Attention-Deficit/Hyperactivity Disorder
Dorothy E. Stubbe MD
Introduction
Attention-deficit/hyperactivity disorder (ADHD) is the single most commonly diagnosed psychiatric disorder of childhood, with an estimated prevalence rate of 4% to 12% of youths in the United States. ADHD is characterized by developmentally inappropriate levels of hyperactivity, inattention, impulsivity, and other deficits of executive function. ADHD is often comorbid with other psychiatric disorders, both externalizing and internalizing, as well as bipolar disorder and learning disabilities. These children frequently experience peer rejection and engage in a broad array of impulsive and disruptive behaviors with subsequent consequences on self-esteem and adaptive coping. This disorder is a major public health problem with enormous negative impact on the child, the family, schools, and society. Billions of dollars are spent annually for school services, mental health services, and increased use of the juvenile justice system for children and adolescents suffering from ADHD. In contrast with historical notions, children do not typically “outgrow” ADHD. Morbidity and disability often persist into adult life.
Background
The conceptualization and diagnostic terminology related to ADHD have changed over the years. Historically, three views of the disorder have dominated: (1) behavioral (e.g., hyperactivity), (2) etiologic (e.g., minimal brain dysfunction), and (3) cognitive (e.g., attention deficit disorder). These changes in conceptualization have led to alterations in diagnostic criteria, research design, prevalence rates, and interventions.
Although initially described in 1902 as “morbid defects of moral control,” the thinking about ADHD as an organic disorder occurred around the time of World War I following the influenza pandemic which left many survivors with high levels of overactivity, impulsivity, and behavioral difficulties. The title “minimal brain dysfunction” was accepted in the 1950s. The next iteration in diagnosis occurred in 1968 with the second edition of the Diagnostic and Statistical Manual of Mental Disorders, 2nd Edition (DSM-II) and the corresponding International Classification of Diseases, 9th Revision (ICD-9) as “hyperkinetic syndrome of childhood.” This disorder remains in the ICD-10 (used clinically in Europe and for billing
coding in the United States) and includes children with pervasive overactivity and inattention, but excludes children with co-occurring conduct difficulties. The DSM criteria used in the United States include children with co-occurring conduct difficulties, thus consisting of a larger population of children.
coding in the United States) and includes children with pervasive overactivity and inattention, but excludes children with co-occurring conduct difficulties. The DSM criteria used in the United States include children with co-occurring conduct difficulties, thus consisting of a larger population of children.
A conceptual shift occurred in the late 1970s in which the disorder was coined “attentiondeficit disorder,” and the core deficiency was postulated to be a failure to regulate attention, arousal, and inhibitory control. The present conceptualization in the fourth edition of the DSM (DSM-IV) published in 1994 consists of three subtypes: predominant symptoms of inattention (ADHD-IA), predominant symptoms of hyperactivity with impulsivity (ADHD-HI), and the combination of the two (ADHD-Combined).
Clinical Features and Differential Diagnosis
ADHD is clinically diagnosed by functional deficits in attention and/or hyperactivity and impulsivity and is most noticeable in the classroom setting. By epidemiological estimates, a classroom with 25 students would be expected to have between 1 and 3 students suffering from functionally impairing ADHD. If there are three ADHD children, the following scenario may be expected: Ms. Jones, the teacher, is discussing the states in New England in the third-grade class. The children have their books open to a map of New England. She asks a question, and Paul’s hand shoots up, he leaps up from his seat in enthusiasm, in the process tipping the desk and causing his pencil and book to fall to the ground. When called on, he looks perplexed and is not able to answer the question. Sam, who is sitting in the back of the class, laughs at Paul and shouts out, “Clutz!” The teacher, in exasperation, calls on Tasha, who is gazing out the window, her book opened to the wrong page. “What was the question?” Tasha asks, coming out of her dreamy state.
As this brief vignette illustrates, children with ADHD may struggle in multiple ways within a classroom. Elementary students most frequently present with ADHD-Combined, which includes functionally interfering symptoms of both inattention and hyperactivity with impulsivity. In the vignette, one might postulate that both Paul and Sam are suffering from this disorder. Tasha, on the other hand, demonstrates symptoms more consistent with ADHD-IA.
Inattention may be thought of as a combination of difficulties with selective attention (difficulties attending to the task at hand), and difficulties with sustained attention and problem solving (distractibility and difficulties considering options). Children with ADHD-IA are often diagnosed at an older age as behavioral difficulties tend to be infrequent and these children are not noted by teachers as disruptive. However, severe underachievement in academic functioning may bring these children to educators’ attention. Parents may be frustrated as distractibility leads to difficulty with organization, and “taking forever” to get ready for school.
