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Methylphenidate has been investigated as a chemical replacement for the treatment of cocaine dependence.<ref name="pmid9408812">{{cite journal |author=Grabowski J, Roache JD, Schmitz JM, Rhoades H, Creson D, Korszun A |title=Replacement medication for cocaine dependence: methylphenidate |journal=J Clin Psychopharmacol |volume=17 |issue=6 |pages=485–8 |year=1997 |month=December |pmid=9408812 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0271-0749&volume=17&issue=6&spage=485}}</ref>
Methylphenidate has been investigated as a chemical replacement for the treatment of cocaine dependence.<ref name="pmid9408812">{{cite journal |author=Grabowski J, Roache JD, Schmitz JM, Rhoades H, Creson D, Korszun A |title=Replacement medication for cocaine dependence: methylphenidate |journal=J Clin Psychopharmacol |volume=17 |issue=6 |pages=485–8 |year=1997 |month=December |pmid=9408812 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0271-0749&volume=17&issue=6&spage=485}}</ref>


Early research began in 2007-8 in some countries on the effectiveness of methylphenidate as a substition agent in refractory cases of cocaine dependence; the fact that it can satisfy cravings for cocaine in a way which is subjectively and pharmacologically equivalent but longer-lasting as well as easier on the body and ''somewhat'' safer and easier to manage has long been part of the 'street lore' associated with stimulants in many parts of the world in much the same way that other substitutionmittel drugs such as methadone, buprenorphine, butorphanol, extended-release oral morphine, dihydrocodeine, and clonidine were amongst opioid users in various times over the past century.
Early research began in 2007-8 in some countries on the effectiveness of methylphenidate as a substition agent in refractory cases of cocaine dependence; the fact that it can satisfy cravings for cocaine in a way which is subjectively and pharmacologically equivalent but longer-lasting as well as easier on the body and ''somewhat'' safer and easier to manage has long been part of the 'street lore' associated with stimulants in many parts of the world in much the same way that other substitutionmittel drugs such as methadone, buprenorphine, butorphanol, extended-release oral morphine, dihydrocodeine, and clonidine were amongst opioid users in various times over the past century.{{clarifyme}}


Given the high co-morbidity between ADHD and autism, a few studies have examined the efficacy and effectiveness of Ritalin in the treatment of autism (e.g., Aman & Langworthy, 2000). However, most these studies examined the effects of Ritalin on attention and hyperactivity symptoms among kids with autism spectrum disorders (ASD). The present study attempted to examine the effects of Methylphenidate on social-communication and self-regulation behaviors among kids with ASDs.
Given the high co-morbidity between ADHD and autism, a few studies have examined the efficacy and effectiveness of Ritalin in the treatment of autism (e.g., Aman & Langworthy, 2000). However, most these studies examined the effects of Ritalin on attention and hyperactivity symptoms among kids with autism spectrum disorders (ASD). The present study attempted to examine the effects of Methylphenidate on social-communication and self-regulation behaviors among kids with ASDs.

Revision as of 11:16, 16 February 2009

"Vitamin R" redirects here. For the Chevelle song, see Vitamin R (Leading Us Along).
Methylphenidate
Clinical data
Pregnancy
category
  • C
Routes of
administration		Oral, Transdermal, IV, Nasal
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability11–52%
Protein binding30%
MetabolismLiver
Elimination half-life2–4 hours
ExcretionUrine
Identifiers
  • methyl 2-phenyl-2-(piperidin-2-yl)acetate
CAS Number
PubChem CID
DrugBank
ChemSpider
CompTox Dashboard (EPA)
ECHA InfoCard100.003.662 Edit this at Wikidata
Chemical and physical data
FormulaC14H19NO2
Molar mass233.31 g/mol g·mol−1
3D model (JSmol)
  • COC(=O)C(C1CCCCN1)c1ccccc1
Indicated for:

Other uses:

Contraindications:
  • Use of tricyclic antidepressants (e.g. desipramine), as methylphenidate may dangerously increase their plasma concentrations, leading to potential toxic reactions (mainly, cardiovascular effects).
  • Use of MAO Inhibitors, such as phenelzine (Nardil) or tranylcypromine (Parnate), and certain other drugs.
  • methylphenidate should not be given to patients who suffer from the following conditions: Severe Arrhythmia, Hypertension or Liver damage.
  • Drug-seeking behaviour
  • Pronounced agitation or nervousness. Other side effects include drowsiness, and mood swings
Side effects:[2][3]

