Guilherme V. Polanczyk

Annual research review: A meta-analysis of the worldwide prevalence of mental disorders in children and adolescents.

BACKGROUND The literature on the prevalence of mental disorders affecting children and adolescents has expanded significantly over the last three decades around the world. Despite the field having matured significantly, there has been no meta-analysis to calculate a worldwide-pooled prevalence and to empirically assess the sources of heterogeneity of estimates. METHODS We conducted a systematic review of the literature searching in PubMed, PsycINFO, and EMBASE for prevalence studies of mental disorders investigating probabilistic community samples of children and adolescents with standardized assessments methods that derive diagnoses according to the DSM or ICD. Meta-analytical techniques were used to estimate the prevalence rates of any mental disorder and individual diagnostic groups. A meta-regression analysis was performed to estimate the effect of population and sample characteristics, study methods, assessment procedures, and case definition in determining the heterogeneity of estimates. RESULTS We included 41 studies conducted in 27 countries from every world region. The worldwide-pooled prevalence of mental disorders was 13.4% (CI 95% 11.3-15.9). The worldwide prevalence of any anxiety disorder was 6.5% (CI 95% 4.7-9.1), any depressive disorder was 2.6% (CI 95% 1.7-3.9), attention-deficit hyperactivity disorder was 3.4% (CI 95% 2.6-4.5), and any disruptive disorder was 5.7% (CI 95% 4.0-8.1). Significant heterogeneity was detected for all pooled estimates. The multivariate metaregression analyses indicated that sample representativeness, sample frame, and diagnostic interview were significant moderators of prevalence estimates. Estimates did not vary as a function of geographic location of studies and year of data collection. The multivariate model explained 88.89% of prevalence heterogeneity, but residual heterogeneity was still significant. Additional meta-analysis detected significant pooled difference in prevalence rates according to requirement of funcional impairment for the diagnosis of mental disorders. CONCLUSIONS Our findings suggest that mental disorders affect a significant number of children and adolescents worldwide. The pooled prevalence estimates and the identification of sources of heterogeneity have important implications to service, training, and research planning around the world.

Epidemiology of attention-deficit/hyperactivity disorder across the lifespan.

Purpose of review Prevalence estimates of the attention-deficit hyperactivity disorder (ADHD) and the rate of persistence of symptoms across the lifespan are heterogeneous, raising questions about the validity of the diagnosis. This review aims to discuss potential reasons for variability in ADHD prevalence estimates and rates of symptom persistence, as well as to present ADHD prevalence rates during the lifespan. Recent findings The best available estimates of ADHD prevalence are around 5.29% for children and adolescents and 4.4% in adulthood. Estimates of ADHD prevalence and rate of symptom persistence over time seem to be highly affected by methodological characteristics of the studies. Summary The review of ADHD epidemiology highlights the need for standardizing study methodologies to make findings comparable. Even so, epidemiological cross-national data seem to support the validity of ADHD.

Childhood Trauma and Children’s Emerging Psychotic Symptoms: A Genetically Sensitive Longitudinal Cohort Study

OBJECTIVE Using longitudinal and prospective measures of trauma during childhood, the authors assessed the risk of developing psychotic symptoms associated with maltreatment, bullying, and accidents in a nationally representative U.K. cohort of young twins. METHOD Data were from the Environmental Risk Longitudinal Twin Study, which follows 2,232 twin children and their families. Mothers were interviewed during home visits when children were ages 5, 7, 10, and 12 on whether the children had experienced maltreatment by an adult, bullying by peers, or involvement in an accident. At age 12, children were asked about bullying experiences and psychotic symptoms. Childrens reports of psychotic symptoms were verified by clinicians. RESULTS Children who experienced mal-treatment by an adult (relative risk=3.16, 95% CI=1.92-5.19) or bullying by peers (relative risk=2.47, 95% CI=1.74-3.52) were more likely to report psychotic symptoms at age 12 than were children who did not experience such traumatic events. The higher risk for psychotic symptoms was observed whether these events occurred early in life or later in childhood. The risk associated with childhood trauma remained significant in analyses controlling for childrens gender, socioeconomic deprivation, and IQ; for childrens early symptoms of internalizing or externalizing problems; and for childrens genetic liability to developing psychosis. In contrast, the risk associated with accidents was small (relative risk=1.47, 95% CI=1.02-2.13) and inconsistent across ages. CONCLUSIONS Trauma characterized by intention to harm is associated with childrens reports of psychotic symptoms. Clinicians working with children who report early symptoms of psychosis should inquire about traumatic events such as maltreatment and bullying.

