Treatment outcomes and patient satisfaction of a virtual partial hospital program: A mixed-method study.

OBJECTIVE: Despite a proliferation of virtual partial hospital programs (PHP) during the COVID-19 pandemic, there is a dearth of research on such programs. In the current study, we compared treatment outcomes and patient satisfaction between an in-person and a virtual PHP. Further, we examined patients' qualitative feedback about the virtual PHP. METHOD: Participants included 282 patients attending a virtual PHP during the COVID-19 pandemic and 470 patients attending an in-person PHP one year prior. Patients completed daily measures of symptom severity, and post-treatment measures of patient satisfaction and treatment outcomes. Patients in the virtual PHP provided feedback about virtual care. Quantitative data were analyzed using multilevel modeling, and qualitative data were analyzed using the principles of inductive analysis. RESULTS: Patients experienced a reduction in depression (b = -.28, p < .001) and anxiety symptoms (b = -.25, p < .001) over time and reported high satisfaction in both the in-person and virtual PHPs. There were no significant differences across programs. Virtual PHP patients identified unique advantages and disadvantages of virtual care. CONCLUSION: Our results suggest that virtual PHPs should be explored as an ongoing model of care that may help to systematically reduce barriers to accessing mental health services.

Voluntary pursuit of negatively valenced stimuli from childhood to early adulthood.

Although common sense suggests that we are motivated to pursue positive and avoid negative experiences, previous research shows that people regularly seek out negative experiences. In the current study, we characterized this tendency from childhood to young adulthood. Due to the known increases in risky behavior and sensation seeking in adolescence, we hypothesized that adolescents would show an increased engagement with negatively valenced stimuli compared to children and adults. Participants aged 4-25 (N = 192) completed a behavioral task assessing motivation to engage with negative, positive, and neutral images. On each trial, participants viewed two small images and selected one to view at a larger size for up to 10s. Trials were organized into three valence conditions: negative versus positive images (matched on arousal), negative versus neutral images, and positive versus neutral images. Although participants chose positive images more than neutral or negative images, participants selected negative images frequently, even when given a positive (28% of trials) or neutral (42% of trials) alternative. Contrary to expectations, the tendency to choose negative images was highest in early childhood and decreased linearly with increasing age, and the tendency to choose positive images increased linearly with age. These results provide insight into how motivation to engage with emotional stimuli varies across age. It is possible that the novelty and rarity of negative experiences drives children to pursue these stimuli. Alternatively, children may find negative images less aversive, which would caution against assuming that these stimuli elicit the same motivational states in individuals of all ages.

Reduced hippocampal and amygdala volume as a mechanism underlying stress sensitization to depression following childhood trauma.

BACKGROUND: Stressful life events are more likely to trigger depression among individuals exposed to childhood adversity. However, the mechanisms underlying this stress sensitization remain largely unknown. Any such mechanism must be altered by childhood adversity and interact with recent stressful life events, magnifying their association with depression. AIM: This study investigated whether reduced hippocampal and amygdala volume are potential mechanisms underlying stress sensitization following childhood violence exposure. METHOD: A sample of 149 youth (aged 8-17 years), with (N = 75) and without (N = 74) exposure to physical abuse, sexual abuse, or domestic violence participated. Participants completed a structural MRI scan and assessments of depression. Approximately 2 years later, stressful life events were assessed along with depression symptoms in 120 participants (57 violence exposed). RESULTS: Childhood violence exposure was associated with smaller hippocampal and amygdala volume. Stressful life events occurring during the follow-up period predicted worsening depression over time, and this association was magnified among those with smaller hippocampal and amygdala volumes. Significant moderated mediation models revealed the indirect effects of violence exposure on increasing depression over time through hippocampal and amygdala volumes, particularly among youths who experienced more stressful life events. CONCLUSIONS: These results provide evidence for reduced hippocampal and amygdala volume as potential mechanisms of stress sensitization to depression following exposure to violence. More broadly, these patterns suggest that hippocampal and amygdala-mediated emotional and cognitive processes may confer vulnerability to stressful life events among children who have experienced violence.

