Can the connection between psychology and neuroscience provide a sufficient framework to support the study of the development of maladaptation and psychopathology? This Special Issue is devoted to papers that address this general issue within their specific domains. If we hope to provide a definitive answer to the question posed above, then it is important to know how cognitive and affective neuroscience arose, what are their distinctive findings to date, and, to the extent possible, predict what future developments can be expected. Before proceeding, we first examine the basic principles inherent to a developmental psychopathology perspective, as well as the multiple disciplines that played a critical role in its evolution as an interdisciplinary science.We are grateful to Mary Rothbart and Sheree L. Toth for their help with this Introduction.

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.The authors were supported by funds from the National Institute of Mental Health (2-ROI-MH36840) and National Institute of Neurological Disorders and Stroke (2-ROI-NS19855) awarded to Eric Courchesne.

Several research groups have identified a network of regions of the adult cortex that are activated during social perception and cognition tasks. In this paper we focus on the development of components of this social brain network during early childhood and test aspects of a particular viewpoint on human functional brain development: “interactive specialization.” Specifically, we apply new data analysis techniques to a previously published data set of event-related potential (ERP) studies involving 3-, 4-, and 12-month-old infants viewing faces of different orientation and direction of eye gaze. Using source separation and localization methods, several likely generators of scalp recorded ERP are identified, and we describe how they are modulated by stimulus characteristics. We then review the results of a series of experiments concerned with perceiving and acting on eye gaze, before reporting on a new experiment involving young children with autism. Finally, we discuss predictions based on the atypical emergence of the social brain network.This work was funded by UK Medical Research Council Programme Grants (G9901005 and G9715587) to M.H.J. and S.B.C. T.F. was supported by a Wellcome Trust Research Fellowship (073985/Z/03/Z).

Event-related potentials (ERPs) were recorded to brief images of caregivers' and strangers' faces for 72 institutionalized children (IG), ages 7–32 months, and compared with ERPs from 33 children, ages 8–32 months, who had never been institutionalized. All children resided in Bucharest, Romania. Prominent differences in four ERP components were observed: early negative (N170), early positive (P250), midlatency negative (Nc), and positive slow wave (PSW). For all but the P250, the amplitude of these components was larger in the never instituionalized group than the institutionalized group; this pattern was reversed for the P250. Typical effects of the Nc (amplitude greater to stranger vs. caregiver) were observed in both groups; in contrast, the IG group showed an atypical pattern in the PSW. These findings are discussed in the context of the role of experience in influencing the neural circuitry putatively involved in recognizing familiar and novel faces.The work reported in this manuscript was supported by a research network (Early Experience and Brain Development) funded by the John D. and Catherine T. MacArthur Foundation (Charles A. Nelson, Network Chair). The Bucharest Early Intervention Core Group consists of Charles H. Zeanah, Anna T. Smyke, and Sebastian F. Koga (Tulane University); Charles A. Nelson (Harvard Medical School); Susan W. Parker (Randolph-Macon College); Nathan A. Fox (University of Maryland); Peter J. Marshall (Temple University); and Hermi R. Woodward (University of Pittsburgh/MacArthur Research Networks). The authors acknowledge the many invaluable contributions of their Romanian partner institutions, the SERA Romania Foundation, the Institute of Maternal and Child Health, and the Bucharest Departments of Child Protection. They are also deeply grateful to their Romanian team, whose hard work and dedication has made this study possible and to Dana Johnson and Mary Jo Spencer for conducting the pediatric screens.

This investigation examined the effects of maltreatment during the first year of life on the neural correlates of processing facial expressions of emotion at 30 months of age. Event-related potentials (ERPs) in response to children passively viewing standardized pictures of female models posing angry, happy, and neutral facial expressions were examined. Four ERP waveform components were derived: early negative (N150), early positive (P260), negative central (Nc), and positive slow wave (PSW). Differences in these waveforms between a group of 35 maltreated and 24 nonmaltreated children were reported. The groups did not differ on the early perceptual negative component (N150), whereas the maltreated children had greater P260 amplitude at frontal leads compared to the nonmaltreated children in response to viewing angry facial expressions. For the Nc component, the nonmaltreated comparison children exhibited greater amplitude while viewing pictures of happy faces compared to angry and neutral faces, whereas the maltreated children showed greater Nc amplitude at central sites while viewing angry faces. For the PSW, the nonmaltreated group showed a greater area score in the right hemisphere in response to viewing angry facial expressions compared to the maltreated group. The results are discussed in terms of brain development and function, as well as their implications for the design and evaluation of preventive interventions.This research was supported by grants from the National Institute of Mental Health (MH067792-02) and the Spunk Fund, Inc. to Dante Cicchetti. We gratefully acknowledge the technical assistance of Rafael Klorman, PhD, and Karen La Due in setting up the ERP laboratory at Mt. Hope Family Center, which was used to carry out this study. Moreover, we appreciate the support and advice provided by Drs. Sheree L. Toth and Fred A. Rogosch. In addition, we are grateful to Karen La Due, Steve Perino, and Shannon O'Hara, as well as other staff at Mt. Hope Family Center, for their assistance in data collection. Finally, we are eternally grateful to those families who participated in this 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.The writing of this paper and the studies reported herein were funded by a grant from the National Institute of Child Health and Human Development (NICHD Grant U19HD34565), which is part of the NICHD Collaborative Program of Excellence in Autism, and a center grant from the National Institute of Mental Health (NIMH Grant U54MH066399), which is part of the NIH STAART Centers Program.