Atypical sensations:

Cardiovascular:

Ear, nose, and throat:

Endocrinal:

  • Appetite loss

Eye:

  • Blurred vision

Gastrointestinal:

  • Nausea/vomiting, abdominal pain

Hematological:

Musculoskeletal:

  • Muscle twitches

Neurological:

Psychological:

Respiratory:

  • Increased respiration rate,


Urogenital and reproductive:

Miscellaneous:

  • Fever

Methylphenidate[4] (MPH) is a prescription stimulant commonly used to treat Attention-deficit hyperactivity disorder, or ADHD, and Attention-deficit disorder, or ADD. It is also one of the primary drugs used to treat the daytime drowsiness symptoms of narcolepsy and chronic fatigue syndrome. The drug is seeing early use to treat cancer-related fatigue.[5] Brand names of drugs that contain methylphenidate include instant-release racemic methylphenidate Ritalin, Ritalina, Rilatine, Attenta (in Australia), Methylin, Penid, and Rubifen; and the sustained release tablets Concerta, Metadate CD, Methylin ER, Ritalin LA, and Ritalin-SR. Focalin is a preparation containing only dextro-methylphenidate, rather than the usual racemic dextro- and levo-methylphenidate mixture of other formulations. A newer way of taking methylphenidate is by using a transdermal patch (under the brand name Daytrana), similar to those used for hormone replacement therapy (HRT), nicotine release and pain relief (Fentanyl).

History

Methylphenidate was patented in 1954 by the CIBA pharmaceutical company (now Novartis) as a potential cure for Mohr's disease.[citation needed] Beginning in the 1960s, it was used to treat children with ADHD or ADD, known at the time as hyperactivity or minimal brain dysfunction (MBD). Today methylphenidate is the most commonly prescribed medication to treat ADHD around the world.[citation needed] Production and prescription of methylphenidate rose significantly in the 1990s, especially in the United States, as the ADHD diagnosis came to be better understood and more generally accepted within the medical and mental health communities.[6]

Most brand-name Ritalin is produced in the United States, and methylphenidate is produced in the United States, Mexico, Argentina and Pakistan. Other generic forms, such as "methylin", are produced by several U.S. pharmaceutical companies. Ritalin is also sold in the United Kingdom, Germany and other European countries (although in much lower volumes than in the United States). These generic versions of methylphenidate tend to outsell brand-name Ritalin four to one.[citation needed] In Belgium the product is sold under the name "Rilatine".

Another medicine is Concerta, a once-daily extended-release form of methylphenidate, which was approved in April 2000. Studies have demonstrated that long-acting methylphenidate preparations such as Concerta are just as effective, if not more effective, than IR (instant release) formulas.[7][8][9][10] Time-release medications are also less prone to misuse[citation needed]

In April 2006, the U.S. Food and Drug Administration (FDA) approved a transdermal patch for the treatment of ADHD called Daytrana.[11]


Indications

Methylphenidate 10 mg Tablet (Mallinckrodt)

Methylphenidate is a central nervous system (CNS) stimulant indicated in the treatment of attention-deficit hyperactivity disorder[12] and narcolepsy.[13] When prescribed at the correct dosage, methylphenidate is usually well tolerated by patients.[7]

In individuals with cancer, methylphenidate is commonly used to counteract opioid-induced somnolence, to increase the analgesic effects of opioids, to treat depression, and to improve cognitive function.[14]

Investigational

A 2006 review assessing the safety of methylphenidate on the developing brain found that in animals with psychomotor impairments, structural and functional parameters of the dopamine system were improved with treatment.[15]

Methylphenidate may reduce the risk of falls in older adults by treating cognitive deficits associated with aging and disease.[16]

Methylphenidate has been investigated as a chemical replacement for the treatment of cocaine dependence.[17]

