Trauma-exposed Women Research Articles

Inflammation, reward circuitry and symptoms of anhedonia and PTSD in trauma-exposed women.

Trauma exposure is associated with increased inflammatory biomarkers (e.g. C-reactive protein [CRP] and cytokines), and inflammation has been shown to impact corticostriatal reward circuitry and increase anhedonia-related symptoms. We examined resting-state functional MRI in a high-trauma inner-city population of African-American women (n= 56), who reported on average five different types of trauma exposures, to investigate whether inflammation correlated with functional connectivity (FC) in corticostriatal reward circuitry in association with symptoms of anhedonia and PTSD. Plasma CRP negatively correlated with bilateral ventral striatum (VS) to ventromedial prefrontal cortex (vmPFC) FC (P< 0.01). In participants where plasma was available to also measure cytokines and their soluble receptors, left (L)VS-vmPFC FC negatively correlated with an inflammatory composite score (previously shown to be increased in plasma and cerebrospinal fluid of depressed patients with high CRP) only in women with significant PTSD symptoms (n= 14; r = -0.582, P= 0.029) and those who experienced moderate-severe childhood trauma (r = -0.595, P= 0.009). Exploratory analyses indicated that LVS-vmPFC FC correlated with anhedonia-related subscales from the Beck Depression Inventory (r = -0.691, P= 0.004) and PTSD Symptom Scale (avoidance/numbness; r = -0.514, P = 0.042) in participants with an inflammatory score over the median (n= 16). Results suggest that inflammation contributes to compromised reward circuitry and symptoms of anhedonia and PTSD in trauma-exposed women.

Examining the cardiovascular response to fear extinction in a trauma-exposed sample

BackgroundTrauma and symptoms of posttraumatic stress disorder (PTSD) have repeatedly been linked to impaired cardiovascular functioning. Poor fear extinction is a well-established biomarker of PTSD that may provide insight into mechanisms underlying cardiovascular risk. The current study probed the cardiovascular response to extinction in a sample of trauma-exposed individuals. MethodsParticipants were 51 trauma-exposed women who underwent a fear conditioning paradigm. Heart rate (HR) during extinction was examined in response to a conditioned stimulus that was previously paired with an aversive unconditioned stimulus (CS+) and one that was never paired (CS-). Heart rate variability (HRV) was calculated at baseline and during the extinction session. ResultsConsistent with fear bradycardia, initial HR deceleration (.5-2s) after CS + onset occurred during early extinction and appeared to extinguish over time. Higher baseline HRV was significantly associated with greater fear bradycardia during early extinction. ConclusionsThis is the first study to demonstrate a pattern of fear bradycardia in early extinction, which was associated with higher HRV levels and decreased over the course of the extinction phase. These results suggest that increased fear bradycardia may be indicative of greater vagal control (i.e., HRV), both of which are psychophysiological biomarkers that may influence cardiovascular and autonomic disease risk in trauma-exposed individuals.

Healthy women with severe early life trauma show altered neural facilitation of emotion inhibition under acute stress.

Across psychopathologies, trauma-exposed individuals suffer from difficulties in inhibiting emotions and regulating attention. In trauma-exposed individuals without psychopathology, only subtle alterations of neural activity involved in regulating emotions have been reported. It remains unclear how these neural systems react to demanding environments, when acute (non-traumatic but ordinary) stress serves to perturbate the system. Moreover, associations with subthreshold clinical symptoms are poorly understood. The present fMRI study investigated response inhibition of emotional faces before and after psychosocial stress situations. Specifically, it compared 25 women (mean age 31.5 ± 9.7 years) who had suffered severe early life trauma but who did not have a history of or current psychiatric disorder, with 25 age- and education-matched trauma-naïve women. Under stress, response inhibition related to fearful faces was reduced in both groups. Compared to controls, trauma-exposed women showed decreased left inferior frontal gyrus (IFG) activation under stress when inhibiting responses to fearful faces, while activation of the right anterior insula was slightly increased. Also, groups differed in brain-behaviour correlations. Whereas stress-induced false alarm rates on fearful stimuli negatively correlated with stress-induced IFG signal in controls, in trauma-exposed participants, they positively correlated with stress-induced insula activation. Neural facilitation of emotion inhibition during stress appears to be altered in trauma-exposed women, even without a history of or current psychopathology. Decreased activation of the IFG in concert with heightened bottom-up salience of fear related cues may increase vulnerability to stress-related diseases.

