The memory trace of an intrusive trauma-analog episode.

Intrusive memories are a core symptom of posttraumatic stress disorder. Compared with memories of everyday events, they are characterized by several seemingly contradictory features: intrusive memories contain distinct sensory and emotional details of the traumatic event and can be triggered by various perceptually similar cues, but they are poorly integrated into conceptual memory. Here, we conduct exploratory whole-brain analyses to investigate the neural representations of trauma-analog experiences and how they are reactivated during memory intrusions. We show that trauma-analog movies induce excessive processing and generalized representations in sensory areas but decreased blood-oxygen-level-dependent (BOLD) responses and highly distinct representations in conceptual/semantic areas. Intrusive memories activate generalized representations in sensory areas and reactivate memory traces specific to trauma-analog events in the anterior cingulate cortex. These findings provide the first evidence of how traumatic events could distort memory representations in the human brain, which may form the basis for future confirmatory research on the neural representations of traumatic experiences.

Psilocybe cubensis extract potently prevents fear memory recall and freezing behavior in short- but not long-term in a rat model of posttraumatic stress disorder.

Psilocybe cubensis is a species of psilocybin mushroom (magic mushroom) of moderate potency whose principal active compounds are psilocybin and psilocin. Recent studies have shown the significant procognitive and mood-enhancer effects of Psilocybe cubensis. However, evidence is so limited, especially in preclinical studies. We aimed to investigate the effect of Psilocybe cubensis extract on posttraumatic stress disorder (PTSD)-like behavior, pain perception, locomotor activity, and anxiety in a rat model of PTSD. Male rats were exposed to three consecutive shocks (0.8 mA, 3 s interval) paired with three sounds broadcasted 3 s before delivering shocks (75 dB, 3 s). After 1, 3, or 21 days, freezing rate was measured in the fear-conditioning apparatus. Open filed test and hot plate were used to assess locomotor activity and anxiety, and pain subthreshold, respectively. Psilocybe cubensis was injected intraperitoneal at the dose of 25 mg/kg (single administration) before (pretrain) or after (posttrain) shocks, or before the test (pretest). Results showed psilocybin potently alleviated PTSD symptom is short- but not long-term after the induction of PTSD. Psilocybe cubensis decreased locomotor activity only in a short period after administration. Psilocybe cubensis also increased pain subthreshold and decreased anxiety. In conclusion, Psilocybe cubensis effects on PTSD-like behavior and locomotor activity seem to be remained in short-term, while Psilocybe cubensis effects on pain subthreshold and anxiety remained long-term. This is the first study evaluating the effect of Psilocybe cubensis on PTSD-like behavior in rats in three different time protocols (1, 3, and 21 days after fear conditioning). (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Altered functional connectivity between cortical networks associated with inhibitory control in trauma-exposed females.

Post-traumatic stress disorder (PTSD) is associated with impaired inhibitory control and alterations in large-scale brain network connectivity. However, few studies to date have examined the construct of inhibitory control as it relates to resting-state functional connectivity (rsFC) in a population with PTSD or trauma-exposure. The present study investigated the relationship between impaired inhibitory control and rsFC within the default mode network (DMN), central executive network (CEN), and salience network (SN) in a sample of females exposed to interpersonal trauma with and without PTSD (n = 67). Participants completed a classic Color-Word Stroop task as a measure of inhibitory control and two resting-state fMRI scans. We conducted voxelwise rsFC analyses with seed regions in the DMN, CEN, and SN and voxelwise linear regression analyses to examine the relationship between inhibitory control and rsFC of these networks across the sample. Better Stroop performance was negatively associated with total self-reported PTSD symptoms. An analysis of PTSD symptom clusters indicated that better Stroop performance was also associated with re-experiencing and hyperarousal symptoms, but not avoidance PTSD symptoms. Decreased coupling between the CEN and the DMN was associated with better inhibitory control in this sample of trauma-exposed females. These findings lend support to the hypothesis that efficient switching between these networks may contribute to better performance on cognitive and attentional tasks in trauma-exposed individuals.

Impact of depression and post-traumatic stress on manual and oculomotor performance in service members with a history of mild TBI.

