Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Methylphenidate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

Effects of methylphenidate on cognition and apathy in normal pressure hydrocephalus: a case study and review.

The psychostimulant methylphenidate has been previously shown to improve cognitive performance in both normal control volunteers and patient populations. In the present case study, the effects of methylphenidate on cognitive and behavioural function were examined in a single patient with idiopathic normal pressure hydrocephalus (NPH) who had undergone ventriculoperitoneal shunting. A double-blind placebo-controlled ABBA drug design was employed, with the administration of two different doses of methylphenidate followed by neuropsychological assessment on a number of psychometric tests and cognitive tasks drawn from the Cambridge Neuropsychological Test Automated Battery (CANTAB). Methylphenidate produced a dose-dependent positive improvement in behavioural measures in the patient associated with a reduction in apathy. It also had a dose-independent enhancing effect on performance of a Spatial Recognition task. These findings require replication in a large sample of patients to determine whether methylphenidate may prove to be generally useful in enhancing cognition and reducing apathy in normal pressure hydrocephalus.

Aged↗

Student perceptions of methylphenidate abuse at a public liberal arts college.

With the ever-increasing diagnosis of attention deficit hyperactivity disorder, methylphenidate has become readily accessible in the college environment. Several properties of methylphenidate indicate abuse liability. A survey regarding the recreational use of methylphenidate was distributed to the student body at a public, liberal arts college. More than 16% of the students reported they had tried methylphenidate recreationally, and 12.7% reported they had taken the drug intranasally. Use of the drug was more common among traditional students than among nontraditional students. Among traditional-age students, reports of methylphenidate use were roughly equivalent to reports of cocaine and amphetamine use. Environmental conditions characteristic of college student life may influence the recreational use of the drug.

Adult↗

Determinants of compliance with methylphenidate therapy in children.

AIM: To get more insight into factors that influence compliance with the use of methylphenidate. METHODS: 22 pharmacies detected children who used methylphenidate. Their parents were sent a questionnaire on the use of methylphenidate. In a case-control study, the influence of patient- and drug-related factors on compliance, as reported by parents, was determined. RESULTS: Parents returned 117 (75%) of 157 questionnaires sent out. Of these, 47.8% of the children missed a dose two times a month or more. Forgetting to take the medication (87.9%) was the most important reason. The case-control study showed that children of 16-18 y were more likely to miss doses. Other patient- and drug-related factors did not influence the missing of doses. CONCLUSION: A number of known determinants for compliance do not influence the missing of doses of methylphenidate. With about 80% of the parents reporting that their child missed doses of methylphenidate less than 5 times per month, compliance was quite good for the majority of the children.

Adolescent↗

The prevalence of attentional problems and the effect of methylphenidate in children with myelomenigocele.

The prevalence of attentional problems, and the effect of methylphenidate was evaluated in a clinic population of children with myelomeningocele. Families of 79 children between the ages of 6 and 15 years were screened for the presence of attention problems in their children, using Conners' questionnaires for parents and teachers, and/or the DSM-IV checklist. Thirty-nine per cent of the children exhibited attention problems, primarily without hyperactivity. Fourteen children with attentional problems were enrolled in a double-blind placebo-controlled trial methylphenidate. Response to methylphenidate was assessed with Conners' questionnaires, Conners' Continuous Performance Test, and a battery of selected neuropsychological tests. No statistically significant response was measured for the group while on methylphenidate. Four children were clinical responders to methylphenidate. The prevalence of attentional problems in children with myelomeningocele is high, and effective medication therapy needs to be studied further.

Adolescent↗

Methylphenidate slows right hemisphere processing in children with attention-deficit/hyperactivity disorder.

