Management of attention deficit hyperactivity disorder

ADHD is a common neurodevelopmental disorder, in Australia, it’s estimated that 6-8% of children and 3-5% of adults have it. [1]

Attention deficit hyperactivity disorder management options are evidence-based practices with established treatment efficacy for ADHD.

The American Academy of Pediatrics (AAP) recommends different treatment paradigms depending on the age of the person being treated. For those aged 4–5, the AAP recommends evidence-based parent- and/or teacher-administered behavioral interventions as first-line treatment, with the addition of methylphenidate if there is continuing moderate-to-severe functional disturbances. For those aged 6–11, the use of medication in combination with behavioral therapy is recommended, with the evidence for stimulant medications being stronger than that for other classes. For adolescents aged 12–17, use of medication along with psychosocial interventions are recommended.[2] Clinical picture of ADHD can be corrected if rehabilitation interventions are started from the early preschool age, when the compensatory capabilities of the brain are great and a persistent pathological stereotype has not yet formed. If symptoms persist at a later age, as the child grows, defects in the development of higher brain functions and behavioral problems worsen, which subsequently lead to difficulties in schooling.[3]

There are a number of stimulant and non-stimulant medications indicated for the treatment of ADHD. The most commonly used stimulant medications include methylphenidate (Ritalin, Concerta), dexmethylphenidate (Focalin, Focalin XR), Serdexmethylphenidate/dexmethylphenidate (Azstarys), mixed amphetamine salts (Adderall, Mydayis), dextroamphetamine (Dexedrine, ProCentra), methamphetamine (Desoxyn), and lisdexamfetamine (Vyvanse). Non-stimulant medications with a specific indication for ADHD include atomoxetine (Strattera), viloxazine (Qelbree), guanfacine (Intuniv), and clonidine (Kapvay). Other medicines which may be prescribed off-label include bupropion (Wellbutrin), tricyclic antidepressants, SNRIs, or MAOIs.[4][5][6] The presence of comorbid (co-occurring) disorders can make finding the right treatment and diagnosis much more complicated, costly, and time-consuming. So it is recommended to assess and simultaneously treat any comorbid disorders.[7]

A variety of psychotherapeutic and behavior modification approaches to managing ADHD including psychotherapy and working memory training may be used. Improving the surrounding home and school environment with parent management training and classroom management can improve behavior and school performance of children with ADHD.[8][9] Specialized ADHD coaches provide services and strategies to improve functioning, like time management or organizational suggestions.[10] Self-control training programs have been shown to have limited effectiveness.[citation needed]

## Contents

* 1 Psychosocial
* 1.1 Parents and classroom
* 1.2 Cognitive training
* 2 Medications
* 2.1 Stimulants
* 2.1.1 Amphetamine
* 2.1.1.1 Methamphetamine
* 2.1.2 Methylphenidate
* 2.2 Non-stimulants
* 2.3 Other
* 2.3.1 Antipsychotic medication
* 2.4 Comparison
* 2.5 Concerns regarding stimulants
* 2.5.1 Increasing use
* 2.5.2 Use in preschoolers
* 2.5.3 Side effects
* 2.5.3.1 Constipation and gastrointestinal pain
* 2.5.3.2 Growth delay and weight loss
* 2.5.3.3 Cardiovascular
* 2.5.3.4 Psychiatric
* 2.5.4 Long-term use
* 2.5.5 Withdrawal and rebound
* 2.5.6 Cancer
* 2.6 History
* 3 Cost-effectiveness
* 4 Alternative medicine
* 4.1 Neurofeedback
* 4.2 Media
* 4.3 Nature
* 4.4 Diet
* 4.5 Exercise
* 5 Comorbid disorders
* 5.1 Tic disorders
* 6 See also
* 7 References
* 8 External links

## Psychosocial[edit | edit source]

See also: Neurobiological effects of physical exercise § Cognitive control and memory

There are a variety of psychotherapeutic approaches employed by psychologists and psychiatrists; the one used depends on the patient and the patient's symptoms. The approaches include psychotherapy, cognitive-behavior therapy, support groups, parent training, meditation, and social skills training. In a 2019 review the effectiveness of social skills training was evaluated in children aged 5 to 18 years. At the time there was little evidence to support or refute this type of training for the treatment of ADHD in this age group.[11]

### Parents and classroom[edit | edit source]

Improving the surrounding home and school environment can improve the behavior of children with ADHD.[8] Parents of children with ADHD often show similar deficits themselves, and thus may not be able to sufficiently help the child with his or her difficulties.[12] Improving the parents' understanding of the child's behavior and teaching them strategies to improve functioning and communication and discourage unwanted behavior has measurable effect on the children with ADHD.[8] The different educational interventions for the parents are jointly called Parent Management Training. Techniques include operant conditioning: a consistent application of rewards for meeting goals and good behavior (positive reinforcement) and punishments such as time-outs or revocation of privileges for failing to meet goals or poor behavior.[8] Classroom management is similar to parent management training; educators learn about ADHD and techniques to improve behavior applied to a classroom setting. Strategies utilized include increased structuring of classroom activities,[13] daily feedback, and token economy.[8] In order for Token Economy to benefit students with ADHD, all staff must be consistent in rewarding the same behaviors. Additionally, establishing classroom routines will help to ensure that students with ADHD remain focused throughout the day.[14]

### Cognitive training[edit | edit source]

A 2013 paper published by two researchers from the University of Oslo concluded that working memory training provides short term improvements, but that there was limited evidence that these improvements were sustained or that they were generalized to improved verbal ability, mathematical skills, attention, or word decoding.[15] A 2014 paper published by a group of researchers from the University of Southampton presented the result of meta analysis study of 14 recently published randomized controlled trials (RCTs). The authors concluded that "more evidence from well-blinded studies is required before cognitive training can be supported as a frontline treatment of core ADHD symptoms".[16]

## Medications[edit | edit source]

### Stimulants[edit | edit source]

Stimulants are the most commonly prescribed medications for ADHD. The stimulant medications indicated to treat ADHD are methylphenidate (Ritalin, Concerta), dexmethylphenidate (Focalin, Focalin XR), Serdexmethylphenidate/dexmethylphenidate (Azstarys), mixed amphetamine salts (Adderall, Mydayis),[17] dextroamphetamine (Dexedrine), lisdexamfetamine (Vyvanse),[18] and in rare cases methamphetamine (Desoxyn).[19] Controlled-release pharmaceuticals may allow once daily administration of medication in the morning. This is especially helpful for children who do not like taking their medication in the middle of the school day. Several controlled-release methods are used.[20][21]

Stimulants used to treat ADHD raise the extracellular concentrations of the neurotransmitters dopamine and norepinephrine, which increases cellular communication between neurons that utilize these compounds. Stimulants increase the availability of synaptic dopamine, reduce the overactivity, impulsivity, and inattention characteristics of patients with ADHD, and improve associated behaviors, including on-task behavior, academic performance, and social functioning.[22]

The therapeutic benefits are due to noradrenergic effects at the locus coeruleus and the prefrontal cortex and dopaminergic effects at the ventral tegmental area, nucleus accumbens, and prefrontal cortex.[23][24]

Stimulant medications are considered safe when used under medical supervision.[8] Nonetheless, there are concerns that the long term safety of these drugs has not been adequately documented,[25][26][27][28] as well as social and ethical issues regarding their use and dispensation. The U.S. FDA has added black-box warnings to some ADHD medications, warning that abuse can lead to psychotic episodes, psychological dependence, and that severe depression may occur during withdrawal from abusive use.[29] Stimulants may be a little harder to be prescribed because they are controlled substances and can be abused easily, an example of this would be Adderall. Studies consistently show that most students report using stimulant medications, legally or illegally to improve academic performance, specifically to increase concentration, organization, and the ability to stay up longer and study.[30] The abuse of this drug has made prescribing it much more meticulous.

Stimulants are some of the most effective medications available for the treatment of ADHD.[31] Seven different formulations of stimulants have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of ADHD: four amphetamine-based formulations, two methylphenidate-based formulations, and dextromethamphetamine hydrochloride. Atomoxetine, viloxazine, guanfacine, and clonidine are the only non-controlled, non-stimulant FDA approved drugs for the treatment of ADHD.[citation needed]

Short-term clinical trials have shown medications to be effective for treating ADHD, but the trials usually use exclusion criteria, meaning knowledge of medications for ADHD is based on a small subset of the typical patients seen in clinical practice.[32] They have not been found to improve school performance and data is lacking on long-term effectiveness and the severity of side effects. Stimulants, however, may reduce the risk of unintentional injuries in children with ADHD.[33][34]

This class of medicines is generally regarded as one unit; however, they affect the brain differently.[35] Some investigations are dedicated to finding the similarities of children who respond to a specific medicine.[35] The behavioral response to stimulants in children is similar regardless of whether they have ADHD or not.[36]

Stimulant medication is an effective treatment[37] for adult attention-deficit hyperactivity disorder[38][39] although the response rate may be lower for adults than children.[40] Some physicians may recommend antidepressant drugs as the first line treatment instead of stimulants[41] although antidepressants have much lower treatment effect sizes than stimulant medication.[42]

