Animal studies reveal that early deprivation impairs regulation of the hypothalamic–pituitary–adrenocortical (HPA) axis, potentially increasing vulnerability to stressors throughout life. To examine early deprivation effects on basal HPA axis activity in humans, basal cortisol levels were examined in 164 internationally adopted children who had experienced varying degrees of preadoption deprivation. Duration of institutional care, age at adoption, and parent ratings of preadoption neglect indexed a latent factor of Deprived Care. Adoption measures of height and weight standardized to World Health Organisation norms indexed a latent factor of Growth Delay that was viewed as another reflection of deprivation. Cortisol samples were collected 3.3–11.6 years postadoption (Md = 7.3 years) at home on 3 days approximately 30 min after wakeup and before bedtime. Both early a.m. levels and the decrease in cortisol across the day were examined. A structural equation model revealed that preadoption Deprived Care predicted Growth Delay at adoption and Growth Delay predicted higher morning cortisol levels and a larger diurnal cortisol decrease.

Psychological disorders co-occur often in children, but little has been done to document the types of conjoint pathways internalizing and externalizing symptoms may take from the crucial early period of toddlerhood or how harsh parenting may overlap with early symptom codevelopment. To examine symptom codevelopment trajectories, we identified latent classes of individuals based on internalizing and externalizing symptoms across ages 3–9 and found three symptom codevelopment classes: normative symptoms (low), severe-decreasing symptoms (initially high but rapidly declining), and severe symptoms (high) trajectories. Next, joint models examined how parenting trajectories overlapped with internalizing and externalizing symptom trajectories. These trajectory classes demonstrated that, normatively, harsh parenting increased after toddlerhood, but the severe symptoms class was characterized by a higher level and a steeper increase in harsh parenting and the severe-decreasing class by high, stable harsh parenting. In addition, a transactional model examined the bidirectional relationships among internalizing and externalizing symptoms and harsh parenting because they may cascade over time in this early period. Harsh parenting uniquely contributed to externalizing symptoms, controlling for internalizing symptoms, but not vice versa. In addition, internalizing symptoms appeared to be a mechanism by which externalizing symptoms increase. Results highlight the importance of accounting for both internalizing and externalizing symptoms from an early age to understand risk for developing psychopathology and the role harsh parenting plays in influencing these trajectories.

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.

The objective of this study was to test a social interactional model of physical aggression. Specifically, this model hypothesizes that the performance of physical aggression has its roots in socialization settings that are characterized by high densities of aversive stimuli and that provide frequent reinforcement for escalation to high intensity aversive behavior during social conflict. Social conflicts were observed during 10 hr of interaction of each of 20 mothers and their 5-year-old sons; half of the sons were selected based on evidence of frequent aggression in home and school settings. Simple descriptive and sequential analyses indicated that aggressive relative to nonaggressive dyad members were more likely to engage in conflict, engaged in longer conflicts, were more likely to escalate to higher levels of aversiveness, and were less likely to de-escalate the intensity of conflict. In aggressive and nonaggressive dyads, the cessation of conflict contingent on the escalation of one dyad member was reliably associated with an increased likelihood of escalation and with escalation to higher levels of aversiveness by that member in the subsequent conflict. However, escalation occurred more frequently and was more likely to result in cessation of conflicts in aggressive than nonaggressive dyads.

Feedback negativity (FN) is an event-related potential elicited by monetary reward and loss; it is thought to relate to reward-related neural activity and has been linked to depression in children and adults. In the current study, we examined the stability of FN, and its relationship with depression in adolescents, over 2 years in 45 8- to 13-year-old children. From Time 1 to Time 2, FN in response to monetary loss and in response to monetary gain showed moderate to strong reliability (rs = .64 and .67, respectively); these relationships remained significant even when accounting for related variables. FN also demonstrated high within-session reliability. Moreover, the relationship between a blunted FN and greater depression observed at Time 1 was reproduced at Time 2, and the magnitude of FN at Time 1 predicted depressive symptomatology at Time 2. These findings are consistent with the hypothesis that FN and its relationship with depression remain consistent over the course of development, and that FN may prospectively predict later depressive symptomatology. The current results suggest that FN may be suitable as a biomarker of depressive symptoms during adolescence.

