Lecture 23 Attention-Deficit Hyperactivity Disorder Lecture Outline I. Introduction II. Background A. Minimal Brain Dysfunction B. Attention Deficits and Psychosocial Variables C. DSM-III and III-R III.Core Features A. Inattention B. Impulsiveness C. Hyperactivity IV. Etiology A. Biological Factors B. Genetics C. Environmental Factors D. Psychosocial Factors V. Course A. Adolescent outcome B. Adult outcome VI. Controversies VII.Conclusion ------------------------------------------- I. Introduction In the last lecture, we discussed the difference between externalizing and internalizing disorders. In today's lecture we will examine an example of an externalizing disorder: Attention-deficit Hyperactivity Disorder (ADHD), or more commonly - "Hyperactivity". Everybody probably knows at least one child considered to be hyperactive (Whalen, 1983) - a child who is overly impulsive, has trouble attending to the task at hand, and in general is exceedingly overactive: a child in perpetual motion, a child who flits around and blurts out but doesn't finish assignments or chores, a child with a short and highly flammable fuse, a child of the present who neither benefits from the past nor plans for the future (Loney, 1980). Hyperactivity is the most common problem among school-age children of normal intelligence, and is the most common problem referred to child guidance clinics in this country (Barkley, 1981, Sleator, 1982). Prevalence rates: common, perhaps in as many as 3% of children (APA, 1987). Sex Ratio: 6 - 9 times more common in males than females (APA, 1987). It is also the most widely studied childhood disorder, as well as one of the most controversial. Debates over diagnosis, etiology, prognosis, and treatment are common (Barkley, 1981). II. Background ADHD has also been called Childhood Hyperactivity, Hyperkinetic Syndrome, Attention Deficit Disorder, and Minimal Brain Dysfunction to name but a few of the more common terms. A. Minimal Brain Dysfunction Modern, scientific interest in what we now know as ADHD began in the 1940's with the work by Alfred Strauss and his colleagues (Schwartz & Johnson, 1985) (although reports about hyperactivity can be found as early as the 1800's [Barkley, 1981]). In a series of studies, Strauss isolated a number of characteristics which he believed could discriminate between groups of mentally retarded children with and without brain damage. Associated with brain damage were aggressiveness, impulsivity, distractibility and hyperactivity. Hyperactivity was seen as the most valid indicator of brain damage (Schwartz & Johnson, 1985). And so, it became widely accepted for many years that children with hyperactive behavior patterns were also brain damaged; the term Minimal Brain Dysfunction (MBD) was widely used to identify these children. Problem: Strauss's reasoning was circular! In effect, he was arguing that hyperactive children were brain damaged because they were hyperactive (Schwartz & Johnson, 1985). Future research failed to find the link between hyperactivity and brain damage. Most children suffering brain damage do not develop hyperactivity, and it's been estimated that fewer than 5% of hyperactive children suffer from brain damage (Rutter, 1977). There was no clear understanding of just what was meant by MBD; some clinicians insisted that restlessness, distractibility, impulsivity, and short attention spans were the key, others insisted it was perceptual/conceptual/learning deficits, and still others saw aggressiveness as the key ((Schwartz & Johnson, 1985). B. Attention Deficits and Psychosocial Variables During the late 60's and early 70's, the focus shifted to the attentional qualities of the disorder. Virginia Douglas and her colleagues at McGill University demonstrated the marked attention deficits seen in these children. Douglas argued that the major deficit was the inability to "stop, look, and listen" (Douglas, 1972) - ie: to sustain attention and inhibit impulsive responding (Barkley, 1981). In the late 70's, the focus broadened: research was indicating that the problems went beyond mere attention deficits. People like Susan Campbell and Charles Cunningham conducted a number of studies on parent-child interaction. It was found that the hyperactive children were noncompliant, attention-seeking and aggressive, and in need of ongoing supervision; and the mothers were overly directive, negative, and less responsive to the child in general (Barkley, 1981). Thus, researchers included social variables into the increasingly complex picture. Compliance and aggressiveness gained diagnostic importance. C. DSM-III and III-R No one could agree on what the primary features were. In 1980, the American Psychiatric Association entered into the debate. The DSM-III was published and it defined a disorder termed Attention Deficit Disorder (ADD), with or without hyperactivity. It was the consensus of the authors of the manual that attention deficits, not overactivity, was the key to the disorder. "Hyperactivity" merely accompanies the disorder as a secondary symptom, and then in only certain children. The DSM-III-R has eliminated the category of Attention Deficit Disorder without hyperactivity, in response to growing research evidence that ADD rarely occurs without hyperactivity - the DSM-III diagnosis of ADD without hyperactivity was rarely made (APA, 1987). The disorder is now termed Attention-deficit Hyperactivity Disorder (ADHD). It is questionable whether attentional disorders without hyperactivity should even be considered as a subtype of attention- deficit disorder. More