ABSTRACT
The neurocardiac circuit is integral to physiological regulation of threat and trauma-related responses. However, few direct investigations of brain-behavior associations with replicable physiological markers of PTSD have been conducted. The current study probed the neurocardiac circuit by examining associations among its core regions in the brain (e.g., insula, hypothalamus) and the periphery (heart rate [HR], high frequency heart rate variability [HF-HRV], and blood pressure [BP]). We sought to characterize these associations and to determine whether there were differences by PTSD status. Participants were N = 315 (64.1 % female) trauma-exposed adults enrolled from emergency departments as part of the prospective AURORA study. Participants completed a deep phenotyping session (e.g., fear conditioning, magnetic resonance imaging) two weeks after emergency department admission. Voxelwise analyses revealed several significant interactions between PTSD severity 8-weeks posttrauma and psychophysiological recordings on hypothalamic connectivity to the prefrontal cortex (PFC), insula, superior temporal sulcus, and temporoparietaloccipital junction. Among those with PTSD, diastolic BP was directly correlated with right insula-hypothalamic connectivity, whereas the reverse was found for those without PTSD. PTSD status moderated the association between systolic BP, HR, and HF-HRV and hypothalamic connectivity in the same direction. While preliminary, our findings may suggest that individuals with higher PTSD severity exhibit compensatory neural mechanisms to down-regulate autonomic imbalance. Additional study is warranted to determine how underlying mechanisms (e.g., inflammation) may disrupt the neurocardiac circuit and increase cardiometabolic disease risk in PTSD.
Subject(s)
Blood Pressure , Heart Rate , Magnetic Resonance Imaging , Stress Disorders, Post-Traumatic , Humans , Stress Disorders, Post-Traumatic/physiopathology , Stress Disorders, Post-Traumatic/diagnostic imaging , Female , Male , Adult , Heart Rate/physiology , Blood Pressure/physiology , Hypothalamus/physiopathology , Hypothalamus/diagnostic imaging , Middle Aged , Young Adult , Cerebral Cortex/diagnostic imaging , Cerebral Cortex/physiopathology , Psychological Trauma/physiopathology , Psychological Trauma/diagnostic imagingABSTRACT
Objective: The purpose of this article is to provide a narrative review synthesizing the literature on differences between women and men in relationships among certain stressors associated with immune system activation and their relationship to cognitive dysfunction and dementia. Method: We review the cycle of stress leading to neuroinflammation via cortisol and neurochemical alterations, cell-mediated immune system activation, and pro-inflammatory cytokines, and how this is implicated in the development of dementia. We follow this by discussing sex differences in stress physiology and immune function. We then review the work on early life adversity (ELA) and adverse childhood experiences (ACEs), post-traumatic stress disorder, acute medical stressors, and their associations with cognitive dysfunction and dementia. Throughout, we emphasize women's presentations and issues unique to women (e.g. trauma disorder prevalence). Conclusions: There is a need for more mechanistic and longitudinal studies that consider trauma accumulation, both physical and emotional, as well as a greater focus on traumas more likely to occur in women (e.g. sexual abuse), and their relationship to early cognitive decline and dementia.
Subject(s)
Dementia , Sex Characteristics , Humans , Dementia/immunology , Dementia/etiology , Female , Male , Psychological Trauma/immunology , Psychological Trauma/physiopathology , Stress, Psychological/immunology , Cognitive Dysfunction/etiology , Cognitive Dysfunction/physiopathology , Cognitive Dysfunction/immunology , Immune System , Stress Disorders, Post-Traumatic/immunology , Stress Disorders, Post-Traumatic/epidemiology , Stress Disorders, Post-Traumatic/physiopathology , Adverse Childhood ExperiencesABSTRACT
BACKGROUND: Traumatic experiences during childhood significantly impact the developing brain and contribute to the development of numerous physical and mental health problems. To date, however, a comprehensive understanding of the functional impairments within the brain associated with childhood trauma histories does not exist. Previous functional magnetic resonance imaging (fMRI) meta-analytical tools required homogeneity of task types and the clinical populations studied, thus preventing the comprehensive pooling of brain-based deficits present in children who have trauma histories. We hypothesized that the use of the novel, data-driven Bayesian author-topic model approach to fMRI meta-analyses would reveal deficits in brain networks that span fMRI task types in children with trauma histories. METHODS: To our knowledge, this is the first study to use the Bayesian author-topic model approach to fMRI meta-analyses within a clinical population. Using PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we present data-driven results obtained by combining activation patterns across heterogeneous tasks from 1428 initially screened studies and combining data from 14 studies that met study criteria (285 children with trauma histories, 297 healthy control children). RESULTS: Altered brain activity was revealed within 2 clusters in children with trauma histories compared to control children: the default mode/affective network/posterior insula and the central executive network. Our identified clusters were associated with tasks pertaining to cognitive processing, emotional/social stress, self-referential thought, memory, unexpected stimuli, and avoidance behaviors in youths who have experienced childhood trauma. CONCLUSIONS: Our results reveal disturbances in children with trauma histories within the modulation of the default mode and central executive networks-but not the salience network-regardless of whether children also presented with posttraumatic stress symptoms.
