Posttraumatic Stress Disorder Subjects Research Articles

Post-Traumatic Stress Disorder Is Associated with Elevated Plasma Cholesterol in Female TT Homozygotes of LDLR rs5925.

To explore the mechanism of inconsistent relationships between plasma lipid profiles and post-traumatic stress disorder (PTSD) reported before, we hypothesized that interplays might exist between PTSD and a variation of rs5925 at low-density lipoprotein receptor (LDLR) gene on plasma lipid profiles. To test our hypothesis, we analyzed the plasma lipid profiles of 709 high school pupils with various genotypes of LDLR rs5925 and with or without PTSD. The results demonstrated that PTSD prevalence in the C allele carriers was higher than that in the TT homozygotes regardless of gender. The C allele carriers had higher levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), ratios of TC to high-density lipoprotein cholesterol (TC/HDL-C) and LDL-C/HDL-C than the TT homozygotes in the male controls, and only higher TC in the female controls, but no differences in the male or female PTSD subjects. PTSD increased TC in the female TT homozygotes but not in the female C allele carriers. PTSD increased TC/HDL-C in the male TT homozygotes but not in the C allele carriers. These results suggest interactions between PTSD and LDLR rs5925 on plasma lipid profiles, which may be among the explanations for previously reported inconsistent relationships between LDLR rs5925 or PTSD and plasma lipid profiles, and facilitate the development of precision medicine interferences in hypercholesterolemia in individuals with different genetic backgrounds and psychiatric status. Psychiatric care or drug supplement may particularly be needed by female hypercholesterolemic subjects with the TT genotype of LDLR rs5925 in Chinese adolescents.

Network Centrality and Modularity of Structural Covariance Networks in Posttraumatic Stress Disorder: A Multisite ENIGMA-PGC Study.

Introduction: Cortical thickness (CT) and surface area (SA) are established biomarkers of brain pathology in posttraumatic stress disorder (PTSD). Structural covariance networks (SCNs) are represented as graphs with brain regions as nodes and correlations between nodes as edges. Methods: We built SCNs for PTSD and control groups using 148 CT and SA measures that were harmonized for site in n = 3439 subjects from Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA)-Psychiatric Genomics Consortium (PGC) PTSD. We compared centrality between PTSD and controls as well as interactions of diagnostic group with age, sex, and comorbid major depressive disorder (MDD) status. We investigated associations between network modularity and diagnostic grouping. Results: Nodes with higher CT-based centrality in PTSD compared with controls included the left inferior frontal sulcus, left fusiform gyrus, left superior temporal gyrus, and right inferior temporal gyrus. Children (<10 years) and adolescents (10-21) with PTSD showed greater centrality in frontotemporal areas compared with young (22-39) and middle-aged adults (40-59) with PTSD, who showed higher centrality in occipital areas. The PTSD diagnostic group interactions with sex and comorbid MDD showed altered centrality in occipital regions, along with greater visual network (VN) modularity in PTSD subjects compared with controls. Conclusion: Structural covariance in PTSD is associated with centrality differences in occipital areas and VN modularity differences in a large well-powered sample. In the context of extensive structural covariance remodeling taking place before and during adolescence, the present findings suggest a process of cortical remodeling that commences with trauma and/or the onset of PTSD but may also predate these events. Impact statement Centrality is a graph theory measure that offers insights into a node's relationship with all other nodes in the brain. Centrality pinpoints the drivers of brain communication within networks and nodes and may be a promising target for treatments such as neuromodulation. Modularity can pinpoint modules that exist within larger networks and quantify the connections between these modules. Centrality and modularity complement functional and structural connectivity measurements within specific brain networks.

Analysis of the Relationship of Attention-Deficit/Hyperactivity Disorder With Posttraumatic Stress Disorder Clarifies Relationship Directionality

In the current issue of Biological Psychiatry, Wendt et al. (1) describe several robust analyses that collectively fill in important knowledge gaps toward understanding the association between attention-deficit/hyperactivity disorder (ADHD) and posttraumatic stress disorder (PTSD). That association is well documented, with a prior meta-analysis of 22 studies reporting increased rates of PTSD in subjects with ADHD and vice versa (2). Studies using control subjects who had experienced trauma found an increased risk of PTSD in individuals with ADHD, suggesting that the association is not entirely due to increased trauma rates in individuals with ADHD (2).

