We describe recent progress in our program of research that aims to use functional magnetic resonance imaging (fMRI) to identify and delineate the brain systems involved in social perception and to chart the development of those systems and their roles as mechanisms supporting the development of social cognition in children, adolescents, and adults with and without autism. This research program was initiated with the intention of further specifying the role of the posterior superior temporal sulcus (STS) region in the network of neuroanatomical structures comprising the social brain. Initially, this work focused on evaluating STS function when typically developing adults were engaged in the visual analysis of other people's actions and intentions. We concluded that that the STS region plays an important role in social perception via its involvement in representing and predicting the actions and social intentions of other people from an analysis of biological-motion cues. These studies of typically developing people provided a set of core findings and a methodological approach that informed a set of fMRI studies of social perception dysfunction in autism. The work has established that dysfunction in the STS region, as well as reduced connectivity between this region and other social brain structures including the fusiform gyrus and amygdala, play a role in the pathophysiology of social perception deficits in autism. Most recently, this research program has incorporated a developmental perspective in beginning to chart the development of the STS region in children with and without autism.
Although allostatic load has been investigated in mood and anxiety disorders, no prior study has investigated developmental change in allostatic load as a precursor to schizotypal personality. This study employed a multilevel developmental framework to examine whether the development of increased allostatic load, as indicated by impaired sympathetic nervous system habituation from ages 3 to 11 years, predisposes to schizotypal personality at age 23 years. Electrodermal activity to six aversive tones was recorded in 995 subjects at age 3 years and again at 11 years. Habituation slopes at both ages were used to create groups who showed a developmental increase in habituation (decreased allostatic load), and those who showed a developmental decrease in habituation (increased allostatic load). Children who showed a developmental increase in allostatic load from ages 3 to 11 years had higher levels of schizotypal personality at 23 years. A breakdown of total schizotypy scores demonstrated specificity of findings to cognitive-perceptual features of schizotypy. Findings are the first to document a developmental abnormality in allostasis in relation to adult schizotypal personality. The relative failure to develop normal habituation to repeated stressors throughout childhood is hypothesized to result in an accumulation of allostatic load and consequently increased positive symptom schizotypy in adulthood.
Earlier age of menarche is believed to confer greater vulnerability to depressive symptoms via increased reactivity to stressors associated with adolescence. In this longitudinal study, we measured depressive symptoms and salivary cortisol levels in 198 boys and 142 girls between the ages of 11 and 13 tested four times during Grade 7 as they transitioned from elementary school to secondary school as per Quebec's education system. Results showed that girls who had already reached menarche before starting secondary school had significantly higher depressive symptoms and salivary cortisol levels across the school year in comparison to girls who had not reached menarche, who in turn presented higher depressive scores than boys. When we divided menarcheal girls as a function of menarcheal timing in subanalyses, we found that girls with early menarche presented consistently elevated depressive symptoms across the school year while girls with on-time menarche presented transient depressive symptoms but no differences in salivary cortisol levels. Collectively, these results show that early menarche is associated with high depressive symptoms and cortisol levels in adolescent girls. This developmental milestone may render girls more vulnerable to environmental stressors and therefore represents a critical period to intervene to promote mental health.
The central feature of schizophrenia is its onset in adolescence. Although this clinical observation is consistent with the view that schizophrenia may be a neurodevelopmental disorder, debate has focused on when the proposed brain maturational deviations may begin and what might be the nature of such defective development. Conflicting models of this illness (e.g., the early and late neurodevelopmental models) have been proposed. In this paper, we will first review concepts from basic developmental neurobiology pertinent to these issues; we then summarize aspects of the neurobiology of schizophrenia that have a particular bearing on the adolescent onset of this illness. We propose that the schizophrenic syndrome may result from early brain adversity and late maturational processes of brain development interacting with adverse humoral, biochemical, and psychosocial factors during adolescence and early adulthood. The onset of schizophrenia in adolescence may be related to the "plasticity switch" secondary to the peripubertal brain maturational changes, perhaps involving an alteration in glutamate receptor function. This loss of plasticity could result in social and nonsocial cognitive deficits that are central to the pathophysiology of schizophrenia; the vulnerable person may therefore utilize prepubertal processing styles that are insufficient to the adaptive and "gistful" abstraction requirements of adult cognition. Schizophrenia onset might occur in the context of psychosocial developmental challenges to a delayed social cognitive capacity among neurodevelopmentally compromised individuals. We review therapeutic implications as well as testable predictions generated by this model, and discuss research strategies that might further our understanding of the brain maturational abnormalities in schizophrenia.
A number of lines of evidence converge in implicating neurodevelopmental processes in the etiology and epigenesis of schizophrenia. In this study we used a prospective, longitudinal design to examine whether adverse obstetric experiences predict schizophrenia and whether there is a deviant functional-developmental trajectory during the first 7 years of life among individuals who manifest schizophrenia as adults. The 9,236 members of the Philadelphia cohort of the National Collaborative Perinatal Project were screened for mental health service utilization in adulthood, and chart reviews were performed to establish diagnoses according to DSM-IV criteria. The risk for schizophrenia increased linearly with the number of hypoxia-associated obstetric complications but was unrelated to maternal infection during pregnancy or fetal growth retardation. Preschizophrenic cases (and their unaffected siblings who were also cohort members) manifested cognitive impairment, abnormal involuntary movements and coordination deficits, and poor social adjustment during childhood. There was no evidence of intraindividual decline in any domain, but preschizophrenic cases did show deviance on an increasing number of functional indicators with age. Together, these findings suggest that both genetic and obstetric factors participate in creating a neural diathesis to schizophrenia, the phenotypic expressions of which are age dependent, probably reflecting the maturational status of a number of interconnected brain systems.