Subject(s)
Brain , Magnetic Resonance Imaging , Humans , Child , Brain/physiopathology , Brain/diagnostic imaging , Adverse Childhood Experiences , Bayes Theorem , Psychological Trauma/physiopathology , Psychological Trauma/diagnostic imaging , Adolescent , Nerve Net/physiopathology , Nerve Net/diagnostic imagingABSTRACT
BACKGROUND AND HYPOTHESES: Affective recovery, operationalized as the time needed for affect to return to baseline levels after daily stressors, may be a putative momentary representation of resilience. This study aimed to investigate affective recovery in positive and negative affect across subclinical and clinical stages of psychosis and whether this is associated with exposure to childhood trauma (sexual, physical, and emotional abuse). STUDY DESIGN: We used survival analysis to predict the time-to-recovery from a daily event-related stressor in a pooled sample of 3 previously conducted experience sampling studies including 113 individuals with first-episode psychosis, 162 at-risk individuals, and 94 controls. STUDY RESULTS: Negative affective recovery (ie, return to baseline following an increase in negative affect) was longer in individuals with first-episode psychosis compared with controls (hazard ratio [HR]â =â 1.71, 95% confidence interval [CI; 1.03, 2.61], Pâ =â .04) and in at-risk individuals exposed to high vs low levels of emotional abuse (HRâ =â 1.31, 95% CI [1.06, 1.62], Pâ =â .01). Positive affective recovery (ie, return to baseline following a decrease in positive affect) did not differ between groups and was not associated with childhood trauma. CONCLUSIONS: Our results give first indications that negative affective recovery may be a putative momentary representation of resilience across stages of psychosis and may be amplified in at-risk individuals with prior experiences of emotional abuse. Understanding how affective recovery contributes to the development of psychosis may help identify new targets for prevention and intervention to buffer risk or foster resilience in daily life.
Subject(s)
Adverse Childhood Experiences , Ecological Momentary Assessment , Psychotic Disorders , Humans , Psychotic Disorders/physiopathology , Female , Male , Adult , Young Adult , Adverse Childhood Experiences/statistics & numerical data , Adolescent , Resilience, Psychological , Affect/physiology , Adult Survivors of Child Abuse , Adult Survivors of Child Adverse Events/statistics & numerical data , Stress, Psychological/physiopathology , Affective Symptoms/physiopathology , Affective Symptoms/etiology , Emotional Abuse/statistics & numerical data , Psychological Trauma/physiopathologyABSTRACT
INTRODUCTION: The relationship between interpersonal trauma and psychosis is well established, and research is now focused on identifying mechanisms that may explain this relationship. Models of trauma and psychosis increasingly emphasize a broad range of affective processes, yet the overall effect of these affective processes is not well understood. AIM: This review systematically examined the effect of any form of long-term affective dysfunction on the relationship between interpersonal trauma and psychosis. Where possible, it used meta-analytic techniques to quantify the overall magnitude of this effect. METHOD: Searches were conducted using PsychINFO, MEDLINE and CINAHL databases, and eligible studies were appraised for methodological quality. Narrative synthesis and meta-analytic methods were used to evaluate evidence. RESULTS: Twenty-nine studies met criteria for inclusion. Five affective mediators were found; depression, anxiety, affective dysregulation, loneliness and attachment. Findings from both the narrative synthesis (n = 29) and meta-analysis (n = 8) indicated that, overall, affect is a small but significant mediator of the relationship between interpersonal trauma and psychosis (pooled Cohen's d = 0.178; pooled 95 % CI: 0.022-0.334). CONCLUSIONS: Overall, findings support affective pathways to psychosis, though highlight the need for further research on broader affective mediators (loneliness, shame). The small effect size found in the meta-analysis also points to the potential importance of non-affective mediators. Clinically, these findings highlight the value of treatment modalities that attend to multiple mechanisms in the relationship between interpersonal trauma and psychosis. Future research should focus on the interplay and causal sequence between these mechanisms to further understand pathways between interpersonal trauma and psychosis.
