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1. Prognostic factors associated with failure of total elbow arthroplasty

Author

Hamoodi, Z., Gehringer, C. K., Bull, L. M., Hughes, T., Kearsley-Fleet, L., Sergeant, J. C., Watts, A. C., Hamoodi, Z., Gehringer, C. K., Bull, L. M., Hughes, T., Kearsley-Fleet, L., Sergeant, J. C., and Watts, A. C.

Abstract

Aims The aims of this study were to identify and evaluate the current literature examining the prognostic factors which are associated with failure of total elbow arthroplasty (TEA). Methods Electronic literature searches were conducted using MEDLINE, Embase, PubMed, and Cochrane. All studies reporting prognostic estimates for factors associated with the revision of a primary TEA were included. The risk of bias was assessed using the Quality In Prognosis Studies (QUIPS) tool, and the quality of evidence was assessed using the modified Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) framework. Due to low quality of the evidence and the heterogeneous nature of the studies, a narrative synthesis was used. Results A total of 19 studies met the inclusion criteria, investigating 28 possible prognostic factors. Most QUIPS domains (84%) were rated as moderate to high risk of bias. The quality of the evidence was low or very low for all prognostic factors. In low-quality evidence, prognostic factors with consistent associations with failure of TEA in more than one study were: the sequelae of trauma leading to TEA, either independently or combined with acute trauma, and male sex. Several other studies investigating sex reported no association. The evidence for other factors was of very low quality and mostly involved exploratory studies. Conclusion The current evidence investigating the prognostic factors associated with failure of TEA is of low or very low quality, and studies generally have a moderate to high risk of bias. Prognostic factors are subject to uncertainty, should be interpreted with caution, and are of little clinical value. Higher-quality evidence is required to determine robust prognostic factors for failure of TEA.

Published
2024

4. Mechanisms underpinning inattention and hyperactivity: Neurocognitive support for ADHD dimensionality

Author

Salum, GA, Sonuga-Barke, E, Sergeant, J, Vandekerckhove, J, Gadelha, A, Moriyama, TS, Graeff-Martins, AS, Manfro, GG, Polanczyk, G, and Rohde, LAP

Subjects
Psychiatry, Neurosciences, Public Health and Health Services, Psychology
Abstract

Background. Taxometric and behavioral genetic studies suggest that attention deficit hyperactivity disorder (ADHD) is best modeled as a dimension rather than a category. We extended these analyses by testing for the existence of putative ADHD-related deficits in basic information processing (BIP) and inhibitory-based executive function (IB-EF) in individuals in the subclinical and full clinical ranges. Consistent with the dimensional model, we predicted that ADHD-related deficits would be expressed across the full spectrum, with the degree of deficit linearly related to the severity of the clinical presentation. Method. A total of 1547 children (aged 6-12 years) participated in the study. The Development and Well-Being Assessment (DAWBA) was used to classify children into groups according to levels of inattention and hyperactivity independently: (1) asymptomatic, (2) subthreshold minimal, (3) subthreshold moderate and (4) clinical ADHD. Neurocognitive performance was evaluated using a two-choice reaction time task (2C-RT) and a conflict control task (CCT). BIP and IB-EF measures were derived using a diffusion model (DM) for decomposition of reaction time (RT) and error data. Results. Deficient BIP was found in subjects with minimal, moderate and full ADHD defined in terms of inattention (in both tasks) and hyperactivity/impulsivity dimensions (in the 2C-RT). The size of the deficit increased in a linear manner across increasingly severe presentations of ADHD. IB-EF was unrelated to ADHD. Conclusions. Deficits in BIP operate at subclinical and clinical levels of ADHD. The linear nature of this relationship provides support for a dimensional model of ADHD in which diagnostic thresholds are defined in terms of clinical and societal burden rather than representing discrete pathophysiological states.

