The impact of similarity in parent and child characteristics on the quality of parenting is underresearched. The current study examined the interaction between mother and child attention-deficit/hyperactivity disorder (ADHD) symptoms on parenting. Two hypotheses were tested: the similarity-fit hypothesis, which predicted that parent and child similarity will improve parenting, and the similarity-misfit hypothesis, which predicted the opposite. Study 1 examined the associations between maternal and child ADHD symptoms and child-specific rearing attitudes of 95 mothers with school-aged children. In Study 2 this analysis was extended to more objective observer-rated mother–child interaction and maternal expressed emotion in 192 mothers of preschool children. Child ADHD symptoms were associated with negative maternal comments and maternal ADHD symptoms with negative expressed emotion. In both studies maternal ADHD symptoms appeared to ameliorate the effects of child ADHD symptoms on negative parenting. Parental response to children with high ADHD symptoms was more positive and affectionate when the mother also had high ADHD symptoms. The results support the similarity-fit hypothesis and highlight the importance of considering both child and maternal ADHD symptoms in studies of parenting.

This paper discusses how converging methods may form a powerful tool in unraveling the neurobiology of attention-deficit/hyperactivity disorder (ADHD). Integrating findings from multiple disciplines can inform us on how different neurobiological and cognitive mechanisms tie together in both typical and atypical development. Examples are discussed of this approach: combining family and genetic approaches with anatomical neuroimaging illustrates how mapping familial effects can bring us closer to understanding the neurobiology of ADHD. Functional neuroimaging has convincingly linked cognitive problems in this disorder with frontostriatal functioning, but also shows that other systems may be involved in some of the symptoms of ADHD. Combining these findings has suggested new avenues for investigation, such as the role of frontocerebellar networks. Furthermore, findings may have practical applications: this paper discusses an example of how converging evidence of striatal dysregulation in ADHD suggests possible directions for treatment that are now being explored in functional imaging studies.

Studies with nonhuman primates and rodents, as well as with human children, have suggested that early separations from caregivers are often associated with changes in the functioning of the hypothalamus–pituitary–adrenal (HPA) axis. On the basis of these findings, we designed a relational intervention that was intended to normalize HPA functioning among children in foster care. This paper presents findings from a randomized clinical trial that assessed the effectiveness of a relational intervention (Attachment and Biobehavioral Catch-up [ABC]) with regard to HPA functioning. The ABC intervention was intended to enhance children's ability to regulate physiology and behavior. The control intervention (Developmental Education for Families) was intended to enhance children's cognitive skills. A comparison group of children who had never been in foster care was also included. Children's cortisol production was assessed upon arrival at the lab, and 15 and 30 min following the Strange Situation. Random effects analyses of variance were performed to assess differences in initial values and change between children in the two intervention groups. Children in the ABC intervention and comparison group children showed lower initial values of cortisol than children in the treatment control group, considering arrival at lab as initial values (p < .05). Groups did not differ significantly in change over time. These results suggest that the ABC intervention is effective in helping children regulate biology in ways more characteristic of children who have not experienced early adversity.

The purpose of this study was to evaluate whether children with a history of disorganized attachment in infancy were more likely than children without a history of disorganized attachment to exhibit symptoms of posttraumatic stress disorder (PTSD) at school age following trauma exposure. The sample consisted of 78 8.5-year-old children from a larger, ongoing prospective study evaluating the effects of intrauterine cocaine exposure (IUCE) on children's growth and development from birth to adolescence. At the 12-month visit, children's attachment status was scored from videotapes of infant–caregiver dyads in Ainsworth's strange situation. At the 8.5-year visit, children were administered the Violence Exposure Scale—Revised, a child-report trauma exposure inventory, and the Diagnostic Interview for Children and Adolescents by an experienced clinical psychologist masked to children's attachment status and IUCE status. Sixteen of the 78 children (21%) were classified as insecure–disorganized/insecure–other at 12 months. Poisson regressions covarying IUCE, gender, and continuity of maternal care indicated that disorganized attachment status at 12 months, compared with nondisorganized attachment status, significantly predicted both higher avoidance cluster PTSD symptoms and higher reexperiencing cluster PTSD symptoms. These findings suggest that the quality of early dyadic relationships may be linked to differences in children's later development of posttraumatic stress symptoms following a traumatic event.

