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PubMed1977

Effects of prior experience and 'functional disturbance' on acute and chronic tolerance to methylphenidate.

The degree of habituation or adaptation an animal has experienced prior to the administration of methylphenidate was found to be more crucial in determining the animal's response to the drug than chronic drug administration alone. Rats allowed to adapt in a Y-maze for 24 days showed less methylphenidate-induced activity than animals receiving chronic administration of saline or methylphenidate but no adaptation, when animals were injected with the drug and tested in the Y-maze on Day 25. Animals also were shown to develop tolerance to the methylphenidate-induced activity.

Adaptation, Psychological↗
PubMed1997

Assessment of endogenous dopamine release by methylphenidate challenge using iodine-123 iodobenzamide single-photon emission tomography.

This double-blind, placebo-controlled study assessed pharmacologically induced endogenous dopamine (DA) release in healthy male volunteers (n=12). Changes in endogenous DA release after injection of the psychostimulant drug methylphenidate were evaluated by single-photon emission tomography (SPET) and constant infusion of iodine-123 iodobenzamide ([123I]IBZM), a D2 receptor radioligand that is sensitive to endogenous DA release. Methylphenidate induced displacement of striatal [123I]IBZM binding, resulting in a significantly decrease in the specific to non-specific [123I]IBZM uptake ratio (average: 8.6%) in comparison with placebo (average: -1.9%). Moreover, injection of methylphenidate induced significant behavioural responses on the following items: excitement, anxiety, tension, and mannerisms and posturing. The results of this study demonstrate the feasibility of using constant infusion of [123I]IBZM and SPET imaging to measure endogenous DA release after methylphenidate challenge and to investigate neurochemical aspects of behaviour.

Adult↗
PubMed1984

Self-control in hyperactive boys in anger-inducing situations: effects of cognitive-behavioral training and of methylphenidate.

The effects of cognitive-behavioral intervention and methylphenidate on anger control in hyperactive boys were investigated in two studies. The anger-inducing stimuli in both studies involved verbal provocation from peers. Study 1 assessed a brief intervention using self-control strategies, while Study 2 employed a longer training period and a control intervention that focused on enhancement of empathy. Both studies included methylphenidate versus placebo comparisons. Methylphenidate reduced the intensity of the hyperactive boys' behavior but did not significantly increase either global or specific measures of self-control. Cognitive-behavioral treatment, when compared to control training, was more successful in enhancing both general self-control and the use of specific coping strategies. There was no advantage for the combination of methylphenidate plus cognitive-behavioral intervention. Implications for intervention to ameliorate the social and interpersonal difficulties of hyperactive children are discussed.

Adolescent↗
PubMed1988

The effects of methylphenidate on levels of processing and laterality in children with attention deficit disorder.

Effects of stimulant medication (methylphenidate) on levels (feature, name, semantic) of word processing by the left and right hemisphere were assessed in 31 attention-deficit-disordered children. In a double-blind procedure, same-different decisions were made to tachistoscopically presented word pairs under medication and placebo. Analysis of manual response times failed to show any negative effects of medication. Feature decisions were faster than name decisions, which were faster than semantic decisions. Methylphenidate induced a right visual field advantage (left hemisphere) for the name decision, which was interpreted as a normalization effect. The results suggest that (1) methylphenidate may selectively improve the phonological level of word processing and (2) methylphenidate's favorable therapeutic effect is produced through inhibition of excessive right hemisphere activity in response to task demands that engage the left hemisphere.

Adolescent↗
PubMed1993

Fenfluramine and methylphenidate in children with mental retardation and attention deficit hyperactivity disorder: laboratory effects.

