Hyperactivity treatment

The rationale behind CDK inhibition during anticancer treatment is to stop hyperactive cell cycles and to inhibit the activity of cyclins that are frequently overexpressed in human cancer. 

Treatment of attention deficit hyperactivity disorder (ADHD) in children with psychostimulants... 

Gibson AP, Bettinger TL, Patel NC, Crismon ML (2006) Atomoxetine versus stimulants for treatment of attention deficit/hyperactivity disorder. Ann Pharmacother 40 1134-1142... 

Somoza EC, Winhusen TM, Bridge TP, et al An open-label pilot study of methylpheni-date in the treatment of cocaine-dependent patients with adult attention deficit/ hyperactivity disorder. J Addict Dis 23 77—92, 2004 Sora 1, Wichems C, Takahashi N, et al Cocaine reward models conditioned place preference can be established in dopamine- and in serotonin-transporter knockout mice. Proc Natl Acad Sci U S A 95 7699-7704, 1998 Soral, Hall FS, Andrews AM, etal Molecular mechanisms of cocaine reward combined dopamine and serotonin transporter knockouts eliminate cocaine place preference. Proc Nad Acad Sci U S A 98 5300-5305, 2001 Spear J, Alderton D Psychosis associated with prescribed dexamphetamine use 0etter). 

The early report by Bradley (1937) on beneficial treatment effects with amphetamine in aggressive, destructive, irritable, and hyperactive boys was repeatedly eonfirmed by double-blind, placebo-controlled studies. Significant reductions in aggressive behavior and improvements in social interactions were found after treatment with 10 to 40 mg/day of d- or /-amphetamine for boys and girls, 5 to 14 years of age, who had been diagnosed as... 

In experiments with mice and squirrel monkeys, we confirmed and extended the antagonism of amphetamine-induced motor hyperactivity by naltrexone at the same time, however, amphetamine s disruption of aggressive and social behavior was not reversed by naltrexone (Winslow and Miczek, in press). Specifically, in mice, the resident s attack and threat behavior toward an intruder was even further reduced by amphetamine after naltrexone pretreatment (figure 7). Squirrel monkeys that are dominant within their social group exhibit significantly lower levels of aggressive display toward other group members and initiate fewer social interactions after amphetamine treatment naltrexone did not block these effects. The interactive effects of amphetamine and naltrexone on locomotor behavior are consistent with the proposed modulation of dopamine-mediated functions by opioids however, the interaction between amphetamine and naltrexone on social behavior appears to involve a different mechanism. 

Winsberg, B.G. Press, M. Bialer, I. and Kupietz, S. Dextroamphetamine and methylphenidate in the treatment of hyperactive/aggressive children. Pediatrics 53 236-241, 1974. 

Comorbid conditions must be addressed in order to maximize desired outcomes. For comorbid bipolar disorder and attention-deficit/hyperactivity disorder when stimulant therapy is indicated, treatment of mania is recommended before starting the stimulant in order to avoid exacerbation of mood symptoms by the stimulant. 

Recommend second-line and/or adjunctive agents that can be effective alternatives in the treatment of attention-deficit hyperactivity disorder when stimulant therapy is less than adequate. 

Treatment goals for attention-deficit hyperactivity disorder are to improve behavior, increase attention/response inhibition (ability to stay on task), and minimize side effects associated with pharmacotherapy. 

Pharmacotherapy is superior to behavioral therapy in the treatment of attention-deficit hyperactivity disorder. Behavior modification provided by parents and teachers in conjunction with pharmacotherapy improves treatment outcomes more than behavior therapy alone. 

American Academy of Pediatrics Subcommittee on Attention-Deficit/Hyperactivity Disorder and Committee on Quality Improvement. Clinical practice guideline Treatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics 2001 108 1033-1044. 

Wolraich ML, Wibbelsman CJ, Brown TE, et al. Attention-deficit/hyperactivity disorder among adolescents A review of the diagnosis, treatment, and clinical implications. Pediatrics 2005 115(6) 1734-1746. 

Brown CS and Cooke SC (1994). Attention deficit hyperactivity disorder, clinical features and treatment options. CNS Drugs, 1, 95-106. 

Reducing problematic behavior to biological causes calls for pharmaceutical solutions and here too powerful corporate interests foster such explanations. The redefinition of hyperactivity as Attention Deficit Disorder (ADD), for example, has significantly benefitted the pharmaceutical industry. The use of Ritalin as a treatment for ADD has doubled since 1995, and it is prescribed to over 4 million children in the US. Production of the drug is up 700 % since 1990, and 90 % of the production is consumed in the US where pharmaco-genomics is a burgeoning field. Europeans have been more cautious, and the International Narcotics Control Board of the UN has expressed concern about the growing tendency to redefine behavior as amenable to pharmaceutical modification. 

The answer is a. (Hardman, p 22L Katzang, p L3L) Methylphenidate is similar to amphetamine and acts as a CN5 stimulant, with more pronounced effects on mental than on motor activities. It is effective in the treatment of narcolepsy and attention-deficit hyperactivity disorders. 

In depressed patients, cortical-hypothalamic-pituitary-adrenal axis hyperactivity can be explained by the hypersecretion of CRF, and secondary pituitary and adrenal gland hypertrophy. Impaired negative feedback at various CNS sites, including the hippocampus and pituitary are also likely to contribute. Downregulation of hippocampal mineralocorticoid receptors and expression is reported in depressed suicides [50]. In bipolar disorder, hyperactivity of the cortical-hypothalamic-pituitary-adrenal axis has been observed [51]. This increase in cortical-hypothalamic-pituitary-adrenal axis activity has also been observed in mixed mood states, mania and in depression in rapidcycling patients. Partial reversal of HPA overactivity is associated with treatment and recovery from depression. 

Dresel, S., Krause, J., Krause, K. H. et al. Attention deficit hyperactivity disorder binding of 99mTc TRODAT-1 to the dopamine transporter before and after methylphenidate treatment. Eur. J. Nucl. Med. 27 1518-1524,2000. 

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