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PubMed1979

Growth of hyperactive children treated with methylphenidate.

This is a study of the growth of 72 hyperactive boys treated continuously with methylphenidate hydrochloride. Major findings were that methylphenidate produces an adverse effect on growth in height and in weight in the first year of treatment, but not in the second year; the first year height deficit is offset in the second year by a greater-than-expected growth rate. No clinical predictors of growth deficits were found; growth in height deficits are not related to total dosage or summer drug holidays, but weight deficits may be related to these factors. Side effects did not correlate with dosage. The temporary growth deficits of the first year are of such minor magnitude as to have little clinical significance.

Body Height↗
PubMed1980

Pemoline, methylphenidate, and placebo in children with minimal brain dysfunction.

An eight-week double-blind comparison between pemoline (Cylert), methylphenidate (Ritalin) hydrochloride, and placebo was carried out on 60 hyperactive children. Measurements of home, school, achievement, cognitive function, and global clinical status were made at baseline, midtreatment, end of treatment, and posttreatment. Both drugs produced improvement in all areas except the achievement measures. One major difference between drugs was the apparently longer action of pemoline, since its effects at home and school tended to persist when the drug was withdrawn, whereas the patients receiving methylphenidate tended to regress to their baseline levels.

Attention Deficit Disorder with Hyperactivity↗
PubMed1983

Growth of hyperactive children on maintenance regimen of methylphenidate.

The growth in height and weight of 86 hyperactive children receiving methylphenidate hydrochloride (average, 40 mg/day for up to four years) was compared with general population norms on recently updated growth charts. A significant decrease in height percentile was apparent after 2, 3, and 4 years of treatment but not after one year. A significant loss in weight percentile occurred onward from the first year of treatment. Dosage was significantly associated with the decrease in height and weight percentile. Greater initial height and weight were associated with greater growth decrements. The use of adjunctive thioridazine hydrochloride (mean, 87 mg/day) did not influence the growth of children receiving methylphenidate. Although the magnitude of the growth suppressant effect in groups was small (dosage accounted for only 2% of the variance in final height), the results suggest that clinicians should monitor the growth of hyperactive children receiving stimulants and consider dosage reduction in individual cases should evidence of growth suppression occur.

Attention Deficit Disorder with Hyperactivity↗
PubMed1988

Hyperactive boys almost grown up. III. Methylphenidate effects on ultimate height.

The height of young adults who were treated with methylphenidate hydrochloride in childhood because of hyperactivity (average daily dose, 45 mg; duration of treatment, six months to five years) was studied. There was no significant difference in height between the treated patients (n = 61) and controls (n = 99); both groups were at the national US norm in stature. The findings indicated that methylphenidate therapy does not compromise final height, even when it has an adverse impact on children's growth rate during the active treatment phase. A compensatory growth rate, or growth rebound, appears to occur following discontinuation of stimulant therapy.

Attention Deficit Disorder with Hyperactivity↗
PubMed2003

Association of the 480 bp DAT1 allele with methylphenidate response in a sample of Irish children with ADHD.

Several studies have implicated the dopamine transporter gene (DAT1) as conferring susceptibility to attention deficit hyperactivity disorder (ADHD), in particular, a VNTR situated at the 3' end of the gene. In addition, the 10-repeat VNTR allele associated with ADHD has been reported to be associated with an over-active transporter protein (DAT). Thus children possessing this variant might be particularly responsive to methylphenidate, a drug known to act by blocking DAT. We have examined this hypothesis and now report an association between the 10-repeat VNTR DAT1 polymorphism and retrospectively rated methylphenidate response in a sample of 119 Irish children with ADHD (chi(2) = 7.918, df = 1, P = 0.005). Our findings suggest a role for the 10-repeat DAT1 risk allele in medication response and may help to predict positive clinical outcome in ADHD.

Attention Deficit Disorder with Hyperactivity↗
PubMed1975

Deanol and methylphenidate in minimal brain dysfunction.

Deanol, a putative acetylcholine precursor, has been used as a treatment for childhood hyperactivity for years. Efficacy has not been satisfactorily established, however. Seventy-four children referred for problems with learning, including many with hyperactivity, were screened for neurological or psychiatric illness, then given deanol, methylphenidate, or placebo in a double-blind fashion for 3 months. Maintenance dose for methylphenidate was 40 mg daily; for deanol, 500 mg. Behavior rating forms, reaction time, and a series of standard psychometric tests were given before and after treatment. Both drugs showed significant improvement on a number of tests; the pattern and degree of change differed slightly for the two. In this paradigm, deanol thus appeared to improve performance in children with learning and behavior disorders. The mechanism of action remains speculative; proof that deanol increases acetylcholine is scanty, and there is a theoretical basis for actually assuming an anticholinergic effect. Further clinical studies on deanol are indicated.

Analysis of Variance↗
PubMedDate not supplied

Deep neck abscesses secondary to methylphenidate (Ritalin) abuse.

