ADHD Research Paper

Outline

I. Introduction

II. Historical Context

III. Description and Diagnosis

A. The Core Symptoms

B. Associated Cognitive Impairments

IV. Theoretical Framework

V. Potential Etiologies

VI. Epidemiology of ADHD

VII. Developmental Course and Adult Outcome

VIII. Diagnostic Criteria

IX. Conclusion

X. Bibliography

I. Introduction

It is not unusual for young children to be energetic and active, or to become bored quickly and move from one activity to another as they explore their environment. A young child’s desire for immediate gratification is to be expected, rather than the restraint or self-control that would be demanded of someone older. However, some children persistently display levels of activity that are far in excess of their age group. Some are unable to sustain their attention to activities, their interest in tasks assigned to them by others, or their persistence in achieving long-term goals as well as their peers.

When a child’s impulse control, sustained attention, and general self-regulation lag far behind expectations for their developmental level, they are likely to be diagnosed as having ADHD. Children with ADHD have a greater probability of experiencing a number of problems in their social, academic, and emotional development and daily adaptive functioning.

Attention Deficit/Hyperactivity Disorder (ADHD) has captured public commentary and scientific interest for more than 100 years. While the diagnostic labels for disorders of inattention, hyperactivity, and impulsiveness have changed numerous times, the actual nature of the disorder has changed little, if at all, from descriptions provided at the turn of the century. During the past century, and especially during the last 30 years, thousands of published scientific papers have focused on ADHD, making it one of the most wellstudied childhood psychiatric disorders.

II. Historical Context of ADHD

Serious clinical interest in children who have severe problems with inattention, hyperactivity, and poor impulse control is first found in three published lectures by the English physician, George Still, presented to the Royal Academy of Physicians in 1902. Still reported on a group of 20 children in his clinical practice whom he defined as having a deficit in “volitional inhibition” or a “defect in moral control” over their own behavior. Still’s observations described many of the associated features of ADHD that would be supported by research almost a century later, such as an overrepresentation of boys compared to girls, the greater incidence of alcoholism, criminal conduct, and depression among the biological relatives, and a familial predisposition to the disorder.

Initial interest in children with these characteristics arose in North America around the time of the great encephalitis epidemics of 1917 and 1918. Children surviving these brain infections were noted to have many behavioral problems similar to those comprising contemporary ADHD. These cases, as well as others known to have arisen from birth trauma, head injury, toxin exposure, and infections, gave rise to the concept of a “brain-injured child syndrome,” often associated with mental retardation. This term was eventually applied to children without a history of brain damage or evidence of retardation but who manifested behavioral problems such as hyperactivity or poor impulse control. This concept would later evolve into that of “minimal brain damage,” and eventually “minimal brain dysfunction” (MBD), as challenges were raised to the label given the lack of evidence of brain injury in many of these cases.

During the 1950s researchers became increasingly interested in hyperactivity. “Hyperkinetic impulse disorder” was attributed to cortical overstimulation resuiting from ineffective filtering of stimuli entering the brain. These studies gave rise to the notion of the “hyperactive child syndrome” typified by daily motor movement that was far in excess of that seen in normal children of the same age.

By the 1970s research findings emphasized the importance of problems with sustained attention and impulse control in addition to hyperactivity in understanding the nature of the disorder. In 1983 Virginia Douglas proposed that the disorder was comprised of major deficits in four areas: (1) the investment, organization, and maintenance of attention and effort; (2) the ability to inhibit impulsive behavior; (3) the ability to modulate arousal levels to meet situational demands; and (4) an unusually strong inclination to seek immediate reinforcement. Douglas’ work, along with numerous subsequent studies of attention, impulsiveness, and other cognitive factors, eventually led to renaming the disorder “Attention Deficit Disorder” (ADD) in 1980.

Just as significant as the renaming of the condition at that time was the distinction made between two types of ADD: those with hyperactivity and those without it. Little research existed at the time on the latter subtype. However, later research suggested that ADD without hyperactivity might be a separate and distinct disorder of a different component of attention (selective or focused) than was the type of inattention seen in those with ADD with hyperactivity (persistence and distractibility). Thus, rather than being related subtypes of a single disorder with a shared, common impairment in attention, future research may show these subtypes to constitute separate disorders of attention altogether.

Within a few years of the creation of the label ADD, concern was raised by Barkley in 1990 and Weiss and Hechtman in 1993 that problems with hyperactivity and impulse control were features critically important to differentiating the disorder from other conditions and to predicting later developmental risks. In 1987 the disorder was renamed Attention Deficit Hyperactivity Disorder. Diagnostic symptoms were identified from a single list of items incorporating all three constructs: hyperactivity, impulsivity, and inattention. The subtype of ADD without Hyperactivity was now renamed Undifferentiated ADD and relegated to minor diagnostic status until further research could clarify its nature and relationship to ADHD.

