Pupil Response to Threat in Trauma-Exposed Individuals With or Without PTSD.
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ABSTRACT:
SUBMITTER: Cascardi M
PROVIDER: S-EPMC4743760 | biostudies-other | 2015 Aug
REPOSITORIES: biostudies-other
Publications
Pupil Response to Threat in Trauma-Exposed Individuals With or Without PTSD.
Cascardi Michele M Armstrong Davine D Chung Leeyup L Paré Denis D
Journal of traumatic stress 20150727 4
An infrequently studied and potentially promising physiological marker for posttraumatic stress disorder (PTSD) is pupil response. This study tested the hypothesis that pupil responses to threat would be significantly larger in trauma-exposed individuals with PTSD compared to those without PTSD. Eye-tracking technology was used to evaluate pupil response to threatening and neutral images. Recruited for participation were 40 trauma-exposed individuals; 40.0% (n = 16) met diagnostic criteria for P ...[more]
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Project description:ImportancePosttraumatic stress disorder (PTSD) is marked by the contrasting symptoms of hyperemotional reactivity and emotional numbing (ie, reduced emotional reactivity). Comprehending the mechanism that governs the transition between neutral and negative emotional states is crucial for developing targeted therapeutic strategies.ObjectivesTo explore whether individuals with PTSD experience a more pronounced shift between neutral and negative emotional states and how the intensity of emotional numbing symptoms impacts this shift.Design, setting, and participantsThis cross-sectional study used hierarchical bayesian modeling to fit a 5-parameter logistic regression to analyze the valence ratings of images. The aim was to compare the curve's slope between groups and explore its association with the severity of emotional numbing symptoms. The study was conducted online, using 35 images with a valence range from highly negative to neutral. The rating of these images was used to assess the emotional responses of the participants. The study recruited trauma-exposed individuals (witnessed or experienced life-threatening incident, violent assault, or someone being killed) between January 17 and March 8, 2023. Participants completed the PTSD Checklist for the Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) (DSM-5) (PCL-5).ExposureOn the basis of DSM-5 criteria (endorsing at least 1 symptom from clusters B and C and 2 from D and E), participants were categorized as having probable PTSD (pPTSD) or as trauma-exposed controls (TECs).Main outcomes and measuresThe main outcome was the slope parameter (b) of the logistic curve fitted to the valence rating. The slope parameter indicates the rate at which emotional response intensity changes with stimulus valence, reflecting how quickly the transition occurs between neutral and negatively valenced states. The secondary outcome was the association between emotional numbing (PCL-5 items 12-14) and the slope parameter.ResultsA total of 1440 trauma-exposed individuals were included. The pPTSD group (n = 445) was younger (mean [SD] age, 36.1 [10.9] years) compared with the TEC group (mean [SD] age, 41.5 [13.3] years; P < .001). Sex distribution (427 women in the TEC group vs 230 in the pPTSD group) did not significantly differ between groups (P = .67). The pPTSD group exhibited a steeper slope (mean slope difference, -0.255; 89% highest posterior density [HPD], -0.340 to -0.171) compared with the controls. Across all individuals (n = 1440), a robust association was found between the slope and emotional numbing severity (mean [SD] additive value, 0.100 [0.031]; 89% HPD, 0.051-0.15). Additional analysis controlling for age confirmed the association between emotional numbing and transition sharpness (mean [SD] additive value, 0.108 [0.032]; 89% HPD, 0.056-0.159), without evidence of an age-related association (mean [SD] additive value, 0.031 [0.033]; 89% HPD, -0.022 to 0.083).Conclusions and relevanceThese findings support that individuals with PTSD undergo rapid transitions between neutral and negative emotional states, a phenomenon intensified by the severity of emotional numbing symptoms. Therapeutic interventions aimed at moderating these swift emotional transitions could potentially alleviate PTSD symptoms.
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Project description:ImportanceRacial 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.ObjectiveTo 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 participantsA 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.ExposuresVarying levels of trauma, PTSD symptoms, and experiences of racial discrimination.Main outcomes and measuresExperiences 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.ResultsIn 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 relevanceThese 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.
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Project description:Recent data have supported the use of an early exposure intervention to promote a reduction in acute stress and posttraumatic stress disorder (PTSD) symptoms after trauma exposure. The present study explored a comprehensive predictive model that included history of trauma exposure, dissociation at the time of the trauma and early intervention, and physiological responses (cortisol and heart rate) to determine which variables were most indicative of reduced PTSD symptoms for an early intervention or treatment as usual.Participants (n = 137) were randomly assigned to the early intervention condition (n = 68) or assessment-only condition (n = 69) while receiving care at the emergency department of a Level 1 trauma center. Follow-up assessments occurred at 4 and 12 weeks posttrauma.Findings suggested that dissociation at the time of the 1st treatment session was associated with reduced response to the early intervention. No other predictors were associated with treatment response. For treatment as usual, cortisol levels at the time of acute care and dissociation at the time of the traumatic event were positively associated with PTSD symptoms.Dissociation at the time at which treatment starts may indicate poorer response to early intervention for PTSD. Similarly, dissociation at the time of the event was positively related to PTSD symptoms in those who received treatment as usual.
