Abstract
In 1963, J. Cotter Hirschberg, in a conference named ‘‘The basic functions of a child psychiatrist in any setting’’, highlighted that one of the several unique contributions which child psychiatrists may make in our work was the understanding of a symptom in the context of development [1]. Three years later, Lee Robins [2] published the landmark longitudinal study ‘‘Deviant children grown up’’, demonstrating the continuity between conduct problems in childhood and antisocial personality disorder in adulthood, and by that, clearly demonstrating to the mental health field the value of tracking people across the lifespan, since childhood, to understand psychopathology. In the following decades, Sroufe and Rutter [3], Garmezy [4], and Cicchetti [5] published influential papers that established the discipline of developmental psychopathology. In parallel, an upsurge of new technologies has unveiled the genome and the brain, paving the way to identify atypical neurodevelopmental processes underlying psychopathology. Today, a developmental perspective is still pivotal in our clinical work as child and adolescent psychiatrists, but not unique to us: a developmental perspective now shapes the current conceptualization and investigation of mental disorders, from those that are apparent in early childhood to senescence [6], and also the avenues to treat them [7]. Our field has benefited tremendously from investigations that took advantage of a developmental framework, and fortunately their number has been increasing dramatically over time. Several important examples have been published in the European Child & Adolescent Psychiatry in the past years, with emphasis on early predictors of later psychopathology [8, 9], continuity and discontinuity of psychopathology across development [10–13], risk and protective factors investigation [14], early intervention [15], and others approaches [16]. In this issue, we see two studies with this same perspective investigating the biological underpinnings of psychopathology. The first study, by Walhovd and colleagues [17] from the University of Oslo, Norway, tested whether the dimensional nature of behavioral symptoms in childhood correlated with brain maturation. Built upon on the finds from Judith Rapoport, Philip Shaw and their team, who beautifully demonstrated that children with attention-deficit/hyperactivity disorder attained a maturational milestone (the peak of cortical thickness) later in comparison to control children [18], Walhovd and colleagues now tested cross-sectionally the association between cortical thickness and hyperactive, inattentive, and conduct symptoms in 107 healthy children from 8 to 19 years. The authors found no evidence of association between hyperactive and inattentive symptoms in healthy children and cortical thickness. Nevertheless, conduct symptoms were associated with cortical thickness controlling for age in left prefrontal and supramarginal areas. This association was being largely driven by younger children, where the interactions between conduct symptoms and age were reflected in regionally thinner frontal and temporal cortices bilaterally. The second study, by Beitchman and colleagues [19] from the University of Toronto, Canada, tested the association between oxytocin genes and behavioral characteristics of children with antisocial behavior. Built upon on an extensive body of work that has demonstrated that oxytocin has important cognitive and behavioral effects, such as to facilitate social memory and afiliative behavior, which are G. V. Polanczyk (&) Department of Psychiatry, University of Sao Paulo Medical School, National Institute of Developmental Psychiatry for Children and Adolescents (INCT-CNPq), Rua Dr. Ovidio Pires de Campos 785, Sao Paulo, SP 05403-010, Brazil e-mail: gvp@usp.br
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