Child maltreatment is a reliable predictor of posttraumatic stress disorder (PTSD) symptoms. However, not all maltreated children develop PTSD symptoms, suggesting that additional mediating variables explain how certain maltreated children develop PTSD symptoms and others do not. The current study tested three potential mediators of the relationship between child maltreatment and subsequent PTSD symptoms: (a) respiratory sinus arrhythmia reactivity, (b) cortisol reactivity, and (c) experiential avoidance, or the unwillingness to experience painful private events, such as thoughts and memories. Maltreated (n = 51) and nonmaltreated groups (n = 59) completed a stressor paradigm, a measure of experiential avoidance, and a semistructured interview of PTSD symptoms. One year later, participants were readministered the PTSD symptoms interview. Results of a multiple mediator model showed the set of potential mediators mediated the relationship between child maltreatment and subsequent PTSD symptoms. However, experiential avoidance was the only significant, specific indirect effect, demonstrating that maltreated children avoiding painful private events after the abuse were more likely to develop a range of PTSD symptoms 1 year later. These results highlight the importance of experiential avoidance in the development of PTSD symptoms for maltreated children, and implications for secondary prevention and clinical intervention models are discussed.

Foster and adoptive parents often face challenges while taking care of children who, due to their adverse early life experiences, are at risk of developing insecure attachment relationships, behavior problems, and stress dysregulation. Several intervention programs have been developed to help foster and adoptive parents to overcome these challenges. In the current study, a series of eight meta-analyses were performed to examine the effectiveness of these intervention programs on four parent outcomes (sensitive parenting, k = 11, N = 684; dysfunctional discipline, k = 4, N = 239; parenting knowledge and attitudes, k = 7, N = 535; parenting stress, k = 18, N = 1,306), three child outcomes (attachment security, k = 6, N = 395; behavior problems, k = 33, N = 2,661; diurnal cortisol levels, k = 3, N = 261), and placement disruption (k = 7, N = 1,100). Results show positive effects for the four parent outcomes and child behavior problems, but not for attachment security, child diurnal cortisol levels, or placement disruption. Indirect effects on child outcomes may be delayed, and therefore long-term follow-up studies are needed to examine the effects of parenting interventions on children.

A short-term longitudinal study during early childhood (N = 301; 155 girls; M = 44.76 months old, SD = 8.20) investigated the prospective associations between peer victimization and aggression subtypes. Specifically, observations of relational and physical victimization as well as teacher reports of the forms (i.e., relational and physical) and functions (i.e., proactive and reactive) of aggression were collected at two time points during an academic year. Within- and between-group gender differences were examined as part of the preliminary analyses. In order to address key study questions, both directions of effect between peer victimization and aggression subtypes were examined. We found that teacher-reported proactive relational aggression predicted decreases in observed relational victimization over time, whereas reactive relational aggression predicted increases in observed relational victimization over time. Ways in which these and other findings extend the literature are discussed.

In this commentary, we (a) discuss logical and empirical limits on the transactional model in accounting for the etiology of any developmental psychopathology, including conduct disorder (CD), and (b) review evidence bearing on whether or not frontal lobe lesions can directly produce CD behavior. Logically, transactions can both decrease and increase phenotypic variance; moreover, there is a mathematical limit (50%) to the amount of variance for which they can account. Empirically, documenting a transactional effect requires (a) that we have unconfounded measures of a child's biotype and social environment, (b) that the biotype and social environment are correlated, and (c) that we have a design (such as an adoption design) that is capable of separating the contribution of this correlation to outcome variance from the main effects of either biotype or social environment considered separately. Given these limits, we should also look for main effects in the etiology of CD. We argue that early damage or dysfunction in the frontal lobes may be one such plausible main effect on CD.

