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Pediatric Attention Deficit Hyperactivity Disorder (ADHD)

  • Author: Maggie A Wilkes, MD; Chief Editor: Caroly Pataki, MD  more...
Updated: Apr 07, 2016

Practice Essentials

Attention deficit hyperactivity disorder (ADHD) is a developmental condition of inattention and distractibility, with or without accompanying hyperactivity.

Signs and symptoms

According to the Diagnostic and Statistical Manual of Mental Health Disorders, Fifth Edition (DSM-5), the 3 types of attention deficit/hyperactivity disorder (ADHD) are (1) predominantly inattentive, (2) predominantly hyperactive/impulsive, and (3) combined. The current DSM-5 criteria are provided below.[1]


This must include at least 6 of the following symptoms of inattention that must have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

  • Often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities
  • Often has difficulty sustaining attention in tasks or play activities
  • Often does not seem to listen to what is being said
  • Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions)
  • Often has difficulties organizing tasks and activities
  • Often avoids or strongly dislikes tasks (such as schoolwork or homework) that require sustained mental effort
  • Often loses things necessary for tasks or activities (school assignments, pencils, books, tools, or toys)
  • Often is easily distracted by extraneous stimuli
  • Often forgetful in daily activities


This must include at least 6 of the following symptoms of hyperactivity-impulsivity that must have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:

  • Fidgeting with or tapping hands or feet, squirming in seat
  • Leaving seat in classroom or in other situations in which remaining seated is expected
  • Running about or climbing excessively in situations where this behavior is inappropriate (in adolescents or adults, this may be limited to subjective feelings of restlessness)
  • Difficulty playing or engaging in leisure activities quietly
  • Unable to be or uncomfortable being still for extended periods of time (may be experienced by others as “on the go” or difficult to keep up with)
  • Excessive talking
  • Blurting out answers to questions before the questions have been completed
  • Difficulty waiting in lines or awaiting turn in games or group situations
  • Interrupting or intruding on others (for adolescents and adults, may intrude into or take over what others are doing)


  • Onset is no later than age 12 years
  • Symptoms must be present in 2 or more situations, such as school, work, or home
  • The disturbance causes clinically significant distress or impairment in social, academic, or occupational functioning
  • Disorder does not occur exclusively during the course of schizophrenia or other psychotic disorder and is not better accounted for by mood, anxiety, dissociative, personality disorder or substance intoxication or withdrawal

See Clinical Presentation for more detail.


Psychometric and educational testing is often important for the diagnosis of ADHD. The patient's initial history may indicate a need for additional tests, as follows:

  • Examine children by using the Conners' Parent and Teacher Rating Scale and examine adolescents according to the Brown Attention Deficit Disorder Scale (BADDS) for Adolescents and Adults [2]
  • Assess impulsivity and inattention using timed computer tests such as the Conners’ Continuous Performance Test (CPT), the Integrated Visual and Auditory (IVA) CPT, or both
  • Assess girls using the Nadeau/Quinn/Littman ADHD Self-Rating Scale for Girls
  • Assess the patient's executive function by using various neuropsychological tests
  • Perform a learning disability evaluation (intelligence quotient [IQ] vs achievement)

See Workup for more detail.


Behavioral and pharmaceutical strategies are the 2 major components in the medical care of patients with ADHD.

Behavioral interventions

Behavioral psychotherapy often is effective when used in combination with medication.[3, 4] Behavioral therapy or modification programs can help diminish uncertain expectations and increase organization. Working with parents and schools through behavioral parent training and behavioral classroom management to ensure environments are conducive to focus and attention is necessary.

Medication regimens

Psychostimulants are effective in patients with ADHD. However, compliance is an issue, particularly in children. Therefore, the use of long-acting medications at once-a-day dosing to treat ADHD has been shown to have advances over shorter-acting drugs. Their use has been marked to higher rates of remission and better adherence, and they have been demonstrated to be less stigmatizing.

See Treatment and Medication for more detail.



The term attention deficit is misleading. In general, the current predominating theories suggest that persons with attention deficit hyperactivity disorder (ADHD), attention deficit disorder (ADD), actually have difficulty regulating their attention; inhibiting their attention to nonrelevant stimuli, and/or focusing too intensely on specific stimuli to the exclusion of what is relevant. In one sense, rather than too little attention, many persons with ADHD (ADD) pay too much attention to too many things, leading them to have little focus.

Three basic forms of ADHD (ADD) are described in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) of the American Psychiatric Association (APA).[1]  They are (1) predominantly inattentive, (2) predominantly hyperactive/impulsive, and (3) combined.

