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PubMed1981

Pharmacokinetics and behavioral effects of methylphenidate in Thoroughbred horses.

In horses given (rapid IV) methylphenidate (Ritalin, alpha-phenyl-2-piperidinacetic acid methyl ester; 0.70 mg/kg), plasma concentrations of the drug decreased rapidly at first, with an apparent alpha half-life of about 19 minutes, and then more slowly, with an apparent beta half-life of about 2.4 hours. These data were well fitted by a 2-compartment open model. In blood, about 40% of the methylphenidate present was in the plasma fraction, and of this, about 80% was plasma-protein bound. If given by subcutaneous or IM injection, plasma concentrations of methylphenidate peaked in about 1 hour and were no longer detectable (cleared) from plasma by 6 hours. Urinary clearance time, however, was longer, and between 12 and 24 hours should be allowed for a dose of methylphenidate to "clear" from urine. Using a variable-interval responding apparatus, methylphenidate was shown to stimulate the responding rate of horses up to 6 times above base line, making it the most potent central stimulant tested in this responding apparatus to date. Peak central stimulation at 30 minutes after IV dosing was seen in horses given 0.4 to 1.0 mg of methylphenidate/kg.

Animals↗
PubMed1996

Methylphenidate augmentation of serotonin selective reuptake inhibitors: a case series.

BACKGROUND: The serotonin selective reuptake inhibitors (SSRIs) are effective in treating major depressive episodes. However, for the subgroups of patients who remain refractory to therapy, augmentation strategies can improve the efficacy of these agents. METHOD: We report the results of an open trial of methylphenidate to augment SSRIs in the treatment of five consecutive cases of DSM-III- R diagnosed major depression. RESULTS: Self-reported symptom reduction was achieved rapidly in all cases, with methylphenidate dosages ranging from 10 to 40 mg/day. Symptom remission was independent of the presence of attention-deficit/hyperactivity disorder. Also, the beneficial effects of the methylphenidate-SSRI combination appeared to be robust and sustained. No patients abused or misused methylphenidate. CONCLUSION: The empirical use of methylphenidate added to ineffective or only partially effective SSRI treatment appeared to be a rapid, safe, and efficacious alternative to existing augmentation strategies for the treatment of major depression. Prospective controlled studies are required to confirm or refute these findings.

Adult↗
PubMed1999

Blockade of striatal dopamine transporters by intravenous methylphenidate is not sufficient to induce self-reports of "high".

The reinforcing effects of cocaine and methylphenidate have been linked to their ability to block dopamine transporters (DAT). Using positron emission tomography (PET), we previously showed that intravenous cocaine induced a significant level of DAT blockade, which was associated with the intensity for self-reports of "high" in cocaine abusers. In this study, we measured DAT occupancies after intravenous methylphenidate and assessed whether they also were associated with the "high". Occupation of DAT by intravenous MP was measured with PET using [11C]cocaine, as a DAT ligand, in eight normal control subjects tested with different methylphenidate doses. The ratio of the distribution volume of [11C]cocaine in striatum to that in cerebellum, which corresponds to Bmax/Kd + 1, was used as measure of DAT availability. In parallel, self-reports of "high" were measured. Methylphenidate produced a dose-dependent blockade of DAT with an estimated ED50 of 0.075 mg/kg. DAT occupancies were significantly correlated with the "high" (p <.03). However, four of the eight subjects, despite having significant levels of DAT blockade, did not perceive the "high". Methylphenidate is as effective as cocaine in blocking DAT in the human brain (cocaine ED50 = 0.13 mg/kg), and DAT blockade, as for cocaine, was also associated with the "high". However, the fact that there were subjects who despite significant DAT blockade did not experience the "high" suggests that DAT blockade, although necessary, is not sufficient to produce the "high".

Adult↗
PubMed1963

Behavioral effects of caffeine, methamphetamine, and methylphenidate in the rat.

It was possible to distinguish three closely-related psychomotor stimulants, caffeine, methamphetamine, and methylphenidate, by means of two operant behavior procedures, fixed interval and fixed number. Under the fixed interval procedure, the percentage change in the number of R(B)s per reinforcement was significantly smaller with caffeine than with methamphetamine or methylphenidate (p < .001). Under the fixed number procedure, the percentage change was significantly smaller with methamphetamine than with caffeine or methylphenidate (p < .001). Thus, methylphenidate had a methamphetamine-like effect under fixed interval and a caffeine-like effect under fixed number.

Animals↗
PubMed1989

Methylphenidate in children with seizures and attention-deficit disorder.

