Pediatric Attention Deficit Hyperactivity Disorder (ADHD) 

Updated: Nov 20, 2018
Author: Maggie A Wilkes, MD; Chief Editor: Caroly Pataki, MD 

Overview

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]

Inattentive

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

Hyperactivity/impulsivity

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)

Other

  • 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.

Diagnosis

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.

Management

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.

Background

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.

Pathophysiology

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.

Epidemiology

Frequency

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.

International

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

Mortality/Morbidity

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.

Sex

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).

Age

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.

 

Presentation

History

The DSM-5 criteria, in conjunction with a thorough clinical interview regarding daily functioning, are important in the diagnosis of attention deficit hyperactivity disorder (ADHD), previously termed attention deficit disorder (ADD).

Diagnostic Criteria (DSM-5)

The DSM-5 criteria are as follows:[1]

Inattentive

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

Hyperactivity/impulsivity

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)

Other

  • 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
  •  
  • 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

Past medical history

Screen for the following medications or supplements that may have negative interactions with ADHD (ADD)-related medications:

  • Anticonvulsant agents

  • Antihypertensive agents

  • Caffeine-containing drugs

  • Pseudoephedrine

  • Ephedra

  • Monoamine oxidase inhibitors (MAOIs)

  • All medications known to be metabolized by means of the cytochrome P450 (CYP) 2D6 hepatic pathway (See the discussion about atomoxetine in the Medication section.)

Screening for medical concerns that may have negative interactions with ADHD (ADD) medications (Drugs of concern are shown in parentheses.)

  • Major arterial disease (stimulants)

  • Narrow-angle glaucoma (stimulants, imipramine, desipramine)

  • Heart disease (clonidine, desipramine, guanfacine, imipramine, stimulants)

  • Heart palpitations (stimulants)

  • Hepatic disease (atomoxetine)

  • Hypertension (stimulants, atomoxetine, bupropion)

  • Orthostasis (atomoxetine, bupropion, stimulants)

  • Pregnancy (all)

  • Renal disease (bupropion, clonidine)

  • Seizure disorder (bupropion, desipramine, imipramine)

  • Urinary retention or hesitancy (atomoxetine, bupropion, stimulants)

Approximately 30-50% of people with ADHD (ADD) have other significant psychiatric comorbidities. Consider screening patients for the following:

  • Anxiety disorders (generalized anxiety disorder [GAD], obsessive-compulsive disorder [OCD], panic disorder, social phobia)

  • Bipolar disorder

  • Communication disorder (receptive, expressive)

  • Conduct disorder (oppositional defiant disorder in children)

  • Depression

  • Dissociative disorders

  • Eating disorder

  • Enuresis/encopresis

  • Learning disability

  • Pervasive developmental disorder including Asperger syndrome

  • Posttraumatic stress disorder (PTSD)

  • Psychotic disorders

  • Sleep disorder (sleep apnea, restless leg syndrome, delayed sleep phase syndrome)

  • Substance-related disorders

  • Thought disorder

  • Tourette syndrome or other tic disorders

  • Somatic comorbidity (No somatic comorbidities are significantly associated with ADHD [ADD].)

Family history

Inquire about a family history of ADHD (ADD) and of the coexistent conditions listed under History of present illness.

Social history

Inquire about the following:

  • Home and family interactions consistent with ADHD (ADD)

    • Disorganization of personal space is the norm.

    • Anger or rage reactions are prevalent.

    • The child usually seems most awake in the late evening.

    • Awakening the child for school causes major problems.

    • The child is often unable to complete what appear to be developmentally appropriate chores.

    • Homework organization and completion are often a problem.

    • High activity level is noted.

    • Completion of multistep directions is difficult.

    • Losing or forgetting material or conversations is observed.

  • Problems with the legal system

    • Arrests

    • Traffic tickets

    • Motor vehicle accidents

  • School performance

    • Report cards

    • Reprimands or notes sent home

    • Homework completion and/or turning homework in on time

    • Extracurricular activities

  • Family dysfunction

    • Drug abuse, alcohol abuse, or both

    • Parent(s) with ADHD (ADD)

    • Physical abuse

    • Sexual abuse

    • Recent death of loved one or friend

    • Severe chronic illness

    • Severe financial problems

  • Social skills

    • Friendships

    • Group cohesion

    • Strengths and interests

  • Pregnancy, potential for pregnancy, or safe-sex practices

    • Previous intercourse

    • Birth control

    • Condom use

  • Work performance

    • Type of work

    • Promptness

    • Overall work performance

  • Abuse of substances by patient or his or her friends (if the patient is an adolescent)

    • Alcohol

    • Caffeine

    • Marijuana

    • Other illicit drugs

    • Snorting stimulants

    • Prescription medications

    • Tobacco (eg, cigarettes, chewing tobacco, snuff)

Physical

A focused physical examination is recommended if none has been performed within the last year or if suggested by history. Although a child or adolescent with ADHD (ADD) may exhibit few symptoms in a clinical setting, careful observation of behavior is important. The following should be included at onset of medication use and periodically to assess for medication-related negative effects:

  • Vital signs

    • Height

    • Weight

    • Blood pressure

    • Pulse

  • General appearance

    • Fidgeting

    • Impulse control

    • State of arousal

  • Mental status examination

    • Affect

    • Cognition

    • Speech patterns

    • Thought patterns

Causes

At present, genetic loading appears to be the primary and perhaps only cause of ADHD (ADD). However, many environmental factors have been correlated with ADHD (ADD), and future research may prove these to be etiologic factors. Morbidity, as evidenced by signs and symptoms in people with ADHD (ADD), may be strongly correlated with the patient's home and school environments.

