Bowlby's attachment theory is a theory of psychopathology as well as a theory of normal development. It contains clear and specific propositions regarding the role of early experience in developmental psychopathology, the importance of ongoing context, and the nature of the developmental process underlying pathology. In particular, Bowlby argued that adaptation is always the joint product of developmental history and current circumstances (never either alone). Early experience does not cause later pathology in a linear way; yet, it has special significance due to the complex, systemic, transactional nature of development. Prior history is part of current context, playing a role in selection, engagement, and interpretation of subsequent experience and in the use of available environmental supports. Finally, except in very extreme cases, early anxious attachment is not viewed as psychopathology itself or as a direct cause of psychopathology but as an initiator of pathways probabilistically associated with later pathology.

Dramatic gains in knowledge have been made in the fields of neuroscience, human development, and developmental psychopathology during the past quarter of a century. Despite the advances that have been achieved in each discipline separately, considerably less progress has occurred in understanding the relation between neurobiological and behavioral development in normal and atypical populations. Research has increasingly demonstrated that abnormalities that occur early in development may result in the emergence of aberrant neural circuitry that eventuates in relatively enduring forms of psychopathology. Knowledge of normal neurobiological development provides a powerful foundation for understanding the contributions that neurodevelopmental processes make to the etiology and sequelae of psychopathology across the life course. An integrated perspective wherein an appreciation of the complex neural, psychological, and social-contextual processes that cohere to bring about normal and pathological outcomes is necessary in order to advance understanding of the genesis and epigenesis of mental disorders. Such an approach will require a reduction of the schisms that so often separate neurobiological and behavioral research.

Elevated corticosterone levels to stress have been found in adult rats exposed prenatally to alcohol, but little is known about the effects of prenatal alcohol exposure on the cortisol response in humans. To date, one study has found that crack/cocaine was related to depressed newborn cortisol levels following a heel prick. In the present study saliva samples were obtained before and after a blood draw from 83 inner-city African American 13-month-old infants exposed prenatally to alcohol, cocaine, and other illicit drugs. Post-blood draw cortisol levels did not differ from basal levels in many of the infants, confirming recent studies indicating adaptation of the adrenocortical response to this type of stress at this age. Maternal depression and emergence of teeth were positively related to cortisol levels. Alcohol exposure was related to elevated basal levels, cocaine to lower basal levels. As predicted from animal findings, heavy alcohol exposure was related to elevated poststress cortisol levels.

In 1996 the Institute of Medicine (IOM, 1996) issued a report on pathways to addiction. Although focused on the use of illegal drugs, the recommendations of the committee are equally applicable to more socially condoned, but still addictive, substances such as alcohol. The IOM (1996) report articulated the types of research that would be needed to expand the understanding of the etiology of drug use disorders, including the following: (a) multidisciplinary research to investigate the combined effects of biological, psychosocial, and contextual factors as they relate to the development of drug use, abuse, and dependence; (b) studies of sufficient duration to enable follow-up of participants in determining the role of risk and protective factors related to the transition from drug use to abuse to dependence; (c) research investigating the role of family factors in the etiology of drug use and abuse; (d) examination of psychopathology as a precursor to drug use and abuse in adolescents and adults; (e) studies of risk and protective factors related to drug use and abuse, especially during discrete developmental stages; and (f) investigation of childhood risk and protective factors that are associated with drug abuse and dependence. In reflecting on these comprehensive goals, striking similarities emerge with respect to these research foci and the field of developmental psychopathology (Cicchetti & Cohen, 1995; Cicchetti & Toth, 1991). Specifically, the principles that guide inquiries conceptualized within a developmental psychopathology framework can be applied toward the conduct of studies designed to address the agenda generated by the IOM (1996) report on substance abuse.

The basic principles of the development of the central nervous system (CNS) are reviewed, and their implications for both normal and abnormal development of the brain are discussed. The goals of this review are (a) to provide a set of concepts to aid in understanding the variety of complex processes that occur during CNS development, (b) to illustrate how these concepts contribute to our knowledge of the normal anatomy of the adult brain, and (c) to provide a basis for understanding how modifications of normal developmental processes by traumatic injury, by environmental or experiential influences, or by genetic variations may lead to modifications in the resultant structure and function of the adult CNS.

The etiology of early age onset substance use disorder (SUD), an Axis I psychiatric illness, is examined from the perspective of the multifactorial model of complex disorders. Beginning at conception, genetic and environment interactions produce a sequence of biobehavioral phenotypes during development which bias the ontogenetic pathway toward SUD. One pathway to SUD is theorized to emanate from a deviation in somatic and neurological maturation, which, in the context of adverse environments, predisposes to affective and behavioral dysregulation as the cardinal SUD liability-contributing phenotype. Dysregulation progresses via epigenesis from difficult temperament in infancy to conduct problems in childhood to substance use by early adolescence and to severe SUD by young adulthood.

