Attention-Deficit/Hyperactivity Disorder
Adults with Tourette’s syndrome with and without attention deficit hyperactivity disorder
Haddad, A. D. M., Umoh, G., Bhatia, V., & Robertson, M. M. (2009). Adults with Tourette's syndrome with and without attention deficit hyperactivity disorder. Acta Psychiatrica Scandinavica, 120(4), 299-307.
Objective: Comorbidity between Tourette’s syndrome (TS) and attention deficit hyperactivity disorder (ADHD) is high.... more
Objective: Comorbidity between Tourette’s syndrome (TS) and attention deficit hyperactivity disorder (ADHD) is high. In children, those with both TS+ADHD fare less well than those with TS-only on measures of both psychopathology and behaviour. The objective of this study was to document such measures in adult patients.
Method: Eighty adults with TS-only were compared to 64 with TS+ADHD using a clinical interview and standardised measures of depression, anxiety and obsessionality.
Results: The two groups were no different on measures of TS severity. TS+ADHD patients had significantly more depression, anxiety, obsessive–compulsive behaviour and maladaptive behaviours than patients with TS-only. There were also significant differences in the incidence of copro- and echo-phenomena and family history of ADHD.
Conclusion: The finding of increased overall behavioural difficulties and psychopathology in adult patients with TS+ADHD when compared with TS-only is in agreement with previous findings in children with TS. Appropriate treatment of ADHD in TS patients during childhood may prevent many behavioural problems in adulthood.
Adolescent impulsivity phenotypes characterized by distinct brain networks
Nature Neuroscience. doi:10.1038/nn.3092
Robert Whelan, Patricia J Conrod, Jean-Baptiste Poline, Anbarasu Lourdusamy, Tobias Banaschewski, Gareth J Barker, Mark A Bellgrove, Christian Büchel, Mark Byrne, Tarrant D R Cummins, Mira Fauth-Bühler, Herta Flor, Jürgen Gallinat, Andreas Heinz, Bernd Ittermann, Karl Mann, Jean-Luc Martinot, Edmund C Lalor, Mark Lathrop, Eva Loth, Frauke Nees, Tomas Paus, Marcella Rietschel, Michael N Smolka, Rainer Spanagel, David N Stephens, Maren Struve, Benjamin Thyreau, Sabine Vollstaedt-Klein, Trevor W Robbins, Gunter Schumann, Hugh Garavan & the IMAGEN Consortium
The impulsive behavior that is often characteristic of adolescence may reflect underlying neurodevelopmental... more The impulsive behavior that is often characteristic of adolescence may reflect underlying neurodevelopmental processes. Moreover, impulsivity is a multi-dimensional construct, and it is plausible that distinct brain networks contribute to its different cognitive, clinical and behavioral aspects. As these networks have not yet been described, we identified distinct cortical and subcortical networks underlying successful inhibitions and inhibition failures in a large sample (n = 1,896) of 14-year-old adolescents. Different networks were associated with drug use (n = 1,593) and attention-deficit hyperactivity disorder symptoms (n = 342). Hypofunctioning of a specific orbitofrontal cortical network was associated with likelihood of initiating drug use in early adolescence. Right inferior frontal activity was related to the speed of the inhibition process (n = 826) and use of illegal substances and associated with genetic variation in a norepinephrine transporter gene (n = 819). Our results indicate that both neural endophenotypes and genetic variation give rise to the various manifestations of impulsive behavior.
