While chronic visual symptom complaints are common among Veterans with a history of mild traumatic brain injury (mTBI), research is still ongoing to characterize the pattern of visual deficits that is most strongly associated with mTBI and specifically, the impact of blast-related mTBI on visual functioning. One area that has not been well explored is the potential impact of blast mTBI on refractive error. While myopic shifts have been documented following head injuries in civilian populations, posttraumatic myopic shifts have not been explored in participants with military mTBI. This study investigated the impact of blast mTBIs on a range of visual function measures including distance acuity and refractive error, in a well-characterized cohort of thirty-one Post-9/11 veterans for whom detailed clinical interviews regarding military and TBI history were available. Seventeen participants had a history of blast-related mTBI (blast mTBI + group) while 14 did not (blast mTBI- group). Results show an increased frequency of convergence insufficiency and myopia in the blast mTBI + group relative to the blast mTBI- group. Linear regression analyses further show that deficits in distance acuity and refractive error are associated with the number of blast mTBIs during military service but not the number of non-blast mTBIs or the number of lifetime non-blast TBIs and cannot be accounted for by PTSD. These results are consistent with long-lasting damage following blast mTBI to subcortical visual structures that support both vergence movements and the accommodative functions needed to see clearly objects at varying distances.

OBJECTIVE: To adapt the Boston Assessment of TBI-Lifetime (BAT-L) interview specifically for female survivors of intimate partner violence (IPV), validate the adapted BAT-L/IPV, and report the prevalence of head injury. SETTING: The BAT-L is the first validated instrument to diagnose traumatic brain injuries (TBIs) throughout the life span for post-9/11 veterans. The BAT-L/IPV was adapted to target diagnostic issues belonging exclusively to IPV while maintaining its life span approach. PARTICIPANTS: Community-dwelling convenience sample of 51 female survivors of IPV with subthreshold (n = 10) or full diagnostic criteria (n = 41) of posttraumatic stress disorder. DESIGN: Standard TBI criteria were evaluated using a semistructured clinical interview. MAIN MEASURES: The BAT-L/IPV is compared with the Ohio State University TBI Identification Method (OSU-TBI-ID) scoring approach as the criterion standard. RESULTS: Correspondence between the BAT-L/IPV and the OSU-TBI-ID score was excellent (Cohen κ = 0.86; Kendall τ-b = 0.89). Sensitivity = 89.3% (95% CI, 81.2-97.4); specificity = 98.3% (95% CI, 95.0-100); positive predictive value = 98.0% (95% CI, 94.2-100); and negative predictive value = 90.6% (95% CI, 83.5-97.7). On the BAT-L/IPV, more than one-third (35.3%) of IPV survivors reported TBI secondary to an IPV-related assault, 76.5% reported IPV subconcussive head injury, 31.4% reported attempted strangulation, and 37.3% reported non-IPV TBI. CONCLUSIONS: The BAT-L/IPV performed well in diagnosing TBI in female IPV survivors as compared with the criterion standard. The prevalence of TBI was frequent; subconcussive head injury was pervasive. Greater awareness for head injury risk and increased diagnostic specificity of TBI in IPV survivors is needed.

OBJECTIVE: Survivors of intimate partner violence (IPV) report significant trauma histories, high rates of posttraumatic stress disorder (PTSD), head injuries and comorbid disorders, and multiple barriers to treatment that often preclude the regular attendance and engagement required in typical therapy protocols. The significant challenges faced by IPV survivors needing treatment may be ameliorated by condensing effective treatments for PTSD, such as cognitive processing therapy (CPT), in an accelerated delivery timeline. METHOD: Using a multiple subject, single case design of six matched pairs of 12 female IPV survivors, we preliminarily tested the relative effectiveness of individual massed CPT delivered over 5 days (mCPT) as compared with standard CPT (sCPT) delivery in women IPV survivors. Assessments included full psychiatric diagnostic interviews, clinical interviews assessing trauma history and head injury prior to treatment, symptom monitoring during treatment, and full repeat assessments at 1 month and 3 months following treatment. RESULTS: No treatment group effect was found for PTSD severity between mCPT and sCPT among intention-to-treat, F(1, 10) = .01, p = .93. Both mCPT and sCPT were associated with significant improvement in PTSD, F(2, 20) = 45.05, p .001, ds = 1.32-2.38). CONCLUSION: Overall, findings indicate mCPT appears effective in reducing psychological symptoms for women IPV survivors and suggest that condensed treatment is both palatable and feasible. Accelerated treatment delivery in this population may provide a necessary lifeline for women with IPV-related PTSD. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Chronic elevation of systemic inflammation is observed in a wide range of disorders including PTSD, depression, and traumatic brain injury, all of which are relatively common in United States Veterans. Although previous work has demonstrated a link between inflammation and various diagnoses separately, few studies have examined transdiagnostic symptoms and inflammation within the same model. The objective of this study was to examine relationships between psychiatric and health variables and systemic inflammation, and to determine whether mild traumatic brain injury (mTBI) and/or exposure to blast munitions moderate these relationships. Confirmatory factor analysis in a large sample (N = 357) of post-9/11 Veterans demonstrated good fit to a four-factor model reflecting traumatic stress, affective, somatic, and metabolic latent variables. Hierarchical regression models revealed that each of the latent variables were associated with higher levels of systemic inflammation. However, the strongest relationship with inflammation emerged among those who had both war-zone blast exposures and metabolic dysregulation, even after adjusting for mental health latent variables. Exploratory analyses showed that blast exposure was associated with metabolic dysregulation in a dose-response manner, with self-reported closer blast proximity associated with the greatest metabolic dysregulation. Together, these results provide greater understanding of the types of symptoms most strongly associated with inflammation, and underscore the importance of maintaining a healthy lifestyle to reduce the impact of obesity and other metabolic symptoms on future chronic disease in younger to middle-aged Veterans.

