Journal of Child Psychology and Psychiatry

Publisher: Association for Child Psychology and Psychiatry, Wiley

Journal description

The Journal of Child Psychology and Psychiatry is internationally recognised to be the leading journal covering both child and adolescent psychology and psychiatry. Articles published include experimental and developmental studies, especially those relating to developmental psychopathology and the developmental disorders. An important function of the Journal is to bring together empirical research, clinical studies and reviews of high quality arising from different theoretical perspectives.

Current impact factor: 6.46

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 6.459
2013 Impact Factor 5.669
2012 Impact Factor 5.422
2011 Impact Factor 4.281
2010 Impact Factor 4.36
2009 Impact Factor 4.983
2008 Impact Factor 4.854
2007 Impact Factor 4.432

Impact factor over time

Impact factor

Additional details

5-year impact 6.68
Cited half-life 9.20
Immediacy index 1.21
Eigenfactor 0.03
Article influence 2.50
Website Journal of Child Psychology and Psychiatry and Allied Disciplines, The website
Other titles Journal of child psychology and psychiatry and allied disciplines (Online), Journal of child psychology and psychiatry
ISSN 1469-7610
OCLC 48799103
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 2 years embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification

Publications in this journal

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: I provide a brief commentary on the brilliant accompanying study of Nikolas et al. concerning risky bicyclist-automobile behavior in ADHD and typical youth. The sophistication of the simulator and procedures and the number and precision of measurements are remarkable and afford us an excellent glimpse into the specific mechanisms by which previously documented injury risk in such natural settings may be increased by ADHD in youth. I also briefly note clinically important implications of these and other research results on accident risk in ADHD.
    Preview · Article · Feb 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: Childhood maltreatment is the most important preventable cause of psychopathology accounting for about 45% of the population attributable risk for childhood onset psychiatric disorders. A key breakthrough has been the discovery that maltreatment alters trajectories of brain development. Methods: This review aims to synthesize neuroimaging findings in children who experienced caregiver neglect as well as from studies in children, adolescents and adults who experienced physical, sexual and emotional abuse. In doing so, we provide preliminary answers to questions regarding the importance of type and timing of exposure, gender differences, reversibility and the relationship between brain changes and psychopathology. We also discuss whether these changes represent adaptive modifications or stress-induced damage. Results: Parental verbal abuse, witnessing domestic violence and sexual abuse appear to specifically target brain regions (auditory, visual and somatosensory cortex) and pathways that process and convey the aversive experience. Maltreatment is associated with reliable morphological alterations in anterior cingulate, dorsal lateral prefrontal and orbitofrontal cortex, corpus callosum and adult hippocampus, and with enhanced amygdala response to emotional faces and diminished striatal response to anticipated rewards. Evidence is emerging that these regions and interconnecting pathways have sensitive exposure periods when they are most vulnerable. Conclusions: Early deprivation and later abuse may have opposite effects on amygdala volume. Structural and functional abnormalities initially attributed to psychiatric illness may be a more direct consequence of abuse. Childhood maltreatment exerts a prepotent influence on brain development and has been an unrecognized confound in almost all psychiatric neuroimaging studies. These brain changes may be best understood as adaptive responses to facilitate survival and reproduction in the face of adversity. Their relationship to psychopathology is complex as they are discernible in both susceptible and resilient individuals with maltreatment histories. Mechanisms fostering resilience will need to be a primary focus of future studies.
    No preview · Article · Feb 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: Although autism spectrum condition (ASC) is strongly genetic in origin, accumulating evidence points to the critical roles of various environmental influences on its emergence and subsequent developmental course. Methods: A developmental psychopathology framework was used to synthesise literature on environmental factors associated with the onset and course of ASC (based on a systematic search of the literature using PubMed, PsychInfo and Google Scholar databases). Particular emphasis was placed on gene-environment interplay, including gene-environment interaction (G × E) and gene-environment correlation (rGE). Results: Before conception, advanced paternal and maternal ages may independently enhance offspring risk for ASC. Exogenous prenatal risks are evident (e.g. valproate and toxic chemicals) or possible (e.g. selective serotonin reuptake inhibitors), and processes endogenous to the materno-foeto-placental unit (e.g. maternal diabetes, enhanced steroidogenic activities and maternal immune activation) likely heighten offspring vulnerability to