research is needed on this. [review DSM-III-R criteria] Note that this is merely a list of characteristics - no particular single feature or subset of features is required to make the diagnosis. Also note that "hyperactivity" is not a necessary feature for the diagnosis ADHD to be made. It was hoped that such flexibility and coverage would improve diagnostic reliability. In addition, these symptoms were selected to better discriminate ADHD from other childhood disorders such as conduct disorder, with which there is often significant overlap (Hinshaw, 1987). Nonetheless, as we have discussed before, constructing a classification scheme without the guidance of theory is little more than a "shot in the dark". A mere list of characteristics, with no underlying theory, is unlikely to ever move us very far in terms of reliability and validity. III. Core Features Even with all the debate concerning the nature of the disorder, three primary features of ADHD are consistently identified by researchers. A. Inattention Inattentiveness is a key symptom of ADHD. Difficulties in attention can take various forms (Barkley, 1981; Levine, 1987): trouble orienting to stimuli failure to even detect stimuli respond to the wrong aspects of a stimulus or to an entirely inappropriate stimulus. failure to sustain attention to task-relevant stimuli, while inhibiting responding to nonrelevant stimuli - they are easily distracted / short attention span In the home: failure to complete chores, homework, etc, to listen to directions, to play for prolonged periods without supervision or attention form others. At school: problems with attending to the teacher and completing in-class assignments. The child is often distracted by other events (what other kids are doing, what's happening outside the window...). However, they may attend at length to these nonrelevant stimuli - so the problem is more than just a short attention span; it often seems to be a problem of allocating the right amount of time and focus to the appropriate information (Levine, 1987). Note: Many children who exhibit deficits in attention alone do not have ADHD (Garfinkel, 1986). Problems with attention may be time limited, due to environmental factors (stressors, significant distractions), physiological variables (fatigue, illness), and mood (irritability, anger). Attention deficits are also seen in other disorders such as depression and mental retardation. So, by itself, attention deficits are not usually sufficient to make the diagnosis of ADHD (Garfinkel, 1986). They must be part of a larger clinical picture. B. Impulsiveness Impulsivity, or the failure to inhibit responding, has also been identified as a primary characteristic. This can take various forms (Barkley, 1981): o quick responding, with numerous errors o do not stop to think about consequences of their actions place themselves in dangerous and risky situations o fail to fully appreciate all aspect of instructions given to them o more likely to respond aggressively (verbally and physically) when frustrated or emotionally hurt by others o do not consider the impact of their actions or statements on others Such actions can lead others to see such children as immature and to their being shunned by others. The impulsive child will also experience more punishment than normal children. C. Hyperactivity Overactivity has also been identified as a key feature of ADHD. The typically picture of such a child is "long on motility and short on restraint" (Loney, 1980); in other words, always on the move, with no apparent regard to rules, directions, or the like. It is thus not surprising that ADHD is often first identified upon the child's entrance to school. It is here that hyperactivity (as well inattentiveness, and impulsivity) is directly incompatible with the structure and goals of the classroom. There is some debate, however, over the significance of excesses in motor behavior. Studies that have actually measured rates of motor activity have found that ADHD children are not necessarily more active than other children, certainly not in all situations. Hyperactivity seems to be most often a problem when the child is in a restrictive environment where concentration is required (eg: a classroom!). Novel or unfamiliar situations seem to elicit the hyperactive behaviors as well (Barkley, 1981). These, then are the core features: Inattentiveness, Impulsivity, and Hyperactivity. The picture is far from clear, however. These characteristics don't always "hang together" - they often fail to correlate with one another (Barkley, 1981). So, it is a question whether or not ADHD represents a single, unified disorder. More likely, ADHD comprises a quite heterogenous group of children, with varying constellations of the above symptoms. IV. Etiology Numerous etiological factors have been identified over the years. Research often produces conflicting findings. Most researchers view ADHD as the final common result of a variety of etiologies - again we are faced with the unlikely prospects of finding a "Unitary explanation". A. Biological factors As we've already noted, ADHD was once thought to be the result of brain damage. Much research has been conducted to find specific organic or neurological factors that could account for ADHD. The "jury is still out", although a number of factors have been hypothesized: 1. Prefrontal cortex abnormalities: This part of the brain plays an important role in inhibiting, modulating, planning, and regulating complex behavior, such as planning for the future and following instructions. People with damage to this part of the brain often exhibit ADHD-like symptoms (inattentive, easily distracted, impulsive, restless, etc). It has thus been hypothesized that ADHD may be caused by abnormalities in this part of the brain (Barkley, 1981). Nevertheless, there is presently no clear direct evidence to support this hypothesis. 