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Background: Childhood maltreatment is robustly associated with increased risk of poor mental health outcome and changes in brain function. The authors investigated whether childhood experience of abuse (e.g. physical, emotional and sexual abuse) and neglect (physical and emotional deprivation) was differentially associated with neural reactivity to threat., Methods: Participants were drawn from an existing study and allocated to one of four groups based on self-report of childhood maltreatment experience: individuals with childhood abuse experiences (n = 70); individuals with childhood neglect experiences (n = 87); individuals with combined experience of childhood abuse and neglect (n = 50); and non-maltreated individuals (n = 207) propensity score matched (PSM) on gender, age, IQ, psychopathology and SES. Neural reactivity to facial cues signalling threat was compared across groups, allowing the differential effects associated with particular forms of maltreatment experience to be isolated., Results: Brain imaging analyses indicated that while childhood abuse was associated with heightened localised threat reactivity in ventral amygdala, experiences of neglect were associated with heightened reactivity in a distributed cortical fronto-parietal network supporting complex social and cognitive processing as well as in the dorsal amygdala. Unexpectedly, combined experiences of abuse and neglect were associated with hypo-activation in several higher-order cortical regions as well as the amygdala., Conclusions: Different forms of childhood maltreatment exert differential effects in neural threat reactivity: while the effects of abuse are more focal, the effects of neglect and combined experiences of abuse are more distributed. These findings are relevant for understanding the range of psychiatric outcomes following childhood maltreatment and have implications for intervention.

A recent study reported a negative association between a putatively functional dopamine (DA) polygenic score, indexing higher levels of DA signaling, and depressive symptoms. We attempted to replicate this association using data from the Duke Neurogenetics Study. Our replication attempt was made in a subsample of 520 non-Hispanic Caucasian volunteers (277 women, mean age 19.78 ± 1.24 years). The DA polygenic score was based on the following five loci: rs27072 (SLC6A3/DAT1), rs4532 (DRD1), rs1800497 (DRD2/ANKK1), rs6280 (DRD3), and rs4680 (COMT). Because the discovery sample in the original study consisted mostly of Asian participants, we also conducted a post hoc analysis in a smaller subsample of Asian volunteers (N = 316, 179 women, mean age 19.61 ± 1.32 years). In the primary sample of non-Hispanic Caucasians, a linear regression analysis controlling for sex, age, socioeconomic status (SES), body mass index, genetic ancestry, and both early and recent life stress, revealed that higher DA polygenic scores were associated with higher self-reported symptoms of depression. This was in contrast to the original association of higher DA polygenic scores and lower depressive symptoms. However, the direction of the association in our Asian subsample was consistent with this original finding. Our results also suggested that compared to the Asian subsample, the non-Hispanic Caucasian subsample was characterized by higher SES, lower early and recent life stress, and lower depressive symptoms. These differences may have contributed to the observed divergence in associations. Collectively, the current findings add to evidence that specific genetic associations may differ between populations and further encourage explicit modeling of race/ethnicity in examining the polygenic nature of depressive symptoms and depression.

Introduction: Previous research has identified specific brain regions associated with regulating emotion using common strategies such as expressive suppression and cognitive reappraisal. However, most research focuses on a priori regions and directs participants how to regulate, which may not reflect how people naturally regulate outside the laboratory., Method: Here, we used a data-driven approach to investigate how individual differences in distributed intrinsic functional brain connectivity predict emotion regulation tendency outside the laboratory. Specifically, we used connectome-based predictive modeling to extract functional connections in the brain significantly related to the dispositional use of suppression and reappraisal. These edges were then used in a predictive model and cross-validated in novel participants to identify a neural signature that reflects individual differences in the tendency to suppress and reappraise emotion., Results: We found a significant neural signature for the dispositional use of suppression, but not reappraisal. Within this whole-brain signature, the intrinsic connectivity of the default mode network was most informative of suppression tendency. In addition, the predictive performance of this model was significant in males, but not females., Conclusion: These findings help inform how whole-brain networks of functional connectivity characterize how people tend to regulate emotion outside the laboratory., (© 2020 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.)

