Altered Metabolic Interrelationships in the Cortico-Limbic Circuitry in Military Service Members with Persistent Post-Traumatic Stress Disorder Symptoms Following Mild Traumatic Brain Injury (original) (raw)

Brain Connectivity

Abstract

INTRODUCTION Comorbid mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) are common in military service members. The aim of this study is to investigate brain metabolic inter-relationships in service members with and without persistent PTSD symptoms following mTBI using 18F-fluorodeoxyglucose positron emission tomography. METHODS Service members (n=408) diagnosed with mTBI were studied retrospectively. Principal component analysis was applied to identify latent metabolic systems, and the associations between metabolic latent systems and self-report measures of post-concussive and PTSD symptoms were evaluated. Participants were divided into two groups based on DSM-IV-TR criteria for PTSD, and structural equation modeling was performed to test a priori hypotheses on metabolic inter-relationships among the brain regions in the cortico-limbic circuitry responsible for top-down control and bottom-up emotional processing. The differences in metabolic inter-relationships between age-matched PTSD-absent (n=204) and PTSD-present (n=204) groups were evaluated. RESULTS FDG uptake in the temporo-limbic system was positively correlated with post-concussive and hyperarousal symptoms. For the bottom-up emotional processing, the insula and amygdala-hippocampal complex in PTSD-present group had stronger metabolic inter-relationships with the bilateral rostral anterior cingulate, left lingual, right lateral occipital, and left superior temporal cortices, but a weaker relationship with the right precuneus cortex, compared to PTSD-absent group. For the top-down control, PTSD-present group had decreased metabolic engagements of the dorsolateral prefrontal cortex on the amygdala. DISCUSSION Our results suggest altered metabolic inter-relationships in the cortico-limbic circuitry in mTBI subjects with persistent PTSD symptoms, which may underlie the pathophysiological mechanisms of comorbid mTBI and PTSD.

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