**4.1 The frontal cortex**

The structural abnormalities in the medial and middle frontal cortex found in VoR with PTSD are supported by previous studies (Shin et al., 2006; Fennema-Notestine et al., 2002; Richert et al., 2006; Hakamata et al., 2007). In addition to such structural findings, functional neuroimaging studies have also shown dysfunction in these cortical areas (Bremner et al., 1999a, 2003; Lanius et al., 2004, 2006; Lindauer et al., 2004b, 2008; Morey et al., 2008). It is therefore possible that altered GMD in the medial and middle frontal cortex may contribute to their hypofunction. However, in the current study, VoR with PTSD had GMD reductions in the left middle frontal cortex and the bilateral medial frontal cortex relative to the HC, but no significant differences relative to VoR without PTSD. This result suggests that severe psychological trauma may change brain gray matter of the medial and middle frontal cortex, but that such plastic changes to these cortical brain structures may not underlie the pathophysiology of PTSD.

Compared to VoR without PTSD and HC, VoR with PTSD had significant bilateral increases in GMD of the pre-central gyrus, which mainly consists of the premotor cortex and the supplementary motor area. Studies indicate the importance of the supplementary motor area in motor tasks that demand retrieval of motor memory (Tanji, 1994). The premotor cortex, located in the pre-central cortex (BA6), seems to play a major role in language (Duffau et al., 2003). Functional neuroimaging studies on PTSD suggest abnormal functional activities in this cortical area. Empirical studies have shown that PTSD groups are characterized by relatively more activation in the pre-central cortex than non-PTSD and healthy comparisons (Bonne et al., 2003; Bremner et al., 1999a; Lanius et al., 2006; Shaw et al., 2002; Jatzko et al., 2006b). These findings suggest that increases in GMD of the precentral cortex may be involved in the neural basis of motor and linguistic PTSD symptomatology.

#### **4.2 The parietal lobule**

The parietal lobule, including the superior and inferior parietal lobule (BA7, BA40) is implicated in memory, recognition, and deductive reasoning (Xie et al., 2004; Knauff et al., 2002). In this study, compared to VoR without PTSD and HC, VoR with PTSD had significant increases in GMD of the inferior parietal lobule. This indicates that the inferior parietal lobule might play an important role in the pathophysiology of PTSD. Additionally, one PET study showed that chronic PTSD patients presented relatively diminished activity in the post-central regions (Molina et al., 2010), which mainly consist of the primary somatic sensory cortex and secondary somatic sensory cortex (Geng et al., 2006). Increases in GMD in the post-central cortex may be associated with the dysfunction related with PTSD.

#### **4.3 The temporal gyrus**

384 Neuroimaging for Clinicians – Combining Research and Practice

Figure 2, and include the left pre-central cortex (E-1), the left inferior parietal lobule (E-2), and the right post-central cortex (E-3). The MNI coordinates, voxel t values, k values (cluster size > 50), and corresponding BA are detailed in Table 3. Regions displayed are for p < .005.

This cross-sectional study employed VBM to examine brain density abnormalities among VoR with PTSD compared to VoR without PTSD and HC in mainland China. The findings of this study support the hypothesis that changes in brain density are associated with the

The structural abnormalities in the medial and middle frontal cortex found in VoR with PTSD are supported by previous studies (Shin et al., 2006; Fennema-Notestine et al., 2002; Richert et al., 2006; Hakamata et al., 2007). In addition to such structural findings, functional neuroimaging studies have also shown dysfunction in these cortical areas (Bremner et al., 1999a, 2003; Lanius et al., 2004, 2006; Lindauer et al., 2004b, 2008; Morey et al., 2008). It is therefore possible that altered GMD in the medial and middle frontal cortex may contribute to their hypofunction. However, in the current study, VoR with PTSD had GMD reductions in the left middle frontal cortex and the bilateral medial frontal cortex relative to the HC, but no significant differences relative to VoR without PTSD. This result suggests that severe psychological trauma may change brain gray matter of the medial and middle frontal cortex, but that such plastic changes to these cortical brain structures may not underlie the

Compared to VoR without PTSD and HC, VoR with PTSD had significant bilateral increases in GMD of the pre-central gyrus, which mainly consists of the premotor cortex and the supplementary motor area. Studies indicate the importance of the supplementary motor area in motor tasks that demand retrieval of motor memory (Tanji, 1994). The premotor cortex, located in the pre-central cortex (BA6), seems to play a major role in language (Duffau et al., 2003). Functional neuroimaging studies on PTSD suggest abnormal functional activities in this cortical area. Empirical studies have shown that PTSD groups are characterized by relatively more activation in the pre-central cortex than non-PTSD and healthy comparisons (Bonne et al., 2003; Bremner et al., 1999a; Lanius et al., 2006; Shaw et al., 2002; Jatzko et al., 2006b). These findings suggest that increases in GMD of the precentral cortex may be involved in the neural basis of motor and linguistic PTSD

The parietal lobule, including the superior and inferior parietal lobule (BA7, BA40) is implicated in memory, recognition, and deductive reasoning (Xie et al., 2004; Knauff et al., 2002). In this study, compared to VoR without PTSD and HC, VoR with PTSD had significant increases in GMD of the inferior parietal lobule. This indicates that the inferior parietal lobule might play an important role in the pathophysiology of PTSD. Additionally, one PET study showed that chronic PTSD patients presented relatively diminished activity in the post-central regions (Molina et al., 2010), which mainly consist of the primary somatic sensory cortex and secondary somatic sensory cortex (Geng et al., 2006). Increases in GMD

in the post-central cortex may be associated with the dysfunction related with PTSD.

**4. Discussion** 

**4.1 The frontal cortex** 

pathophysiology of PTSD.

symptomatology.

**4.2 The parietal lobule** 

pathophysiology of rape-induced PTSD.

Our study showed significant GMD decreases in the left middle temporal gyrus in VoR with PTSD compared to HC. Studies comparing veterans with and without PTSD reveals that those with PTSD had overactivation of the temporal gyrus during the resting state (Molina et al., 2010) and the encoding phase (Geuze et al., 2008b), and underactivation of the bilateral middle temporal gyrus in the retrieval phase (Geuze et al., 2008b). Functional neuroimaging studies reveals significant activation in left middle temporal gyrus in response to empathy judgments in post-therapy PTSD (Farrow et al., 2005) and higher levels of activation in the middle temporal gyrus in dissociative PTSD (Lanius et al., 2006). Empirical evidence suggests that the fusiform cortex is specialized for face processing (Rossion et al., 2000; Rhodes et al., 2004). Research also indicates relatively augmented activity in the fusiform cortex in patients with PTSD (Bonne et al., 2003; Molina et al., 2010). The reduced GMD of the middle temporal gyrus and fusiform cortex found in this study implicates these regions in the dysfunction of memory and dissociative symptoms in PTSD.