ASC. Folate intake is a prenatal protective factor, with a particular window of action around 4 weeks preconception and during the first trimester. These prenatal risks and protective mechanisms appear to involve G × E and potentially rGE. A variety of perinatal risks are related to offspring ASC risk, possibly reflecting rGE. Postnatal social factors (e.g. caregiver-infant interaction, severe early deprivation) during the first years of life may operate through rGE to influence the likelihood of manifesting a full ASC phenotype from a 'prodromal' phase (a proposal distinct to the discredited and harmful 'refrigerator mother hypothesis'); and later postnatal risks, after the full manifestation of ASC, shape life span development through transactions mediated by rGE. There is no evidence that vaccination is a postnatal risk for ASC. Conclusions: Future investigations should consider the specificity of risks for ASC versus other atypical neurodevelopmental trajectories, timing of risk and protective mechanisms, animal model systems to study mechanisms underlying gene-environment interplay, large-sample genome-envirome designs to address G × E and longitudinal studies to elucidate how rGE plays out over time. Clinical and public health implications are discussed.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: There has been little available data to inform the predictors and outcomes of latent class trajectories of depressive symptoms beginning during preschool and continuing throughout school age. Further, the extant literature in this domain has been limited by the use of parent report checklists of nonspecific 'internalizing' psychopathology rather than diagnostic interviews for depression. Methods: To address these gaps in the literature, this study applied growth mixture modeling to depressive symptom severity endorsed by children and/or their caregivers (N = 348) during a structured clinical interview in a 10-year longitudinal dataset spanning from preschool into late school age. Results: Three distinct trajectories of depressive symptom severity were found in boys and girls. For boys, but not girls, the high depression severity latent class increased in depressive symptoms from preschool through school age, followed by a decline in depressive symptom severity during later school age. For girls, the high depression severity latent class remained stable across time. Early childhood social adversity, familial history of affective disorder, preschool-onset ODD/CD, and school age functional impairment differentiated high-risk trajectory classes among both boys and girls. Conclusions: Extending the literature on trajectories of depressive symptoms to the preschool period, these findings incorporate structured clinical interviews of depressive symptom severity and indicate gender differences as well as psychosocial predictors and functional outcomes among children in high severity latent classes. The findings from this study suggest that increased attention to screening for depressive symptoms in early childhood is of significant public health importance.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: More refined dimensions of social-communication impairment are needed to elucidate the clinical and biological boundaries of autism spectrum disorders (ASD) and other childhood onset psychiatric disorders associated with social difficulties, as well as to facilitate investigations in treatment and long-term outcomes of these disorders. Methods: This study was intended to identify separable dimensions of clinician-observed social-communication impairments by examining scores on a widely used autism diagnostic instrument. Participants included verbally fluent children ages 3-13 years, who were given a clinical diagnosis of ASD (n = 120) or non-ASD (i.e. ADHD, language disorder, intellectual disability, mood or anxiety disorder; n = 118) following a comprehensive diagnostic assessment. Exploratory and confirmatory factor analysis examined the factor structure of algorithm items from the Autism Diagnostic Observation Schedule (ADOS), Module 3. Results: Results indicated that a three-factor model consisting of repetitive behaviors and two separate social-communication behavior factors had superior fit compared to a two-factor model that included repetitive behaviors and one social-communication behavior factor. In the three-factor model, impairments in 'Basic Social-Communication' behaviors (e.g. eye contact, facial expressions, gestures) were separated from impairments in 'Interaction quality.' Confirmatory factor analysis in an independent sample of children in the Simons Simplex Collection (SSC) further supported the division of social-communication impairments into these two factors. Scores in Interaction Quality were significantly associated with nonverbal IQ and male sex in the ASD group, and with age in the non-ASD group, while scores in basic social communication were not significantly associated with any of these child characteristics in either diagnostic group. Conclusions: Efforts to conceptualize level, or severity, of social-communication impairment in children with neurodevelopmental disorders might be facilitated by separating the most basic (or proximal) social-communication impairments from those that could arise from a range of other phenotypic variables. Identification of social-communication subdimensions also highlights potential avenues for measuring different types of social-communication impairments for different purposes (e.g. for differential diagnosis vs. response to treatment).
