Chapter 35. Attention-Deficit/Hyperactivity Disorder

DSM-IV-TR Diagnostic Criteria

Attention-Deficit/Hyperactivity Disorder

1. Either (1) or (2):

   1. Six (or more) of the following symptoms of inattention have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level:Inattention

      1. Often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities

      2. Often has difficulty sustaining attention in tasks or play activities

      4. Often does not seem to listen when spoken to directly

      6. 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)

      8. Often has difficulty organizing tasks and activities

      10. Often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework)

      12. Often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils, books, or tools)

      14. Is often easily distracted by extraneous stimuli

      1. Is often forgetful in daily activities

   2. Six (or more) of the following symptoms of hyperactivity-impulsivity have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level: Hyperactivity

      18. Often fidgets with hands or feet or squirms in seat

      20. Often leaves seat in classroom or in other situations in which remaining seated is expected

      22. Often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness)

      24. Often has difficulty playing or engaging in leisure activities quietly

      26. Is often “on the go” or often acts as if “driven by a motor”

      28. Often talks excessively

Impulsivity

1. • • 12. Often blurts out answers before questions have been completed

       14. Often has difficulty awaiting turn

       1. Often interrupts or intrudes on others (e.g., butts into conversations or games)

     2. Some hyperactive-impulsive or inattentive symptoms that caused impairment were present before age 7 years.

2. Some impairment from the symptoms is present in two or more settings (e.g., at school [or work] and at home).

3. There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning.

4. The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder and are not better accounted for by another mental disorder (e.g., Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

Code based on type:

• Attention-Deficit/Hyperactivity Disorder, Combined Type: if both Criteria A1 and A2 are met for the past 6 months
• Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: if Criterion A1 is met but Criterion A2 is not met for the past 6 months
• Attention-Deficit/Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type: if Criterion A2 is met but Criterion A1 is not met for the past 6 months

Epidemiology

Attention-deficit hyperactivity disorder (ADHD) is the most common emotional, cognitive, and behavioral disorder treated in youth. It is a major clinical and public health problem because of its associated morbidity and disability in children, adolescents, and adults. Data from cross-sectional, retrospective, and follow-up studies indicate that youth with ADHD are at risk for developing other psychiatric difficulties in childhood, adolescence, and adulthood including delinquency as well as mood, anxiety, and substance-use disorders.

Early definitions, such as the Hyperkinetic Reaction of Childhood in DSM-II, placed the greatest emphasis on motoric hyperactivity and overt impulsivity as hallmarks of the disorder. The DSM-III represented a paradigm shift as it began to emphasize inattention as a significant component of the disorder. DSM-IV now defines three subtypes of ADHD: predominantly inattentive, predominantly hyperactive–impulsive, and a combined subtype. Criteria for each DSM-IV subtype require six or greater of nine symptoms in each respective category. There are four additional criteria that include age of onset by 7 years, ADHD-specific adaptive impairments, pervasiveness, and separation from other existing conditions. The combined subtype is the most commonly represented subgroup accounting for from 50% to 75% of all ADHD individuals, followed by the inattentive subtype (20–30%), and the hyperactive–impulsive subtype (less than 15%).

Epidemiologic studies indicate that ADHD is a prevalent disorder affecting from 4% to 7% of children worldwide including the United States, New Zealand/Australia, Germany, and Brazil. Although previously thought to remit largely in adolescence, a growing literature supports the persistence of the disorder and/or associated impairment into adulthood in a majority of cases.

Prevalence estimates of childhood ADHD in the United States are estimated to be 5–8%. Estimates vary predictably depending on methodology. Definitions that require both symptom dimensions (hyperactivity/impulsivity and inattention) are more restrictive than those that require only one of these dimensions. Thus, estimates based on pre-DSM III definitions or the ICD codes of hyperkinetic disorder produce lower estimates. In addition the surveys that estimate based on symptoms alone and do not include impairment yield higher estimates. As recently by Faraone et al. (2003), other factors that affect apparent prevalence estimates include pervasiveness criteria, informants (teacher, parent, child), use of rating scales versus clinical interviews as well as ascertainment issues. Community samples have higher rates than school samples.