Background: Childhood maltreatment is one of the most potent predictors of future psychopathology, including internalizing disorders. It remains unclear whether heightened amygdala reactivity to threat and elevated stress exposure may be implicated in the pathogenesis and maintenance of internalizing disorders among individuals with a history of childhood maltreatment., Methods: Using data from a sample of 1,144 young adults, we investigated the contribution of baseline threat-related amygdala reactivity and prospective major stressful life events to internalizing symptoms severity 1 year later (on average) in individuals with a history of maltreatment (n = 100) and propensity score matched nonmaltreated peers (n = 96)., Results: Even after stringently matching for several potentially confounding variables - including baseline internalizing symptoms, socioeconomic status and IQ - childhood maltreatment status predicted increased amygdala reactivity at baseline, elevated post-baseline exposure to major stressful life events and internalizing symptoms at follow-up. We also showed, for the first time, that amygdala reactivity at baseline and also post-baseline exposure to major stressful life events mediated the association between a history of maltreatment and future internalizing symptoms., Conclusions: These findings provide support for the view that maltreatment is a potent developmental insult leading to long-lasting neurocognitive recalibrations of the threat processing system. It is possible that such alterations, over time, may impact mental health functioning by compromising the ability to effectively negotiate everyday challenges (stress susceptibility). These alterations were not, however, found to sensitize an individual to the impact of major stressful life events. The results of this study also lend compelling support to the view that increased psychiatric risk, in the context of childhood maltreatment, follows from an increased propensity to experience major stressful life events (stress generation)., (© 2019 Association for Child and Adolescent Mental Health.)

Amongst a number of negative life sequelae associated with childhood adversity is the later expression of a higher dispositional tendency to experience anger and frustration to a wide range of situations (i.e., trait anger). We recently reported that an association between childhood adversity and trait anger is moderated by individual differences in both threat-related amygdala activity and executive control-related dorsolateral prefrontal cortex (dlPFC) activity, wherein individuals with relatively low amygdala and high dlPFC activity do not express higher trait anger even when having experienced childhood adversity. Here, we examine possible structural correlates of this functional dynamic using diffusion magnetic resonance imaging data from 647 young adult men and women volunteers. Specifically, we tested whether the degree of white matter microstructural integrity as indexed by fractional anisotropy modulated the association between childhood adversity and trait anger. Our analyses revealed that higher microstructural integrity of multiple pathways was associated with an attenuated link between childhood adversity and adult trait anger. Amongst these pathways was the uncinate fasciculus (UF; ΔR 2  = 0.01), which not only provides a major anatomical link between the amygdala and prefrontal cortex but also is associated with individual differences in regulating negative emotion through top-down cognitive reappraisal. These findings suggest that higher microstructural integrity of distributed white matter pathways including but not limited to the UF may represent an anatomical foundation serving to buffer against the expression of childhood adversity as later trait anger, which is itself associated with multiple negative health outcomes., (© 2019 Wiley Periodicals, Inc.)

Compared with neural biomarkers of risk for mental illness, little is known about biomarkers of resilience. We explore if greater executive control-related prefrontal activity may function as a resilience biomarker by "rescuing" risk associated with higher threat-related amygdala and lower reward-related ventral striatum activity. Functional MRI was used to assay baseline threat-related amygdala, reward-related ventral striatum, and executive control-related prefrontal activity in 120 young adult volunteers. Participants provided self-reported mood and anxiety ratings at baseline and follow-up. A moderation model revealed a significant three-way interaction wherein higher amygdala and lower ventral striatum activity predicted increases in anxiety in those with average or low but not high prefrontal activity. This effect was specific to anxiety, with the neural biomarkers explaining ~10% of the variance in change over time, above and beyond baseline symptoms, sex, age, IQ, presence or absence of DMS-IV diagnosis, and both early and recent stress. Our findings are consistent with the importance of top-down executive control in adaptive regulation of negative emotions, and highlight a unique combination of neural biomarkers that may identify at-risk individuals for whom the adoption of strategies to improve executive control of negative emotions may prove particularly beneficial.