Twenty-eight children took part in a double-blind, placebo-controlled, crossover study of fenfluramine and methylphenidate. Fenfluramine dosage was gradually increased to a standardized dose of 1.5 mg/kg per day, whereas methylphenidate was given in doses of 0.4 mg/kg per day. The children were assessed on laboratory tests of selective and sustained attention, visual matching, and color matching, during which seat activity was monitored automatically. Results showed fenfluramine to be superior to placebo on the memory task, whereas methylphenidate reduced commission errors on a continuous performance test. Methylphenidate caused shorter response times, and fenfluramine caused increases, on two of the tests. Examiner behavior ratings indicated significant improvements with both drugs on the domains of attention, activity level, and mood. These findings, together with those from a companion clinical study, suggest that the drugs may have contrasting mechanisms of action, but both appear to have useful clinical effects in these children.

Adolescent↗
PubMed2005

A phase II study of methylphenidate for the treatment of fatigue.

BACKGROUND: Cancer-related fatigue (CRF) is one of the most distressing symptoms patients experience and is seen well after the completion of treatment. Methylphenidate (Ritalin) use includes the treatment of opiate-induced somnolence, depression, and reduced cognition. This phase II study was performed to evaluate the effects of methylphenidate on CRF. PATIENTS AND METHODS: The criteria for the eligibility of patients included the following: a history of breast cancer, absence of disease for greater than 6 months but less than 5 years, a hemoglobin level of >12 g%, less than moderate depression on the Brief Zung Self-administered Depression Scale, and a score of > or =4 on the Brief Fatigue Inventory (BFI). Patients received methylphenidate, 5 mg, orally, twice daily, for 6 weeks, with a dose escalation on week 2 if the BFI score remained > or =4 and no significant toxicities were reported. A response was defined as a decrease in the BFI score of at least two points on weeks 4 and 6 as compared to baseline. RESULTS: Between May 2001 and May 2003, 37 patients were entered and treated. On weeks 4 and 6, 20 of 37 (54%) responded with a decreased BFI score greater than two points, averaging a decrease of 3.5. Although six patients (19%) withdrew due to adverse events, these were reported as grade 1. CONCLUSION: This study suggests that women with breast cancer who are suffering from moderate to severe fatigue may benefit from methylphenidate.

Adult↗
PubMed2006

Does brief, clinically based, intensive multimodal behavior therapy enhance the effects of methylphenidate in children with ADHD?

OBJECTIVE: The additional value of a short-term, clinically based, intensive multimodal behavior therapy to optimally titrated methylphenidate in children with attention-deficit hyperactivity disorder (ADHD) was investigated. METHOD: Fifty children with ADHD (ages 8-12) were randomized to treatment of methylphenidate or treatment with methylphenidate combined with 10 weeks of multimodal behavior therapy. The multimodal behavior therapy consisted of a child and parent behavioral therapy and a teacher behavioral training. Assessments included parent, teacher and child ratings of ADHD symptoms, oppositional and conduct behavior, social skills, parenting stress, anxiety and self-worth. RESULTS: Both treatment conditions yielded significant improvements on all outcome domains. No significant differences were found between both treatments. CONCLUSIONS: No evidence was found for the additive effect of multimodal behavior therapy next to optimally titrated methylphenidate. CLINICAL IMPLICATIONS: This study does not support the expectation that optimally dosed stimulant treated children with ADHD should routinely receive psychosocial treatment to further reduce ADHD- and related symptoms.

Adrenergic Uptake Inhibitors↗
PubMed1991

Behavioral and biochemical effects of methylphenidate in schizophrenic and nonschizophrenic patients.

The authors examined the specific behavioral and biochemical effects of intravenous methylphenidate in a sample of schizophrenic and nonschizophrenic patients. Twenty drug-free patients participated in a double-blind, placebo randomized study of methylphenidate, with multiple samples of plasma homovanillic acid (HVA) and serum growth hormone (GH) obtained during the infusion procedure. Methylphenidate caused a significant increase in positive symptoms that was relatively specific to the schizophrenic patients and was evident even in those with otherwise dormant symptomatology. When behavioral response was correlated with the biochemical responses (i.e., changes in plasma HVA and GH), there was a significant positive relationship between the increase in the BPRS-positive symptoms as well as the hostility/suspiciousness factor, and the increase in GH. These results suggest that the expression of psychotic symptoms may be associated with increased dopaminergic postsynaptic sensitivity, although the nonspecific nature of methylphenidate's actions discourages a stronger interpretation of the results.

