Disease relevance of Attention Deficit Disorder with Hyperactivity

• Catechol O-methyltransferase gene variant and birth weight predict early-onset antisocial behavior in children with attention-deficit/hyperactivity disorder [1].
• In a child with minimal brain dysfunction, we found that chorea was related to the major central effect of methylphenidate and probably to the effect of the drug on central catecholaminergic systems [2].
• BACKGROUND: Impulsivity is a common feature of attention-deficit/hyperactivity disorder (ADHD), and evidence suggests that impulsivity traits may be an indicator of poor prognosis for individuals with bulimia nervosa [3].
• The mouse mutant coloboma (Cm/+), which exhibits profound spontaneous hyperactivity and bears a deletion mutation on chromosome 2, including the gene encoding synaptosomal protein SNAP-25, has been proposed to model aspects of attention-deficit hyperactivity disorder [4].
• Recent studies suggest that children with attention-deficit/hyperactivity disorder (ADHD) and children with traumatic brain injuries (TBI) show changes in similar neuronal networks, including the dopaminergic (DA) and norepinephrinergic (NA) systems [5].

Psychiatry related information on Attention Deficit Disorder with Hyperactivity

• BACKGROUND: Previous research has suggested that substantial comorbidity exists among childhood externalizing disorders, specifically attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) [6].
• In common with previous reports from clinical samples of cocaine abusers, these overall rates were largely accounted for by major depression, minor bipolar conditions (eg, hypomania, cyclothymic personality), anxiety disorders, antisocial personality, and history of childhood attention deficit disorder [7].
• Sixteen trials studied patients with major depressive disorder, and the remaining 8 studied obsessive-compulsive disorder (n = 4), generalized anxiety disorder (n = 2), attention-deficit/hyperactivity disorder (n = 1), and social anxiety disorder (n = 1) [8].
• BACKGROUND: Currently, there is no consensus on the best therapeutic approach to chronic tic disorders and comorbid attention-deficit/hyperactivity disorder (ADHD) [9].
• Psychometrics included the Wender Utah Rating Scale for symptoms of childhood attention-deficit/hyperactivity disorder and the Michigan Alcoholism Screening Test. Veterans also completed the Combat Exposure Scale and subtests of the Wechsler Adult Intelligence Scale-Revised [10].

High impact information on Attention Deficit Disorder with Hyperactivity

• Blood serotonin levels in the attention-deficit disorder [11].
• This suggests a functional deficiency of brain dopamine in the pathogenesis of minimal brain dysfunction [12].
• A dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/impulsive and combined subtypes [13].
• JAMA patient page. Attention-deficit/hyperactivity disorder [14].
• DATA SOURCES: Literature review using a National Library of Medicine database search for 1975 through March 1997 on the terms attention deficit disorder with hyperactivity, methylphenidate, stimulants, and stimulant abuse and dependence [15].

Chemical compound and disease context of Attention Deficit Disorder with Hyperactivity

• Double-blind crossover randomized Latin square comparison of placebo, dextroamphetamine, and levoamphetamine in 31 consecutively diagnosed children with minimal brain dysfunction (MBD) replicated a smaller nonrandom study [16].
• Pemoline, methylphenidate, and placebo in children with minimal brain dysfunction [17].
• The short-term, dose-response effects of methylphenidate hydrochloride were evaluated on academic and social classroom measures in 29 children with attention deficit disorder [18].
• Methylphenidate vs dextroamphetamine vs caffeine in minimal brain dysfunction: controlled comparison by placebo washout design with Bayes' analysis [19].
• In our study, concentrations of plasma HVA and urinary HVA (from 24-hour urine collections) were measured in 20 prepubescent boys who received 3 weeks of placebo, dextroamphetamine sulfate, and fenfluramine hydrochloride in a randomized, double-blind, counterbalanced study of the treatment of attention-deficit disorder [20].