Background: Recent work has indicated that there at least two distinct subtypes of psychopathy. Primary psychopathy is characterized by low anxiety and thought to result from a genetic predisposition, whereas secondary psychopathy is characterized by high anxiety and thought to develop in response to environmental adversity. Primary psychopathy is robustly associated with reduced neural activation to others' emotions and, in particular, distress. However, it has been proposed that the secondary presentation has different neurocognitive correlates., Methods: Primary (n = 50), secondary (n = 100), and comparison (n = 82) groups were drawn from a large volunteer sample (N = 1444) using a quartile-split approach across psychopathic trait (affective-interpersonal) and anxiety measures. Participants performed a widely utilized emotional face processing task during functional magnetic resonance imaging., Results: The primary group showed reduced amygdala and insula activity in response to fear. The secondary group did not differ from the comparison group in these regions. Instead, the secondary group showed reduced activity compared with the comparison group in other areas, including the superior temporal sulcus/inferior parietal lobe, thalamus, pallidum, and substantia nigra. Both psychopathy groups also showed reduced activity in response to fear in the anterior cingulate cortex. During anger processing, the secondary group exhibited reduced activity in the anterior cingulate cortex compared with the primary group., Conclusions: Distinct neural correlates of fear processing characterize individuals with primary and secondary psychopathy. The reduced neural response to fear that characterizes individuals with the primary variant of psychopathic traits is not observed in individuals with the secondary presentation. The neurocognitive mechanisms underpinning secondary psychopathy warrant further systematic investigation., (Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Emotion regulation refers to the use of various strategies, such as cognitive reappraisal and expressive suppression, to help manage our negative experiences, emotions, and thoughts. Although such emotion regulation often occurs within broader social dynamics and interactions, little is known about how social contexts interact with specific regulation strategies to shape the experience of negative emotions. Using data from 544 young adult university students, we provide initial evidence that habitual use of cognitive reappraisal is associated with lower future experience of depression and anxiety primarily through higher perceived social support (PSS). In contrast, expressive suppression is associated with higher future depression and anxiety primarily through lower PSS. These patterns are consistent with the importance of interpersonal influences on emotion regulation and suggest that assessment of social support can help elucidate the mechanisms of successfully regulating negative mood.

Cognitive reappraisal is a commonly used form of emotion regulation that utilizes frontal-executive control to reframe an approaching emotional event to moderate its potential psychological impact. Use of cognitive reappraisal has been associated with diminished experience of anxiety and depressive symptoms, as well as greater overall well-being. Using data from a study of 647 healthy young adults, we provide initial evidence that an association between typical use of cognitive reappraisal in daily life and the experience of anxiety and depressive symptoms is moderated by the microstructural integrity of the uncinate fasciculus, which provides a major anatomical link between the amygdala and prefrontal cortex. Our findings are consistent with the nature of top-down regulation of bottom-up negative emotions and suggest the uncinate fasciculus may be a useful target in the search for biomarkers predicting not only disorder risk but also response to psychotherapy utilizing cognitive reappraisal. (PsycINFO Database Record, ((c) 2018 APA, all rights reserved).)