Genetic causes

Family, twin, adoption, and segregation analysis, as well as molecular genetic studies, show that ADHD (ADD) has a substantial genetic component. Molecular genetic studies have revealed several genes that appear to be associated with ADHD (ADD) because of their effect on dopamine receptors, dopamine transport, and dopamine beta-hydroxylase.

Research by the NIHM has shown that variants of the gene for catecho-O-methyltransferase (COMT) are associated with different levels of prefrontal dopamine activity. COMT metabolizes dopamine.

People with the val/val variant metabolize dopamine rapidly. Because fast metabolism of a substrate decreases the amount of substrate that is biologically available, these people have reduced prefrontal dopamine activity. This reduction, in turn, impairs prefrontal information processing.

Individuals with the val/met variant have fairly efficient prefrontal function.

Patients with the met/met variant have the most efficient prefrontal function. In fact, this variant results in an enzyme that is 3-4 times weaker than the product of the val/val variant.

Environmental causes

No environmental causes have been clearly identified. However, problems with pregnancy (including cigarette smoking during pregnancy) and/or delivery, head injuries, toxin exposure, heavy marijuana use beginning in early adolescence, marital or family dysfunction, and low social class have all been associated with ADHD (ADD).

 

DDx

 

Workup

Laboratory Studies

Workup in attention deficit hyperactivity disorder (ADHD), previously termed attention deficit disorder (ADD), includes the following:

Liver function tests

Liver function tests (LFTs) may be indicated if the patient has a history of hepatic dysfunction.

Amphetamines, methylphenidate, atomoxetine, and tricyclic antidepressants are metabolized hepatically and excreted mainly in the urine.

A cause-and-effect relationship has been established between the use of atomoxetine and reversible hepatic failure. However, no evidence suggests that baseline LFT results assist care with atomoxetine in any way.

Consider checking LFTs if a patient who is taking atomoxetine presents with signs of hepatitis including early signs, such as nausea, vomiting, diarrhea, and muscle aches lasting longer than 5 days.

Determination of CBC counts

A coincident relationship has been reported, but no cause-and-effect relationship has been established between use of methylphenidate and blood dyscrasias.

A few clinical authorities recommend periodic determination of the CBC counts, but their necessity is not generally endorsed, even for patients receiving long-term treatment.

Drug screening

Consider periodic random drug screening by means of urine testing (witnessed) or serum testing (if witnessing of urine testing is not possible) in all patients with a history of chemical abuse or suspected chemical abuse.

Any suspected substances should be investigated.

Imaging Studies

Evidence suggests that MRI and positron emission tomography (PET) may be useful as future diagnostic methods. Current use is appropriate for research purposes only.

At present, no laboratory studies, imaging studies, or procedures help with the diagnosis of ADHD (ADD), unless the patient's history suggests that other pathology must be ruled out.

Other Tests

Psychometric and educational testing is often important for the diagnosis of ADHD (ADD). 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 neuropsychologic tests.

  • Perform a learning disability evaluation (intelligence quotient [IQ] vs achievement).

  • Several well-validated IQ tests are available. The Wechsler tests are the standards. Many believe that untimed tests are most appropriate for persons with ADHD (ADD). A large discrepancy between the patient's IQ and other measures, such as visual or auditory abilities or an ability to work with numbers, is not uncommon, particularly in older children and adolescents

  • Baseline ECG to access the QT interval may be indicated before a tricyclic antidepressant is prescribed.

In 2013, the Neuropsychiatric EEG-Based Assessment Aid (NEBA) System became the first FDA-approved, brain function–based medical device for use in the diagnosis of ADHD in children and adolescents aged 6-17 years. Although it is not meant to be used alone as a means of confirming the presence of ADHD, it can be employed in combination with a complete medical and psychological assessment to help confirm the diagnosis or to indicate the direction that further testing should take. Using electroencephalographic technology, the NEBA system calculates the ratio of theta and beta brain waves, which is comparatively high in children and adolescents with ADHD.[7, 8]

 

Treatment

Medical Care

The first line of treatment for ADHD in children and adolescents is the use of stimulant medications, such as methylphenidate agents and amphetamine/mixed amphetamine salts agents. Educational interventions may be used adjunctively and are helpful in improving academica work habits, organizational skills, and approaches to academic assignments.  The range of psychotropic medications used in the treatment of ADHD is detailed in the Medication section. While behavioral and psychotherapeutic interventions have not been effective in controlling the core features of ADHD in most children, oppositional behaviors, parent-child problems, and social/peer problems that often accompany ADHD can be ameliorated by these approaches.

Most components of behavioral care take place outside of the primary care provider's office. Common components are briefly described below to assist in referral and consultation. Not all components are necessary for every child.

School or education interventions

The age of the child at initial diagnosis and the severity of the symptoms of ADHD (ADD) likely affect the extent to which the child benefits from working with education specialists.

Consultants initially involved with diagnosis and evaluation can also be important in promoting the development of study skills.

Teachers have an important function. Their periodic feedback about the child's school performance through the use of standardized scales, narrative descriptions, and telephone follow-up is generally an indispensable component of ongoing care.

Implementation of academic accommodations and adaptations is often necessary

Psychotherapeutics

Behavioral modification and family therapy are often helpful for concurrent problems with peers and family conflicts in children with ADHD.