ADHD must be differentiated from age-appropriate overactivity and other disorders. For preschool children, this may be difficult. ADHD is most notable in group situations for children who are attending a preschool or a daycare program. These youngsters are usually overly active, but also struggle with “circle-time,” and have a great difficulty sharing, playing cooperatively, and inhibiting impulses. Early diagnosis is helpful in addressing safety, monitoring, teaching parents techniques to help their children, and teaching the children methods to control impulses.
The differential diagnosis for ADHD is extensive. Many medications or other substances may cause overactivity or activation, such as the commonly used bronchodilators to treat asthma. Additionally, other medical disorders such as hearing or vision impairment, seizure disorder, genetic abnormalities, thyroid disorders, and sleep disorders may present with ADHD-type symptoms. Traumatized children and those who have experienced severe psychosocial adversity may be anxious and inattentive. Depressed youths may complain of problems concentrating. Bipolar disorder, manic phase, may mimic the hyperactivity and impulsivity of ADHD. Additionally, any of these disorders and learning difficulties may be comorbid with ADHD, further complicating the clinical diagnosis.
TABLE 4-1 Diagnostic Symptoms of Attention-Deficit/Hyperactivity Disorder | |
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The onset of ADHD impairment must be in early childhood, at least before the age of 7 years, even if it was not diagnosed until later in life. There must be functional impairment in a variety of life settings (home, school, work, etc.). ADHD should not be diagnosed if it presents only concomitantly with a pervasive developmental disorder or a psychotic disorder. Table 4-1 gives diagnostic features and Table 4-2 a comprehensive differential diagnosis for ADHD.
Comorbidity
Individuals with ADHD are at increased risk of suffering from other psychiatric disorders. It is important to diagnose comorbid disorders, as the ADHD child with a comorbid condition may have a different clinical presentation, life course, and response to treatment. The most common disorders comorbid with ADHD are other disruptive behavior disorders and learning disorders, although anxiety disorders and mood disorders (bipolar disorders and major depressive disorders) frequently cooccur. Neurological soft signs (e.g., coordination difficulties and immature reflexes) are also common. Tourette syndrome and other tic disorders frequently present with concomitant ADHD.
It is estimated that 50% of children with ADHD meet criteria for either oppositional defiant disorder (ODD) or conduct disorder (CD). ADHD comorbid with conduct difficulties confers an increase in impairment and risk. In one study, ADHD boys without delinquency were no different from controls on neuropsychological measures, whereas the ADHD delinquents were impaired in the areas of verbal skill, visual motor integration, and visuospatial skills. Additionally, children with ADHD and CD have a much stronger family history of antisocial behavior. Interestingly, there is some evidence that a positive response of ADHD symptoms to stimulant medication may also lead to a decrease in antisocial behaviors.
Learning disabilities are common in children suffering from ADHD—an estimated 20% to 50% suffer from reading, spelling, or arithmetic learning disorders. Both ADHD and reading disorders have strong genetic components but seem to be inherited independently. Children with learning disability alone do not respond to stimulant medications, but children with comorbid ADHD and reading disability show an increase in reading achievement scores when there inattentiveness is successfully controlled with medication.
TABLE 4-2 Differential Diagnosis for Attention-Deficit/Hyperactivity Disorder | ||||||
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Approximately 25% to 30% of children diagnosed with ADHD will meet criteria for an anxiety disorder compared to 5% to 15% of the general population. Children with ADHD and comorbid anxiety report anxiety symptoms that their parents may not have appreciated, as internalizing symptoms may be less overtly noticeable to others especially in the presence of disruptive hyperactive and impulsive behaviors. ADHD-anxious children also tend to report more social difficulties. Factors associated with comorbid ADHD and anxiety include problems during the pregnancy, developmental delays, and stressful life events. Genetic studies suggest that anxiety and ADHD are inherited independently of each other. Major depressive disorder is another internalizing disorder that is diagnosed in some ADHD children, although the prevalence is unknown. Its course is independent of ADHD symptoms.
The prevalence of comorbid bipolar disorder is an area of much controversy. First, the clinician must differentiate the two disorders and then determine whether they are comorbid. Children with comorbid mania demonstrate more grandiosity, elated or irritable mood, racing thoughts, and hypersexuality than children suffering from ADHD alone. These children tend to respond better to mood stabilizers, with or without stimulants, than stimulant medications alone. This issue is complicated and suspicion of bipolar disorder warrants referral to child psychiatry.
Epidemiology
The changing diagnostic criteria over time, different diagnostic schemes used worldwide, and the complex task of integrating diagnostic information from multiple sources complicate epidemiological studies of ADHD. However, based on DSM-IV criteria, prevalence rates seem to be consistent globally, suggesting that ADHD affects 4% to 12% of children worldwide. The male-to-female ratio is about 3:1 in community samples, but as high as 9:1 in the mental health clinical population, most likely due to the higher proportion of disruptive behaviors in ADHD boys which promotes referral for treatment. For the inattentive type of ADHD, the ratio of boys to girls is about equal. Boys tend to demonstrate more hyperactive, impulsive, and other disruptive behaviors, while girls present with more inattention and comorbid anxiety and depression. According the to the American Academy of Child and Adolescent Psychiatry (AACAP), a higher prevalence of ADHD is found in individuals with younger age, lower socioeconomic status, and male gender.