Methylphenidate (Ritalin) abuse has been and continues to be a major medical and social problem. In the past 6 months, we have seen five deep neck abscesses secondary to intravenous Ritalin abuse. This constitutes more than 50% of the deep neck abscesses seen by us in the same time period. The pathogenesis is related to an inflammatory foreign-body reaction to the fillers in the methylphenidate tablets, followed by superinfection by oral or cutaneous flora. Mixed flora infections with weakly pathogenic organisms may also occur.

Abscess↗
PubMed1977

Pharmacokinetics of methylphenidate in the rat using single-ion monitoring GLC-mass spectrometry.

A GLC-mass spectrometric assay for methylphenidate in biological fluids was developed using the ethyl ester homolog of the drug as the internal standard. The procedure has a lower level of sensitivity of 1.2 ng/ml and is based on GLC-mass spectrometic monitoring of the m/e 180 ion common to the mass spectra of the N-trifluoroacetyl derivatives of the drug and internal standard. The brain and plasma levels of methylphenidate in rats were determined after intravenous administration of 0.5 mg/kg of the drug. The two-compartment open pharmacokinetic model fit the data.

Animals↗
PubMed1986

Role of monoamine pathways in attention and effort: effects of clonidine and methylphenidate in normal adult humans.

Methylphenidate (0.65 mg/kg), clonidine (200 micrograms) or placebo were administered to normal adult males undertaking a dichotic monitoring task in which they were required to detect nominated target words and discriminate them from phonemic distractors. Following placebo, performance was better when attention was focused than when divided. Following clonidine, subjects were poorer and slower at discriminating targets during both divided and focused attention and subjectively were withdrawn and reported difficulties with concentration. Methylphenidate had no effect on target discrimination or response time but raised the rate of response and had marked effects on spontaneous behaviour in which an increased attention capacity was generally reported. The effects on attention of the pharmacological agents employed in this study are attributed to their effects on central monoamines. The disparity noted between objective and subjective assessments of attention is discussed in terms of the voluntary allocation of effort.

Adolescent↗
PubMed1986

Methylphenidate and memory: dissociated effects in hyperactive children.

Fourteen children with Attention Deficit Disorder with Hyperactivity (ADD + H) were administered the psychostimulant methylphenidate in a double-blind, placebo-controlled, crossover study. Subjects were evaluated on a well-validated measure of verbal memory and learning with an experimental design comprised of four conditions: placebo and active drug at three doses. Positive memory effects were found in the drug conditions. Significant dose-response relationships were found, indicating enhanced learning from placebo to low to medium to high dose. However, there was a differential drug effect on the memory task; methylphenidate selectively enhanced storage and retrieval mechanisms without affecting immediate acquisition.

Attention Deficit Disorder with Hyperactivity↗
PubMed1988

Low doses of methylphenidate (Ritalin) may alter the delay-of-reinforcement gradient.

The present study investigated effects of methylphenidate on spatio-temporal distributions of responses generated by a fixed interval 60-s schedule of reinforcement. A response panel with 20 different response locations (holes) made it possible to distinguish effects of the drug on the procedurally-correct response (correct according to the contingencies) and effects on other topographically similar responses acting as functionally-adequate responses. Detailed flow charts show how the dynamics of responding changed with dose and segment of the fixed interval. The number of holes visited was increased after low and medium doses, but decreased after high doses. The spatial differences between responses in the initial and the final parts of the fixed interval gradually disappeared after 6 mg/kg or higher doses as the functionally-adequate responses moved to earlier segments of the fixed interval. Few results could, however, be described as response rate dependent. Distributions of responses around the correct hole illustrated differences between procedurally-correct and functionally-adequate classes. The number of holes included in the latter class changed by dose in an inverted U-shaped fashion. Perseverations and stereotyped responding increased with increasing dose. Most of the effects may be described as motor stimulatory. One way of explaining the stimulatory effect is in terms of a lengthened delay-of-reinforcement gradient. The rate-dependent effect of methylphenidate on the procedurally-correct class after some doses may have been due to the combined effects of a lengthened delay gradient increasing the response rates early in the interval and interference from perseverations having their most detrimental effects on the high rates late in the interval.

Animals↗
PubMed1987

Effects of amphetamine, methylphenidate, and apomorphine on regional brain serotonin and 5-hydroxyindole acetic acid.

Electrophysiological and cytofluorometric data suggest that doses of amphetamine which enhance locomotor activity and promote focused stereotypies produce pronounced effects on serotonin pathways in the CNS. However, the biochemical evidence regarding changes in serotonergic function produced by moderate doses of this drug is inconsistent. Therefore, the present study was designed to further examine the effects of amphetamine (1-5 mg/kg) on regional brain serotonin and its metabolite and to compare these effects to behaviorally comparable doses of methylphenidate and apomorphine. At doses which produce a multiphasic behavioral response pattern, including a stereotypy phase consisting primarily of repetitive head movements and occasional oral stereotypies, amphetamine (3 mg/kg) and methylphenidate (30 mg/kg) increased levels of 5HIAA in striatum and frontal cortex, two brain regions which receive serotonergic projections from the dorsal raphe nucleus. In contrast, these drugs decreased or had no effect on 5HIAA levels in hippocampus, a brain region which receives its serotonergic innervation from the median raphe nucleus. A moderate dose of apomorphine (0.5 mg/kg) produced a comparable pattern of neurochemical effects. These data are consistent with electrophysiological and cytofluorometric data suggesting enhanced dorsal raphe serotonergic function following amphetamine-like stimulants. Pretreatment of animals with alpha-methyltyrosine at a dose sufficient to prevent the locomotor stimulation and stereotypy promoted by amphetamine, or by haloperidol, failed to prevent the amphetamine-induced increase in 5HIAA, indicating that these serotonergic effects are not secondary to the amphetamine facilitation of dopaminergic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1975