Adult↗
PubMed1976

Methylphenidate-like effects of the new antidepressant drug nomifensine (HOE 984).

Nomifensine (HOE 984) belongs to a chemically new class of drugs with reported antidepressant properties. Nomifensine, like methylphemidate, d-amphetamine and apomorphine, induces strong, intense stereotypes behaviour in the rat. The nomifensine-induced stereotyped behaviour was completely antagonized by pretreatment with reserpine (7.5 mg/kg, 18 h) but not by short-time pretreatment with alpha-methyltyrosine (250 mg/kg, 2 h.) Nomifensine thus differs from d-amphetamine and apomorphine but resembles methylphenidate on stereotyped behaviour. Nominfensine, M1 (8-amino-2-methyl-4-(4-hydroxyphenyl)-1,2,3,4-tetrahydroisoquinoline fumarate) (Hoechst), methylphenidate and d-amphetamine induced a strong increase in the brain level of homovanillec acid (HVA), whereas the dopamine uptake inhibitor benztropine induced no changes in HVA and cocaine induced only a small increase. Nomifensine and the M1 metabolite, like methylphenidate, also increased 3,4-dihydroxyphenylacetic acid (DOPAC) whereas amphetamine, apomorphine, benztropine and cocaine decreased this dopamine metabolite. This suggests that the stereotyped licking and/or biting activities in the rat are related to dopamine releasing properties of nomifensine, methylphenidate and amphetamine. This is further supported by an inverse relationship between the in vitro dopamine uptake inhibitory concentrations and the sterotypy-inducing dose levels of nomifensine and d-amphetamine. Amphetamine caused a strong, and nomifensine and apormorphine a week increase in brain 3-methoxy-4-hydroxyphenylglycol (MOPEG).

Animals↗
PubMed1985

The effects of surgical and chemical lesions on striatal [3H]threo-(+/-)-methylphenidate binding: correlation with [3H]dopamine uptake.

The specific binding of [3H]threo-(+/-)-methylphenidate to membranes prepared from rat striatum was significantly reduced following either surgical lesions of the medial forebrain bundle or intracerebroventricular administration of 6-hydroxydopamine. The decrease in the density of [3H]threo-(+/-)-methylphenidate binding sites in striatum following chemical or surgical denervation was highly correlated with the decrease in [3H]dopamine uptake. In contrast, intracerebroventricular administration of 5,7-dihydroxytryptamine, AF64A, or chronic parenteral administration of reserpine did not alter either the number of apparent affinity of [3H]threo-(+/-)-methylphenidate binding sites. These data suggest that the specific binding sites for [3H]-threo-(+/-)-methylphenidate in striatum are localized to dopaminergic nerve terminals, and may be associated with the dopamine transport complex.

5,7-Dihydroxytryptamine↗
PubMed1989

Acute and chronic effects of methylphenidate on cortical adrenoceptors in the rat.

The effects of acute and chronic treatments with methylphenidate were examined on cortical adrenoceptors. A single dose of methylphenidate increased the affinity of [3H]prazosin and [3H]idazoxan binding sites. Acute and chronic methylphenidate treatments caused a down-regulation of alpha 1-adrenoceptors. There were no changes in cortical beta-adrenoceptors measured with [3H]dihydroalprenolol nor in endogenous monoamine levels. The alterations in alpha-adrenoceptors can be attributed to an indirect action of methylphenidate possibly through an accrued release of noradrenaline or tyramine.

Animals↗
PubMed1987

Discriminative stimulus effects of caffeine: tolerance and cross-tolerance with methylphenidate.

