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

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

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

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 examining the mediational link between mild traumatic brain injury, acute stress, and post-traumatic stress symptoms following trauma

Background: The presence of mild traumatic brain injury (mTBI) increases post-traumatic stress disorder (PTSD) symptoms in the months following injury. However, factors that link mTBI and PTSD development are still unclear. Acute stress responses after trauma have been associated with PTSD development. mTBI may impair cognitive functions and increase anxiety immediately after trauma. Objective: This research aimed to test the possibility that mTBI increases acute stress symptoms rapidly, which in turn results in PTSD development in the subsequent months. Method: Fifty-nine patients were recruited from the emergency rooms of local hospitals. Post-mTBI, acute stress, and PTSD symptom severity were measured using the Rivermead Post-Concussion Symptoms Questionnaire (RPQ), Acute Stress Disorder Scale (ASDS), and PTSD Checklist for DSM-5 (PCL-5), respectively. Results: Moderated mediation analysis indicated that ASDS, at 2 weeks post-trauma, mediated the relationship between RPQ scores at 2 weeks and PCL-5 scores at 3 months post-trauma, only for patients who met mTBI diagnostic criteria. Conclusions: These findings present preliminary evidence suggesting that acute stress disorder symptoms may be one of the mechanisms involved in the development of PTSD among trauma survivors who have experienced mTBI, which provides a theoretical basis for early intervention of PTSD prevention after mTBI

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

Differences in brain activation in response to fearful faces during appraisal tasks in probable PTSD and non-PTSD groups at two weeks and three months after MVC.

<p>(A) Appraisal of fearful faces vs. neutral faces reveals greater activation in dmPFC (sagittal and axial views) and vmPFC (sagittal view) in the probable PTSD group compared to the non-PTSD group at two weeks. (B) Activation in dmPFC at two weeks after MVC was significantly positively correlated with PCL scores at three months across both groups. (C) Changes over time in dmPFC activation and PCL scores from two weeks to three months were positively correlated in the probable PTSD group. (D) The same contrast reveals greater activation in the probable PTSD group compared to the non-PTSD group in left IC at three months. (E) Activation in left IC was positively correlated with PCL scores at three months across both groups. (F) Summary of significant differences in activation of appraisal of fearful faces between groups at both time points. Initial cut-off voxel level Z > 2.3 (P < 0.01), with whole brain FWE correction at the cluster level of P<0.05.</p

Volume of left SFG.

<p>(A) parcellation of left SFG (shaded in gray) in FreeSurfer partially overlaps with location of the dmPFC activation cluster. (B) Volume of left SFG at two weeks and three months after MVC. *: indicates significant effect of time by group interaction. #: indicates significant decrease in left SFG volume in probable PTSD group over time. The error bars indicate the standard error of the mean.</p

Main effect of appraisal of all emotional faces (fear, angry and neutral) as compared to implicit emotion processing.

<p>(A) A Z statistical map of significant clusters. The clusters are identified by number in the description below. (B) Summary of significant clusters for appraisal activation, initial cut-off voxel level Z > 3.09 (P < 0.001), with whole brain FWE correction at the cluster level of P<0.05.</p

Demographics and symptoms of probable PTSD and non-PTSD groups.

<p>Demographics and symptoms of probable PTSD and non-PTSD groups.</p