For some adolescents, ADHD coaching, participating in a support group, or both can help normalize the disorder and assist them in obtaining well-focused peer feedback and general information.

Psychologists, behavioral developmental pediatricians, clinical social workers, and nurse practitioners who are well familiarized with ADHD can be invaluable in improving social skills, decreasing family and peer conflicts, and increasing prosocial behaviors in children with ADHD.

Given that the majority of children with ADHD often have concurrent conditions such as learning disorders, oppositional and defiant behaviors,and anxiety and mood disorders, these symptoms and disorders should be addressed concurrent to the treatment of ADHD.

Consultations

The timing of consultations depends on the practitioner's degree of knowledge and experience with the evaluation and treatment of ADHD (ADD). Several possible scenarios are described below.

Referral to an ADHD (ADD) specialist, clinic, and/or a psychiatrist or a behavioral developmental pediatrician

In this scenario, the patient may or may not be well known and may have a family member with ADHD (ADD) but no coexistent conditions. However, the clinician feels the patient must be questioned further about ADHD or coexistent conditions.

The patient may or may not be well known and may have no family history of ADHD (ADD) but has a concerning family history of a mood or anxiety disorder.

The patient may or may not be well known and perhaps has other family members with ADHD (ADD) whose condition is stabilized by medications without problems with coexistent conditions; however, ADHD (ADD) cannot be diagnosed and/or coexistent conditions cannot be ruled out with confidence.

A brief consultation with or referral to an ADHD (ADD) specialist or a psychiatrist or behavioral developmental pediatrician

In this scenario, the patient may or may not be well known to the practitioner, and the condition has been stabilized by medications without problems with identified coexistent conditions. However, the medication either no longer works or has started to cause adverse effects, and the medication cannot be adjusted with confidence.

Referral as soon as possible to a specialist or specialty clinic for drug rehabilitation

In this scenario, a patient is being evaluated and is not taking psychostimulants or is being re-evaluated for current psychostimulants and chemical abuse is noted. If the patient is taking psychostimulants and if the medications are being taken properly, a consultation call to decide whether the stimulants should be continued may be more appropriate than simply stopping them.

Diet

No special diet clearly affects ADHD (ADD). Until this situation changes, a healthy diet with minimal, if any, caffeine should be emphasized. Note that, in children, caffeine is often consumed in the form of chocolate candy, chocolate milk, or "energy" drinks.

While additional studies are warranted to verify the data, the results from one study suggest that a restriction diet may reduce ADHD symptoms in some children; food color additives were identified as a possible association with ADHD symptoms.[9]

Activity

No evidence-based studies have been conducted to elucidate the potential role of physical activity in children with ADHD (ADD). However, anecdotal clinical reports commonly attest to improvements in focus and sleep quality associated with regular physical activity and exercise. In addition, regular physical activity is important in patients with some of the common coexistent conditions (eg, depression, anxiety) and helps improve concentration. Therefore, physical activity is often an important component of therapy.

 

Medication

Medication Summary

The 2 major components in the medical care of children with attention deficit hyperactivity disorder (ADHD), previously termed attention deficit disorder (ADD), are behavioral and pharmaceutical therapies. The behavioral component is covered in the Treatment section.

Pediatric dosing of stimulant medications

Dosing of stimulant medications vary among ADHD (ADD) centers throughout the medical community in the United States. The table below is derived from the stimulant trial protocol of The Affinity Center, Inc, a center for the evaluation and treatment of ADHD (ADD) and mood disorders in Cincinnati, Ohio.

Table 1. Pediatric Dosing of Stimulant Medications (Open Table in a new window)

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

Delay-release/extended-release (Jornay PM)

20 mg PO at 8 pm Titrate weekly in increments of 20 mg; not to exceed 100 mg/day Adjust timing of administration between 6:30 pm and 9:30 pm to optimize tolerability and efficacy the next morning and throughout the day 20-mg, 40-mg, 60-mg, 80-mg, 100-mg capsules; can be sprinkled into soft food (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.

Dose conversions

Conversions for psychostimulants are always approximations, especially when one is converting between stimulants, such as methylphenidate and dextroamphetamine. Different forms of the same drug have slightly different pharmacokinetics, and patients often have different responses to them. FDA-recommended conversions between short-acting and long-acting (LA) preparations of the same drug are based on attempts to match serum-concentration curves and not clinical-performance curves.

In clinical practice, ratios for converting among medications vary by ADHD (ADD) manifestations, adverse effects, comorbidities, and the patients' metabolism. Common approximations are described below. Individual patients vary; therefore, close follow-up, and possibly titration, is initially necessary.

For methylphenidate LA, CD, or ER preparations, convert by using a ratio of 2:1 with immediate-release methylphenidate. For example, Ritalin 10 mg q4h is converted to Ritalin LA 20 mg q8h. For a few patients, effects last only 5–6 hours with the LA preparations, although effects last 3.5–4 hours with the IR form. However, a short effect from one 8-hour preparation does not always mean another 8-hour preparation has the same problem.

For XR mixed amphetamine salts (MAS), convert using a ratio of 2:1 with IR MAS. The half-life of MAS widely varies among individuals. Some patients do better with a lower second dose and, thus, may benefit from an IR and XR morning combination.

