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Serotonin syndrome is characterized by the rapid development of hyperthermia, hypertension, myoclonus, rigidity, autonomic instability, mental status changes e. Patients receiving this combination should be monitored for the emergence of serotonin syndrome. If serotonin syndrome occurs, all serotonergic agents should be discontinued and appropriate medical management should be implemented.
There does not appear to be a pharmacokinetic interaction between methylphenidate and TCAs. In one study, use of methylphenidate did not increase plasma concentrations of the CYP2D6 substrate desipramine. Nevertheless, a dose adjustment of the TCA, and monitoring of TCA plasma concentrations when applicable, may be required when initiating or discontinuing methylphenidate. Moderate Both methylphenidate and amoxapine may lower the seizure threshold; therefore, caution is particularly advisable when this combination is administered to patients susceptible to seizures.
In addition, methylphenidate is thought to exert some of its beneficial effects through dopamine re-uptake blockade while amoxapine has central dopamine antagonist properties. In theory, the therapeutic effects of either agent may be reduced. Minor The effects of gastrointestinal pH alterations on the absorption of extended-release methylphenidate Ritalin LA have not been studied. Per the manufacturer of extended-release methylphenidate, the modified release characteristics are pH-dependent.
It is possible that the administration of proton pump inhibitors PPIs or other acid suppressants could alter the release of extended-release methylphenidate, resulting in reduced or increased absorption. Patients receiving a PPI should be monitored for adverse effects and reduced therapeutic efficacy of extended-release methylphenidate.
Severe Amphetamines and methylphenidate should not be coadministered. These drugs represent duplicate treatments for certain conditions. Nervousness, irritability, insomnia, palpitations, arrhythmias, seizures, or other serious stimulant-related adverse effects may occur. Angiotensin II receptor antagonists: Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as angiotensin II receptor antagonists.
Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as angiotensin-converting enzyme inhibitors. Moderate Increased dopaminergic effects may occur during coadministration of methylphenidate, an inhibitor of dopamine reuptake, and dopamine agonists such as pergolide, pramipexole, apomorphine, and ropinirole. Dopaminergic side effects, such as nausea, loss of appetite, weight loss, insomnia, tremor, nervousness, or changes in mood or behavior, are possible.
Moderate Atypical antipsychotics and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine. Methylphenidate blocks central dopamine reuptake, which has the potential to exacerbate psychosis, and antipsychotics, which are central dopamine antagonists, may diminish the effectiveness of methylphenidate.
Major The use of armodafinil with other psychostimulants, including methylphenidate, has not been studied. Patients receiving combination therapy of armodafinil with other psychostimulants should be closely observed for signs of nervousness, irritability, insomnia, arrhythmias, or other stimulant-related side effects. Major Use methylphenidate cautiously in patients receiving atomoxetine, a selective norepinephrine reuptake inhibitor. If coadministration is necessary, monitor patients closely for tachycardia and hypertension.
Although coadministration of methylphenidate and atomoxetine did not increase the cardiovascular effects seen with administration of methylphenidate alone during clinical trials, concurrent use of sympathomimetic agents may result in an increased risk of noradrenergic effects. Also monitor for appropriate clinical response and for any unusual changes in moods or behavior.
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Serotonin syndrome is characterized by the rapid development of various symptoms such as hyperthermia, hypertension, myoclonus, rigidity, hyperhidrosis, incoordination, diarrhea, mental status changes e. Atropine; Hyoscyamine; Phenobarbital; Scopolamine: Moderate Psychostimulants, such as methylphenidate, may lower the seizure threshold, thereby reducing the efficacy of anticonvulsants such as phenobarbital.
In addition, case reports suggest a potential pharmacokinetic interaction between methylphenidate and phenobarbital; however, a kinetic interaction was not confirmed when evaluated at higher sample sizes. Nevertheless, a dose adjustment of phenobarbital and more frequent monitoring of plasma concentrations may be required when initiating or discontinuing methylphenidate. Belladonna Alkaloids; Ergotamine; Phenobarbital: Moderate Bethanechol offsets the effects of sympathomimetics at sites where sympathomimetic and cholinergic receptors have opposite effects.