The recent development of low-risk imaging technologies, such as functional magnetic resonance imaging (fMRI), have had a significant impact on the investigation of psychopathologies in children and adolescents. This review considers what we can infer from fMRI work regarding the development of conduct disorder (CD) and oppositional defiant disorder (ODD). We make two central assumptions that are grounded in the empirical literature. First, the diagnoses of CD and ODD identify individuals with heterogeneous pathologies; that is, different developmental pathologies can receive a CDD or ODD diagnosis. This is indicated by the comorbidities associated with CD/ODD, some of which appear to be mutually exclusive at the biological level (e.g., posttraumatic stress disorder [PTSD] and psychopathic tendencies). Second, two populations of antisocial individuals can be identified: those that show an increased risk for only reactive aggression and those that show an increased risk for both reactive and instrumental aggression. We review the fMRI data indicating that particular comorbidities of CD/ODD (i.e., mood and anxiety conditions such as childhood bipolar disorder and PTSD) are associated with either increased responsiveness of neural regions implicated in the basic response to threat (e.g., the amygdala) or decreased responsiveness in regions of frontal cortex (e.g., ventromedial frontal cortex) that are implicated in the regulation of the basic threat response. We suggest why such pathology would increase the risk for reactive aggression and, in turn, lead to the association with a CD/ODD diagnosis. We also review the literature on psychopathic tendencies, a condition where the individual is at significantly elevated risk for both reactive and instrumental aggression. We show that in individuals with psychopathic tendencies, the functioning of the amygdala in stimulus-reinforcement learning and of the ventromedial frontal cortex in the representation of reinforcement expectancies is impaired. We suggest why such pathology would increase the risk for reactive and instrumental aggression and thus also lead to the association with a CD/ODD diagnosis.

Effortful control was examined as a moderator of the relations of three domains of contextual risk factors to growth in internalizing and externalizing problems in a community sample (N = 189) of children (8–12 years at Time 1). Socioeconomic, maternal, and environmental risk factors were examined as predictors of initial levels and growth in children's adjustment problems across 3 years. The effects of the risk factors depended on children's level of effortful control. For children lower in effortful control, socioeconomic risk was related to significantly higher initial levels of internalizing and externalizing problems and decreases over time. However, children lower in effortful control had higher levels of problems at all three time points than children higher in effortful control. Maternal risk was associated with increases in internalizing for children lower in effortful control, and environmental risk was related to increases in internalizing and externalizing problems for children lower in effortful control, but not those higher in effortful control. Children who were lower in effortful control appeared to experience more adverse effects of contextual risk than those higher in effortful control, suggesting that interventions aimed at improving children's effortful control might serve to protect children from increased risk of adjustment problems associated with contextual risk factors.

Previous studies have documented that smoking during pregnancy (SDP) is associated with offspring externalizing problems, even when measured covariates were used to control for possible confounds. However, the association may be because of nonmeasured environmental and genetic factors that increase risk for offspring externalizing problems. The current project used the National Longitudinal Survey of Youth and their children, ages 4–10 years, to explore the relations between SDP and offspring conduct problems (CPs), oppositional defiant problems (ODPs), and attention-deficit/hyperactivity problems (ADHPs) using methodological and statistical controls for confounds. When offspring were compared to their own siblings who differed in their exposure to prenatal nicotine, there was no effect of SDP on offspring CP and ODP. This suggests that SDP does not have a causal effect on offspring CP and ODP. There was a small association between SDP and ADHP, consistent with a causal effect of SDP, but the magnitude of the association was greatly reduced by methodological and statistical controls. Genetically informed analyses suggest that unmeasured environmental variables influencing both SDP and offspring externalizing behaviors account for the previously observed associations. That is, the current analyses imply that important unidentified environmental factors account for the association between SDP and offspring externalizing problems, not teratogenic effects of SDP.