Around this same time (mid-1980s to 1990s) reports began to appear that challenged the notion that ADHD was primarily a disturbance in attention. Over the previous decade, researchers studying information-processing capacities in children with ADHD were having difficulty demonstrating that the problems these children had with attending to tasks were actually attentional in nature (i.e., related to the processing of incoming information). Problems in response inhibition and preparedness of the motor control system appeared to be more reliably demonstrated. Researchers, moreover, were finding that the problems with hyperactivity and impulsivity were not separate constructs but formed a single dimension of behavior. All of this led to the creation of two separate lists of symptoms for ADHD when the latest diagnostic manual for psychiatry, The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (also known as the DSM-IV) was published by the American Psychiatric Association in 1994. In the DSM-IV, one symptom list now existed for inattention and another for hyperactive-impulsive behavior. The inattention list once again permitted the diagnosis of a subtype of ADHD that consisted principally of problems with attention (ADHD Predominantly Inattentive Type). But two other subtypes were also identified (Predominantly Hyperactive-Impulsive and Combined Types). As of this writing, debate continues over the core deficit(s) involved in ADHD, with increasing emphasis being given to a central problem specifically with behavioral inhibition and more generally with self-regulation or executive functioning.

III. ADHD Description and Diagnosis

A. The Core Symptoms

Problems with attention consist of the child’s inability to sustain attention or respond to tasks or play activities as long as others of the same age or to follow through on rules and instructions as well as others. The child appears more disorganized, distracted, and forgetful than others of the same age. Parents and teachers frequently complain that these children do not seem to listen as well as they should for their age, cannot concentrate, are easily distracted, fail to finish assignments, daydream, and change activities more often than others.

Research corroborates that, when compared to normal children, ADHD children are often more “off-task,” less likely to complete as much work as others, look away more from the activities they are requested to do (including television), persist less in correctly performing boring activities, and are slower and less likely to return to an activity once interrupted. Yet objective research does not find children with ADHD to be generally more distracted by most forms of extraneous events occurring during their task performance, although distractors within the task may prove more disruptive to them than to normal children. Research instead documents that ADHD children are more active than other children, are less mature in controlling motor movements, and have considerable difficulties with stopping an ongoing behavior. They frequently talk more than others and interrupt others’ conversations. They are less able to resist immediate temptations and delay gratification and respond too quickly and too often when they are required to wait and watch for events to happen.

Recent research shows that the problems with behavioral or motor inhibition arise first, at age 3 to 4 years, with those related to inattention emerging somewhat later in the developmental course of ADHD, at age 5 to 7 years. Whereas the symptoms of disinhibition seem to decline with age, those of inattention remain relatively stable during the elementary grades. Yet even the inattentiveness may decline by adolescence in some cases.

A number of factors have been noted to influence the ability of children with ADHD to sustain their attention to task performance, to control their impulses to act, to regulate their activity level, and to produce work consistently. They include: time of day or fatigue; increasing task complexity where organizational strategies are required; extent of restraint demanded for the context; level of stimulation within the setting; the schedule of immediate consequences associated with the task; and the absence of adult supervision during task performance.

It has been shown that children with ADHD are most problematic in their behavior when persistence in work-related tasks is required (i.e., chores, homework, etc.) or where behavioral restraint is necessary, especially in settings involving reduced parental monitoring (i.e., in church, in restaurants, when a parent is on the phone, etc.). Such children are least likely to pose behavioral management problems during free play, when little self-control is required. Fluctuations in the severity of ADHD symptoms have also been documented across a variety of school contexts. In this case, classroom activities involving self-organization and task-directed persistence are the most problematic, with significantly fewer problems posed by contexts involving fewer performance demands (i.e., at lunch, in hallways, at recess, etc.), and even fewer problems posed during highly entertaining special events (i.e., field trips, assemblies, etc.).

B. Associated Cognitive Impairments

Although ADHD is defined by the presence of the two major symptom dimensions of inattention and disinhibition (hyperactivity-impulsivity), research indicates that these children often demonstrate deficiencies in many other abilities. These include: motor coordination and sequencing; working memory and mental computation; planning and anticipation or preparedness for action; verbal fluency and confrontational communication; effort allocation; applying organization strategies; the internalization of self-directed speech; adhering to restrictive instructions; the self-regulation of emotions; and self-motivation. Several studies have also demonstrated what both Still (1902) and Douglas (1983) noted anecdotally years ago–ADHD may be associated with less mature or diminished moral reasoning and the moral control of behavior.

The commonality among most or all of these seemingly disparate abilities is that all fall within the neuropsychological domain described as executive functions. The neurologist Joaquim Fuster wrote in 1989 that these executive abilities are probably mediated by the frontal cortex of the brain, and particularly the prefrontal lobes. Barkley has recently defined executive functions as being those neuropsychological processes that permit or assist with human self-regulation. Self-regulation is then defined as any self-directed form of behavior (both overt and covert) that serves to modify the probability of a subsequent behavior by the individual so as to alter the probability of a later consequence. Such behavior may even involve forgoing immediate rewards for the sake of maximizing delayed outcomes or even exposing oneself to immediate aversive circumstances for this same purpose. Self-regulatory behavior, therefore, includes thinking within this realm of private or covert self-directed behavior. By appreciating the role of the frontal lobes and the prefrontal cortex in these executive abilities, it is easy to see why researchers have repeatedly speculated that ADHD probably arises out of some disturbance or dysfunction of this brain region.