We investigated the relationship of gender to cognitive and affective processing in maltreated youth with posttraumatic stress disorder symptoms using functional magnetic resonance imaging. Maltreated (N = 29, 13 females, 16 males) and nonmaltreated participants (N = 45, 26 females, 19 males) performed an emotional oddball task that involved detection of targets with fear or scrambled face distractors. Results were moderated by gender. During the executive component of this task, left precuneus/posterior middle cingulate hypoactivation to fear versus calm or scrambled face targets were seen in maltreated versus control males and may represent dysfunction and less resilience in attentional networks. Maltreated males also showed decreased activation in the inferior frontal gyrus compared to control males. No differences were found in females. Posterior cingulate activations positively correlated with posttraumatic stress disorder symptoms. While viewing fear faces, maltreated females exhibited decreased activity in the dorsomedial prefrontal cortex and cerebellum I–VI, whereas maltreated males exhibited increased activity in the left hippocampus, fusiform cortex, right cerebellar crus I, and visual cortex compared to their same-gender controls. Gender by maltreatment effects were not attributable to demographic, clinical, or maltreatment parameters. Maltreated girls and boys exhibited distinct patterns of neural activations during executive and affective processing, a new finding in the maltreatment literature.

This is the first review to rigorously examine the mediating role of cognitive factors in the relationship between childhood trauma and subsequent adult psychopathology, and highlight areas for future research. A database search (Child Development & Adolescent Studies, ERIC, Global Health, PsycARTICLES, and PsycINFO) was conducted to identify empirical studies on cognitive factors, explaining the relationship between different types of adverse childhood experiences and adult psychopathology across clinical and nonclinical populations. A narrative synthesis and appraisal of the methodological quality of the studies was conducted. Ninety-eight mediation studies were identified, comprising 4,137 clinical and 28,228 nonclinical participants. Despite great variation in methodological quality of the studies, our narrative synthesis suggests that cognitive factors mediate the relationship between early trauma and later psychopathology. This finding is consistent across different measures of traumatic experiences, psychopathology, and cognitive mediators. Cognitive mediators represent potentially valuable intervention targets for (non)clinical patients who have experienced childhood adversity. Future studies are needed to (a) establish longitudinal causal connections, and (b) assess the effect of interventions that specifically target cognitive change in patients with different levels and types of pathology.

Two disorders of attachment have been consistently identified in some young children following severe deprivation in early life: reactive attachment disorder and disinhibited social engagement disorder. However, less is known about whether signs of these disorders persist into adolescence. We examined signs of reactive attachment disorder and disinhibited social engagement disorder at age 12 years in 111 children who were abandoned at or shortly after birth and subsequently randomized to care as usual or to high-quality foster care, as well as in 50 comparison children who were never institutionalized. Consistent with expectations, those who experienced institutional care in early life had more signs of reactive attachment disorder and disinhibited social engagement disorder at age 12 years than children never institutionalized. In addition, using a conservative intent-to-treat approach, those children randomized to foster care had significantly fewer signs of reactive attachment disorder and disinhibited social engagement disorder than those randomized to care as usual. Analyses within the ever institutionalized group revealed no effects of the age of placement into foster care, but number of caregiving disruptions experienced and the percentage of the child's life spent in institutional care were significant predictors of signs of attachment disorders assessed in early adolescence. These findings indicate that adverse caregiving environments in early life have enduring effects on signs of attachment disorders, and provide further evidence that high-quality caregiving interventions are associated with reductions in both reactive attachment disorder and disinhibited social engagement disorder.

This study examined the developmental cascade of both genetic and environmental influences on toddlers' behavior problems through the longitudinal and multigenerational assessment of psychosocial risk. We used data from the Early Growth and Development Study, a prospective adoption study, to test the intergenerational transmission of risk through the assessment of adoptive mother, adoptive father, and biological parent depressive symptoms on toddler behavior problems. Given that depression is often chronic, we control for across-time continuity and find that in addition to associations between adoptive mother depressive symptoms and toddler externalizing problems, adoptive father depressive symptoms when the child is 9 months of age were associated with toddler problems and associated with maternal depressive symptoms. Findings also indicated that a genetic effect may indirectly influence toddler problems through prenatal pregnancy risk. These findings help to describe how multiple generations are linked through genetic (biological parent), timing (developmental age of the child), and contextual (marital partner) pathways.

