In this paper, we review the history of the concept of neuroplasticity as it relates to the understanding of neuropsychiatric disorders, using schizophrenia as a case in point. We briefly review the myriad meanings of the term neuroplasticity, and its neuroscientific basis. We then review the evidence for aberrant neuroplasticity and metaplasticity associated with schizophrenia as well as the risk for developing this illness, and discuss the implications of such understanding for prevention and therapeutic interventions. We argue that the failure and/or altered timing of plasticity of critical brain circuits might underlie cognitive and deficit symptoms, and may also lead to aberrant plastic reorganization in other circuits, leading to affective dysregulation and eventually psychosis. This “dysplastic” model of schizophrenia can suggest testable etiology and treatment-relevant questions for the future.

Exposure to adversity in childhood is associated with elevations in numerous physical and mental health outcomes across the life course. The biological embedding of early experience during periods of developmental plasticity is one pathway that contributes to these associations. Dimensional models specify mechanistic pathways linking different dimensions of adversity to health and well-being outcomes later in life. While findings from existing studies testing these dimensions have provided promising preliminary support for these models, less agreement exists about how to measure the experiences that comprise each dimension. Here, we review existing approaches to measuring two dimensions of adversity: threat and deprivation. We recommend specific measures for measuring these constructs and, when possible, document when the same measure can be used by different reporters and across the lifespan to maximize the utility with which these recommendations can be applied. Through this approach, we hope to stimulate progress in understanding how particular dimensions of early environmental experience contribute to lifelong health.

The goal of this study was to examine whether growth delay can serve as an index of allostatic load during early development, as it is well known that the activity of stress-mediating systems inhibits growth. The participants were children adopted internationally from institutional care (n = 36), children adopted internationally from foster care (n = 26), and nonadopted children (n = 35). For the adopted children, height for age and weight for height were assessed at adoption; for all children, disinhibited social approach (DSA; termed elsewhere as “indiscriminate friendliness”) and diurnal cortisol were assessed at 6–8 years (M = 6.9 years). For internationally adopted children in general, and postinstitutionalized children specifically, linear growth delay assessed at the time of adoption was associated with more dysregulated behavior in response to an unfamiliar adult (i.e., greater DSA) and a more dysregulated diurnal cortisol rhythm (i.e., higher late afternoon and evening values). Further, among the most growth-delayed children, higher cortisol levels later in the day were correlated with DSA. The potential for using growth delay as an allostatic load indicator and the possible problems and limitations in its use in child populations are discussed.

Past research highlights the importance of considering the sequelae of physical abuse in the context of other risk factors and possible exacerbating circumstances. The present research examines the relative, unique, and interactive effects of physical abuse, sociocultural disadvantage, and cumulative negative life events. Multiple measures and data sources were used to assess the socioeconomic circumstances, exposure to recent negative events, and social, cognitive, and affective adjustment of 19 physically abused and 49 nonabused elementary school-age children. Results indicated that abuse strongly independently predicted problems in children's adjustment with peers, self-perceptions, and depression. Abuse was also related to increased behavioral problems at home and at school, though this relation abated and even reversed itself as social disadvantage increased. Cumulative negative events independently predicted negative self-perceptions and, for girls, increased depression. Socioeconomic hardship was independently related to children's cognitive maturity. In addition, socioeconomic disadvantage qualified the relation between negative events and children's adjustment to peers, such that increased negative events were related to lower peer adjustment among less disadvantaged children but increased peer adjustment of children with more disadvantage. These results support calls for a more contextualized approach to examining the developmental outcomes of physical abuse, one that considers multiple risk factors simultaneously.