Moderate Increased dopaminergic effects may occur during coadministration of methylphenidate, an inhibitor of dopamine reuptake, and dopamine agonists such as bromocriptine. Major Drugs which may lower the seizure threshold, such as methylphenidate, should be used with great caution or avoided in patients taking bupropion. The manufacturer recommends low initial dosing and slow dosage titration of bupropion if this combination must be used concurrently; the patient should be closely monitored.
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One case report describes an adolescent girl who experienced decreases in peak methylphenidate concentrations and reduced methylphenidate efficacy following initiation and dose titration of carbamazepine. Subsequent dose increases of methylphenidate were needed to elicit a therapeutic response. Controlled trials are needed to confirm the case report findings.
Moderate Increased dopaminergic effects may occur during coadministration of methylphenidate, an inhibitor of dopamine reuptake, and medications that increase dopaminergic activity such as levodopa. Moderate Increased dopaminergic effects may occur during coadministration of methylphenidate, an inhibitor of dopamine reuptake, and COMT inhibitors such as tolcapone and entacapone.
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Major Concomitant use of cardiac glycosides with sympathomimetics can cause arrhythmias because sympathomimetics enhance ectopic pacemaker activity. Caution is warranted during co-administration of digoxin and sympathomimetics. Moderate Antipsychotics, such as phenothiazines, and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine.
Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents, including clonidine. Periodic evaluation of blood pressure is advisable during concurrent use of methylphenidate and clonidine, particularly during initial coadministration and after dosage increases of methylphenidate. Minor The modified release characteristics of extended-release methylphenidate are pH-dependent. Administration of H2-blockers could alter the release of methylphenidate. Patients receiving extended-release methylphenidate with acid suppressants should be monitored for adverse effects and therapeutic efficacy.
Major Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and selective serotonin reuptake inhibitors SSRIs. There are rare reports of serotonin syndrome occurring during use of an SSRI and methylphenidate. Minor The response to sympathomimetics may be enhanced by colchicine.
Moderate Inhalational general anesthetics e. While the sympathomimetic effects of methylphenidate are weaker than those of the amphetamines, and evidence of interaction is lacking, caution is advised. The use of Metadate CD is contraindicated on the day of surgery due to the risk of sudden blood pressure increases during administration of halogenated anesthetics.
Major Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and serotonin norepinephrine reuptake inhibitors SNRIs. Serotonin syndrome has been reported during concurrent use of other serotonergic antidepressants i. There is also a case of a neuroleptic malignant syndrome-like reaction occurring in a child on chronic methylphenidate therapy 45 minutes after ingesting a dose of venlafaxine.
It is unclear if the reaction was the result of a drug interaction. Severe Avoid coadministration of methylphenidate and dexmethylphenidate. These drugs represent duplicate treatments. Serious side effects such as nervousness, irritability, arrhythmias, palpitations, seizures, or other stimulant-related adverse effects may occur or get worse during concurrent use. Moderate Concurrent use of dronabinol, THC with sympathomimetics may result in additive hypertension, tachycardia, and possibly cardiotoxicity.
Dronabinol, THC has been associated with occasional hypotension, hypertension, syncope, and tachycardia. In a study of 7 adult males, combinations of IV cocaine and smoked marijuana, 1 g marijuana cigarette, 0 to 2. Major Coadministration of dyphylline with sympathomimetics should be approached with caution.
Coadministration may lead to adverse effects, such as tremors, insomnia, seizures, or cardiac arrhythmias, and should be avoided if possible. Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as eplerenone. Major Sympathomimetics can antagonize the antihypertensive effects of adrenergic agonists when administered concomitantly. Close monitoring of blood pressure or the selection of alternative therapeutic agents may be needed.
Major Ethanol consumption should be avoided during treatment with certain extended-release dosage forms of methylphenidate e. Consumption of ethanol may increases the release rate of methylphenidate. In addition, concurrent use may exacerbate the CNS-related adverse effects of methylphenidate. In addition, concurrent use with alcohol may exacerbate the CNS-related adverse effects of methylphenidate. Moderate Psychostimulants, such as methylphenidate, may lower the seizure threshold, thereby reducing the efficacy of anticonvulsants such as hydantoins.
In addition, case reports suggest a potential pharmacokinetic interaction between methylphenidate and phenytoin; however, a kinetic interaction was not confirmed when evaluated at higher sample sizes. Nevertheless, a dose adjustment of phenytoin and more frequent monitoring of plasma concentrations may be required when initiating or discontinuing methylphenidate.
