Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

In a motor vehicle collision (MVC), survivors often receive mild traumatic brain injuries (mTBI). Although there have been some reports of early white matter changes after an mTBI, much less is known about early cortical structural changes. To investigate early cortical changes within a few days after an MVC, we compared cortical thickness of mTBI survivors with non-mTBI survivors, then reexamined cortical thickness in the same survivors 3 months later. MVC survivors were categorized as mTBI or non-mTBI based on concussive symptoms documented in emergency departments (EDs). Cortical thickness was measured from MRI images using FreeSurfer within a few days and again at 3 months after MVC. Post-traumatic stress symptoms and physical conditions were also assessed. Compared with the non-mTBI group (n=23), the mTBI group (n=21) had thicker cortex in the left rostral middle frontal (rMFG) and right precuneus gyri, but thinner cortex in the left posterior middle temporal gyrus at 7.2±3.1 days after MVC. After 3 months, cortical thickness had decreased in left rMFG in the mTBI group but not in the non-mTBI group. The cortical thickness of the right precuneus region in the initial scans was positively correlated with acute traumatic stress symptoms for all survivors and with the number of reduced activity days for mTBI survivors who completed the follow-up. The preliminary results suggest that alterations in cortical thickness may occur at an early stage of mTBI and that frontal cortex structure may change dynamically over the initial 3 months after mTBI.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140167/1/neu.2014.3492.pd

Subthreshold PTSD and PTSD in a prospective‐longitudinal cohort of military personnel: Potential targets for preventive interventions

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146501/1/da22819_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146501/2/da22819.pd

Early Changes in Cortical Emotion Processing Circuits after Mild Traumatic Brain Injury from Motor Vehicle Collision

Mild traumatic brain injury (mTBI) patients frequently experience emotion dysregulation symptoms, including post-traumatic stress. Although mTBI likely affects cortical activation and structure, resulting in cognitive symptoms after mTBI, early effects of mTBI on cortical emotion processing circuits have rarely been examined. To assess early mTBI effects on cortical functional and structural components of emotion processing, we assessed cortical activation to fearful faces within the first 2 weeks after motor vehicle collision (MVC) in survivors who did and did not experience mTBI. We also examined the thicknesses of cortical regions with altered activation. MVC survivors with mTBI (n = 21) had significantly less activation in left superior parietal gyrus (SPG) (−5.9, −81.8, 33.8; p = 10−3.623), left medial orbitofrontal gyrus (mOFG) (−4.7, 36.1, −19.3; p = 10−3.231), and left and right lateral orbitofrontal gyri (lOFG) (left: −16.0, 41.4, −16.6; p = 10−2.573; right: 18.7, 22.7, −17.7; p = 10−2.764) than MVC survivors without mTBI (n = 23). SPG activation in mTBI survivors within 2 weeks after MVC was negatively correlated with subsequent post-traumatic stress symptom severity at 3 months (r = −0.68, p = 0.03). Finally, the SPG region was thinner in the mTBI survivors than in the non-mTBI survivors (F = 11.07, p = 0.002). These results suggest that early differences in activation and structure in cortical emotion processing circuits in trauma survivors who sustain mTBI may contribute to the development of emotion-related symptoms

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

In a motor vehicle collision (MVC), survivors often receive mild traumatic brain injuries (mTBI). Although there have been some reports of early white matter changes after an mTBI, much less is known about early cortical structural changes. To investigate early cortical changes within a few days after an MVC, we compared cortical thickness of mTBI survivors with non-mTBI survivors, then reexamined cortical thickness in the same survivors 3 months later. MVC survivors were categorized as mTBI or non-mTBI based on concussive symptoms documented in emergency departments (EDs). Cortical thickness was measured from MRI images using FreeSurfer within a few days and again at 3 months after MVC. Post-traumatic stress symptoms and physical conditions were also assessed. Compared with the non-mTBI group (n=23), the mTBI group (n=21) had thicker cortex in the left rostral middle frontal (rMFG) and right precuneus gyri, but thinner cortex in the left posterior middle temporal gyrus at 7.2±3.1 days after MVC. After 3 months, cortical thickness had decreased in left rMFG in the mTBI group but not in the non-mTBI group. The cortical thickness of the right precuneus region in the initial scans was positively correlated with acute traumatic stress symptoms for all survivors and with the number of reduced activity days for mTBI survivors who completed the follow-up. The preliminary results suggest that alterations in cortical thickness may occur at an early stage of mTBI and that frontal cortex structure may change dynamically over the initial 3 months after mTBI

