Methylphenidate

K K Jain MD†

Neuropharmacology & Neurotherapeutics

Updated 06.17.2021
Released 07.06.1999
Expires For CME 06.17.2024

Methylphenidate

Author: K K Jain MD†

See Contributor Disclosures

Methylphenidate

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Introduction

Overview

Methylphenidate, a mild CNS stimulant, is the most commonly used drug for management of attention deficit hyperactivity disorder (ADHD) in children and adults. Methylphenidate may influence several neurotransmitters, especially the release and reuptake of dopamine in the striatum. It enhances cognition by increasing extracellular catecholamine levels. The drug improves cognitive deficits and reduces hyperactivity. Tests are available to identify responders versus nonresponders to methylphenidate.

Key points

	• The mode of action of methylphenidate is not completely understood, but it presumably activates the brain stem arousal system and cortex to produce its stimulant effect.
	• Methylphenidate treatment has been shown to improve the working memory, inhibitory control, and mental flexibility of boys with attention deficit hyperactivity disorder.
	• Effect of methylphenidate on attention deficit hyperactivity disorder patients with comorbid conditions has been studied as well.
	• Clinical trials as well as use in practice has shown that most patients with attention deficit hyperactivity disorder respond to methylphenidate.
	• Nonresponders to methylphenidate can be identified by tests to personalize the therapy for those who are responders.

Historical note and terminology

Methylphenidate was approved by the United States Food and Drug Administration in 1956. It is the most widely used psychostimulant for attention deficit hyperactivity disorder and accounts for 69% of the market for these drugs.

In 2000, the Food and Drug Administration approved an extended release preparation of methylphenidate hydrochloride for once daily dosing. A refined formulation of methylphenidate, dexmethylphenidate hydrochloride, is available. Some controversy has been generated, mostly by public groups, expressing concern at the excessive use of psychostimulants in attention deficit hyperactivity disorders and even raising the possibility of overdiagnosis of this disorder. No scientific evidence has emerged to support this concern.

Pharmacology

Pharmacodynamics. Methylphenidate is a mild central nervous system stimulant. The mode of action is not completely understood, but it presumably activates the brain stem arousal system and cortex to produce its stimulant effect. Methylphenidate appears to exert rate-dependent effects on activity levels and enhance the motor output rather than information processing. Treatment with methylphenidate has been reported to show improvement of declarative memory deficits in adults with attention deficit hyperactivity disorder (33). Methylphenidate treatment has been shown to improve the working memory, inhibitory control, and mental flexibility of boys with attention deficit hyperactivity disorder (05).

Methylphenidate may influence several neurotransmitters, especially the release and reuptake of dopamine in the striatum. Some studies provide direct evidence that oral methylphenidate at doses within the therapeutic range significantly increases extracellular dopamine in the human brain. Because dopamine transporters are increased in patients with attention deficit hyperactivity disorder leading to a reduction in extracellular dopamine, this finding provides an explanation for the therapeutic efficacy of methylphenidate.

Methylphenidate enhances cognition by increasing extracellular catecholamine levels. However, there are individual differences in the cognitive-enhancing effects of methylphenidate in the healthy population. A randomized study showed that methylphenidate improved reward versus punishment learning in high-working memory subjects, whereas it impaired such learning in low-working memory subjects (32).

Positron emission tomography studies of alterations in resting blood flow suggest that methylphenidate modulates brain regions associated with motor function to achieve a reduction in attention deficit hyperactivity disorder symptoms. There is a dopaminergic frontostriatal information processing deficit in attention deficit hyperactivity disorder and methylphenidate-responder patients show an increase in striatal dopamine transporter density on brain imaging studies.

