The influence of the behavioural inhibition system on the development of PTSD-like symptoms after presentation of a traumatic film in healthy subjects

Posttraumatic stress disorder in fibromyalgia syndrome: Prevalence, temporal relationship between posttraumatic stress and fibromyalgia symptoms, and impact on clinical outcome

Posttraumatic Stress Disorder Symptoms During the First Six Months After Traumatic Brain Injury

Posttraumatic stress disorder (PTSD) indicates a chronic stress reaction in response to trauma. This prevalent condition has been identified as a possible risk factor for obesity. Whether PTSD symptoms alter the trajectory of weight gain or constitute a comorbid condition has not been established. To determine whether women who develop PTSD symptoms are subsequently more likely to gain weight and become obese relative to trauma-exposed women who do not develop PTSD symptoms or women with no trauma exposure or PTSD symptoms and whether the effects are independent of depression. The Nurses' Health Study II, a prospective observational study initiated in 1989 with follow-up to 2005, using a PTSD screener to measure PTSD symptoms and time of onset. We included the subsample of the Nurses' Health Study II (54 224 participants; ages 24-44 years in 1989) in whom trauma and PTSD symptoms were measured. Trauma and PTSD symptoms. Development of overweight and obesity using body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) cut points 25.0 and 30.0, respectively; change in BMI during follow-up among women reporting PTSD symptom onset before 1989; and BMI trajectory before and after PTSD symptom onset among women who developed PTSD symptoms in 1989 or during follow-up. Among women with at least 4 PTSD symptoms before 1989 (cohort initiation), BMI increased more steeply (b = 0.09 [SE = 0.01]; P < .001) during the follow-up. Among women who developed PTSD symptoms in 1989 or later, BMI trajectory did not differ by PTSD status before PTSD onset. After PTSD symptom onset, women with at least 4 symptoms had a faster rise in BMI (b = 0.08 [SE = 0.02]; P < .001). The onset of at least 4 PTSD symptoms in 1989 or later was also associated with an increased risk of becoming overweight or obese (odds ratio, 1.36 [95% CI, 1.19-1.56]) among women with a normal BMI in 1989. Effects were maintained after adjusting for depression. Experience of PTSD symptoms is associated with an increased risk of becoming overweight or obese, and PTSD symptom onset alters BMI trajectories over time. The presence of PTSD symptoms should raise clinician concerns about physical health problems that may develop and prompt closer attention to weight status.

Post-Traumatic Stress Disorder (PTSD) is widely known in our society. The symptoms of PTSD are particularly believed to occur predominantly in children. We believe that Yogo teachers, who play a role in maintaining and promoting the health of children, are expected to provide appropriate support for children with a tendency for PTSD. In this study, we investigated the tendency for PTSD in students at University, as well as self-esteem related to depression and anxiety. Furthermore, we clarified the relationship between PTSD and self-esteem and examined the support provided by Yogo teachers. As a result, it was found that the higher the tendency for PTSD, the lower the self-esteem. We believe that the onset of PTSD causes a decline in memory ability and attentional function, which interferes with one’s life and leads to self-denial, resulting in a decline in self-esteem among those with a high tendency for PTSD. These results suggest that Yogo teachers should provide support to prevent the onset of PTSD in child students due to accidents, incidents, natural disasters, etc., as well as support to prevent the decline in self-esteem associated with the onset of PTSD.