Dexedrine Spansule seems to have the greatest interpatient variance when converting the IR form to the CR form. The IR-to-CR ratio for equivalent clinical effects appears to vary from 1:1 to about 1:1.5; however, this conversion has not been well studied. For example, Dextrostat 10 mg q4h is converted to Dexedrine CR 10–15 mg q8h.

Methylphenidate OROS tablets are converted in an 18:5 ratio with methylphenidate. For example, Ritalin 10 mg q4h is converted to Concerta 36 mg. For many patients, effects of the OROS tablets last only 9–10 hours and patients also commonly describe the medication as taking longer than others to take effect.

Methylphenidate OROS tablets are converted in an 18:10 ratio with methylphenidate LA, CD, or ER. For example, Ritalin LA 10 mg q8h is converted to Concerta 18 mg.

Methylphenidate transdermal patch is converted in a 1:1 ratio with methylphenidate IR and a 1:2 ratio with the LA preparations, although the FDA suggests starting with the lowest dose patch and working up.

Lisdexamfetamine dosing conversion may be compared with dextroamphetamine immediate-release (Dexedrine IR). The prescribing information describes a dose of lisdexamfetamine dimesylate 100 mg as equivalent to d-amphetamine sulfate immediate-release 40 mg.

Categories of medications

Psychostimulants are effective in patients with ADHD (ADD). In addition, they have been available for many decades, allowing for a strong appreciation of their lack of major adverse effects when used at therapeutic doses. However, a study published in 2014 suggests that psychostimulants may be associated with increased risk of CV events.[10, 11]

In a longitudinal, prospective cohort study of all children born in Denmark between 1990 and 1999 (mean follow-up 9.5 years), researchers found that use of psychostimulants was associated with nearly two-fold increased risk for a CV event compared with nonuse of the drugs (adjusted hazard ratio [HR], 1.83; 95% confidence interval [CI], 1.10 - 3.04), and the risk among stimulant users with ADHD was even higher (HR, 2.34; 95% CI, 1.15 - 4.75).[10, 11] The actual cardiovascular event rate was low (84 events per 100,000 person-years), the study included a broad definition of cardiovascular events, and the use of other medications was not controlled for, making the clinical significance of the study’s findings uncertain.[10, 11]

In December 2013, the US Food and Drug Administration (FDA) issued a warning that methylphenidate has been linked to rare cases of priapism, with the drug's labeling updated accordingly.[12]

In December 2015, the FDA approved a chewable tablet form of extended-release methylphenidate, to be sold as QuilliChew ER, for treatment of ADHD in patients aged 6 years or older. The tablet comes in strengths of 20, 30, and 40 mg and are scored so they can be split easily. The product is to be taken once daily in the morning.[13]

In May 2013, the FDA approved the stimulant lisdexamfetamine dimesylate (Vyvanse, Shire Plsc) as a maintenance treatment in children and adolescents (aged 6 years and older) with ADHD. The drug was previously approved as a maintenance treatment only in adults.[14]

Approval for lisdexamfetamine dimesylate was based on a 32-week trial designed to evaluate efficacy of the drug in 276 children and adolescents aged 6–17 years. Patients received dosages of 30 mg/day, 50 mg/day, or 70mg/day. Treatment failures at the end point of the 6-week withdrawal period occurred at a significantly lower rate in the drug group (15.8%) than in the placebo group (67.5%). This evidence strongly suggested that patients treated with the drug maintain greater ADHD symptom control.

In June 2017, the FDA approved 2 new ADHD medications, Contempla XR-ODT and Mydayis. Contempla XR-ODT is approved for the treatment of ADHD in children and adolescents between 6 and 17 years of age. It is an oral disintegrating tablet form of extended-release methylphenidate, given once every morning, and is available as a 8.6 mg, 17.3 mg, and 25.9 mg tablet.[15]  Mydayis is also approved for the treatment of ADHD in adolescents and adults aged 13 years or older. It is an extended-release capsule of mixed amphetamine salts administered each morning. It is available as a 12.5 mg, 25 mg, 37.5mg, and 50 mg capsule.[16]

The first bedtime methylphenidate (Jornay PM) was approved by the FDA in 2018. It is indicated for patients with ADHD in adults and children aged 6 years or older. It is administered at 8 PM, although the administration time may be adjusted between 6:30 PM and 9:30 PM to optimize tolerability and efficacy the next morning and throughout the day. The capsule contains 2 functional film coatings that act synergistically to achieve a unique pharmacokinetic profile. The first layer delays the initial release of drug for up to 10 hours, and the second layer helps to control the rate of release of the active pharmaceutical ingredient throughout the day. Compared with placebo, Jornay PM achieved significant improvements in ADHD symptoms as measured by the ADHD rating scale IV (p = 0.002) and the parent rating of evening and morning behavior (revised) scale (p < 0.001).[17]

Blader et al (2009) evaluated the ability of divalproex to reduce aggressive behavior in children with ADHD and a disruptive disorder. Children with persistent aggressive behavior that was underresponsive to psychostimulant therapy were randomly assigned to receive divalproex or placebo in addition to stimulant therapy for 8 weeks. A higher proportion of improved behavior was observed in the divalproex group (8 of 14 [57%]) compared with placebo (2 of 13 [15%]). A larger trial is needed to further study the use of divalproex to ameliorate aggressive behavior in patients with ADHD.[18]

Atomoxetine (Strattera), a nonstimulant selective norepinephrine reuptake inhibitor (SNRI), has been effective in many people with ADHD (ADD). This relatively new medication has the advantages of qd-to-bid dosing and unscheduled status with the Drug Enforcement Agency (DEA). However, cases of reversible hepatic failure have been directly attributed to atomoxetine, and an evaluation of other long-term adverse effects has been limited to data from a few years.