OBJECTIVE: To determine the impact of depression and post-traumatic stress on an automated oculomotor and manual measure of visual attention, compared to conventional neuropsychological assessment. Setting: Military traumatic brain injury (TBI) rehabilitation program. PARTICIPANTS: 188 Active Duty Service Members (ADSM) with a history of mild TBI. DESIGN: A cross-sectional and correlational study with data obtained through an IRB-approved data registry study. Main measures: Bethesda Eye & Attention Measure (BEAM); brief neuropsychological battery; self-reported symptom surveys including Neurobehavioral Symptom Inventory (NSI), Patient Health Questionnaire-8 (PHQ-8), and PTSD Checklist-5 (PCL-5). RESULTS: Small effect sizes were found for partial correlations between both depression and post-traumatic stress and key BEAM metrics. In contrast, small-to-medium effects sizes were found across all traditional neuropsychological test measures. CONCLUSION: This study illustrates the profile of impairments associated with depression and post-traumatic stress on saccadic eye movements and manual responses to BEAM relative to conventional neuropsychological tests. Results demonstrated that among ADSM seen for mTBI, depression and PTS exert a significant negative impact on measures of processing speed, attention, executive function, and memory across saccadic, manual, and conventional neuropsychological tests. However, the unique psychometric features of each of these assessment approaches may assist in distinguishing the effects of psychiatric comorbidities within this population.

Bilateral eye movements disrupt the involuntary perceptual representation of trauma-related memories.

Bilateral eye movement (EM) is a critical component in eye movement desensitization and reprocessing (EMDR), an effective treatment for post-traumatic stress disorder. However, the role of bilateral EM in alleviating trauma-related symptoms is unclear. Here we hypothesize that bilateral EM selectively disrupts the perceptual representation of traumatic memories. We used the trauma film paradigm as an analog for trauma experience. Nonclinical participants viewed trauma films followed by a bilateral EM intervention or a static Fixation period as a control. Perceptual and semantic memories for the film were assessed with different measures. Results showed a significant decrease in perceptual memory recognition shortly after the EM intervention and subsequently in the frequency and vividness of film-related memory intrusions across one week, relative to the Fixation condition. The EM intervention did not affect the explicit recognition of semantic memories, suggesting a dissociation between perceptual and semantic memory disruption. Furthermore, the EM intervention effectively reduced psychophysiological affective responses, including the skin conductance response and pupil size, to film scenes and subjective affective ratings of film-related intrusions. Together, bilateral EMs effectively reduce the perceptual representation and affective response of trauma-related memories. Further theoretical developments are needed to elucidate the mechanism of bilateral EMs in trauma treatment.

A Ventromedial Prefrontal-to-Lateral Entorhinal Cortex Pathway Modulates the Gain of Behavioral Responding During Threat.

BACKGROUND: The ability to correctly associate cues and contexts with threat is critical for survival, and the inability to do so can result in threat-related disorders such as posttraumatic stress disorder. The prefrontal cortex (PFC) and hippocampus are well known to play critical roles in cued and contextual threat memory processing. However, the circuits that mediate prefrontal-hippocampal modulation of context discrimination during cued threat processing are less understood. Here, we demonstrate the role of a previously unexplored projection from the ventromedial region of PFC (vmPFC) to the lateral entorhinal cortex (LEC) in modulating the gain of behavior in response to contextual information during threat retrieval and encoding. METHODS: We used optogenetics followed by in vivo calcium imaging in male C57/B6J mice to manipulate and monitor vmPFC-LEC activity in response to threat-associated cues in different contexts. We then investigated the inputs to, and outputs from, vmPFC-LEC cells using Rabies tracing and channelrhodopsin-assisted electrophysiology. RESULTS: vmPFC-LEC cells flexibly and bidirectionally shaped behavior during threat expression, shaping sensitivity to contextual information to increase or decrease the gain of behavioral output in response to a threatening or neutral context, respectively. CONCLUSIONS: Glutamatergic vmPFC-LEC cells are key players in behavioral gain control in response to contextual information during threat processing and may provide a future target for intervention in threat-based disorders.

The Neurophysiology Behind Trauma-Focused Therapy Modalities Used to Treat Post-Traumatic Stress Disorder Across the Life Course: A Systematic Review.