Twice daily injection of caffeine (30 mg/kg) for 3-1/2 days shifted the caffeine stimulus generalization curve to the right by 3-fold in rats trained to discriminate saline from 30 mg/kg of caffeine, and by 4-fold in rats trained to discriminate saline from 10 mg/kg of caffeine. The latter group was also tested for cross-tolerance with methylphenidate, a drug that generalizes completely with caffeine. Twice daily injection of caffeine (30 mg/kg) for 3-1/2 days increased the ED50 of methylphenidate for caffeine-appropriate responding from 1.5 to 5.5 mg/kg. Conversely, injections of methylphenidate (3.0 mg/kg) increased the ED50 of caffeine from 5.2 to 15 mg/kg. The development of symmetrical cross-tolerance to the discriminative effects of caffeine and to the caffeine-like discriminative effects of methylphenidate supports previous observations suggesting commonalities in the cellular bases of the stimulus properties of these drugs.

Animals↗
PubMed1991

Effects of triadimefon on a multiple schedule of fixed-interval performance: comparison with methylphenidate, d-amphetamine and chlorpromazine.

Triadimefon is a fungicide that has recently been shown to increase motor activity and rates of schedule-controlled responding. These findings indicate that triadimefon resembles psychomotor stimulants and in this respect is a unique pesticide. The present experiment was designed to evaluate triadimefon's effects on performance maintained by a multiple schedule of reinforcement and to compare triadimefon to known psychomotor stimulants. Four rats were trained to perform under a mult FI 1-min FI 5-min schedule of milk reinforcement. They then received a series of dosages of triadimefon (10-170 mg/kg, IP) and of methylphenidate (1-17.3 mg/kg, IP) in a counterbalanced order. Triadimefon increased response rates in both the FI 1-min and FI 5-min components. Methylphenidate did not consistently alter response rates in either component. Temporal patterns of responding were disrupted much more in the FI 5-min component than in the FI 1-min component by both triadimefon and methylphenidate. Performances were then evaluated following a series of dosages of d-amphetamine (0.3-3.0 mg/kg, IP) and chlorpromazine (0.5-2.0 mg/kg, IP). Response rates were increased by d-amphetamine in the FI 1-min component but not in the FI 5-min component. Like triadimefon and methylphenidate, d-amphetamine produced a greater disruption of response patterning in FI 5-min than in FI 1-min. Only chlorpromazine decreased response rates in both components. Chlorpromazine also disrupted FI 5-min response patterning, but left FI 1-min patterning intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The spontaneously hypertensive rat as an animal model of attention-deficit hyperactivity disorder: effects of methylphenidate on exploratory behavior.

Spontaneously hypertensive rats (SHR) show a pervasive hyperactivity in several paradigms. Thus, these rats may be used as an animal model of childhood hyperactivity also called Attention-Deficit Hyperactivity Disorder. This disorder is frequently treated with psychomotor stimulant drugs, but little is known about the effects of such drugs on behavior. The present study investigated the behavioral effects of 1-24 mg/kg methylphenidate (Ritalin) on the exploratory behavior of male SHR and Wistar-Kyoto control rats (WKY) in a two-compartment free-exploration open field. Except following very high doses. SHR spent most of the session time in the field while WKY stayed in the home cage. Low and medium doses were followed by increased activity in the field for SHR and increased activity in the cage for WKY. The response-stimulatory effects of low to medium doses of methylphenidate are less in SHR than in WKY. Starting at medium doses, activity decreased and stereotyped behavior increased progressively by increasing dose. Locomotor activity in the field decreased following lower doses than locomotor activity in the cage, and vertical activity (rearing) was reduced by lower doses than horizontal activity (crossing). The following conclusions were drawn. (i) There is no "paradoxical" inhibition of SHR hyperactivity following methylphenidate. On the contrary, SHR activity is in fact stimulated, albeit to a lesser degree than that of WKY. (ii) The stimulatory effects of low to medium doses are, in general, most pronounced for the kind of exploratory behavior most frequently used by the rat during baseline conditions. (iii) Rearing might be more susceptible to adverse effects of methylphenidate than ambulation.