#### Amphetamine[edit | edit source]

Further information: Amphetamine

Amphetamine pharmaceuticals  Brand
name  | United States
Adopted Name | (D:L) ratio
| Dosage
form  | Marketing
start date  | Sources

|
|
|
|
|

Adderall | Mixed Salts of a Single-Entity Amphetamine Product | 3:1 (salts) | tablet | 1996 | [43][44]
Adderall XR | 3:1 (salts) | capsule | 2001 | [43][44]
Mydayis | 3:1 (salts) | capsule | 2017 | [45]
Adzenys XR | amphetamine | 3:1 (base) | ODT | 2016 | [46][47]
Dyanavel XR | 3.2:1 (base) | suspension | 2015 | [48][49]
Evekeo | amphetamine sulfate | 1:1 (salts) | tablet | 2012 | [50][51]
Dexedrine | dextroamphetamine sulfate | 1:0 (salts) | capsule | 1976 | [43][44]
ProCentra | 1:0 (salts) | liquid | 2010 | [44]
Zenzedi | 1:0 (salts) | tablet | 2013 | [44]
Vyvanse | lisdexamfetamine dimesylate | 1:0 (prodrug) | capsule | 2007 | [43][52]
tablet
Xelstrym | dextroamphetamine | 1:0 (base) | patch | 2022 | [53]

Amphetamine is a chiral compound which is composed of two isomers: levoamphetamine and dextroamphetamine. Levoamphetamine and dextroamphetamine have the same chemical formula but are mirror images of each other, the same way that a person's hands are the same but are mirror images of each other. This mirror difference is enough to produce a small difference in their pharmacological properties; levoamphetamine has a slightly longer half-life than dextroamphetamine, but dextroamphetamine is a more potent central nervous system stimulant. Although it is effective in reducing primary ADHD symptoms such as hyperactivity and inattention, multiple adverse side effects presented. Included in these were headaches, anxiety, nausea and insomnia.[54]

Five different amphetamine-based pharmaceuticals are currently used in ADHD treatment: racemic amphetamine, dextroamphetamine, lisdexamfetamine, and two mixed enantiomer products (Adderall and Dyanavel XR).[43][48][50] Lisdexamfetamine is an inactive prodrug of dextroamphetamine (i.e., lisdexamfetamine itself does not do anything in the body, but it metabolizes into dextroamphetamine).[43] Adderall is a proprietary mixture of (75%) dextroamphetamine and (25%) levoamphetamine salts, which results in very mild differences between their effects.[43] Dyanavel XR contains a similar mixture.[48] Adderall begins to work before dextroamphetamine because of levoamphetamine.[55] Levoamphetamine also provides Adderall with a longer clinical effect than dextroamphetamine. Some children with ADHD and comorbid disorders respond well to levoamphetamine.[35] Amphetamines are modestly more effective than methylphenidate but also potentiate more side effects.[56][57][58]

##### Methamphetamine[edit | edit source]

Further information: Methamphetamine

The body metabolizes methamphetamine into amphetamine (in addition to less active metabolites). A quarter of methamphetamine will ultimately become amphetamine.[59] After comparing only the common ground between dextroamphetamine and dextromethamphetamine, the latter is said to be the stronger stimulant.[60]

#### Methylphenidate[edit | edit source]

Further information: Methylphenidate

Methylphenidate pharmaceuticals  Brand name(s)  | Generic name(s)[lower-alpha 1] | Duration  | Dosage
form

|
|
|

Ritalin  | methylphenidate  | 3–4 hours[65] | tablet
Focalin (US)  | dexmethylphenidate (US)[lower-alpha 2] | 3–4 hours[65] | tablet
Aptensio XR (US);
Biphentin (CA)  | Currently unavailable  | 12 hours[lower-alpha 3] | XR
capsule
Concerta (US/CA);
Concerta XL (UK)  | methylphenidate ER (US/CA);[lower-alpha 4]
methylphenidate ER‑C (CA)[lower-alpha 5] | 12 hours[68] | OROS
tablet
Focalin XR (US)  | dexmethylphenidate XR (US)[lower-alpha 6] | 12 hours[65] | XR
capsule
Quillivant XR (US)  | Currently unavailable  | 12 hours[68] | oral
suspension
Daytrana (US)  | Currently unavailable  | 11 hours[69] | transdermal
patch
Metadate CD (US);
Equasym XL (UK)  | methylphenidate ER (US)[lower-alpha 7] | 8–10 hours[68] | CD/XL
capsule
QuilliChew ER (US)  | Currently unavailable  | 8 hours[70] | chewable
tablet
Ritalin LA (US);
Medikinet XL (UK)  | methylphenidate ER (US)[lower-alpha 8] | 8 hours[68] | ER
capsule
Azstarys  | serdexmethylphenidate /dexmethylphenidate | 13 hours[71] | ER capsule
Ritalin SR (US/CA/UK);
Rubifen SR (NZ)  | Metadate ER (US);[lower-alpha 9]
Methylin ER (US);[lower-alpha 10]
methylphenidate SR (US/CA)[lower-alpha 11] | 5–8 hours[68] | CR
tablet

1. ↑ [61][62][63][64]
2. ↑ Manufactured by Abhai, Novel Laboratories, Sun, Teva, and Tris Pharma.
3. ↑ [66][67]
4. ↑ US generic manufactured by Actavis; CA generics manufactured by Pharmascience and Apotex.
5. ↑ Manufactured by Teva.
6. ↑ Manufactured by Impax, Intellipharmaceutics, Mylan, Par, and Teva.
7. ↑ Manufactured by Impax, Mallinckrodt, and Teva.
8. ↑ Manufactured by Barr and Mayne.
9. ↑ Manufactured by UCB.
10. ↑ Manufactured by Mallinckrodt.
11. ↑ US generics manufactured by County Line Pharmaceuticals and Abhai; CA generic manufactured by Apotex.

Like amphetamine, methylphenidate (MPH) is a chiral compound which is composed of two isomers: d-threo-methylphenidate (also known as dexmethylphenidate, d-methylphenidate, or d-MPH) and l-threo-methylphenidate (also known as l-methylphenidate or l-MPH). Both isomers have the same chemical formula but are mirror images of each other, the same way that a person's hands are the same but are mirror images of each other. Unlike amphetamine, the difference in pharmacological properties between d-MPH and l-MPH is significant, as l-MPH is markedly inferior to d-MPH in its effects, which is due to a number of major differences between the isomers.[72][73]

The effectiveness of methylphenidate is comparable to atomoxetine[74][75][76][77] but modestly lower than amphetamines.[56][57][58]

There are two major medications derived from methylphenidate's isomers: a racemic mixture of half d-threo-methylphenidate and half l-threo-methylphenidate called methylphenidate (Ritalin, Concerta), and an enantiopure formulation containing just d-threo-methylphenidate called dexmethylphenidate (Focalin).[citation needed]

### Non-stimulants[edit | edit source]

Atomoxetine,[78] viloxazine, guanfacine, and clonidine are drugs approved for the treatment of ADHD that have been classified as "non-stimulant".

Atomoxetine
Atomoxetine is a selective norepinephrine reuptake inhibitor.[79] It has comparable efficacy, tolerability and response rate to methylphenidate in children and adolescents; efficacy and discontinuation rate is equivalent in adults.[80][81][82][83] It carries a U.S. FDA black box warning regarding suicidal ideation and is associated with rare cases of liver damage.[84][85]: 5 Controlled studies show increases in heart rate, decreases of body weight, decreased appetite and treatment-emergent nausea.[86]
Viloxazine
Acts as a selective norepinephrine reuptake inhibitor (NRI). However, it may also act as an antagonist of the serotonin 5-HT2B receptor and as an agonist of the serotonin 5-HT2C receptors, actions which may be involved in its therapeutic effects. It was marketed for more than two decades as an antidepressant in Europe before being repurposed as a treatment for ADHD and launched in the United States in April 2021.[87][88]
Guanfacine
The extended release form has been approved by the FDA for the treatment of attention-deficit hyperactivity disorder (ADHD) in children as an alternative to stimulant medications. Its beneficial actions are likely due to its ability to strengthen prefrontal cortical regulation of attention and behavior.[89]
Clonidine
An α2A adrenergic receptor agonist has also been approved in the US. Clonidine was initially developed as a treatment for high blood pressure. Low doses in evenings and/or afternoons are sometimes used in conjunction with stimulants to help with sleep and because clonidine sometimes helps moderate impulsive and oppositional behavior and may reduce tics.[90] It may be more useful for comorbid Tourette syndrome.

### Other[edit | edit source]

Some medications used to treat ADHD are prescribed off-label,[91] outside the scope of their US government approved indications for various reasons. The U.S. FDA requires two clinical trials to prove a potential drug's safety and efficacy in treating ADHD. The drugs below have not been through these tests, so the efficacy is unproven (however these drugs have been licensed for other indications, so have been proven to be safe in those populations) and proper dosage and usage instructions are not as well characterized.[citation needed]

Bupropion
Bupropion is classified as an atypical antidepressant. It is the most common off-label prescription for ADHD.[92] It inhibits the reuptake of norepinephrine, and to a lesser extent dopamine, in neuronal synapses,[93] and has little or no effect on serotonergic reuptake.[94] Bupropion is not a controlled substance. It is commonly prescribed as a timed release formulation to decrease the risk of side effects.[95]
Modafinil
A wakefulness-promoting agent that operates primarily as a selective, relatively weak, and atypical dopamine reuptake inhibitor. Double-blind randomized controlled trials have demonstrated the efficacy and tolerability of modafinil in pediatric ADHD.[96][97] There are risks of serious side effects such as skin reactions, however these are rare and modafinil is not recommended for use in children.[98]: 7 In the United States, it was originally pending marketing on-label as Sparlon, but approval was denied by the FDA due to major concerns over the occurrence of Stevens–Johnson syndrome in clinical trials.[99]
Selegiline
Selegiline acts as a monoamine oxidase inhibitor, and increases levels of monoamine neurotransmitters in the brain. At doses under 20 mg/day, selegiline is a selective and irreversible inhibitor of monoamine oxidase B (MAO-B), increasing levels of dopamine in the brain. In clinical trials, Selegiline has been used in the treatment of attention deficit hyperactivity disorder (ADHD).[100] Selegiline may target specific symptoms of ADHD including: sustained attention, the learning of novel information, hyperactivity, and peer interactions. Selegiline has shown to be relatively effective in treating the inattention subtype of ADHD.[101]