The retention of information represents a defining trait of cognitive systems. The primary function of an organism’s memory is to retain engrams of unique experiences for extended periods, without interrupting memory trace during new learning processes. One of the cardinal unsolved issues in neuroscience lies in unveiling the mechanisms responsible for long-term memory. Despite this, a trustworthy experimental animal model for single-trial long-term memory remains undeveloped. To address this challenge, we aimed to create an animal model to study lifelong memory formation with a single trial. We used a mouse model of post-traumatic stress disorder (PTSD) for this purpose [1]. In this model, mice exposed to a powerful electrical foot shock develop highly persistent traumatic memories, which results in long-term behavioral changes [1]. Our hypothesis was that this model could uncover the mechanisms related to lifelong memory. The primary rationale for adopting the PTSD model as a model of lifelong memory pertains to the heightened durability of traumatic memories in comparison to conventional aversive memories [2]. Protein synthesis inhibitors, which are needed for long-term memory consolidation, can be used as amnesic agents to evaluate memory stability [3]. In a PTSD model using predator scent, the administration of a protein synthesis blocker prior to a traumatic experience disrupts the development of PTSD in mice [4]. However, it remains unclear how traumatic memory impairment affects PTSD development in the footshock model and whether the impairment persists long-term. Based on the evidence that the formation of PTSD necessitates the consolidation of associative memory, which is reliant on protein synthesis and coincides with changes in the stress response system, Siegmund and Watzhek [1] present a two-part proposal concerning the onset of PTSD. The two-part hypothesis regarding PTSD posits that PTSD formation involves sensory conditioning and sensitization processes that mutually reinforce one another. In line with this theorem, we considered the effects of studying context and exposure timing on the development of post-traumatic stress disorder, as it could potentially interfere with sensory conditioning formation [5]. The aim of this study is to create an experimental approach for developing enduring long-term memory through a single trial event on adult mice. We methodically analyzed behavioral expressions and the endurance of normal and traumatic fear memory, as well as their sensitivity to protein synthesis inhibition. Additionally, we investigated the effects of separating the timing of the associative and aversive elements of traumatic memory on PTSD development in a mouse model. The experiment involved male C57Bl/6 mice, aged between 3–4 months and 15–18 months (for an investigation into aged mice), which were placed in an electrified chamber. After 170 seconds, the mice experienced either one footshock (1.5 mA, 2 s) to elicit fear memory or three footshocks (1.5 mA, 10 s) for PTSD induction. After receiving the footshock, the mouse was held in the chamber for 60 seconds before being returned to its home cage. A memory test was conducted seven days later by placing the mice back in the same context. To assess the existence of standard PTSD symptoms, like sensitization and generalization, the creatures were exposed to an unfamiliar context and an unexpected auditory stimulus, respectively. In the experiment, animals were placed in unfamiliar or familiar safe contexts that differed from their previous ones. The duration of freezing was measured to assess fear and evaluate memory retention, sensitization, and generalization. Anxiety levels were evaluated using the elevated plus maze test. In the process of constructing a highly stable long-term memory model, we evaluated the behavioral performance of PTSD-induced (PTSD), fear-conditioned (FC), and active control (AC) groups of animals at 7 days, 1 month, and 3 months after exposure. As a result of PTSD induction, mice displayed increased fear levels for up to 3 months in the training context, along with heightened fear sensitization and generalization at 7 days following exposure, relative to the FC and AC groups. The PTSD group exhibited heightened freezing behavior within a month and a decreased number of entries to the closed arms during the initial three months following exposure when contrasted with the FC and AC groups. We additionally noted that the FC group displayed raised fear levels in contrast to the control animals up to 3 months post-exposure, albeit lower in magnitude than that of the PTSD group. The FC group, similar to the PTSD group, showed increased sensitization and generalization compared to control animals at 1 week post-exposure, but to a lesser extent than we observed in the PTSD group. The findings suggest that traumatic memory remains present for a minimum of three months, whereas fear memory in the fear conditioning paradigm diminishes in intensity during this time. Hence, PTSD induction effectively functions as an animal model of profoundly stable long-term memory, in opposition to the fear conditioning paradigm. As the high stable long-term memory model is designed for testing in senior animals, the impact of aging on traumatic memory formation and storage becomes an important inquiry at six months and one year following exposure. We analyzed the formation of both aversive and traumatic memory in mice aged 15–18 months, one week after footshock exposure. In the study involving older mice, the PTSD group exhibited increased levels of fear memory and sensitization when compared with both the FC and AC groups, in addition to displaying higher levels of generalization and anxiety when compared with the AC group. Furthermore, mice that underwent rear-conditioning showed heightened levels of fear during learning, fear sensitization, and generalization, although not anxiety. These findings demonstrate the formation of traumatic and aversive memory in aged mice, indicating that conducting memory tests six months and a year after exposure is an appropriate approach. To evaluate the durability of traumatic and aversive memory, we administered a protein synthesis inhibitor called cycloheximide (Chm) to interfere with memory formation. Mice were given a cycloheximide solution (95 mg/kg) via intraperitoneal injection 30 minutes before footshock (Chm-PTSD and Chm-FC groups) while control animals received a saline injection (Sal-PTSD, Sal-FC). After training, the Chm-FC group displayed a decrease in freezing rate when compared to the saline-injected group at the 7- and 30-day marks. The Chm-PTSD group exhibited fear levels comparable to those of the Sal-FC group in the training context, and did not display sensitization or generalization of fear. These findings suggest that inhibiting protein synthesis during memory formation resulted in complete amnesia for standard aversive memory and merely weakened traumatic memory. As a result, only the associative component of traumatic memory remained intact, while nonspecific symptoms of PTSD were absent. The strong resilience of memory in the PTSD model to severe disruptions, such as protein synthesis blockade, also confirms its stability, which facilitates exploration of lifelong memory mechanisms in the PTSD model. To examine the timing effect of the associative and aversive component of PTSD development, we evaluated traumatic memory formation when contextual memory formation was absent, and contextual exploration occurred three days before shock cessation. A week after exposure to immediate and intense footshock, mice in the experimental group exhibited lower levels of fear, reduced fear sensitization, and less anxiety compared to those in the PTSD-induced group. If an intense foot shock was preceded by a contextual study three days earlier, the animals exhibited lower levels of fear in an unfamiliar, safe context, and reduced anxiety compared to the mice induced with PTSD. In both cases, the fear level after the shock cessation was identical to that of the mice who experienced an immediate, moderate shock. Based on our findings, we concluded that aversive memory forms in the absence or prior formation of contextual memory in relation to traumatic exposure. However, PTSD induction does not occur under such circumstances. This indicates that contextual memory needs to be formed simultaneously with the traumatic event for the development of traumatic memory in the mouse model of PTSD. In summary, our findings indicate that aversive memory tends to fade over time, while traumatic memory remains stable for a minimum of 3 months following its induction. Therefore, PTSD proves to be a fitting candidate laboratory model for high, stable, and long-term memory. Aged mice aged between 15–18 months display the formation of traumatic memory and experience PTSD symptoms in a manner similar to adult animals aged between 3–4 months in the PTSD model. For the induction of PTSD in mice, contextual memory formation about the traumatic environment and the traumatic event occurrence may coincide, which is crucial.

