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    • Diffusion tensor imaging DTI is particularly powerful for ev

    2018-11-05

    Diffusion tensor imaging (DTI) is particularly powerful for evaluating microstructural integrity of white matter by analyzing the restricted diffusion of water molecules (Catani, 2006). It can detect early neuropathological changes using quantitative indicators such as FA, which is thought to reflect fiber density, axonal diameter and myelination in white matter (Basser et al., 1994a; Basser et al., 1994b). Other DTI parameters that in combination determine FA, such as axial diffusivity (AD, along the axon) and radial diffusivity (RD, perpendicular to the main axonal axis) yield potentially more specific information. In animal studies, AD and RD have been identified as reflecting axonal and myelin integrity, respectively, that underlie changes in FA (Song et al., 2003; Song et al., 2002). Although methodological factors qualify their interpretation (Wheeler-Kingshott and Cercignani, 2009), these parameters provide potentially useful insight into the neurobiology of sirtuins disorders. Few previous DTI studies of PTSD exploited the specific directional diffusivities (AD and RD), or used deterministic tractography to delineate the origins of fibers passing through regions with altered white matter anisotropy. This study used DTI to investigate whole-brain microstructural alterations of white matter in a large sample of PTSD patients and controls, both of whom had survived a major 8.0-magnitude earthquake that occurred near a highly populated region of West China. Those diagnosed with PTSD were compared to those who did not develop the disorder (‘non-PTSD’) to control for general stress effects. The potential power of this study to illuminate the neuropathophysiology of PTSD is enhanced by several factors: 1) the unique characteristic of the trauma event involving a single, discrete period of acute emotional distress, 2) the relatively homogeneous demographic characteristics of the trauma survivors, 3) the use of non-PTSD controls exposed to similar trauma to control for general stress effects, 4) a relatively large study population free from psychotropic medication, and 5) the use of advanced techniques for analyzing the DTI data including the separation of radial and axial diffusivity and deterministic DTI tractography. Our previous functional magnetic resonance imaging (fMRI) studies using some of the present study participants found altered function in prefrontal-limbic system (Jin et al., 2014; Lei et al., 2015a; Yin et al., 2012; Yin et al., 2011a; Yin et al., 2011b). However, anatomic alterations underlying the functional abnormalities were not examined. Based on prior findings from our sample and other laboratories, we hypothesized that there are white matter abnormalities in prefrontal cortex in PTSD patients, and that they are related to PTSD severity.
    Materials and Methods
    Results
    Discussion This FA increase in left superior frontal gyrus is consistent with a previous study that reported increased FA in drug-free PTSD patients who survived a severe coal mine accident at 2 months post-trauma, generally similar to the sample in the present study (Zhang et al., 2011). In contrast, most studies of PTSD patients with multiple, diverse traumatic events and longer symptom duration of several years have reported decreased FA (Daniels et al., 2013; Schuff et al., 2011). For example, Schuff et al. reported decreased FA in the prefrontal cortex in male military veterans with PTSD (mean illness duration: 14 years) (Schuff et al., 2011). This difference in findings between studies of first-episode medication-free patients after specific acute trauma and patients ill with PTSD for several years may be related to a distinct pathophysiology of relatively early illness manifestations, and perhaps also to PTSD that results from a specific single-incident stressor. They also might reflect adaptations and compensations for chronic PTSD, or effects of chronic drug treatment. Another possible explanation for differences in our findings relative to some prior studies of more chronically ill patients may be that we included stressed non-PTSD samples as controls instead of non-exposed community controls. The non-PTSD subjects who were resilient to the same traumatic event may have prior brain characteristics that contributed to the resilience, such as a well-organized DLPFC inhibition system manifest in a FA decrease (Chen et al., 2013). While our findings help understand the brain differences in those who do and do not develop PTSD after major stress, future comparative studies of non-exposed controls within the first year after stress may also be informative for understanding illness consequences and perhaps for identifying general stress effects that do not lead to PTSD. In particular, the observation of FA abnormalities in the present study suggests a critical role of alterations in prefrontal cortex in first-episode medication-free PTSD. However, whether and how white matter alterations in this region may change over the longer term course of illness remains to be determined by longitudinal studies.