Reward anticipation and outcomes in adult males with attention-deficit/hyperactivity disorder

Ströhle, Andreas; Stoy, Meline; Wrase, Jana; Schwarzer, Steffi; Schlagenhauf, Florian; Huß, Michael; Hein, Jakob; Nedderhut, Anke; Neumann, Britta; Gregor, Andreas; Juckel, Georg; Knutson, Brian; Lehmkuhl, Ulrike; Bauer, Michael; Heinz, Andreas

doi:10.1016/j.neuroimage.2007.09.044

Cited by 287 publications

(249 citation statements)

References 34 publications

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“…However, it is plausible that stimulantinduced increases of conformity could contribute to MPH effects on social behavior. An MPH-induced increase in the incentive of conformity, for example, would be consistent with theories and findings that patients with ADHD have reinforcement learning deficits that can be alleviated by stimulant therapy (Frank et al, 2007;Haenlein and Caul, 1987;Luman et al, 2010;Volkow et al, 2005;Wilkison et al, 1995), enhanced responses to raised incentives (Andreou et al, 2007;Kohls et al, 2009;Luman et al, 2005), deficient psychophysical responding to affective stimuli that can be restored by stimulant medication (Conzelmann et al, 2011;Groen et al, 2009), and reduced hemodynamic responses to reward anticipation in the striatum (Plichta et al, 2009;Stark et al, 2011;Strohle et al, 2008). We therefore propose a new working hypothesis that MPH may improve social behavior and acceptance by peers in ADHD patients, in part, by increasing catecholamine-mediated conformity.…”

Section: Discussionsupporting

confidence: 80%

Modulation of Social Influence by Methylphenidate

Campbell-Meiklejohn

Simonsen

Jensen

et al. 2012

Neuropsychopharmacol

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The ability to infer value from the reactions of other people is a common and essential ability with a poorly understood neurobiology. Commonly, social learning matches one's values and behavior to what is perceived as normal for one's social group. This is known as conformity. Conformity of value correlates with neural activity shared by cognitions that depend on optimum catecholamine levels, but catecholamine involvement in conformity has not been tested empirically. Methylphenidate (MPH) is an indirect dopamine and noradrenalin agonist, commonly used for the treatment of attention-deficit hyperactivity disorder for which it reduces undesirable behavior as evaluated by peers and authority figures, indicative of increased conformity. We hypothesized that MPH might increase conformity of value. In all, 38 healthy adult females received either a single oral 20 mg dose of MPH or placebo (PL). Each subject rated 153 faces for trustworthiness followed immediately by the face's mean rating from a group of peers. After 30 min and a 2-back continuousperformance working-memory task, subjects were unexpectedly asked to rate all the faces again. Both the groups tended to change their ratings towards the social norm. The MPH group exhibited twice the conformity effect of the PL group following moderate social conflict, but this did not occur following large conflicts. This suggests that MPH might enhance signals that would otherwise be too weak to evoke conformity. MPH did not affect 2-back performance. We provide a new working hypothesis of a neurocognitive mechanism by which MPH reduces socially disruptive behavior and provides novel evidence of catecholamine mediation of social learning.

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Section: Discussionsupporting

confidence: 80%

Modulation of Social Influence by Methylphenidate

Campbell-Meiklejohn

Simonsen

Jensen

et al. 2012

Neuropsychopharmacol

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“…A recent neuroanatomical study (Carmona et al, 2009) provided clear evidence of alterations in the ventral striatum of children with ADHD. This finding is consistent with recent fMRI data showing ventrostriatal hyporesponsiveness during immediate and delayed reward processing in adults with ADHD Strohle et al, 2008). Tripp and Wickens (2008) proposed the DA transfer deficit theory and suggested that children with ADHD have diminished cellular responses of DA cells to cues that precede reinforcement.…”

Section: Motivationsupporting

confidence: 90%

Understanding the Effects of Stimulant Medications on Cognition in Individuals with Attention-Deficit Hyperactivity Disorder: A Decade of Progress