Early research began in 2007-8 in some countries on the effectiveness of methylphenidate as a substition agent in refractory cases of cocaine dependence; the fact that it can satisfy cravings for cocaine in a way which is subjectively and pharmacologically equivalent but longer-lasting as well as easier on the body and somewhat safer and easier to manage has long been part of the 'street lore' associated with stimulants in many parts of the world in much the same way that other substitutionmittel drugs such as methadone, buprenorphine, butorphanol, extended-release oral morphine, dihydrocodeine, and clonidine were amongst opioid users in various times over the past century.[clarification needed]

Given the high co-morbidity between ADHD and autism, a few studies have examined the efficacy and effectiveness of Ritalin in the treatment of autism (e.g., Aman & Langworthy, 2000). However, most these studies examined the effects of Ritalin on attention and hyperactivity symptoms among kids with autism spectrum disorders (ASD). The present study attempted to examine the effects of Methylphenidate on social-communication and self-regulation behaviors among kids with ASDs.

The sample included 33 children with pervasive developmental disorder (29 boys) with a mean age of 6.93 years (range 5-13). This was a 4-week randomized, double-blind, cross-over placebo study, with treatment changing each week between 4 conditions: placebo, low dose, medium dose, and high dose. In this design, neither the experimenters nor the families know which of the 4 treatments the child is receiving at any given time. In addition, the treatment condition changes randomly each week, without anyone knowing the nature of the old or new condition. This allows the experimenters to assume that consistent changes in behaviors that occur during a particular treatment is truly due to the effect of that treatment and not to the expectation of the treatment (placebo effect).

The results indicate that children showed significantly more joint attention behaviors when receiving Methylphenidate than when receiving the placebo (although the most effective dosage varied by individual). Furthermore, at a group level, the low dose of Methylphenidate resulted in significantly improved joint attention behaviors when compared to the placebo, but no differences were noted between the low, medium, and high doses. Low and medium doses of Methylphenidate also resulted in improved self-regulation behavior when compared to placebo.

The study presents compelling preliminary evidence suggesting that Methylphenidate is effective in improving some social behaviors among children with ASDs.[18]

Pharmacology

Methylphenidate has binding affinity for both the dopamine transporter and norepinephrine transporter, with the Dextromethylphenidate enantiomers displaying a prominent affinity for the norepinephrine transporter. Both the dextro- and levorotary enantiomers displayed receptor affinity for the serotonergic 5HT1A and 5HT2B subtypes, though direct binding to the serotonin transporter was not observed.[19]

The enantiomers and the relative psychoactive effects and CNS stimulation of dextro- and levo-methylphenidate is analogous to what is found in amphetamine, where dextro-amphetamine is considered to have a greater psychoactive and CNS stimulatory effect than levo-amphetamine.

Mode of action

The means by which methylphenidate affects people diagnosed with ADHD are not well understood. Some researchers have theorized that ADHD is caused by a dopamine imbalance in the brains of those affected. Methylphenidate is a norepinephrine and dopamine reuptake inhibitor, which means that it increases the level of the dopamine neurotransmitter in the brain by partially blocking the dopamine transporter (DAT) that removes dopamine from the synapses.[20] This inhibition of DAT blocks the reuptake of dopamine and norepinephrine into the presynaptic neuron, increasing the amount of dopamine in the synapse. It also stimulates the release of dopamine and norepinephrine into the synapse. Finally, it increases the magnitude of dopamine release after a stimulus, increasing the salience of stimulus. An alternate explanation which has been explored is that the methylphenidate affects the action of serotonin in the brain.[21]

It has been established that Ritalin only works in ADHD when levels of an important neurotransmitter called Phenylethylamine is increased. [citation needed]

It is commonly asked why a stimulant should be used to treat hyperactivity, which seems paradoxical. However, CTs of ADHD brains show decreased activity in the brain centers critical to concentration and goal-directed activities.[citation needed] Treatment with methylphenidate (etc.) results in increased activity in those regions, in ADHD patients, and in healthy controls as well. Thus the model explanation is that hyperactive children (and adults) have underactive concentration centers, and stimulating them reduces hyperactivity. Thus the stimulants do not work paradoxically. They stimulate portions of the brain that are underactive by increasing dopamine and norepinephrine in the striatum and prefontal cortex.