2. Neurotransmitter abnormalities: It is known that many (60- 90% [Schwartz & Johnson, 1985]) ADHD children respond to stimulants with reduced ADHD symptoms, a seemingly paradoxical effect. The behavior most improved: attention. For a number of years it was thought that this effect indicated abnormal biochemical processes, especially deficiencies of the neurotransmitters norepinephrine and dopamine (Barkley, 1981). More recent research, however, has shown that ADHD children do not respond differently to stimulant drugs than "normal" children: Stimulants increase attention and concentration for both groups (Schwartz & Johnson, 1985, Yellin, 1986)). There is nothing "paradoxical" about the effects of these drugs: they have the same effects on nonADHD children. This does not necessarily mean neurotransmitters are not etiologically important, only that their importance must be more complex than a simple deficiency model. 3. Neurological Immaturity: An alternative hypothesis is that maturation of central nervous system structures is delayed, rather than actually damaged (Barkley, 1981). Observations of ADHD children make this hypothesis appealing - the children do seem to be acting in immature ways. Some studies of brain activity (especially CNS structures underlying attention and response inhibition) also suggest immature processes. For example, as many as 50% of ADHD children show underaroused EEG (a recording of brain waves) patterns suggestive of cortical immaturity (Barkley, 1981). Nevertheless, the support for this hypothesis is still very far from conclusive. 4. Other signs: Abnormalities have been found in EEG patterns, Event-related potentials, particularly the P300, and skin conductance (Yellin, 1986). In addition, drugs that reduce ADHD symptoms (Ritalin) also normalize the abnormal P300 patterns. These findings all point to deficits in arousal and orienting, in processing information from the environment, or in other words: deficits in "arousal" and "attention". Because ADHD children appear to have a lower than normal state of arousal, some researchers have hypothesized that the children are therefore engaging in extra activity in order to increase their level of stimulation (Schwartz & Johnson, 1985). This could also be why stimulant drugs are effective - they provide the needed stimulation. B. Genetics Studies have found a higher incidence of ADHD in the biological relatives of hyperactive children than in the population at large. This seems to be true even with ADHD children who are adopted. Similarly, there is a high concordance rate for twins (when one twin has ADHD, the other has a higher than average chance of also having ADHD) (Barkley, 1981; Schwartz & Johnson, 1985). These studies all suggest a genetic component to the disorder, although how general and how significant the genetic contribution is remains to be determined. C. Environmental Factors Various toxins and allergy-producing substances in the environment have been identified as possibly relevant to the etiology of ADHD. 1. Lead Poisoning: Lead is found in many substances: paint, automobile fumes (although this is decreasing as unleaded fuel becomes more the standard). A number of studies during the 70's noted an elevated level of lead in the blood of ADHD children. 30 -35% of children with elevated blood lead levels were also hyperactive. So, there does seem to be a connection between lead and at least on symptom of ADHD: hyperactivity (Barkley, 1981: Schwartz & Johnson, 1985). 2. Food Additives and Refined Sugars: For awhile there was a lot of talk about food additives (eg: artificial food colorings and flavorings) and refined sugars as being a cause of ADHD. The interest in this hypothesis was spurred on by the publication of the popular book Why Your Child is Hyperactive, by Feingold, in 1975. While still quite popular as an explanation of the disorder, there is actually very little scientific evidence to support this hypothesis (Barkley, 1981). 3. Other Factors: Various other environmental factors have been suggested, including low-level X-rays emitted by fluorescent lights, maternal smoking during pregnancy, and maternal alcohol consumption during pregnancy. These factors have failed to gain any clear cut support, however (Barkley, 1981). D. Psychosocial Factors Some researchers have claimed that hyperactivity is the result of poor parenting skills: inconsistent rules, over-reliance on punishment, excessive and ill-timed commands. Indeed, treatment programs which teach parents more effective parenting skills have had significant success. Nevertheless, it is not at all clear that these psychosocial factors are the cause of ADHD. For example: such a model fails to explain why ADHD symptoms often occur at a very early age; or why the symptoms are consistent across situations (home, school, play) and thus different forms of child management. In addition, inconsistent or chaotic rules, excessive punishment, and the like are possibly a result of ADHD. There is a concern that parents are being blamed for something that is not their fault (Barkley, 1981). Nevertheless, it is safe to say that for some of these children, parenting styles can have an important influence on maintaining or even