To examine the effects and particularly, any potential detrimental effects of methylphenidate on right hemisphere processing in children with attention-deficit/hyperactivity disorder (ADHD), the performance of 26 children (aged 8-15 years) with ADHD was compared under methylphenidate and placebo on various cognitive tasks in a double-blind within-subjects design. Results indicated that reaction times on a tachistoscopic task were slower on methylphenidate for stimuli that produced a left visual field advantage (reflecting better right hemisphere functioning) but not for stimuli that produced a right visual field advantage (reflecting better left hemisphere functioning) or for bilateral stimuli. It is argued that methylphenidate induces a slower response on tasks involving right hemisphere processing, resulting in slower reaction times and unchanged accuracy rates. Findings on two tasks that more closely reflect classroom-type tasks revealed an improvement in performance on methylphenidate, suggesting that any stimulant-induced benefits on learning style may have overcome detrimental effects on unilateral processing. These findings may help understand the complex, diverse, and sometimes unpredictable effects of psychostimulants on cognitive functioning that are observed clinically in individuals treated for ADHD.

Adolescent↗

Successful desensitization of methylphenidate-induced rash.

OBJECTIVE: Methylphenidate is a cornerstone of attention-deficit/hyperactivity disorder (ADHD) treatment. Cutaneous adverse reactions resulting from methylphenidate may prohibit its usage. We sought a way to continue this therapy in a patient who developed a rash twice following methylphenidate administration. METHODS: In a desensitization protocol, methylphenidate was given in increasing doses, 30 minutes apart, over 10 days, until the therapeutic dose was reached and was continued regularly thereafter. RESULTS: No adverse reactions developed during the desensitization period or during the 6- month follow-up. CONCLUSIONS: In nonlife threatening cutaneous adverse reactions to methylphenidate, a desensitization protocol may enable the continued, safe administration of this drug.

Attention Deficit Disorder with Hyperactivity↗

An enzyme-linked immunosorbent assay (ELISA) for methylphenidate (Ritalin ) in urine.

A direct enyzme-linked immunosorbent assay (ELISA) for urinary immunoreactive methylphenidate (Ritalin), in which a standard 96-well microtiter plate is used, is described. For this ELISA, a methylphenidate-thyroglobulin conjugate is immobilized to the microtiter plate and competes with methylphenidate in the standard or urine sample for antibody-binding sites. After washing, the sheep methylphenidate antibody bound to immobilized methylphenidate is detected with peroxidase-labelled goat antisheep IgG. Following a further wash, tetramethylbenzidine is added, color is developed, and the plate is read at 450 nm on an ELISA plate reader. This method is unaffected by drugs of abuse and is suitable for routine use in the toxicology laboratory.

Animals↗

Fenfluramine and methylphenidate in children with mental retardation and ADHD: clinical and side effects.

Each of 28 nonautistic children with attention-deficit hyperactivity disorder and mental retardation received placebo, methylphenidate (0.4 mg/kg/day), and fenfluramine (gradually increased to 1.5 mg/kg/day) for 4 weeks each in a double-blind, crossover design. Teacher ratings indicated significant improvements with both active drugs on subscales designated as Conduct Problem, Hyperactivity, and Irritability, but methylphenidate alone produced improvements on an Inattention subscale. Parent ratings indicated significant improvements with both drugs on subscales labeled Hyperactivity, Motor Excess, and Conduct Problem. Fenfluramine alone caused improved parent ratings on Irritability and Inappropriate Speech, and on Conners' Abbreviated Symptom Questionnaire. Unlike a previous study, subgroup analyses failed to show a significantly better clinical response to methylphenidate for subjects with higher mental ages, although children with higher IQs responded better than those with IQs less than 45. The active drugs had contrasting effects on heart rate and blood pressure. Fenfluramine caused significant weight reductions relative to both placebo and methylphenidate. These findings suggest that both methylphenidate and fenfluramine have useful, but somewhat different, clinical effects in certain children with attention-deficit hyperactivity disorder and mental retardation.

Adolescent↗

Replacement medication for cocaine dependence: methylphenidate.