One study finds that methylphenidate reduces the increases in brain glucose metabolism during performance of a cognitive task by about 50%. This suggests that, similar to increasing dopamine and norepinephrine in the striatum and prefrontal cortex, methylphenidate may focus activation of certain regions and make the brain more efficient. This is consistent with the observation that stimulant drugs can enhance attention and performance in some individuals. If brain resources are not optimally distributed (for example, in individuals with ADHD or sleep deprivation), improved performance could be achieved by reducing task-induced regional activation. Stimulant delivery when brain resources are already optimally distributed may then adversely affect performance.[22]

Side effects

Common side effects

In children

The following may occur more frequently during the treatment of children:

  • Loss of appetite[23]
  • Abdominal pain[23]
  • Weight loss during prolonged therapy[23]

Less common side effects

Known or suspected risks to health

Researchers have also looked into the role of methylphenidate in affecting stature, with some studies finding slight decreases in height acceleration.[24] Other studies indicate height may normalize by adolescence.[25][26] In a 2005 study, only "minimal effects on growth in height and weight were observed" after 2 years of treatment. "No clinically significant effects on vital signs or laboratory test parameters were observed."[27]

A 2003 study tested the effects of dextromethylphenidate (Focalin), levomethylphenidate, and (racemic) detro-, levomethylphenidate (Ritalin) on mice to search for any carcinogenic effects. The researchers found that all three preparations were non-genotoxic and non-clastogenic; d-MPH, d, l-MPH, and l-MPH did not cause mutations or chromosomal aberrations. They concluded that none of the compounds present a carcinogenic risk to humans.[28] Current scientific evidence supports that long-term methylphenidate treatment does not increase the risk of developing cancer in humans.[29]

The effects of long-term methylphenidate treatment on the developing brains of children with ADHD is the subject of study and debate.[30][31] Although the safety profile of short-term methylphenidate therapy in clinical trials has been well established, repeated use of psychostimulants such as methylphenidate is less clear.

The use of ADHD medication in children under the age of 6 has not been studied. Severe hallucinations may occur. ADHD symptoms include hyperactivity and difficulty holding still and following directions; these are also characteristics of a typical child under the age of 6. For this reason it may be more difficult to diagnose young children, and caution should be used with this age group.[32]

On March 22, 2006 the FDA Pediatric Advisory Committee decided that medications using methylphenidate ingredients do not need black box warnings about their risks, noting that "for normal children, these drugs do not appear to pose an obvious cardiovascular risk."[33] Previously, 19 possible cases had been reported of Cardiac arrest linked to children taking methylphenidate[34] and the Drug Safety and Risk Management Advisory Committee to the FDA recommend a "black-box" warning in 2006 for stimulant drugs used to treat attention deficit/hyperactivity disorder.[35]

According to a small study conducted by the Society of Nuclear Medicine, the use of methylphenidate in certain individuals for reasons outside of its intended clinical applications may adversely affect cognitive performance. Specifically, methylphenidate positively affected brain glucose metabolism in subjects who performed well at baseline on an accuracy-controlled cognitive task, but caused further deterioration of mental processing in subjects who performed poorly at baseline. In other words, certain individuals without ADHD who take the drug to enhance concentration and focus may inadvertently make things worse.[36]

However, in a paper published in Biological Psychiatry (June 24, 2008 online), researchers report that methylphenidate fine-tunes the functioning of neurons in the prefrontal cortex - a brain region involved in attention, decision-making and impulse control - while having few effects outside it. The team studied PFC neurons in rats under a variety of methylphenidate doses, including one that improved the animals' performance in a working memory task of the type that ADHD patients have trouble completing. Using microelectrodes, the scientists observed both the random, spontaneous firings of PFC neurons and their response to stimulation of the hippocampus. When they listened to individual PFC neurons, the scientists found that while cognition-enhancing doses of methylphenidate had little effect on spontaneous activity, the neurons' sensitivity to signals coming from the hippocampus increased dramatically. Under higher, stimulatory doses, on the other hand, PFC neurons stopped responding to incoming information.[37] Another study suggests that methylphenidate improves spatial orientation and working memory in rats on the radial arm maze.