Preschool children are increasingly diagnosed with ADHD. Prevalence has been estimated at 2% to 5% in primary care settings. In a 2008 study by Ghuman and colleagues, up to 59% of preschool children presenting to child guidance clinics met criteria for ADHD, indicating how distressing these symptoms can be even at very young ages. The hyperactive-impulsive type of ADHD is most commonly diagnosed. In general, symptoms related to hyperactivity decline as the child matures. In school-aged children, ADHD-Combined is most commonly diagnosed, while ADHD-IA is increasingly diagnosed in middle school and high school. It is estimated that clinically significant symptoms of ADHD persist into adulthood for about 60% of individuals.
Etiology, Risk, and Resilience Factors
Neurochemistry
Available research suggests that ADHD is a complex disorder resulting from the combined effects of several genes in interactions with the environment. Stahl describes ADHD as primarily a disorder of prefrontal cortex functioning, along with associated interconnections, projections, and circuits to selected parts of the brain regulating attention and motor functioning. Chemically, signals mediated by the neurotransmitters norepinephrine (NE) and dopamine (DA) are thought to be weak in the prefrontal cortex. This is consistent with the idea that the arousal system is deficient and that tonic NE and DA firing rates are too low. Selective attention is hypothesized to be mediated primarily by the anterior cingulate cortex (ACC). Disruptions or inefficient processing by the ACC is related to ADHD or other disorders with impaired ability to attend. Impairments in executive functioning have been postulated by Brown and others to comprise a primary deficit in ADHD. Developmental difficulties with activation, focus, sustained effort, planning and organization, emotion regulation, working memory and behavior regulation are all subsumed under the construct of impairments in executive functioning. Neuropsychological tests have consistently identified deficits in the executive functions of individuals diagnosed with ADHD. Executive functions are thought to involve neural networks that encompass the dorsolateral prefrontal cortex (DLPFC), with connections to the thalamus and basal ganglia. Hyperactive symptoms in ADHD are linked to the prefrontal motor cortex, while impulsive symptoms are thought to be related to the orbital frontal cortex. Barkley postulates that the primary deficit in ADHD-Combined is behavioral disinhibition, which underlies deficits in working memory, self-regulation of affect, motivation, arousal, the capacity for reasoning and reflection, and goal-directed behavior. The cortico-striatal-thalamic-cortical (CSTC) loops are hypothesized to regulate the complex aspects of attention and activity. Inefficiencies anywhere along this loop may cause symptoms of ADHD, and individual patients may vary in symptoms, severity, and type depending upon the unique pattern of neurocircuitry disruption.
NE and DA are intricately involved in modulating prefrontal cortical functioning and are a major focus of treatment. Stimulants approved to treat ADHD include various preparations of methylphenidate and amphetamine, and both are considered to boost NE and DA signals in a number of different ways. It is evident that moderate amounts of these neurotransmitters are essential to prefrontal cortical functioning, and deficits, particularly in the prefrontal cortex, lead to attentional deficiencies. By contrast, very high levels of NE and DA (as found in extreme stress) may impair optimal functioning. Indeed, substance abuse and anxiety disorders are correlated with excess neurotransmission of DA and NE in the prefrontal cortex.
Early neurodevelopmental problems such as obstetrical complications, prematurity, other genetic abnormalities (such as fragile X disorder and others), and exposure in utero to alcohol, cocaine, or other toxins may predispose to ADHD. It is postulated that fetal insults, particularly during the second trimester during the height of neural development, may cause subtle functional abnormalities to the frontal cortex and other brain structures, resulting in the disorder. Soft neurological signs and subtle deficits on electroencephalograms (EEG) findings are also noted in populations of individuals with ADHD compared with controls.
Early findings are also provocative regarding the neuronal-environmental interactions. Specifically, the efficiency of brain functioning may be molded in the perinatal period via neuronal pruning, which is enhanced by appropriate levels of stimulation and nurturance. Efficient CSTC tracks depend upon early activation of these circuits, as is facilitated in an optimally stimulating environment and as is inhibited in a chaotic or deprived environment. Therefore, severe psychosocial adversity in infancy may predispose to less efficient neuronal tracks and potentially to subtle neurodevelopmental disorders such as ADHD. Psychosocial correlates of ADHD include poverty, urban residence, family dysfunction, and parents with psychiatric disorders. These psychosocial risk factors suggest that there may be multiple pathways leading to the development of ADHD in vulnerable children. This information is important for public health prevention efforts and may guide early intervention efforts.
