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PubMed2006

Multisite controlled study of OROS methylphenidate in the treatment of adolescents with attention-deficit/hyperactivity disorder.

BACKGROUND: Despite the persistence of attention-deficit/hyperactivity disorder (ADHD) into adolescence, little is known about the efficacy and tolerability of stimulant medications in this age group. OBJECTIVE: To report the results of a multisite controlled study among adolescents with ADHD evaluating the efficacy and tolerability of osmotic-release oral system (OROS) methylphenidate. DESIGN: Adolescents (N = 220) having a confirmed Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnosis of ADHD underwent dose titration to identify dosages of OROS methylphenidate that improved symptoms to predefined criteria. Subjects successfully completing the dose titration phase (n = 177) (ie, tolerated and responded to treatment and adhered to the protocol) were randomized to receive 2 weeks' treatment with their individualized dosage of OROS methylphenidate (18, 36, 54, or 72 mg once daily) or placebo. Treatment effectiveness was measured using investigator, parent, and adolescent assessments of ADHD. RESULTS: A significant reduction from baseline in the investigator-rated ADHD Rating Scale, the primary efficacy measure, was found with OROS methylphenidate treatment compared with placebo. Similar findings were noted with parent- and adolescent-report measures. Based on a Clinical Global Impression improvement subscale score of much or very much improved, 52% of subjects in the OROS methylphenidate group improved compared with 31% receiving placebo. Thirty-seven percent of subjects required the maximum dosage of 72 mg/d. The incidence of drug-related adverse events was similar between the 2 study groups. CONCLUSION: In adolescents, once-daily OROS methylphenidate significantly reduced ADHD symptoms and was well tolerated using dosages up to 72 mg/d.

Administration, Oral↗
PubMed1995

A double-blind, crossover comparison of methylphenidate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder.

BACKGROUND: There are few controlled studies of methylphenidate hydrochloride in adults with attention-deficit hyperactivity disorder (ADHD), and their results have been equivocal. The discrepancies among these studies may be related to low doses, diagnostic uncertainties, and lack of attention to comorbid disorders. METHODS: We conducted a randomized, 7-week, placebo-controlled, crossover study of methylphenidate in 23 adult patients with DSM-III-R ADHD using standardized instruments for diagnosis, separate assessments of ADHD and depressive and anxiety symptoms, and a robust daily dose of methylphenidate hydrochloride, 1.0 mg/kg per day. RESULTS: We found a marked therapeutic response for methylphenidate treatment of ADHD symptoms that exceeded the placebo response (78% vs 4%, P < .0001). Response to methylphenidate was independent of gender, psychiatric comorbidity with anxiety or moderate depression, or family history of psychiatric disorders. CONCLUSION: Robust doses of methylphenidate are effective in the treatment of adult ADHD.

Adolescent↗
PubMed1997

Clinical efficacy of methylphenidate in conduct disorder with and without attention deficit hyperactivity disorder.

BACKGROUND: Stimulants are not considered appropriate for the treatment of children with conduct disorders (CDs). The postulated differences in stimulant effect between children with attention deficit hyperactivity disorder (ADHD) and CD led to the hypothesis that methylphenidate hydrochloride, which is effective in ADHD, would not significantly improve symptoms of CD. METHODS: We randomly assigned 84 children with CD, between the ages of 6 and 15 years, to receive methylphenidate hydrochloride (up to 60 mg/d) or placebo for 5 weeks. Behavior was evaluated by parent, teacher, and clinician reports and by direct classroom observations. Two thirds of the children also met criteria for ADHD. RESULTS: Contrary to prediction, ratings of antisocial behaviors specific to CD were significantly reduced by methylphenidate treatment. The magnitude of methylphenidate effect indicated meaningful clinical benefit. Partialling out severity of ADHD did not alter the significant superiority of methylphenidate on CD ratings specifically (P < .001). CONCLUSIONS: Methylphenidate has short-term positive effects on children and adolescents with CD. Key aspects of antisocial adjustment appear to be treatment responsive. This effect was independent of severity of the children's initial ADHD symptoms.

Adolescent↗
PubMed2001

Effects of chronic and acute methylphenidate hydrochloride (Ritalin) administration on locomotor activity, ultrasonic vocalizations, and neuromotor development in 3- to 11-day-old CD-1 mouse pups.

