The interdisciplinary science of developmental psychopathology has evolved from its historical roots in a variety of fields including: sociology; epidemiology; embryology; the neurosciences and psychobiology; psychoanalysis; clinical, developmental, and experimental psychology; and psychiatry (Cicchetti, 1990) into an increasingly mature integrative framework within which the contributions of these heretofore largely separate disciplines could be fully realized within the broader context of understanding individual development and functioning, both normal and abnormal (see chapters in Cicchetti & Cohen, 1995a, 1995b; see also Cicchetti & Toth, in press). In one of the early statements concerning the goals of this field, Cicchetti (1990) asserted that: “Developmental psychopathology ... should bridge fields of study, span the life cycle, and aid in the discovery of important new truths about the processes underlying adaptation and maladaptation, as well as the best means of preventing or ameliorating psychopathology. Moreover, this discipline should contribute greatly to reducing the dualisms that exist between the clinical study of and research into childhood and adult disorders, between the behavioral and biological sciences, between developmental psychology and psychopathology, and between basic and applied science” (p. 20).

Developmental psychopathology stands poised at the close of the 20th century on the horns of a major scientific dilemma. The essence of this dilemma lies in the contrast between its heuristically rich open system concepts on the one hand, and the closed system paradigm it adopted from mainstream psychology for investigating those models on the other. Many of the research methods, assessment strategies, and data analytic models of psychology's paradigm are predicated on closed system assumptions and explanatory models. Thus, they are fundamentally inadequate for studying humans, who are unparalleled among open systems in their wide ranging capacities for equifinal and multifinal functioning. Developmental psychopathology faces two challenges in successfully negotiating the developmentalist's dilemma. The first lies in recognizing how the current paradigm encourages research practices that are antithetical to developmental principles, yet continue to flourish. I argue that the developmentalist's dilemma is sustained by long standing, mutually enabling weaknesses in the paradigm's discovery methods and scientific standards. These interdependent weaknesses function like a distorted lens on the research process by variously sustaining the illusion of theoretical progress, obscuring the need for fundamental reforms, and both constraining and misguiding reform efforts. An understanding of how these influences arise and take their toll provides a foundation and rationale for engaging the second challenge. The essence of this challenge will be finding ways to resolve the developmentalist's dilemma outside the constraints of the existing paradigm by developing indigenous research strategies, methods, and standards with fidelity to the complexity of developmental phenomena.

The authors review the constraints of current mental disorder classification systems that rely upon descriptive symptom-based approaches, and weigh the benefits and hazards of these classification and diagnostic strategies. By focusing principally on superficial descriptions of symptoms, current systems fail to address the complex nature of persons' transactions within and adaptations to difficult environments. While attempting to be atheoretical, current systems exclude types of information that may elucidate individuals' functioning across various contexts, often because it is difficult to obtain such data reliably. With current approaches, misdiagnosis is likely, particularly when diagnostic criteria are applied to persons in nonclinical settings. Alternative approaches that take fuller advantage of clinicians' expertise and other forms of clinical data are reviewed, and recommendations are made for the next generation of classification systems. Application of evolutionary theory to psychiatry and psychology, as well as development of a theory and nosology of context in terms of persons' adaptations, are needed to expand our knowledge of normal and abnormal human development and psychopathology.

When maladaptation is viewed as development rather than as disease, a transformed understanding results and a fundamentally different research agenda emerges. Within a developmental perspective, maladaptation is viewed as evolving through the successive adaptations of persons in their environments. It is not something a person “has” or an ineluctable expression of an endogenous pathogen. It is the complex result of a myriad of risk and protective factors operating over time. Key research questions within this framework center on discovery of factors that place individuals on pathways probabilistically leading to later disturbances and factors and processes which maintain individuals on, or deflect them from, such pathways once enjoined. There is an interest in recognizing patterns of maladaptation which, while not properly considered disorder themselves, commonly are precursors of disorder and also in conditions of risk that lie outside of the individual, as well as any endogenous influences. Likewise, there is a focus on factors and processes that lead individuals away from disorder that has emerged, which goes beyond interest in management of symptoms. Finally, many topics that currently are capturing attention in the field, such as “comorbidity” and “resilience,” are seen in new ways from within the perspective of development.

One goal of developmental psychopathology is to understand the origins and course of mental disorders. I argue that pursuit of this goal requires a valid conceptual understanding of disorder and that this understanding can be provided by the “harmful dysfunction” analysis of the concept of disorder. The harmful dysfunction analysis holds that a disorder is a condition that is both harmful according to social values and caused by an internal dysfunction, that is, by a failure of an internal mechanism to perform a function for which it was naturally selected. This analysis explains why many of the distinctive features of developmental psychopathology are appropriate to the study of disorder. It is argued that the harmful dysfunction analysis is a necessary supplement to other proposed criteria for disorder, such as developmental deviation or predictive validity.

There is a growing acceptance of a holistic, interactionistic view in which the individual is seen as an organized whole, functioning and developing as a totality. This view emphasizes the importance of patterns of operating factors. Within this framework, a standard variable-oriented approach, focusing on the variable as the main theoretical and analytical unit, has limitations. A person-oriented approach would often be preferable, where the main theoretical and analytical unit is the specific pattern of operating factors. Such an approach is presented here, focusing on individual development and psychopathology. A brief theoretical and methodological overview is given and a classification approach is emphasized. Empirical examples concerning the longitudinal study of adjustment problems illustrate a number of issues believed to be important to development and psychopathology: problem gravitation, the significance of single variables and of patterns, the developmental study of syndromes (=typical patterns), and the detection of “white spots” in development.