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background and scope: Psychiatric science remains descriptive, with a categorical nosology intended to enhance interobserver reliability. Increased awareness of the mismatch between categorical classifications and the complexity of biological systems drives the search for novel frameworks including discovery science in Big Data. In this review, we provide an overview of incipient approaches, primarily focused on classically categorical diagnoses such as schizophrenia (SZ), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD), but also reference convincing, if focal, advances in cancer biology, to describe the challenges of Big Data and discovery science, and outline approaches being formulated to overcome existing obstacles. Findings: A paradigm shift from categorical diagnoses to a domain/structure-based nosology and from linear causal chains to complex causal network models of brain-behavior relationship is ongoing. This (r)evolution involves appreciating the complexity, dimensionality, and heterogeneity of neuropsychiatric data collected from multiple sources ('broad' data) along with data obtained at multiple levels of analysis, ranging from genes to molecules, cells, circuits, and behaviors ('deep' data). Both of these types of Big Data landscapes require the use and development of robust and powerful informatics and statistical approaches. Thus, we describe Big Data analysis pipelines and the promise and potential limitations in using Big Data approaches to study psychiatric disorders. Conclusion: We highlight key resources available for psychopathological studies and call for the application and development of Big Data approaches to dissect the causes and mechanisms of neuropsychiatric disorders and identify corresponding biomarkers for early diagnosis.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Risk-taking, which involves voluntary choices for behaviors where outcomes remain uncertain, undergoes considerable developmental changes during childhood, adolescence, and early adulthood. In addition, risk-taking is thought to be a key element of many externalizing disorders, such as ADHD, delinquency, conduct disorder, and substance abuse. In this review, we will discuss the potential adaptive and nonadaptive properties of risk-taking in childhood and adolescence. We propose that the changes in brain architecture and function are a crucial element underlying these developmental trajectories. We first identify how subcortical and cortical interactions are important for understanding risk-taking behavior in adults. Next, we show how developmental changes in this network underlie changes in risk-taking behavior. Finally, we explore how these differences can be important for understanding externalizing behavioral disorders in childhood and adolescence. We conclude that longitudinal studies are of crucial importance for understanding these developmental trajectories, and many of these studies are currently underway.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Diagnostic formulations attempt to impose order on the messy reality of psychopathological phenomena. By doing this, so their advocates argue, they provide both the platform necessary for systematic scientific study, and, crucially, the bridge of shared terms and concepts vital if psychiatric science is to be truly translational; where scientific endeavour is guided by clinical priorities and, in-turn, scientific findings innovate clinical practice. The diagnostic schemes we currently work with, taking DSM-5 as the obvious case, are the product of an interesting historical process of ongoing revision – at the same time pragmatic and scientific. On the one hand, it is a process both anchored firmly in historical precedent and constrained by the practical needs of clinicians, patients and health insurance companies. On the other hand, it is a process open to new empirical data about how to best cluster symptomatic expressions and differentiate clinical presentations – so that over historical time diagnostic categories achieve an increasingly accurate mapping of the taxonomy (i.e., underlying structure), and related pathophysiology, of psychiatric phenomenon. Resolving the inevitable tensions that arise when trying to reconcile these pragmatic (economic and professional) and scientific priorities has proved to be both challenging and contentious. The study of heterogeneity as exemplified by the articles highlighted in this editorial indicate a range of different approaches that can be effectively used to refine psychiatric taxonomies by incorporating developmental and pathophysiological data to help identify new putative subtypes of potential therapeutic significance.