The present study examined the effects of chronic and acute treatment with methylphenidate hydrochloride (Ritalin) on isolation-induced ultrasonic vocalizations, spontaneous locomotor activity, and neuromotor coordination in 3- to 11-day-old CD-1 mouse pups. In Experiment 1, 3- to 11-day-old pups received daily injections of saline, 5 mg/kg or 20 mg/kg of methylphenidate hydrochloride, or no injection and were tested on postnatal Days 3, 5, 7, 9, and 11. Both doses of methylphenidate resulted in significant increases in locomotor activity at all ages, but had no significant effect on body weight, neuromotor development, or emission of ultrasonic vocalizations. In Experiment 2, pups were given a single dose of methylphenidate (5 or 20 mg/kg), saline, or no injection on one of postnatal Days 5, 7, 9, or 11. This acute methylphenidate treatment increased locomotor activity, but had no significant effects on ultrasonic vocalizations or neuromotor coordination. These results indicate that short-term, chronic methylphenidate treatment elevates locomotor responses, but has no immediate effects on anxietylike responses or on the development of neuromotor behavior of CD-1 mice in the first 11 days of life.

Animals↗
PubMed2005

Regional cerebral blood flow in children with attention deficit hyperactivity disorder: comparison before and after methylphenidate treatment.

Differences in brain activity of children with attention deficit hyperactivity disorder (ADHD) have been compared to normal healthy controls, suggesting neural correlates of cognitive/behavioral symptoms. Symptoms are improved with methylphenidate treatment but limited sources can be cited to show how brain activity in ADHD is altered after pharmacologic treatment. We investigated how long-term oral medication of methylphenidate affects the resting regional cerebral blood flow (rCBF) in ADHD children, using single photon emission computerized tomography (SPECT). rCBF was decreased in the orbitofrontal cortex and middle temporal gyrus in the right hemisphere whereas it was increased in the dorsomedial prefrontal and somatosensory area bilaterally in drug-naive ADHD children compared to control child subjects. After treatment with methylphenidate, the extent of hyperperfusion in the somatosensory area was reduced and significant reduction of rCBF was found in the right striatum for the first time. Methylphenidate treatment also resulted in rCBF increase in superior prefrontal and reduction in ventral higher visual areas bilaterally. The results indicated that improving ADHD symptom after methylphenidate is associated with normalization of abnormally reduced orbitofrontal activity and abnormally increased somatosensory cortical activity. These changes were accompanied with reduced striatum activity lower than that of normal controls. These changes might be associated with improving ADHD to control attention and motor response to irrelevant environmental stimuli after methylphenidate treatment.

Attention Deficit Disorder with Hyperactivity↗
PubMedDate not supplied

Methylphenidate in children with hyperactivity: review and cost-utility analysis.

OBJECTIVE: To evaluate the effectiveness and cost effectiveness of methylphenidate in the treatment of children with hyperkinetic disorder as defined using ICD-10 criteria. DESIGN: Comprehensive literature review and cost utility analysis comparing methylphenidate treatment with placebo. Costs and effects were estimated from a NHS perspective according to the methodology developed by the previous South and West Development and Evaluation Committee. The number of Quality Adjusted Life Years (QALYs) gained was estimated by using the Index of Health Related Quality of Life to model treatment effects. RESULTS: Evidence from good and medium quality randomized controlled trials shows benefits of methylphenidate over weeks and months respectively. Evidence beyond 6 months is poorer and it is uncertain whether effects of methylphenidate persist into adolescence and adulthood. Methylphenidate is of reasonable cost-effectiveness when considering short- and medium- term benefits with an estimated cost per QALY of 7 pounds 400 to 9 pounds 200 at 1997 prices. CONCLUSIONS: Short-term treatment of hyperkinetic children with methylphenidate is effective and cost effective.

Attention Deficit Disorder with Hyperactivity↗
PubMed1997

Chiral drugs: comparison of the pharmacokinetics of [11C]d-threo and L-threo-methylphenidate in the human and baboon brain.

