Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as an early onset childhood neurodevelopmental disorder. Prevalence in adults is around two-thirds that in childhood, yet longitudinal outcome studies of children with ADHD found a minority continue to meet full criteria in adulthood. This suggests that not all adult cases meet ADHD criteria as children, a conclusion supported by earlier studies relying on retrospective recall in adolescent and adult samples. More recently prospective follow-up of population and control samples suggest that adolescent and young adult ADHD is not always a continuation of childhood ADHD. Here, we review the literature on age of onset, to explore whether late-onset ADHD exists, and if so, examine the evidence for whether this should be considered the same or a different disorder as childhood onset ADHD. We conclude that current evidence supports the view that a significant proportion of young adults meeting criteria for ADHD would not have met full diagnostic criteria for ADHD as children. However, many in the late-onset group show some ADHD symptoms in childhood, or an externalizing disorder such as oppositional defiant disorder. Furthermore, the current studies suggest that most (but not all) cases of late-onset ADHD develop the disorder between the ages of 12-16 and can therefore be considered adolescent or early adult onset ADHD. There is a relative lack of data spanning young to older adulthood to address the question of adult-onset. Currently, there is insufficient data to clarify the extent to which early and late onset ADHD reflect a different balance of genetic and environmental risks or share the same underlying neural mechanisms. Clinicians should be aware that significantly impairing forms of ADHD can emerge beyond the age of 12 years, although perhaps rarely in the context of a complete absence of precursors. The current evidence on treatment responses is limited.
Important advances in understanding traumatic stress reactions in children and young people have been made in recent years. The aim of this review was to synthesise selected recent research findings, with a focus on their relevance to clinical practice. We therefore address: findings on the epidemiology of trauma exposure and Posttraumatic Stress Disorder (PTSD); recent changes to diagnostic classification; implications for screening and assessment of traumatic stress reactions; and treatment outcome studies including interventions for acute and chronic PTSD, dissemination of effective treatments into community settings, and early interventions. We conclude with recommendations for clinical practice and suggestions for future areas of research.
Patrick A. Smith, Tim Dalgleish, Richard Meiser‐Stedman
BACKGROUND: The rate of various anxiety disorders in early childhood and whether they continue into middle childhood or adolescence is not known. We therefore report on the prevalence and stability of DSM-5-defined anxiety disorders and their symptoms, capturing the period from preschool to adolescence. METHODS: By means of interviewer-based clinical interviews, anxiety was measured in a sample of Norwegian children at six measurement points from age 4 to 14 (n = 1,041). To adjust for time-invariant factors, we applied random intercept cross-lagged panel models (RI-CLPMs) capturing within-person changes. RESULTS: Nearly 10% (95% CI = 7.29, 12.63) had an anxiety disorder at some timepoint. Specific phobia was the most prevalent disorder in early and middle childhood, whereas generalized anxiety disorder (GAD) increased in prevalence and became the most common anxiety disorder at age 14 (4.51%, 95% CI = 2.78, 6.23). When time-invariant confounding was adjusted for, homotypic continuity in anxiety symptoms typically first emerged in late middle childhood or adolescence. Even so, such within-person analyses revealed a heterotypic path from increased number of early childhood symptoms of specific phobia to increased number of GAD symptoms in middle childhood (B = .41, 95% CI = .06, .75). Increased separation anxiety in middle childhood predicted increased symptoms of GAD in adolescence (B = .38, 95% CI = .14, .62), and vice versa (B = .05, 95% CI = .00, .09). Only minor gender differences were revealed. CONCLUSIONS: Anxiety disorders are prevalent in childhood. In early childhood, anxiety symptoms generally do not predict later anxiety symptoms. In middle childhood, however, such symptoms are less likely to vanish, indicating this developmental period to be particularly important for preventive and treatment efforts.
For the most part the science of neuro-developmental conditions, such as autism and ADHD, is conducted within a framework defined by a paradigm that assumes that these expressions of neuro-developmental variation are disorders resulting from brain dysfunction. the translational goal being to identify, then target, the source of such dysfunction to reduce disorder and resolve impairment. By shifting this perspective to one that defines such conditions as divergence in thought and action underpinned by brain atypicality, the neurodiversity paradigm offers a fresh scientific vision shaped by a new translational imperative. It shifts the focus of enquiry to understanding the way environments shape experience to either stifle or promote the well-being and development of neurodivergent people. It also encourages the fullest possible participation of neurodivergent people in the scientific process. Together these two elements provide a platform for a new translational science of neurodevelopment.