Protective effect of CRHR1 gene variants on the development of adult depression following childhood maltreatment: Replication and extension

CONTEXT A previous study reported a gene x environment interaction in which a haplotype in the corticotropin-releasing hormone receptor 1 gene (CRHR1) was associated with protection against adult depressive symptoms in individuals who were maltreated as children (as assessed by the Childhood Trauma Questionnaire [CTQ]). OBJECTIVE To replicate the interaction between childhood maltreatment and a TAT haplotype formed by rs7209436, rs110402, and rs242924 in CRHR1, predicting adult depression. DESIGN Two prospective longitudinal cohort studies. SETTING England and New Zealand. PARTICIPANTS Participants in the first sample were women in the E-Risk Study (N = 1116), followed up to age 40 years with 96% retention. Participants in the second sample were men and women in the Dunedin Study (N = 1037), followed up to age 32 years with 96% retention. Main Outcome Measure Research diagnoses of past-year and recurrent major depressive disorder. RESULTS In the E-Risk Study, the TAT haplotype was associated with a significant protective effect. In this effect, women who reported childhood maltreatment on the CTQ were protected against depression. In the Dunedin Study, which used a different type of measure of maltreatment, this finding was not replicated. CONCLUSIONS A haplotype in CRHR1 has been suggested to exert a protective effect against adult depression among research participants who reported maltreatment on the CTQ, a measure that elicits emotional memories. This suggests the hypothesis that CRHR1s protective effect may relate to its function in the consolidation of memories of emotionally arousing experiences.

Is Adult ADHD a Childhood-Onset Neurodevelopmental Disorder? Evidence From a Four-Decade Longitudinal Cohort Study

OBJECTIVE Despite a prevailing assumption that adult ADHD is a childhood-onset neurodevelopmental disorder, no prospective longitudinal study has described the childhoods of the adult ADHD population. The authors report follow-back analyses of ADHD cases diagnosed in adulthood, alongside follow-forward analyses of ADHD cases diagnosed in childhood, in one cohort. METHOD Participants belonged to a representative birth cohort of 1,037 individuals born in Dunedin, New Zealand, in 1972 and 1973 and followed to age 38, with 95% retention. Symptoms of ADHD, associated clinical features, comorbid disorders, neuropsychological deficits, genome-wide association study-derived polygenic risk, and life impairment indicators were assessed. Data sources were participants, parents, teachers, informants, neuropsychological test results, and administrative records. Adult ADHD diagnoses used DSM-5 criteria, apart from onset age and cross-setting corroboration, which were study outcome measures. RESULTS As expected, childhood ADHD had a prevalence of 6% (predominantly male) and was associated with childhood comorbid disorders, neurocognitive deficits, polygenic risk, and residual adult life impairment. Also as expected, adult ADHD had a prevalence of 3% (gender balanced) and was associated with adult substance dependence, adult life impairment, and treatment contact. Unexpectedly, the childhood ADHD and adult ADHD groups comprised virtually nonoverlapping sets; 90% of adult ADHD cases lacked a history of childhood ADHD. Also unexpectedly, the adult ADHD group did not show tested neuropsychological deficits in childhood or adulthood, nor did they show polygenic risk for childhood ADHD. CONCLUSIONS The findings raise the possibility that adults presenting with the ADHD symptom picture may not have a childhood-onset neurodevelopmental disorder. If this finding is replicated, then the disorders place in the classification system must be reconsidered, and research must investigate the etiology of adult ADHD.