Two groups of Romanian children were compared on spectral power and coherence in the electroencephalogram (EEG) in early childhood. One group consisted of previously institutionalized children who had been randomly assigned to a foster care intervention at a mean age of 23 months. The second group had been randomized to remain in institutional care. Because of a policy of noninterference, a number of these children also experienced placement into alternative family care environments. There were minimal group differences between the foster care and institutionalized groups in EEG power and coherence across all measured frequency bands at 42 months of age. However, age at foster care placement within the foster care group was correlated with certain measures of EEG power and coherence. Earlier age at foster care placement was associated with increased alpha power and decreased short-distance EEG coherence. Further analyses separating age at placement from duration of intervention suggest that this effect may be more robust for EEG coherence than EEG band power. Supplementary analyses examined whether the EEG measures mediated changes in intellectual abilities within the foster care children, but no clear evidence of mediation was observed.

Children with narrow phenotype bipolar disorder (NP-BD; i.e., history of at least one hypomanic or manic episode with euphoric mood) are deficient when labeling face emotions. It is unknown if this deficit is specific to particular emotions, or if it extends to children with severe mood dysregulation (SMD; i.e., chronic irritability and hyperarousal without episodes of mania). Thirty-nine NP-BD, 31 SMD, and 36 control subjects completed the emotional expression multimorph task, which presents gradations of facial emotions from 100% neutrality to 100% emotional expression (happiness, surprise, fear, sadness, anger, and disgust). Groups were compared in terms of intensity of emotion required before identification occurred and accuracy. Both NP-BD and SMD youth required significantly more morphs than controls to label correctly disgusted, surprised, fearful, and happy faces. Impaired face labeling correlated with deficient social reciprocity skills in NP-BD youth and dysfunctional family relationships in SMD youth. Compared to controls, patients with NP-BD or SMD require significantly more intense facial emotion before they are able to label the emotion correctly. These deficits are associated with psychosocial impairments. Understanding the neural circuitry associated with face-labeling deficits has the potential to clarify the pathophysiology of these disorders.

Human brain development is created through continuing complex interactions of genetic and environmental influences. The challenge of linking specific genetic or environmental risk factors to typical or atypical behaviors has led to interest in using brain structural features as an intermediate phenotype. Twin studies in adults have found that many aspects of brain anatomy are highly heritable, demonstrating that genetic factors provide a significant contribution to variation in brain structures. Less is known about the relative impact of genes and environment while the brain is actively developing. We summarize results from the ongoing National Institute of Mental Health child and adolescent twin study that suggest that heritability of different brain areas changes over the course of development in a regionally specific fashion. Areas associated with more complex reasoning abilities become increasingly heritable with maturation. The potential mechanisms by which gene–environment interactions may affect heritability values during development is discussed.

Adopting a developmental epidemiology perspective, the current study examines sources of risk heterogeneity for internalizing symptomatology among children of alcoholic parents (COAs). Parent-based factors, including comorbid diagnoses and the number of alcoholic parents in the family, as well as child-based factors, namely child gender, formed the indicators of heterogeneity. Following a novel approach to cross-study methods, we present a three-stage analysis involving measurement development using item response theory, examination of study effects on latent trajectories over time using latent curve modeling, and prediction of these latent trajectories testing our theoretically derived hypotheses in two longitudinal investigations across both mother- and self-reported symptomatology. Specifically, we replicated previous findings that parent alcoholism has a unique effect on child internalizing symptoms, above and beyond those of both parent depression and antisocial personality disorder. However, we also found important subgroup differences, explaining heterogeneity within COAs' risk profile in terms of the number of alcoholic parents in the family, comorbid diagnoses for the alcoholic parent and, for self-reported symptoms, child gender. Such factors serve to refine the definition of risk among COAs, suggesting a more severely impaired target group for preventive interventions, identifying the significance of familial alcoholism in individual differences underlying internalizing symptoms over time, and further specifying the distal risk matrix for an internalizing pathway to alcohol involvement.