Gender and age of the sample also affect estimates prevalence. Girls more commonly have the inattentive type and also less commonly have accompanying ODD/CD, disruptive disorders, factors leading to lower rates of diagnosis. The original descriptions were derived from a child-focused perspective, and do not reflect what are thought to be more salient aspects of adult ADHD: the executive function disorders of poor organization, poor time management, and memory disturbance associated with academic and occupational failure. The lack of appropriate description of adult symptoms may reduce the true prevalence of ADHD in adulthood.

Etiology

Biological Adversity

Several biologic factors have been proposed as contributors to ADHD, including food additives/diet, lead contamination, cigarette and alcohol exposure, maternal smoking during pregnancy, and low-birth weight. Although the Feingold diet for ADHD was popularized by the media and accepted by many parents, systematic studies showed that this diet was ineffective and that food additives do not cause this disorder. Several investigators have shown that lead contamination can cause symptoms of ADHD. However, lead does not account for the majority of ADHD cases, and many children with high-lead exposure do not develop ADHD. An emerging literature documents that maternal smoking and alcohol exposure during pregnancy, low-birth weight, and psychosocial adversity are additional independent risk factors for ADHD.

Pregnancy and delivery complications (i.e., toxemia, eclampsia, poor maternal health, maternal age, fetal postmaturity, duration of labor, fetal distress, low-birth weight, antepartum hemorrhage) appear to have a predisposition for ADHD. Several studies documented that maternal smoking during pregnancy is an independent risk factor for ADHD.

Psychosocial Adversity

Findings of recent studies stress the importance of adverse family–environment variables as risk factors for ADHD. In particular, chronic family conflict, decreased family cohesion, and exposure to parental psychopathology (particularly maternal) are more common in ADHD families compared with control families. It is important to note that, although many studies provide powerful evidence for the importance of psychosocial adversity in ADHD, such factors tend to emerge as universal predictors of children's adaptive functioning and emotional health, rather than specific predictors of ADHD. As such, they can be conceptualized as nonspecific triggers of an underlying predisposition or as modifiers of the course of illness.

Genetics

Because ADHD is believed to be highly genetic, studies of twins have been used to establish its heritability or the degree to which this disorder is influenced by genetic factors. Based on numerous studies of twins, which varied considerably in methodology and definitions of ADHD, the mean heritability for ADHD was shown to be 77%. Seven candidate genes show statistically significant evidence of association with ADHD on the basis of the pooled odds ratio (1.18–1.46) across studies: DRD4, DRD5, DAT, DBH, 5-HTT, HTR1B, and SNAP-25.

Signs & Symptoms

The diagnosis of ADHD is made by careful clinical history. A child with ADHD is characterized by a considerable degree of inattentiveness, distractibility, impulsivity, and often hyperactivity that is inappropriate for the developmental stage of the child. Other common symptoms include low-frustration tolerance, shifting activities frequently, difficulty organizing, and daydreaming. These symptoms are usually pervasive; however, they may not all occur in all settings. Adults must have childhood-onset, persistent, and current symptoms of ADHD to be diagnosed with the disorder. Adults with ADHD often present with marked inattention, distractibility, organization difficulties and poor efficiency, which culminate in life histories of academic and occupational failure.

Rating Scales

Rating scales are extremely helpful in documenting the individual profile of ADHD symptoms as well as assessing the response to treatments. It is important to emphasize that they should not be used for diagnosis without careful clinical confirmation and elicitation of the other criteria necessary for diagnosis. Although neuropsychological testing is not relied upon to diagnose ADHD it may serve to identify particular weaknesses within ADHD or specific learning disabilities co-occurring with ADHD.

Rating scales are available for all age groups and can be useful in assessing and monitoring home, academic and occupational performance. Increasingly, there has been a congruence of opinion in this area with a number of the most widely used scales consisting of Likert ratings of the existing DSM-IV criteria. There are two types of scales in wide use, the so-called “narrow” scales that are specific for ADHD and “broad” scales that measure additional dimensions including comorbidity. The broad scales are useful for separating straightforward and complex cases, and the narrow scales are most useful for honing in on exclusively ADHD dimensions both diagnosis and to monitor specific responses to treatment. In looking to the future, there are proposals to expand the set of diagnostic symptoms to include executive functions (such as time management and multitasking) especially in older individuals.

