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may be involved in the functional compensation for the pathological changes in the neuro-

Earlier studies in the cerebellum of PTSD patients found correlations with abnormal blood flow and glucose absorption (Bonne et al., 2003; Molina et al., 2010) and abnormal volume (Bellis & Kuchibhatla, 2006) in the cerebellum also. This study extends the literature on cerebellum structure involvement in PTSD. This finding, if replicated in larger patient samples, may serve as a marker of brain dysfunction in PTSD, and thus allows for the study of cerebellum pathophysiology before and throughout the course and treatment of PTSD. It should be noted that whilst the sample size (11 VoR with PTSD) of this study meets the threshold of research reported in the literature (Jatzko et al., 2006a; Hou et al., 2007), it was nevertheless limited in terms of its statistical power. A further limitation is the potential for selection bias in both the VoR Group and HC. Given the social stigma attached to VoR in the Chinese cultural context that often results in sexual shame, fear and anxiety over disclosure of the rape, guilt over derogating family honor, self-scrutiny and self-blame after the fact, and even blame of the victim, contribute to the potential selection bias in the VoR Group. Regarding the selection bias in HC, it was not our intention for this group (12 HC) to be representative of the general population, nor were the 65-pooled controls. This group was particularly designed to match the VoR with PTSD regarding the major demographic characteristics. However, given the fact that HC were recruited from healthy workers,

The use of a cross-sectional design is another significant limitation of this study. The shared variance estimated between variables in a cross-sectional design does not allow for a critical examination of causal relationships among them. Consequently, we cannot state categorically whether changes in brain density were the cause or the effect of trauma

The abnormal density of cerebral regions in VoR with PTSD supports the hypothesis that PTSD is associated with structural plastic changes to brain. The results suggest that the medial frontal cortex, pre-central cortex, posterior cingulate cortex, post-central cortex, inferior parietal lobule, and cerebellum are likely to contribute to the neural mechanisms underlying PTSD. These findings suggest that the pre-central cortex of PTSD may be involved in the neural basis of motor and linguistic PTSD symptomatology; the middle temporal gyrus and fusiform cortex may be implicated in the dysfunction of memory and dissociative symptoms in PTSD; the posterior cingulate cortex may underlie pathological symptoms provoked by traumatic reminders of PTSD; the inferior parietal lobule of PTSD might play an important role in the dysfunction of memory, recognition, and deductive reasoning; and the cerebellum may contribute to the functional compensation for the pathological changes in the neuro-circuitry of PTSD. These findings may lead to a better understanding of the basis of brain structure for clinical symptoms with VoR of PTSD. Also,

Future studies call for exploring experiences of rape and associated PTSD symptomatology by using case-control or longitudinal designs, investigating the effect of the specific social and cultural meanings of rape, examining the impact on individuals' posttraumatic response and coping ability, and looking into the relation between brain GMD and PTSD

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**19** 

*Brazil* 

**A Fruitful Encounter** 

*Radiology Clinic – Universidade Federal de São Paulo, SP, Psychotraumatology Clinic - Hospital Perola Byington, SP,* 

Julio F.P. Peres, PsyD, PhD.

**PTSD, Neuroimaging and Psychotherapy:** 

Most of us have dealt with a traumatic event of some kind such as loss, accident, or illness, or will be dealing with one at some point in our lives. Psychological trauma is closely related to the development of posttraumatic stress disorder (PTSD), involving three sets of symptoms: (i) reliving trauma (traumatic memories, nightmares, intrusive thoughts); (ii) emotional avoidance/numbness (affective distance, emotional anaesthesia); and (iii) increased arousal (irritability, insomnia and hypervigilance) (American Psychiatric Association, 1994). Lifetime prevalence of PTSD-triggering traumatic events may be as much as 50–90%, and actual prevalence in the general population is about 8% (Kessler et al., 1995; Vieweg et al., 2006), while partial PTSD (pPTSD) in an at-risk groups have been estimated at approximately 30% (Weiss et al., 1992). After noting that individuals who do not meet the full set of diagnostic criteria for PTSD may suffer from clinically significant symptoms of PTSD (Weiss et al., 1992), the concept of pPTSD or subthreshold PTSD was introduced to describe subsyndromal forms of PTSD (Blanchard et al., 1995; Stein et al. 1997). Thus, exposure to traumatic stressors and psychological trauma is widespread, with a wide range of cognitive and behavioral

One of the main psychological sequelae of traumatic experiences is conditioning of specific fears. In addition to PTSD, traumatic events can significantly influence major depression, somatoform disorders, panic and anxiety disorders, obsessive-compulsive disorders, phobic disorders, and substance abuse (Peres et al., 2009). Although traumatic events are associated with PTSD in the literature, traumatized people do not meet DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) criteria for PTSD in many cases and often present a range of psychoform or somatoform symptoms. Considerable overlap in symptoms and disease comorbidity has been noted for medically unexplained symptoms in the primary care setting, such as chronic fatigue syndrome, low back pain, irritable bowel syndrome, primary headaches, fibromyalgia, temporomandibular joint disorder, major depression, panic attacks, and PTSD (Peres et al., 2009). Epidemiologic surveys increasingly point to a relation between exposure to traumatic events and more health care utilization, adverse health outcomes, onset of specific diseases, and premature death (Corrigan et al., 2005; Keane et al., 2006). Certain characteristics of traumas, particularly peritraumatic cognitive response and related cognitions, appear to heighten the risk for PTSD (Peres et al.,

responses/outcomes among trauma survivors (Peres et al., 2009; 2011).

**1. Introduction** 