Empathic concern for others is an essential motive for challenges of self-regulation at all developmental stages. A child who never develops the capacity for empathic concern may become an ineffective parent, such that developmental psychopathology propagates across generations. We draw on evidence and theory by Panksepp and associates that indicates that infant–mother bonding is mediated by opiate mechanisms. We review the neural systems of pain perception and find these are closely aligned with those for attentional and cognitive self-regulation. Analysis of the limbic and neocortical representations for interpersonal reasoning suggests there are important contributions from visceral, affective, and somatic and cognitive levels. We draw on modern learning theory to propose a critical role for frustration training in development to allow the child to achieve the capacity for tolerating psychological pain that allows effective empathic concern in later relationships.

The circumplex model of affect proposes that all affective states arise from cognitive interpretations of core neural sensations that are the product of two independent neurophysiological systems. This model stands in contrast to theories of basic emotions, which posit that a discrete and independent neural system subserves every emotion. We propose that basic emotion theories no longer explain adequately the vast number of empirical observations from studies in affective neuroscience, and we suggest that a conceptual shift is needed in the empirical approaches taken to the study of emotion and affective psychopathologies. The circumplex model of affect is more consistent with many recent findings from behavioral, cognitive neuroscience, neuroimaging, and developmental studies of affect. Moreover, the model offers new theoretical and empirical approaches to studying the development of affective disorders as well as the genetic and cognitive underpinnings of affective processing within the central nervous system.This work was supported in part by NIMH Grants MH01232, MH59139, MH36197, MHK02-74677, and MH068318; a grant from the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD); NSF Grant BSC-0421702; and funding from the Thomas D. Klingenstein and Nancy D. Perlman Family Fund and the Suzanne Crosby Murphy Endowment at Columbia University.

Interest in the effects of early adversity on children's development reflects contemporary emphases on early experience in the behavioral sciences and plasticity in the neurosciences. Over the past decade, powerful new tools and approaches for understanding the neural circuitry involved in emotion have become increasingly available. Yet, research in developmental psychopathology has not reaped the full benefits of affective neuroscience approaches and methods. Integration of affective neuroscience approaches can excavate developmental mechanisms, thereby advancing knowledge about the etiology, prevention, and treatment of mental health problems in children. Here, we consider two general principles that can guide understanding of plasticity in the neural circuitry of emotion systems and the development of psychopathology.The author was generously supported by the National Institutes of Mental Health (MH 61285, MH 68858) and by the University of Wisconsin. Elizabeth Shirtcliff, Alison Wismer Fries, Jessica Shackman, and Julia Kim–Cohen provided thoughtful comments on an early draft of this paper. The author also thanks Dante Cicchetti and Michael Posner for their critical reviews of the manuscript and Erin Henigan for help with preparation of this manuscript.

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.We thank the children and families that participated in our studies and the staff of the 22q and You Center at the Children's Hospital of Philadelphia. This work was supported by grants from the NIH (R01HD42974 and R01HD46159) and the Philadelphia Foundation to T.J.S., Grant PO1DC02027 to B.S.E., and Grant M01-RR00240 to the Children's Hospital of Philadelphia.

Attention-deficit/hyperactivity disorder (ADHD) is a behavioral syndrome that arises in early childhood, often co-occurs with conduct disorder and leads, developmentally, to antisocial behavior and substance abuse. Models from cognitive and affective neuroscience have been invoked in an effort to understand the development of ADHD, leading to a broad array of interrelated theories and hypothesized mechanisms. In this paper, we highlight core mechanisms that may cut across several theories and constructs, and thus provide some leverage for further study and conceptualization from a neuroscience perspective. We emphasize the joint operations of frontostriatal and frontocerebellar neural loops in detecting and predicting what and when important events in the environment will occur and their interaction with frontoamygdala loops in assigning emotional significance to these events. We note that weaknesses in the development of these basic operations could lead to decrement in the development of cognitive and affective control and other mental operations mediated by prefrontal cortex during development. In turn, such decrement could lead to many of the phenotypic cognitive and neuropsychological features seen in children with ADHD.This work was supported by National Institute of Mental Health Grants R01-MH59105 and R01-MH63146 to J.T.N. and NIMH R01 MH63255 and NIDA R21 DA15882 to B.J.C.