Hippocampal Contribution to Context Encoding across Development Is Disrupted following Early-Life Adversity.

Context can drastically influence responses to environmental stimuli. For example, a gunshot should provoke a different response at a public park than a shooting range. Little is known about how contextual processing and neural correlates change across human development or about individual differences related to early environmental experiences. Children (N = 60; 8-19 years, 24 exposed to interpersonal violence) completed a context encoding task during fMRI scanning using a delayed match-to-sample design with neutral, happy, and angry facial cues embedded in realistic background scenes. Outside the scanner, participants completed a memory test for context-face pairings. Context memory and neural correlates of context encoding did not vary with age. Larger hippocampal volume was associated with better context memory. Posterior hippocampus was recruited during context encoding, and greater activation in this region predicted better memory for contexts paired with angry faces. Children exposed to violence had poor memory of contexts paired with angry faces, reduced hippocampal volume, and atypical neural recruitment on encoding trials with angry faces, including reduced hippocampal activation and greater functional connectivity between hippocampus and ventrolateral prefrontal cortex (vlPFC). Greater hippocampus-vlPFC connectivity was associated with worse memory for contexts paired with angry faces. Posterior hippocampus appears to support context encoding, a process that does not exhibit age-related variation from middle childhood to late adolescence. Exposure to dangerous environments in childhood is associated with poor context encoding in the presence of threat, likely due to greater vlPFC-dependent attentional narrowing on threat cues at the expense of hippocampus-dependent processing of the broader context.SIGNIFICANCE STATEMENT The ability to use context to guide reactions to environmental stimuli promotes flexible behavior. Remarkably little research has examined how contextual processing changes across development or about influences of the early environment. We provide evidence for posterior hippocampus involvement in context encoding in youth and lack of age-related variation from middle childhood to late adolescence. Children exposed to interpersonal violence exhibited poor memory of contexts paired with angry faces and atypical neural recruitment during context encoding in the presence of threatening facial cues. Heightened attention to threat following violence exposure may come at the expense of encoding contextual information, which may ultimately contribute to pathological fear expressed in safe contexts.

The Nonlinear Development of Emotion Differentiation: Granular Emotional Experience Is Low in Adolescence.

People differ in how specifically they separate affective experiences into different emotion types-a skill called emotion differentiation or emotional granularity. Although increased emotion differentiation has been associated with positive mental health outcomes, little is known about its development. Participants ( N = 143) between the ages of 5 and 25 years completed a laboratory measure of negative emotion differentiation in which they rated how much a series of aversive images made them feel angry, disgusted, sad, scared, and upset. Emotion-differentiation scores were computed using intraclass correlations. Emotion differentiation followed a nonlinear developmental trajectory: It fell from childhood to adolescence and rose from adolescence to adulthood. Mediation analyses suggested that an increased tendency to report feeling emotions one at a time explained elevated emotion differentiation in childhood. Importantly, two other mediators (intensity of emotional experiences and scale use) did not explain this developmental trend. Hence, low emotion differentiation in adolescence may arise because adolescents have little experience conceptualizing co-occurring emotions.

Violence exposure and neural systems underlying working memory for emotional stimuli in youth.

