Development Of Posttraumatic Stress Disorder Research Articles

Influencing factors of posttraumatic stress disorder in Shidu parents who have lost their only child: a cross-sectional survey

BackgroundIn China, parents who have lost their only child are referred to as Shidu parents (SDPs). This study aimed to investigate the prevalence and risk factors of post-traumatic stress disorder (PTSD) and investigate the influence of depressive and anxiety symptoms on the development of PTSD.MethodFour hundred and thirty-six SDPs completed assessments of PTSD (Structured Clinical Interview for DSM-IV Disorders, SCID-IV; The Clinician-Administered PTSD Scale-IV, CAPS-IV), depression (Hamilton depression scale), and anxiety (Hamilton Anxiety Scale) via in-person interviews. Logistic regression and hierarchical multiple linear regression analyses were used to explore the association of demographic characteristics, depression, and anxiety symptoms with PTSD.ResultsThe prevalence of PTSD in SDPs was 14.45%. The comorbidity of depression and anxiety symptoms was 87.30% in the SDPs with PTSD. The logistic regression model, which included factors of gender, age, education, depression, and anxiety, which contributed to the development of PTSD, was significant [χ² (11) = 122.47, p < 0.001]. The hierarchical multiple linear regression analysis indicated that female gender and the severity of comorbidities (depression and anxiety) were positively associated with the severity of PTSD.ConclusionThis study found that the severity of depression and anxiety was closely related to the severity of PTSD, supporting that SDPs are highly prone to the co-occurrence of PTSD, depression, and anxiety after bereavement. Our findings may provide more insights into the development of individualized interventions for parents who have experienced the loss of their only child.

Ketamine alleviates PTSD-like effect and improves hippocampal synaptic plasticity via regulation of GSK-3β/GR signaling of rats

BackgroundEach year, 3–4% of the global population experiences post-traumatic stress disorder (PTSD), a chronic mental disorder with significant social and economic repercussions. Although it has been shown that ketamine can effectively alleviate PTSD symptoms in individuals, the specific mechanism of action underlying its anti-PTSD effects remains unclear. In this study, we investigated how a single, low dose of ketamine affected the glycogen synthase kinase 3β (GSK-3β)/glucocorticoid receptor (GR) signaling pathway in a single prolonged stress (SPS)-induced PTSD rat model. MethodsAfter establishing the model, stress-related behavioral alterations in the rats were assessed following intraperitoneal injections of ketamine (10 mg/kg) and GSK-3β antagonist SB216763 (5 mg/kg). In the hippocampus, alterations in the expression of specific proteins implicated in PTSD development, such as GR, brain-derived neurotrophic factor (BDNF), GSK-3β, and phosphorylated glycogen synthase kinase 3β (p-GSK-3β), were assessed. We also measured changes in the mRNA expression levels of GR, BDNF, GSK-3β, FK501 binding protein 51 (FKBP5), and corticotropin-releasing hormone (CRH), as well as synaptic ultrastructure, in the hippocampus, and measured changes in corticosterone levels in the blood. ResultsSPS induced anxiety-like and depression-like behaviors in rats and induced morphological changes in synapse, which were accompanied by higher GSK-3β protein expression and conversely, decreased expression of GR, BDNF, p-GSK-3β, FKBP5 and CRH. Intraperitoneal administration of ketamine (10 mg/kg) after SPS prevented SPS-induced anxiety-like behaviors. Most importantly, ketamine attenuated SPS-induced dysfunctions in GSK-3β/GR signaling and synaptic deficits. Furthermore, treatment with a GSK-3β inhibitor played the same effect as ketamine on behavioral changes of SPS model rats. ConclusionSingle doses of ketamine effectively ameliorate SPS-induced anxiety-like symptoms, potentially by improving synaptic plastic in the hippocampus by regulating GSK-3β/GR signaling.

Protective and vulnerability personality traits associated with PTSD diagnosis after preterm delivery.