Two population enquiries in Walthamstow and Islington, London, have shown that loss of the mother before the age of 17 years, either by death or separation for a year or more, doubles the risk of depressive and anxiety disorders among adult women. Furthermore, there was a particularly high rate of adult depression among those whose mothers died before they were 6 years old, and this was associated with a measure of childhood helplessness. There was no such link of either adult disorder or childhood helplessness with age at loss under 6 years for those losing a mother by separation. Two possible explanations were explored for these contrasting results. That concerning the adequacy of mourning of the mother's death received no support. However, evidence indicated that experience with the mother before the loss (usually affected by ongoing illness) explained the link of adult depression or anxiety with her early death. The failure of age at loss to relate in the separation group was probably due to the fact that among them age of separation was not a good indication of the quality of maternal care before age 6. Indirect evidence emerged which suggested that quality of early attachment (before age 6) to the natural mother before any loss relates to childhood helplessness. This in turn relates to a higher risk of disorder in adult life.

In this investigation, gene–environment–gender interaction effects in predicting child borderline personality disorder symptomatology among maltreated and nonmaltreated low-income children (N = 1,051) were examined. In the context of a summer research camp, adult-, peer-, and self-report assessments of borderline precursor indicators were obtained, as well as child self-report on the Borderline Personality Features Scale for Children. Genetic variants of the oxytocin receptor genotype and the FK506 binding protein 5 gene CATT haplotype were investigated. Children who self-reported high levels of borderline personality symptomatology were differentiated by adults, peers, and additional self-report on indicators of emotional instability, conflictual relationships with peers and adults, preoccupied attachment, and indicators of self-harm and suicidal ideation. Maltreated children also were more likely to evince many of these difficulties relative to nonmaltreated children. A series of analyses of covariance, controlling for age and ancestrally informative markers, indicated significant Maltreatment × Gene × Gender three-way interactions. Consideration of the maltreatment parameters of subtype, onset, and recency expanded understanding of variation among maltreated children. The three-way interaction effects demonstrated differential patterns among girls and boys. Among girls, the gene–environment interaction was more consistent with a diathesis-stress model, whereas among boys a differential-sensitivity interaction effect was indicated. Moreover, the genetic variants associated with greater risk for higher borderline symptomatology, dependent on maltreatment experiences, were opposite in girls compared to boys. The findings have important implications for understanding variability in early predictors of borderline personality pathology.

Views regarding children's influence on their environment and their own development have undergone considerable changes over the years. Following Bell's (1968) seminal paper, the notion of children's influence and the view of socialization as a bidirectional process have gradually gained wide acceptance. However, empirical research implementing this theoretical advancement has lagged behind. This Special Section compiles a collection of new empirical works addressing multiple forms of influential child processes, with special attention to their consequences for children's and others’ positive functioning, risk and resilience. By addressing a wide variety of child influences, this Special Section seeks to advance integration of influential child processes into myriad future studies on development and psychopathology and to promote the translation of such work into preventive interventions.

Previous research has found associations but not established mechanisms of developmental linkage between language ability and inattentive–hyperactive (I-H) behavior problems. The present study examined whether self-regulation mediates the effect of language ability on later I-H behavior problems among young children (N = 120) assessed at 30, 36, and 42 months of age. Cross-lagged panel models tested the direction of effect between language ability and self-regulation and longitudinal effects of language ability on later I-H problems mediated by self-regulation. Language ability was measured by children's scores on the receptive and expressive language subtests of the Differential Ability Scales. Self-regulation was measured by three behavioral tasks requiring inhibitory control. I-H problems were reported by parents and secondary caregivers. Language ability predicted later self-regulation as measured by all three tasks. There was no association, however, between self-regulation and later language ability, suggesting that the direction of effect was stronger from language ability to later self-regulation. Moreover, the effect of language ability on later I-H behavior problems was mediated by children's self-regulation in one of the tasks (for secondary caregivers' but not parents' ratings). Findings suggest that language deficits may explain later I-H behavior problems via their prediction of poorer self-regulatory skills.