Moderate Administer sympathomimetics with caution with beta-agonists such as vilanterol. The cardiovascular effects of beta-2 agonists may be potentiated by concomitant use. Monitor the patient for tremors, nervousness, increased heart rate, or other additive side effects. Moderate The CNS stimulant effects of methylphenidate can be additive when used concurrently with most other psychostimulants, such as caffeine, including foods, herbal or dietary supplement products containing high amounts of caffeine like green tea.
The combination of methylphenidate with other CNS stimulants may increase the incidence of side effects. Patients should avoid excessive caffeine intake, and observe for signs of nervousness, irritability, insomnia, tremor, arrhythmias, or other stimulant-related problems. Patients should be monitored for loss of blood pressure control. Moderate Psychostimulants, such as methylphenidate, may increase blood pressure and reduce the antihypertensive effects of antihypertensive agents, such as guanfacine.
Monitor blood pressure and heart rate periodically when prescribed together. Guanfacine may be used adjunctively to methylphenidate in the treatment of attention deficit hyperactivity disorder ADHD. Pharmacokinetic studies reveal that guanfacine does not influence methylphenidate pharmacokinetics and methylphenidate does not affect guanfacine pharmacokinetics. No dosage adjustments are required when used together.
Patients should be monitored for heart rate, blood pressure, and for sedation during ADHD treatment. Major Caffeine, an active constituent of guarana, is a CNS-stimulant and such actions are expected to be additive when coadministered with other CNS stimulants or psychostimulants. Use of guarana should be avoided with amphetamine, dextroamphetamine, methylphenidate, modafinil, pemoline, pseudoephedrine, beta-agonists or other sympathomimetics.
Moderate Antipsychotics, such as haloperidol, and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine. Major Methylphenidate can reduce the hypotensive effect of antihypertensive agents, including methyldopa. Moderate Clinically significant cardiovascular effects and fatalities have been reported in association with excessive use of inhaled sympathomimetic drugs.
Caution and close observation is needed if indacaterol is used concurrently with other adrenergic sympathomimetics, administered by any route, to avoid potential for increased cardiovascular effects. Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as indapamide. Severe In general, all types of sympathomimetics and psychostimulants should be avoided in patients receiving MAOIs due to an increased risk of hypertensive crisis.
This applies to sympathomimetics including stimulants for ADHD, narcolepsy or weight loss, nasal, oral, and ophthalmic decongestants and cold products, and even respiratory sympathomimetics e. Some local anesthetics also contain a sympathomimetic e. In general, medicines containing sympathomimetic agents should not be used concurrently with MAOIs or within 14 days before or after their use. Moderate Sympathomimetic amines should be used with caution in patients with thyrotoxicosis since these patients are unusually responsive to sympathomimetic amines.
Based on the cardiovascular stimulatory effects of sympathomimetic drugs, the concomitant use of sympathomimetics and thyroid hormones can enhance the effects on the cardiovascular system. Patients with coronary artery disease have an increased risk of coronary insufficiency from either agent. Concomitant use of these agents may increase this risk further. The reduction in TSH secretion is not sustained; hypothyroidism does not occur.
Major Psychostimulants, such as methylphenidate, exhibit sympathomimetic actions and should be avoided with other drugs, such as linezolid, that enhance the pressor response of sympathomimetic agents. A clinically significant rise in systolic blood pressure is possible. In addition, serotonin syndrome has been reported during the concurrent use of linezolid, a non-selective monoamine oxidase inhibitor MAOI , and medications that enhance central serotonergic activity.
Monoamine oxidase MAO is the enzyme responsible for the degradation of norepinephrine, dopamine, and serotonin. Moderate Methylphenidate can occasionally worsen mania in those with bipolar disorder, potentially reducing the overall effectiveness of treatment with mood stabilizers. According to some literature and the product labeling of many stimulants, lithium may antagonize the anorectic and stimulant effects of amphetamines.
Despite this precaution, some data indicate a beneficial effect based upon the clinical circumstances of the patient. Further study is needed to fully assess the benefits and risks that may occur from concomitant administration of methylphenidate and lithium. Close monitoring is advisable when combination therapy is initiated or dosages are increased. Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as loop diuretics. Moderate Antipsychotics, such as loxapine, and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine.