The purpose of this study was to examine the relationship between fathers' alcoholism and the quality of parent-infant interactions during free play. A related goal was to study the potential mediating or moderating role of comorbid parental psychopathology, such as depression and antisocial behavior, difficult infant temperament, and parental aggression. The sample consisted of 204 families with 12-month-old infants (104 alcoholic and 100 control families), recruited from New York State birth records. Results indicated that fathers' alcoholism was associated with a number of other risk factors (depression, antisocial behavior, and family aggression). Fathers' alcoholism was also associated with more negative father-infant interactions as indicated by lower paternal sensitivity, positive affect, verbalizations, higher negative affect, and lower infant responsiveness among alcoholic fathers. As expected, fathers' depression mediated the relationship between fathers' alcoholism and sensitivity, while maternal depression mediated the association between maternal alcohol problems and maternal sensitivity. Parents' psychopathology did not moderate the association between alcoholism and parent-infant interactions. The results from the present study suggest that the origins of risk for later maladjustment among children of alcoholic fathers are apparent as early as infancy and highlight the role of comorbid parental risk factors.
Six and a half years after adoption. 6- to 12-year-old children reared in Romanian orphanages for more than 8 months in their first years of life (RO. n = 18) had higher cortisol levels over the daytime hours than did early adopted (EA, < or = 4 months of age, n = 15) and Canadian born (CB, n = 27) children. The effect was marked, with 22% of the RO children exhibiting cortisol levels averaged over the day that exceeded the mean plus 2 SD of the EA and CB levels. Furthermore, the longer beyond 8 months that the RO children remained institutionalized the higher their cortisol levels. Cortisol levels for EA children did not differ in any respect from those of CB comparison children. This latter finding reduces but does not eliminate concerns that the results could be due to prenatal effects or birth family characteristics associated with orphanage placement. Neither age at cortisol sampling nor low IQ measured earlier appeared to explain the findings. Because the conditions in Romanian orphanages at the time these children were adopted were characterized by multiple risk factors, including gross privation of basic needs and exposure to infectious agents, the factor(s) that produced the increase in cortisol production cannot be determined. Nor could we determine whether these results reflected effects on the limbic-hypothalamic-pituitary-adrenal axis directly or were mediated by differences in parent-child interactions or family stress occasion by behavioral problems associated with prolonged orphanage care in this sample.
Childhood abuse is an important public health problem; however, little is known about the effects of abuse on the brain and neurobiological development. This article reviews the behavioral and biological consequences of childhood abuse and places them in a developmental context. Animal studies show that both positive and negative events early in life can influence neurobiological development in unique ways. Early stressors such as maternal separation result in lasting effects on stress-responsive neurobiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic systems. These studies also implicate a brain area involved in learning and memory, the hippocampus. in the long-term consequences of early stress. Clinical studies of patients with a history of abuse also implicate dysfunction in the HPA axis and the noradrenergic and hippocampal systems; however, there are multiple questions related to chronicity of stress, developmental epoch at the time of the stressor, presence of stress-related psychiatric disorders including posttraumatic stress disorder and depression. and psychological factors mediating the response to trauma that need to be addressed in this field of research. Understanding the effects of abuse on the development of the brain and neurobiology will nevertheless have important treatment and policy implications.
Cortisol regulation was investigated in a sample of school-aged maltreated (n = 175) and demographically comparable low-income nonmaltreated (n = 209) children in the context of a day camp research program. Overall group differences between maltreated and nonmaltreated children were not found for average morning or average afternoon cortisol levels. However, significant variations were found that were based on the subtypes of maltreatment that the children had experienced. Maltreated children who had been both physically and sexually abused (as well as neglected or emotionally maltreated) exhibited substantial elevations in morning cortisol levels; children who had high (>1 SD) cortisol levels in both the morning and afternoon were also overrepresented in the multiple abuse group. Developmental timing of maltreatment did not account for these group differences, whereas the severity of sexual abuse was implicated. In contrast to the multiple abuse group, a subgroup of physically abused children showed evidence of a trend toward lower morning cortisol relative to nonmaltreated children with a significantly smaller decrease in cortisol levels from morning to afternoon. The findings are discussed in terms of the diversity of atypical cortisol regulation patterns that are exhibited among maltreated children.
To date, research involving functional neuroimaging of typical and atypical development has depended on several assumptions about the postnatal maturation of the brain. We consider evidence from multiple levels of analysis that brings into question these underlying assumptions and advance an alternative view. This alternative view, based on an "interactive specialization" approach to postnatal brain development, indicates that there is a need to: obtain data from early in development; focus more on differences in interregional interactions rather than searching for localized, discrete lesions; examine the temporal dynamics of neural processing; and move away from deficits to image tasks in which atypical participants perform as well as typically developing participants.
The genetic and environmental basis of a well-replicated association between antisocial behavior (ASB) and resting heart rate was investigated in a longitudinal twin study, based on two measurements between the ages of 9 and 14 years. ASB was defined as a broad continuum of externalizing behavior problems, assessed at each occasion through a composite measure based on parent ratings of trait aggression, delinquent behaviors, and psychopathic traits in their children. Parent ratings of ASB significantly decreased across age from childhood to early adolescence, although latent growth models indicated significant variation and twin similarity in the growth patterns, which were explained almost entirely by genetic influences. Resting heart rate at age 9-10 years old was inversely related to levels of ASB but not change patterns of ASB across age or occasions. Biometrical analyses indicated significant genetic influences on heart rate during childhood, as well as ASB throughout development from age 9 to 14. Both level and slope variation were significantly influenced by genetic factors. Of importance, the low resting heart rate and ASB association was significantly and entirely explained by their genetic covariation, although the heritable component of heart rate explained only a small portion (1-4%) of the substantial genetic variance in ASB. Although the effect size is small, children with low resting heart rate appear to be genetically predisposed toward externalizing behavior problems as early as age 9 years old.