BackgroundA major obstacle in understanding and treating posttraumatic stress disorder (PTSD) is its clinical and neurobiological heterogeneity. To address this barrier, the field has become increasingly interested in identifying subtypes of PTSD based on dysfunction in neural networks alongside cognitive impairments that may underlie the development and maintenance of symptoms. The current study aimed to determine if subtypes of PTSD, based on normative-based cognitive dysfunction across multiple domains, have unique neural network signatures.MethodsIn a sample of 271 veterans (90% male) that completed both neuropsychological testing and resting-state fMRI, two complementary, whole-brain functional connectivity analyses explored the link between brain functioning, PTSD symptoms, and cognition.ResultsAt the network level, PTSD symptom severity was associated with reduced negative coupling between the limbic network (LN) and frontal-parietal control network (FPCN), driven specifically by the dorsolateral prefrontal cortex and amygdala Hubs of Dysfunction. Further, this relationship was uniquely moderated by executive function (EF). Specifically, those with PTSD and impaired EF had the strongest marker of LN-FPCN dysregulation, while those with above-average EF did not exhibit PTSD-related dysregulation of these networks.ConclusionThese results suggest that poor executive functioning, alongside LN-FPCN dysregulation, may represent a neurocognitive subtype of PTSD.

Elevated serum C-reactive protein (CRP) and possessing an APOE ε4 allele are two of the most prominent risk factors for cognitive and neurological dysfunction in older adults, but little is known about the unique or cumulative effects of these risk factors in young-to-middle-aged adults. To further characterize these potential relationships, measures of cognition and microstructural white matter integrity were examined using data from a sample of 329 post-9/11 war veterans that was collected as part of a comprehensive evaluation that included assessment of neuropsychological functioning, MRI scanning, psychiatric diagnoses, health screening, markers of inflammation, and APOE genotypes. Hierarchical linear regression analyses revealed the CRP and APOE ε4 interaction was associated with global cognition (β = -0.633), executive functioning (β = -0.566), and global fractional anisotropy (β = -0.470), such that elevated CRP was associated with worse cognition and white matter integrity in APOE ε4 carriers. Diffusion tensor imaging (DTI) was used to determine if CRP × APOE ε4 presence was associated with regionally specific fractional anisotropy in white matter tracts. Tract-based spatial statistics revealed CRP × APOE ε4 presence was associated with fractional anisotropy in the corpus callosum, right superior longitudinal fasciculus, right posterior corona radiata, as well as the bilateral anterior and superior corona radiatas. This suggests that APOE ε4 carriers may be uniquely vulnerable to the potentially negative impact of elevated systematic inflammation to cognition and microstructural white matter integrity.

Growing research suggests that posttraumatic stress disorder (PTSD) may be a risk factor for poor cardiovascular health, and yet our understanding of who might be at greatest risk of adverse cardiovascular outcomes after trauma is limited. In this study, we conducted the first examination of the individual and synergistic contributions of PTSD symptoms and blood pressure genetics to continuous blood pressure levels. We harnessed the power of the Psychiatric Genomics Consortium-PTSD Physical Health Working Group and investigated these associations across 11 studies of 72,224 trauma-exposed individuals of European (n = 70,870) and African (n = 1,354) ancestry. Genetic contributions to blood pressure were modeled via polygenic scores (PGS) for systolic blood pressure (SBP) and diastolic blood pressure (DBP) that were derived from a prior trans-ethnic blood pressure genome-wide association study (GWAS). Results of trans-ethnic meta-analyses revealed significant main effects of the PGS on blood pressure levels [SBP: β = 2.83, standard error (SE) = 0.06, p 1E-20; DBP: β = 1.32, SE = 0.04, p 1E-20]. Significant main effects of PTSD symptoms were also detected for SBP and DBP in trans-ethnic meta-analyses, though there was significant heterogeneity in these results. When including data from the largest contributing study - United Kingdom Biobank - PTSD symptoms were negatively associated with SBP levels (β = -1.46, SE = 0.44, p = 9.8E-4) and positively associated with DBP levels (β = 0.70, SE = 0.26, p = 8.1E-3). However, when excluding the United Kingdom Biobank cohort in trans-ethnic meta-analyses, there was a nominally significant positive association between PTSD symptoms and SBP levels (β = 2.81, SE = 1.13, p = 0.01); no significant association was observed for DBP (β = 0.43, SE = 0.78, p = 0.58). Blood pressure PGS did not significantly moderate the associations between PTSD symptoms and blood pressure levels in meta-analyses. Additional research is needed to better understand the extent to which PTSD is associated with high blood pressure and how genetic as well as contextual factors may play a role in influencing cardiovascular risk.