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Seen by:Self-alert training: Volitional modulation of autonomic arousal improves sustained attention
Redmond G. O’Connell, Mark A. Bellgrove, Paul M. Dockree, Adam Lau, Michael Fitzgerald, Ian H. Robertson
Neuropsychologia 2008
The present study examines a new alertness training strategy (Self-Alert Training, SAT) designed to explore the... more
The present study examines a new alertness training strategy (Self-Alert Training, SAT) designed to explore the relationship between the top–down control processes governing arousal and sustained attention. In order to maximally target frontal control systems SAT combines a previously validated behavioural self-alerting technique [Robertson, I. H., Tegner, R., Tham, K., Lo, A., & Nimmo-Smith, I. (1995). Sustained attention training for unilateral neglect: Theoretical and rehabilitation implications. Journal of Clinical and Experimental Neuropsychology, 17, 416–430] with an autonomic arousal biofeedback protocol in which participants learn to modulate their own arousal levels. The SAT protocol was first validated with a group of 23 neurologically healthy participants and then independently tested in a group of 18 adults with ADHD to determine
its clinical utility. Half of the participants in each group were assigned to a placebo condition to control for non-specific effects. All participants performed the sustained attention to response task (SART) during pre- and post-training testing sessions to assess training effects on sustained attention. By the end of SAT all participants were able to modulate their own arousal levels without external prompting. Comparison of pre- and
post-training baseline data indicated that, as predicted, SAT was associated with increased levels of autonomic arousal accompanied by improved accuracy on the SART. In contrast, participants in the placebo condition exhibited a gradual reduction in arousal over time and increased reaction time variability indicative of a vigilance decrement. These data demonstrate that the recruitment of top–down control processes during volitional modulation of arousal leads to improved sustained attention. These findings have important implications for the rehabilitation of attention deficits arising from frontal dysfunction.
The neural correlates of deficient error awareness in attention-deficit hyperactivity disorder (ADHD)
Redmond G. O’Connell, Mark A. Bellgrove, Paul M. Dockree, Adam Lau, Robert Hester, Hugh Garavan, Michael Fitzgerald, John J. Foxe, Ian H. Robertson
Neuropsychologia 2009
The ability to detect and correct errors is critical to adaptive control of behaviour and represents a discrete... more
The ability to detect and correct errors is critical to adaptive control of behaviour and represents a discrete neuropsychological function. A number of studies have highlighted that attention-deficit hyperactivity disorder (ADHD) is associated with abnormalities in behavioural and neural responsiveness to performance errors. One limitation of previous work has been a failure to determine the extent to which these
differences are attributable to failures of conscious error awareness, a process that is dependent on the integrity of the frontal lobes. Recent advances in electrophysiological research make it possible to distinguish unconscious and conscious aspects of error processing. This study constitutes an extensive
electrophysiological investigation of error awareness and error processing in ADHD. A Go/No-Go response inhibition task specifically designed to assess error awareness was administered to a group of adults diagnosed with ADHD and a group of matched control participants. The ADHD group made significantly more errors than the control group but was less likely to consciously detect these errors. An analysis of eventrelated potentials elicited by errors indicated that an early performance monitoring component (early positivity) was significantly attenuated in the ADHD group as was a later component that specifically reflects conscious error processing (Pe). Dipole source modelling suggested that abnormal Pe amplitudes were attributable to decreased activation of the anterior cingulate cortex. Decreased electrodermal activity
in the ADHD group also suggested amotivational insensitivity to performance errors. Our data provide evidence that neuropsychological deficits associated with ADHD can be exacerbated by error processing abnormalities. Error awareness may represent an important cognitive and physiological phenotype for
ADHD.
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Seen by:Clinical Utility of the ADHD Diagnostic Parent Rating Scale Comorbidity Screening Scales
Stephen P. Becker, Joshua M. Langberg, Aaron J. Vaughn, Jeffery N. Epstein
Journal of Developmental & Behavioral Pediatrics, 33, 221-228.
doi: 10.1097/DBP.0b013e318245615b
Objective: To evaluate the clinical utility of the cutoff recommendations for the Vanderbilt ADHD Diagnostic Parent... more
Objective: To evaluate the clinical utility of the cutoff recommendations for the Vanderbilt ADHD Diagnostic Parent Rating Scale (VADPRS) comorbidity screening scales provided by the American Academy of Pediatrics/National Initiative for
Children's Healthcare Quality (AAP/NICHQ) and to examine alternative cutoff strategies for identifying and ruling out disorders commonly comorbid with ADHD.