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: In order to shed more light on the frequent co-occurrence of Autism Spectrum Disorder (ASD) and anxiety in children, the aims of the study were (a) to examine whether ASD and anxiety share familial transmission indicated by cross-symptom associations between parental and children's symptoms (e.g., parental anxiety predicting children's ASD) in addition to associations for similar symptoms; (b) to investigate the possibility that cross-assortative mating (i.e., whether ASD symptoms in one parent are positively associated with anxiety symptoms in the other parent) increases the risk for both ASD and anxiety in children. Method: In 231 families of clinically referred children, parents rated both their own and the other parent's ASD and anxiety symptoms and one parent those of the index child and siblings (n = 447, aged 2.5-18 years). ASD symptoms were assessed using the Social Responsiveness Scale (SRS-2) and anxiety symptoms using the Achenbach System of Empirically Based Assessment (ASEBA) instruments. Results: Parental ASD and anxiety symptoms predicted similar symptoms in children, dependent on the informant type. Additionally, parental anxiety symptoms across both self-report and informant-report predicted children's ASD symptoms and maternal self-reported ASD symptoms predicted children's anxiety symptoms. ASD and anxiety symptoms were correlated within parents, but we found only one cross-symptom association between parents. Conclusions: Cross-symptom associations between parental and children's ASD and anxiety symptoms suggest shared familial transmission of ASD and anxiety, but further research is needed to clarify the underlying mechanisms. Cross-assortative mating does not seem a likely explanation for the co-occurrence of ASD and anxiety in children.
    No preview · Article · Dec 2015 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: Research has suggested that 'risky' family processes have unforeseen negative consequences for health later in life. The purpose of this study was to further understanding of risky family environments and development of health vulnerabilities by (a) examining the likelihood that elevated levels of parental depressive symptoms when children are age 11 forecast accelerated epigenetic aging 9 years later at age 20; (b) determining whether participation in an efficacious family-centered prevention program focused on enhancing supportive parenting and strengthening family relationships will ameliorate this association; and (c) testing a moderation-mediation hypothesis that prevention-induced reductions in harsh parenting across adolescence will account for prevention effects in reducing accelerated epigenetic aging. Methods: In the rural southeastern United States, parents and 11-year-old children from 399 families participated in the Strong African American Families (SAAF) program or a control condition. Parents reported their own depressive symptoms when their children were 11, and both youths and parents reported youth exposure to harsh parenting at ages 11 and 16. Blood was drawn from youths at age 20 to measure accelerated epigenetic aging using a marker derived from the DNA methylation of cells. Results: Elevated parental depressive symptoms forecast accelerated epigenetic aging among youths in the control condition, but not among SAAF participants. Moderated-mediation analyses confirmed that reductions in harsh parenting accounted for SAAF's protective effects on epigenetic aging. Subsequent exploratory analyses indicated that accelerated epigenetic aging forecast emotional distress among young adults in the control condition but not among those who participated in SAAF. Conclusions: This study is unique in using a randomized prevention trial to test hypotheses about the ways risky family processes contribute to accelerated epigenetic aging. The results suggest that developmentally appropriate family-centered interventions designed to enhance parenting and strengthen families can buffer the biological residue of life in a risky family.
    No preview · Article · Dec 2015 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Background: Children with language impairment (LI) show heterogeneity in development. We tracked children from pre-school to middle childhood to characterize three developmental trajectories: resolving, persisting and emerging LI. Methods: We analyzed data from children identified as having preschool LI, or being at family risk of dyslexia, together with typically developing controls at three time points: t1 (age 3;09), t3 (5;08) and t5 (8;01). Language measures are reported at t1, t3 and t5, and literacy abilities at t3 and t5. A research diagnosis of LI (irrespective of recruitment group) was validated at t1 by a composite language score derived from measures of receptive and expressive grammar and vocabulary; a score falling 1SD below the mean of the typical language group on comparable measures at t3 and t5 was used to determine whether a child had LI at later time points and then to classify LIs as resolving, persisting or emerging. Results: Persisting preschool LIs were more severe and pervasive than resolving LIs. Language and literacy outcomes were relatively poor for those with persisting LI, and relatively good for those with resolving LI. A significant proportion of children with average language abilities in preschool had LIs that emerged in middle childhood - a high proportion of these children were at family risk of dyslexia. There were more boys in the persisting and resolving LI groups. Children with early LIs which resolved by the start of formal literacy instruction tended to have good literacy outcomes; children with late-emerging difficulties that persisted developed reading difficulties. Conclusions: Children with late-emerging LI are relatively common and are hard to detect in the preschool years. Our findings show that children whose LIs persist to the point of formal literacy instruction frequently experience reading difficulties.
    No preview · Article · Dec 2015 · Journal of Child Psychology and Psychiatry