This study assessed the safety and efficacy of methylphenidate in children with seizures and attention-deficit disorder. Ten children, aged 6 years 10 months to 10 years 10 months, without seizures while receiving a single antiepileptic drug, were evaluated in a double-blind medication-placebo crossover study with methylphenidate hydrochloride was administered at 0.3 mg/kg per dose and given at 8 AM and 12 PM on school days only. The use of methylphenidate was associated with statistically significant improvements on the Conners' Teacher Rating Scale and on the Finger Tapping Task and with trends toward improvement on the Matching Familiar Figures Test and Discriminant Reaction Time tests. No child had seizures during the study period nor subsequently for those who continued receiving psychostimulants. There were no significant changes of epileptiform features or back-ground activity on electroencephalograms and no alterations in antiepileptic drug levels. Methylphenidate may be a safe and effective treatment for certain children with seizures and concurrent attention-deficit disorder.

Attention Deficit Disorder with Hyperactivity↗
PubMed1976

Methylphenidate effects in learning disabilities. Psychometric changes.

Sixty-one children of average intelligence with appreciable learning lags, but no behaviour disorders, received placedo or methylphenidate hydrochloride for a 12-week period. Methylphenidate was instrumental in improving performance on many psychological tests, but did not affect performance on standardized achievement tests. None of the patient characteristics investigated was stringly predictive of drug effect. Methylphenidate seems to have a specific effect on visualmotor processes, which in turn positively affect performance tasks, but not verbal tasks. Under the conditions of this study, methylphenidate treatment alone did not emerge as a useful agent for the amelioration of reading performance, although the data provide evidence for stimulation effects on children's cognitive functions.

Adolescent↗
PubMed1977

Methylphenidate hydrochloride effects on psychological tests in acute schizophrenic and nonpsychotic patients.

Actively psychotic schizophrenic and nonpsychotic psychiatric inpatients received intravenous methylphenidate hydrochlroide (0.5 mg/kg). Each patient was rated for level of psychosis and talkativeness, and each received the Holtzman projective ink blot tests and the Kent-Rosanoff word-association tests before, during, and after methylphenidate infusion. Minnesota Multiphasic Personality Inventory Goldberg Index scores were also obtained as a general measure of psychosis. For the entire patient group, methylphenidate infusion was followed by a significant increase in talkativeness and psychosis ratings and in pathological responses to the Holtzman ink blot test. There was a significant decrease in common word associations. Since neither of the psychological tests allow more than one response per item, it appears that methylphenidate truly effects pathological thought processes and decreases common word associations as such, rather than merely making these processes more evident by increasing verbalization.

Acute Disease↗
PubMed1978

Methylphenidate vs dextroamphetamine vs caffeine in minimal brain dysfunction: controlled comparison by placebo washout design with Bayes' analysis.

Double-blind crossover comparison of methylphenidate hydrochloride, dextroamphetamine sulfate, and caffeine after placebo washout in 29 children with minimal brain dysfunction (MBD) showed on six ratings that methylphenidate and dextroamphetamine were significantly (P less than .05 to P less than .001) better than placebo and caffeine, but not significantly (P less than .05) different from each other. Placebo, caffeine, and ratings before drug did not differ significantly. Of 26 drug responders, 12 responded best to dextroamphetamine, ten to methylphenidate, and one to caffeine. The latter child showed no improvement at all with either prescription stimulant. Methylphenidate and dextroamphetamine were each efficacious for six children who did not respond to the other stimulant. All three drugs showed significant (P less than .05) weight loss and cardiovascular side effects, the latter possibly spurious. Dextroamphetamine showed a significant (P less than .05) decrease from placebo in "tummyaches."

Attention Deficit Disorder with Hyperactivity↗
PubMed1978

The effect of methylphenidate on serum growth hormone: influence of antipsychotic drugs and diagnosis.

Intravenously administered methylphenidate, 0.5 mg/kg, causes a consistent rise in human serum growth hormone level, with peak values usually occurring 30 minutes after infusion. This rise is attenuated in patients receiving various antipsychotic medications administered on a long-term basis and is decreased in schizophrenic and drug-dependent patients. Methylphenidate causes increases in talkativeness, blood pressure, and pulse that generally parallel increases in serum growth hormone level. However, in contrast to the methylphenidate-induced rise in serum growth hormone level, methylphenidate-induced changes in cardiovascular variables and talkativeness are not altered by antipsychotic medications or diagnostic classification.

Adjustment Disorders↗
PubMed1984

Methylphenidate effects on symptoms of attention deficit disorder in adults.

