The main attention deficit in ADHD appears to be one of sustained attention (Douglas, 1999). When presented with an uninteresting or repetitive task, the performance of a child with ADHD deteriorates over time compared to that of other children. However, findings are not always consistent and may depend on the definitions and tasks used to assess this construct (Hinshaw, 1994). Symptoms of hyperactivity and behavioral impulsivity are best viewed as a single dimension of behavior called hyperactivity-impulsivity (Lahey et al., 1988). The strong link between hyperactivity and behavioral impulsivity has led to suggestions that both are part of a more fundamental deficit in behavioral inhibition (Barkley, 1997; Quay, 1997).
The three core features of ADHD—inattention, hyperac-tivity, and impulsivity—are complex processes. The current view is that hyperactivity-impulsivity is an essential feature of ADHD. In contrast to inattention, it distinguishes children with ADHD from those with other disorders and from normal children (Halperin, Matier, Bedi, Sharma, & Newcorn, 1992). As such, impulsivity-hyperactivity appears to be a specific marker for ADHD, whereas inattention is not (Taylor, 1995). Children with ADHD display a unique constellation and severity of symptoms but do not necessarily differ from comparison children on all types and measures of inattention, hyperactivity, and impulsivity (Barkley, 1998).
DSM-IV-TR specifies three ADHD subtypes based on the child's primary symptoms, which have received growing empirical support (Eiraldi, Power, & Nezu, 1997; Faraone, Biederman, & Friedman, 2000; Gaub & Carlson, 1997a). Children with the combined type display symptoms of both inattention and hyperactivity; those with the predominantly hyperactive-impulsive type display primarily symptoms of hyperactivity-impulsivity; and those with the predominantly inattentive type display primarily symptoms of inattention. Children with the combined and predominantly hyperactive-impulsive types are more likely to display problems in inhibiting behavior and in behavioral persistence than are those who are predominantly inattentive. They are also more likely to be aggressive, defiant, and oppositional; to be rejected by their peers; and to be suspended from school or placed in special education classes (Lahey & Carlson, 1992). Because children who are predominantly hyperactive-impulsive are usually younger than those with the combined type, it is not yet known whether these are actually two distinct subtypes or the same type at different ages (Barkley, 1996).
Children who are predominantly inattentive are described as inattentive and drowsy, daydreamy, spacey, in a fog or easily confused, and they commonly experience a learning disability. They process information slowly and find it hard to remember things. Their main deficits seem to be speed of information processing and selective attention. Growing—but not yet conclusive—evidence suggests that children who are predominantly inattentive constitute a distinct subgroup from other two types (Maedgen & Carlson, 2000). They appear to display different symptoms, associated conditions, family histories, outcomes, and responses to treatment (Barkley, 1998).
The DSM-IV-TR criteria for ADHD have a number of limitations (Barkley, 1996), several of which apply to other childhood disorders as well. First, they are developmentally insensitive, using the same symptom criteria for individuals of all ages—even though some symptoms, such as running and climbing, apply more to young children. In addition, the number of symptoms needed to make a diagnosis is not adjusted for age or level of maturity even though many of these symptoms show a general decline with age. Second, according to DSM-IV-TR, ADHD is a disorder that the child either has or does not have. However, because the number and severity of symptoms are also a matter of degree, children who fall just below the cutoff for ADHD are not necessarily qualitatively different from those who are just above it. In fact, over time, some children move in and out of the DSM-IV-TR category as a result of fluctuations in their behavior. Third, there is some uncertainty about the DSM-IV-TR requirement that symptoms must have an onset prior to age 7. There seems to be little difference between children with an onset of ADHD before or after age 7 (Barkley & Biederman, 1997), and about half of children with ADHD who are predominantly inattentive do not manifest the disorder until after age 7 (Applegate et al., 1997). Finally, the requirement of persistence for 6 months may be too brief for young children. Many preschoolers display symptoms for 6 months, and the symptoms then go away. These limitations highlight the fact that DSM-IV-TR criteria are designed for specific purposes—classification and diagnosis. They help shape our understanding of ADHD and other childhood disorders but are also shaped by—and in some instances lag behind—new research findings.