Patients may significantly benefit more from stimulants than from atomoxetine, but some may have untenable adverse effects with any stimulant product or dose. In the experience of numerous subspecialists, these patients may benefit from a combination of atomoxetine and a stimulant. For many patients, atomoxetine appears to augment the clinical effects of the stimulant, allowing for clinical efficacy with a low dose and decreasing the likelihood of adverse effects.

Antidepressants and alpha-agonists have an important role in some individuals with ADHD (ADD). Most have well-known adverse-effect profiles. Antidepressants and alpha-agonists can cause cardiac adverse effects, and this possibly must be kept in mind.

A cohort study published in the Journal of the American Medical Association in 2011 showed that current or new use of ADHD medications in young and middle-aged adults was not associated with an increased risk of serious cardiovascular events. The limitations of this study included lack of complete information on some potentially important risk factors.[19]

Clonidine extended-release (Kapvay) was approved for children with ADHD in September 2010. The immediate-release clonidine has been used off-label for ADHD; however, sedation was a drawback. The extended-release product provides less fluctuation of serum levels and may be better tolerated.

Modafinil (Provigil), a medication used to treat excessive daytime sleepiness, improves core symptoms in many children with ADHD (ADD). In early studies in children, common adverse affects occurring at rates higher than those of placebo were insomnia (24%) and anorexia (14%).

In August 2006, Cephalon, the manufacturer of modafinil (Sparlon), received a nonapprovable letter from the FDA for the treatment of ADHD (ADD). Cephalon has decided that it will not pursue further development of Sparlon for ADHD (ADD). Modafinil is still available as Provigil, which does have FDA approval to improve wakefulness for adults with narcolepsy, sleep apnea, or shift-work sleep disorders. Many ADHD (ADD) specialists continue to use modafinil in selected patients without problems. To view information from a media briefing describing the FDA decision, see Cephalon Media Briefing.

Transcripts of the FDA Psychopharmacologic Drugs Advisory Committee minutes that describe the rashes observed in clinical trials with modafinil are available. For more information see FDA Psychopharmacologic Drugs Advisory Committee minutes from March 23, 2006 that discuss modafinil for ADHD.

Alpha2-adrenergic Agonists

Class Summary

Alpha2-adrenergic agonists can be helpful in treating hyperactivity, tics, or delayed sleep onset. They have a long history of pediatric use for this indication. Rare cases of sudden death had been reported several years ago in a few children who were given clonidine with concurrent methylphenidate. Reports also described fatal ventricular fibrillation in patients in whom treatment with clonidine was abruptly stopped rather than slowly tapered, as is appropriate. Details of these cases do not substantiate a cause-and-effect association, only concurrence.

The FDA has not stated that these drugs should not be simultaneously used. Nevertheless, a prudent approach is to avoid using these drugs together in any patient with a first-degree relative who died from a sudden cardiac cause without first getting an ECG. Obtaining an ECG in any patient who may benefit from this combination but who has a history of arrhythmia is also prudent. Most experts continue to use clonidine with any of the stimulants when clinically indicated.

The data from one study suggest that morning or evening guanfacine extended release (GXR; ≤4 mg/d) adjunctive to a long-acting psychostimulant resulted in improvement in ADHD symptoms over psychostimulants used alone.[20]

An extended-release clonidine (Kapvay) was approved by the FDA in September 2010 as adjunctive therapy to stimulants for ADHD or as monotherapy.

Guanfacine (Intuniv)

Selectively stimulates alpha2a-adrenoreceptors in brainstem, activating an inhibitory neuron, which reduces sympathetic outflow. This action results in decreased vasomotor tone and HR. The mechanism of action of guanfacine in ADHD is not known. Indicated for ADHD. Effectiveness for long-term use (ie, >9 wk) has not been studied in controlled trials

Clonidine (Kapvay)

Stimulates alpha2-adrenoreceptors in brainstem, activating an inhibitory neuron, which reduces sympathetic outflow. Result is decreased vasomotor tone and HR. Mechanism for ADHD unknown. Extended-release form indicated for ADHD as adjunctive therapy to stimulants or as monotherapy.

Selective norepinephrine reuptake inhibitors (SNRIs)

Class Summary

These are nonstimulant ADHD (ADD) medications generally used as adjuncts to stimulants.

Atomoxetine (Strattera)

SNRI that inhibits presynaptic norepinephrine transporter. Also appears to indirectly stimulant dopamine activity in frontal lobes. Many anecdotal reports state that, when stimulants are not well-tolerated at a dose necessary for efficacy (eg, because of anxiety) and atomoxetine is not efficacious enough alone, the combination of atomoxetine and low dose (tolerable) stimulants is often very effective.

About 5-10% of patients are poor metabolizers of the drug and have increased drug exposure, peak serum levels, and half-lives. If intolerable but benign adverse effects are present at FDA-recommended doses, but not at lower dose, efficacy may be observed at the lower dose; therefore consider a low-dose trial. Usually clinically effective qd despite 5-h half-life (24 h in poor metabolizers); unknown if serum levels are correlated with efficacy.

Antidepressants

Class Summary

Many patients have reported clinically significant improvement with the use of some antidepressants. Although antidepressants are beneficial when added to a stimulant or SNRI in certain clinical situations, a psychostimulant or SNRI is still the medication of choice for most persons with ADHD (ADD) because of its safety profile and superior efficacy.