IV. Theoretical Framework

Many different hypotheses on the nature of ADHD have been proposed over the past century, such as Still’s (1902) notion of defective volitional inhibition and moral regulation of behavior, and Douglas’ (1983) theory of deficient attention, inhibition, arousal, and preference for immediate reward. Few of these have produced models of the disorder that were widely adopted by both scientists and clinicians or that served to drive further programmatic research initiatives. Some of these theories have suggested that ADHD is a deficit in sensitivity to reinforcement, a more general motivational disorder, or a deficit in rule-governed behavior (i.e., the control of behavior by language). Most recently, several theorists working in this area have proposed that ADHD represents a deficit behavioral inhibition; an assertion for which there is substantial evidence, at least for those subtypes that involve hyperactive-impulsive symptoms.

Consistent with these proposals, Barkley outlined a model of ADHD in 1994 that was based upon an earlier theory by Jacob Bronowski first set forth in 1966 on the evolution of the unique properties of human language and their relationship to response inhibition. Bronowski’s model was subsequently combined with that of Juaquim Fuster published in 1989, which specified that the overarching role of the prefrontal cortex is the cross-temporal organization of behavior. Barkley’s hybrid theoretical model of ADHD places behavioral inhibition at a central point and supportive point in relation to four other executive functions dependent upon it for their own effective execution. These functions are working memory, the self-regulation of emotion/motivation, the internalization of speech, and reconstitution (analysis and synthesis of behavioral structures in the service of goal-directed behavioral creativity). The four functions are believed to permit and subserve human self-regulation, bringing behavior progressively under the control of internally represented information, often about the future, and transferring it at least partially away from the control of behavior by more immediate consequences and external events. The executive control of behavior afforded by these functions is proposed to result in a greater capacity for predicting and controlling one’s self and one’s environment so as to maximize future consequences over immediate ones for the individual. And, more generally, the interaction of these executive functions permits far more organized and effective adaptive functioning.

Several assumptions are important in understanding this model as it is applied to ADHD. First, the capacity for behavioral inhibition begins to emerge first in the child’s development, prior to or corresponding with the emergence of the four executive functions. Second, inhibition does not directly cause the activation of these executive functions but sets the occasion for their occurrence and is necessary for their effective performance. Third, these functions probably emerge at different times in the child’s development and may have relatively independent developmental trajectories, although interactive. Fourth, the sweeping cognitive impairments that ADHD creates across these executive functions are secondary to the primary deficit in behavioral inhibition, implying that if inhibition were to be improved, these executive functions would likewise improve.

The deficit in behavioral inhibition is thought to arise principally from genetic and neurodevelopmental origins, rather than from purely social ones, although its expression is certainly influenced by a variety of social factors. The secondary deficits in the executive functions and self-regulation created by the primary deficit in inhibition feedback to contribute to further deficits in behavioral inhibition because self-regulation is required for self-restraint.

Behavioral inhibition is viewed in the model as comprising three related processes: (1) the capacity to inhibit “prepotent” responses prior to their initiation; (2) the capacity to cease ongoing response patterns once initiated such that both (1) and (2) create delays in responding to events; and (3) the protection of this delay and the self-directed (often private or cognitive) actions occurring within it from interference by competing events and their prepotent responses (interference control). Prepotent responses are defined as those for which immediate reinforcement (both positive and negative) is available for their performance or for which there is a strong history of reinforcement in this context. Through the postponement of the prepotent, automatic responses and the creation of this protected period of delay, the occasion is set for the four executive functions to act effectively in modifying the individual’s eventual initial responding to events or modifying their ongoing responses to those events (creating a sensitivity to feedback or errors). The executive system described here may exist so as to achieve a net maximization of both temporally distant and immediate consequences rather than immediate consequences alone. The chain of goal-directed, future-oriented behaviors set in motion by these acts of self-regulation is then also protected from interference during its performance by this same process of inhibition (interference control). Even if disrupted, the individual retains the capacity or intention (via working memory) to return to the goal-directed actions until the outcome is successfully achieved or judged to be no longer necessary.

Space permits here only a brief description of each of the four executive components of this new model of ADHD. The first of these involves working memory, or the capacity for prolonging and manipulating mental representations of events and using such information to control motor behavior. This particular type of memory can be thought of as remembering so as to do and serves to sustain otherwise fleeting information that will be useful in controlling subsequent responding, such as is seen in privately rehearsing a telephone number in mind so as to later dial it accurately. One component of working memory may be related to self-speech (verbal working memory), while a second component is related to perceptual imagery (visual-spatial) and probably involves self-directed sensing, as in visual imagery or covert audition. This retention of information related to past events (retrospection) gives rise to the conjecturing of future events (prospection), which sets in motion a preparedness to act in anticipation of the arrival of these future events (anticipatory set). Out of this continuous referencing or sensing of past and future probably arises the psychological sense of time. These activities taking place in working memory appear to be dependent upon behavioral inhibition. Such working memory processes have been shown to exist in rudimentary form even in young infants permitting them to successfully perform delayed response tasks to a limited degree. As the capacity for inhibition increases developmentally, it probably contributes to the further efficiency and effectiveness of working memory.