Scheduling and abuse potential

It is generally accepted that methylphenidate is the closest pharmaceutical equivalent to cocaine [38], and studies have shown that cocaine addicts cannot distinguish between the two drugs when administered intravenously.[citation needed] However, cocaine has a higher affinity for the dopamine receptor in comparison to methylphenidate, which is thought to be the mechanism of the euphoria associated with the cocaine high.[39]

In the United States, methylphenidate is classified as a Schedule II controlled substance, the designation used for substances that have a recognized medical value but present a high likelihood for abuse because of their addictive potential. Internationally, methylphenidate is a Schedule II drug under the Convention on Psychotropic Substances.[40]

Delivery formulations

Ritalin 10mg Pill (Ciba/Novartis)

All media are in milligrams.

Tablet

  • Ritalin: 5, 10 or 20mg tablets.
  • Ritalin SR: 20mg controlled-release tablets.
  • Attenta: 10mg tablets.
  • Methylin: 5, 10 or 20mg tablets.
  • Methylin ER: 10 and 20mg controlled-release tablets.
  • Metadate ER: 10 and 20mg controlled-release tablets.
  • Concerta: 18, 27, 36 and 54mg controlled-release tablets.[41] (goes off patent in 2018)[42]
  • Equasym: 5, 10, 20 or 30mg tablets.
  • Rubifen: 5, 10 or 20mg tablets.

Capsules

  • Ritalin LA: 10, 20, 30 or 40mg controlled-release capsules.
  • Metadate CD: 10, 20, 30, 40 or 60mg controlled-release capsules.

Patches

  • Daytrana 10, 15, 20 or 30mg controlled-release patches (1.1, 1.6, 2.2 or 3.3 mg/hour for 9 hours).

Criticism

Main article: Attention-deficit hyperactivity disorder controversies
File:Ritalin Bottle.jpg
A Japanese Bottle Of Ritalin

Methylphenidate is frequently used in the treatment for ADHD, and as such criticism of the drug is typically related to the controversy about ADHD.

Generally criticism of methylphenidate revolves around the alleged or established side effects. There are also concerns about illicit use of the drug and the ethics of giving psychotropic drugs to children to reduce ADHD symptoms.[43] In 2002, a study showed that rats treated with methylphenidate are more receptive to the reinforcing effects of cocaine,[39] which seeded doubts if the medication is a gateway drug to substance abuse. However, this contention has since been discredited by multiple sources.[44][45]

According to an article in the Los Angeles Times, "the uproar over Ritalin was triggered almost single-handedly by the Scientology movement."[46] The Citizens Commission on Human Rights, an antipsychiatry group associated with Scientology, conducted a major campaign against Ritalin in the 1980s and lobbied Congress for an investigation of Ritalin.[46] Notwithstanding the LA Times' assertion, however, Ritalin and similar drugs have been criticized by experts and groups not in any way associated with Scientology, such as Dr. Peter Breggin, M.D., Director of the International Center for the Study of Psychiatry and Psychology who testified before House Committee on Education's Subcommittee on Oversight and Investigations Committee on Education and the Workforce[47] and who has also published about "brain-disabling treatments in psychiatry" in numerous peer-reviewed articles and books[48] [49]