Giving birth prematurely is a traumatic event that has many consequences for the mother but also for her baby and their family. Studies have shown that about a quarter of these mothers will suffer from post-traumatic stress disorder (PTSD) as a result. This study aims to identify internal personality factors associated with the development of PTSD in mothers who gave birth before 33 weeks. The results revealed significant correlations between two personality dimensions (neuroticism and extraversion) and the likeliness of developing PTSD in mothers who gave birth prematurely. Neuroticism is positively liked with the disorder while extraversion is negatively correlated with it. Studies should now focus on early detection of PTSD and better interventions for these mothers.

Serum cortisol and neuroticism for post-traumatic stress disorder over 2 years in patients with physical injuries.

This study aimed to explore the relationships between serum cortisol levels, personality traits, and the development of Post-Traumatic Stress Disorder (PTSD) over 2 years among individuals with physical injuries. Participants were consecutively recruited from a trauma center and followed prospectively for 2 years. At baseline, serum cortisol levels were measured, and personality traits were categorized into five dimensions (Extraversion, Agreeableness, Conscientiousness, Neuroticism, and Openness), using the Big Five Inventory-10. The diagnosis of PTSD during follow-up (at 3, 6, 12, and 24 months post-injury) was determined using the Clinician-Administered PTSD Scale for DSM-5. Binary and multinomial logistic regression analyses were conducted to examine the interactions between cortisol levels, personality traits, and PTSD development. Among 923 patients analyzed, 112 (12.1%) were diagnosed with PTSD at some point during the study period, with prevalence rates decreasing from 8.8% at 3 months to 3.7% at 24 months post-injury. Direct associations between cortisol levels or personality traits and PTSD were not observed. However, a significant interaction between lower cortisol levels and higher Neuroticism in relation to PTSD risk was identified, especially during the early follow-up periods (3 to 6 months), but this association waned from the 12-month follow-up onward. Our findings reveal Neuroticism-dependent associations between serum cortisol levels and PTSD development, exhibiting temporal variations. These results suggest that PTSD development may be influenced by a complex, time-sensitive interplay of biological and psychosocial factors, underscoring the importance of considering individual differences in stress reactivity and personality in PTSD research and treatment.

Peritraumatic Dissociation Partially Mediates the Influence of Lifetime Trauma Exposure on Prospective PTSD Symptoms

ABSTRACT Higher lifetime trauma exposure and increased peritraumatic dissociation (PD) are well-known predictors of Post-Traumatic Stress Disorder (PTSD) symptoms following new trauma (prospective PTSD symptoms). The interplay between those factors, however, is not well established. In this study, we aimed to assess whether PD mediates the influence of lifetime trauma exposure on prospective PTSD symptoms. A total of 387 adults visiting five emergency departments who had experienced a traumatic event within 72 hours completed baseline assessments on lifetime trauma exposure count and PD. PTSD symptoms were assessed 1 month later. Structural equation modeling was used to examine the mediation effect of PD in the relationship between lifetime trauma exposure count and 1-month PTSD symptoms. We found that PD mediated the association between lifetime trauma exposure count and 1-month PTSD symptoms, even after accounting for some confounders. However, the mediation was partial, accounting for 17.9% of the lifetime trauma exposure count’s total effect. While this finding is significant, it also suggests that additional mechanisms beyond PD play a role in explaining the influence of higher lifetime trauma exposure on prospective PTSD symptoms. These findings provide valuable insights into the complex dynamics of PTSD development and call for further research to explore complementary factors and preventive strategies.