Violence exposure during childhood is common and associated with poor cognitive and academic functioning. However, little is known about how violence exposure influences cognitive processes that might contribute to these disparities, such as working memory, or their neural underpinnings, particularly for cognitive processes that occur in emotionally salient contexts. We address this gap in a sample of 54 participants aged 8 to 19 years (50% female), half with exposure to interpersonal violence. Participants completed a delayed match to sample task for emotional faces while undergoing functional magnetic resonance imaging scanning. Violence-exposed youth performed worse than controls on happy and neutral, but not angry, trials. In whole-brain analysis, violence-exposed youth had reduced activation in the left middle frontal gyrus and right intraparietal sulcus during encoding and the left superior temporal sulcus and temporal-parietal junction during retrieval compared to control youth. Reduced activation in the left middle frontal gyrus during encoding and the left superior temporal sulcus during retrieval mediated the association between violence exposure and task performance. Violence exposure influences the frontoparietal network that supports working memory as well as regions involved in facial processing during working memory for emotional stimuli. Reduced neural recruitment in these regions may explain atypical patterns of cognitive processing seen among violence-exposed youth, particularly within emotional contexts.

Differential associations of threat and deprivation with emotion regulation and cognitive control in adolescence.

Research on childhood adversity has traditionally focused on single types of adversity, which is limited because of high co-occurrence, or on the total number of adverse experiences, which assumes that diverse experiences influence development similarly. Identifying dimensions of environmental experience that are common to multiple types of adversity may be a more effective strategy. We examined the unique associations of two such dimensions (threat and cognitive deprivation) with automatic emotion regulation and cognitive control using a multivariate approach that simultaneously examined both dimensions of adversity. Data were drawn from a community sample of adolescents (N = 287) with variability in exposure to violence, an indicator of threat, and poverty, which is associated with cognitive deprivation. Adolescents completed tasks measuring automatic emotion regulation and cognitive control in neutral and emotional contexts. Violence was associated with automatic emotion regulation deficits, but not cognitive control; poverty was associated with poor cognitive control, but not automatic emotion regulation. Both violence and poverty predicted poor inhibition in an emotional context. Utilizing an approach focused on either single types of adversity or cumulative risk obscured specificity in the associations of violence and poverty with emotional and cognitive outcomes. These findings suggest that different dimensions of childhood adversity have distinct influences on development and highlight the utility of a differentiated multivariate approach.

Evidence Base Update for Psychosocial Treatments for Children and Adolescents Exposed to Traumatic Events.

Child and adolescent trauma exposure is prevalent, with trauma exposure-related symptoms, including posttraumatic stress, depressive, and anxiety symptoms often causing substantial impairment. This article updates the evidence base on psychosocial treatments for child and adolescent trauma exposure completed for this journal by Silverman et al. (2008). For this review, we focus on 37 studies conducted during the seven years since the last review. Treatments are grouped by overall treatment family (e.g., cognitive behavioral therapy), treatment modality (e.g., individual vs. group), and treatment participants (e.g., child only vs. child and parent). All studies were evaluated for methodological rigor according to Journal of Clinical Child & Adolescent Psychology evidence-based treatment evaluation criteria (Southam-Gerow & Prinstein, 2014), with cumulative designations for level of support for each treatment family. Individual CBT with parent involvement, individual CBT, and group CBT were deemed well-established; group CBT with parent involvement and eye movement desensitization and reprocessing (EMDR) were deemed probably efficacious; individual integrated therapy for complex trauma and group mind-body skills were deemed possibly efficacious; individual client-centered play therapy, individual mind-body skills, and individual psychoanalysis were deemed experimental; and group creative expressive + CBT was deemed questionable efficacy. Advances in the evidence base, with comparisons to the state of the science at the time of the Silverman et al. (2008) review, are discussed. Finally, we present dissemination and implementation challenges and areas for future research.

Glutamatergic regulation prevents hippocampal-dependent age-related cognitive decline through dendritic spine clustering.

