Attention-deficit/hyperactivity disorder (ADHD) is one of the most frequently encountered disorders in pediatric and adolescent medical practice. ADHD is a complex developmental disorder of brain and behavior that makes its initial appearance in preschool ages, persists into adolescence, and, in some individuals, into adult life.1 In 2007, the CDC summary of health statistics for U.S. children indicated that 4.5 million children (7%) between the ages of 3 and 17 years had been diagnosed with ADHD. The rate for boys (11%) was twice the rate for girls (4%).2 While the degree of persistence of this disorder into adulthood is still unclear, estimates from longitudinal studies suggest between 1% and 6% of the adult population has symptoms of ADHD.3
Historically, symptoms of impulsivity, hyperactivity, and inattention were first attributed by Still (1902) to neurological disorder. Therefore, early clinical diagnosis were based upon presumptive “organic” etiological factors such as brain trauma, encephalitis, or other brain conditions that resulted in problems of attention, impulse control, emotional disregulation, and cognition. Gradually, however, the clinical diagnostic emphasis shifted to what Shelton4 labeled “symptom-based” description of the disorder, which preceded current classification systems such as the American Psychiatric Association’s DSM-IV. In 2000, the empirically updated DSM-IV-TR5 was published and provides the current diagnostic criteria and ICD-9 codes for several subtypes of ADHD. These include (1) Attention-Deficit/Hyperactivity Disorder, Combined Type (314.01); (2) Attention-Deficit/ Hyperactivity Disorder, Predominantly Inattentive Type (314.00); (3) Attention-Deficit/Hyperactivity Disorder, Predominantly Hyperactive–Impulsive Type (314.01); and (4) Attention-Deficit/Hyperactivity Disorder, Not Otherwise Specified (314.9). While the first three subtypes are differentiated from each other on the basis of predominant clinical presentation, the fourth subtype is reserved for those patients who, despite the presence of prominent symptoms of inattention or hyperactivity– impulsivity, do not meet full diagnostic criteria for a specific ADHD subtype. Similarly, for adolescents and/or adults who currently have symptoms but no longer meet full criteria, the label “In Partial Remission” would be added to the diagnostic code (eg, 314.01—In Partial Remission). Table 9-1 presents the common signs and symptoms described for diagnostic purposes under the three primary domains of inattention, hyperactivity, and impulsivity.
| Domain: Inattention |
| 1. Poor attention to details or makes careless mistakes inacademic or employment activities |
| 2. Problems in sustained attention |
| 3. Seems not to listen when spoken to |
| 4. Poor follow-through on instructions, tasks, or duties inacademic settings, work, or play |
| 5. Difficulty organizing activities |
| 6. Often avoids tasks requiring sustained concentration or effort |
| 7. Often loses things that are needed |
| 8. Often easily distracted by external stimuli |
| 9. Often forgetful in daily activities |
| Domain: Hyperactivity |
| 1. Often fidgets or squirms in seat |
| 2. Often out-of-seat in classroom or other situations |
| 3. Often runs about or climbs excessively in situations where it is inappropriate |
| 4. Often has difficulty playing or engaging in leisure activities quickly |
| 5. Is often “on the go” or often acts as if “driven by a motor” |
| 6. Often talks excessively |
| Domain: Impulsivity |
| 1. Often blurts out answers before questions have been completed |
| 2. Often has difficulty awaiting turn |
| 3. Often interrupts or intrudes on others |
| Diagnosis Requires: |
| 1. Onset before age 7 years |
| 2. Impairment from symptoms in two or more settings (eg, school, home, work) |
| 3. Clinically significant impairment in social, academic, or occupational functioning |
| 4. Symptoms do not occur exclusively in the course of other psychiatric, mental, or developmental disorder |
Six or more of the symptoms of inattention and six or more of the symptoms of hyperactivity– impulsivity must be present.
Symptoms must have been present for 6 or more months prior to diagnosis.
Some symptoms that have caused impairment must be present before age 7 years.
Symptoms causing some impairment must be present in two or more settings.
There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning.
These symptoms do not occur exclusively during the course of another disorder, such as pervasive developmental disorder and are not better accounted for by another disorder.
There has been considerable controversy about the current diagnostic criteria,6 primarily focused on the age differences in presentation, gender differences in diagnosis, longitudinal course,7,8 and impact of comorbid behavioral, emotional, and cognitive disorders accompanying ADHD.9 What is not controversial is the need for careful, systematic diagnostic approaches to this very complex developmental disorder, and for continued refinement in our understanding of the disorder and its treatment.