This article reviews past research on the parenting characteristics of childhood sexual abuse survivors and presents the results of a qualitative study exploring the women's perspectives on mothering as a survivor. Grounded theory was used in the collection and analysis of the data. Data sources included the narrative responses of 79 women (mean age = 38.2 years) and in-depth interviews of a purposive sample of 15 women (mean age = 39 years). They had an average of 2.2 children, ranging in age from 5 months to young adulthood. The theoretical model identified through analysis of data using the constant comparison method was entitled “The Hard Work of Mothering as a Survivor.” Processes emerged that described the ways participants managed the work of mothering in light of memories of the abuse and attempts to heal from this earlier trauma. The conditions for committing to the work included becoming aware of and accepting the reality of the abuse and how it affected one's life, and taking on the hard work of developing a mothering self. This included expanding awareness, developing and evaluating a personal model of mothering, navigating typical and abuse salient parenting challenges, mothering through the pain of recovery, and battling for balance. The findings highlighted the dynamic, multifaceted nature of recovery and resilience for these mothers and the need for an increased focus on parenting in counseling with childhood sexual abuse survivors. Provision of anticipatory guidance regarding commonly experienced stressors at varying stages of the child's development and the mother's stage of recovery and methods for coping with these challenges, would benefit these mothers and promote parenting competence. Specific implications for psychotherapy and directions for future research are discussed.

This longitudinal study examined personal-accentuation and contextual-amplification models of pubertal timing. In these models, individual and contextual risk factors during childhood and adolescence can magnify the effects of early or late puberty on depression symptoms that occur years later. The moderating role of prepubertal individual factors (emotional problems in late childhood) and interpersonal factors (deviant peer affiliation, early dating, perceived peer popularity, and perceived parental rejection during adolescence) were tested. A representative sample of 1,431 Canadian adolescents between 10–11 and 16–17 years of age was followed biannually. In line with the personal-accentuation model, early puberty has been shown to be a predictor for depression in both girls and boys who presented emotional problems in childhood. This effect was also noted for late maturing boys. Consistent with the contextual-amplification model, early puberty predicted later depression in youth who perceived greater parental rejection. Interpersonal experiences such as early dating in girls and deviant peer affiliation in boys predicted depression in early maturers as well. For girls, early dating was also found to be amplified by childhood emotional problems. In line with biopsychosocial models, results indicate that the effect of pubertal timing on depressive symptoms must be conceptualized through complex interactions between characteristics of adolescents' interpersonal relationships and prepubertal vulnerabilities.

The uneven cognitive phenotype in the adult outcome of Williams syndrome has led some researchers to make strong claims about the modularity of the brain and the purported genetically determined, innate specification of cognitive modules. Such arguments have particularly been marshaled with respect to language. We challenge this direct generalization from adult phenotypic outcomes to genetic specification and consider instead how genetic disorders provide clues to the constraints on plasticity that shape the outcome of development. We specifically examine behavioral studies, brain imaging, and computational modeling of language in Williams syndrome but contend that our theoretical arguments apply equally to other cognitive domains and other developmental disorders. While acknowledging that selective deficits in normal adult patients might justify claims about cognitive modularity, we question whether similar, seemingly selective deficits found in genetic disorders can be used to argue that such cognitive modules are prespecified in infant brains. Cognitive modules are, in our view, the outcome of development, not its starting point. We note that most work on genetic disorders ignores one vital factor, the actual process of ontogenetic development, and argue that it is vital to view genetic disorders as proceeding under different neurocomputational constraints, not as demonstrations of static modularity.

A secondary analysis of the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development was conducted to test the mechanisms by which relational aggression in third grade was associated both directly and indirectly with relational victimization in sixth grade. A large sample (N = 1,035; 522 girls; M = 8.3 years old; SD = 0.23) and multiple informants (teacher, child, and parent report) and methods were used to test several theoretically driven hypotheses. Our path analysis model suggested evidence for both direct and indirect pathways consistent with the sequential social process model of peer harassment. Relational aggression was significantly associated with future relational victimization even after controlling for physical aggression and gender. Loneliness mediated the direct association between relational aggression and peer victimization. A second model testing the reverse direction of effect revealed that relational victimization in third grade predicted relational aggression in sixth grade and was associated with loneliness and depressive symptoms in fifth grade, but there was no evidence for any of the indirect pathways.

Relations between political violence and child adjustment are matters of international concern. Past research demonstrates the significance of community, family, and child psychological processes in child adjustment, supporting study of interrelations between multiple social ecological factors and child adjustment in contexts of political violence. Testing a social ecological model, 300 mothers and their children (M = 12.28 years, SD = 1.77) from Catholic and Protestant working class neighborhoods in Belfast, Northern Ireland, completed measures of community discord, family relations, and children's regulatory processes (i.e., emotional security) and outcomes. Historical political violence in neighborhoods based on objective records (i.e., politically motivated deaths) were related to family members' reports of current sectarian antisocial behavior and nonsectarian antisocial behavior. Interparental conflict and parental monitoring and children's emotional security about both the community and family contributed to explanatory pathways for relations between sectarian antisocial behavior in communities and children's adjustment problems. The discussion evaluates support for social ecological models for relations between political violence and child adjustment and its implications for understanding relations in other parts of the world.