The major neurologic functions disturbed by the neurotransmitter imbalance of ADHD (ADD) fall into the category of executive function. The 6 major tasks of executive function that are most commonly distorted with ADHD (ADD) include (1) shifting from one mindset or strategy to another (ie, flexibility), (2) organization (eg, anticipating both needs and problems), (3) planning (eg, goal setting), (4) working memory (ie, receiving, storing, then retrieving information within short-term memory), (5) separating affect from cognition (ie, detaching one's emotions from one's reason), and (6) inhibiting and regulating verbal and motoric action (eg, jumping to conclusions too quickly, difficulty waiting in line in an appropriate fashion).

Contrary to some media accounts, ADHD (ADD) is not new. In the early 1900s, diagnosis emphasized the hyperactivity component. Today, hyperactivity, impulsivity, and inattention are the areas of focus. However, reports have alluded to disorders involving hyperactivity, impulsivity, and inattention in conjunction with distractibility and inappropriate arousal patterns throughout medical history. What is new is the enhanced awareness of ADHD (ADD) secondary to rapidly accumulating research findings and its addition to the DSM in 1980.



Findings from neuropsychological studies suggest that the frontal cortex and the circuits linking them to the basal ganglia are critical for executive function and, therefore, to attention and exercising inhibition. Many findings support this view, including those described below.

Executive functions are major tasks of the frontal lobes. MRI of the right mesial prefrontal cortex in persons with ADHD (ADD) strongly supports decreased activation (low arousal) during tasks that require inhibition of a planned motor response and timing of a motor response to a sensory cue. MRI in persons with ADHD (ADD) also strongly supports weakened activity in the right inferior prefrontal cortex and left caudate during a task that involves timing of a motor response to a sensory cue.

In an effort to explore neural correlates that mediate response inhibition deficits in children with ADHD, Spinelli, et al (2011) examined functional MRI brain activation patterns of children aged 8-13 years with and without ADHD on a go/no-go task. While lapses in attention preceded response inhibition errors in the children without ADHD, brain circuitry involved in response selection and control was activated prior to errors in the children with ADHD.[5]

The catecholamines are the main neurotransmitters with frontal-lobe function. Catecholamine controlled dopaminergic and noradrenergic neurotransmission appear to be the main targets for medications used to treat ADHD (ADD).

A 10-year study by National Institute of Mental Health (NIMH) demonstrated that the brains of children and adolescents with ADHD (ADD) are 3-4% smaller than those of children without the disorder, and that pharmacologic treatment is not the cause. The more severe patients' ADHD (ADD) symptoms were, as rated by parents and clinicians, the smaller their frontal lobes, temporal gray matter, caudate nucleus, and cerebellum were.

Data from 357 healthy subjects, obtained from the NIH MRI Study of Normal Brain Development, noted that a thinner cortex and slower cortical thinning was associated with higher attention problem scores, suggesting a link between attention and cortical maturation.[6]

In addition to the role of the neurotransmitters most commonly associated with the frontal lobes and the pathways mentioned above, some investigations have begun exploring a possible role for 5-hydroxytryptamine (5-HT). Although the brain’s motor regions are innervated by 5-HT projections, no connection between 5-HT and ADHD (ADD) motor pathology has yet been identified. However, connections have been made to attention-related processes. Altered 5-HT activity does appear to be at least part of the cause for difficulties with perceptual sensitivity and the appropriate recognition of the relative significance of stimulation.




United States

The prevalence of ADHD (ADD) in children appears to be 3-7%. ADHD (ADD) is associated with significant psychiatric comorbidity. Approximately 50-60% of individuals with this disorder meet DSM-5 criteria for at least one of the possible coexisting conditions, which include learning disorders, restless legs syndrome, ophthalmic convergence insufficiency, depression, anxiety disorders, antisocial personality disorder, substance abuse disorder, and conduct disorder. The likelihood of a person having ADHD (ADD) if a family member has ADHD (ADD) or one of the disorders commonly associated with ADHD (ADD) is significant.


People with ADHD (ADD) have been identified in every country studied, with comparable frequency.


The morbidity for ADHD (ADD) widely varies. This range is a function of many factors, including the specific area of deficit, the patient's environmental response to and interaction with the deficits, the therapy provided, and the presence of coexistent conditions.