Pharmacokinetics. Methylphenidate is readily absorbed after oral administration, although the slow-release form is more slowly and extensively absorbed than the regular tablets. Relative bioavailability of the slow-release tablet compared to the regular tablet, as measured by the urinary excretion of its major metabolite (alpha-phenyl-2-piperidine acetic acid), is 105% (49% to 168%) in children and 101% (85% to 152%) in adults. The time-to-peak rate in children is 4.7 hours (1.3 to 8.2 hours) for the slow-release tablets and 1.9 hours (0.3 to 4.4 hours) for the regular tablets. An average of 67% of the slow-release tablet dose is excreted in children as compared to 86% in adults.

CYP2D6 is not involved in the metabolism of methylphenidate. Drugs that are inhibitors of CYP2D6 when taken concurrently with CYP2D6 are not involved in the metabolism of methylphenidate and should not affect its plasma concentration.

Extended-release preparations. Pharmacokinetic/pharmacodynamic studies of extended-release methylphenidate HCl capsules as well as tablets have shown statistically significant different effects on surrogate measures of behavior and performance among children with attention deficit hyperactivity disorder. Superiority at any point in time was achieved by the formulation with the highest expected plasma methylphenidate concentration.

A single-dose, one-period, pharmacokinetic study of methylphenidate multilayer extended-release capsules in preschool-aged children (4 to 6 years) with attention deficit hyperactivity disorder demonstrated the biphasic absorption profile like in those aged 6 to 11 years, apart from a lower volume of distribution and relatively higher systemic methylphenidate levels for children in the preschool group (01).

Osmotic-release methylphenidate. A single dose produces sustained effect on attention and behavior throughout the day in patient with attention deficit hyperactivity disorder. The osmotic-release oral system formulation of methylphenidate has many advantages over the immediate-release formulation, such as avoiding clinical rebound, ease of ingestion, increasing compliance, and reducing the risk of abuse. It has been approved in the United States and Europe for the treatment of attention deficit hyperactivity disorder in children, but it has only been approved for the treatment of adults in the United States and Canada.

Transdermal methylphenidate. The methylphenidate transdermal system patch is approved by the Food and Drug Administration for use in children ages 6 to 12 years with attention deficit hyperactivity disorder. This delivery system permits sustained absorption of the drug through the skin and into the bloodstream. Methylphenidate patches are generally well tolerated in pediatric patients with attention deficit hyperactivity disorder, and treatment-related events are like those reported with oral methylphenidate.

Therapeutic drug monitoring. Monitoring of the parent drug and its major metabolite ritalinic acid in urine is considered necessary to ensure compliance with treatment programs. A rapid, simple, and sensitive liquid chromatography/tandem mass spectrometry assay was developed for the determination of methylphenidate as well as its metabolite in human urine and is being used successfully in clinical practice (21).

Pharmacogenomics/pharmacogenetics. Genotype G1287A of the norepinephrine transporter gene is associated with good response to methylphenidate in Korean children with attention deficit hyperactivity disorder (29). TT genotype at position 2677 in the ABCB1 gene, which plays an important role in the clearance of psychotropic drugs from brain tissues, is associated with adverse drug reactions to osmotic-release oral system (OROS)-methylphenidate (15). Results of 1 study suggest that the norepinephrine transporter gene (SLC6A2) and the synaptosomal-associated protein of the 25-kDa gene (SNAP-25) are involved in good response to OROS-methylphenidate (28).

Clinical trials

At the time methylphenidate was approved, clinical trials were not a requirement. One of the early clinical trial done was a double-blind, placebo-controlled, crossover design in boys aged 7 to 11 years with attention deficit hyperactivity disorder (34). Hyperactivity and conduct problems were significantly reduced during methylphenidate treatment. During the following decade, methylphenidate was found to be effective in several double-blind, placebo-controlled studies in children with attention deficit hyperactivity disorder.

A randomized, double-blind, placebo-controlled, parallel-group study of the methylphenidate transdermal system in pediatric patients with attention deficit hyperactivity disorder showed that it was effective (10).

A randomized, 24-week, double-blind, placebo-controlled, parallel-design study of extended-release methylphenidate showed safety and efficacy in adult individuals with attention deficit hyperactivity disorder (25).