Efficacy of traumatic memory reactivation with or without propranolol in PTSD with high dissociative experiences

ABSTRACT Background: Post-traumatic stress disorder (PTSD) with dissociative symptoms is now a full-fledged subtype of this disorder. The dissociative subtype is associated with a greater number of psychiatric comorbidities. To date, the impact of dissociation on the efficacy of PTSD treatment remains unclear. Objective: The aim of this study was to compare the efficacy of a traumatic memory reactivation procedure with the administration of propranolol or a placebo once a week for six consecutive weeks in reducing PTSD and MDE symptoms between PTSD subjects with or without high dissociative symptoms. Method: For that, we conducted a randomized clinical trial in 66 adults diagnosed with longstanding PTSD and measured the SCID PTSD module, the PTSD Checklist (PCL-S), Beck’s Depression Inventory-II (BDI-II), and the Dissociative Experiences Scale (DES). Results: Patients with and without high dissociative experience had significant improvement in their PCL-S scores over the 6 treatment sessions, and PCL-S scores continued to decline in all patients during the post-treatment period. However, there was no correlation between the presence/absence of high dissociative experiences and no specific effect of propranolol treatment. We found exactly the same results for MDE symptoms. Interestingly, patients with high dissociative experiences before treatment exhibited very significant improvement in their DES scores after the 6 treatment sessions, and patients maintained this improvement 3 months post-treatment. Conclusions: The traumatic memory reactivation procedure is an effective way to treat dissociative symptoms in patients with PTSD, and improvement of these dissociative symptoms was associated with a decrease in both PTSD and depression severity.

Plasma lipidomics in subjects with combat posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) is complex neuropsychiatric disorder triggered by a traumatic event and characterized by the symptoms that represent large burden to patients, as well as to society. Lipidomic approach can be applied as a useful tool for discovery of novel diagnostic, prognostic and therapeutic lipid biomarkers of various disorders, whose etiology is complex and still unknown, including PTSD. Since changes in the levels of lipid metabolites might indicate impairments in various metabolic pathways and cellular processes, the aim of this lipidomic study was to determine altered levels of lipid compounds in PTSD. The study enrolled 235 male patients with combat PTSD and 241 healthy male control subjects. Targeted lipidomic analysis of plasma samples was conducted using reverse-phase liquid chromatography coupled with mass spectrometry. Lipids that have been analyzed belong to the group of ceramides, cholesterol esters, diacylglycerols, lysophosphatidylcholines, lysophosphatidylethanolamines, phosphatidylcholines, phosphatidylethanolamines, sphingomyelins and triglycerides. The levels of fifteen lipid compounds were found to be significantly different between PTSD patients and healthy control subjects, including four phosphatidylcholines, two phosphatidylethanolamines, five sphingomyelins, two cholesterol esters and two ceramides. The lipid metabolites whose levels significantly differed between patients with PTSD and control subjects are associated with various biological processes, including impairments of membrane integrity and function, mitochondrial dysfunction, inflammation and oxidative stress. As these processes might be associated with development and progression of PTSD, altered lipid compounds represent potential biomarkers that could facilitate the diagnosis of PTSD, prediction of the disease, as well as identification of novel treatment approaches in PTSD.

Study on the changes of Structural Covariance Network in post-traumatic stress disorder.

The topological properties of functional brain networks in post-traumatic stress disorder (PTSD) have been thoroughly examined, whereas the topology of structural covariance networks has been researched much less. Based on graph theoretical approaches, we investigated the topological architecture of structural covariance networks among PTSD, trauma-exposed controls (TEC), and healthy controls (HC) by constructing covariance networks driven by inter-regional correlations of cortical thickness. Structural magnetic resonance imaging (sMRI) scans and clinical scales were performed on 27 PTSD, 33 TEC, and 29 HC subjects. Group-level structural covariance networks were established using pearson correlations of cortical thickness between 68 brain areas, and the graph theory method was utilized to study the global and nodal properties. PTSD and HC subjects did not differ at the global level. When PTSD subjects were compared to TEC subjects, they had significantly higher clustering coefficient (p = .014) and local efficiency (p = .031). Nodes having different nodal centralities between groups did not pass the false-discovery rate correction at the node level. According to the structural brain network topological characteristics discovered in this study, PTSD manifests differently compared to the TEC group. In the PTSD group, the SCN keeps the small-world characteristics, but the degree of functional separation is enhanced. The TEC group's reduced small worldness and the tendency for brain network randomization could be signs of trauma recovery.

