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PubMed1987

Sustained release and standard methylphenidate effects on cognitive and social behavior in children with attention deficit disorder.

Two studies were conducted to investigate the relative effects of sustained release methylphenidate (Ritalin [SR-20]) and standard methylphenidate (Ritalin, 10 mg, administered twice daily). In the first study, 13 boys with attention deficit disorder participating in a summer treatment program went through a double-blind, within-subject trial of each form of methylphenidate and placebo. Measures of social and cognitive behavior were gathered in classroom and play settings. Although group analyses of the data showed that both drugs were effective and there were few differences between them, standard methylphenidate was superior to SR-20 on several important measures of disruptive behavior. Furthermore, analyses of individual responsivity showed clearly that most boys responded more positively to standard methylphenidate than to SR-20. The second study involved a partially overlapping group of nine boys with attention deficit disorder participating in the same summer treatment program. Also double-blind, within-subject, and placebo controlled, this study tracked the time courses of the two forms of methylphenidate. Both were shown to have similar time courses on the Abbreviated Conners Rating Scale and other measures, but SR-20 had a slower onset than did the standard drug form on a continuous performance task. Effects of SR-20 were still evident eight hours after ingestion.

Attention Deficit Disorder with Hyperactivity↗
PubMed1986

Testosterone dependent effects of methylphenidate on social investigatory behavior of the rat.

Previous work suggested a sex difference in social investigatory behavior of a novel conspecific during acute exposure to methylphenidate. In contrast to caffeine, which has been observed to increase social investigatory behavior only in males, methylphenidate decreased social investigatory behavior only in females. Testosterone-treated females were comparable to males and were unaffected by methylphenidate. Castrated males were comparable to females in their sensitivity to methylphenidate. Like caffeine, methylphenidate increased locomotor activity in both males and females, suggesting that drug effects on social investigation cannot be attributed to a nonspecific stimulant effect. The combined results reveal a sex-related interaction of circulating testosterone with acute methylphendiate exposure. Interpretations are discussed including the behavioral contrast following exposure to methylphenidate or to caffeine.

Animals↗
PubMed1987

Methylphenidate associated with narcotics for the treatment of cancer pain.

Thirty-two patients with chronic pain due to advanced cancer were treated with methylphenidate (10 mg with breakfast and 5 mg with lunch) for 3 days, versus placebo, in a randomized, double-blind, cross-over study designed to evaluate the capacity of methylphenidate to potentiate the analgesic effect of narcotics and/or to decrease sedation induced by narcotics. In 28 evaluable patients, the intensity of pain (visual analogue 0-100) and intake of extra doses of analgesics (number of doses/day) were 43 +/- 27 and 2.2 +/- 2.4 during methylphenidate, versus 55 +/- 24 (P less than 0.02) and 2.9 +/- 2.9 (P less than 0.002) during placebo, respectively. Activity and drowsiness (visual analogue 0-100) were 57 +/- 25 and 58 +/- 24 after methylphenidate, respectively, versus 41 +/- 26 (P less than 0.05) and 45 +/- 27 (P less than 0.02) after placebo. Upon completion of the study, the investigator and the patient chose methylphenidate blindly as a more useful drug in 23 cases (83%) and 20 cases (70%), respectively (P less than 0.02). No cases of severe toxicity were observed. We conclude that methylphenidate can increase the analgesic effect and decrease sedation of narcotics in this population.

Adult↗
PubMed1982

Methylphenidate treatment of hyperactive children: effects on the hypothalamic-pituitary-somatomedin axis.

To further define the influence of methylphenidate on the growth hormone-somatomedin axis and prolactin secretion, serum growth hormone and prolactin concentrations were assessed over 24 hours and in response to provocative stimuli. The nine hyperactive subjects were all studied during methylphenidate therapy and after drug discontinuation, Diurnal patterns of growth hormone and prolactin concentrations were assessed using an ambulatory, continuous blood withdrawal procedure to ensure that activity, caloric intake, and sleep patterns mimicked normal schedules. No significant difference in integrated concentration of growth hormone, fasting somatomedin concentration, or prolactin integrated concentration was detected between subjects receiving or not receiving methylphenidate. There was a significant increase in peak growth hormone response to arginine stimulation among subjects receiving methylphenidate therapy; however, this appeared to correlate with acute methylphenidate administration. These data do not support the hypothesis that growth defects in hyperactive children treated with methylphenidate are caused by alteration in the hypothalamic-pituitary-somatomedin axis.

Adolescent↗
PubMed1996

Increased methylphenidate usage for attention deficit disorder in the 1990s.