This paper examines critically four habits of social scientists: a reliance on constructs for processes that do not specify the class of agent or the context of action, skepticism toward empirical truths that are inconsistent with political or social goals, a reluctance to use profiles or characteristics that have different weights to classify persons, and an aversion to treating subjects with extreme values as representing special categories. These points are made in the context of the author's research on temperaments in children.

The developmental interplay between nature and nurture is discussed, with particular reference to implications for research in developmental psychopathology. The general principles include individual differences in reactivity to the environment, two-way interplay between intraindividual biology and environmental influences, and the need to consider broader social contextual features. Individuals actively process their experiences; they also act on their environment to shape and select their experiences, and individual characteristics change over time. Key findings on genetic effects include their ubiquitous influence, the multifactorial origin of most psychopathology, the involvement of several genes in most mental disorders, some genetic effects operate through dimensional risk features rather than directly on disorder, some genetic effects are dependent on gene–environment correlations and interactions, and genetic effects increase with age. Key findings on environmental effects include their ubiquitous influence, the genetic mediation of some supposed environmental effects, the importance of passive gene–environment correlations, the paucity of evidence regarding environmental effects on lifetime liability to psychopathology, the lack of understanding of environmental effects on the organism, and the importance of nonshared environmental effects. Research strategies to investigate environmental risk mediation include the range of genetically sensitive designs, migration studies, secular trend investigations, studies of nonfamilial environments, and examination of intraindividual change in relation to measured environmental alterations. Proximal processes involved in person–environment interplay are discussed in relation to person–environment interactions and evocative and active person–environment correlations.

We evaluate the usefulness of 11 key epigenetic concepts from the behavior genetic research paradigm for advancing the field of developmental psychopathology. Key assumptions, empirical examples, and caveats in interpreting results are presented. We emphasize the usefulness of incorporating both dimensional (e.g., temperament trait) and categorical (e.g., diagnosis) variables, environmental measures, direct behavioral assessments, and multiple, theoretically relevant occasions of study into classic twin and family studies. We highlight contemporary techniques for identifying specific chromosomal regions associated with behavioral patterns, and the importance of considering nonmendelizing genetic influences when discerning the panorama of genetic influences on behavior.

The incomplete interface between remediation-oriented research and basic science research has hampered progress toward gaining insight into the etiologies of autism, despite the availability of abundant research data. Investigators of these two research domains differ in their background training and primary goals, which necessarily affect their missions, perspectives, research questions posed, methodologies selected, and interpretation of data from the research. Miscommunication between the two types of researchers has brought about disagreement on nearly every aspect of the research process. We discuss both sides of the impasse: a traditional clinical practice perspective based on the requirement for finding immediate answers to the remediation question and the basic science perspective with the goal of delineating the sequence of biological changes from the initial cause(s) of abnormal development to behavioral outcome. Although remediation-oriented research aims at alleviation of symptoms for today's patients, we propose that a basic science perspective seeks insight into the triggering causes and pathogenesis of the disorder from which better diagnosis and remediation may be devised for patients in the future. We suggest that research in autism can progress beyond the impasse of disagreement and competition toward information integration and insight by means of dialogue, data exchange, discussion, collaboration, and cooperation.

This paper questions the assumption that children's social and emotional competence be placed within the developing child, rather than in the interaction of the child with the range of peer social ecologies in which the children might function. This paper presents a new nonstatistical mathematical approach to modeling children's peer social interaction in small groups using nonlinear difference equations in which both an uninfluenced and an influenced regulatory set point of positive minus negative interaction can be separately estimated. Using this model and the estimation procedure, it is possible to estimate what a focal child and the group initially brings to the group interaction and also how these regulatory set points are influenced by the interaction to determine two influenced regulatory set points. Six-person mainstreamed and specialized groups were established involving three types of unacquainted preschool boys: children with and without developmental delays and a language disordered but intellectually normally functioning group, using a methodology that ensured appropriate matching of child and family characteristics. For each 2-week play group, the social interactions of each child were observed during a designated free play period. Handicapped children were observed in either a specialized or mainstreamed setting. The application made of this modeling process in this paper is generating theory to attempt to understand influence processes. Parameters are introduced that reflect uninfluenced target child and group set points, emotional inertia, and influence functions.

We contrast the current, clinically based framework for behavior disorder against a life course framework, as an alternative structure upon which to map the variations in onset and stability of clinical symptomatology known to take place in adult life. This alternative developmental framework is used as a base around which to understand known variations in rates of alcohol abuse/dependence over the life course and to review existing schemes for the evaluation of developmental variation in “caseness.” From this work, it was proposed that symptom structure be regarded as a mass of greater or lesser breadth, with properties of extensiveness in time and life course invasiveness, as a function of where in the life course the symptomatology first emerged, and the degree to which the mass sustained itself in developmental time. This framework guided the construction of a time-based measure of alcohol related symptomatology, called the Lifetime Alcohol Problems Score (LAPS). The LAPS discriminated among a variety of alcohol-specific and nonalcohol-specific measures of alcohol-related difficulty, including diagnosis of alcohol dependence, having been in treatment, level of other psychopathology, and measures of family disorganization. The measure has potential applicability for prospective studies, and in estimating clinical prognosis. The utility of the paradigm as a framework within which to conceptualize the emergence, ebb, and flow of other behavior disorders is also discussed.