Examination of the stability of the anxiety sensitivity index across the menstrual cycle in trauma-exposed women with and without PTSD

ABSTRACTBackground and Objectives: Anxiety sensitivity (AS), as measured by the Anxiety Sensitivity Index (ASI), has consistently been studied as a trait-level predictor of a variety of emotional and physical health conditions, including premenstrual symptoms. The menstrual cycle influences symptom expression and stress reactivity among anxiety and stress-related disorders. However, research has yet to directly evaluate the stability of AS across the various phases of the menstrual cycle, particularly in clinical populations with high levels of AS and with documented menstrual cycle differences in symptoms such as women with posttraumatic stress disorder (PTSD).Design and Methods: The current study examined whether AS fluctuates as a function of menstrual cycle phase among a community sample of trauma-exposed women (N = 48) with and without PTSD. Participants completed the ASI, including subscales assessing sensitivity to physical, cognitive, and social symptoms of anxiety, during early follicular and mid-luteal menstrual cycle phases.Results: Results revealed that ASI scores remained relatively stable across the different phases of the menstrual cycle assessed; evidence for stability was particularly strong for the subscale assessing sensitivity to physical symptoms of anxiety.Conclusion: This study provides additional support for the conceptualization of AS as a stable, trait-like, cognitive risk factor.

Body mass index in relation to cardiovascular recovery from psychological stress among trauma-exposed women.

Delayed cardiovascular recovery has been associated with greater heart disease risks. However, relative to stress reactivity, cardiovascular recovery has been understudied. Further, few studies have examined associations of recovery with modifiable factors that might inform efforts to enhance recovery. The focus of the present study was whether body mass index (BMI) was associated with recovery following two stress tasks (speech and mental arithmetic). Based on the conceptualization that obesity may lead to impaired post-stress recovery, we also examined whether higher BMI accounted for previously reported associations between elevated PTSD symptoms and delayed recovery. The sample consisted of 50 trauma-exposed civilian women ages 19-49 (M±SD = 30 ± 8). The stress tasks were followed by 15-min post-task rest periods. Cardiovascular recovery was assessed as percentage return to baseline; the recovery measures consisted of heart rate (HR), cardiac output (CO), systolic blood pressure (SBP) and diastolic blood pressure (DBP). PTSD severity was based on structured interview. Higher BMI was associated with significantly less CO recovery from the speech task and less HR recovery from mental arithmetic. Higher BMI was associated with more SBP recovery from the math task, but was not associated with DBP recovery. The indirect effects of BMI in the PTSD/CO recovery relationship based on the Sobel test of mediation were significant. These results partially support the hypotheses that BMI is associated with cardiovascular recovery and that associations of PTSD with recovery may be mediated by BMI.

Trauma Exposure, Posttraumatic Stress Disorder, and Aggression Among Civilian Females.

Trauma exposure and posttraumatic stress disorder (PTSD) have evinced ties to increased risk for aggressive behavior. However, very little information is known regarding the relations between trauma exposure, PTSD, and aggression among non-veteran women. Furthermore, research has not examined the associations between trauma exposure, PTSD symptoms, and aggression using the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5) PTSD criteria. The primary aim of the current study was to investigate the relationships between trauma exposure, PTSD symptoms, and aggression among women. The secondary aim was to examine the specific PTSD symptom clusters in relation to indices of aggression. A total of 217 civilian, trauma-exposed female undergraduate students participated in the study (Mage = 24.30, SD = 6.83, 63.2% White). Higher levels of trauma exposure and PTSD symptoms corresponded with anger (b = .47, 95% CI = [0.11-0.83]; b = .11, 95% CI = [0.05-0.16], respectively) and verbal aggression (b = .50, 95% CI = [0.21-0.78]; b = .06, 95% CI = [0.01-0.10], respectively). PTSD symptoms, but not cumulative trauma exposure, was associated with hostility (b = .23, 95% CI = [0.14-0.59]), whereas physical aggression was only related to trauma exposure (b = .69, 95% CI = [0.31-1.06]). Furthermore, there was a significant indirect effect of cumulative trauma through PTSD symptoms on anger and verbal aggression (b = .15, 95% CI = [0.05-0.32]; b = .09, 95% CI = [0.02-0.20], respectively). Trauma-exposed civilian females with higher levels of PTSD symptoms may be at increased risk for several indices of aggressive behavior. Furthermore, PTSD symptoms may better account for some, but not all, aspects of aggression in trauma-exposed women.