Neuroimaging
Imaging studies of ADHD have focused on the prefrontal cortex, basal ganglia, and cerebellum as these are areas that have been implicated in the pathways that mediate ADHD or are rich in DA. Although results have been mixed, there is evidence of structural and functional differences in the brains of children and adults with ADHD. Volumetric measures have detected smaller right-sided prefrontal regions overall in boys with ADHD. These reductions have been correlated with performance on tasks that require response inhibition, and are consistent with a postulated etiologic role for prefrontal deficits. Girls with ADHD have been found to have smaller left and total caudate volumes. A consistent finding in ADHD has been reduced volume of the posterior-inferior cerebellar vermis, a region that exhibits a high degree of DA receptor reactivity.
Neuroimaging is an important tool to assist in understanding the neurophysiological correlates of ADHD. Functional neuroimaging with positron emission tomography (PET) and single photon emission computerized tomography (SPECT) with adults diagnosed with ADHD has demonstrated decreased frontal cerebral metabolism. Decreased perfusion in the striatum and prefrontal cortex has also been reported. Although functional magnetic resonance imaging (fMRI) has not been conclusive, early results also suggest subtle deficits in frontal lobe and basal ganglia activity. Such results support the notion that catecholamine dysregulation is central to the pathophysiology of ADHD and not just to its treatment. Most interestingly, McNab and colleagues found that when patients conducted mental exercises to train their working memory, an increase in the number of central DA receptors was detected on PET scanning. Despite these intriguing findings, currently there is no clinical role for neuroimaging in diagnosis, determining treatment, or predicting treatment response.
Genetics
It is helpful to conceptualize ADHD as a disorder in which genes may “bias” an individual’s brain circuits toward inefficient information processing and the precipitation of ADHD under adverse environmental circumstances. Data from family, twin, and adoption studies, as well as segregation analyses, show very high heritability coefficients, strongly supporting a genetic etiology for ADHD. Preliminary molecular genetic studies have implicated candidate genes associated with the DA system, including D2 and D4 receptors and the DA transporter. There is also preliminary evidence that genes involved in alpha-2A adrenergic receptors, serotonin receptors, and other proteins may be important. Given the importance of these catecholamines for the modulation of attentional circuits, it is not surprising that alterations in these systems would disrupt attention. Despite these intriguing findings, large genome-wide linkage studies conducted by Castellano and Swanson intended to identify chromosomal regions shared within families with ADHD have been inconsistent. Thus, much work is still needed to clarify the roles of genes and the gene-environment interaction in the etiology of ADHD.
Clinical Course
Although many of the symptoms of ADHD may remit, it has become clear that ADHD is frequently a chronic disorder, which leads to a negative impact on functioning throughout the life cycle. Studies following children with ADHD into adolescence have fairly consistently shown that ADHD children, as compared with controls, exhibit impaired academic functioning, perform more poorly on cognitive tasks, and are characterized by lower self-esteem and poorer social functioning. About three quarters of these children continue to show symptoms of ADHD into adolescence, and serious conduct problems are common.
In general, preschool children demonstrate the highest rates of hyperactivity and impulsivity. Although it is normative for preschool children to interrupt others and have high energy levels, the ability to pay attention and inhibit motor activity can generally differentiate children with functional disability from ADHD and the normal exuberance of preschool children. Children with early-onset severe symptoms, including preschool expulsion, peer rejection, and aggression, may predict a more serious prognosis. Preschool children with ADHD are also at higher risk for corporal punishment, or abuse. These children are challenging to parents, and parents who lack support and effective coping skills may resort to physical discipline.
ADHD-Combined is the most common type of ADHD diagnosed among school-aged children and generally adversely affects their social and academic development. These children have fewer friends and are more often the recipient of disciplinary measures. In general, the hyperactivity tends to wane with maturity, although feelings of restlessness are often reported. Adolescents with ADHD may have less hyperactivity, but they are more prone to school underachievement, substance abuse, and high-risk behaviors. Impulsivity declines after adolescence. The most persistent symptom cluster involves inattention, distractibility, lack of organization, and poor perseverance.
Follow-up studies into adulthood suggest that up to 33% of ADHD teens versus 1% to 9% of controls drop out of high school. ADHD youths complete less education (by 2 to 3 years) and fewer obtain a graduate degree. Likewise, ADHD youths demonstrate lower occupational rankings at the age of 25 years, a higher rate of divorce, increased motor vehicle accidents, poor money management, and a higher rate of unwed pregnancy. Youths with ADHD are also at increased risk for developing antisocial personality disorder and substance-use disorders in adulthood. An estimated 60% of adults continue to suffer from impairing symptoms of ADHD.
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