Journal of Child Psychology and Psychiatry 56:3 (2015), pp 203–205

doi:10.1111/jcpp.12404

Editorial: Capturing the dynamics of development and psychopathology: from neural circuits to global trends Every year, the Journal of Child Psychology and Psychiatry dedicates an entire issue to state-of-theart reviews of the science underpinning our field, conducted by leading international experts. Like last year, the Editors sought to bring together a wide range of topics and thinkers covering many of the major themes that define contemporary child psychology and psychiatry. As always, the result is a veritable treasure trove of data and ideas on some of the most important topics of our times. For the second year running, we also invited commentaries from world-leading experts to accompany each review, and in every case the reviews and their commentaries create a fascinating, forward-looking dialogue about the hurdles that have been overcome, and the challenges that lie ahead.1 We are very grateful to all our authors and commentators for preparing such a rich feast for us. As you read the articles in the this year’s Annual Research Review issue, many common threads will no doubt strike you. To my mind, one notable feature of all the articles was the extent to which elegant research designs, and innovations in technology, have been, and will always be, the key to unlocking some of the central puzzles we are faced with when trying to elucidate the mechanisms of child psychopathology: the innovative use of MRI to reveal the complex structural and functional networks of neuronal organization (V ertes & Bulmore); the importance of well-chosen quasi-experiments to reveal the distinctive sequelae of adverse early care (Zeanah & Gleason), or throw light on the very earliest neurodevelopmental processes implicated in ASD and ADHD (Johnson, Gliga, Jones & Charman); the enormous value of consistent measurement and rigorous epidemiological sampling for charting, and understanding, variations in child psychopathology across nations (Polanczyk, Salum, Sugaya, Caye & Rohde), over the lifespan (Costello & Maughan), and over social periods (Collishaw); the use of rare genetic syndromes for disentangling the common and distinct developmental mechanisms involved in ADHD and other neurodevelopmental disorders (Scerif & Baker), and the major contribution of high-density genotyping, next-generation sequencing and large-scale international collaborative consortia for revealing the hidden heritability problem and pointing to some of the ways it can be tackled (Kiser, Rivero & Lesch). I was also struck by the fact all the authors showed a great willingness to embrace complexity. It is

surely a mark of the growing maturity of our field that there is a greater acknowledgement and acceptance that there will be no simple answers to our questions: no single gene that directly causes disorder, no single experience with wholly predictable and lasting effects, no single phenotype to arise from familial risk, no single pathway or system affected by a rare genetic disorder; no one disorder has a common and inevitable long-term outcome. It must surely be no coincidence that this enthusiasm to take on the challenges of complexity are evident at a time when the field is energetically re-thinking the very nature and structure of psychopathology itself (National Institute of Mental Health, 2014). Each review also shows how, despite the complexity, good science can bring order out of the potential chaos. In doing so, all the reviews speak volumes for the importance of the developmental psychopathology framework for understanding child disorder and maladaptation. The ARR begins with an authoritative review of the nature, development and management of attachment disorders by Zeanah and Gleason1. The authors show just how much progress has been made in this highly complex area, by way of well-designed prospective and interventions studies, and the application of high-quality measurement tools. No doubt a further hidden ingredient in this productive process has been the capacity of those working in the field to ask some tough questions – most importantly: are previously labelled attachment disorders truly disorders of attachment? Here, Bowlby’s clear thinking about the function of attachment behaviour (Bowlby, 1969), and Ainsworth’s elegantly designed instrument for measuring it (Ainsworth, Blehar, Waters, & Wall, 1978), were extremely important for researchers to be able to home in on a relatively clear answer: children diagnosed with Disinhibited Social Engagement Disorder (DSED), as it is now known in DSM-5, may show apparently normal attachment behaviour. That DSED may not be, in a straightforward sense, a disorder of attachment is enormously important for how we think about the assessment and management of these difficulties. The fascinating discussion (in the accompanying commentary) between LyonsRuth and the authors also shows that there is much still to be resolved, particularly about the early causal developmental mechanisms at play and whether attachment plays some part in those. The developmental psychopathology perspective, and the good use of early-in-life prospective longitu-

© 2015 Association for Child and Adolescent Mental Health. Published by John Wiley & Sons Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main St, Malden, MA 02148, USA