Background: The experience of childhood maltreatment is a significant risk factor for the development of depression. This risk is particularly heightened after exposure to additional, more contemporaneous stress. While behavioral evidence exists for this relation, little is known about biological correlates of these stress interactions. Identifying such correlates may provide biomarkers of risk for later depression., Methods: Here, we leverage behavioral, experiential, and neuroimaging data from the Duke Neurogenetics Study to identify potential biomarkers of stress exposure. Based on the past research, we were specifically interested in reward-related connectivity and the interaction of early and more recent stress. We examined psychophysiological interactions between the ventral striatum and other brain regions in relation to these stress variables, as well as measures of internalizing symptomatology (n = 926, participant age range = 18-22 years of age)., Results: We found relatively increased reward-related functional connectivity between the left ventral striatum and the medial prefrontal cortex in individuals exposed to greater levels of childhood maltreatment who also experienced greater levels of recent life stress (β = 0.199, p < 0.005). This pattern of functional connectivity was further associated with elevated symptoms of depression (β = 0.089, p = 0.006). Furthermore, using a moderated mediation framework, we demonstrate that this functional connectivity provides a biological link between cumulative stress exposure and internalizing symptomatology., Conclusions: These findings suggest a novel biomarker linking cumulative stress exposure with the later experience of depressive symptoms. Our results are discussed in the context of past research examining stress exposure in relation to depression.

Background: Trait anger, or the dispositional tendency to experience a wide range of situations as annoying or frustrating, is associated with negative mental and physical health outcomes. The experience of adversity during childhood is one risk factor for the later emergence of high trait anger. This association has been hypothesized to reflect alterations in neural circuits supporting bottom-up threat processing and top-down executive control., Methods: Here, using functional magnetic resonance imaging and self-report questionnaire data from 220 volunteers, we examined how individual differences in top-down prefrontal executive control and bottom-up amygdala threat activity modulate the association between childhood adversity and trait anger during young adulthood., Results: We report that the association between childhood adversity and trait anger is attenuated specifically in young adults who have both relatively low threat-related amygdala activity and high executive control-related dorsolateral prefrontal cortex activity., Conclusions: These brain activity patterns suggest that simultaneous consideration of their underlying cognitive processes-namely, threat processing and executive control-may be useful in strategies designed to mitigate the negative mental health consequences of childhood adversity., (Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Accumulating mental-health research encourages a shift in focus toward transdiagnostic dimensional features that are shared across categorical disorders. In support of this shift, recent studies have identified a general liability factor for psychopathology-sometimes called the 'p factor'- that underlies shared risk for a wide range of mental disorders. Identifying neural correlates of this general liability would substantiate its importance in characterizing the shared origins of mental disorders and help us begin to understand the mechanisms through which the 'p factor' contributes to risk. Here we believe we first replicate the 'p factor' using cross-sectional data from a volunteer sample of 1246 university students, and then using high-resolution multimodal structural neuroimaging, we demonstrate that individuals with higher 'p factor' scores show reduced structural integrity of white matter pathways, as indexed by lower fractional anisotropy values, uniquely within the pons. Whole-brain analyses further revealed that higher 'p factor' scores are associated with reduced gray matter volume in the occipital lobe and left cerebellar lobule VIIb, which is functionally connected with prefrontal regions supporting cognitive control. Consistent with the preponderance of cerebellar afferents within the pons, we observed a significant positive correlation between the white matter integrity of the pons and cerebellar gray matter volume associated with higher 'p factor' scores. The results of our analyses provide initial evidence that structural alterations in corticocerebellar circuitry supporting core functions related to the basic integration, coordination and monitoring of information may contribute to a general liability for common mental disorders.