The dementia of Alzheimer's disease (AD) results primarily from degeneration of neurons that furnish glutamatergic corticocortical connections that subserve cognition. Although neuron death is minimal in the absence of AD, age-related cognitive decline does occur in animals as well as humans, and it decreases quality of life for elderly people. Age-related cognitive decline has been linked to synapse loss and/or alterations of synaptic proteins that impair function in regions such as the hippocampus and prefrontal cortex. These synaptic alterations are likely reversible, such that maintenance of synaptic health in the face of aging is a critically important therapeutic goal. Here, we show that riluzole can protect against some of the synaptic alterations in hippocampus that are linked to age-related memory loss in rats. Riluzole increases glutamate uptake through glial transporters and is thought to decrease glutamate spillover to extrasynaptic NMDA receptors while increasing synaptic glutamatergic activity. Treated aged rats were protected against age-related cognitive decline displayed in nontreated aged animals. Memory performance correlated with density of thin spines on apical dendrites in CA1, although not with mushroom spines. Furthermore, riluzole-treated rats had an increase in clustering of thin spines that correlated with memory performance and was specific to the apical, but not the basilar, dendrites of CA1. Clustering of synaptic inputs is thought to allow nonlinear summation of synaptic strength. These findings further elucidate neuroplastic changes in glutamatergic circuits with aging and advance therapeutic development to prevent and treat age-related cognitive decline.

Childhood abuse and reduced cortical thickness in brain regions involved in emotional processing.

BACKGROUND: Alterations in gray matter development represent a potential pathway through which childhood abuse is associated with psychopathology. Several prior studies find reduced volume and thickness of prefrontal (PFC) and temporal cortex regions in abused compared with nonabused adolescents, although most prior research is based on adults and volume-based measures. This study tests the hypothesis that child abuse, independent of parental education, predicts reduced cortical thickness in prefrontal and temporal cortices as well as reduced gray mater volume (GMV) in subcortical regions during adolescence. METHODS: Structural MRI scans were obtained from 21 adolescents exposed to physical and/or sexual abuse and 37 nonabused adolescents (ages 13-20). Abuse was operationalized using dichotomous and continuous measures. We examined associations between abuse and brain structure in several a priori-defined regions, controlling for parental education, age, sex, race, and total brain volume for subcortical GMV. Significance was evaluated at p < .05 with a false discovery rate correction. RESULTS: Child abuse exposure and severity were associated with reduced thickness in ventromedial prefrontal cortex (PFC), right lateral orbitofrontal cortex, right inferior frontal gyrus, bilateral parahippocampal gyrus (PHG), left temporal pole, and bilateral inferior, right middle, and right superior temporal gyri. Neither abuse measure predicted cortical surface area or subcortical GMV. Bilateral PHG thickness was inversely related to externalizing symptoms. CONCLUSIONS: Child abuse, an experience characterized by a high degree of threat, is associated with reduced cortical thickness in ventromedial and ventrolateral PFC and medial and lateral temporal cortex in adolescence. Reduced PHG thickness may be a mediator linking abuse with externalizing psychopathology, although prospective research is needed to evaluate this possibility.

Perceptual sensitivity to labeling stereotyped emotion expressions: Associations with age and subclinical psychopathology symptoms from childhood through early adulthood.

This study investigates (a) age-related differences in how the intensity of stereotyped facial expressions influence the emotion label children, adolescents, and adults assign to that face and (b) how this perceptual sensitivity relates to subclinical symptoms of psychopathology. In 2015-2016, 184 participants aged 4-25 years viewed posed stereotypes of angry, fearful, sad, and happy expressions morphed with neutral expressions at 10%-90% intensity. Thin plate regression smoothing splines were used to chart nonlinear associations between age and the perceptual threshold participants needed to assign the emotion label expected based on cultural consensus. Results suggest that sensitivity to labeling stereotypical happy faces as "happy" peaked by age 4. Sensitivity to perceiving stereotypical angry faces as "angry" increased from ages 4 to 7 and then plateaued. In contrast, sensitivity to perceiving stereotypical fearful and sad faces demonstrated protracted development, not reaching a plateau until ages 15 and 16, respectively. Reduction in selecting the "I don't know" response was the primary driver of these age-related changes. Stereotyped fear expressions required the highest intensity to be labeled as such and showed the most marked change in perceptual threshold across development. Interestingly, lower intensity morphs of stereotypical fear faces were frequently labeled "sad." Furthermore, perceiving lower intensity fear morphs was associated with fewer internalizing and externalizing symptoms in participants aged 7-19. This study describes the development of perceptual sensitivity to labeling stereotypical expressions of emotion according to cultural consensus and shows that how people perceive and categorize ambiguous facial expressions is associated with vulnerability to psychopathology. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Distress Tolerance as a Mechanism Linking Violence Exposure to Problematic Alcohol use in Adolescence.