This review presents the current state of understanding of trauma-informed modalities in light of current research in neuroscience, analyzing which brain structures and processes are impacted by these modalities. Studies included in the present review met the inclusion criteria of 1) addressing post-traumatic stress disorder (PTSD) in a specific population, 2) treatment of PTSD using any of the evidence-based trauma-informed modalities considered in this review, and 3) presenting functional magnetic resonance imagery (fMRI) data, derived from BOLD signals and voxel-compression maps, of brain structures impacted by these trauma-informed modalities. Articles for this review were collated through PubMed and MEDLINE, using key terms in descending order, such as 'childhood trauma', 'adolescent trauma', and 'adulthood trauma', to 'PTSD', 'fMRI', and so on, depending on the modality in question. Based on these criteria and research methods, 37 studies remained for inclusion in the present review. Among a number of critical findings, this review demonstrates that eye movement desensitization and reprocessing (EMDR) and mindfulness therapy effectively deactivate hindbrain regions implicated in the downregulation of autonomic nervous system (ANS) hyperarousal. This review also shows that trauma-focused cognitive behavioral therapy (TF-CBT) and EMDR activate the hippocampus, anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), and orbitofrontal cortex (OFC)-areas that are implicated in crucial cognitive, affective, and behavioral processes that aid trauma survivors in navigating their challenges.

Assessing Dysfunctional Expectations in Posttraumatic Stress Disorder: Development and Validation of the Posttraumatic Expectations Scale (PTES).

Dysfunctional expectations are a particularly important subset of cognitions that influence the development and maintenance of various mental disorders. This study aimed to develop and validate a scale to assess dysfunctional expectations in posttraumatic stress disorder (PTSD), the "Posttraumatic Expectations Scale" (PTES). In a cross-sectional study, 70 PTSD patients completed the PTES, the Posttraumatic Cognitions Inventory (PTCI), as well as measures of the severity of symptoms of PTSD and depression. The results show that the PTES has excellent internal consistency and correlates significantly with the PTCI and PTSD symptom severity. A regression analysis revealed that the PTES explained variance of PTSD symptom severity above the PTCI, supporting the incremental validity of the PTES. While the original version of the PTES comprises 81 items, short scales were constructed using the BISCUIT (best items scales that are cross-validated, unit-weighted, informative and transparent) method. The current findings provide preliminary psychometric evidence suggesting that the PTES is an internally consistent and valid novel self-report measure in patients with PTSD. However, conclusions about the psychometric properties of the PTES are limited because of the absence of criterion-related validity, factor structure evidence, variability over time/response to intervention, and test-retest reliability. Future research should use the PTES in large-scale longitudinal studies to address these aspects to further validate the scale.

Impairments in Fear Extinction Memory and Basolateral Amygdala Plasticity in the TgF344-AD Rat Model of Alzheimer's Disease Are Distinct from Nonpathological Aging.

Fear-based disorders such as post-traumatic stress disorder (PTSD) steepen age-related cognitive decline and double the risk for developing Alzheimer's disease (AD). Because of the seemingly hyperactive properties of fear memories, PTSD symptoms can worsen with age. Perturbations in the synaptic circuitry supporting fear memory extinction are key neural substrates of PTSD. The basolateral amygdala (BLA) is a medial temporal lobe structure that is critical in the encoding, consolidation, and retrieval of fear memories. As little is known about fear extinction memory and BLA synaptic dysfunction within the context of aging and AD, the goal of this study was to investigate how fear extinction memory deficits and basal amygdaloid nucleus (BA) synaptic dysfunction differentially associate in nonpathologic aging and AD in the TgF344AD (TgAD) rat model of AD. Young, middle-aged, and older-aged WT and TgAD rats were trained on a delay fear conditioning and extinction procedure before ex vivo extracellular field potential recording experiments in the BA. Relative to young WT rats, long-term extinction memory was impaired, and in general, was associated with a hyperexcitable BA and impaired LTP in TgAD rats at all ages. In contrast, long-term extinction memory was impaired in aged WT rats and was associated with impaired LTP but not BA hyperexcitability. Interestingly, the middle-aged TgAD rats showed intact short-term extinction and BA LTP, which is suggestive of a compensatory mechanism, whereas differential neural recruitment in older-aged WT rats may have facilitated short-term extinction. As such, associations between fear extinction memory and amygdala deficits in nonpathologic aging and AD are dissociable.

Interleukine-17 Modulates Neurogenesis and Behavior Following Exposure to Trauma in Mice.