An open-label, extension study of the tolerability and effectiveness of the methylphenidate transdermal system in adolescents diagnosed with attention deficit hyperactivity disorder showed significant improvement (11).

An open-label extension of a randomized, placebo-controlled trial of osmotic release oral system showed that methylphenidate maintained its efficacy for attention deficit hyperactivity disorder, but patients with personality disorder responded poorly (18).

Results of a systematic review of controlled clinical trials of methylphenidate in attention deficit hyperactivity disorder indicate teacher-reported improvement in symptoms as well as general behavior and parent-reported quality of life (30). However, the improvement cannot be properly evaluated because of the risk of bias in these studies and the low quality of outcomes.

A systematic review of randomized controlled trials to assess the efficacy of methylphenidate for attention deficit hyperactivity disorder in children and adolescents with intellectual disability showed that treatment was effective in some but not all subjects with these concomitant disorders (31).

Indications

(1) Attention deficit hyperactivity disorder
(2) Narcolepsy

Off-label uses

	• Depressed or apathetic geriatric patients
	• Treatment of intractable hiccup
	• School-aged children with cerebral palsy
	• Rehabilitation following traumatic brain injury
	• Relief of uncontrolled blepharospasm
	• Results of a randomized, double-blind, placebo-controlled trial showed that methylphenidate reduced symptoms of fatigue associated with depression (14).
	• There is a case report of relief of stuttering after administration of methylphenidate (07).
	• A double-blind, placebo-controlled trial has provided evidence that methylphenidate does not only alter intrinsic connectivity between brain areas involved in sustained attention, but that it also induces significant changes in the cortico-cortical and cortico-subcortical connectivity of many other cognitive and sensory-motor resting state networks (20).
	• A study supports the association of methylphenidate use with a reduced risk of trauma-related emergency department admissions, which are more frequent in children and adolescents affected by attention deficit hyperactivity disorder (17).
	• The long-term intake of methylphenidate by patients with chronic fatigue syndrome with concentration difficulties has a positive effect in about 1 out of 3 patients (04).
	• A metanalysis of studies has shown that methylphenidate may be beneficial for apathy, cognition, and functional performance in patients with Alzheimer disease, but this finding is associated with low-quality evidence (26).
	• Review of literature and various studies indicates a beneficial effect of methylphenidate in relief of fatigue in cancer patient (24).
	• Data from an open study indicate that short-acting methylphenidate can be clinically effective for learning problems in males with Duchenne muscular dystrophy who have attention deficit hyperactivity disorder (16).

Goals and duration of treatment

Duration of treatment. Methylphenidate, a first-line medication for treating attention deficit hyperactivity in children and adults, is used as an integral part of a total treatment program that typically includes other remedial measures: psychological, educational, and social. It should be discontinued periodically to assess the child's condition. Improvement may persist when the drug is discontinued. Drug treatment is not indefinite and may be discontinued after puberty. However, a study has shown that beneficial short-term effects of methylphenidate predict longer-term effects and may, thus, be helpful in the decision for an off-label treatment.

Personalizing treatment with methylphenidate. Despite the effectiveness of methylphenidate for treating attention deficit hyperactivity disorder, up to 30% of individuals with attention deficit hyperactivity disorder show poor responses. Various approaches have been used to identify responders as well as nonresponders to methylphenidate.

Regional cerebral blood flow as determined by single photon emission computed tomography using technetium-99m-hexamethylporphylenamine oxime SPECT in children with attention deficit hyperactivity disorder shows that nonresponders to methylphenidate have different patterns of blood flow than responders, and this may help in making treatment decisions. The results of a 2-year study indicate that hyperactivity improves throughout the first year of treatment, emotional symptoms and behavioral problems improve during the first 6 months of treatment, pro-social symptoms slowly improve over 2 years (23).