Subject(s)
Interpersonal Relations , Psychotic Disorders , Humans , Psychotic Disorders/physiopathology , Psychological Trauma/physiopathology , Object Attachment , Affect/physiologyABSTRACT
ABSTRACT: Urologic chronic pelvic pain syndrome (UCPPS) is a complex, debilitating condition in which patients often report nonpelvic pain in addition to localized pelvic pain. Understanding differential predictors of pelvic pain only vs widespread pain may provide novel pathways for intervention. This study leveraged baseline data from the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network's Symptom Pattern Study to investigate the impact of childhood sexual and nonsexual violent trauma on pelvic and nonpelvic pain sensitivity among adult patients with UCPPS, as well as potential mediators of this association. Study participants who met inclusion criteria for UCPPS completed questionnaires assessing childhood and recent trauma, affective distress, cognitive dysfunction, and generalized sensory sensitivity. Experimental pain sensitivity was also evaluated using standardized pressure pain applied to the pubic region and the arm. Bivariate analyses showed that childhood violent trauma was associated with more nonviolent childhood trauma, more recent trauma, poorer adult functioning, and greater pain sensitivity at the pubic region, but not pain sensitivity at the arm. Path analysis suggested that childhood violent trauma was indirectly associated with pain sensitivity at both sites and that this indirect association was primarily mediated by generalized sensory sensitivity. More experiences of recent trauma also contributed to these indirect effects. The findings suggest that, among participants with UCPPS, childhood violent trauma may be associated with heightened pain sensitivity to the extent that trauma history is associated with a subsequent increase in generalized sensory sensitivity.
Subject(s)
Adverse Childhood Experiences , Chronic Pain , Pain Threshold , Pelvic Pain , Psychological Trauma , Sexual Trauma , Adult , Child , Female , Humans , Male , Middle Aged , Adverse Childhood Experiences/psychology , Chronic Pain/diagnosis , Chronic Pain/physiopathology , Chronic Pain/psychology , Pain Threshold/physiology , Pelvic Pain/diagnosis , Pelvic Pain/physiopathology , Pelvic Pain/psychology , Psychological Trauma/physiopathology , Sexual Trauma/physiopathologyABSTRACT
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.
Subject(s)
Eye Movements , Memory , Psychological Trauma , Visual Perception , Eye Movements/physiology , Memory/physiology , Psychological Trauma/physiopathology , Humans , Affect , Male , Female , Adolescent , Young Adult , Adult , Self Report , Surveys and Questionnaires , Emotions , Visual Perception/physiology , Recognition, Psychology/physiology , Fixation, Ocular/physiology , Eye Movement Desensitization Reprocessing , Stress Disorders, Post-Traumatic/physiopathologyABSTRACT
In humans, traumatic social experiences can contribute to psychiatric disorders1. It is suggested that social trauma impairs brain reward function such that social behaviour is no longer rewarding, leading to severe social avoidance2,3. In rodents, the chronic social defeat stress (CSDS) model has been used to understand the neurobiology underlying stress susceptibility versus resilience following social trauma, yet little is known regarding its impact on social reward4,5. Here we show that, following CSDS, a subset of male and female mice, termed susceptible (SUS), avoid social interaction with non-aggressive, same-sex juvenile C57BL/6J mice and do not develop context-dependent social reward following encounters with them. Non-social stressors have no effect on social reward in either sex. Next, using whole-brain Fos mapping, in vivo Ca2+ imaging and whole-cell recordings, we identified a population of stress/threat-responsive lateral septum neurotensin (NTLS) neurons that are activated by juvenile social interactions only in SUS mice, but not in resilient or unstressed control mice. Optogenetic or chemogenetic manipulation of NTLS neurons and their downstream connections modulates social interaction and social reward. Together, these data suggest that previously rewarding social targets are possibly perceived as social threats in SUS mice, resulting from hyperactive NTLS neurons that occlude social reward processing.
Subject(s)
Neural Pathways , Psychological Trauma , Reward , Septal Nuclei , Social Behavior , Stress, Psychological , Animals , Female , Male , Mice , Brain/pathology , Brain/physiopathology , Calcium/analysis , Calcium/metabolism , Mice, Inbred C57BL , Neurons/metabolism , Neurotensin/metabolism , Optogenetics , Psychological Trauma/pathology , Psychological Trauma/physiopathology , Septal Nuclei/pathology , Septal Nuclei/physiopathology , Stress, Psychological/pathology , Stress, Psychological/physiopathologyABSTRACT
Importance: For Black US residents, experiences of racial discrimination are still pervasive and frequent. Recent empirical work has amplified the lived experiences and narratives of Black people and further documented the detrimental effects of racial discrimination on both mental and physical health; however, there is still a need for further research to uncover the mechanisms connecting experiences of racial discrimination with adverse health outcomes. Objective: To examine neurobiological mechanisms that may offer novel insight into the association of racial discrimination with adverse health outcomes. Design, Setting, and Participants: This cross-sectional study included 102 Black adults who had recently experienced a traumatic injury. In the acute aftermath of the trauma, participants underwent a resting-state functional magnetic resonance imaging scan. Individuals were recruited from the emergency department at a Midwestern level 1 trauma center in the United States between March 2016 and July 2020. Data were analyzed from February to May 2021. Exposures: Self-reported lifetime exposure to racial discrimination, lifetime trauma exposure, annual household income, and current posttraumatic stress disorder (PTSD) symptoms were evaluated. Main Outcomes and Measures: Seed-to-voxel analyses were conducted to examine the association of racial discrimination with connectivity of salience network nodes (ie, amygdala and anterior insula). Results: A total of 102 individuals were included, with a mean (SD) age of 33 (10) years and 58 (57%) women. After adjusting for acute PTSD symptoms, annual household income, and lifetime trauma exposure, greater connectivity between the amygdala and thalamus was associated with greater exposure to discrimination (t(97) = 6.05; false discovery rate (FDR)-corrected P = .03). Similarly, racial discrimination was associated with greater connectivity between the insula and precuneus (t(97) = 4.32; FDR-corrected P = .02). Conclusions and Relevance: These results add to the mounting literature that racial discrimination is associated with neural correlates of vigilance and hyperarousal. The study findings extend this theory by showing that this association is apparent even when accounting for socioeconomic position, lifetime trauma, and symptoms of psychological distress related to an acute trauma.