Method: A sample of 215 children (142 with ADHD), ages 7-11, participated in the study. Parents completed the VADPRS and were administered a diagnostic interview to establish diagnoses of oppositional defiant disorder (ODD), conduct disorder (CD), anxiety, and depression. The clinical utility of the VADPRS comorbidity screening scales were examined.
Results: The recommended AAP/NICHQ cutoff strategies did not have adequate clinical utility for identifying or ruling out comorbidities, with the exception of the VADPRS ODD cutoff strategy which reached adequate levels for ruling out a diagnosis of ODD. An alternative cutoff approach using total sum scores was superior to the recommended cutoff strategies across all diagnoses in terms of ruling out a diagnosis, and this was particularly evident for anxiety/depression. Several individual items on the ODD and CD scales also had acceptable clinical utility for ruling in diagnoses.
Conclusion: The VADPRS comorbidity screening scales may be helpful in determining which children likely do not meet diagnostic criteria for ODD, CD, anxiety, or depression. This study suggests that using a total sum score provides the greatest clinical utility for each of these comorbidities and demonstrates the need for further research examining the use of dimensional assessment strategies in diagnostic decision-making.
The Effect of Group Parent Management Training on Behavioral Disorders of 4-to-10-year-old ADHD Children
Giornale Italiano di Terapia Occupazionale 2011
Functional analysis of intron 8 and 3' UTR variable number of tandem repeats of SLC6A3: differential activity of intron 8 variants.
Hill M, Anney RJ, Gill M, Hawi Z. Functional analysis of intron 8 and 3' UTR variable number of tandem repeats of SLC6A3: differential activity of intron 8 variants. Pharmacogenomics J. 2010 Oct;10(5):442-7. Epub 2009 Dec 22. PubMed PMID: 20029387.
Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder.
Neale BM, Medland SE, Ripke S, Asherson P, Franke B, Lesch KP, Faraone SV, Nguyen TT, Schäfer H, Holmans P, Daly M, Steinhausen HC, Freitag C, Reif A, Renner TJ, Romanos M, Romanos J, Walitza S, Warnke A, Meyer J, Palmason H, Buitelaar J, Vasquez AA, Lambregts-Rommelse N, Gill M, Anney RJ, Langely K, O'Donovan M, Williams N, Owen M, Thapar A, Kent L, Sergeant J, Roeyers H, Mick E, Biederman J, Doyle A, Smalley S, Loo S, Hakonarson H, Elia J, Todorov A, Miranda A, Mulas F, Ebstein RP, Rothenberger A, Banaschewski T, Oades RD, Sonuga-Barke E, McGough J, Nisenbaum L, Middleton F, Hu X, Nelson S; Psychiatric GWAS Consortium: ADHD Subgroup. Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2010 Sep;49(9):884-97. Epub 2010 Aug 1. PubMed PMID: 20732625; PubMed Central PMCID: PMC2928252.
ADHD and DAT1: further evidence of paternal over-transmission of risk alleles and haplotype.
Hawi Z, Kent L, Hill M, Anney RJ, Brookes KJ, Barry E, Franke B, Banaschewski T, Buitelaar J, Ebstein R, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Sonuga-Barke E, Steinhausen HC, Faraone SV, Asherson P, Gill M. ADHD and DAT1: further evidence of paternal over-transmission of risk alleles and haplotype. Am J Med Genet B Neuropsychiatr Genet. 2010 Jan 5;153B(1):97-102. PubMed PMID: 19388000.
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Seen by:Replication of a rare protective allele in the noradrenaline transporter gene and ADHD
Xu X, Hawi Z, Brookes KJ, Anney RJ, Bellgrove M, Franke B, Barry E, Chen W, Kuntsi J, Banaschewski T, Buitelaar J, Ebstein R, Fitzgerald M, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Sonuga-Barke E, Steinhausen HC, Faraone SV, Gill M, Asherson P. Replication of a rare protective allele in the noradrenaline transporter gene and ADHD. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1564-7. PubMed PMID: 18937296; PubMed Central PMCID: PMC2587507.