Other medications which may be prescribed off-label include certain antidepressants such as tricyclic antidepressants (TCAs), SNRIs, SSRIs, or MAOIs.[5][6][4]

#### Antipsychotic medication[edit | edit source]

Atypical antipsychotic medications, which are approved for the treatment of certain behavioral disorders, are sometimes prescribed off-label as a combination therapy with stimulants for the treatment of comorbid (i.e., co-occurring diseases) ADHD and disruptive behavioral disorders.[102][103] Canadian clinical practice guidelines only support the use of dopaminergic antipsychotics with selectivity for D2-type dopamine receptors, particularly risperidone, as a third-line treatment for both disorders following the failure of stimulant monotherapy and psychosocial interventions.[102][104] Combined use of D2-type receptor antagonists and ADHD stimulants for the treatment of ADHD with comorbid behavioral disorders does not appear to have significantly worse adverse effects than ADHD stimulant or antipsychotic monotherapy.[102][105] Research suggests, but has not yet confirmed, the treatment efficacy of antipsychotic and stimulant combination treatment for both disorders;[102] it is unclear if the combination therapy for both disorders is superior to stimulant or antipsychotic monotherapy.[102] There is no evidence to support the use of any subclass of antipsychotics for the treatment of the core symptoms of ADHD (i.e., inattention and hyperactivity) without comorbid behavioral disorders.[106]

Dopaminergic antipsychotics affect dopamine neurons by binding to postsynaptic dopamine receptors, where they function as receptor antagonists.[105] In contrast, ADHD stimulants are indirect agonists of postsynaptic dopamine receptors;[105] in other words, these stimulants increase levels of synaptic dopamine, which then binds to postsynaptic receptors.[105] Stimulants increase the concentration of synaptic dopamine by activating certain presynaptic receptors (i.e., TAAR1) or by blocking or altering the function of reuptake transporters (e.g., DAT, VMAT2) in the presynaptic neuron.[citation needed]

### Comparison[edit | edit source]

Generic Name (INN)  | Brand Name(s)  | TGA-indicated for ADHD?  | MHRA-labelled for ADHD?  | FDA-labelled for ADHD?  | Pharmacological class[107] | Level of support  | Efficacy and miscellany[lower-alpha 1]

|
|
|
|
|
|
|

Central nervous system stimulants
Classical
Amphetamine
(racemic) | Evekeo[50][51] | Not available  | Not available  | Children ≥3 years & adults  | Monoamine reuptake inhibitor & releasing agent | Approved | Highly efficacious; modestly more than methylphenidate[112][113][114][115] with rapid onset of action. 1:1 mix of d-amp & l-amp.
Adderall[lower-alpha 2] | Adderall[116] | Not available  | Not available  | Children ≥3 years & adults  | Monoamine reuptake inhibitor & releasing agent | Approved | Highly efficacious,[117][118] therapeutic effects are usually seen within an hour of oral administration. 3:1 mix of d-amp and l-amp.
Dexamfetamine | Dexedrine,
Dexrostat  | Children ≥3 years & adults  | Children ≥6 years & adults  | Children ≥3 years & adults  | Monoamine reuptake inhibitor & releasing agent | Approved | Highly efficacious,[117][118] therapeutic effects are usually seen within 1–1.5 hours of oral administration.
Lisdexamfetamine | Vyvanse,
Elvanse[119] | Children ≥6 years & adults  | Children ≥6 years & adults  | Children ≥6 years & adults  | Monoamine reuptake inhibitor & releasing agent | Approved | Highly efficacious,[117] therapeutic effects are usually seen within 1–3 hours of oral administration. This is a prodrug formulation of d-amp.
Methamphetamine | Desoxyn[120] | Not available  | Not available  | Children ≥6 years & adults  | Monoamine reuptake inhibitor & releasing agent | Approved | Highly efficacious, therapeutic effects are usually seen within an hour of oral administration.
Methylphenidate | Ritalin,
Concerta[121] | Children ≥6 years & adults  | Children ≥6 years & adults  | Children ≥6 years & adults  | NDRI | Approved | Highly efficacious,[118] comparable to atomoxetine[122][123][124][125] but modestly lower than amphetamines.[126][127][128] Therapeutic effects are usually seen within 0.5–1.5 hours of oral administration (depending on formulation).
Dexmethylphenidate | Focalin[129] | Not available  | Not available  | Children ≥6 years & adults  | NDRI | Approved | Highly efficacious,[118] therapeutic effects are usually seen within 0.5–1.5 hours of oral administration (depending on formulation). No significant advantages over methylphenidate at equipotent dosages.
Non-classical
Atomoxetine | Strattera[130] | Children ≥6 years & adults  | Children ≥6 years & adults  | Children ≥6 years & adults  | NRI | Approved | Highly efficacious; comparable to methylphenidate in children and adolescents and equivalent in adults.[131][132][133][134] It yields a slower onset of action (usually takes at least a couple weeks) but has a lower risk of abuse and dependence than stimulants.
Modafinil | Provigil,
Modavigil[135] | No  | No  | No  | Dopamine reuptake inhibitor | Low  | Rapid onset of action (several hours). Level of support enough to potentially gain approval for pediatric ADHD, however the FDA rejected approval due to concerns over serious skin reactions.[99] Poorly evaluated for adult ADHD as most published research trials focus on pediatric ADHD.[99]
α2 adrenoceptor agonists
Clonidine | Catapres,
Dixarit,
Kapvay[136] | No  | No  | Children ≥6 years  | α2 adrenoceptor agonist | Approved | Delayed onset of action (1 week). Insufficient data to judge its relative efficacy. Only the more sedating, immediate-release formulations are available in some countries, including Australia.[137]
Guanfacine | Intuniv,
Tenex[138] | Children 6 to 17 years  | Children ≥6 years  | Children ≥6 years  | α2 adrenoceptor agonist | Approved | Delayed onset of action (1 week). May be slightly less efficacious than stimulant medications.[117] Not available in many countries.
Antidepressants/Anxiolytics
Amitriptyline | Elavil,
Endep[139] | No  | No  | No  | Tricyclic | Low[140] | Delayed onset of action.
Bupropion | Wellbutrin[141] | No  | No  | No  | NDRI & nAChR antagonist  | High[142] | Delayed onset of action. Is slightly-modestly less efficacious than methylphenidate and atomoxetine.[143]
Buspirone | Buspar[144] | Not available  | No  | No  | 5-HT1A partial agonist | Low[lower-alpha 3] | Delayed onset of action. Being a 5-HT1A receptor partial agonist may afford it the ability to increase dopamine release in the prefrontal cortex.[149][150]
Clomipramine | Anafranil  | No  | No  | No  | Tricyclic | Low[151] | Delayed onset of action.
Desipramine | Norpramin[152] | Not available  | No  | No  | Tricyclic | Moderate[153] | Delayed onset of action.
Duloxetine | Cymbalta[154] | No  | No  | No  | SNRI | Moderate[155] | Delayed onset of action.
Imipramine | Tofranil[156] | No  | No  | No  | Tricyclic | Low[157] | Delayed onset of action.
Milnacipran | Savella,
Ixel[158] | No  | No  | No  | SNRI | Negligible[159] | Delayed onset of action.
Moclobemide | Aurorix  | No | No | Not available  | Reversible MAO-A inhibitor |  Low[160] | Delayed onset of action.
Nortriptyline | Pamelor,
Allegron[161] | No  | No  | No  | Tricyclic | Low[lower-alpha 4] | Delayed onset of action.
Reboxetine | Edronax  | No  | No  | Not available  | Norepinephrine reuptake inhibitor | Low[164] | Delayed onset of action.
Selegiline | Emsam  | No  | No  | No  | Monoamine oxidase inhibitor | Low[165] | Delayed onset of action.
Venlafaxine | Effexor[166] | No  | No  | No  | SNRI | Moderate[167] | Delayed onset of action.
Miscellaneous others
Amantadine | Endantadine,
Symmetrel[168] | No  | No  | No  | NMDA antagonist and dopamine agonist  | Low[169] | ?
Carbamazepine | Equetro,
Tegretol[170] | No  | No  | No  | Sodium channel blocker | Moderate[171] | Use in ADHD is generally considered clinically inadvisable.[172]
Memantine | Namenda[173] | No  | No  | No  | NMDA antagonist | Low[174] | ?

Levels of support

* Approved indicates that the level of evidence to support the use of the drug in the treatment of ADHD is sufficient for at least one regulatory agency to have already approved it.
* Very high indicates at least six randomised double-blind placebo-controlled trials support the use of the drug in the treatment of ADHD.
* High indicates that at least three positive randomised double blind placebo-controlled trials have been performed evaluating the efficacy of the drug.
* Moderate indicates that at least one moderately/large-sized (≥30 people) positive randomised double-blind placebo-controlled clinical trial has been performed to evaluate the efficacy of the drug.
* Low indicates that at least one positive open-label or double-blind non-placebo-controlled clinical trial has been performed to evaluate the efficacy of the drug, or a controlled trial that was inadequately sized (<30 participants) or poorly designed.
* Very low. At least two case reports have documented the successful use of the drug in the treatment of ADHD.
* Negligible. One positive case report and additional theoretical (e.g. based on the mechanism of action of the drug in question) support.