A number of different causes of the brain dysfunctions that result in ADHD have been examined in the search for the etiology of this disorder. Among these are (1) differences in brain morphology and development, (2) differences in neurotransmitter activity, (3) differences in neuroelectrophysiology, (4) differences in genetics, and (5) interactions of genetic risk and environmental factors. Structural differences in the brains of children and adults with ADHD compared to normal control have included anterior and posterior regions of the corpus callosum, basal ganglia and related frontal-striatal structures, caudate nucleus, and prefrontal versus occipital volumes.10,11 Whether smaller volumes in these anatomic sites for ADHD result in the symptoms assumes that smaller size equates to less functional capabilities. However, there appears to be some support for the importance of prefrontal-striatal systems in development of behavioral response inhibition. More recently, longitudinal imaging studies have also supported the role of delayed maturation of superior and dorsolateral prefrontal cortex and in the middle and superior temporal cortex in children diagnosed with ADHD.12
Studies have employed functional neuroimaging techniques in order to assess for differences in brain activity in selected structures of the brains of children and adults with ADHD. Studies of dorsolateral prefrontal cortex and ventrolateral prefrontal cortex, dorsal anterior cingulate cortex, and striatum predominate because these anatomic areas have been implicated in functions such as vigilance, selective and divided attention behavioral inhibition, and aspects of executive functioning including planning, response selection, and response initiation. Support for hypofunction in dorsal anterior and posterior cingulate cortex has been demonstrated in a number of recent FMRI studies.13 Earlier PET and SPECT studies of ADHD subjects, although methodologically flawed due to lack of control groups, found increased regional cerebral blood flow in dorsolateral prefrontal cortex, caudate, and thalamus when methylphenidate was administered.13
Neuroelectrophysiological studies utilizing quantitative EEG (QEEG) and event-related potentials (ERPs), while problematic compared to MRI in terms of spatial resolution, have also been utilized to study brain functioning in ADHD subjects compared to controls. Results, however, have not yet enabled these two methodologies to explicitly address the specific anatomic substrates involved in the problems of inattention, impulsivity, and executive control functions in ADHD subjects. Genetic studies have focused upon the familial pedigree of individuals diagnosed with ADHD. Current views suggest that ADHD results from polygenetic rather than a single gene mode of inheritance with approximately 70% to 95% variance in symptoms. Concordance rates for identical twins are considerably higher compared to concordance rates in fraternal twins (70%-80% vs. 30%-40%). Specific dopamine receptor genes identified include DRD2 and DRD5, the dopamine transport gene DAT1, and potentially defective alleles of the dopamine beta hydroxylase enzyme (DBH) that is important in the dopamine-to-norepinepherine conversion.14 Recently, a large-scale assessment of 51 candidate genes in pathways related to dopamine, norepinepherine, and serotonin supported earlier reports of the role of DRD4 and DAT genes in the ADHD phenotype as well as 16 other potential genes, lending further support for the polygenetic model of ADHD.
A final group of studies have focused upon environmental factors, genetic profiles, and specific subtypes of ADHD. Previously, a number of acquired risk factors for the development of ADHD have been identified. These include pregnancy and birth complications, low birth weight, traumatic brain injury, prenatal substance exposure, and lead exposure. However, these factors likely carry less influence in the likelihood of developing ADHD, or at least are responsible for fewer cases, than genetic factors. Recently, Swanson and associates15 presented a potential model that addresses gene–environment interactions that may affect fetal adaptations in development of dopamine neurons and contribute to development of different subtypes of ADHD. The authors critically review the research literature that provides support for the dopamine deficit theory underlying ADHD, and suggests future studies, in particular those needed to address the emergence of the ADHD phenotype over time.
The clinical presentation of ADHD varies by age. Children from age 3 years through the adolescent years and even adults can present with symptoms of overactivity, inattention, and impulsivity. Parents of children 7 years or younger may report the presence of overactivity, impulsivity leading to sometimes risky behavior, sleep disorders (eg, difficulty falling asleep, disruptive sleep, and early morning awakening), short attention spans, and inability to sustain focused attention. Some of these behavioral problems may have been noticed in the preschool years but emerged as clearly problematic upon entry to prekindergarten or kindergarten classes. Once in the school environment, teacher reports are also included in the presentation. Typical teacher reports focus on problems such as failure to follow classroom rules, frequent out-of-seat behavior, difficulty completing assigned work, interrupting others, easily distracted, distracting other students trying to do classroom activities, failure to turn in assignments, and less frequently, aggression towards other students or arguing with others.
During the primary grades, problems in academic functioning and achievement may lead to questions regarding a learning disability in reading, mathematics, or spelling/writing. While research has suggested that both boys and girls may exhibit some or all of these behavioral problems, a subset of children (more commonly girls than boys) present with parental and school complaints of failure to complete assigned school work, inattentive (sometimes “spacey”) behaviors, slowness in initiating or completing assignments, and disorderly school papers and work habits.
In general, most research has reported that primary symptoms of hyperactivity may diminish during adolescence and into adult years. However, continuing problems in short attention span, difficulties with sustained attention and distractibility, inattention to detail, problems meeting deadlines, and excessive daydreaming have been reported. For some adolescents and adults, impulsivity remains a problem that can lead to poor decision making and risk-taking behaviors. Employment and/or educational/vocational underachievement may lead to depressive and anxiety complaints. Higher rates of alcohol and substance abuse, marital discord, and legal problems have been described in some longitudinal studies of childhood ADHD.16,17
In 2007, the American Academy of Child and Adolescent Psychiatry issued practice parameters for the assessment and treatment of children, adolescents, and adults with attention-deficit/hyperactivity disorder.18 The report was an update of an earlier set of guidelines published in 1997 and complements the guideline issued by the American Academy of Pediatrics in 2000.19 The following recommendations were made:
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