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dinal studies, was much in evidence in the review of the common and distinct developmental mechanisms in ASD and ADHD by Johnson and colleagues Indeed, the reviews of Johnson et al., Scerif and Baker and Kiser et al. form something of a trio, all focusing, from different points of view, and using different tools, on the neurodevelopmental disorders. All three reviews gather together evidence indicating that ADHD, ASD and in the latter two cases, intellectual disabilities, may share common (and distinct) underlying mechanisms. The Johnson et al. and Scerif and Baker reviews both draw attention to the critical point that populations already diagnosed with ASD or ADHD pose challenges for disentangling aetiological processes because symptoms, risk factors and underlying mechanisms are often correlated and conflated. Johnson and colleagues show how prospective studies of at-risk infants have revealed many early cognitive precursors to ASD and are beginning to indicate some potential early-appearing neurocognitive commonalities between ASD and ADHD. Prospective studies of at-risk infants have been exceptionally important for understanding the developmental origins of ASD, and even suggesting possible modes of early intervention (see Green et al., 2015), and Johnson and colleagues make a compelling case that the time is ripe for similar investigations of ADHD. Scerif and Baker tackle a related problem by focusing on relatively rare disorders of known genetic origin. The elegance of this approach for understanding ADHD is several-fold: (1) causal inferences about the role of genes in the phenotypic and endophenotypic profiles of these disorders are relatively secure (despite the likely complex intervening pathways involved), (2) common behavioural, cognitive or biological features amongst genetically distinct disorders provide evidence of equifinality – multiple biological pathways giving rise to similar developmental outcomes; (3) by focusing on known genetic disorders investigators can study development prior to the emergence of symptoms, and (4) by studying affected groups with different profiles it becomes possible to identify dissociable mechanisms that might otherwise be correlated and hard to disentangle in idiopathic ADHD. One intriguing conclusion the authors draw is that seemingly similar superficial symptoms may be underpinned by distinct neurocognitive mechanisms. Like Johnson et al., Scerif and Baker encourage us to think of these disorders as arising from developmental processes beginning in early life, involving numerous pathways, influenced by multiple genetic, environmental and epigenetic factors. These early changes may have cascading (and compensatory) effects as they unfold over time. The baton is then passed to Kiser and colleagues, who present a wide-ranging perspective on the genetics of neurodevelopmental disorders. Based on different sources of evidence, Kiser et al. seem

J Child Psychol Psychiatry 2015; 56(3): 203–5

to draw somewhat similar conclusions to Johnson et al. and Scerif and Baker, in that they suggest there may be a common ‘neurogenetic’ backbone to ADHD, ASD and intellectual disability (and possibly beyond), resulting from numerous overlapping neuroregulatory genes affecting, pleiotropically, a wide range of unfolding neurodevelopmental processes, a theme also picked up by Doyle in her commentary on Scerif and Baker. The picture they paint of the connections between genes and disorders is a far cry from the now-outdated notion that a gene or several genes cause a disorder. One comes away from reading these three reviews with some humility for the complexity of development and the scale of the task in hand, as well as a sense of excitement that the tools, methods and ideas are there to enable us to make a good start. The review by V ertes & Bulmore provides an elegant overview of one such approach that fits well with the kinds of complex, dynamic, developmental models suggested by the Johnson, Scerif and Kiser reviews. Growth connectomics, and the graph-theoretic approach that is a critical element of it, is a way of thinking about the structural and functional organization of the developing brain, which of course arises as a result of wildly complex multi-level intrinsic and extrinsic interactions. One of the most appealing features of this way of thinking is that it provides a biologically plausible framework for describing brain function and development that is coherent at all levels of analysis – from microscopic local networks of neurons, right up to the high-level orchestrated interactions that must occur between the neurocognitive modules necessary for complex behaviour and thought. A fascinating idea to arise from this way of thinking is that disturbances in the normative development of key ‘hubs’ in network organization may be critical in the emergence of psychopathology. Last but not least, we end the Annual Research Review with three beautifully complementary systematic reviews of epidemiological studies of childhood disorder. In the first, Costello and Maughan review the evidence concerning the long-term adult outcomes of childhood psychopathology. Inspired by work on optimal outcomes in ASD (e.g., Fein et al., 2013), Costello and Maughan use longitudinal cohort studies to investigate the extent of recovery among adults who had experienced diagnosed psychiatric difficulties in childhood. Not only is it vitally important to know the long-term prognosis of childhood disorder, but demonstrating the degree of variability in outcomes focuses attention on the factors that distinguish optimal from sub-optimal outcomes. Understanding how those factors work is obviously of great importance when thinking about intervention. The conclusions the authors draw are cause for optimism, but also an important reminder that the absence of disorder is not the same thing as a fulfilling, productive and happy life. © 2015 Association for Child and Adolescent Mental Health.