The effects of methylphenidate and haloperidol on the heart rate and blood pressure of hyperactive children with special reference to time of action.

Twelve hyperactive-aggressive children were given single acute doses of placebo, methylphenidate (0.3 mg/kg) and haloperidol (0.035 mg/kg) on three separate occasions in a double blind crossover design with drug order randomized across subjects. Resting heart rates and systolic and diastolic blood pressures were obtained at nine intervals up to 7 hrs and electrocardiograms at 150 min after ingestion. Methylphenidate caused a small trend toward an increment in heart rate and a significant increment in blood pressure, while the changes with haloperidol were minimal. There were no EKG changes. Changes in heart rate were of a minimal nature as compared with those occurring with digestion which tended to obscure drug effects.

Analysis of Variance↗
PubMed1975

Differential effects of methylphenidate on reticular formation and thalamic neuronal activity.

Intravenous administration of methylphenidate (1 or 2 mg/kg) markedly attenuated the unit discharge rate in the mesencephalic reticular formation of rats and cats. Concurrently this drug enhanced the neural activity in the primary sensory nuclei of the thalamus. The differential effect of methylphenidate on these two neural systems suggest a possible mechanism by which it may improve attentive processes in hyperkinesis.

Acoustic Stimulation↗
PubMed1976

Tolerance in methylphenidate-induced locomotion in prairie dogs (Cynomys ludovicianus).

After a five-day adaptation period in activity wheels, four prairie dogs were assigned to a methylphenidate group (2.5 mg/kg, s.c.) and four prairie dogs were assigned to a saline group for ten consecutive daily injections. Half-revolutions of locomotor activity were recorded during seven measurement periods taken daily. During the third measurement period, from 1-3 hrs following injection, the methylphenidate group declined in locomotor activity over the first three days of drug administration.

Animals↗
PubMed1977

Comparative effects of d-amphetamine, l-amphetamine, and methylphenidate on mood in man.

The comparative effects of d-amphetamine, l-amphetamine, and methylphenidate were assessed in 16 normal subjects, using a double-blind, crossover placebo-controlled design. Within the dose range tested, the efficacy ratio of d-amphetamine:l-amphetamine was about 2:1, and graphic presentation of dose response scores indicated a relatively small difference in potency between the amphetamine isomers. Methylphenidate was intermediate in efficacy between d-amphetamine and l-amphetamine. The efficacy ratios for d-amphetamine:l-amphetamine on increasing euphoric mood in man were similar to the previously reported ratios of there two isomers in inducing or exacerbating psychosis in humans. These findings do not support the suggestion, made by Snyder and others, that the differential effects of d-amphetamine vs. l-amphetamine on a specific type of behavior in man could be utilized to infer the predominance of noradrenergic vs. dopaminergic mediation of amphetamine's effects on this behavior.

Adult↗
PubMed1978

Haloperidol and lithium blocking of the mood response to intravenous methylphenidate.

The euthymic manic-d-pressive patients with therapeutic plasma lithium levels were each given two i.f. infusions of 30 mg of methylphenidate. The infusions were separated by at least 3 days. Before one infusion each patient was given 5 mg of haloperidol i.v. and before the other infusion each was given an identical volume of saline. A psychiatric observer was blind to the nature of the pretreatment and the order of pretreatment was randomized. Saline pretreated patients showed marked activation and euphoriant responses despite therapeutic lithium levels. Haloperidol pretreatment reduced this response in three patients and eliminated the euphoriant and activating response in the remaining seven patients. These results agree with the existence of a dopaminergic step in the induction of methylphenidate-induced activation and euphoria.

Adult↗
PubMed1978

The effects of methylphenidate on repeated acquisition of serial discrimination reversals.

Rats were trained to bar-press for sucrose solution in the presence of one of two stimulus conditions. On each daily training session, the stimulus during which bar-pressing was reinforced was reversed. The subjects were trained in this Serial Discrimination Reversal procedure until successive acquisitions of the discrimination had stabilized. Drug treatments consisting of saline or 0.25, 1.0, 2.0, 4.0, 6.0 or 8.0 mg/kg of methylphenidate were then administered 20 min prior to the daily training sessions. Acquisition of the discrimination was enhanced by low doses of methylphenidate (1,2, and 4 mg/kg) and attentuated by higher doses (6 and 8 mg/kg).

Animals↗