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Differences in culture, education, family life, peers and media provide considerable diversity for the environments in which children grow up. This volume discusses the environments surrounding children as an essential piece of development.

This paper reports on three studies on the development and validation of the Parental Reflective Functioning Questionnaire (PRFQ), a brief, multidimensional self-report measure that assesses parental reflective functioning or mentalizing, that is, the capacity to treat the infant as a psychological agent. Study 1 investigated the factor structure, reliability, and relationships of the PRFQ with demographic features, symptomatic distress, attachment dimensions, and emotional availability in a socially diverse sample of 299 mothers of a child aged 0-3. In Study 2, the factorial invariance of the PRFQ in mothers and fathers was investigated in a sample of 153 first-time parents, and relationships with demographic features, symptomatic distress, attachment dimensions, and parenting stress were investigated. Study 3 investigated the relationship between the PRFQ and infant attachment classification as assessed with the Strange Situation Procedure (SSP) in a sample of 136 community mothers and their infants. Exploratory and confirmatory factor analyses suggested three theoretically consistent factors assessing pre-mentalizing modes, certainty about the mental states of the infant, and interest and curiosity in the mental states of the infant. These factors were generally related in theoretically expected ways to parental attachment dimensions, emotional availability, parenting stress, and infant attachment status in the SSP. Yet, at the same time, more research on the PRFQ is needed to further establish its reliability and validity.

Although most resilience science has focused on individual-level psychosocial factors that promote individual resilience, theorists and researchers have begun to examine neurobiological and systems-level factors implicated in resilience. In this commentary we argue that the development of effective interventions to enhance resilience necessitates understanding that resilience in the individual is dependent on multiple layers of society. Further, we suggest that there is a bidirectional relationship between systems-level resilience (i.e., resilience of romantic partners, family members, neighborhoods, and larger social contexts) and individual resilience. We suggest directions for future research and interventions, with the goal of stimulating research efforts that address these questions among trauma-exposed individuals.

It has been reported previously that infant faces elicit enhanced attentional allocation compared to adult faces in adult women, particularly when these faces are emotional and when the participants are mothers, as compared to non-mothers [1]. However, it remains unclear whether this increased salience of infant faces as compared to adult faces extends to children older than infant age, or whether infant faces have a unique capacity to elicit preferential attentional allocation compared to juvenile or adult faces. Therefore, this study investigated attentional allocation to a variety of different aged faces (infants, pre-adolescent children, adolescents, and adults) in 84 adult women, 39 of whom were mothers. Consistent with previous findings, infant faces were found to elicit greater attentional engagement compared to pre-adolescent, adolescent, or adult faces, particularly when the infants displayed distress; again, this effect was more pronounced in mothers compared to non-mothers. Pre-adolescent child faces were also found to elicit greater attentional engagement compared to adolescent and adult faces, but only when they displayed distress. No preferential attentional allocation was observed for adolescent compared to adult faces. These findings indicate that cues potentially signalling vulnerability, specifically age and sad affect, interact to engage attention. They point to a potentially important mechanism, which helps facilitate caregiving behaviour.