Psychological Testing

Psychological testing is not necessary for the routine diagnosis of ADHD and does not readily distinguish children with and without ADHD. Nonetheless, psychometric testing can be valuable in narrowing the differential diagnosis and identifying comorbid learning difficulties. Many children with ADHD have difficulties with abstract reasoning, mental flexibility, planning, and working memory, a collection of skills broadly categorized as executive functioning skills. They can also present with verbal and nonverbal performance skills and/or visual–spatial processing deficits. In such circumstances, neuropsychological assessments can be valuable and may help to clarify the diagnosis. Children with learning, language, visual–motor, or auditory processing problems usually perform poorly only in their particular problem area, whereas children with ADHD may perform poorly in several areas of evaluation.

Nonroutine laboratory studies are not indicated unless the history or physical examination is suggestive of seizures, neurodevelopmental regression, or localizing neurologic signs, or if an acute or chronic medical disorder is suspected.

Neuroimaging

The neurobiology of ADHD is not completely understood, although imbalances in dopaminergic and noradrenergic systems have been implicated in the core symptoms that characterize this disorder. Many brain regions are candidates for impaired functioning in ADHD. Prefrontal hypotheses in ADHD have primarily involved the dorsolateral prefrontal cortex, associated with organizational, planning, working memory, and attentional dysfunctions and Orbital lesions associated with social disinhibition and impulse control disorders.

Structural imaging studies, using computerized tomography or magnetic resonance imaging found evidence of structural brain abnormalities among ADHD patients, with the most common findings being smaller volumes in frontal cortex, cerebellum, and subcortical structures. Castellanos and colleagues found smaller total cerebral brain volumes from childhood through adolescence. This work suggested that genetic or early environmental influences on brain development in ADHD are fixed, nonprogressive, and unrelated to stimulant treatment. Numerous fMRI studies have reported Dorsal Anterior Cingulate Cortex (dACC) hypofunction in ADHD on tasks of inhibitory control

Brain imaging studies fit well with the concept that dysfunction in fronto-subcortical pathways occurs in ADHD. Three subcortical structures implicated by the imaging studies (i.e., caudate, putamen, and globus pallidus) are part of the neural circuitry underlying motor control, executive functions, inhibition of behavior, and the modulation of reward pathways. These frontal–striatal–pallidal–thalamic circuits provide feedback to the cortex for the regulation of behavior.

The fronto-subcortical systems pathways associated with ADHD are rich in catecholamines, which are involved in the mechanism of action of stimulant medications used to treat this disorder. A plausible model for the effects of medications in ADHD suggests that, through dopaminergic and/or noradrenergic pathways, these agents increase the inhibitory influences of frontal cortical activity on subcortical structures.

Imaging studies also implicate the cerebellum and corpus callosum in the pathophysiology of ADHD. The cerebellum contributes significantly to cognitive functioning, presumably through cerebellar–cortical pathways involving the pons and thalamus. The corpus callosum connects homotypic regions of the two cerebral hemispheres. Size variations in the callosum and volume differences in number of cortical neurons may degrade communication between the hemispheres, which may account for some of the cognitive and behavioral symptoms of ADHD.

Samples ascertained before the publication of DSM-III relied on earlier definitions that highlighted hyperactivity as a hallmark of ADHD. Since it is hyperactivity that wanes earliest, it may be that older samples were enriched with subjects more likely to remit from ADHD than individuals identified today. There is evidence for this hypothesis in the data. In a recent analysis, the persistence rate was lowest in studies ascertained according to DSM-II ADD and highest in those studies ascertained according to DSM-III-R ADHD. The available data also suggests a continuation of childhood behavior problems and emerging antisocial behavior among many in this group of children. For example, researchers have noted the rate of conduct disorders among children with ADHD to range between 25% and 50% at follow-up during adolescence. Reports also suggest that a majority of children with ADHD continue to exhibit deficits in attention and/or activity level in adulthood, with only about 30% of children evidencing a remission of symptoms by adolescence and early adulthood. Recent work also suggests that ADHD youth disproportionately become involved with cigarettes, alcohol, and then drugs. Individuals with ADHD, independent of comorbidity, tend to maintain their addiction longer compared to their non-ADHD peers.