Published
2014

8. European guidelines on managing adverse effects of medication for ADHD

Author

Graham, J., Banaschewski, T., Buitelaar, J., Coghill, D., Danckaerts, M., Dittmann, R. W., Döpfner, M., Hamilton, R., Hollis, C., Holtmann, M., Hulpke-Wette, M., Lecendreux, M., Rosenthal, E., Rothenberger, A., Santosh, P., Sergeant, J., Simonoff, E., Sonuga-Barke, E., Wong, I. C. K., Zuddas, A., Steinhausen, H.-C., Taylor, E., and (for the European Guidelines Group)

Published
2011
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10. Additional file 1 of Symptoms in first-degree relatives of patients with rheumatoid arthritis: evaluation of cross-sectional data from the symptoms in persons at risk of rheumatoid arthritis (SPARRA) questionnaire in the PRe-clinical EValuation of Novel Targets in RA (PREVeNT-RA) Cohort

Author

Costello, R. E., Humphreys, J. H., Sergeant, J. C., Haris, M., Stirling, F., Raza, K., van Schaardenburg, D., and Bruce, Ian N.

Subjects
musculoskeletal diseases, skin and connective tissue diseases
Abstract

Additional file 1:. Symptoms in Persons At Risk of Rheumatoid Arthritis (SPARRA) Questionnaire

Published
2021
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11. Additional file 2 of Symptoms in first-degree relatives of patients with rheumatoid arthritis: evaluation of cross-sectional data from the symptoms in persons at risk of rheumatoid arthritis (SPARRA) questionnaire in the PRe-clinical EValuation of Novel Targets in RA (PREVeNT-RA) Cohort

Author

Costello, R. E., Humphreys, J. H., Sergeant, J. C., Haris, M., Stirling, F., Raza, K., van Schaardenburg, D., and Bruce, Ian N.

Abstract

Additional file 2: Table 1 Specific details of seropositivty. Table 2 Characteristics and associations with symmetrical and small joint pain in females only. Table 3: Symptoms and associations with symmetrical and small joint pain in females only (N=631)

Published
2021
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12. A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16

Author

Asherson, P, Zhou, K, Anney, R J L, Franke, B, Buitelaar, J, Ebstein, R, Gill, M, Altink, M, Arnold, R, Boer, F, Brookes, K, Buschgens, C, Butler, L, Cambell, D, Chen, W, Christiansen, H, Feldman, L, Fleischman, K, Fliers, E, Howe-Forbes, R, Goldfarb, A, Heise, A, Gabriëls, I, Johansson, L, Lubetzki, I, Marco, R, Medad, S, Minderaa, R, Mulas, F, Müller, U, Mulligan, A, Neale, B, Rijsdijk, F, Rabin, K, Rommelse, N, Sethna, V, Sorohan, J, Uebel, H, Psychogiou, L, Weeks, A, Barrett, R, Xu, X, Banaschewski, T, Sonuga-Barke, E, Eisenberg, J, Manor, I, Miranda, A, Oades, R D, Roeyers, H, Rothenberger, A, Sergeant, J, Steinhausen, H-C, Taylor, E, Thompson, M, and Faraone, S V

Published
2008
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16. Co-transmission of conduct problems with attention-deficit/hyperactivity disorder: familial evidence for a distinct disorder

Author

Christiansen, H., Chen, W., Oades, R. D., Asherson, P., Taylor, E. A., Lasky-Su, J., Zhou, K., Banaschewski, T., Buschgens, C., Franke, B., Gabriels, I., Manor, I., Marco, R., Müller, U. C., Mulligan, A., Psychogiou, L., Rommelse, N. N. J., Uebel, H., Buitelaar, J., Ebstein, R. P., Eisenberg, J., Gill, M., Miranda, A., Mulas, F., Roeyers, H., Rothenberger, A., Sergeant, J. A., Sonuga-Barke, E. J. S., Steinhausen, H.-C., Thompson, M., and Faraone, S. V.

Published
2008
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19. The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder: association signals in DRD4, DAT1 and 16 other genes

Author

Brookes, K, Xu, X, Chen, W, Zhou, K, Neale, B, Lowe, N, Aneey, R, Franke, B, Gill, M, Ebstein, R, Buitelaar, J, Sham, P, Campbell, D, Knight, J, Andreou, P, Altink, M, Arnold, R, Boer, F, Buschgens, C, Butler, L, Christiansen, H, Feldman, L, Fleischman, K, Fliers, E, Howe-Forbes, R, Goldfarb, A, Heise, A, Gabriëls, I, Korn-Lubetzki, I, Marco, R, Medad, S, Minderaa, R, Mulas, F, Müller, U, Mulligan, A, Rabin, K, Rommelse, N, Sethna, V, Sorohan, J, Uebel, H, Psychogiou, L, Weeks, A, Barrett, R, Craig, I, Banaschewski, T, Sonuga-Barke, E, Eisenberg, J, Kuntsi, J, Manor, I, McGuffin, P, Miranda, A, Oades, R D, Plomin, R, Roeyers, H, Rothenberger, A, Sergeant, J, Steinhausen, H-C, Taylor, E, Thompson, M, Faraone, S V, Asherson, P, and Johansson, L

Published
2006
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27. The relationship between ADHD and key cognitive phenotypes is not mediated by shared familial effects with IQ

Author

Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., and Kuntsi, J.