Animals↗
PubMed1991

Characterisation of methylphenidate and nomifensine induced dopamine release in rat striatum using in vivo brain microdialysis.

The in vivo effects of methylphenidate (50 mg/kg) and nomifensine (20 mg/kg) on dopamine release and metabolism in the rat striatum were studied using brain microdialysis. Dialysate catecholamine content was measured by high pressure liquid chromatography with electrochemical detection. Both compounds increased the dialysate content of dopamine (430% and 320% of basal efflux, respectively). Release was inhibited by reducing extracellular calcium levels and by infusion of tetrodotoxin (2 microM) via the dialysis probe (calcium free-39 +/- 18% of control, methylphenidate; 40 +/- 17% of control, nomifensine; tetrodotoxin-35 +/- 19% of control, methylphenidate; 40 +/- 14% of control, nomifensine) and also by prior depletion of dopamine storage pools using reserpine (5 mg/kg) (15 +/- 12% of control, methylphenidate; 19 +/- 9% of control, nomifensine). Dialysate levels of dihydroxyphenylacetic acid were not altered by either drug whereas homovanillic acid levels increased. These data suggest that both drugs increase dialysate dopamine content by facilitating Ca2(+)-dependent vesicular release most probably by inhibition of dopamine reuptake.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Omega-conotoxin GVIA inhibits the methylphenidate-induced but not methamphetamine-induced behavior.

We investigated the effects of antagonists for omega-conotoxin GVIA (omega-CTX)-sensitive N-type voltage-sensitive calcium channels (N-channels) on methylphenidate- and methamphetamine-induced behavior. I.c.v. injection of omega-CTX or neomycin, both N-channel antagonists, caused a dose-dependent inhibition of methylphenidate-induced hypermotility in mice but failed to inhibit methamphetamine-induced hyperactivity. Further, omega-CTX inhibited the circling behavior induced by methylphenidate in rats that had kainic acid-induced unilateral striatal lesions. These results suggest that calcium influx through omega-CTX-sensitive N-channels plays an important role in methylphenidate-induced behavior.

Animals↗
PubMed1994

Simultaneous detection of methylphenidate and its main metabolite, ritalinic acid, in doping control.

Two analytical methods for the simultaneous detection in urine of methylphenidate and its main metabolite, ritalinic acid, are described. Both procedures are based on solid-phase extraction of urine samples on Bond Elut Certify columns, and capillary gas chromatographic-mass spectrometric detection of O-trimethylsilyl, N-trifluoroacetyl derivatives. The former method is used as a general screening procedure for the detection of basic polar nitrogen-containing compounds in urine such as stimulants, narcotic and adrenergic drugs. The latter procedure is proposed as a specific method to confirm methylphenidate ingestion. The two methods are sensitive enough to detect methylphenidate and ritalinic acid in urine at least for 24 h after administration of a therapeutic dose (20 mg oral dose) of methylphenidate.

Gas Chromatography-Mass Spectrometry↗
PubMed1989

Differential effects of methylphenidate and dextroamphetamine on the motor activity level of hyperactive children.

An acceleration-sensitive device was used to measure motor activity continuously through the day in 18 hyperactive boys in a day hospital program. The children received methylphenidate, dextroamphetamine, or placebo daily after breakfast and lunch in an 11-week double-blind crossover trial. Differential effectiveness of the two drugs in lowering motor activity was found. Methylphenidate significantly lowered activity measurements in a morning structured classroom and in less structured activities in the afternoon. Dextroamphetamine effects on activity were similar, although they did not differ significantly from placebo effects between 11:00 AM and noon in our classroom setting. Methylphenidate produced a greater decrement in motor activity than did dextroamphetamine between 11:00 AM and 1:00 PM. There were no significant differences in activity level between drug doses within each drug phase across the dose ranges used (for methylphenidate 0.45 to 1.25 mg/kg given twice daily, and for dextroamphetamine 0.2 to 0.6 mg/kg given twice daily). Plasma drug concentrations did not correlate with decrements in activity for either drug.

Child↗