Parent of origin effects in attention/deficit hyperactivity disorder (ADHD): analysis of data from the international multicenter ADHD genetics (IMAGE) program
Anney RJ, Hawi Z, Sheehan K, Mulligan A, Pinto C, Brookes KJ, Xu X, Zhou K, Franke B, Buitelaar J, Vermeulen SH, Banaschewski T, Sonuga-Barke E, Ebstein R, Manor I, Miranda A, Mulas F, Oades RD, Roeyers H, Rommelse N, Rothenberger A, Sergeant J, Steinhausen HC, Taylor E, Thompson M, Asherson P, Faraone SV, Gill M. Parent of origin effects in attention/deficit hyperactivity disorder (ADHD): analysis of data from the international multicenter ADHD genetics (IMAGE) program. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1495-500. PubMed PMID: 18163388.
Conduct disorder and ADHD: Evaluation of conduct problems as a categorical and quantitative trait in the international multicentre ADHD genetics study
Anney RJ, Lasky-Su J, O'Dúshláine C, Kenny E, Neale BM, Mulligan A, Franke B, Zhou K, Chen W, Christiansen H, Arias-Vásquez A, Banaschewski T, Buitelaar J, Ebstein R, Miranda A, Mulas F, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Sonuga-Barke E, Steinhausen H, Asherson P, Faraone SV, Gill M. Conduct disorder and ADHD: evaluation of conduct problems as a categorical and quantitative trait in the international multicentre ADHD genetics study. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1369-78. PubMed PMID: 18951430.
Genome‐wide association scan of the time to onset of attention deficit hyperactivity disorder
Lasky-Su J, Anney RJ, Neale BM, Franke B, Zhou K, Maller JB, Vasquez AA, Chen W, Asherson P, Buitelaar J, Banaschewski T, Ebstein R, Gill M, Miranda A, Mulas F, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Sonuga-Barke E, Steinhausen HC, Taylor E, Daly M, Laird N, Lange C, Faraone SV. Genome-wide association scan of the time to onset of attention deficit hyperactivity disorder. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1355-8. PubMed PMID: 18937294; PubMed Central PMCID: PMC2605611.
Genome‐wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate gene associations
Lasky-Su J, Neale BM, Franke B, Anney RJ, Zhou K, Maller JB, Vasquez AA, Chen W, Asherson P, Buitelaar J, Banaschewski T, Ebstein R, Gill M, Miranda A, Mulas F, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Sonuga-Barke E, Steinhausen HC, Taylor E, Daly M, Laird N, Lange C, Faraone SV. Genome-wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate gene associations. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1345-54. PubMed PMID: 18821565.
Genome‐wide association scan of attention deficit hyperactivity disorder
Neale BM, Lasky-Su J, Anney RJ, Franke B, Zhou K, Maller JB, Vasquez AA, Asherson P, Chen W, Banaschewski T, Buitelaar J, Ebstein R, Gill M, Miranda A, Oades RD, Roeyers H, Rothenberger A, Sergeant J, Steinhausen HC, Sonuga-Barke E, Mulas F, Taylor E, Laird N, Lange C, Daly M, Faraone SV. Genome-wide association scan of attention deficit hyperactivity disorder. Am J Med Genet B Neuropsychiatr Genet. 2008 Dec 5;147B(8):1337-44. PubMed PMID: 18980221; PubMed Central PMCID: PMC2831205.
Case-control genome-wide association study of attention-deficit/hyperactivity disorder
Neale BM, Medland S, Ripke S, Anney RJ, Asherson P, Buitelaar J, Franke B, Gill M, Kent L, Holmans P, Middleton F, Thapar A, Lesch KP, Faraone SV, Daly M, Nguyen TT, Schäfer H, Steinhausen HC, Reif A, Renner TJ, Romanos M, Romanos J, Warnke A, Walitza S, Freitag C, Meyer J, Palmason H, Rothenberger A, Hawi Z, Sergeant J, Roeyers H, Mick E, Biederman J; IMAGE II Consortium Group. Case-control genome-wide association study of attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2010 Sep;49(9):906-20. Epub 2010 Aug 5. PubMed PMID: 20732627; PubMed Central PMCID: PMC2928577.