Chronic elevations of endogenous cortisol levels have been shown to alter medial temporal cortical structures and to be accompanied by declarative memory impairments and depressive symptoms in human adults. These effects of elevated endogenous levels of cortisol have not been directly studied in adolescents. Because adolescents with Cushing syndrome show endogenous elevations in cortisol, they represent a unique natural model to study the effects of prolonged hypercortisolemia on brain function, and memory and affective processes during this developmental stage. Using functional magnetic resonance imaging (fMRI), we compared 12 adolescents with Cushing syndrome with 22 healthy control adolescents on amygdala and anterior hippocampus activation during an emotional faces encoding task. None of these adolescents manifested depressive symptoms. Encoding success was assessed using a memory recognition test performed after the scan. The fMRI analyses followed an event-related design and were conducted using the SPM99 platform. Compared to healthy adolescents, patients with Cushing syndrome showed greater left amygdala and right anterior hippocampus activation during successful face encoding. Memory performance for faces recognition did not differ between groups. This first study of cerebral function in adolescents with chronic endogeneous hypercortisolemia due to Cushing syndrome demonstrates the presence of functional alterations in amygdala and hippocampus, which are not associated with affective or memory impairments. Such findings need to be followed by work examining the role of age and related brain maturational stage on these effects, as well as the identification of possible protective factors conferring resilience to affective and cognitive consequences in this disease and/or during this stage of cerebral development.

Drug abuse research and theory has become much more sophisticated over the last 2 decades, and some of the advancements parallel concepts that are part of the developmental psychopathology approach. The application of the developmental psychopathology perspective to recent drug abuse research findings can provide a greater understanding of that information and point to important areas of future research. Among the drug abuse research areas discussed here and viewed from this perspective are antecedent and co-occurring psychopathological conditions and other problem behaviors; the diversity of the nature of, paths to, and processes and outcomes related to drug abuse; the role of intermediary influences; the interaction of individual and environmental predisposing and protective factors; the role of families and other social institutions in intervention; and developmental stage characteristics. Directions for future research are also discussed.

Functional neuroimaging recently has been used to localize brain dysfunction in borderline personality disorder (BPD). Initial studies have examined baseline activity or emotional reactivity, and our group has investigated what we consider to be a crucial interaction between negative emotion and behavioral (dys)control. This research is beginning to identify abnormal frontolimbic circuitry likely underlying core clinical features of this condition. We review the evidence for dysfunction in specific frontolimbic regions, leading to a mechanistic model of symptom formation in BPD. In addition, we offer an integration of these neuroimaging findings with developmental perspectives on the emergence of borderline psychopathology, focusing on the ways in which early psychosocial experience may interact with developing brain systems. We also consider possible mechanisms of psychotherapeutic change at the neural systems level in BPD. Finally, we propose that future neuroimaging studies of BPD should integrate multiple levels of observation (structural, functional, neurochemical, genetic, and clinical) in a model-driven fashion to further understand the dynamic relationship between biological and psychological factors in the development and treatment of this difficult condition.

Guided by an evolutionary model of allostatic load, this study examined the hypothesis that the association between interparental aggression and subsequent changes in children's cortisol reactivity to interparental conflict is moderated by their temperamental dispositions. Participants of the multimethod, longitudinal study included 201 2-year-old toddlers and their mothers. These children experienced elevated levels of aggression between parents. Consistent with the theory, the results indicated that interparental aggression predicted greater cortisol reactivity over a 1-year period for children who exhibited high levels of temperamental inhibition and vigilance. Conversely, for children with bold, aggressive temperamental characteristics, interparental aggression was marginally associated with diminished cortisol reactivity. Further underscoring its implications for allostatic load, increasing cortisol reactivity over the one year span was related to concomitant increases in internalizing symptoms but decreases in attention and hyperactivity difficulties. In supporting the evolutionary conceptualization, these results further supported the relative developmental advantages and costs associated with escalating and dampened cortisol reactivity to interparental conflict.

