| Summary: | 碩士 === 國立陽明大學 === 腦科學研究所 === 99 === Background: The neurobiological basis of severe acute respiratory syndrome (SARS)-related post-traumatic stress disorder (PTSD) has never been studied. This study aimed at investigation of brain structure changes that caused by SARS-related hypoxia and PTSD.
Methods: Gray matter volume (GMV) changes were detected using voxel-based morphometry analysis (VBM) for each pair of groups, including SARS-related PTSD (s-PTSD), non-SARS-related PTSD (ns-PTSD), healthy control (HC), severe hypoxia patients (sHyp) and slight hypoxia patients (slHyp) (s-PTSD, n=15; ns-PTSD, n=14; HC, n=15; sHyp, n= 7; slHyp, n= 8). The sHyp and slHyp were separated by a pressure of oxygen in artery and fraction of inspired oxygen ratio. Each participant underwent the MR scanning to acquire the brain T1-weighted images from a 1.5-Tesla MRI unit.
Results: The atrophied right hippocampus was found in contrast between s-PTSD and ns-PTSD. GMV losses were found in the right thalamus and right precuneus in contrast between Hyp and nHyp. In contrast with HC, s-PTSD had a GMV loss in the left superior orbital frontal cortex (OFC), and several decreased volumes were found in ns-PTSD, including the left superior OFC, right middle OFC, bilateral precentral and left anterior insula. The significant negative correlation was observed between Pittsburgh sleep quality index (PSQI) and right thalamus.
Conclusions: Based on the findings of cellular damage in the hippocampus caused by hypoxia in the previous study and no reduced GMV of ns-PTSD in our study, we inferred the atrophied right hippocampus in s-PTSD might be caused by SARS-related hypoxemia. The negative correlation between PSQI and the right thalamus implicated that the GMV loss of the right thalamus may be related to poor sleep quality. The OFC was reported to be related to affective response of the integration, regulation, extinction memory and a top-down control of amygdala. The atrophied OFC in both PTSD patients might be lead to the above functions into dysfunction.
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