Post-traumatic stress disorder (PTSD) is a psychiatric disorder accompanied by deficits in cognitive and social skills. Adult hippocampal neurogenesis is a lifelong phenomenon, with new neurons being formed in the granular cell layer of the dentate gyrus. Impaired neurogenesis is associated with multiple behavioral disorders including Alzheimer's disease and schizophrenia. PTSD patients often present hippocampal atrophy and animal models clearly present impaired neurogenesis. Previous studies on PTSD patients demonstrated elevated levels of Th17 cells and plasma levels of the pro-inflammatory cytokine interleukin-17A (IL-17A). Since IL-17A can impair neurogenesis in mice, we thus hypothesized that decreasing the serum levels of IL-17A will increase hippocampal neurogenesis and alleviate symptoms in a murine model of PTSD. Surprisingly, our results showed that attempting to neutralize IL-17A with an antibody resulted in increased serum levels of IL-17A, while targeting IL-23, the upstream regulator of IL-17, did lower the levels of IL-17A in trauma-exposed mice. As expected, increased levels of serum IL-17A (in anti-IL-17A treated mice) resulted in impaired neurogenesis, reflected by reduced number of proliferating Ki67+ neural progenitors and newly formed DCX+ neurons, which was correlated with increased expression of Hes1. Nevertheless, increased maturation was noted by the expression of Slit2 and Ache. In contrast, treatment with anti-IL-23 indeed resulted in increased neurogenesis. Behaviorally, both treatments did not affect trauma-related freezing behavior but did affect trauma-related social deficits. Unexpectedly, increased levels of serum IL-17A (in anti-IL-17A treated mice) prevented social deficits in trauma-exposed mice while anti-IL-23 exacerbated these deficits. We thus conclude that IL-17 is involved in regulating neurogenesis following exposure to stress but may be important in maintaining social behavior.

Utility of 7,8-dihydroxyflavone in preventing astrocytic and synaptic deficits in the hippocampus elicited by PTSD.

Astrocytic functions and brain-derived neurotrophic factor (BDNF)-tyrosine kinase receptor B (TrkB) signaling pathways are impaired in stress-related neuropsychiatric diseases. Previous studies have reported neuroprotective effects of 7,8-dihydroxyflavone (7,8-DHF), a TrkB activator. Here, we investigated the molecular mechanisms underlying pathogenesis of post-traumatic stress disorder (PTSD) using a modified single-prolonged stress (SPS&S) model and the potential beneficial effects of 7,8-DHF. SPS&S reduced the hippocampal expression of glial fibrillary acidic protein (GFAP), a marker of astrocytes, and induced morphological changes in astrocytes. From the perspective of synaptic function, the SPS&S model displayed reduced expression of BDNF, p-TrkB, postsynaptic density protein 95 (PSD95), AMPA receptor subunit GluR1 (GluA1), NMDA receptor subunit N2A/N2B ratio, calpain-1, phosphorylated protein kinase B (Akt) and phosphorylated mammalian target of rapamycin (mTOR) and conversely, higher phosphatase and tension homolog (PTEN) expression in the hippocampus. Acute or continuous intraperitoneal administration of 7,8-DHF (5 mg/kg) after SPS&S procedures prevented SPS&S-induced fear memory generalization and anxiety-like behaviors as well as abnormalities of hippocampal oscillations. Most importantly, 7,8-DHF attenuated SPS&S-induced abnormal BDNF-TrkB signaling and calpain-1-dependent cascade of synaptic deficits. Furthermore, treatment with a TrkB inhibitor completely blocked while an mTOR inhibitor partially blocked the effects of 7,8-DHF on behavioral changes of SPS&S model mice. Our collective findings suggest that 7,8-DHF effectively alleviates PTSD-like symptoms, including fear generalization and anxiety-like behavior, potentially by preventing astrocytic and synaptic deficits in the hippocampus through targeting of TrkB.

Functional MRI-based study of emotional experience in patients with psychogenic non-epileptic seizures: Protocol for an observational case-control study-EMOCRISES study.