Preliminary Study of Acute Changes in Emotion Processing in Trauma Survivors with PTSD Symptoms

Accumulating evidence suggests traumatic experience can rapidly alter brain activation associated with emotion processing. However, little is known about acute changes in emotion neurocircuits that underlie PTSD symptom development. To examine acute alterations in emotion circuit activation and structure that may be linked to PTSD symptoms, thirty-eight subjects performed a task of appraisal of emotional faces as their brains were functionally and structurally studied with MRI at both two weeks and three months after motor vehicle collision (MVC). As determined by symptoms reported in the PTSD Checklist at three months, sixteen survivors developed probable PTSD, whereas the remaining 22 did not meet criteria for PTSD diagnosis (non-PTSD). The probable PTSD group had greater activation than the non-PTSD group in dorsal and ventral medial prefrontal cortex (dmPFC and vmPFC) while appraising fearful faces within two weeks after MVC and in left insular cortex (IC) three months after MVC. dmPFC activation at two weeks significantly positively correlated with PTSD symptom severity at two weeks (R = 0.462, P = 0.006) and three months (R = 0.418, p = 0.012). Changes over time in dmPFC activation and in PTSD symptom severity were also significantly positively correlated in the probable PTSD group (R = 0.641, P = 0.018). A significant time by group interaction was found for volume changes in left superior frontal gyrus (SFG, F = 6.048, p = 0.019) that partially overlapped dmPFC active region. Between two weeks and three months, left SFG volume decreased in probable PTSD survivors. These findings identify alterations in frontal cortical activity and structure during the early post-trauma period that appear to be associated with development of PTSD symptoms

A Comparison of Methods to Harmonize Cortical Thickness Measurements Across Scanners and Sites

Results of neuroimaging datasets aggregated from multiple sites may be biased by site-specific profiles in participants’ demographic and clinical characteristics, as well as MRI acquisition protocols and scanning platforms. We compared the impact of four different harmonization methods on results obtained from analyses of cortical thickness data: (1) linear mixed-effects model (LME) that models site-specific random intercepts (LME INT), (2) LME that models both site-specific random intercepts and age-related random slopes (LME INT+SLP), (3) ComBat, and (4) ComBat with a generalized additive model (ComBat-GAM). Our test case for comparing harmonization methods was cortical thickness data aggregated from 29 sites, which included 1,340 cases with posttraumatic stress disorder (PTSD) (6.2–81.8 years old) and 2,057 trauma-exposed controls without PTSD (6.3–85.2 years old). We found that, compared to the other data harmonization methods, data processed with ComBat-GAM was more sensitive to the detection of significant case-control differences (Χ 2(3) = 63.704, p < 0.001) as well as case-control differences in age-related cortical thinning (Χ 2(3) = 12.082, p = 0.007). Both ComBat and ComBat-GAM outperformed LME methods in detecting sex differences (Χ 2(3) = 9.114, p = 0.028) in regional cortical thickness. ComBat-GAM also led to stronger estimates of age-related declines in cortical thickness (corrected p-values < 0.001), stronger estimates of case-related cortical thickness reduction (corrected p-values < 0.001), weaker estimates of age-related declines in cortical thickness in cases than controls (corrected p-values < 0.001), stronger estimates of cortical thickness reduction in females than males (corrected p-values < 0.001), and stronger estimates of cortical thickness reduction in females relative to males in cases than controls (corrected p-values < 0.001). Our results support the use of ComBat-GAM to minimize confounds and increase statistical power when harmonizing data with non-linear effects, and the use of either ComBat or ComBat-GAM for harmonizing data with linear effects

Underlying Dimensions of DSM-5 Posttraumatic Stress Disorder and Major Depressive Disorder Symptoms

This study examined the relationship between the underlying latent factors of major depression symptoms and DSM-5 posttraumatic stress disorder (PTSD) symptoms (American Psychiatric Association, 2013). A nonclinical sample of 266 participants with a trauma history participated in the study. Confirmatory factor analyses were conducted to evaluate the fit of the DSM-5 PTSD model and dysphoria model, as well as a depression model comprised of somatic and nonsomatic factors. The DSM-5 PTSD model demonstrated somewhat better fit over the dysphoria model. Wald tests indicated that PTSD’s negative alterations in cognitions and mood factor was more strongly related to depression’s nonsomatic factor than its somatic factor. This study furthers a nascent line of research examining the relationship between PTSD and depression factors in order to better understand the nature of the high comorbidity rates between the two disorders. Moreover, this study provides an initial analysis of the new DSM-5 diagnostic criteria for PTSD