A Study of PTSD and Trauma Control Subjects with PET/MR

Objectives The amygdala (AMY) and prefrontal cortex (PFC) are implicated in PTSD, but the underlying neural mechanisms are incompletely understood. Using Siemens PET/MR scanner we studied trauma-exposed subjects with (n=11) and without (n=15) PTSD using FDG PET and structural MR.

Methods Diagnosis of PTSD was confirmed using Structured Clinical Interview. Clinical ratings used Montgomery Asberg Depression Rating Scale (MADRS), Hamilton Anxiety Rating Scale (Ham-A) and the Clinician-Administered PTSD scale (CAPS) to measure PTSD symptoms. PET scans were acquired for 60 min after injection of [¹⁸F]FDG with simultaneous MR scans. A Dixon sequence was used for attenuation. The PET reconstructions were performed using the e7tools (Siemens). The structural images were processed using Freesurfer (FS)(http://surfer.nmr.mgh.harvard.edu/) providing segmentation of cortical and subcortical structures. The FS masks were applied to PET data after coregistration of MR to PET. Evaluation of FDG was based on an SUV ratio (SUVR) using the whole brain SUV to normalize each subject (SUVs were based on uptake from 45 to 60 min). Correlation coefficients of regional SUVR with PTSD symptoms were calculated using matlab.

Results Results. Among regions associated with PTSD negative correlations with symptom measures were found for PFC for all measures ( r=-.44 to -.53, p ranging from .005 to .025). AMY showed a positive correlation with depression (r=.406 p=.04).

Conclusions These data substantiate a role for PFC (and possibly AMY) in mediating the PTSD phenotype. These data extend the existing literature showing abnormal PFC (and AMY) glucose metabolism in trauma survivors with PTSD also in the absence of specific trauma reminders.

Research Support Steven and Alexandra Cohen Veterans Center