OBJECTIVE: To estimate the increased use and the prevalence of methylphenidate (Ritalin) treatment of youth with attention deficit disorder (ADD) during the 1990s. DESIGN: Using time-trend findings from two large population-based data sources, three pharmaceutical databases, and one physician audit, a best-fit estimate of the usage and the usage trends for methylphenidate treatment over the half decade from 1990 through 1995 was sought. SETTING: Five regions in the United States (US) and the nation as a whole. PATIENTS: Youths on record as receiving methylphenidate for ADD. RESULTS: The findings from regional and national databases indicate that on average, there has been a 2.5-fold increase in the prevalence of methylphenidate treatment of youths with ADD between 1990 and 1995. In all, approximately 2.8% (or 1.5 million) of US youths aged 5 to 18 were receiving this medication in mid-1995. The increase in methylphenidate treatment for ADD appears largely related to an increased duration of treatment; more girls, adolescents, and inattentive youths on the medication; and a recently improved public image of this medication treatment. CONCLUSION: The database findings presented serve to correct exaggerated media claims of a 6-fold expansion of methylphenidate treatment, although they do not clarify the issue of the appropriateness of this treatment.

Adolescent↗
PubMed1978

Methylphenidate in 6-hydroxydopamine-treated developing rat pups. Effects on activity and maze performance.

In order to better devine the relationship between brain catecholaminergic mechanisms and the clinical syndrome of minimal brain dysfunction, we have developed an experimental model that has many of the features of the disorder seen in children. This model is effected by the preferential depletion of brain dopamine in 5-day-old rat pups following the intracisternal administration of 6-hydroxydopamine, and in the present investigation, we have examined the effects of methylphenidate hydrochloride (0.25 to 2.0 mg/kg) on activity levels and cognitive performance in normal and 6-hydroxydopamine treated animals. Methylphenidate therapy resulted in a significant increase in activity levels of normal rat pups 12 and 19 days of age; in contrast, methylphenidate administered to 6-hydroxydopamine-treated animals did not increase activity at 12 days of age and significantly reduced activity at 19 and 26 days. Methylphenidate had no effect on T-maze performance in normals, but significantly improved performance in 6-hydroxydopamine-treated animals. Our results suggest that the "paradoxical" response to methylphenidate found in 6-hydroxydopamine-treated rat pups may be the result of central denervation supersensitivity.

Age Factors↗
PubMed1976

Methylphenidate, dextroamphetamine, and levamfetamine. Effects on schizophrenic symptoms.

Methylphenidate hydrochloride dextroamphetamine sulfate, and levamfetamine succinate have potential as pharmacologic tools for the indirect evaluation of the role of neurotransmitters in schizophrenia. In actively ill schizophrenic patients, methylphenidate administered intravenously causes a brief but clear intensification of preexisting psychotic symptoms, such as hallucinations and delusions. In our study, methylphenidate, dextroamphetamine, and levamfetamine were administered in equimolar doses to schizophrenic patients. Methylphenidate was a more effective activator of symptoms than dextroamphetamine, which in turn was more effective than levamfetamine. Levodopa (L-dopa) given orally also reportedly produces a temporary worsening of schizophrenic symptoms. While these findings augment a body of information suggesting that dopamine and norepinephrine may play a role in the activation of schizophrenic symptoms, our findings with methylphenidate (reportedly weak in eliciting stereotyped behaviour in rat) and our review of the literature indicate complexities that remain to be resolved. There is some utility of the procedure for differential diagnosis and selective therapy, but this is still of occasional and limited potential.

Acute Disease↗
PubMed1976

Comparative effects of methylphenidate and thioridazine in hyperkinetic children. I. Clinical results.

The effects of three pharmacological treatments, methylphenidate hydrochloride, thioridazine hydrochloride, a methylphenidate/thioridazine combination, and placebo were studied in outpatient hyperkinetic children rated hyperactive both in school and at home or clinic. Active treatment lasted 12 weeks; placebo lasted four weeks. Significant clinical improvement was obtained in a variety of settings--all treatments were superior to placebo on ratings filled out by parents, teachers, and clinic staff. Though initially the combination of methylphenidate and thioridazine tended to produce greater clinical improvement, it was not superior to methylphenidate alone after 12 weeks of treatment. Methylphenidate alone and the methylphenidate/thioridazine combination were more effective than thioridazine alone. The salient side effects with methylphenidate treatment were decrease in appetite, difficulty in falling asleep, and increased mood sensitivity. In contrast, thioridazine administration was associated with appetite increase and enuresis.

Administration, Oral↗
PubMed1985

Stimulants, urinary catecholamines, and indoleamines in hyperactivity. A comparison of methylphenidate and dextroamphetamine.