The maternal experience of stressful events during pregnancy has been associated with a number of adverse consequences for behavioral development in offspring, but the measurement and interpretation of prenatal stress varies among reported studies. The Raine Study recruited 2900 pregnancies and recorded life stress events experienced by 18 and 34 weeks' gestation along with numerous sociodemographic data. The mother's exposure to life stress events was further documented when the children were followed-up in conjunction with behavioral assessments at ages 2, 5, 8, 10, and 14 years using the Child Behavior Checklist. The maternal experience of multiple stressful events during pregnancy was associated with subsequent behavioral problems for offspring. Independent (e.g., death of a relative, job loss) and dependent stress events (e.g., financial problems, marital problems) were both significantly associated with a greater incidence of mental health morbidity between age 2 and 14 years. Exposure to stressful events in the first 18 weeks of pregnancy showed similar associations with subsequent total and externalizing morbidity to events reported at 34 weeks of gestation. These results were independent of postnatal stress exposure. Improved support for women with chronic stress exposure during pregnancy may improve the mental health of their offspring in later life.
Previous work based on observations of home videotapes indicates that differences can be detected between infants with autism spectrum disorder and infants with typical development at 1 year of age. The present study addresses the question of whether autism can be distinguished from mental retardation by 1 year of age. Home videotapes of first birthday parties from 20 infants later diagnosed with autism spectrum disorder, 14 infants later diagnosed with mental retardation (without autism), and 20 typically developing infants were coded by blind raters with respect to the frequencies of specific social and communicative behaviors and repetitive motor actions. Results indicated that 1-year-olds with autism spectrum disorder can be distinguished from 1-year-olds with typical development and those with mental retardation. The infants with autism spectrum disorder looked at others and oriented to their names less frequently than infants with mental retardation. The infants with autism spectrum disorder and those with mental retardation used gestures and looked to objects held by others less frequently and engaged in repetitive motor actions more frequently than typically developing infants. These results indicate that autism can be distinguished from mental retardation and typical development by 1 year of age.
Moffitt's theory regarding two types of adolescent antisocial behavior was investigated using a prospective, longitudinal study of normal and abnormal development in a primarily low socioeconomic status, ethnically diverse sample. Results supported the presence of an early-onset/persistent (EOP) group and an adolescence-onset (AO) group. Groups were most reliably and significantly distinguished by indices of socioemotional history within the first 3 years, but no significant differences were found on early measures of temperament or neuropsychological functioning. EOPs scored significantly lower than other groups on measures of neuropsychological functioning only during late childhood and adolescence, suggesting that the declines in verbal functioning that have been so reliably found in this and other samples of early-starting antisocial adolescents are progressive and consequent to adverse experience. In adolescence, AOs were significantly more likely to report high levels of internalizing symptoms and life stress, suggesting that AO antisocial behavior is not a benign phenomenon. Implications of these findings for etiologic theories of adolescent antisocial behavior are discussed.
The purpose of the present study is to identify child and adult correlates that differentiate (a) individuals with persistent alcohol dependence from individuals with developmentally limited alcohol dependence and (b) individuals with adult-onset alcohol dependence from individuals who never diagnose. There are 1,037 members of the Dunedin Longitudinal Study, which is a birth cohort followed prospectively from birth until age 32. Past-year DSM-IV alcohol dependence diagnoses are ascertained with structured diagnostic interviews at ages 18, 21, 26, and 32. Individuals are classified as developmentally limited, persistent, or adult-onset subtypes based on their time-ordered pattern of diagnoses. The persistent subtype generally exhibits the worst scores on all correlates, including family psychiatric history, adolescent and adult externalizing and internalizing problems, adolescent and adult substance use, adult quality of life, and coping strategies. The prospective predictors that distinguished them from the developmentally limited subtype involved family liability, adolescent negative affectivity, daily alcohol use, and frequent marijuana use. Furthermore, young people who develop the persistent subtype of alcohol dependence are distinguished from the developmentally limited subtype by an inability to reduce drinking and by continued use despite problems by age 18. The adult-onset group members are virtually indistinguishable from ordinary cohort members as children or adolescents; however, in adulthood, adult-onset cases are distinguished by problems with depression, substance use, stress, and strategies for coping with stress. Information about age of onset and developmental course is fundamental for identifying subtypes of alcohol dependence. Subtype-specific etiologies point to targeted prevention and intervention efforts based on the characteristics of each subtype.
This study examined the relationship between paternal alcoholism and toddler behavior problems from 18 to 36 months of age, as well as the potential moderating effects of 12-month infant-mother attachment security on this relationship. Children with alcoholic fathers had higher levels of internalizing and externalizing behavior than children of nonalcoholic fathers. Simple effects testing of an interaction effect of child age, group, and attachment security with mothers on externalizing behaviour suggested that at 24 and 36 months of age mother-infant attachment security moderated the relationship between alcohol group status and externalizing behaviour. Namely, within the alcohol group, those children with secure relationships with their mothers had significantly lower externalizing than insecure children of alcoholics. A similar pattern was noted for internalizing behavior at 36 months of age. Implications for intervention are discussed.
This study examined the association between maternal cocaine use and children's emotional regulation. Using a brief separation procedure, we observed 78 18-month-old at-risk children and their mothers from three defined maternal groups: no drug use; no cocaine use but a positive history for alcohol, tobacco, and/or marijuana; and cocaine use with or without alcohol, tobacco, and/or marijuana. Coded videotaped behavior identified three maternal constructs (separation style, physical engagement, and emotional engagement) and three child constructs (negative reactivity to separation, initial regulatory activity, and follow-up positive emotional engagement). Cocaine-using mothers displayed less emotional engagement than other mothers. Children with cocaine-using mothers displayed less negative reactivity and follow-up positive emotional engagement than their counterparts. Child reactivity was connected to maternal drug use, whereas emotional engagement during reunion was linked to birthweight and maternal behavior. Results suggest a possible impairment or restriction of emotional expression and regulation in the face of stress and/or maternal disengagement that is more common among cocaine-exposed children with their mothers.