Subject(s)
Amygdala/physiopathology , Black People/psychology , Cerebral Cortex/physiopathology , Emotional Regulation/physiology , Psychological Trauma/physiopathology , Stress Disorders, Post-Traumatic/diagnostic imaging , Adult , Amygdala/diagnostic imaging , Cerebral Cortex/diagnostic imaging , Cross-Sectional Studies , Female , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Psychological Trauma/diagnostic imaging , Severity of Illness Index , Trauma Severity Indices , United StatesABSTRACT
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.
Subject(s)
Prolonged Grief Disorder , Psychological Trauma , Stress Disorders, Post-Traumatic , Adult , Aged , Diagnostic and Statistical Manual of Mental Disorders , Factor Analysis, Statistical , Female , Humans , Male , Middle Aged , Psychological Trauma/classification , Psychological Trauma/complications , Psychological Trauma/physiopathology , Stress Disorders, Post-Traumatic/classification , Stress Disorders, Post-Traumatic/etiology , Stress Disorders, Post-Traumatic/physiopathologyABSTRACT
Background: Peritraumatic dissociation is purported to emerge together with attenuated autonomic arousal, immobility, and staring. However, empirical evidence is scarce and heterogeneous. Moreover, it is still a matter of debate whether these responses predict intrusion formation. Objective: The present trauma-analogue study examined associations between peritraumatic dissociation, autonomic activation, facial movements, staring, and intrusion formation. Method: Seventy-one healthy women watched a highly aversive film, while autonomic activation (heart rate, respiratory sinus arrhythmia, skin conductance level), facial movements (temporal variations in corrugator electromyography), and staring (fixation duration, tracklength) were assessed. Afterwards, participants rated the intensity of dissociation during film viewing and reported intrusions and associated distress in a smartphone application for 24 hours. Results: Peritraumatic dissociation was linked to higher autonomic arousal (higher heart rate and, on a trend-level, lower respiratory sinus arrhythmia), increased facial movements, and staring (lower tracklength). Peritraumatic dissociation, higher autonomic arousal (higher heart rate and lower respiratory sinus arrhythmia), staring (higher fixation duration), and, on a trend-level, more facial movements were linked to higher intrusion load (number x distress of intrusions) and together explained 59% of variance. Skin conductance level was neither linked to peritraumatic dissociation nor intrusion load. Conclusions: Our results suggest that, at low-dissociation-levels observed in trauma-analogue studies, peritraumatic dissociation may occur together with heightened autonomic arousal and facial movements, indexing increased negative affect. Staring might, irrespectively of dissociation-levels, serve as objective marker for dissociation. Together, peritraumatic dissociation and its psychophysiological correlates might set the stage for later intrusion formation.