Incidence and risk factors for post-traumatic stress disorder in a population affected by a severe flood

This study examined the prevalence of lifetime traumatic events and current symptoms of posttraumatic stress disorder (PTSD) among treatment-seeking cocaine-dependent outpatients and compared patients with and without PTSD on current substance use, psychopathology, and sociodemographic characteristics. The subjects were 122 adult cocaine-dependent outpatients participating in a treatment outcome study of psychosocial therapy. In addition to standard self-report and interview measures of psychopathology and substance use, the subjects completed the Trauma History Questionnaire and the PTSD Checklist before entering treatment. These patients experienced a large number of lifetime traumatic events (mean = 5.7); men experienced more general disasters and crime-related traumas than women, and women experienced more physical and sexual abuse than men. According to self-report measures, 20.5% of the subjects currently met the DSM-III-R criteria for PTSD; the rate of PTSD was 30.2% among women and 15.2% among men. Patients with PTSD had significantly higher rates of co-occurring axis I and axis II disorders, interpersonal problems, medical problems, resistance to treatment, and psychopathology symptoms than patients without PTSD. Psychopathology symptoms represented the most consistent difference between the two groups and provided the best prediction of PTSD status in a logistic regression. However, the groups did not differ significantly in current substance use or sociodemographic characteristics. These findings underscore the value of screening substance abusers for PTSD, because it can identify a small but substantial number who might require additional treatment. Further studies of the relationship between PTSD and substance abuse appear warranted.

PTSD and Combat-Related Injuries: Functional Neuroanatomy

Military personnel experience posttraumatic stress disorder (PTSD), which is associated with differential DNA methylation across the whole genome. However, the relationship between these DNA methylation patterns and clinically relevant increases in PTSD severity is not yet clearly understood. The purpose of this study was to identify differences in DNA methylation associated with PTSD symptoms and investigate DNA methylation changes related to increases in the severity of PTSD in military personnel. In this pilot study, a cross-sectional comparison was made between military personnel with PTSD (n = 8) and combat-matched controls without PTSD (n = 6). Symptom measures were obtained, and genome-wide DNA methylation was measured using methylated DNA immunoprecipitation (MeDIP-seq) from whole blood samples at baseline and 3 months later. A longitudinal comparison measured DNA methylation changes in military personnel with clinically relevant increases in PTSD symptoms between time points (PTSD onset) and compared methylation patterns to controls with no clinical changes in PTSD. In military personnel with elevated PTSD symptoms 3 months following baseline, 119 genes exhibited reduced methylation and 8 genes exhibited increased methylation. Genes with reduced methylation in the PTSD-onset group relate to the canonical pathways of netrin signaling, Wnt/Ca+ pathway, and axonal guidance signaling. These gene pathways relate to neurological disorders, and the current findings suggest that these epigenetic changes potentially relate to PTSD symptomology. This study provides some novel insights into the role of epigenetic changes in PTSD symptoms and the progression of PTSD symptoms in military personnel.