Published
2011

36. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder

Author

Demontis, D, Walters, R, Martin, J, Mattheisen, M, Als, T, Agerbo, E, Baldursson, G, Belliveau, R, Bybjerg-Grauholm, J, Baekvad-Hansen, M, Cerrato, F, Chambert, K, Churchhouse, C, Dumont, A, Eriksson, N, Gandal, M, Goldstein, J, Grasby, K, Grove, J, Gudmundsson, O, Hansen, C, Hauberg, M, Hollegaard, M, Howrigan, D, Huang, H, Maller, J, Martin, A, Martin, N, Moran, J, Pallesen, J, Palmer, D, Pedersen, C, Pedersen, M, Poterba, T, Poulsen, J, Ripke, S, Robinson, E, Satterstrom, F, Stefansson, H, Stevens, C, Turley, P, Walters, G, Won, H, Wright, M, Andreassen, O, Asherson, P, Burton, C, Boomsma, D, Cormand, B, Dalsgaard, S, Franke, B, Gelernter, J, Geschwind, D, Hakonarson, H, Haavik, J, Kranzler, H, Kuntsi, J, Langley, K, Lesch, K, Middeldorp, C, Reif, A, Rohde, L, Roussos, P, Schachar, R, Sklar, P, Sonuga-Barke, E, Sullivan, P, Thapar, A, Tung, J, Waldman, I, Medland, S, Stefansson, K, Nordentoft, M, Hougaard, D, Werge, T, Mors, O, Mortensen, P, Daly, M, Faraone, S, Borglum, A, Neale, B, Albayrak, O, Anney, R, Arranz, M, Banaschewski, T, Bau, C, Biederman, J, Buitelaar, J, Casas, M, Charach, A, Crosbie, J, Dempfle, A, Doyle, A, Ebstein, R, Elia, J, Freitag, C, Focker, M, Gill, M, Grevet, E, Hawi, Z, Hebebrand, J, Herpertz-Dahlmann, B, Hervas, A, Hinney, A, Hohmann, S, Holmans, P, Hutz, M, Ickowitz, A, Johansson, S, Kent, L, Kittel-Schneider, S, Lambregts-Rommelse, N, Lehmkuhl, G, Loo, S, McGough, J, Meyer, J, Mick, E, Middletion, F, Miranda, A, Mota, N, Mulas, F, Mulligan, A, Nelson, F, Nguyen, T, Oades, R, O'Donovan, M, Owen, M, Palmason, H, Ramos-Quiroga, J, Renner, T, Ribases, M, Rietschel, M, Rivero, O, Romanos, J, Romanos, M, Rothenberger, A, Royers, H, Sanchez-Mora, C, Scherag, A, Schimmelmann, B, Schafer, H, Sergeant, J, Sinzig, J, Smalley, S, Steinhausen, H, Thompson, M, Todorov, A, Vasquez, A, Walitza, S, Wang, Y, Warnke, A, Williams, N, Witt, S, Yang, L, Zayats, T, Zhang-James, Y, Smith, G, Davies, G, Ehli, E, Evans, D, Fedko, I, Greven, C, Groen-Blokhuis, M, Guxens, M, Hammerschlag, A, Hartman, C, Heinrich, J, Hottenga, J, Hudziak, J, Jugessur, A, Kemp, J, Krapohl, E, Murcia, M, Myhre, R, Nolte, I, Nyholt, D, Ormel, J, Ouwens, K, Pappa, I, Pennell, C, Plomin, R, Ring, S, Standl, M, Stergiakouli, E, St Pourcain, B, Stoltenberg, C, Sunyer, J, Thiering, E, Tiemeier, H, Tiesler, C, Timpson, N, Trzaskowski, M, van der Most, P, Vilor-Tejedor, N, Wang, C, Whitehouse, A, Zhao, H, Agee, M, Alipanahi, B, Auton, A, Bell, R, Bryc, K, Elson, S, Fontanillas, P, Furlotte, N, Hinds, D, Hromatka, B, Huber, K, Kleinman, A, Litterman, N, McIntyre, M, Mountain, J, Northover, C, Pitts, S, Sathirapongsasuti, J, Sazonova, O, Shelton, J, Shringarpure, S, Tian, C, Vacic, V, Wilson, C, ADHD Working Grp Psychiat Genomics, Early Lifecourse Genetic, 23andMe Res Team, Institute for Molecular Medicine Finland, Centre of Excellence in Complex Disease Genetics, Psychiatrie & Neuropsychologie, RS: MHeNs - R3 - Neuroscience, Psychiatry, ADHD Working Group of the Psychiatric Genomics Consortium (PGC), 23andme Research Team, University of St Andrews. Cellular Medicine Division, University of St Andrews. Institute of Behavioural and Neural Sciences, University of St Andrews. School of Medicine, Child and Adolescent Psychiatry / Psychology, Erasmus MC other, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Life Course Epidemiology (LCE), Clinical Neuropsychology, Biological Psychology, APH - Health Behaviors & Chronic Diseases, APH - Mental Health, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Personalized Medicine, Clinical Child and Family Studies, LEARN! - Child rearing, and APH - Methodology