Distinct saliva DNA methylation profiles in relation to treatment outcome in youth with posttraumatic stress disorder

In youth with posttraumatic stress disorder (PTSD) non-response rates after treatment are often high. Epigenetic mechanisms such as DNA methylation (DNAm) have previously been linked to PTSD pathogenesis, additionally DNAm may affect response to (psychological) therapies. Besides investigating the direct link between DNAm and treatment response, it might be helpful to investigate the link between DNAm and previously associated biological mechanisms with treatment outcome. Thereby gaining a deeper molecular understanding of how psychotherapy (reflecting a change in the environment) relates to epigenetic changes and the adaptability of individuals. To date, limited research is done in clinical samples and no studies have been conducted in youth. Therefore we conducted a study in a Dutch cohort of youth with and without PTSD (n = 87, age 8–18 years). We examined the cross-sectional and longitudinal changes of saliva-based genome-wide DNA methylation (DNAm) levels, and salivary cortisol secretion. The last might reflect possible abbreviations on the hypothalamic–pituitary– adrenal (HPA) axis. The HPA-axis is previously linked to DNAm and the development and recovery of PTSD. Youth were treated with 8 sessions of either Eye Movement Reprocessing Therapy (EMDR) or Trauma Focused Cognitive behavioral Therapy (TF-CBT). Our epigenome wide approach showed distinct methylation between treatment responders and non-responders on C18orf63 gene post-treatment. This genomic region is related to the PAX5 gene, involved in neurodevelopment and inflammation response. Additionally, our targeted approach indicated that there were longitudinal DNAm changes in successfully treated youth at the CRHR2 gene. Methylation at this gene was further correlated with cortisol secretion pre- and post-treatment. Awaiting replication, findings of this first study in youth point to molecular pathways involved in stress response and neuroplasticity to be associated with treatment response.

Delayed effects of alcohol consumption on the association between serum BDNF levels and post-traumatic stress disorder development over two-years

BackgroundsThis study aimed to examine the individual and combined effects of serum BDNF (sBDNF) levels and alcohol consumption status, assessed shortly after a physical injury, on the development of post-traumatic stress disorder (PTSD) over two years. MethodsParticipants were consecutively recruited from a trauma center and followed prospectively for two years. At baseline, sBDNF levels and alcohol consumption history were assessed. A range of socio-demographic and clinical covariates were also collected. PTSD diagnosis during follow-up (3, 6, 12, and 24 months post-injury) was established using the Clinician-Administered PTSD Scale for DSM-5. Binary and multinomial logistic regression analyses were employed to investigate the relationships between sBDNF levels, alcohol consumption status, and PTSD onset. ResultsOut of 923 participants analyzed, 112 (12.1%) developed PTSD at some point during the study, with prevalence rates of 8.8% at 3 months, 7.6% at 6 months, 4.8% at 12 months, and 3.7% at 24 months. The study found no individual associations between sBDNF levels or alcohol consumption status and PTSD development. However, lower sBDNF levels significantly predicted PTSD in individuals who consumed alcohol, a relationship not observed in non-drinkers, with significant interaction terms. This pattern was consistent at later follow-up points from 12 to 24 months, but not at earlier assessments at 3 and 6 months. LimitationsThe study's reliance on participants from a single trauma center with moderate to severe injuries may limit the generalizability of the findings. ConclusionsA significant interaction between sBDNF levels and alcohol consumption in relation to PTSD development was observed, particularly in the long term. These findings highlight the necessity of considering both sBDNF levels and alcohol consumption in strategies aimed at preventing PTSD among individuals with physical injuries, underscoring the need for tailored approaches based on these factors.

New recognition of the heart-brain axis and its implication in the pathogenesis and treatment of PTSD.

Post-traumatic stress disorder (PTSD) is a complex psychological disorder provoked by distressing experiences, and it remains without highly effective intervention strategies. The exploration of PTSD's underlying mechanisms is crucial for advancing diagnostic and therapeutic approaches. Current studies primarily explore PTSD through the lens of the central nervous system, investigating concrete molecular alterations in the cerebral area and neural circuit irregularities. However, the body's response to external stressors, particularly the changes in cardiovascular function, is often pronounced, evidenced by notable cardiac dysfunction. Consequently, examining PTSD with a focus on cardiac function is vital for the early prevention and targeted management of the disorder. This review undertakes a comprehensive literature analysis to detail the alterations in brain and heart structures and functions associated with PTSD. It also synthesizes potential mechanisms of heart-brain axis interactions relevant to the development of PTSD. Ultimately, by considering cardiac function, this review proposes novel perspectives for PTSD's prophylaxis and therapy.