Methylphenidate (Ritalin) is the most commonly prescribed psychoactive medication for children in the US where it is used for the treatment of attention deficit hyperactivity disorder. Methylphenidate is marketed as a racemic mixture of the d-threo and l-threo enantiomers. It is believed that the d enantiomer is responsible for the therapeutic effect of methylphenidate. In this study we labeled the individual enantiomers with carbon-11 and compared their binding and pharmacokinetics in the human and baboon brain. Microdialysis studies in the rat were performed to compare their potency in elevating striatal dopamine concentration. Positron emission tomographic (PET) studies with [11C]d-threo-methylphenidate ([11C]d-threo-MP) demonstrated highest regional uptake in basal ganglia. In contrast, [11C]l-threo-methylphenidate ([11C]l-threo-MP) displayed similar uptakes in all brain regions. The ratios of distribution volumes at the steady-state for the basal ganglia to cerebellum (DVBG/DVCB) ranged from 2.2 to 3.3 for [11C]d-threo-MP in baboon and human, and only 1.1 for [11C]l-threo-MP. Pretreatment with unlabeled methylphenidate (0.5 mg/kg) or GBR12909 (1.5 mg/kg) markedly reduced the striatal but not the cerebellar uptake of [11C]d-threo-MP, whereas there was no effect on DVBG/DVCB for [11C]l-threo-MP. In the rat, d-threo-MP increased extracellular dopamine concentration by 650% whereas l-threo-MP did not affect dopamine levels. These results indicate that pharmacological specificity of MP resides entirely in the d-threo isomer and directly show that binding of the l-isomer in human brain is mostly nonspecific.

Aged↗
PubMed1994

Methylphenidate and nortriptyline in the treatment of poststroke depression: a retrospective comparison.

The hospital charts of elderly stroke patients with major depression, as determined by DSM-III-R criteria, who were treated with either methylphenidate (n = 28) or nortriptyline (n = 30) were retrospectively reviewed. Fifty-three percent of the methylphenidate patients experienced complete remission of depressive symptoms. Similarly, 43% of the patients in the nortriptyline group showed remission of depressive symptomatology. Whereas the response rates between the two treatment groups were not significantly different in the patients who did respond to treatment (chi 2 = .608, df = 1, p = NS), the speed of response was significantly better in the methylphenidate group (t[13] = 15.9, p < .001). The average peak response time for the methylphenidate patients was 2.4 days compared to 27 days for the nortriptyline group. This finding is consistent with previous reports suggesting a rapid response to methylphenidate and other psychostimulants, typically between 24 and 72 hours. Adverse side effects, such as cardiac changes, did not differ between groups, generally falling in the mild range of severity. These data suggest that the rapid effects of methylphenidate may be especially useful to speed recovery from depression so that patients can participate more fully in rehabilitation programs.

Aged↗
PubMed1994

Binding of bromine-substituted analogs of methylphenidate to monoamine transporters.

We synthesized the o-, m- and p-bromo derivatives of dl-threo-methylphenidate from the corresponding bromophenylacetonitriles by modification of the literature synthesis of methylphenidate (Panizzon, Helv. Chim. Acta 1944, 27, 1748). In in vitro binding assays all three dl-threo bromo compounds had higher affinities than methylphenidate for dopamine transporter sites labeled with [3H]2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane ([3H]WIN 35,428; IC50 = 13, 4, 20 and 82 nM for o-, m-, and p-bromo compounds, and unsubstituted methylphenidate, respectively). They also bound more strongly than methylphenidate to norepinephrine reuptake sites labeled with [3H]nisoxetine (IC50 = 32, 20, 31 and 440 nM, respectively), but were weak ligands (IC50 > or = 1 microM) at the serotonin transporter labeled with [3H]paroxetine. In addition, the bromine substituted derivatives demonstrated similar activity to methylphenidate in vivo in rodents in terms of inhibition of heart uptake of [3H](-)-norepinephrine, elevation of striatal extracellular dopamine, and stimulation of locomotor activity.

Animals↗
PubMed1995

Binding of d-threo-[11C]methylphenidate to the dopamine transporter in vivo: insensitivity to synaptic dopamine.