ADHD (ADD) is more frequently diagnosed in boys than in girls. Most estimates of the male-to-female ratio range between 3:1 and 4:1 in clinic populations. However, many community-based samples produce a ratio of 2:1. Recognition of ADHD (ADD) has improved over the last decade, and the male-to-female ratio has been decreasing; this may be the result of the increased recognition of inattentive ADHD (ADD).


Data concerning the likelihood that a child with ADHD (ADD) will also have the disorder as an adult are conflicting. As definitions of ADHD (ADD) subtypes improve, some subtypes that cause more adult dysfunction than others will likely be found.

Approximately 30-80% of children with ADHD (ADD) have the disorder as adults. Most experts believe that the rate is well above 50%.

Hyperactive symptoms may decrease with age because of developmental trends toward self-control and changes in brain composition (ie, pruning of abundant neural connections) that occur during late adolescence. However, persons with ADHD (ADD) developmentally mature later than the average population. Inattentive symptoms do not appear to have a similar developmental advantage and tend to remain constant into adulthood.

Contributor Information and Disclosures

Maggie A Wilkes, MD Resident Physician, Department of Psychiatry, Medical University of South Carolina College of Medicine

Maggie A Wilkes, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.


Eve G Spratt, MD, MSc Professor of Pediatrics and Psychiatry, Division of Developmental Pediatrics, Medical University of South Carolina; Director, Pediatric Consultation Liaison Psychiatry, Medical University of South Carolina Children's Hospital at Charleston

Eve G Spratt, MD, MSc is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry

Disclosure: Nothing to disclose.

Stacey M Cobb, MD Fellow in Developmental and Behavioral Pediatrics, Clinical Instructor, Department of Pediatrics, Medical University of South Carolina College of Medicine

Stacey M Cobb, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, Society for Developmental and Behavioral Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Caroly Pataki, MD Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, Physicians for Social Responsibility

Disclosure: Nothing to disclose.


Zainab P Contractor, MD Medical Director, The Affinity Center

Disclosure: Nothing to disclose.

Chet Johnson, MD Professor and Chair of Pediatrics, Associate Director, Developmental Pediatrician, Center for Child Health and Development, Shiefelbusch Institute for Life Span Studies, University of Kansas School of Medicine; LEND Director, University of Kansas Medical Center

Chet Johnson, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Christine A Mayhall, PhD Clinical Psychologist, The Affinity Center

Christine A Mayhall, PhD is a member of the following medical societies: American Psychological Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Table 1. Pediatric Dosing of Stimulant Medications
Medication Initial Pediatric Dose Pediatric Dosage Range and Maximum Dose* Common Pediatric Dose* Preparations
Methylphenidate immediate release (IR) (Ritalin, Methylin, generic) 2.5-5 mg 0.1-0.8 mg/kg/dose PO qd to 5 times/d; not to exceed 60 mg/d 0.3-0.5 mg/kg/dose PO tid/qid All preparations available as 5-mg, 10-mg, or 20-mg scored tabs; Methylin also available as 2.5-mg, 5-mg, or 10-mg chewable tab and PO solution (5 mg/5 mL and 10 mg/mL)
Methylphenidate sustained-release (SR) (Ritalin LA, Metadate CD) Convert from IR or use 10 mg. 0.2-1.4 mg/kg/dose PO qd/tid; not to exceed 60 mg/d 0.6-1 mg/kg/dose PO qd/bid 10-mg, 20-mg, 30-mg, or 40-mg tabs (Metadate also has 50-mg and 60-mg tabs.); can be sprinkled into soft food (Do not cut, crush, or chew.)
Methylphenidate extended release (ER)‡ (Ritalin SR, Methylin ER, Metadate ER, Quillivant XR, generic SR) Convert from IR

May initiate treatment with Quillivant XR

0.2-1.4 mg/kg/dose PO qd/tid; not to exceed 60 mg/d

Quillivant XR: Once daily dosing

0.6-1 mg/kg/dose PO qd/bid 20-mg Spansules (Do not cut, crush, or chew)