The neural underpinnings of impaired consciousness and of the variable severity of behavioural deficits from one absence seizure to the next are not well understood. We aimed to measure functional MRI (fMRI) and electroencephalography (EEG) changes in absence seizures with impaired task performance compared with seizures in which performance was spared. In this cross-sectional study done at the Yale School of Medicine, CT, USA, we recruited patients from 59 paediatric neurology practices in the USA. We did simultaneous EEG, fMRI, and behavioural testing in patients aged 6–19 years with childhood or juvenile absence epilepsy, and with an EEG with typical 3–4 Hz bilateral spike-wave discharges and normal background. The main outcomes were fMRI and EEG amplitudes in seizures with impaired versus spared behavioural responses analysed by t test. We also examined the timing of fMRI and EEG changes in seizures with impaired behavioural responses compared with seizures with spared responses. 93 patients were enrolled between Jan 1, 2005, and Sept 1, 2013; we recorded 1032 seizures in 39 patients. fMRI changes during seizures occurred sequentially in three functional brain networks. In the default mode network, fMRI amplitude was 0·57% (SD 0·26) for seizures with impaired and 0·40% (0·16) for seizures with spared behavioural responses (mean difference 0·17%, 95% CI 0·11–0·23; p<0·0001). In the task-positive network, fMRI amplitude was 0·53% (SD 0·29) for seizures with impaired and 0·39% (0·15) for seizures with spared behavioral responses (mean difference 0·14%, 95% CI 0·08–0·21; p<0·0001). In the sensorimotor-thalamic network, fMRI amplitude was 0·41% (0·25) for seizures with impaired and 0·34% (0·14) for seizures with spared behavioural responses (mean difference 0·07%, 95% CI 0·01–0·13; p=0·02). Mean fractional EEG power in the frontal leads was 50·4 (SD 15·2) for seizures with impaired and 24·8 (6·5) for seizures with spared behavioural responses (mean difference 25·6, 95% CI 21·0–30·3); middle leads 35·4 (6·5) for seizures with impaired, 13·3 (3·4) for seizures with spared behavioural responses (mean difference 22·1, 95% CI 20·0–24·1); posterior leads 41·6 (5·3) for seizures with impaired, 24·6 (8·6) for seizures with spared behavioural responses (mean difference 17·0, 95% CI 14·4–19·7); p<0·0001 for all comparisons. Mean seizure duration was longer for seizures with impaired behaviour at 7·9 s (SD 6·6), compared with 3·8 s (3·0) for seizures with spared behaviour (mean difference 4·1 s, 95% CI 3·0–5·3; p<0·0001). However, larger amplitude fMRI and EEG signals occurred at the outset or even preceding seizures with behavioural impairment. Impaired consciousness in absence seizures is related to the intensity of physiological changes in established networks affecting widespread regions of the brain. Increased EEG and fMRI amplitude occurs at the onset of seizures associated with behavioural impairment. These finding suggest that a vulnerable state might exist at the initiation of some absence seizures leading them to have more severe physiological changes and altered consciousness than other absence seizures. National Institutes of Health, National Institute of Neurological Disorders and Stroke, National Center for Advancing Translational Science, the Loughridge Williams Foundation, and the Betsy and Jonathan Blattmachr Family.

Diminished responsivity to reward incentives is a key contributor to the social-communication problems seen in autism spectrum disorders (ASDs). Social motivation theories suggest that individuals with ASD do not experience social interactions as rewarding, leading to negative consequences for the development of brain circuitry subserving social information. In this study, we examined neural responses to social and non-social reward anticipation in 35 typically developing young adults, examining modulation of reward sensitivity by level of autistic traits. Using an Event-related potential incentive-delay task incorporating novel, more ecologically valid forms of reward, higher expression of autistic traits was associated with an attenuated P3 response to the anticipation of social (simulated real-time video feedback from an observer), but not non-social (candy), rewards. Exploratory analyses revealed that this was unrelated to mentalizing ability. The P3 component reflects motivated attention to reward signals, suggesting attenuated motivation allocation specific to social incentives. The study extends prior findings of atypical reward anticipation in ASD, demonstrating that attenuated social reward responsiveness extends to autistic traits in the range of typical functioning. Results support the development of innovative paradigms for investigating social and non-social reward responsiveness. Insight into vulnerabilities in reward processing is critical for understanding social function in ASD.

Social exclusion inherently involves an element of expectancy violation, in that we expect other people to follow the unwritten rule to include us in social interactions. In this functional magnetic resonance imaging (fMRI) study, we employed a unique modification of an interactive virtual ball-tossing game called “Cyberball” (Williams et al., 2000) and a novel paradigm called “Cybershape,” in which rules are broken in the absence of social exclusion, to dissociate brain regions that process social exclusion from rule violations more generally. Our Cyberball game employed an alternating block design and removed evoked responses to events when the participant was throwing the ball in inclusion to make this condition comparable to exclusion, where participants did not throw. With these modifications, we replicated prior findings of ventral anterior cingulate cortex (vACC), insula, and posterior cingulate cortex activity evoked by social exclusion relative to inclusion. We also identified exclusion-evoked activity in the hippocampi, left ventrolateral prefrontal cortex, and left middle temporal gyrus. Comparing social exclusion and rule violation revealed a functional dissociation in the active neural systems as well as differential functional connectivity with vACC. Some overlap was observed in regions differentially modulated by social exclusion and rule violation, including the vACC and lateral parietal cortex. These overlapping brain regions showed different activation during social exclusion compared to rule violation, each relative to fair play. Comparing activation patterns to social exclusion and rule violation allowed for the dissociation of brain regions involved in the experience of exclusion versus expectancy violation. ►Social exclusion activated vACC, PCC, hippocampus, and insula. ►Rule violation activated dorsal medial and lateral PFC and parietal cortex. ►vACC showed different patterns of functional connectivity in social exclusion and rule violation. ►Rule violation and Social exclusion showed a dorsal-ventral distinction in mPFC, respectively. ►Social exclusion and rule violation recruit distinct networks of brain activation.

