Proton Magnetic Resonance Spectroscopy Investigation of the Right Frontal Lobe in Children With Attention-Deficit/Hyperactivity Disorder

Yeo, Ronald A.; Hill, Dina E.; Campbell, Richard A.; Vigil, Janet; Petropoulos, Helen; Hart, Blaine L.; Zamora, Leona; Brooks, William M.

doi:10.1097/00004583-200303000-00010

Cited by 96 publications

(60 citation statements)

References 34 publications

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“…For example, MRS has been used with some success to identify biochemical abnormalities in ADHD (Bush et al, 2005;Carrey et al, 2003;Courvoisie et al, 2004;Jin et al, 2001;Kronenberg et al, 2008;MacMaster et al, 2003;Perlov et al, 2007Perlov et al, , 2008Sun et al, 2005;Yeo et al, 2003), but has been limited because of previous requirements that restricted (Duzel et al, 2009;Goldstein et al, 2009). Improved PET receptor characterization studies would permit in vivo dopamine receptor identification, which could synergistically improve functional and connectivity studies by refining our understanding of neuromodulatory effects.…”

Section: Multimodal Imaging and Technique Refinementmentioning

confidence: 99%

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Bush

2009

Neuropsychopharmacol

289

251

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Research attempting to elucidate the neuropathophysiology of attention-deficit/hyperactivity disorder (ADHD) has not only shed light on the disorder itself, it has simultaneously provided new insights into the mechanisms of normal cognition and attention. This review will highlight and integrate this bidirectional flow of information. Following a brief overview of ADHD clinical phenomenology, ADHD studies will be placed into a wider historical perspective by providing illustrative examples of how major models of attention have influenced the development of neurocircuitry models of ADHD. The review will then identify major components of neural systems potentially relevant to ADHD, including attention networks, reward/feedbackbased processing systems, as well as a 'default mode' resting state network. Further, it will suggest ways in which these systems may interact and be influenced by neuromodulatory factors. Recent ADHD imaging data will be selectively provided to both illustrate the field's current level of knowledge and to show how such data can inform our understanding of normal brain functions. The review will conclude by suggesting possible avenues for future research.

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Section: Multimodal Imaging and Technique Refinementmentioning

confidence: 99%

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Bush

2009

Neuropsychopharmacol

289

251

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“…Structural and functional imaging studies have revealed that working memory is primarily controlled by the dorsolateral prefrontal cortex and basal ganglia (D'Esposito et al 1995;Smith et al 1998) and that patients with ADHD have an altered architecture and less activation of these areas compared to controls (Zametkin et al 1990;Castellanos et al 1996;Aman and Carmichael 1997;Rubia et al 1999;Yeo et al 2003;Dickstein et al 2006). Inhibition is primarily mediated by the fronto-striatal circuitry and this circuitry has also been found to be involved in the pathology of ADHD (Durston et al 2003;Schulz et al 2004).…”

Section: Introductionmentioning

confidence: 99%

“…Remaining fixated on the fixation cross while the target is presented in the peripheral visual field requires top-down control processes, mediated by the superior frontal, inferior parietal and superior temporal brain areas (Hopfinger et al 2000). Since several of these brain areas and dopaminergic transmission have also been found altered in patients with ADHD (Zametkin et al 1990;Castellanos et al 1996;Aman and Carmichael 1997;Rubia et al 1999;Durston et al 2003;Yeo et al 2003;Schulz et al 2004;Dickstein et al 2006), it is hypothesized that children with ADHD will have difficulty executing memory-guided saccades and remaining fixated during the fixation period.…”

Section: Introductionmentioning

confidence: 99%

Deficits in visuo-spatial working memory, inhibition and oculomotor control in boys with ADHD and their non-affected brothers

et al. 2008

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Summary. Few studies have assessed visuo-spatial working memory and inhibition in attention-deficit=hyperactivity disorder (ADHD) by recording saccades and consequently little additional knowledge has been gathered on oculomotor functioning in ADHD. Moreover, this is the first study to report the performance of non-affected siblings of children with ADHD, which may shed light on the familiality of deficits. A total of 14 boys with ADHD, 18 non-affected brothers, and 15 control boys aged 7-14 years, were administered a memory-guided saccade task with delays of three and seven seconds. Familial deficits were found in accuracy of visuospatial working memory, percentage of anticipatory saccades, and tendency to overshoot saccades relative to controls. These findings suggest memory-guided saccade deficits may relate to a familial predisposition for ADHD.