The differential effects of PTSD, MDD, and dissociation on CRP in trauma-exposed women

ObjectiveC-reactive protein (CRP), a marker of systemic inflammation, has been associated with psychiatric disorders including major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). Some research suggests that exposure to trauma can trigger increased activity in the inflammatory system. Dissociation is associated with chronic trauma exposure and may be an important factor in understanding the risk for psychiatric outcomes associated with inflammation. The main objective of the current study was to understand how CRP was related to trauma, dissociation, PTSD and MDD in a sample of 55 traumatized African American women with type 2 diabetes mellitus recruited from an urban hospital. MethodHigh sensitivity CRP (hsCRP) was assayed through blood samples; psychiatric disorders were assessed with structured clinical interviews, dissociation was assessed with the Multiscale Dissociation Inventory, and exposure to trauma in childhood and adulthood was assessed with the Childhood Trauma Questionnaire and the Traumatic Events Inventory, respectively. ResultsCorrelational results showed a significant association between higher concentrations of hsCRP and child abuse (p < 0.05), overall dissociation severity (p < 0.001), and PTSD symptoms (p < 0.01). ANOVA results showed significantly higher levels of hsCRP in those with current MDD, current PTSD, and remitted PTSD. A hierarchical linear regression model demonstrated a significant association between dissociation symptoms and greater hsCRP levels independent of childhood abuse, PTSD, and MDD (R2∆ = 0.11, p = 0.001) and independent of emotion dysregulation (p < 0.05). ConclusionThese findings suggest that dissociation symptoms among those with a history of trauma may be particularly associated with higher levels of inflammation.

A trauma-informed substance use and sexual risk reduction intervention for young South African women: a mixed-methods feasibility study

ObjectivesSexual and physical trauma and substance use are intersecting risks for HIV among young women. This study assesses the feasibility, acceptability and preliminary effects of a novel trauma-informed substance use...

Not all posttraumatic stress disorder symptoms are equal: fear, dysphoria, and risk of developing hypertension in trauma-exposed women.

Posttraumatic stress disorder (PTSD) is associated with higher risk of incident hypertension, but it is unclear whether specific aspects of PTSD are particularly cardiotoxic. PTSD is a heterogeneous disorder, comprising dimensions of fear and dysphoria. Because elevated fear after trauma may promote autonomic nervous system dysregulation, we hypothesized fear would predict hypertension onset, and associations with hypertension would be stronger with fear than dysphoria. We examined fear and dysphoria symptom dimensions in relation to incident hypertension over 24 years in 2709 trauma-exposed women in the Nurses' Health Study II. Posttraumatic fear and dysphoria symptom scores were derived from a PTSD diagnostic interview. We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each symptom dimension (quintiles) with new-onset hypertension events (N = 925), using separate models. We also considered lower-order symptom dimensions of fear and dysphoria. Higher levels of fear (P-trend = 0.02), but not dysphoria (P-trend = 0.22), symptoms were significantly associated with increased hypertension risk after adjusting for socio-demographics and family history of hypertension. Women in the highest v. lowest fear quintile had a 26% higher rate of developing hypertension [HR = 1.26 (95% CI 1.02-1.57)]; the increased incidence associated with greater fear was similar when further adjusted for biomedical and health behavior covariates (P-trend = 0.04) and dysphoria symptoms (P-trend = 0.04). Lower-order symptom dimension analyses provided preliminary evidence that the re-experiencing and avoidance components of fear were particularly associated with hypertension. Fear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.

Sex differences in intrusive memories following trauma.