Notes

1. ↑ References:[108][109][110][111]
2. ↑ Unlike most drugs, Adderall has no generic (USAN, INN, or BAN) name.
3. ↑ References:[145][146][147][148]
4. ↑ References:[153][162][163]

### Concerns regarding stimulants[edit | edit source]

Main article: Attention-deficit hyperactivity disorder controversies § Concerns about medication

Some parents and professionals have raised questions about the side effects of drugs and their long-term use.[91]

#### Increasing use[edit | edit source]

Outpatient treatment rates held steady in the U.S. from the late 1990s to early 2000s. Prior to this, outpatient treatment for ADHD in the U.S. grew from 0.9 children per 100 in 1987 to 3.4 per 100 in 1997.[175] A survey conducted by the Centers for Disease Control and Prevention in 2011–2012 found 11% of children between the ages of 4 and 17 were reported to have ever received a health care provider diagnosis of ADHD at some point (15% of boys and 7% of girls),[176] a 16% increase since 2007 and a 41% increase over the last decade.[177] The CDC notes that community samples suggest the incidence of ADHD in American children is higher than the five percent stated by the American Psychiatric Association in DSM-5, with 8.8% of U.S. children having a current diagnosis in the 2011 survey.[177][178] However, only 6.1% of children in the 2011 survey were taking ADHD medication, suggesting as many as 17.5% of children with current ADHD were not receiving treatment.[177]

#### Use in preschoolers[edit | edit source]

Parents of children with ADHD note that they usually display their symptoms at an early age. There have been few longitudinal studies on the long-term effects of stimulant use in children.[179] The use of stimulant medication has not been approved by the FDA for children under the age of six.[180] A growing trend is the diagnosis of younger children with ADHD. Prescriptions for children under the age of 5 rose nearly 50 percent from 2000 to 2003.[181][182] Research on this issue has indicated that stimulant medication can help younger children with "severe ADHD symptoms" but typically at a lower dose than older children. It was also found that children at this age are more sensitive to side effects and should be closely monitored.[180] Evidence suggests that careful assessment and highly individualized behavioural interventions significantly improve both social and academic skills,[183] while medication only treats the symptoms of the disorder. "One of the primary reasons cited for the growing use of psychotropic interventions was that many physicians realize that psychological interventions are costly and difficult to sustain."[184]

#### Side effects[edit | edit source]

##### Constipation and gastrointestinal pain[edit | edit source]

Central nervous system stimulants such as lisdexamfetamine may be associated with occurrences of constipation, diarrhea, nausea, and stomach pain.[185]

##### Growth delay and weight loss[edit | edit source]

There is some evidence of mild reductions in growth rate with prolonged stimulant treatment in children, but no causal relationship has been established and reductions do not appear to persist long-term.[186] Weight loss almost always corresponds with loss of appetite, which may result from the medication. Severe weight loss is very uncommon though. Loss of appetite is very temporary and typically comes back as daily effects of stimulants wear off. Nausea, dizziness, and headaches, other side effect, can also indirectly affect appetite and result in weight loss.[187]

##### Cardiovascular[edit | edit source]

There is concern that stimulants and atomoxetine, which increase the heart rate and blood pressure, might cause serious cardiovascular problems.[188][189] Recent extremely large-scale studies by the FDA indicate that, in children, young adults, and adults, there is no association between serious adverse cardiovascular events (sudden death, myocardial infarction, and stroke) and the medical use of amphetamine, methylphenidate, or other ADHD stimulants.[190][191][192][193]

##### Psychiatric[edit | edit source]

Many of these drugs are associated with physical and psychological dependence.[194][page needed] Sleep problems may occur.[195]

Methylphenidate can worsen psychosis in psychotic patients, and in very rare cases it has been associated with the emergence of new psychotic symptoms.[196] It should be used with extreme caution in patients with bipolar disorder due to the potential induction of mania or hypomania.[197] There have been very rare reports of suicidal ideation, but evidence does not support a link.[186] The long-term effects on mental health disorders in later life of chronic use of methylphenidate is unknown.[198]

A 2009 FDA review of 49 clinical trials found that approximately 1.5% of children in clinical trials of medications for ADHD had experienced signs or symptoms of psychosis or mania. Postmarketing reports were also analyzed, with nearly half of them involving children under the age of eleven. Approximately 90% of cases had no reported previous history of similar psychiatric events. Hallucinations involving snakes, worms or insects were the most commonly reported symptoms.[199]

#### Long-term use[edit | edit source]

Long-term methylphenidate or amphetamine exposure in some species is known to produce abnormal dopamine system development or nerve damage,[200][201] but humans experience normal development and nerve growth.[202][203][204] Magnetic resonance imaging studies suggest that long-term treatment with amphetamine or methylphenidate decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function of the right caudate nucleus.[202][203][204]

Reviews of clinical stimulant research have established the safety and effectiveness of long-term amphetamine use for ADHD.[205][206] Controlled trials spanning two years have demonstrated continuous treatment effectiveness and safety.[206][207] One review highlighted a nine-month randomized controlled trial of amphetamine in children that found an average increase of 4.5 IQ points and continued improvements in attention, disruptive behaviors, and hyperactivity.[207]

There is some evidence that ADHD itself may protect the brain against the natural aging process later in life,[208] perhaps by exercising the brain, and helping maintain volume. It is unknown how long term medication treatment effects the trajectory of brain volume decline in the aging ADHD brain.[208]

#### Withdrawal and rebound[edit | edit source]

Tolerance to the therapeutic effects of stimulants can occur,[209] and rebound of symptoms may occur when the dose wears off.[210] Rebound effects are often the result of the stimulant dosage being too high or the individual not being able to tolerate stimulant medication. Signs that the stimulant dose is too high include irritability, feeling stimulated or blunting of affect and personality.[211]

Stimulant withdrawal or rebound reactions can occur and can be minimised in intensity via a gradual tapering off of medication over a period of weeks or months.[212] A small study of abrupt withdrawal of stimulants did suggest that withdrawal reactions are not typical, and may only occur in susceptible individuals.[213]

#### Cancer[edit | edit source]

Concerns about chromosomal aberrations and possible cancer later in life was raised by a small-scale study on the use of methylphenidate, though a review by the Food and Drug Administration (FDA) found significant methodological problems with the study.[214] A follow-up study performed with improved methodology found no evidence that methylphenidate might cause cancer, stating "the concern regarding a potential increase in the risk of developing cancer later in life after long-term MPH treatment is not supported."[215]

### History[edit | edit source]

The first reported evidence of stimulant medication used to treat children with concentration and hyperactivity problems came in 1937.[216] Charles Bradley in Providence, Rhode Island, reported that a group of children with behavioral problems improved after being treated with the stimulant Benzedrine.[216][217] In 1954, the stimulant methylphenidate (Ritalin, which was first produced in 1944) became available; it remains one of the most widely prescribed medications for ADHD. Initially the drug was used to treat narcolepsy, chronic fatigue, depression, and to counter the sedating effects of other medications. The drug began to be used for ADHD in the 1960s and steadily rose in use.[216]

In 1975, pemoline (Cylert) was approved by the U.S. FDA for use in the treatment of ADHD. While an effective agent for managing the symptoms, the development of liver failure in 14 cases over the next 27 years would result in the manufacturer withdrawing this medication from the market. New delivery systems for medications were invented in 1999 that eliminated the need for multiple doses across the day or taking medication at school. These new systems include pellets of medication coated with various time-release substances to permit medications to dissolve hourly across an 8–12 hour period (Metadate CD, Adderall XR, Focalin XR) and an osmotic pump that extrudes a liquid methylphenidate sludge across an 8–12 hour period after ingestion (Concerta).[citation needed]

In 2003, atomoxetine (Strattera) received the first FDA approval for a nonstimulant drug to be used specifically for ADHD.[218] In 2007, lisdexamfetamine (Vyvanse) became the first prodrug[219] for ADHD to receive FDA approval.[220] In March 2019, a Purdue Pharma subsidiary received approval from the FDA for Adhansia XR, a methylphenidate medication to treat ADHD.[221]

## Cost-effectiveness[edit | edit source]

Combined medical management and behavioral treatment is the most effective ADHD management strategy, followed by medication alone, and then behavioral treatment.[31] In terms of cost-effectiveness, management with medication has been shown to be the most cost-effective, followed by behavioral treatment, and combined treatment.[31] The individually most effective and cost-efficient way is with stimulant medication. Additionally, long-acting medications for ADHD, in comparison to short-acting varieties, generally seem to be cost-effective.[222] Comorbid (relating to two diseases that occur together, e.g. depression and ADHD) disorders makes finding the right treatment and diagnosis much more costly than when comorbid disorders are absent.[citation needed]

## Alternative medicine[edit | edit source]

Caffeine is sometimes used to manage ADHD symptoms.