The impact of environmental risk on toddlers' cognitive and linguistic development was investigated in a longitudinal study of 78 high-risk families. The risk factors examined were family social status, mother's psychosocial functioning, and quality of dyadic involvement at 1 year of age (including measures of mother-infant interaction and infant-mother attachment security). Child outcome measures included the Bayley MDI (at 24 months) and the Preschool Language Scale (at 36 months). The data indicate that dyadic involvement was an important mediator in the relation between environmental risk and subsequent child competence. Specific relations among early interactive experiences, infant attachment security, and subsequent cognitive and linguistic gain were examined within a framework of risk and protective factors. The results suggest that secure attachment may operate as a protective factor, but only among the more extreme cases in this exclusively high-risk sample.

Infant-parent psychotherapy in the second year of life presents specific challenges related to the child's developmental characteristics. The concept of projective identification is discussed as a mechanism for understanding the toddler's specific contribution to attachment disorders with the parent. A versatile clinical format is recommended including joint parent-child sessions, individual work with the toddler and the parents, and the use of therapeutic modes of communication specifically geared to the toddler's needs (“toddlerese”). Clinical examples and research applications are given to illustrate these points.

Dermatoglyphic asymmetry of fingertip ridge counts is more frequent in schizophrenia patients than normal controls, and may reflect disruptions in fetal development during Weeks 14–22 when fingerprints develop. However, there are no data in humans linking specific adverse events at specific times to dermatoglyphic asymmetries. Our objective was to determine whether prenatal exposure to a natural disaster (1998 Quebec ice storm) during Weeks 14–22 would result in increased dermatoglyphic asymmetry in children, and to determine the roles of maternal objective stress exposure, subjective stress reaction, and postdisaster cortisol. Ridge counts for homologous fingers were scored for 77 children (20 target exposed [Weeks 14–22] and 57 nontarget exposed [exposed during other gestation weeks]). Children in the target group had more than 0.50 SD greater asymmetry than the nontarget group. Within the target group, children whose mothers had high subjective ice storm stress had significantly greater asymmetry than those with lower stress mothers, and maternal postdisaster cortisol had a significant negative correlation with the children's dermatoglyphic asymmetry (r = −.56). Prenatal maternal stress during the period of fingerprint development results in greater dermatoglyphic asymmetry in their children, especially in the face of greater maternal distress.

This article is about the course of depressive symptoms during a classroom-based randomized preventive field trial aimed at improving reading achievement among first-grade children in an urban population of mixed ethnicity and lower middle to low socioeconomic status. In the fall, children reported high levels of depressive symptoms, a risk factor for major depressive disorder. There was a linear relationship in the fall between depressive symptoms and achievement test scores. Among male children in intervention classrooms whose gain in achievement was at least the national average, depression from fall to spring was decreased, compared to those whose achievement gain was lower. Among female children both in the control and in the intervention classrooms, there was also a significant relationship between gain in achievement and the course of depression.

A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families participated in this study, including 69 with child welfare documentation of moderate to severe maltreatment in the past 6 months. The children, who ranged in age from 3 to 5 years, were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors; and a composite variable assessed the number exposures to these adversities. Methylation of two sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p < .05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p < .05). FKBP5 alters glucocorticoid receptor responsiveness, and FKBP5 gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children.

Building upon prior findings of elevated problems among East Coast suburban youth through the 11th grade, this study establishes disproportionately high incidence of maladjustment across three disparate samples: East Coast Suburban youth at the end of their senior year in high school, and 11th and 12th graders in (a) a Northwest suburb and (b) an East Coast city. Both East Coast samples showed pronounced elevations in substance use, whereas the Northwest suburban sample showed marked vulnerability in serious internalizing and externalizing symptoms. Across all samples, parents’ low perceived containment for substance use (lax repercussions on discovering use) was a major vulnerability factor, followed by parents’ knowledge of their teens’ activities. Overall, adolescents’ symptom levels were more strongly related to their relationships with mothers than with fathers. An exception was boys’ apparent vulnerability to fathers’, but not mothers’, perceived depressive symptoms. As with affluent eighth graders, we found that “overscheduling” in extracurriculars is not a critical vulnerability factor among these high school students. Finally, youth reports suggested that most affluent parents do not indiscriminately bail their children out of all problem situations (although a small subset, apparently, do). Results are discussed along with the implications for practice and for future research.