As many as one half of all clinic-referred children display ADHD symptoms either alone or in combination with other disorders, making it one of the most common referral problems in North America (Barkley, 1998). The best estimate is that about 3-7% of all school-age children in North America have ADHD (APA, 2000; Jensen et al., 1999). However, as with other disorders, estimates can and do vary widely because informants in different settings do not always agree on symptoms or may emphasize different symptoms. Teachers, for example, are especially likely to rate a child as inattentive when oppositional symptoms are also present (Abikoff, Courtney, Pelham, & Koplewicz, 1993). Because adults may disagree, prevalence estimates are much higher when based on just one person's opinion than they are when based on a consensus (Lambert, Sandoval, & Sassone, 1978).
ADHD occurs much more frequently in boys than in girls, with estimates ranging from 6-9% for boys and from 2-3% for girls in the 6- to 12-year age range. In adolescence, overall rates of ADHD drop for both boys and girls, but boys still outnumber girls by the same ratio of 2:1 to 3:1. This ratio is even higher in clinic samples, in which boys outnumber girls by 6:1 or more—most likely because boys are referred more frequently due to their defiance and aggression (Szatmari, 1992). ADHD in girls may go unrecognized and unreported because teachers may fail to recognize and report inattentive behavior unless it is accompanied by the disruptive symptoms normally associated with boys (McGee & Feehan, 1991). In fact, many of the DSM-IV-TR symptoms, such as excessive running around, climbing, and blurting out answers in class are generally more common in boys than in girls. Thus, sampling, referral, and definition biases may be a factor in the greater reported prevalence of ADHD in boys than in girls.
In the past, girls with ADHD were a highly under-studied group (Arnold, 1996). However, recent findings show that girls with ADHD are more likely to have conduct, mood, and anxiety disorders; lower IQ and school achievement scores; and greater impairment on measures of social, school, and family functioning than are girls without ADHD (Biederman et al., 1999; Greene et al., 2001; Rucklidge & Tannock, 2001). In addition, the expression, severity of symptoms, family correlates, and response to treatment are similar for boys and girls with ADHD (Faraone et al., 2000; Silverthorn, Frick, Kuper, & Ott, 1996). When gender differences are found, boys show more hyperactivity, more accompanying aggression and antisocial behavior, and greater impairment in executive functions, whereas girls show greater intellectual impairment (Gaub & Carlson, 1997b; Seidman, Biederman, Faraone, & Weber, 1997).
The symptoms of ADHD are probably present at birth, although reliable identification is difficult until the age of 3-4 years when hyperactive-impulsive symptoms become increasingly more salient (Hart, Lahey, Loeber, Applegate, & Frick, 1996). Preschoolers with ADHD act suddenly without thinking, dashing from activity to activity, grabbing at immediate rewards; they are easily bored and react strongly and negatively to routine events (Campbell, 1990; DuPaul, McGoey, Eckert, & VanBrakle, 2001). Symptoms of inattention emerge at 5-7 years of age, as classroom demands for sustained attention and goal-directed persistence increase (Hart et al., 1996). Symptoms of inattention continue through grade school, resulting in low academic productivity, dis-tractibility, poor organization, trouble meeting deadlines, and an inability to follow through on social promises or commitments to peers (Barkley, 1996).
The child's hyperactive-impulsive behaviors that were present in preschool continue, with some decline, during the years from 6 to 12. During elementary school, oppositional defiant behaviors may also develop (Barkley, 1998). By 8-12 years, defiance and hostility may take the form of serious problems, such as lying or aggression. Through the school years, ADHD increasingly takes its toll as children experience problems with self-care, personal responsibility, chores, trustworthiness, independence, social relationships, and academic performance (Koplowicz & Barkley, 1995; Stein, Szumoski, Blondis, & Roizen, 1995). Although hyperactive-impulsive behaviors decline significantly by adolescence, they still occur at a level higher than in 95% of same-age peers (Barkley, 1996). The disorder continues into adolescence for at least 50% or more of clinic-referred elementary school children (Barkley, Fisher, Edelbrock, & Smallish, 1990; Weiss & Hechtman, 1993). Childhood symptoms of hyperactivity-impulsivity (more so than those of inattention) are generally related to poor adolescent outcomes (Barkley, 1998). Some youngsters with ADHD either outgrow their disorder or learn to cope with it. However, many continue to experience problems, leading to a lifelong pattern of suffering and disappointment (Mannuzza & Klein, 1992).