Motor dysfunction is associated with schizophrenia, and recent longitudinal studies indicate that it precedes the onset of clinical symptoms. Of particular interest is the heightened occurrence of involuntary movements, which are apparent as early as infancy and suggest the presence of subcortical brain abnormalities. In this article, we present the results of a study of spontaneous movements in adolescents with schizotypal personality disorder (SPD). SPD is a syndrome that has been shown to be genetically linked with schizophrenia and is often observed prior to the early adult onset of schizophrenia. Systematic coding of videotapes of diagnostic interviews revealed that the SPD group showed significantly more involuntary movements of the head, trunk, and upper limbs than did normals and adolescents with other personality disorders. There were no diagnostic group differences in the rate of voluntary movements. Salivary cortisol, measured before the interview, was positively correlated with involuntary movements. Taken together, the findings provide further support for the hypothesized etiologic relation between SPD and schizophrenia. Based on a neural diathesis-stress model, potential underlying mechanisms are discussed.

Mundy and Sigman (1989) note that a problem arises in reconciling the existence of joint-attention deficits in autism with Leslie's (1987) theory that autistic children lack an innate, late-appearing metarepresentational capacity. Such a theory fails to encompass earlier rooted and perhaps more basic manifestations of autistic children's impairments in interpersonal coordination and intersubjective communication. The account provided by Mundy and Sigman, while promising, fails to address a critical question: How is it that autistic children have limited understanding that other people are subjects of experience with whom things can be shared? 1 suggest that an answer emerges only when we pay due regard to the nature of normal and autistic interpersonal relations. Here the authors' cognitive-behavioral analysis of affective exchanges between people leaves out the heart (and much of the mind) of the matter.

Maternal depression has a number of adverse effects on children. In the present study, maternal depressive symptoms were assessed (using the Center for Epidemiological Studies Depression Scale) when their child was 3 months, 6 months, 1 year, 2 years, 4.25 years, 6 years, 7 years, 8 years, and 10 years of age. At 9.5 years of age, children's (94 females, 82 males) depressive symptoms as well as cardiovascular and cortisol levels during baseline and two psychologically stressful tasks were measured. Using multilevel modeling, maternal depressive symptom trajectories were considered in relation to their child's adrenocortical and cardiovascular responses to acute stress. Our goal was to determine maternal depressive symptom trajectories for children with elevated cardiovascular and cortisol reactivity to acute stress and elevated depressive symptoms. In general, those mothers with chronically elevated depressive symptoms over their child's life span had children with lower initial cortisol, higher cardiac output and stroke volume in response to acute stress, lower vascular resistance during acute stress tasks, and significantly more depressive symptoms at 9.5 years of age. These results are discussed in the context of established associations among hypothalamic–pituitary–adrenal axis dysregulation, depression, and cardiovascular disease.

The purpose of this study was to ascertain the effectiveness of the Relational Psychotherapy Mothers' Group (RPMG), a supportive parenting group intervention for substance abusing women. Sixty mothers receiving RPMG were compared to 67 women receiving recovery training (RT); both treatments supplemented treatment in the methadone clinics. At the end of the 6-month treatment period, RPMG mothers showed marginally significant improvement on child maltreatment (self-reported) and cocaine abuse based on urinalyses when compared with RT mothers; notably, children of RPMG mothers reported significantly greater improvement in emotional adjustment and depression than children of RT mothers. At 6 months follow-up, however, treatment gains were no longer apparent. Overall, the findings suggest that whereas supportive parenting interventions for substance abusing women do have some preventive potential, abrupt cessation of the therapeutic program could have deleterious consequences.Preparation of the manuscript was funded in part by grants from the National Institutes of Health (RO1-DA10726, RO1-DA11498, R01-DA14385, and K23DA14606), the William T. Grant Foundation, and the Spencer Foundation.