Hypothesis 1: On fMRI scanning, frontoparietal activation during performance of executive function tasks of working memory, inhibitory control processes, and stimulus-response interference will exhibit greater signal intensity, a wider spatial extent, and more bilateral activation in chronic MTBI than chronic OI participants. Hypothesis 2: DTI changes, characterized by lower FA and higher MD at the gray-white junction, corpus callosum, central semiovale, and internal capsule, will be seen in MTBI but not in OI subjects. Hypothesis 3: Increased fMRI activation in chronic MTBI will be correlated with location and severity of disrupted fiber tracks that subserve neural networks associated with each fMRI activation task. Hypothesis 4: Performance on computerized neuropsychological testing (ANAM) and reaction time measures on fMRI tasks will better discriminate MTBI from OI than standard paper-and pencil tests. Hypothesis 5: The combination of fMRI, DTI, and ANAM will better discriminate MTBI from OI than each individual method. Hypothesis 6: More severe brain pathology in MTBI, as measured by neuroimaging (fMRI, DTI) and ANAM test scores, will be associated with less severe PTSD and symptoms.
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Brain activation on Stop Signal Reaction Time Task (SSRT)
Timeframe: 12-24 months post-injury
Brain activation on Sternberg Item Recognition Task (SIRT)
Timeframe: 12-24 months post-injury