Most studies of attention-deficit/hyperactivity disorder (ADHD) have focused on the combined type and emphasized a core problem in response inhibition. It is proposed here that the core problem in the truly inattentive type of ADHD (not simply the subthreshold combined type) is in working memory. It is further proposed that laboratory measures, such as complex-span and dual-task dichotic listening tasks, can detect this. Children with the truly inattentive type of ADHD, rather than being distractible, may instead be easily bored, their problem being more in motivation (underarousal) than in inhibitory control. Much converging evidence points to a primary disturbance in the striatum (a frontal–striatal loop) in the combined type of ADHD. It is proposed here that the primary disturbance in truly inattentive-type ADHD (ADD) is in the cortex (a frontal–parietal loop). Finally, it is posited that these are not two different types of ADHD, but two different disorders with different cognitive and behavioral profiles, different patterns of comorbidities, different responses to medication, and different underlying neurobiologies.Preparation of this manuscript was supported by grants from NIDA (R01 DA19685-16A2) and the McDonnell Foundation (JSMF Grant 21002016). The author gratefully thanks Russ Barkley, Dante Cicchetti, Michael Posner, and Margaret Weiss for comments on an earlier draft of the manuscript. Of course, only the author bears responsibility for any errors in this paper.

From an affective neuroscience perspective, the goal of achieving a deeper, more mechanistic understanding of the development of depression will require rigorous models that address the core underlying affective changes. Such an understanding will necessitate developing and testing hypotheses focusing on specific components of the complex neural systems involved in the regulation of emotion and motivation. In this paper, we illustrate these principles by describing one example of this type of approach: examining the role of disruptions in neural systems of positive affect in major depressive disorder in school-age children and adolescents. We begin by defining positive affect, proposing that positive affect can be distinguished from negative affect by its neurobehavioral features. We provide an overview of neural systems related to reward and positive affect, with a discussion of their potential involvement in depression. We describe a developmental psychopathology framework, addressing developmental issues that could play a role in the etiology and maintenance of early-onset depression. We review the literature on altered positive affect in depression, suggesting directions for future research. Finally, we discuss the treatment implications of this framework.This research was supported by a Klingenstein Third Generation Foundation Postdoctoral Fellowship, NIMH Training Grant T32 MH018269, and NIMH Research Network R24 MH67346. We thank David J. Kupfer for his compelling suggestions about clinical course and development across the life span, and we thank Anna Lotze for help with references.

Reflective thinking occurs when information stored in long-term memory (LTM) is not sufficient to allow one to respond “automatically” to an object or event. Instead, stored information must be entered into working memory and a novel response or solution produced. In this article I argue that mental imagery plays a central role in this process, and that over the course of normal cognitive development the process of reflective thinking “programs” LTM so that an increasingly large number of tasks can be performed without reflective thinking. Normal cognitive development thus results in a decreasing reliance on imagery. However, if highly emotional images are formed, additional retrieval cues can be entered into LTM, making such images more likely to occur in the future. Such images induce arousal, similar to that induced by the actual event. This line of thinking leads to a novel perspective on the neurocognitive deficits that underlie the development of posttraumatic stress disorder, and may also help to explain some symptoms seen in hyperactivity, impulsiveness, and difficulties in self-control.The work summarized in this paper was supported in part by NSF ROLE Grant REC-0106760 and NIH Grant 5 R01 MH60734. Portions of this article were adapted from a draft of Kosslyn (2005). I thank the Editors and Robin Rosenberg for helpful comments on earlier drafts.

Four models of psychopathy (frontal lobe dysfunction, response set modulation, fear dysfunction, and violence inhibition mechanism hypotheses) are reviewed from the perspective of cognitive neuroscience. Each model is considered both with respect to the psychopathy data and, more importantly, for the present purposes, with respect to the broader cognitive neuroscience fields to which the model refers (e.g., models of attention with respect to the response set modulation account and models of emotion with respect to the fear dysfunction and violence inhibition mechanism models). The paper concludes with an articulation of the more recent integrated emotion systems model, an account inspired both by recent findings in affective cognitive neuroscience as well as in the study of psychopathy. Some directions for future work are considered.