Adolescents exposed to violence are at elevated risk of developing most forms of psychopathology, including depression, anxiety, and alcohol abuse. Prior research has identified emotional reactivity and difficulties with emotion regulation as core mechanisms linking violence exposure with psychopathology. Scant research has examined behavioral responses to distress as a mechanism in this association. This study examined the association of violence exposure with distress tolerance-the ability to persist in the face of distress-and whether lower distress tolerance linked violence exposure with subsequent increases in depression, anxiety, and alcohol abuse problems during adolescence. Data were collected prospectively in a sample of 287 adolescents aged 16-17 (44.3% male; 40.8% White). At Time 1, participants provided self-report of demographics, violence exposure, and psychopathology, and completed a behavioral measure of distress tolerance, the Paced Auditory Serial Addition Task. Four months later, participants (n = 237) repeated the psychopathology assessments. Violence exposure was associated with lower distress tolerance (ß = -.21 p = .009), and elevated concurrent psychopathology (ß = .16-.45, p = .001-.004). Low distress tolerance was prospectively associated with greater likelihood of abusing alcohol over time (OR = .63, p = .021), and mediated the association between violence exposure and greater levels (ß = .02, 95% CI [.001, .063]) and likelihood (OR = .03, 95% CI [.006, .065]) of alcohol use over time. In contrast, low distress tolerance was not associated concurrently or prospectively with internalizing symptoms. Results persisted after controlling for socio-economic status. Findings suggest that distress tolerance is shaped by early experiences of threat and plays a role in the association between violence exposure and development of problematic alcohol use in adolescence.

Developmental Variation in the Associations of Attention Bias to Emotion with Internalizing and Externalizing Psychopathology.

Attention biases to emotion are associated with symptoms of internalizing and externalizing psychopathology in children and adolescents. It is unknown whether attention biases to emotion and their associations with different symptoms of psychopathology vary across development from early childhood through young adulthood. We examine this age-related variation in the current study. Participants (N = 190; ages: 4-25) completed survey-based psychopathology symptom measures and a dot-probe task to assess attention bias to happy, sad, and angry relative to neutral faces. We tested whether linear or non-linear (e.g., spline-based models) associations best characterized age-related variation in attention to emotion. We additionally examined whether attention biases were associated with depression, anxiety, and externalizing symptoms and whether these associations varied by age. No age-related differences in attention biases were found for any of the emotional faces. Attention biases were associated with psychopathology symptoms, but only when examining moderation by age. Biased attention to angry faces was associated with greater symptoms of anxiety and depression in adolescents and young adults, but not children. Similarly, biased attention to happy faces was associated with externalizing symptoms in adolescents and young adults, but not in children. In contrast, biased attention to happy faces was associated with greater anxiety symptoms in children, but not in adolescents or young adults. Biased attention toward social threat and reward becomes more strongly coupled with internalizing and externalizing symptoms, respectively, during the transition to adolescence. These findings could inform when interventions such as attention bias modification training may be most effective.

Charting the development of emotion comprehension and abstraction from childhood to adulthood using observer-rated and linguistic measures.