Assessment of Post-traumatic Stress Disorder Risk Factors Among Law Enforcement Staff: A Case-Control Study

Background: Given the inherent nature of their job, law enforcement staff regularly confront major stressors. Objectives: The prevalence of post-traumatic stress disorder (PTSD) among law enforcement staff is about twice that of the general population. We conducted this study to assess PTSD risk factors among this population. Methods: This prospective case-control study was conducted on patients with PTSD working as law enforcement staff as the case group, and their comrades with no PTSD as the control group. We used a questionnaire, including possible factors contributing to the development of PTSD, to gather the data. Binomial logistic regression was used to calculate the odds ratio (OR) and 95% confidence intervals. Results: A total of 84 participants were included in the study. We found that some factors could be protective against PTSD, including marriage (OR: 0.270, 95% CI: 0.087 - 0.839, P-value: 0.024), having an academic degree (OR: 0.333, 95% CI: 0.114 - 0.978, P-value: 0.045), higher income (R2: 0.081; OR: 0.849, 95% CI: 0.721 - 1.000, P-value: 0.050), and receiving satisfactory family support (OR: 0.413, 95% CI: 0.171 - 0.999, P-value: 0.050). Furthermore, logistic regression showed that a positive psychological history (OR: 2.562, 95% CI: 1.025 - 6.406, P-value: 0.044), a positive familial psychological history (OR: 2.667, 95% CI: 1.099 - 6.406, P-value: 0.030), and encountering trauma (aside from the current trauma) after 18 years of age (OR: 2.643, 95% CI: 1.038 - 6.731, P-value: 0.041) are risk factors for PTSD. Conclusions: Our results showed that marriage, having an academic degree, higher income, and receiving satisfactory family support are protective factors. In addition, the risk factors for PTSD include a positive psychological history, a positive familial psychological history, and encountering trauma (aside from the current trauma) after 18 years of age. However, given our limitations, further studies should be conducted before drawing solid conclusions.

Posttraumatic stress disorder in the aftermath of the Turkey earthquake: exploring the role of demographics, level of exposure, and personality traits

ABSTRACT Background and Objectives Post-Traumatic Stress Disorder (PTSD) is an important mental disorder that can develop after mass traumas such as earthquakes. In our study, we aimed to investigate the development of PTSD after the Turkey earthquake (6 February 2023) and its association with some demographic variables, personality traits, and psychological vulnerability. Method 547 participants completed assessments of personality, disaster exposure, and PTSD symptoms. Multiple regression analyses were used to identify predictors of PTSD symptoms. Results PTSD scores were higher in women, single people, those with low educational level, those who witnessed someone else's injury or death, those who were injured, and those whose homes were destroyed. Physical injury, conscientiousness, marital status, income, and agreeableness predicted PTSD. Among these variables, physical injury was the strongest predictor of PTSD. Conclusions Psychological vulnerability, conscientiousness, physical injury, employment, witnessing someone else's injury, gender, and emotional stability predicted PTSD score in a significant way. Physical injury, conscientiousness, marital status, income, agreeableness predicted PTSD in a significant way.

Social Determinants of Mental Health for Posttraumatic Stress Disorder

Recognizing and addressing the social determinants of mental health (SDoMH) for posttraumatic stress disorder (PTSD) is essential for the effective practice of psychiatry. Experiencing traumatic events and subsequent development of PTSD profoundly affects individuals, families, and society, making it one of the most common mental health disorders with substantial psychiatric comorbidity. This article delves into the bidirectional aspects of the SDoMH in PTSD and reviews the diagnostic criteria, prevalence rates, and repercussions of PTSD on both an individual level and within society. PTSD assessment, interventions, and treatment are reviewed, including Prolonged Exposure, Cognitive Processing Therapy, Eye Movement, Desensitization and Reprocessing, trauma-focused and grief therapy. Primary prevention of PTSD, public health considerations, and positive psychiatry tenets are reviewed. [ Psychiatr Ann . 2024;54(7):e209–e215.]