Antecedentes: Se supone que la disociación peritraumática surge junto con la activación autonómica atenuada, la inmovilidad y la mirada fija. Sin embargo, la evidencia empírica es escasa y heterogénea. Además, sigue siendo objeto de debate si estas respuestas predicen la formación de intrusiones.Objetivo: El presente estudio análogo al trauma examinó las asociaciones entre la disociación peritraumática, la activación autonómica, los movimientos faciales, la mirada fija y la formación de intrusiones.Método: Setenta y una mujeres sanas vieron una película altamente aversiva mientras se evaluaba la activación autonómica (frecuencia cardíaca, arritmia sinusal respiratoria, nivel de conductancia de la piel), los movimientos faciales (variaciones temporales en la electromiografía del corrugador) y la mirada fija (duración de la fijación, longitud del seguimiento). Posteriormente, las participantes calificaron la intensidad de la disociación durante la visualización de la película e informaron sobre las intrusiones y la angustia asociada en una aplicación para teléfonos inteligentes durante 24 horas.Resultados: La disociación peritraumática se relacionó con una mayor activación autonómica (mayor frecuencia cardíaca y, a nivel de tendencia, menor arritmia sinusal respiratoria), mayores movimientos faciales y mirada fija (menor duración del seguimiento). La disociación peritraumática, la mayor activación autonómica (mayor frecuencia cardíaca y menor arritmia sinusal respiratoria), la mirada fija (mayor duración de la fijación) y, en un nivel de tendencia, más movimientos faciales estaban vinculados a una mayor carga de intrusiones (número x angustia de intrusiones) y juntos explicaban el 59% de la varianza. El nivel de conductancia de la piel no se relacionó con la disociación peritraumática ni con la carga de intrusión.Conclusiones: Nuestros resultados sugieren que, a niveles bajos de disociación observados en estudios de trauma análogos, la disociación peritraumática puede ocurrir junto con una mayor activación autonómica y movimientos faciales, lo que indica un aumento del afecto negativo. La mirada fija, independientemente de los niveles de disociación, podría servir como marcador objetivo de disociación. En conjunto, la disociación peritraumática y sus correlatos psicofisiológicos podrían sentar las bases para la formación posterior de intrusiones.
Subject(s)
Autonomic Nervous System/physiopathology , Dissociative Disorders/physiopathology , Psychological Trauma/physiopathology , Adolescent , Adult , Arousal/physiology , Eye Movement Measurements , Facial Muscles/physiology , Female , Galvanic Skin Response , Heart Rate/physiology , Humans , Male , Respiratory Sinus Arrhythmia/physiology , Young AdultABSTRACT
ABSTRACT: Trauma exposure has been repeatedly linked to psychophysiological threat reactivity, although the directionality of this association has been inconsistent. Several factors likely contribute to inconsistent findings including type of trauma and threat paradigm. The present study therefore examined the impact of trauma type on psychophysiological reactivity to predictable (P-) and unpredictable (U-) threat in young adults (N = 112). Participants were classified into three groups: history of interpersonal or noninterpersonal trauma, or no history of trauma. Startle eyeblink potentiation was recorded during a well-validated threat-of-shock paradigm. Results indicated individuals with interpersonal trauma exposure displayed exaggerated startle reactivity to U-threat (only) compared with both other groups. In contrast, individuals with noninterpersonal trauma exhibited blunted startle reactivity to U-threat (only) compared with both other groups. Findings reveal that trauma and threat type influence threat reactivity and that those with a history of interpersonal trauma may uniquely display exaggerated sensitivity to stressors that are uncertain.
Subject(s)
Anticipation, Psychological/physiology , Fear/physiology , Psychological Trauma/physiopathology , Reflex, Startle/physiology , Violence , Adolescent , Adult , Female , Humans , Interpersonal Relations , Male , Young AdultABSTRACT
BACKGROUND: Endometrial tissue plays an important role in the regulation of female fertility and there is evidence that endometrial pathology (including endometriosis) is closely related to endocrine disorders. On the other hand, various neuroendocrine changes can be significantly affected by psychosocial stress. In connection with these findings, we tested the relationship between neuroendocrine changes, sexual dysfunction, psychosocial/traumatic stress, and dissociative symptoms in women with endometriosis. METHODS: A total of 65 patients with endometriosis were included in the study. Clinical examinations were focused on the biochemical analysis of neuroendocrine markers of endometriosis (cancer antigen 125 [CA 125] and cancer antigen 19-9 [CA 19-9]), estradiol, psychometric evaluation of sexual dysfunction, psychosocial/traumatic stress, and dissociative symptoms. RESULTS: The results showed significant Spearman correlations between the values of the revised range of sexual difficulties for sexual dysfunction (Revised Female Sexual Distress Scale), psychosocial/traumatic stress (Trauma Symptoms Checklist) (Râ=â0.31), and dissociative symptoms (Somatoform Dissociation Questionnaire) (Râ=â0.33). Positive correlations were also found between CA 125 and CA 19-9 (Râ=â0.63), and between CA 125 and the results of the values of the revised scale of sexual difficulties for sexual dysfunction (Revised Female Sexual Distress Scale) (Râ=â0.29). Also psychosocial/traumatic stress (Trauma Symptoms Checklist) significantly correlated with CA 125 (Râ=â0.38) and with CA 19-9 (Râ=â0.33). CONCLUSION: These results represent the first findings regarding the relationship of the neuroendocrine markers CA 125 and CA 19-9 and sexual dysfunction with trauma/stress-related symptoms and dissociative symptoms in women with endometriosis.