Genetic and Epigenetic Association of Hepatocyte Nuclear Factor-1α with Glycosylation in Post-Traumatic Stress Disorder.

Post-traumatic stress disorder (PTSD) is a complex trauma-related disorder, the etiology and underlying molecular mechanisms of which are still unclear and probably involve different (epi)genetic and environmental factors. Protein N-glycosylation is a common post-translational modification that has been associated with several pathophysiological states, including inflammation and PTSD. Hepatocyte nuclear factor-1α (HNF1A) is a transcriptional regulator of many genes involved in the inflammatory processes, and it has been identified as master regulator of plasma protein glycosylation. The aim of this study was to determine the association between N-glycan levels in plasma and immunoglobulin G, methylation at four CpG positions in the HNF1A gene, HNF1A antisense RNA 1 (HNF1A-AS1), rs7953249 and HNF1A rs735396 polymorphisms in a total of 555 PTSD and control subjects. We found significant association of rs7953249 and rs735396 polymorphisms, as well as HNF1A gene methylation at the CpG3 site, with highly branched, galactosylated and sialyated plasma N-glycans, mostly in patients with PTSD. HNF1A-AS1 rs7953249 polymorphism was also associated with PTSD; however, none of the polymorphisms were associated with HNF1A gene methylation. These results indicate a possible regulatory role of the investigated HNF1A polymorphisms with respect to the abundance of complex plasma N-glycans previously associated with proinflammatory response, which could contribute to the clinical manifestation of PTSD and its comorbidities.

Reduced Platelet MAO-B Activity Is Associated with Psychotic, Positive, and Depressive Symptoms in PTSD.

Post-traumatic stress disorder (PTSD) is a trauma-related disorder. Platelet monoamine oxidase (MAO-B) is a peripheral biomarker associated with various symptoms in different psychopathologies, but its role in PTSD or different symptoms in PTSD is not clear. This study elucidated the association between platelet MAO-B activity and clinical symptoms occurring in PTSD. Platelet MAO-B activity was determined in 1053 male Caucasian subjects: 559 war veterans with PTSD (DSM-5 criteria), 62 combat exposed veterans who did not develop PTSD, and 432 non-combat exposed healthy controls. Clinical symptoms in PTSD were determined using CAPS and PANSS. Platelet MAO-B activity, controlled for the effect of smoking, was significantly increased in PTSD with severe versus mild and moderate traumatic symptoms, and was significantly decreased in PTSD subjects with severe versus mild positive, psychotic, and depressive symptoms. This finding was further confirmed with reduced platelet MAO-B activity in PTSD veterans with severe versus mild individual items of the PANSS-depressed, PANSS-psychotic, and PANSS-positive subscales. Altered platelet MAO-B activity, controlled for the possible confounders, was associated with the development and severity of different symptoms occurring in PTSD. These findings confirmed the role of platelet MAO-B activity as a peripheral marker of various psychopathological symptoms.

Machine learning for post-traumatic stress disorder identification utilizing resting-state functional magnetic resonance imaging.

Early detection of post-traumatic stress disorder (PTSD) is essential for proper treatment of the patients to recover from this disorder. The aligned purpose of this study was to investigate the performance deviations in regions of interest (ROI) of PTSD than the healthy brain regions, to assess interregional functional connectivity and applications of machine learning techniques to identify PTSD and healthy control using resting-state functional magnetic resonance imaging (rs-fMRI). The rs-fMRI data of 10 ROI was extracted from 14 approved PTSD subjects and 14 healthy controls. The rs-fMRI data of the selected ROI were used in ANOVA to measure performance level and Pearson's correlation to investigate the interregional functional connectivity in PTSD brains. In machine learning approaches, the logistic regression, K-nearest neighbor (KNN), support vector machine (SVM) with linear, radial basis function, and polynomial kernels were used to classify the PTSD and control subjects. The performance level in brain regions of PTSD deviated as compared to the regions in the healthy brain. In addition, significant positive or negative functional connectivity was observed among ROI in PTSD brains. The rs-fMRI data have been distributed in training, validation, and testing group for maturity, implementation of machine learning techniques. The KNN and SVM with radial basis function kernel were outperformed for classification among other methods with high accuracies (96.6%, 94.8%, 98.5%) and (93.7%, 95.2%, 99.2%) to train, validate, and test datasets, respectively. The study's findings may provide a guideline to observe performance and functional connectivity of the brain regions in PTSD and to discriminate PTSD subject using only the suggested algorithms.