Sleep disturbances represent one risk factor for depression. Reward-related brain function, particularly the activity of the ventral striatum (VS), has been identified as a potential buffer against stress-related depression. We were therefore interested in testing whether reward-related VS activity would moderate the effect of sleep disturbances on depression in a large cohort of young adults. Data were available from 1129 university students (mean age 19.71 ± 1.25 years; 637 women) who completed a reward-related functional MRI task to assay VS activity and provided self-reports of sleep using the Pittsburgh Sleep Quality Index and symptoms of depression using a summation of the General Distress/Depression and Anhedonic Depression subscales of the Mood and Anxiety Symptoms Questionnaire-short form. Analyses revealed that as VS activity increased the association between sleep disturbances and depressive symptoms decreased. The interaction between sleep disturbances and VS activity was robust to the inclusion of sex, age, race/ethnicity, past or present clinical disorder, early and recent life stress, and anxiety symptoms, as well as the interactions between VS activity and early or recent life stress as covariates. We provide initial evidence that high reward-related VS activity may buffer against depressive symptoms associated with poor sleep. Our analyses help advance an emerging literature supporting the importance of individual differences in reward-related brain function as a potential biomarker of relative risk for depression. SIGNIFICANCE STATEMENT Sleep disturbances are a common risk factor for depression. An emerging literature suggests that reward-related activity of the ventral striatum (VS), a brain region critical for motivation and goal-directed behavior, may buffer against the effect of negative experiences on the development of depression. Using data from a large sample of 1129 university students we demonstrate that as reward-related VS activity increases, the link between sleep disturbances and depression decreases. This finding contributes to accumulating research demonstrating that reward-related brain function may be a useful biomarker of relative risk for depression in the context of negative experiences., (Copyright © 2017 the authors 0270-6474/17/379724-06$15.00/0.)

Calculating math problems from memory may seem unrelated to everyday processing of emotions, but they have more in common than one might think. Prior research highlights the importance of the dorsolateral prefrontal cortex (dlPFC) in executive control, intentional emotion regulation, and experience of dysfunctional mood and anxiety. While it has been hypothesized that emotion regulation may be related to 'cold' (ie. not emotion-related) executive control, this assertion has not been tested. We address this gap by providing evidence that greater dlPFC activity during 'cold' executive control is associated with increased use of cognitive reappraisal to regulate emotions in everyday life. We then demonstrate that in the presence of increased life stress, increased dlPFC activity is associated with lower mood and anxiety symptoms and clinical diagnoses. Collectively, our results encourage ongoing efforts to understand prefrontal executive control as a possible intervention target for improving emotion regulation in mood and anxiety disorders.

The experience of child maltreatment is a significant risk factor for the development of later internalizing disorders such as depression and anxiety. This risk is particularly heightened after exposure to additional, more contemporaneous stress. While behavioral evidence exists for such "stress sensitization," little is known about the mechanisms mediating such relationships, particularly within the brain. Here we report that the experience of child maltreatment independent of recent life stress, gender, and age is associated with reduced structural integrity of the uncinate fasciculus, a major white matter pathway between the amygdala and ventromedial prefrontal cortex, in young adults. We further demonstrate that individuals with lower uncinate fasciculus integrity at baseline who subsequently experience stressful life events report higher levels of internalizing symptomatology at follow-up. Our findings suggest a novel neurobiological mechanism linking child maltreatment with later internalizing symptoms, specifically altered structural connectivity within the brain's threat-detection and emotion-regulation circuitry.

Impulsivity is a complex trait associated with a range of maladaptive behaviors, including many forms of psychopathology. Previous research has implicated multiple neural circuits and neurotransmitter systems in impulsive behavior, but the relationship between impulsivity and organization of whole-brain networks has not yet been explored. Using graph theory analyses, we characterized the relationship between impulsivity and the functional segregation ("modularity") of the whole-brain network architecture derived from resting-state functional magnetic resonance imaging (fMRI) data. These analyses revealed remarkable differences in network organization across the impulsivity spectrum. Specifically, in highly impulsive individuals, regulatory structures including medial and lateral regions of the prefrontal cortex were isolated from subcortical structures associated with appetitive drive, whereas these brain areas clustered together within the same module in less impulsive individuals. Further exploration of the modular organization of whole-brain networks revealed novel shifts in the functional connectivity between visual, sensorimotor, cortical, and subcortical structures across the impulsivity spectrum. The current findings highlight the utility of graph theory analyses of resting-state fMRI data in furthering our understanding of the neurobiological architecture of complex behaviors.