According to this model of ADHD, behavioral inhibition also sets the stage for the development of the second executive component of this model, that being the self-regulation of emotion in children. The inhibition of the initial prepotent response includes the inhibition of the initial emotional reaction that it may have elicited. It is not that the child does not experience emotion; rather, the behavioral reaction to or expression of that emotion is delayed along with any motor behavior associated with it. The delay in responding this creates allows the child time to engage in self-directed behaviors that will modify both the eventual response to the event as well as the emotional reaction that may accompany it. Because emotions are themselves forms of both motivational and arousal states, the model argues that deficits in the self-regulation of emotion should be associated with deficits in self-motivation and the self-control of arousal, particularly in the service of goal-directed behavior.

The internalization of self-directed speech, as originally described by Vygotsky, forms the third executive component of this model of ADHD. During the early preschool years, speech, once developed, is initially employed for communication with others. As behavioral inhibition progresses, language becomes turned on the self. It now is not just a means of influencing the behavior of others but provides a means of reflection as well as a means for controlling one’s own behavior (instruction).

The fourth component of this model involves the capacity to rapidly take apart and recombine units of behavior, including language. The delay in responding that behavioral inhibition permits allows time for information related to the event to be mentally prolonged and then dissassembled so as to extract more information about the event that will aid in preparing a response to it. In a related fashion, previously learned response patterns can also be broken down into smaller units of behavior. This internal decomposition of information and its associated response patterns permits the complementary process to occur, that being synthesis, or the invention of novel combinations of behavioral structures, including words and ideas, in the service of goal-directed action. This gives a highly creative or generative character as well as a hierarchically organized nature to human goal-directed behavior.

Finally, the internally represented information and motivation generated by these four executive functions is used to control a separate unit within the model, that being motor behavior itself. Such information serves to program, execute, and sustain behavior directed toward goals and the future, giving human behavior an intentional or purposive quality. Task-irrelevant movement is now more effectively suppressed, goal-directed behavior better sustained, and this pattern of behavior more efficiently reengaged should disruption of the behavioral pattern occur because of the control afforded by the internal information being generated from the four executive functions.

The impairment in behavioral inhibition occurring in ADHD is hypothesized to disrupt the efficient execution of these executive functions, thereby limiting the capacity of these individuals for self-regulation. The result is an impairment in the cross-temporal organization of behavior, in the prediction and control of one’s own behavior and environment, and inevitably in the maximization of long-term consequences for the individual.

How does this model account for the problems with attention believed to exist in ADHD? According to this model, it is critical to distinguish between two forms of sustained attention that are traditionally confused in the research literature on ADHD. The first is called contingency-shaped attention. This refers to continued responding in a situation or to a task as a function of the immediate available contingencies of reinforcement provided by the task or its context. Responding that is maintained under these conditions then is directly dependent on the immediate environmental contingencies. Many factors affect this form of sustained attention or responding: the novelty of the task, the intrinsic interest the activity may hold for the individual, the immediate reinforcement it provides for responding in the task, the state of fatigue of the individual, and the presence or absence of an adult supervisor (or other stimuli which signal other consequences for performance that are outside the task itself). The model predicts that this type of sustained attention relatively unaffected by ADHD as it is behavior under the control of external events.

As children mature, however, a second form of sustained attention emerges described in the model as goal-directed persistence. This form of sustained responding arises as a direct consequence of the development of self-regulation or the control of behavior by internally represented information. Such persistence derives from the development of a progressively greater capacity by the child to hold events, goals, and plans in mind (working memory), to adhere to rules governing behavior and to formulate and follow such rules, to self-induce a motivational state supportive of the plans and goals formulated by the individual so as to maintain goal-directed behavior, and even to create novel behaviors in the service of the goal’s attainment. The capacity to initiate and sustain chains of goal-directed behavior in spite of the absence of immediate environmental contingencies for their performance is predicted to be the form of sustained attention disrupted by ADHD.

Apart from this heuristically valuable distinction in forms of sustained attention, this theoretical model of ADHD makes numerous predictions about the cognitive and behavioral deficits likely to be found in those with the disorder (i.e., impaired working memory and sense of time, delayed internalization of speech, etc.), many of which have received little or no attention in research on ADHD. It also provides a framework by which to better organize and understand the numerous cognitive deficits identified in previous studies of children with ADHD than does the current view of ADHD as being chiefly an attention deficit.

V. Potential Etiologies of ADHD

The precise causes of ADHD are unknown at the present time. Numerous causes have been proposed, but evidence for many has been weak or lacking entirely. However, a number of factors have been shown to be associated with a significantly increased risk for ADHD in children.

The vast majority of the potentially causative factors associated with ADHD that are supported by empirical research seem to be biological in nature; that is, they are factors known to be related to or to have a direct effect on brain development and/or functioning. The precise causal pathways by which these factors lead to ADHD, however, are simply not known at this time.