Post-traumatic stress disorder and childhood emotional abuse are markers of subthreshold bipolarity and worse treatment outcome in major depressive disorder.

Post-traumatic stress disorder (PTSD) and childhood maltreatment (CMT: parental neglect; emotional, physical and sexual abuse) have been linked to bipolar disorder but they are also common in major depressive disorder (MDD). Our objective was to investigate their association with the bipolar spectrum and antidepressant treatment outcome in 482 outpatients with DSM-IV MDD treated in the Combining Medications to Enhance Depression Outcomes trial for 28 weeks Bipolar spectrum score included age of onset <21 years, subthreshold hypomania (a period of elated or irritable mood with at least two concurrent hypomanic symptoms, which did not fulfill DSM criteria for hypomanic/manic episode) and depressive mixed state (DMX). PTSD subjects (n = 107; 22%) had more severe depression (P < 0.0001), work and social impairment (P = 0.0031), comorbid anxiety disorders (P < 0.0001) and increased suicidality (P = 0.0003). Bipolar spectrum score was higher with PTSD comorbidity (P = 0.0063) and childhood emotional abuse (P = 0.0001). PTSD comorbidity was associated with residual suicidality (P = 0.0218) after 6 weeks of antidepressant use whereas childhood emotional abuse [odds ratio (OR), 1.01-2.22], subthreshold hypomania (OR, 1.04-4.09) and DMX (OR, 1.00-4.19) were predictors of mood switch. These results corroborate the role of PTSD and childhood emotional abuse as markers of bipolar spectrum and prognostic factors during antidepressant treatment.

Working memory, cortical dopamine tone, and frontoparietal brain recruitment in post-traumatic stress disorder: a randomized controlled trial

Post-traumatic stress disorder (PTSD) leads to impairments in both cognitive and affective functioning. Animal work suggests that chronic stress reduces dopamine tone, and both animal and human studies argue that changes in dopamine tone influence working memory, a core executive function. These findings give rise to the hypothesis that increasing cortical dopamine tone in individuals with greater PTSD symptomatology should improve working memory performance. In this pharmacological functional magnetic resonance imaging (fMRI) study, 30 US military veterans exhibiting a range of PTSD severity completed an emotional working memory task. Each subject received both placebo and the catechol-O-methyl transferase inhibitor tolcapone, which increases cortical dopamine tone, in randomized, double-blind, counterbalanced fashion. Mnemonic discriminability (calculated with d′, an index of the detectability of working memory signals) and response bias were evaluated in the context of task-related brain activations. Subjects with more severe PTSD showed both greater tolcapone-mediated improvements in d′ and larger tolcapone-mediated reductions in liberally-biased responding for fearful stimuli. FMRI revealed that tolcapone augmented activity within bilateral frontoparietal control regions during the decision phase of the task. Specifically, tolcapone increased cortical responses to fearful relative to neutral stimuli in higher severity PTSD subjects, and reduced cortical responses to fearful stimuli for lower severity PTSD subjects. Moreover, tolcapone modulated prefrontal connectivity with areas overlapping the default mode network. These findings suggest that enhancing cortical dopamine tone may represent an approach to remediating cognitive and affective dysfunction in individuals with more severe PTSD symptoms.

Platelet serotonin concentration and trait aggression in veterans with post-traumatic stress disorder: a preliminary study

Animal and human studies suggest that aggressive behavior may be modulated by brain serotonergic system. Serotonergic (5-HT) dysfunction is associated with post-traumatic stress disorder (PTSD), but also with increased aggression and impulsivity, hallmarks of PTSD. The aim of the study was to investigate the association of platelet 5-HT concentration and various types of aggression and impulsivity in veterans with PTSD. A group of 42 male combat-related PTSD subjects entered the study. Four different aggression facets were measured by the Buss and Perry's Aggression Questionnaire (BPAQ). Verbal and physical types of impulsive aggressive behavior were measured by the subscales of the Žužul's Aggressiveness Inventory A-87. Impulsivity was determined using Eysenck's IVE questionnaire. PTSD severity was evaluated by Watson’s PTSD questionnaire. Platelet serotonin concentration was determined spectrofluorimetrically. Confounding variables were: age, body mass, alcohol use, comorbid depression, and tobacco use. Platelet 5-HT concentration and PTSD severity were independently associated only with impulsive types of aggression, as higher platelet 5-HT concentration and more severe PTSD were related to more impulsive aggression. These results strongly recommend distinguishing between specific types of aggression facets, and advise the importance of theory-based concepts of aggression facets when evaluating the biological correlates of aggression.