Subject(s)
CA-125 Antigen/blood , CA-19-9 Antigen/blood , Endometriosis , Psychological Trauma , Sexual Dysfunction, Physiological , Somatoform Disorders , Adult , Correlation of Data , Dissociative Disorders/diagnosis , Dissociative Disorders/psychology , Endometriosis/blood , Endometriosis/complications , Endometriosis/psychology , Female , Humans , Neurosecretory Systems/metabolism , Psychological Techniques , Psychological Trauma/complications , Psychological Trauma/diagnosis , Psychological Trauma/physiopathology , Psychology , Sexual Dysfunction, Physiological/blood , Sexual Dysfunction, Physiological/psychology , Somatoform Disorders/diagnosis , Somatoform Disorders/physiopathology , Somatoform Disorders/psychologyABSTRACT
Recent studies suggest that reward anticipation decreases individuals' acute stress responses. However, individuals who have experienced early life stress (ELS) may have a blunted capacity for reward anticipation, which reduces its buffering effect on psychosocial stress responses. To investigate this phenomenon, 66 young adults completed the Trier Social Stress Test following a reward anticipation task, and their ELS levels were measured using the Childhood Trauma Questionnaire (CTQ). Meanwhile, the current study collected biological and psychological measures of stress by analysing cortisol levels, heart rates, heart rate variability (HRV) as well as subjective stress levels, in response to the Trier Social Stress test. Results showed that reward anticipation successfully decreased acute stress responses in general, and it also improved participants' HRV. However, this effect was more evident in individuals with low ELS than those with high ELS. These findings help us deepen understanding of the role of reward anticipation in fostering resilience under stress and the potentially important implications for individuals who have been exposed to ELS are also discussed.
Subject(s)
Adverse Childhood Experiences , Anticipation, Psychological/physiology , Autonomic Nervous System/physiopathology , Heart Rate/physiology , Psychological Trauma/physiopathology , Reward , Stress, Psychological/physiopathology , Adult , Female , Humans , Male , Young AdultABSTRACT
Importance: Racial discrimination has a clear impact on health-related outcomes, but little is known about how discriminatory experiences are associated with neural response patterns to emotionally salient cues, which likely mediates these outcomes. Objective: To examine associations of discriminatory experiences with brainwide response to threat-relevant cues in trauma-exposed US Black women as they engage in an attentionally demanding task. Design, Setting, and Participants: A cross-sectional study was conducted from May 1, 2014, to July 1, 2019, among 55 trauma-exposed US Black women to examine associations of racial discrimination experiences with patterns of neural response and behavior to trauma-relevant images in an affective attentional control task. Posttraumatic stress disorder (PTSD) symptoms and trauma exposure were entered as covariates to isolate variance associated with experiences of racial discrimination. Exposures: Varying levels of trauma, PTSD symptoms, and experiences of racial discrimination. Main Outcomes and Measures: Experiences of Discrimination Questionnaire (EOD) (range, 0-9) for count of the number of situations for which each participant reported having unfair treatment for a racial reason. Experiences of trauma and PTSD symptoms were assessed with the Traumatic Events Inventory (TEI) (number of times the person was exposed to trauma; score range, 0-112) and PTSD Symptom Scale (PSS) (score range, 0-51). Response to trauma-relevant vs neutral distractor cues were assessed via functional magnetic resonance imaging during performance of an affective Stroop (attentional control) task. Statistical analyses were conducted at a whole-brain, voxelwise level with familywise error correction. Results: In this study of 55 Black women in the US (mean [SD] age, 37.7 [10.7] years; range, 21-61 years), participants reported a mean (SD) TEI frequency of 33.0 (18.8) and showed moderate levels of current PTSD symptoms (mean [SD] PSS score, 15.4 [12.9]). Mean (SD) EOD scores were 2.35 (2.44) and were moderately correlated with current PTSD symptoms (PSS total: r = 0.36; P=.009) but not with age (r = 0.20; P = .15) or TEI frequency (r = -0.02; P = .89). During attention to trauma-relevant vs neutral images, more experiences of racial discrimination were associated with significantly greater response in nodes of emotion regulation and fear inhibition (ventromedial prefrontal cortex) and visual attention (middle occipital cortex) networks, even after accounting for trauma and severity of PTSD symptoms (brainwide familywise error corrected; r = 0.33 for ventromedial prefrontal cortex; P = .02). Racial discrimination was also associated with affective Stroop task performance; errors on trials with threat-relevant stimuli were negatively correlated with experiences of racial discrimination (r = -0.41; P = .003). Conclusions and Relevance: These findings suggest that experiences of racial discrimination associate with disproportionately greater response in brain regions associated with emotion regulation and fear inhibition and visual attention. Frequent racism experienced by Black individuals may potentiate attentional and regulatory responses to trauma-relevant stressors and lead to heightened modulation of regulatory resources. This may represent an important neurobiological pathway for race-related health disparities.