Minimizing Survey Questions for PTSD Prediction Following Acute Trauma.

Traumatic experiences have the potential to give rise to post-traumatic stress disorder (PTSD), a debilitating psychiatric condition associated with impairments in both social and occupational functioning. There has been great interest in utilizing machine learning approaches to predict the development of PTSD in trauma patients from clinician assessment or survey-based psychological assessments. However, these assessments require a large number of questions, which is time consuming and not easy to administer. In this paper, we aim to predict PTSD development of patients 3 months post-trauma from multiple survey-based assessments taken within 2 weeks post-trauma. Our objective is to minimize the number of survey questions that patients need to answer while maintaining the prediction accuracy from the full surveys. We formulate this as a feature selection problem and consider 4 different feature selection approaches. We demonstrate that it is possible to achieve up to 72% accuracy for predicting the 3-month PTSD diagnosis from 10 survey questions using a mean decrease in impurity-based feature selector followed by a gradient boosting classifier.

Risk factors for PTSD symptoms following PICU admission for childhood septic shock.

ObjectivePaediatric intensive care unit (PICU) admission represents a traumatic event for many children. Follow-up studies have found post-traumatic stress disorder (PTSD) rates of 10-30%, with a particular prevalence following admission for sepsis. Dysregulated inflammatory responses are associated with PTSD. Sepsis involves a marked inflammatory response but the relationship between this and PTSD have not been clearly established. In this study we investigate associations between the inflammatory response, psychosocial risk factors, and PTS symptoms following PICU admission for septic shock.We investigate the outcomes for children aged > 3 years, discharged from one PICU following admission for septic shock between 2010 and 2017. The study was a retrospective analysis of PICU-specific PTS symptoms reported by parents at any time since discharge via the Trauma and Behavior Health screen. Demographics, pre-morbid health characteristics, and exposure to other traumatic events were assessed. Clinical characteristics and blood test results at admission and at 48 h were recorded from clinical records. Multiple linear regression was used to investigate relationships between PTS symptom scores and predictor variables.Data for 65 participants (48% male, median assessment age 8.0 years) was available. Median time since admission was 5.1 years. 30.8% children scored at risk of PTSD at any time since discharge Symptoms were significantly associated with acute CRP rise (p 0.03), other trauma exposures (p = 0.01), and female gender (p =0.04).PTS symptoms in children who have survived septic shock are prevalent. These findings support a possible contribution of acute inflammatory changes, cumulative traumatic exposure, and female gender in post-PICU PTSD development.

Inhibition of Protein Synthesis Attenuates Formation of Traumatic Memory and Normalizes Fear-Induced c-Fos Expression in a Mouse Model of Posttraumatic Stress Disorder.

Posttraumatic stress disorder (PTSD) is a debilitating psychosomatic condition characterized by impairment of brain fear circuits and persistence of exceptionally strong associative memories resistant to extinction. In this study, we investigated the neural and behavioral consequences of inhibiting protein synthesis, a process known to suppress the formation of conventional aversive memories, in an established PTSD animal model based on contextual fear conditioning in mice. Control animals were subjected to the conventional fear conditioning task. Utilizing c-Fos neural activity mapping, we found that the retrieval of PTSD and normal aversive memories produced activation of an overlapping set of brain structures. However, several specific areas, such as the infralimbic cortex and the paraventricular thalamic nucleus, showed an increase in the PTSD group compared to the normal aversive memory group. Administration of protein synthesis inhibitor before PTSD induction disrupted the formation of traumatic memories, resulting in behavior that matched the behavior of mice with usual aversive memory. Concomitant with this behavioral shift was a normalization of brain c-Fos activation pattern matching the one observed in usual fear memory. Our findings demonstrate that inhibiting protein synthesis during traumatic experiences significantly impairs the development of PTSD in a mouse model. These data provide insights into the neural underpinnings of protein synthesis-dependent traumatic memory formation and open prospects for the development of new therapeutic strategies for PTSD prevention.