doi:10.1111/jcpp.12404

Polanczyk and colleagues examine the world-wide prevalence of childhood psychiatric disorders using meta-analysis. The review adds to the now-burgeoning work on global mental health for children, which has really gathered momentum over the last 8– 10 years. The findings of the meta-analysis are remarkable in the relative consistency of the prevalence estimates they reveal around the world. Methodology, it seems, may be a more important factor in explaining between-study differences in rates of child disorder than geography. With that in mind, there is an interesting tension implicit in the contrast between the review by Polanczyk et al. and the one that follows by Collishaw. Collishaw presents a systematic review of secular trends in rates of childhood disorder. Like the other epidemiological articles in this issue, Collishaw carefully details the methodological assumptions and caveats required to interpret this literature, and despite those, finds evidence of seemingly real changes appearing over time, particularly for conduct problems and depression. A crucial question is how these secular changes relate to concomitant changes in exposure to causal –presumably environmental – influences. And it is there that the apparent tension lies between the Collishaw and Polanczyk reviews: if real rates of disorder change over time within countries, then one would tend to expect divergence in prevalence rates across countries. Unless, that is, the causal factors involved are changing in a rather synchronized fashion around the world. While one can imagine some mechanisms that might operate like that, it would be surprising if these accounted for the majority of secular change. Methodological or analytical issues look like the obvious contenders here. Ultimately, it might only be possible to resolve these kinds of matters with large, multi-cohort studies involving many nations around the world, using precisely the same sampling and measurement methodology from one cohort to the next. I feel an international consortium coming on. . ..

© 2015 Association for Child and Adolescent Mental Health.

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On behalf of my fellow Editors of the Journal of Child Psychology and Psychiatry, I hope you enjoy this year’s Annual Research Review.

Pasco Fearon Editor, Annual Research Reviews Acknowledgements P.F. has disclosed interests in relation to his role as an Associate Editor of JCPP and the Annual Research Reviews coordinating Editor as detailed below, but has no specific competing or potential conflicts of interest in relation to this Editorial. Chair in Developmental Psychopathology,University College London, UK. Honorary associate professorship at Yale University (2007 – present). Associate Editor of the journals Attachment and Human Development and Mental Health and Prevention.

Note 1. Articles that are in this ARR issue (with italicized names on first and second significant mention) can be found at: http://onlinelibrary.wiley.com/ doi/10.1111/jcpp.2015.56.issue-3/issuetoc.

References Ainsworth, M.S., Blehar, M.C., Waters, E., & Wall, S. (1978). Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Lawrence Erlbaum. Bowlby, J. (1969). Attachment and loss, Vol. 1: Attachment. London: Hogarth Press and the Institute of Psycho-Analysis. Fein, D., Barton, M., Eigsti, I.M., Kelley, E., Naigles, L., Schultz, R.T.,  & Tyson, K. (2013). Optimal outcome in individuals with a history of autism. Journal of Child Psychology and Psychiatry, 54, 195–205. Green, J., Charman, T., Pickles, A., Wan, W.M., Elsabbagh, M., Slomis, V., & BASIS Team (2015). Parent-mediated intervention versus no intervention for infants at high risk of autism: a parallel, single-blind, randomised trial. Lancet Psychiatry, 2, 133–140. National Institute of Mental Health (2014). Research Domain Criteria (RDoC). Available from: http://www.nimh.nih.gov/ research-priorities/rdoc/index.shtml [last accessed 5 February 2015].

Editorial: Capturing the dynamics of development and psychopathology: from neural circuits to global trends.

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