Major Sympathomimetics can antagonize the effects of vasodilators when administered concomitantly. Patients should be monitored for reduced efficacy if taking macitentan with a sympathomimetic. Moderate Psychostimulants, such as methylphenidate, may lower the seizure threshold, thereby reducing the efficacy of barbiturates such as mephobarbital in treating seizures.
In addition, case reports suggest a potential pharmacokinetic interaction between methylphenidate and barbiturates such as phenobarbital; however, a kinetic interaction was not confirmed when evaluated at higher sample sizes. Nevertheless, a dose adjustment of the barbiturate may be required when initiating or discontinuing methylphenidate. Moderate In theory, metoclopramide and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine.
Patients receiving this combination should be monitored for loss of effectiveness of either agent. Methylphenidate blocks central dopamine reuptake, which increases central dopaminergic functioning, while metoclopramide is a dopamine antagonist. Moderate Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and mirtazapine. Major The use of modafinil with other psychostimulants, including methylphenidate, has not been extensively studied.
Patients receiving combination therapy of modafinil with other psychostimulants should be closely observed for signs of nervousness, irritability, insomnia, arrhythmias, or other CNS stimulant-related side effects. Single dose studies of methylphenidate combined with modafinil noted that the rate of absorption of modafinil was delayed up to one hour by the presence of methylphenidate; no changes occurred in the metabolism and extent of absorption of either medication. Moderate Antipsychotics, such as molindone, and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine.
Moderate Concurrent use of nabilone with sympathomimetics e. In a study of 7 adult males, combinations of cocaine IV and smoked marijuana 1 g marijuana cigarette, 0 to 2. Moderate Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and nefazodone. Major Concomitant use of nitrates with sympathomimetics can result in antagonism of the antianginal effects of nitrates.
In addition, amyl nitrite can block the alpha-adrenergic effects of epinephrine, possibly precipitating tachycardia and severe hypotension. Major Use of medications that lower the seizure threshold should be carefully evaluated when considering the use of intrathecal radiopaque contrast agents. Methylphenidate should be discontinued at least 48 hours before myelography and should not be resumed for at least 24 hours postprocedure. Major Pimozide should not be used in patients taking drugs that may, themselves, cause motor and phonic tics e.
Once this issue is excluded, use together may proceed with caution. Pimozide and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine. Moderate Psychostimulants, such as methylphenidate, may lower the seizure threshold, thereby reducing the efficacy of anticonvulsants such as primidone. In addition, case reports suggest a potential pharmacokinetic interaction between methylphenidate and primidone; however, a kinetic interaction was not confirmed when evaluated at higher sample sizes.
Nevertheless, a dose adjustment of primidone and more frequent monitoring of plasma concentrations may be required when initiating or discontinuing methylphenidate. Major Because procarbazine exhibits some monoamine oxidase inhibitory MAOI activity, sympathomimetic drugs should be avoided. As with MAOIs, the use of a sympathomimetic drug with procarbazine may precipitate hypertensive crisis or other serious side effects.
In the presence of MAOIs, drugs that cause release of norepinephrine induce severe cardiovascular and cerebrovascular responses. In general, do not use a sympathomimetic drug unless clinically necessary e. If use is necessary within 2 weeks of the MAOI drug, in general the initial dose of the sympathomimetic agent must be greatly reduced. Patients should be counseled to avoid non-prescription OTC decongestants and other drug products, weight loss products, and energy supplements that contain sympathomimetic agents.
Moderate The concomitant use of rasagiline and sympathomimetics was not allowed in clinical studies; therefore, caution is advised during concurrent use of rasagiline and sympathomimetics including stimulants for ADHD and weight loss, non-prescription nasal, oral, and ophthalmic decongestants, and weight loss dietary supplements containing Ephedra. Although sympathomimetics are contraindicated for use with other non-selective monoamine oxidase inhibitors MAOIs , hypertensive reactions generally are not expected to occur during concurrent use with rasagiline because of the selective monoamine oxidase-B MAO-B inhibition of rasagiline at manufacturer recommended doses.
One case of elevated blood pressure has been reported in a patient during concurrent use of the recommended dose of rasagiline and ophthalmic tetrahydrozoline. One case of hypertensive crisis has been reported in a patient taking the recommended dose of another MAO-B inhibitor, selegiline, in combination with ephedrine. It should be noted that the MAO-B selectivity of rasagiline decreases in a dose-related manner as increases are made above the recommended daily dose and interactions with sympathomimetics may be more likely to occur at these higher doses.