Subject(s)
Black or African American/ethnology , Emotional Regulation/physiology , Fear/physiology , Prefrontal Cortex , Psychological Trauma , Racism/ethnology , Stress Disorders, Post-Traumatic , Adult , Brain Mapping , Cross-Sectional Studies , Humans , Magnetic Resonance Imaging , Middle Aged , Nerve Net/diagnostic imaging , Nerve Net/physiopathology , Occipital Lobe/diagnostic imaging , Occipital Lobe/physiopathology , Patient Acuity , Prefrontal Cortex/diagnostic imaging , Prefrontal Cortex/physiopathology , Psychological Trauma/diagnostic imaging , Psychological Trauma/ethnology , Psychological Trauma/physiopathology , Stress Disorders, Post-Traumatic/diagnostic imaging , Stress Disorders, Post-Traumatic/ethnology , Stress Disorders, Post-Traumatic/physiopathology , United States , Young AdultABSTRACT
ABSTRACT: Research has shown that women are more prone to childhood trauma and this state is associated with somatic symptoms. Also, people who have been exposed to traumatic experiences use experiential avoidance to reduce negative emotions. However, the mediating role of experiential avoidance in the relationship between childhood trauma and somatic symptoms is not clear, so, the present study investigated whether the relationships among different types of childhood trauma and somatic symptoms could be explained by experiential avoidance in female college students. In a cross-sectional study, 251 Iranian female college students with somatic symptoms were recruited from the University of Tabriz. Participants completed self-report scales, including the Persian version of Child Abuse Self-Reported Scale, Acceptance and Action Questionnaire-II (AAQ-II), and the Patient-health questionnaire (PHQ-15). A path analysis was used to empirically explore the relationships. Structural equation modeling analyses confirmed a partial mediation model. Study participants who had a higher level of emotional trauma reported higher levels of somatic symptoms. Emotional and neglect trauma showed significant positive relations with experiential avoidance. Bootstrapping results showed that experiential avoidance partially mediated the relationship between emotional trauma and somatic symptoms. Moreover, the association between neglect and somatic symptoms was fully mediated by experiential avoidance. These findings suggest that experiential avoidance might be one mechanism explaining how adverse emotional and neglect experiences influence somatic symptoms. Interventions addressing experiential avoidance through methods such as emotion-focused therapy and mindfulness are discussed as potential future directions for treating somatic symptoms in females who experienced emotional and neglect trauma.
Subject(s)
Adverse Childhood Experiences , Avoidance Learning/physiology , Medically Unexplained Symptoms , Psychological Trauma/physiopathology , Adolescent , Adult , Cross-Sectional Studies , Female , Humans , Iran , Students , Universities , Young AdultABSTRACT
Chronic pain and post-traumatic stress disorder (PTSD) frequently co-occur, and research suggests that these 2 conditions exacerbate one another producing greater impact on normal functioning in combination than separately. The influence of traumatic experiences on both pain and PTSD has been shown, but the nature of this interplay remains unclear. Although Criterion A trauma is required for the diagnosis of PTSD, whether the association between PTSD and chronic pain is dependent on Criterion A is underexplored. In this observational cohort study, we examined the association between pain and PTSD-like symptoms in the context of Criterion A trauma in 5,791 men from the Vietnam Era Twin Registry. Correlations and mixed-effects regression models were used to evaluate the relationship between PTSD Checklist-Civilian Version symptoms and multiple indicators of pain from the Short Form McGill Pain Questionnaire across trauma history and chronic pain conditions. 53.21% of the participants experienced trauma consistent with DSM-IV Criterion A for PTSD. The associations between pain indicators and PTSD-like symptoms was stronger for individuals with a history of trauma but remained robust for individuals without trauma history. Small but significant interactions between past trauma and pain indicators and PTSD-like symptoms were observed. Findings were similar in a subsample of participants with history of chronic pain conditions. The relationship between PTSD-like symptoms and indicators of pain were largely independent of trauma consistent with Criterion A, highlighting the need to better understand and address stressful life events in chronic pain patients and pain concerns in individuals reporting trauma. PERSPECTIVE: This article demonstrates that the relationship between PTSD-like symptoms and indicators of pain is largely independent of trauma consistent with Criterion A. This finding highlights the need to better understand and address stressful life events in chronic pain patients and pain concerns in individuals reporting trauma.