Moderating Effects of BDNF Genetic Variants and Smoking on Cognition in PTSD Veterans.

Posttraumatic stress disorder (PTSD) is frequently associated with cognitive disturbances and high prevalence of smoking. This study evaluated cognition in war veterans with PTSD and control subjects, controlled for the effect of smoking and brain derived neurotrophic factor (BDNF) rs6265 and rs56164415 genotypes/alleles. Study included 643 male war veterans with combat related PTSD and 120 healthy controls. Genotyping was done by real time PCR. Cognitive disturbances were evaluated using the Positive and Negative Syndrome Scale (PANSS) cognition subscale and the Rey-Osterrieth Complex Figure (ROCF) test scores. Diagnosis (p < 0.001), BDNF rs56164415 (p = 0.011) and smoking (p = 0.028) were significant predictors of the cognitive decline in subjects with PTSD. BDNF rs56164415 T alleles were more frequently found in subjects with PTSD, smokers and non-smokers, with impaired cognition, i.e., with the higher PANSS cognition subscale scores and with the lower ROCF immediate recall test scores. Presence of one or two BDNF rs56164415 T alleles was related to cognitive decline in PTSD. The T allele carriers with PTSD had advanced cognitive deterioration in smokers and nonsmokers with PTSD, and worse short-term visual memory function. Our findings emphasize the role of the BDNF rs56164415 T allele and smoking in cognitive dysfunction in war veterans with PTSD.

Efficacy and Underlying Mechanism of Acupuncture in the Treatment of Posttraumatic Stress Disorder: A Systematic Review of Animal Studies.

Acupuncture is a nonpharmacological intervention that can be useful in the clinical management of posttraumatic stress disorder (PTSD), especially in situations with a lack of medical resources, including large-scale PTSD events such as disasters. Some clinical studies have reported the clinical effect of acupuncture in improving PTSD symptoms, but the underlying therapeutic mechanism has yet to be explored. Therefore, this review summarized the underlying therapeutic mechanisms of acupuncture in animal PTSD models. A comprehensive search was conducted in 14 electronic databases, and two independent researchers performed study selection, data extraction, and the methodological quality assessment. Twenty-four relevant studies were included in this review and summarized according to the proposed main mechanisms. In behavioral evaluation, acupuncture, including manual acupuncture and electro-acupuncture, reduced anxiety and fear responses and weakened fear conditioning, improved sleep architecture, reduced depressive symptoms, and alleviated disturbance of spatial learning and memory of PTSD animal models. The therapeutic mechanisms of acupuncture proposed in the included studies could be classified into two categories: (1) regulation of stress responses in the neuroendocrine system and (2) promotion of neuroprotection, neurogenesis, and synaptic plasticity in several brain areas. However, the methodological quality of the included animal studies was not high enough to produce robust evidence. In addition, mechanistic studies on specific aspects of acupuncture that may affect PTSD, including expectancy effects, in human PTSD subjects are also needed.

FDG PET imaging of vascular inflammation in post-traumatic stress disorder: A pilot case–control study

The prevalence of cardiovascular diseases (CVD) is increased in subjects with post-traumatic stress disorder (PTSD). Vascular inflammation mediates CVD and may be assessed by 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. In this pilot study, we investigated whether subjects with PTSD have enhanced vascular and systemic inflammation compared to healthy controls, as assessed by FDG PET imaging. MethodsA prospective group of 16 subjects (9 PTSD and 7 controls, age 34 ± 7) without prior history of CVD underwent FDG PET/CT imaging. The presence of PTSD symptoms at the time of the study was confirmed using PTSD checklist for DSM-5 (PCL5) questionnaire. Blood samples were collected to determine blood glucose, lipid and inflammatory biomarkers (tumor necrosis factor α, interleukin-1β, and interleukin-6) levels. FDG signal in the ascending aorta, amygdala, spleen and bone marrow was quantified. ResultsThe two groups matched closely with regards to cardiovascular risk factors. The inflammatory biomarkers were all within the normal range. There was no significant difference in FDG signal in the aorta (target to background ratio: 2.40 ± 0.29 and 2.34 ± 0.29 for control and PTSD subjects, difference: − 0.06, 95% confidence interval of difference: − 0.38 to 0.26), spleen, bone marrow, or amygdala between control and PTSD subjects. There was no significant correlation between aortic and amygdala FDG signal. However, a significant positive correlation existed between amygdala, splenic, and bone marrow FDG signal. ConclusionThis pilot, small study did not reveal any difference in vascular or systemic inflammation as assessed by FDG PET imaging between PTSD and healthy control subjects. Because of the small number of subjects, a modest increase in vascular inflammation, which requires larger scale studies to establish, cannot be excluded. The correlation between FDG signal in amygdala, spleen and bone marrow may reflect a link between amygdala activity and systemic inflammation.