The degree to which infant regulatory behaviors, together with infant reactivity to novelty, predicted anxious behavior at 2.5 years, and the moderating effect of maternal behavior were tested. Sixty-four low-risk mothers and infants participated. Mothers rated infant negative reactivity and anxious behavior; infant and maternal behaviors were observed at 6 months postpartum. Based on results of hierarchical, multiple regressions, infant regulatory behaviors (i.e., attention control, withdrawal) moderated associations between reactivity to novelty and later anxious behavior, but predictions depended also on maternal behavior. High reactivity to novelty, in conjunction with withdrawal and with poor attention control, predicted anxious behavior only when mothers were less engaged or less sensitive, suggesting that maternal behavior alters developmental trajectories associated with infant temperament.
The clinical concept of psychopathy ("psychopathic personality") is generally considered to entail persistent behavioral deviancy in the company of emotional-interpersonal detachment. However, longstanding debates continue regarding the appropriate scope and boundaries of the concept. Here, we review alternative historic descriptions of the disorder together with empirical findings for the best-established assessment instruments in use with adolescents and youth as a basis for formulating an integrative, triarchic model of psychopathy. The essence of the triarchic model is that psychopathy encompasses three distinct phenotypic constructs: disinhibition, which reflects a general propensity toward problems of impulse control; boldness, which is defined as the nexus of social dominance, emotional resiliency, and venturesomeness; and meanness, which is defined as aggressive resource seeking without regard for others ("dysaffliated agency"). These differing phenotypic components are considered in terms of relevant etiologic and developmental pathways. The triarchic conceptualization provides a basis for reconciling and accommodating alternative descriptive accounts of psychopathy, and a framework for coordinating research on neurobiological and developmental processes contributing to varying manifestations of the disorder.
As the US population becomes more diverse in the 21st century, researchers face many conceptual and methodological challenges in working with diverse populations. We discuss these issues for racially and ethnically diverse youth, using Spencer's phenomenological variant of ecological systems theory (PVEST) as a guiding framework. We present a brief historical background and discuss recurring conceptual flaws in research on diverse youth, presenting PVEST as a corrective to these flaws. We highlight the interaction of race, culture, socioeconomic status, and various contexts of development with identity formation and other salient developmental processes. Challenges in research design and interpretation of data are also covered with regard to both assessment of contexts and developmental processes. We draw upon examples from neighborhood assessments, ethnic identity development, and attachment research to illustrate conceptual and methodological challenges, and we discuss strategies to address these challenges. The policy implications of our analysis are also considered.
Empirical investigations of resilience over the past 30 years have examined a wide range of psychosocial correlates of, and contributors to, this phenomenon. Thus far, theoretical treatments of resilience have focused almost exclusively on psychosocial levels of analysis to derive explanatory models. However, there have been no formal discussions of either theory or research that have examined the biological contributors to, or correlates of, competent functioning despite the experience of adversity. This paper seeks to fill this gap and sets forth a preliminary theoretical framework and outline of empirical strategies for studying the biological underpinnings of resilience. The initial sections of the paper discuss the particular suitability of a transactional organizational theoretical perspective as a conceptual foundation for including a biological level of analysis within the extant theoretical framework of resilience. Subsequently, other important theoretical considerations for the inclusion of a biological perspective on resilience are discussed, including the avoidance of an approach that would reduce resilience to merely a biological process, the application of the constructs of multifinality and equifinality to a biological perspective on resilience, as well as a general discussion of the potential for utilization of brain imaging and other technologies in the study of resilience. The possible relation between the mechanisms of neural plasticity and resilience are examined in some detail, with specific suggestions concerning research questions needed to examine this association. Sections of the paper discuss the likely relation of several areas of brain and biological functioning with resilience, including emotion, cognition, neuroendocrine and immune functioning, and genetics. The paper concludes with a discussion of the implications of a biological perspective on resilience for preventive interventions.
Largely because of the influence of Moffitt's useful distinction between adolescence-limited and life-course persistent antisocial behavior, it has become increasingly common to view problem behavior that makes its first appearance in adolescence as developmentally normative. This study prospectively examined the lives of individuals in the NICHD Study of Early Child Care and Youth Development whose patterns of antisocial behavior varied with respect to age of onset and stability from kindergarten through age 15. Consistent with past research, early-onset, persistently deviant youth experienced more contextual adversity and evinced higher levels of intraindividual disadvantages than their peers from infancy through midadolescence. However, relative to youth who never showed significantly elevated antisocial behavior through age 15, children who showed antisocial behavior primarily in adolescence also were more disadvantaged from infancy forward, as were youth who only demonstrated significant externalizing problems in childhood. Findings generally replicated across sex and did not vary as a function of whether antisocial behavior groups were defined using T-scores normed within sex or identified using an empirically driven grouping method applied to raw data.
We present a multilevel approach to developing potential explanations of cognitive impairments and psychopathologies common to individuals with chromosome 22q11.2 deletion syndrome. Results presented support our hypothesis of posterior parietal dysfunction as a central determinant of characteristic visuospatial and numerical cognitive impairments. Converging data suggest that brain development anomalies, primarily tissue reductions in the posterior brain and changes to the corpus callosum, may affect parietal connectivity. Further findings indicate that dysfunction in "frontal" attention systems may explain some executive cognition impairments observed in affected children, and that there may be links between these domains of cognitive function and some of the serious psychiatric conditions, such as attention-deficit/hyperactivity disorder, autism, and schizophrenia, that have elevated incidence rates in the syndrome. Linking the neural structure and the cognitive processing levels in this way enabled us to develop an elaborate structure/function mapping hypothesis for the impairments that are observed. We show also, that in the case of the catechol-O-methyltransferase gene, a fairly direct relationship between gene expression, cognitive function, and psychopathology exists in the affected population. Beyond that, we introduce the idea that variation in other genes may further explain the phenotypic variation in cognitive function and possibly the anomalies in brain development.