We aimed to assess comprehensively the prevalence of perinatal risks experienced by a potentially high-risk yet understudied population of children domestically adopted in the United States. Data are from participant report and medical records from mothers (n = 580) who completed a domestic adoption placement with nonrelatives at or near birth (Mean placement age = 7 days). We describe a comprehensive measure of perinatal risks, including divergences from previous assessment tools and the incorporation of multiple reporters, and report the prevalence of various types of perinatal risks. The prevalence of each specific risk factor was generally low, although several risks were more prevalent in this sample than estimates from nationally representative publicly available data. Nearly the entire sample (99%) experienced some type of risk exposure. Birth mothers who placed their children for adoption domestically in the US experience higher levels of perinatal risks than the national average, but not for all specific types of risk. Thus, the developmental trajectories of children adopted domestically may systematically differ from the general population to the extent that these specific perinatal risks impact development.

Social exclusion is a potent elicitor of distress. Previous studies have shown that medial frontal theta oscillations are modulated by the experience of social exclusion. Using the Cyberball paradigm, we examined event-related dynamics of theta power in the EEG at medial frontal sites while children aged 8–12 years were exposed to conditions of fair play and social exclusion. Using an event-related design, we found that medial frontal theta oscillations (4–8Hz) increase during both early (i.e., 200–400ms) and late (i.e., 400–800ms) processing of rejection events during social exclusion relative to perceptually identical “not my turn” events during inclusion. Importantly, we show that only for the later time window (400–800ms) slow-wave theta power tracks self-reported ostracism distress. Specifically, greater theta power at medial frontal sites to “rejection” events predicted higher levels of ostracism distress. Alpha and beta oscillations for rejection events were unrelated to ostracism distress at either 200–400ms or 400–800ms time windows. Our findings extend previous studies by showing that medial frontal theta oscillations for rejection events are a neural signature of social exclusion, linked to experienced distress in middle childhood. •Medial frontal theta oscillations increase for rejection events in social exclusion.•Medial frontal theta at 400–800ms is neural signature of ostracism distress.•Medial frontal alpha/beta oscillations in exclusion are unrelated to distress.•“Not my turn” events are unrelated to ostracism distress.

Anxiety disorders represent a common but often debilitating form of psychopathology in both children and adults. While there is a growing understanding of the etiology and maintenance of these disorders across various research domains, only recently have integrative accounts been proposed. While classical attachment history has been a traditional core construct in psychological models of anxiety, contemporary attachment theory has the potential to integrate neurobiological and behavioral findings within a multidisciplinary developmental framework. The current paper proposes a modern attachment theory-based developmental model grounded in relevant literature from multiple disciplines including social neuroscience, genetics, neuroendocrinology, and the study of family factors involved in the development of anxiety disorders. Recent accounts of stress regulation have highlighted the interplay between stress, anxiety, and activation of the attachment system. This interplay directly affects the development of social-cognitive and mentalizing capacities that are acquired in the interpersonal context of early attachment relationships. Early attachment experiences are conceptualized as the key organizer of a complex interplay between genetic, environmental, and epigenetic contributions to the development of anxiety disorders - a multifactorial etiology resulting from dysfunctional co-regulation of fear and stress states. These risk-conferring processes are characterized by hyperactivation strategies in the face of anxiety. The cumulative allostatic load and subsequent \"wear and tear\" effects associated with hyperactivation strategies converge on the neural pathways of anxiety and stress. Attachment experiences further influence the development of anxiety as potential moderators of risk factors, differentially impacting on genetic vulnerability and relevant neurobiological pathways. Implications for further research and potential treatments are outlined.