Measurement of regional brain volume by MRI has shown that poor responders to methylphenidate have smaller regional volumes of the left putamen as well as larger precuneus volumes compared to good responders at baseline (06). The machine learning approach in this study showed that volumetric information among these 2 regions alongside the left frontoparietal regions, occipital lobes, and posterior/inferior cerebellum could predict clinical responses to methylphenidate in individuals with attention deficit hyperactivity disorder.

A study was conducted to examine whether reaction time parameters in adult patients with attention deficit hyperactivity disorder could predict their response to methylphenidate (Fredericksen et al 2021b). In addition to traditional Continuous Performance Test II, the authors extracted intraindividual raw data and analyzed time series using linear and nonlinear mathematical models. Clinical responders, assessed with the Clinical Global Impression-Improvement scale, showed significant normalization of target failures, reduced variability, and increased complexity of reaction time series after 6 weeks of treatment with methylphenidate, whereas nonresponders showed no significant changes. Approaches to identify responders versus nonresponders help to personalize treatment of attention deficit hyperactivity disorder with methylphenidate.

Special considerations

Patients with comorbid disorders. The FDA has a "black box" warning for methylphenidate drugs about an increased risk of sudden death and serious cardiovascular problems. Methylphenidate should be used cautiously in patients with hypertension. Blood pressure should be monitored at appropriate intervals in all patients, especially those with hypertension.

Comorbid tic disorder. Methylphenidate is listed as contraindicated in patients with tics. However, some unpublished studies show that slow-release once-a-day formulations of methylphenidate do not aggravate tics and have even been shown to improve tics. Based on results of clinical trials, methylphenidate and clonidine (particularly in combination) are considered effective for attention deficit hyperactivity disorder in children with comorbid tics. Immediate-release methylphenidate is considered a safe and effective short-term treatment for attention deficit hyperactivity disorder in children with chronic tic disorder, but the possibility of tic exacerbation in susceptible individuals warrants careful monitoring of all patients.

Comorbid substance abuse disorder. Adult patients with attention deficit hyperactivity disorder and comorbid substance abuse disorder may be treated with methylphenidate. Use of A Quick Test of Cognitive Speed (AQT) has shown that adults with attention deficit hyperactivity disorder and concomitant substance abuse disorder have lower rate of response to methylphenidate than adults with attention deficit hyperactivity disorder without concomitant substance abuse disorder (03). A clinical application of AQT is for adjustment of dose of methylphenidate.

Sleep disorders in adults with attention deficit hyperactivity disorder (ADHD). Attention deficit hyperactivity disorder is associated with disrupted sleep and circadian rhythm. There is a theoretical concern that methylphenidate, a CNS stimulant, may aggravate sleep-disturbances. On the other hand, beneficial effects of methylphenidate on attention deficit hyperactivity disorder may contribute to improved sleep. To resolve these issues, a pilot study examined effects of first-time methylphenidate treatment on objective and subjective sleep characteristics in adult attention deficit hyperactivity disorder patients with pretreatment sleep problems, but without any primary sleep disorder (13). Subjects on methylphenidate showed an increased percentage of stage 2 sleep compared to their nontreated baseline. Otherwise, there were no significant changes in polysomnography variables. Because of the limitations of a small number of subjects in an open study, larger controlled trials are needed.

Epilepsy and ADHD. More than 30% of children with epilepsy have been reported to develop ADHD whereas the incidence in a control population is about 6%. Methylphenidate, a CNS stimulant, has not been proven to exacerbate seizures and can be used for management of ADHD in epileptic children as discussed under the section on adverse effects of methylphenidate.

Anesthesia. No contraindications have been found in for anesthesia in patients under treatment with methylphenidate.