This article reports a comparison on outcomes of 26-year-old males who were defined several years ago in the Dunedin longitudinal study as exhibiting childhood-onset versus adolescent-onset antisocial behavior and who were indistinguishable on delinquent offending in adolescence. Previous studies of these groups in childhood and adolescence showed that childhood-onset delinquents had inadequate parenting, neurocognitive problems, undercontrolled temperament, severe hyperactivity, psychopathic personality traits, and violent behavior. Adolescent-onset delinquents were not distinguished by these features. Here followed to age 26 years, the childhood-onset delinquents were the most elevated on psychopathic personality traits, mental-health problems, substance dependence, numbers of children, financial problems, work problems, and drug-related and violent crime, including violence against women and children. The adolescent-onset delinquents at 26 years were less extreme but elevated on impulsive personality traits, mental-health problems, substance dependence, financial problems, and property offenses. A third group of men who had been aggressive as children but not very delinquent as adolescents emerged as low-level chronic offenders who were anxious, depressed, socially isolated, and had financial and work problems. These findings support the theory of life-course-persistent and adolescence-limited antisocial behavior but also extend it. Findings recommend intervention with all aggressive children and with all delinquent adolescents, to prevent a variety of maladjustments in adult life.
Efforts to understand the etiology of adult mental disorders by studying children has produced unanticipated changes in our understanding of pathology, individual development, and the role of social context. Among these are the blurring of the division between mental illness and mental health, the need to attend to patterns of adaptation rather than personality traits, and the powerful influences of the social world on individual development. Current developmental views place deviancy in the dynamic relation between individuals and their contexts. At another level, when we view the history of developmental psychopathology, dialectical developmental processes are evident as we trace how patterns of adaptation of researchers, expressed in theoretical models and empirical paradigms. increasingly have come to match the complexities of human mental health and illness.
Researchers have long been interested in whether particular temperamental traits in childhood connote risk for depressive disorders. For example, children characterized as having high negative emotionality (NE; sadness, fear, anger) and low positive emotionality (PE; anhedonia, listlessness, and lack of enthusiasm) are hypothesized to be at risk for depression. Few studies, however, have examined whether (and how) these two temperamental dimensions interact to confer risk. In a sample of 329 preschoolers, the present study addressed this question by examining the relation between PE and NE and asymmetry in resting EEG activity in frontal and posterior regions, which are putative biomarkers for depression. Using a laboratory battery to define temperament, we found an interaction of PE and NE on posterior asymmetry. Specifically, when PE was high, NE was associated with greater relative right activity. When PE was low, NE was not related to posterior asymmetry. These results were driven by differences in EEG activity in right posterior regions, an area associated with emotional processing and arousal, and were specific to girls. We found no relation between temperament and frontal asymmetry. These findings suggest that, at least for girls, PE and NE may have an interactive effect on risk for depression.
We examined the course of maternal depressive symptoms and children's attachment security at 36 months in a large sample of mother-child pairs from 10 sites across the country participating in the NICHD Study of Early Child Care (N = 1077). Maternal depressive symptoms predicted higher rates of insecure attachment. Women who reported intermittent symptoms across the first 36 months had preschoolers who were more likely to be classified as insecure C or D; women with chronic symptoms were more likely to have preschoolers who were classified as insecure D. Symptoms reported only during the first 15 months were not associated with elevated rates of later insecurity. After controlling for potentially confounding demographic variables, maternal sensitivity (observed at 6, 15, 24, and 36 months) did not meaningfully account for links between attachment security and patterns of depressive symptoms. However, the course and timing of maternal depressive symptoms interacted with maternal sensitivity to predict insecurity. Women with late, intermittent, or chronic symptoms who were also low in sensitivity were more likely to have preschoolers who were insecure, in contrast to symptomatic women who were high in sensitivity. These data have implications for understanding the combined impact of maternal depressive symptoms and maternal sensitivity on children's socioemotional development.
Nongenetic factors have a major influence on psychopathology. Knowledge on specific psychosocial risk and protective mechanisms is more limited because of inadequate attention to measurement issues, person effects on the environment, and the possibility of genetic mediation. Nevertheless, a range of research strategies may be used to provide rigorous tests of causal hypotheses; these have shown the importance of environmentally mediated risks. Challenges for the future include greater use of such research strategies, improved measures of psychosocial risks that can be applied to large samples, investigation of origins of risks, identification of causes of time trends in levels of psychopathology, delineation of psychosocial effects on lifetime liability, understanding of environmental effects on the organism, appreciation of processes involved in developmental programming, and understanding of individual differences in susceptibility.
This is a critical review of the literature related to the neurodevelopmental hypothesis of schizophrenia which posits that the illness is related to abnormal brain development. The review focuses on data deriving from clinical studies, and it is organized according to the life phase from which the data were collected: conception and birth, infancy and childhood up to the onset of the illness, after illness onset, and postmortem. The neurodevelopmental hypothesis is supported by several pieces of evidence, including increased frequency of obstetric complications in patients with schizophrenia: the presence of minor physical anomalies; the presence of neurological, cognitive, and behavioral dysfunction long before illness onset; a course and outcome of the illness itself that is incompatible in most cases with a degenerative illness; the stability of brain structural measures over time; and the absence of postmortem evidence of neurodegeneration. A historical perspective on how this research accumulated and a section addressing important areas of future investigation are also provided. We conclude that schizophrenia is certainly not a degenerative brain disorder, and that it is likely that a brain insult in utero or at birth plays a role in its expression. Current evidence cannot completely exclude the role of environmental variables after birth. In addition, it is possible that other psychiatric disorders may also have a neurodevelopmental component.
This article examines the role of adolescent social relationships in fostering the occurrence and co-occurrence of depression and substance abuse, using two waves of data from a community sample of adolescents (N = 900). Multinomial logistic response models were estimated to identify the extent to which risk and protective features of youths' family and peer relations were differentially linked with depressive symptoms, substance abuse, and their co-occurrence. Taking a within-person, configurational approach to adolescent adaptation, contrasts involved four subgroups of adolescents: those high on both depressed mood and substance abuse, those who experience neither problem, those evidencing high levels of depressive symptoms only, and those high on substance abuse only. Risk for depressive symptoms was differentiated by its association with conflict and lack of support in the friendship domain. Substance abuse was associated with negative peer pressure, but these youth were otherwise little different from youths with no problems. Whereas co-occurrence of depression and substance use was associated with more difficulties in both the family and peer environments, the most distinctive risk was that of low family support. Discussion centers on the developmental antecedents of co-occurring problems and family relations during adolescence.