BACKGROUND: Psychogenic non epileptic seizures (PNES) are a frequent, disabling and costly disorder for which there is no consensual caring. They are considered as a dissociative disorder and they share many common characteristics with post-traumatic stress disorder (PTSD). Nevertheless, their pathophysiology is still unclear. In this study, we plan to obtain new data comparing functional brain activity of participants suffering from PNES, from PTSD and healthy controls via functional brain MRI during resting state and under emotional visual stimulation. The protocol presented hereunder describes an observational study with no direct treatment implication. Nevertheless, it could lead to a better understanding of PNES and to identifying targets for specialised cares of post-traumatic or dissociative disorders, like repetitive transcranial magnetic stimulation. METHODS & ANALYSIS: This is a prospective, single-centre, interventional, non-randomized, open, controlled and exploratory clinical study. It will involve 75 adult French, right-handed women in 3 groups, either suffering from PNES or PTSD, or healthy controls. An informed consent will be signed by each participant. All of them will be given psychiatric tests to assess dissociation and alexithymia, psychopathological profile and history, and emotional recognition. Each participant will undergo a functional brain MRI. We will record anatomical images and five functional imaging sequences including emotional periodic oscillatory stimulation, standard emotional stimulation, Go / No Go task under emotional stimulation, and resting state. Analysis will include a descriptive analysis of all participants and the treatment for functional magnetic resonance imaging images of each sequence. REGISTRATION, ETHICS & DISSEMINATION: This study was approved the regional Protection of Persons Committee under the reference 16.10.01 and by the French National Medical Security Agency under the reference 2016-A01295-46. The protocol and results will be published in peer-reviewed academic medical journals and disseminated to research teams, databases, specialised media and concerned patients' organisations.

Propofol improves learning and memory in post-traumatic stress disorder (PTSD) mice via recovering hippocampus synaptic plasticity.

AIMS: Propofol, the most commonly used intravenous anesthetic, is known for its protective effect in various human and animal disease models such as post-traumatic stress disease (PTSD). However, it still needs efforts to clarify the effect of propofol on fear memory extinction and the relevant mechanisms. METHODS: Fear memory extinction was examined in PTSD mice model. Thirty-six mice were randomly divided into three groups: a shock + propofol group (sh + Pro), shock + normal saline group (sh + NS), and sham group. The mice were treated with propofol (150 mg/kg) or normal saline (of the same volume) intraperitoneally 30 min after the conditioning. These mice's behavior was analysed with contextual test, sucrose preference test (SPT) and Morris water maze (MWM). Additionally, the synaptic plasticity of the hippocampus was examined by long-term potentiation (LTP) and long-term depression (LTD). KEY FINDINGS: Compared with the sham group, the sh + NS group showed increased freezing time and depressive behavior, meanwhile the sh + Pro group showed minor behavioral changes. What's more, we found that propofol rescued the impaired long-term potentiation (LTP) and long-term depression (LTD) in hippocampus of PTSD mice. All these suggest that propofol can accelerate fear memory extinction and change synaptic plasticity of PTSD mice. SIGNIFICANCE: The study proved that propofol can protect the mice from PTSD by reserving synaptic plasticity and brought a new insight into PTSD treatment indicating that propofol maybe a potential cure for PTSD.

Associations between telomere length and symptoms of posttraumatic stress disorder and appetitive aggression in trauma-exposed men.

Exposure to community violence is common in South Africa and negatively impacts on biopsychosocial health. Posttraumatic stress disorder (PTSD) is characterised by symptoms of intrusion, avoidance, hypervigilance and negative alterations in cognition and mood, and can develop consequent to trauma exposure. Individuals who repeatedly experience and witness violence may also come to view it as appealing and rewarding. This appetitive aggression (AA) increases the likelihood of perpetrating violence. Telomeres are repetitive nucleotide sequences that protect the ends of chromosomes. Telomere length (TL) attrition is a stress-sensitive marker of biological aging that has been associated with a range of psychiatric disorders. This study investigated the cross-sectional relationship between TL and symptoms of PTSD and AA in South African men residing in areas with high community violence. PTSD and AA symptom severity was assessed in 290 men using the Posttraumatic Stress Disorder Symptom Scale - Interview (PSS-I) and Appetitive Aggression Scale (AAS), respectively. Quantitative polymerase chain reaction was performed on DNA extracted from saliva and used to calculate relative TL (rTL). Regression models were used to assess the relationships between rTL and PSS-I and AAS scores. Network analyses using EBIC glasso methods were performed using rTL and items from each of the AAS and PSS-I measures. Both PSS-I (p = 0.023) and AAS (p = 0.016) scores were positively associated with rTL. Network analyses indicated that rTL was weakly related to two PSS-I and five AAS items but performed poorly on indicators of centrality and was not strongly associated with measure items either directly or indirectly. The positive association between rTL and measures of AA and PTSD may be due to the induction of protective homeostatic mechanisms, which reduce TL attrition, following early life trauma exposure.

Neurocircuitry basis of the opioid use disorder-post-traumatic stress disorder comorbid state: conceptual analyses using a dimensional framework.