Agonists, or "replacement medications," are useful adjuncts in treatment of opiate and nicotine dependence. They have not been systematically examined in cocaine dependence. Results of early open trials with methylphenidate for treatment of cocaine dependence were equivocal. Twenty-four cocaine-dependent subjects were enrolled in an 11-week double-blind, placebo-controlled study of methylphenidate. Assignment was random. Intake included a 2-day human laboratory procedure in which subjects received initial doses of methylphenidate or placebo. Subjects attended the clinic Monday through Friday and received oral doses of methylphenidate (5 mg plus 20-mg sustained release) or placebo at 8:00 a.m., with afternoon and weekend take-home doses (20 mg sustained-release or placebo) provided in Medication Events Monitoring System bottles to monitor compliance. Clinic visits included therapy sessions, electrocardiograms, self-report measures, and twice-weekly urine screens. The two groups were equivalent in terms of retention (methylphenidate 48% and placebo 42%) and had similar cocaine use outcomes (40% benzoylecgonine-positive urine screens). There were no significant adverse effects. The doses were sufficient to permit detection of psychoactive effects ("stimulant," "more energy") and side effects ("jitteriness," "eating less") without increased "craving." Additional medications with different effects profiles are being studied to further evaluate the replacement model in cocaine dependence.

Adult↗

Biphasic inotropic effects of methamphetamine and methylphenidate on ferret papillary muscles.

Methamphetamine and methylphenidate are structurally related agents that have direct negative inotropic (NIEs) and indirect positive inotropic effects (PIEs) in cardiac tissues. This study was designed to determine and compare cellular mechanisms of the NIEs of methamphetamine and methylphenidate by using a mammalian animal model. Isometric tension was measured in ferret papillary muscles in physiologic salt solution. A subset of muscles was loaded with the bioluminescent calcium indicator, aequorin. Further, to investigate the NIE of methamphetamine, the dose-response relations to isoproterenol, histamine, and calcium were measured with or without methamphetamine (2 x 10(-4) M), after adrenergic neuronal blockade with reserpine. Both methamphetamine and methylphenidate had direct NIEs at higher doses (>10(-4) M). A shift in the slope of the isoproterenol dose-response curve suggested involvement of the beta-adrenoceptor pathways. The direct NIE of methylphenidate was more prominent. Our results suggest that the negative inotropic effects of methamphetamine and methylphenidate may be important with clinically used and abused concentrations of these drugs and may be difficult to reverse with beta-adrenergic inotropic agents in cases of toxicity.

Adrenergic Agents↗

Effects of methylphenidate on subtypes of attention-deficit/hyperactivity disorder.

OBJECTIVE: To compare the effects of methylphenidate on attention-deficit/hyperactivity disorder (ADHD) subtypes. METHOD: Nineteen ADHD/inattentive (ADHD/I) and 22 ADHD/combined (ADHD/C) 6- to 12-year-old children entered a 6-week, double-blind trial of placebo and methylphenidate in divided doses (0.94 +/- 0.02 mg/kg/day = 33.06 +/- 1.40 mg/day). ADHD children received a restricted arithmetic task without medication before the trial and after their noon dose on the last day of each phase. Thirty-four unmedicated controls were tested at comparable time points. Parents and teachers rated ADHD children before and after each phase of the trial; parents rated controls before the study. RESULTS: Controls had marginally better arithmetic performance than children with ADHD/C who outperformed ADHD/I children. Unmedicated children with ADHD exceeded controls in task-incompatible behaviors during restricted arithmetic. Under methylphenidate, both ADHD subtypes reached control levels of arithmetic performance and task-incompatible behavior. Before the trial, parents rated children with both ADHD subtypes higher than controls on inattention, hyperactivity, and oppositionality/aggression and parents and teachers rated ADHD/C children higher than ADHD/I children on hyperactivity and oppositionality/aggression but not inattention. Methylphenidate lowered parent and teacher ratings of inattention and hyperactivity for those with both ADHD subtypes, but ratings of children with ADHD/C decreased more in hyperactivity and aggression. CONCLUSIONS: Methylphenidate ameliorated task-incompatible behavior, arithmetic performance, and inattention comparably in both ADHD subtypes, whereas medication reduced hyperactivity and aggression largely in children with ADHD/C.

Aggression↗

Methylphenidate and interpersonal relationships of children with attention deficit hyperactivity disorder.