A group of 164 children from different infant temperament categories were seen at 7 years of age for a laboratory battery that included behavioral and physiological measurements. The major results indicated that children who had been classified as high reactive infants at 4 months of age, compared with infants classified as low reactive, (a) were more vulnerable to the development of anxious symptoms at age 7 years, (b) were more subdued in their interactions with a female examiner, (c) made fewer errors on a task requiring inhibition of a reflex, and (d) were more reflective. Further, the high reactives who developed anxious symptoms differed from the high reactives without anxious symptoms with respect to fearful behavior in the second year and, at age 7 years, higher diastolic blood pressure, a narrower facial skeleton, and greater magnitude of cooling of the temperature of the fingertips to cognitive challenge. Finally, variation in magnitude of interference to fearful or aggressive pictures on a modified Stroop procedure failed to differentiate anxious from nonanxious or high from low reactive children.

A model of the effects of children's temperament (negative and positive emotionality, impulsivity and attention focusing) on post-divorce threat appraisals, coping (active and avoidant), and psychological symptoms (depression and conduct problems) was investigated. The study utilized a sample of 223 mothers and children (ages 9 to 12 years) who had experienced divorce within the last two years. Evidence was found of direct effects of child-report negative emotionality on children's threat perceptions and of child-report positive emotionality and impulsivity on children's coping. Indirect effects of negative emotionality on active and avoidant coping through threat appraisal were found. Direct effects of the temperament variables on symptoms were also found. Cross group analyses indicated that the models were robust to age differences, but gender differences were found in the relation between negative emotionality and depression. The results of this study indicate that temperament and threat appraisals are important predictors of children's post-divorce symptoms, and that temperament is a predictor of children's appraisal and coping process.

The hypothesis was tested that weak theory of mind (ToM) and/or emotion recognition (ER) abilities are specific to subjects with autism. Differences in ToM and ER performance were examined between autistic (n = 20), pervasive developmental disorder—not otherwise specified (PDD-NOS) (n = 20), psychiatric control (n = 20), and normal children (n = 20). The clinical groups were matched person-to-person on age and verbal IQ. We used tasks for the matching and the context recognition of emotional expressions, and a set of first- and second-order ToM tasks. Autistic and PDD-NOS children could not be significantly differentiated from each other, nor could they be differentiated from the psychiatric controls with a diagnosis of ADHD (n = 9). The psychiatric controls with conduct disorder or dysthymia performed about as well as normal children. The variance in second-order ToM performance contributed most to differences between diagnostic groups.

During the past 10 years nearly 80 studies on disorganized attachment involving more than 6,000 infant–parent dyads have been carried out. The current series of meta-analyses have established the reliability and discriminant validity of disorganized infant attachment. Although disorganized attachment behavior is necessarily difficult to observe and often subtle, many researchers have managed to become reliable coders. Furthermore, disorganized attachment shows modest short- and long-term stability, in particular in middle class environments, and it is not just a concomitant of constitutional, temperamental, or physical child problems. The predictive validity of disorganized attachment is established in terms of problematic stress management, the elevated risk of externalizing problem behavior, and even the tendency of disorganized infants to show dissociative behavior later in life. In normal, middle class families, about 15% of the infants develop disorganized attachment behavior. In other social contexts and in clinical groups this percentage may become twice or even three times higher (e.g., in the case of maltreatment). Although the importance of disorganized attachment for developmental psychopathology is evident, the search for the mechanisms leading to disorganization has just started. Frightening parental behavior may play an important role but it does not seem to be the only causal factor involved in the emergence of disorganized attachment.

Within the last decade, many investigators have focused on the physical, neurodevelopmental, and neuropsychological effects of prenatal cocaine exposure on infants and young children. Although inconclusive on many crucial issues, published studies reveal the beginnings of a profile of possible cocaine-related effects on neuropsychological functions subserving arousal and attention regulation. That profile is informed by preclinical studies in which important factors such as duration and type of exposure as well as environmental conditions may be more adequately controlled. In the developing brain, there are a number of candidate mechanisms that account for how prenatal cocaine exposure may interfere with neural ontogeny. This review focuses on the monoamine system, one of the primary sites of action of cocaine in the adult. In the developing organism, monoamines play critical trophic roles through all phases of central nervous system (CNS) ontogeny—cell proliferation, neural migration, growth, maturation, and synaptogenesis. Because of their trophic role in CNS ontogeny, cocaine effects on developing nervous system may be mediated in part through effects on monoamine system ontogeny. In turn, these effects may be expressed behaviorally in disrupted patterns of arousal and attention regulation given that these domains are connected intimately to monoaminergic systems.

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.

The prediction of young-adult adjustment from early adolescent conduct problems and depressive symptoms was examined for an at-risk sample of approximately 200 males. Conduct problems and depressive symptoms were expected to show stability to young adulthood. It was predicted that early adolescent conduct problems would be associated with a broad range of adjustment problems in young adulthood due to cumulative adjustment failures. Early adolescent depressive symptoms were expected particularly to predict poor relationships with parents and peers. Additive and interactive effects of the two predictors were examined. Conduct problems and depressive symptoms showed significant stability to young adulthood. Conduct problems were associated with a broad range of adjustment problems including continuing problems in peer associations, substance use, self-esteem, relationships with parents, and new problems in noncompletion of education, unemployment, driver's license suspensions, and causing pregnancies. Depressive symptoms predicted particularly to problems in social relationships. Higher levels of both conduct problems and depressive symptoms in early adolescence did not predict to increased difficulties for any one outcome over either problem alone, either due to main or interaction effects. Such co-occurrence, however, did result in problem outcomes in multiple areas, thus, the poorest adjustment overall.