This study examined two facets of emotion development: emotion word comprehension (knowing the meaning of emotion words such as "anger" or "excitement") and emotion concept abstraction (representing emotions in terms of internal psychological states that generalize across situations). Using a novel emotion vocabulary assessment, we captured how a cross-sectional sample of participants aged 4-25 (N = 196) defined 24 emotions. Smoothing spline regression models suggested that emotion comprehension followed an emergent shape: Knowledge of emotion words increased across childhood and plateaued around age 11. Human coders rated the abstractness of participants' responses, and these ratings also followed an emergent shape but plateaued significantly later than comprehension, around age 18. An automated linguistic analysis of abstractness supported coders' perceptions of increased abstractness across age. Finally, coders assessed the definitional strategies participants used to describe emotions. Young children tended to describe emotions using concrete strategies such as providing example situations that evoked those emotions or by referring to physiological markers of emotional experiences. Whereas use of these concrete strategies decreased with age, the tendency to use more abstract strategies such as providing general definitions that delineated the causes and characteristics of emotions or by providing synonyms of emotion words increased with age. Overall, this work (a) provides a tool for assessing definitions of emotion terms, (b) demonstrates that emotion concept abstraction increases across age, and (c) suggests that adolescence is a period in which emotion words are comprehended but their level of abstraction continues to mature. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Low Emotional Awareness as a Transdiagnostic Mechanism Underlying Psychopathology in Adolescence.

The ability to identify and label one's emotions is associated with effective emotion regulation, rendering emotional awareness important for mental health. We evaluated how emotional awareness was related to psychopathology and whether low emotional awareness was a transdiagnostic mechanism explaining the increase in psychopathology during the transition to adolescence and as a function of childhood trauma-specifically violence exposure. In Study 1, children and adolescents (N=120, aged 7-19 years) reported on emotional awareness and psychopathology. Emotional awareness was negatively associated with psychopathology (p-factor) and worsened across age in females but not males. In Study 2 (N=262, aged 8-16 years), we replicated these findings and demonstrated longitudinally that low emotional awareness mediated increases in p-factor as a function of age in females and violence exposure. These findings indicate that low emotional awareness may be a transdiagnostic mechanism linking adolescent development, sex, and trauma with the emergence of psychopathology.

Impaired hippocampus-dependent associative learning as a mechanism underlying PTSD: A meta-analysis.

Smaller hippocampal volume is associated with increased risk for PTSD following trauma, but the hippocampal functions involved remain unknown. We propose a conceptual model that identifies broad impairment in hippocampus-dependent associative learning as a vulnerability factor for PTSD. Associative learning of foreground cues and background context is required to form an integrated representation of an event. People with poor associative learning may have difficulty remembering who or what was present during a trauma, where the trauma occurred, or the sequence of events, which may contribute to PTSD symptoms. We argue that associative learning difficulties in PTSD exist for cues and context, regardless of the emotional nature of the information. This contrasts with PTSD models that focus exclusively on threat-processing or contextual-processing. In a meta-analysis, people with PTSD exhibited poor associative learning of multiple information types compared to those without PTSD. Differences were of medium effect size and similar magnitude for neutral and negative/trauma-related stimuli. We provide evidence for associative learning difficulties as a neurocognitive pathway that may contribute to PTSD.

Altered development of hippocampus-dependent associative learning following early-life adversity.

Little is known about how childhood adversity influences the development of learning and memory and underlying neural circuits. We examined whether violence exposure in childhood influenced hippocampus-dependent associative learning and whether differences: a) were broad or specific to threat cues, and b) exhibited developmental variation. Children (n = 59; 8-19 years, 24 violence-exposed) completed an associative learning task with angry, happy, and neutral faces paired with objects during fMRI scanning. Outside the scanner, participants completed an associative memory test for face-object pairings. Violence-exposed children exhibited broad associative memory difficulties that became more pronounced with age, along with reduced recruitment of the hippocampus and atypical recruitment of fronto-parietal regions during encoding. Violence-exposed children also showed selective disruption of associative memory for threat cues regardless of age, along with reduced recruitment of the intraparietal sulcus (IPS) during encoding in the presence of threat. Broad associative learning difficulties may be a functional consequence of the toxic effects of early-life stress on hippocampal and fronto-parietal cortical development. Difficulties in the presence of threat cues may result from enhanced threat processing that disrupts encoding and short-term storage of associative information in the IPS. These associative learning difficulties may contribute to poor life outcomes following childhood violence exposure.