Even so, far less evidence is available to support any purely psychosocial etiology of ADHD. In the vast majority of cases where such psychosocial risks have been found to be significantly associated with ADHD or hyperactivity, more careful analysis has shown these to be either the result of ADHD in the child or, far more often, to be related to aggression or conduct disorder rather than to ADHD. For instance, the child management methods used by parents, parenting stress, marital conflict, or parental psychopathology have now been shown to be far more strongly associated with aggressive and antisocial behavior than with ADHD. The strong hereditary influence in ADHD may also contribute to an apparent link between ADHD and poor child management by a parent — a link that may be attributable to the parent’s own ADHD. The environment in which the child is raised and schooled probably plays a larger role in determining the outcomes of children with the disorder and a much lesser role in primary causation.

Throughout the century, investigators have repeatedly noted the similarities between symptoms of ADHD and those produced by lesions or injuries to the frontal lobes of the brain, particularly the prefrontal cortex. Both children and adults suffering injuries to the certain regions of prefrontal cortex demonstrate deficits in sustained attention, inhibition, working memory, the regulation of emotion and motivation, and the capacity to organize behavior across time.

Numerous other lines of evidence have been suggestive of a neurological origin to the disorder. Several studies have examined cerebral blood flow in ADHD and normal children. They have consistently shown decreased blood flow to the prefrontal regions of the brain and the striatum with which these regions are richly interconnected, particularly in its anterior portion. More recently, studies using positron emission tomography (PET) to assess cerebral glucose metabolism have found diminished metabolism in adults and adolescent females with ADHD although not in adolescent males with ADHD. However, significant correlations have been noted between diminished metabolic activity in the left anterior frontal region of the brain and severity of ADHD symptoms in adolescent males with ADHD. This demonstration of an association between the metabolic activity of certain brain regions and symptoms of ADHD is critical in demonstrating a connection between the findings pertaining to brain activation and the behavior comprising ADHD.

More detailed analysis of brain structures using high resolution magnetic resonance imaging (MRI) devices has also suggested differences in some brain regions in those with ADHD. Initial studies that focused on reading-disabled children and used ADHD children as a contrast group examined the region of the left and right temporal lobes (the planum temporale). These regions are thought to be involved with auditory detection and analysis and, therefore, with certain subtypes of reading disabilities. For some time, researchers studying reading disorders have focused on these brain regions because of their connection to the rapid analysis of speech sounds. Children with ADHD and children with reading disabilities were found to have smaller right hemisphere plana temporale than the control group, while only the reading disabled children had a smaller left plana temporale. In another study, the corpus callosum was examined in subjects with ADHD. This structure assists with the interhemispheric transfer of information. Those with ADHD were found to have a smaller callosum, particularly in the area of the genu and splenium and that region just anterior to the splenium. An attempt to replicate this finding, however, failed to show any differences between ADHD and control children in the size or shape of the entire corpus callosum with the exception of the posterior portion of the splenium, which was significantly smaller in subjects with ADHD. Two additional studies examining the corpus callosum, however, documented smaller anterior (rostral) regions in children with ADHD; findings more consistent with prior studies of brain anatomy and functioning in children with ADHD. Most recently, two studies using larger samples of ADHD and normal children and MRI technology have both documented a smaller right prefrontal cortex and smaller right striatum and right basal ganglia (of which the striatum is a part) in ADHD children. Thus, despite some inconsistencies in findings across some of the earlier studies of brain morphology and functioning in ADHD, more recent studies are increasingly identifying the prefrontal regions of the brain and certain regions of the basal ganglia, such as the striatum, as probably being involved in the disorder.

None of these studies found evidence of frank brain damage in any of these structures in those with ADHD. This is consistent with past reviews of the literature conducted by Michael Rutter in 1983 suggesting that brain damage was related to less than 5% of those with hyperactivity. It is also consistent with more recent studies of twins suggesting that nonshared environmental factors, such as pre-, peri-, and postnatal neurological insults, among other factors, account for approximately 15 to 20% of the differences among individuals in the behavioral pattern associated with ADHD (inattention and hyperactive-impulsive behavior). Where differences in brain structures are found, they are probably the result of abnormalities that arise in brain development (embryology) within these particular regions, the causes of which are not known but may have to do with particular genes responsible for the construction of these brain regions.

No evidence exists to show that ADHD is the result of abnormal chromosomal structures (as in Down’s Syndrome), their fragility (as in Fragile X) or transmutation, or of extra chromosomal material (as in XXY syndrome). Children with such chromosomal abnormalities may show greater problems with attention, but such abnormalities are very uncommon in children with ADHD.

By far, the preponderance of research evidence suggests that ADHD is a trait that is highly hereditary in nature, making heredity one of the most well substantiated among the potential etiologies for ADHD. Multiple lines of research support such a conclusion. For years, researchers have noted the higher prevalence of psychopathology in the parents and other relatives of children with ADHD. In particular, higher rates of ADHD, conduct problems, substance abuse, and depression have been repeatedly observed in these studies. Research such as that by Joseph Biederman and colleagues at the Harvard Medical School (Massachusetts General Hospital) shows that between 10 and 35% of the immediate family members of children with ADHD are also likely to have the disorder, with the risk to siblings of the ADHD children being approximately 32%. More recent studies even suggest that if either parent has ADHD, the risk to offspring for the disorder may be as high as 50%.

Another line of evidence for genetic involvement in ADHD has emerged from studies of adopted children, which have found higher rates of hyperactivity in the biological parents of hyperactive children than in adoptive parents of hyperactive children. Biologically related and unrelated pairs of international adoptees also identified a strong genetic component to the behavioral dimension underlying ADHD.