Adolescence is a period marked by increases in risk taking, sensation seeking, and emotion dysregulation. Neurobiological models of adolescent development propose that lagging development in brain regions associated with affect and behavior control compared to regions associated with reward and emotion processing may underlie these behavioral manifestations. Cross-sectional studies have identified several functional brain networks that may contribute to risk for substance use and psychopathology in adolescents. Determining brain structure measures that prospectively predict substance use and psychopathology could refine our understanding of the mechanisms that contribute to these problems, and lead to improved prevention efforts. Participants (N = 265) were healthy substance-naïve adolescents (ages 12–14) who underwent magnetic resonance imaging and then were followed annually for up to 13 years. Cortical thickness and surface area measures for three prefrontal regions (dorsolateral prefrontal cortex, inferior frontal gyrus, and orbitofrontal cortex) and three cortical regions from identified functional networks (anterior cingulate cortex, insular cortex, and parietal cortex) were used to predict subsequent binge drinking, externalizing symptoms, and internalizing symptoms. Thinner dorsolateral prefrontal cortex and inferior frontal cortex in early adolescence predicted more binge drinking and externalizing symptoms, respectively, in late adolescence (ps < .05). Having a family history of alcohol use disorder predicted more subsequent binge drinking and externalizing symptoms. Thinner parietal cortex, but not family history, predicted more subsequent internalizing symptoms (p < .05). This study emphasizes the temporal association between maturation of the salience, inhibition, and executive control networks in early adolescence and late adolescent behavior outcomes. Our findings indicate that developmental variations in these brain regions predate behavioral outcomes of substance use and psychopathology, and may therefore serve as prospective biomarkers of vulnerability.

The present study applies an allostatic load framework to an examination of the relationship between maternal psychosocial risk factors and maladaptive parenting behaviors. Specifically, the implications of low socioeconomic status and maternal depressive symptoms for maternal sympathovagal functioning during young children's distress were examined, as well as whether that functioning was, in turn, associated with maternal insensitivity, hostility, intrusiveness, and disengagement during mother–child dyadic interaction. Consistent with an allostatic framework, three patterns of sympathovagal functioning were expected to emerge: normative arousal, hyperarousal, and hypoarousal profiles. Furthermore, meaningful associations between maternal psychosocial risk factors, maladaptive parenting behaviors, and the three profiles of sympathovagal functioning were anticipated. Participants included 153 mother–toddler dyads recruited proportionately from lower and middle socioeconomic status backgrounds. Mothers’ sympathovagal response to their child's distress was assessed during the Strange Situation paradigm, and mothers’ parenting behavior was assessed during a dyadic free-play interaction. As hypothesized, normative arousal, hyperarousal, and hypoarousal profiles of maternal sympathovagal functioning were identified. Maternal depressive symptomatology predicted the hyperarousal profile, whereas socioeconomic adversity predicted hypoarousal. Moreover, allostatic load profiles were differentially associated with problematic parenting behaviors. These findings underscore the role of physiological dysregulation as a mechanism in the relationship between proximal risk factors and actual maladaptive parenting behaviors.

The longitudinal associations of older sibling substance use as well as dyadic sibling conflict and collusion to younger sibling substance use were examined in a community-based sample of 244 same-sex sibling pairs. Indirect effects of older siblings on younger sibling substance use were hypothesized via younger sibling deviant peer affiliation and conflict with friends. Adolescents, parents, friends, and teachers completed measures of substance use, conflict, and deviant peer involvement. Observational data were used for both measures of collusion and conflict. Findings suggest that older sibling substance use has a direct effect on younger sibling use, but relationship dynamics and reinforcement played a significant role as well. Specifically, collusion and conflict in the sibling relationship both had indirect effects through younger siblings’ deviant peer affiliation. Findings validate the powerful socializing role of both siblings and peers, and elucidate the complex mechanisms through which socialization occurs. Furthermore, data underscore the importance of considering how multiple dimensions of socialization operate in the elaboration of antisocial behavior.