Imipramine (Tofranil)

Inhibits reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neuron.

Bupropion (Wellbutrin)

Inhibits neuronal dopamine reuptake. Weak blocker of serotonin and norepinephrine reuptake.

Desipramine (Norpramin)

May increase synaptic concentration of norepinephrine in CNS by inhibiting reuptake by presynaptic neuronal membrane. May have effects in the desensitization of adenyl cyclase and downregulation of beta-adrenergic and serotonin receptors. Adjust dose to response and serum level.

Stimulants

Class Summary

Psychostimulants stimulate the areas of decreased activation to a higher state of arousal. The spectrums of therapeutic efficacy and adverse effects of all the FDA-scheduled category II psychostimulants for ADHD (ADD) are similar. For any individual, therapeutic efficacy may vary greatly among drugs, preparations, or formulations (generic vs brand name).

The most common adverse effects include anorexia, sleep disturbances, mild anxiety, and rebound (eg, post-therapeutic agitation, anger, lethargy). Most individuals who take psychostimulants for ADHD (ADD) develop tolerance for the adverse effects within a few weeks. Although adverse-effect profiles, akin to therapeutic profiles, are similar for all psychostimulants, patients have their own positive and negative responses, which vary among the drugs.

Individuals with certain current or latent coexistent psychiatric disorders (eg, psychosis, bipolar disorder, some disorders of anxiety or depression) are particularly vulnerable to the adverse effects of stimulants if they do not receive concurrent medication, psychological counseling, or both for the coexistent condition.

The following contains FDA-approved dosing information and FDA-stated contraindications. Of note, many experts question the FDA's maximums for most stimulant medications (see the Table above for ranges). Experts also question several comorbidities thought to be contraindications because evidence suggests that tics may be as likely to improve with stimulants as worsen with them. Furthermore, blood pressure improves in some individuals with hypertension receiving stimulants, whereas others simply need a slight increase in their dose of antihypertensive. Finally, although the FDA lists glaucoma as a contraindication, the specific concern is only narrow-angle glaucoma.

Dextroamphetamine (Dexedrine, Dexedrine Spansules, Dextrostat)

Increases amount of circulating dopamine and norepinephrine in cerebral cortex by blocking reuptake of norepinephrine or dopamine from synapse. Short-acting brands fairly similar in cost; generic is 50-60% less expensive. Dexedrine available as 5-mg scored tab. Dextrostat available as 5-mg or 10-mg scored tab. Dexedrine Spansules (CR) available as 5-mg, 10-mg, or 15-mg Spansules

Methylphenidate (Aptensio XR, Concerta, Cotempla XR-ODT, Jornay PM)

Stimulates cerebral cortex and subcortical structures. Generic and branded-generic (Methylin and Metadate regular or ER) formulations 50-60% less expensive than Ritalin. LA preparations more expensive than short-acting preparations. Concerta (LA) tends to be more expensive than other preparations; 1 cap of Concerta, similar to other stimulants, costs the same whatever dose.

Although clinical difference between generic drug and branded-generics or Ritalin has not been verified, many patients have enough variability among preparations that they are willing to pay the price difference. Many experts observed enough variability that they do not prescribe plain generic products unless patient (or insurance) insists. FDA allows for 20% variability in certain parameters between generics and brands and determines equivalence solely by pharmacokinetics and not data from clinical studies.

Dextroamphetamine and amphetamine mixture (Adderall, Mydayis)

Produce CNS and respiratory stimulation. CNS effect may occur in cerebral cortex and reticular activating system. May have direct effect on alpha-receptor and beta-receptor sites in peripheral system and release stores of norepinephrine in adrenergic nerve terminals. Mixture contains various salts of amphetamine and dextroamphetamine. Adderall is available as 5-mg, 7.5-mg, 10-mg, 12.5-mg, 15-mg, 20-mg, or 30-mg scored IR tabs and 10-mg, 20-mg, and 30-mg XR caps. Mydayis is also available as 12.5 mg, 25 mg, 37.5 mg, 50 mg extended release caps.

Dexmethylphenidate (Focalin, Focalin XR)

Contains pharmacologically active d-enantiomer of racemic methylphenidate. Blocks norepinephrine and dopamine reuptake into presynaptic neuron and increases release of these monamines into extraneuronal space.

Methylphenidate transdermal patch (Daytrana)

CNS stimulant. Therapeutic action for ADHD (ADD) not known but thought to block norepinephrine and dopamine reuptake into presynaptic neuron and to increase release of these monoamines into extraneuronal space. Racemic mixture composed of the d-enantiomer and l-enantiomer. The d-enantiomer is more pharmacologically active than the l-enantiomer. Transdermal administration exhibits minimal first-pass effect compared with PO administration; consequently, lower dose of transdermal methylphenidate (on mg/kg basis) compared with PO dose of methylphenidate may still produce higher d-methylphenidate level.

Available in 4 dosage strengths. Different-sized patches contain different amounts of methylphenidate and deliver different amounts over 9-h dose period. Respective patch sizes, methylphenidate content per patch, and dose delivered over 9 h are 12.5, 18.75, 25, and 37.5 cm2; 27.5, 41.3, 55, and 82.5 mg; and 10, 15, 20, and 30 mg. Onset of desired effect occurs approximately 2 h after application and persists 3-4 h after removal.