Studies of twins conducted in the United States, Australia, and the United Kingdom provide a third avenue of evidence for a genetic contribution to ADHD. In general, these studies suggest that if one twin is diagnosed with ADHD, the concordance for the disorder in the second twin may be as high as 81 to 92% in monozygotic twins but only 29 to 35% in dizygotic twins.

Quantitative genetic analyses of a large sample of families studied in Boston by Joseph Biederman and his colleagues suggest that a single gene may account for the expression of the disorder. The focus of research recently has been on the dopamine type 2 gene, given findings of its increased association with alcoholism, Tourette’s Syndrome, and ADHD. However, difficulties have arisen in the replication of this finding. More recent studies have implicated the dopamine transporter gene as being involved in ADHD as might the D4D repeator gene, which has shown an association with novelty-seeking and risk-taking personality traits. Clearly, research into the genetic mechanisms involved in the transmission of ADHD across generations will prove an exciting and fruitful area of research endeavor over the next decade as the human genome is mapped and better understood and as more sophisticated genetic technologies arising from this project come to be applied to the study of the genetics of ADHD.

Pre-, peri-, and postnatal complications, and malnutrition, diseases, trauma, and other neurologically compromising events may occur during the development of the nervous system before and after birth. Among these various biologically compromising events, several have been repeatedly linked to risks for inattention and hyperactive behavior. Elevated body lead burden has been shown to have a small but consistent and statistically significant relationship to the symptoms comprising ADHD. However, even at relatively high levels of lead, less than 38% of these children are rated as hyperactive on teacher rating scales, implying that most lead-poisoned children do not develop symptoms of ADHD. Other types of environmental toxins found to have some relationship to inattention and hyperactivity are prenatal exposure to alcohol and tobacco smoke.

VI. Epidemiology of ADHD

The prevalence of ADHD, as reviewed by Peter Szatmari in 1992, using large epidemiological studies ranges from a low of 2 % to a high of 6.3 %, with most falling within the range of 4.2 to 6.3 %. Most studies have found similar prevalence rates in elementary school-aged children. Differences in prevalence rates are due in part to different methods of selecting these populations, to the criteria used to define a case of ADHD, and to the age range of the samples. For instance, prevalence rates may be 2 to 3% in females but 6 to 9% in males during the 6 to 12-year-old age period, but fall to 1 to 2% in females and 3 to 4.5 % in males by adolescence.

While the declining prevalence of ADHD with age may reflect real recovery from the disorder, it may also involve, at least in part, an artifact of methodology. This artifact results from the use of items in the diagnostic symptom lists across the life span that are were developed upon and chiefly applicable to young children. These items may reflect the underlying constructs of ADHD very well at younger ages but may be increasingly less appropriate for older age groups. This could create a situation where individuals remain impaired by ADHD characteristics as they mature, but outgrow the diagnostic symptom list for the disorder, resulting in an illusory decline in prevalence over development. Until more age-appropriate symptoms are studied for adolescent and adult populations, this issue remains unresolved.

Gender appears to play a significant role in determining prevalence of ADHD within a population. On average, males are between 2 and 6 times more likely than females to be diagnosed with ADHD in epidemiological samples of children, with the average being roughly 3:1. Within clinic-referred samples, the sex ratio can rise to 6:1 to 9:1, suggesting that males with ADHD are far more likely to be referred to clinics than females, especially if they have an associated oppositional or conduct disorder. It is unclear at this time why males should be more likely to have ADHD than females. This could result partly from an artifact of the relationship between male gender and more aggressive and oppositional behavior; such behavior is known to increase the probability of referral to mental health centers. Because such behavior is often associated with ADHD, clinic-referred males are also more likely to have ADHD. The greater preponderance of males might also, in part, be an artifact of applying a set of diagnostic criteria developed primarily on males to females. Using a predominantly male population to set diagnostic criteria as was done for the DSM-IV (see below) could create a higher threshold for diagnosis for females relative to other females than for males relative to other males. Such a circumstance argues for the eventual examination of whether separate diagnostic criteria (symptom thresholds) ought to be considered for each gender.

ADHD occurs across all socioeconomic levels. Where differences in prevalence rates are found across levels of social class, they may be artifacts of the source used to define the disorder or of the association of ADHD with other disorders known to be related to social class, such as aggression and conduct disorder. No one, however, has made the argument that the nature or qualitative aspects of ADHD differ across social classes.

Hyperactivity or ADHD is present in all countries studied so far, such as New Zealand, Japan, Italy, Germany, India, and Australia. While it may not receive the same diagnostic label in each country, the behavior pattern comprising the disorder appears to be present internationally. ADHD arises also in all ethnic groups studied so far.

VII. Developmental Course and Adult Outcome

Major follow-up studies of clinically referred hyperactive children have been ongoing during the last 25 years at five sites: Montreal, New York City, Iowa City, Los Angeles, and Milwaukee. Follow-up studies of children identified as hyperactive during epidemiological screenings of general populations have also been conducted in the United States, Australia, New Zealand, and England.

