident when predicting IL-10 at a follow-up assessment (indirect std. ß = -0.018, p(adj)  = 0.04) controlling for baseline IL-10. CONCLUSIONS: Given that AIM2 methylation mediated the association between PTSD symptoms and multiple inflammatory and neuropathology markers, our results suggest that AIM2 methylation may offer clinical utility for indexing risk for adverse health outcomes associated with these peripheral indices of inflammation and neuropathology. Results also suggest a possible shared etiology underlying the frequent co-occurrence of inflammation and neuropathology.

OBJECTIVE: More than one-third of women in the United States experience intimate partner violence (IPV) in their lifetime, increasing their risk for traumatic brain injury (TBI). Despite the prevalence of TBI among IPV survivors, research is sparse in comparison with parallel populations (eg, military, accidents, sports). This pilot study aimed to provide a preliminary investigation of the effect of TBI on brain morphometry and resting-state functional connectivity in women who experience IPV. PARTICIPANTS: A total of 45 community-dwelling women survivors of IPV who screened positive for posttraumatic stress disorder (PTSD). DESIGN: Participants completed comprehensive assessments of trauma exposure, PTSD, TBI history, and brain neurological health. Twenty-three participants (51.1%) met diagnostic criteria for lifetime TBI. Of these, 15 participants experienced 1 or more TBIs resulting from IPV. The remaining participants experienced TBI from non-IPV exposures (eg, sports/motor vehicle accident). Surface-based neuroimaging analyses were performed to examine group differences in cortical thickness and in functional connectivity of amygdala and isthmus cingulate seeds to examine emotion regulation and the default mode network, respectively. MAIN MEASURES: Boston Assessment of Traumatic Brain Injury-Lifetime for Intimate Partner Violence (BAT-L/IPV); Clinician Administered PTSD Scale (CAPS); structural and functional neuroimaging. RESULTS: History of lifetime TBI in women IPV survivors was associated with differences in cortical thickness as well as functional connectivity between the isthmus cingulate seed and a variety of regions, including superior parietal and frontal cortices. Individuals with IPV-related TBI showed lower cortical thickness in the right paracentral gyrus than individuals with TBI from other non-IPV etiologies. CONCLUSION: Significant differences in brain structure and connectivity were observed in individuals with IPV and TBI. A lower mean cortical thickness of the paracentral gyrus was associated with TBI due to IPV than TBI from other etiologies. Although preliminary, findings from this pilot study present a step toward identifying potential mechanisms by which IPV and TBI secondary to IPV impact brain health in women.

Mild traumatic brain injury (mTBI) is among the most common injuries sustained by post-9/11 veterans; however, these injuries often occur within the context of psychological trauma. Blast exposure, even in the absence of a diagnosable TBI, leads to changes in neural connectivity and congitive functioning. Therefore, considering clinical comorbidities and injury characteristics is critical to understanding the long-term effects of mTBI. Research is moving towards identifying diagnostic and prognostic blood-based biomarkers for TBI; however, few studies include other prevalent clinical and medical comorbidities related to deployment. Here, we present the initial cross-sectional relationships between plasma biomarkers, clinical, and medical comorbidities in a well-characterized longitudinal sample of 550 post-9/11 veteran men and women. We examined biomarkers associated with inflammation (interleukin 6 and 10, tumor necrosis factor α, and eotaxin) and neurodegeneration (neurofilament light, glial fibrillary acidic protein (GFAP), tau, brain derived neurotrophic factor, amyloid ß 40 and 42, phosphorylated neurofilament heavy chain, and neuron specific enolase). Univariate analyses of covariance (ANCOVA) were conducted to determine mean level differences between close blast (blasts that occur within 0-10 meters) and mTBI groups. Our primary findings were twofold: (1) Inflammatory markers were consistently higher in participants exposed to close blasts and were strongly related to deployment-related psychopathology. (2) GFAP was consistently lower in participants exposed to blast and mTBI and lower GFAP was associated with more severe psychological symptoms. More research is clearly needed; however, our findings indicate that chronic increased inflammation and decreased GFAP may be related to close blast exposure.