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	Methylphenidate is a former featured article candidate. Please view the links under Article milestones below to see why the nomination failed. For older candidates, please check the archive.
Article milestones Date Process Result January 27, 2010 Featured article candidate Not promoted

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Addiction and dependence are not signs of an overdose. Thus should not be a subheading of that. Doc James ( talk · contribs · email) 05:53, 17 May 2019 (UTC) reply

In fact abuse and dependence are block box warnings. We include these under side effects generally. [1] Doc James ( talk · contribs · email) 05:59, 17 May 2019 (UTC) reply

The original placement under the overdose heading was compliant with MOS:MED#Drugs, treatments, and devices. It is, therefore, acceptable. Also, the only reason that adverse effects is listed as a potential location for that section is that some drugs - and by some drugs I mean opiates (addiction and dependence) and benzos (dependence) - produce one or both of addiction and dependence at commonly prescribed doses for certain conditions (opiate addiction is really only a possibility in the case of end of life care though). I know for certain that this was the intended approach based upon the sectioning specified in the MOS because I'm the one who proposed listing "Adverse effects" and "Overdose" as potential locations for that subsection in the MOS way back when. Therefore, I'm moving it back.

The black box warning doesn't specify how methylphenidate addiction develops; don't read into something that's not there. Seppi333 ( Insert 2¢) 06:06, 17 May 2019 (UTC) reply

No it does not make sense. Overdose is not simple just excessive usage. And actually placing under "Side effects" was fully compliant with WP:MEDMOS Doc James ( talk · contribs · email) 06:32, 17 May 2019 (UTC) reply

RfC about placement of content

First ref says "Our findings suggest that methylphenidate may be associated with a number of serious adverse events as well as a large number of non-serious adverse events in children " [3]

Second ref says "the low quality of the underpinning evidence means that we cannot be certain of the magnitude of the effects." [4]

The text was supported. Doc James ( talk · contribs · email) 11:40, 1 November 2019 (UTC) reply

I've been made aware of a medication called Jornay PM (Methylphenidate HCl). It looks like an extended-release form of Methylphenidate but patients take it at night. It has FDA approval and is currently available in the US. Does it belong as a mention in Extended-release section? I'd add it myself but I'm having trouble finding the right references for how long it lasts and if it's available outside the US, etc. Wirewad ( talk) 18:13, 5 December 2019 (UTC) reply

I can't find anyone summing it up with a single number or range, either. The chart on their FDA efficacy paperwork suggests a 12-hour active period (following the 8-10 hour delayed release) and their description of the active effect includes phrasing like "from morning until bedtime," but they don't interpret the chart for us. https://www.ironshorepharma.com/labeling.pdf

However, they do indicate that dosing can be increased to ensure that the medication remains effective until the end of the day. https://www.jornaypm-pro.com/dosing

Additionally, a review of the medication in Pharmacy Times suggests that Jornay PM takes advantage of existing ER technology, and that the innovation is simply the pairing of that with existing DR technology (delayed/extended release). So, it would be reasonable to assume that the ER piece of this is basically the same as other ER meds, and put down 8-12 hours as a broad range accounting for 2 standard deviations (or more) from the mean. https://www.pharmacytimes.com/view/stimulant-medication-with-evening-dosing-to-address-earlymorning-functioning-impairments-in-adhd

Regardless, Jornay PM is a very notable addition to existing options. I hope someone adds it to the page, even if they feel compelled to leave some of the sections on the table blank or simply quote the manufacture saying "all day" (or whatever exact phrasing) instead of putting a number. It's a shame to not see it here. 162.129.250.22 ( talk) 16:58, 18 April 2022 (UTC) reply

Ref says "Stimulant medications cause a modest increase in average blood pressure (about 2-4 mmHg) and average heart rate (about 3-6 bpm), and individuals may have larger increases... Cardiac: angina, arrhythmia, palpitations, pulse increased or decreased, tachycardia"