Self-organization can be approached in terms of developmental processes occurring within and between component systems of temperament. Within-system organization involves progressive shaping of cortical representations by subcortical motivational systems. As cortical representations develop, they feed back to provide motivational systems with enhanced detection and guidance capabilities. These reciprocal influences may amplify the underlying motivational functions and promote excessive impulsivity or anxiety. However, these processes also depend upon interactions arising between motivational and attentional systems. We discuss these between-system effects by considering the regulation of approach motivation by reactive attentional processes related to fear and by more voluntary processes related to effortful control. It is suggested than anxious and impulsive psychopathology may reflect limitations in these dual means of control, which can take the form of overregulation as well as underregulation.
Preliminary work indicates that cognitive vulnerability to depression may be associated with variants of the serotonin transporter promoter polymorphism (5-HTTLPR) and the valine to methionine at position 66 (val66met) polymorphism of the brain-derived neurotrophic factor (BDNF) gene; however, existing reports come from small samples. The present study sought to replicate and extend this research in a sample of 375 community-dwelling children and their parents. Following a negative mood induction, children completed a self-referent encoding task tapping memory for positive and negative self-descriptive traits. Consistent with previous work, we found that children with at least one short variant of the 5-HTTLPR had enhanced memory for negative self-descriptive traits. The BDNF val66met polymorphism had no main effect but was moderated by maternal depression, such that children with a BDNF methionine allele had a heightened memory for negative self-descriptive traits when mothers had experienced depression during children's lifetimes; in contrast, children with a methionine allele had low recall of negative traits when mothers had no depression history. The findings provide further support for the notion that the 5-HTTLPR is associated with cognitive markers of depression vulnerability and that the BDNF methionine allele moderates children's sensitivity to contextual factors.
The "unresolved" state of mind with respect to loss or trauma as assessed in the Adult Attachment Interview is common in clinical and forensic groups, as well as in mothers whose infants are classified as disorganized in their attachment relationship to them. However, questions remain about what the unresolved state represents and what factors predict the unresolved state. This case controlled study reports on 64 women who had suffered stillbirth and who were pregnant with their next child. The study explores attachment, psychiatric, and social factors associated with the unresolved state or higher unresolved scores with respect to stillbirth. Women who had experienced stillbirth were more likely to be unresolved than control women. Although a similar number of stillbirth and control women had experienced childhood trauma, only women who had experienced stillbirth were unresolved with respect to this trauma, suggesting the unresolved state may be evoked or reevoked by subsequent traumatic loss. Higher unresolved scores in relation to stillbirth were predicted by childhood trauma, poor support from family after the loss, and having a funeral for the infant. The results are discussed in terms of the woman's sense of being causal in the loss.
This study examined the abilities of 40 Latina mothers and their 6- to 11-year-old children (20 girls, 20 boys) to recognize and produce emotion expressions and how these abilities differed as a function of maternal depressive symptoms. The results indicated that depressively symptomatic mothers were less accurate at recognizing basic emotions (e.g., happy, sad, etc.) and some mixed emotions (e.g., scared/ok combinations) than nonsymptomatic mothers, but there were no group differences for emotion production. In contrast, children of symptomatic mothers posed fewer recognizable sad expressions than their peers. Error pattern analyses also revealed that children of symptomatic mothers were more likely to mistakenly recognize happiness and to avoid posing sadness (across all basic emotions). Children's ability to pose emotions was related to their mothers' emotion production, and this was not moderated by maternal depressive symptoms. The discussion focuses on the possible interpersonal consequences of these biases and deficits in the emotion-related abilities of symptomatic mothers and their children and on the need to conduct research on the familial and cultural processes that might underlie these findings.
Williams syndrome is a rare genetic disorder in which, it is claimed, language abilities are relatively strong despite mild to moderate mental retardation. Such claims have, in turn, been interpreted as evidence either for modular preservation of language or for atypical constraints on cognitive development. However, this review demonstrates that there is, in fact, little evidence that syntax, morphology, phonology, or pragmatics are any better than predicted by nonverbal ability, although performance on receptive vocabulary tests is relatively good. Similarly, claims of an imbalance between good phonology and impaired or atypical lexical semantics are without strong support. There is, nevertheless, consistent evidence for specific deficits in spatial language that mirror difficulties in nonverbal spatial cognition, as well as some tentative evidence that early language acquisition proceeds atypically. Implications for modular and neuroconstructivist accounts of language development are discussed.
We present an analysis of the role of emotions in normal and abnormal development and preventive intervention. The conceptual framework stems from three tenets of differential emotions theory (DET). These principles concern the constructs of emotion utilization; intersystem connections among modular emotion systems, cognition, and action; and the organizational and motivational functions of discrete emotions. Particular emotions and patterns of emotions function differentially in different periods of development and in influencing the cognition and behavior associated with different forms of psychopathology. Established prevention programs have not emphasized the concept of emotion as motivation. It is even more critical that they have generally neglected the idea of modulating emotions, not simply to achieve self-regulation, but also to utilize their inherently adaptive functions as a means of facilitating the development of social competence and preventing psychopathology. The paper includes a brief description of a theory-based prevention program and suggestions for complementary targeted interventions to address specific externalizing and internalizing problems. In the final section, we describe ways in which emotion-centered preventions can provide excellent opportunities for research on the development of normal and abnormal behavior.
An understanding of developmental phenomena demands a relational or coactive concept of causality, as opposed to a conceptualization that assumes that singular causes can act in isolation. In this article we present a developmental psychobiological systems view of relational (bidirectional, coactional) causality, in which it is proposed that developmental outcomes are a consequence of at least two specific components of coaction from the same or different levels of a developmental system. The levels are genetic, neural, behavioral, and environmental; the latter level includes the cultural, social, and physical aspects of an organism's environment. We show the applicability of this view to the understanding of the development of normal and abnormal behavioral and psychological phenotypes through illustrations from the existing animal and human literature. Finally, we discuss future possibilities and potential stumbling blocks in the implementation of a more fully realized bidirectional, coactional perspective in developmental psychopathological research.