Pregnancy. Adequate animal reproduction studies to establish safe use of methylphenidate during pregnancy have not been conducted. The FDA has assigned methylphenidate to pregnancy category of C. Methylphenidate should not be used by women of childbearing age unless the potential benefits outweigh the possible risks. In a study of 180 children exposed to methylphenidate in utero during the first trimester, 4 children with major malformations were identified (09). According to the authors, methylphenidate exposure during pregnancy does not appear to be associated with a substantial, ie, more than 2-fold, increased risk of congenital malformations. A further study by these authors also concluded that first trimester in utero exposure to methylphenidate is not associated with a substantially increased overall risk of major congenital malformations (22). Results of a prospective, comparative, multicenter observational study suggest that methylphenidate does not seem to increase the risk for major malformations, but further studies are required to establish its safety in pregnancy and its possible association with miscarriages (08).

Methylphenidate is excreted in breast milk only in small amounts, and there are no reports of breastfed infants demonstrating any adverse effects, but there are no adequate studies of long-term neurodevelopmental effects (19).

Pediatric. Safety and efficacy in children under the age of 4 years has not been established.

Geriatric. Methylphenidate is not used in elderly patients.

Adverse effects

Growth retardation. Although a causal relationship has not been established, suppression of growth (ie, weight gain, height gain, or both) has been reported with the long-term use of stimulants in children. Therefore, patients requiring long-term therapy should be carefully monitored.

Cardiovascular effects. Cardiovascular complications of methylphenidate include rise in blood pressure and tachyarrhythmias. Acute cardiomyopathy and pericarditis have been reported following the use of methylphenidate.

Seizures. There are reports of seizures associated with use of methylphenidate during the first month of treatment, but 4 large observational studies have shown that it may be safely used in children and adolescents, even those with a history of epilepsy (02). Safe concomitant use of anticonvulsants and methylphenidate has not been established. If seizures occur, the drug should be discontinued. The risk of potential triggers of a seizure during the first month of treatment needs to be reexamined in future studies.

Hallucinations. A small number of children taking methylphenidate may suffer hallucinations that usually feature insects, snakes, or worms. Treatment is withdrawal of methylphenidate rather than the use of a second drug to treat the hallucinations caused by the stimulant action.

Abuse. Like other psychostimulants, methylphenidate has a potential for abuse. Its behavioral pharmacological similarities to methamphetamine and cocaine have created concern for its potential as a drug of abuse. Cerebral lacunar infarction has been reported following chronic oral abuse of methylphenidate. In 2019, the Food and Drug Administration emphasized the abuse of methylphenidate as a public health concern. The U.S. Drug Enforcement Administration has placed stringent schedule II controls on the manufacture, distribution, and prescription of methylphenidate. Special licenses are required for these activities, and prescription refills are not allowed. Development of abuse deterrent formulations of methylphenidate is warranted (27).