Doc James ( talk · contribs · email) 10:27, 29 January 2020 (UTC) reply

Support the 2019 proposal to merge to brand Daytrana to the generic name for the drug. Klbrain ( talk) 17:34, 18 April 2020 (UTC) reply

• Support merge to generic. Doc James ( talk · contribs · email) 23:32, 18 April 2020 (UTC) reply

Done Doc James ( talk · contribs · email) 07:06, 21 May 2020 (UTC) reply

I am not able to contribute professional knowledge to this article, but I would like to share some personal experience. Methylphenidate was a psychiatric "magic bullet" for me. After decades of crippling clinical depression, my current psychiatric care provider (the most recent in a series of at least six) suggested it. The improvement in my symptoms was immediate, intense, and lasting. I had run through the gamut of conventional depression treatments prior to this, including ECT, with no relief, and did not know that methylphenidate was an option. I suspect that many of my former providers did not know either, or considered it a last resort.

If someone could expand this section and include some links to academic or medical sources it would be of enormous value to other people who are struggling with treatment-resistant depression. It is difficult as a layman or patient to find information about this use of methylphenidate, and heathcare providers seem to be gun-shy about recommending it. 216.30.159.93 ( talk) 23:38, 11 September 2020 (UTC) reply

depression treatment usually depends on monoamine theory. SSRI or other antidepressants(except atypicals and maoi's) increase monoamines but mostly serotonin basicly. Atypical depression and ADHD related depression (and some other types of depression) can be reversed by stimulants because of their distinct mechanism. But as a dopamine reuptake inhibitor methylphenidate mostly treats fatigue and anhedonia associated with depression or other medical conditions. my situation is same with you. ssri's can make depression worse if depression associated with other conditions. primary depression is more type of "melancholy" rather than "just anhedonia". but there is also some types of depression that depend on anhedonia but they respond ssri/snri's unlike those with ADHD. RoyaleKingdom78 ( talk) 12:19, 9 December 2021 (UTC) reply

Adding some sources. The prescriber’s guide to classic MAO inhibitors (phenelzine, tranylcypromine, isocarboxazid) for treatment-resistant depression and MAOIs and CNS Stimulants

Currently it is: "It is not a Cocaine derivate nor analogue. Cocaine is analgesic and ligand channel blocker with SNDRI action while Methylphenidate is NDRI with 2-3 fold DAT selectivity over NET. Cocaine also more potent in SERT rather than NDRI site. [7]"

But it should be as follows: It is not a Cocaine derivate nor an analog. Cocaine is an analgesic and ligand channel blocker with SNDRI action while Methylphenidate is an NDRI with 2-3 fold DAT selectivity over NET. Cocaine is also more potent in SERT rather than NDRI sites. [7]"

(First time posting on wiki hope I did it right)

I noticed that too, upon a first reading of the article. I made the corrections that you suggested. Thank you! And yes, you posted correctly here on the talk page!-- FeralOink ( talk) 12:54, 2 January 2022 (UTC) reply

Not exactly "grammar", but in the Available Forms/Extended Release section, "Metadate ER" and "Methylin ER" are brand names, but appear in the Generic Names column.

This sentence under Other medical uses, "However, the use of stimulants such as methylphenidate in cases of treatment-resistant depression is controversial.[42]", references a journal article from 1992.

Kraus MF, Burch EA (October 1992). "Methylphenidate hydrochloride as an antidepressant: controversy, case studies, and review". Southern Medical Journal. 85 (10): 985–991. doi:10.1097/00007611-199210000-00012. PMID 1411740

30 years later, it's relatively common to use Methylphenidate to augment other medications in treatment-resistant depression. Therefore, I believe that either this sentence needs to be reevaluated for whether it's necessary, and/or more recent references are needed to back up this claim. Alteredtome ( talk) 04:14, 12 April 2022 (UTC) reply

To all who contributed to writing this Article, all I can say is might just be the best article I’ve read on the entire site. Which is thousands so it’s saying a lot for me. Well done. 2601:644:8F83:D7A0:79B2:28C7:ECD2:4397 ( talk) 01:08, 1 October 2022 (UTC) reply