Neuroimaging and behavioral studies have shown that children and adults with autism have impaired face recognition. Individuals with autism also exhibit atypical event-related brain potentials to faces, characterized by a failure to show a negative component (N170) latency advantage to face compared to nonface stimuli and a bilateral, rather than right lateralized, pattern of N170 distribution. In this report, performance by 143 parents of children with autism on standardized verbal, visual-spatial, and face recognition tasks was examined. It was found that parents of children with autism exhibited a significant decrement in face recognition ability relative to their verbal and visual spatial abilities. Event-related brain potentials to face and nonface stimuli were examined in 21 parents of children with autism and 21 control adults. Parents of children with autism showed an atypical event-related potential response to faces, which mirrored the pattern shown by children and adults with autism. These results raise the possibility that face processing might be a functional trait marker of genetic susceptibility to autism. Discussion focuses on hypotheses regarding the neurodevelopmental and genetic basis of altered face processing in autism. A general model of the normal emergence of social brain circuitry in the first year of life is proposed, followed by a discussion of how the trajectory of normal development of social brain circuitry, including cortical specialization for face processing, is altered in individuals with autism. The hypothesis that genetic-mediated dysfunction of the dopamine reward system, especially its functioning in social contexts, might account for altered face processing in individuals with autism and their relatives is discussed.
In this paper I review evidence and viewpoints on developmental plasticity in the cerebral cortex. Although there is some degree of plasticity in the cortex during early postnatal life in the human infant, this plasticity is constrained by various factors. Three working hypotheses about postnatal cortical specialization of function are advanced, and some specific predictions about the limits and extent of plasticity are assessed through both empirical evidence from infants and simulations on simple cortical network models.
Growing epidemiological, genetic, and clinical neurobiological evidence indicates that abnormalities in brain development play determining roles in the pathobiology of schizophrenia. Neuropathological research has made significant progress in delineating cellular and molecular abnormalities in schizophrenia that have relevance to neurodevelopment. This paper reviews the neurodevelopmental processes of neurogenesis, neuronal migration, differentiation, synaptogenesis, neuron and synaptic pruning, and myelination and the reported neuropathological findings in schizophrenia that may be a consequence of disturbances in these processes. While many neuropathological findings in schizophrenia are controversial or await confirmation, reported abnormalities in neuron density, number and morphology, cytoarchitecture, dendritic arbors and spines, synapse-related proteins, and the well-established absence of gliosis or any other evidence of neurodegeneration or neural injury all provide support for the neurodevelopmental model of schizophrenia.
Autistic symptoms begin in the first years of life, and recent magnetic resonance imaging studies have discovered brain growth abnormalities that precede and overlap with the onset of these symptoms. Recent postmortem studies of the autistic brain provide evidence of cellular abnormalities and processes that may underlie the recently discovered early brain overgrowth and arrest of growth that marks the first years of life in autism. Alternative origins and time tables for these cellular defects and processes are discussed. These cellular and growth abnormalities are most pronounced in frontal, cerebellar, and temporal structures that normally mediate the development of those same higher order social, emotional, speech, language, speech, attention, and cognitive functions that characterize autism. Cellular and growth pathologies are milder and perhaps nonexistent in other structures (e.g., occipital cortex), which are known to mediate functions that are often either mildly affected or entirely unaffected in autistic patients. It is argued that in autism, higher order functions largely fail to develop normally in the first place because frontal, cerebellar, and temporal cellular and growth pathologies occur prior to and during the critical period when these higher order neural systems first begin to form their circuitry. It is hypothesized that microstructural maldevelopment results in local and short distance overconnectivity in frontal cortex that is largely ineffective and in a failure of long-distance cortical-cortical coupling, and thus a reduction in frontal-posterior reciprocal connectivity. This altered circuitry impairs the essential role of frontal cortex in integrating information from diverse functional systems (emotional, sensory, autonomic, memory, etc.) and providing context-based and goal-directed feedback to lower level systems.
Recently, a series of studies demonstrated false belief understanding in young children through completely nonverbal measures. These studies have revealed that children younger than 3 years of age, who consistently fail the standard verbal false belief test, can anticipate others' actions based on their attributed false beliefs. The current study examined whether children with autism spectrum disorder (ASD), who are known to have difficulties in the verbal false belief test, may also show such action anticipation in a nonverbal false belief test. We presented video stimuli of an actor watching an object being hidden in a box. The object was then displaced while the actor was looking away. We recorded children's eye movements and coded whether they spontaneously anticipated the actor's subsequent behavior, which could only have been predicted if they had attributed a false belief to her. Although typically developing children correctly anticipated the action, children with ASD failed to show such action anticipation. The results suggest that children with ASD have an impairment in false belief attribution, which is independent of their verbal ability.
The present study, utilizing both a child protective services and high school sample of midadolescents, examined the issue of self-report of maltreatment as it relates to issues of external validity (i.e., concordance with social worker ratings). reliability (i.e.. overlap with an alternate child maltreatment self-report inventory; association of a self-labeling item as "abused" with their subscale item counterparts), and construct validity (i.e., the association of maltreatment with posttraumatic stress symptomatology and dating violence). Relevant theoretical work in attachment, trauma, and relationship violence points to a mediational model, whereby the relationship between childhood maltreatment and adolescent dating violence would be expected to be accounted for by posttraumatic stress symptomatology. In the high school sample, 1329 adolescents and, in the CPS sample, 224 youth on the active caseloads completed comparable questionnaires in the three domains of interest. For females only, results supported a mediational model in the prediction of dating violence in both samples. For males, child maltreatment and trauma symptomatology added unique contributions to predicting dating violence. with no consistent pattern emerging across samples. When considering the issue of self-labeling as abused. CPS females who self-labeled had higher posttraumatic stress symptomatology and dating violence victimization scores than did their nonlabeling, maltreated counterparts for emotional maltreatment. These results point to the need for ongoing work in understanding the process of disclosure and how maltreatment experiences are consciously conceptualized.