The objectives of this study were (1) to determine whether attention deficit disorder (ADD) is a specific diagnostic entity in adulthood; (2) to evaluate, using a double-blind crossover design, the efficacy of methylphenidate hydrochloride in adults with evidence of residual ADD with hyperactivity (ADD-H) (N = 26); and (3) to evaluate the specificity of drug response by also administering methylphenidate to patients with similar adult symptoms but no childhood history of ADD-H (N = 35). Results indicated success in differentiating relatively distinct groups. However, no overall benefit from methylphenidate was evident, regardless of childhood history of ADD-H. Approximately 25% of the sample appeared clinically to benefit from methylphenidate, but no clear-cut predictors of drug response were identified; history of drug abuse (polydrug) appeared to be the best predictor. Even among the responders, benefit was generally not as marked nor as clinically valuable as in childhood ADD-H.

Adolescent↗
PubMed1995

Efficacy of methylphenidate for attention-deficit hyperactivity disorder in children with tic disorder.

BACKGROUND: The findings from case reports and patient questionnaire surveys have been interpreted as indicating that administration of stimulants is ill-advised for the treatment of attention-deficit hyperactivity disorder in children with tic disorder. METHODS: Thirty-four prepubertal children with attention-deficit hyperactivity disorder and tic disorder received placebo and three dosages of methylphenidate hydrochloride (0.1, 0.3, and 0.5 mg/kg) twice daily for 2 weeks each, under double-blind conditions. Treatment effects were assessed using direct observations of child behavior in a simulated (clinic-based) classroom and using rating scales completed by the parents, teachers, and physician. RESULTS: Methylphenidate effectively suppressed hyperactive, disruptive, and aggressive behavior. There was no evidence that methylphenidate altered the severity of tic disorder, but it may have a weak effect on the frequency of motor (increase) and vocal (decrease) tics. CONCLUSION: Methylphenidate appears to be a safe and effective treatment for attention-deficit hyperactivity disorder in the majority of children with comorbid tic disorder.

Attention Deficit Disorder with Hyperactivity↗
PubMed2000

Negative ion chemical ionization for the determination of methylphenidate in human plasma by stable isotope dilution gas chromatography/mass spectrometry.

A sensitive and specific method for the determination of methylphenidate in human plasma is presented. Methylphenidate was extracted from plasma by solvent extraction with hexane at pH 9.3 and derivatized to its heptafluorobutyrate derivative. The derivative was measured by gas chromatography/negative ion chemical ionization mass spectrometry without any further purification. Using this detection mode, a diagnostically useful fragment ion at m/z 369 was obtained at high relative abundance. (18)O(2)-labelled methylphenidate was used as an internal standard and its rapid and facile preparation from the unlabeled compound is described. Calibration graphs were linear within the range 0.14-18.25 ng ml(-1). The inter-assay precision was 8.7% (0.14 ng ml(-1)) and 3.1% (4.56 ng ml(-1)) and the intra-assay variability was 1.3% (0.14 ng ml(-1)) and 0.4% (4.56 ng ml(-1)). Accuracy determinations showed deviations of +0.7% (0.14 ng ml(-1)) and -2.5% (4.56 ng ml(-1)). The method is rugged, rapid and robust and has been applied to the batch analysis of methylphenidate during pharmacokinetic profiling of the drug.

Central Nervous System Stimulants↗
PubMed1975

A reproducible gas chromatographic mass spectrometric assay for low levels of methylphenidate and ritalinic acid in blood and urine.

A rapid, sensitive method of analysis for methylphenidate and ritalinic acid in blood and urine has been developed using gas chromatography mass spectrometry and selected ion monitoring for separation and detection. The methylphenidate is isolated by solvent extraction into chloroform and the ritalinic acid is isolated by salting out into isopropyl alcohol, followed by methylation and subsequent solvent extraction. The method has been applied to the study of methylphenidate metabolism and excretion in adults and hyperactive children undergoing treatment with methylphenidate.

Adult↗
PubMed2006

Oral methylphenidate fails to elicit significant changes in extracellular putaminal dopamine levels in Parkinson's disease patients: positron emission tomographic studies.