See also

References

  1. ^ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA. Retrieved 22 Oct 2023.
  2. ^ "Methylphenidate - Oral (Ritalin) side effects, medical uses and drug interactions". Retrieved 2007-11-02.
  3. ^ "Ritalin (methylphenidate) Side Effects and Abuse". Retrieved 2007-11-02.
  4. ^ Pronunciation
  5. ^ "An Old Drug May Give Cancer Patients a Lift". ACS News Center. American Cancer Society. 2002-01-24. Retrieved 2008-02-24.
  6. ^ "News from DEA, Congressional Testimony, 05/16/00". Retrieved 2007-11-02.
  7. ^ a b Steele, M., et al. (2006). "Template:PDFlink". Can J Clin Pharmacol. 2006 Winter;13(1):e50-62.
  8. ^ Pelham, W.E., et al. (2001). "Once-a-day Concerta methylphenidate versus three-times-daily methylphenidate in laboratory and natural settings". Pediatrics. 2001 Jun;107(6):E105.
  9. ^ Keating, G.M., McClellan, K., Jarvis, B. (2001). "Methylphenidate (OROS formulation)". CNS Drugs. 2001;15(6):495-500; discussion 501-3.
  10. ^ Hoare, P., et al. (2005). "Template:PDFlink". Eur Child Adolesc Psychiatry. 2005 Sep;14(6):305-9.
  11. ^ Peck, P. (2006, 7 April). FDA Approves Daytrana Transdermal Patch for ADHD. MedPage today. Retrieved April 7, 2006, from http://www.medpagetoday.com/ProductAlert/Prescriptions/tb/3027.
  12. ^ Fone KC (2005). "Stimulants: use and abuse in the treatment of attention deficit disorder". Current opinion in pharmacology. 5 (1): 87–93. doi:10.1016/j.coph.2004.10.001. PMID 15661631. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  13. ^ Fry JM (1998). "Treatment modalities for narcolepsy". Neurology. 50 (2 Suppl 1): S43–8. PMID 9484423. {{cite journal}}: Unknown parameter |month= ignored (help)
  14. ^ Rozans M, Dreisbach A, Lertora JJ, Kahn MJ (2002). "Palliative uses of methylphenidate in patients with cancer: a review". J. Clin. Oncol. 20 (1): 335–9. PMID 11773187. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  15. ^ Grund T., et al. "Influence of methylphenidate on brain development - an update of recent animal experiments", Behav Brain Funct. 2006 January 10;2:2.
  16. ^ [1]
  17. ^ Grabowski J, Roache JD, Schmitz JM, Rhoades H, Creson D, Korszun A (1997). "Replacement medication for cocaine dependence: methylphenidate". J Clin Psychopharmacol. 17 (6): 485–8. PMID 9408812. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  18. ^ A review of: Laudan B. Jahromi, Connie L. Kasari, James T. McCracken, Lisa S-Y. Lee, Michael G. Aman, Christopher J. McDougle, Lawrence Scahill, Elaine Tierney, L. Eugene Arnold, Benedetto Vitiello, Louise Ritz, Andrea Witwer, Erin Kustan, Jaswinder Ghuman, David J. Posey (2008). Positive Effects of Methylphenidate on Social Communication and Self-Regulation in Children with Pervasive Developmental Disorders and Hyperactivity Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-008-0636-9
  19. ^ Markowitz JS "et al." (2006). "A Comprehensive In Vitro Screening of d-, l-, and dl-threo-Methylphenidate: An Exploratory Study". "J Child Adolesc Psychopharmacol". 2006 Dec;16(6):687-98.
  20. ^ Volkow N., et al. (1998). "Dopamine Transporter Occupancies in the Human Brain Induced by Therapeutic Doses of Oral Methylphenidate". Am J Psychiatry 155:1325-1331, October 1998.
  21. ^ Gainetdinov, Raul R. (2001). "Genetics of Childhood Disorders: XXIV. ADHD, Part 8: Hyperdopaminergic Mice as an Animal Model of ADHD". Journal of the American Academy of Child & Adolescent Psychiatry. 40 (3): 380–382. Retrieved 2006-11-11. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  22. ^ Volkow, ND (2008). "Methylphenidate decreased the amount of glucose needed by the brain to perform a cognitive task". 'PLoS ONE'. 3 (4): e2017. PMID 18414677. Retrieved 2008-11-26. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  23. ^ a b c d e f g h i j k l m n o p q r s Methylphenidate Official FDA info and side effects
  24. ^ Rao J.K., Julius J.R., Breen T.J., Blethen S.L. (1996). "Response to growth hormone in attention deficit hyperactivity disorder: effects of methylphenidate and pemoline therapy". Pediatrics. 1998 Aug;102 (2 Pt 3):497-500.
  25. ^ Spencer, T.J., et al. (1996)."Growth deficits in ADHD children revisited: evidence for disorder-associated growth delays?". J Am Acad Child Adolesc Psychiatry. 1996 Nov;35(11):1460-9.
