Attention-deficit/hyperactivity disorder: a therapeutic update

Kirby, Kelly; Rutman, Lori; Bernstein, Henry H.

doi:10.1097/00008480-200204000-00017

Cited by 13 publications

(3 citation statements)

References 21 publications

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“…Attention-deficit hyperactivity disorder (ADHD) is a heterogeneous syndrome, which is characterized by behavioral and cognitive dysfunctions, including inattention, impulsivity and hyperactivity (Kirby et al 2002; Krain and Castellanos 2006; Pasini et al 2007; Goldman et al 1998). Clinical studies have emphasized a genetic predisposition; however, more recently there is evidence that adverse environmental factors, such as chronic family conflicts, decreased family cohesion and parental psychopathology also may play a significant role (Biederman et al 1995; Counts et al 2005; Miller et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Early life stress induces attention-deficit hyperactivity disorder (ADHD)-like behavioral and brain metabolic dysfunctions: functional imaging of methylphenidate treatment in a novel rodent model

et al. 2016

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In a novel animal model Octodon degus we tested the hypothesis that, in addition to genetic predisposition, early life stress (ELS) contributes to the etiology of attention-deficit hyperactivity disorder-like behavioral symptoms and the associated brain functional deficits. Since previous neurochemical observations revealed that early life stress impairs dopaminergic functions, we predicted that these symptoms can be normalized by treatment with methylphenidate. In line with our hypothesis, the behavioral analysis revealed that repeated ELS induced locomotor hyperactivity and reduced attention towards an emotionally relevant acoustic stimulus. Functional imaging using (14C)-2-fluoro-deoxyglucose-autoradiography revealed that the behavioral symptoms are paralleled by metabolic hypoactivity of prefrontal, mesolimbic and subcortical brain areas. Finally, the pharmacological intervention provided further evidence that the behavioral and metabolic dysfunctions are due to impaired dopaminergic neurotransmission. Elevating dopamine in ELS animals by methylphenidate normalized locomotor hyperactivity and attention-deficit and ameliorated brain metabolic hypoactivity in a dose-dependent manner.

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Section: Introductionmentioning

confidence: 99%

Early life stress induces attention-deficit hyperactivity disorder (ADHD)-like behavioral and brain metabolic dysfunctions: functional imaging of methylphenidate treatment in a novel rodent model

et al. 2016

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“…Attention-deficit/hyperactivity disorder (ADHD) is a neuropsychiatric disorder commonly diagnosed during childhood, characterized by excessive levels of inattentiveness, impulsivity, and hyperactivity (1). Ritalin hydrochloride (methylphenidate hydrochloride), as a mild central nervous system (CNS) stimulant, is available in the form of 5, 10, and 20 mg tablets for oral administration; Ritalin-SR is available as sustained-release tablets of 20 mg for oral administration.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of histopathologic and histomorphometric changes of testicular tissue and gonadotropin levels following consumption of methylphenidate in male mice

Fazelipour¹,

Tootian²,

Saremi³

et al. 2014

Turk J Med Sci

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“…Attention Deficit Hyperactivity Disorder (ADHD), one of the most common neurobehavioral disorders of human childhood, is a heterogeneous syndrome that includes behavioral and cognitive dysfunctions, such as inattention, impulsivity, and hyperactivity (Goldman et al, 1998;Kirby et al, 2002). Since dopaminergic dysfunctions appear to contribute to ADHD, the most frequently used drug to treat symptoms of ADHD is methylphenidate (MP) (Kirby et al, 2002;Bolanos et al, 2003), which exerts its action mainly via the dopaminergic system (Volkow et al, 2001;Seeman and Madras, 2002). Animal models of ADHD, such as the spontaneously hypertensive rat (Sagvolden, 2000), the dopamine transporter knockout mouse (Gainetdinov and Caron, 2001), and others (see Davids et al, 2003) are focused on the genetic background of ADHD.…”

Section: Introductionmentioning

confidence: 99%

Methylphenidate treatment recovers stress‐induced elevated dendritic spine densities in the rodent dorsal anterior cingulate cortex

Zehle

Bock

Jezierski

et al. 2007

Developmental Neurobiology

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Exposing pups of the rodent species Octodon degus to periodic separation stress during the first three postnatal weeks leads to behavioral alterations, which include reduced attention towards an emotional stimulus and motoric hyperactivity. These behavioral changes, which are reminiscent of symptoms of attention deficit hyperactivity disorder (ADHD), are paralleled by synaptic changes in the dorsal anterior cingulate cortex (ACd), a limbic cortex region, which plays a key role in the modulation of attentional and executive functions. ADHD is typically treated with methylphenidate (MP), a drug acting on the dopaminergic system. However, the effect of chronic MP-treatment on neuronal and synaptic maturation in the developing brain is unknown. Applying the Golgi-Cox stainining technique, we tested in which way chronic MP-treatment interferes with dendritic and synaptic development in the ACd and whether this treatment can restore the stress-induced changes of neuronal connectivity. We found that chronic treatment with 1 mg/kg MP recovers stress-induced changes of spine densities in the ACd. Furthermore, MP-treatment resulted in increased dendritic length and complexity in both, stressed as well as unstressed control animals. These results indicate that synaptic reorganization as well as dendritic growth in the prefrontal cortex continue into prepuberty and are modulated by MP-treatment.

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Attention-deficit/hyperactivity disorder: a therapeutic update

Cited by 13 publications

References 21 publications

Early life stress induces attention-deficit hyperactivity disorder (ADHD)-like behavioral and brain metabolic dysfunctions: functional imaging of methylphenidate treatment in a novel rodent model

Early life stress induces attention-deficit hyperactivity disorder (ADHD)-like behavioral and brain metabolic dysfunctions: functional imaging of methylphenidate treatment in a novel rodent model

Evaluation of histopathologic and histomorphometric changes of testicular tissue and gonadotropin levels following consumption of methylphenidate in male mice

Methylphenidate treatment recovers stress‐induced elevated dendritic spine densities in the rodent dorsal anterior cingulate cortex

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