Background: Stressful life events are among the most reliable precipitants of major depressive disorder; yet, not everyone exposed to stress develops depression. It has been hypothesized that robust neural reactivity to reward and associated stable levels of positive affect (PA) may protect against major depressive disorder in the context of environmental adversity. However, little empirical data exist to confirm this postulation. Here, we test the hypothesis that individuals with relatively low ventral striatum (VS) reactivity to reward will show low PA levels in the context of recent life stress, while those with relatively high VS reactivity will be protected against these potentially depressogenic effects., Methods: Differential VS reactivity to positive feedback was assessed using blood oxygen level-dependent functional magnetic resonance imaging in a sample of 200 nonpatient young adults. Recent life stress, current depressive symptoms, and PA were assessed via self-report. Linear regression models were used to investigate the moderating effects of VS reactivity on the relationship between recent stress and state PA across participants., Results: Recent life stress interacted with VS reactivity to predict self-reported state PA, such that higher levels of life stress were associated with lower PA for participants with relatively low, but not for those with high, VS reactivity. These effects were independent of age, gender, race/ethnicity, trait PA, and early childhood trauma., Conclusions: The current results provide empirical evidence for the potentially protective role of robust reward-related neural responsiveness against reductions in PA that may occur in the wake of life stress and possibly vulnerability to depression precipitated by stressful life events., (Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Objective: Self-administered by spouses and other collateral informants, the nationally normed Older Adult Behavior Checklist (OABCL) provides standardized data on diverse aspects of older adult psychopathology and adaptive functioning. We tested the validity of the Older Adult Behavior Checklist (OABCL) scale scores in terms of associations with diagnoses of dementia of the Alzheimer's type (DAT) and mood disorders (MD) and with nine measures of psychopathology, cognitive performance, and adaptive functioning., Method: Informants completed OABCLs for 727 60-97-year-olds recruited from a memory disorders clinic, geriatric psychiatry clinic, and community-dwelling seniors. OABCL scale scores were tested for associations with DAT and MD diagnoses, as well as with scores on the Neuropsychiatric Inventory, Mini-Mental State Exam (MMSE), Clock Drawing Test, Alzheimer's Disease Assessment Scale, Geriatric Depression Scale, Clinical Dementia Rating, Dementia Severity Rating Scale, Trail Making Test Part A, and Instrumental Activities of Daily Living., Results: OABCL scales had medium to large correlations with the nine other indices of functioning and significantly augmented MMSE discrimination between patients with DAT versus MD. OABCL scales also discriminated significantly between patients diagnosed with DAT versus MD and both these groups versus nonclinical subjects., Conclusions: Multiple OABCL scales had medium to large associations with diverse indices of functioning based on other kinds of data. The nationally normed OABCL provides new ways to integrate informant and self-report data to improve assessment of older adults. Specifically, the OABCL can provide discrimination between those who qualify for diagnoses of DAT versus MD versus neither diagnosis., (Copyright © 2010 John Wiley & Sons, Ltd.)

To determine clinical and sociodemographic factors that are associated with major neuropsychiatric illnesses among brain tumor patients, we administered a modified version of the Brief Patient Health Questionnaire and a demographic data form to 363 adult neuro-oncology patients. Responses were analyzed to assess for associations between demographic variables, clinical variables, and symptoms consistent with diagnoses of generalized anxiety disorder and/or depression. Multivariate logistic regression analyses showed that female gender was associated with the presence of symptoms of anxiety, depression, and combined anxiety and depression. Lower WHO tumor grade classifications, lower education level, and a history of psychiatric illness also emerged as important predictors of symptoms consistent with anxiety and/or depression. Marital status and presence of past/current medical illness trended toward being significantly associated with depression alone. Patient use of psychiatric medication was not associated with any study variables. Results of the present study suggest several hypotheses to test with neuro-oncology patients in further longitudinal analyses, which would benefit from the inclusion of a wider range of neuropsychiatric symptoms in conjunction with neurocognitive and functional impairment variables.