Swanson

Baler

Volkow

2010

Neuropsychopharmacol

213

165

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The use of stimulant drugs for the treatment of children with attention-deficit hyperactivity disorder (ADHD) is one of the most widespread pharmacological interventions in child psychiatry and behavioral pediatrics. This treatment is well grounded on controlled studies showing efficacy of low oral doses of methylphenidate and amphetamine in reducing the behavioral symptoms of the disorder as reported by parents and teachers, both for the cognitive (inattention and impulsivity) and noncognitive (hyperactivity) domains. Our main aim is to review the objectively measured cognitive effects that accompany the subjectively assessed clinical responses to stimulant medications. Recently, methods from the cognitive neurosciences have been used to provide information about brain processes that underlie the cognitive deficits of ADHD and the cognitive effects of stimulant medications. We will review some key findings from the recent literature, and then offer interpretations of the progress that has been made over the past decade in understanding the cognitive effects of stimulant medication on individuals with ADHD. Neuropsychopharmacology Reviews (2011) 36, 207-226; doi:10.1038/npp.2010; published online 29 September 2010Keywords: methylphenidate; amphetamine; dopamine; prefrontal cortex; executive function; cognitive enhancement INTRODUCTIONCognitive deficits and behavioral symptoms associated with attention-deficit/hyperactivity disorder (ADHD) have been studied intensively and are well documented in the literature. Stimulant drugs (methylphenidate (MP) and amphetamine (AMP)) are particularly effective for the clinical treatment of ADHD, and accordingly, pediatricians and psychiatrists have been prescribing them for over seven decades (Bradley, 1937). Clear reductions in symptoms justify treatment with stimulant medications (MTA, 1999b), but the cognitive effects are less clear. Here, we will review the current understanding of some underlying neural processes that may account for the ADHD symptoms of inattention and impulsivity, and we will review evidence from neuropsychological and neuroimaging studies about how stimulant medications may affect these processes. To focus our review, we will not revisit related topics that are addressed elsewhere: the medical use of non-stimulant drugs to treat ADHD (Dopheide and Pliszka, 2009;Waxmonsky, 2005), the non-medical use of stimulants and non-stimulants for cognitive enhancement (Sahakian and Morein-Zamir, 2007;Stix, 2009), and nonmedical alternative treatments based on neurofeedback (Gevensleben et al, 2009) and working memory training (Klingberg et al, 2005) that have recently been evaluated and have gained some support in randomized clinical trials.In the Diagnostic and Statistical Manual (DSM) of the American Psychiatric Association, Version IV (APA, 1994(APA, , 2000, the cognitive symptoms of ADHD are grouped into two domains: inattention and hyperactivity/impulsivity. Currently, nine are specified for inattention (poor attending to details, sustaining attention, lis...

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“…As left ventral striatal hyporesponsiveness during reward anticipation has been repeatedly shown in patients with adult ADHD, 51,52 NPY overexpression may result in deviant reward-related neural processing in duplication carriers. Moreover, the relative hypoactivity within the left posterior insula during the anticipation of monetary loss in carriers could reflect anxiolytic effects of NPY.…”

Section: Discussionmentioning

confidence: 83%

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

et al. 2010

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Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental syndrome characterized by hyperactivity, inattention and increased impulsivity. To detect micro-deletions and micro-duplications that may have a role in the pathogenesis of ADHD, we carried out a genome-wide screen for copy number variations (CNVs) in a cohort of 99 children and adolescents with severe ADHD. Using high-resolution array comparative genomic hybridization (aCGH), a total of 17 potentially syndrome-associated CNVs were identified. The aberrations comprise 4 deletions and 13 duplications with approximate sizes ranging from 110 kb to 3 Mb. Two CNVs occurred de novo and nine were inherited from a parent with ADHD, whereas five are transmitted by an unaffected parent. Candidates include genes expressing acetylcholine-metabolizing butyrylcholinesterase (BCHE), contained in a de novo chromosome 3q26.1 deletion, and a brain-specific pleckstrin homology domaincontaining protein (PLEKHB1), with an established function in primary sensory neurons, in two siblings carrying a 11q13.4 duplication inherited from their affected mother. Other genes potentially influencing ADHD-related psychopathology and involved in aberrations inherited from affected parents are the genes for the mitochondrial NADH dehydrogenase 1 a subcomplex assembly factor 2 (NDUFAF2), the brain-specific phosphodiesterase 4D isoform 6 (PDE4D6) and the neuronal glucose transporter 3 (SLC2A3). The gene encoding neuropeptide Y (NPY) was included in a B3 Mb duplication on chromosome 7p15.2-15.3, and investigation of additional family members showed a nominally significant association of this 7p15 duplication with increased NPY plasma concentrations (empirical family-based association test, P = 0.023). Lower activation of the left ventral striatum and left posterior insula during anticipation of large rewards or losses elicited by functional magnetic resonance imaging links gene dose-dependent increases in NPY to reward and emotion processing in duplication carriers. These findings implicate CNVs of behaviour-related genes in the pathogenesis of ADHD and are consistent with the notion that both frequent and rare variants influence the development of this common multifactorial syndrome.

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Reward anticipation and outcomes in adult males with attention-deficit/hyperactivity disorder

Cited by 287 publications

References 34 publications

Modulation of Social Influence by Methylphenidate

Modulation of Social Influence by Methylphenidate

Understanding the Effects of Stimulant Medications on Cognition in Individuals with Attention-Deficit Hyperactivity Disorder: A Decade of Progress

Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree

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