Major Coadministration of methylphenidate and reserpine should be avoided if possible. Methylphenidate and reserpine may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on neurotransmitters. Methylphenidate blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increases the release of these monoamines into the extraneuronal space while reserpine depletes stores of serotonin and norepinephrine in the brain, adrenal medulla, and other tissues, and reduces the reuptake of catecholamines by adrenergic nerve terminals.
Reserpine binds tightly to catecholamine storage vesicles in the adrenergic neuron, eventually destroying these vesicles so that the terminals cannot concentrate or store norepinephrine or dopamine. This process also occurs in vesicles that store serotonin. Patients should be monitored for reduced efficacy if taking riociguat with a sympathomimetic. Severe Safinamide is contraindicated for use with methylphenidate due to the risk of serotonin syndrome.
Safinamide is a selective inhibitor of monoamine oxidase B, the enzyme which metabolizes dopamine. At high doses, diminished metabolism of serotonin and norepinephrine are also possible through inhibition of MAO-A. There is some evidence that the alteration of dopamine transport systems by methylphenidate may indirectly augment the action of serotonin. Selective serotonin reuptake inhibitors: Patients should be monitored for reduced efficacy if taking selexipag with a sympathomimetic. Serotonin norepinephrine reuptake inhibitors: Major The use of methylphenidate with sibutramine should be approached with great caution, due to the risk for serotonin syndrome.
Blood pressure and heart rate will require periodic monitoring, since additive effects may occur. Sibutramine has not been studied in combination with stimulants that are not used for weight loss, such as methylphenidate. Sibutramine may cause serotonin syndrome, and serotonin syndrome has been rarely reported with methylphenidate-type agents. Serotonin syndrome risk increases when 2 or more drugs with this effect are used together. Moderate The stimulant effects of methylphenidate can be additive when used concurrently with other psychostimulants, such as sodium oxybate.
The combination may increase the incidence of side effects; if these combinations cannot be avoided the patient should be closely observed for signs of nervousness, irritability, insomnia, arrhythmias, or other stimulant-related problems. Sodium oxybate has the potential to induce seizures; it has been speculated that this effect may be mediated through the action of sodium oxybate at GABA receptors.
Although convulsant effects occur primarily at high dosages, sodium oxybate should be used cautiously with psychostimulants that are known to lower seizure threshold. Note that CNS stimulants, including methylphenidate, are frequently used in the treatment of narcolepsy, and clinical trials involving the use of psychostimulants with sodium oxybate have not found the combinations to be unsafe.
Pharmacodynamic interactions cannot be ruled out, however. John's Wort, Hypericum perforatum: Moderate Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and St. Moderate Psychostimulants, such as methylphenidate, exhibit sympathomimetic actions and may interact with other drugs, such as tedizolid, that enhance the pressor response of sympathomimetic agents. In addition, serotonin syndrome has been reported during the concurrent use of linezolid, which is structurally related to tedizolid, and medications that enhance central serotonergic activity.
Tedizolid inhibits monoamine oxidase MAO , the enzyme responsible for the degradation of norepinephrine, dopamine, and serotonin. If serotonin syndrome occurs, all serotonergic agents should be discontinued and appropriate medical management should be implemented Terazosin: Moderate Concurrent administration of theophylline or aminophylline with some sympathomimetics can produce excessive stimulation and effects such as nervousness, irritability, or insomnia.
Moderate Methylphenidate can reduce the hypotensive effect of antihypertensive agents such as thiazide diuretics. Moderate Antipsychotics, such as thiothixene, and methylphenidate may interact pharmacodynamically to diminish the therapeutic effects of either agent through opposing effects on dopamine.
Major Sympathomimetics can antagonize the antihypertensive effects of vasodilators when administered concomitantly. Also, vasodilators can antagonize pressor responses to epinephrine. Patients should be monitored to confirm that the desired antihypertensive effect is achieved. Moderate Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and vilazodone.