The regional distribution of [11C]d-threo-methylphenidate in mouse brain was very similar to that of [3H]WIN 35,428 ((-)-2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane), and the two radioligands were displaced from striatum similarly after administration of the potent cocaine analog RTI-55 ((-)-2 beta-carbomethoxy-3 beta-(4-iodophenyl)tropane). However, while striatal [3H]WIN 35,428 increased between 5 and 30 min, striatal [11C]d-threo-methylphenidate halved. Thus [11C]d-threo-methylphenidate binds similarly to but more reversibly than [3H]WIN 35,428. The methyl ester of L-DOPA (L-3,4-dihydroxyphenylalanine; 200 mg/kg) plus benserazide plus clorgyline, which markedly elevates rat striatal extracellular dopamine (Wachtel and Abercrombie, 1994, J. Neurochem. 63, 108), decreased the mouse striatum-to-cerebellum ratio for [11C]d-threo-methylphenidate at 30 min by 13% (P < 0.05). In positron emission tomographic (PET) baboon studies [11C]d-threo-methylphenidate binding was insensitive to drugs expected to lower endogenous dopamine. These experiments suggest that normal synaptic dopamine does not compete for binding with [11C]d-threo-methylphenidate, and will not affect PET measures of dopamine transporter availability.

Animals↗
PubMed1996

Affinities of methylphenidate derivatives for dopamine, norepinephrine and serotonin transporters.

We have synthesized several derivative of dl-threo-methylphenidate (Ritalin) bearing substituents on the phenyl ring. IC50 values for binding these compounds to rat brain monoamine transporters were assessed using [3H]WIN 35,428 (striatal membranes, dopamine transporters, DAT), [3H]nisoxetine (frontal cortex membranes, norepinephrine transporters, NET) and [3H]paroxetine (brain stem membranes, 5HT transporters, 5HTT). Affinities (1/Ki) decreased in the order: DAT > NET >> 5HTT. Substitution at the para position of dl-threo-methylphenidate generally led to retained or increased affinity for the dopamine transporter (bromo > iodo > methoxy > hydroxy). Substitution at the meta position also increased affinity for the DAT (m-bromo > methylphenidate; m-iodo-p-hydroxy > p-hydroxy). Substitution at the ortho position with bromine considerably decreased affinity. Similar IC50 values for binding of o-bromomethylphenidate to the dopamine transporter were measured at 0, 22 and 37 degrees. N-Methylation of the piperidine ring of methylphenidate also considerably reduced affinity. The dl-erythro isomer of o-bromomethylphenidate did not bind to the DAT (IC50 > 50,000 nM). Affinities at the dopamine and norepinephrine transporters for substituted methylphenidate derivatives were well correlated (r2=0.90). Abilities of several methylphenidate derivatives to inhibit [3H]dopamine uptake in striatal synaptosomes corresponded well with inhibition of [3H]WIN 35, 428 binding. None of the compounds examined exhibited significant affinity to dopamine D1 or D2 receptors (IC50 > 500 or 5,000 nM, respectively), as assessed by inhibition of binding of [3H]SCH 23390 or [123I]epidepride, respectively, to striatal membranes.

Animals↗
PubMed1979

Methylphenidate and d-amphetamine: effects and interactions with alphamethyltyrosine and tetrabenazine on DRL performance in rats.

The effects of d-amphetamine and methylphenidate and their interactions with amine-depleting drugs were examined in rats trained to press a lever to obtain water reinforcement on a schedule that differentially reinforced responding at low rates (DRL). Both methylphenidate (2.5-20.0 mg/kg) and d-amphetamine (0.375-3.0 mg/kg) increased the rate of responding and decreased the frequency of reinforcement on the DRL schedule. Both drugs also shifted the interresponse time (IRT) distributions to the left such that the modal IRT occurred well below the minimum IRT required for reinforcement (d-amphetamine was abut eight times more potent than methylphenidate for each of these effects). The effects of both d-amphetamine and methylphenidate on DRL performance were attenuated by administration of alphamethyltyrosine (AMT) (150 mg/kg) and both drugs attenuated the response rate-suppressing effects of tetrabenazine (TBZ) (4.0 mg/kg). The similarity of the drug interactions between methylphenidate or amphetamine and AMT or TBZ suggest that the doses of methylphenidate and d-amphetamine examined act on similar catecholaminergic pools with the central nervous system to influence DRL performance.