Understanding the interface between opioid use disorder (OUD) and post-traumatic stress disorder (PTSD) is challenging. By use of a dimensional framework, such as research domain criteria, convergent and targetable neurobiological processes in OUD-PTSD comorbidity can be identified. We hypothesise that, in OUD-PTSD, circuitry that is implicated in two research domain criteria systems (ie, negative valence and cognitive control) underpins dysregulation of incentive salience, negative emotionality, and executive function. We also propose that the OUD-PTSD state might be systematically investigated with approaches outlined within a neuroclinical assessment framework for addictions and PTSD. Our dimensional analysis of the OUD-PTSD state shows how first-line therapeutic approaches (ie, partial µ-type opioid receptor [MOR1] agonism) modulate overlapping neurobiological and clinical features and also provides mechanistic rationale for evaluating polytherapeutic strategies (ie, partial MOR1 agonism, κ-type opioid receptor [KOR1] antagonism, and α-2A adrenergic receptor [ADRA2A] agonism). A combination of these therapeutic mechanisms is projected to facilitate recovery in patients with OUD-PTSD by mitigating negative valence states and enhancing executive control.

Inescapable footshocks induce molecular changes in the prefrontal cortex of rats in an amyloid-beta-42 model of Alzheimer's disease.

Alzheimer's disease (AD) affects several brain areas, including the prefrontal cortex (PFC) involved in execution, working memory, and fear extinction. Despite these critical roles, the PFC is understudied in AD pathology. People with post-traumatic stress disorder (PTSD) have twice the risk of developing AD, and the underlying mechanisms linking these two diseases are less understood. Here, we investigated the effect of footshock stress on behavioural vis-a-vis molecular changes in the PFC of an amyloid-beta (Aß)-42 lesion rat model of AD. Trauma-like conditions were induced by exposing the animals to several footshocks. AD-like condition was induced via intra-hippocampal injection of Aß-42 peptide. Following Aß-42 injections, animals were tested for behavioural changes using the Open Field Test (OFT) and Y-maze test. The PFC was later harvested for neurochemical analyses. Our results showed an interactive effect of footshocks and Aß-42 lesion on: reduced percentage alternation in the Y-maze test, suggesting memory impairment; reduced number of line crosses and time spent in the centre square of the OFT, indicating anxiogenic responses. Similarly, there was an interactive effect of footshocks and Aß-42 lesion on: increased FK506 binding protein 51 (FKBP5) expression, which can be associated with stress-induced anxiogenic behaviours; and increased neuronal apoptosis in the PFC of the animals. In addition, footshocks, as well as Aß-42 lesion, reduced superoxide dismutase levels and Bridging Integrator-1 (BIN1) expression in the PFC of the animals, which can be linked to the observed memory impairment. In conclusion, our findings indicate that footshocks exaggerate PFC-associated behavioural and molecular changes induced by an AD-like pathology.

Complex PTSD in survivors of intimate partner violence: risk factors related to symptoms and diagnoses.

Background: In 2018, the World Health Organization proposed a new diagnosis entitled Complex Posttraumatic Stress Disorder (CPTSD) in the ICD-11. It is a diagnosis that encompasses the classic symptoms of PTSD, along with symptoms of disturbances in self-organization (DSO). Although this disorder has been studied in several countries and populations, research on the population of women survivors of intimate partner violence (IPV) is scarce. Objectives: 1) To analyse the prevalence of CPTSD and PTSD according to ICD-11 criteria; 2) To analyse the associations between CPTSD symptomatology and severity of violence, level of fear, resilience and strategies of emotion regulation; 3) To analyse which risk factors (severity of violence, level of fear, resilience and strategies of emotion regulation) may differ between female survivors with CPTSD or PTSD. Method: 162 women IPV survivors who completed a socio-demographic and violence-related interview, as well as questionnaires to assess PTSD and CPTSD, severity of violence, resilience and emotion regulation strategies. Results: The results showed a higher prevalence of CPTSD (39.50%), compared to PTSD (17.90%). Moreover, a high level of fear was related to re-experiencing in the here and now, avoidance, current sense of threat and disturbances in relationships. Low levels of resilience and maladaptive emotion regulation strategies such as expressive suppression were related to affective dysregulation, negative self-concept and disturbances in relationships. Finally, the results showed that maladaptive emotion regulation strategies differentiated between meeting CPTSD and PTSD criteria in women survivors of IPV. Conclusion: The findings of this study indicated that CPTSD was twice as prevalent as PTSD within the sample. Moreover, maladaptive emotion regulation strategy as expressive suppression was the main variable related to experiencing CPTSD, in contrast to PTSD. These findings may have important implications for the design of specific treatments aimed at women survivors of IPV, who also suffer CPTSD.