Children with attention deficit disorder with hyperactivity were given either methylphenidate hydrochloride or dextroamphetamine sulfate to compare the effects on urinary excretion of catecholamines, indoleamines, and phenylethylamine (PEA). Methylphenidate's effects were distinctly different from those of dextroamphetamine. After methylphenidate administration, both norepinephrine (NE) and normetanephrine (NMN) concentrations were significantly elevated, and there was a 22% increase in excretion of 3-methoxy-4-hydroxyphenylglycol (MHPG). In contrast, after dextroamphetamine treatment, MHPG excretion was significantly reduced and NE and NMN values were unchanged. Excretion of dopamine and metabolites was unchanged by either drug. Urinary PEA excretion was not significantly changed after methylphenidate treatment, but increased 1,600% in response to dextroamphetamine. Methylphenidate treatment did not significantly alter serotonin or 5-hydroxyindoleacetic acid excretion. Effects of dextroamphetamine were not tested.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Methylphenidate and growth in hyperactive children. A controlled withdrawal study.

The effect of stimulants on growth has been controversial. Among hyperactive children receiving long-term methylphenidate hydrochloride treatment, we examined the effects of methylphenidate withdrawal on the growth of hyperactive children randomly assigned to be taken off, or remain on, the medication regimen over two consecutive summers. After one summer, no group difference in height was found, but weight was higher in the group that had been taken off methylphenidate therapy. In contrast, two summers of being off methylphenidate treatment had a significant positive effect on height but not on weight. The results document a linkage between exposure to methylphenidate and reduction in growth velocity. However, they do not address whether the medication has long-term effects on height.

Adolescent↗
PubMed2006

Absence of association with DAT1 polymorphism and response to methylphenidate in a sample of adults with ADHD.

A polymorphism in the dopamine transporter gene (DAT1) has been previously associated with ADHD and methylphenidate has been hypothesized to block the dopamine transporter. The goal of this study was to examine whether a 40-bp variable number of tandem repeats (VNTR) of DAT1 moderate response and adverse effects associated with methylphenidate treatment of adults with ADHD. Subjects were 106 adults with ADHD enrolled in 6-week randomized placebo-controlled parallel design trials of methylphenidate (OROS and immediate release preparations). There was no evidence of an association between DAT1 VNTR and response to methylphenidate (F(2,100) = 0.04, P = 0.9). Similarly, there was no pattern of statistically significant association with DAT1 VNTR and cardiovascular or spontaneously reported adverse effects. We failed to identify an association with DAT1 and the response or tolerability of methylphenidate in adults with ADHD.

Adult↗
PubMed1979

A chemical ionization selected ion monitoring assay for methylphenidate and ritalinic acid.

A methane chemical ionization quantitative assay for methylphenidate and its major metabolite, ritalinic acid, is described. Methylphenidate and the internal standard, ethylphenidate, were extracted from plasma samples and derivatized to prevent thermal decomposition in the gas chromatography. Ritalinic acid was esterified with diazomethane and extracted as methylphenidate. The intensity of the protonated molecular ion of the derivatized drug and internal standard was measured by selected ion monitoring. Calibration curves were prepared from drug standards dissolved in drug-free plasma, and the lower limit of the curves extended to 0.5 ng methylphenidate per ml plasma. The method was used to generate plasma decay curves for pediatric patients undergoing methylphenidate therapy.

Child↗
PubMed1984

Methylphenidate, apomorphine, THIP, and diazepam in monkeys: dopamine-GABA behavior related to psychoses and tardive dyskinesia.

In eight monkeys (Cercopithecus aethiops), previously treated with haloperidol for 4-14 months, we have examined the behavioral effect of: (1) methylphenidate vs apomorphine; (2) 4,5,6,7-tetrahydroisoxazolo-(5,4-c)-pyridin-3-ol(THIP, a GABA agonist) vs diazepam; and (3) THIP and diazepam in methylphenidate-induced behavior. Methylphenidate (0.5-5.0 mg/kg) and apomorphine (0.1-0.5 mg/kg) both increased locomotion, but otherwise exhibited different behavioral profiles. Methylphenidate induced repetitive movements of head, limbs, and trunk, and hallucinatory-like behavior, but not oral hyperkinesia (licking and gnawing), whereas apomorphine preferentially caused oral hyperkinesia. THIP produced a syndrome of bradykinesia, dystonia, ataxia, myoclonus, sedation, and decreased responsiveness, whereas diazepam produced only bradykinesia, ataxia, sedation, and decreased responsiveness, but not dystonia and myoclonus. Methylphenidate-induced locomotion and repetitive movements were reduced by THIP and diazepam, whereas hallucinatory-like behavior was markedly aggravated by THIP, but not by diazepam.

