PTSD is increasingly recognized as a common, disabling mental health problem after trauma. Neuroimaging studies suggest that PTSD is related to abnormal brain function and structure, but the development of such abnormalities is poorly understood. Advanced neuroplasticity research demonstrates that the adult brain is capable of dynamically altering its function and structure. Based on this evidence, PTSD can be conceptualized as a form of maladaptation to trauma. The current study will examine this idea by testing for progressive changes during the initial weeks after a traumatic motor vehicle collision (MVC). The working hypothesis is that brain function and structure in survivors who do and in survivors who do not develop PTSD will change differently during the early post-trauma weeks. Survivors of MVCs recruited at the Emergency Department (ED) will be longitudinally studied, starting within the initial days (up to 2 weeks) and again at approximately 12 weeks after the MVC. Neural activity associated with characteristic deficits in down-regulation of negative emotion in PTSD patients will be studied using a Reappraisal Emotion Regulation Task (RERT) and a Shifted-attention Emotion Appraisal Task (SEAT) during functional magnetic resonance imaging (fMRI). In addition, high-resolution structural MRI (sMRI) scans will be used to examine cortical thickness. The differences in activation associated with emotional tasks and in cortical thickness between scan sessions at initial days and 12 weeks will be used to define progressive functional and structural changes over this period. Group differences in progressive brain changes in PTSD and non-PTSD survivors will be used to identify differences in brain function and structure that contribute to PTSD. The proposed work fills an important gap in current models of PTSD development by identifying factors that differentiate a natural recovery following traumatic stress from a maladaptive recovery that leads to PTSD. The findings can help develop early interventions to prevent and treat PTSD. Preliminary data have been collected from MVC survivors scanned within days (9?4 days) and 12 weeks after an MVC. Preliminary results suggest that cortical thickness in frontal and temporal cortices changed over the initial weeks in trauma exposed groups, but not in trauma free controls over a comparable time interval. Brain activation associated with emotional processing increased in left prefrontal and visual cortices, but decreased in left supramarginal gyrus and parahippocampus. These preliminary results provide initial indications of functional and structural changes over this perid in several brain areas, including FC regions. The proposed research extends this work.
PTSD is increasingly recognized as a public health problem because of the substantial suffering, medical costs and lost productivity associated with PTSD debilitation. This longitudinal study fulfills strategic objectives of NIMH in that it will apply neuroimaging research to explore neural bases of PTSD, including the trajectory of initial PTSD development. This proposal merits consideration for the NIH Exploratory Developmental Research Grant Program (PA-11-261) for its potential to contribute to better interventions for PTSD, and to improve neuroimaging methodologies for the study of the causes of mental disorders.