Biological context of Attention Deficit Disorder with Hyperactivity

• A common haplotype of the dopamine transporter gene associated with attention-deficit/hyperactivity disorder and interacting with maternal use of alcohol during pregnancy [21].
• An association of the dopamine receptor D4 (DRD4) gene located on chromosome 11p15.5 and attention deficit/hyperactivity disorder (ADHD) has been demonstrated and replicated by multiple investigators [22].
• Three groups have previously performed genome scans in attention-deficit/hyperactivity disorder (ADHD); linkage to chromosome 5p13 was detected in all of the respective studies [23].
• Over the past few decades, functional neuroimaging techniques have begun to provide unprecedented windows on the neurobiology of attention-deficit/hyperactivity disorder (ADHD) and the neural effects of medications used to treat the disorder [24].
• The past decade has witnessed the establishment of several now well-replicated findings in the neuropsychology of attention-deficit/hyperactivity disorder (ADHD), which have been confirmed by meta-analyses [25].

Anatomical context of Attention Deficit Disorder with Hyperactivity

• BACKGROUND: Symptoms of attention-deficit/hyperactivity disorder (ADHD) have been associated with frontal lobe deficits [26].
• Blockade of norepinephrine alpha-2-adrenoceptors in prefrontal cortex markedly impairs prefrontal cortex function and mimics most of the symptoms of attention-deficit/hyperactivity disorder, including impulsivity and locomotor hyperactivity [27].
• Cerebrospinal fluid homovanillic acid predicts behavioral response to stimulants in 45 boys with attention deficit/hyperactivity disorder [28].
• BACKGROUND: Thyroid abnormalities have been associated with attention deficit/hyperactivity disorder (ADHD) and with other childhood psychiatric disorders [29].
• OBJECTIVE: To examine the relation between specific frontostriatal structures (prefrontal cortex and basal ganglia) and response inhibition deficits observed in attention-deficit/hyperactivity disorder (ADHD) [30].

Gene context of Attention Deficit Disorder with Hyperactivity

• CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is a common heritable childhood behavioral disorder [21].
• Associations have been reported of the seven-repeat (7R) allele of the human dopamine receptor D4 (DRD4) gene with both attention-deficit/hyperactivity disorder and the personality trait of novelty seeking [31].
• Joint analysis of the DRD5 marker concludes association with attention-deficit/hyperactivity disorder confined to the predominantly inattentive and combined subtypes [32].
• These data support the involvement of GSK-3 as an important mediator of DA and lithium action in vivo and suggest that modulation of the Akt/GSK-3 pathway might be relevant to DA-related disorders, such as attention deficit hyperactivity disorder and schizophrenia [33].
• Attention-deficit/hyperactivity disorder (ADHD) is the most commonly diagnosed behavioral disorder in childhood and likely represents an extreme of normal behavior [34].

Analytical, diagnostic and therapeutic context of Attention Deficit Disorder with Hyperactivity

• Twenty boys (mean age, 9 +/- 2 years) with attention deficit disorder with hyperactivity received three weeks each of dextroamphetamine sulfate (0.5 mg/kg/d), fenfluramine hydrochloride (0.6 mg/kg/d increased to 2.0 mg/kg/d), and placebo in a double-blind, random-order, crossover design [35].
• The tentative results of this study confirm the primary position of sympathomimetics in the pharmacotherapy of minimal brain dysfunction and, in addition, suggest the involvement of dopamine pathways in this disorder [36].
• Diagnosis of attention deficit disorder in a 35-year-old man and treatment with pemoline substantially improved his response to alcoholism treatment and aftercare [37].
• Although the efficacy of medications for attention-deficit/hyperactivity disorder (ADHD) is well demonstrated in clinical trials, substantial numbers of patients fail to remain on therapy, and there is tremendous variability in tolerability and treatment acceptance [38].
• This study investigated EEG differences between children with two subtypes of Attention-Deficit/Hyperactivity Disorder (ADHD) and normal control subjects [39].

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