Blog
About

  • Record: found
  • Abstract: found
  • Article: not found

Attention-deficit/hyperactivity disorder.

Read this article at

ScienceOpenPublisherPubMed
Bookmark
      There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

      Abstract

      Attention-deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder that affects 5% of children and adolescents and 2.5% of adults worldwide. Throughout an individual's lifetime, ADHD can increase the risk of other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. In most cases ADHD arises from several genetic and environmental risk factors that each have a small individual effect and act together to increase susceptibility. The multifactorial causation of ADHD is consistent with the heterogeneity of the disorder, which is shown by its extensive psychiatric co-morbidity, its multiple domains of neurocognitive impairment and the wide range of structural and functional brain anomalies associated with it. The diagnosis of ADHD is reliable and valid when evaluated with standard criteria for psychiatric disorders. Rating scales and clinical interviews facilitate diagnosis and aid screening. The expression of symptoms varies as a function of patient developmental stage and social and academic contexts. Although there are no curative treatments for ADHD, evidenced-based treatments can markedly reduce its symptoms and associated impairments. For example, medications are efficacious and normally well tolerated, and various non-pharmacological approaches are also valuable. Ongoing clinical and neurobiological research holds the promise of advancing diagnostic and therapeutic approaches to ADHD. For an illustrated summary of this Primer, visit: http://go.nature.com/J6jiwl.

      Related collections

      Most cited references 233

      • Record: found
      • Abstract: found
      • Article: not found

      Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis.

      Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories. We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia. We analysed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders in 33,332 cases and 27,888 controls of European ancestory. To characterise allelic effects on each disorder, we applied a multinomial logistic regression procedure with model selection to identify the best-fitting model of relations between genotype and phenotype. We examined cross-disorder effects of genome-wide significant loci previously identified for bipolar disorder and schizophrenia, and used polygenic risk-score analysis to examine such effects from a broader set of common variants. We undertook pathway analyses to establish the biological associations underlying genetic overlap for the five disorders. We used enrichment analysis of expression quantitative trait loci (eQTL) data to assess whether SNPs with cross-disorder association were enriched for regulatory SNPs in post-mortem brain-tissue samples. SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10(-8)) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2. Model selection analysis supported effects of these loci for several disorders. Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity. Polygenic risk scores showed cross-disorder associations, notably between adult-onset disorders. Pathway analysis supported a role for calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of cross-disorder association were enriched for brain eQTL markers. Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology. These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause. National Institute of Mental Health. Copyright © 2013 Elsevier Ltd. All rights reserved.
        Bookmark
        • Record: found
        • Abstract: found
        • Article: not found

        Validity of the executive function theory of attention-deficit/hyperactivity disorder: a meta-analytic review.

        One of the most prominent neuropsychologic theories of attention-deficit/hyperactivity disorder (ADHD) suggests that its symptoms arise from a primary deficit in executive functions (EF), defined as neurocognitive processes that maintain an appropriate problem-solving set to attain a later goal. To examine the validity of the EF theory, we conducted a meta-analysis of 83 studies that administered EF measures to groups with ADHD (total N = 3734) and without ADHD (N = 2969). Groups with ADHD exhibited significant impairment on all EF tasks. Effect sizes for all measures fell in the medium range (.46-.69), but the strongest and most consistent effects were obtained on measures of response inhibition, vigilance, working memory, and planning. Weaknesses in EF were significant in both clinic-referred and community samples and were not explained by group differences in intelligence, academic achievement, or symptoms of other disorders. ADHD is associated with significant weaknesses in several key EF domains. However, moderate effect sizes and lack of universality of EF deficits among individuals with ADHD suggest that EF weaknesses are neither necessary nor sufficient to cause all cases of ADHD. Difficulties with EF appear to be one important component of the complex neuropsychology of ADHD.
          Bookmark
          • Record: found
          • Abstract: not found
          • Article: not found

          Grand challenges in global mental health.

            Bookmark

            Author and article information

            Affiliations
            [1 ] Departments of Psychiatry and of Neuroscience and Physiology, State University of New York (SUNY) Upstate Medical University, Syracuse, New York 13210, USA.
            [2 ] K.G. Jebsen Centre for Psychiatric Disorders, Department of Biomedicine, University of Bergen, 5020 Bergen, Norway.
            [3 ] Social Genetic and Developmental Psychiatry, Institute of Psychiatry Psychology and Neuroscience, King's College London, London, UK.
            [4 ] Department of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
            [5 ] Department of Psychiatry, Harvard Medical School, Massachusetts General Hospital, Pediatric Psychopharmacology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
            [6 ] Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Department of Cognitive Neuroscience and Karakter Child and Adolescent Psychiatry University Centre, Nijmegen, The Netherlands.
            [7 ] ADHD Program, Department of Psychiatry, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
            [8 ] Biomedical Network Research Centre on Mental Health (CIBERSAM), Barcelona, Spain.
            [9 ] Department of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
            [10 ] ADHD Outpatient Program, Hospital de Clinicas de Porto Alegre, Department of Psychiatry, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
            [11 ] National Institute of Developmental Psychiatry for Children and Adolescents, Sao Paulo, Brazil.
            [12 ] Department of Psychology, University of Southampton, Southampton, UK.
            [13 ] Department of Experimental Clinical and Health Psychology, Ghent University, Ghent, Belgium.
            [14 ] Neuroscience and Mental Health Research Program, Research Institute of The Hospital for Sick Children, Toronto, Canada.
            [15 ] Department of Applied Psychology and Human Development, Ontario Institute for Studies in Education, University of Toronto, Toronto, Ontario, Canada.
            [16 ] Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Human Genetics and Psychiatry, Nijmegen, The Netherlands.
            Journal
            Nat Rev Dis Primers
            Nature reviews. Disease primers
            Springer Nature
            2056-676X
            2056-676X
            August 06 2015
            : 1
            27189265
            nrdp201520
            10.1038/nrdp.2015.20

            Comments

            Comment on this article