This study investigated pupillary and behavioral responses to an emotional word valence identification paradigm among 32 pre-/early pubertal and 34 mid-/late pubertal typically developing children and adolescents. Participants were asked to identify the valence of positive, negative, and neutral words while pupil dilation was assessed using an eyetracker. Mid-/late pubertal children showed greater peak pupillary reactivity to words presented during the emotional word identification task than pre-/early pubertal children, regardless of word valence. Mid-/late pubertal children also showed smaller sustained pupil dilation than pre-/early pubertal children after the word was no longer on screen. These findings were replicated controlling for participants' age. In addition, mid-/late pubertal children had faster reaction times to all words, and rated themselves as more emotional during their laboratory visit compared to pre-/early pubertal children. Greater recall of emotional words following the task was associated with mid-/late pubertal status, and greater recall of emotional words was also associated with higher peak pupil dilation. These results provide physiological, behavioral, and subjective evidence consistent with a model of puberty-specific changes in neurobehavioral systems underpinning emotional reactivity.

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 effects of childhood abuse are diverse, and although pathology is not the only outcome, psychiatric illness, including posttraumatic stress disorder (PTSD), can develop. However, adult PTSD is less common among those who experienced single-event traumas as children than it is among those who experienced childhood abuse. In addition, PTSD is more common among adults than children who experienced childhood abuse. Such evidence raises doubt about the direct, causal link between childhood trauma and adult PTSD. The experience of childhood trauma, and in particular abuse, has been identified as a risk factor for subsequent development of PTSD following exposure to adult trauma, and a substantial literature identifies revictimization as a factor that plays a pivotal role in this trajectory. The literature on the developmental effects of childhood abuse and pathways to revictimization, when considered in tandem with the biological effects of early stress in animal models, may provide some explanations for this. Specifically, it seems possible that permanent sensitization of the hypothalamic–pituitary–adrenal axis and behavioral outcomes are a consequence of childhood abuse, and these combine with the impact of retraumatization to sustain, perpetuate, and amplify symptomatology of those exposed to maltreatment in childhood.

Although the construct of regulation is usually applied to ongoing behavior, it also has implications for ongoing cognition and the development of cognitive representations. We propose that subcortical motivational systems influence cortical representations in two general ways. First, they regulate response processes, promoting a general selection of information to which the child is exposed. Second, motivational systems regulate attention, promoting a more selective stabilization of representations for motivationally relevant sources of information. Together with the environment, these regulatory processes shape the child's developing representations. Individual differences in these processes result in cortical representational systems that enhance the motivational systems* ability to detect relevant inputs and to guide behavior in light of them. Examples are provided that focus on fearful children, discussing how their self-representation may contribute to anxious psychopathology.

Recent empirical and theoretical work on both normal and pathological development has led to the formulation of the metarepresentational conjecture for autism. This account of autistic development links the core impairments in imaginative abilities, communicative skills, and social competence to dysfunction of a single set of underlying cognitive mechanisms. In this context, Mundy and Sigman (1989) argue that the impairment of early gestural communication in autism cannot be accounted for by the metarepresentational theory. On the contrary, this early communication impairment in autism is highly consistent with a faulty theory-of-mind module. In normal development, this module is available from around the first year to handle estensive communication – shared pretense being a prime, though slightly later, example. We briefly consider the role in communication of perceptual processes that may trigger metarepresentation. This early theory-of-mind module, with its metarepresentational processes, provides the specific developmental basis for later versions of the child's theory of mind.

Recent research has suggested that autistic social impairment (ASI) is continuously distributed in nature and that subtle autistic-like social impairments aggregate in the family members of children with pervasive developmental disorders (PDDs). This study examined the longitudinal course of quantitatively characterized ASI in 3- to 18-year-old boys with and without PDD. We obtained assessments of 95 epidemiologically ascertained male–male twin pairs and a clinical sample of 95 affected children using the Social Responsiveness Scale (SRS), at two time points, spaced 1–5 years apart. Longitudinal course was examined as a function of age, familial loading for PDD, and autistic severity at baseline. Interindividual variation in SRS scores was highly preserved over time, with test–retest correlation of 0.90 for the entire sample. SRS scores exhibited modest general improvement over the study period; individual trajectories varied as a function of severity at baseline and were highly familial. Quantitative measurements of ASI reflect heritable traitlike characteristics. Such measurements can serve as reliable indices of phenotypic severity for genetic and neurobiologic studies, and have potential utility for ascertaining incremental response to intervention.