References

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02: Andrade C. Methylphenidate and the risk of new-onset seizures. J Clin Psychiatry 2020;81(4):20f13586.** PMID 32726522
03: Arvidsson M, Dahl ML, Franck J, Wiig EH, Nielsen NP. Methylphenidate effects on processing speed in a clinical sample of adults with ADHD and substance use disorder: a pilot study. Nord J Psychiatry 2019;73(2):118-24. PMID 30861357
04: Blockmans D, Persoons P. Long-term methylphenidate intake in chronic fatigue syndrome. Acta Clin Belg 2016;71(6):407-14. PMID 27351244
05: Bolfer C, Pacheco SP, Tsunemi MH, Carreira WS, Casella BB, Casella EB. Attention-deficit/hyperactivity disorder: the impact of methylphenidate on working memory, inhibition capacity and mental flexibility. Arq Neuropsiquiatr 2017;75(4):204-8. PMID 28489138
06: Chang JC, Lin HY, Lv J, Tseng WI, Gau SS. Regional brain volume predicts response to methylphenidate treatment in individuals with ADHD. BMC Psychiatry 2021;21(1):26.** PMID 33430830
07: Devroey D, Beerens G, Van De Vijver E. Methylphenidate as a treatment for stuttering: a case report. Eur Rev Med Pharmacol Sci 2012;16 Suppl 4:66-9. PMID 23090813
08: Diav-Citrin O, Shechtman S, Arnon J, et al. Methylphenidate in pregnancy: a multicenter, prospective, comparative, observational study. J Clin Psychiatry 2016;77(9):1176-81. PMID 27232650
09: Dideriksen D, Pottegård A, Hallas J, Aagaard L, Damkier P. First trimester in utero exposure to methylphenidate. Basic Clin Pharmacol Toxicol 2013;112(2):73-6. PMID 23136875
10: Findling RL, Bukstein OG, Melmed RD, et al. A randomized, double-blind, placebo-controlled, parallel-group study of methylphenidate transdermal system in pediatric patients with attention-deficit/hyperactivity disorder. J Clin Psychiatry 2008;69(1):149-59. PMID 18312050
11: Findling RL, Katic A, Rubin R, Moon E, Civil R, Li Y. A 6-month, open-label, extension study of the tolerability and effectiveness of the methylphenidate transdermal system in adolescents diagnosed with attention-deficit/hyperactivity disorder. J Child Adolesc Psychopharmacol 2010;20(5):365-75. PMID 20973707
12: Fredriksen M, Egeland J, Haavik J, Fasmer OB. Individual variability in reaction time and prediction of clinical response to methylphenidate in adult ADHD: a prospective open label study using Conners' Continuous Performance Test II. J Atten Disord 2021b;25(5):657-71.** PMID 3076245
13: Fredriksen M, Golparian N, Beiske K, Stavem K. Impact of methylphenidate on sleep problems in adults with ADHD: a pilot polysomnography study. Nord J Psychiatry 2021a;75(3):234-38.** PMID 33100096
14: Kerr CW, Drake J, Milch RA, et al. Effects of methylphenidate on fatigue and depression: a randomized, double-blind, placebo-controlled trial. J Pain Symptom Manage 2012;43(1):68-77. PMID 22208450
15: Kim SW, Lee JH, Lee SH, Hong HJ, Lee MG, Yook KH. ABCB1 c.2677G>T variation is associated with adverse reactions of OROS-methylphenidate in children and adolescents with ADHD. J Clin Psychopharmaco 2013;33(4):491-8. PMID 23771192
16: Lionarons JM, Hellebrekers DMJ, Klinkenberg S, Faber CG, Vles JSH, Hendriksen JGM. Methylphenidate use in males with Duchenne muscular dystrophy and a comorbid attention-deficit hyperactivity disorder. Eur J Paediatr Neurol 2019;23(1):152-7. PMID 30287260
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19: Marchese M, Koren G, Bozzo P. Is it safe to breastfeed while taking methylphenidate? Can Fam Physician 2015;61(9):765-6. PMID 26623462
20: Mueller S, Costa A, Keeser D, et al. The effects of methylphenidate on whole brain intrinsic functional connectivity. Hum Brain Mapp 2014;35(11):5379-88. PMID 24862742
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22: Pottegård A, Hallas J, Andersen JT, et al. First-trimester exposure to methylphenidate: a population-based cohort study. J Clin Psychiatry 2014;75(1):e88-93. PMID 24502866
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Methylphenidate

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Methylphenidate

Methylphenidate

Introduction

Overview

Key points

Historical note and terminology

Pharmacology

Clinical trials

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Author

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to access the full version.

Questions or Comment?

Also in This Category

Wilson disease

Anti-LGI1 encephalitis

Fatal familial insomnia

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Methylphenidate

Introduction

Overview

Key points

Historical note and terminology

Pharmacology

Clinical trials

Indications

Off-label uses

Contraindications

Goals and duration of treatment

Dosing

Special considerations

Interactions

Adverse effects

References

Contributors

Author

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Wilson disease

Anti-LGI1 encephalitis

Fatal familial insomnia

Acupuncture

Hyperventilation syndrome

Apraxia

Neurologic disorders associated with behavioral symptoms

Cortical blindness

This is an article preview.
Start a Free Account
to access the full version.