Animal and human research suggests that the development of posttraumatic stress disorder (PTSD) may involve the overconsolidation of memories of a traumatic experience. Previous studies have attempted to use pharmaceutical agents, especially the β-adrenergic blocker propranolol, to reduce this overconsolidation. In this randomized, placebo-controlled study of the efficacy of propranolol in reducing the development of PTSD, we optimized dosages and conducted both psychophysiological and clinical assessments 1 and 3 months after the traumatic event. Forty-one emergency department patients who had experienced a qualifying acute psychological trauma were randomized to receive up to 240 mg/day of propranolol or placebo for 19 days. At 4 and 12 weeks post-trauma, PTSD symptoms were assessed. One week later, participants engaged in script-driven imagery of their traumatic event while psychophysiological responses were measured. Physiological reactivity during script-driven traumatic imagery, severity of PTSD symptoms, and the rate of the PTSD diagnostic outcome were not significantly different between the two groups. However, post hoc subgroup analyses showed that in participants with high drug adherence, at the 5-week posttrauma assessment, physiological reactivity was significantly lower during script-driven imagery in the propranolol than in the placebo subjects. The physiological results provide some limited support for a model of PTSD in which a traumatic conditioned response is reduced by posttrauma propranolol. However, the clinical results from this study do not support the preventive use of propranolol in the acute aftermath of a traumatic event.

Toward the Predeployment Detection of Risk for PTSD

ObjectiveTo evaluate the relationship among personality (according to Cloninger’s psychobiological model), posttraumatic stress disorder (PTSD) symptoms, trait resilience and quality of life (QoL) in people who were exposed to the Kiss nightclub fire.Methods188 participants were assessed with the Posttraumatic Checklist–civilian version (PCL-C), the Resilience Scale (RS), the Temperament and Character Inventory (TCI), the World Health Organization Quality of Life–Bref (WHOQOL-Bref), and the WHOQOL-100 Spirituality, religiousness, and personal beliefs (WHOQOL-100-SRPB). Data were analyzed in a dimensional approach, with correlation analysis, multiple linear regression and Structural Equation Modeling (SEM), with PCL-C, RS, and WHOQOL-Bref dimensions as dependent variables.ResultsMultiple linear regression showed that PTSD symptoms were predicted by harm avoidance (β = .34, p < .001), self-directedness (β = -.28, p < .01), and self-transcendence (β = .24, p < .01). Trait resilience was predicted by harm avoidance (β = -.38, p < .01), self-directedness (β = .20, p < .05), and self-transcendence (β = .18, p < .05). Also, PTSD symptoms had considerable negative effect on all dimensions of QoL. Self-transcendence was a positive predictor of subjective and spiritual QoL. SEM showed that QoL was predicted by PTSD symptoms (β = -.52, p < .001), trait resilience (β = .30, p < .001), cooperativeness (β = .135, p = 0.40), and self-directedness (β = .27, p < .01). The effect of self-directedness on QoL was mediated by PTSD symptoms and trait resilience. PTSD symptoms also mediated the relationship between trait resilience and QoL, and RS mediated the relationship of personality and PTSD symptoms.ConclusionThe study gives insights on prediction of PTSD severity, trait resilience and QoL from temperament and character traits, in a sample of people exposed to the Kiss nightclub fire. Harm avoidance was the most influent trait on PTSD symptoms and trait resilience. Self-directedness was the most import trait related to QoL, still that it was more related to PTSD severity than personality traits. Self-transcendence had positive effects on both PTSD symptoms and trait resilience, indicating a coping style that may coexist with psychopathology.