  26. ^ Klein R.G. & Mannuzza S. (1988). "Hyperactive boys almost grown up. III. Methylphenidate effects on ultimate height". Arch Gen Psychiatry. 1988 Dec;45(12):1131-4.
  27. ^ Wilens, T., et al. (2005). ADHD treatment with once-daily OROS methylphenidate: final results from a long-term open-label study". J Am Acad Child Adolesc Psychiatry. 2005 Oct;44(10):1015-23.
  28. ^ Teo, S.K., et al. (2003). "D-Methylphenidate is non-genotoxic in vitro and in vivo assays". Mutat Res. 2003 May 9;537(1):67-79.
  29. ^ Walitza, Susanne (2007). "Does Methylphenidate Cause a Cytogenetic Effect in Children with Attention Deficit Hyperactivity Disorder?". Environmental Health Perspectives. 115 (6): 936–940. doi:10.1289/ehp.9866. {{cite journal}}: Unknown parameter |authors= ignored (help); Unknown parameter |month= ignored (help)
  30. ^ "ADHD & Women's Health - Attention-deficit hyperactivity disorder National Women's Health Report". 2003. Retrieved 2007-11-03. Although methylphenidate is perhaps one of the best-studied drugs available, with thousands of studies attesting to its longterm safety over the past 50 years, that hasn't stopped critics from raising alarms about the drug's long-term use on children's developing brains, particularly given research that finds the numbers of children taking the drug skyrocketing in recent years. {{cite journal}}: Cite journal requires |journal= (help); Unknown parameter |month= ignored (help)
  31. ^ "Nonpharmacological Interventions for Preschoolers With ADHD: The Case for Specialized Parent Training" (PDF). Infants & Young Children. 19 (2): 142–153. Retrieved 2008-12-30. While most recent studies suggest that methylphenidate is relatively well-tolerated by young children, some suggest that side effects might be more marked in preschoolers than in school-aged children (Firestone, Musten, Pisterman, Mercer, & Bennett, 1998). Furthermore, some researchers have argued that there is the potential for negative long-term effects on the developing brains of young children chronically medicated (Moll, Rothenberger, Ruther, & Huther, 2002). {{cite journal}}: Unknown parameter |authors= ignored (help)
  32. ^ Attention Deficit Hyperactivity Disorder (ADHD)
  33. ^ Minutes of the FDA Pediatric Advisory Committee. March 22, 2006.
  34. ^ New Scientist 18 February 2006
  35. ^ Minutes of the FDA Pediatric Advisory Committee, March 22, 2006
  36. ^ Popular Stimulant's Role In Brain Function Deterioration Is Cause For Concern, According To Researchers
  37. ^ Study Uncovers How Ritalin Works in Brain to Boost Cognition, Focus Attention Newswise, Retrieved on June 24, 2008.
  38. ^ http://learn.genetics.utah.edu/content/addiction/issues/ritalin.html Ritalin and Cocaine
  39. ^ a b http://www.udel.edu/chemo/teaching/CHEM465/SitesF02/Prop26b/Rit%20Page4.html Pretreatment with methylphenidate sensitizes rats to the reinforcing effects of cocaine
  40. ^ Template:PDFlink 23rd edition. August 2003. International Narcotics Board, Vienna International Centre. Retrieved 2 March 2006
  41. ^ Full Prescribing Information for Concerta. (215 KiB)
  42. ^ Generic Concerta
  43. ^ Lakhan SE; Hagger-Johnson G. The impact of prescribed psychotropics on youth. Clinical Practice and Epidemiology in Mental Health 2007;3(21).
  44. ^ Wilens, T.E.., et al. (2003). "Does Stimulant Therapy of Attention-Deficit/Hyperactivity Disorder Beget Later Substance Abuse? A Meta-analytic Review of the Literature". PEDIATRICS. 2003 Vol. 111 No. 1:pp. 179-185
  45. ^ Russell A. Barkley, PhD,et al. (2003). "Does the Treatment of Attention-Deficit/Hyperactivity Disorder With Stimulants Contribute to Drug Use/Abuse? A 13-Year Prospective Study". PEDIATRICS. 2003 Vol. 111 No. 1: pp. 97-109
  46. ^ a b Sappell, Joel (1990-06-29). "Suits, Protests Fuel a Campaign Against Psychiatry". Los Angeles Times. p. A48:1. Retrieved 2006-11-29. {{cite news}}: Unknown parameter |coauthors= ignored (|author= suggested) (help) Backup copy link here
  47. ^ Dr. Peter Breggin's testimony to the House Committee on Education
  48. ^ "Psychiatric Drug Adverse Reactions (Side Effects) and Medication"
  49. ^ Psychostimulants in the treatment of children diagnosed with ADHD: Risks and Mechanisms of Action

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