See also: Alternative therapies for developmental and learning disabilities

Most alternative therapies do not have enough supporting evidence to recommend them.[223][224] Moreover, when only the best conducted studies are taken into account results tend to be similar to placebo.[224]

### Neurofeedback[edit | edit source]

Neurofeedback (NF) or EEG biofeedback is a treatment strategy used for children, adolescents and adults with ADHD.[225] The human brain emits electrical energy which is measured with electrodes. Neurofeedback alerts the patient when beta waves are present. This theory believes that those with ADHD can train themselves to decrease ADHD symptoms.[citation needed]

No serious adverse side effects from neurofeedback have been reported.[226] Research into neurofeedback has been mostly limited and of low quality.[226] While there is some indication on the effectiveness of biofeedback it is not conclusive: several studies have yielded positive results, however the best designed ones have either shown reduced effects or non-existing ones.[failed verification][226][227] In general no effects have been found in the most blinded ADHD measures, which could be indicating that positive results are due to the placebo effect.[228]

### Media[edit | edit source]

Preliminary studies have supported the idea that playing video games is a form of neurofeedback, which helps those with ADHD self-regulate and improve learning.[229][230] Memory, multitasking, fluid intelligence, and other cognitive talents may be improved by certain computer programmes and video games.[231] On the other hand, ADHD may experience great difficulty disengaging from the game, which may in turn negate any benefits gained from these activities,[232] and time management skills may be negatively impacted as well.[233]

### Nature[edit | edit source]

Children who spend time outdoors in natural settings, such as parks, seem to display fewer symptoms of ADHD, which has been dubbed "Green Therapy".[234] But it may be due to reverse causation.[clarification needed]

### Diet[edit | edit source]

Main article: Diet and attention deficit hyperactivity disorder

There is insufficient evidence to support dietary changes in ADHD and thus they are not recommended by the American Academy of Pediatrics as of 2019.[235] Perhaps the best known of the dietary alternatives is the Feingold diet which involves removing salicylates, artificial colors and flavors, and certain synthetic preservatives from children's diets.[236] However, studies have shown little if any effect of the Feingold diet on the behavior of children with ADHD.[237]

Results of studies regarding the effect of eliminating artificial food coloring from the diet of children with ADHD have been very varied. It has been found that it might be effective in some children but as the published studies have been of low quality results can be more related to research problems such as publication bias.[238] The UK Food Standards Agency (FSA) has called for a ban on the use of six artificial food colorings[239] and the European Union (EU) has ruled that some food dyes must be labeled with the relevant E number as well as this warning: "may have an adverse effect on activity and attention in children."[240] Nevertheless, existing evidence neither refutes nor supports the association between ADHD and food colouring.[241]

Dietary supplements, self-medication,[242] and specialized diets are sometimes used by people with ADHD with the intent to mitigate some or all of the symptoms. However a 2009 article in the Harvard Mental Health Letter states, "Although vitamin or mineral supplements [micronutrients] may help children diagnosed with particular deficiencies, there is no evidence that they are helpful for all children with ADHD. Furthermore, megadoses of vitamins, which can be toxic, must be avoided."[citation needed] In the United States, no dietary supplement has been approved for the treatment for ADHD by the FDA.[243]

Some popular supplements used to manage ADHD symptoms:

* Caffeine – ADHD is associated with increased caffeine consumption, and caffeine's stimulant effects on cognition may have some benefits for ADHD.[244] Limited evidence suggests a small therapeutic effect that is markedly inferior to standard treatments like methylphenidate and dextroamphetamine while still producing similar or greater side effects.[244][245]
* Nicotine – The association between ADHD and nicotine intake is well known, and limited evidence suggests that nicotine may help improve some of the symptoms of ADHD, although the effect is generally small.[246][247][248]
* Omega-3 fatty acids – There is no evidence that supplementation with omega-3 or other polyunsaturated fatty acids provides any improvement in the symptoms of ADHD in children or adolescents.[249] A 2011 meta analysis found a "small but significant benefit", with benefits being "modest compared to the efficacy of currently available pharmacological treatments for ADHD".[250] The review concluded that supplementation may be worth consideration as an augmentative treatment in combination with medication due to its "relatively benign side-effect profile", but not as a primary treatment.[250] Most research on omega-3 fatty acids is considered to be of very poor quality with widespread methodological weaknesses.[249][250]
* Zinc – Although the role of zinc in ADHD has not been elucidated, there is a small amount of limited evidence that lower tissue zinc levels may be associated with ADHD.[251] In the absence of a demonstrated zinc deficiency (which is rare outside of developing countries), zinc supplementation is not recommended as a treatment option for ADHD.[252]
* In the 1980s vitamin B6 was promoted as a helpful remedy for children with learning difficulties including inattentiveness; however, a study of large doses of vitamins with ADHD children showed that they were ineffective in changing behavior.[253]

### Exercise[edit | edit source]

Regular physical exercise, particularly aerobic exercise, is an effective add-on treatment for ADHD in children and adults, particularly when combined with stimulant medication (although the best intensity and type of aerobic exercise for improving symptoms are not currently known).[254][255][256] The long-term effects of regular aerobic exercise in ADHD individuals include better behavior and motor abilities, improved executive functions (including attention, inhibitory control, and planning, among other cognitive domains), faster information processing speed, and better memory.[254][255][256] Parent-teacher ratings of behavioral and socio-emotional outcomes in response to regular aerobic exercise include: better overall function, reduced ADHD symptoms, better self-esteem, reduced levels of anxiety and depression, fewer somatic complaints, better academic and classroom behavior, and improved social behavior.[254] Exercising while on stimulant medication augments the effect of stimulant medication on executive function.[254] It is believed that these short-term effects of exercise are mediated by an increased abundance of synaptic dopamine and norepinephrine in the brain.[254]

## Comorbid disorders[edit | edit source]

Because ADHD comorbidities are diverse and the rate of comorbidity is high, special care must dedicated to certain comorbidities. The FDA is not set up to address this issue, and does not approve medications for comorbidities, nonetheless certain such topics have been extensively researched.

### Tic disorders[edit | edit source]

Patients with Tourette syndrome who are referred to specialty clinics have a high rate of comorbid ADHD. Patients who have ADHD along with tics or tic disorders may also have problems with disruptive behaviors, overall functioning, and cognitive function, accounted for by the comorbid ADHD.[257]

The treatment of ADHD in the presence of tic disorders has long been a controversial topic. Past medical practice held that stimulants could not be used in the presence of tics, due to concern that their use might worsen tics;[258] however, multiple lines of research have shown that stimulants can be cautiously used in the presence of tic disorders.[259][213] Several studies have shown that stimulants do not exacerbate tics any more than placebo does, and suggest that stimulants may even reduce tic severity.[260] A 2011 Cochrane Collaboration review concluded that most major ADHD medications were effective in children with tics, and that stimulants did not generally worsen tics outside of individual cases.[261] Methylphenidate, guanfacine, clonidine, and desipramine were associated with improvement of tic symptoms.[261] Controversy remains, and the PDR continues to carry a warning that stimulants should not be used in the presence of tic disorders, so physicians may be reluctant to use them. Others are comfortable using them and even advocate for a stimulant trial when ADHD co-occurs with tics, because the symptoms of ADHD can be more impairing than tics.[258][262]

The stimulants are the first line of treatment for ADHD, with proven efficacy, but they do fail in up to 20% of cases, even in patients without tic disorders.[263] Current prescribed stimulant medications include: methylphenidate, dextroamphetamine, and mixed amphetamine salts (Adderall). Other medications can be used when stimulants are not an option. These include the alpha-2 agonists (clonidine and guanfacine), tricyclic antidepressants (desipramine and nortriptyline), and newer antidepressants (bupropion and venlafaxine). There have been case reports of tics worsening with bupropion. There is good empirical evidence for short-term safety and efficacy for the use of desipramine, bupropion and atomoxetine.[263]