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“…It has been shown that ADHD patients have altered architecture and less activation in the PFC [47][48][49] . Persistent working-memory problems are the main cognitive defi cit in ADHD [40,41,50,51] .…”

Section: Prefrontal Cognitive Dysfunctions In Adhdmentioning

confidence: 99%

“…In this paper, we review research progress in the relevant fi elds, focusing on the potential relationship between prefrontal α 2A -adrenoceptors and ADHD in nonhuman primates [35][36][37][38][39] . including poor attention regulation [40] , limited working memory [41] , and inability to inhibit inappropriate motor activity [42] .Working memory is a fundamental higher-order function, underlies a wide range of executive functional processes [43,44] , and is primarily controlled by the PFC [45,46] .It has been shown that ADHD patients have altered architecture and less activation in the PFC [47][48][49] . Persistent working-memory problems are the main cognitive defi cit in ADHD [40,41,50,51] .…”

mentioning

confidence: 99%

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

Sun

Luo

et al. 2015

Neurosci. Bull.

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Attention deficit and hyperactivity disorder (ADHD), a prevalent syndrome in children worldwide, is characterized by impulsivity, inappropriate inattention, and/or hyperactivity. It seriously afflicts cognitive development in childhood, and may lead to chronic under-achievement, academic failure, problematic peer relationships, and low self-esteem. There are at least three challenges for the treatment of ADHD. First, the neurobiological bases of its symptoms are still not clear. Second, the commonly prescribed medications, most showing short-term therapeutic efficacy but with a high risk of serious side-effects, are mainly based on a dopamine mechanism. Third, more novel and effi cient animal models, especially in nonhuman primates, are required to accelerate the development of new medications. In this article, we review research progress in the related fi elds, focusing on our previous studies showing that blockade of prefrontal cortical α 2A -adrenoceptors in monkeys produces almost all the typical behavioral symptoms of ADHD.Keywords: prefrontal cortex; α 2A -adrenoceptors; cognitive functions; attention defi cit and hyperactivity disorder; animal models ·Review· IntroductionAttention deficit and hyperactivity disorder (ADHD) is one of the most prevalent childhood neurodevelopmental conditions, affecting 3-5% of grade-school children worldwide [1] . It is characterized by i nappropriate levels of inattention, i mpulsivity, and/or hyperactivity [2][3][4] . These symptoms develop in childhood, and can persist into adolescence and adulthood [5] . ADHD seriously affects cognitive development [6][7][8] , and, without appropriate treatment, has consequences for the risk of anxiety, substance abuse, and depression in adulthood [ 2, 5, 9] .T he neurobiological bases o f ADHD symptoms are still not clear [10] . Clarifying them can help better understand the biological vulnerabilities that may underlie ADHD in a specifi c patient and how to modulate the responses to treatment, thereby contributing to better and more effective therapy.It has been suggested that the symptoms involve a dopaminergic mechanism in the prefrontal cortex (PFC) and striatum [11, 12] . Experimentally decreased dopamine (DA) release in the PFC results in ADHD-like symptoms [13, 14] .To date, DA dysregulation is thought to be central to the neurobiology of ADHD, and its pharmacological treatment, such as m ethylphenidate (MPH, i.e. Ritalin) [15][16][17] , levels the DA c oncentration in the synapse and extrasynaptic space in the PFC as a blocker of the DA transporter. MPH ameliorates inappropriate inattention [18][19][20] , decreases impulsivity [21] , and enhances inhibitory control [22] . However, as MPH is a prescription psychostimulant, there are strong concerns over drug dependence, paranoia, schizophrenia, and behavioral sensitization that might be caused by longterm therapy, similar to other stimulants [23][24][25].Converging evidence indicates that the pathophysiology of ADHD has multiple origins [26][27][28][29][30][31][32] ; for i...

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Proton Magnetic Resonance Spectroscopy Investigation of the Right Frontal Lobe in Children With Attention-Deficit/Hyperactivity Disorder

Cited by 96 publications

References 34 publications

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Deficits in visuo-spatial working memory, inhibition and oculomotor control in boys with ADHD and their non-affected brothers

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

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