Previous research has suggested that changes in the manifestations of the nonverbal learning disabilities syndrome (NLD) occur over the lifespan and that they do so in a manner that is consistent with the tenets of the NLD model (Rourke, 1989). Although the model would predict that age-related changes would also be evident within the childhood years, no study has yet examined this possibility. Based on the tenets of the model, specific predictions were formulated regarding developmental changes in the features of the NLD syndrome that would be expected to occur across the middle childhood and early adolescent years. The pattern of neurocognitive and socioemotional changes observed within the context of the cross-sectional data provided strong support for the predictions. Due to methodological limitations, no firm conclusions regarding the developmental manifestations of the NLD syndrome could be derived from the results of the longitudinal study. At most, these results suggested that some improvements in areas of neurocognitive deficiency may occur with the implementation of an appropriate remedial intervention program.

The course of severe depressive symptoms from pregnancy to 6 months postpartum, as well as the occurrence of severe paranoid symptoms prenatally, were examined by the Millon Clinical Multiaxial Inventory I and the Beck Depression Inventory, in 78 women who were heavy, chronic cocaine users and who retained custody of their children after birth. Six months postpartum, the quality of caregiving was observed and assessed in the home, and the children were assessed on the Bayley MDI Index in the laboratory. Mothers who were depressed and paranoid prenatally, regardless of whether the depression continued to 6 months postpartum, were less sensitive in caregiving than women without severe symptoms of paranoia or depression during pregnancy or those who reported only depression that lifted by 6 months postpartum. Mothers who were depressed prenatally and continued to be depressed by 6 months postpartum, regardless of the presence or absence of paranoia, had infants who earned lower Bayley MDI scores than the offspring of women without severe psychological symptoms or women whose depression had lifted. Severe depressive symptoms during pregnancy, if they did not continue to 6 months postpartum, did not appear to adversely influence either caregiving or infant functioning.

Extensive research has established a positive association between caregiver-child behavioral synchrony and child developmental functioning. Burgeoning research examining physiological synchrony has yet to elucidate its impact for children’s developing self-regulation. The objectives of this systematic review were to: 1) determine whether there is evidence that caregiver-child physiological synchrony promotes positive child development, 2) examine developmental differences in physiological synchrony and its correlates, and 3) explore whether context, risk, and/or stress influence patterns of synchrony. Sixty-nine studies met the following criteria on PubMed and PsycINFO: 1) peer-reviewed empirical articles in English that 2) examine autonomic, hypothalamic-pituitary-adrenocortical, and/or central nervous system activity 3) for caregivers and children 4) in response to a task and 5) directly examine the association between caregiver and child physiology. Findings varied based on developmental period and current behavioral context. Functional differences may exist across physiological systems and contexts. Synchrony may have different developmental consequences for dyads with and without certain risk factors. Few studies examine physiological synchrony across multiple systems or contexts, nor do they measure child characteristics associated with synchrony. Statistical and methodological challenges impede interpretation. Findings generally support the idea that physiological synchrony may support children’s developing self-regulation. Longitudinal research is needed to examine child developmental outcomes over time.

Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match–mismatch model (an evolutionary–developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field.

Individuals who have experienced high levels of childhood stress are at increased risk for a wide range of behavioral problems that persist into adulthood, yet the neurobiological and molecular mechanisms underlying these associations remain poorly understood. Many of the difficulties observed in stress-exposed children involve problems with learning and inhibitory control. This experiment was designed to test individuals' ability to learn to inhibit responding during a laboratory task. To do so, we measured stress exposure among a community sample of school-aged children, and then followed these children for a decade. Those from the highest and lowest quintiles of childhood stress exposure were invited to return to our laboratory as young adults. At that time, we reassessed their life stress exposure, acquired functional magnetic resonance imaging data during an inhibitory control task, and assayed these individuals' levels of methylation in the FK506 binding protein 5 (FKBP5) gene. We found that individuals who experienced high levels of stress in childhood showed less differentiation in the dorsolateral prefrontal cortex between error and correct trials during inhibition. This effect was associated only with childhood stress exposure and not by current levels of stress in adulthood. In addition, FKBP5 methylation mediated the association between early life stress and inhibition-related prefrontal activity. These findings are discussed in terms of using multiple levels of analyses to understand the ways in which adversity in early development may affect adult behavioral adaptation.