The onset of ADHD symptoms has been found to be generally in the preschool years, typically by age 3 or 4, and usually by entry into formal schooling. First to arise in many cases is the pattern of hyperactive-impulsive behavior and, in some cases, oppositional and aggressive conduct. Preschool-aged children with significant degrees of inattentive and hyperactive behavior who are difficult to manage for their parents or teachers and whose pattern of such behavior is persistent for at least a year or more are highly likely to have ADHD and to retain their symptoms into the elementary school years.

By the time ADHD children move into the age range of 6 to 12 years, the problems with hyperactive-impulsive behavior are increasingly associated with difficulties with the form of sustained attention referred to above as goal-directed persistence and distractibility (poor interference control). These symptoms of inattention appear to arise by the age of 5 to 7 years and may emerge out of the increasing difficulties ADHD children are having with self-regulation. The inattentiveness evident in children having ADD without Hyperactivity (Predominantly Inattentive Type of ADHD) may be of a qualitatively different form (focused or selective attention) and may not emerge or be impairing of the child’s school performance until even later, such as mid-to-late childhood.

When ADHD is present in clinic-referred children, the likelihood is that 50 to 80% will continue to have their disorder into adolescence. Although severity levels of symptoms are declining over development, this does not mean hyperactive children are necessarily outgrowing their disorder relative to normal children; like mental retardation, the disorder of ADHD is defined by a developmentally relative deficiency, rather than an absolute one, that persists in many children over time.

The persistence of ADHD symptoms across childhood as well as into early adolescence appears to be associated with the initial degree of hyperactive/impulsive behavior in childhood, the co-existence of conduct problems or oppositional/hostile behavior, poor family relations and conflict in parent-child interactions, as well as maternal depression. These predictors have also been associated with the development and persistence of oppositional and conduct disorder into adolescence.

The Montreal follow-up study of Weiss and Hechtman reported in 1993 that at least half of their subjects were still impaired by some symptoms of the disorder in adulthood. The New York City longitudinal study by Salvatore Mannuzza and Rachel Klein suggested that 18 to 30% of hyperactive children continue to have significant symptoms of ADHD into adulthood. Most recently, the Milwaukee follow-up study by Barkley and Fischer suggests that the source of information about the symptoms may be a significant factor in establishing the persistence of the disorder into adulthood. Less than 25 % of ADHD children reported having significant symptom levels of the disorder in adulthood when asked about themselves as young adults while their parents indicated that more than 60% of these subjects continued to have clinically significant degrees of the disorder as young adults. Until more studies report adult outcomes for ADHD children using clinical diagnostic criteria appropriate for adults and collecting information not only from the adult but from a parent or an immediate family member who knows them well, the true persistence of the disorder into adulthood will remain a matter of some controversy. At the very least, current research suggests it may be 30 to 50%, although the percentage may be higher among clinic-referred children followed to adulthood.

VIII. Diagnostic Criteria

The most recent diagnostic criteria for ADHD are defined in the DSM-IV (1994). They stipulate that individuals have had their symptoms of ADHD for at least 6 months, that these symptoms exist to a degree that is developmentally deviant, and that they have developed by 7 years of age. From the Inattention item list, six of nine items must be endorsed as developmentally inappropriate. Likewise, from the Hyperactive-Impulsive item list, six of nine items must be endorsed as deviant. Depending upon whether criteria are met for either or both symptom lists will determine the type of ADHD that is to be diagnosed: Predominantly Inattentive, Predominantly Hyperactive-Impulsive, or Combined Type.

These diagnostic criteria are empirically derived and are the most rigorous ever available in the history of clinical diagnosis for this disorder. They were developed by a committee of some of the leading experts in the field, a literature review of research on ADHD, an informal survey of rating scales assessing the behavioral dimensions related to ADHD by the committee, and from statistical analyses of the results of a field trial of the items using a large sample of children from 10 different sites in North America.

Controversy continues over whether ADHD-Predominantly Inattentive Type represents a true subtype of ADHD. It is unclear if these children share a common attentional disturbance with the Combined Type and are distinguished simply by the relative absence of significant hyperactivity-impulsivity or whether they have a qualitatively different impairment in attention from that seen in the Combined Type. Several recent reviews of the literature have suggested that this is not in fact a true subtype but actually a separate, distinct disorder having a different attentional disturbance than the one present in ADHD-Combined Type. However, evidence for this subtype’s existence was at least strong enough to place it within the DSM-IV while awaiting more research on its course and treatment responsiveness to help clarify its status. The very limited research available to date suggests that Predominantly Inattentive ADHD children have more problems in the focused or selective component of attention, appear sluggish in their speed of information processing, and may have memory retrieval problems; in contrast, those with ADHD-Combined Type have more problems with persistence and distractibility as well as with poor inhibition.

The research criteria from the International Classification of Diseases (ICD-10) for Hyperkinetic Disorders closely resemble the DSM-IV in stressing two lists of symptoms related to inattention and overactivity and in requiring that pervasiveness across settings be demonstrated. The specific item contents, manner of presenting these symptoms lists within the home and school setting, requirement for office observation of the symptoms, and the earlier age of onset (age 6 years) clearly differs from the DSM-IV, as does the specification of a lower bound of IQ below which the diagnosis should not be given.