Pathological doubt, a prominent feature of obsessive-compulsive disorder (OCD), may be related to difficulty tolerating ambiguous or uncertain situations. This is thought to be particularly true of those patients with checking compulsions. Intolerance of uncertainty (IU) has been studied extensively within the domains of worry and generalized anxiety; however, it has received relatively little empirical attention in OCD patients. We administered the Intolerance of Uncertainty Scale [Personality and Individual Differences 17 (1994) 791] to 55 clinic patients with OCD, 43 of whom had checking compulsions, and 14 nonanxious controls. OC checkers showed greater IU than did OC noncheckers and NACs. The latter two groups did not differ from each other. Furthermore, both repeating and checking rituals were associated with IU. Pathological doubt may be understood not only in terms of knowledge-based constructs, but also patients' emotional reaction to feelings of uncertainty. We discuss the implications for increasing tolerance via cognitive-behavioral therapy.

Pathological doubt, often found in individuals with obsessive-compulsive disorder (OCD), has been theoretically linked to memory deficits, but empirical evidence for such deficits has been mixed. In contrast, many studies suggest that individuals with OCD have low confidence in their memories. The present study aimed to build upon previous research by measuring memory accuracy and confidence in OCD using ecologically valid, idiographically-selected stimuli. Individuals with OCD (OCs), anxious controls (ACs), and nonanxious controls (NACs) were exposed to a set of objects that the OCs had identified as safe, unsafe, or neutral. Participants were then asked to recall as many objects as possible and to rate their confidence in each memory. This process was repeated 6 times, using the same stimuli for each trial. Contrary to hypothesis, no group differences emerged in memory accuracy. However, OCs' memory confidence for unsafe objects showed a progressive decline over repeated trials. This pattern was not observed among NACs or ACs. Furthermore, OCs with primary checking reported lower confidence in long-term memory than did OCs without primary checking. These results suggest that when OCs are repeatedly exposed to threat-related stimuli (such as repeated checking), their level of confidence in remembering these stimuli paradoxically decreases.

Laboratory studies using word-list paradigms have provided evidence that nontraumatized individuals falsely recall or recognize events that never occurred. In the present study, H. L. Roediger and K. B. McDermott's false-memory paradigm (1995) was utilized to examine possible source monitoring deficits in individuals with PTSD. Traumatized individuals with PTSD were compared with traumatized individuals without PTSD and with nontraumatized control participants. Participants heard lists of related words (e.g., bed, night) that were associates of a critical nonpresented word (e.g., sleep) and were given immediate free recall and later recognition tests. Traumatized participants with and without PTSD generated more false recalls of critical nonpresented words than did nontraumatized participants. False recall was related to trait anxiety and PTSD severity. The results are consistent with a general source-monitoring deficit in trauma-exposed individuals.

This study examines the relationship among features of social relationships, both negative and positive, and later posttrauma pathology. Using a prospective design, 142 female victims of sexual or nonsexual assault were assessed at both 2 weeks and 3 months following the assault. We examined self-reported perceptions of how often the participant has been the recipient of socially supportive actions by others and how often the participant has been engaged in interpersonal friction with others. Degree of interpersonal friction shortly after the assault predicted PTSD severity 3 months later. On the contrary, positive social support did not predict later PTSD severity. These results are consistent with previous studies that underscore the association between negative features of social relationships and PTSD.

In the present study, individuals with obsessive-compulsive disorder (OCD) who also had excessive health concerns (n = 56) were compared with OCD individuals without such concerns (n = 343) regarding their OCD symptom severity, types of obsessions and compulsions, insight into the irrationality of their obsessions, and prevalence of generalized anxiety disorder. While the presence of health concerns did not affect the severity of OCD symptoms, the groups differed with respect to the types of symptoms displayed: those with health concerns had more somatic and harm obsessions, and checking compulsions: whereas those without such concerns had more contamination obsessions and washing compulsions. The insight of both groups ranged from poor to excellent, yet the number of individuals with poor insight was greater among those with health concerns than those without. Generalized anxiety disorder was also more prevalent among OCD individuals with excessive health concerns.