Firstly this article reads in parts like an advert instead of a normal article on substances. Secondly, the delphic analyis which includes police and legal services is not useful in estimating addictive, deadly, or dangerous potential, rather it can only indicate attitudes instead of expert opinion due to the inclusion of police. Given that the police involved in this study are engaged in a drug war which generally treats pharmaceuticals as arbitrarily less dangerous, it's an obvious bias. This diagramm is misleading and should be deleted as should references to it. 77.188.117.198 ( talk) 16:21, 23 January 2023 (UTC) reply

Are bupropion and methylphenidate TAAR-active? Requesting binding profile. -- 0dorkmann ( talk) 08:16, 11 February 2023 (UTC) reply

No. Here is the relevant discussion from Dr. Faraone in 2018;

“The direct effects of MPH include inhibition of the DAT and NET ( 113, 114, 118, 120, 123, 128), an affinity for and agonist activity at the 5-HT_1A receptor ( 119, 120), and redistribution of VMAT-2 ( 88, 125). As a consequence of these interactions, MPH elevates extracellular DA and NE levels ( 58, 71, 94, 107). The enhanced efflux of DA and NE associated with MPH exposure results in increased availability of DA and NE to bind to their respective transporters (ie, the DAT or NET) or to DA or NE receptors, as evidenced by reductions in ligand binding in PET and SPECT studies ( 112, 113, 117, 122- 124, 127).

Although increases in extracellular levels of striatal DA in rats measured using microdialysis are less pronounced with MPH than with AMP, both compounds have been shown to exhibit similar magnitude of effects with regard to reductions in DA binding potential as measured by PET in rodents and nonhuman primates ( 94). Multiple studies have demonstrated that MPH also directly interacts with adrenergic receptors ( 109, 115, 119, 120). Through activation of α₂adrenergic receptors, MPH has been demonstrated to stimulate cortical excitability ( 109). Further evidence for the interaction of MPH with α₂ adrenergic receptors comes from data indicating that the procognitive effects of MPH in a working memory task are blocked by the α₂ adrenergic antagonist idazoxan ( 115). The effects of MPH on α₂ adrenergic receptors are notable given that two α₂ adrenergic receptor agonist drugs (extended-release forms of guanfacine and clonidine) are indicated for the treatment of ADHD ( 196)”.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8063758/ JoeBo82 ( talk) 01:58, 8 July 2023 (UTC) reply

To me it seems superfluous and it might be found confusing to readers. Gutten på Hemsen ( talk) 15:59, 15 April 2023 (UTC) reply

From Adverse Effects:

"Ophthalmologic adverse effects may include blurred vision caused by pupil dilatation and dry eyes, with less frequent reports of diplopia and mydriasis"

This seems to be saying that mydriasis is less common than dilated pupils. These terms are synonymous. Is this a syntactical issue I'm missing or is it contradictory? his seems to be saying that dilated pupils are less common than 2603:7081:1603:A300:2CC4:A198:82DB:C8BF ( talk) 02:44, 28 September 2023 (UTC) reply

"In children over age 6 and adolescents, the short-term benefits and cost-effectiveness of methylphenidate are well established. A number of reviews have established the safety and effectiveness for individuals with ADHD over several years." Several narrative reviews, the newest of which is 12 years old, are cited in support of this passage. By contrast, a recent Cochrane review concludes that the quality of randomized controlled trials of methylphenidate is too poor to make conclusions about the effectiveness or harms of methylphenidate. This review is actually cited a paragraph below. It seems strange to leave up these contradictory statements. I would suggest that more information about the conclusions of the Cochrane review be included and the older text deleted. Feline negativity ( talk) 18:12, 4 November 2023 (UTC) reply

Methylphenidate and amphetamines are still first-line treatment for ADHD so I don't think nothing's changed since that source. Not sure why you want a latest source when the scientific fact do not change/update. -- WikiLinuz ( talk) 05:45, 12 February 2024 (UTC) reply

WP:OLDSOURCES applies when newer evidence falsifies the older facts from the old source (but this doesn't seem to be the case here, unless I misunderstood what you mean). -- WikiLinuz ( talk) 05:48, 12 February 2024 (UTC) reply

The majority of the claims made in the two paragraphs removed are based on research from the early 2000s, in flawed (narrative) reviews which typically did not bother to review to quality of the trials on which they were based. Three separate Cochrane reviews of methylphenidate, by three different research groups, have found that the quality of the RCT evidence base is too poor to draw conclusions regarding the safety and efficacy of methylphenidate in the treatment of ADHD.

