Qualitative methods are well suited to advance the understanding of the role of social context in the development of maladaptation and psychopathology. However, they have not been widely used by developmental psychopathologists, despite being utilized in related fields, particularly in the sociological study of crime and delinquency. This article assesses the potential for the increased use of qualitative methods in developmental psychopathology and addresses the challenges involved in integrating them with quantitative research strategies. The interplay of qualitative and quantitative methods in the study of juvenile delinquency is reviewed for relevant lessons about both the utility and the difficulties of integrating the two types of methods. The problem of assessing continuities and discontinuities over the life course in patterns of antisocial behavior is discussed as an example of the challenge of integrating methodological paradigms. Schools of thought about qualitative methods and their relationship to quantitative research paradigms are identified and compared. Examples are discussed of narrative life history interviewing and qualitative observational techniques and of recent research endeavors integrating these qualitative techniques with quantitative data analyses.

The utility and flexibility of recent advances in statistical methods for the quantitative analysis of developmental data—in particular, the methods of individual growth modeling and survival analysis—are unquestioned by methodologists, but have yet to have a major impact on empirical research within the field of developmental psychopathology and elsewhere. In this paper, we show how these new methods provide developmental psychpathologists with powerful ways of answering their research questions about systematic changes over time in individual behavior and about the occurrence and timing of life events. In the first section, we present a descriptive overview of each method by illustrating the types of research questions that each method can address, introducing the statistical models, and commenting on methods of model fitting, estimation, and interpretation. In the following three sections, we offer six concrete recommendations for developmental psychopathologists hoping to use these methods. First, we recommend that when designing studies, investigators should increase the number of waves of data they collect and consider the use of accelerated longitudinal designs. Second, we recommend that when selecting measurement strategies, investigators should strive to collect equatable data prospectively on all time-varying measures and should never standardize their measures before analysis. Third, we recommend that when specifying statistical models, researchers should consider a variety of alternative specifications for the time predictor and should test for interactions among predictors, particularly interactions between substantive predictors and time. Our goal throughout is to show that these methods are essential tools for answering questions about life-span developmental processes in both normal and atypical populations and that their proper use will help developmental psychopathologists and others illuminate how important contextual variables contribute to various pathways of development.

Posttraumatic stress disorder is the pathological replay of emotional memory formed in response to painful, life-threatening, or horrifying events. In contrast, depression is often precipitated by more social context-related stressors. New data suggest that different types of life experiences can differentially impact biochemistry, physiology, anatomy, and behavior at the level of changes in gene expression. Repeated separation of neonatal rat pups from their mother results in many long-lasting alterations in biology and behavior paralleling that in depression, including hypercortisolism. The role of the amygdala in modulating emotional memory is highlighted, as well as some of its unique properties such as metaplasticity (i.e., the differential direction of long-term adaptation, either potentiation or depression) in response to the same input as a function of the prior history of stimulation. The implications of these emerging data on the physiological and molecular mechanisms underlying emotional memory emphasize the particular importance of prevention and early intervention.

This article reviews memory-related impairments in trauma survivors with posttraumatic stress disorder and their possible association to neuroendocrine alterations seen in this disorder. The neuroendocrine profile in PTSD first described in chronically ill combat veterans is characterized by lower basal cortisol levels, higher glucocorticoid receptor number, enhanced sensitivity to exogenous steroids, and increased variation in basal cortisol levels over the diurnal cycle. The generalizability and time course of these neuroendocrine alterations are explored in longitudinal studies and studies in other traumatized populations. These studies suggest that at least some aspects of this neuroendocrine profile can also be seen in other populations, including women, children, and victims of childhood trauma. Additionally, the alterations may be present early in the course of illness, perhaps even in the immediate aftermath of trauma, and may continue to be manifest in elderly trauma survivors. The mechanisms by which these neuroendocrine alterations may influence the formation and processing of traumatic memories are discussed.

Studies in animals showing hippocampal atrophy and associated memory deficits in stress and aging have implications for stress and aging in humans. Clinical studies in traumatized human populations with posttraumatic stress disorder (PTSD) have replicated studies in animals, showing reduction in volume of the hippocampus measured with magnetic resonance imaging and associated memory deficits. Trauma at different stages of development (early childhood abuse versus trauma in later life due to combat) may influence the nature of memory deficits and hippocampal atrophy. Studies in aging human subjects are consistent with animal studies, although future research is needed in this area. The similarities between biological findings related to cortisol and the hippocampus in stress and aging in both animal and human studies raises the question of whether PTSD can be seen as a form of accelerated aging. Evidence that stress affects the hippocampus and the capacity for learning has broad implications for public health policy, underlying the need for additional resources in this important area and a reexamination of our understanding of factors influencing academic achievement.