Antecedentes: En 2018, la Organización Mundial de la Salud propuso en la CIE-11 un nuevo diagnóstico denominado trastorno de estrés postraumático complejo (TEPTC). Se trata de un diagnóstico que engloba los síntomas clásicos del TEPT y los síntomas de alteraciones de la auto-organización (AAO). Aunque este trastorno se ha estudiado en varios países y poblaciones, la investigación en la población de mujeres supervivientes de violencia de género (VG) es escasa.Objetivos: 1) Analizar los porcentajes de TEPTC y TEPT según los criterios de CIE-11; 2) Analizar las asociaciones entre los síntomas de TEPTC con la gravedad de la violencia, nivel de miedo, resiliencia y estrategias de regulación emocional; 3) Analizar qué factores de riesgo (gravedad de la violencia, nivel de miedo, resiliencia y estrategias de regulación emocional) diferencian entre sufrir TEPTC o TEPT en mujeres supervivientes de VG.Método: Las participantes fueron 162 mujeres supervivientes de VG que completaron una entrevista sociodemográfica y de violencia, así como cuestionarios para evaluar el TEPT y el TEPTC, gravedad de la violencia, resiliencia y estrategias de regulación emocional.Resultados: Los resultados mostraron una mayor prevalencia de TEPTC (39,50%) que de TEPT (17,90%). Además, un alto nivel de miedo se relacionó con la reexperimentación en el aquí y ahora, evitación, sensación actual de amenaza y alteraciones en las relaciones. Bajos niveles de resiliencia y estrategias desadaptativas de regulación emocional como la supresión de la expresión, se relacionaron con los síntomas de desregulación afectiva, autoconcepto negativo y alteraciones en las relaciones. Por último, los resultados mostraron que las estrategias desadaptativas de regulación emocional diferenciaban entre cumplir los criterios de TEPTC y TEPT en mujeres supervivientes de VG.Conclusión: Este estudio mostró que el TEPTC es dos veces más prevalente que el TEPT en la presente muestra de mujeres supervivientes de VG. Además, la estrategia desadaptativa de regulación emocional de supresión de la expresión fue la principal variable relacionada con presentar TEPTC en contraste con el TEPT. Estos hallazgos podrían tener importantes implicaciones para el diseño de tratamientos específicos dirigidos a las mujeres supervivientes de VG que sufren TEPTC.

DSM-5-TR prolonged grief disorder and DSM-5 posttraumatic stress disorder are related, yet distinct: confirmatory factor analyses in traumatically bereaved people.

Background: Prolonged grief disorder (PGD) is newly included in the text revision of the DSM-5 (DSM-5-TR). So far, it is unknown if DSM-5-TR PGD is distinguishable from bereavement-related posttraumatic stress disorder (PTSD). Prior research examining the distinctiveness of PTSD and pathological grief focused on non-traumatic loss samples, used outdated conceptualizations of grief disorders, and has provided mixed results. Objective: In a large sample of traumatically bereaved people, we first evaluated the factor structure of PTSD and PGD separately and then evaluated the factor structure when combining PTSD and PGD symptoms to examine the distinctiveness between the two syndromes. Methods: Self-reported data were used from 468 people bereaved due to the MH17 plane disaster (N = 200) or a traffic accident (N = 268). The 10 DSM-5-TR PGD symptoms were assessed with the Traumatic Grief Inventory-Self Report Plus (TGI-SR+). The 20-item Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5) was used to tap PTSD symptoms. Confirmatory factor analyses were conducted. Results: For PTSD, a seven factor, so-called 'Hybrid' model yielded the best fit. For PGD, a univariate factor model fits the data well. A combined model with PGD items loading on one factor and PTSD items on seven factors (associations between PGD and PTSD subscales r ≥ .50 and ≤.71), plus a higher-order factor (i.e. PTSD factors on a higher-order PTSD factor) (association between higher-order PTSD factor and PGD factor r = .82) exhibited a better fit than a model with all PGD and PTSD symptom loading on a single factor or two factors (i.e. one for PGD and one for PTSD). Conclusions: This is the first study examining the factor structure of DSM-5-TR PGD and DSM-5 PTSD in people confronted with a traumatic loss. The findings provide support that PGD constitutes a syndrome distinguishable from, yet related with, PTSD.