The mediating effect of sleep quality on exposure to community violence and posttraumatic stress symptoms in the United States

ObjectivesThe role of sleep quality is not yet fully understood in the context of posttraumatic stress disorder (PTSD) following exposure to community violence. Thus, the primary aim of this study is to examine the mediating effect of sleep quality in the relationship between community violence exposure and posttraumatic stress symptoms. MethodsUtilizing a cross-sectional survey administered to an online opt-in panel of adults in the United States in 2023 (age ≥ 18 years) (N = 342), respondents reported on their exposure to community violence, sleep quality, and posttraumatic stress symptoms. Covariate-adjusted regressions were used to test these relationships. ResultsDirectly experiencing community violence was associated with poorer sleep quality (β = 0.11, 95 % CI [0.02, 0.20], p = 0.022) and posttraumatic stress symptoms (β = 0.33, 95 % CI [0.17, 0.48], p = < 0.001), and poorer sleep quality predicted greater posttraumatic stress symptoms (β = 0.74, 95 % CI [0.58, 0.91], p = 0<.001). Further, sleep quality was a partial mediator (β = 0.24, 95 % CI [0.04, 0.50], p = 0.028), accounting for 24 % of the relationship. ConclusionsFindings from this study help deepen understanding of the processes that contribute to the development of PTSD and provide insights into possible interventions, including treatment for sleep problems in the aftermath of violence exposure as a means for lessening the mental health burdens of community violence.

Early pharmacological interventions for prevention of post-traumatic stress disorder (PTSD) in individuals experiencing acute traumatic stress symptoms.