Oppositional Defiant Disorder and Conduct Disorder

There are important nosologic distinctions between attention and hyperactivity per se and that of associated symptoms common to the disruptive behavioral disorder category. Oppositional defiant disorder (ODD) is characterized by a pattern of negativistic, hostile and defiant behavior. ADHD and ODD/CD have been found to co-occur in 30–50% of cases in both epidemiologic and clinical samples. In contrast, conduct disorder (CD) is a more severe, and less common, disorder of habitual rule breaking defined by a pattern of aggression, destruction, lying, stealing, or truancy. While CD is a strong predictor of substance abuse, ODD without CD is not.

Mood Disorders

Unipolar depression in a child may be apparent from a sad or irritable mood, a persistent loss of interest, or pleasure in the child's favorite activities. Other signs and symptoms include physiologic disturbances such as in changes in appetite and weight, abnormal sleep patterns, psychomotor abnormalities, fatigue, and diminished ability to think, as well as feelings of worthlessness or guilt and suicidal preoccupation.

Classical mania in adults is characterized by euphoria, elation, grandiosity, and increased energy. However, in many adults and most children, mania is more commonly manifested by extreme irritability or explosive mood with associated poor psychosocial functioning that is often devastating to the patient and family. In milder conditions, additional symptoms include unmodulated high energy such as a decreased sleep, over talkativeness, racing thoughts, or increased goal-directed activity (social, work, school, sexual) or an associated manifestation of markedly poor judgment such as thrill-seeking or reckless activities.

In epidemiologic studies and several controlled, prospective studies, higher rates of depression were found in ADHD. A baseline diagnosis of major depression predicted lower psychosocial functioning, a higher rate of hospitalization as well as impairments in interpersonal and family functioning. Similarly, higher rates of mania were detected in follow-up studies. ADHD children with comorbid mania at either baseline or follow-up assessment had other correlates expected in mania including additional psychopathology, psychiatric hospitalization, severely impaired psychosocial functioning as well as a greater family history of mood disorders.

Childhood Anxiety Disorders

Childhood anxiety disorders are often not suspected in an overactive child, just as ADHD is often not assessed in inhibited children. When present, both contribute to social, behavioral, and academic dysfunction. In addition anxiety may be associated with intense intrapsychic suffering. Thus, having both ADHD and anxiety disorders may substantially worsen the outcome of children with both disorders. In the MGH follow-up study, ADHD children with comorbid anxiety disorder had increased psychiatric treatment, more impaired psychosocial functioning as well as a greater family history of anxiety disorders.

Cognitive Performance and Learning Disabilities

Children with ADHD perform more poorly than controls on standard measures of intelligence and achievement. In addition, children with ADHD perform more poorly in school than do controls, as evidenced by more grade repetitions, poorer grades in academic subjects, more placements in special classes, and more tutoring. The reported degree of overlap varies by definition, the more restrictive definition has a rate of 20–25%.

ADHD Plus Tics

Children with ADHD have higher rates of Tic disorders that may contribute additional dysfunction due to distractions and social impairments directly attributable to the movements or vocalizations themselves. A number of studies have noted that anti-ADHD treatment is highly effective for ADHD behaviors, aggression, and social skill deficits in children with TS or chronic tics.

Substance-Use Disorders

Combined data from retrospective accounts of adults and prospective observations of youth indicates that juveniles with ADHD are at increased risk for cigarette smoking and substance abuse during adolescence.

The ADHD adolescent and young adult is at risk for school failure, emotional difficulties, poor peer relationships, and trouble with the law. Factors identifiable in younger youth that predict the persistence of ADHD into adulthood include familiality with ADHD and psychiatric comorbidity—particularly aggression or delinquency problems. Although the literature provides compelling evidence that the diagnosis of ADHD in childhood predicts persistent ADHD and poor outcome in adolescence, these findings also suggest that such a comprised outcome is not shared by all ADHD children. The discussion thus far has not addressed a related clinical question: Can the functioning of ADHD children normalize in the context of persistent ADHD? We analyzed data from a 4-year longitudinal study of referred children and adolescents with ADHD, to assess normalization of functioning and its predictors among boys with persistent ADHD.

Using indices of emotional, educational, and social adjustment, we found that 20% of children with persistent ADHD functioned poorly at follow-up in all three domains, 20% did well in all three domains, and 60% had intermediate outcomes. These findings suggested that the syndromatic persistence of ADHD is not associated with a uniform functional outcome but leads instead to a wide range of emotional, educational, and social adjustment outcomes that can be partially predicted by exposure to maternal psychopathology, larger family size, psychiatric comorbidity, and impulsive symptoms.