Patients receiving this combination should be monitored closely for toxicity. Moderate Because of the potential risk and severity of serotonin syndrome, caution should be observed when coadministering drugs that have serotonergic properties such as methylphenidate and vortioxetine. Patients receiving methylphenidate with vortioxetine should be monitored for the emergence of serotonin syndrome. Moderate Case reports suggest a potential interaction between methylphenidate and coumarin anticoagulants; however, pharmacokinetic interactions were not confirmed when explored at higher sample sizes.
Nevertheless, a dose adjustment of warfarin and more frequent monitoring of the INR may be required when initiating or discontinuing methylphenidate. Methylphenidate exhibits activity similar to that of the amphetamines, although the underlying pharmacology for these two drug classes may differ. Methylphenidate exerts many of its effects through dopamine uptake blockade of central adrenergic neurons, in contrast to the amphetamines and cocaine that increase catecholamine release as a primary mechanism.
Specifically, methylphenidate blocks dopamine transport or carrier proteins. As a result, sympathomimetic activity in the central nervous system is increased. There is some evidence that the alteration of dopamine transport systems by methylphenidate may indirectly augment the action of serotonin, but further pharmacologic research is needed to understand these processes.
The main sites of CNS activity appear to be the brain stem arousal system and the cerebral cortex, including the subcortical structures of the thalamus. Methylphenidate-induced CNS stimulation produces a decreased sense of fatigue, an increase in motor activity and mental alertness, mild euphoria, and brighter spirits. A mild anorexic effect may occur. Unlike the amphetamines and cocaine, physical dependence is infrequent with normal clinical use at therapeutic doses. Chronic use of methylphenidate may lead to tolerance of side-effects and psychic dependence, similar to other psychostimulants.
Psychic dependence and addiction are more likely with parenteral or inhalational abuse, and are usually noted with illicit street use. In the periphery, the sympathomimetic actions of methylphenidate are minimal at therapeutic doses, and are less than those of the amphetamines or cocaine. Because methylphenidate slowly blocks the dopamine-transport proteins, methylphenidate appears less likely than the amphetamines or cocaine to increase systolic and diastolic blood pressure or cause respiratory stimulation.
Heart rate typically increases slightly with normal therapeutic doses of stimulants about 3—6 bpm ; however, a reflexive decrease in heart rate in response to increased blood pressure can also occur. At high doses, such as in overdoses, stimulants can cause significant hypertension, tachycardia, arrhythmias, and other serious complications. The mechanism s of action of the treatment of mental and behavioral conditions in ADHD are not established. Improved attention spans, decreased distractibility, increased ability to follow directions or complete tasks, and decreased impulsivity and aggression have been noted when stimulants are prescribed for the treatment of ADHD.
Current research suggests that the modulation of serotonergic pathways via changes in dopamine transport may contribute to the calming effects in the treatment of this disorder, but precise pharmacologic mechanisms have yet to be elucidated. Methylphenidate is administered orally and transdermally. Distribution in humans is unknown, but it does cross the blood-brain-barrier.
Metabolism occurs in the liver via de-esterification to the primary metabolite alpha-phenyl-piperidine acetic acid also known as ritalinic acid , which is inactive. Small amounts of the hydroxylated metabolites e. Therapeutic activity is primarily due to the parent compound. In studies with tablet and extended-release capsule Ritalin LA formulations, the average elimination half-life in adults was about 3.
Affected cytochrome P isoenzymes and drug transporters: The rapid half-life of immediate-release oral preparations may result in unmeasurable concentrations of the drug between the morning and midday doses; extended release preparations reduce these peak and trough variances. Extended-release once-daily oral preparations minimize the fluctuations between peak and trough concentrations associated with immediate-release formulations.
The transdermal form of methylphenidate bypasses the liver upon first pass, unlike the oral formulation, resulting in higher serum concentrations with lower initial doses. Additionally, the concentration of l-methylphenidate is roughly equal to that of d-methylphenidate with patch administration, whereas with oral administration little l-methylphenidate is available due to first pass metabolism.
However, the pharmacological activity of l-methylphenidate is less than d-methylphenidate. Immediate-release and extended-release dosage forms dosed more than once per day: Peak serum concentrations are achieved in about 1. The duration of action ranges from 3 to 6 hours with regular tablets and about 8 hours with the extended-release tablets. These extended-release tablets for once daily administration follow a biphasic pharmacokinetic profile to provide day-long medication availability.
