Evidence-based pharmacotherapy for attention-deficit hyperactivity disorder

Biederman, Joseph; Spencer, Thomas; Wilens, Timothy E.

doi:10.1017/s1461145703003973

Cited by 217 publications

(125 citation statements)

References 119 publications

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“…Methylphenidate is an effective treatment for the behavioral and cognitive deficits associated with ADHD when administered orally at therapeutic doses (Greenhill, 2001;Volkow and Swanson, 2003;Biederman et al, 2004). Thus, one potential caveat of the present study is that methylphenidate was administered via subcutaneous injections, which may have produced a more rapid onset of action than orally administered methylphenidate as used in clinical settings.…”

Section: Discussionmentioning

confidence: 91%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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Stimulant drugs, including D-amphetamine, cocaine, and methylphenidate, increase cigarette smoking in controlled human laboratory experiments. Although the mechanism(s) underlying this effect are unknown, it is possible that stimulants may enhance directly the abuse-related effects of nicotine. In the present study, we characterized the behavioral pharmacological interactions between methylphenidate and nicotine in the intravenous self-administration, drug discrimination, and locomotor cross-sensitization procedures. Adult male Sprague-Dawley rats were trained to respond for intravenous nicotine (0.01 or 0.03 mg/kg/infusion) or sucrose, and the acute effects of methylphenidate (1.25-10 mg/kg) were determined; in addition, separate groups of rats were treated with methylphenidate (2.5 mg/kg) or saline before 12 consecutive nicotine (0.03 mg/kg/infusion) self-administration sessions. Next, the discriminative stimulus effects of nicotine (0.03-0.3 mg/kg) and methylphenidate (1.25-10 mg/kg), alone and in combination with a low nicotine dose (0.056 mg/kg), were tested in nicotine-trained rats. Finally, the locomotor effect of repeated methylphenidate (2.5 mg/kg) was tested in rats previously treated with nicotine (0.2-0.8 mg/kg). Results indicated that acute methylphenidate increased the rate of nicotine self-administration at doses that reduced sucrose-maintained responding; furthermore, tolerance to this effect was not apparent following repeated methylphenidate. Methylphenidate, while not substituting for nicotine alone, dose-dependently enhanced the discriminative stimulus effect of a low nicotine dose. In addition, repeated nicotine exposure promoted the development of locomotor sensitization to methylphenidate. Taken together with recent clinical findings, these results suggest that methylphenidate may enhance the abuse-related behavioral effects of nicotine, perhaps increasing vulnerability to tobacco dependence.

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Section: Discussionmentioning

confidence: 91%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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“…Furthermore, psychosocial treatments, such eas parental training and behavioral therapy seem to be effective only during its delivery, and their effects are rarely sustained long-term [7][8][9]. Considering the significant limitations of current available interventions, it has become a consensus among clinicians that new treatment options for ADHD are needed.…”

mentioning

confidence: 99%

Evidence-Based Information on the Clinical Use of Neurofeedback for ADHD

et al. 2012

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Summary Neurofeedback (NF) is a training to enhance selfregulatory capacity over brain activity patterns and consequently over brain mental states. Recent findings suggest that NF is a promising alternative for the treatment of attention-deficit/hyperactivity disorder (ADHD). We comprehensively reviewed literature searching for studies on the effectiveness and specificity of NF for the treatment of ADHD. In addition, clinically informative evidence-based data are discussed. We found 3 systematic review on the use of NF for ADHD and 6 randomized controlled trials that have not been included in these reviews. Most nonrandomized controlled trials found positive results with medium-to-large effect sizes, but the evidence for effectiveness are less robust when only randomized controlled studies are considered. The direct comparison of NF and sham-NF in 3 published studies have found no group differences, nevertheless methodological caveats, such as the quality of the training protocol used, sample size, and sample selection may have contributed to the negative results. Further data on specificity comes from electrophysiological studies reporting that NF effectively changes brain activity patterns. No safety issues have emerged from clinical trials and NF seems to be well tolerated and accepted. Follow-up studies support long-term effects of NF. Currently there is no available data to guide clinicians on the predictors of response to NF and on optimal treatment protocol. In conclusion, NF is a valid option for the treatment for ADHD, but further evidence is required to guide its use.

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“…Sampling time-points were set at 0, 3,6,12,24,48,72,96,120,144,168,192,216, and 240 h. The patch was removed after 168 h. Blood samples were collected from the ear vein. Plasma samples were separated by centrifugation (3500 rpm) for 10 min, processed using the solid extraction cartridge for extraction of clonidine as described above, and analyzed using the LC-MS method.…”

Section: Measurement Of Clonidine In Plasma Using Lc-msmentioning

confidence: 99%