| Summary: | Rationale/statement of the problem: Because posttraumatic stress disorder (PTSD) and blast-mild traumatic brain injury (mTBI) commonly are comorbid in veterans of the wars in Iraq and Afghanistan, attributing persistent behavioral or other symptoms to one or the other entity remains controversial. Here, we asked if multimodal neuroimaging would reveal persistent functional or structural abnormalities in veterans who had experienced blast-mTBIs in Iraq and/or Afghanistan and, if so, could any such abnormalities be attributed to comorbid PTSD. Methods: Thirty-four blast-mTBI veterans (26 with PTSD and 8 without PTSD) and 16 Iraq and/or Afghanistan-deployed veterans without blast or blunt impact mTBI or PTSD were studied. Each veteran underwent magnetic resonance diffusion tensor (DTI) and magnetization transfer/cross-relaxation imaging (MT-CRI), as well as fluorodeoxyglucose positron emission tomography (FDG-PET); structured clinical assessments of blast and combat exposure, psychiatric diagnoses, and posttraumatic stress disorder symptoms; neurologic evaluations; and self-report scales of postconcussive symptoms (PCS), combat exposure, depression, sleep quality, and alcohol use. Results: Blast-mTBI veterans exhibited reduced fractional anisotropy in the genu and splenium of the corpus callosum on DTI; reduced macromolecular-bound proton fraction (a brain putative measure of myelin integrity) in white and gray matter and multiple regions of interest on MT-CRI; and parietal, somatosensory, and visual cortex hypometabolism on FDG-PET. The presence of PTSD in mTBI veterans had no effect on DTI or MT-CRI structural brain biomarkers. The only effect of PTSD on FDG-PET functional biomarkers was lower glucose metabolism in visual cortices bilaterally. Conclusions: Iraq and Afghanistan combat veterans with blast-mTBI exhibit abnormalities of brain white matter structural integrity and macromolecular organization and regional cortical glucose metabolism years after blast exposure. Although comorbid PTSD was associated with lower visual cortex metabolism, it had no effect on structural biomarkers. These findings are consistent with recent neuropathologic evidence of cortical tauopathy and neuronal degeneration in a small sample of Veterans with blast-mTBI.
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