Subject(s)
Chronic Pain/physiopathology , Psychological Trauma/physiopathology , Registries , Stress Disorders, Post-Traumatic/physiopathology , Stress, Psychological/physiopathology , Veterans , Aged , Chronic Pain/epidemiology , Comorbidity , Humans , Life Change Events , Male , Middle Aged , Psychological Trauma/epidemiology , Stress Disorders, Post-Traumatic/epidemiology , Stress, Psychological/epidemiology , United States/epidemiologyABSTRACT
ABSTRACT: Refugees experience distress from premigration trauma, often exacerbated by postmigration difficulties. To develop effective interventions, risk factors for mental health symptoms need to be determined. Male Iraqi refugees (N = 53) to the United States provided background information and reported predisplacement trauma and psychological health within 1 month of their arrival. An inflammatory biomarker-C-reactive protein (CRP) was assessed approximately 1.5 years after arrival, and a contextual factor-acculturation-and psychological health were assessed 2 years after arrival. We tested whether acculturation and CRP were associated with posttraumatic stress disorder (PTSD) and depression symptoms at the 2-year follow-up, controlling for baseline symptoms, age, body mass index, and predisplacement trauma. Acculturation was inversely related to depression, and CRP was positively related to both PTSD and depression at the 2-year follow-up. Interventions targeting acculturation could help reduce the development of depression symptoms in refugees. The role of CRP in the development of PTSD and depression symptoms warrants further research.
Subject(s)
Acculturation , C-Reactive Protein/metabolism , Depression , Psychological Trauma , Refugees , Stress Disorders, Post-Traumatic , Adolescent , Adult , Depression/blood , Depression/ethnology , Depression/physiopathology , Follow-Up Studies , Humans , Iraq/ethnology , Male , Middle Aged , Psychological Trauma/blood , Psychological Trauma/ethnology , Psychological Trauma/physiopathology , Stress Disorders, Post-Traumatic/blood , Stress Disorders, Post-Traumatic/ethnology , Stress Disorders, Post-Traumatic/physiopathology , United States/ethnology , Young AdultABSTRACT
BACKGROUND: Between unaffected mental health and diagnosable psychiatric disorders, there is a vast continuum of functioning. The hypothesized link between striatal dopamine signaling and psychosis has guided a prolific body of research. However, it has been understudied in the context of multiple interacting factors, subclinical phenotypes, and pre-postsynaptic dynamics. METHOD: This work investigated psychotic-like experiences and D2/3 dopamine postsynaptic receptor availability in the dorsal striatum, quantified by in vivo [11C]-raclopride positron emission tomography, in a sample of 24 healthy male individuals. Additional mediation and moderation effects with childhood trauma and key dopamine-regulating genes were examined. RESULTS: An inverse relationship between nondisplaceable binding potential and subclinical symptoms was identified. D2/3 receptor availability in the left putamen fully mediated the association between traumatic childhood experiences and odd beliefs, that is, inclinations to see meaning in randomness and unfounded interpretations. Moreover, the effect of early adversity was moderated by a DRD2 functional variant (rs1076560). The results link environmental and neurobiological influences in the striatum to the origination of psychosis spectrum symptomology, consistent with the social defeat and diathesis-stress models. CONCLUSIONS: Adversity exposure may affect the dopamine system as in association with biases in probabilistic reasoning, attributional style, and salience processing. The inverse relationship between D2/3 availability and symptomology may be explained by endogenous dopamine occupying the receptor, postsynaptic compensatory mechanisms, and/or altered receptor sensitivity. This may also reflect a cognitively stabilizing mechanism in non-help-seeking individuals. Future research should comprehensively characterize molecular parameters of dopamine neurotransmission along the psychosis spectrum and according to subtype profiling.
Subject(s)
Adverse Childhood Experiences , Dopamine D2 Receptor Antagonists/pharmacokinetics , Dopamine/metabolism , Neostriatum/metabolism , Psychological Trauma/metabolism , Psychotic Disorders/metabolism , Receptors, Dopamine D2/metabolism , Adult , Adult Survivors of Child Adverse Events , Female , Humans , Male , Neostriatum/diagnostic imaging , Positron-Emission Tomography , Psychological Trauma/diagnostic imaging , Psychological Trauma/physiopathology , Psychotic Disorders/diagnostic imaging , Psychotic Disorders/physiopathology , Raclopride/pharmacokinetics , Receptors, Dopamine D2/genetics , Receptors, Dopamine D3/metabolismABSTRACT
ABSTRACT: Although catatonia is related to several medical conditions, catatonia as a response to trauma and posttraumatic stress disorder (PTSD) is less clear. The aim of this review is to explore the small emerging body of preliminary evidence that suggests a possible correlation between psychological trauma and catatonia. Initial data suggests a correlation between episodes of intense fear associated with trauma and PTSD and some forms of catatonic responses. Although this relationship is still speculative to be causative, it can have important implications if confirmed. This is especially salient when it is examined alongside existing studies of the response to fear in animals and the phenomenon of tonic immobility, which bears a striking resemblance to catatonia in humans. If prospective studies further support the initial findings, it could change our conceptual understanding of the etiology of a subtype of catatonia substantially while pointing to likely targets of further research to understand the biological mechanisms that underlie the illness.