Thirty-seven families who had a child between the ages of 8 and 15 (mean age = 12.0 years) and had at least one parent who had experienced a recent episode of affective disorder were assigned randomly to one of two psychoeducational interventions. The interventions (clinician-facilitated or lecture-group discussion) were designed to prevent childhood depression and related problems through decreasing the impact of related risk factors and encouraging resiliency-promoting behaviors and attitudes. They were similar in content but differed in the level of the children's involvement and the degree to which the families' individual life experiences were linked to the educational material. Assessments included standard diagnostic and social functioning instruments and interviews designed specifically for this project to assess behavior and attitude change. Each parent and child was individually assessed by separate assessors who were blind to information about the other family members. Parent participants in both groups reported being satisfied with the intervention. Clinician group participants reported a significantly larger number of overall changes, as well as higher levels of change regarding communications about the illness with their children and increased understanding by the children of their illness. Significantly more children in the clinician group also reported they gained a better understanding of parental affective illness as a result of their participation in the project.

To examine the effects of early emotional neglect on children's affective development, we assessed children who had experienced institutionalized care prior to adoption into family environments. One task required children to identify photographs of facial expressions of emotion. A second task required children to match facial expressions to an emotional situation. Internationally adopted, postinstitutionalized children had difficulty identifying facial expressions of emotion. In addition, postinstitutionalized children had significant difficulty matching appropriate facial expressions to happy, sad, and fearful scenarios. However, postinstitutionalized children performed as well as comparison children when asked to identify and match angry facial expressions. These results are discussed in terms of the importance of emotional input early in life on later developmental organization.The authors thank Paul Ekman and Linda Camras for making their facial expression stimuli available to us. Dirk Wilker, Ziggy Bialzik, and Craig Rypstat provided invaluable assistance with computer programming and the computerized implementation of the tasks reported in this article. We also appreciate the assistance of Gabrielle Sowle, Marna Brown, Justin Martin, Susan Perlman, Kristi Johnson, Anne Kolan, Erin Eatough, and Sarah Pluck in the collection of these data. Linda Camras provided very helpful comments on an earlier version of this manuscript. These experiments would not be possible without the participation of many children and their families, for whose collaboration we are extremely appreciative. A preliminary version of these data were presented at the 2003 Biennial Meeting of the Society for Research in Child Development. This research was supported by grants from the National Institute of Mental Health to Seth Pollak (MH 68858 and MH 61285). Alison Wismer Fries was also supported by a National Institutes of Health Training Program in Emotion Research (MH 18931).

Theories of borderline personality disorder (BPD) postulate that high-risk transactions between caregiver and child are important for the development and maintenance of the disorder. Little empirical evidence exists regarding the reciprocal effects of parenting on the development of BPD symptoms in adolescence. The impact of child and caregiver characteristics on this reciprocal relationship is also unknown. Thus, the current study examines bidirectional effects of parenting, specifically harsh punishment practices and caregiver low warmth, and BPD symptoms in girls aged 14–17 years based on annual, longitudinal data from the Pittsburgh Girls Study (N = 2,451) in the context of child and caregiver characteristics. We examined these associations through the use of autoregressive latent trajectory models to differentiate time-specific variations in BPD symptoms and parenting from the stable processes that steadily influence repeated measures within an individual. The developmental trajectories of BPD symptoms and parenting were moderately associated, suggesting a reciprocal relationship. There was some support for time-specific elevations in BPD symptoms predicting subsequent increases in harsh punishment and caregiver low warmth. There was little support for increases in harsh punishment and caregiver low warmth predicting subsequent elevations in BPD symptoms. Child impulsivity and negative affectivity, and caregiver psychopathology were related to parenting trajectories, while only child characteristics predicted BPD trajectories. The results highlight the stability of the reciprocal associations between parenting and BPD trajectories in adolescent girls and add to our understanding of the longitudinal course of BPD in youth.