This article examines how bipolar symptoms emerge during development, and the potential role of psychosocial and pharmacological interventions in the prevention of the onset of the disorder. Early signs of bipolarity can be observed among children of bipolar parents and often take the form of subsyndromal presentations (e.g., mood lability, episodic elation or irritability, depression, inattention, and psychosocial impairment). However, many of these early presentations are diagnostically nonspecific. The few studies that have followed at-risk youth into adulthood find developmental discontinuities from childhood to adulthood. Biological markers (e.g., amygdalar volume) may ultimately increase our accuracy in identifying children who later develop bipolar I disorder, but few such markers have been identified. Stress, in the form of childhood adversity or highly conflictual families, is not a diagnostically specific causal agent but does place genetically and biologically vulnerable individuals at risk for a more pernicious course of illness. A preventative family-focused treatment for children with (a) at least one first-degree relative with bipolar disorder and (b) subsyndromal signs of bipolar disorder is described. This model attempts to address the multiple interactions of psychosocial and biological risk factors in the onset and course of bipolar disorder.

Relations between maternal and paternal problem drinking symptoms and destructive marital conflict, parenting problems, and children's internalizing and externalizing problems were investigated. Participants were community families with a child in kindergarten who completed questionnaire measures at baseline (N = 235), 1 year later (N = 227), and 2 years later (N = 215). Structural equation modeling revealed that paternal problem drinking at Time 1 was associated with greater destructive marital conflict 1 year later. In turn, destructive marital conflict was related to decreased parental warmth and increased parental psychological control; these parenting problems were associated with greater child internalizing and externalizing problems at the third time point. Further analyses revealed that the indirect effects of paternal drinking on children's adjustment were significant, and that relations remained even after including autoregressive effects. Findings are discussed in terms of family process models for relations between parental drinking and child adjustment problems.

The study assessed conduct and emotional difficulties in a group of Romanian adoptees at age 11, and serves as a follow-up to assessments made when the children were 6 years old. It was found that there was a significant increase in emotional difficulties, but not conduct problems, for the Romanian sample since age 6. It was also found that emotional difficulty was significantly more prevalent at age 11 in the Romanian group than in a within-UK adoptee group. Emotional difficulties in the Romanian adoptee group were found to be significantly and strongly related to previous deprivation-specific problems (disinhibited attachment, cognitive impairment, inattention/overactivity and quasi-autism); however, the presence of such early problems did not account fully for the onset of later emotional problems. Five contrasting hypotheses concerning possible mediators for later onset of emotional difficulties for the Romanian group were examined. No links were found to duration of deprivation or other deprivation-related indices, stresses/difficulties in the postadoption family environment, or educational attainment and self-esteem. There was some evidence that emotion recognition might play a role in the emergence of these problems, but other measures of social competence and theory of mind showed no associations with the onset of emotional problems.

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.

This paper examines interrelations between biological and social influences on the development of self-regulation in young children and considers implications of these interrelations for the promotion of self-regulation and positive adaptation to school. Emotional development and processes of emotion regulation are seen as influencing and being influenced by the development of executive cognitive functions, including working memory, inhibitory control, and mental flexibility important for the effortful regulation of attention and behavior. Developing self-regulation is further understood to reflect an emerging balance between processes of emotional arousal and cognitive regulation. Early childhood educational programs that effectively link emotional and motivational arousal with activities designed to exercise and promote executive functions can be effective in enhancing self-regulation, school readiness, and school success.