Hippocampal Volume Differences in Gulf War Veterans with Current Versus Lifetime Posttraumatic Stress Disorder Symptoms

We sought to identify common risk factors associated with posttraumatic stress disorder (PTSD) onset and course, including delayed, persistent, and remitted PTSD following a major traumatic exposure. Based on a prospective study of New York City adults following the World Trade Center disaster (WTCD), we conducted baseline interviews with 2,368 persons one year after this event and then at follow-up 1 year later to evaluate changes in current PTSD status based on DSM-IV criteria. Baseline analysis suggested that current PTSD, defined as present if this occurred in the past 12 months, was associated with females, younger adults, those with lower self-esteem, lower social support, higher WTCD exposure, more lifetime traumatic events, and those with a history of pre-WTCD depression. At follow-up, current PTSD was associated with Latinos, non-native born persons, those with lower self-esteem, more negative life events, more lifetime traumatic events, and those with mixed handedness. Classifying respondents at follow-up into resilient (no PTSD time 1 or 2), remitted (PTSD time 1, not 2), delayed (no PTSD time 1, but PTSD time 2), and persistent (PTSD both time 1 and 2) PTSD, revealed the following: compared to resilient cases, remitted ones were more likely to be female, have more negative life events, have greater lifetime traumatic events, and have pre-WTCD depression. Delayed cases were more likely to be Latino, be non-native born, have lower self-esteem, have more negative life events, have greater lifetime traumas, and have mixed handedness. Persistent cases had a similar profile as delayed, but were the only cases associated with greater WTCD exposures. They were also likely to have had a pre-WTCD depression diagnosis. Examination of WTCD-related PTSD at follow-up, more specifically, revealed a similar risk profile, except that handedness was no longer significant and WTCD exposure was now significant for both remitted and persistent cases. PTSD onset and course is complex and appears to be related to trauma exposure, individual predispositions, and external factors not directly related to the original traumatic event. This diagnostic classification may benefit from additional conceptualization and research as this relates to changes in PTSD status over time.

Post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) are associated with functional impairments, yet little is known about their influence on HIV pre-exposure prophylaxis (PrEP) motivation among women survivors of intimate partner violence (IPV). Understanding how PTSD and MDD symptoms influence PrEP motivation is particularly important given survivors of IPV have an increased risk for HIV acquisition. The present study assessed the association between PrEP motivation with latent profiles of PTSD and MDD symptoms among women survivors of IPV. Data were collected from a sample of 285 women from Baltimore, MD, and New Haven, CT. Latent profile analysis (LPA) was performed to identify distinct patterns of depressive and PTSD symptoms among women survivors of IPV. Binary logistic regression was performed to examine the association of profile membership on PrEP motivation. A six-profile solution was determined to best fit the data. Profiles were characterized by: Profile 1, very low depressive and very low PTSD symptoms (28.07%); Profile 2, average depressive symptoms and low (below the mean) PTSD symptoms (21.05%); Profile 3, high depressive symptoms and low (below the mean) PTSD symptoms (9.8%); Profile 4, moderate depressive symptoms and high PTSD symptoms (15.78%); Profile 5, high PTSD avoidance and average depressive symptoms (17.1%); Profile 6, high depressive and high PTSD symptoms (8%). We found that, the odds of being in Stage 3 of the PrEP Motivational Cascade (PrEParation; defined by having access to a medical provider to prescribe PrEP, be willing to take PrEP, and self-identifying as an appropriate candidate for PrEP) compared to Stage 1 of the PrEP Motivational Cascade (Precontemplation; defined by being eligible for PrEP, but not willing to take PrEP and/or not self-identifying as an appropriate candidate for PrEP) were lower for women assigned to the low depressive symptoms and low PTSD symptoms profile (Profile 1 of the LPA) compared to women in the high depressive symptoms and High PTSD symptoms profile (Profile 6 of the LPA, OR = 0.22, 95% CI = 0.06-0.76, p = 0.02). Women assigned to the low PTSD symptoms and average depressive symptoms profile (Profile 2 of the LPA) had lower odds of being in Stage 3 (PrEParation) compared to Stage 1 (Precontemplation) compared to women assigned to the high depressive symptoms and High PTSD symptoms profile (Profile 6 of the LPA, OR = 0.25, 95% CI = 0.07-0.92, p = 0.037). Women survivors of IPV with higher PTSD and MDD symptoms expressed greater motivation to engage in PrEP compared to women survivors with low PTSD and low MDD symptoms. Findings support the CDC's clinical PrEP recommendations to integrate depression screening into PrEP services, but there is a critical need to also include PTSD screening. Further, MDD and PTSD symptoms may present differential barriers to PrEP motivation among women survivors of IPV. Precision care could synchronize trauma-informed practices and mental health treatment to engage survivors in PrEP services.