The same conclusion has been reached by the WHO Essential Medicines Committee, which has twice rejected methylphenidate from the list on the same grounds: namely, that safety, efficacy, and the harm-benefit ratio have not been adequately established. It therefore seems to me that the information on the page is indeed outdated, as it has been contradicted by newer, high-quality reviews. Why would outdated information from uncritical reviews be preferred to the reports of recent Cochrane systematic reviews, which have been supported by a WHO Committee? I believe it is Wikipedia policy to prefer the highest-quality recent systematic reviews on a medical topic. Feline negativity ( talk) 22:17, 12 February 2024 (UTC) reply

I disagree with your removal of the two paragraphs in question. I am interpreting/reformulating your primary argument against the paragraphs and their sources as follows: "The sources cited are narrative reviews from over a decade ago that do not take into account the quality of the available evidence; more recent systematic reviews are superior in this aspect, and because the two source groups and their associated claims contradict each other, the more critical recent reviews should be given WP:DUEWEIGHT over the older ones." Is this an accurate representation of your argument?

Assuming it is, I have multiple issues with it. First of all, there are recent systematic reviews that take into account the evidence quality and nonetheless come to the conclusion that methylphenidate is an effective ADHD treatment ( Cortese et al. 2018 Taking into account both efficacy and safety, evidence from this meta-analysis supports methylphenidate in children and adolescents...for the short-term treatment of ADHD, Elliott et al. 2020 Overall, we found that ADHD pharmacotherapies, as a class, improved clinical response relative to placebo; although the latter does not specifically state that specifically methylphenidate is effective, it was one of the medications looked at in the analysis). This suggests that it's a matter of disagreement between the sources on what conclusions can be made with the evidence, not which evidence was available (unless there was a drastic shift in available evidence in those few years between these sources and yours) nor whether the evidence quality was analyzed; in other words, different sources had mostly the same evidence, analyzed it in mostly the same way, and came to different conclusions on what could be said about the effectiveness of methylphenidate.

Second, the non-inclusion of a medication in the list of WHO essential medicines doesn't say much about whether a medication is effective or not; for the version of the list where it was rejected in the source you cite, only 460 medications made it onto the list at all (and even today it has just 591). The clue is in the name: only the most essential medicines for the most important needs of a healthcare system are included. Plenty of safe and effective medications aren't included, and this is by design. I don't have the full text, but from what I can tell about the WHO source, it is not a systematic review; this is fine, but by that token recent narrative reviews and clinical practice guidelines could be cited as well.

Thirdly, you seem to be implying either that there is a contradiction between the newer sources and the older paragraphs, that the claims of the newer sources are not given sufficient weight/coverage in the article, or both (correct me if I'm wrong though). As I understand it, the core issue of the newer sources – what they primarily dispute – is not the existence of such evidence but the quality of the evidence (see my first point). It's clear there is an effect, but as our article states itself (citing one of the newer critical sources): "[t]he precise magnitude of improvement in ADHD symptoms and quality of life produced by methylphenidate treatment remains uncertain" [emphasis mine]. The effect size and evidence quality are the two main loci of scientific debate. That's what those sources have investigated, and that's what's already in the article.