Quillivant XR 5 mg/mL suspension

Methylphenidate OROS tablets (Concerta) Convert from IR or use 18 mg. 0.3-2 mg/kg PO qd; not to exceed 54 mg/d 0.8-1.6 mg/kg PO qd 18-mg, 27-mg, 36-mg, and 54-mg tabs (Do not cut, crush, or chew.)
Methylphenidate transdermal patch (Daytrana) Convert from IR or use 10 mg (12.5 cm2 patch) released over 9 h and titrate up prn. 0.3-2 mg/kg released over 9 h; not to exceed one 30-mg patch 10-30 mg released over 9 h 10-mg, 15-mg, 20-mg, 30-mg patches, applied to the hip
Dexmethylphenidate IR (Focalin) 2.5-5-mg 0.1-0.5 mg/kg/dose PO qd to qid; not to exceed 20 mg/d 0.2-0.3 mg/kg/dose PO bid/tid 2.5-mg, 5-mg, or 10-mg scored tabs (Do not cut, crush, or chew.)
Dexmethylphenidate extended release (Focalin-XR) 5-10-mg 0.2-1 mg/kg/dose PO qd to bid; not to exceed 20 mg/d 0.4-0.6 mg/kg/dose PO qd/bid 5-mg, 10-mg, or 20-mg scored tabs; can be sprinkled into soft food (Do not cut, crush, or chew.)
Dextroamphetamine (Dexedrine, Dextrostat) 2.5-5 mg 0.1-0.7 mg/kg/dose PO qd/qid; not to exceed 60 mg/d 0.3-0.5 mg/kg/dose PO qd/tid Dexedrine: 5-mg scored tabs; Dextrostat: 5-mg and 10-mg scored tabs
Dextroamphetamine Spansules (Dexedrine CR) 5 mg 0.1-0.75 mg/kg/dose PO qd/bid; not to exceed 60 mg/d 0.3-0.6 mg/kg/dose PO qd/bid 5-mg, 10-mg, or 15-mg Spansules; can be sprinkled into soft food (Do not cut, crush, or chew.)
Mixed amphetamine salts IR (Adderall, generic) 2.5-5 mg 0.1-0.7 mg/kg/dose PO qd/qid; not to exceed 40 mg/d 0.3-0.5 mg/kg/dose PO tid/qid 5-mg, 7.5-mg, 10-mg, 12.5-mg, 15-mg, 20-mg, or 30-mg scored tabs
Mixed amphetamine salt XR (Adderall-XR) Convert from IR or use 5-10 mg 0.2-1.4 mg/kg/dose PO qd/tid

Not to exceed 30 mg/d

0.6-1 mg/kg/dose PO qd/bid 5-mg, 10-mg, 15-mg, 20-mg, 25-mg, or 30-mg Spansules; can be sprinkled into soft food (Do not cut, crush, or chew.)
Lisdexamfetamine (Vyvanse) 30 mg PO qam 30-70 mg PO qam Data limited 20-mg, 30-mg, 40-mg, 50-mg, 60-mg, or 70-mg caps (Swallow cap whole, sprinkle into soft food, or dissolve contents in glass of water and drink immediately.)Risk of apnea in patients with chronic pulmonary disease; closely monitor these patients, when initiating and titrating therapy; alternatively, consider the use of alternative non-opioid analgesics in these patients (see Black Box Warnings and Contraindications)
Amphetamine (Evekeo, Dyanavel XR), Adzenys XR-ODT Evekeo: 2.5 mg PO BID/TID


Dyanavel XR: 2.5-5 mg PO once daily


Adzenys XR-ODT: 6.3 mg PO qAM

Evekeo: 2.5 mg BID/TID; only in rare cases is it necessary to exceed 40 mg/day


Dyanavel XR: 2.5-5 mg/day; not to exceed 20 mg/day


Adzenys XR-ODT: Not to exceed 18.8 mg/day (aged 6-12 y) or 12.5 mg/day (aged 13-17 y)

Data limited Evekeo: 5-mg, 10-mg tablets


Dyanavel XR: 2.5-mg/mL extended-release oral suspension (do not substitute oral suspension for other amphetamine products on a milligram-per-milligram basis)


Adzenys XR-ODT: 3.1-mg, 6.3-mg, 9.4-mg, 12.5-mg, 15.7-mg, 18.8-mg extended-release oral disintegrating tablets

Note. In general, when the terms methylphenidate, Dexedrine, and Ritalin are used without abbreviations for extended-release preparations (eg, continuous release [CR], SR, osmotic-release oral system [OROS]), a short-acting, IR preparation is implied.

* Maximum pediatric dose suggested by the US Food and Drug Administration (FDA). Although some children benefit greatly from doses greater than these, benefit from use of either the lowest and highest ends of the dose range is uncommon.

†The methylphenidate patch contains a different total methylphenidate dose than the name implies because it is designed to last 12 hours (eg, 10-mg patch [patch size 12.5 cm2] delivers about 10 mg over 9 h [estimated delivery rate is 1.1 mg/h for this particular patch]). Delivery rate varies depending on patch size.

‡Many patients describe their experience with methylphenidate SR preparations as erratic and uncomfortable.

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