Psychopharmacologic Interventions

Medications remain a mainstay of treatment for children, adolescents, and adults with ADHD. In fact, recent multisite studies support that medication management of ADHD is the most important variable in outcome in context to multimodal treatment. For example, in a large prospective and randomized long-term trial of ADHD youth, those receiving stimulants alone were observed to have similar improvement in core ADHD symptoms at 14 months follow-up compared to those randomized to receive stimulants plus psychotherapy. Of interest, both medicated groups had a better overall outcome than those receiving extensive psychotherapy without stimulants. The stimulants, specific norepinephrine reuptake inhibitors (SNRIs), certain antidepressants, and certain antihypertensives comprise the available agents for ADHD. Stimulants, SNRIs, and antidepressants have been demonstrated to have similar pharmacological responsivity across the lifespan including school-aged children, adolescents, and adult groups with ADHD.

Stimulants

The stimulants are the most commonly prescribed agents for pediatric and adult groups with ADHD. The most commonly used compounds in this class include methylphenidate (Ritalin, Concerta, Metadate, Focalin, and others) and amphetamine (Dexedrine, Adderall). Stimulants are sympathomimetic drugs, which increase intrasynaptic catecholamines (mainly dopamine) by inhibiting the presynaptic reuptake mechanism and releasing presynaptic catecholamines. Whereas methylphenidate specifically blocks the dopamine transporter protein, amphetamines also release dopamine stores and cytoplasmic dopamine directly into the synaptic cleft. Recent data suggests that acute tolerance to stimulants may develop rapidly necessitating an ascending- or pulsing-pharmacokinetic profiles for ADHD efficacy.

Methylphenidate and d-amphetamine are both short-acting compounds, with an onset of action within 30–60 minutes and a peak clinical effect usually seen between 1 and 2 hours after administration lasting 2–5 hours. The amphetamine compounds (Adderall) and sustained release preparations of methylphenidate and dextroamphetamine are intermediate-acting compounds with an onset of action within 60 minutes and duration of 6–8 hours.

Given the need to additionally treat ADHD outside of academic settings (i.e., social, homework) and to reduce the need for in school dosing and likelihood for diversion, there has been great interest in extended release preparations of the stimulants. Extended release preparations greatly reduce untoward peak adverse effects of stimulants such as headaches and moodiness, as well as essentially eliminating afternoon wear off and rebound.

A new generation of highly sophisticated, well-developed, safe and effective long-acting preparations of stimulant drugs has reached the market and revolutionized the treatment of ADHD. These compounds employ novel delivery systems to overcome acute tolerance termed “tachyphylaxis.” There are several long-acting methylphenidate formulations and a long-acting methylphenidate formulation. While Concerta is a 12-hour formulation, Metadate-CD and Ritalin LA are 8-hour methylphenidate formulations. In addition Adderall XR is a 12-hour amphetamine formulations. Methylphenidate as a secondary amine gives rise to four optical isomers: d-threo, l-threo, d-erythro, and l-erythro. Recently the active stereoisomer, d-threo-methylphenidate compound has been available in an immediate release and long-acting form as Focalin and Focalin XR.

Stimulants appear to work in all age groups of individuals with ADHD. Studies in preschoolers report improvement in ADHD symptoms, structured tasks as well as mother–child interactions; however, there may be a higher side effect burden compared to other age groups. Similarly, in adolescents response has been reported as moderate to robust, with no abuse or tolerance noted. In addition, stimulant treatment has been found to be effective in adults with ADHD.

Predictable short-term adverse effects include reduced appetite, insomnia, edginess, and GI upset. In adults, elevated vital signs may emerge necessitating baseline and on-drug monitoring. There are a number of controversial issues related to chronic stimulant use. Although stimulants may produce anorexia and weight loss, their effect on ultimate height remains less certain. While initial reports suggested that there was a persistent stimulant-associated decrease in growth in height in children, other reports have failed to substantiate this finding, and still others question the possibility that growth deficits may represent maturational delays related to ADHD itself rather than to stimulant treatment. Stimulants may precipitate or exacerbate tic symptoms in ADHD children. Recent work suggests that the majority of ADHD youth with tics can tolerate stimulant medications; however, up to one third of children with tics may have worsening of their tics with stimulant exposure. Current consensus suggests that stimulants can be used in youth with comorbid ADHD plus tics with careful monitoring for stimulant-induced tic exacerbation.