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Project description:Background: Alexithymia, an inability to recognise one's emotions, has been associated with trauma-exposure and posttraumatic stress disorder (PTSD). Previous research suggests involvement of the oxytocin system, and socio-emotional neural processes. However, the paucity of neurobiological research on alexithymia, particularly in trauma-exposed populations, warrants further investigation.Objective: Explore associations between alexithymia, endogenous oxytocin levels, and socio-emotional brain function and morphometry in a trauma-exposed sample.Method: Dutch trauma-exposed police officers with (n = 38; 18 females) and without PTSD (n = 40; 20 females) were included. Alexithymia was assessed with the Toronto Alexithymia Scale (TAS-20). Endogenous salivary oxytocin was assessed during rest, using radioimmunoassay. Amygdala and insula reactivity to socio-emotional stimuli were assessed with functional MRI, amygdala and insula grey matter volume were derived using Freesurfer.Results: Alexithymia was higher in PTSD patients compared to trauma-exposed controls (F(1,70) = 54.031, p < .001). Within PTSD patients, alexithymia was positively associated with PTSD severity (ρ(36) = 0.497, p = .002). Alexithymia was not associated with childhood trauma exposure (β = 0.076, p = .509), police work-related trauma exposure (β = -0.107, p = .355), oxytocin levels (β = -0.164, p = .161), insula (β = -0.170, p = .158) or amygdala (β = -0.175, p = .135) reactivity, or amygdala volume (β = 0.146, p = .209). Insula volume was positively associated with alexithymia (β = 0.222, p = .016), though not significant after multiple testing corrections. Bayesian analyses supported a lack of associations.Conclusions: No convincing neurobiological correlates of alexithymia were observed with any of the markers included in the current study. Yet, the current study confirmed high levels of alexithymia in PTSD patients, independent of trauma-exposure, substantiating alexithymia's relevance in the clinical phenotype of PTSD.
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Project description:Behavioural, structural, and functional neuroimaging have implicated the hippocampus as a critical brain region in posttraumatic stress disorder (PTSD) pathogenesis. Recent work in a normative, primarily European, sample identified 15 unique genetic loci contributing to structural variability in six hippocampal subfield volumes. We explored the relevance of these loci in two samples (Mental Illness Research Education and Clinical Centre [MIRECC] and Grady; n = 290) of trauma-exposed individuals enriched for PTSD and of diverse ancestry. Four of the previous loci demonstrated nominal evidence of replication in the MIRECC dataset, primarily within non-Hispanic whites (NHW). One locus replicated in the Grady cohort, which was composed exclusively of non-Hispanic blacks (NHB). Our data supported genetic interactions with diagnosis of lifetime PTSD and genetic interactions with childhood trauma in the MIRECC sample, but not the Grady sample. Given the racial, diagnostic, and trauma-exposure differences with the original genome-wide association study (GWAS) report, we conducted a full GWAS in the MIRECC and Grady datasets. Interactions between genetic variants and lifetime PTSD or childhood trauma were interrogated for single nucleotide polymorphisms (SNPs) with evidence of main effects. Genetic associations surpassed false discovery rate (FDR)-correction within hippocampal subfields in fimbria, subiculum, cornu ammonis-1 (CA1), and hippocampal amygdala transition area (HATA). One association was replicated in the Grady cohort (rs12880795 in TUNAR with left (L)-HATA volume). The most significant association in the MIRECC dataset was between rs6906714 in LINC02571 and right (R)-fimbria volume (p = 5.99×10-8, q = 0.0056). Interestingly, the effect of rs6906714 on R-fimbria volume increased with exposure to childhood trauma (gene*environment [G*E] interaction p = 0.022). These preliminary results argue for G*E interactions between genetic loci with PTSD and childhood trauma on hippocampal phenotypes. Our results underscore the need for larger neuroimaging-genetic studies in PTSD, trauma, and ancestrally diverse populations.
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Project description:A subtype of the posttraumatic stress disorder diagnosis for children 6 years and younger (PTSD-6Y) was introduced in the Diagnostic and Statistical Manual, Fifth Edition (DSM-5). This study utilized confirmatory factor analytic techniques to evaluate the proposed DSM-5 PTSD-6Y factor structure and criterion and convergent validity against competing models. Data for N = 284 (3-6 years) trauma-exposed young children living in New Orleans were recruited following a range of traumas, including medical emergencies, exposure to Hurricane Katrina and repeated exposure to domestic violence. The model was compared to DSM-IV, a 4-factor 'dysphoria' model that groups symptoms also associated with anxiety and depression, and alternate 1- and 2- factor models. Convergent validity was established against the Child Behavior Checklist (CBCL). Criterion related validity was established by comparing each model to a categorical rating of impairment. The Dysphoria and PTSD-6Y models offered the better accounts of symptom structure, although neither satisfied minimum requirements for a good fitting model. These two models also only showed small levels of convergence with CBCL dimensions. The 1-factor model offered the most compelling balance of sensitivity and specificity, with the 2-factor model and the Dysphoria model following closely behind. These CFA results do not support the symptom clusters proposed within the DSM-5 for PTSD-6Y. Although a 4-factor Dysphoria model offers a better overall account of clustering patterns (relative to alternate models), alongside acceptable sensitivity and specificity for detecting clinical impairment, it also falls short of being an adequate model in this younger age group.