This is a report on the research design and findings of a 23-year longitudinal study of the impact of intrafamilial sexual abuse on female development. The conceptual framework integrated concepts of psychological adjustment with theory regarding how psychobiological factors might impact development. Participants included 6- to 16-year-old females with substantiated sexual abuse and a demographically similar comparison group. A cross-sequential design was used and six assessments have taken place, with participants at median age 11 at the first assessment and median age 25 at the sixth assessment. Mothers of participants took part in the early assessments and offspring took part at the sixth assessment. Results of many analyses, both within circumscribed developmental stages and across development, indicated that sexually abused females (on average) showed deleterious sequelae across a host of biopsychosocial domains including: earlier onsets of puberty, cognitive deficits, depression, dissociative symptoms, maladaptive sexual development, hypothalamic-pituitary-adrenal attenuation, asymmetrical stress responses, high rates of obesity, more major illnesses and healthcare utilization, dropping out of high school, persistent posttraumatic stress disorder, self-mutilation, Diagnostic and Statistical Manual of Mental Disorders diagnoses, physical and sexual revictimization, premature deliveries, teen motherhood, drug and alcohol abuse, and domestic violence. Offspring born to abused mothers were at increased risk for child maltreatment and overall maldevelopment. There was also a pattern of considerable within group variability. Based on this complex network of findings, implications for optimal treatments are elucidated. Translational aspects of extending observational research into clinical practice are discussed in terms that will likely have a sustained impact on several major public health initiatives.
Borderline personality disorder (BPD) is a paradigmatic disorder of adult attachment, with high rates of antecedent childhood maltreatment. The neurocognitive correlates of both attachment disturbance and maltreatment are both presently unknown in BPD. This study evaluated whether dimensional adult attachment disturbance in BPD is related to specific neurocognitive deficits, and whether childhood maltreatment is related to these dysfunctions. An outpatient BPD group (n=43) performed nearly 1 SD below a control group (n=26) on short-term recall, executive, and intelligence functions. These deficits were not affected by emotionally charged stimuli. In the BPD group, impaired recall was related to attachment-anxiety, whereas executive dysfunction was related to attachment-avoidance. Abuse history was correlated significantly with executive dysfunction and at a trend level with impaired recall. Neurocognitive deficits and abuse history exhibited both independent and interactive effects on adult attachment disturbance. These results suggest that (a) BPD patients' reactivity in attachment relationships is related to temporal-limbic dysfunction, irrespective of the emotional content of stimuli, (b) BPD patients' avoidance within attachment relationships may be a relational strategy to compensate for the emotional consequences of frontal-executive dysregulation, and (c) childhood abuse may contribute to these neurocognitive deficits but may also exert effects on adult attachment disturbance that is both independent and interacting with neurocognitive dysfunction.
We used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene-environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.
In this study we investigated the development of the hypothalamic-pituitary-adrenal (HPA) axis in 21 group-living rhesus monkeys infants that were physically abused by their mothers in the first few months of life and in 21 nonabused controls. Cortisol and adrenocorticotropin hormone (ACTH) responses to a corticotropin-releasing hormone (CRH) challenge were assessed at 6-month intervals during the subjects' first 3 years of life. Abused infants exhibited greater cortisol responses to CRH than controls across the 3 years. Abused infants also exhibited blunted ACTH secretion in response to CRH, especially at 6 months of age. Although there were no significant sex differences in abuse experienced early in life, females showed a greater cortisol response to CRH than males at all ages. There were no significant sex differences in the ACTH response to CRH, or significant interactions between sex and abuse in the ACTH or cortisol response. Our findings suggest that early parental maltreatment results in greater adrenocortical, and possibly also pituitary, responsiveness to challenges later in life. These long-term alterations in neuroendocrine function may be one the mechanisms through which infant abuse results in later psychopathologies. Our study also suggests that there are developmental sex differences in adrenal function that occur irrespective of early stressful experience. The results of this study can enhance our understanding of the long-term effects of child maltreatment as well as our knowledge of the development of the HPA axis in human and nonhuman primates.
The purpose of the present research was to examine Deese-Roediger-McDermott false memory for trauma-related and nontrauma-related lists in adolescents and adults with and without documented histories of child sexual abuse (CSA). Individual differences in psychopathology and adult attachment were also explored. Participants were administered free recall and recognition tests after hearing CSA, negative, neutral, and positive Deese-Roediger-McDermott lists. In free recall, CSA and negative lists produced the most false memory. In sharp contrast, for recognition, CSA lists enjoyed the highest d' scores. CSA-group adolescents who evinced greater posttraumatic stress disorder (PTSD) symptoms had higher rates of false memory compared to (a) non-CSA group adolescents with higher PTSD symptom scores (free recall), and (b) CSA-group adolescents with lower PTSD symptom scores (recognition). Regression analyses revealed that individuals with higher PTSD scores and greater fearful-avoidant attachment tendencies showed less proficient memory monitoring for CSA lists. Implications for trauma and memory development and for translational research are discussed.
The authors tested whether emerging borderline personality disorder (BPD) symptoms mediated the association between childhood physical abuse (CPA) and aggression among incarcerated girls. Participants were 121 incarcerated adolescent girls (13-19 years old). Three forms of aggression (relational, overt, and violent offending behavior) and exposure to CPA by a parental figure were assessed using self-report inventories, whereas BPD symptoms were evaluated using a structured interview. Mediation models, including tests of indirect effects, were conducted in which each form of aggression was predicted from CPA with BPD symptoms entered as a mediator. A divergent pattern emerged in which BPD symptoms mediated the relationship between CPA and violent offending, but not less severe forms of overt aggression. Relational aggression, although correlated with CPA, was not associated with BPD symptoms. Implications for the conceptualization and treatment of girls' aggression within the context of interpersonal functioning are discussed.