Following oral administration of Concerta, plasma concentrations of methylphenidate increase rapidly reaching an initial maximum at about 1 hour, followed by a gradual increase in concentration over the next 5 to 9 hours. Thereafter, concentrations gradually decrease. Tmax across all doses occurs between 6 to 10 hours. The half-life of methylphenidate in adults and adolescents after oral administration of Concerta is about 3. These extended-release capsules for once-daily administration follow a biphasic pharmacokinetic profile to provide day-long medication availability.
The product demonstrates an initial peak plasma level at about 1. The Metadate CD capsule, when opened and sprinkled on a tablespoon of cool applesauce, is bioequivalent to the intact capsule. The effects of altered gastric pH on the absorption of Ritalin LA have not been studied. Interactions with antacids or acid blockers are possible.
The product demonstrates an initial peak plasma level at about 1 to 3 hours and a second peak at about 5 to 8 hours after dosing. There were no differences in pharmacokinetic parameters when this formulation was given with applesauce, but a high fat breakfast may delay absorption time. However, the capsules may be taken with food without clinically significant effects. The Ritalin LA capsule, when opened and sprinkled on a tablespoon of cool applesauce, is bioequivalent to the intact capsule.
Aptensio XR follows an extended-release biphasic pharmacokinetic profile to provide day-long medication availability with once daily administration. After oral administration, an initial peak plasma concentration occurs at about 2 hours, with a gradual descending concentration over the next 4 to 6 hours, after which a gradual increase begins reaching a second peak at about 8 hours. The pharmacokinetic profile of Aptensio XR administered as a whole capsule or opened and sprinkled onto applesauce under fasting conditions is similar.
After a single dose administered to healthy adults under fasting conditions, the following pharmacokinetic parameters were calculated: After a single 40 mg dose under fasting conditions, Cmax was obtained at a median time of 5 hours. Plasma methylphenidate concentrations declined monophasically. The mean elimination half-life was 5. The presence of alcohol increases release of methylphenidate.
This extended-release suspension for once-daily administration provides a mean peak plasma concentration of Food has no clinically significant effect on the bioavailability of the suspension. After a single Administration with a high-fat meal shorted the median time to peak concentration Tmax by 0. The mean elimination half-life was about 4 hours in healthy volunteers.
The presence of alcohol potentially increases release of methylphenidate. Transdermal Route The extent of methylphenidate systemic absorption after patch administration is dependent on the length of time the patch is worn and the patch size. Peak plasma concentrations of methylphenidate are reached approximately 8 hours after patch application. Cmax and AUC increase significantly with repeated daily administration compared to single-dose administration.
In children 6 to 12 years of age, mean peak concentrations of transdermal methylphenidate were roughly 1. However, the Cmax of single dose administration of transdermal methylphenidate is comparable to the Cmax from a single dose of the once daily oral formulations. Transdermal absorption of methylphenidate may increase over time with chronic therapy; these changes cannot be explained by changes in clearance or rate of elimination.
On average, steady-state is achieved after approximately 14 days of dosing. The time until any transdermally administered d-methylphenidate is detectable in the circulation averages 3. The absorption rate and extent is increased when methylphenidate patch is applied to inflamed skin or exposed to heat. Absorption characteristics in areas other than the hip are not known. Once the methylphenidate patch is removed after 9 hours of wear time, methylphenidate plasma concentrations decline in a biexponential manner most likely due to distribution of methylphenidate from the skin after patch removal.
The pharmacological activity of l-methylphenidate is less than d-methylphenidate. With transdermal administration in children and adolescents, the mean elimination half-life of l-methylphenidate was shorter than for d-methylphenidate and ranged from 1. Your Name Your name is required. Recipient's Email Separate multiple email address with a comma Please enter valid email address Recipient's email is required.
Your email has been sent. For once-daily product dosing. Oral dosage extended-release once-daily tablets; e. Adults up to 65 years not currently taking methylphenidate. Children and Adolescents 6 years and older not currently taking methylphenidate. Oral dosage extended-release once-daily capsules; e. Adults not currently taking methylphenidate. Adults currently taking other dosage forms of methylphenidate.
Children and Adolescents 6 years and older currently taking other dosage forms of methylphenidate. Children and Adolescents 6 years and older. Oral dosage extended-release once-daily chewable tablets; e. Oral dosage extended-release once-daily suspension; e.