Autism symptoms in attention-deficit/hyperactivity disorder: a familial trait which correlates with conduct, oppositional defiant, language and motor disorders
Mulligan A, Anney RJ, O'Regan M, Chen W, Butler L, Fitzgerald M, Buitelaar J, Steinhausen HC, Rothenberger A, Minderaa R, Nijmeijer J, Hoekstra PJ, Oades RD, Roeyers H, Buschgens C, Christiansen H, Franke B, Gabriels I, Hartman C, Kuntsi J, Marco R, Meidad S, Mueller U, Psychogiou L, Rommelse N, Thompson M, Uebel H, Banaschewski T, Ebstein R, Eisenberg J, Manor I, Miranda A, Mulas F, Sergeant J, Sonuga-Barke E, Asherson P, Faraone SV, Gill M. Autism symptoms in Attention-Deficit/Hyperactivity Disorder: a familial trait which correlates with conduct, oppositional defiant, language and motor disorders. J Autism Dev Disord. 2009 Feb;39(2):197-209. Epub 2008 Jul 19. Erratum in: J Autism Dev Disord. 2009 Feb;39(2):210-1. PubMed PMID: 18642069.
Déficit de atención e hiperactividad en adultos con adicción a sustancias: ¿TDAH o síndrome secundario al abuso de sustancias?
by José María Ruiz Sánchez de León
Attention deficit and hyperactivity in adults addicted to substances: ADHD or syndrome secondary to substance abuse? [In Spanish] Revista Española de Drogodependencias 2009, 34(1), 32-45.
Resumen:
Existe un cuerpo de investigación, sometido a fuertes intereses comerciales, para considerar la... more
Resumen:
Existe un cuerpo de investigación, sometido a fuertes intereses comerciales, para considerar la existencia del trastorno por déficit de atención e hiperactividad (TDAH) en adultos, que informa de presuntas prevalencias muy elevadas en población adicta. Otros estudios sugieren cifras mucho menores y más acordes con las observadas en población infantil, utilizando todos, y no sólo algunos, de los criterios diagnósticos establecidos. Puesto que el diagnóstico en el momento actual debe ser meramente sindrómico, los síntomas manifestados por los afectados son de interés crucial. A partir de diversos autoinformes de síntomas de TDAH (ASRS de la OMS), de disfunción ejecutiva (DEX, FrSBe) y de condiciones asociadas (MCMI-II, DII-Short), los datos del presente estudio muestran que es más probable que los síntomas de inatención e hiperactividad observados en sujetos adictos en tratamiento se deban a efectos derivados de la adicción que a condiciones mórbidas previas al abuso de sustancias.
Palabras clave:
TDAH, adicción, síndrome disejecutivo, funciones ejecutivas, cambio de personalidad, lóbulo frontal.
Abstract:
There is a substantial amount of research, related to strong commercial interests, defending the existence of the attention deficit and hyperactivity disorder (ADHD) in adults. This line of scientific research usually displays a high prevalence of this disorder in addicted individuals. On the other hand, some studies show smaller percentages, in agreement with those found in children, applying all of the established diagnosis criteria. As current diagnosis can only be established in a syndromic way, there is a core interest in those symptoms mentioned by affected individuals. Subjects in this study were asked to fill several self-assessment questionnaires about different ADHD symptoms (WHO’s ASRS), executive dysfunction (DEX, FrSBe) and associate conditions (MCMI-II, DII-Short). Resulting data showed a higher probability that observed symptoms of lack of attention and hyperactivity in addicted subjects may be related to addiction itself, rather than any previous morbid condition.
Key words:
ADHD, addiction, executive functions, dysexecutive syndrome, personality change, frontal lobe.