Child Trauma Exposure and Psychopathology: Mechanisms of Risk and Resilience.

Exposure to trauma in childhood is associated with elevated risk for multiple forms of psychopathology. Here we present a biopsychosocial model outlining the mechanisms that link child trauma with psychopathology and protective factors that can mitigate these risk pathways. We focus on four mechanisms of enhanced threat processing: information processing biases that facilitate rapid identification of environmental threats, disruptions in learning mechanisms underlying the acquisition of fear, heightened emotional responses to potential threats, and difficulty disengaging from negative emotional content. Supportive relationships with caregivers, heightened sensitivity to rewarding and positive stimuli, and mature amygdala-prefrontal circuitry each serve as potential buffers of these risk pathways, highlighting novel directions for interventions aimed at preventing the onset of psychopathology following child trauma.

Increasing verbal knowledge mediates development of multidimensional emotion representations.

How do people represent their own and others' emotional experiences? Contemporary emotion theories and growing evidence suggest that the conceptual representation of emotion plays a central role in how people understand the emotions both they and other people feel.1-6 Although decades of research indicate that adults typically represent emotion concepts as multidimensional, with valence (positive-negative) and arousal (activating-deactivating) as two primary dimensions,7-10 little is known about how this bidimensional (or circumplex) representation arises.11 Here we show that emotion representations develop from a monodimensional focus on valence to a bidimensional focus on both valence and arousal from age 6 to age 25. We investigated potential mechanisms underlying this effect and found that increasing verbal knowledge mediated emotion representation development over and above three other potential mediators: (i) fluid reasoning, (ii) the general ability to represent non-emotional stimuli bidimensionally, and (iii) task-related behaviors (e.g., using extreme ends of rating scales). These results suggest that verbal development facilitates the expansion of emotion concept representations (and potentially emotional experiences) from a "positive or negative" dichotomy in childhood to a multidimensional organization in adulthood.

Maltreatment Exposure, Brain Structure, and Fear Conditioning in Children and Adolescents.

Alterations in learning processes and the neural circuitry that supports fear conditioning and extinction represent mechanisms through which trauma exposure might influence risk for psychopathology. Few studies examine how trauma or neural structure relates to fear conditioning in children. Children (n=94) aged 6-18 years, 40.4% (n=38) with exposure to maltreatment (physical abuse, sexual abuse, or domestic violence), completed a fear conditioning paradigm utilizing blue and yellow bells as conditioned stimuli (CS+/CS-) and an aversive alarm noise as the unconditioned stimulus. Skin conductance responses (SCR) and self-reported fear were acquired. Magnetic resonance imaging data were acquired from 60 children. Children without maltreatment exposure exhibited strong differential conditioning to the CS+ vs CS-, based on SCR and self-reported fear. In contrast, maltreated children exhibited blunted SCR to the CS+ and failed to exhibit differential SCR to the CS+ vs CS- during early conditioning. Amygdala and hippocampal volume were reduced among children with maltreatment exposure and were negatively associated with SCR to the CS+ during early conditioning in the total sample, although these associations were negative only among non-maltreated children and were positive among maltreated children. The association of maltreatment with externalizing psychopathology was mediated by this perturbed pattern of fear conditioning. Child maltreatment is associated with failure to discriminate between threat and safety cues during fear conditioning in children. Poor threat-safety discrimination might reflect either enhanced fear generalization or a deficit in associative learning, which may in turn represent a central mechanism underlying the development of maltreatment-related externalizing psychopathology in children.