Etiological and clinical features of childhood psychotic symptoms: results from a birth cohort

CONTEXT It has been reported that childhood psychotic symptoms are common in the general population and may signal neurodevelopmental processes that lead to schizophrenia. However, it is not clear whether these symptoms are associated with the same extensive risk factors established for adult schizophrenia. OBJECTIVE To examine the construct validity of childrens self-reported psychotic symptoms by testing whether these symptoms share the risk factors and clinical features of adult schizophrenia. DESIGN Prospective, longitudinal cohort study of a nationally representative birth cohort in Great Britain. PARTICIPANTS A total of 2232 twelve-year-old children followed up since age 5 years (retention, 96%). Main Outcome Measure Childrens self-reported hallucinations and delusions. RESULTS Childrens psychotic symptoms are familial and heritable and are associated with social risk factors (eg, urbanicity); cognitive impairments at age 5; home-rearing risk factors (eg, maternal expressed emotion); behavioral, emotional, and educational problems at age 5; and comorbid conditions, including self-harm. CONCLUSIONS The results provide a comprehensive picture of the construct validity of childrens self-reported psychotic symptoms. For researchers, the findings indicate that children who have psychotic symptoms can be recruited for neuroscience research to determine the pathogenesis of schizophrenia. For clinicians, the findings indicate that psychotic symptoms in childhood are often a marker of an impaired developmental process and should be actively assessed.

Is the α-2A adrenergic receptor gene (ADRA2A) associated with attention-deficit/hyperactivity disorder?

Attention‐Deficit/Hyperactivity Disorder (ADHD) is a complex childhood‐onset psychiatric disorder characterized by marked symptoms of inattention, hyperactivity, and impulsivity. The role of genetic factors in its etiology is strongly supported by family, adoption, and twin studies. Although most of the molecular studies have investigated the dopamine D4 receptor gene (DRD4) and the dopamine transporter gene (DAT1) genes in its etiology, pharmacological and brain imaging evidences seem to indicate that genes of the adrenergic system could also be attractive for association studies. We investigated a sample of 96 Brazilian ADHD children and adolescents and their parents for the ADRA2A MspI polymorphism. Although no association with either MspI allele was observed through the haplotype relative risk (HRR) analysis, effects of the ADRA2A gene on inattention and combined (inattention + hyperactivity/impulsivity) symptom scores were detected (U = 222.5, z = 2.19, P = 0.03; and U = 208.5, z = 2.32, P = 0.02, respectively). Our results suggest that the ADRA2A gene might have a small effect on ADHD susceptibility or that this gene might modulate the severity of the disorder. They are also consistent with the noradrenergic theories of ADHD, suggesting a role for the α2A adrenergic receptors in the disorder.

Evaluation of the Persistence, Remission, and Emergence of Attention-Deficit/Hyperactivity Disorder in Young Adulthood