Lisdexamfetamine (Vyvanse)

Inactive prodrug of dextroamphetamine. Elicits CNS stimulant activity. Blocks norepinephrine and dopamine reuptake in presynaptic neurons and increases release of these monoamines in extraneuronal space. It is indicated for initial and maintenance treatment of ADHD in children aged 6-17 years and adults.

Amphetamine (Dyanavel XR, Evekeo)

Noncatecholamine, sympathomimetic amine that elicits CNS stimulant activity. The precise mechanism by which amphetamines produce mental and behavioral effects are unclear. Available as short-acting tablets (Evekeo) that need 2-3 doses/day in children aged 3 y or older. It is also available as a long-acting, once daily oral suspension (Dyanavel XR) or extended release oral disintegrating tablets (Adzenys XR-ODT) for patients aged 6 y or older.

 

Follow-up

Further Outpatient Care

Follow-up for attention deficit hyperactivity disorder (ADHD), previously termed attention deficit disorder (ADD), varies and depends on the patient's profile, the clinician's experience, and the access to healthcare providers.

After the patient's condition is stabilized, a follow-up frequency of every 6-12 weeks is often appropriate for the first year.

After that, patients whose conditions are stable may do best with visits every 4 months to assess their medications.

Psychotherapy may need to be continued for months to years.

Complications

Coexisting neuropsychiatric disorders and learning disorders can complicate the diagnosis and treatment of ADHD (ADD). See History.

Prognosis

The prognosis for patients with ADHD (ADD) is excellent if the following conditions are present:

  • The patient has no major comorbidity.

  • Medication management takes into account minor comorbidities and the great range of individual responses.

  • Patients and caregivers receive appropriate education about ADHD (ADD) and ADHD (ADD) management.

  • Adherence to therapy continues.

  • Any and all coexisting learning disabilities are diagnosed, and remediation is scheduled and undertaken.

  • Any and all coexisting emotional problems are investigated and treated appropriately by a primary care provider or the patient is referred to a mental health professional.

Patient Education

Provide information about the pathophysiology in lay terms.

Provide information about complementary therapeutic approaches to medication (eg, involvement of education specialists, counseling or coaching, school accommodations, parent training).

Provide clinical medication information.

Include appropriate follow-up parameters.

Attend to administrative issues related to medication (eg, prescription writing and safety, compliance with state laws).

Provide emergency information.

Seek school accommodations.

Provide contact information for local and national support organizations.

Provide literature or written resources (eg, books, periodicals).

For excellent patient education resources, visit eMedicineHealth's Mental Health Center. Also, see eMedicineHealth's patient education article Attention Deficit Hyperactivity Disorder.

 

Questions & Answers

Overview

What is attention deficit hyperactivity disorder (ADHD)?

What are the types of pediatric attention deficit hyperactivity disorder (ADHD)?

What are the diagnostic criteria for predominantly inattentive attention deficit hyperactivity disorder (ADHD)?

What are the diagnostic criteria for predominantly hyperactive/impulsive attention deficit hyperactivity disorder (ADHD)?

Which diagnostic criteria are associated with all types of pediatric attention deficit hyperactivity disorder (ADHD)?

Which tests are useful in the diagnosis of pediatric attention deficit hyperactivity disorder (ADHD)?

What are the 2 main treatment strategies for pediatric attention deficit hyperactivity disorder (ADHD)?

How does the attention deficit component of attention deficit hyperactivity disorder (ADHD) manifest?

What are the 3 forms of attention deficit hyperactivity disorder (ADHD)?

Which neurologic/executive functions are disrupted in attention deficit hyperactivity disorder (ADHD)?

How long has ADHD been recognized as a medical diagnosis?

Which areas of the brain are responsible for executive function and what changes in those areas manifest as attention deficit hyperactivity disorder (ADHD)?

What is the role of neural correlates that mediate response inhibition deficits in children with attention deficit hyperactivity disorder (ADHD)?

Which neurotransmitters are targeted by attention deficit hyperactivity disorder (ADHD) medications?

What differences in brain structure can be observed in children who have attention deficit hyperactivity disorder (ADHD) compared with children who do not have ADHD?

What is the role of 5-hydroxytryptamine (5-HT) in the pathophysiology of attention deficit hyperactivity disorder (ADHD)?

What is the prevalence of pediatric attention deficit hyperactivity disorder (ADHD) and its comorbidities in the US?

How does the prevalence of attention deficit hyperactivity disorder (ADHD) in the US compare with the prevalence in other countries?

What factors influence the morbidity of pediatric attention deficit hyperactivity disorder (ADHD)?

Is attention deficit hyperactivity disorder (ADHD) more common in in boys or in girls?

How does pediatric attention deficit hyperactivity disorder (ADHD) evolve over time and into adulthood?

Presentation

Which diagnostic criteria are used for pediatric attention deficit hyperactivity disorder (ADHD)?

What are the DSM-5 diagnostic criteria for inattentive pediatric attention deficit hyperactivity disorder (ADHD)?

What are the DSM-5 diagnostic criteria for hyperactive/impulsive pediatric attention deficit hyperactivity disorder (ADHD)?

Which diagnostic criteria are applicable to all types of pediatric attention deficit hyperactivity disorder (ADHD) other than inattentiveness and hyperactivity/impulsivity?

Which medications and supplements may have negative interactions with attention deficit hyperactivity disorder (ADHD)-related medications?