## See also[edit | edit source]

* List of investigational attention deficit hyperactivity disorder drugs

## References[edit | edit source]

1. ↑ "Australian Evidence-Based Clinical Practice Guidelines For ADHD FACTSHEET: For General Practitioners (GPs)" (PDF). aadpa.com.au. Archived (PDF) from the original on 18 May 2024. Retrieved 3 June 2024.
2. ↑ Wolraich, Mark L.; Hagan, Joseph F.; Allan, Carla; Chan, Eugenia; Davison, Dale; Earls, Marian; Evans, Steven W.; Flinn., Susan K.; Froehlich, Tanya; Frost, Jennifer; Holbrook, Joseph R.; Lehmann, Christoph Ulrich; Lessin, Herschel Robert; Okechukwu, Kymika; Pierce, Karen L. (October 2019). "Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents". Pediatrics. 144 (4): e20192528. doi:10.1542/peds.2019-2528. PMC 7067282. PMID 31570648. Archived from the original on 22 April 2024. Retrieved 18 April 2024.
3. ↑ Khaletskaya, O. V. Синдром дефицита внимания и гиперактивности в детском возрасте. Archived from the original on 16 December 2023. Retrieved 18 April 2024.
4. ↑ 4.0 4.1 Stein, Mark A. (July 2004). "Innovations in attention-deficit/hyperactivity disorder pharmacotherapy: long-acting stimulant and nonstimulant treatments". American Journal of Managed Care. 10 (4 Suppl): S89–98. PMID 15352535. Archived from the original on 8 March 2020. Retrieved 18 April 2024.
5. ↑ 5.0 5.1 Christman AK, Fermo JD, Markowitz JS (August 2004). "Atomoxetine, a novel treatment for attention-deficit-hyperactivity disorder". Pharmacotherapy. 24 (8): 1020–36. doi:10.1592/phco.24.11.1020.36146. PMID 15338851. S2CID 43053256.
6. ↑ 6.0 6.1 Hazell, P (October 2005). "Do adrenergically active drugs have a role in the first-line treatment of attention-deficit/hyperactivity disorder?". Expert Opinion on Pharmacotherapy. 6 (12): 1989–98. doi:10.1517/14656566.6.12.1989. PMID 16197353. S2CID 13346726.
7. ↑ Waxmonsky, James (October 2003). "Assessment and treatment of attention deficit hyperactivity disorder in children with comorbid psychiatric illness". Current Opinion in Pediatrics. 15 (5): 476–482. doi:10.1097/00008480-200310000-00006. PMID 14508296. S2CID 36186879.
8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 American Academy of Pediatrics Subcommittee on Attention-Deficit/Hyperactivity Disorder; American Academy of Pediatrics Committee on Quality Improvement (October 2001). "Clinical practice guideline: treatment of the school-aged child with attention-deficit/hyperactivity disorder". Pediatrics. 108 (4): 1033–44. doi:10.1542/peds.108.4.1033. PMID 11581465.
9. ↑ Tresco, Katy E.; Lefler, Elizabeth K.; Power, Thomas J. (2010). "Psychosocial Interventions to Improve the School Performance of Students with Attention-Deficit/Hyperactivity Disorder". Mind & Brain: The Journal of Psychiatry. 1 (2): 69–74. ISSN 2042-468X. PMC 2998237. PMID 21152355.
10. ↑ Ahmann, Elizabeth; Tuttle, Lisa Joy; Saviet, Micah; Wright, Sarah D. (2018). "A Descriptive Review of ADHD Coaching Research: Implications for College Students" (PDF). Journal of Postsecondary Education and Disability. 31 (1): 17–39. Archived (PDF) from the original on 10 March 2024. Retrieved 18 April 2024.
11. ↑ Storebø, Ole Jakob; Elmose Andersen, Mette; Skoog, Maria; Joost Hansen, Signe; Simonsen, Erik; Pedersen, Nadia; Tendal, Britta; Callesen, Henriette E.; Faltinsen, Erlend; Gluud, Christian (21 June 2019). "Social skills training for attention deficit hyperactivity disorder (ADHD) in children aged 5 to 18 years". The Cochrane Database of Systematic Reviews. 2019 (6): CD008223. doi:10.1002/14651858.CD008223.pub3. ISSN 1469-493X. PMC 6587063. PMID 31222721.
12. ↑ Kazdin, Alan E. Parent management training: treatment for oppositional, aggressive, and antisocial behavior in children and adolescents. Oxford University Press, 2005
13. ↑ "Guidelines for better facilitation in school for students with ADHD". Helpseeker.net. Archived from the original on 26 February 2021. Retrieved 10 December 2020.
14. ↑ Landolfi, Anna-Maria (April 2014). "Inclusive Classroom Communities: Supporting Students with Characteristics of Attention Deficit Hyperactivity Disorder" (PDF). Ontario Institute for Studies in Education of the University of Toronto. Archived (PDF) from the original on 26 February 2024. Retrieved 18 April 2024.
15. ↑ Melby-Lervåg M, Hulme C (February 2013). "Is working memory training effective? A meta-analytic review". Dev Psychol. 49 (2): 270–91. CiteSeerX 10.1.1.281.7759. doi:10.1037/a0028228. PMID 22612437. S2CID 12370312.
16. ↑ Sonuga-Barke, E; Brandeis, D; Holtmann, M; Cortese, S (October 2014). "Computer-based Cognitive Training for ADHD: A Review of Current Evidence". Child and Adolescent Psychiatric Clinics of North America. 23 (4): 807–824. doi:10.1016/j.chc.2014.05.009. PMID 25220088.
17. ↑ Sulzer D, Sonders MS, Poulsen NW, Galli A (April 2005). "Mechanisms of neurotransmitter release by amphetamines: a review". Progress in Neurobiology. 75 (6): 406–33. doi:10.1016/j.pneurobio.2005.04.003. PMID 15955613. S2CID 2359509.
18. ↑ Howland RH (August 2008). "Lisdexamfetamine: a prodrug stimulant for ADHD". Journal of Psychosocial Nursing and Mental Health Services. 46 (8): 19–22. doi:10.3928/02793695-20080801-05. PMID 18777964.
19. ↑ National Toxicology Program (July 2005). "NTP-CERHR monograph on the potential human reproductive and developmental effects of amphetamines". NTP Cerhr Mon (16): vii–III1. PMID 16130031.
20. ↑ "ADHD Medications: How They Work & Side Effects". Cleveland Clinic. Archived from the original on 9 April 2024. Retrieved 8 January 2024.
21. ↑ Mechler, Konstantin; Banaschewski, Tobias; Hohmann, Sarah; Häge, Alexander (1 February 2022). "Evidence-based pharmacological treatment options for ADHD in children and adolescents". Pharmacology & Therapeutics. 230: 107940. doi:10.1016/j.pharmthera.2021.107940. ISSN 0163-7258. PMID 34174276.
22. ↑ Faraone, Stephen V; Biederman, Joseph; Spencer, Thomas J; Aleardi, Megan (5 October 2006). "Comparing the Efficacy of Medications for ADHD Using Meta-analysis". Medscape General Medicine. 8 (4): 4. ISSN 1531-0132. PMC 1868385. PMID 17415287.
23. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapters 10 and 13". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 266, 318–323. ISBN 978-0-07-148127-4.
24. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 148, 154–157. ISBN 978-0-07-148127-4.
25. ↑ King, S; Griffin, S; Hodges, Z (July 2006). "A systematic review and economic model of the effectiveness and cost-effectiveness of methylphenidate, dexamfetamine and atomoxetine for the treatment of attention deficit hyperactivity disorder in children and adolescents". Health Technology Assessment. 10 (23): iii–iv, xiii–146. doi:10.3310/hta10230. PMID 16796929.
26. ↑ Murphy, Kevin R; Barkley, Russell A (2005). Attention-Deficit Hyperactivity Disorder: A Clinical Workbook (Third ed.). New York: Guilford Press. ISBN 978-1-59385-227-6.
27. ↑ Stern HP, Stern TP (September 2002). "When children with attention-deficit/hyperactivity disorder become adults". South. Med. J. 95 (9): 985–91. doi:10.1097/00007611-200209000-00011. PMID 12356139.
28. ↑ Lerner M, Wigal T (January 2008). "Long-term safety of stimulant medications used to treat children with ADHD". Pediatric Annals. 37 (1): 37–45. doi:10.3928/00904481-20080101-11. PMID 18240852.
29. ↑ "Full U.S. Concerta Prescribing Information". Janssen Pharmaceuticals, Inc. 15 July 2014. Archived from the original on 26 November 2014. Retrieved 6 September 2014.
30. ↑ Advokat, Claire (1 July 2010). "What are the cognitive effects of stimulant medications? Emphasis on adults with attention-deficit/hyperactivity disorder (ADHD)". Neuroscience & Biobehavioral Reviews. 34 (8): 1256–1266. doi:10.1016/j.neubiorev.2010.03.006. ISSN 0149-7634. PMID 20381522. S2CID 20105233. Archived from the original on 22 June 2017. Retrieved 18 April 2024.
31. ↑ 31.0 31.1 31.2 Jensen; Garcia, JA; Glied, S; Crowe, M; Foster, M; Schlander, M; Hinshaw, S; Vitiello, B; Arnold, LE (2005). "Cost-Effectiveness of ADHD Treatments: Findings from the Multimodal Treatment Study of Children With ADHD". American Journal of Psychiatry. 162 (9): 1628–1636. doi:10.1176/appi.ajp.162.9.1628. hdl:1811/51178. PMID 16135621. S2CID 18620849.
32. ↑ Weiss MD, Gadow K, Wasdell MB (2006). "Effectiveness outcomes in attention-deficit/hyperactivity disorder". J Clin Psychiatry. 67 (Suppl 8): 38–45. PMID 16961429.
33. ↑ Ruiz-Goikoetxea, Maite; Cortese, Samuele; Aznarez-Sanado, Maite; Magallón, Sara; Alvarez Zallo, Noelia; Luis, Elkin O.; de Castro-Manglano, Pilar; Soutullo, Cesar; Arrondo, Gonzalo (2018). "Risk of unintentional injuries in children and adolescents with ADHD and the impact of ADHD medications: A systematic review and meta-analysis". Neuroscience & Biobehavioral Reviews. 84: 63–71. doi:10.1016/j.neubiorev.2017.11.007. hdl:10171/45012. ISSN 0149-7634. PMID 29162520.
34. ↑ Dalsgaard, Søren; Leckman, James F.; Mortensen, Preben Bo; Nielsen, Helena Skyt; Simonsen, Marianne (1 August 2015). "Effect of drugs on the risk of injuries in children with attention deficit hyperactivity disorder: a prospective cohort study". The Lancet. Psychiatry. 2 (8): 702–709. doi:10.1016/S2215-0366(15)00271-0. ISSN 2215-0374. PMID 26249301.
35. ↑ 35.0 35.1 35.2 Arnold, LE (2000). "Methylphenidate vs Amphetamine: Comparative Review". Journal of Attention Disorders. 3 (4): 200–211. doi:10.1177/108705470000300403.
36. ↑ Rapoport JL, Inoff-Germain G (2002). "Responses to methylphenidate in Attention-Deficit/Hyperactivity Disorder and normal children: update 2002". J Atten Disord. 6 (Suppl 1): S57–60. doi:10.1177/070674370200601s07. PMID 12685519. S2CID 24320882.
37. ↑ Dusan Kolar; Amanda Keller; Maria Golfinopoulos; Lucy Cumyn; Cassidy Syer; Lily Hechtman (February 2008). "Treatment of adults with attention-deficit/hyperactivity disorder". Neuropsychiatr Dis Treat. 4 (1): 107–121. doi:10.2147/ndt.s1747. PMC 2515906. PMID 18728812.
38. ↑ Spencer TJ (April 2007). "Pharmacology of adult ADHD with stimulants". CNS Spectr. 12 (4 (Suppl 6)): 8–11. doi:10.1017/S1092852900026018. PMID 17715564. S2CID 32723902.
39. ↑ Rostain, Anthony L. (September 2008). "ADHD in Adults: Attention-Deficit/Hyperactivity Disorder in Adults: Evidence-Based Recommendations for Management". Postgraduate Medicine. 120 (3): 27–38. doi:10.3810/pgm.2008.09.1905. PMID 18824823. S2CID 23171226. Archived from the original on 19 July 2009. Retrieved 17 February 2022.
40. ↑ Spencer, Thomas; Biederman, Joseph; Wilens, Timothy (June 2004). "Stimulant treatment of adult attention-deficit/hyperactivity disorder". Psychiatric Clinics of North America. 27 (2): 361–372. doi:10.1016/j.psc.2003.12.002. PMID 15064002. Archived from the original on 24 October 2016. Retrieved 18 April 2024.
41. ↑ Higgins ES (January 1999). "A comparative analysis of antidepressants and stimulants for the treatment of adults with attention-deficit hyperactivity disorder". J Fam Pract. 48 (1): 15–20. PMID 9934377.
42. ↑ Verbeeck W, Tuinier S, Bekkering GE (February 2009). "Antidepressants in the treatment of adult attention-deficit hyperactivity disorder: a systematic review". Adv Ther. 26 (2): 170–184. doi:10.1007/s12325-009-0008-7. PMID 19238340. S2CID 5975939.
43. ↑ 43.0 43.1 43.2 43.3 43.4 43.5 43.6 Heal DJ, Smith SL, Gosden J, Nutt DJ (June 2013). "Amphetamine, past and present – a pharmacological and clinical perspective". J. Psychopharmacol. 27 (6): 479–496. doi:10.1177/0269881113482532. PMC 3666194. PMID 23539642.
44. ↑ 44.0 44.1 44.2 44.3 44.4 "National Drug Code Amphetamine Search Results". National Drug Code Directory. United States Food and Drug Administration. Archived from the original on 16 December 2013. Retrieved 16 December 2013.
45. ↑ "Mydayis Prescribing Information" (PDF). United States Food and Drug Administration. Shire US Inc. June 2017. pp. 1–21. Archived (PDF) from the original on 9 June 2019. Retrieved 8 August 2017.
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227. ↑ Lofthouse N, Arnold LE, Hurt E (October 2012). "Current status of neurofeedback for attention-deficit/hyperactivity disorder". Curr Psychiatry Rep. 14 (5): 536–42. doi:10.1007/s11920-012-0301-z. PMID 22890816. S2CID 37075142.