IMPORTANCE Attention-deficit/hyperactivity disorder (ADHD) is now recognized to occur in adulthood and is associated with a range of negative outcomes. However, less is known about the prospective course of ADHD into adulthood, the risk factors for its persistence, and the possibility of its emergence in young adulthood in nonclinical populations. OBJECTIVE To investigate childhood risk factors and young adult functioning of individuals with persistent, remitted, and late-onset young adult ADHD. DESIGN, SETTING, AND PARTICIPANTS The study sample was the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins born in England and Wales from January 1, 1994, to December 4, 1995. Evaluation of childhood ADHD (ages 5, 7, 10, and 12 years) included prenatal and perinatal factors, clinical characteristics, and aspects of the family environment. Among participants aged 18 years, ADHD symptoms and associated impairment, overall functioning, and other mental health disorders were examined. Data analysis was conducted from February 19 to September 10, 2015. MAIN OUTCOMES AND MEASURES Attention-deficit/hyperactivity disorder according to DSM-IV diagnostic criteria in childhood and DSM-5 diagnostic criteria in young adulthood. RESULTS Of 2232 participants in the E-Risk Study, 2040 were included in the present analysis. In total, 247 individuals met diagnostic criteria for childhood ADHD; of these, 54 (21.9%) also met diagnostic criteria for the disorder at age 18 years. Persistence was associated with more symptoms (odds ratio [OR], 1.11 [95% CI, 1.04-1.19]) and lower IQ (OR, 0.98 [95% CI, 0.95-1.00]). At age 18 years, individuals with persistent ADHD had more functional impairment (school/work: OR, 3.30 [95% CI, 2.18-5.00], home/with friends: OR, 6.26 [95% CI, 3.07-12.76]), generalized anxiety disorder (OR, 5.19 [95% CI, 2.01-13.38]), conduct disorder (OR, 2.03 [95% CI, 1.03-3.99]), and marijuana dependence (OR, 2.88 [95% CI, 1.07-7.71]) compared with those whose ADHD remitted. Among 166 individuals with adult ADHD, 112 (67.5%) did not meet criteria for ADHD at any assessment in childhood. Results from logistic regressions indicated that individuals with late-onset ADHD showed fewer externalizing problems (OR, 0.93 [95% CI, 0.91-0.96]) and higher IQ (OR, 1.04 [95% CI, 1.02-1.07]) in childhood compared with the persistent group. However, at age 18 years, those with late-onset ADHD demonstrated comparable ADHD symptoms and impairment as well as similarly elevated rates of mental health disorders. CONCLUSIONS AND RELEVANCE We identified heterogeneity in the DSM-5 young adult ADHD population such that this group consisted of a large, late-onset ADHD group with no childhood diagnosis, and a smaller group with persistent ADHD. The extent to which childhood-onset and late-onset adult ADHD may reflect different causes has implications for genetic studies and treatment of ADHD.

Factor and Latent Class Analysis of DSM-IV ADHD Symptoms in a School Sample of Brazilian Adolescents

OBJECTIVE To evaluate the validity of the multidimensional construct proposed by DSM-IV for the diagnosis of attention-deficit/hyperactivity disorder (ADHD) in a school sample of young Brazilian adolescents. METHOD An instrument including all 18 DSM-IVADHD symptoms was administered to 1,013 students aged 12 to 14 years at 64 state schools by trained research assistants. Each symptom was rated on a Likert scale with five levels of severity (never, almost never, sometimes, frequently, and always). RESULTS Using an exploratory factor analytic approach (principal components analysis), two factors were extracted. Factor I (hyperactivity-impulsivity) comprised eight DSM-IV hyperactive-impulsive symptoms with loadings > or =0.40. Factor II (inattention) included also eight DSM-IV symptoms of inattention. The two factors explained 34% of the total variance and had an interfactor correlation of 0.45. Latent class analysis demonstrated similar classes in males and females, but class structures were markedly different from previous analyses of parent report data. CONCLUSION The findings support the appropriateness of the multidimensional construct introduced by DSM-IV in the diagnosis of ADHD in a different culture but emphasize the possible impact of different reporters on the results of structural model-testing.

Evidence-based information on the clinical use of neurofeedback for ADHD.

SummaryNeurofeedback (NF) is a training to enhance self-regulatory capacity over brain activity patterns and consequently over brain mental states. Recent findings suggest that NF is a promising alternative for the treatment of attention-deficit/hyperactivity disorder (ADHD). We comprehensively reviewed literature searching for studies on the effectiveness and specificity of NF for the treatment of ADHD. In addition, clinically informative evidence-based data are discussed. We found 3 systematic review on the use of NF for ADHD and 6 randomized controlled trials that have not been included in these reviews. Most nonrandomized controlled trials found positive results with medium-to-large effect sizes, but the evidence for effectiveness are less robust when only randomized controlled studies are considered. The direct comparison of NF and sham-NF in 3 published studies have found no group differences, nevertheless methodological caveats, such as the quality of the training protocol used, sample size, and sample selection may have contributed to the negative results. Further data on specificity comes from electrophysiological studies reporting that NF effectively changes brain activity patterns. No safety issues have emerged from clinical trials and NF seems to be well tolerated and accepted. Follow-up studies support long-term effects of NF. Currently there is no available data to guide clinicians on the predictors of response to NF and on optimal treatment protocol. In conclusion, NF is a valid option for the treatment for ADHD, but further evidence is required to guide its use.