BackgroundA key mechanism thought to underlie Posttraumatic Stress Disorder (PTSD) is enhanced emotional memory consolidation. Recent evidence in healthy controls revealed that women have greater negative memory consolidation following stress relative to men. This study examined emotional memory consolidation in women and men with PTSD, and in trauma-exposed and non-trauma controls to test the hypothesis that emotionally negative memory consolidation would be greater in women with PTSD.MethodOne hundred and forty-seven men and women (47 with PTSD, 49 trauma-exposed controls, and 51 non-trauma controls) completed an emotional memory task where they looked at negative, neutral and positive images from the International Affective Picture System (IAPS). Delayed recall and an intrusive memory diary were completed two days later.ResultsWomen displayed greater recall, and reported more negative intrusive memories than men. A gender x group interaction effect showed that both women with PTSD and trauma-exposed women reported more intrusive memories than women without trauma exposure or men.ConclusionThis study provided preliminary evidence of sex differences in intrusive memories in those with PTSD as well as those with a history of trauma exposure. Future research should include measures of sex hormones to further examine sex differences on memory consolidation in the context of trauma exposure and PTSD.

Resting amygdala connectivity and basal sympathetic tone as markers of chronic hypervigilance

BackgroundChronic hypervigilance, a state of sustained alertness and hyperarousal in the absence of threat, has been shown to predict poorer clinical outcomes post-trauma. An exaggerated and persistent amygdala alerting response to affective information has been proposed as a reactivity-based, and thus indirect, marker of hypervigilance. However, because chronic hypervigilance is a persistent rather than reactive state, it should be directly observable under resting-state conditions without the need for exposure to affectively charged stimuli. ObjectiveWe tested resting amygdala connectivity and basal sympathetic and hypothalamic-pituitary-adrenal axis activity as direct neural and neuroendocrine markers of chronic hypervigilance. Participants24 trauma-exposed women (age M = 22.9, SD = 5.5) and 20 no-trauma controls (age M = 21.1, SD = 3.2). MeasuresAmygdala connectivity was measured using functional magnetic resonance imaging at rest and during viewing of novel and familiar affective scenes. Elevated amygdala connectivity during the viewing of novel scenes (exaggerated alerting response) and familiar scenes (persistent alerting response) was used as a reactivity-based index of hypervigilance. Resting amygdala connectivity and basal salivary alpha-amylase (sAA) and cortisol were tested as neural and neuroendocrine markers of hypervigilance, respectively. ResultsCompared to no-trauma controls, trauma-exposed women showed greater connectivity between the left amygdala and the ventral anterior cingulate cortex (vACC) both during affective processing and at rest. Exaggerated neural novelty response was associated with greater resting left amygdala-vACC connectivity and higher basal sAA, but not cortisol. ConclusionsGreater synchronization of threat-detection circuitry in the absence of threat and basal sympathetic tone might serve as complementary resting-state markers of the cognitive and physiological components of chronic hypervigilance, respectively.

Cardiovascular risks in relation to posttraumatic stress severity among young trauma-exposed women

BackgroundPosttraumatic stress is associated with elevated risk for cardiovascular disease (CVD). Relatively little research, particularly among women, has documented mechanisms by which PTSD might confer CVD risk during early adulthood. The purpose of the present study was to examine whether the number and relative levels of CVD risk factors are associated with posttraumatic stress symptom severity among young, trauma-exposed women. MethodsParticipants were premenopausal women ages 19–49 with varying levels of posttraumatic stress and no history of chronic medical illness (n = 54), and were recruited from mental health clinics and the general community. Posttraumatic stress severity was assessed with a structured clinical interview (Clinician-Administered PTSD Scale). The CVD risk factors assessed were lipids (total cholesterol, triglycerides, high- and low-density lipoproteins), resting blood pressure (BP), body mass index (BMI), no exercise in typical week, and cigarette smoking. ResultsPosttraumatic stress severity was associated with lower high-density lipoprotein levels and higher triglycerides, greater systolic and diastolic BP, greater BMI, and a greater number of total CVD risk factors. LimitationsThe main limitation is the limited number of participants who displayed clinical levels on some of the CVD risk factors (e.g., BP). Nonetheless, most participants exhibited more than one CVD risk factor, indicating the potential for many of the women in this relatively young sample to progress toward greater risk later in life. ConclusionsThe present results support the contention that, in the absence of medical illness, posttraumatic stress symptom severity among young women is associated with several CVD risk factors early in life.

Impact of Traumatic Stress on Sleep and Management Options in Women.