Antecedentes: El trastorno de duelo prolongado (PGD en su sigla en inglés) se incluyó recientemente en la revisión del texto del DSM-5 (DSM-5-TR). Hasta ahora, se desconoce si el PGD del DSM-5-TR se puede distinguir del trastorno de estrés postraumático (TEPT) relacionado con el duelo. Investigaciones anteriores que examinaron el carácter distintivo del trastorno de estrés postraumático y el duelo patológico se centraron en muestras con pérdidas no traumáticas, utilizaron conceptualizaciones obsoletas de los trastornos del duelo y arrojaron resultados mixtos.Objetivo: En una muestra grande de personas en duelo traumático, primero evaluamos la estructura factorial de TEPT y PGD por separado y luego evaluamos la estructura factorial al combinar los síntomas de TEPT y PGD para examinar la distinción entre los dos síndromes.Métodos: Se utilizaron datos autoreportados de 468 personas en duelo debido al desastre del avión MH17 (N = 200) o un accidente de tráfico (N = 268). Los 10 síntomas de PGD del DSM-5-TR se evaluaron con el Inventario de Autoreporte de Duelo Traumático Plus (TGI-SR +). Se utilizó la lista de chequeo de 20 ítems para el trastorno de estrés postraumático para el DSM-5 (PCL-5) para examinar los síntomas del TEPT. Se realizaron análisis factoriales confirmatorios.Resultados: Para el TEPT, un modelo de siete factores, llamado modelo 'híbrido', produjo el mejor ajuste. Para el PGD, un modelo de factor univariado se ajusta bien a los datos. Un modelo combinado con elementos de PGD que cargan en un factor y elementos de TEPT en siete factores (asociaciones entre las subescalas de PGD y TEPT r ≥ 50 y ≤ .71), más un factor de orden superior (es decir, factores de TEPT en un factor de TEPT de orden superior)) (asociación entre el factor TEPT de orden superior y el factor PGD r = .82) mostró un mejor ajuste que un modelo con toda la carga de síntomas de PGD y TEPT en un solo factor o dos factores (es decir, uno para PGD y otro para TEPT).Conclusiones: Este es el primer estudio que examina la estructura factorial del PGD según DSM-5-TR y el TEPT según DSM-5 en personas que enfrentan una pérdida traumática. Los hallazgos respaldan que el PGD constituye un síndrome que se distingue del TEPT, pero que está relacionado con él.

New Metabolic, Digestive, and Oxidative Stress-Related Manifestations Associated with Posttraumatic Stress Disorder.

Posttraumatic stress disorder (PTSD) represents a pressing and generally invalidating syndrome that is triggered by a terrifying or stressful experience, relying on recurrently reliving the traumatic event feelings associated to it, which is subsequently linked to ongoing activations of stress-related neurobiological pathways and is often associated with neurodegeneration. In this paper, we examine what lies beneath this disorder, reviewing evidence that connects PTSD with a wide array of mechanisms and its intertwined pathways that can lead to the decompensation of different pathologies, such as cardiovascular disease, gastrointestinal ailments, autoimmune disorders, and endocrine diseases. Also, the significance of the oxidative stress in this frame of reference is debated. Thus, knowing and identifying the main features of the distressing experience, the circumstances around it, as well as the neuropsychological and emotional characteristics of people prone to develop PTSD after going through disturbing incidents can offer an opportunity to anticipate the development of potential destructive consequences in several psychological dimensions: cognitive, affective, relational, behavioral, and somatic. We can also observe more closely the intricate connections of the disorder to other pathologies and their underlying mechanisms such as inflammation, oxidative stress, bacterial overgrowth syndrome, irritable bowel syndrome, metabolic disorders, oxytocin, and cortisol in order to understand it better and to optimize the course of treatment and its management. The complex foundation PTSD possesses is supported by the existing clinical, preclinical, and experimental data encompassed in the current review. Different biological systems and processes such as the hypothalamic-pituitary-adrenal axis, sympathetic nervous system, oxidative stress, inflammation, and microbiome suffer modifications and changes when it comes to PTSD; that is why targeted therapies exert tremendous alleviations of symptoms in patients diagnosed with this disorder. Therefore, this implies that PTSD is not restricted to the psychiatric domain and should be viewed as a systemic condition.