Subjects
Netherlands Twin Register (NTR), Male, Trastorns per dèficit d'atenció amb hiperactivitat en els infants, LD SCORE REGRESSION, Medizin, Genome-wide association study, US CHILDREN, Genoma humà, Attention deficit disorder with hyperactivity in children, Medical and Health Sciences, Cohort Studies, 0302 clinical medicine, 2.1 Biological and endogenous factors, POLYGENIC RISK, Aetiology, Child, IDENTIFIES 11, SEXUAL-BEHAVIOR, Early Lifecourse & Genetic Epidemiology (EAGLE) Consortium, Pediatric, 0303 health sciences, education.field_of_study, Genome, Genetic Predisposition to Disease/genetics, 1184 Genetics, developmental biology, physiology, Brain, 3rd-DAS, Single Nucleotide, Biological Sciences, Polymorphism, Single Nucleotide/genetics, 3. Good health, Mental Health, Meta-analysis, Child, Preschool, Genetic Loci/genetics, Genome-Wide Association Study/methods, Trastorns per dèficit d'atenció amb hiperactivitat en els adults, Attention Deficit Disorder (ADD), Female, Attention Deficit Disorder with Hyperactivity/genetics, RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry, SDG 4 - Quality Education, Clinical psychology, Risk, Adolescent, DEFICIT HYPERACTIVITY DISORDER, Concordance, Population, PROVIDES INSIGHTS, QH426 Genetics, Biology, Quantitative trait locus, Brain/physiology, Polymorphism, Single Nucleotide, 23andMe Research Team, behavioral disciplines and activities, Gene Expression Regulation/genetics, Article, 150 000 MR Techniques in Brain Function, GENETIC ARCHITECTURE, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, Clinical Research, Behavioral and Social Science, mental disorders, medicine, Genetics, Attention deficit hyperactivity disorder, Humans, Genetic Predisposition to Disease, Polymorphism, education, Preschool, QH426, 030304 developmental biology, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], ASSOCIATION METAANALYSIS, Prevention, Human Genome, Case-control study, MAJOR DEPRESSION, medicine.disease, Attention Deficit Hyperactivity Disorder (ADHD), Genetic architecture, Brain Disorders, ADHD Working Group of the Psychiatric Genomics Consortium, Gene Expression Regulation, Attention Deficit Disorder with Hyperactivity, Genetic Loci, RC0321, Attention deficit disorder with hyperactivity in adults, 3111 Biomedicine, 030217 neurology & neurosurgery, Genome-Wide Association Study, Developmental Biology
Abstract

Attention deficit/hyperactivity disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, finding important new information about the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes and around brain-expressed regulatory marks. Analyses of three replication studies: a cohort of individuals diagnosed with ADHD, a self-reported ADHD sample and a meta-analysis of quantitative measures of ADHD symptoms in the population, support these findings while highlighting study-specific differences on genetic overlap with educational attainment. Strong concordance with GWAS of quantitative population measures of ADHD symptoms supports that clinical diagnosis of ADHD is an extreme expression of continuous heritable traits. Postprint