Animals↗
PubMed1978

Methylphenidate and serum prolactin in man.

Methylphenidate induces psychostimulation and increases cardiovascular parameters, and its psychostimulant effects have been proposed to occur via a dopaminergic mechanism. The effect of methylphenidate on serum prolactin was utilized as a method of evaluating methylphenidate's central dopamimergic effects. Methylphenidate was not found to exhibit a consistent effect on serum prolactin. Thus, its effect on serum prolactin does not parallel its behavioral activating properties, suggesting that such activation may not involve dopamine. Possibly, norepinephrine or other noncatecholaminergic neurotransmitters are involved in methylphenidate-induced behavioral activation.

Adult↗
PubMed1978

Comparison of oral and intravenous methylphenidate.

Oral methylphenidate (1.0 mg/kg) and intravenous methylphenidate (0.5 mg/kg) were compared as to their ability to increase behavioral activation, pulse, blood pressure, and serum growth hormone. Intravenous methylphenidate was considerably more effective than oral methylphenidate in activating behavior and in increasing pulse and blood pressure. Although oral methylphenidate appeared to increase behavioral activation, this effect was not statistically significant.

Administration, Oral↗
PubMed1980

Flurazepam effects on methylphenidate-induced stereotyped behavior.

The effects of flurazepam (0.0, 0.5, and 3.0 mg/kg) on methylphenidate-induced increases in stereotypy, gnawing, sniffing, and locomotion were evaluated in Swiss-Webster mice in daytime and nighttime experiments. Methylphenidate (50 mg/kg) increased overall stereotypy and stereotyped gnawing behavior; two doses of methylphenidate (25 mg/kg and 50 mg/kg) increased locomotion and sniffing behavior. Flurazepam 3.0 mg/kg augmented methylphenidate-induced stereotyped gnawing behavior and stereotypy. Flurazepam significantly decreased locomotion and sniffing, but did not interact with methylphenidate's effects on locomotion and sniffing.

Animals↗
PubMed1996

Does haloperidol block methylphenidate? Motivation or attention?

The effect of methylphenidate preceded by a moderate dose of haloperidol on reaction times over the duration of a continuous performance test (CPT), was investigated in ten male children, with a DSM-III diagnosis of attention deficit disorder with hyperactivity disorder (ADDH). Using a within-subject double-blind design, the effects of methylphenidate preceded by haloperidol on reaction time during the first and second blocks of CPT test were compared. Methylphenidate maintained a significantly improved reaction time in the second block of the CPT test. When methylphenidate, preceded by placebo, was preceded by haloperidol this effect was not observed, suggesting opposing effects on attentional systems by methylphenidate versus haloperidol. The study is the first to examine the "blocking" effect of haloperidol over the course of a CPT. The results suggest that dopamine systems are involved in the maintenance of the CPT response, and support an "incentive motivation" theory of sustained attention.

Analysis of Variance↗
PubMed2002

The effects of methylphenidate on prepulse inhibition during attended and ignored prestimuli among boys with attention-deficit hyperactivity disorder.

RATIONALE AND OBJECTIVES: The present study investigated attentional modification of prepulse inhibition of startle among boys with and without attention-deficit hyperactivity disorder (ADHD). Two hypotheses were tested: (1) whether ADHD is associated with diminished prepulse inhibition during attended prestimuli, but not ignored prestimuli, and (2) whether methylphenidate selectively increases prepulse inhibition to attended prestimuli among boys with ADHD. METHODS: Participants were 17 boys with ADHD and 14 controls. Participants completed a tone discrimination task in each of two sessions separated by 1 week. ADHD boys were administered methylphenidate (0.3 mg/kg) in one session and placebo in the other session in a randomized, double-blind fashion. During each series of 72 tones (75 dB; half 1200-Hz, half 400-Hz), participants were paid to attend to one pitch and ignore the other. Bilateral eyeblink electromyogram startle responses were recorded in response to acoustic probes (50-ms, 102-dB white noise) presented following the onset of two-thirds of tones, and during one-third of intertrial intervals. RESULTS: Relative to controls, boys with ADHD exhibited diminished prepulse inhibition 120 ms after onset of attended but not ignored prestimuli following placebo administration. Methylphenidate selectively increased prepulse inhibition to attended prestimuli at 120 ms among boys with ADHD to a level comparable to that of controls, who did not receive methylphenidate. CONCLUSIONS: These data are consistent with the hypothesis that ADHD involves diminished selective attention and suggest that methylphenidate ameliorates the symptoms of ADHD, at least in part, by altering an early attentional mechanism.

Arousal↗