In order to clarify the effects of methylphenidate on interpersonal relationships of children with attention deficit hyperactivity disorder (ADHD), data from sociometric tests conducted in 28 classes to which ADHD children belonged was analyzed, comparing patients who had a history of methylphenidate treatment with those who had not. It was suggested that ADHD children with a history of methylphenidate treatment had more favorable votes and fewer unfavorable ones than those without it. However, there were more isolated children among ADHD children with methylphenidate treatment than in those without it. The results are discussed in the light of previous findings in the literature and a hypothesis for methylphenidate induced isolation is proposed.

Attention Deficit Disorder with Hyperactivity↗

Methylphenidate alters vesicular monoamine transport and prevents methamphetamine-induced dopaminergic deficits.

It has been hypothesized that high-dose methamphetamine treatment rapidly redistributes cytoplasmic dopamine within nerve terminals, leading to intraneuronal reactive oxygen species formation and well characterized persistent dopamine deficits. We and others have reported that in addition to this persistent damage, methamphetamine treatment rapidly decreases vesicular dopamine uptake, as assessed in purified vesicles prepared from treated rats; a phenomenon that may contribute to aberrant intraneuronal dopamine redistribution proposedly caused by the stimulant. Interestingly, post-treatment with dopamine transporter inhibitors protect against the persistent dopamine deficits caused by methamphetamine; however, mechanisms underlying this phenomenon have not been elucidated. Also of interest are findings that dopamine transporter inhibitors, including methylphenidate, rapidly increase 1) vesicular dopamine uptake, 2) vesicular monoamine transporter-2 (VMAT-2) ligand binding, and 3) VMAT-2 immunoreactivity in a vesicular subcellular fraction prepared from treated rats. Therefore, we hypothesized that methylphenidate post-treatment might protect against the persistent striatal dopamine deficits caused by methamphetamine by rapidly affecting VMAT-2 and vesicular dopamine content. Results reveal that methylphenidate post-treatment both prevents the persistent dopamine deficits and reverses the acute decreases in vesicular dopamine uptake and VMAT-2 ligand binding caused by methamphetamine treatment. In addition, methylphenidate post-treatment reverses the acute decreases in vesicular dopamine content caused by methamphetamine treatment. Taken together, these findings suggest that methylphenidate prevents persistent methamphetamine-induced dopamine deficits by redistributing vesicles and the associated VMAT-2 protein and presumably affecting dopamine sequestration. These findings not only provide insight into the neurotoxic effects of methamphetamine but also mechanisms underlying dopamine neurodegenerative disorders, including Parkinson's disease.

Adrenergic Uptake Inhibitors↗

Three-month treatment course of methylphenidate increases plasma levels of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone-sulfate (DHEA-S) in attention deficit hyperactivity disorder.

Methylphenidate is considered by many to be the treatment of choice for attention deficit hyperactivity disorder (ADHD). Methylphenidate exerts its therapeutic effects through the dopaminergic, serotonergic and noradrenergic systems, however its effects on other neurophysiological systems, such as the neurosteroidal system, remain unknown. Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEA-S) are neuroactive steroids with effects on several neurophysiological and behavioral processes. The purpose of the present study was to determine the effect of 3 months of treatment with methylphenidate on circulatory DHEA, DHEA-S, and cortisol in children with ADHD. The study population consisted of 15 boys (aged 11.5 +/- 1.6 years) with ADHD, combined type. Subjects were evaluated before and after methylphenidate treatment with a specific rating scale for the assessment of inattention and impulsivity in ADHD. Results show that treatment led to significant clinical improvement in all subjects. Furthermore, following 3 months of treatment, there was a significant increase in serum levels of DHEA and DHEA-S but not in circulatory levels of cortisol. The mean rate of increase in DHEA levels was 23 and 53.6% in DHEA-S. Our findings suggest that DHEA and DHEA-S may play a role in the therapeutic effects of methylphenidate. Several mechanisms to explain this action are proposed, including involvement of the serotonergic, GABA-ergic and noradrenergic pathways.

Attention Deficit Disorder with Hyperactivity↗

Effects of methylphenidate on functional MRI blood-oxygen-level-dependent contrast.