Published
2019
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38. Test-retest reliability and correlations of 5 global measures addressing at-work productivity loss in patients with rheumatic diseases

Author

Leggett, S, Van Der Zee-Neuen, A, Boonen, A, Beaton, D, Bojinca, M, Bosworth, A, Dadoun, S, Fautrel, B, Hagel, S, Hofstetter, C, Lacaille, D, Linton, D, Mihai, C, Petersson, I, Rogers, P, Sergeant, J, Scire, C, Verstappen, S, Leggett S., Van Der Zee-Neuen A., Boonen A., Beaton D. E., Bojinca M., Bosworth A., Dadoun S., Fautrel B., Hagel S., Hofstetter C., Lacaille D., Linton D., Mihai C., Petersson I. F., Rogers P., Sergeant J. C., Scire CA., Verstappen S. M. M., Leggett, S, Van Der Zee-Neuen, A, Boonen, A, Beaton, D, Bojinca, M, Bosworth, A, Dadoun, S, Fautrel, B, Hagel, S, Hofstetter, C, Lacaille, D, Linton, D, Mihai, C, Petersson, I, Rogers, P, Sergeant, J, Scire, C, Verstappen, S, Leggett S., Van Der Zee-Neuen A., Boonen A., Beaton D. E., Bojinca M., Bosworth A., Dadoun S., Fautrel B., Hagel S., Hofstetter C., Lacaille D., Linton D., Mihai C., Petersson I. F., Rogers P., Sergeant J. C., Scire CA., and Verstappen S. M. M.

Abstract

Objective. Several global measures to assess at-work productivity loss or presenteeism in patients with rheumatic diseases have been proposed, but the comparative validity is hampered by the lack of data on test-retest reliability and comparative concurrent and construct validity. Our objective was to test-retest 5 global measures of presenteeism and to compare the association between these scales and health-related well-being. Methods. Sixty-five participants with inflammatory arthritis or osteoarthritis in paid employment were recruited from 7 countries (UK, Canada, Netherlands, France, Sweden, Romania, and Italy). At baseline and 2 weeks later, 5 global measures of presenteeism were evaluated: the Work Productivity Scale-Rheumatoid Arthritis (WPS-RA), Work Productivity and Activity Impairment Questionnaire (WPAI), Work Ability Index (WAI), Quality and Quantity questionnaire (QQ), and the WHO Health and Performance Questionnaire (HPQ). Agreement between the 2 timepoints was assessed using single-measure intraclass correlations (ICC) and correlated between each other and with visual analog scale general well-being scores at followup by Spearman correlation. Results. ICC between measures ranged from fair (HPQ 0.59) to excellent (WPS-RA 0.78). Spearman correlations between measures were moderate (Qquality vs WAI, r = 0.51) to strong (WPS-RA vs WPAI, r = 0.88). Correlations between measures and general well-being were low to moderate, ranging from-0.44 ? r ? 0.66. Conclusion. Test-retest results of 4 out of 5 global measures were good, and the correlations between these were moderate. The latter probably reflect differences in the concepts, recall periods, and references used in the measures, which implies that some measures are probably not interchangeable. The Journal of Rheumatology.

Published
2016

40. A Stages-of-Information Approach to Hyperactivity.

Author

Sergeant, J. A. and Scholten, C. A.

Abstract

In a memory search task with context recognition, three groups of children were examined: hyperactives, somewhat hyperactives, and controls. Both groups of hyperactive-rated children were slower in their cognitive processing than controls. (MP)

Published
1983

41. Using Smartphones for Research Outside Clinical Settings:How Operating Systems, App Developers, and Users Determine Geolocation Data Quality in mHealth Studies

Author

Beukenhorst, A L, Schultz, D M, McBeth, J, Lakshminarayana, R, Sergeant, J C, and Dixon, W G

Subjects
Journal Article
Abstract

Smartphones that collect user geolocation provid opportunities for mobile Health (mHealth). Although granularity of geolocation data may be high, data completeness depends on the device's operating system, application developer decisions, and user actions. We investigate completeness of geolocation data collected via smartphones of 5601 people that self-reported daily chronic pain symptoms on 349,293 days. On 17% of these days, hourly geolocation data is reported, but days with 0 (16%), 1 (14%) and 2 (13%) geolocations are common. Android phones collect geolocation more often than iPhones (median 17 versus 2 times a day). Factors on operating system level and individual user level influence completeness of geolocation data collected with smartphones. mHealth researchers should be aware of these factors when designing their studies. The mHealth research community should devise standards for reporting geolocation data quality, analysing systematic differences in data quality between participant groups, and methods for data imputation.