The pursuit of rewarding experiences motivates everyday human behavior, and can prove beneficial when pleasurable, positive consequences result (e.g., satisfying hunger, earning a paycheck). However, reward seeking may also be maladaptive and lead to risky decisions with potentially negative long-term consequences (e.g., unprotected sex, drug use). Such risky decision making is often observed during adolescence, a time in which important structural and functional refinements occur in the brain's reward circuitry. Although much of the brain develops before adolescence, critical centers for goal-directed behavior, such as frontal corticobasal ganglia networks, continue to mature. These ongoing changes may underlie the increases in risk-taking behavior often observed during adolescence. Further, typical development of these circuits is vital to our ability to make well-informed decisions; atypical development of the human reward circuitry can have severe implications, as is the case in certain clinical and developmental conditions (e.g., attention-deficit/hyperactivity disorder). This review focuses on current research probing the neural correlates of reward-related processing across human development supporting the current research hypothesis that immature or atypical corticostriatal circuitry may underlie maladaptive behaviors observed in adolescence.

Children's behavior problems may stem from ineffective cortical mechanisms for regulating negative emotions, and the success of interventions may depend on their impact on such mechanisms. We examined neurophysiological markers associated with emotion regulation in children comorbid for externalizing and internalizing problems before and after treatment. We hypothesized that treatment success would correspond with reduced ventral prefrontal activation, and increased dorsomedial prefrontal activation, at the time point of an event-related potential (ERP) associated with inhibitory control. Twenty-seven 8- to 12-year-old children (with usable data) were tested before and after a 14-week community-based treatment program and assessed as to improvement status. Fifteen 8- to 12-year-olds from the normal population (with usable data) were tested over the same interval. All children completed an emotion-induction go/no-go task while fitted with a 128-channel electrode net at each test session. ERP amplitudes, and estimates of cortical activation in prefrontal regions of interest, were measured at the peak of the “inhibitory” N2 and compared between improvers, nonimprovers, and nonclinical children. ERP amplitudes showed no group differences. However, improvers showed an overall reduction in ventral prefrontal activation from pretreatment to posttreatment, bringing them in line with nonclinical children, whereas ventral activation remained high for nonimprovers. Both improvers and nonimprovers showed high dorsal activation relative to nonclinical children. Supplementary analyses indicated that only ventral prefrontal regions, and only within the N2 time window, showed decreased activity from pre- to posttreatment, suggesting changes in regulatory processes rather than in overall emotional arousal. These cortically mediated changes may permit a reduction in the overengaged, rigid style of emotion regulation characteristic of children with behavior problems.

The current investigation addresses the manner through which trauma affects basic memory and self-system processes. True and false recall for self-referent stimuli were assessed in conjunction with dissociative symptomatology among abused (N = 76), neglected (N = 92), and nonmaltreated (N = 116) school-aged children. Abused, neglected, and nonmaltreated children did not differ in the level of processing self-schema effect or in the occurrence and frequency of false recall. Rather, differences in the affective valence of false recall emerged as a function of maltreatment subtype and age. Regarding dissociation, the abused children displayed higher levels of dissociative symptomatology than did the nonmaltreated children. Although abused, neglected, and nonmaltreated children did not exhibit differences in the valence of their self-schemas, positive and negative self-schemas were related to self-integration differently among the subgroups of maltreatment. Negative self-schemas were associated with increased dissociation among the abused children, whereas positive self-schemas were related to increased dissociation for the neglected children. Thus, positive self-schemas displayed by the younger neglected children were related to higher dissociation, suggestive of defensive self-processing. Implications for clinical intervention are underscored.

Callous-unemotional (CU) traits in antisocial youth have been associated with deficits in the processing of emotionally distressing stimuli in a number of past studies. In the current study, we investigated moderators of this association in a sample of 88 ethnically diverse detained boys (mean age = 15.57, SD = 1.28). Overall, emotional processing of distressing stimuli using a dot-probe task was not related to CU traits and there was no moderating effect of ethnicity. However, CU traits were related to deficits in emotional processing in youth high on aggression and youth high on exposure to community violence. Further, youth high on CU traits but with enhanced orienting to distressing stimuli had stronger histories of abuse, supporting the possibility that there may be environmentally influenced pathways in the development of these traits.