Despite case reports of stimulant misuse, there is a paucity of scientific data supporting that stimulant-treated ADHD individuals abuse their medication; however, data suggests that diversion of stimulants to non-ADHD youth continues to be a concern. Families should closely monitor stimulant medication and college students receiving stimulants should be advised to carefully store their medication. Despite the findings on efficacy of the stimulants, studies have also reported consistently that typically one third of ADHD individuals do not respond or cannot tolerate this class of agents.

Specific Norepinephrine Reuptake Inhibitors (Atomoxetine)

Atomoxetine (Strattera) is one of a new class of compounds, known as SNRIs. Currently atomoxetine is the only nonstimulant that is FDA approved for ADHD. Atomoxetine may be particularly useful in stimulant failures, or when oppositionality, anxiety, or tics co-occur within ADHD. After extensive testing, atomoxetine has been found to be generally safe and well tolerated. However, there have been rare (2 out of 3 million patients) reports of liver injury.

Antidepressants

A subgroup of antidepressants are second-line drugs of choice for ADHD. The tricyclic antidepressants (TCAs) as well as bupropion (Wellbutrin) block the reuptake of neurotransmitters including norepinephrine. In contrast, the serotonin reuptake inhibitors are not useful for ADHD. The TCAs are effective in controlling abnormal behaviors and improving cognitive impairments associated with ADHD, but less so than the majority of stimulants. As minor increases in heart rate and the ECG intervals are predictable with TCAs, ECG monitoring at baseline and at therapeutic dose is suggested, but not mandatory.

Antihypertensives

The antihypertensives clonidine (Catapress) and guanfacine (Tenex) are alpha-adrenergic agonists, which have been primarily used in the treatment of hypertension. These compounds have been shown to be useful in the treatment of ADHD. Guanfacine is longer acting and less sedating than clonidine. The antihypertensives have been used for the treatment of ADHD as well as associated tics, aggression, and sleep disturbances, particularly in younger children.

Modafinil

Modafinil is an antinarcoleptic agent, which is structurally and pharmacologically different than other agents approved to treat ADHD. Testing in children has reported effectiveness in ADHD. While generally safe and well-tolerated there has been concerns about uncommon occurrences of a severe rash possibly related to Stevens Johnson syndrome.

Psychotherapeutic Interventions

The largest-scale study examining the relative and combined effectiveness of medical and nonmedical interventions for ADHD is the NIMH Multimodal Treatment Study for ADHD Study (MTA). In this 5-year, 6-site project, 579 elementary-age children with ADHD were randomly assigned to one of four 14-month treatment conditions: behavioral treatment, medication management (mostly methylphenidate), combined behavioral treatment and medication management, and a community comparison group. Children in the Behavioral Treatment arm received a very intensive combination of treatments, including school consultation, a classroom aide, an 8-week summer treatment program, and 35 sessions of parent management training. Findings from the MTA study at 14 months indicate that medical intervention was significantly more effective than behavioral and community treatments; that behavioral treatment only modestly enhanced the effect of medication alone; and that behavioral treatment alone was no more effective than the treatment received by children in the community comparison group on core symptoms of ADHD.

If adult ADHD is a clinically significant disorder, then ADHD adults should show functional impairments in multiple domains. Several studies suggest this to be true. These studies have shown that ADHD adults had lower socioeconomic status, more work difficulties, and more frequent job changes. The ADHD adults had fewer years of education and lower rates of professional employment. Similarly, others have shown that among patients with substance-use disorders, ADHD predicts social maladjustment, immaturity, fewer social assets, lower occupational achievement, and high rates of separation and divorce.

ADHD is a prevalent worldwide, heterogeneous disorder that frequently persists into adult years. The disorder is associated with significant impairment in occupational, academic, social, and intrapersonal domains necessitating treatment. Converging data strongly support a neurobiological and genetic basis for ADHD with catecholaminergic dysfunction as a central finding. While psychosocial interventions such as educational remediation and cognitive–behavioral approaches should be considered in the management of ADHD, an extensive literature supports the effectiveness of pharmacotherapy not only for the core behavioral symptoms of ADHD but also improvement in linked impairments including cognition, social skills, and family function.