aggravating the ADHD symptoms (Wicks-Nelson & Israel, 1984). V. Course Relatively few studies have examined the course of ADHD: What happens to the child as s/he grows up. Clinical lore often suggests that the symptoms fade away. The studies that have been conducted do not, however, support this conclusion (Lambert, 1988; Schwartz & Johnson, 1985; Weiss & Hechtman, 1986). A. Adolescent outcome Most studies indicate the core features persist; however, they are frequently no longer the most obvious complaint. Instead, the following become salient: poor school performance social deviancy relationship difficulties with peers and adults delinquency low self-esteem significant under-achievement nervousness, restlessness aggressive/easily angered alcohol/drug use or abuse There is also some indication that a significant percentage of ADHD adolescents (about 25%) have a history of antisocial behavior. It has been suggested that adults with Antisocial Personality Disorder may have been hyperactive as children. B. Adult outcome As many as 1/3 to 1/2 of hyperactive children continue to be troubled by symptoms of ADHD in adulthood. Continued problems seem particularly likely if antisocial behavior and drug use/abuse was present in their childhood/adolescence. Adulthood problems include: 20% or more have Antisocial Personality Disorder low self-esteem impaired social skills inferior work status (held jobs for a shorter duration, laid off/quit more frequently, inferior work performance) VI. Controversies The topic of ADHD is fraught with controversies. The major treatment of the disorder is with stimulant drugs, such as Ritalin. It is estimated that 60 - 90% respond favorably to these drugs (Schwartz & Johnson, 1985). But there has been concern that these drugs are being administered merely to keep children quite and to facilitate classroom management, and that hyperactivity is simply a myth constructed to justify this control: the natural vigor of youth is being denied. Recently, there has been a lot of media attention given to the Church of Scientology's national campaign against ADHD and Ritalin treatments. This campaign, under the Church's Citizen's Commission on Human Rights (CCHR) has claimed that Ritalin commonly leads children to suicide, murder, seizures and brain damage, addiction, and permanent emotional disturbance. Such a highly visible and emotional campaign is disturbing to many because it is based on little firm scientific data. In well controlled studies, side effects, in fact, appear to be quite limited. For example (Barkley, 1988) (See Handout 23-1): 82 ADHD children (ages 5 to 16) underwent an objective double blind, placebo controlled evaluation of two doses of Ritalin (0.3 and 0.5 mg/kg twice daily). Results: None of the severe side effects claimed by CCHR occurred. Of the side effects that did occur (see handout), many also occurred in the placebo group as well. What this suggests is that many of the supposed side effects of Ritalin may in fact be pre- existing behavioral or emotional problems. It seems likely that such problems could be mistaken for Ritalin side effects. most common side effects: decreases in appetite, insomnia, stomachaches and headaches - all of which were rated as quite mild (form 0 to 3 on a 9 point scale). other side effects: 10% developed mild nervous tics one child developed mild psychotic symptoms These symptoms, however, disappeared shortly after medication was stopped. In response to the medication, 87% of the 82 children displayed improvements in school behavior and performance. In short: Even when significant side effects occur, they are transient, abating within hours after stopping medication. For the majority of children, improvements occurred. While the CCHR campaign is provocative and has a certain simplistic appeal, such a hypothesis is not supported by the available data, and it hardly accounts for the numerous physical, behavioral, cognitive and social impairments that these children suffer (Barkley, 1981). However...one real problem here is that there are no clear norms concerning what is appropriate in childhood behavior. How active does one have to be to be considered hyperactive? Without such norms, how can we be certain that we are not also, inadvertently, medicating normal children? [Again, we are confronted with the ever-present question: What is it that we mean by "normal" and "abnormal"?]. VII. Conclusion Today we have looked at an example externalizing disorder: Attention deficit Hyperactivity Disorder. If you are left with the feeling that there are more questions than answers about this disorder, you are correct. We have yet to pin-down exactly what ADHD is, what causes it, let alone how to treat it. Yet it remains a phenomenon of real concern to teachers and parents, and it is frequently seen in child guidance clinics and pediatricians' offices.Handout 23-1 Percentage of 82 ADHD Children Experiencing Each Side Effect of Ritalin at Two Dose Levels (0.3 and 0.5 mg/kg twice daily) Possible Placebo Low Dose Moderate Dose Side Effect % Sev.* % Sev. % Sev. Decreased Appetite 15 0.4 52 1.8 56 2.6 Insomnia 40 1.5 62 2.7 68 3.1 Stomachaches 18 0.5 39 1.0 35 1.5 Headaches 11 0.3 26 0.6 21 0.8 Prone to Crying 49 1.8 59 2.3 54 2.0 Tics/Nervous Movements 18 0.7 18 0.9 28 1.2 Nailbiting 22 1.1 26 1.1 29 1.3 Talks Excessively 16 0.4 20 0.6 22 0.9 Irritable 72 3.2 65 2.6 66 2.7 Sadness 43 1.6 48 1.9 41 1.8 Stares Excessively 40 1.3 38 1.2 38 1.0 *Sev. = Mean Severity Rating of this side effect using a scale from 0 (not at all) to 9 (severe). (Barkley, 1988)