Whether internalizing symptoms increase or remain at similar levels throughout childhood is currently not well understood. Moreover, the association between vagal regulation of cardiac activity and internalizing symptoms across childhood needs to be clarified. We used a multilevel conceptual framework to examine how children's vagal regulation of cardiac activity and mothers' internalizing symptoms were jointly associated with children's developmental trajectories of internalizing symptoms from ages 4 to 10 years old. Data came from 384 children who participated in an ongoing longitudinal study. Children and their mothers came to the research laboratory at ages 4, 5, 7, and 10. Mothers reported their children's and their own internalizing symptoms. Children's vagal regulation of cardiac activity was assessed during quiet baseline tasks and during challenge tasks. Multilevel models revealed that child internalizing symptoms increased from ages 4 to 10 years old, but only in females, and especially between ages 7 and 10. More vagal withdrawal in response to challenge was associated with more internalizing symptoms, particularly with more somatic symptoms. Associations between children's physiological regulation and internalizing symptoms differed by children's age, sex, and presence of maternal internalizing symptoms. Understanding associations between vagal regulation of cardiac activity and internalizing symptoms during childhood calls for fine-grained developmental analyses that take into account the heterogeneity of internalizing symptoms, as well as developmental phase, context, and gender.

A diathesis-stress interaction model is used to describe multifinality in adolescent internalizing and risky behavioral outcomes. Problematic behavior associated with adolescent insecure preoccupation (a diathesis) was expected to interact with the level of maternal autonomous discourse (a stressor) to predict specific adolescent outcomes. Assessments of adolescent preoccupied attachment organization, observations of maternal displays of autonomy in mother–adolescent interactions, and adolescent reports of internalizing symptoms and risky behaviors were obtained at age 16. As predicted, maternal autonomy in the mother–adolescent relationship helped to explain multifinality in dysfunctional symptoms among preoccupied adolescents. Adolescent preoccupation was more strongly linked to internalizing behavior when mothers demonstrated low levels of autonomy in interactions with their adolescents and more strongly linked to risky behavior when mothers displayed extremely high levels of autonomy. Implications for autonomy processes in increasing our understanding of how adolescent insecure–preoccupation relates to profiles of specific problems during adolescence are discussed as is the importance of exploring the role of attachment in different contexts.

A longitudinal prospective design was used to test the generalizability of low levels of social preference and high levels of antisocial peer involvement as risk factors for delinquent behavior problems to African American (AA) and European American (EA) boys and girls (N = 384). Social preference scores were computed from peer reports in middle childhood (ages 6–9). Parents and adolescents reported antisocial peer involvement in early adolescence (ages 13–16) and adolescents reported on their own delinquent behavior in late adolescence (ages 17 and 18). Analyses tested for differences across four groups (AA boys, EA boys, AA girls, EA girls) in construct measurement, mean levels, and associations among variables. Few measurement differences were found. Mean-level differences were found for social preference and delinquent behavior. AA boys were least accepted by peers and reported the highest level of delinquent behavior. EA girls were most accepted by peers and reported the lowest level of delinquent behavior. Associations among peer experiences and delinquent behavior were equivalent across groups, with lower levels of social preference and higher levels of antisocial peer involvement associated with more delinquent behavior. Person-centered analyses showed the risk associated with low social preference and high antisocial peer involvement to be similar across groups, providing further evidence of the generalizability of the peer relationship experiences as risk factors for subsequent delinquent behavior problems.This research was supported by grants from the National Institute of Mental Health (MH 42498, MH 57095) and the National Institute of Child Health and Human Development (HD 30572 to G.S.P., K.A.D., and J.E.B.). We are grateful to the Child Development Project families for their participation. Special thanks to Jennifer Burczyk–Brown for her help in managing the analyses and to Michael M. Criss for his comments on an early version of the manuscript. This article has been approved for publication by the Director of the Louisiana Agricultural Experiment Station (manuscript 03-36-104).