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Project description:BackgroundPost-traumatic stress disorder (PTSD) is an established comorbidity in Bipolar Disorder (BD), but little is known about the characteristics of psychological trauma beyond a PTSD diagnosis and differences in trauma symptoms between BD-I and BD-II.Objective(1) To present characteristics of a trauma-exposed BD sample; (2) to investigate prevalence and trauma symptom profile across BD-I and BD-II; (3) to assess the impact of a lifetime PTSD diagnosis vs. a history of trauma on BD course; and (4) to research the impacts of sexual and physical abuse.MethodsThis multi-center study comprised 79 adult participants with BD with a history of psychological trauma and reports baseline data from a trial registered in Clinical Trials (https://clinicaltrials.gov; ref: NCT02634372). Clinical variables were gathered through clinical interview, validated scales and a review of case notes.ResultsThe majority (80.8%) of our sample had experienced a relevant stressful life event prior to onset of BD, over half of our sample 51.9% had a lifetime diagnosis of PTSD according to the Clinician Administered PTSD scale. The mean Impact of Event Scale-Revised scores indicated high levels of trauma-related distress across the sample, including clinical symptoms in the PTSD group and subsyndromal symptoms in the non-PTSD group. Levels of dissociation were not higher than normative values for BD. A PTSD diagnosis (vs. a history of trauma) was associated with psychotic symptoms [2(1) = 5.404, p = 0.02] but not with other indicators of BD clinical severity. There was no significant difference between BD-I and BD-II in terms of lifetime PTSD diagnosis or trauma symptom profile. Sexual abuse significantly predicted rapid cycling [2(1) = 4.15, p = 0.042], while physical abuse was not significantly associated with any clinical indicator of severity.ConclusionTrauma load in BD is marked with a lack of difference in trauma profile between BD-I and BD-II. Although PTSD and sexual abuse may have a negative impact on BD course, in many indicators of BD severity there is no significant difference between PTSD and subsyndromal trauma symptoms. Our results support further research to clarify the role of subsyndromic PTSD symptoms, and highlight the importance of screening for trauma in BD patients.
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Project description:Individuals admitted to inpatient psychiatry for suicide-related concerns are at increased risk of suicide post-discharge, necessitating an understanding of factors, such as posttraumatic stress disorder (PTSD), that are associated with suicide-related hospitalizations. In this study, we examined if individuals admitted for suicide-related concerns were more likely than those admitted for other reasons to have elevated PTSD symptoms or a probable PTSD diagnosis. We also examined the moderating role of impulsivity. Participants were 188 trauma-exposed adult psychiatric inpatients (M [SD]age = 33.6 y [11.7 y], 63.3% male, 46.3% white). We used the Life Events Checklist for DSM-5, PTSD Checklist for DSM-5, Beck Scale for Suicide Ideation, and Barratt Impulsiveness Scale-11 to assess trauma exposure, PTSD symptoms, suicidal ideation severity, and impulsivity, respectively. We controlled for trauma load, number of psychiatric diagnoses, and comorbid depressive and substance use disorders. Patients admitted for suicide-related concerns (55.3%; n = 104), compared with those admitted for other reasons (44.7%; n = 84), had more severe PTSD symptoms, corresponding to medium-to-large effect sizes; associations were stronger at higher levels of impulsivity. Additionally, patients admitted for suicide-related concerns were nearly four times more likely than their counterparts to screen positive for a provisional PTSD diagnosis. Among the subset of individuals admitted for suicide-related concerns, greater PTSD symptoms were associated with more severe suicidal ideation. In sum, PTSD symptoms are elevated among psychiatric inpatients admitted for suicide-related concerns, and among this subgroup, greater PTSD symptom severity covaries with suicidal ideation severity. Screening for and treating PTSD, and attending to cooccurring impulsivity, in psychiatric inpatients may reduce suicide risk.
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Project description:BackgroundTheoretical models of self-conscious emotions indicate that shame is elicited through internal, stable, and global causal attributions of the precipitating event. The current study aimed to investigate whether these negative attributions are related to trauma-related shame and PTSD symptom severity.MethodA total of 658 participants aged 18 to 89 (M = 33.42; SD = 12.17) with a history of trauma exposure completed a range of self-report measures assessing trauma exposure, negative trauma-related attributions, shame, and PTSD symptoms.ResultsHigher levels of internal, stable, and global trauma-related attributions were significantly associated with shame and PTSD. Shame mediated the association between trauma-related attributions and PTSD symptom severity, even after controlling for the effects of number of trauma exposures, worst index trauma and depression.ConclusionsThe present results suggest that negative attributions are a critical cognitive component related to shame and in turn, PTSD symptom severity. Future research should aim to replicate these findings in a clinical sample and extend these findings using prospective designs.
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