Which medical conditions and treatments may have negative interactions with medications used to manage attention deficit hyperactivity disorder (ADHD)?

What psychiatric comorbidities are associated with attention deficit hyperactivity disorder (ADHD)?

What behavioral, social, and family history inquiries should be made in the evaluation of pediatric attention deficit hyperactivity disorder (ADHD)?

What is the role of a physical exam in children presenting with pediatric attention deficit hyperactivity disorder (ADHD)?

Which assessments are useful in monitoring for adverse effects of medications used to treat pediatric attention deficit hyperactivity disorder (ADHD)?

What is the primary cause of attention deficit hyperactivity disorder (ADHD) and which factors are believed to contribute to it?

What role does genetics play in pediatric attention deficit hyperactivity disorder (ADHD)?

What role do environmental factors play in the etiology of pediatric attention deficit hyperactivity disorder (ADHD)?

DDX

What are the differential diagnoses for Pediatric Attention Deficit Hyperactivity Disorder (ADHD)?

Workup

What is the role of liver function tests in the workup of pediatric attention deficit hyperactivity disorder (ADHD) and when are they indicated?

What is the relationship between the use of methylphenidate to treat pediatric attention deficit hyperactivity disorder (ADHD) and blood dyscrasias?

When is drug screening recommended in attention deficit hyperactivity disorder (ADHD)?

Are lab and imaging studies or procedures indicated in the diagnosis of pediatric attention deficit hyperactivity disorder (ADHD)?

Which psychometric and educational tests are useful in the diagnosis of pediatric attention deficit hyperactivity disorder (ADHD)?

What is the Neuropsychiatric EEG-Based Assessment Aid (NEBA) System and how is it used in the diagnosis of pediatric attention deficit hyperactivity disorder (ADHD)?

Treatment

What are the main components of the treatment strategy for pediatric attention deficit hyperactivity disorder (ADHD)?

What role do teachers have in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

What psychotherapeutic options may be beneficial in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

When and how often are consultations necessary in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

When is consultation unnecessary in the management of pediatric attention deficit hyperactivity disorder (ADHD)?

When is referral to an attention deficit hyperactivity disorder (ADHD) specialist necessary in the management of pediatric attention deficit hyperactivity disorder (ADHD)?

What changes in medication treatment efficacy merit a consultation with an attention deficit hyperactivity disorder (ADHD) specialist or psychiatrist?

When should a patient being treated for attention deficit hyperactivity disorder (ADHD) be referred to a specialist or specialty clinic for drug rehabilitation?

What role does diet play in the management of pediatric attention deficit hyperactivity disorder (ADHD)?

What role does physical activity play in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

Medications

Is there a standard protocol for the use of stimulant medications in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

What factors should be considered when converting from one medication to another in the treatment of attention deficit hyperactivity disorder (ADHD)?

What is the conversion ratio for adjusting methylphenidate preparations in pediatric attention deficit hyperactivity disorder (ADHD)?

What is the conversion ratio for adjusting extended-release (XR) mixed amphetamine salts (MAS) in pediatric attention deficit hyperactivity disorder (ADHD)?

What is the conversion ratio when switching from dextroamphetamine (Dexedrine Spansule) immediate release (IR) to controlled-release (CR) in the treatment of in pediatric attention deficit hyperactivity disorder (ADHD)?

What are the common conversion ratios for methylphenidate osmotic-release oral system (OROS) tablets to other preparations of methylphenidate (LA, CD, ER) in pediatric attention deficit hyperactivity disorder (ADHD)?

What is the conversion ratio when switching from methylphenidate immediate release (IR) or LA to the transdermal patch in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

How is lisdexamfetamine dosing converted in the treatment of pediatric attention deficit hyperactivity disorder (ADHD)?

What are the cardiovascular risks of psychostimulants in the treatment of attention deficit hyperactivity disorder (ADHD)?

Does methylphenidate cause any adverse effects?

Is a chewable form of methylphenidate available for the treatment of attention deficit hyperactivity disorder (ADHD)?

Which psychostimulants are FDA approved for the treatment of attention deficit hyperactivity disorder (ADHD) in children?

Is divalproex effective in reducing aggressive behavior in attention deficit hyperactivity disorder (ADHD)?

How safe and effective is atomoxetine (Strattera) in patients with attention deficit hyperactivity disorder (ADHD)?

Are antidepressants and alpha-agonists safe in patients with attention deficit hyperactivity disorder (ADHD)?

Do attention deficit hyperactivity disorder (ADHD) medications increase risk of cardiovascular events in young and middle-aged adults?

Is clonidine extended-release (Kapvay) used to treat pediatric attention deficit hyperactivity disorder (ADHD)?

Is modafinil (Provigil) effective in treating the symptoms of attention deficit hyperactivity disorder (ADHD) symptoms?

Is modafinil used in the treatment of attention deficit hyperactivity disorder (ADHD)?

Which medications in the drug class Alpha2-adrenergic Agonists are used in the treatment of Pediatric Attention Deficit Hyperactivity Disorder (ADHD)?

Which medications in the drug class Selective norepinephrine reuptake inhibitors (SNRIs) are used in the treatment of Pediatric Attention Deficit Hyperactivity Disorder (ADHD)?

Which medications in the drug class Antidepressants are used in the treatment of Pediatric Attention Deficit Hyperactivity Disorder (ADHD)?

Which medications in the drug class Stimulants are used in the treatment of Pediatric Attention Deficit Hyperactivity Disorder (ADHD)?