Acute traumatic stress symptoms may develop in people who have been exposed to a traumatic event. Although they are usually self-limiting in time, some people develop post-traumatic stress disorder (PTSD), a severe and debilitating condition. Pharmacological interventions have been proposed for acute symptoms to act as an indicated prevention measure for PTSD development. As many individuals will spontaneously remit, these interventions should balance efficacy and tolerability. To assess the efficacy and acceptability of early pharmacological interventions for prevention of PTSD in adults experiencing acute traumatic stress symptoms. We searched the Cochrane Common Mental Disorders Controlled Trial Register (CCMDCTR), CENTRAL, MEDLINE, Embase and two other databases. We checked the reference lists of all included studies and relevant systematic reviews. The search was last updated on 23 January 2023. We included randomised controlled trials on adults exposed to any kind of traumatic event and presenting acute traumatic stress symptoms, without restriction on their severity. We considered comparisons of any medication with placebo, or with another medication. We excluded trials that investigated medications as an augmentation to psychotherapy. We used standard Cochrane methodological procedures. Using a random-effects model, we analysed dichotomous data as risk ratios (RR) and calculated the number needed to treat for an additional beneficial/harmful outcome (NNTB/NNTH). We analysed continuous data as mean differences (MD) or standardised mean differences (SMD). Our primary outcomes were PTSD severity and dropouts due to adverse events. Secondary outcomes included PTSD rate, functional disability and quality of life. We included eight studies that considered four interventions (escitalopram, hydrocortisone, intranasal oxytocin, temazepam) and involved a total of 779 participants. The largest trial contributed 353 participants and the next largest, 120 and 118 participants respectively. The trials enrolled participants admitted to trauma centres or emergency departments. The risk of bias in the included studies was generally low except for attrition rate, which we rated as high-risk. We could meta-analyse data for two comparisons: escitalopram versus placebo (but limited to secondary outcomes) and hydrocortisone versus placebo. One study compared escitalopram to placebo at our primary time point of three months after the traumatic event. There was inconclusive evidence of any difference in terms of PTSD severity (mean difference (MD) on the Clinician-Administered PTSD Scale (CAPS, score range 0 to 136) -11.35, 95% confidence interval (CI) -24.56 to 1.86; 1 study, 23 participants; very low-certainty evidence), dropouts due to adverse events (no participant left the study early due to adverse events; 1 study, 31 participants; very low-certainty evidence) and PTSD rates (RR 0.59, 95% CI 0.03 to 13.08; NNTB 37, 95% CI NNTB 15 to NNTH 1; 1 study, 23 participants; very low-certainty evidence). The study did not assess functional disability or quality of life. Three studies compared hydrocortisone to placebo at our primary time point of three months after the traumatic event. We found inconclusive evidence on whether hydrocortisone was more effective in reducing the severity of PTSD symptoms compared to placebo (MD on CAPS -7.53, 95% CI -25.20 to 10.13; I2 = 85%; 3 studies, 136 participants; very low-certainty evidence) and whether it reduced the risk of developing PTSD (RR 0.47, 95% CI 0.09 to 2.38; NNTB 14, 95% CI NNTB 8 to NNTH 5; I2 = 36%; 3 studies, 136 participants; very low-certainty evidence). Evidence on the risk of dropping out due to adverse events is inconclusive (RR 3.19, 95% CI 0.13 to 75.43; 2 studies, 182 participants; low-certainty evidence) and it is unclear whether hydrocortisone might improve quality of life (MD on the SF-36 (score range 0 to 136, higher is better) 19.70, 95% CI -1.10 to 40.50; 1 study, 43 participants; very low-certainty evidence). No study assessed functional disability. This review provides uncertain evidence regarding the use of escitalopram, hydrocortisone, intranasal oxytocin and temazepam for people with acute stress symptoms. It is therefore unclear whether these pharmacological interventions exert a positive or negative effect in this population. It is important to note that acute traumatic stress symptoms are often limited in time, and that the lack of data prevents the careful assessment of expected benefits against side effects that is therefore required. To yield stronger conclusions regarding both positive and negative outcomes, larger sample sizes are required. A common operational framework of criteria for inclusion and baseline assessment might help in better understanding who, if anyone, benefits from an intervention. As symptom severity alone does not provide the full picture of the impact of exposure to trauma, assessment of quality of life and functional impairment would provide a more comprehensive picture of the effects of the interventions. The assessment and reporting of side effects may facilitate a more comprehensive understanding of tolerability.

Downregulation of lncRNAs Gomafu, NONMMUT033604.2, and NONMMUT064397.2 in the hippocampus of mice with model of post-traumatic stress disorder

Objectives Molecular mechanisms of post-traumatic stress disorder (PTSD) development have been analysed by evaluati-ng changes in the expression level of long non-coding RNA (lncRNA) as a potential biomarker of the disease and as one of the molecular aspects associated with the disease development. Methods In our study, we used quantitative polymerase chain reaction (qPCR) to evaluate changes in the expression level of long non-coding RNA – Gomafu, NONMMUT033604.2, and NONMMUT064397.2 – in the hippocampus of mice that were subjected to an artificially induced middle single prolonged stress (mSPS) model of post-traumatic stress disorder. Results We found a significant reduction in the expression levels of each of the three lncRNAs tested: Gomafu in 45.4 times, NONMMUT033604.2 in 53.4 times, and NONMMUT064397.2 in 5.2 times. The results of the present study provide evidence that the mSPS model effectively induces PTSD-like behaviour in mice leading to a significant decrease in the expression level of Gomafu, NONMMUT033604.2 and NONMMUT064397.2 lncRNA in mice hippocampus. Conclusions This data provides evidence that the three studied lncRNAs could be potential biomarkers of PTSD development.