As many as 80% of children with ADHD have a co-occurring disorder (Jensen, Martin, & Cantwell, 1997). About 25% or more have a specific learning disorder (Cantwell & Baker, 1992; Semrud-Clikeman et al., 1992) and 30-60% have impairments in speech and language (Baker & Cantwell, 1992; Cohen et al., 2000). About half of all children with ADHD— mostly boys—also meet criteria for oppositional defiant disorder (ODD) by age 7 or later, and 30-50% eventually develop conduct disorder (CD; Barkley, 1998; Biederman, Faraone, & Lapey, 1992). ADHD, ODD, and CD tend to run in families, which suggests a common causal mechanism (Biederman et al., 1992). However, ADHD is usually associated with cognitive impairments and neurodevelopmental difficulties, whereas conduct problems are more often related to family adversity, parental psychopathology, and social disadvantage (Schachar & Tannock, 1995).
About 25% of children with ADHD—usually younger boys—experience excessive anxiety (Tannock, 2000). It is interesting to note that the overall relationship between ADHD and anxiety disorders is reduced or eliminated in adolescence. The co-occurrence of an anxiety disorder may inhibit the adolescent with ADHD from engaging in the impulsive behaviors that characterize other youngsters with ADHD (Pliszka, 1992). As many as 20% of children with ADHD experience depression, and even more eventually develop depression or another mood disorder by early adulthood (Mick, Santangelo, Wypij, & Biederman, 2000; Willcutt, Pennington, Chhabildas, Friedman, & Alexander, 1999). The association between ADHD and depression may be a function of family risk for one disorder's increasing risk for the other (Biederman et al., 1995).
Children with ADHD display many associated cognitive, academic, and psychosocial deficits. They consistently show deficits in executive functions—particularly those related to motor inhibition (Pennington & Ozonoff, 1996). Most children with ADHD are of at least normal overall intelligence, but they experience severe difficulties in school nevertheless (Fischer, Barkley, Edelbrock, & Smallish, 1990). In fact, the academic skills of children with ADHD have been found to be impaired even before they enter the first grade (Mariani & Barkley, 1997).
The association between ADHD and general health is uncertain at this time (Barkley, 1998; Daly et al., 1996), although a variety of health problems have been suggested (e.g., upper respiratory infections, asthma, allergies, bed-wetting, and other elimination problems). Instability of the sleep-wake system is characteristic of children with ADHD, and sleep disturbances are common (Gruber, Sadeh, & Raviv, 2000). Resistance to going to bed and fewer total hours may be the most significant sleep problems (Wilens, Biederman, & Spencer, 1994), although the precise nature of the sleep disturbance in ADHD is not known (Corkum, Tannock, & Moldofsky, 1998). Up to 50% of children with ADHD are described as accident-prone, and they are more than twice as likely as other children to experience serious accidental injuries, such as broken bones, lacerations, severe bruises, poisonings, or head injuries (Barkley, 1998). As young adults, they are at higher risk for traffic accidents and offenses (Nada-Raja et al., 1997) as well as for substance abuse (Wilens, Biederman, Mick, Faraone, & Spencer, 1997) and risky sexual behaviors such as multiple partners and unprotected sex (Barkley, Fisher, & Fletcher, 1997).
Families of children with ADHD experience many difficulties, including interactions characterized by negativity, child noncompliance, high parental control, and sibling conflict (Whalen & Henker, 1999). Parents may experience high levels of distress and related problems; the most common ones are depression in mothers and antisocial behavior (i.e., substance abuse) in fathers. Further stress on family life stems from the fact that parents of children with ADHD may themselves have ADHD and other associated conditions (Johnston & Mash, 2001). It is critical to note that high levels of family conflict and the links between ADHD and parental psychopathol-ogy and marital discord seem to be related to the child's co-occurring conduct problems rather than to ADHD alone.