Animals↗
PubMed1991

Discriminative stimulus properties of triadimefon: comparison with methylphenidate.

Two groups of rats (N = 4 each) were trained to discriminate either triadimefon (40 mg/kg) or methylphenidate (4 mg/kg) from saline in a two-lever, milk-reinforced drug discrimination paradigm. Dose-response functions were determined during 5-min extinction sessions. Both agents produced a dose-related increase in the percentage of responses that occurred on the drug lever. In the substitution phase of the study, rats trained to discriminate triadimefon were tested with methylphenidate and rats trained to discriminate methylphenidate were tested with triadimefon. Triadimefon substituted completely for methylphenidate and methylphenidate substituted completely for triadimefon. These results indicate that triadimefon can function as a discriminative stimulus and that it shares discriminative stimulus properties with methylphenidate.

Animals↗
PubMed1983

Regional localization of [14C] methylphenidate in rabbit brain.

1. Neuroanatomical distribution of [14C] methylphenidate has been examined in rabbit brain following intracerebroventricular administration. 2. After about a week of implantation of cannula, in lateral ventricle, in albino rabbits, [14C] methylphenidate was injected through the cannula. The distribution of [14C] methylphenidate was examined at 15, 60 and 180 min after the injection in twelve brain regions. 3. The highest levels were observed at the first sampling time (15 min), in medulla and cervical spinal cord. Pons, caudate, tegmentum and hypothalamus also showed significant uptake of [14C] methylphenidate. Cerebral cortex and thalamus showed very low uptake. 4. The uneven distribution suggests a special affinity of methylphenidate for certain brain regions. The implications of this finding for the central actions of methylphenidate are discussed.

Animals↗
PubMed1995

Experimental studies on the long-term effects of methylphenidate hydrochloride.

Toxicology and carcinogenesis studies of methylphenidate hydrochloride, a drug used in the treatment of attention-deficient disorders, were performed in F344 rats and B6C3F1 mice. In these studies, methylphenidate hydrochloride was administered for 2 years at doses of 0, 100, 500 or 1000 ppm in the feed to rats and at doses of 0, 50, 250, 500 ppm to mice in groups that consisted of 50 animals/dose/sex/species. The average amount of methylphenidate consumed per day was estimated to be 4-47 mg/kg/day for rats and 5-67 mg/kg/day for mice. Survival was similar in dosed and control groups. An increase in benign tumors of the liver and increased liver weights were observed in male and female mice at the high dose. An increase in hepatoblastomas was also seen in high dose male mice. Methylphenidate was not mutagenic in the Salmonella assay system, and it is hypothesized that this tumorigenic effect might be due to nongenotoxic effects of the chemical such as an increase in cell proliferation. Increased incidences of neoplasms were not seen in rats. However, there was a notable decrease in mammary gland fibroadenomas in female rats and a marginal decrease in benign pheochromocytomas in male rats. Epidemiology studies of methylphenidate have found no evidence of a carcinogenic effect in humans and like our findings in rats, report a less than expected rate of cancers in patients taking methylphenidate.

Adenoma, Liver Cell↗
PubMed1992

Neuropsychological effects of methylphenidate in patients receiving a continuous infusion of narcotics for cancer pain.

Twenty consecutive patients with cancer pain receiving a continuous subcutaneous infusion of narcotics were admitted to a double-blind, crossover trial designed to assess the effects of methylphenidate on neuropsychological functions. After a baseline assessment, patients were randomized to receive methylphenidate orally at 08.00 h for 2 consecutive days or placebo. During day 3, a crossover took place and patients received the alternate treatment for 2 more days. At the end of the trial, both patients and investigators were asked to choose blindly the most effective treatment. Cognitive tests (finger tapping, FT 10 and 30 sec; arithmetics, A; reverse memory of digits, RM; and visual memory, VM) were performed in all patients before and 45 min after their morning dose of narcotics for 2 consecutive days. Mean percentual change in FT 10 sec, FT 30 sec, A, RM, and VM after the narcotic dose were 89 +/- 12%, 98 +/- 15%, 108 +/- 17%, 101 +/- 17%, and 97 +/- 21% in the placebo group versus 119 +/- 16 (P less than 0.001), 130 +/- 19 (P less than 0.001), 78 +/- 21 (P less than 0.001), 125 +/- 28 (P less than 0.01), and 128 +/- 26 (P less than 0.001) in the methylphenidate group, respectively. After completion of the trial, methylphenidate was chosen blindly by the patient and investigator in 13 and 14 cases, placebo in 3 and 2 cases, a "no choice" in 3 and 3 cases, respectively (P less than 0.01). Our results suggest that methylphenidate is capable of improving cognitive function in patients receiving high doses of opiates subcutaneously. More research is necessary in order to determine the duration of cognitive improvement after each dose of methylphenidate as well as the best type and dose of amphetamine.