Published
2017
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42. Glutamatergic and GABAergic gene sets in attention-deficit/hyperactivity disorder: association to overlapping traits in ADHD and autism

Author

Naaijen, Jilly, Bralten, Janita, Poelmans, Geert, Faraone, Stephen, Asherson, Philip, Banaschewski, T, Buitelaar, J., Franke, B, Ebstein, R P, Gill, M., Miranda, A., Oades, R.D., Roevers, H., Rothenberger, A, Sergeant, J., Barke, Edmund James, Anney, R., Mulas, F, Steinhausen, H C, Glennon, JC, and Buitelaar, JK

Subjects
0301 basic medicine, Male, Candidate gene, Adolescent, Autism Spectrum Disorder, Medizin, Glutamic Acid, Nerve Tissue Proteins, Impulsivity, Receptors, Metabotropic Glutamate, Receptors, N-Methyl-D-Aspartate, Severity of Illness Index, behavioral disciplines and activities, 150 000 MR Techniques in Brain Function, 03 medical and health sciences, Cellular and Molecular Neuroscience, Glutamatergic, 0302 clinical medicine, mental disorders, medicine, Attention deficit hyperactivity disorder, Humans, Receptors, AMPA, Autistic Disorder, Child, Biological Psychiatry, gamma-Aminobutyric Acid, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Fusion Regulatory Protein 1, Light Chains, Calcium-Binding Proteins, Glutamate receptor, Amino Acid Transport System y+L, medicine.disease, Receptors, GABA-A, Psychiatry and Mental health, 030104 developmental biology, Schizophrenia, Attention Deficit Disorder with Hyperactivity, Child, Preschool, Autism, GABAergic, Original Article, Female, medicine.symptom, Psychology, Neuroscience, 030217 neurology & neurosurgery
Abstract

Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorders (ASD) often co-occur. Both are highly heritable; however, it has been difficult to discover genetic risk variants. Glutamate and GABA are main excitatory and inhibitory neurotransmitters in the brain; their balance is essential for proper brain development and functioning. In this study we investigated the role of glutamate and GABA genetics in ADHD severity, autism symptom severity and inhibitory performance, based on gene set analysis, an approach to investigate multiple genetic variants simultaneously. Common variants within glutamatergic and GABAergic genes were investigated using the MAGMA software in an ADHD case-only sample (n=931), in which we assessed ASD symptoms and response inhibition on a Stop task. Gene set analysis for ADHD symptom severity, divided into inattention and hyperactivity/impulsivity symptoms, autism symptom severity and inhibition were performed using principal component regression analyses. Subsequently, gene-wide association analyses were performed. The glutamate gene set showed an association with severity of hyperactivity/impulsivity (P=0.009), which was robust to correcting for genome-wide association levels. The GABA gene set showed nominally significant association with inhibition (P=0.04), but this did not survive correction for multiple comparisons. None of single gene or single variant associations was significant on their own. By analyzing multiple genetic variants within candidate gene sets together, we were able to find genetic associations supporting the involvement of excitatory and inhibitory neurotransmitter systems in ADHD and ASD symptom severity in ADHD.

Published
2017
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44. Erratum: The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder: association signals in DRD4, DAT1 and 16 other genes

Author

Brookes, K, Xu, X, Chen, W, Zhou, K, Neale, B, Lowe, N, Anney, R, Franke, B, Gill, M, Ebstein, R, Buitelaar, J, Sham, P, Campbell, D, Knight, J, Andreou, P, Altink, M, Arnold, R, Boer, F, Buschgens, C, Butler, L, Christiansen, H, Feldman, L, Fleischman, K, Fliers, E, Howe-Forbes, R, Goldfarb, A, Heise, A, Gabriëls, I, Korn-Lubetzki, I, Johansson, L, Marco, R, Medad, S, Minderaa, R, Mulas, F, Müller, U, Mulligan, A, Rabin, K, Rommelse, N, Sethna, V, Sorohan, J, Uebel, H, Psychogiou, L, Weeks, A, Barrett, R, Craig, I, Banaschewski, T, Sonuga-Barke, E, Eisenberg, J, Kuntsi, J, Manor, I, McGuffin, P, Miranda, A, Oades, R D, Plomin, R, Roeyers, H, Rothenberger, A, Sergeant, J, Steinhausen, H-C, Taylor, E, Thompson, M, Faraone, S V, and Asherson, P