Social critics have charged that professionals have been too quick to label energetic and exuberant children as having this mental disorder and that educators also may be using these labels simply as an excuse for poor educational environments. This would imply that children who are hyperactive or are diagnosed with ADHD are actually normal but are being labelled as mentally disordered because of parent and teacher intolerance. If this were actually true, then we should find no differences of any cognitive, behavioral, or social significance between ADHD children and normal children. We should also find ADHD is not associated with any significant later risks in development for maladjustment within any domains of adaptive functioning, social, or school performance. Furthermore, research on potential etiologies for the disorder should also come up empty-handed. This is hardly the case. It should become clear from the totality of information on ADHD presented here and elsewhere in reviews such as those by Barkley in 1990 and Hinshaw in 1994 that those with ADHD have significant deficits in behavioral inhibition and associated executive functions that are critical for effective self-regulation, that these deficits are significantly associated with various biological factors, and particularly genetic and neurodevelopmental ones, and that ADHD symptoms and other associated disorders pose substantial risks for these individuals over the life span.

IX. Conclusion

Future research needs to address the nature of the attentional problems in ADHD given that current research seriously questions whether these problems are actually within the realm of attention at all. Most studies of ADHD point to impairment within the motor, output, or motivational systems of the brain being most closely affiliated with ADHD rather than deficiencies in the sensory processing systems where attention has been traditionally thought to reside. Even the problem with sustained attention may represent a deficiency in a more complex form of goal-directed persistence that arises out of poor self-regulation rather than representing a disturbance in the more primitive form of sustained responding that is contingency shaped. Our understanding of the very nature of the disorder of ADHD is at stake in how research comes to resolve these issues.

Key to understanding ADHD is the notion that it is actually a disorder of behavioral performance and not one of skill; of how and when one’s intelligence comes to be applied in everyday effective adaptive functioning and not in that knowledge itself; of doing what one knows how to do rather than of knowing what to do. The concepts of time, timing, and timeliness are likely to prove increasingly crucial in deepening our understanding of ADHD. In particular, psychological time, how it is sensed, and how it is used in the crosstemporal organizing of complex, goal-directed behavior and in self-regulation may come to be a critical element in models of ADHD. Undoubtedly, research on brain function and structure is likely to further our understanding of the unique role of the prefrontal cortex and the midbrain structures with which it is closely associated in ADHD. But advances in theoretical models must also occur in order to better understand the nature and organization of the executive functions subserved by these brain regions and even the relationship of genetics, which builds these brain regions in embryological development, to ADHD and the deficits it produces in behavioral performance. And the current body of twin studies further suggests that while such genetic influences are important, there exists a lesser but still important role for unique (nonshared) environmental influences on the differences among individuals in symptoms of ADHD and its underlying behavioral traits. Some of these influences are no doubt social in nature while others are likely to be nongenetic pre-, peri-, and postnatal factors affecting brain development. Such studies, not only on the basic psychological nature of ADHD but also on its basic neuroanatomic and neurogenetic origins and the influence of unique social factors upon them, forebode further significant and exciting advances to come in the understanding and treatment of this fascinating developmental disorder.

Bibliography:

1. American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.
2. Barkley, R. A. (1997a). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121, 65-94.
3. Barkley, R. A. (1977b). ADHD and the nature of self-controI. New York: Guilford.
4. Barkley, R. A. (1994). Impaired delayed responding: A unified theory of attention deficit hyperactivity disorder. In D. K. Routh (Ed.), Disruptive behavior disorders: Essays in honor of Herbert Quay (pp. 11-57). New York: Plenum.
5. Barkley, R. A. (1990). Attention deficit hyperactivity disorder: A handbook for diagnosis and treatment. New York: Guilford.
6. Biederman, J., Faraone, S. V., Keenan, K., & Tsuang, M. T. (1991 ). Evidence of a familial association between attention deficit disorder and major affective disorders. Archives of General Psychiatry, 48, 633-642.
7. Bronowski, J. (1977). Human and animal languages. A sense of the future (pp. 104-131 ). Cambridge, MA: MIT Press.
8. Denckla, M. B. (1994). Measurement of executive function. In G. R. Lyon (Ed.), Frames of reference for the assessment of learning disabilities: New view on measurement issues (pp. 117-142). Baltimore, MD: Paul H. Brookes.
9. Douglas, V. I. (1983). Attention and cognitive problems. In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 280-329). New York: Guilford.
10. Fuster, J. M. (1989). The prefrontal cortex. New York: Raven.
11. Hinshaw, S. P. (1994). Attention deficits and hyperactivity in children. Thousand Oaks, CA: Sage.
12. Rutter, M. (1983). Introduction: Concepts of brain dysfunction syndromes. In M. Rutter, (Ed.), Developmental neuropsychiatry (pp. 1-14). New York: Guilford.
13. Szatmari, P. (1992). The epidemiology of ADHD. In G. Weiss (Ed.), Child and adolescent psychiatric clinics of North America (Vol. 1, pp. 361-372). Philadelphia: W. B. Saunders.
14. Weiss, G. & Hechtman, L. (1993). Hyperactive children grown up. New York: Guilford.