BACKGROUND: Low educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself. METHODS: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended-family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi-experimental extended children-of-twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self-reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old. RESULTS: Children of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations. CONCLUSIONS: Associations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems.
Fartein Ask Torvik, Espen Moen Eilertsen, Tom A. McAdams et al.
BACKGROUND: There has been recent systematic review of key evidence in psychosocial intervention in autism but little review of biological treatments. METHODS: We analyse the current literature from the perspective of intervention and mechanism targets across social and biological development. RESULTS: The overall quality of trials evidence in autism intervention remains relatively low, despite some recent progress. Many treatments in common use have little or no evidence base. This is very concerning in such an important disorder. A variety of psychosocial interventions can show effect to improve some short-term effects on children's immediate dyadic social interactions, for instance with caregivers. But showing true effectiveness in this developmental disorder requires generalisation of such effects into wider social contexts, on autism symptoms and in long-term progress in development. Only a few interventions so far have begun to show this. A number of early phase interventions on biological targets have shown real promise, but none has yet progressed to larger scale effectiveness trials on behavioural or symptom outcomes. CONCLUSIONS: There has been enough progress in psychosocial intervention research now to be able to begin to identify some evidence-based practice in autism treatment. To consolidate and improve outcomes, the next phase of intervention research needs improved trial design, and an iterative approach building on success. It may also include the testing of potential synergies between promising biological and psychosocial interventions.
BACKGROUND: Adolescence is a transition period characterized by heightened emotional reactivity, which for some sets the stage for emerging depressive symptoms. Prior studies suggest that adolescent depression is associated with deviant cortical and subcortical brain structure. Longitudinal studies are, however, currently scarce, but critical to detect which adolescents are at risk for developing depressive symptoms. METHODS: In this longitudinal study, a community sample of 205 participants underwent magnetic resonance imaging (MRI) in three biennial waves (522 scans) spanning 5 years across ages 8-25 years. Depressive symptomatology was assessed using self-report at the third time point. Mixed models were used to examine the relations between structural brain development, specifically regional change in cortical thickness, surface area and subcortical volumes (hippocampus and amygdala), and depressive symptoms. RESULTS: Accelerated frontal lobe cortical thinning was observed in adolescents who developed depressive symptoms at the third time point. This effect remained after controlling for parent-reported affective problems at the first time point. Moreover, the effect was driven by specific lateral orbitofrontal and precentral regions. In addition, differential developmental trajectories of parietal cortical thickness and surface area in several regions were found for participants reporting higher depressive symptomatology, but these results did not survive correction for multiple comparisons. Volumes or developmental volume changes in hippocampus or amygdala were not related to depressive symptoms. CONCLUSIONS: This study showed that emerging depression is associated with cortical thinning in frontal regions within individuals. These findings move beyond detecting cross-sectional correlations and set the stage for early detection, which may inform future intervention.
Marieke Geerte Nynke Bos, Sabine Peters, Ferdi C. van de Kamp et al.
BACKGROUND: Identifying low-cost and easy to implement measures of infant markers of later psychopathology may improve targeting of early intervention for prevention. Because of their early manifestation, relative stability and overlap with constructs central to affect-based dimensions of child and adolescent psychopathology, negative emotionality and self-regulation have been the focus of this research. We conducted a meta-analysis of longitudinal studies examining the prospective association between infant temperament measured with parent ratings and child/adolescent psychopathology. METHODS: A systematic literature search for prospective longitudinal studies, which included measures of questionnaire-assessed infant temperament (negative emotionality, self-regulation, behavioural inhibition, surgency/extraversion, activity level) and symptoms of child or adolescent mental health (externalising, internalising) and neurodevelopmental problems (attention deficit/hyperactivity disorder [ADHD], autism spectrum disorder [ASD]), was conducted. Standardised estimates of association were calculated and pooled in meta-analyses. RESULTS: Twenty-five studies (n = 28,425) met inclusion criteria. Small associations were seen between psychopathology aggregated across all domains and infant negative emotionality (r = .15; p < .001) and self-regulation (r = -.19; p = .007). Effects were also significant but weaker for behavioural inhibition (r = .10; p = .027) and activity level (r = .08; p = .016). Surgency/extraversion was not significantly associated with psychopathology in general (r = -.04; p = .094); however, it was negatively associated with ASD (r = -.10, p = .015). Significant correlations were observed with some outcomes isomorphic with predictors, internalising problems and behavioural inhibition (r = .10; p = .013), ADHD symptoms and activity level (r = .19; p = .009). CONCLUSION: Questionnaire-based assessments of infant negative emotionality may have transdiagnostic potential to contribute to a risk index of later childhood psychopathology. Behavioural inhibition, surgency/extraversion and activity ratings may provide more specific predictive power. More data from prospective studies are required before the potential of self-regulation and surgency/extraversion can be properly gauged.