Published
2006
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45. [Long-acting medications for the treatment of hyperkinetic disorders - a systematic review and European treatment guideline. Part 1: overview and recommendations]

Author

Banaschewski, T., Coghill, D., Santosh, P., Zuddas, A., Philip Asherson, Buitelaar, J., Danckerts, M., Dopfner, M., Faraone, S. V., Rothenberger, A., Sergeant, J., Steinhausen, H. C., Sonuga-Barke, E. J. S., and Taylor, E.

Subjects
Cognitive neurosciences [UMCN 3.2], Perception and Action [DCN 1], Neuroinformatics [DCN 3], Mental health [NCEBP 9]
Abstract

Item does not contain fulltext A panel of experts from several European countries has accomplished a systematic review of published and unpublished data on the use of long-acting medications in ADHD and hyperkinetic disorder. Based on this analysis detailed recommendations about the use of these drugs in practice have been developed: (1) Long-acting preparations should be licensed and used; (2) They should not completely replace short-acting drugs (which will be the initial treatment for many children in view of cost and the greater flexibility of dosing). Individual clinical choices are necessary. (3) Both ATX and extended-release stimulants should be available. In addition, detailed recommendations will be made with regard to the criteria to be applied in choosing a preparation for the individual patient.

Published
2008
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48. The relationship between ADHD and key cognitive phenotypes is not mediated by shared familial effects with IQ

Author

Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., Kuntsi, J., Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., and Kuntsi, J.

Abstract

Background Twin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ. Method Multivariate familial models were run on data from 1265 individuals aged 6-18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice-delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI). Results Significant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41-0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80-87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ. Conclusions The aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD

Published
2017

49. Predictability of oppositional defiant disorder and symptom dimensions in children and adolescents with ADHD combined type

Author

Aebi, M., Müller, U. C., Asherson, P., Banaschewski, T., Buitelaar, J., Ebstein, R., Eisenberg, J., Gill, M., Manor, I., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Sergeant, J., Sonuga-Barke, E., Thompson, M., Taylor, E., Faraone, S. V., Steinhausen, H.-C, Aebi, M., Müller, U. C., Asherson, P., Banaschewski, T., Buitelaar, J., Ebstein, R., Eisenberg, J., Gill, M., Manor, I., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Sergeant, J., Sonuga-Barke, E., Thompson, M., Taylor, E., Faraone, S. V., and Steinhausen, H.-C

Abstract

Background Oppositional defiant disorder (ODD) is frequently co-occurring with attention deficit hyperactivity disorder (ADHD) in children and adolescents. Because ODD is a precursor of later conduct disorder (CD) and affective disorders, early diagnostic identification is warranted. Furthermore, the predictability of three recently confirmed ODD dimensions (ODD-irritable, ODD-headstrong and ODD-hurtful) may assist clinical decision making. Method Receiver-operating characteristic (ROC) analysis was used in order to test the diagnostic accuracy of the Conners' Parent Rating Scale revised (CPRS-R) and the parent version of the Strength and Difficulties Questionnaire (PSDQ) in the prediction of ODD in a transnational sample of 1093 subjects aged 5-17 years from the International Multicentre ADHD Genetics study. In a second step, the prediction of three ODD dimensions by the same parent rating scales was assessed by backward linear regression analyses. Results ROC analyses showed adequate diagnostic accuracy of the CPRS-R and the PSDQ in predicting ODD in this ADHD sample. Furthermore, the three-dimensional structure of ODD was confirmed by confirmatory factor analysis and the CPRS-R emotional lability scale significantly predicted the ODD irritable dimension. Conclusions The PSDQ and the CPRS-R are both suitable screening instruments in the identification of ODD. The emotional lability scale of the CPRS-R is an adequate predictor of irritability in youth referred for ADHD

Published
2017

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