In this study, we assessed the changes of endogenous dopamine (DA) levels in response to methylphenidate in 5 patients with idiopathic Parkinson's disease (PD) and 6 healthy controls. Three-dimensional positron emission tomography was performed with the D2 receptor antagonist [11C]raclopride (RAC) at baseline and 1 hour following the administration of oral methylphenidate (0.8 mg/kg) to assess changes in dopamine levels indirectly. Oral methylphenidate produced no significant change in extracellular DA levels in the putamen, as estimated by comparing changes in RAC binding at baseline and 1 hour following its administration in PD subjects and healthy controls. However, there were small changes in RAC binding of opposite direction in caudate and ventral striatal regions compared between the two groups. Although there was no consistent improvement in motor function in the PD group, some patients did experience a subjective high in response to methylphenidate (MP). Failure of oral MP to alter extracellular DA levels in putamen could result from degeneration of presynaptic dopaminergic terminals, with consequent severe reductions in the levels of endogenous DA and dopamine transporter in PD subjects. Our data provide in vivo neurochemical support for the lack of clinical efficacy following MP in PD patients and are also in keeping with reduced DA release following amphetamine in PD subjects.

Administration, Oral↗
PubMed1994

Mercuric chloride and p-chloromercuriphenylsulfonate exert a biphasic effect on the binding of the stimulant [3H]methylphenidate to the dopamine transporter.

Mercuric chloride was found to have a biphasic effect on the binding of the radiolabeled stimulant [3H]methylphenidate to membranes from a crude synaptosomal preparation of rat striatal tissue. Binding was enhanced at low concentrations of HgCl2, reaching a maximum of 62% above control values at 2.5 microM HgCl2. It was inhibited in a dose-dependent manner at concentrations greater than 5 microM HgCl2, with an IC50 of 7.2 microM. The increase in binding observed at the low concentrations of HgCl2 was shown by Scatchard analysis to be due to an increase in the affinity of [3H]methylphenidate for its binding site on the dopamine transporter, while a decrease in both affinity and Bmax accompanied the reduction of [3H]methylphenidate binding observed at the higher concentrations of the inorganic mercury compound. The sodium salt of the organic mercurial p-chloromercuriphenylsulfonic acid also caused an increase in [3H]methylphenidate binding (159% above controls at 2,000 microM), followed by an immediate decrease in binding at higher concentrations of the reagent. Because both of these mercury-containing compounds have a high propensity for interacting with sulfhydryl groups, these data suggest that the cysteine residues in the dopamine transporter molecule may play an important role in the regulation of stimulant binding to the uptake complex.

4-Chloromercuribenzenesulfonate↗
PubMed1995

A randomized, crossover evaluation of methylphenidate in cancer patients receiving strong narcotics.

Sedation may be a dose-limiting side-effect of opioid therapy in some cancer patients. This study was designed to evaluate further the use of the psychostimulant, methylphenidate, an agent that has been reported to counter-act opioid-induced sedation, in patients with cancer-related pain. Patients receiving a stable dose of an opioid for cancer-related pain were recruited for this randomized, double-blind, crossover clinical trial. In addition to their regular dose of narcotics, they received 5 days of methylphenidate followed by 5 days of placebo, or vice versa. Our data did not definitively demonstrate any statistically significant benefit for methylphenidate, but did suggest that this drug could mildly decrease narcotic-induced drowsiness and could increase night-time sleep. These data, in conjunction with other published data, suggest that methylphenidate can counteract narcotic-induced daytime sedation to a limited degree.

Adolescent↗
PubMed1977

The effect of methylphenidate on test performance in the cognitively impaired aged.

It was hypothesized that a central nervous system stimulant with relatively weak peripheral effects would facilitate test performance in the cognitively impaired aged. Twelve elderly subjects participated in a counter-balanced, crossover comparison of 10 mg methylphenidate, 30 mg methylphenidate and placebo. All treatments were administered double-blind as a single dose of oral medication. Neither dosage of active medication was found to effect psychomotor or psychological test performance, subjective report, heart rate or blood pressure. A subsequent open trial of 45 mg methylphenidate resulted in heart rate, blood pressure and subjective changes in two of eight subjects but no effects on test performance. The results suggest that cognitive performance in the moderately impaired aged is unimproved following administration of methylphenidate, and perhaps similar sympathomimetic amines, below a dosage level associated with clinically significant peripheral effects.

Aged↗
PubMed1982

State-dependent learning in children receiving methylphenidate.

Methylphenidate state-dependent learning was investigated using a paired-associate learning task of 16 pairs of pictures. Subjects were 15 children for whom methylphenidate was currently being prescribed. Each child was seen for two learning sessions and two testing sessions. Learning took place under placebo and under the child's regular dosage of methylphenidate. During retention testing all combinations of learning drug-state and testing drug-state were observed for each child. Data were analyzed using contrast variables which took into account the repeated-measures nature of the design. The results indicated that there was a trend in the direction of state-dependence in the whole sample. Significant symmetrical state-dependent effects were obtained in those subjects whose original learning was facilitated by methylphenidate.

Adolescent↗