Katarzyna Kostyrka‐Allchorne, Sam V. Wass, Edmund J. S. Sonuga-Barke
BACKGROUND: Child mental health problems are common. Previous studies have examined secular changes in their prevalence but have not assessed whether later outcomes have changed. We therefore aimed to test whether outcomes of child mental health problems have changed over a 40-year period. METHODS: Three cohorts were utilized: The National Child Development Study (NCDS: N = 14,544, aged 7 in 1965), the Avon Longitudinal Study of Parents and Children (ALSPAC: N = 8,188, aged 7 in 1998), and the Millennium Cohort Study (MCS: N = 13,192, aged 7 in 2008). Mental health problems at age 7 were identified using the parent-reported Rutter-A scale (NCDS) and Strengths and Difficulties Questionnaire (ALSPAC and MCS). Associated outcomes were compared across cohorts: age 11 social functioning, age 16 exam attainment and age 16 mental health. RESULTS: Child mental health problems were common in each cohort (boys: 7.0%-9.7%; girls: 5.4%-8.4%). Child mental health problems became more strongly associated with social functioning problems (boys: NCDS OR = 1.95 (1.50, 2.53), MCS OR = 3.77 (2.89, 4.92); interaction p < .001; girls: NCDS OR = 1.69 (1.22, 2.33), MCS OR = 3.99 (3.04, 5.25), interaction p < .001), lower academic attainment for boys (NCDS OR = 0.49 (0.31, 0.78), ALSPAC OR = 0.30 (0.22, 0.41), interaction p = .009), and age 16 mental health problems (boys: NCDS d' = 0.55 (0.38, 0.72), ALSPAC d' = 0.95 (0.73, 1.16); interaction p = .004; girls: NCDS d' = 0.50 (0.34, 0.65), ALSPAC d' = 0.99 (0.78, 1.20); interaction p < .001). CONCLUSIONS: Child mental health problems have become more strongly associated with negative social, educational and mental health outcomes in recent generations.
Ruth Sellers, Naomi Warne, Andrew R. Pickles et al.
BACKGROUND: Children with autism spectrum disorder (ASD) often have co-occurring symptoms of attention-deficit/hyperactivity disorder (ADHD) and/or anxiety. It is unclear whether these disorders arise from shared or distinct developmental pathways. We explored this question by testing the specificity of early-life (infant and toddler) predictors of mid-childhood ADHD and anxiety symptoms compared to ASD symptoms. METHODS: Infants (n = 104) at high and low familial risk for ASD took part in research assessments at 7, 14, 24 and 38 months, and 7 years of age. Symptoms of ASD, ADHD and anxiety were measured by parent report at age 7. Activity levels and inhibitory control, also measured by parent report, in infancy and toddlerhood were used as early-life predictors of ADHD symptoms. Fearfulness and shyness measured in infancy and toddlerhood were used as early-life predictors of anxiety symptoms. Correlations and path analysis models tested associations between early-life predictors and mid-childhood ADHD and anxiety symptoms compared to mid-childhood ASD symptoms, and the influence of controlling for ASD symptoms on those associations. RESULTS: Increased activity levels and poor inhibitory control were correlated with ADHD symptoms and not ASD or anxiety; these associations were unchanged in path models controlling for risk-group and ASD symptoms. Increased fearfulness and shyness were correlated with anxiety symptoms, but also ASD symptoms. When controlling for risk-group in path analysis, the association between shyness and anxiety became nonsignificant, and when further controlling for ASD symptoms the association between fearfulness and anxiety became marginal. CONCLUSIONS: The specificity of early-life predictors to ADHD symptoms suggests early developmental pathways to ADHD might be distinct from ASD. The overlap in early-life predictors of anxiety and ASD suggests that these disorders are difficult to differentiate early in life, which could reflect the presence of common developmental pathways or convergence in early behavioural manifestations of these disorders.
Elizabeth Shephard, Rachael Bedford, Bosiljka Milosavljevic et al.