228. ↑ Holtmann, M; Sonuga-Barke, E; Cortese, S; Brandeis, D (October 2014). "Neurofeedback for ADHD: A Review of Current Evidence". Child and Adolescent Psychiatric Clinics of North America. 23 (4): 789–806. doi:10.1016/j.chc.2014.05.006. hdl:1854/LU-5841198. PMID 25220087. Archived from the original on 17 January 2021. Retrieved 18 April 2024.
229. ↑ Jenks, Susan (9 March 2006). "ADHD patients play video games as part of treatment". USA Today. Archived from the original on 10 January 2021. Retrieved 18 April 2024.
230. ↑ Butnik S.M. (2005). "Neurofeedback in adolescents and adults with attention deficit hyperactivity disorder". Journal of Clinical Psychology. 61 (5): 621–625. doi:10.1002/jclp.20124. PMID 15723361. S2CID 25108272.
231. ↑ Small, Gary W.; Lee, Jooyeon; Kaufman, Aaron; Jalil, Jason; Siddarth, Prabha; Gaddipati, Himaja; Moody, Teena D.; Bookheimer, Susan Y. (June 2020). "Brain health consequences of digital technology use". Dialogues in Clinical Neuroscience. 22 (2): 179–187. doi:10.31887/DCNS.2020.22.2/gsmall. ISSN 1958-5969. PMC 7366948. PMID 32699518.
232. ↑ Shaw R.; Grayson A.; Lewis V. (2000). "Inhibition, ADHD, and computer games: The inhibitory performance of children and ADHD on computerized tasks and games". Journal of Attention Disorders. 8 (4): 160–168. doi:10.1177/1087054705278771. PMID 16110046. S2CID 21265539.
233. ↑ Tolchinsky A.; Jefferson, S.D. (2011). "Problematic video game play in a college sample and its relationship to time management skills and Attention-Deficit/Hyperactivity disorder symptomology". Cyberpsychology, Behavior, and Social Networking. 14 (9): 489–496. doi:10.1089/cyber.2010.0315. PMID 21288135.
234. ↑ Rojas, NL; Chan, E (2005). "Old and new controversies in the alternative treatment of attention-deficit hyperactivity disorder". Mental Retardation and Developmental Disabilities Research Reviews. 11 (2): 116–30. doi:10.1002/mrdd.20064. PMID 15977318.
235. ↑ Wolraich, ML; Hagan JF, Jr; Allan, C; Chan, E; Davison, D; Earls, M; Evans, SW; Flinn, SK; Froehlich, T; Frost, J; Holbrook, JR; Lehmann, CU; Lessin, HR; Okechukwu, K; Pierce, KL; Winner, JD; Zurhellen, W; Subcommittee on Children and Adolescents with attention-deficit/hyperactive disorder (October 2019). "Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents". Pediatrics. 144 (4): e20192528. doi:10.1542/peds.2019-2528. PMC 7067282. PMID 31570648.
236. ↑ Schnoll, R; Burshteyn, D; Cea-Aravena, J (March 2003). "Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect". Applied Psychophysiology and Biofeedback. 28 (1): 63–75. doi:10.1023/A:1022321017467. PMID 12737097. S2CID 7783422.
237. ↑ Krummel DA, Seligson FH, Guthrie HA (1996). "Hyperactivity: is candy causal?". Critical Reviews in Food Science and Nutrition. 36 (1–2): 31–47. doi:10.1080/10408399609527717. PMID 8747098. S2CID 32631191.
238. ↑ Nigg JT, Lewis K, Edinger T, Falk M (January 2012). "Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives". J Am Acad Child Adolesc Psychiatry. 51 (1): 86–97.e8. doi:10.1016/j.jaac.2011.10.015. PMC 4321798. PMID 22176942.
239. ↑ "Food coloring ban in the UK but usage continues for USA". BioHealthBase BRC Team. 23 October 2014. Archived from the original on 2 November 2014.
240. ↑ "Modernising the Rules on Food Additives and Labelling of Azo Dyes". FLEXNEWS: Business News for the Food Industry. Global Data Systems. European Parliament. 9 July 2008. Archived from the original on 2 December 2008.
241. ↑ Kleinman RE, Brown RT, Cutter GR, Dupaul GJ, Clydesdale FM (June 2011). "A research model for investigating the effects of artificial food colorings on children with ADHD". Pediatrics. 127 (6): e1575–84. doi:10.1542/peds.2009-2206. PMID 21576306.
242. ↑ Wilson, JJ; Levin, FR (December 2001). "Attention deficit hyperactivity disorder (ADHD) and substance use disorders". Current Psychiatry Reports. 3 (6): 497–506. doi:10.1007/s11920-001-0044-8. PMID 11707164. S2CID 46121828.
243. ↑ "FDA Asks Attention-Deficit Hyperactivity Disorder (ADHD) Drug Manufacturers to Develop Patient Medication Guides". Food and Drug Administration. 21 September 2007. Archived from the original on 21 February 2008. Retrieved 13 April 2009.
244. ↑ 244.0 244.1 Ioannidis, K; Chamberlain, SR; Müller, U (September 2014). "Ostracising caffeine from the pharmacological arsenal for attention-deficit hyperactivity disorder—was this a correct decision? A literature review". Journal of Psychopharmacology. 28 (9): 830–6. doi:10.1177/0269881114541014. PMID 24989644. S2CID 13465319.
245. ↑ Schechter, MD; Timmons, GD (1985). "Objectively measured hyperactivity—II. Caffeine and amphetamine effects". Journal of Clinical Pharmacology. 25 (4): 276–80. doi:10.1002/j.1552-4604.1985.tb02838.x. PMID 4008672. S2CID 33184695.
246. ↑ Toledano A, Alvarez MI, Toledano-Díaz A (September 2010). "Diversity and variability of the effects of nicotine on different cortical regions of the brain – therapeutic and toxicological implications". Central Nervous System Agents in Medicinal Chemistry. 10 (3): 180–206. doi:10.2174/1871524911006030180. hdl:10261/61750. PMID 20528766.
247. ↑ McClernon, FJ; Kollins, SH (October 2008). "ADHD and smoking: from genes to brain to behavior". Annals of the New York Academy of Sciences. 1141 (1): 131–47. Bibcode:2008NYASA1141..131M. doi:10.1196/annals.1441.016. PMC 2758663. PMID 18991955.
248. ↑ Potter, AS; Schaubhut, G; Shipman, M (December 2014). "Targeting the nicotinic cholinergic system to treat attention-deficit/hyperactivity disorder: rationale and progress to date". CNS Drugs. 28 (12): 1103–13. doi:10.1007/s40263-014-0208-9. PMC 4487649. PMID 25349138.
249. ↑ 249.0 249.1 Gillies D, Leach MJ, Perez Algorta G (April 2023). "Polyunsaturated fatty acids (PUFA) for attention deficit hyperactivity disorder (ADHD) in children and adolescents". Cochrane Database Syst Rev. 2023 (4): CD007986. doi:10.1002/14651858.CD007986.pub3. PMID 37058600.
250. ↑ 250.0 250.1 250.2 Bloch MH, Qawasmi A (October 2011). "Omega-3 fatty acid supplementation for the treatment of children with attention-deficit/hyperactivity disorder symptomatology: systematic review and meta-analysis". J Am Acad Child Adolesc Psychiatry. 50 (10): 991–1000. doi:10.1016/j.jaac.2011.06.008. PMC 3625948. PMID 21961774.
251. ↑ Arnold LE, DiSilvestro RA (2005). "Zinc in attention-deficit/hyperactivity disorder". Journal of Child and Adolescent Psychopharmacology. 15 (4): 619–27. doi:10.1089/cap.2005.15.619. hdl:1811/51593. PMID 16190793.
252. ↑ Bloch, MH; Mulqueen, J (October 2014). "Nutritional supplements for the treatment of ADHD". Child and Adolescent Psychiatric Clinics of North America. 23 (4): 883–97. doi:10.1016/j.chc.2014.05.002. PMC 4170184. PMID 25220092.
253. ↑ Haslam RH, Dalby JT, Rademaker AW (1984). "Effects of megavitamin therapy on children with attention deficit disorders". Pediatrics. 74 (1): 103–111. doi:10.1542/peds.74.1.103. PMID 6234505. S2CID 24645872.
254. ↑ 254.0 254.1 254.2 254.3 254.4 Den Heijer AE, Groen Y, Tucha L, Fuermaier AB, Koerts J, Lange KW, Thome J, Tucha O (February 2017). "Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: a systematic literature review". Journal of Neural Transmission. 124 (Suppl 1): 3–26. doi:10.1007/s00702-016-1593-7. PMC 5281644. PMID 27400928. "Beneficial chronic effects of cardio exercise were found on various functions as well, including executive functions, attention and behavior."
255. ↑ 255.0 255.1 Kamp CF, Sperlich B, Holmberg HC (July 2014). "Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters". Acta Paediatrica. 103 (7): 709–714. doi:10.1111/apa.12628. PMID 24612421. S2CID 45881887. "We may conclude that all different types of exercise ... attenuate the characteristic symptoms of ADHD and improve social behaviour, motor skills, strength and neuropsychological parameters without any undesirable side effects. Available reports do not reveal which type, intensity, duration and frequency of exercise is most effective"
256. ↑ 256.0 256.1 Rommel AS, Halperin JM, Mill J, Asherson P, Kuntsi J (September 2013). "Protection from genetic diathesis in attention-deficit/hyperactivity disorder: possible complementary roles of exercise". Journal of the American Academy of Child and Adolescent Psychiatry. 52 (9): 900–910. doi:10.1016/j.jaac.2013.05.018. PMC 4257065. PMID 23972692. "The findings from these studies provide some support for the notion that exercise has the potential to act as a protective factor for ADHD."
257. ↑ Sukhodolsky DG, Scahill L, Zhang H, et al. (January 2003). "Disruptive behavior in children with Tourette's syndrome: association with ADHD comorbidity, tic severity, and functional impairment". J Am Acad Child Adolesc Psychiatry. 42 (1): 98–105. doi:10.1097/00004583-200301000-00016. PMID 12500082. S2CID 24550481.
Hoekstra PJ, Steenhuis MP, Troost PW, et al. (August 2004). "Relative contribution of attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and tic severity to social and behavioral problems in tic disorders". J Dev Behav Pediatr. 25 (4): 272–9. doi:10.1097/00004703-200408000-00007. PMID 15308928. S2CID 22578353.
Carter AS, O'Donnell DA, Schultz RT, et al. (February 2000). "Social and emotional adjustment in children affected with Gilles de la Tourette's syndrome: associations with ADHD and family functioning. Attention Deficit Hyperactivity Disorder". J Child Psychol Psychiatry. 41 (2): 215–23. doi:10.1111/1469-7610.00602. PMID 10750547.
Spencer, T; Biederman, J; Harding, M; O'Donnell, D; Wilens, T; Faraone, S; Coffey, B; Geller, D (October 1998). "Disentangling the overlap between Tourette's disorder and ADHD". J Child Psychol Psychiatry. 39 (7): 1037–44. doi:10.1111/1469-7610.00406. PMID 9804036.
258. ↑ 258.0 258.1 Freeman, Roger D. "Tourette's Syndrome: minimizing confusion". Archived from the original on 11 April 2006. Retrieved 8 February 2006. RD Freeman, MD, is Clinic Head of Neuropsychiatry Clinic at British Columbia Children's Hospital, Vancouver, professional advisory board member of Tourette Syndrome Foundation of Canada, and former member of the Tourette Syndrome Association Medical Advisory Board. Freeman has over 180 journal-published articles on PubMed. Archived 24 July 2008 at the Wayback Machine
259. ↑ Palumbo, D; Spencer, T; Lynch, J; Co-Chien, H; Faraone, SV (Summer 2004). "Emergence of tics in children with ADHD: impact of once-daily OROS methylphenidate therapy". Journal of Child and Adolescent Psychopharmacology. 14 (2): 185–94. doi:10.1089/1044546041649138. PMID 15319016.
Kurlan, Roger (July 2003). "Tourette's syndrome: are stimulants safe?". Current Neurology and Neuroscience Reports. 3 (4): 285–8. doi:10.1007/s11910-003-0004-2. PMID 12930697. S2CID 35508887.
Law, SF; Schachar, RJ (August 1999). "Do typical clinical doses of methylphenidate cause tics in children treated for attention-deficit hyperactivity disorder?". Journal of the American Academy of Child and Adolescent Psychiatry. 38 (8): 944–51. doi:10.1097/00004583-199908000-00009. PMID 10434485.
260. ↑ Tourette's Syndrome Study Group (February 2002). "Treatment of ADHD in children with tics: a randomized controlled trial". Neurology. 58 (4): 527–36. doi:10.1212/WNL.58.4.527. PMID 11865128. S2CID 224482.
261. ↑ 261.0 261.1 Osland, Sydney T.; Steeves, Thomas Dl; Pringsheim, Tamara (26 June 2018). "Pharmacological treatment for attention deficit hyperactivity disorder (ADHD) in children with comorbid tic disorders". The Cochrane Database of Systematic Reviews. 2018 (6): CD007990. doi:10.1002/14651858.CD007990.pub3. ISSN 1469-493X. PMC 6513283. PMID 29944175.
262. ↑ Zinner, Samuel H. (November 2000). "Tourette disorder". Pediatrics in Review. 21 (11): 372–83. doi:10.1542/pir.21-11-372. PMID 11077021. S2CID 7774922.
263. ↑ 263.0 263.1 Scahill, L; Erenberg, G; Berlin, CM; Budman, C; Coffey, BJ; Jankovic, J; Kiessling, L; King, RA; Kurlan, R; Lang, Anthony; Mink, Jonathan; Murphy, Tanya; Zinner, Samual; Walkup, John (April 2006). Tourette Syndrome Association Medical Advisory Board: Practice Committee. "Contemporary assessment and pharmacotherapy of Tourette syndrome". NeuroRx. 3 (2): 192–206. doi:10.1016/j.nurx.2006.01.009. PMC 3593444. PMID 16554257.