Children and adolescents with ADHD display little of the give and take, cooperation, and sharing that characterize other children (Dumas, 1998; Henker & Whalen, 1999). They are disliked and uniformly rejected by peers, have few friends, and are often unhappy (Gresham, MacMillan, Bocian,
Ward, & Forness, 1998; Landau, Milich, & Diener, 1998). Their difficulties in regulating their emotions (Melnick & Hinshaw, 2000) and the aggressiveness that frequently accompanies ADHD often lead to conflict and negative peer reputation (Erhardt & Hinshaw, 1994).
Current research into causal factors provides strong evidence for ADHD as a disorder with neurobiological determinants (Biederman & Spencer, 1999; Tannock, 1998). However, biological and environmental risk factors together shape the expression of ADHD symptoms over time following several different pathways (Johnston & Mash, 2001; Taylor, 1999). ADHD is a complex and chronic disorder of brain, behavior, and development; its cognitive and behavioral outcomes affect many areas of functioning (Rapport & Chung, 2000). Therefore, any explanation of ADHD that focuses on a single cause and single outcome is likely to be inadequate (Taylor, 1999).
Several sources of evidence point to genetic influences as important causal factors in ADHD (Kuntsi & Stevenson, 2000). First, about one third of immediate and extended family members of children with ADHD are also likely to have the disorder (Faraone, Biederman, & Milberger, 1996; Hechtman, 1994). Of fathers who had ADHD as children, one third of their offspring have ADHD (Biederman et al., 1992; Pauls,
1991). Second, studies of biologically related and unrelated pairs of adopted children have found a strong genetic influence that accounts for nearly half of the variance in attention-problem scores on child behavior rating scales (van den Oord, Boomsma, & Verhulst, 1994). Third, twin studies report heri-tability estimates of ADHD averaging .80 or higher (Tannock, 1998). Both the symptoms and diagnosis of ADHD show average concordance rates for identical twins of 65%—about twice that of fraternal twins (Gilger, Pennington, & DeFries,
1992). Twin studies also find that the greater the severity of ADHD symptoms, the greater the genetic contributions (Stevenson, 1992).
Finally, genetic analysis suggests that specific genes may account for the expression of ADHD in some children (Faraone et al., 1992). Preliminary studies have found a relation between the dopamine transporter (DAT) gene and ADHD (Cook et al., 1995; Gill, Daly, Heron, Hawi, & Fitzgerald, 1997). Studies have also focused on the gene that codes for the dopamine receptor gene (DRD4), which has been linked to the personality trait of sensation seeking (high levels of thrill-seeking, impulsive, exploratory, and excitable behavior; Benjamin et al., 1996; Ebstein et al., 1996). Findings that implicate specific genes within the dopamine system in ADHD are intriguing, and they are consistent with a model suggesting that reduced dopaminergic activity may be related to the behavioral symptoms of ADHD (Faraone et al., 1999; Winsberg & Comings, 1999). However, other genetic findings indicate that the serotonin system also plays a crucial role in mediating the hyperactive-impulsive components of ADHD (Quist & Kennedy, 2001). As with other disorders of childhood, it is important to keep in mind that in the vast majority of cases, the heritable components of ADHD are likely to be the result of multiple interacting genes on several different chromosomes. Taken together, the findings from family, adoption, twin, and specific gene studies suggest that ADHD is inherited, although the precise mechanisms are not yet known (Edelbrock, Rende, Plomin, & Thompson, 1995; Tannock, 1998).