Adult↗
PubMed2006

Does methylphenidate reduce the symptoms of chronic fatigue syndrome?

PURPOSE: Chronic fatigue syndrome is a clinical entity consisting of prolonged and debilitating fatigue in which concentration disturbances are very frequent. Until now, no medical treatment has shown any efficacy. The objectives of this study were to investigate the short-term effects of methylphenidate, an amphetamine derivative, on fatigue, concentration disturbances, and quality of life. SUBJECTS AND METHODS: A double-blind randomized placebo-controlled crossover study was conducted in 60 patients who fulfilled the 1994 Centers for Disease Control criteria for chronic fatigue syndrome and had concentration difficulties. Patients were enrolled between March 2003 and March 2004 at the outpatient department of a university hospital referral center for chronic fatigue syndrome patients. Random assignment to 4 weeks treatment with methylphenidate 2 x 10 mg/day, followed by 4 weeks of placebo treatment, or 4 weeks of placebo treatment, followed by methylphenidate treatment. Fatigue and concentration were measured with a Checklist Individual Strength (CIS) and a Visual Analogue Scale (VAS). RESULTS: Fatigue scores fell significantly during methylphenidate intake in comparison with baseline (mean difference: -0.7, P = .010 for VAS; mean difference: -11.8, P <.0001 for CIS) and in comparison with placebo (mean difference: -1.0, P = .001 for VAS; mean difference: -9.7, P <.0001 for CIS). Concentration disturbances, measured with a VAS improved significantly under methylphenidate treatment compared with baseline (mean difference: -1.3, P <.0001) and compared with placebo (mean difference: -1.1, P <.0001). A clinical significant effect (> or =33% improvement or CIS < or =76) on fatigue was achieved in 17% of patients, who were considered responders; on concentration in 22% of patients. CONCLUSIONS: Methylphenidate at a dose of 2 x 10 mg/day is significantly better than placebo in relieving fatigue and concentration disturbances in a minority of chronic fatigue syndrome patients. Further studies are needed to investigate the long-term effects of this treatment.

Adult↗
PubMed2006

Cognitive effects of immediate-release methylphenidate in children with attention-deficit/hyperactivity disorder.

A growing body of literature has examined the cognitive effects of immediate-release methylphenidate in children with attention-deficit/hyperactivity disorder (ADHD). However, a clear understanding of the types and magnitude of such effects are difficult to discern from such a large and varied collection of published reports. This review evaluated a total of 40 relevant placebo-controlled studies published since Rapport and Kelly's [1993. Psychostimulant effects on learning and cognitive function. In: Matson, J.L. (Ed.), Handbook of Hyperactivity in Children. Allyn & Bacon, Boston, pp. 97-136] original review of cognitive effects of methylphenidate in children with ADHD. Of these published studies, 63.5% identified some improvement in cognitive function following methylphenidate treatment. Methylphenidate improved performance on saccadic eye movement, planning/cognitive flexibility, attention/vigilance, and inhibitory control tasks in 83.3%, 71.4%, 70.6%, and 69.7% of studies, respectively. A total 58.3% and 50% of studies that evaluated the effect of methylphenidate on tasks of memory and working memory/divided attention, respectively, noted improvement. Variability of findings across studies may be explained by differential effects of methylphenidate on brain function, intra- and inter-individual variability in medication response, methodological limitations, and problems associated with repeated neuropsychological assessment and metric properties of commonly utilised neuropsychological instruments.

Attention Deficit Disorder with Hyperactivity↗