OBJECTIVE: The authors' goal was to determine potential hemodynamic consequences of methylphenidate on functional magnetic resonance imaging (MRI) blood-oxygen-level-dependent (BOLD) contrast. METHOD: BOLD and perfusion changes were recorded from the motor cortex of six healthy subjects while they performed flexion-extension movements of the right index finger (finger tapping) at varying rates before and after oral methylphenidate administration. RESULTS: Functional MRI signals increased monotonically with faster movement rates. Subjects' heart rates increased modestly after methylphenidate administration, but no changes in finger tapping performance or functional MRI signals were observed. CONCLUSIONS: Methylphenidate does not alter BOLD neural-hemodynamic coupling. Consequently, functional MRI can be used to map neural systems that subserve cognitive operations (e.g., attention and executive processes) in subjects taking methylphenidate.

Adult↗

Bone mineral density and turnover in children with attention-deficit hyperactivity disorder receiving methylphenidate.

Attention-deficit hyperactivity disorder (ADHD) is the most common behavior disorder among children; methylphenidate is a drug frequently prescribed for the control of its symptoms. One of the potential side effects of methylphenidate that concerns parents is its impact on the growth of children, since the mechanism by which methylphenidate might influence growth is not known. As linear growth is associated with an increase in bone mineral density and turnover, this study was undertaken to evaluate bone mineral density by dual photon absorptiometry and bone turnover by measuring serum bone-specific alkaline phosphatase and the urinary deoxypyridinoline excretion rate in children treated with methylphenidate for 1 to 2 years as compared to a control group. There were no significant differences in bone mineral density at either the lumbar spine or femoral neck in the study group (0.662 +/- 0.04 and 0.735 +/- 0.07 g/cm2, respectively) as compared to the controls (0.675 +/- 0.05 g/cm2 and 0.734 +/- 0.07 g/cm2, respectively). Furthermore, there were no significant differences in serum bone-specific alkaline phosphatase in the study group (58 +/- 22 U/L) as compared to the control children (71 +/- 34 U/L) or in urinary deoxypyridinoline in the study group (34 +/- 38 nM/mM), as compared to the control group (27 +/- 12 nM/mM). In conclusion, our data do not support a significant effect of methylphenidate on bone mineral density turnover in children when used for 1 to 2 years.

Attention Deficit Disorder with Hyperactivity↗

Quantitative electroencephalography in frontotemporal dementia with methylphenidate response: a case study.

Frontotemporal dementia is an underdiagnosed illness with predominant behavioral and executive manifestations. Historically, diagnosis has been based on a combination of clinical history, neuropsychological testing, and brain imaging. No effective treatment currently exists for this disorder. A case is presented using quantitative EEG with methylphenidate challenge correlated with SPECT. The patient underwent neuropsychological testing, a SPECT brain study, and a quantitative EEG, which was repeated after methylphenidate administration. SPECT was significant for hypoperfusion to the bilateral frontotemporal regions, with left-sided hypoperfusion greater than homologous right as demonstrated by LORETA analysis. QEEG correlated with SPECT, and demonstrated profound left greater than right bi-frontotemporal slowing, which normalized partially after methylphenidate administration. The patient has remained on methylphenidate as an outpatient, and has had significant behavioral improvement. Quantitative EEG may provide both diagnostic and therapeutic data with regard to frontotemporal dementia. Further studies of methylphenidate in this population are needed to confirm these data.

Aged↗

Methylphenidate-induced chorea: case report and pharmacologic implications.

In a child with minimal brain dysfunction, we found that chorea was related to the major central effect of methylphenidate and probably to the effect of the drug on central catecholaminergic systems. Also, after 3 weeks of treatment with methylphenidate, guinea pigs showed a hypersensitive response to apomorphine, suggesting that chronic administration of methylphenidate leads to hypersensitivity of receptor sites. Chorea beginning shortly after initiation of methylphenidate therapy probably is related to the central dopaminergic effect of the drug; when choreic movements appear after chronic methylphenidate administration, altered responsiveness of striatal dopamine receptor sites may be responsible.

Animals↗