English

BACKGROUND Post-traumatic stress disorder (PTSD) is a mental health condition that is triggered by a terrifying event either experiencing it or witnessing it. Although the pathogenesis is still unknown, some researches indicate inflammatory background and liver dysfunction as a part of the disease. We wanted to determine inflammatory markers' levels and investigate the correlation with liver enzymes in PTSD patients. METHODS This cross-sectional study included 60 male subjects aged between 40 - 60 years. Subjects were divided into two groups: a group of veterans with combat exposure and PTSD according to DSM-IV criteria and a control group of healthy subjects without combat exposure. WBC count, leucocytes ratios, levels of inflammatory markers (C reactive protein- CRP, fibrinogen, and erythrocyte sedimentation rateESR), and liver enzymes (aspartate aminotransferase- AST, alanine aminotransferase- ALT, creatine kinase- CK, and gamma-glutamyl transferase- GGT) were determined in all respondents. RESULTS The concentrations of CRP, fibrinogen, ESR, platelet-lymphocyte ratio and monocytelymphocyte ratio in subjects with PTSD were statistically significantly higher than those in the control group. Levels of AST and GGT in PTSD subjects were statistically significantly higher than of those in the control group subjects. Statistically significant positive correlation was found between serum AST and CRP concentration (Rho = 0.416; P = 0.022), as well as GGT and CRP concentration (Rho = 0.395; P = 0.031). CONCLUSIONS Results indicate the relationship between liver pathology and inflammation in the complex pathogenesis of PTSD. These can be used in future researches and development of a new diagnostic approach and treatment that may lead to a longer lifespan of PTSD patients. KEY WORDS PTSD, Inflammation, Liver Enzymes

PTSD and Suicidal Behaviors Amongst L'Aquila 2009 Earthquake Young Survivors

Background: Post-traumatic stress disorder (PTSD) is one of the most frequent and severe psychiatric consequences of natural disasters, frequently associated with suicidality. The aim of this study was at examining the possible relationships between suicidal behaviors and full-blown or partial PTSD, in a sample of young earthquake survivors. The second aim was at investigating the specific role of PTSD symptoms on suicidality.Methods: A total of 475 young adults who survived the L'Aquila 2009 earthquake, one of the most severe Italian disasters of the last decades, were recruited and assessed after 21 months from the catastrophe. Participants were evaluated by two questionnaires assessing subthreshold psychopathology, the Trauma and Loss Spectrum Self-Report (TALS-SR) to investigate both full and partial PTSD, and two specific Mood Spectrum Self-Report (MOODS-SR) sub-domains exploring suicidality, namely suicidal ideation and suicide attempts.Results: The ensuing findings showed that suicidal ideation and suicide attempts were present, respectively, in 40 (8.4%) and 11 (2.3%) survivors. Rates of suicidal ideation were significantly more elevated in full-blown PTSD subjects (group 1), as compared with those suffering from partial (group 2) or no PTSD (group 3). Interestingly, group 2 subjects showed significantly more suicidal ideation than healthy individuals, and less than those of group 1, while the frequency of suicide attempts was similar across the three groups. Suicidal ideation was associated with higher scores in the following TALS-SR domains: grief-reactions, re-experiencing, avoidance and numbing, maladaptive coping, and personal characteristics/risk factor.Conclusions: The results of the present study support and extend previous findings on the role of PTSD symptoms in suicidality after a severe earthquake. However, as compared with available literature, they also highlight the significant impact of sub-threshold PTSD manifestations in increasing the suicide risk in survivors of a mass disaster.

Cortical volume abnormalities in posttraumatic stress disorder: an ENIGMA-psychiatric genomics consortium PTSD workgroup mega-analysis.