## External links[edit | edit source]

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Attention deficit hyperactivity disorder (ICD-10 Chapter V: Mental and behavioural disorders#(F90–F98) Behavioural and emotional disorders with onset usually occurring in childhood and adolescence, F90, 314)

Main articles|

* History of ADHD
* ADHD in adults
* ADHD controversies
* ADHD management
* Social construct theory of ADHD
* ADHD coaching
* Epidemiology of ADHD
* Diet and ADHD

* Major characteristics: Attention
* Hyperactivity
* Impulsivity

Sub-types|

* ADHD predominantly inattentive (ADHD-I, formerly ADD)
* ADHD predominantly hyperactive (ADHD-H, formerly ADHD)
* ADHD combined type (ADHD-C)

Medications|

Stimulants:

* Methylphenidate (Ritalin, Concerta, and others)
* Dexmethylphenidate (Focalin, Focalin XR)
* Amphetamine (Evekeo, Adderall, Adzenys XR, Dyanavel XR)
* Dextroamphetamine (Dexedrine, Zenzedi, ProCentra, and others)
* Lisdexamfetamine (Vyvanse)

Non-stimulant:

* Atomoxetine (Strattera)
* Guanfacine (Tenex (off-label), Intuniv)
* Clonidine (Catapres (off-label), Kapvay)

Related or outdated topics|

* Deferred gratification
* Auditory processing disorder
* Deficits in attention, motor control and perception
* Developmental coordination disorder
* Low arousal theory
* Sluggish cognitive tempo
* Sensory processing disorder
* Hunter vs. farmer hypothesis

* Category

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Amphetamine

Main articles
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pharmaceuticals|

| Amphetamine|

* Adzenys ER
* Adzenys XR-ODT
* Dyanavel XR
* Evekeo
* Evekeo ODT
* Mixed amphetamine salts
* Adderall
* Adderall XR
* Mydayis

|

Levoamphetamine|

N/A

Dextroamphetamine|

* Dexedrine
* ProCentra
* Zenzedi

Lisdexamfetamine|

* Vyvanse

Neuropharmacology|

| Biomolecular targets|

* TAAR1 (full agonist)
* CART (mRNA inducer)
* 5-HT1A receptor (low affinity ligand)
* MAO (weak competitive inhibitor)
* Carbonic anhydrases hCA4, hCA5A, hCA5B, hCA7, hCA12, hCA13, and hCA14 (enzyme activator)

|

Inhibited transporters|

* DAT
* NET
* SERT
* VMAT1
* VMAT2
* EAAT3
* SLC22A3
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Active metabolites|

* 4-Hydroxyamphetamine
* 4-Hydroxynorephedrine
* Norephedrine

Related articles|

* ADHD
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* Amphetamine psychosis
* Benzedrine in popular culture
* Dopamine
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* Category

*[XR]: extended-release
*[OROS]: Osmotic [Controlled] Release Oral [Delivery] System
*[CD/XL]: controlled-delivery/extended-release
*[ER]: extended-release
*[CR]: controlled-release
*[d-amp]: dextroamphetamine
*[l-amp]: levoamphetamine
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*[mRNA]: messenger RNA