Paeoniflorin exerts anti-PTSD effects in adult rats by modulating hippocampus and amygdala histone acetylation modifications in response to early life stress

Early life stress (ELS) can cause long-term changes by epigenetic factors, especially histone acetylation modification, playing a crucial role, affect normal cognition, mood, and behavior, and increase susceptibility to post-traumatic stress disorder (PTSD) in adulthood. It has been found that paeoniflorin (PF) can cross the blood-brain barrier to exert anti-PTSD effects on adult PTSD rats. However, whether PF can alleviate the harmful effects caused by ELS in adulthood has not yet been reported. Therefore, to explore the relationship between ELS and PTSD susceptibility in adulthood and its mechanism, in this study, SPS was used as a stressor of ELS, and the mathematical tool Z-normalization was employed as an evaluation criterion of behavioral resilience susceptibility. To investigate the regulatory mechanism of PF on histone acetylation in the hippocampus and amygdala of ELS rats in adulthood, using changes in HATs/HDACs as the entry point, meanwhile, the epigenetic marks (H3K9 and H4K12) in the key brain regions of ELS (hippocampus and amygdala) were evaluated, and the effects of PF on behavioral representation and PTSD susceptibility were observed. This study found that ELS lead to a series of PTSD-like behaviors in adulthood and caused imbalance of HATs/HDACs ratio in the hippocampus and amygdala, which confirms that ELS is an important risk factor for the development of PTSD in adulthood. In addition, paeoniflorin may improve ELS-induced PTSD-like behaviors and reduce the susceptibility of ELS rats to develop PTSD in adulthood by modulating the HATs/HDACs ratio in the hippocampus and amygdala.

Functional anatomy of the limbic system structures involved in the development of post-traumatic stress disorder: analysis of anatomical and clinical studies

We present an analysis of anatomical and clinical studies investigating the morphological and functional characteristics of various structures of the limbic system involved in the development of post-traumatic stress disorder (PTSD). Understanding the structural organization and functional interactions of this system will provide new insights into the mechanisms underlying PTSD. The results of various morphological and clinical studies are considered, including information on the architecture and interconnections of the structures of the limbic system and their alteration by traumatic events. The generalized results provide new data on the role of the individual structures of the limbic system in the development of PTSD, enabling more accurate prediction of the development of PTSD and prompt appropriate measures to alleviate the course of this disorder

Neuroimaging of posttraumatic stress disorder in adults and youth: progress over the last decade on three leading questions of the field.

Almost three decades have passed since the first posttraumatic stress disorder (PTSD) neuroimaging study was published. Since then, the field of clinical neuroscience has made advancements in understanding the neural correlates of PTSD to create more efficacious treatment strategies. While gold-standard psychotherapy options are available, many patients do not respond to them, prematurely drop out, or never initiate treatment. Therefore, elucidating the neurobiological mechanisms that define the disorder can help guide clinician decision-making and develop individualized mechanisms-based treatment options. To this end, this narrative review highlights progress made in the last decade in adult and youth samples on three outstanding questions in PTSD research: (1) Which neural alterations serve as predisposing (pre-exposure) risk factors for PTSD development, and which are acquired (post-exposure) alterations? (2) Which neural alterations can predict treatment outcomes and define clinical improvement? and (3) Can neuroimaging measures be used to define brain-based biotypes of PTSD? While the studies highlighted in this review have made progress in answering the three questions, the field still has much to do before implementing these findings into clinical practice. Overall, to better answer these questions, we suggest that future neuroimaging studies of PTSD should (A) utilize prospective longitudinal designs, collecting brain measures before experiencing trauma and at multiple follow-up time points post-trauma, taking advantage of multi-site collaborations/consortiums; (B) collect two scans to explore changes in brain alterations from pre-to-post treatment and compare changes in neural activation between treatment groups, including longitudinal follow up assessments; and (C) replicate brain-based biotypes of PTSD. By synthesizing recent findings, this narrative review will pave the way for personalized treatment approaches grounded in neurobiological evidence.