The problems with the two removed paragraphs are ultimately solvable with the use of more recent sources. On the other hand, their removal appears to slant the article's coverage away from the mainstream academic consensus regarding the effectiveness of ADHD medications. Coolclawcat ( talk) 11:11, 13 February 2024 (UTC) reply

Thanks for your comments. I believe that the use of narrative reviews from the early 2000s is problematic (unfortunately they seem to be all over Wikipedia), as they were often written before journals had stringent COI policies, before peer-reviewers were well versed in the techniques of EBM, and before there was a widespread knowledge of the deeply flawed nature of many industry-sponsored drug trials. (Eminent medical historian Edward Shorter has described this period as the nadir of the corruption of academic medicine by industry.) I think that the language in the removed paragraphs was heavily promotional, based on an uncritical appraisal of the literature, and that the paragraphs should be replaced with similar information from newer and superior sources.

There is indeed another major recent systematic review on the topic, Cortese et al, which drew conclusions opposed to the review of Storebø et al. The crux of the matter is how the quality and risk of bias of the included trials are assessed. The two research groups behind the reviews have been going back and forth quarreling over which of them is doing this correctly for around 8 years now. This article has citations to all or most of their commentary on the Storebø review, and here are critical letters on Cortese's. Ultimately I believe Storebø's review is to be preferred, although a note about the controversy would certainly be warranted. Storebø et al. is more recent, underwent a very extensive peer-review for inclusion in the Cochrane Library, and was explicitly preferred by the Expert Committee and the peer-reviewers for the WHO, who received both meta-analyses for review. It is certainly true that methylphenidate doesn't have to be an "essential medicine" to be an effective one, but look at the commentary of the WHO as to why it was rejected: because the poor quality of the trials makes the efficacy, safety, and cost-effectiveness of methylphenidate unclear. Obviously this is not what the article had previously said: the section opened with very strong and positive assertions about the effects of methylphenidate, and relegated the assessment of the Cochrane review and the WHO to the role of a minor quibble, rather than calling into doubt the evidence base on which the preceding claims were made. Feline negativity ( talk) 20:38, 13 February 2024 (UTC) reply

There is an interesting discussion of the WHO's decision and rationale in the pages of this month's Lancet Psychiatry. It is another point in Storebø's favor, in my view, that the authors do not have conflicts of interest, whereas many of the authors on the Cortese review and on the critical commentaries on Storebø have very extensive financial ties to industry, which has been shown to be a significant issue, including in systematic reviews. There is a useful review I have found of the issues involved in the dispute, which could provide some background for discussion here and could also be worth citing in the main article. Feline negativity ( talk) 23:54, 13 February 2024 (UTC) reply

I've had the time now to take a look at the other systematic review you brought up, Elliott et al. This review actually extensively raises very similar concerns with regard to risk of bias as the Cochrane reviews of methylphenidate in adults by Cândido et al. and Boesen et al. The sentence you quote from the Discussion section continues, "however, the clinical importance of these changes is unclear, and when the analyses were restricted to studies at low risk of bias due to blinding, there was no significant difference between ADHD pharmacotherapy and placebo in the meta-analysis, and few differences were evident in the network meta-analyses...the certainty of the findings for all outcomes was very low to low." In Table 3 you can see that Elliott et al. have classified all the evidence for the various outcomes with methylphenidate as being of "very low" quality. It is perhaps worth noting that a previous Cochrane review on methylphenidate in adults was retracted for, amongst other reasons, an inadequate assessment of bias in the literature. Feline negativity ( talk) 06:39, 14 February 2024 (UTC) reply

agree w/ Feline negativity-- Ozzie10aaaa ( talk) 13:57, 15 February 2024 (UTC) reply

Methylphenidate and MAOIs are perfectly safe to use concomitantly, despite common dogma to the contrary. MPH is not a releaser of norepinephrine unlike DEX and especially mixed AMP salts (due to the presence of levoamphetamines which have strong peripheral effects). There is virtually no risk of precipitating a hypertensive crisis if titrated/managed properly. The prescriber’s guide to classic MAO inhibitors (phenelzine, tranylcypromine, isocarboxazid) for treatment-resistant depression and MAOIs and CNS Stimulants 206.194.253.145 ( talk) 04:44, 21 January 2024 (UTC) reply