After exposure to traumatic stress, women are at greater risk than men for developing symptoms of some psychiatric disorders, including insomnia and nightmares. Sleep disturbance is one of the most refractory symptoms of posttraumatic stress disorder. Women were included in a few studies that examined efficacy of psychological or pharmacologic interventions for trauma-related sleep disturbances. Studies demonstrated preliminary evidence for efficacy of cognitive behavioral therapy for insomnia, imagery rehearsal therapy, and combinations of these techniques in treating insomnia and nightmares in trauma-exposed women. Prazosin as an adjunct to ongoing treatment is a potentially efficacious strategy for treating trauma-related nightmares in women.

Methods to reduce false reporting of substance abstinence in clinical research

Substance use may influence study results in human subjects research. This study aims to report the concordance between self-report and biochemical assessments of substance use and test the effect of methods to reduce false reports of abstinence in trauma-exposed women participating in a research study. In this pilot study, substance use was assessed during telephone prescreening and via self-report and biochemical verification (i.e., urine toxicology and alcohol breathalyzer tests) at an in-person evaluation. Due to the high number of participants who tested positive for substances despite self-reporting abstinence during prescreening, study procedures were modified to disincentivize false self-reports of substance use two thirds of the way through recruitment. New potential participants were explicitly informed during prescreening and informed consent that a positive drug or alcohol test during screening would result in exclusion from the study and withholding of payment. Prior to modifying study methods, 20% of participants who had reported abstinence during the telephone prescreen had a positive substance use test at the in-person visit. Modifying study procedures resulted in an 81% decrease in positive substance use assessments. Adoption of this methodology may decrease inadvertent confounding of clinical research outcomes by undetected and/or misreported substance use.

Generalisation of fear in PTSD related to prolonged childhood maltreatment: an experimental study.

Fear responses are particularly intense and persistent in post-traumatic stress disorder (PTSD), and can be evoked by unspecific cues that resemble the original traumatic event. Overgeneralisation of fear might be one of the underlying mechanisms. We investigated the generalisation and discrimination of fear in individuals with and without PTSD related to prolonged childhood maltreatment. Sixty trauma-exposed women with (N = 30) and without (N = 30) PTSD and 30 healthy control participants (HC) underwent a fear conditioning and generalisation paradigm. In a contingency learning procedure, one of two circles of different sizes was associated with an electrical shock (danger cue), while the other circle represented a safety cue. During generalisation testing, online risk ratings, reaction times and fear-potentiated startle were measured in response to safety and danger cues as well as to eight generalisation stimuli, i.e. circles of parametrically varying size creating a continuum of similarity between the danger and safety cue. The increase in reaction times from the safety cue across the different generalisation classes to the danger cue was less pronounced in PTSD compared with HC. Moreover, PTSD participants expected higher risk of an aversive event independent of stimulus types and task. Alterations in generalisation constitute one part of fear memory alterations in PTSD. Neither the accuracy of a risk judgement nor the strength of the induced fear was affected. Instead, processing times as an index of uncertainty during risk judgements suggested a reduced differentiation between safety and threat in PTSD.

A community-based randomized controlled trial of Mom Power parenting intervention for mothers with interpersonal trauma histories and their young children.

We conducted a study to evaluate the effectiveness of Mom Power, a multifamily parenting intervention to improve mental health and parenting among high-risk mothers with young children in a community-based randomized controlled trial (CB-RCT)design. Participants (N=122) were high-risk mothers (e.g., interpersonal trauma histories, mental health problems, poverty) and their young children (age <6years), randomized either to Mom Power, a parenting intervention (treatment condition), or weekly mailings of parenting information (control condition). In this study, the 13-session intervention was delivered by community clinicians trained to fidelity. Pre- and post-trial assessments included mothers' mental health symptoms, parenting stress and helplessness, and connection to care. Mom Power was delivered in the community with fidelity and had good uptake (>65%) despite the risk nature of the sample. Overall, we found improvements in mental health and parenting stress for Mom Power participants but not for controls; in contrast, control mothers increased in parent-child role reversal across the trial period. The benefits of Mom Power treatment (vs. control) were accentuated for mothers with interpersonal trauma histories. Results of this CB-RCT confirm the effectiveness of Mom Power for improving mental health and parenting outcomes for high-risk, trauma-exposed women with young children. ClinicalTrials.gov Identifier: NCT01554215.

Posttraumatic stress disorder and accelerated aging: PTSD and leukocyte telomere length in a sample of civilian women.