Many factors that compromise the development of the nervous system before and after birth—such as pregnancy and birth complications, low birth weight, malnutrition, early neurological insult or trauma, and diseases of infancy—may be related to ADHD symptoms (Milberger, Biederman, Faraone, Chen, & Jones, 1996; Milberger, Biederman, Faraone, Guite, & Tsuang, 1997). Although these early factors predict later symptoms of ADHD, there is little evidence that they are specific to ADHD because they also predict later symptoms of other disorders as well. A mother's use of cigarettes, alcohol, or other drugs during pregnancy can have damaging effects on her unborn child. Mild or moderate exposure to alcohol before birth may lead to inattention, hyperactivity, impulsivity, and associated impairments in learning and behavior (Streissguth, Bookstein, Sampson, & Barr, 1995). Other substances used during pregnancy—such as nicotine or cocaine—can adversely affect the normal development of the brain and lead to higher than normal rates of ADHD (Weissman et al., 1999).
There is both indirect and direct support for neurobiologi-cal causal factors in ADHD (Barkley, 1998; Faraone & Biederman, 1998). There are known associations between events or conditions known to be related to neurological status and symptoms of ADHD. Among these are peri- and postnatal events and diseases; environmental toxins such as lead; language and learning disorders; and signs of neurological immaturity, such as clumsiness, poor balance and coordination, and abnormal reflexes. Other sources of indirect support include the improvement in ADHD symptoms produced by stimulant medications known to affect the central nervous system, the similarity between symptoms of ADHD and symptoms associated with lesions to the pre-frontal cortex (Grattan & Eslinger, 1991), and the deficient performances of children with ADHD on neuropsychological tests associated with prefrontal lobe functions (Barkley, Grodzinsky, & DuPaul, 1992).
Neuroimaging studies have found that children with ADHD have a smaller right prefrontal cortex than do those without ADHD (Filipek et al., 1997) and show structural abnormalities in several parts of the basal ganglia (Semrud-Clikeman et al., 2000). Although simple and direct relations cannot be assumed between brain size and abnormal function, anatomic measures of frontostriatal circuitry are related to children's performance on response inhibition tasks (Casey et al., 1997). In adults with ADHD and in adolescent girls with ADHD, positron-emission tomography (PET) scan studies have found reduced glucose metabolism in the areas of the brain that inhibit impulses and control attention (Ernst et al., 1994). Significant correlations have also been found between diminished metabolic activity in the left anterior frontal region and severity of ADHD symptoms in adolescents (Zametkin et al., 1993). Taken together, the findings from neuroimaging studies suggest the importance of the frontostriatal region of the brain in ADHD. These studies tell us that in children with ADHD, there is a structural difference or less activity in certain regions of the brain, but they don't tell us why.
Genetic studies find that psychosocial factors in the family account for only a small amount of the variance (less than 15%) in ADHD symptoms (Barkley, 1998), and explanations of ADHD based exclusively on negative family influences have received little support (Silverman & Ragusa, 1992; Willis & Lovaas, 1977). Nevertheless, family influences are important in understanding ADHD for several reasons (Johnston & Mash, 2001; Whalen & Henker, 1999). First, family influences may lead to ADHD symptoms or to a greater severity of symptoms. In some circumstances, ADHD symptoms may be the result of interfering and insensitive early caregiving practices (Jacobvitz & Sroufe, 1987). In addition, for children at risk for ADHD, family conflict may raise the severity of their hyperactive-impulsive symptoms to a clinical level (Barkley, 1996). Second, family problems may result from interacting with a child who is impulsive and difficult to manage (Mash & Johnston, 1990). The clearest support for this child-to-parent direction of effect comes from double-blind placebo control drug studies in which children's ADHD symptoms were decreased using stimulant medications. Decreases in children's ADHD symptoms produced a corresponding reduction in the negative and controlling behaviors that parents had previously displayed when their children were unmedicated (Barkley, 1988; Humphries, Kinsbourne, & Swanson, 1978). Third, family conflict is probably related to the presence, maintenance, and later emergence of associated ODD and CD symptoms. Many interventions for ADHD try to change patterns of family interaction to head off an escalating cycle of oppositional behavior and conflict (Sonuga-Barke, Daley, Thompson, Laver-Bradbury, & Weeks, 2001). Family influences may play a major role in determining the outcome of ADHD and associated problems even if such influences are not the primary cause of ADHD (Johnston & Mash, 2001).
Was this article helpful?