The purpose of this study was to use the Attachment Q-Set to create categories of attachment organization that were conceptually consistent with organizational categories derived from other attachment assessments, reliable, and valid. We were particularly interested in creating categories that would describe insecure attachment organizations in children from difficult life circumstances. Our sample of relationships included 3062 teacher–child relationships. Children ranged in age from toddlers to kindergartners and were diverse in ethnic background. Two percent of the children were diagnosed with severe social and emotional problems and enrolled in a therapeutic preschool. Sixteen percent were enrolled in intervention programs on the basis of family poverty and another 34% of the children attended subsidized child care programs for low-income children. All of the children's child–teacher relationships were assessed with the Attachment Q-Set (AQS). Independent observers observed or rated children's peer play. Teachers completed behavior problem questionnaires and Student Teacher Relationships Scales. Using the AQS we created five subscales and six attachment organizational categories. These subscales and organizational categories were associated in theoretically meaningful ways with measures of behavior problems, social competence with peers, and teacher perceptions of child–teacher relationship.

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.

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.

Our findings in the Helsinki Influenza Study and the Danish Forty Year Study lead us to conclude that a 2nd-trimester maternal influenza infection may increase risk for adult schizophrenia or adult major affective disorder. More recently we have also reported an increase of unipolar depression among offspring who were exposed prenatally to a severe earthquake (7.8 on the Richter scale) in Tangshan, China. Among the earthquake-exposed males (but not the females), we observed a significantly greater depression response for those individuals exposed during the 2nd trimester of gestation. These findings suggest that maternal influenza infection and severe maternal stress may operate (in different ways) as teratogens, disrupting the development of the fetal brain and increasing risk for developing schizophrenia or depression in adulthood.

We examined how family and child risk factors jointly affected stability and change in externalizing behavior over time in a prospective study of eventual alcohol use disorder. Study participants were community-recruited alcoholic and control families, and their initially preschool-aged male and female children (N = 335). Family risk varied as a function of both parental alcoholism (ALC) and antisocial personality disorder (ASPD) and was evaluated for both parents. Child risk was characterized by a set of risky temperament attributes pertaining to high activity, high reactivity, and low attention span. Externalizing behavior was used as the proxy indicator for later alcohol problems. For children in the high family risk group (involving current ALC in both parents or current ALC + ASPD comorbidity or both), child risk when children were 3–5 years old (Wave 1) directly predicted externalizing behavior when children were 6–8 years old (Wave 2), even when Wave 1 child risk was controlled for. In addition, parents' negative interaction with children at Wave 1 mediated the effect of child risky temperament on Wave 2 externalizing behavior. No such pattern was observed in the low family risk group, where only autostability effects were predictive of outcomes at Wave 2. The importance of nesting structure as an ingredient in the epigenesis of risk was discussed. Its particular relevance in understanding the process of risk transmission among offspring from antisocial alcoholic families was emphasized.

Few studies have examined the association between attachment and psychopathology in samples of clinically diagnosed children or the relation between attachment variables and the continuity of clinical symptoms. Clinic-referred preschool boys (n = 80) with early onset conduct problems (as indicated by diagnoses of Oppositional Defiant Disorder) were compared with a case-matched group of 80 nonproblem boys to determine whether observed attachment behaviors could: (a) differentiate the groups, (b) explain concurrent variation in problem severity within the clinic group, and (c) predict the outcomes of clinic boys 1 and 2 years later. Over half of the clinic boys with early onset conduct problems (54%) exhibited an insecure attachment strategy during reunion, as opposed to 18% of comparison group boys. All insecure patterns were overrepresented in the clinic group. Clinic boys were more likely than comparison boys to engage in provocative behavior when separated from their mothers. Contrary to our hypothesis, attachment variables showed little ability to explain concurrent or future variation in the problem severity or diagnostic status of clinic boys. We conclude that observable attachment behaviors exhibited during the preschool years are related to the initial identification of early onset conduct problems but may have little value by themselves in predicting the subsequent course and severity of problems in the 2 years following clinic referral.

The role of peer relations in childhood and behavioral and family characteristics in early adolescence as risk factors for adolescent childbearing was investigated. Sociometric surveys across third, fourth, and fifth grade and parent and child measures of behavioral and family functioning at sixth and eighth grade were collected in a lower income, urban sample of 308 African American females. Results replicated earlier findings on the role of childhood aggression as a predictor of teen motherhood. In addition, girls who displayed stable patterns of childhood aggression were at significantly higher risk not only to have children as teenagers but to have more children and to have children at younger ages. Results also indicated that females who were depressed in midadolescence were at greater risk to become parents between age 15 and 19 years. These findings demonstrate the need to take a differentiated approach to understanding teen childbearing and varying developmental pathways in the prediction of teen motherhood.