Studies in male combat veterans have suggested posttraumatic stress disorder (PTSD) is associated with shorter telomere length (TL). We examined the cross-sectional association of PTSD with TL in women exposed to traumas common in civilian life. Data are from a substudy of the Nurses' Health Study II (N = 116). PTSD and subclinical PTSD were assessed in trauma-exposed women using diagnostic interviews. An array of health behaviors and conditions were assessed. DNA was extracted from peripheral blood leukocytes (collected 1996-1999). Telomere repeat copy number to single gene copy number (T/S) was determined by quantitative real-time PCR telomere assay. We used linear regression models to assess associations and examine whether a range of important health behaviors (e.g., cigarette smoking) and medical conditions (e.g., hypertension) previously associated with TL might explain a PTSD-TL association. We further examined whether type of trauma exposure (e.g., interpersonal violence) was associated with TL and whether trauma type might explain a PTSD-TL association. Relative to not having PTSD, women with a PTSD diagnosis had shorter log-transformed TL (β = -.112, 95% confidence interval (CI) = -0.196, -0.028). Adjustment for health behaviors and medical conditions did not attenuate this association. Trauma type was not associated with TL and did not account for the association of PTSD with TL. Our results add to growing evidence that PTSD may be associated with more rapid cellular aging as measured by telomere erosion. Moreover, the association could not be explained by health behaviors and medical conditions assessed in this study, nor by type of trauma exposure.

Post-traumatic Stress Disorder and 20-Year Physical Activity Trends Among Women.

Post-traumatic stress disorder (PTSD) may be associated with physical inactivity, a modifiable lifestyle factor that contributes to risk of cardiovascular and other chronic diseases; however, no study has evaluated the association between PTSD onset and subsequent physical activity (PA) changes. Analyses were conducted between October 2014 and April 2016, using data from the ongoing Nurses' Health Study II (N=50,327). Trauma exposure and PTSD symptoms were assessed using two previously validated measures, the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD. Average PA (hours/week) was assessed using self-report measures at six time points across 20 years (1989-2009). Linear mixed models with time-updated PTSD assessed differences in PA trajectories by trauma/PTSD status. Among a subsample of women whose trauma/PTSD onset during follow-up, group differences in PA patterns before and after onset were assessed using linear spline models. PA decreased more steeply over time among trauma-exposed women reporting four or five (β= -2.5E-3, SE=1.0E-3, p=0.007) or six or seven PTSD symptoms (β= -6.7E-3, SE=1.1E-3, p<0.001) versus women without trauma exposure, adjusting for potential confounders. Among a subsample of women whose trauma/PTSD symptoms onset during follow-up, no differences in PA were observed prior to onset; after onset, women with six or seven PTSD symptoms had a steeper decline (β= -17.1E-3, SE=4.2E-3, p<0.001) in PA over time than trauma-exposed women without PTSD. Decreases in PA associated with PTSD symptoms may be a pathway through which PTSD influences cardiovascular and other chronic diseases.

PTSD and Alcohol Associations Among Trauma-Exposed Women: Critical Questions for the Field.

PTSD and Alcohol Associations Among Trauma-Exposed Women: Critical Questions for the Field.

Persistent amygdala novelty response is associated with less anterior cingulum integrity in trauma-exposed women.

ObjectivesWe investigated the potential role of cingulum and uncinate fasciculus integrity in trauma-related neural hypervigilance, indexed by less discrimination between amygdala activation to novel and familiar affective images.Participants22 women (mean age 21.7 ± 3.9 years) with a history of trauma, and 20 no-trauma controls (mean age 21.9 ± 4.8 years).MeasuresTrauma exposure and trauma-related symptoms were assessed during structured clinical interview. White matter integrity in the anterior cingulum, parahippocampal cingulum, and uncinate fasciculus was measured using diffusion weighted imaging. Amygdala response to novel and familiar affective scenes was measured with functional magnetic resonance imaging.ResultsTrauma-exposed women showed less discrimination between novel and familiar negative images in the amygdala compared to no-trauma controls. In trauma-exposed women, less amygdala discrimination between novel and familiar affective images was associated with less structural integrity in the anterior cingulum, but was not associated with structural integrity of the parahippocampal cingulum or the uncinate fasciculus.ConclusionsThe anterior cingulum might play an important role in impaired novelty discrimination for affective information in the amygdala. This impairment is potentially driven by inefficient habituation and could contribute to persistent behavioral hypervigilance following trauma exposure.