Studies of posttraumatic stress disorder (PTSD) report volume abnormalities in multiple regions of the cerebral cortex. However, findings for many regions, particularly regions outside commonly studied emotion-related prefrontal, insular, and limbic regions, are inconsistent and tentative. Also, few studies address the possibility that PTSD abnormalities may be confounded by comorbid depression. A mega-analysis investigating all cortical regions in a large sample of PTSD and control subjects can potentially provide new insight into these issues. Given this perspective, our group aggregated regional volumes data of 68 cortical regions across both hemispheres from 1379 PTSD patients to 2192 controls without PTSD after data were processed by 32 international laboratories using ENIGMA standardized procedures. We examined whether regional cortical volumes were different in PTSD vs. controls, were associated with posttraumatic stress symptom (PTSS) severity, or were affected by comorbid depression. Volumes of left and right lateral orbitofrontal gyri (LOFG), left superior temporal gyrus, and right insular, lingual and superior parietal gyri were significantly smaller, on average, in PTSD patients than controls (standardized coefficients = -0.111 to -0.068, FDR corrected P values < 0.039) and were significantly negatively correlated with PTSS severity. After adjusting for depression symptoms, the PTSD findings in left and right LOFG remained significant. These findings indicate that cortical volumes in PTSD patients are smaller in prefrontal regulatory regions, as well as in broader emotion and sensory processing cortical regions.

Common and distinct patterns of gray matter alterations in borderline personality disorder and posttraumatic stress disorder: A dual meta-analysis

BackgroundBorderline personality disorder (BPD) and posttraumatic stress disorder (PTSD) are severe psychiatric disorders and often co-occur, either of the two will seriously threaten to public health. However, we lack ample evidences to understand the potential pathophysiologic mechanisms of gray matter (GM) alterations in the two disorders. MethodsWe performed a meta-analysis in both BPD (15 datasets including 442 BPD subjects versus 441 healthy controls) and PTSD (11 datasets including 214 PTSD subjects versus 258 healthy controls) applying anisotropic effect-size-based algorithms (AES-SDM) method. ResultsConjunction analysis found relative GM volume reductions in both disorders in the orbitofrontal gyrus and anterior cingulate cortex, contrarily, differences were predominantly observed that GM volume increased in the posterior cingulate gyrus and precuneus in BPD subjects, and GM volume decreased in the amygdala-hippocampal fear circuit, fusiform gyrus in PTSD subjects. ConclusionsGroup comparisons and conjunction analyses in BPD and PTSD identified same regions of GM volume reductions in the orbitofrontal gyrus and anterior cingulate cortex, which may provide clues for the neurobiological mechanisms and clinical diagnosis underpinning two disorders.

Cortical Transcriptomic Alterations in Association With Appetitive Neuropeptides and Body Mass Index in Posttraumatic Stress Disorder.

BackgroundThe molecular pathology underlying posttraumatic stress disorder (PTSD) remains unclear mainly due to a lack of human PTSD postmortem brain tissue. The orexigenic neuropeptides ghrelin, neuropeptide Y, and hypocretin were recently implicated in modulating negative affect. Drawing from the largest functional genomics study of human PTSD postmortem tissue, we investigated whether there were molecular changes of these and other appetitive molecules. Further, we explored the interaction between PTSD and body mass index (BMI) on gene expression.MethodsWe analyzed previously reported transcriptomic data from 4 prefrontal cortex regions from 52 individuals with PTSD and 46 matched neurotypical controls. We employed gene co-expression network analysis across the transcriptomes of these regions to uncover PTSD-specific networks containing orexigenic genes. We utilized Ingenuity Pathway Analysis software for pathway annotation. We identified differentially expressed genes (DEGs) among individuals with and without PTSD, stratified by sex and BMI.ResultsThree PTSD-associated networks (P < .01) contained genes in signaling families of appetitive molecules: 2 in females and 1 in all subjects. We uncovered DEGs (P < .05) between PTSD and control subjects stratified by sex and BMI with especially robust changes in males with PTSD with elevated vs normal BMI. Further, we identified putative upstream regulators (P < .05) driving these changes, many of which were enriched for involvement in inflammation.ConclusionsPTSD-associated cortical transcriptomic modules contain transcripts of appetitive genes, and BMI further interacts with PTSD to impact expression. DEGs and inferred upstream regulators of these modules could represent targets for future pharmacotherapies for obesity in PTSD.